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Wednesday, 18 January 2017

New Discovery of How Eukaryotes originated from Prokaryotes

From Cell to Man (Image: Cosmology)

Origin of life is known to exist about 2billion years ago from simplest organisms like single celled bacteria and archaea. Eukaryotes which are complex life forms known to originate from these tiny organisms. This evolutionary leap is considered to be an important step in the history behind origin of life. But the question about these complex cells arise from simple single celled microbes still remained mystery.

A recent study that published in the journal Nature provided new insights about how the deemed 'marvel microbes' shed light over evolutionary transition from simple to complex life forms.

Dr. Thijs Ettema from Uppsala University in Sweden who led the study mentioned The Huffington Post, "“Our new paper tells what our microbial ancestors might have looked like. We humans are eukaryotes, and our cells are big and complex. In contrast, the cells of bacteria and archaea are tiny and simple. The main question is how the big and complex cells of eukaryotes have evolved from the smaller and simpler prokaryotic cells.”

Asgard archaea (named after Norse gods) form a group with the eukaryotes.  (Image: Nature)


The research findings are based on the work framed by Carl Woose who had shown that eukaryotes origated from Archaea. Here a new type of archaea called the Asgard archaea fall in one of the four known lineages named after Norse gods (view figure). They are usually seen in ocean floor, sea beds, lakes and hot springs. Interestingly even though Asgard is prokarote it has several eukaryotic genes in their genome and this provides a deep insight about how eukaryotes originated from simplest life forms.

“They (Asgard archaea) represent a sister group of eukaryotes in the tree of life,” Etterma said. “In addition to that, their genomes contain a lot of important eukaryotic genes. Altogether, the discovery of these Asgard archaea tells us that eukaryotes, and hence humans as well, share a common ancestry.”



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Tuesday, 17 January 2017

The Power of Predatory Bacteria can be Harnessed as a 'living antibiotic'

Predatory bacteria is one of the new therapeutic approaches that scientist are starting to look at. These are bacteria that requires a prey to finish their life cycle and thus are called predatory bacteria. A naturally occurring predatory bacterium is able to work with the immune system to clear multi-drug resistant Shigella infections in zebrafish, according to a study published in Current Biology. It is the first time the predatory bacterium Bdellovibrio bacteriovorus has been successfully used as an injected anti-bacterial therapy and represents an important step in the fight against drug-resistant infections, or 'superbugs'. Shigella infection is responsible for over 160 million illnesses and over 1 million deaths every year - and is a common cause of 'travellers’ diarrhoea. Cases of drug-resistant Shigella are also on the rise as, although the diarrhoea usually clears up without treatment, antibiotics are often used even in mild cases to stop the diarrhoea faster. Resistance to antibiotics has prompted a team of researchers from Imperial College London and Nottingham University to look to the natural environment for creative solutions to this problem.

To investigate Bdellovibrio's ability to control drug resistant Gram-negative infections, researchers injected zebrafish larvae with a lethal dose of Shigella flexneri strain M90T, resistant to both streptomycin and carbenicillin antibiotics. Bdellovibrio was then injected into the larvae's infection site, and a decrease in the number of Shigella was seen. In the absence of Bdellovibrio, zebrafish were unable to control the replication of Shigella and levels of the bacteria rose. Wellcome Research Career Development Fellow Dr Serge Mostowy, co-lead author from Imperial College London said: "This study really shows what a unique and interesting bacterium Bdellovibrio is as it presents this amazing natural synergy with the immune system and persists just long enough to kill prey bacteria before being naturally cleared. It's an important milestone in research into the use of a living antibiotic that could be used in animals and humans."


Bdellovibrio can invade and kill a range of Gram-negative bacteria, such as E. coli and Salmonella, in the natural environment. Previous research has shown that it can reduce pathogen numbers in the stomach of chickens when taken as an oral therapy, but there is growing need to develop therapies to target infections in wounds and organs. Successful use of Bdellovibrio highlights its potential uses in tackling a range of drug-resistant Gram-negative bacterial infections that can develop in hospital patients.

Professor Liz Sockett, co-lead author from The University of Nottingham said: "This has been a truly ground-breaking collaboration that shows therapeutic Bdellovibrio in action inside the translucent living zebrafish. The predatory action of the Bdellovibrio breaks the Shigella-pathogen cells and this stimulates the white blood cells; redoubling their 'efforts' against the pathogen and leading to increased survival of the zebrafish 'patients'." Remarkably, Bdellovibrio is also able to reduce pathogen load in immunocompromised zebrafish larvae that have been depleted of white blood cells. However, survival is significantly greater in immune-competent zebrafish, showing that Bdellovibrio's maximum therapeutic benefit comes from its ability to work cooperatively with the host's own immune system.

