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Markers of heart and Vessel diseases

 

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K291            K250


K291 TnI                                                                                                New 1 step version


During the last decade cardiac TnI has been proved to be one of the most specific and sensitive
markers of acute myocardial infarction (AMI), perioperative myocardial infarction, and other types
of myocardial tissue damage.
TnI is a protein with molecular weight 22.5 kDa and comprises a component of troponin complex,
or simply troponin. Troponin plays an important role in the regulation of striated and cardiac
muscle contraction and consists of three components - troponin C (TnC), troponin I (TnI) and
troponin T (TnT), each of them performing specific functions. Three isoforms of TnI are known
for human muscular tissue - two isoforms are characteristic for skeletal muscles and one isoform
is strictly cardiac-specific. The structural differences enable to discriminate between skeletal and
cardiac isoforms of TnI by immunological methods.
TnI appears in the bloodstream within 4-6 hours after onset of the chest pain attack and reaches
its peak level during the first 16-20 hours. Within the first day after AMI cardiac TnI is released from
necrotic myocardial tissue showing similar pattern to CKMB - the ‘golden’ AMI marker of the last
decade. However, while CKMB remains elevated for two-three days after onset of the chest pain,
TnI can be detected in serum or plasma for up to one week after the first symptoms of the AMI.
Therefore, TnI can be used not only for rapid diagnostics of AMI, but also for late evaluation, if serum
testing was non-available during the acute phase.
This utility of TnI assay makes TnI resemble TnT - another representative of the troponin
family among cardiac markers. But recently it has been demonstrated that TnT (as well as
CKMB) concentrations are frequently increased in chronic dialysis patients and in patients with chronic
skeletal muscle disease even in the absence of ischaemic heart disease. This fact is explained
by expression of cardiac isoform of TnT and CKMB in abnormal skeletal muscle in such groups of
patients. On the contrary, no expression of cardiac TnI was detected in skeletal muscles of the
patients with chronic renal and skeletal muscle diseases and the concentration of this analyte in such
groups of patients mostly remains within the cut-off level.

 

Sample type: serum, plasma                             Incubation: 60/15’, 370С                    Control sample: 1
Sample volume: 50 μl                                      Calibrators: 5 (0-10 ng/ml)                 Shelf life: 12 months
Sensitivity: 0.25 ng/ml
 

 

K250 CRP ultra EIA

С–reactive protein (CRP) is a pentamerous protein with a MM ca. 100 kDa. CRP is one of the most
ancient factors of humoral immunity. CRP has high affinity to a number of internal antigens –
phosphoethanolamine, phosphorilcholine, histones, fibronectin, laminine and poly-cationic compounds.
CRP may bind to cell wall polysaccarides of streptococci and staphylococci, takes part in plasma
clearance from apoptotic and necrotic detrite by promoting their phagocytosis. CRP may activate
classical complement cascade and stimulate phagocytic activity of macrophages. A sharp rise (up to
1000-fold) of circulating CRP level is a sensitive but not specific marker of acute inflammation induced
by interleukin 6. Recently it has been found that a long-term elevation of plasma CRP level (3 – 10
mg/l) is associated with a high risk of coronary disease. Elevated basal plasma CRP level is found in
menopausal women treated by replacing hormonal therapy as well as in smokers.

 

Sample type: serum, plasma                             Sensitivity: 0.2 mg/l                          Control sample: 1
Sample predilution: 1:101                                 Incubation: 30’/30’/15’, 370С              Shelf life: 12 months
Sample volume: 25 μl                                       Calibrators: 6 (0-25 mg/l)                  Normal range, mg/l: 0-5.0
 

 

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Last modified: 05/29/09