The TrkB agonist 7,8-dihydroxyflavone improves sensory-motor performance and reduces lipid peroxidation in old mice.

7,8-Dihydroxyflavone (7,8-DHF) is a natural flavonoid compound that act as Trk-B agonist. 7,8-DHF is also a potent antioxidant. When applied systematically, 7,8-DHF can pass through blood-brain barrier and exhibit potential therapeutic effects in several animal models of neurodegenerative disorders. This study investigates the remedial effects of 7,8-DHF on behavioral impairments and biochemical changes associated with aging with a species emphasis on cortex. For this purpose three experimental groups were formed which are young control group, old group and old-DHF groups. 5 mg/kg 7,8-DHF was administered intraperitoneally to old-DHF group for 3 weeks. We assessed the hang wire and adhesive removal performances of mice. Also, oxidative stress, neuroinflammation and synaptic protein levels in the cortex were measured. We observed that chronic administration of 7,8-DHF improved behavioral performance of old mice. Besides, 7,8-DHF reversed MDA level which was increased in old control animals. However, 3 weeks application of 7,8-DHF failed to recover the levels of neuroinflammation markers (TNF-α and IL-6) and synaptic proteins (PSD-95 and Synaptophysin) which were reduced in old group. These findings demonstrate that improvement of age-dependent behavioral impairments and MDA levels by 7,8-DHF could be attributed to its antioxidant actions.

The effect of homocysteine on the expression of CD36, PPARγ, and C/EBPα in adipose tissue of normal and obese mice.

The purpose of this study was to investigate the effect of homocysteine (Hcy) on CD36, PPARγ, and C/EBPα gene and protein expression in adipose tissue obtained from normal and high-calorie diet obesity models. CD36, PPARγ, and C/EBPα gene expression and protein levels in adipose tissue specimens were determined using the RT-PCR and ELISA methods, respectively. Significantly increased CD36 gene expression was observed in adipose tissue from obese mice, while Hcy significantly reduced CD36 gene expression in adipose tissue from normal and obese mice. PPARγ and C/EBPα gene expression levels decreased significantly in all groups compared to the normal group. In addition, levels of both PPARγ and C/EBPα gene expression were lower with Hcy supplementation compared to their own controls. In conclusion, Hcy's reduction of CD36 gene expression in adipose tissue may be one probable factor in hyperhomocysteinemia representing an independent risk factor for cardiovascular diseases.

Endoplasmic reticulum stress markers are of no value in predicting cardiopulmonary resuscitation success and survival in out-of hospital cardiac arrest: A nested case-control study.

OBJECTIVES: The purpose of this study was to determine the value of the endoplasmic reticulum (ER) stress markers glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and PERK in predicting the success of cardiopulmonary resuscitation (CPR) or post-CPR survival. MATERIALS AND METHODS: Non-traumatic out-of-hospital CA patients were included in this prospective, nested case-control study. Standard CPR and post-resuscitative care were applied. Levels of ER stress markers were measured at presentation and were investigated to determine whether they might constitute a marker predicting return of spontaneous circulation (ROSC) or sustained ROSC, and of 24-h, and 1 and 3-month survival. RESULTS: Fifty-two out of 99 non-traumatic CA patients were enrolled. ROSC was determined at a level of 25%, sustained ROSC at 23%, 24-h survival at 7%, and 1- and 3-month survival at 4.6%. No difference was determined in terms of ER stress markers between patients with and without ROSC or sustained ROSC. Only PERK levels were higher in surviving patients than non-surviving subjects in terms of 24-h survival (p = 0.01). Otherwise, no stress markers differed between surviving and non-surviving patients at any survival time point. CONCLUSION: ER stress markers are of no value in determining establishment of ROSC or sustained ROSC, success of CPR, or survival. Only PERK levels may be valuable in terms of 24-h survival.

Autoantibodies Against Carbonic Anhydrase I and II in Patients with Acute Myeloid Leukemia.

OBJECTIVE: Cancer, one of the principal causes of death, is a global social health problem. Autoantibodies developed against the organism's self-antigens are detected in the sera of subjects with cancer. In recent years carbonic anhydrase (CA) I and II autoantibodies have been shown in some autoimmune diseases and carcinomas, but the mechanisms underlying this immune response have not yet been explained. The aim of this study was to evaluate CA I and II autoantibodies in patients with acute myeloid leukemia (AML) and to provide a novel perspective regarding the autoimmune basis of the disease. MATERIALS AND METHODS: Anti-CA I and II antibody levels were investigated using ELISA in serum samples from 30 patients with AML and 30 healthy peers. RESULTS: Anti-CA I and II antibody titers in the AML group were significantly higher compared with the control group (p=0.0001 and 0.018, respectively). A strong positive correlation was also determined between titers of anti-CA I and II antibodies (r=0.613, p=0.0001). CONCLUSION: Our results suggest that these autoantibodies may be involved in the pathogenesis of AML. More extensive studies are now needed to reveal the entire mechanism.