Behavioral patterns tell us more than we listen. Human reactions to situations and behavioral decisions affect their hormonal rhythms . A well known study in this regard, is the release of Testosterone in Chimpanzees under stress conditions.  Changing hormonal levels have a direct impact on metabolism and thus can trigger the onset off metabolic syndrome disorders.  If we react to a stressful situation aggressively, then a set of hormones are active; but if we react to the similar situation rather passively or by social manipulation an entirely different set of hormones are triggered. Hence how we behave decides our susceptibility to endocrine disorders. Observing behavioral patterns thus offers interesting opportunities to predict onset of various metabolic syndrome disorders such as Diabetes, Hypertension, Hypercholesterolemia and cardiovascular (CV) diseases. Precisely put, metabolic syndrome disorders find their roots in neuro-behavioural rather than dietary or metabolic origins . The neuro-behavioural origins hypothesis suggests that there should be detectable behavioural differences between people with and without metabolic syndrome disorders. Here we test whether the economic behaviour of individuals with any of the metabolic syndrome disorders differs from that of healthy age matched controls using the ultimatum bargaining game. 

To test the same, we selected a simple bargaining game that has been used extensively in economics and behavioural science, namely ultimatum game (Thaler, 1988). Ultimatum game was selected owing to its simplicity and a consistent demonstration that levels of certain hormones are associated with the behavioural outcome in the game (Emanuele et al, 2008). The ultimatum game is a two-player bargaining game. The two players are unknown to each other. One player (player 1) plays the role of allocator and the other player (player 2) plays the role of recipient. Player 1 is promised some money and is asked to divide it between himself and the other player. The rules stipulate that player 1 must make an offer, and player 2 can either accept the offer or reject it. If player 2 accepts the offer, player 1 receives the promised money and will have to give the offered fraction to player 2. If player 2 rejects the offer, none of them gets any money. The ultimatum game was played by 59 persons with at least one of the four metabolic syndrome disorders namely type 2 diabetes (T2D), hypertension, hypercholesterolemia and cardiovascular disease (MS group). The results were then compared to a healthy age matched control consisting of 71 persons. 

As expected, the MS group gave significantly lower ultimatum game offers than the control group. When tested for individual disorders, type 2 diabetics gave significantly lower offers than the non-diabetic group. In binary logistic regression, ultimatum game offer was a better predictor of MS and T2D than Body Mass Index (BMI). 

To conclude, there are detectable behavioural differences between individuals with metabolic syndrome disorders as compared to age matched healthy controls. The results are compatible with the neurobehavioral origins hypothesis and demonstrate further the association between metabolic states and social and economic behaviour. 

Find the whole research article here.

Press mention: 

https://timesofindia.indiatimes.com/city/pune/Behaviour-may-decide-proneness-to-diabetes-Study/articleshow/6193235.cms 

The association of σ factors with the RNA polymerase dictates the expression profile of a bacterial cell. Major changes to the transcription profile are achieved by the use of multiple factors that confer distinct promoter selectivity to the holoenzyme. The cellular concentration of a σ factor is regulated by diverse mechanisms involving transcription, translation and post-translational events. The number of σ factors varies substantially across bacteria. The diversity in the interactions between σ factors also varies- ranging from collaboration, competition or partial redundancy in some cellular or environmental contexts. These interactions can be rationalized by a mechanistic model referred to as the partitioning of σ space model of bacterial transcription. The structural similarity between different σ/anti-σ complexes despite poor sequence conservation and cellular localization reveals an elegant route to incorporate diverse regulatory mechanisms within a structurally conserved scaffold. These features are described here with a focus on σ/anti-σ complexes from Mycobacterium tuberculosis. In particular, we discuss recent data on the conditional regulation of σ/anti-σ factor interactions. Specific stages of M. tuberculosis infection, such as the latent phase, as well as the remarkable adaptability of this pathogen to diverse environmental conditions, can be rationalized by the synchronized action of different factors.

