A new use for the breast cancer drug tamoxifen could bring new hope for HIV/AIDS patients affected by the fungus Cryptococcosis. This fungus causes either pneumonia or the brain infection meningoencephalitis and manifests mainly in HIV/AIDS patients due to their immunosuppressed status. It causes more deaths in this population than, for example, tuberculosis. Overall, it is responsible for approximately 620,000 deaths internationally each year. The study, led by researchers in the laboratory of Dr Damian Krysan in the University of Rochester in the USA, was a response to the fact that therapies for this disease have not substantially advanced since the 1950s and that the gold standard treatment of amphotericin B and 5-flucytosine is not readily available in areas like sub-Saharan Africa where it is most needed. In these areas, fluconazole is standardly used for treatment of Cryptococcosis, being cheaper and more readily available, but unfortunately it is also much less effective.

The current study, to be published in mBio®, the online open-access journal of the American Society for Microbiology (ASM.), follows a growing trend of re-examining old drugs to see if they are effective against targets different from their normal uses. Tamoxifen is a breast cancer drug, but in clinical microbiological tests Dr Krysan’s group discovered that it was effective in killing Cryptococcus. Importantly, it acted synergistically with fluconazole; combining the drugs resulted in four-times greater effectiveness than using either alone. The study also showed that tamoxifen uses a different strategy in killing Cryptococcus compared to how it works against breast cancer. It targets calmodulin-related proteins. This offers an important clue as to the types of strategies that may be important developing newer drugs to target Cryptococcus; the researchers found that if tamoxifen was modified to be more effective in interfering with calmodulin, it also became more effective in killing the fungus.

Dr Krysan concluded that: "This work sets the stage for additional animal studies to see if tamoxifen can be used as a drug in people and will allow us to design new drugs related to tamoxifen that are better antifungals".

Sources

http://www.eurekalert.org/pub_releases/2...020614.php

hello,has anyone given gate 2014 biotechnology?
if so,please give the reviews.

The efficacy of vaccination against the influenza virus has been sharply demonstrated in a report published online today in the American Journal of Respiratory and Critical Care Medicine. The report shows that of flu patients presenting for care at Duke University Hospital, patients who had not been vaccinated were most severely affected and required the most intensive treatment. The study was carried out between November 2013 and early January 2104 on 55 patients. Of these 22 required intensive care, however only two of these had been vaccinated. The majority of the 55 patients were infected with the H1N1 virus that caused the 2009 pandemic. Young, previously healthy adults were particularly hard-hit by the flu outbreak.

The lead author on the paper, Dr Cameron Wolfe, commented that: "Our observations are important because they reinforce a growing body of evidence that the influenza vaccine provides protection from severe illness requiring hospitalizations….The public health implications are important, because not only could a potentially deadly infection be avoided with a $30 shot, but costly hospitalizations could also be reduced."
Previously on this site we have described a flu forecasting website for the United States set up by infectious disease experts at Columbia's Mailman School of Public Health (http://www.biotechnologyforums.com/thread-2914.html). Dr Jeffrey Shaman, who led the development of this forecasting website commented that it may help “foster greater awareness of influenza activity and risk around the country, and motivate individuals to take measures, such as vaccination, to protect themselves against the virus". Studies such as today’s American Journal of Respiratory and Critical Care Medicine paper would seem to support a strategy whereby flu outbreaks are predicted and vaccination programmes initiated in a timely manner. The study also highlighted problems associated with false negative results obtained with a rapid test for influenza which resulted in some patients not receiving anti-virals at an early stage in their illness.

Dr Wolfe concluded that: "Together, our observations during this influenza season support a high prevalence of the H1N1 virus affecting young adults and requiring ICU care, high false negative rates of rapid flu tests, and delay in starting antiviral treatment……Added to the finding of very low vaccination rates among both hospitalized and ICU admissions, our observations support previous findings that vaccination reduces the severity of disease and vaccinations should be encouraged as recommended by the U.S. Centers for Disease Control and Prevention."

Sources

http://www.eurekalert.org/pub_releases/2...021014.php [Accessed 10 February 2014].

