Improvement of hyperphagia by activation of cerebral I(1)-imidazoline receptors in streptozotocin-induced diabetic mice.

Imidazoline I1-receptors (I1R) are known to regulate blood pressure and rilmenidine, an agonist, is widely used as antihypertensive agent in clinic. However, the role of I1R in feeding behavior is still unclear. In the present study, we used the agonist of I1R to investigate the effect on hyperphagia in streptozotocin (STZ)-induced diabetic mice. Rilmenidine decreased the food intake of STZ-diabetic mice in a dose-dependent manner. The reduction of food intake was abolished by pretreatment with efaroxan at the dose sufficient to block I1R. Intracerebroventricular (icv) administration of rilmenidine into STZ-diabetic mice also significantly reduced hyperphagia, which was reversed by icv administration of efaroxan. In addition, similar results were observed in STZ-diabetic mice, which received chronic treatment with rilmenidine 3 times daily (t.i.d.) for 7 days. Moreover, the hypothalamic neuropeptide Y (NPY) level was reduced by rilmenidine that was also reversed by pretreatment with efaroxan. In conclusion, the obtained results suggest that rilmenidine can decrease food intake in STZ-diabetic mice through an activation of I1R to lower hypothalamic NPY level.

Activation of imidazoline I-2B receptors by allantoin to increase glucose uptake into C2C12 cells.

Allantoin, an active principle of the yam, belongs to the group of guanidinium derivatives and has been reported to lower plasma glucose in diabetic animals. Recent evidence indicates that activation of the imidazoline I(2B) receptor (I(2B)R) by guanidinium derivatives also increases glucose uptake; however, the effect of allantoin on I(2B)R is still unknown. Glucose uptake into cultured C2C12 cells was determined using 2-[¹4C]-deoxy-D-glucose as a tracer. The changes in 5'-AMP-activated protein kinase (AMPK) expression were also identified by Western blotting analysis. The allantoin-induced glucose uptake action was dose-dependently blocked by BU224, a specific I2R antagonist, in C2C12 cells. Moreover, AMPK phosphorylation by allantoin was found to be dose-dependently increased in C2C12 cells using AICAR treatment as a reference. In addition, both actions of allantoin, the increases in glucose uptake and AMPK phosphorylation, were dose-dependently attenuated by amiloride in C2C12 cells. Moreover, compound C at concentrations sufficient to inhibit AMPK blocked the allantoin-induced glucose uptake and AMPK phosphorylation. Thus, we suggest that allantoin can activate I(2B)R to increase glucose uptake into cells, and propose I(2B)R as a new target for diabetic therapy.

Effects of fish oil and vitamin E on the antioxidant defense system in diet-induced hypercholesterolemic rabbits.

This study was designed to investigate the effects of fish oil and vitamin E on the antioxidant defense system in hypercholesterolemic rabbits. A high fat and cholesterol diet, with or without supplement by fish oil and/or a vitamin E supplement, was fed to rabbits for 6 weeks. Compared to the reference diet of regular laboratory rabbit chow, a high fat and cholesterol-enriched diet increased atheroma formation, plasma lipid and peroxide levels, decreased blood glutathione levels, and reduced plasma glutathione reductase, glutathione peroxidase, and catalase activities. Fish oil supplementation significantly reduced atheroma and increased glutathione reductase and glutathione peroxidase activities and blood glutathione levels, but increased plasma lipid peroxide levels. Vitamin E supplementation of the fish oil diet enhanced the beneficial effects by increasing glutathione reductase activity and decreasing peroxide levels. These results indicate that a high fat and cholesterol diet attenuates blood glutathione levels and plasma antioxidant enzyme activities, which may account for some of its atherogenic properties. Consumption of fish oil enhances antioxidative defenses against the oxidative stress imposed by hypercholesterolemia, and vitamin E further enhances these beneficial effects.

