Tag: microbiology

200+ Papers by Annamalai Univ Scientists Contain Plagiarism, Manipulation

Multiple researchers in the country, from obscure to prominent, are regularly caught plagiarising.

At least 200 academic papers published by researchers at Annamalai University, in Chidambaram, Tamil Nadu, contain plagiarised text, manipulated images and fudged data – all pointing to research misconduct and, potentially, fraud. The list of offending papers includes at least 14 in which the university’s incumbent vice-chancellor, Velayutham Murugesan, is also an author.

The finding is courtesy Elisabeth Bik, a science integrity consultant who regularly scans the scientific literature for signs of misconduct and manipulation, and publishes the results on Twitter. Bik is by training a microbiologist. She wrote in a blog post, published on November 5, that she spent nearly three months examining these papers as well as that she has alerted the editors of nearly 150 journals in which these papers had appeared.

The Wire reached out to the VC for comment but received no response. K. VijayRaghavan, the principal scientific adviser to the Government of India, said in a tweet that he’d follow up (Bik had clarified in her post that its contents were only “her opinions”). VijayRaghavan elaborated on his comment to The Print, saying he’d bring the matter to the notice of the university’s “chancellor and funding agencies”.

“In this particular case at Annamalai, the research misconduct was very widespread, and also appear to have affected the current vice-chancellor, who is ultimately responsible for research conducted at his university,” Bik wrote in her post. She also said she had “little hope” vis-à-vis accountability considering the VC himself was implicated.

Text plagiarism is the easiest to spot, using comparative analysis. Image manipulation is a more labour-intensive process, as Bik’s own Twitter feed suggests: she regularly posts images containing repetitively copy-pasted elements and asks her followers if they can spot them.

In some of the papers in which the VC, Murugesan, is an author, Bik found multiple instances where the same image had been used in different papers discussing different experimental results. She also reported manipulation within a single image, where a pattern that shouldn’t have repeated was in fact repeated.

On the data front, she found researchers – i.e. the authors of the problem papers – had reached “highly unusual” conclusions. For example, in one of them that included analysis of standard deviations, she found that nearly all the deviations came to 7.5% of the (statistical) mean. “Such a narrow range of SDs is highly unusual in biological measurements,” Bik wrote.

Multiple researchers in the country, from obscure to prominent, are regularly caught plagiarising. One of the more common reasons this happens is that research institutions and universities had enforced a ‘publish or perish’ paradigm, in which academics are required to publish papers in order to qualify for promotions, etc., for a long time without excluding those who hadn’t signed up for research – but had for teaching, e.g. As a result, desperate academics resorted to publishing anything at all, aided by a crop of journals prepared to publish anything in exchange for a not insubstantial fee.

However, this can’t be an excuse for research misconduct, and many eminent scientists have expressed concern that a lack of proper sanctions against such practices has cultivated numerous mediocre scientists who pass on their lax attitude to their students as well. For example, as Pushpa Mitra Bhargava told The Wire after The Wire reported that Appa Rao Podile, the former VC of Hyderabad University, had admitted to plagiarising text in his papers:

Because of the low standard of our scientists, they are unable to produce research output of any originality. Plagiarism then becomes an easy route to be recognised. The situation is made worse by the absence of proper penalties for plagiarism. As regards the VCs, they are also derived from the same pool of mediocrity.

Indeed, apart from Appa Rao, other prominent researchers who have plagiarised in their papers include former Pondicherry University VC Chandra Krishnamurthy, former Kumaon University VC B.S. Rajput, former Delhi University VC Deepak Pental, Bharat Ratna recipient C.N.R. Rao, director of IISER Thiruvananthapuram V. Ramakrishnan, and a clutch of researchers recently appointed to Jawaharlal Nehru University. Earlier this year, the research output of some important labs around the country were called into question after journalists and investigators uncovered evidence of image manipulation in nearly 200 papers.

Pushkar, director of the International Centre Goa, wrote in The Wire in June 2015, that “plagiarism was not considered, at least until quite recently, as something wrong”. The University Grants Commission (UGC) approved the country’s first formal ruleset to fight plagiarism among researchers only in late 2018. Further, the UGC invited proposals in May this year to undertake a qualitative scrutiny of PhD theses published in India; plagiarism is expected to top the list of problems.

Sewage Surveillance is the Next Frontier in the Fight Against Polio

Polio can be circulating through a community long before anyone is paralysed. Monitoring sewage for the virus lets public health officials short-circuit this ‘silent transmission’.