Catania, J., Que, L.G., Govert, J.A., Hollingsworth, J.W. and Wolfe, C.R., 2014. High ICU admission rate for 2013-2014 Influenza is associated with a low rate of vaccination. American Journal of Respiratory and Critical Care Medicine, Feb. 10, 2014. http://www.atsjournals.org/doi/abs/10.11...vlM57avnIU [Accessed 10 February 2014].

1-Week Hands-on Workshop on Human/Cancer Cell Culture Techniques & MTT Assay

Organisers: Prof. Dr. Sheo Mohan Singh, Director, International Centre for Stem Cells, Cancer and Biotechnology (ICSCCB)

Dates: March 9th – 15th and April 6th-12th 2014

Location: ICSCCB, Pune, India

Website: http://icsccb.org/workshops/cellcultureworkshop/
The website gives all the necessary information on registration, programme, accommodation, fees and other important details.

Who should attend?
UG/PG/PhD students, faculty, scientists as well as people working in industry in the field of Biotechnology, Bioinformatics, Life Sciences, Medical Sciences, Pharmaceutical Sciences, Chemical Sciences and related subject areas

Purpose of the workshop
There will be a series of 1-Week workshops in which practical hands-on training on the basic cell culture techniques will be provided. These include; media preparation; genomic DNA isolation, estimation and agarose gel electrophoresis; RNA extraction, cDNA preparation, PCR and agarose gel electrophoresis; protein extraction, estimation, SDS-PAGE and Coomassie staining of proteins; freezing and thawing of cells; and MTT Assay for proliferation/cytotoxicity.

The workshop is aimed at beginners to teach and train them in animal cell culture and molecular techniques using human/cancer cell lines. It will be supported by some theoretical classes on basic cell culture techniques, media preparation, gene/protein expression and interaction networks in hematopoietic stem cells (HSCs) and cancer cells.

A new genomic study on people living in the Tibetan plateau has identified a novel mechanism of population adaptation to local environments, in this case specifically to high altitudes. The study, in Nature Communications, found that genetic adaptations beneficial for survival at high altitudes arose approximately 30,000 years ago in ancestors of contemporary Sherpas. Admixture then allowed these genes to be passed on to more recent migrants originating at lower elevations. These advantageous genetic adaptations were amplified by natural selection in the gene pool of modern Tibetans.

The study was carried out by researchers in the University of Chicago, Oxford University Clinical Research Unit in Kathmandu, Nepal, the Mountain Medicine Society of Nepal, Howard Hughes Medical Institute, Maryland and Case Western Reserve University in Ohio. It examined genome-wide data from 69 Nepalese Sherpa, an ethnic group related to Tibetans compared to 96 unrelated individuals from high-altitude regions of the Tibetan plateau. Comparisons were also performed to genomes derived from HapMap3 and the Human Genome Diversity Panel and from Indian, Central Asian and two Siberian populations.

Modern Tibetans have physiological traits that make them well equipped to cope with high altitudes. This includes relatively low haemoglobin levels. Two of the genes which were already to be known to be variant in this population were EGLN1 and EPAS1, which are key to oxygen homeostasis. Previous studies had hypothesised that variants in these genes arose approximately 3000 years ago, but this was at odds with archaeological evidence as well as studies on mitochondrial DNA and Y chromosome evidence. In the current study, the researchers were able to confirm that high-altitude adaptations in the EGLN1 and EPAS1 genes, associated with lower haemoglobin concentration, arose approximately 30,000 years ago and that these adaptations are enriched in the modern Tibetan genome. This suggests that the more recent migrants from lower altitudes acquired the advantageous high altitude variations upon interbreeding with highlanders via admixture. This is a novel mechanism of adaptation of a population to local environment which is independent of selection of new mutations. On a genomic level, modern Tibetans have traits in common with modern Sherpas and with Han Chinese. Apart from the already recognised EGLN1 and EPAS1 genes, the researchers identified other genes not previously known to be associated with high altitude adaptation, including HYOU1, which is enhanced in response to low oxygen and HMBS, which is involved in the production of haem. Dr Anna Di Rienzo, the lead author on the study, concluded that "There is a strong possibility that these genes are adaptations to high altitude…They represent an example of how the ancestry-based approach used in this study will help make new discoveries about genetic adaptations."