Socio-economic disparities in preterm birth: causal pathways and mechanisms.

Preterm birth is the leading cause of infant mortality in industrialised societies. Its incidence is greatly increased among the socially disadvantaged, but the reasons for this excess are unclear and have been relatively unexplored. We hypothesise two distinct sets of causal pathways and mechanisms that may explain social disparities in preterm birth. The first set involves chronic and acute psychosocial stressors, psychological distress caused by those stressors, increased secretion of placental corticotropin releasing hormone (CRH), changes in sexual behaviours or enhanced susceptibility to bacterial vaginosis and chorioamnionitis, cigarette smoking or cocaine use, and decidual vasculopathy. The second hypothesised pathway is a gene-environment interaction based on a highly prevalent mutation in the gene for methylenetetrahydrofolate reductase (MTHFR), combined with low folate intake from the diet and from prenatal vitamin supplements, consequent hyperhomocysteinemia, and decidual vasculopathy. We propose to test these hypothesised pathways and mechanisms in a nested case-control study within a prospectively recruited and followed cohort of pregnant women with singleton pregnancies who deliver at one of four Montreal hospitals that serve an ethnically and socio-economically diverse population. Following recruitment during the late first or early second trimester, participating women are seen at 24-26 weeks, when a research nurse obtains a detailed medical and obstetric history; administers several scales to assess chronic and acute stressors and psychological function; obtains blood samples for CRH, red blood cell and plasma folate, homocysteine, and DNA for the MTHFR mutation; and performs a digital and speculum examination to measure cervical length and vaginal pH and to obtain swabs for bacterial vaginosis and fetal fibronectin. After delivery, each case (delivery at < 37 completed weeks following spontaneous onset of labour or prelabour rupture of membranes) and two controls are selected for placental pathological examination, hair analysis of cotinine, cocaine, and benzoylecgonine, and analysis of stored blood and vaginal specimens. Statistical analysis will be based on multiple logistic regression and structural equation modelling, with sequential construction of models of potential aetiological determinants and covariates to test the hypothesised causal pathways and mechanisms. The research we propose should improve understanding of the factors and processes that mediate social disparities in preterm birth. This improved understanding should help not only in developing strategies to reduce the disparities but also in suggesting preventive interventions applicable across the entire socio-economic spectrum.

Different fast-gate regulation by external Cl(-) and H(+) of the muscle-type ClC chloride channels.

The fast gate of the muscle-type ClC channels (ClC-0 and ClC-1) opens in response to the change of membrane potential (V). This gating process is intimately associated with the binding of external Cl(-) to the channel pore in a way that the occupancy of Cl(-) on the binding site increases the channel's open probability (P(o)). External H(+) also enhances the fast-gate opening in these channels, prompting a hypothesis that protonation of the binding site may increase the Cl(-) binding affinity, and this is possibly the underlying mechanism for the H(+) modulation. However, Cl(-) and H(+), modulate the fast-gate P(o)-V curve in different ways. Varying the external Cl(-) concentrations ([Cl(-)](o)) shifts the P(o)-V curve in parallel along the voltage axis, whereas reducing external pH mainly increases the minimal P(o) of the curve. Furthermore, H(+) modulations at saturating and nonsaturating [Cl(-)](o) are similar. Thus, the H(+) effect on the fast gating appears not to be a consequence of an increase in the Cl(-) binding affinity. We previously found that a hyperpolarization-favored opening process is important to determine the fast-gate P(o) of ClC-0 at very negative voltages. This [Cl(-)](o)-independent mechanism attracted little attention, but it appears to be the opening process that is modulated by external H(+).

Pulmonary structural maturation and pulmonary artery remodeling after reversible fetal ovine tracheal occlusion in diaphragmatic hernia.

