Posted by Kasra
There has been too much work overload in the current days, not letting me blog as often as I want to. Meanwhile, have a look at and share this well done infographic about Lyme disease. Click here for the source, more info and also other infographics.
Source: Nursing School Hub
Posted by Kasra:
I often think of how Richard Feynman so simply and truly describes the beauty or extra-beauty that science brings to everything around us. I believe what Feynman says is more or less obvious to scientists or people somehow involved in science. We enjoy asking questions and seeking answers that naturally lead to more questions. Then why is it that we can’t convey this feeling to more people? Why the general consensus is that “Science is boring?” Is it because it solves riddles and demystifies magic? Or is it because of the overused and misused jargon? Or mazybe it is because it replaces a preferred presumption with hard truth? With all the discoveries and advancements and technologies surrounding us, why would some people still think science is boring? Maybe science communication should not be just writing about cool stuff that happen in science, but also discussing why we find them cool and fascinating. Feynman elegantly describes the way a scientist would look at nature.
I tried to read only little bit about the interaction of pollinators and flowering plants and was overwhelmed with its complexity. At least one way that I find science fascinating is how it explains the complexity of nature by enhancing its details. It reveals and explains hidden patterns and interactions, at the end making it even more complex that it originally was, nevertheless more beautiful. Here is just a glimpse of this beauty, ultraviolet vision of butterflies and nectar guides of flowers.
Posted by Kasra
This is in continuation of a post by my old friend and classmate in his new exciting blog Genophoria. He expressed his rightful concerns about the rise of “Entertainment Science”, where he says scientists are coming out of their Ivory towers and shouting out their impressive and sometimes controversial findings to the public. It often happens that these controversial findings, or at least their conclusions in that regard are wrong. Scientists can accept that. Science is by nature self-correcting. But at the same time, for the public, they lose their credibility as truth-seekers which they claim to be.
It just happens that at this very time, PNAS has published a study on the statistics of retracted publications. Let’s not exaggerate. The percentage of retracted papers compared to number of publications is very very small. Still, their results were a bit surprising at least to me: 67% of them were retracted due to misconduct, either fraud or suspected fraud. Only 20% or so were due to error. Many questions arise: Has it always been like this? Only is it because there are more publications now and more screening? What percentage goes unnoticed? Most importantly, what were the underlying reasons for these fraudulent publications? Were they desperate Postdocs or PIs trying to win a Cell or a Nature to renew a fellowship or a grant? Or were they seeking something further, a socioeconomical, political or cultic purpose beyond science? These questions seek immediate attention and hopefully clear answers. Without any doubt, the fight for budget has become fiercer; and no, most scientists can no longer live in ivory towers, indifferent to the public and their attention – if they ever did. By the way, hadn’t you said earlier that by turning away from the public we turned from high-ranked academics into socially excluded geeks? We need to interact with the public, to rebuke false claims and promote logical thinking. I guess as you say, we are doing it wrong.
If the scientific community is willing to share the excitement of discoveries and controversies with the public, it should be more stringent in the peer-reviewing process of such claims. In retrospect, how many of the fraudulent retracted papers can be labelled as editorial or peer-review failures? Publishing in high-impact journals is getting harder and harder. But maybe during the peer-review, there should be a new focus on skepticism and a shrewd eye for biased claims, besides asking for more and more control experiments. At the same time, when presenting discoveries to the press, more transparency and accuracy about their nature and details are needed, so that a susceptibility SNP doesn’t turn into a cancer gene and an in vitro-tested compound into its ultimate cure.
Fang FC, Steen RG, & Casadevall A (2012). Misconduct accounts for the majority of retracted scientific publications. Proceedings of the National Academy of Sciences of the United States of America PMID: 23027971
Posted by Kasra
I’ve been struck down with a cold for quite some days now and haven’t been able to put my thoughts together for my next post. During the healing process, I would like to introduce two eloquently written Immunology blogs that I accidentally stumbled upon on Researchblogging. I am appreciating this website more and more both as a general science reader as well as a science blogger. Regular or once a while visits are definitely recommended. Now the blogs:
Memory Reactivation discusses recent research mostly around adaptive immunity and interactions among immune cells. The technical language might be difficult for those not in the field, but definitely a pleasant read for immunologists.