Sources

http://www.eurekalert.org/pub_releases/2...020714.php

JEONG, C., ALKORTA-ARANBURU, G., BASNYAT, B., NEUPANE, M., WITONSKY, D.B., PRITCHARD, J.K., BEALL, C.M. AND DI RIENZO, A., 2014. Admixture facilitates genetic adaptations to high altitude in Tibet. Nature Communications 5, Article number: 3281; doi:10.1038/ncomms4281

An international research collaboraration between the laboratory of Prof. Padraic Fallon in Trinity College Dublin, Ireland with researchers in the University of Edinburgh and the University of Erlangen has uncovered a potential new mechanism behind development of idiopathic pulmonary fibrosis (IPF). The study, published recently in the Proceedings of the National Academy of Sciences (PNAS) has identified the cytokine IL-25 and the novel immune cell type, the type 2 innate lymphoid cell (ILC2) as previously unsuspected players in development of IPF.

IPF is a distressing condition whereby lungs of patients become irreversibly scarred, leading to difficulty in breathing. The condition is chronic and progressive with a poor prognosis due to the lack of understanding of the underlying mechanisms and hence lack of effective therapies. Thus research efforts to advance understanding of this condition are all the more important. The disease has been linked to factors such as cigarette smoking and occupational exposure to substances such as gases and dust. It can also arise as a complication of other pulmonary diseases such as asthma. Current hypotheses suggest that the scarring is a result of repeated injuries to the alveolar epithelial cells resulting in release of pro-fibrotic regulators including transforming growth factor β (TGF β), which results in a knock-on effect on fibroblasts, which produce collagen, leading to the scarring.

The PNAS study used both in vivo mouse models and lung samples from patients with IPF in order to examine the mechanisms of IPF. The murine models implicated IL-25 as a major player in IPF generation. The mechanism identified involved IL-25 mediated release of IL-13 from ILC2 cells directly resulting in collagen deposition in the lungs of the challenged mice. In order to link the findings to human disease, lung samples were collected from IPF patients. Interestingly, these samples had increased expression of IL-25 when compared to control samples and also featured a population of ILC2 cells that was missing from control samples. The authors of the study concluded that their findings suggest an innate, T-cell independent mechanism for IPF generation that opens up previously unsuspected therapeutic avenues targeting IL-25 and ILC2.

IPF is not the only disease identified by Prof. Fallon’s research group to potentially feature ILC2 cells and IL-25. In a collaboration with researchers in the University of Oxford, UK and LMB Cambridge, UK, they published a recent study in The Journal of Experimental Medicine implicating ILC2 and IL-25 in the development of atopic dermatitis (eczema) while the first author of the PNAS paper, Dr. Emily Hams, is also examining their role in regulation of obesity. Thus targeting of IL-25 and ILC2 may have far-reaching implications for new therapies for a wide range of diseases.

Sources

Press release:http://www.sfi.ie/news-resources/press-releases/scientists-discover-new-cellular-process-leading-to-lung-fibrosis.html [Accessed 10 February 2014].

HAMS, E., ARMSTRONG, M., BARLOW, J., SAUNDERS, S., SCHWARTZ, C., COOKE, G., FAHY, R.J., CROTTY, T.B., HIRANI, N., FLYNN, R.J., VOEHRINGER, D., MCKENZIE, A.N., DONNELLY, S.C. and FALLON, P. (2014). IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis. Proceedings Of The National Academy Of Sciences Of The United States Of America, 111(1), 367-372. doi:10.1073/pnas.1315854111

SALIMI, M., BARLOW, J., SAUNDERS, S., XUE, L., GUTOWSKA-OWSIAK, D., WANG, X., HUANG, L., JOHNSON, D., SCANLON, S., MCKENZIE, A., FALLON, P., and OGG, G 2013, A role for IL-25 and IL-33-driven type-2 innate lymphoid cells in atopic dermatitis. The Journal Of Experimental Medicine, 210, 13, pp. 2939-2950

Have recently returned to my background in molecular biology/biochemistry.
Specifically, I have interest in the marine cyanobacteria that produce oxygen, ethylene and both. Seeking the top producers and would like to know which members cultivate these
Some of the culture labs did not answer virtually any of my emailed queries.

Guidance sought

Hello...I m in my second year of biotechnology. It would be nice if anyone tell me about what is the pka of Dna and why it has that pka??Thank you..