PURPOSE: Congenital diaphragmatic hernia (CDH) is associated with thickened pulmonary arteries (PA) contributing to pulmonary hypertension. In the current study, the effects of antenatal glucocorticoids and reversible tracheal occlusion (TO) on PA structure were assessed in a hypoplastic lung model. METHODS: A left-sided CDH was created in fetal lambs at 80 days gestation, TO at 108 days, and release of the occlusion (TR) at 129 days. All were given 1 dose of maternal glucocorticoids at 135 days. At 136 days (term, 145 days), the fetus was delivered by cesarian section. CDH (n = 7), CDH + TO (n = 6), CDH + TO + TR (n = 6), and unoperated twin controls (n = 16) were compared. Outcome measurements were (1) lung growth, represented by lung weight to body weight ratio (LW/BW), (2) lung structural maturation, which is inversely proportional to mean terminal bronchiole density (MTBD), (3) PA medial and adventitial areas (square micrometers), (4) lung capillary load, which is the ratio of vessel surface area (SA) to tissue SA ratio. RESULTS: CDH lungs were hypoplastic with a low LW/BW and high MTBD. The small PAs (<75 microm) of CDH had an increased medial area, indicating increased muscle mass and an increased adventitial area. CDH + TO +/- TR increased LW/BW and achieved normal structural lung maturity with a low MTBD. Only CDH + TO thinned the PA medial area closer to control values. The adventitial area remained thick in CDH +/- TO +/- TR when compared with controls. All 4 groups had similar capillary load. CONCLUSIONS: TO may be especially important for PA remodeling in the latter part of gestation, because TR 1 week before delivery prevents thinning of the small PAs in CDH. The shaping achieved by TO in terms of lung growth, structural maturity, and pulmonary artery medial area thinning may prove beneficial in lessening the severity of the associated pulmonary hypertension in CDH.

Effect of n-3 fatty acids on the composition and binding properties of lipoproteins in hypertriglyceridemic patients.

BACKGROUND: Treatment of hyperlipidemic patients with fish oil results in an increase in plasma LDL cholesterol despite a marked decrease in the LDL precursor, VLDL. OBJECTIVE: We studied the relation between VLDL composition and LDL concentrations. DESIGN: Fourteen hypertriglyceridemic patients were treated with encapsulated fish oil (containing 1.45 g eicosapentaenoic acid and 1. 55 g docosahexaenoic acid/d) for 4 wk. Venous blood samples were collected before and after treatment. Eleven normolipidemic subjects served as a control group. RESULTS: Fish oil effectively lowered plasma lipid and apolipoprotein (apo) E concentrations in the hypertriglyceridemic patients, whereas apo B concentrations increased. The lipid and apolipoprotein content of VLDL decreased, whereas LDL cholesterol and LDL apo B increased. Fractionation of VLDL by heparin-affinity chromatography showed that before treatment hypertriglyceridemic patients had more VLDL in the 0.05-mol NaCl/L subfraction and less in the 0.20-mol/L subfraction than did control subjects (P < 0.05), whereas the subfraction distribution pattern was normalized after fish-oil treatment. Nevertheless, plasma concentrations of the 0.05-mol NaCl/L subfraction were decreased and those of the 0.20-mol/L subfraction were increased in hypertriglyceridemic patients after fish-oil treatment (P < 0.05). Fish-oil treatment both enhanced VLDL binding and lowered LDL binding to fibroblasts. CONCLUSION: Treatment of hypertriglyceridemic patients with fish oil caused differential effects on VLDL subfractions and decreased LDL binding to fibroblast receptors, which may have contributed to the paradoxical increase in LDL-cholesterol concentrations.

Therapeutic effect of sheng-ji-san on pressure ulcers.

