Which way are we going?

We need rule of law, not rule of mafia. Young population of UP had expected a lot from Akhilesh Yadav, but he failed totally and worst even than Mulayam Singh Yadav. Mayawati did worst that's why public refused her, now Akhilesh Yadav is on same track and within one year lost his ground as exemplified by exit polls. Parliamentary election will teach him. If Durga Shakti Nagpal (IAS officer) demolished an illegal construction, then before suspending her government should show courage to declare it legal first. It's court instruction to stop any such construction on government property, then Akhilesh should suspend that judge first who gave this instruction because by his sentence the judge broke communal harmony. These kind of opportunistic politics is destroying the democracy. 

People should think about their future and respond accordingly. By corruption one can make money in short-term and can defend it by manipulating his deeds, but in the long-term it's fatal even for his children. Please you must think about this. Come out of caste-based politics and make India safe and secured for everyone.

Jai Hind !!!

Professor Obaid Siddiqi, National Research Professor at the National Centre for Biological Sciences, Tata Institute of Fundamental Research (TIFR) passed away

Obaid Siddiqi FRS, National Research Professor at the National Centre for Biological Sciences, Tata Institute of Fundamental Research (TIFR) passed away on 26 July 2013. He is survived by his wife Asiya, sons Imran and Kalim, and daughters Yumna and Diba.

 

Obaid Siddiqi was born in 1932 in Uttar Pradesh and received his early education at Aligarh Muslim University. He obtained his Phd from the University of Glasgow, working on microbial genetics with Guido Pontecorvo. He carried out post-doctoral research with Alan Garen at the Cold Spring Harbor Laboratory and University of Pennsylvania. This work led to the discovery of stop codons in the genetic code and the mechanism of chain termination during protein synthesis.

In 1962, at the invitation of Homi Bhabha, he set up the Molecular Biology Unit at the Tata Institute of Fundamental Research in Mumbai. The formation of this unit is widely regarded as a transformational event in the landscape of modern biology research in India. Thirty years later, he would become the founding director of the TIFR National Center for Biological Sciences in Bangalore.

In the early seventies, Siddiqi began to study the genetic basis of behaviour using Drosophila as a model. Working with Seymour Benzer at Caltech he discovered a set of temperature sensitive paralytic mutants that exhibited defects in the electrical activity of nerves and muscles. This discovery led to a deeper understanding of the mechanistic basis of neuronal function and heralded the dawn of the field of Behavioral Genetics.

In the nineteen eighties, Siddiqi and his students at TIFR, Mumbai carried out pioneering work on the genetic basis of taste and smell in Drosophila. These discoveries paved the way for the modern understanding of how senses such as taste and smell are detected and encoded in the brain. He was active in this area of research till the end of his life, maintaining an active laboratory as an Emeritus Professor at NCBS.

Obaid Siddiqi's contributions have been widely recognized both nationally and internationally. He was an elected member of the Royal Society, London (FRS), the US National Academy of Sciences, The World Academy of Sciences, Trieste, the Indian Academy of Sciences, Bangalore (President 1986-89), National Academy of Sciences (India), Allahabad, and Maharashtra Academy of Sciences.

He has been honoured with the Padma Vibhushan, Padma Bhushan, Bhatnagar Prize, INSA Golden Jubilee Medal, Birla Samarak Kosh National Award, Goyal Foundation Prize, Aryabhatta Medal by INSA, Bhasin Foundation Prize, Science Congress Plaque of Honours, BC Roy Award for Biomedical Research and Firodia Award for Basic Sciences.

Obaid Siddiqi has held visiting professorships at Yale University, the Massachusetts Institute of Technology, the California Institute of Technology and Cambridge University. He was twice Sherman Fairchild Distinguished Scholar at Caltech and was a life member of Clare Hall, Cambridge. Aligarh Muslim University, Banaras Hindu University, Jamia Hamdard, Kalyani University, IIT Bombay, Jamia Millia Islamia and Central University of Hyderabad have conferred upon him the honorary degree of D.Sc.

In the words of K VijayRaghavan, former director of NCBS: "There are a daring few who define new intellectual quests, and whose courage and leadership create a culture...today, we celebrate Obaid Siddiqi whose foresight, determination and quiet courage has transformed research in molecular biology in India at least twice and whose scientific successes span many fields of biology. While establishing institutional excellence and instilling an iconoclastic culture of independence and freethinking, these pioneering efforts have led to wide appreciation, both of the beauty and value of Obaid's science and of his leadership in institution building, as models to emulate."

