Volume 2 • July 2019
Editor-in-Chief: Arunima Bhattacharya
Associate Editor: Nabhonil Chatterji
Journal Editorial Committee
Ankur Rao • Attrayee Chakraborty • Vaidehi Roy Chowdhury •
Gayatri Dutt • Arkopriyo Banerjee • Shubham Dutta •
Pallavi Chakraborty • Padmanava Dasgupta
Published by: InquiScitive
Website: www.inquiscitive.wordpress.com
Cover Page Design: Arkopriyo Banerjee
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CONTENTS CONTENTS PAGE
NUMBER
Message from
Prof. David Law
Dr. Souvik Roy
An Appeal from InquiScitive
Editorial
Feature Article:
An Investigation on Nitrification in Aquaria & Its Social Importance
Rwik Suvro Roy
1
Bacteriophage Therapy: An Alternative Approach to Treat Antibiotic
Resistant Superbugs
Rajarshi Roy
5
Heart-Type Fatty Acid-Binding Protein as a Biomarker for Atherosclerotic
Heart Disease
Vipin Kumar Sharma
10
Learning Linguistic Lucidity
Arunima Bhattacharya and Debava Chaudhuri 15
Relation of Pentose Phosphate Pathway and Cancer
Jyoti Sangwan and Vipin Kumar Sharma 18
Novel Proteins to Nobel Prize
Shubham Dutta 25
“Achoo”, Culprit: The Sun
Leena Bhadra 30
CRISPR Baby
Avirup Chakraborty 33
Black Holes
Rituraj Bhattacharjee 36
Time Ticking Back
Souptik Ghosh 39
The Numbers are on Our Side!
Abhinaba Chakraborty 45
Chemical Combat
Rajarshi Chanda and Arunima Bhattacharya 49
Mystery Microbes in Space
Souraj Banerjee 56
The Balancing Act
Nilanjan Das 59
Dreams Decoded
Nabhonil Chatterji and Tannishtha Das 62
At the Sutardja Center for Entrepreneurship & Technology(SCET) at the University of California, Berkeley, westrive to change the way students are educated. Deep skillsand scientific rigor are important but they are not enough. Ifwe expect students, like the editors, contributors and readersof InquiScitive, to change the world, we must develop themindsets, behaviors and judgment required for innovativeapplication of science and technology. And you don’t have towater down the academics to achieve this.
As Director of Global Academic Programs at SCET, I have the privilege to work with the beststudents from around world that come to Berkeley and SCET to broaden their perspectives,culturally and academically. This past semester, I had the pleasure of hosting a number ofstudents from SRM Institute of Science & Technology representing both campuses, Chennaiand Amravati.
The diversity of experience and technical skill each student brought to the classroomprepared them for their journey. The learning vehicle was the application of skills to a real-world challenge. It is this process of experimenting, failing, and reflecting that sharpens self-awareness. It is a process that impresses upon students a sense of agency while pursuingtheir academic goals. Students who embrace this responsibility will thrive.
I’m encouraged by your thoughtful pursuits at InquiScitive and I know readers willappreciate being joined in debate in an approachable manner, being educated on newapproaches, and come away with a sense that we are in the capable hands of a newgeneration of mindful technologists and innovators.
David Law is the Director of Global Academic programs at SCET Berkeley. He overseesthe development and design of technology entrepreneurship programs for internationalstudents and visiting researchers at the undergraduate, graduate and doctoral level.David is also and instructor at SCET and has taught Challenge Lab at Berkeley andinternationally. Prior to joining UC Berkeley, David spent 20 years in the softwareindustry at executive levels in finance, operations and strategy. He is co-founder of VentureDojo Private Limited, an online hybrid platform designed for instructors and students oftechnology entrepreneurship. David received his BBA in Finance and Economics at JamesMadison University and his Masters in International Management at Thunderbird Schoolof Global Management at Arizona State University.
“Persistence in scientific research leads to what I callinstinct for truth.” — Louis Pasteur
When Sir Albert Einstein and Gurudev Rabindranath Tagoremet on July 14th 1930, what followed thereafter is one of themost intellectually engrossing conversations on the archaicfriction between science and religion. A small excerpt* fromthe conversation between the two greatest stalwarts of alltimes:
TAGORE: “When our universe is in harmony with Man, the eternal, we know it as Truth, wefeel it as beauty.”EINSTEIN: “This is the purely human conception of the universe.”TAGORE: “There can be no other conception. This world is a human world — the scientificview of it is also that of the scientific man. There is some standard of reason and enjoymentwhich gives it Truth……………”
As the Bard most rightly said, all our scientific ventures and research adventures shouldculminate in a ‘Truth’ being unraveled. The cobweb of complex, entangled problems shouldbe unwound finely through the pin-pointed addressal of scientific queries, and certainly notby dreamy reveries. And therein lays the seed of the much-coveted tree of hope for anyscientifically-inclined society.
While writing a Foreword for the second issue of the much-popular e-journal of‘InquiScitive’, I am being overwhelmed by nostalgia. The blog of ‘InquiScitive’, over thisone year, has bloomed from a tiny bud to a flower with petals as colorful as the variousbranches of Science and Technology it addresses to. I heartily congratulate one and allassociated in this unique gesture of promoting correct scientific thoughts in a much lucidlanguage. I deeply wish that this e-journal and the blog successfully walk down the path oftheir wonderful journey not only this year, but for many more years to come.
Souvik Roy, B.Sc. (Gold-Medalist), M.Sc. (Gold-Medalist), M.Phil. Ph.D.Assistant Professor,Post-Graduate Department of Biotechnology,St. Xavier’s College (Autonomous),30 Mother Teresa Sarani, Kolkata - 700 016, India.
[*Information Courtesy: https://factordaily.com/rabindranath-tagore-einstein-birth-anniversary/]
AN APPEAL FROM INQUISCITIVE…
“Science is simply the word we use to describe amethod of organizing our curiosity” – Tim Minchin
It was in March 2017 that InquiScitive(www.inquiscitive.wordpress.com) was launched with thehumble aim of creating an interdisciplinary forum tocommunicate and discuss about the latest discoveries in thevarious fields of Science & Technology. We thought of makingit a destination to satiate the doubts of the unknown, theimpossible. We wanted to disseminate the knowledge ofcurrent scientific advancements which largely remains lockedup in laboratories to the public at large.
As the Head, it is my pleasure to launch the second edition of our digital publication,InquiScitive Journal: An e-magazine of latest scientific developments. A numberof young science graduates have published their articles and reviews in this volume. I hopethat the readers will appreciate our effort, and encourage us to continue to publish thismagazine in future.
We dream of growing bigger. We dream of making our journal truly successful by reaching alarge number of readers and scientists globally. For this we would need shared responsibility,as also register our magazine with an ISSN number.
We at InquiScitive are striving to bridge the gap between scientific giants and the commonreaders, with practically no source of funding – it is totally a non-profit initiative. In order tosustain our initiative, just to reach science to the general public, we need your financialsupport and moral assurance. If you want to help us, please write to [email protected].
Nilanjan Das is the Founder and Head of InquiScitive. He is a Postgraduate inBiotechnology from St. Xavier’s College (Autonomous), Kolkata, and is currently ResearchObserver at Institute of Post-Graduate Medical Education & Research, Kolkata.
EDITORIAL‘Always question, always wonder.’
It is often said that answers lie with those who have the courage to ask. It is precisely with thisoutlook towards life that a group of science enthusiasts started the science blog – InquiScitive,a conflation of recent scientific developments, infused with a simple, yet earnest approach ofgenerating awareness about the same, in the readers. Science is not only about facts and figures.Science is about innovation, it is about the power to imagine and hence, create. Keeping this inmind, the approach has been to avoid the toning down of articles by the black and whiterepresentation of facts, but instead, add vibrant strokes of the authors’ own opinion to thecanvas, thus, making it unique and original.
We would also like to take this opportunity to thank our dynamic core team, without whoseguidance and support, this publication would have been a difficult milestone to reach. We alsothank the zealous members of our editorial committee, who have worked tirelessly to put this e-journal together, page by page. Finally, our heartfelt gratitude to the many members of our teamwho have been inquisitive, in the truest sense of the word, delving deep into the many mysteriesof science, attempting to provide solutions for pressing issues of the day using novel methodsand technology and above all, channelizing their passion towards the correct exploitation ofscience.
The contents of this e-journal are not mere articles, but the embodiment of the passions, creativeexpression and outlook of an entire generation of budding scientists who are sure torevolutionize the world, with their work, in the years to come. Every person who has contributedan article to this e-journal has already advanced on his or her journey to make the world a betterplace than it is now. The selection process has been exceptionally trying; every article on ourblog being worthy of publication. However, the few articles that have featured in this e-journalare those, whose words have left a profound imprint on our minds and hence, have carved aspecial niche for themselves. Yet it is you, the reader, who reserves the right to judge ourcreation, so allow us to leave that part of this publication to you. We wish all our readers some oftheir most pleasurable hours, as they browse through our creation. Happy Reading!
Arunima BhattacharyaEditor-in-Chief, InquiScitive Journal
Nabhonil ChatterjiAssociate Chief Editor, InquiScitive Journal
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Feature Article
AN INVESTIGATION ON
NITRIFICATION IN AQUARIA &
ITS SOCIAL IMPORTANCE RWIK SUVRO ROY
2nd Year, M.Sc. in Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected]
1. Introduction
Nitrification is a biological process that is commonly seen in plants. It’s the biological
oxidation of ammonium/ammonia to nitrite followed by the oxidation of nitrite to
nitrate. Nitrification is considered as a very important step in nitrogen cycle, but its
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relevance in the aquarium ignites my research interest, as keeping fresh water fish
aquarium is my hobby.
We have all seen aquaria and how fish-keepers love feeding their ornamental fishes
with hands. But not only as a hobby, aquaria are widely considered by the scientists
and researchers as stress reducing element. Staring at the movement of the fishes for
at least 8 minutes can help us calm down our minds. Aquarium observers tend to
experience a decrease in pulse rate and muscle tension and an increase in skin
temperature (De Schriver and Riddick, 1990). According to a research published in the
journal ‘Environment & Behaviour’, people who spend time in watching aquaria and
fish tanks could see improvements in their physical and mental wellbeing (Cracknell
et al. 2015).
The most essential element to a healthy synthetic aquatic environment is its filtration.
Filtration is the heart of any aquarium. This is where the nitrification and the
microorganisms that are involved in the process come into play. In science journals
and literature various experiments have been found which enquire about the role of
nitrification both in marine as well as fresh water aquaria. Paul. C. Burrell et al. (2001)
have shown that under freshwater nitrifying conditions the AOB that is most efficient,
is Nitrosomonas marina. Timothy et al. (1998) suggested through their studies that
Nitrobacter was not the dominant nitrifying bacteria in freshwater aquaria. Laura
Muha (2007) wanted to clarify some aspects concerning how delicate they are and how
fast they colonize in our tanks. She also wrote on the effects of antibiotics and chlorine
on the nitrifying bacteria. Sauder et al. (2011) used quantitative real time PCR to
quantify the ammonia mono oxygenase and 16S RNA genes of bacteria and
thaumarchacota in fresh water aquarium bio-filter.
Biological filtration includes filtration techniques that utilizes biological (living)
organisms to remove impurities from the wastewater. Filter media selection is critical
in the operation to achieve effluent quality requirements. The most important is to
choose the correct types of filter media. Sajuni et al. (2010) conducted laboratory
studies to evaluate the optimum ammonia removal performance using four different
types of filter media (Ceramic Ring A, Ceramic Ring B, Japanese Filter Mat and Filter
Wool) at different ammonia loading rates. Ceramic Ring A has been found to give the
best performance with respect to their efficiency of ammonia removal because of high
surface area and characteristic roughness. The research result shows that nitrification
is most efficient at pH levels ranging from about 7.5 to 9.0. Water temperature was
kept between 27°C and 30°C. Nitrification efficiency is slower at lower temperatures.
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2. Research Questions and Objective of Study:
Our research enquiry is centrally to investigate the simple way which can make the
keeping of fish simple and affordable to a fish keeper. The filtration process in an
aquarium can be categorized into: mechanical, biological and chemical filtration
categories. The biological filtration deals with Nitrification. Aquatic animals like fishes
are ammonotelic. The ammonia thus released in the water makes it toxic for fishes,
threatening their survival. Ammonia can cause fatal skin of the fishes and gill burn
even in a concentration as low as 0.25 ppm. The biological filtration aims at growth of
nitrifying bacteria in the filter media which helps to combat with the ammonia rich
environment.
One of the nitrifying bacteria, Nitrosomonas, oxidises ammonia to nitrite. Nitrite is less
toxic than ammonia but can be fatal to fishes in a concentration above 0.25 ppm. The
other bacteria involved, i.e. Nitrospira like bacteria, oxidises Nitrite to Nitrate. In
normal ecosystem this conversion is carried on by Nitrobacter, but studies reveal that
Nitrospira like bacteria are predominant in freshwater aquaria. Nitrate is the least toxic
among the three other intermediates and can be tolerated by fishes in a concentration
not more than 40 ppm. Nitrates can be kept in control by partial water change, twice
every week. Another of our research question is to trace out from where all these
bacteria are coming and growing inside the aquarium.