In the present study, the effectiveness of sheng-ji-san (SJS) in promoting the healing of pressure ulcers was evaluated. Thirty-two patients with pressure ulcers were divided into two groups. The treated group received routine medical care combined with SJS treatment and the control group received only routine medical care. After three weeks, the treated group showed a significant reduction in both surface area and depth grade, while the control group showed no significant change. The reduction ratio of the surface area of the ulcer and the effectiveness ratio for the treated group were significantly higher than for the control group. Multiple Linear Regression Analysis revealed that only the SJS treatment was significantly associated with the reduction of surface area and that the use of SJS could independently explain the observed high effectiveness ratio and a relatively high Odds Ratio of 9.539. These results indicate that SJS is effective in promoting the healing of pressure ulcers and should be considered as an adjuvant to routine therapy.

Aminoguanidine attenuates hemodynamic and microcirculatory derangement in rat intestinal ischemia and reperfusion.

BACKGROUND: Nitric oxide (NO) participates in the regulation of hemodynamic and microcirculatory changes in intestinal ischemia and reperfusion (I/R). However, the nature of the involvement of an inducible NO release has been controversial. This study evaluates the impact of an inducible NO synthase inhibitor, aminoguanidine, used as a treatment in a rat intestinal I/R model. METHODS: We investigated the hemodynamics by measuring the mean arterial pressure (MAP), and the microcirculatory responses of the intestine and liver to systemically administered aminoguanidine by use of laser-Doppler flowmetry (LDF), in vivo microscopy, and flow cytometry. RESULTS: During the 30-min ischemia of the selected 20-cm ileal segment, no MAP change was noted. At reperfusion, a marked decrease of MAP was noted and the lowest levels were noted 3 hours after reperfusion (67 +/- 4% vs. 99 +/- 5% in sham-operated control animals). A marked decrease in liver perfusion as measured by LDF was noted 1 hour after reperfusion and remained low at 5 hours (72 +/- 4% vs. 97 +/- 3% in sham-operated control animals). A marked decrease in intestine perfusion was noted by using LDF 1 hour after reperfusion and remained low at 5 hours (43 +/- 3% vs. 92 +/- 4% in sham-operated control animals). The flow velocity of the postcapillary venules of the intestine was markedly decreased (1.01 +/- 0.62 vs. 2.67 +/- 0.34 mm/s in sham-operated control animals) at 5 hours after reperfusion. The flow velocity of the postsinusoidal venules of the liver was also markedly decreased (1.01 +/- 0.62% vs. 2.67 +/- 0.34% in sham-operated control animals). Leukocyte-endothelial interaction (adhesion) was increased in the postcapillary venules of the intestine (54 +/- 12 vs. 6 +/- 4/microm2 in sham-operated control animals) and in the postsinusoidal venules of the liver (32 +/- 8 vs. 2 +/- 2/microm2 in sham-operated control animals). Concomitantly, the granulocyte count was increased (9.1 +/- 0.6 vs. 2.1 +/- 0.3% of total circulating leukocytes in sham-operated control animals), with an increase of CD 11b expression. Aminoguanidine administration (1 mg/kg) 0.5 hour before ischemia and 1 hour after reperfusion significantly increased MAP, increased intestine and liver perfusion, decreased adhesion, and decreased circulating granulocytes and CD 11b expression. CONCLUSION: Inhibition of an inducible NO release by aminoguanidine in intestinal I/R can attenuate hemodynamic and microcirculatory derangement.

Anticonvulsant effect of Uncaria rhynchophylla (Miq) Jack. in rats with kainic acid-induced epileptic seizure.