Dr Michael Chew, Science Portfolio Advisor at Wellcome said: "It may be unusual to use a bacterium to get rid of another, but in the light of the looming threat from drug resistant infections the potential of beneficial bacteria-animal interactions should not be overlooked. We are increasingly relying on last line antibiotics, and this innovative study demonstrates how predatory bacteria could be an important additional tool to drugs in the fight against resistance."


Source: LabRoots Inc. Newsletter
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Monday, 16 January 2017

Analysis of Human Microbiome Yields Potential new Antibiotics

Rising antibiotic resistance is considered a major public health threat one that the United Nations has taken notice of, prompting warnings about the danger it poses. Utilizing computational power, researchers looked to bacteria to find candidate compounds they were then able to synthesize. Two potential new antibiotics have been produced using this strategy.

A research team at Rockefeller University led by Sean Brady, head of the Laboratory of Genetically Encoded Small Molecules, interrogated public databases containing the genomes of bacteria that live in the human body. They wanted to find clusters of genes that were predicted to produce molecules, non-ribosomal peptides, which are the basis of myriad antibiotics.
 
There are genes within the genome of a microbe that are antimicrobial, but using bacteria to produce those compounds is fraught with challenges. Many bacterial strains are difficult to grow in a lab. Scientists would also have to determine how to manipulate the proper genes of a bacterium to make them express the antimicrobial molecules. Using computational methods avoided those problems.
 
In doing so, the team found 57 candidate gene clusters, from which 30 were chosen. Using a technique called solid-phase synthesis, 25 compounds were produced. Those compounds were then tested with human pathogens, enabling the investigators to identify the two antibiotics the scientists named humimycin A and humimycin B. The findings were published in Nature Chemical Biology.

Humimycin A and B are closely related and from a family of bacteria named Rhodococcus, which have not previously yielded anything resembling the humimycins when grown with typical laboratory protocols. The humimyics proved very effective combating Staphylococcus and Streptococcus bacteria, microbes that can result in serious infections in humans and tend to become antibiotic resistant.
 
Experiments determined that the humimycins act to inhibit an enzyme that aids in buildings cell walls in bacteria; without that cell-wall-building power, the bacteria die. Beta-lactams are a commonly used class of antibiotics that have a diminishing effect as bacteria build resistance to them. The researchers found, however, that humimycins can actually re-sensitize bacteria to the action of beta-lactams they had become resistant to.
 
Staphylococcus microbes that were resistant to beta-lactam died after being exposed to a beta-lactam antibiotic in combination with humimycin A. Incredibly, that effects was still seen even if there had been little effect from using humimycin A by itself. Brady suggested that is because both compounds work by disrupting different parts of the same biological pathway.
 
"It's like taking a hose and pinching it in two spots," he says. Even if neither kink halts the flow altogether on its own, "eventually, no more water comes through."
 
The scientists went a step further and used a common cause of antibiotic-resistant infections, Staphylococcus aureus, to infect mice. After being dosed with the strain, which was beta-lactam resistant, the mice were treated with either humimycin A, a beta-lactam antibiotic, or a combination of both. The mice treated with both drugs had the best outcome, and that discovery could pave the way toward therapeutics for human use.
 
Brady is hopeful that this work will inspire others to pursue a similar line of reasoning to find other potential therapies. He plans to apply the strategy to bacterial species outside of the human microbiome, and eventually, even to those bacterial species whose genomes have not yet been sequenced.




Source: Via labroots
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Fasting could Stunt Leukaemia into Remission

Leukaemia a malignant progressive disease in which the bone marrow and other blood-forming organs produce increased numbers of immature or abnormal leucocytes  which invariably suppresses the production of normal blood cells, leading to anaemia and other symptoms. The newest leukaemia research findings suggest that intermittent fasting may literally starve the cancer cells. The study, by the University of Texas Southwestern Medical Center, explores different pathways by which acute lymphoblastic leukaemia may be targeted more successfully.

Though considered a rare disease, acute lymphoblastic leukaemia which is the most common form of childhood cancer, peaking in early childhood between the ages of 2 and 4. The cancer involves the overproduction of immature white blood cells in the bone marrow. These cancerous cells invade the blood and other organ systems, causing massive cell death and damage in a short amount of time. Based on previous research that suggests fasting may augment chemotherapy outcome, researchers at University of Texas Southwestern decided to investigate this line of treatment in several mouse models of Acute Lymphoblastic Leukaemia (ALL). The mice received either normal feeding or were subject to a dietary restriction consistent with intermittent fasting.