The substrate, walls of our tank, plants and other ornamentals provide a media for the
bacterial colony to grow on. The bacteria always prefer to colonize on a media with
greater surface area. There are several synthetic Medias found in the market that are
made to have an enormous surface area for the bacteria to grow on.
The bacterial colony tends to grow from scratch under ammonia rich conditions. It is
therefore recommended to cycle your tank in ammonia rich condition before letting
the fish in, because a new tank doesn’t house the beneficial bacteria. Fish food and
often liquid ammonia are used to cycle a tank. A minimum of one month is required
for the nitrifying bacteria to colonize the media before the fishes are added.
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3. Conclusion:
The basic knowledge of nitrogen cycle can thus help in establishment of a healthy
aquarium and the nitrifying bacteria can be used to reduce the toxic effects of fish
waste, thus preventing mortality of ornamental fishes.
References:
[1] Mary M. DeSchriver and Carol Cutler Riddick (1990). Effects of Watching Aquariums on
Elders' Stress, Anthrozoos A Multidisciplinary Journal of The Interactions of People &
Animals 4(1):44-48, DOI: 10.2752/089279391787057396
[2] Crystal Ponti (2018). Watching Fish Swim Is an Odd But Effective Way to Relax, MENTAL
HEALTH, TONIC, https://tonic.vice.com/en_us/article/qvep4q/aquarium-therapy-
good-for-health accessed on 2nd April, 2018.
[3] N.R. Sajuni, A.L. Ahmad and V.M. Vadivelu, 2010. Effect of Filter Media Characteristics,
pH and Temperature on the Ammonia Removal in the Wastewater. Journal of Applied
Sciences, 10: 1146-1150.
Mr. Rwik Suvro Roy is a 2nd year student in the Postgraduate department of Biotechnology, St. Xavier's
College (Autonomous), Kolkata.
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BACTERIOPHAGE THERAPY:
AN ALTERNATIVE APPROACH
TO TREAT ANTIBIOTIC RESISTANT
SUPERBUGS
RAJARSHI ROY
M.Sc. in Microbiology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected]
In recent years, therapeutic uses of bacteriophages have witnessed a renewed interest.
This is due to the increased difficulties in the treatment of antibiotic-resistant strains
of bacteria also known as superbugs. Phage therapy involves the treatment of
superbugs with lytic phage which interacts with its target bacterial cells, invade them,
introduce its own viral genome within the bacterial host, override its replication
machinery, divide within it and finally lyse and kill the target cell.
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Fig 1. Lytic cycle of bacteriophage killing a target
According to the Review on Antimicrobial Resistance (O’Neill, 2014) it is estimated that
by the year 2050, 10 million people annually could be at risk of losing their lives due
to drug resistant infections, overtaking deaths caused by cancer in just over three
decades.
Fig 2. Statistics on deaths relating to antibiotic resistant infections.
[Picture Courtesy: statista.com/chart/amp/3095/drug-resistant-infections/]
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There are multiple ways in which bacteria can adapt to become resistant against
antibiotics: -
1. Modification and degradation of the antibiotics.
2. Expansion of the antimicrobial agents using efflux pumps.
3. Modification of antimicrobial targets within the bacteria
Advantages of bacteriophage therapy over the contemporary treatment of infections
using antibiotics include: -
1. Bacteriophages are bactericidal in nature they infect and kill the bacterial cells
2. Species-specific and do not harm non target cells
3. They do not harm Eukaryotic cells, that is they will not harm human cells as we
don’t have the specific receptors for them to interact with
4. They do not induce cross-resistance like antibiotics
5. Phages are constantly evolving which can kill bacteria that have become resistant.
Franzon et al. (2016) reports in the paper “Long-term effects of single and combined
introductions of antibiotics and bacteriophages on populations of Pseudomonas”, some
promising results on use bacteriophages as a promising alternative to antibiotics.
Fig 3. Pseudomonus aeruginosa
[Picture Courtesy: ehagroup.com/resources/pathogens/pseudomonas-aeruginosa/]
The bacteria Pseudomonas aeruginosa was inoculated in fresh media containing LKD16
phage (Podoviridae family) only, antibiotic only and phage-antibiotic conditions. As
expected the addition of phage or antibiotic had a strong negative effect on bacterial
density during the experiment. There was a synergistic effect which was observed
when the bacteria was treated with both antibiotic as well as bacteriophage
simultaneously, the results indicated action of the phage combined with high doses of
carbenicillin reduces the long term growth of bacteria.
The results have been shown next.
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Fig 4. Optical density measures of different experiments on P. aeruginosa with different
concentrations of different antibiotics in either the presence or absence of bacteriophage.
[Picture Courtesy: Franzon et al. Long-term effects of single and combined introductions of
antibiotics and bacteriophages on populations of Pseudomonas aeruginosa.]
So in an era where antibiotic-resistant bacterial infections are steadily on the rise,
bacteriophages could provide numerous advantages, such as:-
1. They can help in the treatment of antibiotic-resistant infections which are caused
by methicillin-resistant Staphylococcus aureus as well as Pseudomonas aeruginosa
which cause multitudes of different kinds of diseases including diseases pertaining
to the respiratory tract, the gastrointestinal tract and many others.
2. They are used to treat victims of ulcers and severe skin burns
3. Phages have the ability to cross the brain blood barrier as a result of which they
can reach the areas of the human body normal antibiotics cannot.
Apart from a few tiny obstacles to the advancement of phage therapy in the future,
which involves, if not restricted to, approvals for commercialized human trials and
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also mega-corps yet to take up this noble undertaking, I firmly believe that phage
therapy certainly deserves the opportunity to demonstrate its worth in the medical
community.
References:
[1] Blaise Franzon, Marie Vasse and Michael E. Hochberg (2016) Long-term effects of single
and combined introductions of antibiotics and bacteriophages on populations of
Pseudomonas. Evolutionary Applications ISSN 1752-4571. doi:10.1111/eva.12364
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831460/)
[2] Deaths From Drug-Resistant Infections Set To Skyrocket by Niall McCarthy
(https://www.google.com/amp/s/www.statista.com/chart/amp/3095/drug-resistant-
infections/)
[3] Jim O’Neill (2014) The Review on Antimicrobial Resistance. HM Government and
Wellcome Trust.
Mr. Rajarshi Roy has just completed his M.Sc. in Microbiology from St. Xavier's College, Kolkata. His
interests range from cancer biology to alternative modes of treatment for antibiotic resistant infections.
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HEART-TYPE FATTY ACID-
BINDING PROTEIN AS A
BIOMARKER FOR
ATHEROSCLEROTIC HEART
DISEASE VIPIN KUMAR SHARMA
2nd Year, M.Sc., Department of Biochemistry
Central University of Haryana,
Adalpur, Haryana 123029, India.
Email: [email protected]
Atherosclerotic Heart Disease (AHD) or Coronary Artery Disease (CAD) can be
caused by the excessive deposition of cholesterol and other insoluble compounds on
the inner wall of the coronary artery (artery that sends blood to the heart muscles).
This plaque formation narrows down the arterial lumen and blocks it. This causes the
heart to put in extra effort to pump blood from these vessels resulting in pain and
often heart attacks. As cases of cardiac diseases are increasing day by day, it is
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becoming essential to develop a simple yet vigorous and dependable diagnostic bio-
marker for the diagnosis of such risks. In emergency instances, a simple and accessible
diagnostic assay can provide accurate diagnosis with minimum errors in minimal
possible time. Such bio-marker based tests need to be easy to handle, highly efficient,
sensitive and specific in nature. The conventionally used Troponin-T (Trop-T) is
utilized as a biomarker to spot acute coronary syndromes; however it may not rise
until 6-7 hours after the arrival of manifestations and has to be repeated within 8-12
hours after the genesis of pain in order to verify the diagnosis. Hence, very precise
and dependable biomarkers are needed that can detect cardiac disease without much
delay. Plasma levels of Heart-type Fatty Acid-Binding Protein (H-FABP) can resolve
this if they are utilized as an early marker whereas the Trop-T can be utilized as a late
marker.
1. Heart-type Fatty Acid-Binding Protein (H-FABP):
The fatty Acid Binding Protein-3 (FABP-3) gene is present on chromosome number -1
and at 1p33-p32 locus codes for the H-FABP protein which is also called mammary-
derived growth inhibitor. H-FABP is 51.2kDa cytosolic protein which is formed of 133
amino acids and is liberated from myocardial cells following ischemia (insufficient
blood supply in cardiac muscles). Ten FABPs involved in fatty acid metabolism
actively have been identified till date. They transport the fatty acids from the plasma
membrane to mitochondria for oxidation purpose. These FABPs are presumed to be
engaged in the intracellular metabolism and uptake and transport of polyunsaturated
fatty acids (PUFAs). FABPs have regulatory effects on cell growth, division of cell and
halting the growth of mammary epithelial cells.
Immunoreactivity of H-FABP was recognized in both ventricles and atria, the parietal
cells in the stomach, many striated muscles, renal epithelial cells, ductal and acinar
cells in the breast, ductal cells of the salivary gland, corpus luteum, Leydig cells of the
testis, vascular endothelial cells, adipocytes and terminally differentiated epithelia of
intestinal, respiratory and urinogenital tracts.
H-FABP was not noticed in old infarcted (local necrosis occurring due to hindered
blood supply) muscles of the heart. In fact the morphologically usual heart muscle
cells do not exhibit H-FABP one hour after perilous ischemic lesions indicating that
these heart muscle cells which were appearing to be normal were actually non-viable
cells. In the context of H-FABP, it is very important to note that when primary cultures
of neonatal heart muscle cells of the rat were subjected to saturated fatty acids
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(palmitic acid; C16:0 and Stearic acid; C18:0), it resulted in death but monounsaturated
(Oleic acid; C18:1) and polyunsaturated (Linoleic acid; C18:2, Linolenic acid; C18:3
and Arachidonic acid; C20:4) fatty acids did not show the same result.
Additionally, the PUFAs increased the expression of FABPs and the ruinous effect of
saturated fatty acids was neutralized by unsaturated fatty acids indicating that one of
the major functions of H-FABP can be the transportation of PUFAs to heart muscle
cells to preserve their integrity. This is proved by observing that the mice lacking the
H-FABP showed drastic defects in PUFA utilization; their hearts were not able take
up plasma PUFAs and use it as the main fuel with efficacy. The deficiency of H-FABP
also causes exercise intolerance (decreased ability to do physical tasks) and localized
cardiac hypertrophy (size enlargement). All the data discussed above show that H-
FABP is required for cardiac intra-cellular lipid transportation and selection of fuel
and therefore, plays a vital role in metabolic homeostasis.
H-FABP is released as a result of ischemic injury which aggravates the cardiac muscle
cell’s function and survival due to the reduction of H-FABP. This leads to inept
transportation and utilization of PUFAs as fuel. Those who consume high quantities
of saturated fatty acids and trans-fats are more prone to cardiac risks and aggravation
of heart muscle damage as saturated fatty acids and trans-fats are toxic to heart muscle
cells. Therefore, the consumption of PUFAs is always recommended as they neutralize
the toxic effects of saturated fatty acids on heart muscle cells.
2. Measurement of H-FABP in Atherosclerotic Heart Disease:
Since H-FABP plays a significant role in the functioning of heart muscles, measuring
the plasma and urine levels of H-FABP becomes a promising assay for myocardial
ischemia. Sandwich enzyme-linked immune sorbent assay (S-ELISA) which is desired
for the detection of antigen sandwiched between the two layers of antibodies was
developed in 1995 for H-FABP and depicted that the assay range was 0-250 ng/ml.
The least detection limit of this assay was 1.25 ng/ml, and the standard levels of H-
FABP plasma and urine of healthy subjects were 3.65+1.81 ng/ml to 3.65-1.81 ng/ml
and 3.20+2.70 ng/ml to 3.20-2.70 ng/ml respectively.
Some other studies have demonstrated that H-FABP serves as a reliable and early bio-
marker for the confirmation of acute myocardial infarction (AMI) just after the arrival
of symptoms. Due to this great reliability and efficiency of H-FABP as an early
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detection biomarker, several tests to measure the concentration of H-FABP in urine
and blood were designed. Researchers are even trying to implement the dual
biomarker strategy for most realistic results i.e. H-FABP and Trop-T for diagnosing
early AMI. Therefore the H-FABP of each and every patient with acute chest pain is
necessary to confirm AMI or AHD. Such tests must be promoted in small and rural
hospitals (strip test as for glucose in emergency departments) so that maximum
cardiac patients can be benefitted. Akash Manoj from India has developed a non-
invasive and inexpensive technique to determine the levels of FABP-3. This is a
breakthrough in cardiology research. His device looks just like a regular glucose strip
test and can help a lot of people with asymptomatic heart issues.
