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  • S. Karger AG  (5)
  • English  (5)
  • 1995-1999  (5)
  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 1999
    In:  Digestion Vol. 60, No. 1 ( 1999), p. 63-68
    In: Digestion, S. Karger AG, Vol. 60, No. 1 ( 1999), p. 63-68
    Abstract: The distribution of tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, was investigated immunohistochemically in various organs of the gastrointestinal tract and compared with that of neuroendocrine markers. While immunoreactivity for serotonin and chromogranin A was restricted to enterochromaffin cells, positive staining for tryptophan hydroxylase was detected in normal enterocytes lining the epithelium of the small intestine. Tryptophan hydroxylase was localized in the supranuclear cytoplasm of absorptive cells, and was absent from the terminal web. The enterocytes of the exfoliation zone at the tips of the villi demonstrated a strong immunoreactivity similar to those at the slope of the villi. Mucus-containing Goblet cells, Paneth cells and stromal cells of the lamina propria remained unlabelled. The duodenal glands of Brunner revealed only sporadically a weak immunostaining for tryptophan hydroxylase. The monooxygenase was also detected in numerous secretory tubules of the pyloric mucosa, where the proportion of positive cells decreased progressively from the crypts towards the upper parts of the gastric glands. No significant immunoreactivity was demonstrated in colon, adrenal cortex, liver, pancreas, and mesenteric lymph nodes. The demonstration of tryptophan hydroxylase in normal enterocytes suggested that epithelial cells of the small intestine are able to synthesize 5-hydroxytryptophan.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
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    Language: English
    Publisher: S. Karger AG
    Publication Date: 1999
    detail.hit.zdb_id: 1482218-0
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  • 2
    In: Digestion, S. Karger AG, Vol. 58, No. 5 ( 1997), p. 469-475
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1997
    detail.hit.zdb_id: 1482218-0
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  • 3
    Online Resource
    Online Resource
    S. Karger AG ; 1997
    In:  Cardiology Vol. 88, No. 3 ( 1997), p. 296-299
    In: Cardiology, S. Karger AG, Vol. 88, No. 3 ( 1997), p. 296-299
    Type of Medium: Online Resource
    ISSN: 1421-9751 , 0008-6312
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1997
    detail.hit.zdb_id: 1482041-9
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  • 4
    In: Cardiology, S. Karger AG, Vol. 90, No. 4 ( 1998), p. 286-294
    Abstract: 〈 b 〉 Background: 〈 /b 〉 Recent studies have suggested that positive troponin I tests are associated with an increased risk of cardiac death during short-term follow-up. However, it is unknown if troponin I tests alone or in addition to CK-MB measurements are superior to predict unfavorable outcome during long-term follow-up. 〈 b 〉 Patients and Methods: 〈 /b 〉 In a prospective, double-blind study we assessed the prevalence and prognostic value of combined troponin I and CK-MB tests in an unselected cohort of patients (n = 292) admitted to the emergency department for acute chest discomfort. Patients were grouped according to the diagnosis on discharge in those with acute myocardial infarction (1), unstable angina (2), and noncardiac chest pain (3). Six months after enrollment, death rates were obtained and follow-up interviews were performed with respect to survival, recurrence of chest pain, and myocardial infarction. 〈 b 〉 Results: 〈 /b 〉 In patients with evidence of coronary heart disease, the mortality rate for abnormal troponin I and normal CK-MB levels was 5.0%. Baseline troponin I and elevated CK-MB levels were associated with a mortality rate of 4.0%. However, the mortality rate was significantly higher (11.1%) in patients presenting with elevated troponin I and CK-MB values. In patients without myocardial infarction on admission, 10.5% with positive troponin I tests died compared to 1.6% with negative tests. The mortality rate in patients without myocardial infarction was 2.7% for patients with elevated CK-MB but normal troponin I values. In patients with both markers elevated a significantly higher mortality rate (16.7%) was found, representing a 6-fold increase in the death event rate. With the additional knowledge of troponin I values, it could be demonstrated that certain cases were misclassified as having noncardiac chest pain. At least some of the latter patients with above-normal values of troponin I were retrospectively to be reclassified as unstable angina. Acute non-Q-wave myocardial infarctions were occasionally misdiagnosed as either angina pectoris or nonischemic chest pain. 〈 b 〉 Conclusions: 〈 /b 〉 Our data suggest the superiority of combined CK-MB and troponin I measurements in clinical practice for the early risk stratification of patients presenting with acute chest pain. In nonmyocardial infarctions, both CK-MB and troponin I convey independent prognostic information with regard to fatal outcome. Troponin I tests in addition to CK-MB measurements contribute to a lower rate of misdiagnoses.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1482041-9
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  • 5
    In: Experimental and Clinical Immunogenetics, S. Karger AG, Vol. 15, No. 3 ( 1998), p. 130-133
    Abstract: Variants of the mannose-binding lectin (MBL) have been shown to be associated with low serum concentrations of the protein and to predispose to bacterial, fungal and viral infections. A recent small study on 33 Caucasian patients had suggested that a mutation at codon 52 of the MBL gene is associated with chronic hepatitis B virus (HBV) infection. Exon 1 of the MBL gene was amplified by PCR in 61 patients with chronic HBV infection, 28 patients with acute infection and in 60 controls. MBL variants were detected by subsequent restriction enzyme digestion and agarose gel electrophoresis. The occurrence of the codon 52 mutation in patients with chronic HBV infection did not differ significantly from that in controls or patients with acute infection (9 vs. 7%), nor were there any significant differences for the codon 54 mutation. The frequency of MBL variants at codon 52 and 54 is not increased in patients with chronic HBV infection. Thus, the previously reported association of MBL deficiency with chronic HBV infection in adults could not be confirmed.
    Type of Medium: Online Resource
    ISSN: 0254-9670 , 1421-9948
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1482283-0
    detail.hit.zdb_id: 605860-7
    SSG: 12
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