Hi everyone! It has been an exciting week in science, and since it is Sunday evening, I thought I’d give you a brief overview of what has been happening in the scientific world this week.
Scientists have discovered a new exoplanet that closely resembles our solar system’s Jupiter, using the Gemini Planet Imager. The Gemini Planet imager, a high-contrast imaging instrument, went live in 2013 and allows direct imaging of distant planets (as opposed to using indirect observations, like small wobbles in star orbits, to deduce their existence). The new planet, named 51 ERI B is located around a star called 51 Eridani, located a little less than 100 lightyears away from earth. This discovery is particularly interesting because 51 Eridani is a really young star, only about 20 million years old (the sun and the solar system are estimated to be around 4.5 billion years old, by comparison), and studying it can give us vital clues about the origin of Jupiter and other gas giants. The new planet is about twice the size of Jupiter, has a surface temperature of 600 – 750 Kelvin, and has large amounts of methane and water vapor.
This week also marks the completion of the 1000 genomes project. This project, started in January, 2008, mapped the genomes of 2504 participants, spread over 26 populations, and coming from a multitude of ethnicities. Five of the six inhabited continents were represented (Australia being the exception). The project aimed to identify all variations that occurred at a frequency of least 1% in the population (i.e. existed in at least 1 out of 100 individuals). The project identified over 88 million DNA sequence variants, and have published their results in the current issue of Nature. The data they collected is freely available on their website. On a similar note, the UK10K project, which plans to sequence the genomes of 10000 individuals in the UK from diseased as well as healthy backgrounds to identify potential disease-causing or biomedically relevant variants, also published their results in the same issue.
This next story has the makings of a spy movie. AIDS is caused by the retrovirus, HIV (human immunodeficiency virus). The virus infects human cells and spreads by making many copies of itself (called virions) by hijacking the host cell’s protein synthesis machinery, and budding off from the host cell’s membrane. Now, the host cell is not completely defenseless. It expresses proteins known as SERINCs (SERINC3 and SERINC5), which hide in the plasma membrane and surreptitiously sneak into the newly formed virion particles while they are budding. Once they are there, these sneaky double agents prevent the virion particles from infecting other target cells. But the virus has one more trick up its sleeve. Scientists show for the first time that HIV viruses produce a protein called Nef, which recognizes the host cells SERINs, and sequesters them into harmless endosomal compartments inside the cell, effectively ‘jailing’ them, and stopping them from reducing the infectivity of the viruses.
More (literal) cloak and dagger stuff here. Since the advent of nanotechnology, one of the fastest growing areas of research has focused on its potential biomedical applications. In particular, scientists have hoped to use nanoparticles for effective and targeted drug delivery. But one issue that has plagued researchers is that since these particles are essentially foreign objects introduced into the body, the immune system tends to recognize them as such, and this may lead to unpleasant consequences. Additionally, synthetic substances often tend to react unpredictably with biological material, if left alone. Scientists over at University of California, San Diego, took a different approach. They used the cell membrane of human platelets (a type of small blood cells that help in blood clotting) to ‘cloak’ nanoparticles, and used these nanoparticles to deliver drugs to rodents which modelled heart disease and bacterial infection. The nanoparticles, following cloaking, not only showed better effectiveness in treating disease, but also avoided the immune system better. This opens up a new frontier in biointerfacing and nano-scale biomedical research.
This has also been a good week for research on Malaria. Malaria is a tropical disease that kills hundreds of thousands of people each year, primarily in developing countries. It is caused by a protozoan parasite called Plasmodium, which is transmitted by female Anopheles mosquitoes. Africa is one of biggest centers for this disease, and certain mutations have been found in the populations there that provide a degree of resistance to the disease (the sickle cell anemia gene being a famous example). A new study published in Nature this week carried out genome wide association studies in over 10000 African children, and discovered a new gene locus for variation that confers about 33 % resistance against malaria. The locus is located very close to the cluster of glycophorin genes which code for proteins located on the red blood cell surface which allow entry of the parasite.
The most common strategy for preventing malaria (since no vaccine exists) is to kill/prevent breeding of the mosquitoes themselves. A problem with using insecticides to achieve this is that many mosquitoes develop tolerance or resistance to insecticides. Interestingly, a study this week reported that coating the insecticides with electrostatic charge using netting, increased the effectivity of these insecticides, killing even resistant mosquitos. The authors think that this might be used later in trapping devices or to coat walls or curtains to eliminate mosquitos.
The most interesting study regarding malaria that I found though, is one that does not involve humans as well. While we tend to view the mosquitoes as the main culprits in causing and spreading malaria, the truth is that they too are victims of the wily Plasmodium parasite. The mosquito has an immune system that actively fights the parasite, with the help of a protein called TEP1. Now, TEP1 isn’t equally effective for all mosquitoes as there are different alleles (variants) of the TEP1 genes in the population. Different variants leave the mosquitoes either susceptible or resistant to the parasite. One would think that the susceptible variants would get weeded out over time, until all individuals left alive are carrying the resistant allele – but this clearly is not the case. Scientists appear to have solved this mystery by showing that the TEP1 gene has a second function – it removes damaged sperm cells, improving male fertility. And surprisingly, the allele which leaves individuals susceptible to the malaria parasite, is the one that improves fertility the most. For the mosquitoes therefore, it is a tradeoff between reproduction and immunity.
This does not begin to scratch the surface of all the interesting research published this week. Scientists have traced the origins of enamel (the hard coating that covers our teeth) to the coated scales of an ancient bony fish, they have found that exposing migratory birds to traffic noises by using speakers reduces their body condition and stopover efficiency, and that person-to-person variation in judging faces as attractive is determined largely by the environment and not by our genes. And lots more.
Over here, at the Scientific Lens, the second post in the ‘Demystifying the brain‘ series was published. If you haven’t read it yet, I’d suggest you give it a try – this week’s post talked about the brains of our ancestors and how the human brain may have evolved.
So, that’s all for now. Let me know if you want me to cover any of these studies in more detail. I hope you all had a great week and are now enjoying a well-deserved weekend. See you next week!