References:
[1] Vupputuri A, Shekar S, Krishnan S, et al. Heart-type fatty acid-binding protein (H-FABP)
as an early diagnostic biomarker in patients with acute chest pain. Ind Heart J.
2015;67:538–542.
[2] Kleine AH, Glatz JF, Van Nieuwenhoven FA, Van der Vusse GJ. Release of heart fatty acid-
binding protein into plasma after acute myocardial infarction in man. Mol Cell Biochem.
1992;116:155–162.
[3] Watanabe K, Wakabayashi H, Veerkamp JH, Ono T, Suzuki T. Immunohistochemical
distribution of heart-type fatty acidbinding protein immunoreactivity in normal human
tissues and in acute myocardial infarct. J Pathol. 1993;170:59–65.
[4] Zschiesche W, Kleine AH, Spitzer E, Veerkamp JH, Glatz JF. Histochemical localization of
heart-type fatty-acid binding protein in human and murine tissues. Histochem Cell Biol.
1995;103:147–156.
[5] de Vries JE, Vork MM, Roemen TH, et al. Saturated but not mono-unsaturated fatty acids
induce apoptotic cell death in neonatal rat ventricular myocytes. J Lipid Res. 1997;38:
1384–1394.
[6] Van Bilsen M, de Vries JE, Van der Vusse GJ. Long-term effects of fatty acids on cell
viability and gene expression of neonatal cardiac myocytes. Prostaglandins Leukot Essent
Fatty Acids. 1997;57:39–45.
[7] Binas B, Danneberg H, McWhir J, Mullins L, Clark AJ. Requirement for the heart-type fatty
acid binding protein in cardiac fatty acid utilization. FASEB J. 1999;13:805–812.
[8] Ohkaru Y, Asayama K, Ishii H, et al. Development of a sandwich enzyme-linked
immunosorbent assay for the determination of human heart type fatty acid-binding
protein in plasma and urine by using two different monoclonal antibodies specific for
human heart fatty acidbinding protein. J Immunol Methods. 1995;178:99–111.
[9] "TEDx Gateway 2018: Akash Manoj, child prodigy, solved a problem that renowned
innovators couldn't". Free Press Journal
[10] Xie PY, Li YP, Chan CP, Cheung KY, Cautherley GW, Renneberg R. A one-step
immunotest for rapid detection of heart-type fatty acid-binding protein in patients with
acute coronary syndromes. J Immunoassay Immunochem. 2010;31:24–32.
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[11] Li CJ, Li JQ, Liang XF, et al. Point-of-care test of heart-type fatty acid-binding protein
for the diagnosis of early acute myocardial infarction. Acta Pharmacol Sin. 2010;31:307–
312.
[12] Bank IE, Dekker MS, Hoes AW, et al. Suspected acute coronary syndrome in the
emergency room: Limited added value of heart type fatty acid binding protein point of
care or ELISA tests: The FAME-ER (Fatty Acid binding protein in Myocardial infarction
Evaluation in the Emergency Room) study. Eur Heart J Acute Cardiovasc Care. 2015, Apr
23. pii: 2048872615584077.
Image Reference:
https://www.ocregister.com/2015/05/01/identifying-sudden-cardiac-issues-in-young-
athletes/
Mr. Vipin Kumar Sharma is pursuing M.Sc. in Biochemistry from Central University of Haryana. He
is also a Youtuber at Vipin Sharma Biology Tutorials (Silver Play Awardee), Author at Altis Vortex,
Biology Mentor at Unacademy Studios-Placebo and Former Director of VSBT.
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LEARNING LINGUISTIC
LUCIDITY
ARUNIMA BHATTACHARYA and DEBAVA CHAUDHURI
3rd Year, M.Sc. in Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected],
Being fluent in an additional or multiple foreign languages, other than one’s maternal language is the new thing “en vogue” in this generation. English being the most preferred language to be taught after the mother tongue, Spanish, French, Arabic, Chinese and Russian (basically, the official languages identified by the United Nations), too remain the most coveted languages to be mastered by the ever-competitive youth of the world today.
But what is it with the student community and foreign-language learning? Is it indeed true that the teenage brain can process languages better than the adult one? Scientists have mixed opinions.
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To begin with, let it be kept in mind that sensory information enters the brain by way
of the thalamus, travels through the limbic system, and finally arrives to the cerebral
cortex, where it is stored in different localizations or modularities. Although it is true
that neurons cannot be regenerated, the brain is capable of building new neuronal
connections by virtue of cortical pyramidal cells. These grow by addition of dendrites,
which on appropriate stimulation, branch and re-branch: an exciting upcoming field
of research called Neuroplasticity. Besides, as is known and believed, the Broca’s area
in the left frontal lobe controls the execution
of speech sounds, the Wernicke’s area in the
left temporal lobe analyses the meaning of
words and phrases and helps in cognition,
while the amygdala in the thalamus controls
the emotional response to learning of the
language. Despite the dominance of the left
hemisphere, linguistic processing and
behaviour (i.e. cognition and communication)
are the results of unconscious and seamless
coordination of the activities between both
the hemispheres via the cerebral
commissures.
Language processing includes a typical cycle of the following five aspects:
Vision → Emotion → Attention → Learning and memory → Repetition
So what difference does it make to the brain when it can process multiple languages,
compared to when it processes only a single language? The answer lies in the
overlapping of cortical regions. Each language that one learns and uses in a lifetime is
generally stored and processed in associated yet different cortical regions of the brain.
When different languages are processed by different cortical regions, the commissures
too undergo adaptive changes in response to organization of the languages, as a
requirement of “linguistic switching”. This observation was hugely based on
experiments conducted by temporary neural disruption of the left Dorsolateral
Prefrontal Cortex (DLPFC) in volunteers (by inhibitory theta-burst Transcranial
Magnetic Stimulation), who were then subjected to repeating audio-visual syllable
sequences in a Hebb-repetition* learning task. According to results, the DLPFC-
disrupted group had better ability to retain the sequences, compared to those who
relied on DLPFC (the control group). These results hinted at the fact that a mature pre-
frontal cortex faced a lot of competition with the implicit learning of word-forms,
which further stresses on the belief that teenagers pick up new languages way more
easily than mature adults.
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Further studies on images of sections of the midsagittal corpus callosum showed that
the anterior midbody to total corpus callosum midsagittal area ratio was higher in
multilingual individuals, with respect to monolingual individuals :stressing on the
possibility that callosal adaptation facilitates interhemispheric transfer by increased
myelination, providing greater cortical connectivity.
Although the brain never really stops addition of new
words, many researchers postulate that after a critical
period, brain plasticity gradually becomes ineffective
and less equipped, owing to experiental effects.
So if you’re in the last years of your teens and are looking
forward to pick up a new language, do hurry up! And if
that age is just gone, nevermind : the brain is tuned to be
unique for every individual and as the saying goes, “Practice makes (everything)
perfect.”
*Hebb repetition task : For further details, visit
https://www.sciencedirect.com/science/article/pii/S0749596X13000570 (Inspired
by Still Alice, a film by Richard Glatzer and Wash Westmoreland)
References:
[1] 50 ideas you really need to know the human brain by Moheb Costandi
[2] Eleonore H.M. Smalle, et. al. (2017): Language learning in the adult brain: disrupting the
dorsolateral prefrontalcortex facilitates word-form learning. Nature, DOI:
10.1038/s41598-017-14547-x.
[3] Teresa J. Kennedy (2006): Language Learning and Its Impact on the Brain: Connecting
Language Learning with the Mind Through Content-Based Instruction. Foreign Language
Annals, Volume 39, Number 3, Fall 2006.
[4] https://www.bing.com/images/search?q=Brain+Plasticity&FORM=RESTAB
Ms. Arunima Bhattacharya is a 3rd year student of M.Sc. in Biotechnology from St. Xavier's College,
Kolkata, and is the Editor-in-Chief of InquiScitive Journal. She has also completed DALF C1 in French
from Alliance Française du Bengale.
Mr. Debava Chaudhuri is a 3rd year student of M.Sc. in Biotechnology from St. Xavier's College,
Kolkata.
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RELATION OF PENTOSE
PHOSPHATE PATHWAY AND
CANCER JYOTI SANGWAN and VIPIN KUMAR SHARMA
2nd Year, M.Sc., Department of Biochemistry
Central University of Haryana,
Adalpur, Haryana 123029, India.
Email: [email protected],
In recent years, the interest of people towards cancer metabolism has increased. The pentose phosphate Pathway (PPP) or phosphogluconate pathway or hexose monophosphate pathway (HMP) is a major source of NADPH and is required for the synthesis of nucleic acids. Cells of skin, bone marrow or rapidly dividing cells use the ribose-5-phosphate (pentose sugar) to make DNA, RNA and coenzymes such as NADH, FADH, ATP etc. NADPH is required for the reductive biosynthesis and scavenging of Reactive Oxygen Species (ROS). Thus, PPP plays a pivotal role in regulating cancer cells to meet their anabolic demands. The article summarizes the deregulatory mechanism of PPP and its importance in cancer cell growth and survival.
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1. Introduction to Pentose Phosphate Pathway (PPP):
The PPP is branched from glycolysis. The branching point of glycolysis is the first priming step i.e. phosphorylation of glucose to glucose-6-phophate (G-6-P), which is catalyzed by hexokinase. The PPP is divided into two main biochemical phases viz. oxidative phase and non-oxidative phase. The oxidative phase carries out the oxidation and decarboxylation at first carbon (C-1) of G-6-P and converts it into Ribose-5-phosphate, carbon dioxide and reduces NADP+ to NADPH. NADPH is a major scavenger of ROS and is required for the generation of reduced Glutathione (GSH) which is also termed as the master antioxidant of our body. Ribose-5-phophate acts as a precursor for nucleotide biosynthesis or it can be metabolized through non-oxidative phase of PPP which converts Ribose-5-phosphate to G-3-P, which begins the cycle again.
The non-oxidative phase involves the intermediates Fructose-6-phosphate (F-6-P), sedoheptulose and erythrose which results in the production of the precursors for amino acid biosynthesis. Two enzymes transketolase and transaldolase are unique to interconversions of non-oxidative phase of PPP.
Fig 1: Pentose Phosphate Pathway. PPP is divided into two main biochemical phases viz. oxidative
and non-oxidative phase. Glucose-6-phosphate dehydrogenase (G-6-PD) catalyzes the irreversible
oxidation of Glucose-6-phosphate into phosphoglucolactone which is an intramolecular ester. Ribose-
5-phosphate is then converted into Ribose-5-phosphate by Ribose-5-phosphate isomerase (RPI) and
then ribose-5-phosphate is converted into Xylulose-5-phosphate by enzyme Ribulose-5-phosphate
epimerase (RPE). Transketolase (TKT) and Transaldolase (TALDO) are mainly responsible for the
complex interconvesion within the non-oxidative phase of PPP.
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Normally differentiated non-dividing cells depend on mitochondrial oxidative phosphorylation to generate ATP while in human cancer cells, the glucose metabolism occurs through glycolysis (Warburg effect) producing pyruvate and lactate as the final metabolites in cells.
2. Enzymes of PPP and their oncogenic regulations:
Glucose-6-phosphate dehydrogenase (G-6-PD): It is the very first and rate-limiting enzyme of oxidative phase of PPP which catalyzes the irreversible oxidation of Glucose-6-phosphate into phosphoglucolactone. First NADPH will be scavenging the cellular ROS and will also play crucial roles in antioxidant defense. G-6-PD acts a “gate keeper” of PPP as it determines the flux partitioning between the PPP and glycolysis. G-6-PD is overexpressed in cancer cells. It has two cellular isomers: a dimer and a tetramer. Low pH and ionic strength are beneficial for the tetramer synthesis, whereas high pH generates a shift towards the dimer synthesis. p53 is a tumor suppressor which binds to G-6-PD, inhibits the formation of active dimer and suppresses production of NADPH, glucose biosynthesis and consumptions, thereby inhibiting PPP.
Polo like kinase-1 (PLK-1) promotes the formation of G-6-PD dimer and thus promotes the cancer cell cycle growth and progression. P21-activated kinase H promotes G-6-PD activity by increasing Mdm2 mediated p53 ubiquitination and degradation. Suppression of G-6-PD decreases NADPH production and reduces the capacity to scavenge ROS. These results show that G-6-PD is a potential biomarker and represent a promising therapeutic target in cancer cells.
6-Phosphogluconate dehydrogenase (6-PGD) will catalyse the decarboxylation and oxidation of 6-phosphogluconate to form ribulose-5-phosphate (Ketopentose) and CO2. Second molecule of NADPH is generated during this reaction. 6-PGD enzyme is commonly activated by lysine acetylation in human cancer cells which promotes reduction of NADP+ and hence the activity of 6-PGD. Thus the activated 6-PGD enhances the oxidative branch of PPP which plays a crucial role in maintaining intracellular Ribulose-5-phosphate at a physiological level that is enough to fulfill the metabolic requirements of growing cancer cells.
