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Cmb assignment

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Siddhartha Asthana 16111017

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Metabolic changes in cells can occur at the earliest stages of disease. In most cases, knowledge of those signals is limited, since we usually detect disease only after it has done significant damage. Now, a team led by engineers at Tufts University School of Engineering has opened a window into the cell by developing an optical tool that can read metabolism at subcellular resolution, without having to perturb cells with contrast agents, or destroy them to conduct assays. As reported today in Science Advances, the researchers were able to use the method to identify specific metabolic signatures that could arise in diabetes, cancer, cardiovascular and neurodegenerative diseases.

The method is based on the fluorescence of two important coenzymes (biomolecules that work in concert with enzymes) when excited by a laser beam. The coenzymes -- nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) -- are involved in a large number of metabolic pathways in every cell. To find out the specific metabolic pathways affected by disease or stress, the Tufts scientists looked at three parameters: the ratio of FAD to NADH, the fluorescence "fade" of NADH, and the organization of the mitochondria as revealed by the spatial distribution of NADH within a cell (the energy producing "batteries" of the cell).

The first parameter -- the relative amounts of FAD to NADH -- can reveal how well the cell is consuming oxygen, metabolizing sugars, or producing or breaking down fat molecules. The second parameter -- the fluorescence "fade" of NADH -- reveals details about the local environment of the NADH. The third parameter -- the spatial distribution of NADH in the cells -- shows how the mitochondria split and fuse in response to cellular growth and stress.

"Taken together, these three parameters begin to provide more specific, and unique metabolic signatures of cellular health or dysfunction," said Irene Georgakoudi, Ph.D., corresponding author of the study and a professor of biomedical engineering in the School of Engineering at Tufts. "The power of this method is the ability to get the information on live cells, without the use of contrast agents or attached labels that could interfere with results."

Other methods exist for non-invasively tracking the metabolic signatures of disease, such as the PET scan, which is often used in research. But while PET scans provide low resolution information with excellent depth penetration into living tissues, the optical method introduced by the Tufts researchers detects metabolic activity at the resolution of single cells, although mostly near the surface.

That is not necessarily a limitation. Many diseases can be detected at the surface of tissues, including cancer, while many pre-clinical studies are performed with animal models and engineered three-dimensional tissues that can benefit from being monitored non-destructively. The method developed by Georgakoudi and colleagues may prove to be a powerful research tool for understanding their metabolic signatures.

Journal Reference:

Liu, Z., Pouli, D., Alonzo, C.A., Varone, A., Karaliota,S., Quinn, K.P., Münger, K., Karalis, K.P., Georgakoudi, I. Mapping metabolic changes by noninvasive, multiparametric, high-resolution imaging using endogenous contrast. Sci. Adv., 2018 DOI: 10.1126/sciadv.aap9302

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stem cells; fitness; diseases and conditions; biotechnology and bioengineering; veterinary medicine; biology; biochemistry; batteries; civil engineering

# data[].attributes.attachment_link.title
Optical tools to detect metabolic changes linked to disease: Discovery suggests the possibility of non-invasive metabolic monitoring for use in research and development of improved therapeutics

# data[].attributes.attachment_link.description
A team led by engineers has opened a window into the cell by developing an optical tool that can read metabolism at subcellular resolution, without having to perturb cells with contrast agents, or destroy them to conduct assays. The researchers were able to use the method to identify specific metabolic signatures that could arise in diabetes, cancer, cardiovascular and neurodegenerative diseases.

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Subham Gupta
16111018

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Rohit Kumar
16111013

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Yaadwinder Singh
Roll No. 16111024

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Ashok https://thebioscientist.org/2018/03/05/new-approach-boost-immune-system-using-personal-cancer-vaccine/

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Anureet kaur
16111003
Biotechnology 2nd year

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Manisha

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Researchers may be able to stop the replication of Ebola virus by mutating its most important protein, according to a paper published in the Journal of Biological Chemistry.

Researchers were able to mutate Viral Protein 40 (VP40) in a way that changed the residues of the protein, blocking the budding and replication of Ebola virus in a model system.

VP40 is a peripheral membrane protein that regulates viral budding from the plasma membrane. It interacts with a human plasma-membrane lipid, phosphatidylserine, to facilitate replication of the virus. All animal viruses have to cross membranes for cell entry and exit.

The research team, led by Robert Stahelin of Purdue University, found the specific parts of VP40 that bind with the lipid: a cationic patch on the end of an amino acid chain. This site controls the ability of the protein to form a lipid envelope, the layer that protects the virus from the outside environment.