After 4 months I'm going to complete my studies (B.Sc. BIOINFORMATICS ) but now I'm confused. I want to know, is it better to do M.Sc. Bioinformatics after B.Sc.?? Is there any scope (jobs) in this field??

A study led by a research group in the University of Washington has found that inherited (germline) mutations in genes known to be involved in ovarian cancer are present in 20% of women with no known family history or predisposition to ovarian cancer. The study, published yesterday in Nature Communications, also revealed the presence of germline mutations in genes not previously associated with ovarian cancer. The results of this study suggest that screening of women for ovarian cancer needs to take into account the fact that genetic susceptibility to ovarian cancer may not be obvious from a look at family history. While more than 20000 women are estimated to be afflicted with ovarian cancer, often it is not diagnosed until the cancer has spread due to a lack of definitive symptoms. As a result, there is a poor five –year survival rate for this cancer. The germline mutations identified in this study may not in themselves necessarily lead to cancer, however when linked to acquired (somatic) genetic changes that may occur during a woman’s life, these germline mutations would be sufficient to tip the balance. The authors consider the 20% figure to be conservative as on-going research is expected to reveal further mutations.

The study used large-scale exome-wide analysis to examine both tumour DNA and the woman’s own DNA from 429 ovarian carcinoma cases and 557 controls. These ovarian cancer cases were considered to have arisen sporadically, in the absence of any known familial susceptibility. By comparing the sequences, the researchers were able to identify the somatic mutations that had been acquired in the tumour. In addition, they could compare the ovarian cancer patients’ own DNA samples to those of control subjects to determine if there were germline variants in the cancer patients related to susceptibility to ovarian cancer. This genetic detective work revealed that in 20% of these apparently sporadic ovarian cancer cases, there were germline truncation variants and large deletions in genes belonging to the Fanconi pathway. This pathway is associated with cell division and repair of damaged or mutated DNA and includes the genes BRCA1 (breast cancer type 1 susceptibility protein) and BRCA2 (breast cancer type 2 susceptibility protein), which are widely known to be associated with predisposition to both ovarian and breast cancer. The study found that the ovarian cancer patients carried germline mutations in these genes which would lead to shortened (truncated) protein product, as well as mutations in another gene in this pathway, PALB2 (Partner and localizer of BRCA2). As well as these mutations which were already familiar in the field of ovarian cancer susceptibility, mutations were found in several other genes not previously known in this context, including NF1 (Neurofibromin), MAP3K4 (Mitogen-activated protein kinase kinase kinase 4), CDKN2B (Cyclin-dependent kinase 4 inhibitor B) and MLL3 (Histone-lysine N-methyltransferase 2C).

In all, the findings of this important paper should encourage better integration of knowledge of both inherited and acquired mutations in causing ovarian cancer and contribute to changes in screening practices for this devastating disease. The lead author of the paper, Dr. Li Ding, said: “We’re now able to obtain a fuller picture of the way cancer develops in a particular patient. More studies are needed, but our findings could have important implications for developing better screening strategies for ovarian cancer and improving early detection.”

Sources

Kanchi KL, Johnson KJ, Lu C, Raphael BJ, Wilson RK, Ding L et al. Integrated analysis of germline and somatic variants in ovarian cancer. Nature Communications. Jan. 22, 2014. (Available at
http://www.nature.com/ncomms/2014/140122...affil-auth

Press release: https://news.wustl.edu/news/Pages/26399.aspx

Hello I will tell you about my first experiment idea it will be a breeding project that will have the purpose of creating better organization and weapons among bacteria and viruses to fight cells and medicine I am open to Ideas I will discuss mine with you!

I am basically from biotech background and interested in doing training in bioinformatics. Please tell me about the uses of microarray data analysis .

Studies on the white-throated sparrow have given a rare insight into how a chromosomal rearrangement resulting in genetic polymorphism directly impacts behaviour in a vertebrate. The study, led by researchers in Emory University, was published in early edition this week in the Proceedings of that National Academy of Sciences in the United States of America (PNAS). It has linked differences in parenting and aggression behaviour in two different white-throated sparrow phenotypes to the oestrogen receptor ER-alpha.

