An experimental model of hemolysis-induced acute pancreatitis.

The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirty-three of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.

An experimental model of hemolysis-induced acute pancreatitis

The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20 percent. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20 percent (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20 percent ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70 percent) of 50 rats, moderate hemolysis in seven (14 percent), and no hemolysis in eight (16 percent). Thirty-three of 35 (94.2 percent) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8 percent) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80 percent of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines

The association of dehydroepiandrosterone, obesity, waist-hip ratio and insulin resistance with fatty liver in postmenopausal women--a hyperinsulinemic euglycemic insulin clamp study.

BACKGROUND/AIMS: The relationship between insulin resistance and the occurrence of fatty acid has been documented. Recently DHEA (dehydroepiandrosterone) was shown to have a protective effect against development of fatty liver in rats. We aimed to investigate the association of nonalcoholic fatty liver and serum levels of DHEA, obesity, fat distribution and insulin resistance and to evaluate the effect of DHEA on fatty liver, obesity and insulin resistance. METHODOLOGY: Thirteen postmenopausal women with nonalcoholic fatty liver and 14 postmenopausal women with normal liver histology were included into the study. Body mass index, waist-hip ratio, serum DHEA, DHEAS, triglyceride, cholesterol levels and insulin resistance were determined. Fatty liver was determined by ultrasound and established by liver biopsy and histology. Hyperinsulinemic euglycemic clamp studies were performed. RESULTS: The subjects in both groups were age matched (p > 0.05). Body mass index showed obesity in patients with fatty liver but not in control group (p = 0.01). Central obesity was present in women with fatty liver (p = 0.039). As expected, insulin resistance was significantly present in patients with fatty liver (p = 0.001). DHEA and DHEAS levels of women with fatty liver were greater than those of control group (p1 = 0.001 and p2 = 0.0001, respectively). DHEA and DHEAS were positively correlated with both body mass index and waist-hip ratio. However, glucose disposal rate was inversely and significantly correlated with DHEA and DHEAS levels. CONCLUSIONS: These data do not support the hypothesis that DHEA or DHEAS protect post-menopausal women against fatty liver, diabetes and obesity. Indeed, DHEA and DHEAS may be the cause of fatty liver, obesity (especially abdominal obesity) and diabetes in estrogen-deficient women.

Functional dyspepsia: relationship between clinical subgroups and Helicobacter pylori status in Western Turkey.

The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-alpha (TNF-alpha) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-alpha and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.

Functional dyspepsia: relationship between clinical subgroups and Helicobacter pylori status in Western Turkey

The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6 percent), motility disorder-like (ML), 281 (31.2 percent), and the combination (C) of these symptoms, 298 (33.1 percent). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-alpha (TNF-alpha) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-alpha and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups

Influence of an abrupt increase in blood pressure on the blood-brain barrier permeability during acute hypertension and epileptic seizures.

The interrelationship between the breakdown of the blood-brain barrier according to the Evans-blue passage and an abrupt increase in blood pressure (DeltaP) was studied in rats subjected to adrenaline-induced acute hypertension and also pentylenetetrazol-induced seizures. Arterial blood pressure was increased by adrenaline, then immediately i.v. nifedipine was injected and subsequently decreased to the control value in the acute hypertensive group. Arterial blood pressure was increased by pentylenetetrazol, then immediately GABA (gamma-aminobutiric acid) was injected and the blood pressure was decreased to the control value in the seizure group. The animals were divided into five groups. Group I: control; Group II: acute hypertension; Group III: acute hypertension + nifedipine; Group IV: seizure; Group V: seizure + GABA. The Evans-blue dye content was found to be 0.25 +/- 0.01 mg% in the whole brain in the control animals, and 0.803 +/- 0.1 mg% in the acute hypertensive group. This difference between these groups was found to be significant: P< 0.01. In the nifedipine group (Group III) the Evans-blue content was 0.30 +/- 0.1 mg% in the whole brain; and there was no significant difference between control values and nifedipine-treated animals (P> 0.5). The Evans-blue content was 1.6 +/- 0.2 mg% in the whole brain during seizure, and decreased to 0.36 +/- 0.1 mg% after GABA injection was administered. There was also no significant difference between the control value and the GABA-treated animals (P> 0.5). These results have shown that an abrupt increase in blood pressure (DeltaP) did not change the blood-brain barrier permeability in both acute hypertension and seizures.

Salicylic acid derivatives form stable complexes with scandium(III) ion in aqueous solution.

The stability constants of 5-nitrosalicylic acid (5-NSA) and 5-sulfosalicylic acid (5-SSA) complexes of Sc(III) were determined by potentiomeric pH titration. ML and ML2 type first and second complexes were observed in the solutions of 5-NSA and 5-SSA with Sc(III) at 25 degrees C in I=0.1 M ionic medium. The stability constants of Sc(III)-5NSA and Sc(III)-5SSA systems were also investigated by spectrophotometry to determine the stoichiometries of the complexes formed in the reactions. Our results showed that Sc(III)-5SSA complexes are more stable than the Sc(III)-5NSA complexes in aqueous solutions.

Heat-induced changes in nuclear-associated proteins in normal and thermotolerant HeLa cells.

In the present study we used one-dimensional 7-10% gradient SDS polyacrylamide gels to resolve the proteins associated with nuclei isolated from normal and heat-shocked cells. By analyzing the relative optical density of 27-30 polypeptide bands as a function of the duration of the heat shock or the time of incubation after heating, we were able to observe the following regarding heat-induced alterations in nuclear protein binding. Various proteins show an increased nuclear association in terms of their nuclear protein content, but the kinetics of this association is not identical for individual proteins. Moreover, the changes in these associations are differentially affected in nuclei from thermotolerant cells. This type of analysis demonstrates the possibility that the cellular effects of hyperthermia could be correlated with the altered binding and/or increased presence of specific proteins associated with the nucleus in heated cells.

Heat-shock-induced changes in nuclear protein and cell killing in thermotolerant HeLa cells.

The correlation between the protein content of nuclei and heat-induced cell killing was determined for HeLa cells with various levels of thermotolerance. Thermotolerance was induced by heating cells at 45 degrees C for 15 or 30 min and then incubating them at 37 degrees C for 5 or 24 h. This procedure resulted in four different levels of thermotolerance requiring up to 5 h of heat at 45 degrees C to kill more than 90% of the most resistant cells. Upon exposure to 45 degrees C, the increase in the protein content of isolated nuclei was proportionally less for thermotolerant cells. The difference between the initial increase in nuclear protein content for normal and thermotolerant cells was relatively small for shorter heating times but became clearly evident for longer heating exposures. The correlations between cell killing and nuclear protein content were not statistically different from controls for any of the various levels of thermotolerance. The correlation was measured over survival levels below 0.1 in thermotolerant cells. Because thermotolerant HeLa cells are very resistant to heat, previous studies had not tested the correlation to survival levels below a half-decade of cell killing. These results should resolve some of the conflicting observations reported in the literature and are consistent with the suggestion that heat-induced changes in binding of nuclear protein play a key role in the lethal effects of hyperthermia.