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  • 1
    Electronic Resource
    Electronic Resource
    Observer variability in the histologic assessment of oral premalignant lesions (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 24 (1995), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Histopathologic examination of oral leukoplakias has a major impact on the assessment of prognosis and treatment planning. We investigated the extent of agreement in grading epithelial dysplasia between pathologists with the same or different educational backgrounds. Two general pathologists and two oral pathologists were each given 100 sections of oral leukoplakia to grade from no dysplasia to carcinoma in-situ. The interobserver agreement rates were in the range of 49% to 69%. The calculated kappa values were in the range of 27% to 45%), showing poor to moderate agreement between the pathologists. When comparing the kappa values between the two pairs of pathologists with the same education, these values did not diverge from the general level of kappa values, indicating that the interobserver variability was due to individual differences rather than to educational background.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1995.tb01166.x
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  • 2
    Electronic Resource
    Electronic Resource
    Systemic high-dose ranitidine in the treatment of psoriasis: an open prospective clinical trial (1995)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 133 (1995), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We report the results of an open, prospective study on the efficacy of systemic ranitidine in the treatment of psoriasis. Twenty patients suffering from moderate to severe psoriasis were included in the study. The median pretreatment PASI score was 15·7 (range 6·0-24·7). The patients were treated with oral ranitidine 300 mg twice a day for 6 months; no other medication was allowed during the study period. Eighteen patients completed the study. The median PASI score was reduced from 15·7 to 14·5. 9·1 and 5·7. after 1, 3 and 6 months of treatment, respectively (P〈0·00001). A significant reduction in PASI score was evident at 3 months of treatment. A mild to moderate deterioration occurred in 15 patients within the first month of treatment, but this was followed by improvement during prolonged treatment in most patients. No other clinical and/or biochemical side-effects were observed. Eight patients continued therapy with ranitidine after the study was completed, and none of these patients relapsed during a follow-up period of 12–18 months. The results of the present study suggest that ranitidine may be a beneficial and safe treatment for psoriasis. In addition, high-dose, long-term ranitidine treatment appears to be free from severe adverse effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2133.1995.tb06923.x
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  • 3
    Electronic Resource
    Electronic Resource
    Transient optical emission from the error box of the γ-ray burst of 28 February 1997 (1997)
    [s.l.] : Nature Publishing Group
    Nature 386 (1997), S. 686-689 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] GRB970228 was detected9 with the Gamma-ray Burst Monitor10 on board the Italian-Dutch BeppoSAX satellite11 on 1997 February 28, UT 02h58minOls. The event lasted -80s and reached peak fluxes of 4 X 106, 6 X 10"6 and 107 ergcirT2 s"1 in the 40-600 keV, 40-1,000 keV and ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/386686a0
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  • 4
    Electronic Resource
    Electronic Resource
    Multiple defects of both hepatic and peripheral intracellular glucose processing contribute to the hyperglycaemia of NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 326-336 
    Details
    ISSN: 1432-0428
