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NIH scientists find microbes on the skin of mice promote tissue healing, immunity | National Institutes of Health (NIH)

NIH scientists find microbes on the skin of mice promote tissue healing, immunity | National Institutes of Health (NIH)

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NIH scientists find microbes on the skin of mice promote tissue healing, immunity

Insights may inform wound management techniques.

What

Beneficial bacteria(link is external) on the skin of lab mice work with the animals’ immune systems to defend against disease-causing microbes and accelerate wound healing, according to new research from scientists at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. Researchers say untangling similar mechanisms in humans may improve approaches to managing skin wounds and treating other damaged tissues. The study was published online today in Cell.
Like humans and other mammals, mice are inhabited by large, diverse microbial populations collectively called the microbiome. While the microbiome is believed to have many beneficial functions across several organ systems, little is known about how the immune system responds to these harmless bacteria.
To investigate, NIAID scientists led by Yasmine Belkaid, Ph.D., chief of the Mucosal Immunology Section of NIAID’s Laboratory of Parasitic Diseases, observed the reaction of mouse immune cells to Staphylococcus epidermidis, a bacterium regularly found on human skin that does not normally cause diseaseTo their surprise, immune cells recognized S. epidermidis using evolutionarily ancient molecules called non-classical MHC molecules, which led to the production of unusual T cells(link is external) with genes associated with tissue healing and antimicrobial defense. In contrast, immune cells recognize disease-causing bacteria with classical MHC molecules, which lead to the production of T cells that stoke inflammation.
 Researchers then took skin biopsies from two groups of mice—one group that had been colonized by S. epidermidis and another that had not. Over five days, the group that had been exposed to the beneficial bacteria experienced more tissue repair at the wound site and less evidence of inflammation. Dr. Belkaid’s team plans to next probe whether non-classical MHC molecules recognize friendly microbes on the skin of other mammals, including humans, and similarly benefit tissue repair. Eventually, mimicking the processes initiated by the microbiome may allow clinicians to accelerate wound healing and prevent dangerous infections, the researchers note.

Article

J Linehan et al. Non-classical immunity controls microbiota impact on skin immunity and tissue repair. Cell DOI: 10.1016/j.cell.2017.12.033 (2018).

Who

Yasmine Belkaid, Ph.D., Mucosal Immunology Section Chief in NIAID’s Laboratory of Parasitic Diseases and study co-author, is available for comment.

Contact

To schedule interviews, please contact Judith Lavelle, (301) 402-1663, judith.lavelle@nih.gov(link sends e-mail).
NIAID conducts and supports research — at NIH, throughout the United States, and worldwide — to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.  
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
NIH…Turning Discovery Into Health®

A Guide to Cognitive Fitness - Harvard Health

A Guide to Cognitive Fitness - Harvard Health

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What is cognitive reserve?



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An important concept that is crucial to the understanding of cognitive health is known as cognitive reserve. You can think of cognitive reserve as your brain's ability to improvise and find alternate ways of getting a job done. Just like a powerful car that enables you to engage another gear and suddenly accelerate to avoid an obstacle, your brain can change the way it operates and thus make added recourses available to cope with challenges. Cognitive reserve is developed by a lifetime of education and curiosity to help your brain better cope with any failures or declines it faces.
Get your copy of A Guide to Cognitive Fitness

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In this Special Health Report, Harvard Medical School doctors share a six-step program that can yield important and lasting results. Together these “super 6” can strengthen your intellectual prowess, promote your powers of recall, and protect the brain-based skills that are essential for full, rewarding, and independent living. From simple and specific changes in eating to ways to challenge your brain, this is guidance that will pay dividends for you and your future.

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The concept of cognitive reserve originated in the late 1980s, when researchers described individuals with no apparent symptoms of dementia who were nonetheless found at autopsy to have brain changes consistent with advanced Alzheimer's disease. These individuals did not show symptoms of the disease while they were alive because they had a large enough cognitive reserve to offset the damage and continue to function as usual.
Since then, research has shown that people with greater cognitive reserve are better able to stave off the degenerative brain changes associated with dementia or other brain diseases, such as Parkinson's disease, multiple sclerosis, or a stroke. A more robust cognitive reserve can also help you function better for longer if you're exposed to unexpected life events, such as stress, surgery, or toxins in the environment. Such circumstances demand extra effort from your brain—similar to requiring a car to engage another gear. When the brain cannot cope, you can become confused, develop delirium, or show signs of disease. Therefore, an important goal is to build and sustain your cognitive reserve. You can get a rough idea of your cognitive reserve simply by gauging how much your education, work, and other activities have challenged your brain over the years. Our six-step program will help you improve your cognitive reserve.
To learn more about staying mentally sharp and fit, read Cognitive Fitness, a Special Health Report from Harvard Medical School.