Water-attracting residues at this site are critical for membrane penetration and budding. Substituting those residues with alanine, which is hydrophobic, reduced lipid binding by 40-fold and stopped localization to the plasma membrane.

VP40 is a transformer protein, capable of rearranging itself into different structures: monomer, dimer and octamer. These various structures interact with the lipid differently, according to the paper. The dimer is best equipped to facilitate replication, performing twice as well as the monomer, and nearly 10 times better than the octamer.

"It's exciting to learn that these different oligomeric structures bind differently with the human lipid cells," Stahelin said. "That might explain why there are different roles for this protein in the viral replication cycle."

There are currently no FDA-approved vaccines or therapeutics available for Ebola virus. Outbreaks are rare but deadly, with fatality rates as high as 90 percent. Knowing how and where the protein interacts with the lipid could allow researchers to better target it with therapeutics.

"This helps us understand how the virus uses human cell membranes to replicate and form new virus particles. The virus needs this one lipid to form the new particle and infect other cells," Stahelin said. "We've been targeting human cells with therapeutics that modulate the way the cell makes lipids, and we like to target the human cell because it isn't likely to mutate and become resistant to the drug.

Cellular and in vitro models were used in this study. In vitro models were used to quantify how well VP40 binds to synthetic membranes. The researchers mutated the DNA code to change the amino acid sequence of VP40, purified those proteins to homogeneity and compared their bindings to that of the original VP40.

In cellular experiments, live cell imaging was used to monitor VP40 localization in human cells. The movement of the mutant VP40 and the original VP40 were compared to see how they bind to the human cell plasma membrane, the site of viral replication.

Stahelin collaborated with researchers from Florida International University, The Scripps Research Institute and the University of Notre Dame. The work was supported by National Institutes of Health (NIH) Grants AI081077 and AI121841, and NIH Health CBBI Predoctoral Training Fellowship T32GM075762.

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viruses; ebola; hiv and aids; human biology; cell biology; genetics; molecular biology; virology

# data[].attributes.attachment_link.title
Mutating Ebola's key protein may stop replication: Researchers may be able to stop the replication of Ebola virus by mutating its most important protein.

# data[].attributes.attachment_link.description
Researchers may be able to stop the replication of Ebola virus by mutating its most important protein, according to a paper published in the Journal of Biological Chemistry. Researchers were able to mutate Viral Protein 40 (VP40) in a way that changed the residues of the protein, blocking the budding and replication of Ebola virus in a model system.

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Jashaninder Singh

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Sukhdeep bawa

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Publisher's note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

References

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Liu, M. et al. A DNA tweezer-actuated enzyme nanoreactor. Nat. Commun. 4, 2127 (2013).

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Hwang, Y.-C., Chen, W. & Yates, M. V. Use of fluorescence resonance energy transfer for rapid detection of enteroviral infection in vivo. Appl. Environ. Microbiol. 72, 3710-3715 (2006).

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Erbs, P. et al. In vivo cancer gene therapy by adenovirus-mediated transfer of a bifunctional yeast cytosine deaminase/uracil phosphoribosyltransferase fusion gene. Cancer Res. 60, 3813-3822 (2000).

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Austin, E. A. & Huber, B. E. A first step in the development of gene therapy for colorectal carcinoma: cloning, sequencing, and expression of Escherichia coli cytosine deaminase. Mol. Pharmacol. 43, 380-387 (1993).

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Acknowledgements

We thank S. Michnick for providing the split yCD constructs. This work was supported by grants from National Science Foundation (CBET1510817 and MCB1543838).

Author information

These authors contributed equally: Rebecca P. Chen and Daniel Blackstock.

Affiliations

Department of Chemical and Biomolecular Engineering, University of Delaware, Newark, DE, USA

Rebecca P. Chen

, Daniel Blackstock

, Qing Sun

& Wilfred Chen

Contributions

R.P.C., D.B. and W.C. conceived the project. R.P.C., D.B., Q.S. and W.C. designed experiments. R.P.C. and D.B. performed the FRET experiments. R.P.C. and Q.S. performed the enzyme cascade experiments. R.P.C. performed the split yCD experiments. R.P.C., D.B., Q.S. and W.C. analysed the data. R.P.C., D.B., Q.S. and W.C. wrote the paper. All authors discussed the results and commented on the manuscript.

Competing interests

The authors declare no competing interests.

Corresponding author

Correspondence to Wilfred Chen.

