Solar cells that work in rain

Solar cells that work in rain Image
In case you have read my last month’s guest post about harvesting solar energy in rust, you would be delighted to know that there has been yet another breakthrough in our attempt to harness solar energy.  For many years, solar energy has been targeted for being unavailable at night and during rains. The problem of utilizing solar energy at night can be resolved with the help of metal oxide cells as elaborated in my above post (do read it, if you have not done so already). And now researchers at the Ocean University in China have addressed the second problem and developed solar cells that can actually use rain drops to generate electricity.

Published in the German journal Angewandte Chemie, the paper titled, A Solar Cell Triggered by Sun and Rain, opens a new realm of possibilities when harnessing solar energy. Coating the solar cell with a thin film of graphene allows the cell to function even when it is raining. Graphene is nothing but reduced form of graphite that consists of a honeycomb arrangement of carbon atoms in a two dimensional matrix. Although known to us for over 50 years, graphene was rarely studied until recently in 2004, where it was studied in greater depth and its abundant properties were brought to the fore. A good conductor of heat and electricity, it is almost transparent and yet stronger than steel. Showing bipolar transistor effect, graphene has also found its way into modern electronics such as computers, smartphones, TVs etc. and is making strides in biological research to be used as a biosensor for detecting cancers and also as electrode to engage with neurons.

Rain drop creating a difference in potential when it impacts the graphene layer,
thus acting as a pseudocapacitor. Image credit:

Prof. Qunwei Tang and his team of researchers used graphene’s property of binding to positively charged ions to generate minute amounts of electricity from their modified solar cell. Raindrops carry some impurities with them as they descend from the sky. These impurities are usually in the form of certain salts that are made up of common elements such as sodium, calcium, ammonium etc. When dissolved in water, these salts dissociate into their respective ions and upon impact with a solar cell containing a thin graphene layer, form a pseudocapacitor, that has positively charged ions of water on side and the negatively charged electrons of graphene on the other, creating a potential difference (in microvolts) that is sufficient to generate electric current and hence electricity.

The experiments done by the researchers are still in their early phases but have managed to convert 6.53% of solar energy into electricity. Although this might not sound like a lot, considering the fact that rain drops were deterrent to working of a solar cell, this is huge accomplishment and paves way for further work to be done to increase the effectiveness of solar cells. As mentioned in our previous post about solar cells, currently solar cells are able to convert 10-15% of solar energy into electric energy and a simple layering of graphene on them should enable boosting of this capacity.

But this is not all. Researchers at University of Surrey were also able to use graphene to utilise the diffused sunlight that we get inside our homes and never utilise. Coating walls with graphene films could also help us harness more solar energy than we ever have.

If you would like to read more of these interesting stories from the world of science, subscribe to our  blog and we will send you an email every time we post something new and interesting. Alternatively, you can follow us on social media such as FacebookTwitter or Google Plus!


Tang, Q., Wang, X., Yang, P., & He, B. (2016). A Solar Cell That Is Triggered by Sun and Rain Angewandte Chemie DOI: 10.1002/ange.201602114

Anguita JV, Ahmad M, Haq S, Allam J, & Silva SR (2016). Ultra-broadband light trapping using nanotextured decoupled graphene multilayers. Science advances, 2 (2) PMID: 26933686

Apple vs Samsung like patent war in the genomics industry

Image credit:

