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Body Weight Ratio (body + weight_ratio)
Selected AbstractsEvaluation of passive integrated transponder tags for marking the bullhead (Cottus gobio), a small benthic freshwater fish: effects on survival, growth and swimming capacityECOLOGY OF FRESHWATER FISH, Issue 3 2007G. Knaepkens Abstract,,, This study examined potential adverse effects of surgically implanted passive integrated transponder (PIT) tags (12 × 2.1 mm) on bullhead (Cottus gobio L.) of three different length-classes (I: 50,64 mm, II: 65,79 mm, III: 80,94 mm). During a 7-week laboratory experiment, the rate of PIT tag loss, incision closure time, survival, growth and swimming capacity were tested. The PIT tag weight to fish body weight ratio varied between 1.04% and 4.85%. The mean incision closure time differed significantly among length-classes and varied between 2.8 (I) and 4.3 (III) weeks. Nevertheless, PIT tag retention did not differ among length-classes and was ,90%. The survival of untagged, sham-tagged and PIT-tagged bullheads was ,90% and did not differ within or among length-classes. Finally, within each length-class, there was no difference in growth and swimming capacity among treatments. Hence, these results suggest the applicability of PIT tags for individually tagging bullheads ,50 mm. [source] Chronic effects of type 2 diabetes mellitus on cardiac muscle contraction in the Goto-Kakizaki ratEXPERIMENTAL PHYSIOLOGY, Issue 6 2007F. C. Howarth Type 2 diabetes mellitus accounts for more than 90% of all cases of diabetes mellitus, and cardiovascular complications are the major cause of mortality and death in diabetic patients. The chronic effects of type 2 diabetes mellitus on heart function have been investigated in the Goto-Kakizaki (GK) rat. Experiments were performed in GK rats and age-matched Wistar control rats at 18 months of age. The progressive effects of diabetes on glucose metabolism were monitored periodically by application of the glucose tolerance test. Ventricular action potentials were measured in isolated, perfused heart. Shortening and intracellular Ca2+ were measured in electrically stimulated ventricular myocytes. The GK rats displayed mild fasting hyperglycaemia and progressively worsening glucose tolerance. At 18 months of age and 180 min after intraperitoneal injection of glucose (2 g (kg body weight),1), blood glucose was 436 ± 47 mg dl,1 in GK rats compared with 153 ± 18 mg dl,1 in control animals. Heart weight to body weight ratio was significantly increased in GK rats (4.10 ± 0.09 mg g,1, n= 5) compared with control animals (3.36 ± 0.22 mg g,1, n= 4). Spontaneous heart rate was slightly reduced in GK rats compared with control rats. Although the amplitude of shortening was not altered, the amplitude of the Ca2+ transient was significantly increased in myocytes from GK rats (0.78 ± 0.11 ratio units) compared with control rats (0.50 ± 0.06 ratio units). Despite progressively worsening glucose metabolism, at 18 months of age the contractile function of the heart appears to be well preserved. [source] Modulation of glycosphingolipid metabolism significantly improves hepatic insulin sensitivity and reverses hepatic steatosis in mice,HEPATOLOGY, Issue 5 2009Nora Bijl Nonalcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance, and type 2 diabetes. The hyperinsulinemia that occurs as a consequence of insulin resistance is thought to be an important contributor to the development of fatty liver. We have shown that the iminosugar N-(5'-adamantane-1'-yl-methoxy)-pentyl-1-deoxynojirimycin (AMP-DNM), an inhibitor of the enzyme glucosylceramide synthase, is a potent enhancer of insulin signaling in rodent models for insulin resistance and type 2 diabetes. The present study was designed to assess the impact of AMP-DNM on insulin levels, liver triglyceride synthesis, and gene expression profile. Treatment of ob/ob mice with AMP-DNM restored insulin signaling in the liver, corrected blood glucose values to levels found in lean mice, and decreased insulin concentration. The expression of sterol regulatory element-binding protein 1c target genes involved in fatty acid synthesis normalized. AMP-DNM treatment significantly reduced liver to body weight ratio and reversed hepatic steatosis, comprising fat as well as inflammatory markers. In addition, AMP-DNM treatment corrected to a large extent the gene expression profile of ob/ob mice livers