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CCNY’s Nir Krakauer in monsoon research breakthrough

CCNY’s Nir Krakauer in monsoon research breakthrough

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Credit: Nir Krakauer


With average precipitation of 35 inches per four-month season over an area encompassing most of the Indian subcontinent, the South Asia summer monsoon is intense, only partly understood, and notoriously difficult to predict. Until now, according to findings by Nir Y. Krakauer, a City College of New York civil engineer.

Because of the monsoon’s enormous impact on these sectors, his research is of importance to a range of activities, including agriculture, industry, fishing and hydropower.

A frequent visitor to the region, stretching from Nepal to Sri Lanka, Krakauer has devised a methodology that allows forecasts potentially up to a year in advance. Currently, most predictions are made about two months in advance of the South Asia monsoon season that runs from June to September, but it is not known how far ahead skillful forecasts might be possible.

“People usually use one or two predictors for forecasts,” said the Grove School of Engineering associate professor who is also affiliated with the CCNY-based NOAA-CREST. “Many of these predictors are one or another pattern of sea surface temperatures. My question was how do you find which patterns are important for forecasting the monsoon – the amount of rain and where it will be?”

Unlike other forecasters who use only the sea surface temperature readings from neighboring waters, Krakauer looked at the predictive potential of all the common patterns in the sea surface temperature map. He developed prediction methods using global sea surface temperature and monsoon precipitation data from between 1901 to 1996, and tested the performance of his prediction methods on data from 1997-2017.

“What I found is that two methods seem to do a good job of forecasting the monsoon. I looked at the sea surface temperatures at the beginning of the monsoon, and going back as far as four years before.”

His finding was that, generally, the closer to the beginning of the monsoon season, the more accurate forecasts that are based on sea surface temperature can be. But predictions with some accuracy can be made as far as a year in advance.

Getting a better sense of how much water will be available is particularly important given that the rainfall is getting more intense in South Asia while the total amount remains constant, meaning that more rain is falling in a shorter period. This could be problematic for farmers in the region.

Entitled “Year-ahead predictability of South Asian Summer Monsoon Precipitation,” Krakauer’s research appears in the journal Environmental Research Letters.

His work in South Asia has been partly supported by USAID, most recently as part of the US-Pakistan Center for Advanced Studies on Water program.

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Source: New feed

This Biotech Accelerates Stem Cell Therapy Development

This Biotech Accelerates Stem Cell Therapy Development

Mogrify is the new kid on the block for stem cell therapy. Based in Cambridge, UK, it boasts technology that could speed up the development of stem cell therapies by predicting the best protein recipe to transform mature adult cells into other cell types.

stem cell therapy mogrify disley

Mission: To use next-generation sequencing and gene expression data to develop more cost-effective stem cell therapies for regenerative medicine fields such as cardiac repair and cartilage regeneration.

Many cell therapies require taking adult cells such as fibroblasts, reverting the cells back to a stem cell stage, and then program them into the therapeutic cell that you want. This is not a simple process, and it can take significant amounts of time and money.

The stem cell stage can be skipped in a process called transdifferentiation, directly changing one mature cell, such as a liver cell, to another cell type, such as a pancreatic islet cell. Doing so could save a huge amount of effort for researchers developing cell therapies from scratch, as well as saving many costs in the development and manufacturing process. However, researchers have to carry out extensive trial-and-error approaches to make it work.

Mogrify aims to make this transdifferentiation process easier. The company has developed a software tool that combines data from next-generation sequencing and gene regulation studies to predict which proteins and small molecules they need to transdifferentiate the cells.

The Mogrify algorithm has not only confirmed many previously discovered cell conversions, but it has also already validated over a dozen cell conversions in vitro,” Darrin Disley, the CEO of Mogrify told me.

The cell therapies that Mogrify develops could be the first to convert adult cell types into other types without needing to enter the stem cell stage.

Additionally, once discovered, each cellular conversion can be iteratively tweaked to achieve optimal therapeutic effect, safety and manufacturability,” said Disley. “None of these capabilities have been reported to date.

stem cell therapy mogrify disley stem cell

The company is planning to commercialize this software tool by licensing it out and forming partnerships with other companies. In addition, Mogrify has plans to develop its own therapies using the software, with applications in fields such as regenerating cartilage in osteoarthritis, and cardiac tissue repair in heart disease.