Chengcheng Zhang the study lead author who is an associate professor at UT Southwestern, said “Strikingly, we found that in models of ALL, a regimen consisting of six cycles of 1 day of fasting followed by 1 day of feeding completely inhibited cancer development," Within 7 weeks on the fasting diet, the mice had undetectable levels of leukaemia cells in the bone marrow and spleen, a promising sign of disease remission. By contrast, mice on the normal diet regimen contained nearly 70 percent of cancerous cells in the affected organs.
"Although initially cancerous, the few fluorescent cells that remained in the fasted mice after 7 weeks appeared to behave like normal cells. Mice in the ALL model group that ate normally died within 59 days, while 75 percent of the fasted mice survived more than 120 days without signs of leukaemia,” reported Zhang.

The exact mechanism behind this effect is yet to be fully understood. However, Zhang’s team suspect it involves leptin, a “satiety hormone” released to inhibit the hunger sensation. "We found that fasting decreased the levels of leptin circulating in the bloodstream as well as decreased the leptin levels in the bone marrow," said Zhang. "These effects became more pronounced with repeated cycles of fasting," he adds. "After fasting, the rate at which the leptin levels recovered seemed to correspond to the rate at which the cancerous ALL cells were cleared from the blood."


This outstanding result implies that fasting augmented with normal treatment will be helpful, but as it is now, it hasn’t been clinically tested in human. For this reason patients or caretakers should not yet consider fasting as a treatment plan.
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Wednesday, 11 January 2017

Novel Wound-healing Technology Developed

Based on the online edition of npj Biofilms and Microbiomes a WSU research team has successfully used a mild electric current to take on and beat drug-resistant bacterial infections, a technology that may eventually be used to treat chronic wound infections. The researchers have filed a patent application and are working to commercialize the process. Already several companies have contacted WSU to discuss commercialization. They also hope to begin conducting clinical tests.

Haluk Beyenal and Paul Hohenschuh; Distinguished Professor in the Gene and Linda Voiland School of Chemical Engineering and Bioengineering, led the research team by using an antibiotic in combination with the electric current to kill all of the highly persistent Pseudomonas aeruginosa PAO1 bacteria in their samples. P. aeruginosa is a bacteria that is responsible for chronic and serious infections in people with lung diseases, such as cystic fibrosis, chronic wounds and it’s implicated as the cause of pneumonia for people who are on ventilators and infections in burn victims. "I didn't believe it. Killing most of the persister cells was unexpected," said Beyenal, when he first saw the results. "Then we replicated it many, many times."
Bacterial resistance is a growing problem around the world. While antibiotics were a miracle drug of the 20th century, their widespread use has led to drug-resistant strains. In the U.S. at least two million infections and 23,000 deaths are now attributable to antibiotic-resistant bacteria each year, according to the Centers for Disease Control. When doctors use antibiotics to treat a bacterial infection, many of the bacteria die. Bacteria that form a slime layer (called a biofilm), however, are more difficult to kill because antibiotics only partially penetrate this protective layer. Subpopulations of "persister" cells survive treatment and are able to grow and multiply, resulting in chronic infections.


In the new study, the researchers used an "e-scaffold," a sort of electronic band-aid made out of conductive carbon fabric, along with an antibiotic to specifically tackle these persister cells. The e-scaffold creates an electrical current that produces a low and constant concentration of hydrogen peroxide, an effective disinfectant, at the e-scaffold surface. The hydrogen peroxide disrupts the biofilm matrix, damages the bacterial cell walls and DNA, allowing better antibiotic penetration and efficacy against the bacteria. "It turns out the hydrogen peroxide is really hard on biofilms,'' said Doug Call, a professor in the Paul Allen School of Global Animal Health and co-author on the paper.

Researchers have tried electrical stimulation as a method to kill bacteria for more than a century but with only mixed results. Beyenal's team determined the conditions necessary for the electrochemical reaction to produce hydrogen peroxide. The current has to be carefully controlled, however, to assure the correct reaction at an exact rate. Their method also does not damage surrounding tissue, and the bacteria are unable to develop resistance to such an electrochemical treatment. "We pushed past the observation and got to the mechanism,'' said Call.  "If you can explain why it works, then you can move forward, describe the limitations, and hopefully augment the effect."