The world is at the brink of eradicating polio. Only three countries now have ongoing transmission: Nigeria, Afghanistan and Pakistan. And in 2017, there were only a couple dozen cases of paralytic wild polio reported worldwide – a massive decrease from the estimated 350,000 cases reported across 125 countries in 1988. Development of the polio vaccine and global vaccination efforts are at the heart of this monumental public health achievement.

Epidemiologists typically detect polio transmission based on reported cases of acute flaccid paralysis (AFP). The World Health Organisation certifies a country as polio-free if there are no reports of AFP for three years. But AFP is a severe outcome that occurs in a very small fraction of polio infections. It’s just the tip of the iceberg – one case of AFP indicates substantial underlying polio transmission in a population.

This is why now, as the world approaches the final stages of polio eradication, environmental surveillance becomes key. Looking for poliovirus in sewage is more sensitive than counting up cases of AFP. It can detect virus shed in the faeces of non-paralysed people infected with polio – what epidemiologists call the silent circulation of polio.

Also watch: Does India Have the Funds to Run the World’s Largest Healthcare Scheme?

Environmental microbiologists have studied pathogens in sewage for decades, but its use as a public health surveillance tool is relatively new. As epidemiologists who specialise in modelling the spread of disease, we wondered if we could estimate the intensity of infection in a population by analysing counts of virus in its sewage. The discovery of polio transmission in Israel in 2013 – the first in that country since 1988 – provided a way for us to test whether our model, coupled with environmental surveillance data from different parts of the world, could be used to assess how much silent transmission is still happening globally.

Characterising a polio outbreak in Israel

Given all the progress made toward polio eradication, it was disturbing to realise polio was actively being transmitted in Israel in 2013. A sewage surveillance system – set up in 1989 by the Israeli health department to detect poliovirus – sounded the alarm. The Ministry of Health worked quickly to vaccinate the public, and fortunately none of the infections resulted in paralysis.

To track polio in human waste in Israel, samples are automatically collected from sewage trunk lines and treatment plants approximately weekly. Back at the country’s Central Virology Laboratory, they’re checked for poliovirus.

Most of the positive sewage samples during the 2013 outbreak came from the Negev region of Israel, and most of those from predominantly Bedouin communities. Based on molecular characteristics of the virus isolated from the sewage, scientists know that the virus originated in Pakistan, then traveled into the region, diverging into Egypt, Israel and Syria. For a virus, even tightly guarded geopolitical borders are fluid.

To understand what kept the polio transmission going, we needed to better characterise Bedouin movement patterns. Where people travel provides pathways for them to potentially spread the virus. For example, larger Jewish communities such as Beer Sheva are economic hubs; Bedouins from communities throughout the region travel there daily. In addition, many communities send children to regional schools, another potential hub of transmission.

Poor sanitary conditions provide an important route for the poliovirus to move from host to host – remember, infected people excrete viable virus in their faeces. Epidemiologists knew surprisingly little about the water and sanitation infrastructure of these Bedouin communities, beyond that they were highly variable and often poor compared to nearby Jewish communities.

Also read: With Over 20 Cases of Zika in Jaipur, Health Ministry Begins Monitoring

Creating a model for how polio spread

The Central Virology Laboratory and Ministry of Health recognised the potential in their data, but no one had developed a theory to convert environmental surveillance into public health metrics. Because of our experience in modelling environmentally transmitted infectious diseases, we met with Central Virology Laboratory and Ministry of Health officials on the ground during the later stages of the epidemic and began collaborating on a new approach to the problem.

A mathematical model allows epidemiologists to use what we know about a situation’s underlying biological mechanisms to better interpret or extract more information from data. We knew a number of things in this case: the relative levels of poliovirus in various communities’ sewage over time, the coverage of the vaccination campaigns, and the differences in transmission between the wild virus and the attenuated vaccine virus. Our goal was to come up with a model that would explain how the disease was transmitted through the population in Israel that would match the observed changes in sewage polio levels over time.

Using new analytical methods, we estimated that in Rahat, the largest predominantly Bedouin community that sustained significant transmission, 56% of the at-risk population – primarily children under 10 – was infected.

Positive polio samples from the environment only alert public health officials that transmission is happening. Our model provides additional information about how many people were infected. Without a model, researchers would have no way of estimating the extent of the outbreak – the poliovirus in the sewage could have been collected from many people shedding a little or a few people shedding a lot. But because outbreaks follow recognisable patterns, the dynamic changes in polio concentration can actually tell us a lot about how the disease is moving through the population.