toward the profile of lean mice. Conclusion: Pharmacological lowering of glycosphingolipids with the iminosugar AMP-DNM is a promising approach to restore insulin signaling and improve glucose homeostasis as well as hepatic steatosis. (HEPATOLOGY 2009.) [source] Hepatic venous outflow obstruction in pediatric living donor liver transplantation using left-sided lobe grafts: Kyoto university experience,LIVER TRANSPLANTATION, Issue 10 2010Seisuke Sakamoto The goals of this study were to evaluate the incidence of hepatic venous outflow obstruction (HVOO) in pediatric patients after living donor liver transplantation (LDLT) using left-sided lobe grafts and to assess the therapeutic modalities used for the treatment of this complication at a single center. Four hundred thirteen primary LDLT procedures were performed with left-sided lobe grafts between 1996 and 2006. All transplants identified with HVOO from a cohort of 380 grafts with survival greater than 90 days were evaluated with respect to the patient demographics, therapeutic intervention, recurrence, and outcome. Seventeen cases (4.5%) were identified with HVOO. Eight patients experienced recurrence after the initial balloon venoplasty. Two patients finally required stent placement after they experienced recurrence shortly after the initial balloon venoplasty. A univariate analysis revealed that a smaller recipient-to-donor body weight ratio and the use of reduced grafts were statistically significant risk factors. The cases with grafts with multiple hepatic veins had a higher incidence of HVOO. In conclusion, the necessity of repeated balloon venoplasty and stent placement was related to poor graft survival. Therefore, the prevention of HVOO should be a high priority in LDLT. When grafts with multiple hepatic veins and/or significant donor-recipient size mismatching are encountered, the use of a patch graft is recommended. Stent placement should be carefully considered because of the absence of data on the long-term patency of stents and stent-related complications. New stenting devices, such as drug-eluting and biodegradable stents, may be promising for the management of HVOO. Liver Transpl 16:1207,1214, 2010. © 2010 AASLD. [source] Small-for-size liver syndrome after auxiliary and split liver transplantation: Donor selectionLIVER TRANSPLANTATION, Issue 9 2003Nigel Heaton Small-for-size liver grafts can be defined by a recognizable clinical syndrome that results from the transplantation of too small a functional mass of liver for a designated recipient. A graft to recipient body weight ratio less than 0.8, impaired venous inflow, and enhanced metabolic demands in patients with poor clinical conditions must be considered as main factors leading to the small-for-size syndrome (SFSS) when using living and cadaveric partial grafts such as split and auxiliary liver grafts. Increased risk of graft dysfunction is currently observed in fatty infiltration of more than 30%, abnormal liver test results (especially bilirubin and gamma glutaryl transferase), and other donor risk factors such as high inotrope administration and donor stay in the intensive care unit (>5 days). Older donors are especially vulnerable to prolonged cold ischemia and high inotrope levels, giving rise to early graft dysfunction and prolonged cholestasis. Increased metabolic need on a functionally small-for-size graft predisposes to surgical and septic complications and poorer survival. Splitting livers into right and left lobe grafts increases the potential risk of small-for-size grafts for both recipients. Several techniques of venous outflow reconstruction/implantation have been proposed to reduce the risk of obstruction postoperatively. Prevention and management of SFSS will improve in parallel with the increased experience, allowing us optimum usage of available organs and reducing overall morbidity and mortality. (Liver Transpl 2003;9:S26-S28.) [source] The effect of fetal tracheal occlusion on lung tissue mechanics and tissue composition,PEDIATRIC PULMONOLOGY, Issue 2 2009Jacques C. Jani MD Abstract Fetal tracheal occlusion (TO) is currently used to treat severe cases of congenital diaphragmatic hernia (DH). Clinical and experimental studies suggest an improved postnatal outcome, but lung tissue mechanics after TO have not been studied. We determined the effect of TO on mechanical impedance and lung tissue components in a rabbit model for DH. At 23 days of