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The medicinal properties of Cinnamon cassia (C. cassia) bark have been reported for their clinical importance for many diseases including diabetes. However, there is no clear evidence so far regarding dose selection for its hepato- and nephroprotective effect in diabetic condition. Hence, the present study aims at evaluating in vitro antioxidant activity, the acute toxicity, and dose fixation of C. cassia bark for their effective medicinal values in streptozotocin (STZ)-induced rats. All the extracts exhibited potential in vitro antioxidant activity and showed a dose-dependent (1000, 2000, 3000, 4000, and 5000 mg/kg BW) acute toxicity by in vivo model. The levels of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), urea, and creatinine showed a significant elevation in animals treated with the highest dose. In further studies along with histopathological studies, animals treated with STZ (60 mg/kg BW) followed by a different dose (300, 400, and 500 mg/kg BW) of ethanolic extract of the C. cassia bark and glibenclamide (3 mg/kg BW) revealed that the altered level of mitochondrial enzymes, hepatic, and renal marker in STZ-induced animals were restored in C. cassia bark extract-treated group as of control. These results could be of scientific support for the use of the ethanolic extract of the C. cassia bark in folk medicine for the management of diabetes and its associated complications. [ABSTRACT FROM AUTHOR]

Impairment of hand functions in individuals with spinal cord injury (SCI) severely disrupts activities of daily living. Recent advances have enabled rehabilitation assisted by robotic devices to augment the residual function of the muscles. Traditionally, electromyography-based muscle activity sensing interfaces have been utilized to sense volitional motor intent to drive robotic assistive devices. However, the dexterity and fidelity of control that can be achieved with electromyography-based control have been limited due to inherent limitations in signal quality. We have developed and tested a muscle-computer interface (MCI) utilizing sonomyography to provide control of a virtual cursor for individuals with motor-incomplete spinal cord injury. We demonstrate that individuals with SCI successfully gained control of a virtual cursor by utilizing contractions of muscles of the wrist joint. The sonomyography-based interface enabled control of the cursor at multiple graded levels demonstrating the ability to achieve accurate and stable endpoint control. Our sonomyography-based muscle-computer interface can enable dexterous control of upper-extremity assistive devices for individuals with motor-incomplete SCI.

Background: Nonalcoholic fatty liver disease (NAFLD) is one of the most common etiologies of chronic liver disease worldwide. The pathogenesis of metabolic syndrome associated with NAFLD is still under debate. AIM OF THE SCOPE: This study has investigated the hepatic biochemical and histological changes and also insulin resistance in metabolic syndrome associated with NAFLD., Methods: Young male Wistar rats fed a high-fat diet (HFD 42.2% beef tallow) together with N ( ω )-nitro-L-arginine methyl ester (L-NAME; 80 mg/L in drinking water) for 8 weeks and subsequently with 2% d-limonene for the final 4 weeks., Results: HFD-fed rats treated with L-NAME showed increased systolic blood pressure, heart rate, fasting blood glucose, plasma insulin, hepatic marker enzymes, hepatic lipids, circulatory lipid peroxidation by-products, and hepatic phase I enzyme activities with decreased circulatory nonenzymic antioxidant concentrations and hepatic phase II enzyme activities. Dietary supplementation with d-limonene reversed the HFD and L-NAME-induced changes and restored pathological alteration of liver and pancreas., Conclusions: These data provide new insights into the therapeutic approach of d-limonene against the development of the metabolic syndrome associated with NAFLD.

The present study was designed to investigate the effect of rutin on ethanol-induced hepatotoxicity in a dose-dependent manner in rats. Male albino rats were divided into six groups. Group 1 rats served as control and group 2 rats received rutin 100 mg/kg body weight. Hepatotoxicity was induced in groups 3-6 rats (20% ethanol) for 60 days. In addition, groups 4-6 rats received rutin at doses of 25, 50, 100 mg/kg body weight, respectively for the last 30 days of the experiment. We observed a significant increase in the activities of liver marker enzymes, serum amino transferases, alkaline phosphatase, γ-glutamyl transpeptidase the levels of thiobarbituric acid reactive substances, conjugated dienes, lipid hydroperoxides, and a decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione and its related enzymes, vitamins C and E when compared to ethanol-fed rats. Rutin supplementation along with ethanol significantly decreased the levels of liver marker enzymes, lipid peroxidation and significantly elevated the activities of liver SOD, CAT, GSH, glutathione peroxidase, vitamins C and E when compared to untreated ethanol supplemented rats. Among the three doses, 100 mg/kg body weight of rutin was found to exert a more pronounced hepatoprotective effect against ethanol-induced toxicity. Our results were also confirmed by the histopathologic observations., (© 2010 The Authors Fundamental and Clinical Pharmacology © 2010 Société Française de Pharmacologie et de Thérapeutique.)