Supplementary Information

Supplementary Materials and Methods, Supplementary Figures and Supplementary Tables

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Dynamic protein assembly by programmable DNA strand displacement

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The construction of dynamic protein-DNA nano-assemblies suitable for modulating protein proximities and activities has now been demonstrated. This approach uses DNA strand displacement and can enable control of enzyme activity to be programmed using logic gates. As a demonstration, a split enzyme capable of activating a prodrug is triggered is by cancer-specific miRNAs.

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BOSTON- Despite enormous efforts over more than 30 years, HIV/AIDS researchers have yet to develop either a vaccine or cure for the disease. But they have made progress in monkey experiments, and two studies reported here this week at the largest annual U.S. HIV/AIDS conference created serious buzz.

Several AIDS vaccines have had some success in monkey models, which typically use SIV, a simian cousin of HIV that causes AIDS in rhesus macaques. But one vaccine has long stood out from the pack. Designed by Louis Picker and colleagues at Oregon Health & Science University's Vaccine and Gene Therapy Institute in Beaverton, the vaccine stitches SIV genes into a harmless Trojan horse, cytomegalovirus. Picker's team has given the vaccine to more than 200 monkeys and then "challenged" them with injections of a particularly nasty strain of SIV. All told, 55% of the animals became temporarily infected and then completely controlled the virus for years or even cleared it. Two stubborn questions remain, however: Picker and co-workers have yet to nail down the immune responses that explain the vaccine's success, and they also can't explain why it frequently fails.

At the meeting this week-the Conference on Retroviruses and Opportunistic Infections- immunologist Michael Gale Jr. of the University of Washington in Seattle described how his group explored these questions by taking a big picture view of active genes in the protected and unprotected animals. Specifically, the researchers identified and compared clusters of genes in the two groups of animals that were turned on high or tamped down low. These clusters control the production of various interleukins (biochemicals that communicate messages between immune cells), cell growth, and inflammation. They drilled down to 234 genes that had different expression levels in the two groups at day 3 and found that by looking at these alone, they could predict with 91% accuracy whether the vaccine injection would protect an animal. "This is the most interesting talk at the whole meeting," says Mario Clerici, an immunologist at the University of Milan in Italy who long has focused on why some humans handle the virus better than others.

Picker says these findings offer him new ways to tweak his vaccine. "Obviously the vaccine is tickling something, and maybe the critical issue is tickling a certain pathway a little bit stronger," he says. As an example, he points to the genes that collectively control interleukin-10 production, which were turned on much higher in protected animals. "If that signal turns out to be critical, I can manipulate it," he says. Picker has co-founded a company, Vir Biotechnology in San Francisco, California, that plans to start testing the vaccine in humans next year.

On the cure front, immunologist Dan Barouch, who directs the Center for Virology and Vaccine Research at Beth Israel Deaconess Medical Center-Harvard Medical School in Boston, threw the kitchen sink at the virus. His team first infected 44 monkeys with a hybrid of SIV and HIV called SHIV. One week later, the scientists began treating all the animals with antiretrovirals (ARVs) and continued for 2 years. In all 44 monkeys, the virus dropped to undetectable levels on standard blood tests. The researchers then divided the animals into four groups that received either nothing (the controls), a potent HIV antibody, a drug that binds to toll-like receptor 7 (TLR7) that studs innate immune system cells, or the antibody plus the TLR7 drug. Sixteen weeks later, they stopped all ARVs.

In humans who control HIV with ARVs to the point that researchers cannot find the virus in their blood or tissues, the virus always comes screaming back, usually within a few weeks, once they stop taking drugs. That's precisely what happened in all 11 control animals. In the monkeys given the TLR7 drug or the antibody, 20 of 22 no longer could suppress the SHIV. But in the group that received the antibody plus the TLR drug, five of 11 animals did not see the SHIV return after 6 months (the experiment is ongoing) and the others have low levels of the virus. "We're very encouraged by this preliminary proof of concept study," Barouch says.

A key obstacle to curing an HIV infection is that even when people have undetectable levels of virus, a reservoir remains of cells that hold chromosomes laced with "latent" viral DNA, which doesn't produce progeny and thus lies under the radar of the immune system-but can suddenly kick into gear and cause mayhem. Earlier monkey studies showed that the TLR7 drug can "shock" lately infected cells to produce the virus, setting them up for elimination. Many groups have attempted "shock-and-kill" experiments in monkeys and humans. "This is the first evidence that shock-and-kill works," Picker says.