Remember the year 2012, when all we could hear from the smartphone industry was the on-going litigation between Apple and Samsung. Well, after a recent move from Illumina, the world’s largest next generation sequencing instrument provider, we can expect 2016 to be a similar year of litigation in the genomics industry. Except that unlike Apple’s opponent Samsung, who were busy selling smartphones around the world, Illumina’s opponent is a young company based in UK, Oxford Nanopore Technologies just venturing out in the real world. To understand, why Illumina would take such a step, we first need to go back in time, where all this began.
The Human Genome Project was an ambitious project taken up by the
National Human Genome Research Institute (NHGRI) and
funded by the National Institute of Health (NIH)
Back in 2003, with the then available method of sequencing (Sanger Sequencing), it took the researchers 13 years and $2.7 billion to publish the Human Genome. At this rate, sequencing would be the luxury of just a few people on the planet and would eventually die. To harness the potential of the genetics and make the genome “the transformative textbook of medicine”  as Francis Collins, the then director of NHGRI called it, sequencing had to be cheaper and affordable for all. Sanger Sequencing had its own limitations and therefore, there was a need for a cheaper, better, faster method of sequencing. But this was not some late realization that had struck after the HGP was completed.
Companies were already work on the next generation of sequencing (NGS) technology and as early as 2005, 454 Life Science launched its 454 sequencing platform, which was closely followed by Solexa that launched its Genome Analyzer in 2006 and AgenCourt that launched SOLiD (Sequencing by Oligo Ligation Detection) the same year. Larger companies like Roche and Applied Biosystems were quick to harp on the potential of these companies and bought out the companies, 454 and AgenCourt along with their technologies. Illumina, that was looking at its BeadArray Technology to offer genotyping services using microarrays, bought off Solexa to get into the NGS arena. (Source:
Types of Next Gen Sequencing. Image credit:
A quick comparison of the different types of sequencing platforms
454 is now owned by Roche, SOLiD by Thermo Scientific and Solexa by Illumina.
The years that followed brought out iterations of these technologies, promising longer reads, faster turn around, reduction in costs etc. Illumina, however, were quick to realise that costing was the single largest factor that would determine the adoption of this new technology and therefore, since 2009, has been constantly reducing their prices for complete genome sequencing from $48000 to $19,500 a year later and then reducing it to $4000 per individual while testing their Hi Seq machines. This dramatic decrease in pricing even forced the X Prize organizers to cancel their Genomics X Prize, a first in their history, where the goal of the prize was outpaced by innovation. With their HiSeq X machines (cost of $10 million each), which is 10 Hi Seq sequencers in a single behemoth unit, Illumina claims to sequence genomes for $1000 (Just that the machine is capable of sequence genomes of about 50 people a day and is busy convincing governments to do so).
Hi Seq X Ten machine. Image source:
HiSeq X Ten, the behemoth sequencer! 

But the smartest company of 2014, as suggested by MIT Technology Review, did not put all its eggs in one basket. Apart from the high end sequencers, Illumina also has a range of bench top sequencers called MiniSeq that at approx.. $50,000 are affordable for regular sized labs. Apart from its popular sequencing technology, it has also invested its efforts in non-invasive prenatal testing and aims to be the one stop solution for the genomics needs of a family. Illumina, which also promotes, other sequencing technologies (at least 6 others) that it owns, in 2009 tied up with UK based company, Oxford Nanopore Technologies to further develop the nanopore sequencing technique that held potential to reduce sequencing costs further. 
Oxford nanopore, the new generation sequencers
The new generation sequencers! 

Just like the mobile giants, Apple and Samsung,  who were collaborators once upon a time, the relationship ended in 2013 on a bitter note after Oxford Nanopore Technologies revealed their plan of going to the market with nanopore sequencing technology but on their own range of instruments. By this time, Illumina was already controlling 70% of the market share with its sequencers and with products like HiSeq X in the pipeline, there seemed to be little to worry about. Nevertheless, they pursued their interest in nanopore sequencing separately and later that year also licensed a version of nanopore sequencing from University of Alabama at Birmingham (UAB) (will come back to this later).
Oxford Nanopore were yet to even hand out their prototypes to their early adopters and Illumina were probably confident that they would have their newly owned nanopore technology products ready before the British company would reach out to the markets. Delays due to technical glitches hit Oxford Nanopore’s prospects even further and the prototypes were further delayed but in April of 2014, selected researchers got their hands on the first MinION sequencers, which changed the story entirely.
MinION sequencer. Image credit:
True to its name, the MinION sequencer, from Oxford Nanopore Technologies! 

