Prevention of the rehaemorrhage of bleeding peptic ulcers: effects of Helicobacter pylori eradication and acid suppression.

AIM: This study aimed to investigate the consequences of Helicobacter pylori eradication and acid suppression on rehaemorrhage caused by bleeding peptic ulcers. METHODS: A total of 320 patients who had been diagnosed with bleeding peptic ulcers between January 1994 and December 2001 were included in the study. Cases between 1994 and 1997, prior to the introduction of eradication therapy, were assigned to group A, whereas those between 1998 and 2001, after the eradication therapy, were assigned to group B. RESULTS: Of the 320 cases, 162 were designated as group A (113 gastric ulcers and 49 duodenal ulcers) and 158 as group B (116 and 42, respectively). Rehaemorrhage occurred in 24 cases (15%) and five cases (3%) in groups A and B, respectively, presenting a significantly decreased rate of rehaemorrhage in group B. Among those without eradication, rehaemorrhage was observed in 15 of 128 cases (12%) that received treatment with histamine(2)-receptor antagonist (famotidine), and 14 of 142 cases (10%) treated with proton-pump inhibitors, with no significant difference between the two. CONCLUSIONS: Helicobacter pylori eradication lowered the rates of rehaemorrhage. Treatment with histamine(2)-receptor antagonist or proton-pump inhibitors did not produce a difference in the rate of rehaemorrhage.

Effects of antioxidative agents on apoptosis induced by ischaemia-reperfusion in rat intestinal mucosa.

BACKGROUND AND AIM: We have previously demonstrated that ischaemia-reperfusion induces apoptosis in the intestinal mucosa. To evaluate that reactive oxygen species enhanced intestinal apoptosis after ischaemia-reperfusion, we examined whether antioxidants reduced apoptosis. METHODS: Rats were infused through a duodenal tube with antioxidative agents, glutathione, rebamipide and dymethylsulfoxide during 2 h before an ischaemic insult. The superior mesenteric artery was occluded for 60 min, followed by 60 min reperfusion. Apoptosis was evaluated by percentage fragmented DNA (fragmented DNA/total DNA) and immunochemical staining. RESULTS: Increase in apoptosis in the intestinal mucosa after ischaemia-reperfusion was attenuated by intraduodenal infusion of antioxidative agents, but was not completely abolished. CONCLUSION: Scavenging effects of the antioxidative agents attenuated increases in intestinal apoptosis, indicating that oxidative stress after ischaemia-reperfusion plays an important role in induction of apoptosis in the intestinal mucosa.

Food texture differences affect energy metabolism in rats.

Dietary factors such as taste and nutrients are known to affect satiety and energy balance. We hypothesized that food texture might contribute to the regulation of energy metabolism through the process of mastication in the oral cavity as well. The effects of long-term feeding of different-textured pellets on body weight gain, adiposity, and thermogenesis were assessed. From weaning at 4 wks, rats were divided into 2 groups fed on either standard (controls) or soft pellets (soft-fed) that required less chewing with the same nutritional composition. At 26 wks, the soft-fed rats showed greater adiposity than did the controls. Daily food intake did not differ between the 2 groups. The increase in body temperature following feeding was significantly lower in the soft-fed rats. These results suggested that food texture affected energy metabolism by changing post-prandial thermogenesis. The long-term deficiency of thermogenesis associated with soft foods resulted in a greater tendency toward obesity.

Antigenic and functional analyses of glycoprotein of rabies virus using monoclonal antibodies.

Thirty-five monoclonal antibodies (MAbs) against glycoprotein (G protein) of the RC-HL strain of the rabies virus have been established. Using these MAbs, two antigenic sites (I and II) were delineated on the G protein of the RC-HL strain in a competitive binding assay. Of these, 34 MAbs recognized the epitopes on site II. Site II was further categorized into 10 subsites according to their patterns in a competitive binding assay. Each site II-specific MAb showed 5 to 23 nonreciprocal competitions. The reactivities of 35 MAbs to rabies and rabies-related viruses in an indirect immunofluorescent antibody test showed that six MAbs in group A binded to rabies and rabies-related viruses and eight MAbs in group E reacted only with rabies viruses, considering that the former represent the genus-specific of Lyssavirus and the latter are rabies virus-specific. From biological assays, 28 of the 35 MAbs showed neutralization activity, 31 showed hemagglutination inhibition (HI) activity, and 18 showed immunolysis (IL) activity. The MAbs recognizing neutralization epitopes fell into at least three groups: those exhibiting both HI and IL activity, those showing only HI activity, and those showing neither HI nor IL activity. All IL epitopes overlap with HA epitopes. Five of the nine MAbs which reacted with the antigen treated by sodium dodecyl sulfate in ELISA were not reduced, or reduced only slightly, in the titer. None of the MAbs reacted with 2-mercaptoethanol-treated antigen. Only one MAb that recognized site I reacted with the denatured G protein in a Western blotting assay, indicating that its epitope is linear. These results suggest that almost all of the epitopes on the G protein of the rabies virus are conformation-dependent and the G protein forms a complicated antigenic structure.