Diagnosis and management of transthyretin familial amyloid polyneuropathy in Japan: red-flag symptom clusters and treatment algorithm | Orphanet Journal of Rare Diseases | Full Text

Diagnosis and management of transthyretin familial amyloid polyneuropathy in Japan: red-flag symptom clusters and treatment algorithm | Orphanet Journal of Rare Diseases | Full Text







Diagnosis and management of transthyretin familial amyloid polyneuropathy in Japan: red-flag symptom clusters and treatment algorithm

  • Yoshiki Sekijima,
  • Mitsuharu Ueda,
  • Haruki Koike,
  • Sonoko Misawa,
  • Tomonori Ishii and
  • Yukio AndoEmail author
Orphanet Journal of Rare Diseases201813:6
Received: 31 July 2017
Accepted: 23 November 2017
Published: 17 January 2018

Abstract

Hereditary ATTR (ATTRm) amyloidosis (also called transthyretin-type familial amyloid polyneuropathy [ATTR-FAP]) is an autosomal-dominant, adult-onset, rare systemic disorder predominantly characterized by irreversible, progressive, and persistent peripheral nerve damage. TTR gene mutations (e.g. replacement of valine with methionine at position 30 [Val30Met (p.Val50Met)]) lead to destabilization and dissociation of TTR tetramers into variant TTR monomers, which form amyloid fibrils that deposit in peripheral nerves and various organs, giving rise to peripheral and autonomic neuropathy and several non-disease specific symptoms.
Phenotypic and genetic variability and non–disease-specific symptoms often delay diagnosis and lead to misdiagnosis. Red-flag symptom clusters simplify diagnosis globally. However, in Japan, types of TTR variants, age of onset, penetrance, and clinical symptoms of Val30Met are more varied than in other countries. Hence, development of a Japan-specific red-flag symptom cluster is warranted. Presence of progressive peripheral sensory-motor polyneuropathy and ≥1 red-flag sign/symptom (e.g. family history, autonomic dysfunction, cardiac involvement, carpal tunnel syndrome, gastrointestinal disturbances, unexplained weight loss, and immunotherapy resistance) suggests ATTR-FAP. Outside of Japan, pharmacotherapeutic options are first-line therapy. However, because of positive outcomes (better life expectancy and higher survival rates) with living donor transplant in Japan, liver transplantation remains first-line treatment, necessitating a Japan-specific treatment algorithm.
Herein, we present a consolidated review of the ATTR-FAP Val30Met landscape in Japan and summarize findings from a medical advisory board meeting held in Tokyo on 18th August 2016, at which a Japan-specific ATTR-FAP red-flag symptom cluster and treatment algorithm was developed. Beside liver transplantation, a TTR-stabilizing agent (e.g. tafamidis) is a treatment option. Early diagnosis and timely treatment using the Japan-specific red-flag symptom cluster and treatment algorithm might help guide clinicians regarding apt and judicious use of available treatment modalities.

Keywords

Disease-modifying agentTafamidisLiver transplantationHereditary ATTR amyloidosisFamilial amyloid polyneuropathyAmyloidosis neuropathyCarpal tunnel syndromeCardiomyopathyRed-flag symptom clusters

Ahead of Print -Ceftriaxone-Resistant Neisseria gonorrhoeae, Canada, 2017 - Volume 24, Number 3—March 2018 - Emerging Infectious Disease journal - CDC

Ahead of Print -Ceftriaxone-Resistant Neisseria gonorrhoeae, Canada, 2017 - Volume 24, Number 3—March 2018 - Emerging Infectious Disease journal - CDC