These USB stick like devices were given away for an early adopter’s price of $1000 and later that year, publications begun to pour out, which had used MinION as its sequencing platform. The portability of the device was is largest USP and as researchers were able to use this simple sequencers on the field to track the spread of Ebola in Guinea and a nosocomial infection of Salmonella in the UK. These success stories were hailed across the world and suddenly, the bench top sequencer of Illumina, started to look like a gigantic unnecessity. Why bother using an externally powered hard disk drive, when you can use a USB powered flash drive.
MinION’s strength does not lie only in its small size. Along with the fact, it lowers sequencing costs further than what Illumina currently offers, the MinION is capable of reading long sequences of DNA that has never been achieved before (>5000 bp) and sequence detection is done in real time and lets the researcher access the sequencing data in real time as opposed to the 11-24 hour wait on Illumina’s machines.  If MinION’s capabilities were not good enough, Oxford Nanopore is now promoting, what we can call, its flagship product, PromethION, a benchtop sequencer, which packs the power of 48 MinIONs that the user can choose to use individually or altogether and a direct competitor to the MiSeq machines that are Illumina’s popular product.
Coming back to the present, Illumina has now filed a case of patent infringement on part of Oxford Nanopore Technologies and accuses them of stealing ideas from the patent they hold (the one they licensed from UAB in 2013). The basis of the complaint is that Illumina strongly believes that the nanopore used in MinION and PromethION match those derived from Mycobacterium smegmatis. What MinION uses to carry out its sequencing is a secret held very closely by Oxford Nanopore but Illumina are certain that it is some derivative of M.smegmatis.

Nanopore GIF. Image credit:
Representation of how a nanopore works and gives out sequencing data.

On the basis of this conjecture, Illumina have requested the Court of California to stop the import of equipment made by Oxford Nanopore on US soil. Interestingly, they also claim that if a void, is created in the area of genomic services as a result of this ban, Illumina and other sequencing providers (Roche, who are planning to close down their sequencing business, Applied Biosystems, who are now part of Thermo Scientific and boast of ION torrent sequencers, based on SOLiD technology and Pacific Biosciences, whose latest sequencers is bigger and more expensive than llumina’s ) will be able to address it.

With their revolutionary technology, these guys are looking to sequence genomes of
300 dead people. Why? Read this blog post to know.
Taking into consideration that Illumina has recently attacked their biggest clients BGI  before they took over Complete Genomics, who also boast of a revolutionary sequencing technology  , it is no surprise, that Illumina are fighting this legal battle, purely because Oxford Nanopore Technologies is a potential competitor now. Oxford Nanopore do not have regular customers but are valued at $1.4 billion dollars not very far from the Illumina, who have worked over a decade to reach this far. It, therefore, seems that this litigation is only to put a cog in the wheel and slow the progress of Oxford Nanopore. Illumina are probably working on a nanopore sequencer and its nearing completion and would like it be available along with the PromethION, so that they do not lose market share. Probably, the story is much worse. Illumina have nothing in the pipeline in terms of a nanopore sequencer but just a HiSeq 50 or 100 and as always, the MinION is ruining their best laid plans.
While Oxford Nanopore have not said much about how they are going to react to this litigation, they too have multiple patents relating to this technology, some of which precede the patent that Illumina is fighting with. A countersuit might be on the cards and we will probably see, the two companies slug it out in the courts rather than in the market, where the real challenge is.
We have to just wait and see, how this battle takes shape, but researchers around the world want just one confirmation. Like Apple and Samsung did, keep rolling out new products every year and bringing down costs of genome sequencing. A $100 genome anyone?

Paper citation:

Liu, L., Li, Y., Li, S., Hu, N., He, Y., Pong, R., Lin, D., Lu, L., & Law, M. (2012). Comparison of Next-Generation Sequencing Systems Journal of Biomedicine and Biotechnology, 2012, 1-11 DOI: 10.1155/2012/251364

Why Sci-Hub’s story is so crucial to science?

why is sci-hub so important? Image credit:

On the 28th of October 2015, Judge Robert Sweet in his ruling at the New York district court declared that the website be blocked with immediate effect and managed to stop hundreds and thousands of researchers and science enthusiasts from accessing the holy grail of today’s science, the research paper.