Satiation and masticatory function modulated by brain histamine in rats.

Both the ventromedial hypothalamus (VMH) and the mesencephalic trigeminal sensory nucleus (Me5) are densely innervated by histaminergic neurons. The depletion of neuronal histamine (HA) from the Me5 by the bilateral microinfusion of 448 nmol/rat alpha-fluoromethylhistidine (FMH), a specific suicide inhibitor of histidine decarboxylase, reduced the eating speed and prolonged meal duration, while leaving the meal size unaffected. HA depletion from the VMH increased the size of the meal and prolonged its duration, but not the eating speed. When the HA turnover rate was measured at 15 min after the scheduled feeding following fasting for less than 24 hr, the rate increased in the region including the Me5, but not in the hypothalamus. The turnover rate reached higher levels at 60 min in both regions. Gastric intubation of an isocaloric liquid diet or an equivolume of water with the liquid diet abolished the increase in HA turnover both in the Me5 region and the hypothalamus. The present findings indicate that brain HA thus modulates satiation through both the VMH and masticatory function as well as due to the action of the Me5. The HA function activated by mastication began earlier in the Me5 and later in the hypothalamus due to a signal originating from the oral proprioceptors and initiated by chewing.

Food consistency modulates eating volume and speed through brain histamine in rat.

Changes in meal parameters of rats fed with different consistency of food were examined using hard and soft pellets. Meal size and eating speed of the first meal after 1800 h increased significantly in rats fed with soft pellets compared to those fed with hard pellets. Effects of histamine depletion on meals treated with hard or soft pellets were investigated after an intraperitoneal injection of 0.11 mmol/kg alpha-fluoromethylhistidine (FMH), a specific suicide inhibitor of the histamine synthesizing decarboxylase enzyme. When rats were fed with hard pellets, FMH significantly decreased eating speed and prolonged meal duration without affecting meal size. When rats were fed with soft pellets, FMH increased meal size and duration, but not eating speed. The meal parameter of eating speed was significantly decreased and meal size and duration were increased in obese Zuckers, a hereditary histamine-depleted animal model, when compared to their lean littermates. These results indicate that proprioceptive sensation from the oral cavity may regulate meal parameters through histaminergic neurons in the brain.

Effects of endurance training under hyperoxia on serum and tissue lipid levels in rats.

Effects of 6 weeks endurance training (5 days per week) under hyperoxia (60% O2 plus 40% N2) on serum and tissue lipid levels were investigated in male rats. Rats were divided into 4 groups: normoxia-control (NC), hyperoxia-control (HC), normoxia-training (NT), and hyperoxia-training (HT). NT and HT groups were run on a treadmill in a chamber at 20 m per min with a 6 degree gradient for 30 min. The chamber was perfused with hyperoxic gas. After training under hyperoxia, high density lipoprotein cholesterol (HDL-C) was higher (p less than 0.01) than in the normoxic condition, but there were no changes in serum lipids and glucose, or liver and aorta cholesterol. Skeletal muscle TG and liver glycogen in hyperoxic condition tended to show the higher values. Basal lipolysis of adipose tissue was increased (p less than 0.05) by hyperoxia, and decreased (p less than 0.01) by training, but there was no change of norepinephrine induced lipolysis in any group. The results suggest that endurance training or resting under hyperoxia induces increased HDL-C or lipolytic activity of adipose tissue. These effects might be caused by greater fat oxidation during exercising or resting under hyperoxia.

Three distinctive activities of human triceps surae muscle during the stance phase in treadmill walking and running.

Activity of human triceps surae muscle (TS) during locomotion was investigated in relation to the muscle shortening and lengthening contractions. Length changes in the TS were presumed from its girth recorded using a mercury-in-silastic gauge wrapped around the muscle belly. The muscle girth during the stance phase resulted in three peaks corresponding to the actions of heel contact, weight support and toe kick. These peak heights were apparently larger than the girth level in the perpendicular standing posture. Three girth increases in running appeared in the process of ankle dorsiflexion. During walking, girth increases on weight support and toe kick were seen in the same phase. The TS through the stance phase is considered to always contract into a shortening state less than the muscle length in the perpendicular standing posture. These muscle activities are probably imposed to resist the muscle stretching. Therefore, it was suggested that the TS contracts eccentrically, with no lengthening contraction.

Microcalorimetric measurements of heat production in isolated rat brown adipocytes.

Heat production, oxygen consumption, and lipolysis in isolated interscapular brown adipocytes from the rat were investigated. Epinephrine, norepinephrine, and isoproterenol increased heat production in a concentration-dependent manner, showing, about 6-, 4-, and 5-fold higher effects than controls, respectively. The concentration of isoproterenol for threshold heat production and glycerol release were 10(-10) M and 10(-9) M, respectively. The fact that 10(-9) M isoproterenol increased heat production by about 3-fold while glycerol release had no effect at all indicates that calorimetry is more appropriate for investigation of brown adipocytes. At least the method is more sensitive than that of measuring glycerol release.