gestation (term,=,31 days) either a sham thoracotomy or a diaphragmatic defect was induced. DH fetuses were randomly assigned to undergo 5 days later TO. Fetuses were delivered by term cesarean section to determine lung to body weight ratio (LBWR), dynamic lung mechanics and lung impedance. Airway resistance (Raw), elastance (HL), tissue damping (GL) and hysteresivity (GL/HL) were calculated from impedance data. Collagen I and III and elastin were quantified histologically. LBWR was significantly increased by TO compared to DH (P,<,0.001) and resistance and compliance of the respiratory system (Rrs, Crs) were improved as well. TO resulted in a significant decrease of Raw comparable to observations in sham-fetuses, without effect on lung tissue mechanics HL, GL and hysteresivity. This coincides with a significant decrease of collagen I, III and elastin in comparison to DH fetuses. In this first report on lung tissue mechanics in a rabbit model of DH, TO had a substantial effect on tissue morphology yet this was not mirrored in lung mechanics. We conclude that the effect of TO on lung mechanics without in utero reversal of occlusion, is dominated by airway remodeling. Pediatr Pulmonol. 2009; 44:112,121. © 2009 Wiley-Liss, Inc. [source] Disrupted galectin-3 causes non-alcoholic fatty liver disease in male miceTHE JOURNAL OF PATHOLOGY, Issue 4 2006K Nomoto Abstract Galectin-3, a ,-galactoside-binding animal lectin, is a multifunctional protein. Previous studies have suggested that galectin-3 may play an important role in inflammatory responses. Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a liver condition that may progress to end-stage liver disease and based on the known functions of galectin-3, it was hypothesized that galectin-3 might play a role in the development of NAFLD. Thus, this study investigated the role of galectin-3 in NAFLD by comparing galectin-3 knockout (gal3,/,) mice and wild-type (gal3+/+) mice. The livers of gal3,/, male mice at 6 months of age histologically displayed mild to severe fatty change. The liver weight per body weight ratio, serum alanine aminotransferase levels, liver triglyceride levels, and liver lipid peroxide in gal3,/, mice were significantly increased compared with those in gal3+/+ mice. Furthermore, the hepatic protein levels of advanced glycation end-products (AGE), receptor for AGE (RAGE), and peroxisome proliferator-activated receptor , (PPAR,) were increased in gal3,/, mice relative to gal3+/+ mice. In conclusion, this study suggests that the absence of gal3 can cause clinico-pathological features in male mice similar to those of NAFLD. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Hepatoprotective Activity of Polyherbal Formulation (Normeta®) in Oxidative Stress Induced by Alcohol, Polyunsaturated Fatty Acids and Iron in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2009Shilpa N. Patere The present study was carried out to evaluate the effects of oral treatment with polyherbal formulation Normeta® (2 ml and 4 ml/kg) on hepatic damage induced by alcohol 10,30% (blood alcohol was maintained at levels between 150 and 350 mg/dl), thermally oxidized oil (polyunsaturated fatty acids) (15% of diet) and carbonyl iron (1.5,2% of diet) for 30 days in rats. In vitro studies with 1, 1-Diphenyl, 2-Picrylhydrazyl (DPPH), Nitric oxide and Ferric chloride (Fe+3 ions) showed that Normeta® possesses antioxidant and metal chelating activity. Alcohol, polyunsaturated fatty acids and iron feeding produced an increase in serum levels of iron, serum glutamate pyruvate transaminase and decrease in serum proteins. It was also associated with elevated lipid peroxidation (thiobarbituric acid reactive substances) and disruption of antioxidant defence mechanism in liver, decreased body weight and increased liver to body weight ratio. Oral administration of Normeta® along with alcohol, polyunsaturated fatty acids and iron decreased the serum iron, serum glutamate pyruvate transaminase levels and increased serum protein levels. The levels of liver thiobarbituric acid reactive substances were decreased and the activities of antioxidant enzymes superoxide dismutase and catalase were increased. Improvement in body weight and liver to body weight ratio was also observed. The effects of Normeta® on physico-metabolic parameters were comparable with silymarin. This indicates that Normeta® has favourable effect in bringing down the severity of