Founded in 2016, Mogrify raised a seed round of €3.3M ($3.7M) this week to help fund the commercialization of its software. The company also hopes to close a Series A round of up to €26M ($30M) by the end of 2019.

One of the top biotech leaders around London, Oxford and Cambridge, Disley is a well-known figure in the medical biotech world, having previously been the CEO of the UK gene editing company Horizon Discovery for 11 years.

What we think:

Mogrify’s technology could help to advance regenerative medicine by guiding the transdifferentiation of adult cells in the lab. Overall, this could cut a lot of R&D from the drug development time, which can easily take ten years or more.

Stem cell therapy is a field with a lot of potential. Last year, the stem cell therapy Alofisel from the Belgian biotech TiGenix was approved in Europe for the treatment of Crohn’s disease. The Czech biotech Bioinova is also taking stem cells from bone marrow to encourage wound healing and amyotrophic lateral sclerosis.     

“There is a long way to go,” noted Disley. “The Mogrify approach could dramatically accelerate the quest for new cell therapies, which are currently limited by the lack of available sources of cells with suitable efficacy, safety and manufacturing profiles.” 


Images from Shutterstock

The post This Biotech Accelerates Stem Cell Therapy Development appeared first on Labiotech.eu.


Source: Labiotech

Stroke Recovery May Be Assisted by HIV Drug, Suggests Study of “Missing” Gene

Stroke Recovery May Be Assisted by HIV Drug, Suggests Study of “Missing” Gene

Hints have been accumulating that maraviroc, a drug for slowing HIV, could benefit patients who have suffered mild stroke. A few years ago, maraviroc was shown to improve learning and memory in mice. And a new study, also in mice, indicates that the drug enhances motor recovery after stroke and improves cognitive function after traumatic brain injury. The new study also presents information from a unique patient population to strengthen the case that maraviroc could lessen stroke’s harms in people.

The people evaluated in the current study carry a mutated version of the CCR5 gene, which expresses a cell receptor protein that can be blocked by maraviroc. When CCR5 is expressed on human immune cells, it can serve as an entry point for HIV. CCR5, it happens, can also be expressed in cortical neurons, but only during or after stroke.

Carriers of mutated CCR5, the new study indicates, have better outcomes after stroke. Details appeared February 21 in the journal Cell, in an article titled, “CCR5 Is a Therapeutic Target for Recovery after Stroke and Traumatic Brain Injury.” The fruit of a collaboration between scientists based at UCLA and Hebrew University, the article speculates that inhibiting the expression of CCR5 promotes recovery by enhancing plasticity, the ability of the brain to rewire itself after injury.

“Recovery is associated with preservation of dendritic spines, new patterns of cortical projections to contralateral pre-motor cortex, and upregulation of CREB and DLK signaling,” the article’s authors wrote. “Administration of a clinically utilized FDA-approved CCR5 antagonist, devised for HIV treatment, produces similar effects on motor recovery post stroke and cognitive decline post-traumatic brain injury.”

When the UCLA team, led by S. Thomas Carmichael, MD, PhD, chair and professor of neurology, decided to evaluate whether targeting CCR5 with maraviroc could accelerate recovery from stroke, it teamed with pharmacologist Esther Shohami, PhD, at Hebrew University to test the drug’s effectiveness in suppressing CCR5 in a mouse model.

“We found that maraviroc blocked CCR5 in mice and boosted the animals’ recovery from traumatic brain injury and stroke,” said Carmichael. “The big question left to answer was whether eliminating CCR5 would produce the same results in people.”

Knowing that CCR5 deletion is common in Ashkenazi Jews, Carmichael and his team reached out to researchers at Tel Aviv University. In a lucky coincidence, the Israeli scientists were already following 446 stroke patients in an observational study.

Led by neuroscientist Einor Ben Assayag, PhD, the study focused only on patients who had suffered mild or moderate strokes. Her team documented the patients’ improvements in walking, arm and leg control, and other types of movement.

“Einor’s lab had the patients’ blood samples and was evaluating their recovery from stroke after intervals of six months, one year, and two years,” said Carmichael. “People missing the CCR5 gene showed significantly greater recovery in motor skills, language, and sensory function.”

One year after stroke, patients missing CCR5 also scored higher in tests assessing memory, verbal function, and attention.