Picker and others stress several important caveats. It's possible that the virus will return in these five monkeys-humans presumed to be cured have had HIV show up more than 2 years after stopping ARVs. And in this experiment, ARV treatment was started a week after infection; it rarely happens that soon in people. SHIV is also easier for monkeys to naturally control than the SIV used in Picker's studies. With all that in mind, Jeffrey Lifson, who does SIV studies at the U.S. National Cancer Institute in Frederick, Maryland, says the findings are "interesting, provocative, and potentially important."

Steven Deeks, a clinician who does cure trials at the University of California, San Francisco, says he soon plans to test a similar combination of a TLR drug and a potent antibody in patients who have been fully suppressed for several years. "There's no clear mechanism here, but as a clinician, I don't really care," he says. "It's all a big black box: You have something that goes in and something that goes out. What comes out here is no virus."

doi:10.1126/science.aat5439

Jon is a staff writer for Science.

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HIV, the virus that causes AIDS, has a secret life. Though anti-retroviral therapy can reduce its numbers, the virus can hide and avoid both treatments and the body's immune response.

Researchers at UC Davis Health, together with colleagues at UC San Francisco and the University of North Carolina at Chapel Hill, have found that increased crotonylation, an epigenetic mechanism that governs gene expression, might be the key to making HIV come out of hiding and become susceptible to anti-HIV drugs. Their study is published in The Journal of Clinical Investigation.

"We have been working on mechanisms that could be used to disrupt HIV latency," said Satya Dandekar, chair of the UC Davis Department of Medical Microbiology and Immunology and senior author on the paper. "The goal is to force the virus to be expressed so it is visible to the immune system and can be targeted through immuno-therapeutics. This is the first study to identify histone crotonylation as a driver for HIV transcription and de-crotonylation of histone as an epigenetic marker for HIV silencing."

While medical science has transformed HIV/AIDS from a deadly disease to a chronic one, there are still millions of people living with the virus. HIV's ability to become dormant makes it invisible to both the immune system and treatments. Researchers have dedicated years to deciphering the mechanisms that help HIV hide and finding ways to reverse that process.

In this study, the researchers focused on histone crotonylation, an epigenetic mechanism that modifies the proteins that package DNA, affecting gene expression.

"Histone crotonylation regulates HIV latency," said UC Davis associate project scientist Guochun Jiang, first author on the paper. "If we can modulate that, the virus can be more efficiently flushed out."

To better understand this mechanism, the team focused on an enzyme called ACSS2, which plays an important role in fatty acid metabolism in the gut. HIV has often been linked to impairment of lipid metabolism, making ACSS2 a promising potential target for an HIV cure.

To test it out, the researchers studied peripheral blood samples from HIV-infected patients and several HIV latency cell models. Activating the ACSS2 enzyme increased viral transcription manifold. The results from patient samples were particularly encouraging.

"We examined well-characterized cell models of HIV latency and immune cells from HIV patients who had been undergoing antiretroviral therapy and had undetectable viral loads," Dandekar said. "In those samples, we were able to disrupt the HIV silencing by inducing histone crotonylation."

To further validate the results, the researchers treated samples with an ACSS2 inhibitor, which reduced detectable virus levels, highlighting the important role of decrotonylation in establishing HIV latency.

One of the more intriguing findings in the study was that increasing histone crotonylation works synergistically with other known anti-HIV latency molecules, such as the protein kinase C agonist PEP005 and the HDAC inhibitor vorinostat. Dandekar and her colleagues are now searching for more molecules that attack viral latency to develop an overall strategy of combining therapeutic agents to compel HIV expression.

"We are looking for synergistic disruption, by combining histone crotonylation with other mechanisms to reactivate HIV," Dandekar said. "This research positions us to screen and identify small molecules, which can be optimized to carry out HIV modification."

Journal Reference:

Guochun Jiang, Don Nguyen, Nancie M. Archin, Steven A. Yukl, Gema Méndez-Lagares, Yuyang Tang, Maher M. Elsheikh, George R. Thompson, Dennis J. Hartigan-O'Connor, David M. Margolis, Joseph K. Wong, Satya Dandekar. HIV latency is reversed by ACSS2-driven histone crotonylation. Journal of Clinical Investigation, 2018; 128 (3): 1190 DOI: 10.1172/JCI98071

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hiv and aids; infectious diseases; viruses; std; virology; epigenetics research; genetics; biotechnology

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HIV, the virus that causes AIDS, has a secret life. Though anti-retroviral therapy can reduce its numbers, the virus can hide and avoid both treatments and the body's immune response.