    Keywords: Key words Hepatic glucose production ; glucose fatty acid cycle ; Cori cycle ; muscle glucose metabolism ; glycogen synthase.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetic (NIDDM) patients were studied during a modified euglycaemic state when fasting hyperglycaemia was normalized by a prior (–210 to –150 min) – and later withdrawn (–150–0 min) – intravenous insulin infusion. Glucose metabolism was assessed in NIDDM patients (n = 10) and matched control subjects (n = 10) using tritiated glucose turnover rates, indirect calorimetry and skeletal muscle glycogen synthase activity determinations. Total and non-oxidative exogenous glycolytic flux rates were measured using appearance rates of tritiated water. A + 180 min euglycaemic hyperinsulinaemic (40 mU · m–2· min–1) clamp was performed to determine the insulin responsiveness of the various metabolic pathways. Plasma glucose concentration increased spontaneously during baseline measurements in the NIDDM patients (-120 to 0 min: 4.8 ± 0.3 to 7.0 ± 0.3 mmol/l; p 〈 0.01), and was primarily due to an elevated rate of hepatic glucose production (3.16 ± 0.13 vs 2.51 ± 0.16 mg · kg FFM–1· min–1; p 〈 0.01). In the NIDDM subjects baseline glucose oxidation was decreased (0.92 ± 0.17 vs 1.33 ± 0.14 mg · kg FFM–1· min–1; p 〈 0.01) in the presence of a normal rate of total exogenous glycolytic flux and skeletal muscle glycogen synthase activity. The simultaneous finding of an increased lipid oxidation rate (1.95 ± 0.13 vs 1.61 ± 0.07 mg · kg FFM–1· min–1; p = 0.05) and increased plasma lactate concentrations (0.86 ± 0.05 vs 0.66 ± 0.03 mmol/l; p = 0.01) are consistent with a role for both the glucose-fatty acid cycle and the Cori cycle in the maintenance and development of fasting hyperglycaemia in NIDDM during decompensation. Insulin resistance was demonstrated during the hyperinsulinaemic clamp in the NIDDM patients with a decrease in the major peripheral pathways of intracellular glucose metabolism (oxidation, storage and muscle glycogen synthase activity), but not in the pathway of non-oxidative glycolytic flux which was not completely suppressed during insulin infusion in the NIDDM patients (0.55± 0.15 mg · kg FFM–1· min–1; p 〈 0.05 vs 0; control subjects: 0.17 ± 0.29; NS vs 0). Thus, these data also indicate that the defect(s) of peripheral (skeletal muscle) glucose processing in NIDDM goes beyond the site of glucose transport across the cell membrane. [Diabetologia (1995) 38: 326 –336]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400638
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  • 5
    Electronic Resource
    Electronic Resource
    Low birth weight is associated with NIDDM in discordant monozygotic and dizygotic twin pairs (1997)
    Springer
    Diabetologia 40 (1997), S. 439-446 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Twins ; non-insulin-dependent diabetes mellitus ; birth weight ; intrauterine malnutrition.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous studies have demonstrated an association between low weight at birth and risk of later development of non-insulin-dependent diabetes mellitus (NIDDM). It is not known whether this association is due to an impact of intrauterine malnutrition per se, or whether it is due to a coincidence between the putative “NIDDM susceptibility genotype” and a genetically determined low weight at birth. It is also unclear whether differences in gestational age, maternal height, birth order and/or sex could explain the association. Twins are born of the same mother and have similar gestational ages. Furthermore, monozygotic (MZ) twins have identical genotypes. Original midwife birth weight record determinations were traced in MZ and dizygotic (DZ) twins discordant for NIDDM. Birth weights were lower in the NIDDM twins (n = 2 × 14) compared with both their identical (MZ; n = 14) and non-identical (DZ; n = 14) non-diabetic co-twins, respectively (MZ: mean ± SEM 2634 ± 135 vs 2829 ± 131 g, p 〈 0.02; DZ: 2509 ± 135 vs 2854 ± 168 g, p 〈 0.02). Using a similar approach in 39 MZ and DZ twin pairs discordant for impaired glucose tolerance (IGT), no significantly lower birth weights were detected in the IGT twins compared with their normal glucose tolerant co-twins. However, when a larger group of twins with different glucose tolerance were considered, birth weights were lower in the twins with abnormal glucose tolerance (NIDDM + IGT; n = 106; 2622 ± 45 g) and IGT (n = 62: 2613 ± 55 g) compared with twins with normal glucose tolerance (n = 112: 2800 ± 51 g; p = 0.01 and p = 