Read more at Biomolecular Forms and Functions 

Mycobacterium tuberculosis encounters diverse host microenvironments including acidification of phagosomes, nitrogen intermediates, reactive oxygen species, nutrient starvation, DNA damage, phosphate deprivation and hypoxia (Stallings and Glickman, 2010).  Extracytoplasmic Function (ECF) σ factors, that are non-essential and stress inducible, contribute significantly to bacterial survival alongside one- and two-component systems (Helmann, 2002).  M. tuberculosis has ten ECF σ factors- of which four are localized in an inactive complex with membrane associated anti-σ factors (Rodrigue et al, 2006; Sachdeva et al, 2009).  The membrane associated anti-σ factors (RsdA, RsmA, RskA and RslA in M. tuberculosis) share a common structural organization comprising of an extra-cytoplasmic domain that is a receptor for environmental stress connected to the cytoplasmic anti-σ domain by a single trans-membrane helix (Figure 3.1).  The stress-induced release of an ECF σ factor from the σ/anti-σ factor complex governs the intra-cellular levels of these transcription initiation factors and thereby the expression of their cognate regulons.  The relative cellular abundance of different σ factors dictates the expression profile- best described by a mechanistic model referred to as the partitioning of σ factor space (Gruber and Gross, 2003).  Indeed, the number of different σ factors is correlated with the diversity of environmental conditions encountered by the bacterium (Gruber and Gross, 2003).  

The intracellular release of an ECF σ factor from the inactive membrane-associated σ/anti-σ complex is governed by a proteolytic cascade referred to as the Regulated Intra-membrane Proteolysis (RIP) pathway (Heinrich and Wiegert, 2009).  This cascade is initiated by the action of a so-called site-1 protease that acts on the extracytoplasmic domain of the anti-σ factor (Heinrich and Wiegert, 2009).  This triggers the activity of a trans-membrane protease (site-2 protease) that dissociates the σ/anti-σ complex from the membrane.  The anti-σ factor is then degraded by energy-dependent proteolytic complexes to release the bound ECF σ factor that can associate with the RNA polymerase and initiate transcription (Figure 3.1A).  The specific intracellular proteolysis of the anti-σ factor is primarily governed by ClpXP in Escherichia coli, although other proteolytic assemblies also contribute to this process (Chaba et al, 2007).  The specific degradation of E. coli RseA from the σE/RseA complex is also influenced by an adaptor protein, SspB (Flynn et al, 2004).  E. coli SspB mediated interactions are specific and crucial for effective degron recognition- while E. coli ClpX interacts with residues 9-11 at the C terminus of the ssrA degron, SspB interacts with residues 1-4 and 7 (Flynn et al, 2001).  Other E. coli ClpX adaptors that have been characterized are RssB and UmuD (Dougan et al, 2002; Neher et al, 2003).  The presence of different adaptors suggested a mechanism for the specific recruitment of diverse substrates for the ClpX unfoldase to initiate targeted degradation along with the serine protease ClpP in the ClpXP proteolytic complex (Dougan et al, 2002).  

ClpX comprises of a small N-terminal domain flexibly attached to the unfoldase module consisting of a small and large AAA+ domain (Miller and Enemark, 2016).  The AAA+ domains have multiple conserved sequence features including Walker A and Walker B motifs for ATP binding, a second region of homology (SRH) segment involved in ATP hydrolysis and sensor 2 and 3 residues that propagate conformational changes upon ATP hydrolysis to stabilize the ATP binding conformation of the unfoldase (Miller and Enemark, 2016; Wojtyra et al, 2003; Donaldson et al, 2003; Glynn et al, 2009, Hanson and Whiteheart, 2005).  The orientation of the large and small AAA+ domains varies considerably in the hexameric ClpX ring (Glynn et al, 2009).  With the two domains functioning in a concerted manner, ClpX can translocate and unfold a diverse range of substrates (Flynn et al, 2003).  Analysis of E. coli ClpX substrates suggested five distinct degron motifs (Flynn et al, 2003).  Apart from adaptor proteins that enforce specificity, the N-terminal domain of E. coli ClpX is also involved in substrate recognition (Wojtyra et al, 2003).  The role of the ClpX N-terminal domain, however, differs across substrates.  While the N-terminal domain substantially influences E. coli ClpX action on substrates like λO and MuA, it is much less so for Green Fluorescent Protein (GFP) substrates with a small stable RNA gene A (ssrA) degron (Wojtyra et al, 2003).  