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Kushal saini 2

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Bacteriophages, known informally as phages, are viruses that can attack and kill specific bacteria. They occur everywhere in the natural world. Precisely because they are matched to just one specific type of bacteria, researchers and medics hope that phages can be engineered to combat certain bacterial infections. For example, the food industry is already using these phages to destroy pathogens in food products by natural methods.

However, genetically engineering phages in order to customise them for specific applications continues to be a very challenging and time-consuming process. It is particularly difficult to modify phages to combat Gram-positive bacteria such as Staphylococcus. Incorporating a synthetic phage genome into Gram-positive bacteria has so far been very problematic, as their cell walls are so thick.
Custom designing phages
A new era may now be dawning in the use of bacteriophages, however, as a team of researchers led by Martin Loessner, Professor of Food Microbiology at ETH Zurich, has just presented a novel technology platform in a paper published in the journal PNAS. This enables scientists to genetically modify phage genomes systematically, provide them with additional functionality, and finally reactivate them in a bacterial "surrogate" -- a cell-wall deficient Listeria cell, or L-form.

The new phage workbench allows such viruses to be created very quickly and the "toolbox" is extremely modular: it allows the scientists to create almost any bacteriophages for different purposes, with a great variety of functions.

"Previously it was almost impossible to modify the genome of a bacteriophage," Loessner says. On top of that, the methods were very inefficient. For example, a gene was only integrated into an existing genome in a tiny fraction of the phages. Isolating the modified phage was therefore often like searching for a needle in a haystack.

"In the past we had to screen millions of phages and select those with the desired characteristics. Now we are able to create these viruses from scratch, test them within a reasonable period and if necessary modify them again," Loessner stresses.
Planning phages on the computer
Samuel Kilcher, a specialist in molecular virology, has played a key role in the breakthrough: he used synthetic biology methods to plan the genome of a bacteriophage on the drawing board and assemble it in a test tube from DNA fragments. At the same time new, additional functions were incorporated in the phage genome, such as enzymes to dissolve the bacterial cell wall. In addition, Kilcher is able to remove genes that give a phage unwanted properties, such as the integration into the bacterial genome or the production of cytotoxins.

In order to reactivate a phage from synthetic DNA, the genome was introduced into spherical, cell wall-deficient but viable forms of the Listeria bacterium (L-form Listeria). Based on the genetic blueprint, these bacterial cells then produce all the components of the desired phage and ensure that the virus particles are assembled correctly.

The researchers also discovered that spherical Listeria cells are not only capable of creating their own specific phages, but also those able to attack other bacteria. Usually, a host only generates its own specific viruses. L-form Listeria are therefore suitable as a virtually universal incubator for bacteriophages.

If the Listeria cells are then brought to the point where they rupture (lysis), the bacteriophages are released and can be isolated and multiplied for use in therapy or diagnostics.
Only virulent phages are suitable
"A key prerequisite for using effective synthetic bacteriophages is that their genome is unable to integrate into the host's genome," Kilcher emphasises. If this happens, the virus no longer presents a threat to the bacterium. Using this new method, however, the scientists were able to simply reprogram such integrative phages so that they become interesting again for antibacterial applications.

The two researchers are not particularly worried about potential resistances against the phages. And even if there were any, for example due to a bacterium changing its surface structures to prevent the virus from attaching, the new technology makes it possible to develop a suitable phage against which a bacterium has not yet developed resistance.

The researchers also think the danger of unintended release is very small: because the bacteriophages -- both natural and synthetic -- are extremely host-specific, they cannot survive for long without their host. This high specificity also prevents the bacteriophages from switching to a new host bacterium. "Adapting to the surface structure of a different host would take an awful long time in nature," Loessner says.
Close to a practical application
With this new technology, Loessner's team has made a giant stride towards applying synthetic bacteriophages for use in therapy, diagnostics or the food industry. The scientists are thus managing to overcome constraints associated with the use of naturally occurring phages. "Our toolbox could help to exploit the potential of phages," Loessner says. The researchers have applied for a patent for their technology. Now they hope to find licensees to produce the phages for therapy and diagnostics.

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The accumulation of mutations in the human genome is at the origin of cancers, as well as the development of resistance to treatments. The Cyclin E and Myc genes are active in the control of cell division. When they are mutated, for example in response to a carcinogen, these genes induce cells to start replicating their DNA prematurely during the cell cycle. This abnormal cell division causes a tumor to develop. Why is this the case? Biologists from the University of Geneva (UNIGE), Switzerland, show that precocious entry of the genome into the replication phase leads to molecular collisions occurring on the DNA and induces new mutations. These results, published in the journal Nature, could be used to develop new therapeutic approaches.