[Usefulness of ceftazidime in intractable respiratory tract infections].

Usefulness of ceftazidime (CAZ) was studied in 56 cases of intractable respiratory tract infections. CAZ was administered at a daily dose of 2-4 g in 2 divided doses by intravenous drip infusion for 3-15 days. 1. Analysis was carried out in 38 cases and the following result was obtained. Efficacy rate was: 68% (17/25) in pneumonia, 60% (3/5) in chronic bronchitis and 67% (4/6) in secondary infections in chronic respiratory disease cases, and the overall efficacy rate was 63.2% (24/38). 2. In bacteriological study, 68.2% (15/22) of eradication rate was obtained. Against Staphylococcus aureus, eradication was obtained in all strains (4 strains). Against Pseudomonas aeruginosa, eradication occurred in 4 strains out of 10, and decrease in number in 2 strains. 3. As for adverse effects, mild hepatic disorder was observed in 2 cases (3.6%) out of 56. 4. From the above result, CAZ is considered to be very useful when used as monotherapy for aged patients and in the treatment of severe and intractable infections accompanied by underlying diseases.

Effects of swimming exercise at two different water temperature on hepatic lipid and lipoprotein levels in experimental fatty liver rats.

The present study was aimed at demonstrating the effects of exercising in water at two different temperatures on lipid-lipoprotein metabolism in experimental fatty liver rats. The rats were fed a high fat, high cholesterol (CHL) diet for 6 weeks, then returned to standard chow. The fatty liver rats were then divided at random into three groups, two for swimming in 20 degrees C (20SWG) and 30 degrees C (30SWG) water, 5 days/week, 30 min/day for 6 weeks, and a sedentary control group (SG). The concentrations of serum triglyceride (TG) and CHL were significantly lower (p less than 0.01) in both the 20SWG and 30SWG than in the SG. The serum concentration of very low density lipoprotein (VLDL)-CHL was clearly less in the 20SWG than in the SG (p less than 0.05) or the 30SWG (p less than 0.01). Compared to the SG, the two swimming groups had significantly lower levels (p less than 0.01) of low density lipoprotein (LDL)-CHL. The LDL-CHL in the 30SWG was significantly lower (p less than 0.01) than that in the 20SWG. There were no significant differences among the three groups in high density lipoprotein (HDL)/CHL. However, the ratio of HDL to CHL was over 10% greater in the two swimming groups than in the SG. Hepatic CHL ester and TG were significantly lower (p less than 0.05) in the 20SWG than in the SG. These results indicate that swimming in water at the lower temperature was more stimulating to lipid-lipoprotein metabolism in fatty liver than swimming in the higher temperature water.

Dependence of lipid-lipoprotein metabolism on exercise intensity in experimental fatty liver rats.

To develop experimental fatty liver, Wistar male rats were fed a high fat, high cholesterol (Cho) diet for 6 weeks after which their diet was changed to standard chow. The animals were then divided by random selection into a sedentary group (SG) and four treadmill exercise groups for 6 weeks as follows: walking group (WG, 10 m/min, 60 min); low-speed running group (LRG, 20 m/min, 30 min); middle-speed running group (MRG, 30 m/min, 20 min) and high-speed running group (HRG, 40 m/min, 15 min). The serum concentration of very low density lipoprotein (VLDL) and low density lipoprotein (LDL)-Cho decreased, and high density lipoprotein (HDL)-Cho increased in WG compared with the other three exercise groups. Hepatic triglyceride (TG) was significantly lower (P less than 0.05) in WG than in SG. Hepatic Cho was lower in HRG than in the other three exercise groups, and Cho in the aortic wall was higher. The results suggest that light exercise, such as walking might be more beneficial to lipid-lipoprotein metabolism than strong exercise, such as high-speed running. This is consistent with suggestion that light exercise might be effective in clinical treatment for hyperlipidemia, arteriosclerosis or fatty liver.

Effects of long-term exercise and high-cholesterol diet on lipid-lipoprotein metabolism in rats.

To accelerate the synthesis of endogenous lipids, Wistar male rats were administered sucrose solution and standard chow diet for 5 weeks. The diet was then changed to tap water plus a high-cholesterol (Cho) diet and the animals were subjected to treadmill running for 5 weeks. The concentrations of serum triglyceride (TG) and very low density lipoprotein (VLDL)-cho in the group that had endurance exercise and was fed high-Cho diet were significantly lower than those in the non-exercise group that was fed high-Cho diet. However, the exercise-high-Cho group accumulated quantities of lipids in the liver similar to the non-exercise-high-Cho group and developed a markedly fatty liver. In conclusion, it is suggested that long-term exercise did not accelerate hepatic lipid metabolism and seemed to suppress synthesis and release of VLDL in the liver.