The PNAS study examined white-throated sparrows (Zonotrichia albicollis) with two different, long-recognised phenotypes caused by a rearrangement in a chromosome sequence known as chromosomal polymorphism ZAL2/2m. This polymorphism results in two readily distinguishable forms of the sparrow, the tan-striped morph and the white-striped morph, respectively. The attached picture clearly shows how they can be distinguished by their plumage (copyright/credit Brent Horton, http://esciencecommons.blogspot.ie/2014/...ocial.html). Sparrows with the rearranged ZAL2m polymorphism (white-striped) are recognised to be more aggressive and less parental than the tan-striped birds.

In the study, parenting behaviour was assessed in the wild by monitoring frequency with which the birds returned to the nest to feed their young while aggression monitoring was based on analysis of song rate in the presence of a perceived threat to the sparrow’s territory. Such patterns of behaviour are thought to be mediated by sensitivity to sex steroids in vertebrates. An examination of the polymorphic region revealed various candidate genes, among them ESR1, the gene for oestrogen receptor ER-alpha. Levels of expression of this receptor affect sensitivity to sex hormones including testosterone. The study demonstrated that in the region of the ESR1 gene that controls its expression, known as the promoter, there were fixed differences (polymorphisms) between the tan-striped and white-striped birds. These polymorphisms affected the transcription of ESR1 in vitro. When expression of the ESR1 protein product, ER-alpha, was examined in brain regions associated with aggression, white-striped birds (the more aggressive ZAL2m polymorphism type) had three times the level of ER-alpha than the tan-striped birds. By correlating behavioural data and lab data, the researchers were able to show that expression of ER-alpha in that region and others predicted variation in territorial aggression and parenting.

This is an unusual example of a study being able to demonstrate directly how a chromosomal rearrangement causes behavioural difference in a vertebrate. The authors are currently examining a suite of further neuroendocrine genes captured by the chromosome rearrangement to examine their impact on behaviour.

Sources
HORTON, B.M., HUDSON, W.H., ORTLUND, E.A., SHIRK, S., THOMAS, J.W., YOUNG, E.R., ZINZOW-KRAMER, W.M. and MANEY, D.L., 2014. Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes. Proceedings of the National Academy of Sciences. 2014 Jan; Available from: http://dx.doi.org/10.1073/pnas.1317165111.

Press release: http://esciencecommons.blogspot.ie/2014/...ocial.html

Researchers from KU Leuven in Belgium have identified a ‘short-circuit’ mechanism in chemosensors called transient receptor potential (TRP) channels that can paradoxically lead to increased pain in response to candidate painkillers targeting these channels. The work, published online in last week’s Nature Chemical Biology focused on one member of the TRP family called TRPM3.

Pain provides with a vital ‘warning’ system alerting us to the dangers of, for example, extreme heat or cold. A network of sensory nerves, for example in the skin and mucosa, relays pain signals from around the body to the brain. Around these nerves are ion channels such as the TRP family. The TRP family act as primary chemosensors. Upon binding of a ligand, a cation conducting pore opens in the middle of the TRP channel. This results in a tiny electrical signal which when it is transmitted to the brain is interpreted as pain. The Belgian group’s work involved study of candidate painkillers which would target the TRPM3. This channel detects heat and the hormone pregnenolone sulfate, a pain and inflammation trigger. TRPM3 can be gated by combinding drugs such as endogenous neurosteroids and exogenous chemicals such as clotrimazole.

In an in vivo mouse model, the Belgian study found that an alternative pathway was mediated via TRPM3 when channels were closed by a number of different mechanisms including desensitization, blockade, mutagenesis and chemical modification of the central pore. This pathway therefore did not depend on an open ion channel. Instead, it involved a ‘short circuit’ whereby the stimulus found a different route; rather than using the central pore, it carved a path through the surrounding material and activated the nearby pain nerves, sending a pain signal to the brain. The overall result was to exacerbate TRPM3-dependent pain. The researchers maintain that this mechanism may explain the pain-enhancing side effects of drugs such as clotrimazole and thy hope that it will shed new light on TRP channel function and pharmacology.