Lucas Tafur takes a comprehensive look at research on relationships among diet, metabolism and immune function, an area of immunology that I personally find very interesting and informative.
Enjoy reading and come back soon!
There is no argument against the beauty and complexity of life under the microscope. The Pretty Protozoa microblog provides solid proof.
Posted by Kasra
I had seen parts of this animation that beautifully shows the central dogma of molecular biology, without knowing the creator and his other pieces of work. I finally discovered Drew Berry, the artist behind this work through his TED talk. There, he shares his passion and inspirations and shows pieces of his original and recent animations. Excited by the talk, I Googled him and found that has also produced a video describing the life cycle of Plasmodium. The first and second parts of this short but entertaining and educational video can be watched here and here. This video and similar works by this animator can and should be used as powerful teaching aids.
Drew Berry has tried to be as scientifically accurate as possible by getting protein structures from the protein data bank (PDB) and reading research papers to correctly animate the mechanisms according to them. Read more about his work on his website.
Posted by Kasra
It has been more than a year since my last post. Apparently doing science has taken over writing about science. I am going to try to put more frequent updates which means that I get to explore research being done on parasites again! I would also like to state again that parasite diary would gladly accept your diaries as well. May it be your own research, or work by somebody else that you find fascinating. It doesn’t need to be recently published either. I am pretty sure nobody has read everything about everything. Therefore, all stories about parasites (whether eukaryotic or not) can be exciting and informative to read. If you are interested in participating, send us your diaries to parasitediary AT gmail DOT com and we will publish them under your name.
As a start to the new era of the parasite diary, I would like to introduce a podcast that I think anyone with the slightest interest in parasites should not miss. This Week in Parasitism (TWIP) is narrated by Dr. Vincent Racaniello and Dr. Dickson Despommier from Columbia University. This podcast teaches you about ecology, physiology and behaviour of eukaryotic parasites and tells you stories that you have never heard before about their history and impact on human life. Their enthusiasm for research and for parasites pumps up your energy to continue doing your boring benchwork while listening! I need say no more. Check out TWIP and its sisters (or brothers?) TWIV (Virology) and TWIM (Microbiology).
P.S. The picture in the logo of TWIP is of the nematode Trichinella spiralsis sitting comfortably inside its nurse cell in the muscle tissue.
Posted by Kasra Hassani
I am appointed to do a review paper for a ‘Reading and Conference’ course on Fungi. I chose the opportunistic pathogen Aspergillus fumigatus as the focus of my review. Having studied only on Trypanosomes and innate immune cells so far, my background in mycology is close to zero. So I decided to start from scratch. I stepped upon a surprisingly neatly written review that gave me exactly as much background I needed on Aspergillus before I would go more in depth on the subject. “Aspergillus: A primer for the novice” by Dr. Joan Bennett includes scientifically exciting and still critical detail about various species of Aspergillus, their commercial, historical and culinary(yes!) importance. For once after a long time I read the whole review paper and not only the section that interested my research focus. If interested to learn more about the ubiquitous fungus Aspergillus, you can also enjoy reading this paper alongside your favorite afternoon beverage here.
Bennett JW (2009). Aspergillus: a primer for the novice. Medical mycology : official publication of the International Society for Human and Animal Mycology, 47 Suppl 1 PMID: 19253144
Posted by: Kasra Hassani
Many pathogens are unable to live outside the host. Therefore, before killing or completely using up their host, they should ensure that they will be successfully transfered to another one, or one may say, those who did not never made it through evolution. Depending on their life-cycle and type, strategies to ensure transmission diffes among pathogens. In a comment for Nature Reviews in Immunology Sacks and Yazdanbakhsh comparatively discuss these strategies among air-borne pathogens, protozoan vector borne pathogens and also multicellular pathogens. Air-borne bacteria and viruses can easily spread after an acute infection and do not necessarily need to modulate immune response to avoid the up-coming sterilizing immunity. On the other hand, vector-borne parasites such as Plasmodium or the Trypanosomes require more time for efficient transmission. Therefore, parasites have developed strategies to delay life-long immunity. For instance, in African Trypanosomes (T. brucei) continuous variation of the surface glycoprotein (correctly named the variable surface glycoprotein or VSG) hiders development of a protective immune response and allows the parasite to reside in the blood for a long time. Alternatively, Leishmania infections co-inside with presence of regulatory T cells and considerable amounts of IL-10 which down-regulates the protective Th1 response. In larger parasites such as helminths rapid movement from immune-sensitive areas such as the skin or acquiring and presentation of host antigens are among the strategies that are used for delaying the immune response and buying time for transmission.