According to Satyajit Mayor, current Director of NCBS: "Obaid Siddiqi was one of the finest biologists India has ever had. His contribution to the growth of Molecular Biology in India is unparalleled. Throughout his career, Obaid always set an example for doing science at its most creative. He pioneered efforts in establishing the field of Behavioral Genetics based on his own research on the genetics of olfactory sensation in Drosophila. At the same time in his gentle but persuasive style he motivated a legion of younger colleagues by doing excellent science himself whilst in India. In 1992 he established the National Centre for Biological Sciences as a Centre of TIFR, to achieve excellence and to nurture fundamental curiosity to explore new frontiers in biological research. The realization and embodiment of these core principles, through the growth of the Centre over twenty years, is yet again a testimony to the foresight of this visionary man. Establishing an institution that promotes enquiry at all scales of Biology is indeed a pioneering experiment in how research in biological sciences may be conducted in the modern era of molecular biology.

It is not a surprise that Obaid Siddiqi was also one of India most decorated scientists. We will miss our friend, philosopher and muse deeply, and hope to cherish his dreams and ambitions in the way we would know he would want us to- by building on the edifice he has left us, and doing even more creative science."

Source: NCBS News

Nitish Kumar's media management

Now a days politicians started a new trend called as "media management" to favor their work and not to criticize. This is fatal to our democracy because media play a critical role to bring issues impartially to people and subsequently people make their views for the particular government. Media also has become a key player of corruption. 

Nitish Kumar spent Rs.182 crores of public money on media to advertise his "sushasan". Please read full report of BeyondHeadlines in this regard obtained by RTI.

Please click here to read.

Japanese team creates cancer-specific killer T cells from induced pluripotent stem cells

Researchers from the RIKEN Research Centre for Allergy and Immunology in Japan report today that they have succeeded for the first time in creating cancer-specific, immune system cells called killer T lymphocytes, from induced pluripotent stem cells (iPS cells). To create these killer cells, the team first had to reprogram T lymphocytes specialized in killing a certain type of cancer, into iPS cells. The iPS cells then generated fully active, cancer-specific T lymphocytes. These lymphocytes regenerated from iPS cells could potentially serve as cancer therapy in the future.

Previous research has shown that killer T lymphocytes produced in the lab using conventional methods are inefficient in killing cancer cells mainly because they have a very short life-span, which limits their use as treatment for cancer. To overcome these problems, the Japanese researchers led by Hiroshi Kawamoto and presenting their results in the journal Cell Stem Cell online today, reprogramed mature human killer T lymphocytes into iPS cells and investigated how these cells differentiate.

The team induced killer T lymphocytes specific for a certain type of skin cancer to reprogram into iPS cells by exposing the lymphocytes to the 'Yamanaka factors'. The 'Yamanaka factors' is a group of compounds that induce cells to revert back to a non-specialized, pluripotent stage. The iPS cells obtained were then grown in the lab and induced to differentiate into killer T lymphocytes again. This new batch of T lymphocytes was shown to be specific for the same type of skin cancer as the original lymphocytes: they maintained the genetic reorganization enabling them to express the cancer-specific receptor on their surface. The new T lymphocytes were also shown to be active and to produce the anti-tumor compound interferon-γ.

"We have succeeded in the expansion of antigen-specific T cells by making iPS cells and differentiating them back into functional T cells. The next step will be to test whether these T cells can selectively kill tumor cells but not other cells in the body. If they do, these cells could be directly injected to patients for therapy. This could be realized in the not-so-distant future." explains Dr Kawamoto. 

Reference

• Raul Vizcardo, Kyoko Masuda, Daisuke Yamada, Tomokatsu Ikawa, Kanako Shimizu, Shin-ichiro Fujii, Haruhiko Koseki, Hiroshi Kawamoto "Regeneration of human tumor antigen-specific T cells from iPS cells derived from mature CD8+ T cells." Cell Stem Cell, 2013. doi: 10.1016/j.stem.2012.12.006

Nanoparticles help disrupt tumor blood supply, destroy tumors

In recent years, cancer researchers have been developing agents that destroy the blood vessels surrounding tumors with the goal of starving tumors to death. Some of these agents, such as tumor necrosis factor-alpha (TNF-α) have shown promising results, but often their toxicity has proven too great to be clinically useful. Using gold nanoparticles as a delivery vehicle for TNF-α has reduced this toxicity and the resulting construct has already completed a phase I clinical trial in humans.