Volume 24, Number 3—March 2018

Letter

Ceftriaxone-Resistant Neisseria gonorrhoeae, Canada, 2017

To the Editor: I read with great interest the report by Lefebvre et al. about a Neisseria gonorrhoeae isolate identified in Canada demonstrating a ceftriaxone MIC of 1 mg/L (1). The authors note: “As of October 15, 2017, only 5 ceftriaxone-resistant Neisseria gonorrhoeae isolates had been reported worldwide (MIC range 0.5–2 mg/L).” The authors cite published reports from Spain, Japan, Australia, and France.
I would like to clarify that additional N. gonorrhoeae isolates have been identified with ceftriaxone MICs >0.5 mg/L. Since 1987, as part of the Gonococcal Isolate Surveillance Project, the Centers for Disease Control and Prevention has been testing N. gonorrhoeae isolates for ceftriaxone susceptibility. During 1987–2016, the Centers for Disease Control and Prevention identified and reported 5 isolates with ceftriaxone MICs of 0.5 mg/L in the United States. These isolates were found in San Diego, California (1987); Cincinnati, Ohio (1992 and 1993); Philadelphia, Pennsylvania (1997); and most recently, Oklahoma City, Oklahoma (2012) (2). Therefore, although the number of N. gonorrhoeae isolates with ceftriaxone MICs >0.5 mg/L identified globally to date has been small, these Gonococcal Isolate Surveillance Project findings should be acknowledged. Continued and enhanced global surveillance of gonococcal isolates for antimicrobial susceptibility testing is imperative.
Alan R. KatzComments to Author 
Author affiliation: University of Hawaii, Honolulu, Hawaii, USA

References

  1. Lefebvre BMartin IDemczuk WDeshaies LMichaud SLabbe ACet al. Ceftriaxone-resistant Neisseria gonorrhoeae, Canada, 2017. [cited 2017 Nov 19].Epub ahead of print.
  2. Centers for Disease Control and Prevention. Sexually transmitted diseases surveillance 2016 [cited 2017 Nov 19]. https://www.cdc.gov/std/stats16/CDC_2016_STDS_Report-for508WebSep21_2017_1644.pdf
Suggested citation for this article: Katz AR. Ceftriaxone-resistant Neisseria gonorrhoeae, Canada, 2017. Emerg Infect Dis. 2018 Mar [date cited]. http://dx.doi.org/10.3201/eid2403.171892


DOI: 10.3201/eid2403.171892

Correction: Vol. 23, No. 10 - Volume 24, Number 2—February 2018 - Emerging Infectious Disease journal - CDC

Correction: Vol. 23, No. 10 - Volume 24, Number 2—February 2018 - Emerging Infectious Disease journal - CDC





Volume 24, Number 2—February 2018

Correction

Correction: Vol. 23, No. 10

The author list has been corrected for Enterovirus D68–Associated Acute Flaccid Myelitis in Immunocompromised Woman, Italy (E. Giombini et al.). The article has been corrected online (https://wwwnc.cdc.gov/eid/article/23/10/17-0792_article).
Cite This Article

DOI: 10.3201/eid2402.C12402

Etymologia: Parvovirus - Volume 24, Number 2—February 2018 - Emerging Infectious Disease journal - CDC

Etymologia: Parvovirus - Volume 24, Number 2—February 2018 - Emerging Infectious Disease journal - CDC





Volume 24, Number 2—February 2018

Etymologia

Etymologia: Parvovirus

Eduardo K.U.N. FonsecaComments to Author 

Parvovirus [pahr′ vo-vi′′res]

Thumbnail of This electron micrograph depicts a number of parvovirus H-1 virions of the Parvoviridae family of DNA viruses. Photo CDC/ R. Regnery; E. L. Palmer, 1981.
Figure. This electron micrograph depicts a number of parvovirus H-1 virions of the Parvoviridae family of DNA viruses. Photo CDC/ R. Regnery; E. L. Palmer, 1981.
Viruses of the family Parvoviridae (Latin parvum [meaning small or tiny]) are among the smallest viruses described, 18–28 nm in diameter (Figure). There are 2 subfamilies of the family ParvoviridaeParvovirinae and Densovirina (Latin denso [thick or compact]). Parvovirinae may infect humans, but Densovirina infect only arthropods (1). Structurally, these viruses are nonenveloped, icosahedral viruses that contain a single-stranded linear DNA genome (2,3).
The small size of these viruses might account for their late discovery. In 1974, the first pathogenic human parvovirus was discovered and named B19 from the coding of a serum sample, number 19 in panel B, that gave anomalous results during testing for hepatitis B (4). Although human B19 infections are more often asymptomatic or lead to mild rash illnesses and arthralgias, they can also cause severe anemia in fetuses and in persons with underlying hemoglobinopathies (5).