“When you suffer a stroke, part of your brain dies, severing those cells’ connections with neurons in other regions. That’s why stroke patients often suffer paralysis or lose speech,” Carmichael said. “When CCR5 is missing or blocked, neurons can make new connections and rewire the brain, enabling patients to regain some lost function.”

The scientists’ next step will be to launch a clinical trial testing the effectiveness of the drug maraviroc on stroke patients with the CCR5 gene.

Source: Genengnews

Triclosan Added to Consumer Products Dramatically Decreases Antibiotic Efficacy

Triclosan Added to Consumer Products Dramatically Decreases Antibiotic Efficacy

Antibacterial products have encompassed consumer products for many years, but only recently have we begun to see the potential negative effects surrounding the widespread use of these compounds. The antimicrobial triclosan, for instance, is incorporated into a wide range of products from oral hygiene, soaps, and cosmetics to baby toys and clothing. While the idea was to reduce bioburdens and prevent illness, new research from investigators at Washington University in St. Louis (WUSTL) finds that the chemical is actually making bacteria stronger and more capable of surviving antibiotic treatment.

“In order to effectively kill bacterial cells, triclosan is added to products at high concentrations,” explained senior study investigator Petra Levin, PhD, professor of biology at WUSTL.

Findings from the new study—published recently in Antimicrobial Agents & Chemotherapy through an article titled “The widely used antimicrobial triclosan induces high levels of antibiotic tolerance in vitro and reduces antibiotic efficacy up to 100-fold in vivo”—suggests that triclosan exposure may inadvertently drive bacteria into a state in which they are able to tolerate normally lethal concentrations of antibiotics.

In 2017, the U.S. Food and Drug Administration cited both safety concerns and lack of efficacy when it recommended against adding triclosan to consumer soaps, but these guidelines have not discouraged companies from adding it to other products. What’s more, Levin said, “Triclosan is very stable. It lingers in the body and in the environment for a long time.”

This new study in mice uncovers the extent to which triclosan exposure limits the body’s ability to respond to antibiotic treatment for urinary tract infection. It also sheds new light on the cellular mechanism that allows triclosan to interfere with antibiotic treatment.

The WUSTL team were particularly interested in bactericidal antibiotics—those that can kill bacterial cells and are typically prescribed by doctors to treat bacterial infections. They wanted to know whether triclosan could protect bacteria from death in the presence of killing antibiotics. The researchers treated bacterial cells with bactericidal antibiotics and tracked their ability to survive over time. In one group, the bacteria were exposed to triclosan prior to being given the bactericidal antibiotic. In the other group, they were not.

“Triclosan increased the number of surviving bacterial cells substantially,” Levin noted. “Normally, one in a million cells survive antibiotics, and a functioning immune system can control them. But triclosan was shifting the number of cells. Instead of only one in a million bacteria surviving, one in 10 organisms survived after 20 hours. Now, the immune system is overwhelmed.”

Triclosan exposure allowed the bacteria to escape death by antibiotics. And the protective property was not limited to any single family of antibiotics. In fact, multiple antibiotics that are considered unique in how they kill cells were less effective at killing bacteria exposed to triclosan.

“Triclosan increased tolerance to a wide breadth of antibiotics,” explained lead study investigator Corey Westfall, a postdoctoral scholar in the Levin lab. “Ciprofloxacin (also known as Cipro) was the most interesting one to us because it is a fluoroquinolone that interferes with DNA replication and is the most common antibiotic used to treat UTIs.”

UTIs occur when bacteria, primarily Escherichia coli (E. coli), enter and infect the urinary tract. Antibiotics such as Cipro are commonly used to kill the bacteria and treat the infection.

UTIs are common, as is exposure to triclosan. A shocking percentage—about 75%—of adults in the United States have detectable levels of triclosan in their urine. About 10% of adults have levels high enough to prevent E. coli from growing. Could triclosan’s presence in the body interfere with treating UTIs?

Interestingly, the researchers found that mice who drink triclosan-spiked water have urine triclosan levels similar to those reported in humans.

“This result meant we could actually test the impact that human urine levels of triclosan have during antibiotic treatment of UTIs in mice,” Levin said.