3-Phosphoglycerate (3-PG) inhibits the activity of 6-PGD. Malic enzyme increases 6-PGD activity by forming a physiological hetero-oligomer with 6-PGD.
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Fig 2. Oncogenic regulation of different enzymes of PPP
Ribose-5-phosphate isomerase (RPI) converts Ribose-5-phosphate into Ribose-5-phosphate and Ribose-5-phosphate epimerase (RPE) converts ribose-5-phosphate into Xylulose-5-phosphate. It has been demonstrated that RPLA regulates tumor genesis and cancer growth which is also significantly overexpressed in Hepatocellular carcinoma (HCC).
Transketolase (TKT) and Transaldolase (TALDO) are majorly responsible for the complex interconvesion within the non-oxidative phase of PPP. TKT transfers C-1 and C-2 of Xylulose-5-Phosphate to Ribose-5-phosphate and then forming 7C product. The remaining 3C fragment from Xylulose forms glyceraldehyde-3-phosphate. TALDO catalyzes the transfer a 3C fragment from Sedoheptulose-7-phosphate to Glyceraldehyde-3-phosphate and leads to the formation of Fructose-6-phosphate and Erythrose-4-phophate. Combination of Ascorbic acid and arginine decreases intercellular NADPH by reducing TALDO activity in non-oxidative PPP. Overexpression of TALDO is noticed in gastric adenocarcinoma.
Hexokinase (HK) phosphorylates glucose in the first step of glycolysis (irreversible regulatory step). Upregulation of HK is required to maintain the Warburg effect in cancer cells. HK exist in 4 isoforms (HK-1 to HK-4). HK-2 has a 100 fold higher glucose affinity than HK-1, HK-3 and HK-4. Elevation in expression of HK-2 promotes glycolysis and inhibits the mitochondrial mediated apoptosis in cancer cells. HLF-1 induces the expression of the HK-2.
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Phosphofructokinase (PFK-1) irreversibly phosphorylates fructose-6-phosphate into fructose-1,6-biphosphate which is the rate limiting step in glycolysis. Enhanced PFK-1 activity has been demonstrated in cancer cell lines and PFK-1 expression is upregulated in liver and breast cancers. In hypoxic condition, PFK-1 activity is suppressed by O-GlcNAcylation and redirects the glucose towards oxidative phase of PPP, which enhances the cancer cell growth. P53 inhibitor of TIGAR activation (PITA) is a kruppel- associated box type zinc finger protein, which is a selective regulator of P53. PITA exhibits increased PFK1 activity. PFKP (PFK-1 platelet isoform) is overexpressed in human glioblastoma cells and promotes brain cancer cell proliferation. In Leukemic cells, CDK6 phosphorylates PFKP and suppresses the activity of PFKP and thus, shifting the glucose derived carbon into the PPP and enhances the NADPH production to neutralize reactive oxygen species.
Snail-1 (transcriptional repressor of epithelial mesenchyme) represses PFKP, thus leading to the switching of glucose derived carbon to PPP, and then leads to generation of NADPH. The dynamic regulations of PFK-1 platelet isoforms enhance the survival of cancer cells which are undergoing metabolic stress.
Pyruvate kinase (PK) carry out the third irreversible reaction of glycolysis which is the conversion of PEP into pyruvate. PK also plays an important role in control of cancer cell metabolism. Two isoforms i.e. M-1 and M-2 of PK are generated by alternative splicing of PK. The expressions of PKM-1 and PKM-2 are time and location dependent. In cancer cells PKM-2 is preferentially expressed. In human lung cancer cells, increased intracellular ROS leads to the inhibition of PKM-2 by oxidation of Cys358. Cys358 requires the transfer of glucose derived carbon to PPP or glucose flux into the PPP which leads to the ROS detoxification.
3. PPP in various types of cancers:
HCC ( Hepatocellular carcinoma) is the most common cancer in the world and Breast cancer stands second in the race whereas Lung cancer leads to the highest mortality in the world. One of the main features of these three types of cancer is glucose metabolism alteration. Understanding of metabolic alterations in cancer cells may provide potential therapeutic strategies for different types of cancer. Elevated expression of G-6-PD has been demonstrated in patients with HCC. BAG directly interacts with G-6-PD and then suppresses the PPP flux and HCC cell growth. The major difference between normal hepatocyte cells and HCC cells is the difference in vital enzymes catalyzing the first step of glycolysis. In normal hepatocytes, the first step of glycolysis is catalyzed by Glucokinase whereas this step is catalyzed by HK-2 in HCC cells. G-6-PD is also closely associated with breast cancer and it has been demonstrated that G-6-PD silencing reduces lipid biosynthesis and increases glycolytic flux in breast cancer cells. TKT silencing reduces glycolysis flux in breast cancer cells.
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In breast cancer, NSD-2 overexpression induces cancer resistance by upregulating HK-2 and G-6-PD expression which also enhances PPP flux.
In lung cancer, G-6-PD inhibition enhances cancer cell sensitivity to cisplastin by inducing oxidative stress while resistance to cis-platin is promoted by 6-PGD in lung cancer, by decreasing the expression of miR-613 and miR-206. HK-2 is essential for lung cancer tumorigenesis in vivo and lung cancer cell growth in vitro.
4. Main therapeutic target in cancer cells is G-6-PD:
Antimalarial drugs such as primaquine or divicine lead to drug-induced hemolytic anemia. It was demonstrated that individuals with lowered GSH (reduced form of GS) and primaquine-sensitive hemolysis were route for NADPH generation. Thus, the erythrocytes with G-6-PD deficiency are more vulnerable to oxidative stress. G-6-PD Class-II deficiencies have less than 10% activity compared to the wild type. G-6-PD plays a pivotal role in PPP flux and ROS detoxification by producing NADPH so its deficiency leads to irreversible correlation with cancer evidence and mortality. It was reported that G-6-PD deficient individuals have lower chances of cancer mortality from all cancers.
Based on epidemiological evidence of metabolic characteristic of PPP in human cancer and G-6-PD deficiency, it was understood that G-6-PD is a potential target of synthetic lethal approach for various types of cancer combined with targeted therapeutics. ALDH (aldehyde dehydrogenase), glutamine metabolism and fatty acid oxidation are also considered in combinatory therapeutics to inhibit G-6-PD in cancer and hence provide new insights to clinical benefit of cancer treatment.
References:
[1] Jiang P, Du W and Wu M. Regulation of the pentose phosphate pathway in cancer. Protein Cell 2014, 5(8):592–602 DOI 10.1007/s13238-014-0082-8
[2] Cho ES, Cha YH, Kim HS et. al. The Pentose Phosphate Pathway as a Potential Target for Cancer Therapy. Biomol Ther 26(1), 29-38 (2018)
[3] Patra KC and Hay N. The pentose phosphate pathway and cancer. Trends Biochem Sci. 2014 August ; 39(8): 347–354. doi:10.1016/j.tibs.2014.06.005.
[4] Jin L and Zhou Y. Crucial role of the pentose phosphate pathway in malignant tumors. Oncology Letters 17: 4213-4221, 2019
[5] Vazquez A, Kamphorst JJ, Markert EK, Schug ZT, Tardito S and Gottlieb E: Cancer
metabolism at a glance. J Cell Sci 129: 3367‑3373, 2016.
[6] Weber GF: Metabolism in cancer metastasis. Int J Cancer 138: 2061‑2066, 2016. [7] Lu J, Tan M and Cai Q: The Warburg effect in tumor progression: Mitochondrial oxidative
metabolism as an anti‑metastasis mechanism. Cancer Lett 356: 156‑164, 2015. [8] Vander Heiden MG, Cantley LC and Thompson CB: Understanding the Warburg effect:
The metabolic requirements of cell proliferation. Science 324: 1029‑1033, 2009.
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[9] Martinez‑Outschoorn UE, Peiris‑Pagés M, Pestell RG, Sotgia F and Lisanti MP: Cancer
metabolism: A therapeutic perspective. Nat Rev Clin Oncol 14: 11‑31, 2017.
Ms. Jyoti Sangwan and Mr. Vipin Kumar Sharma are pursuing M.Sc. in Biochemistry from Central
University of Haryana.
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NOVEL PROTEINS TO NOBEL
PRIZE SHUBHAM DUTTA
2nd Year, M.Sc. in Virology,
National Institute of Virology,
20/ A, Dr. Ambedkar Road, Post Box No. 11, Pune 411001, India.
Email: [email protected]
“Healthy is just precancerous condition”– these words by stand-up comedian Drew
Hastings echoed the thoughts many scientists in the 1980’s had. Laboratories in USA
enthusiastically started studying cancer at the molecular level more vigorously than
before. Most importantly, the National Institute of Health (NIH) raised huge funds to
drive fundamental research on cancer biology with respect to public health. At this
time, a lab in University of California (Berkley) observed a game changing
phenomenon regarding the immune system in perspective of cancer biology. James P.
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Allison from this lab observed a protein CTLA-4 residing on the surface of T-cell
acting as a brake on latter and the idea of using this strategy in a negatively regulated
way generated in his mind. Let’s have a quick look on this CTLA-4 (Cytotoxic T-
lymphocyte-associated protein 4) protein-
It is also known as CD152, a protein receptor and most interestingly an immune
checkpoint that downregulates immune response.
Apart from being present at T-cell surface, it has been also found on the dendritic
cell.
CTLA-4 may also function via modulation of cell motility and/or signaling
through PI3 kinase, that reverses TCR-induced ‘Stop signal’needed for firm contact
between T cells and antigen-presenting cells (APCs).
Dr. Allison was able to express this protein on the surface of splenic T cells,
Thymocytes,T cell tumors but not on B cells. Taking all observations and inferences
into account he and his team published CTLA-4 as the murine homologue of human
CD28 antigen. But his idea of CTLA-4 blockade and disengaging T-cell brake
unleashed the immune system to attack cancer cells. Therefore, in 1994 along with Dr.
Krummel, Allison came to a conclusion that CTLA-4 instead served as a negative
regulator of T cell activation. This was initially interpreted as an intrinsic effect on T-
cell, where CTLA-4 induced negative signal blocking co-stimulatory receptors. The
complicated mechanism behind this negative co-stimulation by CTLA-4 is given in
the form of a simple diagram:
Fig 1. Molecular mechanisms of CTLA4 and PD-1 attenuation of T-cell activation. Schematic of
the molecular interactions and downstream signaling induced by ligation of CTLA4 and PD-1 by their
respective ligands. The possibility of additional downstream cell-intrinsic signaling mechanisms is
highlighted for both CTLA4 and PD-1.
[Ref: ‘Fundamental Mechanisms of Immune Checkpoint Blockade Therapy’- A Review by Spencer
C. Wei, Colm R. Duffy and James P. Allison (Cancer Discovery-2018)]
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It is very commonly said that great men think alike. Allison’s finding was resonated
with another great scientist from Kyoto University, when Tasuku Honjo and
colleagues assumed that PD-1 identified by subtractive hybridization to isolate
mRNAs overexpressed in dying mouse cells, would be involved in pathways
regulating apoptosis.Programmed cell death protein 1 (PD-1)and CD279 (Cluster of
differentiation 279), is a protein on the surface of cells that has a role in regulating the
immune system’s response to the cells of the human body by down-regulating the
immune system and promoting self-tolerance by suppressing T cell inflammatory
activity. In 2002, Honjo lab published a paper where they explained that, PD-1/PD-
L1 blockade triggers the killing of cancer and/or tumor cells as CTLA-4 does:
Fig 2. The discovery by Tasuku Honjo and coworkers, the identification of the PD-1 surface
protein, recognizing its role as an inhibitor of activation and developing antibodies to release the
brake. The graph shows the effect of anti-PD1 treatment in mice with metastasizing melanoma
compared to untreated controls.
[Ref: ‘The Scientific Background- Discovery of cancer therapy by inhibition of negative immune
regulation’ (2018)]
Let’s have a look on the comparative study between the mechanistic pathway of these
two proteins in regulating immune response that paves the way of killing the cancer
cells.
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Fig 3. The role of CTLA-4 and PD-1 as inhibitors of activation (upper panels) and the effect
oreleasing the corresponding brakes using antibodies (lower panels).
[from ‘The Scientific Background- Discovery of cancer therapy by inhibition of negative immune
regulation’ (2018)]
After 2010, knowledge of these kinds of mechanism motivated many other groups to
develop the combined therapeutic strategy involving anti-CTLA4 and anti–PD-1
antibodies simultaneously to the dendritic cell suspension. In 2010, even a human trial
was conducted on advance staged myeloma patients which resulted in tremendous
success. However, the enhanced efficacy of combined therapy is mechanistically
unrevealed; we do not know whether this is driven by cellular additives from
monotherapies or not. One can make out how fascinating Dr. Allison’s work is from
his statement: “The Reason I’m thrilled about this is I’m a basic scientist. I didn’t get
into these studies to cure cancer. I wanted to know how T-cells work”.
