Fouth generation troponin T (cTnT) and the high-sensitivity TnT (hsTnT) assays now are widely used in emergency room as a indicator of AMI. Troponin levels continue to determine the therapy of those patients who are presenting with a possible acute coronary syndrome.Evidence also are found on these patients with ACS but with non-ST-elevation in ECG.
An elevated troponin concentration is determined by a value greater than the 99th percentile of a normal population. Thses values were hardly to be exceeded when using the troponin assays in the early stage, except in the condition of AMI. Historically, the two sensitive troponin assays are now gold standard and reference assays for AMI diagnosis. Other biomarkers for AMI such as CK, CK-MB, etc, since they aspartate amino transferase and lactate dehydrogenase which are not as stable as troponin lead them to limited importance.
Fouth generation troponin T (cTnT) and the high-sensitivity TnT (hsTnT) assays are first developed more than 20 years ago. With each new generation of troponin assays, clinicians have to do clinical trials to determine the utility of this biomarker in clinical practice. The list of causes for an abnormally elevated troponin has increased, in another hand, the improvements in the assays and the more sensitive detection limits. Elevations could be observed in several pathological conditions, including heart disease, renal impairment and pulmonary embolism, but might also be seen in extreme exertion, such as marathon runners.
So, how should the high sensitive troponin assay be used in clinicals? Normally in ER, assays are used to rule-in AMI which has been already recognized. Perhaps a greater interest lies in the ability of hs-Tn assay to allow the earlier rule-out AMI in early stage, but is is not identified yet. Verification of this will allow accelerated assessment protocols to be developed, with patients rapidly progressing
to provocative testing for inducible ischaemia at a much earlier time, even same day, following negative serial
biomarkers and ECGs.
Monday, July 30, 2012
Human Immunodeficiency Virus
This topic will focus on
the virus which is in my profile picture!
Introduction Human immunodeficiency virus
(HIV) is a lentivirus which
causes acquired immunodeficiency
syndrome (AIDS), a condition in humans in which progressive failure of
the immune system allows life-threatening opportunistic infections and cancers
to thrive.
Mechanism
Viruses such as HIV cannot grow or reproduce on their own, they need to infect
the cells of a living organism in order to replicate (make new copies of
themselves). Ex: HIV could infect T helper cells, especially CD4+ T
cells, macrophages, and dendritic cells. HIV infection leads to low levels of
CD4+ T cells by three mechanisms: First, direct viral killing of
infected cells; second, increased rates of apoptosis in infected cells; and
third, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes
that recognize infected cells. When CD4+ T cell numbers decline
below a critical level, cell-mediated immunity is lost, and the body becomes
progressively more susceptible to opportunistic infections.
Treatment Antiretroviral drugs keep the levels of HIV in the body at a low level, so that the immune system is able to recover and work effectively. Antiretroviral drugs enable many HIV positive people to live long and healthy lives.
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