Suppression of TLR4/MyD88/TAK1/NF-κB/COX-2 Signaling Pathway in the Central Nervous System by Bexarotene,a Selective RXR Agonist,Prevents Hyperalgesia in the Lipopolysaccharide-Induced Pain Mouse Model

Neurochemical Research - A selective RXR agonist, bexarotene, has been shown to have anti-inflammatory, anti-nociceptive, and neuroprotective effects in several models of numerous neurological...     

Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart

We investigated whether 8-week treadmill training strengthens antioxidant enzymes and decreases lipid peroxidation in rat heart. The effects of acute exhaustive exercise were also investigated. Male rats (Rattus norvegicus, Sprague-Dawley strain) were divided into trained and untrained groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h day(-1), 5 days week(-1) for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted. Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats. The activities of glutathione peroxidase and glutathione reductase enzymes decreased by both acute exercise and training. Glutathione S-transferase and catalase activities were not affected. Total and non-enzymatic superoxide scavenger activities were not affected either. Superoxide dismutase activity decreased by acute exercise in untrained rats; however, this decrease was not observed in trained rats. Our results suggested that rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited.     

Prevalence of known mutations in the MEFV gene in a population screening with high rate of carriers

The Familial Mediterranean Fever (FMF) shows an autosomal recessive pattern of inheritance and affects certain ethnic groups. Disease is caused by mutations in MEFV gene and more than 180 mutations have been defined in affected individuals. Current study aimed to determine the frequency-type of the mutations for MEFV gene in Sivas??middle Anatolian city. The cohort was composed of 3340 patients. MEFV gene mutations were studied by multiplex PCR based reverse hybridization stripAssay method. Patients?? clinical features were; family history: 68%, erysipelas-like erythema: 17.6%, fever: 89.9%, abdominal pain: 84.2%, peritonitis: 90.2%, arthritis: 33%, pleuritis: 14.2%, parental consanguinity: 21.2%. Current results revealed that M694V is the most frequent mutation (43.12%), followed by E148Q (20.18), M680I(G/C) (15.00%) and V726A (11.32%). The study population has a high rate of carriers and the E148Q mutation frequency was found to be highest when compared to the other regions of Turkey and other Mediterranean groups.     

Molecular identification and distribution of Anopheles maculipennis complex in the Mediterranean region of Turkey

The present study was set to identify the members of An. maculipennis complex, which includes effective malaria vectors, throughout the Mediterranean region of Turkey using the second internal transcribed spacer of ribosomal DNA (rDNA-ITS2) sequences from 200 specimens. Resulting sequences of this complex from the Mediterranean region revealed the presence of three species belonging to the An. maculipennis complex, namely An. sacharovi, An. maculipennis s.s. and An. melanoon. The lengths of ITS2 region were 284, 294 and 306 bp in length for An. maculipennis s.s., An. melanoon and An. sacharovi respectively. While no sequence divergence was observed within any species, An. sacharovi was the most distantly related species from An. maculipennis s.s. and An. melanoon with a sequence divergence of 15.1% and 15.4%, respectively. While An. melanoon was the rare species, An. maculipennis s.s., was the most abundant and An. sacharovi was the most wide spread one.     

Effects of nicotine and vitamin E on carbonic anhydrase activity in some rat tissues in vivo and in vitro

Effects of nicotine, nicotine + vitamin E and nicotine + Hippophea rhamnoides L. extract (HRe-1) on muscle, heart, lungs, testicle, kidney, stomach, brain and liver carbonic anhydrase (CA; EC 4.2.1.1.) enzyme activities were investigated in vivo. Groups of rats were given nicotine (0.5 mg/kg/day, i.p.), nicotine + vitamin E (75 mg/kg/day, i.g.), nicotine + HRe-1 (250 mg/kg/day, i.g.) and a control group vehicle only. The results showed that nicotine inhibited the heart, lung, stomach and liver CA enzyme activities by approximately 80% (p < 0.001), approximately 94% (p < 0.001), approximately 47% (p < 0.001) and approximately 81% (p < 0.001) respectively, and activated muscle and kidney, but had no effects on the testicle and brain CA activities. Nicotine + vitamin E inhibited the heart and liver CA enzyme activities by approximately 50% (p < 0.001), and approximately 50% (p < 0.001), respectively, and nicotine + vitamin E activated the muscle CA activity. However, nicotine + vitamin E had no effect on lung, testicle, kidney, stomach and brain CA activities. Nicotine + HRe-1 inhibited the heart and stomach CA enzyme activities by approximately 51% (p < 0.001), and approximately 32% (p < 0.002), respectively, and activated the muscle and brain CA activities, but had no effects on the lung, testicle, kidney, and liver CA activities. In vitro CA inhibition results for similar experiments correlated well with the in vivo experimental results in lungs, testicles, kidney, stomach, brain and liver tissues.