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Reference:
[1] ‘The murine homologue of the T lymphocyte antigen CD28. Molecular cloning and cell
surface expression.’ (Journal of Immunology- 1990) ; JANE A. GROSS, TOM ST. JOHN
AND JAMES P. ALLISON.
[2] ‘Fundamental Mechanisms of ImmuneCheckpoint Blockade Therapy’ (Review); Cancer
Discovery (2018) Spencer C. Wei , Colm R. Duffy and James P. Allison.
[3] ‘The Scientific Background- Discovery of cancer therapy by inhibition of negative immune
regulation’ (2018).
[4] Wikipedia
Mr. Shubham Dutta is currently pursuing M.Sc. in Virology from NIV, Pune, and is a B.Sc. in
Microbiology from Ramkrishna Mission Vidyamandira, Belur. He is a Member of Editorial Committee,
InquiScitive Journal. He is also a singer.
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“ACHOO”, CULPRIT: THE SUN LEENA BHADRA
2nd Year, M.Sc. Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected]
“Achoo!” the awkward sweet sound that a person makes when one sneezes making the nose wrinkle and one’s face look so weird. That moment when there’s pin-drop silence and everyone is busy with their own work and suddenly someone goes “Achoo”, all pairs of eyes in the room turn to that person and that poor guy helplessly wishes that the Invisibility Cloak from the Wizarding World of Harry Potter was real. Sneezing can’t be controlled. It is simply one of the body’s unavoidable reflexes. It is typically associated with the irritation of the nose. How does this happen? When we feel any particular irritant in our nose, the signal from there is sent via neural pathways to the brain, resulting in a powerful release of air through the mouth and nose. This helps not only in the expulsion of mucus or irritants from the nasal passage at the earliest, but also contracts a bunch of muscles in the body, including the eyelids and trachea giving rise to a confused expression.
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But there’s one more dangerous culprit who can cause us to sneeze- The Sun. Although not as dramatic as bursting into flames like the vampires without their sun-protection voodoo rings in L.J. Smith’s novels, for some people sudden exposure to sunlight produces an unexpected reflex resulting in sneezing. According to some informal surveys, 17-35% of the world’s population are sun-sneezers. How to avoid it? Wear sunglasses.
Sun-sneezers have always existed among us. People knew about this for a long time. Even the Greek philosopher, Aristotle mentioned sun-sneezers in his Book of Problems, Chapter ‘Nose’. The question he raised was, "Why does the heat of the Sun provoke sneezing, and not the heat of the fire?" This phenomenon is called the Photic Sneeze Reflex. The reflex has nothing to do with the kind of wavelength or color of light, but the intensity of light. It appears to have been the result of some cross wiring along the trigeminal nerve. The trigeminal nerve is the 5th cranial nerve and is the largest and most complex paired nerve in the head. The nerve has three major branches leading to the eyes, nasal cavity and the jaw. Being a crowded place in terms of nervous signaling, it comes as no surprise that the trigeminal nerve would occasionally get the reflexes wrong. Bright light causes the pupils to contract and the signal might be erroneously sent to the nose as well. There’s also another hypothesis that states that the sun-sneezes occur thanks to ‘parasympathetic generalization.’ Parasympathetic generalization is a process caused when one part of the parasympathetic nervous system, like the pupil is excited by a stimulus and happens to activate other parts of the system as well, such as the membranes in the nose.
Even though it might be a misfiring of the nervous system, scientists have recently discovered the underlying genetic cause of sun-sneezing. Thus, one is born to be a sun-sneezer. These people are now said to have the “Achoo”. As hilarious as the acronym may sound, Achoo stands for Autosomal Dominant Compelling Helio-opthalmic Outburst. It is ‘autosomal' because the affiliated gene is located on one of the non-sex-linked chromosomes, and 'dominant' because you only need to inherit it from one of your parents to express the trait. When a Genome Wide Association Study was conducted in 2010, it was found that these people had a Cytosine base instead of a Thymine in the concerned gene. The 2nd chromosome in the body is said to contain the gene responsible for the photic sneeze reflex. So, just a single base pair mutation is capable of causing such a major change.
Even though commonly associated with the sun, photic sneeze reflex can also happen in response to exposure to any other light suddenly. Scientists are yet to discern whether sun-sneezing has any evolutionary benefit. So, “Achoo” is pretty harmless and sun-sneezers are unique people.
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References:
[1] The Sun Sneeze Gene- http://ve42.co/23andme [2] Photic sneeze reflex- Wikipedia [3] Why does bright light cause some people to sneeze?- http://www.scientificamerican.com [4] Definition of Photic Sneeze reflex- http://www.medicinenet.com [5] A genome-wide association study of photic sneeze reflex- http://www.nature.com [6] BBC-Future-Why looking at the light makes us sneeze- http://bbc.com [7] Reversing Photic Sneeze Reflex: Overcoming Cravings- The Raw Vegan Plant-Based
Detoxification & Regeneration Workbook for Healing Patients- Volume 3 [8] ACHOO Syndrome- Medical Genetic Summaries- https://www.ncbi.nlm.nih.gov
Ms. Leena Bhadra is a student of Biotechnology (M.Sc. 2nd Year) at St. Xavier’s College (Autonomous),
Kolkata.
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CRISPR BABY
AVIRUP CHAKRABORTY
2nd Year, M.Sc. in Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected]
Every moment, we are exposed to innumerable pathogens and, to add to our miseries,
our genetic and systemic constitution harbors several factors that are their allies in this
constant conspiracy. A fundamental question that would naturally arise is: How are
we alive? Is it only because of the pulsating heart or the breathing lungs or any similar
organ? And how are those deadly factors regulated or kept inactivated?
Let us, therefore, talk about one of the most important of such factors – the caspases,
that program death for us upon activation, triggering apoptosis. The genes controlling
the different apoptotic factors are carefully kept inactivated to ensure our cells to be
alive and are activated only when their further survival can cause harm to us, e.g. if
they are harboring a virus within themselves. Then there are oncogenes which are
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stimulatory for growth but can cause uncontrolled proliferation upon hyperactivation,
leading to carcinogenesis. The human genome is too diverse and has a normal
tendency to get mutated and infected, scripting our funeral.
In accordance to this, there are genes which normally promote HIV (human
immunodeficiency virus) infection and replication. It is quite evident that if the gene
is edited or modified by any means then this nature of the gene to promote HIV
infection may be inhibited and the individual will be immune to HIV. If this inhibition
is done in the embryo way before the baby is born then it would be immune to HIV
ever since birth. This milestone was achieved by the Chinese scientist Dr. Jiankui He
from University of Shenzen. He claims to have created the two “first-s":
1. genetically edited babies, and
2. HIV immune babies.
For this editing process, He et al. utilized Clustered Regularly Interspaced Short
Palindromic Repeats (CRISPR) which form a part of the internal defense system in
bacteria. The exact name to this technology is though, CRISPR-Cas9, which takes into
action the work of enzyme Cas9.
CRISPR is a family of DNA sequences found within the prokaryotic genome. These
sequences are derived from DNA fragments from viruses that have previously
infected the prokaryote and are used to detect and destroy DNA from similar viruses
during subsequent infections. Cas9 is an enzyme that uses CRISPR sequences as a
guide to recognize and cleave specific strands of DNA that are complementary to the
CRISPR sequence. A simple version of CRISPR-Cas9 has been modified to edit
genomes. By delivering the Cas9 nuclease complexed with a synthetic guide RNA
(gRNA) into a cell, the cell’s genome can be cut at a desired location, allowing existing
genes to be removed and/or new ones to be added. In this way, not only can a baby
be made immune to HIV but the genes responsible for other predictable illnesses that
may plague the baby in future can also be edited and designer babies may be formed
who will be immune to all possible genetic maladies.
The target gene for the research work in question was that expressing CCR5 or
chemokine receptor type 5 on the surface of WBCs. HIV-1 most commonly uses the
chemokine receptors to enter target immunological cells. Thus if the CCR5 gene is
genetically edited blocking or inactivating its gene product from interacting with HIV-
1 virus, then the baby can be made immune to HIV infection throughout its lifetime
unless any other mutagenic substance happens to activate it again, which is yet to be
answered.
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The team initially worked with eight Chinese couples of HIV positive men and HIV
negative women. At first, the sperms were washed to ensure that HIV was not present.
Then they injected the sperms along with CRISPR-Cas9 enzymes into unfertilized
eggs. This produced a total of 30 fertilized embryos, of which 19 were viable and
appeared healthy. Two of the four embryos from one couple contained modifications
to CCR5 and these two modified embryos were implanted in the woman, even though
one embryo also had an intact copy of CCR5 gene. It was found that the first baby that
was genetically edited was born with a twin. But only one of the genetically modified
babies would be resistant to HIV, because gene editing caused removal of both copies
of her CCR5 gene. The other twin could still be susceptible to infection because the
gene editing process inadvertently left one copy of her CCR5 gene intact.
This research work has shed light upon future programs on gene editing and
modifications that could lead to resistance to many genetic deformities. Still it leaves
many questions unanswered, such as: whether prospective parents were properly
informed of the risks; why CCR5 modification was chosen as a remedy when there are
other proven methods for HIV prevention; why the experiments were carried out on
couples having HIV positive men although HIV positive women have a higher chance
of passing the virus onto their children and many more. Most importantly, the
reception of this technology of creation of designer babies by the skeptics in the
scientific world on ethical grounds is largely questionable. But again, every coin has
two sides and this time, both sides are quite unclear. Only further research with
CRISPR technology would be able to answer these questions and pave the way
towards a secure human health without any illness and worry.
References:
[1] Nature 564, 13-14 (2018) doi: 10.1038/d41586-018-07573-w
[2] https://www.nature.com/articles/d41586-018-07573-w
[3] https://www.bgr.in/news/crispr-gene-edited-babies-scientist-genes-human-dna-
resistant-hiv-
aids/?fbclid=IwAR1_vrP5CYlegB3m3kgqsFsGM7sGlrDprLhBgHD3A2euxgrcTAKY9Lzt
M2k
Mr. Avirup Chakraborty is a 2nd year student of the Department of Biotechnology, St. Xavier's College
(Autonomous), Kolkata and a science enthusiast.
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BLACK HOLES RITURAJ BHATTACHARJEE
4th Year, B.Tech. in Electronics and Communication Engineering,
Swami Vivekananda Institute of Science and Technology,
Dakshin Gobindapur, Kolkata, West Bengal 700145.
Email: [email protected]
One of the most impressive and mysterious objects in the universe, Black Holes have
captured much attention from both Astronomers and the general populace alike. But
what are they, really? An all-consuming darkness or something far more interesting?
Let us explore the incredible physics of black holes, in the simplest way possible
through this article.
Let us begin with what exactly a black hole is. In the simplest possible terms, it is the
collapsed core of a really, really big star. A star is spherical because of two forces; the
force of its own gravity which tries to crush it, and the force of the thermonuclear
fusion reaction at its core, which tries to blow it apart. At a certain distance, which is
essentially the star’s radius, these forces balance each other. Since it is more or less
equal on all sides, the star remains spherical. For really large stars which are at least
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four times the mass of the Sun, when the fuel of the core is spent, the gravitational
forces completely dominate and crush the core. This tremendous pressure first results
in a type 1b or type 2 supernovae which are arguably the brightest objects in the
universe though for a short period of time.
These tremendous explosions are followed by the rapid collapse of the stellar core,
until the gravity near its surface becomes so strong not even light can escape. This
creates what is called the Event Horizon or the boundary of the black hole. The core
continues to collapse beyond the event horizon, but the nature of that collapse cannot
be determined because no electromagnetic radiation penetrates the Event Horizon.
Relativity tells us that the core continues to collapse into a singularity, an infinitely
small and infinitely dense point of space time as a whole.
This brings us to the incredible things that relativity predicts the black hole hides
inside and around the Event Horizon. One cannot survive a fall into a black hole. This
is because of a very well-known effect of gravity called Tidal Forces. It is due to this
effect that the Moon causes tides on Earth. The Earth’s gravity also applies tidal forces
on you by pulling your legs a little more strongly that it pulls your sides or your head
when you stand. However, the force of gravity of the Earth is so weak and because
our bodies have adapted, this force is almost imperceptible. Near a Black Hole
however, the force of Gravity is so great that tidal forces will continue to stretch one
until, well, snap. There’s a rather funny name for this: Spaghettification. This is because
before the snap, one basically becomes spaghetti.
In the event that one survives this and falls into a black hole, what would one see?
Time near a black hole is slowed down, so an orbiting observer would see you fall
slower and slower until your image stops at the Event Horizon. The orbiting person
would see you stuck at the Event Horizon for all of eternity. But what about the person
who has fallen? Time will initially pass normally. At the event horizon itself, nothing
can be seen. Light is trapped here, so the photons cannot reach the eyes. For an instant,
they would become blind. Once inside, relativity says that time itself becomes a spatial
dimension which sort of means they would see all the possible pasts, presents and
futures of the Universe. Everything that has ever occurred or hasn’t occurred.
