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The Top 3 Tonsil Stone Causes – Plus, Getting Rid of Them Forever!


Tonsil stones wreck lives. Dramatic as that might sound, those little white spots at the back of your throat probably have you shying away from social situations, embarrassed of your bad breath. Just one simple tonsil stone causes anxiety and self consciousness. Though rarely painful, you may feel constantly self conscious about your breath, searching for remedies and trying different medications to get rid of them. Well, you’re not alone. Tonsillitis is extremely common.

Learning about tonsil stone causes will ultimately help in your quest to get back to a normal life.

They are basically a mixture of mucus, bacteria tiny food particles. Each of these ingredients, naturally occurring in the throat, gets caught in little pockets on the surface of the tonsils and mixes together to create the trademark white spots which causes the associated problems.

The top 3 most common causes of tonsil stones are:

Bacteria. Everyone has oral bacteria, it helps in breaking down food and is present in our saliva. Bad bacteria can be banished by practicing good oral hygiene. Brush your teeth frequently, preferably after eating, and use a mouth wash to help keep your bacteria healthy.

Diet. A bad diet has also been attributed to tonsil stone causes. Eating healthy foods is extremely important. It has also been suggested that dairy products may be associated with the development of tonsillitis.

Genetics. Health issues are often genetic, tonsillitis is no exception. If you have a history of tonsillitis in your family, chances are you may also get them. Now, unfortunately there’s not a great deal you can do about that, but if you are unlucky enough to have tonsil stones in your genes, or for any other reason, help is at hand.



Source by Kerry Jarman

Findings suggest the possibility of manipulating gut microbiome to treat disease — ScienceDaily


CagA, a protein produced by the bacterium Helicobacter pylori, can alter the population of microbes living in the fruit fly gut, leading to disease symptoms, according to new research published in PLOS Pathogens by Tiffani Jones and Karen Guillemin of the University of Oregon.

Microbes living in the human gut normally help keep people healthy, but disruptions to this microbial community can promote disease. Infections with specific microbial species can disrupt the gut microbiome, but it is unclear how such disruption occurs and whether it promotes disease.

In the new study, Jones and her colleagues used Drosophila fruit flies to test the effects of infection with H. pylori, which can cause gastric cancer in humans. They hypothesized that a protein associated with H. pylori called CagA disrupts the fruit fly gut microbiome and contributes to disease.

To test their hypothesis, the researchers genetically engineered fruit flies to express the CagA protein in their intestines, without being infected by H. pylori. This allowed them to disentangle the specific effects of CagA from the overall effects of H. pylori infection.

They found that CagA expression in the fruit fly gut caused excess growth of intestinal cells and promoted immune system responses that are associated with H. pylori infection. However, these symptoms did not occur in CagA-expressing flies that were raised without microbes, suggesting the importance of the gut microbiome.

Indeed, further investigation revealed that CagA expression was associated with a disrupted gut microbiome in the flies. Exposure to the CagA-expressing flies caused the same microbiome disruptions in normal flies, which was sufficient to cause the same symptoms of excess cell growth and immune response seen in the genetically altered flies.

Overall, these findings show that CagA can indirectly cause disease symptoms by altering the gut microbiome. This raises the possibility that the harmful effects of infection with H. pylori — and other microbes that may function similarly — could be mitigated by manipulating the balance of microbes in the gut.

“Our work demonstrates for the first time that a bacterial virulence factor like CagA can alter commensal microbial communities to cause disease,” the author explain. “This work also reveals that commensal microbial communities may participate in the progression of H. pylori mediated gastric cancer.”

Story Source:
Materials provided by PLOS. Note: Content may be edited for style and length.



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A day dedicated to research


Springer Nature organizes the first Research Day in Rome at La Sapienza University

This guest blog comes from Nick Barber, Library Director, Southern Europe, Springer 

 

On Oct 3 2017 Springer Nature held the first “Research Day” in coordination with La Sapienza University Library System in Rome and in collaboration with CARE.