hepatotoxicity. [source] Hepatic venous outflow reconstruction in adult living donor liver transplants without portal hypertensionCLINICAL TRANSPLANTATION, Issue 2 2004Diego Bogetti Abstract:, Graft congestion is one of the causes of poor graft function in segmental liver transplantation. Three factors are implicated in segmental graft congestion: graft size, hepatic venous outflow and portal inflow. The graft size must be matched to the body weight, which is conventionally done by using graft to body weight ratio. Hepatic blood outflow must be optimized by hepatic vein reconstruction, which can be complicated. High portal blood flow has been shown to be detrimental to small-for-size grafts. These factors are strictly connected to each other. They can all contribute to graft congestion and poor function, while one factor can compensate for the others and decrease congestion. Ideally, all the accessory veins should be reconstructed, if possible, to maximize the outflow. In the absence of portal hypertension and with an adequate sized graft, complex venous reconstruction may not be necessary. We present a case report of an adult living donor liver transplant with the favorable conditions of normal portal pressure and a large sized graft, but complicated by the presence of several accessory hepatic veins. A simple hepatic vein anastomosis was sufficient for adequate outflow and prompt graft function. [source] Neostigmine and pilocarpine attenuated tumour necrosis factor , expression and cardiac hypertrophy in the heart with pressure overloadEXPERIMENTAL PHYSIOLOGY, Issue 1 2008Jessica Freeling The inflammatory cytokine tumour necrosis factor , (TNF,) is known to be a major factor contributing to cardiac remodelling and dysfunction. Parasympathetic nervous system cholinergic function can inhibit TNF, expression during systemic infection. In the present study, we tested the effects of a cholinesterase inhibitor, neostigmine, and a muscarinic cholinergic agonist, pilocarpine, on cardiac hypertrophy and TNF, levels during pressure overload. Rats with transverse aortic constriction exhibited elevated TNF, protein levels in the heart, increased heart weight to body weight ratios (an index of cardiac hypertrophy) and decreased left ventricular diastolic function. Two weeks of infusion with neostigmine (6 ,g kg,1 day,1) or pilocarpine (0.3 mg kg,1 day,1) significantly reduced cardiac hypertrophy, reduced TNF, levels and elevated interleukin-10 levels in heart tissues, and improved ventricular function in rats with transverse aortic constriction. Neither of these treatments significantly changed ventricular pressure load. Furthermore, in primary cultured neonatal cardiac cells, treatment with pilocarpine attenuated adrenergic agonist phenylephrine-induced increased TNF, expression and [3H]leucine (a marker of protein synthesis) incorporation in the cells. Collectively, both cholinergic agents decreased TNF, levels and attenuated cardiac hypertrophy. Since both agents potentially enhanced cholinergic function, the anti-inflammatory action may be involved in the cardioprotective effect of the treatments with these agents. [source] Alcohol-induced free radicals in mice: Direct toxicants or signaling molecules?HEPATOLOGY, Issue 5 2001Ming Yin Tumor necrosis factor , (TNF-,) and free radicals are produced in early alcohol-induced liver injury. Recently, pathology caused by alcohol was blocked nearly completely in tumor necrosis factor , receptor 1 (TNF-R1) knockout mice. With this model, it is now possible to evaluate whether free radicals are directly toxic or act as redox regulators of TNF-, production. Specifically, if free radicals were directly toxic, a parallel decrease in free radicals and pathology in TNF-R1 knockout mice would be predicted. If they only affect TNF-, production, radicals would be expected to remain high while pathology is diminished. Accordingly, free radical production in TNF-R1 knockout mice was studied here. The enteral alcohol delivery model used mice lacking TNF-R1 (p55) and wild-type control C57Bl/6J mice. Animals received a liquid diet continuously with either ethanol or isocaloric maltose-dextrin as control for 4 weeks. Urine ethanol levels fluctuated from 10 to 500 mg/dL in a cyclic pattern in mice receiving ethanol. Ethanol elevated liver:body weight ratios, serum alanine transaminase (ALT) levels, and pathology scores in wild-type mice. These parameters were blunted nearly