Now, a team at the University of Minnesota headed by John Bischof, has shown that they can use this gold nanoparticle-TNF-α system to enhance the effects of either thermal therapy or cryosurgery. Moreover, the researchers demonstrated that they can use standard magnetic resonance imaging technology to visualize tumor destruction. Dr. Bischof and his colleagues reported their findings in the journal Molecular Pharmaceutics.

 Experiments in a mouse model of human prostate cancer showed that the gold nanoparticle-TNF-α system disrupted blood flow into tumors within 90 minutes of injection, an effect that lasted up to six hours. Using a technique known as dynamic contrast-enhanced MRI, Dr. Bischof's team was able to clearly image the changes in blood flow into and around the tumor following nanoparticle treatment. The researchers note that in human patients, a simple five-minute MRI scan would be sufficient to detect a meaningful change in tumor blood vessel function.

 Once the tumor blood vessels had been "preconditioned," Dr. Bischof and his collaborators treated the animals with either thermal therapy or cryosurgery, both of which produced marked reductions in tumors. They noted that none of the animals treated with thermal therapy died, an important finding given that an equivalent dose of TNF-α with no gold nanoparticle attached followed by thermal therapy was found to be lethal in a large percentage of animals. The researchers also showed that nanoparticle-delivered TNF-α did not trigger inflammatory reactions associated with activated neutrophils, something that does occur when tumors are treated with native TNF-α.

 This work, which was supported in part by the National Cancer Institute, is detailed in a paper titled, "Nanoparticle delivered vascular disrupting agents (VDAs): use of TNF-α conjugated gold nanoparticles for multimodal cancer therapy." Investigators for the University of Arkansas for Medical Sciences also participated in this study. An abstract of this paper is available at the journal's website.

Scientists discover kill-switch controls immune-suppressing cells

Scientists have uncovered the mechanism that controls whether cells that are able to suppress immune responses live or die.

The discovery of the cell death processes that determine the number of 'regulatory T cells' an individual has could one day lead to better treatments for immune disorders.

Regulatory T cells are members of a group of immune cells called T cells. Most T cells actively respond to clear the body of infections. By contrast, regulatory T cells are considered to be immune-suppressing cells because they can 'switch off' immune response to a particular molecule. This immune suppression is important for preventing the inappropriate immune attack of the body's own tissues, which is the underlying cause of autoimmune diseases such as lupus and type 1 diabetes.
 

A shortage of regulatory T cells is linked with the development of autoimmune and inflammatory conditions, while some people with higher than normal numbers of regulatory T cells cannot fight infections properly.



Scientists have uncovered the mechanism that controls whether cells that are able to suppress immune responses live or die. Dr Daniel Gray (right) and Ms Antonia Policheni from Melbourne's Walter and Eliza Hall Institute of Medical Research were part of a research team that made the discovery, which could one day lead to better treatments for immune disorders. Credit: Walter and Eliza Hall Institute of Medical Research.

Dr Daniel Gray and Ms Antonia Policheni from the Walter and Eliza Hall Institute's Molecular Genetics of Cancer and Immunology divisions made the discovery about how regulatory T cell numbers are controlled as part of an international team of researchers jointly led by Dr Gray and Dr Adrian Liston who is head of the Flanders Institute for Biotechnology (VIB) Laboratory for Autoimmune Genetics at the University of Leuven, Belgium. They found that regulatory T cells are constantly being produced in the body, but their numbers are held steady by a process of cell death. The findings are published today in the journal Nature Immunology.

Cell death, or apoptosis, is important in many immune cell types for the removal of excess, defective or damaged cells. The decision of these cells on whether to live or die is controlled by a family of proteins called the 'Bcl-2 protein family'. This includes proteins that can either promote cell survival or trigger cell death, in response to many different stimuli.