The M. tuberculosis RIP pathway is only partially characterised.  The site-1 protease that initiates the proteolytic cascade in the RIP pathway has not been identified in M. tuberculosis.  The site-2 protease Rip1 (Rv2869c) acts on all membrane associated anti-σ factors (RskA, RsmA, RslA and RsdA) (Sklar et al, 2010; Schneider et al, 2014).  For comparison, in E. coli, the first two proteolytic steps are performed by DegS and YaeL (Alba et al, 2002; Kanehara et al, 2002).  However, straightforward extension from the E. coli model for the subsequent steps is difficult as there are four membrane-associated σ/anti-σ complexes in M. tuberculosis (σD/RsdA, σK/RskA, σL/RslA and σM/RsmA) as opposed to one (σE/RseA) in E. coli (Figure 3.4A).  The cytosolic step of the cascade involving intracellular proteolytic complexes is also substantially different in M. tuberculosis than either E. coli or B. subtilis (Flynn et al, 2003; Heinrich et al, 2009).  For example, M. tuberculosis has two ClpP protease components- ClpP1 and ClpP2 (Raju et al, 2012).  Furthermore, targeted protein degradation in E. coli by the ClpXP complex is achieved by specific interactions conferred by adaptor proteins between the substrate with an accessible degron and ClpX.  Unlike E. coli, no SspB homologue or adaptor of M. tuberculosis ClpX has been annotated or experimentally identified thus far.  Nonetheless, previous studies revealed that the cytoplasmic domain of RsdA was recognised and cleaved by the M. tuberculosis ClpXP2P1 complex (Jaiswal et al, 2013).  The degron in M. tuberculosis RsdA is VAA, identical to that in E. coli RseA.  RslA, however, was found to be resistant to ClpXP2P1 degradation, despite having the ssrA-like degron (Jaiswal et al, 2013).  Another aspect that can modulate the cellular abundance of ECF σ factors is the diversity in release mechanisms of the ECF σ from an inactive σ/anti-σ complex.  For example, M. tuberculosis RslA was shown to release σL under oxidative stress conditions (Thakur et al, 2010).  In this case, the receptor for the redox stimulus was the Zinc binding CXXC motif in the anti-σ factor, RslA.  M. tuberculosis RskA also was shown to dissociate under reducing conditions from σK; the redox sensor in this case, however, is the σ factor σK (Shukla et al, 2014).  

In the regulated proteolytic cascade, the targeted proteolysis of an anti-σ factor by the ClpXP proteolytic complex is the last step in signal transduction to effect changes in gene expression in response to environmental stress.  The cytosolic domains of four M. tuberculosis anti-σ factors with the ssrA-like degron provided a set of natural variants to understand the basis for substrate selection in M. tuberculosis ClpX.  We note that while the N-terminal domain of ClpX is not involved in degron recognition, it influences the unfoldase activity.  We also describe biochemical experiments which reveal that the degron sequence governs both- the substrate binding affinity as well as the kinetics of unfolding.  The variation in the dwell time of the substrate on ClpX was also seen to have a direct bearing on the proteolytic degradation of the anti-σ substrates by the ClpXP2P1 complex to release free ECF σ factors that can initiate transcription.  In effect, M. tuberculosis ClpX translates variation in the degron sequence into differential unfoldase activity.  These degron-dependent differences in last step in the M. tuberculosis RIP cascade are thus likely to provide an additional regulatory layer for nuanced changes in the transcriptional profile in response to a stress stimulus.  

Find the whole research article here.

Tuberculosis kills around 1.5 million people in the world every year and is caused by the bacteria Mycobacterium tuberculosis.  Although TB is curable, rise of multidrug-resistant (MDR) and extremely drug-resistant (XDR) strains of Mycobacterium tuberculosis (Mtb) pose a serious health threat.  Current drug regimens are longer, costlier, have hazardous side effects and lower prospects of treatment success.  Thus, for the effective treatment of MDR and XDR TB there is an urgency to not only develop new drugs but also better treatment regimens- combination therapy. 

Mtb is an obligate aerobe that depends vitally on the Electron Transport chain (ETC) to produce energy via oxidative phosphorylation.  Energy metabolism lies at the crux of Mtb infection, highlighting the importance of the enzymes in the ETC.  Bedaquline (BDQ) a drug against ATP synthase (complex IV ETC) is one of the only novel drugs approved by the FDA in the last 40 years.  Other drugs like Q203 and Clofazimine (Cfz) targeted towards the cytochrome bc1 oxidase (complex III ETC) and NADH dehydrogenase (ETC enzyme NADH2) respectively are currently under development.  Recent studies, however, demonstrate the ability of Mtb to undergo metabolic remodelling in response to BDQ.  It has also been seen that the inactivation of either of the two terminal oxidases of the ETC, cytochrome bc1 and cytochrome bd has a synergistic effect on the action of BDQ.  Moreover, the metabolic response of Mtb to Q203 and Cfz are still not well characterised.  