There is always uncertainty in model predictions, so corroboration with multiple data sources is important. In this outbreak, we were able to compare to crude estimates of infection based on community stool samples.

Monitoring environment for silent transmission

As we approach the final stages of polio eradication, environmental measures will become the only feasible way to detect polio transmission. And this silent spread of the virus must be halted to fully eradicate the disease. Waiting until there’s a paralytic case means there’s a lot of polio around and containing it with vaccination efforts becomes more difficult.

 Environmental surveillance efforts are growing in all three polio-endemic countries. Indeed, since the success seen in Israel in identifying and quickly containing transmission by administering oral polio vaccine, many countries have begun to implement polio environmental surveillance. WHO is working toward developing organised environmental surveillance standards akin to the well-established standards for acute flaccid paralysis.

Beyond polio, environmental surveillance can and should be extended to other infectious diseases shed into sewage – enteroviruses, typhoid and cholera are prime candidates. Epidemiologists can then use modelling approaches to translate surveillance data to describe population patterns, allowing public health officials to respond rapidly to outbreaks.The Conversation

Marisa Eisenberg, Associate Professor of Complex Systems, Epidemiology, and Mathematics, University of Michigan; Andrew Brouwer, Research Investigator in Epidemiology, University of Michigan, and Joseph Eisenberg, Professor and Chair of Epidemiology, University of Michigan

This article was originally published on The Conversation . Read the original article.

I, Holobiont. Are You and Your Microbes a Community or a Single Entity?

Scientists have discovered more and more plants and animals that are accompanied by a jostling menagerie of internal and external fellow-travellers and a species called holobiont, a unique combination of a host, plus all of the resident microbes that live in it and on it.

Cicadas might be a pest, but they’re special in a few respects. For one, these droning insects have a habit of emerging after a prime number of years (7, 13, or 17). They also feed exclusively on plant sap, which is strikingly low in nutrients. To make up for this deficiency, cicadas depend on two different strains of bacteria that they keep cloistered within special cells, and that provide them with additional amino acids. All three partners – the cicadas and the two types of microbes – have evolved in concert, and none could survive on its own.

These organisms together make up what’s known as a holobiont: a combination of a host, plus all of the resident microbes that live in it and on it. The concept has taken off within biology in the past ten years, as we’ve discovered more and more plants and animals that are accompanied by a jostling menagerie of internal and external fellow-travellers. Some of the microorganisms kill each other with toxins, while others leak or release enzymes and nutrients to the benefit of their neighbours. As they compete for space and food, cohabiting microbes have been found to affect the nutrition, development, immune system and behaviour of their hosts. The hosts, for their part, can often manipulate their resident microbiota in many ways, usually via the immune system.

You yourself are swarming with bacteria, archaea, protists and viruses, and might even be carrying larger organisms such as worms and fungi as well. So are you a holobiont, or are you just part of one? Are you a multispecies entity, made up of some human bits and some microbial bits – or are you just the human bits, with an admittedly fuzzy boundary between yourself and your tiny companions? The future direction of medical science could very well hinge on the answer.

The American evolutionary theorist Lynn Margulis, who popularised the theory of symbiosis, first coined the term ‘holobiont’ in 1991. She was interested in long-term, tightly integrated associations such as those evident in lichens – the crusty-looking growths found on rocks and trees, made up of fungus conjoined with algae. Margulis thought that there was a tight analogy between an egg and a sperm coming together to form a new organism, and the coming together of two species to form a new symbiotic consortium, which she called a holobiont.

Margulis argued that the interactions within a holobiont aren’t too different from the life cycle of sexually reproducing organisms. The partners are integrated wholes that die and reproduce as one. But instead of sending out tiny cells to reproduce, holobionts send out individual organisms of different species.

With this framing in mind, when biologists began to use the term in the 1990s, they applied it to a few (usually two) organisms. But the word took on a very different cast in the hands of the American coral reef biologist Forest Rohwer and his colleagues, who defined a holobiont as a host and all of its associated microorganisms.

