Microbiology - Viruses (Structure, Types and Bacteriophage Replication)
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Microbiology - Viruses (Structure, Types and Bacteriophage Replication) - Video

The Compost Tea Experiment: In the Making
I #39;m ecstatic to finally orchestrate this experiment and find out if compost tea definitively works. I hope to bring to light the facts and benefits of using ...

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The Compost Tea Experiment: In the Making - Video

NEW YORK, Aug. 7, 2013 /PRNewswire/ -- Reportlinker.com announces that a new market research report is available in its catalogue:

In Vitro Diagnostic (IVD) Market [Instruments, Reagents & Data Management Systems] [Technique (Immunoassay, Clinical Chemistry, Molecular Diagnostics, Haematology) & Applications (Diabetes, Infectious Diseases, Cancer & Cardiology)] Systems, End Users] http://www.reportlinker.com/p01593771/In-Vitro-Diagnostic-IVD-Market-%5BInstruments-Reagents--Data-Management-Systems%5D-%5BTechnique-Immunoassay-Clinical-Chemistry-Molecular-Diagnostics-Haematology--Applications-Diabetes-Infectious-Diseases-Cancer--Cardiology%5D-Systems-End-Users%5D-.html#utm_source=prnewswire&utm_medium=pr&utm_campaign=In_Vitro_Diagnostic

In Vitro Diagnostic (IVD) Market [Instruments, Reagents & Data Management Systems] [Technique (Immunoassay, Clinical Chemistry, Molecular Diagnostics, Haematology) & Applications (Diabetes, Infectious Diseases, Cancer & Cardiology)] Systems, End Users] Forecast To 2017

The global in vitro diagnostics market was valued at $49.2 billion in 2012. The factors likely to fuel the growth of the market include ongoing developments in analytical laboratory automation, swift progress in various fields of diagnosis such as point-of-care testing, molecular diagnosis, immunoassays, hematology, flow cytometry, and microbiology; and finally, the geographical market expansion within emerging countries.

The most important trend witnessed recently in the in vitro diagnostic industry is the trend of self-testing as opposed to patients visiting hospitals. This is one of the biggest factors responsible for the growth of point-of-care testing, as patients prefer self-testing so as to avoid unnecessary visits to the hospital. However, factors such as stringent regulatory frameworks and a shortage of budget are restraining the growth of this market. The global in vitro disgnostics market is expected to reach $69.1 billion by 2017, at a CAGR of 7% from 2012 to 2017.

In 2012, the Americas had accounted for the largest share of the global in vitro diagnostic market, followed by Europe. However, the BRIC countries represent the fastest-growing markets due to the economic growth, the rising number of chronic diseases, and an increasing awareness about the use of IVD tests to control the spread of diseases. Moreover, the economic slowdown, pricing pressures, and high competition in mature countries will compel companies to focus on emerging markets.

Scope of the Report This research report categorizes the global IVD (In vitro diagnostic) market on the basis of technique, product type, application, and end-users. These markets are broken down into segments and sub-segments, providing exhaustive value analysis for 2010, 2011 and 2012, as well as forecast up to 2017. Each of the devices market is comprehensively analyzed at a granular level by geography (North America, Europe, BRIC, Japan and Rest of the World) to provide in-depth information on the global scenario. These regions are further analyzed at major country levels.

Global IVD Market, by Technique: Immunochemistry Clinical Chemistry Molecular Diagnostics Hematology Microbiology Coagulation Other Clinical Instruments (clinical centrifuges, sample processers, washers, histology, cytology, and flow cytometry)

Global IVD Market, by Product Type: Reagents Instruments Services Data Management System Software/Hardware

Global IVD Market, by Application: Diabetes Infectious Diseases Oncology Cardiology HIV/AIDS Autoimmune Diseases Drug Testing Nephrology Others (endocrine tests, blood analysis tests, pregnancy tests, and general clinical applications)

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In Vitro Diagnostic (IVD) Market [Instruments, Reagents & Data Management Systems] [Technique (Immunoassay, Clinical ...

Newswise BUFFALO, N.Y. The bacteria Streptococcus pneumoniae harmlessly colonizes the mucous linings of throats and noses in most people, only becoming virulent when they leave those comfortable surroundings and enter the middle ears, lungs or bloodstream. Now, in research published in July in mBio, University at Buffalo researchers reveal how that happens.