What should be a simple means to communicate to the world one’s research findings, has become a currency of some sort. A ticket to a researcher’s professional success, a magnet for an investigator to attract funding for his lab and the elusive piece of the puzzle that the publishing group can hold you ransom for, until you cough up some good cash ($30 or above for a single article and thousands of dollars for a bundled annual subscription)

What Judge Sweet termed as a “disservice (to) public interest”, is actually a small website that allows you access to scientific research, old and new, and for free. Sci- Hub. Org, started in 2011, as a trusted place to access research data for free without any bias. It simply did not matter to Sci-Hub who its users were and where they came from, if you had a scientific interest in a topic, then Sci-Hub would help you dwell into further, for free!

Alexandra Elbakyan, founder of Sci-Hub Image credit:
Alexandra Elbakyan, founder of Sci-Hub

After losing its original domain to the court ruling, Sci- Hub has moved to another domain and continues to do its good work tirelessly.  Its founder, Alexandra Elbakyan, told Simon Oxenham at Big Think that

“we are not going to stop our activities, and plan to expand our database.” 

The website that was originally launched in Russian and looked primitive for most of its lifetime has now blossomed after the court ruling and is available for users in English as well.

Sci-Hub, in 2014 Image credit:

Why do whales wash ashore?

The following post was accepted as our guest post at the Science Log, the English version of the  popular Hindi Science website, Scientific World. Below is the introduction to this post. 

Last month, about 100 whales were washed ashore along the coastline of Tiruchendur, in the southern state of Tamil Nadu. While locals in the area were successful in pushing back 36 of these whales using various methods, 45 of these creatures succumbed on the shore. Just a couple of weeks after this incident, a 30 foot whale was washed ashore on the western coast. Although,  we still await formal reasons for these incidents, you might have come across a lot of theories put out by experts as well on non-experts through various media channels as to why these whales might have reached the shores. Through this post, however, we will look at well investigated reasons why these sea creatures might leave the sanctity of their homes and travel to shallow waters.

To read the complete post, please click here to go to the post on Science Log

RotM: Interview with Prof. Steve Winder

For our recent Researcher of the Month, we spoke to Professor Steve Winder, Professor of Molecular Cell Biology, at the Department of Biomedical Science, The University of Sheffield. His laboratory focuses on the study of dystroglycan, a protein that plays an important role in cell adhesion and signalling. His recent paper in Human Molecular Genetics speaks about the a FDA approved drug, currently being used for treating leukemia as a treatment for Duchenne Muscular Dystrophy (DMD). Here is Professor Winder telling us more about his lab's findings and how we might cure DMD in the near future. 

CTS : For the benefit of our readers, could you please tell us more about your  findings in the recent study. 
SW: Identification of a systemically acting and universal small molecule therapy for  Duchenne muscular dystrophy would be an enormous advance for this condition. Based on evidence gained from studies on mouse genetic models, we have identified tyrosine phosphorylation and degradation of β-dystroglycan as a key event in the aetiology of Duchenne muscular dystrophy. Thus, preventing tyrosine phosphorylation and degradation of β-dystroglycan presents itself as a potential therapeutic strategy. 

Using the dystrophic sapje zebrafish, we have investigated the use of tyrosine kinase and other inhibitors to treat the dystrophic symptoms in this model of Duchenne muscular dystrophy.
Dastanib or Sprycel may be used to cure Duchenne Muscular Dystrophy Image credit: Wikipedia
Molecular Structure of Dasatinib, a drug produced by Bristol-Myers Squibb and marketed as Sprycel
Dasatinib, a potent and specific Src tyrosine kinase inhibitor, was found to decrease the levels of β-dystroglycan phosphorylation on tyrosine and to increase the relative levels of non-phosphorylated β-dystroglycan in sapje zebrafish. Furthermore, dasatinib treatment resulted in the improved physical appearance of the sapje zebrafish musculature and increased swimming ability as measured by both duration and distance of swimming of dasatinib-treated fish compared with control animals. These data suggest great promise for pharmacological agents that prevent the phosphorylation of β-dystroglycan on tyrosine and subsequent steps in the degradation pathway as therapeutic targets for the treatment of Duchenne muscular dystrophy.