Sources

Vriens, J., Held, K., Janssens, A., Tóth, B., Kerselaers, S., Nilius, B., Vennekens, R., & Voets, T., 2014, 'Opening of an alternative ion permeation pathway in a nociceptor TRP channel', Nature Chemical Biology, viewed 14 January 2014

Press release: http://www.kuleuven.be/english/news/shor...ifies-pain

A flu forecasting website for the United States set up by infectious disease experts at Columbia's Mailman School of Public Health may help “foster greater awareness of influenza activity and risk around the country, and motivate individuals to take measures, such as vaccination, to protect themselves against the virus" according to Jeffrey Shaman, PhD, who led the site’s development. The URL is cpid.iri.columbia.edu. The system reports predictions every Friday during the flu season for 94 US cities.

The latest data reported was for the week from December 29th 2013 to January 4th 2014. It reported in which cities flu was expected to arise and when it would peak and also in which cities seasonal flu is likely to have already peaked. Overall, the system predicted that the 2013-2014 flu season would peak later with fewer cases than in 2012-2013 but with considerably more severe cases than in 2011-2012 season.

According to a press release from Colombia, the website boasts features including:
• Interactive map of the United States the displays the relative severity of seasonal flu in cities across the country flu and incidence numbers for each.
• Influenza incidence predictions by city for the coming weeks.
• Map that illustrates the proportion of flu cases by region.
• Charts that compare the timing and severity of the four most recent flu seasons.
• Exportable data for each week of the flu season (beginning in 9/29 for the 2013-2014 season).

The scientifically validated system adapts techniques used in weather forecasting to convert real-time, Web-based estimates of influenza infection into local forecasts of the future influenza incidence by locality. It is hoped that access to the website may have a positive public health impact by influencing the public in terms of accessing vaccination and exercising care around people sneezing and coughing. It should also have a positive impact on public health officials by helping inform decisions on vaccine stockpiling and distribution and measures such as school closures. It is to be hoped that in the future this type of system may become available internationally.

   
This is a screenshot of cpid.iri.columbia.edu. Credit: cpid.iri.columbia.edu

Source
http://www.eurekalert.org/pub_releases/2...011314.php

Research published in last week's Nature Communications suggests that the microRNA miR-181a may be a useful prognostic marker for predicting response to therapy of epithelial ovarian cancer (EOC). The study, from research groups in Case Western Reserve University and Mount Sinai Medical Centre, both in the USA, and the Mario Negri Institute of Pharmaceutical Research in Milan, examined expression of miR-181a in 80 human EOC samples. They also used both in vitro and preclinical in vivo ovarian mouse models to elucidate function and pathways of miR-181a. According to Analisa DiFeo of Case Comprehensive Cancer Center and lead investigator on the study, their findings showed that “miR-181a was one of the top expressing microRNAs in tumours from patients who recurred within the first six months after treatment" and that there were “higher levels in recurrent tumours compared to primary tumours" in their patient population.

MicroRNAs such as miR-181a are short, single stranded RNA molecules which help control expression of up to 60% of all protein encoding genes. In the current study, in vivo and in vitro studies indicated that the target for miR-181a was the Smad7 gene. SMAD7 protein is an inhibitor of the TGF-β signalling pathway, a potent metastases inducer. Inhibition of SMAD7 by miR-181a would therefore remove the brake on TGF-β and encourage metastases.

However, the story of miR-181a in cancer is not straightforward, and it appears to have more than one target protein, suggesting caution should be applied in any consideration of miR-181a in EOC therapy. MiR-181a has been associated with poor prognosis in colorectal cancer (CRC) and enhances the chemoresistance and resistance to radiation of human cervical squamous cell carcinoma. In contrast, in breast cancer decreased serum miR-181a has been proposed as a potential biomarker and miR-181a has been shown, for example, to enhance drug sensitivity in mitoxantone-resistant breast cancer cells. In this case, the target for miR-181a is the breast cancer resistance protein (BCRP/ABCG2). On the other hand, the target in CRC was expression of the tumour suppressor, phosphatase and tensin homolog (PTEN) while in human cervical squamous cell carcinoma cells it targeted the apoptosis inhibitor PRKCD.

Given the number of targets for miR-181a that have been identified in various cancer cells and the differing effects of the microRNA in breast cancer as opposed to ovarian, cervical and colorectal cancer, a lot of work lies ahead in any potential therapeutic use of miR-181a. This is particularly relevant, for example, for women with hereditary breast–ovarian cancer syndromes. However, the study in Nature Communications does suggest a prognostic value for miR-181a in predicting response to therapy and recurrence for EOC.