Everything that is occurring or isn’t occurring. Everything that will occur or won’t
occur. But before you start dreaming of reveling in this godly ability, I did mention
that you cannot survive a fall into a black hole.
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Even if you (hypothetically) survive Spaghettification, the singularity will eventually
crush you into nothingness, and maybe eject your particles (i.e. your ¬fundamental
particles like electrons) into another part of the universe.
Hence, it is important to avoid black holes nearby and to “see” it coming, the Accretion
Disc is a good indicator. The Accretion disc is a gigantic circle of dust and gas around
the BH. Basically stars or the stellar dust near a black hole forms an unstable orbit
around it. The black hole feeds off this dust and gas, gaining mass. Now, near the
black hole, this disc will be speeding around at ridiculous speeds, at good percentages
of the speed of light. This generates incredible friction, which in turn, generates
incredible heat. This makes the accretion disk glow very bright in all spectrums of the
electromagnetic wavelength. In case of rotating black holes called “Kerr Black Holes”,
there will also be a plume of ejected luminous gas hundreds of thousands of light
years in length from the poles of the BH.
Mr. Rituraj Bhattacharjee in an Electrical Engineering student at Swami Vivekananda Institute of
Science and Technology, and an Analyst in InquiScitive. He is also a cartoonist and Founding Member
of Last Page Doodles.
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TIME TICKING BACK SOUPTIK GHOSH
2nd Year, M.Sc. in Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected]
Haven’t we all wanted to go back in time at some point or the other? Be it to complete
a lengthy examination paper or simply to live out the fantasies born out of reading
sci-fi novels? In 21st Century, this may not be a distant dream anymore for scientists
have apparently succeeded in “reversing time” using Quantum Computing.
To start with, let us get a simplified idea of Quantum Computing. Quantum
Computing refers to a field where computer technologies are developed using the
principles of Quantum Theory, which in turn explains the behavior and nature of
energy and matter at quanta, i.e., at atomic and subatomic levels. The main advantage
of a Quantum Computer is that it has enormous processing power which enables it to
be available in multiple states and perform multiple tasks using all possible
permutations simultaneously.
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Another important aspect of this Computing is Temporal Asymmetry. If we go by a
real-life example rather than the formal definition, then it shall be easier to
comprehend. A glass shatters into a number of pieces when it falls down on the floor;
the pieces can never be united to regain the original object. This phenomenon is
known as Temporal Asymmetry and it has continued to baffle scientists for long.
Scientists from the Moscow Institute of Physics and Technology (MIPT), along with
researchers from the United States and Switzerland, have tackled this problem by
combining two different disciplines, which includes computational and quantum
mechanics. The results illustrate that the asymmetry could emerge due to the forcing
of classical causal explanations on the observations in a fundamentally quantum
world.
The scientists commenced with assessing the Physical Laws which can distinguish
between the past and the future. Most laws in Physics make no separate distinction
between these two time determinants. For example, let one equation describe the
collision and rebound of 2 identical billiard or pool balls. If the event is recorded
initially and then played in reverse, the same equation can still be used to represent it.
Also, it's impossible to tell the two events apart without the recording. Each of the
variations appears equally practicable, whether you examine the actual occasion or
it’s opposite. It would seem that the pool balls defy the intuitive sense of time.
However, let’s imagine a cue ball, after being struck, breaking a pool pyramid, with
the other balls scattering in all directions (see figure, next page). In that case, it shall be
easy to distinguish the actual-existence situation from the reverse playback. What
makes the latter look so absurd is our intuitive understanding of the second law of
thermodynamics—an isolated system of matter either remains static or evolves
toward a state of chaos rather than order.
“The actual experiment involving four stages on a quantum computer mirror the stages of the
thought experiment involving an electron in space and the imaginary analogy with pool balls.
At the beginning of the experiment, each of the three systems initially evolves from order
toward chaos, but then a perfectly timed external disturbance reverses this process.”
Most other laws of physics do not prevent infused tea from flowing back into the tea
bag, rolling billiard balls from assembling into a pool pyramid, or a volcano from
"erupting" in reverse. But these phenomena are not seen, because they would require
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an isolated system to assume a more ordered state without any outside intervention,
and that is a direct contradiction to the second law.
The nature of this law has not been explained in full detail, but researchers have made
great headway in understanding the basic principles behind it.
Quantum physicists from MIPT set out to examine if time may at all reverse itself for
something as minimal as a single particle and for a fraction of a second. Instead of
colliding pool balls, they examined a solitary electron in an empty interstellar space.
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"Suppose the electron is localized once we begin observing it. This means that we're
pretty certain regarding its position in space. The laws of quantum physics hinder the
researchers from knowing it with absolute preciseness, however, we are able to define
a tiny region wherever the electron is localized," says study co-author Andrey
Lebedev from MIPT and ETH Zurich.
The team tried to calculate the probability of observing an electron "smeared out" over
a fraction of a second instantly localizing into its recent past. It showed that even
across the complete lifetime of the universe—13.7 billion years—observing 10 billion
freshly localized electrons every second, the reverse evolution of the particle's state
would happen only once. And even then, the electron would travel no greater than a
mere one ten-billionth of a second into the past.
Large-scale phenomena involving pool balls and volcanoes clearly unfold on more
abundant bigger timescales and feature an astounding range of electrons and different
particles. This explains why we do not observe old people growing younger or an ink
blot disappearing from stained paper.
The researchers then tried to reverse time during a four-stage experiment. In place of
an electron, they determined the state of a quantum computer product of 2 and later
3 basic components known as superconducting qubits.
A qubit is a unit of information described by a “one”, a “zero”, or a mixed
“superposition” of both states.
Stage 1: Order-Each qubit is initialized within the ground state, denoted as zero. This
extremely ordered configuration corresponds to an electron localized in a very little
region, or a rack of billiard balls before the break.
Stage 2: Degradation- The order is lost. Exactly like the electron that gets smeared out
over a progressively massive region of space, or the rack broken on the pool table, the
state of the qubits becomes a constantly changing advanced dynamic pattern of zeros
and ones. This result is achieved by concisely launching the evolution program on the
quantum computer. Actually, an analogous degradation would occur by itself because
of interactions with the surroundings. However, the controlled program of
autonomous evolution can modify the last stage of the experiment.
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Stage 3: Time reversal - A special program is used to modify the state of the quantum
computer in a way that it would then evolve "backwards" from chaos toward order.
This operation is akin to the random microwave background fluctuation in the case of
the electron, but this time, it is deliberately induced. A clearly far-fetched analogy for
the Pool example would be somebody giving the table a strong and perfectly
calculated kick.
Stage 4: Regeneration- The evolution program from the second stage is launched once
more. Provided that the "kick" has been delivered with success, the program doesn't
end in a lot of chaos however rather rewinds the state of the qubits into the past,
similar to the way a smudged electron would be localized or the Pool balls would
retrace their trajectories in reverse playback eventually forming a triangle.
The researchers found that in eighty five percent of the cases, the two-qubit quantum
computer came back into the initial state. When 3 qubits were concerned, plenty of
errors took place, ensuing in a roughly 50 percent success rate. According to the
authors, these errors occur because of imperfections within the actual quantum device.
As a lot of advanced gadgets are designed, the error rate is anticipated to drop.
Interestingly, the time reversal algorithmic program itself might prove helpful for
making quantum computing a lot more precise. “Our algorithmic program can be
updated and accustomed check programs written for quantum computers and
eliminate noise and errors,” Lebedev explained.
Now let us come to the actual question. Did the scientists actually reverse the time?
The answer is No, they did not! This gives rise to the question: If they did not reverse
the time, what did they actually do?
They carried out the experiment as if they were rewinding a video. A close example
can be of a lens, which is used to focus light “reversing” the dispersal of light that had
gone out of focus. The authors of the paper, from the MIPT, Argonne National
Laboratory in Illinois, and ETH Zurich, said that their methodology and results might
be useful for testing quantum programs. This is correct, but that’s a lot less interesting
than a time machine. Despite all the controversy surrounding the experiment, there is
no denying the fact that a day will come when we will actually be able to reverse time.
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References:
[1] https://www.technologyreview.com/s/613123/no-ibm-didnt-just-reverse-time-with-a-
quantum-computer/
[2] https://www.independent.co.uk/life-style/gadgets-and-tech/news/time-reverse-
quantum-computer-science-study-moscow-a8820516.html
[3] https://www.nature.com/articles/s41598-019-40765-6
Image Reference:
https://3c1703fe8d.site.internapcdn.net/newman/gfx/news/hires/2019/1-physicistsre.jpg
Mr. Souptik Ghosh is a student of 2nd Year, Postgraduate Department of Biotechnology, St. Xavier’s
College (Autonomous), Kolkata. He is a regular quizzer and has won several laurels. He is interested
in recent scientific developments and other current affairs.
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THE NUMBERS ARE ON OUR
SIDE! ABHINABA CHAKRABORTY
M.Sc. in Botany (Specialized in Microbiology),
Visva-Bharati University,
Bolpur, West Bengal 731235, India.
Email: [email protected]
1. Background:
Ever since the discovery of penicillin by Alexander Fleming in 1928, antibiotics have
been a great weapon against pathogenic bacteria. However, with time, antibiotic
resistant bacterial strains have become more and more common and their treatment
with conventional therapies often prove to be futile.
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To become resistant to antibiotics, bacteria only needs a few genes, which they obtain
by Horizontal gene transfer in the form of selfish genetic elements, such as,
conjugative plasmids. A single element can confer multiple antibiotic resistance. Even
in the absence of antibiotics, the plasmids spread and persist within the population,
making the situation messier.
The ability of bacteriophages to kill and lyse the specific bacteria, minimally
disrupting the normal flora, inspired researchers to use these viruses as antibacterial
agents to kill antibiotic resistant bacterial strains. This application of phages as drugs
to treat bacterial disease became popularized as Phage therapy.
However, the initial excitement faded away when researchers found that bacteria even
within a very small population could become resistant to phage infection which is
often manifested by alteration of the surface proteins to which phage bind or the
development of adaptive immunity via interfering CRISPR sequences. Also, the
frequency of bacteria reversing to phage susceptibility is very low.
Though the mechanism of bacterial resistance to phage infection differs from that of
antibiotic resistance, the outcome was the same i.e. inability of the therapeutic agent
to cease bacterial proliferation. So, advocates of phage therapy hypothesized the use
of phage cocktail (a cocktail of different phages infecting same host) in which case, it
was less likely for the bacteria to develop resistance against all the phages used.
However, a few argued in favor of using a single lytic phage instead of a cocktail of
phages to prevent the development of a broad host range cocktail resistant strains.
2. The Problem and the Solution:
Phages drive bacterial evolution by causing selective pressure in a population or by
providing beneficial features to specific bacteria within a very narrow host range.
Keeping these in mind, it is suspected there will be difficulties in isolating phages
effective against potentially multi-phage-resistant bacterial strains in future. Thus, the
long term viability of phage therapy is questionable.
By antagonistic co-evolutionary cycles, phages affect the bacterial evolution. In the
course of evolution, viruses evolve to re-infect hosts that have already become
resistant to earlier types of the same virus.
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As the surface components are utilized by the phages for attachment with the bacteria,
it has been seen that bacteria evolve their surface components more rapidly than other
parts. Even in laboratory conditions, the rate of molecular evolution of co-evolving
bacteria and their lytic phages is accelerated when there is an arms race going on
between them. So, even if all the phages do not seem to be able to adapt to infect
resistant hosts, there will be some, which will remain infective by constantly evolving
along with their hosts.
Pre-defined phage cocktails used globally in a manner similar to that of antibiotics
may result in over-evolved bacterial hosts. Use of phage cocktails will substantially
delay the evolution of bacterial superbugs, resistant to a broad range of phages. So,
though it sounds hypothetical, phage therapy may face the same fate as antibiotic
therapy in future. However, it can also be argued that co-evolved phages, adapted in
due to course of evolution along with the bacterial host, may still remain infective in
the days of broad spectrum phage resistant superbugs.
Despite the above-mentioned observations on bacterial evolution, several studies
have suggested that the evolution of phage-resistant superbugs is not going to occur.
Viral adaptation to evolved hosts has been studied in the laboratory as well as in their
natural habitats. It has been observed that bacteria in their natural habitat were more
resistant to their contemporary phages than to past or future phages. Meta-analysis of
interactions among host and phage performed by Flores et al. concluded that phages
can often remain infective to many different host strains from different origins.
Therefore, now is the time to isolate phages against all the potential pathogenic,
antibiotic resistant bacteria because in future when all antibiotics are rendered useless,
we will be able to use these phages as weapons in war against pathogens. And, with
the numbers on our side, we’ll win the battle.
References:
[1] Bennett PM, 2009, Plasmid encoded antibiotic resistance: acquisition and transfer of
antibiotic resistance genes in bacteria. Br J Pharmacol.153:S347–S357.
[2] Jalasvuori M, Friman V-P, Nieminen A, Bamford JKH, Buckling A, 2011, Bacteriophage
selection against a plasmid-encoded sex apparatus leads to the loss of antibiotic-resistance
plasmids. Biol Lett.7:902–905.