Two protagonists just aren’t enough when it comes to explaining the evolutionary success of corals. They are made up of clusters of polyps, tiny wiggling things that get by with just a few tentacles and a toothless maw. Coral polyps reproduce by cloning themselves, and then sticking together to form large colonies, supported by a jointly fashioned skeleton. The most spectacular corals work hand-in-hand with photosynthetic algae that they host within their own cells. The algae provide nutrients via photosynthesis, while the coral gives the algae both food and protection. And those simple little polyps don’t end their symbiotic relationships there. Corals don’t possess a complicated immune system to fend off pathogens; instead, they seem to selectively cultivate helpful or benign bacteria, which crowd out the harmful microbes. Corals also produce mucus that appears to be able to trap phages, viruses that infect and kill only bacteria. An enemy of an enemy is a friend, after all.

Rohwer and colleagues, unaware of Margulis’s idea, introduced the term holobiont to capture the dynamics of coral physiology. As a result, by the early 2000s, the scientific literature contained two contrasting definitions. One picked out an organism-like symbiotic pair that reproduced, while the other identified an ecological community of microbes indexed to a host.

For a time, the ecological account prevailed. But Margulis’s physiological conception of holobionts was revitalised in the late 2000s as part of a new theory: what’s known as the hologenome theory of evolution. Advocates merged both versions of holobiont into something a bit more conceptually loaded. On this view, the ecological notion of holobiont (the host and all its resident microbes) is given additional properties. It’s an entity that’s coherent enough to have its own hologenome, made up of the host genome plus all the microbial genomes. A major implication of this theory is that natural selection doesn’t just act on the genome of individual organisms: it acts on the hologenome of holobionts, which are seen as single units that can evolve at the level of the holobiont.

Today, researchers engage in fierce debate over which forces shape holobionts and host-microbiome systems. They can be roughly split into two factions, the ecological and the evolutionary. On the ecological side, holobionts are seen as complex and dynamic ecosystems, in constant flux shaped by individual interactions from the bottom up. So you are part of a holobiont. But this stands in opposition to the evolutionary account, which casts holobionts as higher-level entities akin to organisms or units of selection, and believes that they are shaped as a whole from the top down. On this view, you are a holobiont.

The ecological and evolutionary views make for very different predictions about how a holobiont will change over time. Evolutionary theory predicts that the parts of a unit of selection will tend to cooperate: to sacrifice their own interests for the good of the whole. Ecological theory, by contrast, predicts competition and exploitation: parts will cooperate only insofar as it benefits them. Think of the differences between an ant colony and a motley assortment of insects fighting over scarce resources.

A dominant view in medicine treats the body as a battleground where any invaders are bad and must be exterminated. But in an ecosystem, there are no bad guys, just species playing different roles. If the ecological account of holobionts is true, a human host is more like a habitat to be managed, with the right balance and competition between different kinds of microbes being an important consideration. What counts as healthy can depend on what kinds of services we want out of our attendant ecosystem. If the microbes in a holobiont are more like ants in a colony, or genes in a genome, they are parts of a larger integrated whole. So we might expect stable co-adapted partners living in concert across holobiont generations.

However, the evolutionary version of holobionts gives us reason to stick to an expanded version of the ‘us versus them’ picture of medicine. It’s just that now we have a few more allies on our side that we need to take care of. The evolutionary framework might also provide some justification for the calls for a return to a palaeomicrobiome that existed before the modern diet – for that would literally help to return a missing part of ourselves.

As things stand, the evidence leans heavily towards a more ecological interpretation of holobionts. Most of the partners come together anew each generation, and don’t interact in the ways that are necessary for higher-level integration into organismic wholes. The theoretical bar for making that transition is high, and getting over it is going to be rare. But it potentially varies from holobiont to holobiont. There is still a long and exciting scientific road ahead, as researchers begin to unravel the secret lives and complex effects of microbes on the development, behaviour and evolution of their hosts.Aeon counter – do not remove

Derek J. Skillings is a biologist and philosopher of science and currently a lecturer in philosophy at the University of Pennsylvania.

This article was originally published at Aeon and has been republished under Creative Commons.

Listen: The Drug-Resistant Superbug That May Have Taken a Flight from India to Paris

Multi-drug resistant bacteria are growing more powerful each day with microbiologists struggling to find a way to combat these pathogens.

Multi-drug resistant bacteria are growing more powerful each day with microbiologists struggling to find a way to combat these pathogens.

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Credit: John Voo/Flickr, CC BY 2.0

Thirty-nine volunteers, 59 countries, 136 airports. With 400 swabs collected over three years. That is what it took for researchers to determine the course of bacteria that affect thousands of people worldwide. Multi-drug resistant bacteria are growing more powerful each day with microbiologists struggling to find a way to combat these pathogens. Samanth Subramanian and Padmaparna Ghosh talk to Frieder Schaumburg, the microbiologist who ran this study to understand the fight against these superbugs.