Dr Gray said the team had discovered that Bcl-2 family proteins were important determinants of regulatory T cell numbers. "Regulatory T cell death is highly dependent on the activity of two opposing Bcl-2 family proteins, called Mcl-1 and Bim," he said. "Mcl-1 is required for regulatory T cell survival, allowing them to suppress unhealthy immune responses, while Bim triggers the death of regulatory T cells. Without Mcl-1 activity, regulatory T cell numbers fall, provoking lethal autoimmune disease. Conversely, if Bim activity is lost, regulatory T cells accumulate in abnormally high numbers."

Dr Liston said the finding was exciting, because it opened up new ways to control regulatory T cell numbers in disease. "Already, there is considerable interest in a new class of agents, called 'BH-3 mimetics' that target Bcl-2-like molecules including Mcl-1," he said. "If agents that can influence regulatory T cell survival can be developed, we could see new ways to suppress autoimmune disease, by boosting regulatory T cell numbers, or to enhance beneficial immune responses, by silencing regulatory T cells."

Source: Walter and Eliza Hall Institute

Novel bacterial 'language' discovered

In nature, bacteria are no mavericks but live in close association with neighboring bacteria. They have evolved specific cell-cell communication systems that allow them to detect the presence of others and even to build up cooperative networks.

LMU microbiologist PD Dr. Ralf Heermann and Professor Helge Bode of the Goethe-University in Frankfurt have just reported the discovery of a previously unknown bacterial "language". Their findings are detailed in the latest issue of the journal Nature Chemical Biology. "Our results demonstrate that bacterial communication is much more complex than has been assumed to date," Heermann says.

The bacterial communication system that is currently best understood uses N-acylhomoserine lactones (AHLs) as signals. These compounds are made by enzymes that belong to the group of LuxI-family synthases. Transmitting cells secrete the signal and neighboring cells recognize the concentration via a LuxR-type receptor. Signal perception changes the pattern of gene expression in the receiving cells, which results in alterations in their functional properties or behavior. However, many bacteria have LuxR receptors but lack any LuxI homolog, so that they cannot produce AHLs. These receptors are referred to as LuxR solos.

A new class of bacterial signaling molecules
Ralf Heermann and Helge Bode have now discovered a type of ligand that binds to LuxR solos. As model system, they chose the species Photorhabdus luminescens, a pathogenic bacterium that is lethal to insects.

Bacteria communicate by means of chemical processes. LMU microbiologist PD Dr. Ralf Heermann and Professor Helge Bode of the Goethe-University Frankfurt have identified a novel bacterial cell-cell communication system that uses alpha-pyrones …more
 

"We have identified a new class of bacterial signaling molecules, which are produced by a previously unknown biochemical route," explains Helge Bode, Merck Professor of Molecular Biotechnology at Goethe-Universität Frankfurt. It turns out that a LuxR solo of this bacterium responds to compounds called alpha-pyrones, specifically to photopyrones. Furthermore, the researchers have identified the pyrone synthase (PpyS) that catalyzes the biosynthesis of photopyrones. The pyrone-based signaling system allows the bacteria to recognize one another, whereupon they produce a surface factor that causes cell clumping. Heermann and Bode assume that this collective behavior makes the cells less vulnerable to the insect's innate immune system, and then allows them to kill their victims by the production of various of toxins." P. luminescens is a useful model organism, because it is related to many human pathogens, including coliform bacteria such as enterohemorrhagic E. coli (EHEC) and well as plague bacteria," Heermann points out.

Read the article The microbiota controls the shape of immunity.