We were asking, what is the mechanism behind what makes us sick? explains Anders P. Hakansson, PhD, assistant professor of microbiology and immunology in the UB School of Medicine and Biomedical Sciences. We are looking to find ways to interfere with the transition to disease. Few have looked at the specific mechanism that suddenly makes these bacteria leave the nose where they typically prefer to reside and travel into the lungs or the middle ear where they cause disease. If we can understand that process, then maybe we can block it.

Hakansson and his colleagues had previously found that when the pneumococci colonize the nose, they form sophisticated, highly structured biofilm communities.

In the current study, the research team grew biofilms of pneumococci on top of human epithelial cells, where the bacteria normally grow. They then infected these bacteria with influenza A virus or exposed them to the conditions that typically accompany the flu, including increased temperature to mimic fever, increased concentrations of ATP (the energy molecule in cells), and the stress hormone norepinephrine, released during flu infection. All three stimuli triggered a sudden release and departure of bacteria from the biofilm in the nose into otherwise normally sterile organs, such as the middle ears and lungs or into the bloodstream. At the same time, the researchers found that the gene expression profile of the bacteria that had dispersed from the biofilms revealed far more virulence.

Hakansson says the research demonstrates how the mammalian and bacterial kingdoms interact. Humans are the only natural hosts for these bacteria, he explains, when the viral infection comes in, there is this interkingdom signaling, where the bacteria respond to host molecules. If we can find ways to interrupt that signaling, we might be able to prevent disease.

Hakansson is affiliated with the Witebsky Center for Microbial Pathogenesis and Immunology and the New York State Center of Excellence in Bioinformatics and Life Sciences, both at UB. The major portion of the work was conducted by co-author Laura R. Marks, an MD/PhD candidate in the UB Department of Microbiology and Immunology, with co-authors Bruce A. Davidson, research assistant professor of anesthesiology and Paul R. Knight, III, MD, PhD, professor of anesthesiology and microbiology and immunology.

The work was funded by the UB Department of Microbiology and Immunology.

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From Harmless Colonizers to Virulent Pathogens: UB Microbiologists Identify What Triggers Disease

Aug. 6, 2013 The bacteria Streptococcus pneumoniae harmlessly colonizes the mucous linings of throats and noses in most people, only becoming virulent when they leave those comfortable surroundings and enter the middle ears, lungs or bloodstream. Now, in research published in July in mBio, University at Buffalo researchers reveal how that happens.

"We were asking, what is the mechanism behind what makes us sick?" explains Anders P. Hakansson, PhD, assistant professor of microbiology and immunology in the UB School of Medicine and Biomedical Sciences. "We are looking to find ways to interfere with the transition to disease. Few have looked at the specific mechanism that suddenly makes these bacteria leave the nose where they typically prefer to reside and travel into the lungs or the middle ear where they cause disease. If we can understand that process, then maybe we can block it."

Hakansson and his colleagues had previously found that when the pneumococci colonize the nose, they form sophisticated, highly structured biofilm communities.

In the current study, the research team grew biofilms of pneumococci on top of human epithelial cells, where the bacteria normally grow. They then infected these bacteria with influenza A virus or exposed them to the conditions that typically accompany the flu, including increased temperature to mimic fever, increased concentrations of ATP (the energy molecule in cells), and the stress hormone norepinephrine, released during flu infection. All three stimuli triggered a sudden release and departure of bacteria from the biofilm in the nose into otherwise normally sterile organs, such as the middle ears and lungs or into the bloodstream. At the same time, the researchers found that the gene expression profile of the bacteria that had dispersed from the biofilms revealed far more virulence.

Hakansson says the research demonstrates how the mammalian and bacterial kingdoms interact. "Humans are the only natural hosts for these bacteria," he explains, "when the viral infection comes in, there is this interkingdom signaling, where the bacteria respond to host molecules. If we can find ways to interrupt that signaling, we might be able to prevent disease."

Hakansson is affiliated with the Witebsky Center for Microbial Pathogenesis and Immunology and the New York State Center of Excellence in Bioinformatics and Life Sciences, both at UB. The major portion of the work was conducted by co-author Laura R. Marks, an MD/PhD candidate in the UB Department of Microbiology and Immunology, with co-authors Bruce A. Davidson, research assistant professor of anesthesiology and Paul R. Knight, III, MD, PhD, professor of anesthesiology and microbiology and immunology.

The work was funded by the UB Department of Microbiology and Immunology.

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From harmless colonizers to virulent pathogens: Microbiologists identify what triggers disease