References

  1. Tattersall PCotmore SF. Parvoviruses. In: Topley WW, Wilson GS, editors. Topley & Wilson’s microbiology and microbial infections. Vol. 1, 10th ed. London: Hodder Arnold; 2005. p. 407−39.
  2. Pattison JRB19 virus—a pathogenic human parvovirus. Blood Rev1987;1:5864DOIPubMed
  3. Servey JTReamy BVHodge JClinical presentations of parvovirus B19 infection. Am Fam Physician2007;75:3736.PubMed
  4. Cossart YEField AMCant BWiddows DParvovirus-like particles in human sera. Lancet1975;1:723DOIPubMed
  5. Young NSBrown KEParvovirus B19. N Engl J Med2004;350:58697DOIPubMed

Figure

Cite This Article

DOI: 10.3201/eid2402.ET2402

In the Company of Microbes: Ten Years of Small Things Considered - Volume 24, Number 2—February 2018 - Emerging Infectious Disease journal - CDC

In the Company of Microbes: Ten Years of Small Things Considered - Volume 24, Number 2—February 2018 - Emerging Infectious Disease journal - CDC





Volume 24, Number 2—February 2018

Books and Media

In the Company of Microbes: Ten Years of Small Things Considered

Moselio Schaechter
ASM Press
ISBN-13: 978-1555819590;
ISBN-10: 1555819591
Pages: 292; Price: $20.00
In 2006, Elio Schaechter began a blog, titled Small Things Considered, about the microbial world for the American Society for Microbiology (ASM). The book, In the Company of Microbes: Ten Years of Small Things Considered, is a selected compilation of 70 of the more than 1,000 blog entries that were posted through 2015. Contributions from 33 writers in addition to Dr. Schaechter are included. These writers are past presidents of ASM and microbiologists from academic institutions around the world. The selections were chosen mostly because they were the authors’ personal or historical reflections on interactions with microbes. As such, these are aimed to be enjoyable reads, without bogging the reader down in obscurely technical scientific, often ephemeral, data.
The pieces are divided into 7 sections, including personal musings of microbiologists, historical reviews, specifics of the microbial world, thoughts on being a microbiologist, teaching, and technical essays. The blog entries cover a breadth of information but have been selected because they emphasize the unusual or unexpected, often prompting a reaction of surprise, amusement, or curiosity to the reader. Interspersed throughout are Dr. Schaechter’s finely detailed questions, designed to provoke further thought and discussion. For example: “Given so many bacteria are intimately associated with animals and plants, why are so relatively few pathogenic?” “How does Clostridium botulinum benefit from making botulinum toxin?” “Is global warming likely to result in a significant net increase, decrease, or no change in the microbial biomass?” “Why are there so many species of microbes on earth?”
Because these are blogs, by design, they are very readable short selections; the book can be picked up and read and put down again and again without missing a beat. It certainly makes for good reading while traveling, sipping coffee, or during other quiet times.
Microbiologists shouldn’t be the only readers of this book. Anyone interested in the microbial world, including those in public health and clinical medicine, will appreciate many of the essays. There are some selections that those with less knowledge of molecular biology or microbial ecology will not understand and thus not benefit from reading. However, because this a collection of blog essays, a reader can simply move on to the next selection. Only a few readings relate closely to infectious diseases, including some on medical microbiology, typhus, retroviruses, fecal transplants, and HIV vaccines.
Modern microbiology is a wide field that has rapidly progressed during the past 50 years, encompassing the gamut from basic biology, biochemical engineering, applied mathematics, and theoretical physics. Centered on the ubiquity of the microbial world, these discussions touch everyone in the field and others interested in the disease effects of microbes on humans. This collection of well-written short essays is a notable accomplishment.
Richard DanilaComments to Author 
Author affiliation: Minnesota Department of Health, Infectious Disease Epidemiology, Prevention and Control, St. Paul, Minnesot
Cite This Article

DOI: 10.3201/eid2402.171664