When a cell divides into two daughter cells, it must replicate its entire genome and transcribe part of it to make new proteins. Cell division is notably regulated by specific genes, including the proto-oncogenes Cyclin E and Myc. Their overexpression or mutation into oncogenes, following exposure of cells to a carcinogen for example, leads to uncontrolled proliferation of cells and promotes the formation of cancer. "We wanted to understand why numerous mutations accumulate in cells with activated oncogenes," explains Thanos Halazonetis, Professor at the Department of Molecular Biology of the UNIGE Faculty of Science.
Replication must begin between two genes
In order to replicate its entire DNA, that is to say nearly 6.4 billion pairs of nucleotides in just a few hours, the cell organizes the preparation of this process at thousands of sites on each chromosome simultaneously. The position and spacing of these sites, called 'replication origins', must be controlled to ensure that replication takes place in a smooth and efficient way.

The UNIGE researchers have developed a method to identify the origins of replication on all chromosomes. This consists of isolating and sequencing the newly synthesized DNA from cells that have just entered the replication phase, in order to map on the genome the sites where replication has begun. This method, specifically developed for human cells, offers high degrees of sensitivity and resolution.

"Initially, the cell identifies all potential replication origins with a molecular marker. We have discovered that in normal cells, the aberrant replication origins are subsequently eliminated. This is the case for those that are located inside a gene, whereas they should be outside the genes so that the integral message of each gene is preserved," explains Morgane Macheret, a researcher at the Department of Molecular Biology at UNIGE and first author of the article.
When the cells skip steps
The activation of the oncogenes Cyclin E or Myc, on the other hand, induces the cells to begin replication of their DNA prematurely, without having had time to eliminate all the replication origins present in the genes. "The replication and transcription machineries are therefore active simultaneously on genes carrying a replication origin, which causes conflicts. Our analyses show that these conflicts induce DNA breakdowns, chromosomal rearrangements and, therefore, mutations," says Thanos Halazonetis.

Do these results explain the genomic instability present in different types of cancers? In order to answer this question, the biologists have studied an array of more than 500'000 chromosomal rearrangements already characterized in a wide range of tumors. "We observed that these chromosomal defects are particularly common in the conflict zones we described. We hope that the discovery of the mechanism that partly or totally explains the genesis of this genomic instability will eventually lead to the development of new therapeutic strategies," concludes Morgane Macheret.

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NEWS: GREEN BATTERY
Ramya Veerubhotla, research scholar at IIT Kharagpur’s Department of Biotechnology, along with her partner, has developed a disposable and flexible battery made from paper that could generate power from the bacteria present in sewage water. They have grabbed worldwide attention for their innovation in developing ‘Paper Battery’ from sewage bacteria .
➡For the environment-friendly battery cell to start energy production, sewage water containing bacteria needs to be injected into it.
➡The uniqueness of her innovation is that the device is made on a paper platform unlike other batteries, which are heavy.
➡The battery is made using air cathode, and the anode can be prepared from any simple carbon based material.
➡Usually Microbial Fuel Cells (MFCs) take a couple of days to start power production as the bacteria needs to adjust to the environment. But for this device, the power production starts within 10 seconds.
➡The power generated from one cell is in the range of a few microwatts. More cells mean more power.
➡It may be difficult to power household devices with this, but it can power certain electronic components.
➡ The device is flexible and can be stacked together. For more power, you can make more units, stack them and fold them in a compact shape.”
➡This research presented by IIT Kharagpur’s ‘Team Electrodes’ at KPIT Sparkle 2018,an innovation recognition competition held in partnership with the Department of Science and Technology of the government of India, in Pune has won the first prize and a cash award of Rs. 10 lakh while competing with 12000 students from across the country.
➡The Platinum Award received by Ramya was decided on the basis of novelty, affordability and commercial viability of the proposed idea by an international panel of judges.

➡Ramya’s PhD supervisor, Professor Debabrata Das, an authority on MFCs, is confident that this invention would have tremendous use in bio-electric toilets.
➡One of the best advantages of the device is that it is 100% biodegradable and environment-friendly, which is not the case with chemical batteries.

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This week's headlines include: Cancer Immunotherapy is getting even better, Sunovion Parkinson's Drug Heads to FDA, Setting Up Battle With Acorda, FDA agrees to quick review of smallpox drug, Abcam, Molecular Devices join forces to develop immunoassays for researchers, Cobra Biologics and Symbiosis granted £1.9 million from Innovate UK, Corning and CytoSMART collaborate to simplify cell counting in laboratories, and Bristol-Myers' positive cancer data still lags Merck.