All of the mice with the infection received Cipro to treat the UTI. Only some of the mice drank triclosan-spiked water. After antibiotic treatment, mice with triclosan exposure had a large number of bacteria in their urine and stuck to the bladder—mice without exposure had significantly lower bacterial counts.

“The magnitude of the difference in bacterial load between the mice that drank triclosan-spiked water and those that didn’t is striking,” Levin said.

“If the difference in the number of bacteria between the groups was less than tenfold, it would be difficult to make a strong case that the triclosan was the culprit,” Levin added. “We found 100 times more bacteria in the urine of triclosan-treated mice—that is a lot.”

This striking result has an equally striking message—antibiotics are less effective at treating UTIs when triclosan is around, at least in mice.

But how exactly is triclosan is interfering with antibiotic treatment? The WUSTL team was determined to find that mechanism.

Levin and her colleagues found that triclosan works with a cell growth inhibitor, a small molecule nicknamed ppGpp, to render cells less sensitive to antibiotics.

“We report that clinically relevant concentrations of triclosan increased E. coli and MRSA tolerance to bactericidal antibiotics as much as 10,000-fold in vitro and reduced antibiotic efficacy up to 100-fold in a mouse urinary tract infection model,” the authors wrote. “Genetic analysis indicated that triclosan-mediated antibiotic tolerance requires alarmone guanosine tetraphosphate (ppGpp) synthesis but is independent of growth. These data highlight an unexpected and certainly unintended consequence of adding high concentrations of antimicrobials in consumer products, supporting an urgent need to reevaluate the costs and benefits of the prophylactic use of triclosan and other bacteriostatic compounds.”

During times of stress, ppGpp responds by shutting down the biosynthetic pathways that make the building blocks—DNA, RNA, protein, and fat—that ultimately become new cells. This response helps divert resources away from growth and towards survival.

“There is a rule in medicine that you don’t give drugs that slow cell growth before drugs that kill cells,” Levin said.

Bactericidal antibiotics kill by targeting specific biosynthetic pathways. Ampicillin targets the enzymes that make the bacterial cell wall, for example, while Cipro targets DNA synthesis. When these pathways are shut down, bactericidal antibiotics have trouble doing their job.

While clinical studies would be required to definitively prove that triclosan is interfering with antibiotic treatments in humans, Levin said, “my hope is that this study will serve as a warning that will help us rethink the importance of antimicrobials in consumer products.”

Source: Genengnews

AbbVie, Voyager Launch $1.5B+ Gene Therapy Collaboration Aimed at Parkinson’s, Other Synucleinopathies

AbbVie, Voyager Launch .5B+ Gene Therapy Collaboration Aimed at Parkinson’s, Other Synucleinopathies

AbbVie and Voyager Therapeutics said today they will launch a potentially $1.5 billion-plus gene therapy collaboration—the companies’ second billion-dollar-plus alliance in as many years, with the new partnership focused on treating Parkinson’s disease and other diseases characterized by abnormal accumulation of misfolded alpha-synuclein protein.

The companies said they plan to develop “one or more” treatments that apply Voyager’s vectorized antibody platform and approach to delivering antibodies across the blood-brain barrier.

Voyager uses adeno-associated virus (AAV) capsids designed for a one-time intravenous delivery of genes that encode antibodies that target and bind to the alpha-synuclein protein. Voyager says its approach could deliver higher levels of therapeutic antibodies in the brain compared with current systemic administration of antibodies.

“Our scientific platform allows us to develop unique AAV gene therapies that are designed to knock down disease-causing gene expression, increase the expression of missing proteins, or enable the expression of therapeutic antibodies through vectorization,” Voyager president and CEO Andre Turenne said in a statement. “We are excited to expand our efforts towards pathological species of alpha-synuclein given its role in the progression of disease, and AbbVie is the ideal partner to advance this new target and therapeutic modality.”

Parkinson’s is a key disease area of focus for Voyager. Just last month, Neurocrine Biosciences agreed to develop and commercialize Voyager’s gene therapy programs for Parkinson’s disease and Friedreich’s ataxia, plus two other programs to be determined, through a collaboration that could generate more than $1.865 billion for Voyager.