Anti-viral enzyme contributes to several forms of cancer

Researchers at the University of Minnesota have discovered that a human antiviral enzyme causes DNA mutations that lead to several forms of cancer. The discovery, reported in the July 14 issue of Nature Genetics, follows the team's earlier finding that the enzyme, called APOBEC3B, is responsible for more than half of breast cancer cases. The previous study was published in Nature in February.
APOBEC3B is part of a family of antiviral proteins that Harris has studied for more than a decade. His effort to understand how these proteins work has led to these surprising discoveries that APOBEC3B is a broadly important cancer mutagen.
"We are very excited about this discovery because it indicates that a single enzyme is one of the largest known contributors to cancer mutation, possibly even eclipsing sources such as UV rays from the sun and chemicals from smoking," says Reuben Harris, a professor of Biochemistry, molecular biology and biophysics based in the College of Biological sciences. Harris, who led the study, is also a member of the Masonic Cancer Center, University of Minnesota.
For the current study, Harris, along with colleagues Michael Burns and Alpay Temiz, analyzed tumor samples from 19 different types of cancer for the presence of APOBEC3B and 10 related proteins. Results showed that APOBEC3B alone was significantly elevated in six types (bladder, cervix, two forms of lung cancer, head & neck, and breast). Levels of the enzyme, which is present in low levels in most healthy tissues, were elevated in several other types of cancer as well.
A second key finding was that the mutational signature of APOBEC3B is a close match to the actual mutation pattern in these cancers. "Much like we each have unique written signatures, these enzymes each leave a unique mark," Harris says.
Findings from both studies are counterintuitive because the enzyme, which is produced by the immune system, is supposed to protect cells from HIV and other viruses, not harm our own genomic DNA.
While it's well known that sunlight and chemical carcinogens can mutate DNA, and that mutations are essential for cancer to develop, Harris is the first to discover that this human enzyme is a major cause mutation in cancer. He believes that APOBEC3B is a biological "double-edged sword" that protects some cells from viruses such as HIV and produces mutations that give rise to cancer in others.
Harris hopes to find a way to block APOBEC3B from mutating DNA, just as sunscreen blocks mutations that lead to melanoma. Many cancer mutations have been identified, but discovering a common source of mutation such as APOBEC3B is expected to help researchers to move "upstream" and look for a way to stop carcinogenesis closer to its source, he says, "like damming a river before it wreaks havoc on downstream areas." It's also possible that a simple test for APOBEC3B could be used to detect cancer earlier.
Harris is a professor in the Department of Biochemistry, molecular biology and Biophysics, which is a joint department of the College of Biological sciences and the Medical School. He is also a member of the Masonic Cancer Center, University of Minnesota, which is part of the National Cancer Institute's network of Comprehensive Cancer Centers. Harris and colleagues are grateful for support from the National Institutes of Health, the Department of Defense Breast Cancer Research Program, the Jimmy V Foundation, and the Minnesota Ovarian Cancer Alliance.

Source: University of Minnesota

Be religious, not just an practitioner of a particular religion

Religion is the soft target in everyone's talking. It has been said that religion is the weapon by which a society can be bound with love and simultaneously it can also be used to kill others. It's a very sensitive issue in every field of life. Do you think that religion has a name, and if yes should it be given a name? Whenever I sit alone, this question always comes in my mind. Here, I shared my opinion. It's quite possible that you may not agree with me but it can't stop me here; may be others like it. One should respect others opinion, everyone should have right to put own views in public. One can criticize my views, I will take it with healthy mind. Everything should be discussed in a civilized society, sometimes we get something better out of it.

Does only practicing a named religion (e.g. Hinduism, Islam, Christianity, Sikhism, Judaism, Jainism, Buddhism, and many more) make you religious? I see huge difference between "true religion" and "practicing a named religion". Practicing a named religion doesn't always make you religious. For example, if I say "help everyone who needs you", which religion does oppose it? Answer is 'no one'. You can ask many questions with yourself, you will find the same answer. Religion doesn't have any name. Given name of a religion only describe a path or group of followers. A name can define its followers to differentiate them but cannot define a religion. Every religion teaches us to be a human and respect humanity. Then, why should it be given a name? Every path takes us to a single religion. I born in a Hindu family I became a Hindu, if I would have born in a Muslim family I would have been following Islam; similar for other named religions. Where is my opinion? Having the born identity we start hating others who follow different named religions. Why is this, did you think about? Actually, we have never been a religious person. A religious person can never hate others. What is behind this hatred mindset? Answer is very simple, we do not have knowledge about other named religions and its teachings, and unfortunately we shield ourselves for such source of knowledge. We only know them by media and tailored stories. Why don't we try to learn by ourselves?

God says to be a human and serve humanity for others. He never says that you follow particular path. If one says that a particular path is the only way to reach the God, he is only making you fool. God only wants you to be helpful and loving to others, He doesn't need a particular path to be followed. God cannot be a "God" if He says you to follow a particular path, it could be sentence of a dictator but not of "God". God doesn't run an empire. We all are associated with Him only, He does not rule us but He is merciful.

There should be an open teaching of every religion for our children, this will make them a complete knowledge of other religions too. It will minimize hatred mindset for others. These children will make a healthy society in which there will be love for everyone.

Be religious for humanity not only a practitioner, it will make a better world for everyone.