In Case You Missed It, Recent Articles on Cell Culture Dish and Downstream Column:

We recently finished our Ask the Expert discussion, " Ask the Expert - Implementation of Continuous Manufacturing Strategies for Protein Therapeutics." During this Ask the Expert session, we covered several common questions related to continuous biomanufacturing, including PAT initiatives, expected timelines, potential cost savings, optimization, process parameters, and lot release and how it compares with traditional fed-batch processes....

Chimeric antigen receptor (CAR)-T cells which are engineered to recognize tumor cell-specific surface antigens, have shown promise to affect complete remission in patients with B-cell malignancies. With the recent FDA approval of Novartis' Kyrmriah™ and Gilead Science's Yescarta™, CAR-T cell therapy could be on target to become the standard treatment for blood cancers ¹. However, utilizing the CAR approach to treat solid tumors has not been as successful because many of the surface antigens upregulated in solid tumor cells, and thus chosen as targets for CAR-T cells, are present at significant levels in normal tissues ². This has resulted in significant adverse effects in clinical studies including toxicity to healthy tissues and at worst, has proven fatal ³. Methods for testing different models of CAR-T cells in vitro can provide further insight into viable antigen targets before first-in-man studies that utilize such models. The latest advancements in drug discovery screening, especially for cancer therapeutics, utilize three-dimensional (3D) cell culture models which more closely mimic the in vivo tumor microenvironment. For example, 3D multicellular tumor spheroids develop hypoxic cores, demonstrate gradients of various soluble factors, and a diffusion profile for drugs similar to tumors ⁴. Here we demonstrate an HTS-compatible system to assay CAR-T cells against tumor spheroids by combining Corning ® spheroid 384-well ultra-low attachment microplates, which enables the reproducible formation of a single spheroid in each well, and the DiscoverX KILR ® Cytotoxicity assay, which provides a non-radioactive, dye-free method to specifically measure target cell death in a co-culture using luminescence...

In this podcast and accompanying article, we interviewed Silke Bergheim-Pietza, Global Product Manager Depth Filtration, Pall. We discussed challenges faced in the cell harvesting step, in particular, selecting the best cell harvesting method based on the cell density and feed turbidity of the process and meeting the demand of increasing cell densities. Download the cell harvesting technology selection guide and use the guide to compare the latest single-use harvesting technologies...

Biomanufacturing contamination due to Mycoplasma is a very real concern, as it poses a potential health risk for patients. As such, regulatory agencies require biopharmaceutical companies to test for the presence of mycoplasma both during the manufacturing process and in the final product. While any contamination can be extremely challenging and costly, mycoplasma contamination is particularly difficult...

In this podcast and accompanying article, we interviewed Jonathan Royce, Business Leader, Chromatography Resins, GE Healthcare Life Sciences, about the biggest challenges in Downstream biomanufacturing including overcoming bottlenecks, changing antibody structures and bioburden control. Jonathan shared how a purification platform can address some of these issues and discusses purification challenges that still need to be resolved.

I have compiled a list of our most popular 25 blogs, podcasts, and webinars for 2017 listed in alphabetical order...

In this podcast and accompanying article, we interviewed Jonathan Royce, Business Leader, Chromatography Resins, GE Healthcare Life Sciences, about the evolution of Protein A including the latest developments in Protein A chromatography resins. We also discussed what the future holds for this purification mainstay and how it can continue to address the changing needs of biopharma...

Process economics are frequently discussed with respect to continuous biomanufacturing implementation. More specifically, are the potential cost benefits worth making a manufacturing change and in which situations are the benefits greatest? At Biotech Week Boston in September, there was a very interesting talk titled " Cost modeling of the downstream bioprocessing design space," presented by Mark Schofield, Ph.D., Senior R&D Manager, Pall Life Sciences. In the talk, Dr. Schofield shows data related to cost modeling the downstream bioprocess design space. He also describes some of the challenges facing biomanufacturing including cost pressure, competition, and the rise of biosimilars, and how implementing integrated continuous operations can address several of these challenges...