CTS: Of all Src inhibitors available, Why was dastanib chosen?
SW:We actually used the zebrafish system to screen many compounds and drugs. Dasatinib was just picked as an exemplar for publication. 

Image credit: doi: 10.1093/hmg/ddv469
Image showing significantly reduced movement in sapje fish in terms of distance covered when compared to their siblings A, results of movement tracking when compared, B, and improvement in movement when treated with dastanib, C. Image credit: Prof.Steve Winder and Human Molecular Genetics. 

CTS: Korner et al 2014 carried out a similar study with a compound called bortezomib. How different would you say is this study from theirs? 
SW: Korner et al used a mouse model of congenital muscular dystrophy(CMD) and treated it with a proteasome inhibitor, whereas we used a mouse model of DMD and a Src inhibitor. Interestingly the same group have recently shown that the same drug is not effective against a different mousemodel of the same disease.

CTS: So, would you be working on a different model of zebrafish to ensure that that your findings are reproducible?
SW: Given that we have already advanced our studies in mdx mice with some apparent success, there seems little need to go back to zebrafish at this stage.

CTS: Your lab has worked on mouse models earlier, why shift to zebrafish for this study?
SW: The mouse model demonstrated the importance of tyrosine phosphorylation in the aetiology of DMD. The shift to fish was simply for the purposes of screening many candidate compounds. Drug screening is much quicker, cheaper and easier in fish than in mice.

CTS:What happens next? Since this is an approved drug, can we skip the human trials altogether? 
SW:No, trials are still needed. Although dasatinib is approved clinically and the safety testing has been done, we will still need to demonstrate efficacy against DMD in people.

CTS: So, would your lab be involved in the clinical trials for Duchenne Muscular Dystrophy?
SW: The initial discovery is patented with us as inventors, however pharma involvement would be needed in order to obtain the drugs for the trial. The trial could be investigator led, or pharma could choose to do it. 

Prof. Steve Winder, University of Sheffield
Just a regular day at the office.
Image credit: Professor Steve Winder
CTS: Looking at the treatments in the future, isn't gene therapy a more robust answer to a genetic disease like DMD. When perfected, it holds promise of 100% recovery. Is your lab looking at gene replacement therapies as well?
SW: Whilst DMD is a monogenic disease, there are hundreds of different mutations. There is currently no single genetic therapy that is capable of correcting all the defects, and those that there are, are far from 100% perfect. Delivering these sorts of therapies to muscle remains problematic. CRISPR-Cas9 mediated gene editing would appear to be one way around that. 

However, we are not pursuing gene therapy approaches since that is not our current area of expertise.For the moment, a systemic small molecule inhibitor could be an answer. So although at present we are still working up the pharmacological approach, but ultimately a combinatorial regimen of pharmacological and genetic therapy may give greatest efficacy.

Readers interested to know about Duchenne Muscular Dystrophy would like to read our other post, Exception to the thumb rule.

If you would like to read more of these interesting stories from the world of science, subscribe to our  blog and we will send you an email every time we post something new and interesting. Alternatively, you can follow us on social media such as FacebookTwitter or Google Plus!