This study investigated the anticonvulsant effect of Uncaria rhynchophylla (UR) and the physiological mechanisms of its action in rats. A total of 70 male Sprague-Dawley (SD) rats were selected for study. Thirty four of these rats were divided into 5 groups as follows: 1) CONTROL GROUP (n = 6): received intraperitoneal injection (i.p.) of kainic acid (KA, 12 mg/kg); 2) UR1000 group (n = 10), 3) UR500 group (n = 6) 4) UR250 group, received UR 1000, 500, 250 mg/kg i.p. 30 min prior to KA administration, respectively; 5) Contrast group: received carbamazepine 20 mg/kg i.p. 30 min prior to KA administration. Behavior and EEG were monitored from 15 min prior to drug administration to 3 hours after KA administration. The number of wet dog shakes were counted at 10 min intervals throughout the experimental course. The remaining 36 rats were used to measure the lipid peroxide level in the cerebral cortex one hour after KA administration. These rats were divided into 6 groups of 6 rats as follows: 1) Normal group: no treatment was given; 2) CONTROL GROUP: received KA (12 mg/kg) i.p.; 3) UR1000 group, 4) UR500 group, 5) UR250 group, received UR 1000, 500, 250 mg/kg i.p. 30 min prior to KA administration, respectively; 6) Contrast group: received carbamazepine 20 mg/kg i.p. 30 min prior to KA administration. Our results indicated that both UR 1000 and 500 mg/kg decreased the incidence of KA-induced wet dog shakes, no similar effect was observed in the UR 250 mg/kg and carbamazepine 20 mg/kg group. Treatment with UR 1000 mg/kg, 500 mg/kg, or 250 mg/kg and carbamazepine 20 mg/kg decreased KA-induced lipid peroxide level in the cerebral cortex and was dose-dependent. These findings suggest that the anticonvulsant effect of UR possibly results from its suppressive effect on lipid peroxidation in the brain.

The role of vitamin E on the anti-atherosclerotic effect of fish oil in diet-induced hypercholesterolemic rabbits.

The role of vitamin E on the anti-atherosclerotic effect of fish oil in diet-induced hypercholesterolemic rabbits was studied in male New Zealand white rabbits. The animals were randomly divided into six groups of 14 each according to the chow given them. Group I, control, rabbits were fed regular laboratory rabbit chow. In addition to the regular chow, Group II rabbits were fed a high (1%) cholesterol-enriched diet. Group III had the same diet as Group II plus 450 mg vitamin E/1000 g chow. Group IV also had the same diet as Group II plus 10% fish oil, but without vitamin E. Group V's diet contained 1% cholesterol, 10% fish oil, and 450 mg vitamin E/1000 g chow. Group VI had the same diet as Group V, but with 150 mg vitamin E/1000 g chow. At the end of a 6-week feeding, the ascending aorta from seven rabbits from each group was harvested for the analysis of prostanoid production, thiobarbituric acid reactive substances (TBARS), superoxide dismutase activity, and cholesterol and vitamin E levels; the same tissue from the other seven rabbits from each group was obtained for the delineation of atherosclerotic lesions by planimetry after the Sudan IV stain. The high cholesterol diet-treated rabbits had worse prostanoid synthesis and higher TBARS levels, which paralleled the severity of the atherosclerosis. Vitamin E or fish oil supplementation in a high cholesterol diet had beneficial prostanoid production, reduced aortic TBARS levels, and attenuated atherosclerotic lesions; these effects were potentiated when vitamin E and fish oil were combined together. The atherosclerotic lesion reduction in rabbits treated with high cholesterol plus fish oil and 450 mg vitamin E/1000 g chow reached statistical significance (P < 0.05) compared to high cholesterol and the same dose of vitamin E-treated rabbits. The rabbits treated with high cholesterol plus fish oil, but without vitamin E or with 150 mg vitamin E/1000 g chow showed an increased plasma creatine kinase activity at 4 (P < 0.01 and 0.05, respectively) and 6 (P < 0.001 and 0.01, respectively) week of feeding. These results suggest that vitamin E and/or fish oil attenuate atherosclerosis in high cholesterol-fed rabbits; vitamin E and fish oil potentiated the effect of each other. Furthermore, without sufficient vitamin E supplementation, rabbits treated with high cholesterol plus fish oil will show an elevation of plasma creatine kinase activity.

The correlation between skin electrical conductance and the score of qi vacuity.