This is the latest episode of The Intersection, a fortnightly podcast on Audiomatic. For more such podcasts visit audiomatic.in.

A Cancer Biologist Moving With the Cells

“I’ve been lucky to have had mentors who don’t look at us as women but as scientific colleagues. That’s why you aim for areas of excellence because that’s where you find people like that.”

“I’ve been lucky to have had mentors who don’t look at us as women but as scientific colleagues. That’s why you aim for areas of excellence because that’s where you find people like that.”

Radhika Nair. Source: Nandita Jayaraj/TLoS

Radhika Nair. Source: Nandita Jayaraj/TLoS

The Life of Science – Funny, candid, humble and wise, Radhika Nair makes life in research look good. Before she moved to the Rajiv Gandhi Centre for Biotechnology (RGCB) in Trivandrum earlier this year, the molecular biologist had worked in Cambridge and then in Sydney, where she found her calling – cancer biology.

More specifically, Radhika studies why cancer cells ‘move’ or metastasise. Metastasis is when cancer becomes serious because it marks the spread of the cancerous cells from their origin to other parts of the body. Only some (about 0.1%) cancer cells are able to successfully make the transition – they need to jump aboard the blood stream, get out of the tumour, then lodge at a new site and enter a new organ.

Summing her research questions, Radhika said: “Metastasis is a long journey for cells, through many nasty environments in the body. Only a few cells can make it. Is it a predetermined quality of a cell that makes it able to metastasise? If it is, then we can target such cells and stop them. Or is it random?” And that’s not all. Why do the drugs that work on primary tumours not work on cells that have moved to other places?

Secondary tumour deposits in the liver from a primary cancer of the pancreas. Credit: Wikimedia Commons

Secondary tumour deposits in the liver from a primary cancer of the pancreas. Credit: Wikimedia Commons

A circuitous route

To answer these questions more efficiently, Radhika swears by her pet technique which is based on single cell technologies, i.e. studying individual cells that have metastasised rather than the traditional way of studying bulk cells. It’s an expensive method, she said, but one that enables us to finally answer these critical questions (see previous para) and move on to therapeutic solutions.

Radhika calls her path to cancer biology unconventional and rather twisted. A project on malaria vaccine that she worked on at the Tata Institute of Fundamental Research (TIFR), Mumbai, while doing her master’s degree convinced her that research is what she wanted to do, though she wasn’t as yet sure of which area.

Her initial plans to study further in the US didn’t materialise as she did not get the full scholarship that she was adamant about. However, she did manage to procure a PhD position at National Institute of Immunology (NII) in Delhi. “NII was a [damned] good programme, a great experience scientifically and personally too.” Radhika worked there on germ cell death, an area that she notes is sort of the opposite of cancer (where cells grow uncontrollably). “When I think abt it now, maybe my journey was making its way then.”

During the final stages of her Ph.D., Radhika got married and had a child, so upon completion, she decided to take a break to spend more time with her six-month-old son. When they moved to the UK with her surgeon husband after a couple years, Radhika decided to start reapplying.

To science as a mother

“People say there is no bias against women who’ve taken a break but believe me there is.” Radhika admits that now that she is on the side that is hiring, sometimes this hesitancy is legitimate: “The thing is, if you take a break for maternity in science, it’s not just the one year you miss out on because by the time you can restart it takes twice as long. It’s so competitive that two years can be a lifetime.” She adds that in India women continue to be the primary caregivers so working women have to be smart about their choices. “It’s not easy; you literally have to be changing diapers in the morning and then come back to high-pressure science.”

However, Radhika does not see why worthy candidates are still given such a hard time. “You’d think that if a woman wants to come back, applies to places like Cambridge, gets the fellowship, then it means she has something in her!” While she believes that selection processes are better these days, she acknowledges the need for more. “Everyone says the right things but if you scratch the surface they are worried if women will be able to cope – but we can do it. There are enough of us who are living proof.”

Things eventually worked out well for Radhika, who earned herself a spot as a postdoctoral scholar at the Medical Research Council at Cambridge University. She laughingly recalled how her boss there used to push her to the forefront during equal opportunity seminars. “I ticked all the wrong boxes. He used to say look at her – Asian, woman, under-30, with child – I’ve hired her, I’m totally equal opportunity!”