What I find more interesting among all of this is the evolution of the host in the same direction. In many parasitic infections, the immune response does not lead to complete parasite clearance, rather to a residual infection with minimum or no pathology yet still transmissibility. Read et al. have argued in a Primer in PLoS Biology that this ‘tolerance’ is a type of immunity that can arise in the host-parasite co-evolution as an alternative to ‘resistance’ where complete of the pathogen clearance occurs. Firstly, complete clearance of the pathogen can be too costly compared to its control. Secondly, In the dynamic co-evolution of the host and the parasite, genes who confer tolerance against a pathogen could be favored to those who confer resistance. Evolution of tolerance does not harm or might even favor parasite existence since tolerant host are reservoirs of the parasites within the population. Therefore, they do not prompt counter-adaptation by the parasites.
Sacks and Yazdanbakhsh conclude their comment by mentioning that these immune strategies should be taken into consideration when designing vaccines for parasitic diseases. They suggest that instead of trying to override this desire of the immune system for tolerance rather than resistance, vaccines could induce tolerance where minimal pathology is caused by a controlled persistence of the parasites. A classic example of a vaccination strategy in this line is Leishmanization wherein live Leishmania parasites used to be inoculated in soldiers or children in risk of infection and would confer immunity to further infections. With regard to development of immunological tolerance to leishmaniasis, not resistance, these types of vaccines need reconsideration.
Identification of Key Cytosolic Kinases Containing Evolutionarily Conserved Kinase Tyrosine-based Inhibitory Motifs (KTIMs).
Posted by: Issa Abu-Dayyeh
I have posted an earlier article to talk about our PLoS NTD paper where we have described a novel strategy by which Leishmania was able to inhibit TLR-mediated macrophage activation through its ability to inhibit IRAK-1 kinase activity by activating the protein tyrosine phosphatase (PTP) SHP-1.
We have identified the site of binding between SHP-1 and IRAK-1 to be an evolutionarily conserved ITIM-like motif, which we called a kinase tyrosine-based inhibitory motif (KTIM). In this newly-published paper in Developmental and Comparative Immunology, Abu-Dayyeh et al. present evolutinary as well as experimental data that propose that KTIMs could potentially represent a novel regulatory site involved in the control of the kinase activity of many key kinases involved in siganlling pathways of immune cells. Although this work awaits to be further explored by other researches, I believe this work could open various doors towards many important discoveries in the field of immunology.
Here is the abstract of the paper:
We previously reported that SHP-1 regulates IRAK-1 activity by binding to an ITIM-like motif found within its kinase domain, which we named Kinase Tyrosine-based Inhibitory Motif (KTIM). Herein, we further investigated the presence, number, location, and evolutionary time of emergence of potential KTIMs in many cytosolic kinases, all known to play important roles in the signalling and function of immune cells. We unveil that several kinases contain potential KTIMs, mostly located within their kinase domain and appearing predominantly at the level of early vertebrates becoming highly conserved thereafter. Regarding the KTIMs that were found conserved in both vertebrates and invertebrates, we provide experimental data suggesting that such motifs may have constituted readily-available sites that performed new regulatory functions as soon as their binding partners (e.g. SHP-1) appeared in vertebrates. We thus propose KTIMs as novel regulatory motifs in kinases that function through binding to SH2 domain-containing proteins such as SHP-1. Copyright © 2009. Published by Elsevier Ltd.