In traditional Chinese medicine, the syndrome of qi vacuity means that the patient's body has a low level of energy to react to stress. Recently, we used a score, the QV score, by scaling the severity of symptoms and signs of qi vacuity in patients with tiredness. The aim of this study was to investigate the relationship between QV score and skin electrical conductance in patients with tiredness. One hundred and forty-three healthy controls and 103 patients with tiredness were involved. Each subject received a weak electrical stimulation with constant voltage (1.75 volt), and conductance was measured between two different limbs. The mean value of skin conductance among four limbs was calculated and expressed by a special unit, namely Chin. The correlation between the skin conductance and QV score was analyzed by a linear regression analysis. The results showed that skin electrical conductance of healthy controls was negatively correlated with age (r-coefficient = -0.51, P = 0.000). The skin conductance of patients with tiredness was significantly lower than that of healthy controls with matching age (P = 0.000 by Student's t-test). Moreover, there was a positive correlation between the decrease of skin conductance and the QV score in patients with tiredness (r-coefficient = +0.68, P = 0.000). These results suggest that a decrease in skin electrical conductance may be closely related to the severity of qi vacuity. The skin conductance test is a simple, reliable, and quantitative method for detection of syndrome of qi vacuity.

Vitamin E supplementation attenuates myointimal proliferation of the abdominal aorta after balloon injury in diet-induced hypercholesterolemic rabbits.

The effects of vitamin E supplementation in a dose of 450 mg/1000 g chow on the myointimal proliferation of the abdominal aorta after balloon injury were studied in 4 groups of rabbits (24 each). The animals were fed regular diet, regular diet plus vitamin E, 1% cholesterol-enriched diet, and 1% cholesterol-enriched diet plus vitamin E. Each animal underwent a balloon injury of the abdominal aorta and left common iliac artery after 2 weeks of feeding. The animals remained on their respective diets thereafter. In 8 balloon-injured and 8 sham-operated animals of each group, the abdominal aortas were harvested 3 days after the procedure for the analysis of prostacyclin and thromboxane A2 synthesis, thiobarbituric acid reactive substances (TBARS) levels, enzyme activities of glutathione reductase (GR) and glutathione peroxidase (GP) as well as reduced (GSH) and oxidized (GSSG) glutathione levels, 3H-thymidine uptake, cholesterol as well as vitamin E contents. In the other 8 balloon-injured rabbits of each group, the tissue was harvested 3 weeks later for the morphometric study. In dependent of high cholesterol feeding, the vitamin E-treated rabbits had lower aortic production of thromboxane B2, higher 6-keto-PGF1 alpha and higher 6-keto-PGF1 alpha/thromboxane B2 ratios in both procedures. The aortic TBARS levels of the rabbits treated high cholesterol alone were significantly higher than the other three groups in both procedures. Balloon injury had a trend to increase TBARS levels and had significantly higher 3H-thymidine uptake (each p < 0.001) than sham operation in each group. Vitamin E supplement to high cholesterol diet or regular chow reduced aortic TBARS levels (p < 0.005 and 0.01, respectively) and 3H-thymidine uptake (p < 0.05 and 0.01, respectively), as well as attenuated myointimal proliferation of the abdominal aorta and left common iliac artery after balloon injury; but only supplement to high cholesterol diet reached statistical significances (both p < 0.05 compared to rabbits fed high cholesterol alone). These results suggest that vitamin E supplement changes prostanoid metabolism to a favorable pattern and reduces lipid peroxidation of the abdominal aortic wall, thus attenuates myointimal proliferation after balloon injury; these presentations are particularly obvious in diet-induced hypercholesterolemic rabbits.

Hyperbaric oxygen therapy attenuates pancreatic microcirculatory derangement and lung edema in an acute experimental pancreatitis model in rats.