0.03, respectively). Furthermore, the twins with the lowest birth weights among the two co-twins had the highest plasma glucose concentrations 120 min after the 75-g oral glucose load (n = 86 pairs: 9.6 ± 0.6 vs 8.0 ± 0.4 mmol/l, p = 0.03). In conclusion, the association between low birth weight and NIDDM in twins is at least partly independent of genotype and may be due to intrauterine malnutrition. IGT was also associated with low birth weight in twins. However, the possibility cannot be excluded that the association between low birth weight and IGT could be due to a coincidence with a certain genotype causing both low birth weight and IGT in some subjects. [Diabetologia (1997) 40: 439–446]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050698
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  • 6
    Electronic Resource
    Electronic Resource
    Risk and mechanism of dexamethasone-induced deterioration of glucose tolerance in non-diabetic first-degree relatives of NIDDM patients (1997)
    Springer
    Diabetologia 40 (1997), S. 1439-1448 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Minimal model analysis ; insulin secretion ; insulin resistance ; relatives of NIDDM patients ; steroids ; glucose intolerance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We tested the hypothesis that glucose intolerance develops in genetically prone subjects when exogenous insulin resistance is induced by dexamethasone (dex) and investigated whether the steroid-induced glucose intolerance is due to impairment of beta-cell function alone and/or insulin resistance. Oral glucose tolerance (OGTT) and intravenous glucose tolerance tests with minimal model analysis were performed before and following 5 days of dex treatment (4 mg/day) in 20 relatives of non-insulin-dependent diabetic (NIDDM) patients and in 20 matched control subjects (age: 29.6 ± 1.7 vs 29.6 ± 1.6 years, BMI: 25.1 ± 1.0 vs 25.1 ± 0.9 kg/m2). Before dex, glucose tolerance was similar in both groups (2-h plasma glucose concentration (PG): 5.5 ± 0.2 [range: 3.2–7.0] vs 5.5 ± 0.2 [3.7–7.4] mmol/l). Although insulin sensitivity (Si) was significantly lower in the relatives before dex, insulin sensitivity was reduced to a similar level during dex in both the relatives and control subjects (0.30 ± 0.04 vs 0.34 ± 0.04 10–4 min–1 per pmol/l, NS). During dex, the variation in the OGTT 2-h PG was greater in the relatives (8.5 ± 0.7 [3.9–17.0] vs 7.5 ± 0.3 [5.7–9.8] mmol/l, F-test p 〈 0.05) which, by inspection of the data, was caused by seven relatives with a higher PG than the maximal value seen in the control subjects (9.8 mmol/l). These “hyperglycaemic” relatives had diminished first phase insulin secretion (Ø1) both before and during dex compared with the “normal” relatives and the control subjects (pre-dex Ø1: 12.6 ± 3.6 vs 26.4 ± 4.2 and 24.6 ± 3.6 (p 〈 0.05), post-dex Ø1: 22.2 ± 6.6 vs 48.0 ± 7.2 and 46.2 ± 6.6 respectively (p 〈 0.05) pmol · l–1· min–1 per mg/dl). However, Si was similar in “hyperglycaemic” and “normal” relatives before dex (0.65 ± 0.10 vs 0.54 ± 0.10 10−4 · min–1 per pmol/l) and suppressed similarly during dex (0.30 ± 0.07 vs 0.30 ± 0.06 10−4 · min–1 per pmol/l). Multiple regression analysis confirmed the unique importance of low pre-dex beta-cell function to subsequent development of high 2-h post-dex OGTT plasma glucose levels (R 2 = 0.56). In conclusion, exogenous induced insulin resistance by dex will induce impaired or diabetic glucose tolerance in those genetic relatives of NIDDM patients who have impaired beta-cell function (retrospectively) prior to dex exposure. These subjects are therefore unable to enhance their beta-cell response in order to match the dex-induced insulin resistant state. [Diabetologia (1997) 40: 1439–1448]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050847
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  • 7
    Electronic Resource
    Electronic Resource
    Multiple defects of both hepatic and peripheral intracellular glucose processing contribute to the hyperglycaemia of NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 326-336 
    Details
    ISSN: 1432-0428