Webinars:
New Webinar Available On Demand!
The cost of goods of an Integrated Continuous Bioprocessing (ICB) platform for the manufacturing of a mAb from fed-batch cell harvest has been evaluated using BioSolve Process, a modeling software from BioPharm Services. The costs associated with the ICB platform were compared to those of stainless steel and single-use batch processes. These downstream processes were evaluated across sets of clinical and commercial production scenarios. For both sets of scenarios, 27 different cases were modeled by varying 3 factors: bioreactor titer, volume, and number of batches per year. By taking this approach, the cost-benefits of the ICB platform could be seen across a wide range of manufacturing scales.

In this webinar, participants will learn:

The findings of the full-factorial modeling exercise.

The cost-benefits of continuous bioprocessing at many scales of manufacturing.

Podcasts:

Check out our podcast channel. We have 15 great podcasts covering drug discovery, stem cell culture, upstream and downstream biomanufacturing and more!

Click below to download through iTunes or Google play:

Headlines:

"Last year, the Food and Drug Administration approved two new immunotherapies to treat certain leukemias and lymphomas. Now, in a study published in the New England Journal of Medicine, researchers detail who is most likely to benefit from the treatments, called CAR T cell therapy..."

"Another drug that may help alleviate some of the debilitating symptoms of Parkinson's disease is on its way to an FDA review, setting up a possible commercial battle between two drug developers, Sunovion Pharmaceuticals and Acorda Therapeutics. Sunovion, of Marlborough, MA, said late Monday that its experimental Parkinson's drug, APL-130277, succeeded in a 109-patient Phase 3 trial. The drug helped improve the motor function of adult Parkinson's patients suffering "off" episodes, meaning their medications aren't working. Sunovion plans to file for FDA approval in the spring..."

"A Corvallis biotech firm is on a fast track toward approval of the world's first treatment for smallpox. Siga Technologies announced on Wednesday that the Food and Drug Administration has accepted its new drug application for the oral formulation of Tpoxx, the company's pill for treating smallpox infection, and has promised to complete its review in six months rather than the usual 10..."

"Abcam, a supplier of protein research material and kits, has teamed up with bioanalytical measurement solutions expert Molecular Devices to develop screening tools for the life science industry. The initial focus of this transatlantic collaboration is on creating new high-sensitivity fluorescent enzyme-linked immunosorbent assay (ELISA) kits. These immunoassays are used to detect and quantify substances such as peptides and proteins in basic research, high throughput screening and diagnostics..."

"This grant will be used by the companies to establish commercial viral vector manufacturing capabilities within the UK as part of their joint investment project (costing £4.8 million in total). The whole project is aimed at developing world leading capabilities for clinical and commercial production of gene and immunotherapy viral vectors for both drug substance and drug product manufacturing. Additionally, it will support a larger investment in the production capabilities of both companies..."

"Corning Incorporated and CytoSMART Technologies BV today announced an agreement that will simplify mammalian cell counting in laboratories around the world. Cell counting is a critical step in subcultivation in the cell culture workflow..."

"Bristol-Myers Squibb Co (BMY.N) on Monday provided some positive data on its immuno-oncology drugs for the most lucrative lung cancer market but it fell short of giving clarity on its ability to compete with a rival treatment from Merck & Co Inc..."

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The Dish's Weekly Biotechnology News Wrap Up - February 9, 2018 - Cell Culture Dish

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This week's headlines include: Cancer Immunotherapy is getting even better, Sunovion Parkinson's Drug Heads to FDA, Setting Up Battle With Acorda, FDA agrees to quick review of smallpox drug, Abcam, Molecular Devices join forces to develop immunoassays for researchers, Cobra Biologics and Symbiosis granted £1.9 million from Innovate UK, Corning and CytoSMART collaborate to simplify cell ...

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Will More Of Biotech's Top Brass Soon Come On Board?

One Biotech Company Has Begun to Capitvate Investors & A New CEO At The Helm Could Be Presenting Near Term Opportunity!

What Is The Buzz Surrounding Sorrento Therapeutics Inc (NASDAQ:SRNE)?

Effective February 5, 2018, Sorrento Therapeutics Inc (NASDAQ:SRNE) and Yuhan Corporation reported that the South Korean MFDS has permitted ImmuneOncia Therapeutics' IND for the commencement of clinical studies for company-discovered IMC-001, which is solely licensed to ImmuneOncia for selected regional markets by company.

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Biotech Stocks Newsletter - February 23, 2018

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Will More Of Biotech's Top Brass Soon Come On Board? One Biotech Company Has Begun to Capitvate Investors & A New CEO At The Helm Could Be Presenting Near Term Opportunity! What Is The Buzz Surrounding Sorrento Therapeutics Inc (NASDAQ:SRNE)?