Mtb Cytochrome bd oxidase plays a crucial in energy homeostasis and enhances resistance to oxidative and nitrosative stress inside the host.  Cytochrome bd oxidase is also shown to influence the potency of cytochrome bc1-aa3 inhibitors.  However, our understanding of the metabolic function and role of this oxidase remains incomplete.  Thus, our aim is to biochemically and biophysically characterise Mtb cytochrome bd oxidase.  These studies would prove essential to improve novel inhibitors that are currently being developed for cytochrome bd oxidase.  In depth analysis of the protein-drug interaction through structural studies would aid in the design and improvement of these drugs.  

The coronavirus pandemic of 2020 started unusually slowly but has now infected 5 million people worldwide and accounted for more than 300 thousand deaths. The outbreak of the coronavirus disease (COVID-19) originally started in Wuhan, China in late 2019 and increasingly spread to Europe and across the globe by February this year. What was more surprising was the alarming rate at which this viral infection was contagious and the increased number of asymptomatic carriers. This not only made it difficult for the health care personnel to identify positively infected people but also for the government trying to curb down these ever-increasing numbers. Today the healthcare systems are under enormous pressure delaying regular healthcare for people with different illnesses such as tuberculosis (TB) making the situations in nursing homes worrisome. The entire world has stood together to come up with strategies to fight against this disease and is collaborating across borders. While we will come up with new vaccines and medicines for the novel coronavirus and win this war it is important to address the impacts of this crisis on the health care systems in the post-pandemic world, especially in countries with high TB burden. 

Read more on the blog. 

“Water is scarce, and climate is changing. Forests are fast depleting; granaries are empty, and industries are shutting down! Kautilya has called upon his fellow ministers Parashar, Varahamihira and Bharadwaj for an emergency meeting. If right actions are not taken, it is game over for all of us. Will their decisions and policies be able to keep India draught free and restore the balance?” Welcome to the world of “Meghdoot””, a novel monsoon strategy board game.

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A hundred thousand years ago the world was a very different place. Civilisations flourished and gave rise to traditions, cultures and distinct lifestyles. Today years later, we find ourselves, the modernised versions surrounded by new avenues of science and technology. Mankind has benefitted immensely due to the advances in science and has been gifted a comfortable lifestyle. But is this very comfort pushing us towards uncertain boundaries? Lately, several lifestyle related disorders like Cancer, Diabetes, Alzheimers, Hypertension, Cardiac disease etc are resurfacing. Cancer especially is a serious concern because of its high fatality rates and ever-increasing incidence. But is Cancer really the disease of the modern world, was it prevalent in ancient times and can a perfectly balanced lifestyle still encounter this devil?

The first ever mentions of Cancer can be found in ancient Indian books on Ayurveda dating back to 2nd millennium BCE. References to Cancer can be found in both, Charaka sanhita and the Sushruta nidansthana. It is exciting to notice how accurately are they mentioned alongside their types, prognosis, and various cures and surgical protocols. Charaka described cancer as a growing lump or mass, called ‘Arbuda’ caused due to imbalance in doshas (Vatta, Pitta and Kapha). He classified Arbuda (tumours) into two categories: Saumya (benign) and Ghataka (malignant). According to the descriptions in Sushruta nidansthana, cancer is a gradually increasing mass of definite size, is globular in shape, deep rooted in structure and usually does not suppurate. Arbudas (tumours) are generally painful and can occur in any part of the body. Arbuda can involve ‘mansa’ and ‘rakta’ caused by a disparity in the tridoshas (Vatta, Pitta and Kapha).

Following are the excerpts from Charaka sanhita and the Sushruta nidansthana:

‘Arbuda’ is defined as Aram-sheeghram- (which is fast) bundati-gyapayati- (appearing) mansochhrayam- (originating in flesh)-swarupam-gatrapradeshe- (in body)-sammurchhitai-doshairrmansasruk- pradushanad- (formed due to imbalanced blood and flesh); yat-tad-arbudam (is termed as arbudam).

Urbundara nishamne, mulvibhujadeeh, prushodaradisch yadva arbati-gachhati gatrapradeshe-kutrapi-yad arb gatau (one which has a pervading , omnipresent/potent deep seated root in the  body) - Udach; yadva-arbudgirisadrusham (raised like a mountain)  vruttakaram sthiram mahad analpmulam (rounded, immobile, large, deeply spreaded root) cha yattjayate-tatsadrushyad idamapi.