completely in TNF-R1 knockout mice. Ethanol treatment increased free radical production in wild-type mice compared with animals fed a high-fat control diet. There were no differences in intensity of free radical signals regardless of the presence or absence of TNF-R1; however, pathology differed markedly between these groups. These findings are consistent with the hypothesis that free radicals act as redox signals for TNF-, production and do not directly damage cells in early alcohol-induced hepatic injury. [source] Effect of oral administration of arabic gum on cisplatin-induced nephrotoxicity in ratsJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2003Abdulhakeem A. Al-Majed Abstract It has been recently postulated from our laboratory that Arabic gum (AG) offers a protective effect in the kidney of rats against nephrotoxicity induced by gentamicin via inhibiting lipid peroxidation. It has also recently shown a powerful antioxidant effect through scavenging superoxide anions. In this study we utilized a rat model of cisplatin (CP)-induced nephrotoxicity to determine its peak time following (1, 2, 5, and 7 days) of a single CP (7.5 mg/kg, i.p.) injection. Also, a possible protective effect of cotreatment with AG (7.5 g/kg/day p.o.) on CP-induced nephrotoxicity was investigated. Biochemical as well as histological assessments were carried out. CP-induced nephrotoxicity was manifested by significant elevations of the functional parameters blood urea, serum creatinine, and kidney/body weight ratio. Maximum toxic effects of CP were observed 5 days after its injection, while it started after day 1 in the biochemical parameters, such as glutathione depletion in the kidney tissue with concomitant increases in lipid peroxides and platinum content. Additionally, severe necrosis and desquamation of tubular epithelial cells in renal cortex as well as interstitial nephritis were observed after 5 days in CP-treated animals. Five days after AG cotreatment with CP did not protect the kidney from the damaging effects of CP. However, it significantly reduced CP-induced lipid peroxidation. These findings suggest that lipid peroxidation is not the main cause of CP-induced nephrotoxicity but it is rather more dependent on other factors such as platinum disposition in renal interstitial tubules. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:146,153, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10072 [source] Endothelial-Independent Prevention of High Blood Pressure in L-Name-Treated Rats by Angiotensin II type I Receptor Antisense Gene TherapyEXPERIMENTAL PHYSIOLOGY, Issue 4 2003Phyllis Y. Reaves It has previously been established that a single systemic administration of retroviral vector containing angiotensin II type I receptor antisense (AT1R-AS) in the neonatal spontaneously hypertensive rat (SHR) prevents development of hypertension, and in addition cardiac hypertrophy and endothelial dysfunction. However, these studies could not determine whether the effects of AT1R-AS on high blood pressure (BP) and endothelial function were independent. Angiotensin receptor blockers have been shown to reduce BP in the L-NAME (N , -nitro-L-arginine methyl ester hydrochloride)-induced rat model of hypertension. Our objective in the present study was to use the L-NAME model of hypertension to determine whether AT1R-AS treatment would lower high BP and attenuate cardiac hypertrophy under conditions of permanent endothelial damage. A single bolus of LNSV-AT1R-AS viral particles in neonatal Wistar-Kyoto (WKY) rats was without affect on basal BP. Efficacy of the transgene incorporation was assessed by observing a significant reduction in angiotensin-induced dipsogenic response in the AT1R-AS-treated animals. Introduction of L-NAME in the drinking water for 10 weeks resulted in the establishment of hypertension only in the WKY rats treated with vector alone. These hypertensive (BP, 179 ± 4 mmHg) animals showed a 17% increase in heart weight/body weight ratio and a 60% reduction in ACh-induced vasorelaxation in phenylephrine-preconstricted arteries. The L-NAME-induced high BP and cardiac hypertrophy were attenuated in rats expressing AT1R-AS. However, endothelial dysfunction could not be prevented with the antisense therapy. These observations demonstrate that attenuation of endothelial dysfunction is not a prerequisite for the antihypertensive effects of AT1R-AS treatment. [source] | |||||||||||||