Among gene therapy candidates covered by that collaboration are Voyager’s lead candidate, VY-AADC for Parkinson’s. Neurocrine has agreed to fund the Phase II/III pivotal program for VY-AADC, which has advanced to the Phase II RESTORE-1 trial (NCT03562494). RESTORE-1 dosed its first patient in December 2018. The following month, after a Type B meeting with the FDA, Voyager agreed to increase RESTORE-1’s target number of patients to between 75 and 100, and conduct a staggered-parallel Phase 3 trial (RESTORE-2) of similar size and design to RESTORE-1.

Earlier $1.1B tau partnership

The new collaboration comes a year and two days after AbbVie and Voyager launched a potentially $1.1-billion-plus partnership focused on developing and commercializing gene therapies for tau-related neurodegenerative diseases that include Alzheimer’s disease, frontotemporal dementia, and progressive supranuclear palsy.

That partnership is in its lead candidate selection phase, Voyager states on its website.

“The expansion of AbbVie’s partnership with Voyager represents the potential we see in the ability of its vectorized antibody platform to surpass the blood-brain barrier and more effectively deliver biologic therapies,” said Jim Summers, PhD, vice president, discovery neuroscience research, AbbVie. “We are hopeful that Voyager’s technology will enable further development of transformative treatments for patients with neurodegenerative diseases.”

In the new partnership, AbbVie agreed to pay Voyager $65 million upfront and up to $245 million in preclinical and Phase I development option payments. AbbVie may exercise one or more exclusive development options to select up to a total of four research compounds and their corresponding product candidates to proceed to development, Voyager stated in a regulatory filing.

AbbVie also agreed to pay Voyager up to an additional $728 million in payments tied to achieving development and regulatory milestones for each alpha-synuclein vectorized antibody compound developed, and up to $500 million in commercial milestone payments.

In addition, Voyager is eligible to receive tiered royalties from AbbVie on the global commercial net sales of each alpha-synuclein vectorized antibody developed.

Investors responded to Voyager’s expanded partnership with AbbVie with a buying surge that sent Voyager’s share price rising about 18% from yesterday’s closing price of $10.68, to $12.58 in early market trading this morning as of 10:01 a.m.

Source: Genengnews

Colorectal Cancer Stem Cell Growth Driven by High-Fat Diet and Altered Bile Acid Profile

Colorectal Cancer Stem Cell Growth Driven by High-Fat Diet and Altered Bile Acid Profile

Studies by Salk Institute scientists have suggested how high-fat diets may fuel the early development of colorectal cancer in people who have a common genetic mutation. Findings from the studies in mouse models and human cells, and reported in Cell, indicate that a high-fat diet and genetics combine to change bile acid balance in the gut, which in turn impacts on bile acid hormonal signaling to stem cells and lets potentially cancerous cells survive. The team, headed by Ronald Evans, PhD, who holds Salk’s March of Dimes chair in molecular and developmental biology, in addition, showed that chemically activating farsenoid X receptor (FXR) signaling in the gut counteracted the effect of unbalanced bile acids in both mouse organ models and in human colon cancer cell lines.

The studies hint that high-fat diets could help to explain why deaths from colorectal cancer in people under 55 years of age are on the increase, even though overall cancer death rates are falling. “It could be that when you’re genetically prone to get cancer, something like a high-fat diet is a second hit,” added Ruth Yu, PhD, a staff researcher at the Gene Expression Laboratory at Salk, and co-author of the team’s published paper. “This study provides a new way to lower inflammation, restore intestinal health, and to dramatically reduced tumor progression,” suggested Evans, who is also director of the Gene Expression Laboratory, and Howard Hughes Medical Institute investigator. The researchers’ published paper is titled, “FXR Regulates Intestinal Cancer Stem Cell Proliferation.”

High-fat diets, lack of exercise, obesity, diabetes, and high serum levels of toxic bile acids are all risk factors for colorectal cancer (CRC). The gastrointestinal tract contains a population of intestinal stem cells (ISCs) that replenish the cells lining the gut, but this process can be disrupted by diet, the team pointed out. “Dietary fatty acids have been implicated in enhancing the self-renewal capacity of ISCs and progenitor cells, as well as the tumor-initiating potential of cancer stem cells (CSCs).”

Mutations in the adenomatous polyposis coli (APC) gene, which normally acts as a tumor suppressor in these stem cells, can remove the gene’s control on stem cell replication and allow them to become cancerous, the authors explained. In fact, most CRC patients carry APC mutations. “Although the majority of CRC cases are sporadic, ~85% of patients have mutations in the adenomatous polyposis coli (APC) gene, a crucial negative regulator of Wnt signaling,” the team wrote.