Gatra pradeshe kwachidev doshaha

Sammurchhita mansamasruk pradushva.

Vruttam sthiram mandrujam

Mahantamanalpmulam chirvruddhvapakam

Kurvanti mansocchravamatyagaadham

Tadarbudam shastravido vadanti. [Su.Ni. 11]

meaning;

Due to the vitiation of flesh and blood by imbalanced and aggravated doshas (Vatta, Pitta and Kapha) a large vegetation of flesh appears at any part of the body which becomes rounded, immovable, slightly painful and has its root considerable deep in the flesh (affected part). This growth is termed is ‘Arbuda’ by the learned physicians.

Rogaschotsedh samanyaadhimansarbudadayaha [Ch]

meaning;

Arbuda (tumour) is a disease wherein swelling (utsedh) is a common feature.

Types of Arbuda:

Arbudas have been described to be of six types based on the origin of the imbalanced doshas and vitiation of blood, flesh and fat. Of the six, the mansa and rakta belong to the Ghatak (malignant) category and are considered incurable (asadhya). The rest of them are Saumya (benign) and curable. These are slow growing (cheervruddhi) and do not metastasize (aprasaranshil) [Ch.Chi.12]. 

Doshaha pradusto rudhiram shirastu

sampidya sankochya gatastu pakam

Sasraavamannuhyati manspindam

Mansankurrairachittamaashuvruddhim

Sravatyajasram rudhiram

pradustamasadhyametadrudhiratmak syat

Raktakshayopdravpeedittvaat

Pandurbhavetpeeditastu. [Su.Ni. 11]

meaning;

Imbalanced doshas contract and compress the vessels (sira) and blood (rudhir) of affected part, raise a slightly suppurated (paakam) exuding tumour covered with small warts and fleshy tubercules and is called as Raktarbuda. This tumour is rapidly growing, exuding constant flow of vititated blood. It is considered incurable (asashya) due to its origin in blood. The patient looks pale and yellow because of disturbance and depletive actions due to haemorrhage.

Mushtipraharadibhiradite ange

Mansapradustam prakaroti shofam

Avedanam snigdhamananyavarnam

Apakamashmopmamaprachalyam

Pradustmanasasyu narasya

Baaddhmetanbhavenmans parayansya.

Mansarbudam tvetadasadhyamuktam.

Meaning;

When the flesh of any body part gets vitiated due to an external force it gives rie to swelling (shofam) and is called as Mansarbuda. It is painless, glossy, of same colour as the surrounding and is non-supporting, stony hard and immobile. If such a tumour appears in a person addicted to meat diet (mansparayan), the tumour (mansarbud) gets deep seated and is incurable.

While the above excerpts are just a sneak peek of the vast knowledge of Cancer in ancient literature, it goes without saying that Cancer is as old as man himself. Despite the changes in lifestyle, food habits, and exposure to carcinogens, it’s a disease that prevails. It was there before when there were seemingly less carcinogens, exercise was in the routine and fresh, organic food was a norm. With all the challenges of the new lifestyle of today, its incidence just rises. Even if we believe we practice a perfectly well-balanced lifestyle, cancer occurrence cannot be denied. With each passing day as cancer research advances and we come closer to winning this battle, acceptance and awareness stay the prime tools for an effective cure. Afterall, a stitch in time, saves nine!

All the above Sanskrit verses and their translations have been retrieved from- The truth about Cancer (http://cancerfundamentaltruth.in/index.htm).

-Dr. Anuja Joshi

The above article is in collaboration with Dr. Sharada Umarani (Onco-Physiotherapist, Pune, Maharashtra). Please visit https://www.instagram.com/p/CBI842Mjc7q/?igshid=1ptip08wbxi8m  for more information on cancer awareness. 

2011 World cup finals…Dhoni…. executes his favorite scoop-helicopter shot to hit a six and India wins the World cup!... and celebrations begin on ground. I am sure those moments are etched on your heart as they are on mine. While we can’t forget the crucial innings played by Dhoni on that battleground, we all remember the essential and important contribution each player made towards that historic win. If we zoom out successively, we can even say that the beginning of that win started at the exit of 2007 world-cup loss. While Dhoni was the end effect hitting six on that day, every bit of the net practice, fitness regime, diet and discipline that the whole team of 15 and support staff followed throughout were behind the success. Let us remember that 3 players out of those 15 did not even play that final game, but their availability was equally crucial in our win. Now you will wonder, why am I reminding you of that wonderful memory from ‘C’ricket even though out topic today is ‘C’ancer and ‘C’limate change. The reason is that there is a lot more in-common between Cricket, Cancer and Climate change than we ‘C’.  We can only win as a team and only after sustained efforts!