InquiScitive Journal: An e-magazine on recent scientific developments
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[3] Loc-Carrillo C, Abedon ST, 2011, Pros and cons of phage therapy. Bacteriophage
2011;1:111–114.
[4] Lenski Re, 1984, Two-step Resistance by Escherichia Coli B to Bacteriophage T2.
Genetics;107.
[5] Hyman P, Abedon ST, 2010, Bacteriophage Host Range and Bacterial Resistance. Adv
Appl Microbiol,70:217–248.
[6] Capparelli R, Nocerino N, Iannaccone M, Ercolini D, Parlato M, et al, 2010,Bacteriophage
Therapy of Salmonella enterica: A Fresh Appraisal of Bacteriophage Therapy. J Infect
Dis,201:52–61.
[7] Gu J, Liu X, Li Y, Han W, Lei L, et al, 2012, A Method for Generation Phage Cocktail with
Great Therapeutic Potential. PLoS One, 7:e31698.
[8] Chan BK, Abedon ST. Phage Therapy Pharmacology: Phage Cocktails,2012, Adv Appl
Microbiol,78:1–23.
[9] Krylov V, Shaburova O, Krylov S, Pleteneva E, Krylov V, et al. 2012, A Genetic Approach
to the Development of New Therapeutic Phages to Fight Pseudomonas Aeruginosa in
Wound Infections. Viruses,5:15–53.
[10] Paterson S, Vogwill T, Buckling A, Benmayor R, Spiers AJ, et al. 2010, Antagonistic
coevolution accelerates molecular evolution. Nature 464:275–278.
[11] Marston MF, Pierciey FJ, Shepard A, Gearin G, Qi J, et al. 2012, Rapid diversification
of coevolving marine Synechococcus and a virus. Proc Natl Acad Sci U S A 109:4544–9.
[12] Scanlan PD, 2017, Bacteria–Bacteriophage Coevolution in the Human Gut:
Implications for Microbial Diversity and Functionality. Trends Microbiol, 25:614–623.
[13] Dennehy JJ. 2012, What Can Phages Tell Us about Host-Pathogen Coevolution? Int J
Evol Biol, 2012:396165.
[14] Kashiwagi A, Yomo T, 2011, Ongoing Phenotypic and Genomic Changes in
Experimental Coevolution of RNA Bacteriophage Qβ and Escherichia coli. PLoS
Genet,7:e1002188.
[15] Clokie MRJ, Millard AD, Letarov A V, Heaphy S. 2011, Phages in nature.
Bacteriophage,1:31–45.
[16] Gómez P, Buckling A. 2013, Coevolution with phages does not influence the evolution
of bacterial mutation rates in soil. ISME J ,7:2242–2244.
[17] Flores CO, Meyer JR, Valverde S, Farr L, Weitz JS. 2011,Statistical structure of host-
phage interactions. Proc Natl Acad Sci U S A,108:E288-97.
Mr. Abhinaba Chakraborty has qualified M.Sc. in Botany (specialization in Microbiology) from Visva-
Bharati University, Shantiniketan.
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CHEMICAL COMBAT RAJARSHI CHANDA1 and ARUNIMA BHATTACHARYA2
1 3rd Year, UG Department of Life Sciences,
Presidency University,
86/1, College Street Road, Kolkata 700073, India.
2 3rd Year, M.Sc. in Biotechnology,
St. Xavier’s College (Autonomus),
30, Mother Teresa Sarani, Kolkata 700016, India.
Email: [email protected] , [email protected]
The use of the cytotoxic properties of chemical substances as weapons has been in use
for quite some time. Also termed as chemical warfare, this is not considered to be a
very conventional weapon. Chemical, biological and nuclear warfare are, in fact,
collectively called Weapons of Mass Destruction (WMDs). However, the use of
chemical weapons is prohibited under customary international humanitarian law.
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Fig 1. WMDs
[Source: https://www.trtworld.com/mea/the-global-guide-of-using-chemicals-as-a -weapon-of-war-
331604]
Looking back at the history of chemical warfare, we have seen use of chemicals in
wars even in ancient mythological ages, dating back to almost 600 BCE.
The earliest archaeological evidence of gas warfare is during the Roman-Persian Wars
– in the collapsed tunnels of Dura-Europos in Syria, there has been evidence that in
the third century AD, the Sassanians used bitumen and sulfur crystals. Dense clouds
of choking sulfur dioxide gases were given off due to the ignition, which killed 19
Roman soldiers in two minutes.
Fig 2. Schematic view of Dura Europos tunnel
[ Source : http://www.romeacrosseurope.com/wp-content/uploads/2017/01/Tunnel-warfare-in-Dura-
Europos.jpg e ]
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The use of cytotoxic chemicals as weapons dates back thousands of years, but the first
large scale use of chemical weapons was seen during World War I.
Primarily used to injure, kill and demoralize the defending troops, the static and slow-
moving gases where the most effective among the chemical weapons. Disabling gases
such as tear gas, as well as lethal ones, like phosgene, chlorine and mustard gas were
used. This chemical warfare was a major component of the first global war and the
first total war of the 20th century. The extent of such use was so massive that the First
World War is often termed as The Chemist’s War.
Quite naturally, major health concerns, including fatality were raised, and on ethical
grounds, the use of poison and/or poisonous gases was banned according to the 1899
Hague Declaration Concerning Asphyxiating Gases and the 1907 Hague Convention
on Land Warfare and was considered to be a war crime.
Consequently, due to the widespread horror and public revulsion at the use of gases
in the first war, the combatants in the Second World War stood firm in refusing any
such use as a part of their war strategies.
The Timeline of Use of Chemical Warfare:
1. 1899
The Hague Convention : Countries agree to ban the use of projectiles to diffuse
‘asphyxiating or deleterious gases’.
2. 22 April 1915
168 tons of chlorine gas are released near Ypres, Belgium, by German troops against
the French in the Second Battle of Ypres.
3. 1917
Mustard gas is initially introduced by German forces, prior to the Third Battle at Ypres.
4. 1925
The Geneva Protocol : The use of asphyxiating poisonous, or other gases , and
bacteriological warfare in war is prohibited.
5. 1935
Italy uses sulfur mustard throughout its invasion of Federal Democratic Republic of
Ethiopia.
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6. 1937-1945
Japan uses a variety of poisonous gases in China
7. 1962-1971
The United States of America uses herbicides, including Agent Orange, and tear gas
in Vietnam.
8. 1980-1988
Iraq uses mustard gas and the nerve agent Tabun against Iranian forces.
9. 1988
Iraq uses a poisonous gas attack on its own city of Halabja, killing up to 5000 Kurds,
most of them being civilians.
10. 1992
Chemical Weapons Convention : It prohibits the development , production ,
stockpiling, transfer , or use of chemical weapons and requires signatures to destroy
chemical weapon stockpiles. OPCW (Organization for the Prohibition of Chemical
Weapons) is formed.
11. 1995
The Aum Shinrikyo doomsday cult launches an organophosphate nerve agent attack
in the subway of Tokyo.
12. 2012-2018
Chemical weapons repeatedly strike rebel-held areas throughout Syria’s war.
Major Gases Used During World War I
Tear Gas
The earliest military uses of chemicals throughout World War 1.
The French army was the first to employ tear gas, using 26 mm grenades filled with
tear gas (ethyl bromoacetate) , not even detected by the Germans.
Mustard gas
The most effective chemical agent of the First World War was sulfur mustard, known
as “mustard gas”. It is a volatile oily liquid, introduced as a vesicant (an agent that
causes blistering), by Germany in 1917.
It was also called the Yellow Cross because the Germans marked their shells yellow
for mustard gas.
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Symptoms included sore eyes, nausea, skin blisters, internal and external bleeding
and heavy exposure might lead to death.
Phosgene
It is a pulmonary agent and is also known as the Green Cross (phosgene and/or
diphosgene).
Green Cross is also a generic World War I German marking for artillery shells with
pulmonary agents (chemical payload affecting the lungs).
The tip of the projectile with the fuse end is painted green and a green cross at the
bottom of the cartridge.
It was first used on May 31, 1915 in a German offensive in Ypres. It contained a mixture
of chlorine and phosgene in the ratio 95:5.
Bromine based gases
Many bromine derived gases were used in World War I. Some of them are
bromoacetone (BA), bromobenzyl cyanide (Camite), bromomethyl ethyl ketone
(homomartonite, Bn-stoff), chloroacetone (Tonite, A-stoff), ethyl bromoacetate,
and/or xylyl bromide.
These bromine derivatives were also called The White Cross. White Cross was a
generic code name used by the German Army for artillery shells with an irritant
chemical payload.
It primarily affected the eyes and mucous membranes.
World War II
The Second World War did not see use of chemical agents in combat. There was use
of chemical agents by the German forces but not in war. In fact, the Nazis accidentally
discovered the toxic nerve agent, Sarin gas, and gas chambers (with hydrogen cyanide
based fumigant Zyklon B) were enormously used to mercilessly kill thousands of
Jewish people, but the propagation of such chemical warfare was not seen in the
battlefield. It is often speculated that such a decision on Hitler’s part had a link to his
own personal experiences in the Battles of Ypres of the First World War, where he had
been a soldier – however there has been no certain verification.
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Fig 3. Interior of a Holocaust gas chamber. The Prussian blue stains on the walls of the chamber
can be traced back to the use of hydrogen cyanide based Zyklon B.
[Source : https://i.pinimg.com/originals/cd/71/9f/cd719f9aa88215da23e5e7ad4b5aeb04.jpg ]
The use of chemical agents as destructive agents are, without a doubt, morally wrong.
But with the aim of outdoing each other, the fronts did extensive research and due to
that many beneficial characteristics of certain gases were also discovered, some of
them proving to be very useful even in the scientific field. Similar arguments can be
drawn with respect to nuclear and biological warfare too, but what remains the crux
of the issue is that the cost in each such case is huge: life. Not only is the contemporary
generation affected, some lethal chemicals have effects that may be passed on to future
generations. Although such weapons constitute essential war strategies, we can never
deny John F. Kennedy’s words, which hinted that if we do not abolish such weapons,
a day may come when these abolish the entire human race.
References:
[1] https://www.americanheritage.com/content/why-we-didn%E2%80%99t-use-
poison-gas-world-war-ii
[2] https://www.sciencehistory.org/distillations/magazine/a-brief-history-of-
chemical-war
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[3] https://owlcation.com/humanities/The-Gruesome-Military-Tactics-of-World-
War-I
[4] https://www.history.com/news/the-nazis-developed-sarin-gas-but-hitler-was-
afraid-to-use-it
Mr. Rajarshi Chanda is a 3rd year student of the UG Department of Life Sciences, Presidency
University. He has also completed DELF A1 in French from Alliance Française du Bengale.
Ms. Arunima Bhattacharya is a 3rd year student of M.Sc. in Biotechnology from St. Xavier's College,
Kolkata, and is the Editor-in-Chief of InquiScitive Journal. She has also completed DALF C1 in French
from Alliance Française du Bengale.
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MYSTERY MICROBES IN
SPACE SOURAJ BANERJEE
M.Sc. in Microbiology,
University of Calcutta,
35, Ballygunge Circular Road, Kolkata 700019, India.
Email: [email protected]
“Intelligence is the ability to adapt to change.”
—Stephen Hawking
The microbes, in the truest sense, can be considered highly intelligent if we follow the
words of this legendary physicist, for recent investigations have shown that they have
stepped into the shoes of an astronaut, shifting their niche from this chaotic earth to
the space! This cosmopolitan nature of such microbes has turned out to be a boon for
astronauts, providing a crucial tool in diagnosing astronaut illness as well as
functional in providing an insight into the investigation of life amidst the vastness of
the outer space.
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This revolutionary work of identifying the microbes aboard the International Space
Station, and tracing their lineage using several aspects of DNA sequencing strategies,
carried out by “Genes in Space-3” team, will continue to serve for long as an important
milestone in the ever expanding realm of space exploration along with that of
microbiology. The group led by NASA astronaut Peggy Whitson conducted the
experiment in the orbiting laboratory, while on earth it was investigated by a team of
scientists led by Sarah Wallace, NASA Microbiologist.
Whitson et al. collected the microorganisms from the orbiting space station by
exposing the petri dishes at several places throughout the entire laboratory,
transferring the bacterial colonies from the petri plates to miniature test tubes, a rare
event which paved the way for further research work yet to be carried out in the
microgravity. The next step taken was to amplify their genetic material using PCR and
isolating the DNA for downstream sequencing. The credit of conducting PCR for the
1st time in space goes to “Genes in Space-1” team, where they amplified DNA using
miniPCR thermal cycler followed by MinION device to carry out the DNA sequencing.
These two findings coupled together, successfully completed the characterization of
microbes found in the orbiting space station.