Work in Evans’ lab has for the last 40 years been investigating the roles of the 30 or so bile acids that help to digest food and absorb cholesterol, fats, and fat-soluble nutrients. The researchers had discovered that bile acids send hormonal signals to gastrointestinal stem cells via the FXR receptor, which acts as “the master regulator of BA homeostasis, governing synthesis, efflux, influx, and detoxification throughout the gut-liver axis,” they wrote. The researchers’ new work builds on their previous findings, and demonstrates how high-fat diets can impact on that hormonal signaling.

Work by Salk postdoctoral fellow Ting Fu, PhD, who is first author on the published paper, focused on a mouse model with an APC mutation that develops early colorectal cancer. She found that levels of bile acids that interact with FXR increased at the same time as the animals started to develop cancer. The presence of additional bile acids further speeded cancer progression. “We saw a very dramatic increase in cancer growth correlated to bile acid,” said Michael Downes, PhD, a senior staff scientist at Salk and co-corresponding author of the study. “Our experiments showed that maintaining a balance of bile acids is key to reducing cancer growth.”

Colon cancer growth, as measured by the number of dividing cells shown in green, is dramatically increased when the FXR-regulated gene network is disrupted by specific bile acids or a high-fat diet. [Salk Institute]

Adding a high-fat diet into the mix further speeded cancer progression. The high-fat diets led to increased levels of two bile acids in particular, T-βMCA and DCA, which depressed FXR activity, allowing specific populations of stem cells to replicate without control and accumulate DNA damage. “Total BA levels and levels of T-βMCA and DCA tracked with tumor load suggestive of a causal link,” the researchers stated.

Further in vivo studies suggested that T-βMCA was the main driver of CRC progression. “These findings imply that T-βMCA can effectively recapitulate the ability of HFD to promote CRC progression,” they added. “We knew that high-fat diets and bile acids were both risk factors for cancer, but we weren’t expecting to find they were both affecting FXR in intestinal stem cells,” noted Annette Atkins, PhD, a staff researcher at Salk and co-author of the study.

The mutant APC mouse model commonly develops adenomas that only slowly, if at all, develop into malignant adenocarcinomas. This process of adenoma to adenocarcinoma conversion was found to be much faster in animals fed a high-fat diet. The researchers then used a Salk-developed FXR agonist molecule called FexD, to activate the receptor. Administration of FexD reversed the effects of unbalanced bile acids in mouse organoids and in human colon cancer-derived organoids. FexD administration also delayed tumor progression in the mouse model of CRC, and prolonged survival. “… selective activation of intestinal FXR retards the progression of adenomas and adenocarcinomas,” they stated. “… survival studies revealed profound improvements upon FexD treatment.”

The researchers concluded that FXR acts as “a point of convergence of heredity (H) and environmental (E) risk factors for CRC … Our studies demonstrate that the APC mutation and high-fat diet independently and cooperatively increase the BA pool that results in the repression of FXR signaling in intestinal stem cells.”

From left: Annette Atkins, Tae Gyu Oh, Ting Fu, Ronald Evans, Eiji Yoshihara, Fritz Cayabyab, Michael Downes, and Ruth Yu. [Salk Institute]

The study findings also hint at the potential to use drugs to hold back development of colon cancer. “While colon cancer is considered ‘incurable,’ Ting’s work opens up an entirely new frontier in the understanding and treatment of the disease,” said Evans. The researchers acknowledge that further tests will be needed before considering the potential to test FexD in humans, but they point out that one FXR agonist has already been approved and others are moving through clinical trials for treating liver disease, so “rapid translation of these findings into CRC patients is foreseeable.”


Source: Genengnews

BioTecNika on WhatsApp | Get Latest Bioscience Alerts in WhatsApp

BioTecNika on WhatsApp | Get Latest Bioscience Alerts in WhatsApp

BioTecNika on WhatsApp BioTecNika on WhatsApp for all Biotecnikans, A Few Months ago we had launched BioTecNika on WhatsApp and today we are proud to say that it has been a huge success so far. Our New service has been widely appreciated & adopted. However, we noticed that some of you have still not opted […]

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