 Let us for a moment consider the problem of Climate Change. The apparent symptoms that we all observe are that the temperatures are getting warmer as a whole, there is a rise in the number of extreme weather events, sea level is rising and glaciers are melting at high rate to name a few. But fundamentally, it is due to the imbalance in the equilibrium of our mother earth. In this sense, we can think of the mountains, glaciers, earth’s atmosphere and oceans all as different organs of our earth.  Life is sustained on earth only on  account of a delicate balance amongst these different organs. Our artificial interventions, such as emission of carbon-dioxide at an unprecedented rate, change the composition of the earth system and introduce a small imbalance. The nature of this imbalance is such that it grows rapidly and uncontrollably to ultimately manifest into those worrisome symptoms we all talk about. I am sure you all by now figured that this is in-fact is a  very similar story to the way cancer attacks our body. 

The common thread is that an apparently small imbalance in terms of misbehaving cells grows on to multiply rapidly to ultimately culminate into a problem. Furthermore, both our body and our earth, are so complex systems with a fine balance in their functioning that an early detection of the problem is a tricky business. And when we detect it, treating the problem locally in isolation is even a bigger challenge!

What did we do when Indian cricket coach Greg Chapel was introducing an imbalance in the Indian cricket team during 2005-2006? In the whole drama, Saurav Ganguly was the face of the conflict and suffered the most. He even lost his place in the team for a short while. Ultimately, the team collectively raised a voice to throw Greg Chapel out. They carefully eliminated the habits which were hurting the team-spirit…and there began the march towards an ultimate world-cup win in 2011. Bingo!! There you go…there lies the key to solving the problem of Cancer or  Climate Change. 

The irony is that a sole person suffers in cancer or only a certain community on the island or a river-delta faces the grave consequences of the sea-level rise through climate change. But the cause lies in our collective unsustainable habits. In case of cancer, they could be carcinogens we inhale through air, we unknowingly intake through food or through our leisurely habits such as chewing tobacco. In case of Climate Change, the habits could be our leisurely air travels, coal based carbon-dioxide emitting energy generation or pollution though vehicles. It is rare that we recognize that these problems need to be sorted out at the community / country level. 

We as a community need to seek for strict policies and should make their implementation our top priority. We need to be aware that the unsustainable habits and their consequences in terms of Cancer or Climate Change are tightly linked. We need to talk to each other about these problems and educate ourselves on the possible solutions. The solutions could be uncompromising policy about the emissions of carcinogens in our environments, in our food or stricter taxes on well-known products such as tobacco. Or for climate change they could be, a quicker transition to renewable energy sources, adherence to stricter pollution norms or mindful change in our policy towards reduce, reuse and recycle. Such a change could be our magic moment and a beginning of a future victory over these problems. 

Individual awareness and collective action needs to be our mantra!

We know we all can do it. Take the example of our Aussie friends. As they carved out an almost invincible cricket team during 1990-2000’s so did they chalk out a rock-solid plan to fight skin cancer. When it was scientifically established that skin cancer is caused by the action of excess UV rays that escape through rarified ozone layer, Aussies studied it carefully to form a “Cancer Council”. On one hand they designed public campaigns to make a common Aussie aware about this and implemented stricter policies, but on the other, they raised a global movement to reduce the emission of harmful CFC’s that cause ozone hole. Kudos to the efforts of the Aussies in significant reduction of Skin cancer and ours globally in reducing the ozone hole. As Aussies can do it so can we all after sustained efforts as a community!

-Dr. Vishal Dixit

(Edited by Dr. Anuja Joshi)

The above article is in collaboration with Dr. Vishal Dixit (Assistant Professor, Interdisciplinary Program in Climate Studies, IIT Bombay, India)  and Dr. Sharada Umarani (Onco-Physiotherapist, Pune, Maharashtra). Please visit https://www.instagram.com/p/CBI842Mjc7q/?igshid=1ptip08wbxi8m  for more information on cancer awareness.