Sources

Press release: http://www.eurekalert.org/pub_releases/2...010814.php [Accessed 8 January 2014]

Guo, L., & Zhang, Q., 2012, 'Decreased serum miR-181a is a potential new tool for breast cancer screening', International Journal Of Molecular Medicine, 30, 3, pp. 680-686,

Chen, Y., Ke, G., Han, D., Liang, S., Yang, G., & Wu, X., 2014, 'MicroRNA-181a enhances the chemoresistance of human cervical squamous cell carcinoma to cisplatin by targeting PRKCD', Experimental Cell Research, 320, 1, pp. 12-20,

[b]Parikh, A., Lee, C., Joseph, P., Marchini, S., Baccarini, A., Kolev, V., Romualdi, C., Fruscio, R., Shah, H., Wang, F., Mullokandov, G., Fishman, D., D'Incalci, M., Rahaman, J., Kalir, T., Redline, R., Brown, B, Narla, G., & Difeo, A., 2014, 'microRNA-181a has a critical role in ovarian cancer progression through the regulation of the epithelial-mesenchymal transition', Nature Communications, 5, p. 2977

Nishimura, J., Handa, R., Yamamoto, H., Tanaka, F., Shibata, K., Mimori, K., Takemasa, I., Mizushima, T., Ikeda, M., Sekimoto, M., Ishii, H., Doki, Y., & Mori, M., 2012, 'microRNA-181a is associated with poor prognosis of colorectal cancer', Oncology Reports, 28, 6, pp. 2221-2226

Ke, G., Liang, L., Yang, J., Huang, X., Han, D., Huang, S., Zhao, Y., Zha, R., He, X., & Wu, X., 2013, 'MiR-181a confers resistance of cervical cancer to radiation therapy through targeting the pro-apoptotic PRKCD gene', Oncogene, 32, 25, pp. 3019-3027

Jiao, X., Zhao, L., Ma, M., Bai, X., He, M., Yan, Y., Wang, Y., Chen, Q., Zhao, X., Zhou, M., Cui, Z., Zheng, Z., Wang, E., & Wei, M., 2013, 'MiR-181a enhances drug sensitivity in mitoxantone-resistant breast cancer cells by targeting breast cancer resistance protein (BCRP/ABCG2)', Breast Cancer Research And Treatment, 139, 3, pp. 717-730

Pichler, M., Winter, E., Ress, A., Bauernhofer, T., Gerger, A., Kiesslich, T., Lax, S., Samonigg, H., & Hoefler, G., 2013, 'miR-181a is associated with poor clinical outcome in patients with colorectal cancer treated with EGFR inhibitor', Journal Of Clinical Pathology,

The analysis of polyacrylamide gels is currently carried out manually or automatically. In the automatic method, there are limitations related to the acceptable degree of distortion of lane and band continuity. The available software cannot deal satisfactorily with this type of situations. Therefore, the paper presents an original image analysis method devoid of the aforementioned drawbacks.

more to read at:
http://www.biomedical-engineering-online...nt/12/1/68

It is possible to carry out this method of DNA polymorphism analysis on distorted images of polyacrylamide gels. The method is fully automatic and does not require any operator intervention. Compared with other methods, it produces the best results and the resulting image is easy to interpret. The presented method of measurement is used in the practical analysis of polyacrylamide gels in the Department of Genetics at the University of Silesia in Katowice, Poland.

Hi All,

I have done my graduation in computer science two years back,I wish to study my Post graduation in Bioinformatics as I am well interested in this course moreover I did my 12th in Bio-Science.I look forward to become a Bioinformatics Research Scientist.Please request you to provide the scope of this course in India and abroad

Thank you.

The findings of a new study from the University of Eastern Finland may suggest that including sources of vitamin E in the diet, such as vegetable oils including palm oil, sunflower, corn, soybean and olive oil or using vitamin E supplements, could confer an advantage in avoiding memory disorders in later life. The study, published in Experimental Gerontology, found that elevated serum levels of various vitamin E forms was associated with decreased risk of development of cognitive impairment. Vitamin E is a fat-soluble vitamin in eight forms, four tocopherols and four tocotrienols and is an important anti-oxidant. To date one form, α-tocopherol , which is found in many vitamin E supplements, has been focused on in studies of cognitive impairment and Alzheimer's disease. However the Finnish study suggests that other forms of vitamin E, including γ-tocopherol, β-tocotrienol and total tocotrienols, are associated with the observed protective effect.

