No abstract

Our results indicate that treatment with oral glucosamine sulfate in a rat OA model (1) attenuates the development of OA, (2) concomitantly reduces nociception, and (3) modulates chondrocyte metabolism, possibly through inhibition of cell p38 and JNK and increase of ERK expression.

Bile duct ligation (BDL) induces primary biliary cirrhosis characterized by cholestasis, impaired liver function, and cognition. Young male Sprague-Dawley rats were used: rats underwent laparotomy without BDL ͓sham-control (SC) group͔; rats had restricted diets supply ͓diet-control (DC) group͔; rats underwent BDL for 2 wk (BDL group); BDL rats with melatonin (500 g/kg/d) intraperitoneally for 2 wk ͓melatonin (500 g/kg/d) (M500) group͔; and BDL rats with melatonin (1000 g/kg/d/intraperitoneally) for 2 wk ͓melatonin (1000 g/kg/d) (M1000) group͔. All the surviving rats were assessed for spatial memory and blood was tested for biochemical study. Liver, brain cortex, and hippocampus were collected for determination of malondialdehyde (MDA) and glutathione (GSH)/ oxidized glutathione (GSSG) ratios. BDL group rats had significantly higher plasma direct/total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), MDA values and higher liver MDA values and lower GSH/GSSG ratios when compared with SC group. In addition, BDL group rats had impaired spatial performance. After melatonin treatment, cholestatic rats' plasma MDA levels, liver MDA levels, and liver GSH/GSSG ratios approached to the values of SC group. Only high dose of melatonin improved spatial performance. Results of this study indicate cholestasis in the developing rats increase oxidative stress and cause spatial memory deficits, which are prevented by melatonin treatment.

Our results indicate that local intra-articular administration of MgSO(4) following collagenase injection in an experimental rat OA model (1) modulates chondrocyte metabolism through inhibition of cell NMDA receptor phosphorylation and apoptosis, (2) attenuates the development of OA, and (3) concomitantly reduces nociception.

Identifying and treating kidney injury in cirrhosis is important. Bile duct ligation (BDL) is a commonly used cholestatic liver disease model. We hypothesized that asymmetric dimethylarginine (ADMA) is involved in BDL-induced oxidative stress and kidney injury, which can be prevented by melatonin. We also intended to elucidate whether increased ADMA is due to increased protein arginine methyltransferase-1 (PRMT1, ADMA-synthesizing enzyme) and/or decreased dimethylarginine dimethylaminohydrolase (DDAH, ADMA-metabolizing enzyme). Three groups of young rats were studied, sham (N = 7), untreated BDL rats (N = 9), and melatonin-treated BDL rats (N = 6, BDL + M). Melatonin-treated BDL rats received daily melatonin 1 mg/kg/day via intraperitoneal injection. One-third of the young BDL rats died compared with none in the BDL + M group. All surviving rats were killed 14 days after surgery. BDL rats had higher plasma aspartate aminotransferase, alanine aminotransferase, direct and total bilirubin, and ammonia levels than shams. They also had kidney injury characterized by increased tubulointerstitial injury scores and plasma creatinine and symmetric dimethylarginine levels, which melatonin prevented. Plasma ADMA levels were elevated in BDL rats, combined with increased hepatic PRMT1 and decreased renal DDAH activity. In addition, melatonin increased hepatic DDAH2 expression, increased DDAH activity and concomitantly decreased ADMA contents in both the liver and kidney. In conclusion, melatonin therapy decreased mortality and prevented kidney injury induced by BDL via reduction of ADMA (by increasing DDAH activity) and oxidative stress.

Nitric oxide (NO) regulates placental blood flow and actively participates in trophoblast invasion and placental development. Asymmetric dimethylarginine (ADMA) can inhibit NO synthase, which generates NO. ADMA has been associated with uterine artery flow disturbances such as preeclampsia. Substantial experimental evidence has reliably supported the hypothesis that an adverse in utero environment plays a role in postnatal physiological and pathophysiological programming. Growing evidence suggests that the placental nitrergic system is involved in epigenetic fetal programming. In this review, we discuss the roles of NO and ADMA in normal and compromised pregnancies as well as the link between placental insufficiency and epigenetic fetal programming.

ObjectiveTo describe the epidemiological characteristics of infantile hypertrophic pyloric stenosis (IHPS) in ethnic Chinese children.Materials and MethodsWe reviewed the National Health Insurance claims database and analyzed data from children less than one year of age who had been diagnosed with IHPS (ICD-9-CM 750.5) and had undergone pyloromyotomy (ICD-9-CM 43.3). We analyzed the incidence, gender, age at diagnosis, length of hospital stay, seasonal variation and cost of IHPS from data collected between January 1997 and December 2007.ResultsA total of 1,077 infants met inclusion criteria, including 889 boys and 188 girls. The annual incidence of IHPS ranged from 0.30 to 0.47 per 1,000 live births with a mean incidence of 0.39 per 1,000 live births. Between 2002 and 2007, the incidence showed a declining trend (P = 0.025) with coincidentally increasing trends for both exclusive breastfeeding (P = 0.014) and breastfeeding plus bottle feeding (P = 0.004). The male-to-female rate ratio was dynamic and increased from 3.03 during the first two weeks of life to 8.94 during the 8th through 10thweeks of life. The overall male-to-female rate ratio was 4.30. The mean age at diagnosis was 43.1±2.4 days. After analyzing the months of birth and hospital admission, no seasonal variation associated with IHPS was detected. The mean length of hospital stay was 8.28±7.10 days.ConclusionsThe incidence of IHPS in Taiwan, a country with a majority ethnic Chinese population, was lower than observed incidences in Caucasian populations living in Western countries. Breastfeeding campaigns and low maternal smoking rates may contribute to the lower incidence of IHPS in Taiwan. However, additional studies with longer follow-up periods are needed.

No abstract