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

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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 ...

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

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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

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

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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

LAB: FOOD MICROBIOLOGY – Video

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LAB: FOOD MICROBIOLOGY
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By: Varakorn Koschakosai

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LAB: FOOD MICROBIOLOGY - Video

Medical Microbiology

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Medical Microbiology Diagnosis Journals OMICS Publishing Group
This video belongs to Medical Microbiology which is the branch of Microbiology which deals with the study of microorganisms including bacteria, viruses, fung...

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Medical Microbiology

Plant Pathology

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Plant Pathology Microbiology Journals OMICS Publishing Group
This video is by OMICS Publishing Group of Plant pathology also called as phytopathology which is the scientific study of plant diseases caused by pathogens ...

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Plant Pathology

Siemens Shows Labs How to “Test Smarter. Run Faster.” at AACC 2013

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HOUSTON--(BUSINESS WIRE)--

Siemens Healthcare Diagnostics is showcasing its latest innovations that unite clinical and workflow excellence to help laboratories Test smarter. Run faster. at the 2013 AACC and ASCLS Annual Meeting and Clinical Lab Expo in Houston, July 28 August 1 (Booth #3449). This years exhibit visually recreates the various clinical environments in which Siemens proven solutions can be found, including the central, microbiology, and molecular lab, emergency department, intensive care unit (ICU) and physicians office/clinic.

Whether conducted in a lab, a doctors office or even at a patients bedside, clinical diagnostic testing will continue to increase in importance for optimizing patient care, especially in light of increasing pressure on healthcare systems, said Michael Reitermann, CEO, Siemens Healthcare Diagnostics. At this years AACC, Siemens is proud to demonstrate how we are leveraging our scientific, technological and business acumen to meet our customers needs from a workflow and clinical perspective.

Central Laboratory Solutions

Siemens AACC 2013 presence once again highlights the companys pioneering advances in central laboratory automation, including the unveiling of the VersaCellX3 Solution1, a unique sample management solution for low and medium volume labs that increases flexibility and advances workflow capabilities for up to three connected Siemens analyzers. Using advanced robotics with dynamic STAT management for the optimal mix of chemistry and/or immunoassay analytics along with one-touch sample management, the VersaCell X3 Solution enables labs to streamline a non-automated environment without the resource requirements of track-based automation. For the higher volume market, the Siemens Aptio Automation1 unified solution helps address the changing workload and expanding needs of todays growing clinical laboratory, while delivering innovation for better patient care.

Leadership in the central lab innovation extends to Siemens IT platforms, including the CentraLink Data Management System1, which displays clinical data and manages workflow across multiple disciplines and platforms, including the VersaCell X3 Solution and Aptio Automation. Attendees are also learning how the new syngo Lab Inventory Manager2 leverages cloud-based technology to streamline and automate the inventory management process. Additionally, information is available about how Siemens Remote Service for Diagnostics provides proactive customer support by optimizing system performance to enhance lab efficiency.

Multiple Siemens central lab instruments and assays are also highlighted including the compact, fully automated SysmexCA-660 System1,3 for hemostasis testing, along with the random access high-volume SysmexCS-5100 System1,3,4 coagulation analyzer, which enables first-run accuracy by identifying and managing unsuitable test specimens prior to analysis. Visitors are also getting a closer look at the CellaVisionDM96 Digital Morphology System1,5, used for automated blood cell microscopy analysis, and accessing the companys robust test menu via touch screens. Featured assays include the IMMULITE2000 Systems Anti-CCP IgG assay1 for rheumatoid arthritis, ADVIACentaur Vitamin D Total assay1,6 and Dimension VistaLOCIVitamin B12 assay1.

Emergency Room and ICU Solutions

Nearby in the Emergency Department/ICU, Siemens spotlights several of its latest near-patient critical care testing solutions, including the RAPIDLab348EX Blood Gas System1,4, a cost-effective blood gas analyzer for smaller labs that generates reliable results in approximately 60 seconds with a minimum of operator interaction. Steps away is the StratusCS Analyzer1, which delivers quantitative cardiac assays for fast patient evaluation, along with the RAPIDPoint500 Blood Gas System1 with the newly available pleural fluid pH test1.

Physicians Office and Clinic Solutions

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Siemens Shows Labs How to “Test Smarter. Run Faster.” at AACC 2013

Methamphetamine increases susceptibility to deadly fungal infection

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Public release date: 30-Jul-2013 [ | E-mail | Share ]

Contact: Jim Sliwa jsliwa@asmusa.org 202-942-9297 American Society for Microbiology

Methamphetamine use can make a person more susceptible to the lung infection cryptococcosis, according to a study published in mBio, the online open-access journal of the American Society for Microbiology.

Researchers found that injected methamphetamine (METH) significantly enhanced colonization of the lungs by Cryptococcus neoformans and accelerated progression of the disease and the time to death in mouse models. C. neoformans is usually harmless to healthy individuals, but METH causes chinks in the blood-brain barrier that can permit the fungus to invade the central nervous system, where it causes a deadly brain infection.

"The highest uptake of the drug is in the lungs," says corresponding author Luis Martinez of Long Island University-Post, in Brookville, New York and of Albert Einstein College of Medicine in The Bronx. "This may render the individual susceptible to infection. We wanted to know how METH would alter C. neoformans infection."

Thirteen million people in the US have abused METH in their lifetimes, and regular METH users numbered approximately 353,000 in 2010, the most recent year for which data are available. A central nervous system stimulant that adversely impacts immunological responses, recent studies show that injected METH accumulates in various sites in the body, but the lungs seem to accumulate the highest concentrations, says Martinez, which could well impact how the lung responds to invading pathogens.

To study the impact this accumulation might have on pulmonary infection, Martinez and his colleagues injected mice with doses of METH over the course of three weeks, then exposed those mice to the C. neoformans fungus. In humans, C. neoformans initially infects the lungs but often crosses the blood-brain barrier to infect the central nervous system and cause meningitis. In their experiments, METH significantly accelerated the speed with which the infected mice died, so that nine days after infection, 100% of METH treated mice were dead, compared to 50% of the control mice.

Using fluorescent microscopy to examine lung tissue in METH-treated and control mice, the researchers found that METH enhanced the interaction of C. neoformans with epithelial cells in the lining of the lung. Seven days after exposure to the fungus, the lungs of METH-treated mice showed large numbers of fungi surrounded by vast amounts of gooey polysaccharide in a biofilm-like arrangement. METH-treated mice also displayed low numbers of inflammatory cells early during infection and breathed faster than controls, a sign of respiratory distress.

Martinez says this greater ability to cause disease in the lung may be due in part to simple electrical attraction. Their analysis shows that METH imparts a greater negative charge on the surface of the fungal cells, possibly lending them a greater attraction to the surface of the lung and an enhanced ability to form a biofilm that can protect its members from attack by the immune system. The fungus also releases more of its capsular polysaccharide in METH-treated mice, which can help the organism colonize and persist in the lung.

"When the organism senses the drug, it basically modifies the polysaccharide in the capsule. This might be an explanation for the pathogenicity of the organism in the presence of the drug, but it also tells you how the organism senses the environment and that it will modify the way that it causes disease," Martinez says.

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Methamphetamine increases susceptibility to deadly fungal infection


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