The study focused on a sample of 140 Finnish people over the age of 65 who had no memory impairment at the beginning of the 8-year study. The study population was drawn from participants in the more extensive Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study, which examines links between cardiovascular disease and memory impairment. For the purposes of the study, cognitive impairment was defined as development of mild cognitive impairment (MCI) or Alzheimer's dementia. Lower risk of cognitive impairment was observed in subjects with higher absolute serum levels of γ-tocopherol, β-tocotrienol, and total tocotrienols. The study highlights the importance of considering all forms of vitamin E when considering vitamin E status and suggests a further benefit of including vitamin E in the diet.

Sources

MANGIALASCHE, F., SOLOMON, A., KÅREHOLT, I., HOOSHMAND, B., CECCHETTI, R., FRATIGLIONI, L., SOININEN, H., LAATIKAINEN, T., MECOCCI, P. and KIVIPELTO, M., 2013. Serum levels of vitamin E forms and risk of cognitive impairment in a Finnish cohort of older adults. Experimental Gerontology, 48 (12): 1428 DOI: 10.1016/j.exger.2013.09.006

University of Eastern Finland. "Several forms of vitamin E protect against memory disorders, study says." ScienceDaily, 7 Jan. 2014. [Accessed 8 Jan. 2014].

Scientists in the University of Washington have used nanoparticle technology to immunise mice with what they term ‘just-in-time’ vaccines in a process that could revolutionise distribution and accessibility of vaccines if successfully extended to humans in the future. Current technologies rely on making batches of vaccines centrally and then distributing them to centres where they need to be used, with refrigeration required at all steps. The University of Washington researchers used rudimentary equipment and a single-pot process to produce their vaccine. If this could be extended to humans, it raises the possibility of making vaccines at the site at which they are needed. This would be especially advantageous in the developing world, allowing doctors and scientists locally to act to produce the necessary vaccines cheaply and easily at the first signs of an epidemic.

The University of Washington study, published this week in the journal Nanomedicine: Nanotechnology, Biology and Medicine, used a fusion protein created between ovalbumin, which is often used as a model antigen in animal studies, and a calcium phosphate binding domain. This effectively created a mineralised biocompatible adjuvant in a single step. When administered to mice, this nanoparticle induced the production of an ovalbumin-specific antibody response and class-switch recombination. Importantly, when the mice were subsequently challenged with an influenza virus containing an ovalbumin-derived peptide, the mice produced substantially higher levels of ovalbumin-specific CD8 T cells- protective killer cells of the immune system- and a cytokine called interferon-gamma (IFN-gamma) which is toxic to invading pathogens, compared to mice which received the protein in the absence of the nanoparticle. A robust immune response was observed 8 months after vaccination. The mechanism of action of the nanoparticle appears to reside in its ability to ferry antigen to the secondary lymph nodes, where immune reactions can be mounted. There they are detected by specialised immune cells called dendritic cells, which in turn can then present antigen to the immune killer cells such as CD8 T cells.

The strength of this technology lies in its simplicity, with production possible using rudimentary equipment, and lack of reliance on transport and refrigeration of vaccines. Production costs would be much lower and production could be tailored to match the vaccines to the relevant specific infectious agents at local level. Additionally, there is the possibility of administering vaccine via alternative methods to injection, such as a disposable patch. There is a long road ahead for this technology in terms of human testing but one day it may have a positive impact on vaccination programmes worldwide.

Sources

Zhou, W., Moguche, A.O., Chiu, D., Murali-Krishna, K. and Baneyx, F., 2013. Just-in-time vaccines: Biomineralized calcium phosphate core-immunogen shell nanoparticles induce long-lasting CD8 T cell responses in mice. Nanomedicine: Nanotechnology, Biology and Medicine, 2013; DOI: 10.1016/j.nano.2013.11.007

University of Washington. "On-demand vaccines possible with engineered nanoparticles." [/align], 7 Jan. 2014. [Accessed 8 Jan. 2014]