    Keywords: Hepatic glucose production ; glucose fatty acid cycle ; Cori cycle ; muscle glucose metabolism ; glycogen synthase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetic (NIDDM) patients were studied during a modified euglycaemic state when fasting hyperglycaemia was normalized by a prior (−210 to −150 min) — and later withdrawn (−150–0 min) — intravenous insulin infusion. Glucose metabolism was assessed in NIDDM patients (n=10) and matched control subjects (n=10) using tritiated glucose turnover rates, indirect calorimetry and skeletal muscle glycogen synthase activity determinations. Total and non-oxidative exogenous glycolytic flux rates were measured using appearance rates of tritiated water. A+180 min euglycaemic hyperinsulinaemic (40 mU·m−2·min−1) clamp was performed to determine the insulin responsiveness of the various metabolic pathways. Plasma glucose concentration increased spontaneously during baseline measurements in the NIDDM patients (−120 to 0 min: 4.8±0.3 to 7.0±0.3 mmol/l; p〈0.01), and was primarily due to an elevated rate of hepatic glucose production (3.16±0.13 vs 2.51±0.16 mg·kg FFM−1·min−1; p〈0.01). In the NIDDM subjects baseline glucose oxidation was decreased (0.92±0.17 vs 1.33±0.14 mg·kg FFM−1·min−1; p〈0.01) in the presence of a normal rate of total exogenous glycolytic flux and skeletal muscle glycogen synthase activity. The simultaneous finding of an increased lipid oxidation rate (1.95±0.13 vs 1.61±0.07 mg·kg FFM−1·min−1; p=0.05) and increased plasma lactate concentrations (0.86±0.05 vs 0.66±0.03 mmol/l; p=0.01) are consistent with a role for both the glucose-fatty acid cycle and the Cori cycle in the maintenance and development of fasting hyperglycaemia in NIDDM during decompensation. Insulin resistance was demonstrated during the hyperinsulinaemic clamp in the NIDDM patients with a decrease in the major peripheral pathways of intracellular glucose metabolism (oxidation, storage and muscle glycogen synthase activity), but not in the pathway of non-oxidative glycolytic flux which was not completely suppressed during insulin infusion in the NIDDM patients (0.55±0.15 mg·kg FFM−1·min−1; p〈0.05 vs 0; control subjects: 0.17±0.29; NS vs 0). Thus, these data also indicate that the defect(s) of peripheral (skeletal muscle) glucose processing in NIDDM goes beyond the site of glucose transport across the cell membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400638
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  • 8
    Electronic Resource
    Electronic Resource
    Lymphocyte proliferation in response to exercise (1997)
    Springer
    European journal of applied physiology 75 (1997), S. 375-379 
    Details
    ISSN: 1439-6327
    Keywords: Key words Exercise  ;  Lymphocytes  ;  Mitogens  ; Proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lymphocyte proliferative responses are often used to evaluate the functional capacity of the immune system in response to exercise. Blood mononuclear cells (BMNC) are stimulated in vitro with polyclonal mitogens and the incorporation of 3H-thymidine into the DNA reflects cell proliferation. The BMNC are most often stimulated with either phytohaemagglutinin (PHA), poke weed mitogen (PWM), concanavalin A (Con-A), interleukin-2 (IL-2), or purified derivative of tuberculin (PPD). The literature concerning lymphocyte proliferation and exercise is reviewed with respect to the type and intensity of exercise, and also the effect of training status. The proliferative responses to exercise are highly heterogeneous, the most consistent finding being that PHA-stimulated cell responses decrease during exercise which may reflect a decreased fraction of CD3+ cells. In contrast, reduced, elevated or even unchanged lymphocyte proliferative response to PHA, PWM, Con-A, IL-2 and PPD have been demonstrated in the recovery period following exercise. Also variable responses are present in trained athletes compared to less fit subjects. Even though this may reflect that the time of 3H-thymidine incorporation into lymphocytes varies, we conclude that a functional evaluation of the immune system in response to exercise cannot be based solely upon measurements of lymphocyte proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004210050175
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