Körner Z, Fontes-Oliveira CC, Holmberg J, Carmignac V, & Durbeej M (2014). Bortezomib partially improves laminin α2 chain-deficient muscular dystrophy. The American journal of pathology, 184 (5), 1518-28 PMID: 24631023

Körner Z, & Durbeej M (2016). Bortezomib Does Not Reduce Muscular Dystrophy in the dy2J/dy2J Mouse Model of Laminin α2 Chain-Deficient Muscular Dystrophy. PloS one, 11 (1) PMID: 26731667

Lipscomb L, Piggott RW, Emmerson T, & Winder SJ (2016). Dasatinib as a treatment for Duchenne muscular dystrophy. Human molecular genetics, 25 (2), 266-74 PMID: 26604135

Genes don't call all the shots, your environment does to.

The usage of the terms such as 'DNA' and 'genes' has exploded in recent years and is  commonly used to denote characteristics and traits in people, features of products and even as lyrics for a song. The theory of genetics that genes assign traits to individuals has been rooted so deeply into our psyche, that we fail to see the other side of the story completely. The role of the environment in shaping how our genes function is a fact that is unheard by many people and is something I would like to shed a little light on in this post.
Image credit:

The public understanding about genetics is more or less like the way people follow astrology . If the newspaper predicts that the day at work will not go well, we tend to blame the stars/ sun sign for everything that goes wrong that day. Similarly, the presumption that genes control the way we function and act, has set the tone for genes to be solely in control of everything that is happening inside our cells. However, this is not how genes work. There is a machinery that allows genes to adapt to their surroundings without actually changing the DNA sequence. These are not mutations that are stopping gene function or restarting them, these are minor changes that can increase or decrease gene expression, introduced as a result of conditions in the organisms environment. Called epigenetics, these changes are inheritable and can be passed on to future generations as well. 

In the past, there have been many studies that have shown how epigenetic changes can be brought about in genes. Methylation of DNA, role of non-coding RNA and modification of histone proteins are a few of the epigenetic methods that we have been able to unearth so far. A recent study published in Science by Daniel Simola and colleagues studied histone protein modification in carpenter ants and were able to externally amend behaviour in these ants.

Description: This image shows a Carpenter ant ...
A Carpenter ant (Camponotus ligniperda)
(Photo credit: Wikipedia)
The colony of a carpenter ant consists of a queen, her brood and several thousands of workers. We know that all worker ants are genetically the same but are given different tasks in their colonies. There is no exception in carpenter ants as well, where smaller ants or minors are assigned the task of taking care of the young and forage for food, whereas the larger ants or majors defend the colony. Using drugs that affect acetylation of histone proteins (Histone deacetylases or HDAC, the researchers saw an increase in scouting and foraging activity in minor ants. Thus, lower the acetylation, larger was foraging activity seen in the ants. Conversely, this increased foraging could be dropped by using a inhibitor of histone acetyltransferase (HATi). 

Diagram showing behavioral differences in major and minor carpenter ants when treated with HATi and HDACs.
Image credit: Simola et al., 2016. doi:10.1126/science.aac6633
Using this information, the researchers were able to induce foraging behaviour in major ants (who are built to defend and protect) and retain them for up to 50 days of age. This goes to show that even though these ants are genetically programmed to carry out a certain task, their behaviour can be modified using external factors. Since a large number of these proteins and enzymes are common among insects and even vertebrates, it is safe to assume that such epigenetic change in behaviour can be brought about in vertebrates as well. 

The study also found that there is a window of opportunity, where epigenetic changes can result in behaviour modification and there is a lot of work to be done to understand this window, right from why it exists, how it functions to why it closes as the animal matures. Nevertheless, the study manages to show that genes are not in complete control and your environment has say too. 

If you liked reading this post, you might also like our other post about cells not being ruled by genes.

If you would like to read more of these interesting stories from the world of science, subscribe to our  blog and we will send you an email every time we post something new and interesting. Alternatively, you can follow us on social media such as FacebookTwitter or Google Plus!


Simola DF, Graham RJ, Brady CM, Enzmann BL, Desplan C, Ray A, Zwiebel LJ, Bonasio R, Reinberg D, Liebig J, & Berger SL (2016). Epigenetic (re)programming of caste-specific behavior in the ant Camponotus floridanus. Science (New York, N.Y.), 351 (6268) PMID: 26722000