This study was designed to investigate hyperbaric oxygen (HBO) therapy as a treatment for managing animals with induced acute pancreatitis. Forty-five anesthetized male Sprague-Dawley rats were studied. A severe acute pancreatitis model was established by combining an intravenous infusion of cerulein (15 microg/kg/h) and an intraductal injection of 0.1 ml of glycodeoxycholic acid (5 mM). Pathology, serum amylase level, pancreatic malondiadehyde levels and water content of the lungs and the pancreas were used to evaluate the severity of disease. Moreover, an in vivo microscopic technique was used to investigate microcirculatory derangement in the pancreas, i.e., flow velocity and leukocytes sticking in postcapillary venules. HBO was delivered in three regimens, i.e., 100% oxygen at 2.5 absolute atmospheric pressure (AAP), 40% oxygen at 2.5 AAP, and 100% oxygen at 1 AAP, 6 h after the initiation of induction of acute pancreatitis. All animals survived until the end of the experiments. HBO significantly improved the pathologic conditions and pancreatic malondiadehyde levels. Concomitantly, it also significantly lessened the severity of lung edema and improved the microcirculatory environment in the pancreas. Our results support the findings that HBO therapy has a beneficial effect on pancreatic microcirculation and lung edema during acute pancreatitis in rats.

Hyperbaric oxygen pretreatment attenuates hepatic reperfusion injury.

Microcirculatory derangement, energy depletion and lipid peroxidation have been related to development of ischemia-reperfusion injury in the liver. This study investigates the effects of hyperbaric oxygen (HBO) on hepatic ischemia-reperfusion injury. Adult, male Sprague-Dawley rats were used. Three groups were evaluated: 1) sham-operated control (laparotomy only, no ischemia, no HBO), n=8; 2) ischemia control (1-h ischemia, 2-h reperfusion, no HBO), n=8; and 3) HBO pretreatment (100%, oxygen, 2.5 atm absolute, 90 min) plus ischemia (1-h ischemia, 2-h reperfusion), n=8. An in vivo microscope was used to investigate hepatic microcirculation. Tissue malondialdehyde (MDA) and adenosine triphosphate (ATP) were determined. In comparison with the ischemia control group, HBO significantly improved harmful insults following ischemia-reperfusion. HBO lessened adherent leukocyte count (6.00+/-1.31 cells/200 microm vs 11.38+/-2.88 cells/200 microm), and improved flow velocity (1.72+/-0.26 mm/s vs 0.83+/-0.19 mm/s) in post-sinusoidal venules. HBO also reduced MDA (1.04+/-0.24 nmol/mg protein vs 2.24+/-0.49 micromol/g protein), and increased ATP (2.03+/-0.17 micromol/g wet wt vs 0.73+/-0.11 micromol/g wet wt) levels. This study demonstrates that HBO before ischemia may ameliorate the ischemia-reperfusion injury of the liver in the rat model.

Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type.

OBJECTIVES: To determine the prevalence of plasma thiamine deficiency in patients referred to a memory disorder clinic and to compare plasma thiamine levels with red blood cell (RBC) thiamine levels. To determine if patients with senile dementia of the Alzheimer's type (SDAT) differ from those without SDAT in either plasma or RBC thiamine levels. DESIGN: Case-control study. SETTING: Ambulatory care referral center. PATIENTS: Consecutive sample of 34 patients; 17 patients who met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for probable Alzheimer's disease and 17 patients with other forms of dementia. METHODS: Plasma and RBC thiamine levels were determined in all patients with the use of a microbiologic assay known for its specificity to biological forms of thiamine. Vitamin supplementation was determined by chart review. OUTCOME MEASURES: Plasma and RBC thiamine levels. RESULTS: Patients with SDAT were found to have significantly lower plasma thiamine levels than patients without SDAT. Low plasma thiamine levels were detected in a significantly larger proportion of patients with SDAT than in patients without SDAT. Red blood cell thiamine levels did not correlate with the clinical diagnosis of SDAT. Vitamin supplementation did not correlate with diagnosis and plasma or RBC thiamine levels. CONCLUSIONS: A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status.