Similar to the way that penicillin was discovered by accident, the research to develop the e-scaffold actually came out of Beyenal's group's failed attempt to improve fuel cells, he said. When the researchers figured out they could only produce a small amount of electric current for their fuel cell cathode, they decided to see if they could use the process for a different purpose. "As engineers, we are always trying to find solutions to a problem, so we decided to use bad cathodes to control biofilm growth, and it worked. Our inspiration came from the fundamental work to understand its mechanism" he said.


This brought to mind a question – “should we publish our negative result as a growing researcher?”
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Bacteria That Evades Drug Treatment

One of the major concern for scientist and medical practitioners is the issue of bacteria that is resistant to standard treatments. ‘superbugs’ as they are often referred to are not just the one of concern or of great threat to public health, but chronic bacterial infections that evade treatment which afflict many people. For this reason scientists are looking for new ways to exploit weaknesses in bacteria, and trying to develop new treatment strategies. In the quest for this, researchers at the BASP Centre, University of Copenhagen have reported finding strategies utilized by bacteria in order to survive antibiotic treatment and as aptly named it persister cells. A complete understanding of this phenomenon will help the development of better drug treatments, and could potentially initiate the creation of novel antibiotics that would aim at these tenacious, pathogenic persister bacteria.


Alexander Harms and colleagues in their publication in the journal of science described this newly identified molecular mechanisms that helps the bacteria endure and survive antibiotic treatment in such a way that they can later cause infections that become recurrent and chronic. Such infections can be forced down with typical therapeutic regimens, only to re-surface especially when the immune system is vulnerable. In their words “This amazing resilience is often due to hibernation in a physiological state called persistence where the bacteria are tolerant to multiple antibiotics and other stressors. Bacterial cells can switch into persistence by activating dedicated physiological programs that literally pull the plug of important cellular processes. Once they are persisters, the bacteria may sit through even long-lasting antibiotic therapy and can resuscitate to cause relapsing infections at any time after the treatment is abandoned.”

Recent work published by investigators working in the field has revealed the molecular underpinnings of several cellular cascades that drive the formation of bacterial persisters. Scientists have been able to confirm what scientists have long thought, that persistence is very closely related to dormancy or slow growth. Analogies to bacterial persistence can therefore be found in nature, such as animals that go into hibernation, slowing metabolism during periods when their environment is not ideal for survival. Another example is the tough, persistent spores that many mushrooms and plants produce to propagate themselves.
In an event seen in many different kinds of bacteria, a special compound, referred to as "magic spot" – the molecule guanosine-tetraphosphate or ppGpp, regulates dormancy pathways, giving it a central function in the bacterial persistence phenomenon. Many of these findings were achieved at the BASP Centre, and hopefully will aid in the future development of better drug treatment strategies, or even the eventual creation of novel antibiotics. Major and most important goal is now how to design drug, probably a secondary one that will be effective when the bacteria persist i.e. switch to a dormant mode.


For further reading on bacteria associated with chronic infections, the journal Virulence will be helpful.
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26 Deaths reported in Madagascar Plague Outbreak

Bipolar staining of a plague smear prepared from lymph aspirated from an adenopathic lymph node, or bubo, of a plague patient. (Source: CDC)


In early December 2016, a suspected plague was reported by Ministry of Health in Madagascar to World Health Organization. The affected district Befotaka, south-east of the country known to be endemic and till now no such plague cases were reported since 1950.

Based on the record on 27th December 2016, 62 cases (6 confirmed, 5 probably and 51 suspected) including 26 deaths were reported. The fatality rate is about 42 percent.

Of 11 samples, 5 were tested positive by rapid diagnostic test and 6 then confirmed by Institut Pasteur Laboratory. Among 11 samples, 5 were classified as pneumonic plague and remaining as bubonic plague.
Investigations have reported that the outbreak was started since mid of August 2016. The affected zone is known to be remote and hence insecurity slows down investigations.

Key response activities that have been included now are (Source: Outbreak News):

  • ·        Epidemiological investigations including active case finding and rapid diagnostic testing
  • ·        Training of community health workers on community-based surveillance and early detection of cases
  • ·        Clinical Management of suspected cases
  • ·        Identification, follow up and chemoprophylaxis of contacts
  • ·        Vector and reservoir control through the use of Kartman boxes
  • ·        Sensitization of the population
  • ·        Strengthening the community based surveillance
  • ·        Free treatment of other diagnosed disease such as malaria
  • ·        Strengthening early detection in neighbouring districts
  • ·        Laboratory confirmation

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