“These are very benign microbes and are commonly observed in human-occupied
areas and have been identified in samples returned from the ISS previously. Neither
of the two species are considered pathogens” quoted by Dan Huot, NASA
spokesperson, on identifying the microbes isolated from space as, Staphylococcus
capitis and Staphylococcus hominis.
This extraordinary piece of work, mastered almost single-handedly by NASA
astronauts, overcoming several barriers and adverse climatic conditions, will be
instrumental in serving the future course of space research, by securing the health of
astronauts against deadly pathogens and with knowledge of microbial diversity
across the vast galaxies, which is yet to be elucidated, will surely instil passion in the
young minds of budding scientists and would-be-researchers, to take up a challenging
role in unravelling the mysteries clinging to this vast universe.
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References:
[1] Sarah Lewin. (2018) Astronauts Identify Mystery Microbes in Space for the 1st time.
Space.com.
[2] Jenny Howard. (2017) Genes in Space-3 Successfully Identifies Unknown Microbes in
Space. International Space Station Program Science Office. Johnson Space Centre.
Mr. Souraj Banerjee has just completed his M.Sc. in Microbiology from University of Calcutta. He is
the Campus Ambassador of InquiScitive in CU.
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THE ‘BALANCING’ ACT NILANJAN DAS
M.Sc. in Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700 016, India.
Email: [email protected]
The Système international d’unités (S.I.)is the modern form of the metric system and has seven base units. They are usually defined by quantities that are fixed and invariant in nature. Often certain artefacts have been used to define the units of dimensions.
History is yet again the witness to a moment of transfiguration in Physics. It’s been 130 years since the kilogram (kg), the S.I. unit of mass, was defined by a lump of platinum in a vault in Paris, scientific democracy has prevailed over the old definition. The Conférence générale des poids et mesures (CGPM), the supreme authority of the International Bureau of Weights and Measures, in Versailles have unanimously voted for a change, and thus the global measure of mass will now be defined in terms of a fundamental constant of nature called the Plank’s constant.
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According to the director of the International Bureau of Weights and Measures, Prof. Martin Milton, the redefinition is a landmark moment in scientific progress.
Earlier, the kg was defined by the mass of the international prototype kilogram (IPK) or Le Grand K− a platinum alloy cylinder commissioned in 1889 − having a mass equal to the mass of 1 dm3 of water at 1 atm pressure and a temperature of 4°C.
The kilogram is one of the fundamental units of dimension in metrology and so it is a paramount consideration that the defining quantity is immutable itself, in order to stable foundation in Science. The weight of IPK was long known to fluctuate over time. The slightest abrasion can make it lighter, while air pollution can coat the surface and over time make it heavier.
The new system defines the S.I. unit of mass through the electrical force that is required to balance the weight of 1 kg on a machine called the Kibble balance. The electrical force itself is linked to the Planck constant (h) through quantum electric effects described by two Nobel Prize winners, Brian Josephson and Klaus von Klitzing. Planck’s constant is the quantum of action, which relates the energy carried by a photon to its frequency. The accepted redefinition of the constant h is exactly 6.62607015×10−34 kgm2s−1, thereby defining the kilogram in terms of the second and the meter. And since the meter is defined as a time fraction of the speed of light in vacuum, thus kilogram is defined in terms of the time only.
Fig 1. Kibble Balance: electromechanical instrument that measures the ‘electrical mass’ by producing
a balancing force equal to the strength of the electric current and voltage.
Some other S.I. base units has be redefined as a result of the vote. The units for electric current (ampere), temperature (kelvin) and amount of substance (mole) all become linked to invariant constants of nature, namely the electronic charge (e), the Boltzmann constant (kB) and the Avogadro number (NA) respectively.
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The unit of time, second (s), is now defined by taking the fixed numerical value of the unperturbed ground-state hyperfine transition frequency of caesium, ∆νCs = 9192631770 s–1.
Similarly, length unit metre (m), is now defined by taking the fixed numerical value of the speed of light in vacuum, c =299792458 m/s. The S.I. unit of electric current, ampere (A), is defined by taking the fixed numerical value of the elementary charge e to be 1.602176634 ×10–19 A s. The S.I. unit of temperature, kelvin (K), is defined by taking the fixed numerical value of the Boltzmann constant kB = 1.380649 × 10– 23 kg m2s–2K–1. The amount of substance, defined by mole, is exactly equal to Avogadro number of elementary entities, where NA = 6.02214076 × 1023 mol–1.
While the conference of Physicists make fundamental corrective changes in the System of International units, it would have zero impact on the way consumables are weighed at the market (and won’t reduce even a kg of your body weight!). It, however, links the physical quantities to constants woven into the fabric of the universe. The modified definitions has been effective from the World Metrology Day on 23rd March 2019.
References:
[1] Bureau International des Poids et Mesures: Information for users about the proposed revision of the SI https://www.bipm.org/utils/common/pdf/SI-statement.pdf
[2] https://en.wikipedia.org/wiki/2019_redefinition_of_SI_base_units [3] https://www.dailyo.in/technology/the-new-definition-of-kilogram-weight-
measurements-physics/story/1/27950.html
Mr. Nilanjan Das has just passed M.Sc. in Biotechnology from St. Xavier’s College (Autonomous),
Kolkata, and is currently working as a Research Observer on PCOS, at IPGME&R, Kolkata. His
Master’s Dissertation was on ovarian cancer metabolism. He is the Founder and Head of InquiScitive,
He is interested in wide range of subjects, from Biology to Psychology to national and international
politics.
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DREAMS DECODED NABHONIL CHATTERJI and TANNISHTHA DAS
2nd Year, M.Sc. in Biotechnology,
St. Xavier’s College (Autonomous),
30, Mother Teresa Sarani, Kolkata 700016, India.
Email: [email protected],
“For in dreams, we enter a world that is entirely our own. Let them swim in the deepest ocean and glide over the highest cloud.”
—Albus Dumbledore
(Harry Potter and the Prisoner of Azkaban, J.K. Rowling)
A dream is generally defined as a succession of images, ideas and emotions that the mind expresses in certain stages of sleep. Dreams typically involve elements from waking lives—known people or familiar locations—but often take on a fantastical feel. Dreams are frequently interesting, and can allow people to act out certain scenarios that would never be possible in real life. However, dreams are not expressed in a linear fashion. Instead, they are non-linear and chaotic, and do not always make much sense. Humans typically have multiple dreams per night that grow longer as sleep draws to a close.
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A number of hypotheses have been suggested in order to explain the neurobiological rationale behind the appearance of certain scenes in our dreams. One of them is the Activation Synthesis Model put forward by Hobson and McCarley, which believes that dreams do not essentially have any implications or meanings. Instead, they are thought of as mere electrical impulses, caused by the random misfiring of neurons that pull random images from our memory. They believed that our dreams are nothing, but cobbled attempts of our brain at making sense of them.
Another such theory is the Continual Activation Theory. It proposes that dreams occur as a result of continuous neural activation in the brain. This hypothesis believes that the primary function of sleep is the encoding and conversion of short term memories into long term memories by a process called consolidation. This theory is based on an underlying assumption that during REM sleep (discussed later), the unconscious part of the brain processes the procedural memory (implicit and long term memory, related to motor skills, frequently residing below the level of conscious awareness.) As the sensory inputs do not reach the brain, at this time, the activation in the conscious part of the brain decreases manifold, triggering a ‘continual activation’ mechanism generating a data stream that flows from the memory stores to the conscious part of the brain.
On the psychological front, Sigmund Freud, postulated that our dreams are a manifestation of our innermost desires or conflicts. He compartmentalized the content of our dreams into two parts, the manifest content which comprises the actual images and visuals seen in the dream, while the latent content represents the hidden psychological interpretation of the manifest content.
It is often said that while the conscious mind sleeps, the unconscious mind dreams. The research of the day serves to disprove any possible biological function of dreams, along with the possibility of dreams occurring as a result of random misfiring. Instead, dreams are simply assumed to be a result of ‘sleep thinking’, wherein the organized neural network within the brain functions to think, similar to the way it does when we are awake.
Our sleep cycle can be distinctly divided into two major parts; Rapid Eye Movement (REM) Sleep and Non Rapid Eye Movement (NREM) Sleep. The dreams that are usually recalled, on waking up, are usually associated with the REM stage of sleep. This is also indicated by an Electroencephalogram taken during REM sleep, which shows that brainwaves pattern during this time, are most similar to those obtained in the wakeful state of the person.
When a person begins to fall asleep, the serotonin levels in the body increase, resulting in the triggering of NREM sleep. There is a subsequent release of acetylcholine by the
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pons, which then travels towards the forebrain, causing cholinergic activation there, resulting in the synthesis of the apparently meaningless visual clips that appear in our dreams and thus resulting in the generation of REM sleep. During REM sleep, the two most active regions of the brain are the hippocampus and the amygdala, which are both parts of the limbic system. The hippocampus is responsible for the tuning of short term memories into long term ones while the amygdala is involved with fear and aggression, explaining the phenomenon called ‘nightmares’. Interestingly, dreamers are not aware of the fact that they are dreaming, while doing so and tend to become uncritical during dreams, accepting impossible events as though they are real. This can be attributed to the decreased activity of the prefrontal cortex (the region of the brain responsible for planning and logical reasoning) while dreaming. The cortex is responsible for the content of dreams. Since we are highly visual animals the visual cortex, right at the back of the brain, is especially active, but so are many other parts.
On the other hand, NREM sleep is associated with more static dreams and this stage of sleep is generated by neurons present in the preoptic region of the hypothalamus and the basal forebrain. The sharp contrast in the neurochemical patterns during REM and NREM sleep suggest that the representation of the dreaming self can be established as a function of the sleeping state. Dream data suggests the presence of at least two representative selves; the Aggressive self, characteristic of REM sleep and the Friendly self-characteristic of NREM sleep. However, the reason behind the dreaming mind creating two diametrically opposite selves, using contradictory behavioral strategies to combat a hostile situation, continues to leave researchers baffled.
Fig 1. Brain areas involved with long-term memory & emotion are highly active during REM
[Source: https://images.app.goo.gl/G6SotriUQbTdg7856]
It is said that every person dreams but not all of them can remember it the next day. It varies from person to person. Few remember the entire dream, some remember parts of it while others don’t remember dreaming at all. Norepinephrine, which aids
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in remembering is present in low levels during dreaming and so is the electrical activity in the prefrontal cortex which is associated with long-term memory. We have a better chance of remembering a dream if we wake straight out of it. A recent study showed that people who have more theta brain-wave activity in their prefrontal cortex after waking from REM sleep have a better chance of recalling a dream. It is also believed that alpha waves represent a wakeful period during sleep and has some role in consolidating dreams. A new study has discovered that heightened blood flow activity within certain regions of the brain could help explain why some people remember dreams better than others. In general, recalling a dream is thought to require intermittent wakefulness during the night for the vision to be incorporated in longer-term memory. But what causes some people to wake up more than others is not known yet.
Fig 2. Sleep stage and Dream Recall
[After Dement (1976); Source: https://images.app.goo.gl/rNdcKSzgzgDDB4eT9]
Dreams involving emotions and organized storyline are remembered more frequently. Nightmares and other vivid, emotional dreams are most likely to be retained and result in a greater arousal of brain and body and are therefore more likely to wake us up.
In addition to throwing light on the functions of hippocampal and neocortical circuits in the consolidation of episodic memory, and to the content of dreams, research also points towards intriguing possibilities about creativity and the generation of novel thoughts. One stage of consolidation possibly involves the integration of information with pre-existing knowledge and associating these with known realms. We dream when we become aware of these activated memories, which are usually discontinuous images and sounds coupled with motor activity.
Although accurate recall is mostly adaptive, there may be a positive side to a process that produces fragmentation—both in the wakeful state and during sleep. All new ideas are based upon previously acquired information. These patches of knowledge, are used to recall information about personal experience. If these bonds are weakened, this information may be recombined, either in the form of dreams or that of
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misremembered episodes and may even result in leading us down unusual paths towards creative insights and new ideas.
References: [1] https://www.semanticscholar.org/paper/The-brain-as-a-dream-state-generator%3A-
an-hypothesis-Hobson-McCarley/f1af886bfac2ee058ddaf1a6fb61dabe08e19b08 [2] https://www.scientificamerican.com/article/what-processes-in-the-brain-allow-you-to-
remember-dreams/ [3] https://www.semanticscholar.org/paper/Brain-reactivity-differentiates-subjects-with-
high-Eichenlaub-Bertrand/11eba66487396c69eba590a2e66437cc6120ce9f [4] https://www.medicalnewstoday.com/articles/284378.php [5] https://www.psychologytoday.com/us/basics/dreaming
Mr. Nabhonil Chatterji is a 2nd year student in the Postgraduate Department of Biotechnology, St.
Xavier's College (Autonomous), Kolkata. He is also the Secretary of the St. Xavier's College Science
Association and the Associate Chief Editor of InquiScitive.
Ms. Tannishtha Das is a 2nd year student in the Postgraduate Department of Biotechnology, St.
Xavier's College (Autonomous), Kolkata.
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