Choosing cancer

The next step in Radhika’s career came with her relocation to Sydney. It is here, while working with Alexander Swarbrick at the Garvan Institute of Medical Research, that she started focusing on cancer.

Radhika with her lab members at Sydney.

Radhika with her lab members at Sydney.

But it took a rather tragic event to make Radhika realise that breast cancer research is what she wanted to dedicate her life to. Her friend Nidhi, a neurologist, was diagnosed with the same disease. Sadly Nidhi didn’t make it, but Radhika used this shock to fuel her fire. “Until then I had no idea what I would do. I made a promise to Nidhi that I would keep going. Not that I’m going to find a cure or anything but it keeps me going when things get hard.” Such lessons in life have influenced Radhika, even in her teaching style. “I make my students go to oncology meetings to put a face to the disease. It’s important to not see them as just samples but to know the suffering the person is going through.”

She described one of her significant findings while in Sydney: “There are genes that predispose you to breast cancer. One type of cancer, the her2-type cancer, is marked by huge over-expression of the mic gene. Patients who over-expressed both mic and her2 did much worse than those who over-expressed only one gene.” With her research group, she wondered, was there an interaction? Their experiments proved that there was.

They found that another molecule was driving this interaction between her2 and mic. If they knocked down this molecule the model mice, the ones they did the experiments on, did much better. In the course of her time there, Radhika became known for developing cutting edge in-vitro (in lab conditions) and in-vivo (in living cell conditions) models for breast cancer.

Radhika is not shy in admitting that she relied heavily on her family to take care of her son on those important days. “It’s tough, especially in the first few years of having a child. My parents were around, so I had incredible support,” she said. “My mother jokingly calls herself IAS – Indian Ayah Service.” (‘Ayah’ is Tamil/Malayalam for ‘caregiver’.)

Finding her way back

But she soon realised the scenario was starting to get a bit unfair for her parents. “It’s a long journey for my parents to visit us so often.” The alternative was a scary one. “I was so settled in Sydney. Things couldn’t be better, they were finally chugging along, but the time had come to make a choice.” In 2010, the family began discussing the possibility of a return to India.

Once it was decided, Radhika had to make preparations by giving talks in India over the next two years, applying and eventually being awarded the Ramanujan Fellowship (constituted to bring back scientific talent to India) and building a network.

India is finally opening up. More and more scientists abroad are returning to India – the funding situation in the US is also getting tough, many fear they will be stuck as eternal post-docs – so there is competition. The scene is slightly better in India, said Radhika, who is now setting up her lab at RGCB in Thiruvananthapuram. “You get less money of course. You may have to downsize your science a bit. There’s a wait before your research can build up.”

With her project assistant Reshma Murali at RGCB.

With her project assistant Reshma Murali at RGCB.

Radhika has a plan. “I’ve given myself five years. It takes two to set stuff up – models, equipment, cells, assays, etc., then in year three I want to start publishing. I hope to start recruiting PhDs by the end of this year.”

Radhika came to India with her eyes wide open. “Indian institutes are so understaffed and underfunded. I want to transfer my skills and train another set of students the same way I was lucky to be trained. I love the UK and Australia but this is home. I’ll be here, see where it takes me, till they kick me out,” she laughs.

India as a scientific destination

India has a huge requirement for breast cancer research and awareness. “Though India has fewer cases than the US, 50% of them don’t make it because they come into healthcare so late.” But Radhika feels this depressing scenario can be corrected. “Surveillance programmes can help, as can teaching girls at a young age to check their breasts. The shame has to go. There’s nothing wrong with your body and you know it best.”

Students pursuing science in India have it good, she believes, but you have to aim for the top. “In the beginning, a woman may have to be ready to work twice as hard but at a point, it becomes a level playing field. There are boys clubs but I don’t care about that. I’ve been lucky to have had mentors who don’t look at us as women but as scientific colleagues. That’s why you aim for areas of excellence because that’s where you find people like that.”

Another piece of advice Radhika has for young researchers is to be a little more open to their definitions of success. “In India, it’s still considered a failure if you don’t become a PI [Principal Investigator]. But not everyone is meant to be a PI, some are meant to be Project Assistants. Do what fits you, what you’re happy with.”

This piece was originally published by The Life of Science. The Wire is happy to support this project by Aashima Dogra and Nandita Jayaraj, who are traveling across India to meet some fantastic women scientists.