Scavenging effects of Mallotus repandus on active oxygen species.

The active oxygen species scavenging potencies of Mallotus repandus (Willd.) Muell.-Arg. extracts were evaluated by the electron spin resonance (ESR) spin-trapping technique. Superoxide radical (O2.-) and hydroxyl radical (OH.) were supplied enzymatically from hypoxanthine-xanthine oxidase (HPX-XOD) reaction and hydrogen peroxide-ferrous sulfate (Fenton reaction), respectively, to the assay system. The ethyl acetate fraction of Mallotus repandus (stem) showed the greatest superoxide radical scavenger activity and the n-hexane fraction of Mallotus repandus (stem as well as root) the greatest hydroxyl radical scavenger activity.

Radical scavenger and antihepatotoxic activity of Ganoderma formosanum, Ganoderma lucidum and Ganoderma neo-japonicum.

The free radical scavenging and antihepatotoxic activity from Ganoderma lucidum, Ganoderma formosanum and Ganoderma neo-japonicum were studied. Treatment with the water extract of Ganoderma lucidum, Ganoderma formosanum and Ganoderma neo-japonicum caused a marked decrease in the CCl4-induced toxicity in rat liver, made evident by their effect on the levels of glutamic oxaloacetic transaminase (GOT) and lactic dehydrogenase (LDH) in the serum. The scavenging potency of the water extracts of the crude drugs was evaluated in terms of their ability to reduce the peaks of spin adducts using electron spin resonance (ESR) spin-trapping techniques. The results indicated that Ganoderma formosanum showed the greatest antihepatotoxic activity and the greatest free radical scavenging activity.

Cruciferous vegetables and glutathione: their effects on colon mucosal glutathione level and colon tumor development in rats induced by DMH.

The effect of a diet containing 10-40% lyophilized cabbage or broccoli as cruciferous vegetable or 10-40% lyophilized potato as noncruciferous vegetable fed for 14 days on the colon mucosal glutathione (GSH) level was studied in male rats. The GSH levels of the duodenum mucosa and the liver were also measured. Cabbage and broccoli enhanced the colon and duodenum mucosal GSH levels in a dose-related manner; potato had no effect. All three vegetables had no effect on the liver GSH level. The effect of GSH on colon tumorigenesis induced by 1,2-dimethylhydrazine (DMH) was also examined in rats. Male Sprague-Dawley rats were injected with DMH (20 mg/kg body wt) weekly for 20 weeks. DMH lowered the colon mucosal GSH level. GSH (100 mg/day/rat) dissolved in the drinking water and given to rats during and after DMH injections had little or no effect on tumor incidence and total number of colon tumors. Tumors were larger in rats that received GSH than in those that received water. This study shows that the colon mucosal GSH level can be enhanced by feeding rats a diet high in cabbage or broccoli and that GSH added to the drinking water did not affect DMH-induced colon tumorigenesis under the experimental conditions used.

The anti-inflammatory effects of Chinese crude drug prescriptions on experimental arthritis.

San-Miao-Warn (SMW), Tuhwo-Jih-Shen-Tang (TJS) and Dang-Quei-Nian-Tong-Tang (DGT) are Chinese traditional prescriptions. In this study, we evaluated the anti-inflammatory activities of these crude drug prescriptions in carrageenan-induced acute arthritis and complete Freund's adjuvant (CFA)-induced chronic arthritis in rats. It was found that pretreatment with SMW, TJS or DGT at a dosage of 100 mg/kg or 300 mg/kg, significantly inhibited carrageenan-induced acute arthritis. Moreover, these crude drugs also significantly suppressed the development of chronic arthritis induced by CFA. These results suggest that SMW, TJS and DGT are potential anti-inflammatory agents and may be considered as alternatives for non-steroid anti-inflammatory drugs (NSAID).