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or
0032 (0)16 41 44 07
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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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