The seminar examined the changing face of research today, seeking to understand the evolving needs of research and researchers themselves, and consider the role that academic and research libraries are increasingly required to adapt to.

Furthermore, the spotlight was on approaches and innovations proposed by scientific and academic publishers, including how they can respond to these changes and bring more clarity to the complex publishing process many researchers now face.

In Italy, CARE/CRUI is the principal group responsible for coordinating access to electronic resources for the higher education and research communities, and linked to the Conference of University Rectors CARE. This event in Rome was directed at a mixed audience of librarians, university rectors for research and researchers.

Founded in 1303, La Sapienza University is the largest university in Italy, as well as its top-ranking academic institution in terms of the number of published articles, according to Clarivate Analytics’ InCites 2012-2016.

A call for collaboration

Keynote speakers provided lively presentations, addressing the main issues and topics concerning the changing role of libraries and research over the past several years. This resulted in a passionate call for more collaboration and partnership at all levels to respond to the challenges we all face.

The morning continued with experts from Springer Nature, who discussed various related topics.

  • Dan Penny, Head of Market Intelligence, presented some of the innovations that Springer Nature is now incorporating in its publishing workflows.
  • Grace Baynes, Director, Data and New Product Development, spoke on the increasing presence and importance of ‘big data’ in scientific research, the need to make it open, and how to make the various open data policy requirements increasingly required for article submissions more transparent.

A presentation of Springer Nature SciGraph, given by Grace Baynes, provided further insights into open data initiatives.

  • Elisa De Ranieri, Head of Editorial Process and Data Analytics, Nature journals, provided insights into how publishers are seeking to overcome nagging challenges in terms of integrity, efficiency, reproducibility and the speed of communication of research.

Panel discussion

In the afternoon a lively round table discussion followed, taking a closer look at various questions. A summary of the discussions will be shared on this blog soon.

All presentations are available here and a recorded version of the parallel webinar can be found here.

We invite you to submit any comments or questions on Research Day (in Italian or English) here. (elisa.magistrelli@springer.com)



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H7N9 influenza is both lethal and transmissible in animal model for flu — ScienceDaily


In 2013, an influenza virus that had never before been detected began circulating among poultry in China. It caused several waves of human infection and in late 2016, the number of people to become sick from the H7N9 virus suddenly started to rise. As of late July 2017, nearly 1,600 people had tested positive for avian H7N9. Nearly 40 percent of those infected had died.

In early 2017, Yoshihiro Kawaoka, professor of pathobiological sciences at the University of Wisconsin-Madison School of Veterinary Medicine, received a sample of H7N9 virus isolated from a patient in China who had died of the flu. He and his research team subsequently began work to characterize and understand it. The first of those results are published today (Oct. 19, 2017) in Cell Host & Microbe.

For the first time, Kawaoka says, his team has identified an influenza virus strain that is both transmissible between ferrets (the best animal model proxy for human influenza infections) and lethal, both in the animal originally infected and in otherwise healthy ferrets in close contact with these infected animals.

“This is the first case of a highly pathogenic avian virus that transmits between ferrets and kills them,” Kawaoka says. “That’s not good for public health.”

Everyone in the influenza field knew it was only a matter of time before the virus became pathogenic in chickens, which is to say that it became capable of causing disease, but Kawaoka says it took several years. It was initially hard to detect because, unlike some other influenza viruses such as H5N2 — which is highly lethal in chickens and caused significant outbreaks on poultry farms across the U.S. and elsewhere in 2015 — H7N9 was not killing the chickens it infected.

Instead, it remained silent, passing unknown from chicken to chicken and, occasionally, infecting humans that came into contact with the birds.

Influenza viruses are well known for their propensity to adapt. With each new infection of a host, small changes take place within the genomes of influenza viruses. Sometimes these mutations occur in key regions and lead to significant alterations to the original virus, rendering it capable of infecting new hosts, making hosts sick, causing greater illness, and becoming resistant to the drugs typically used to treat them.

Kawaoka and his team observed this within the sample isolated from the deceased patient, who while alive had been treated with the common flu drug Tamiflu. Using a technique to read the genetic identity of the virus population that had infected the patient, Kawaoka’s team learned the virus had started to mutate: The sample contained a population of H7N9 virus that was sensitive to Tamiflu and a population that was resistant.

So the team created two viruses virtually identical to those isolated from the patient, one sensitive to Tamiflu and the other bearing the mutation that conferred resistance to the drug. Comparing this to a low-pathogenic version of the H7N9 virus that Kawaoka and others had previously studied, the research team assessed how well each virus grows in human respiratory cells, where most influenza viruses take up residence in the body. They found that each grew efficiently, though the resistant strain was less effective than the other two.

The team also found that each virus infects and causes illness, to varying degrees, in several animal models for influenza — mice, ferrets and macaques.

To test whether the virus was transmissible between mammals, the researchers set up experiments in which ferrets were housed alone in individual cages separated by a barrier that allowed respiratory droplets to pass from one cage to the next. In each pair, one ferret was deliberately infected with the virus while the other was placed into the cage healthy.

Each of the three virus types were transmitted from infected ferrets to the previously uninfected animals. Two of three ferrets infected with the nonresistant strain of H7N9 — the strain currently circulating in China — died, as did the animals to which they passed the virus.

“Without additional mutations, the virus transmitted and killed ferrets,” says Kawaoka, noting that further alterations to the virus may not be necessary to make it a potential public health threat, though human-to-human transmission has thus far remained limited.

The team also confirmed the drug-resistant H7N9 did not respond to oseltamivir, the active agent in Tamiflu. It did respond to another drug called a protease inhibitor, but Kawaoka says it is a drug currently approved only in Japan and only for use in pandemic situations.

“I don’t want to cause alarm,” Kawaoka says, but “it’s only a matter of time before the resistant virus acquires a mutation that allows it to grow well, (rendering it) more likely to be lethal at the same time it is resistant.”

However, Kawaoka and his team are currently unable to better understand what mutations may enable this transition, at least in the United States, where a moratorium on work that might cause a pathogen to take on a new function not currently known in nature has been in place for several years.

“We can’t do the experiments to find out why,” Kawaoka says. “We really need to understand why H7N9 is lethal and transmissible, and what is different in this one resistant H7N9. If we knew that, because there are multiple viruses circulating, we could narrow down efforts to those that are lethal and transmissible.”

He recently published a commentary in the Proceedings of the National Academy of Sciences, co-authored with two colleagues who are also experts in influenza, in which they explain the challenges this moratorium creates for understanding the potential of viruses like H7N9 to become pandemic.

“Results from (gain-of-function) studies would almost certainly help in understanding the pandemic potential of influenza viruses and produce public health benefits, such as the prioritization and development of pre-pandemic vaccines and antiviral drugs,” the authors write. Fundamental (gain-of-function) research on transmissibility, host-range restriction, drug resistance, immunogenicity, pathogenicity, and replicative ability would also benefit global public health.”

The H7N9 virus is likely to continue to mutate as it infects humans, resulting in adaptations that enhance the viruses’ pathogenicity or ability to pass from person to person, Kawaoka adds. In other words, nature is already performing its own gain-of-function experiments, with potentially serious consequences.

It has, however, become a bit easier recently to detect when poultry are infected with H7N9, thereby allowing people to limit their exposure. That’s because the virus has begun to kill birds in China, too. But unlike in the U.S., where farmers cull their flocks to limit the spread of infectious disease, China relies on vaccines. This worries Kawaoka, given how well the virus has been shown to grow.

For now, he says: “We should improve our surveillance.”

10.1016/j.chom.2017.09.008



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