Serum pro-inflammatory cytokines may play an important role in the association between periodontal disease and hyperlipidaemia.

Calorie restriction (CR) has attracted increased interest since CR enhances lifespan and alters age-related decline in hippocampal-dependent cognitive functions. Obesity is associated with poor neurocognitive outcome including impaired hippocampal synaptic plasticity and cognitive abilities such as learning and memory. N-Methyl-D-aspartate receptors (NMDARs) are linked to hippocampal-dependent learning and memory, which may be stabilized by CR. In the present study, we aimed to establish the effects of CR on NMDARs in CA1 region of hippocampus in obese and non-obese rats. In addition, malondialdehyde (MDA) levels were determined as a marker for lipid peroxidation (LPO) in hippocampus. Four groups were constituted as control group (C, n = 9), obese group (OB, n = 10), obese calorie-restricted group (OCR, n = 9), and non-obese calorie-restricted group (NCR, n = 10). OCR and NCR were fed with a 60% CR diet for 10 weeks. After 10 weeks of CR, the MDA levels significantly decreased in the calorie-restricted groups. Obesity caused significant decreases in NR2A and NR2B subunit expressions in the hippocampus. The hippocampal NR2A and NR2B levels significantly increased in the OCR group compared with the OB group (P < 0.05). In contrast, the hippocampal NR2A and NR2B levels significantly decreased in the NCR group compared with the C group (P < 0.05). Oxidative stress can be prevented by CR, and these data may provide a molecular and cellular mechanism by which CR may regulate NMDAR-mediated response against obesity-induced changes in the hippocampus.

This brief review summarizes some of the publications that document the preventive role of melatonin in kidney damage caused by carcinogens such as 2-nitropropane, arsenic, carbon tetrachloride, nitrilotriacetic acid and potassium bromate. Numerous chemicals generate excessive free radicals that eventually induce renal worsening. Melatonin partially or totally prevents free radical mediated tissue damages induced by many carcinogens. Protective actions of melatonin against the harmful effects of carcinogens are believed to stem from its direct free radical scavenging and indirect antioxidant activities. Dietary or pharmacologically given melatonin may attenuate the oxidative stress, thereby mitigating the subsequent renal damage.

Early chelating age will negatively influence the VEGF level, which increases angiogenesis, however, early starting transfusion age and regular blood transfusion will positively influence the VEGF level, which decreases angiogenesis in thalassemic patients.

We suggested that walnut supplementation may have protective effects against the decline of cognitive functions by regulating NMDAR and lipid peroxidation levels in the hippocampus. The study provides evidence that selected dietary factors (polyunsaturated fatty acids, melatonin, vitamin E, and flavonoids) within walnut may help to trigger hippocampal neuronal signal transduction for the formation of learning and memory.

We suggested that walnut supplementation may have protective effects against the decline of cognitive functions by regulating NMDAR and lipid peroxidation levels in the hippocampus. The study provides evidence that selected dietary factors (polyunsaturated fatty acids, melatonin, vitamin E, and flavonoids) within walnut may help to trigger hippocampal neuronal signal transduction for the formation of learning and memory.

Introduction: Thalassemia major (TM) is an important cause of severe anemia that necessitates regular blood transfusion to prevent the profound weakness and cardiac decompensation caused by the anemia. However, iron overloading is an inevitable consequence of prolonged transfusion therapy. In addition, extramedullary hematopoiesis and hemosiderosis cause spleen, liver and marrow enlargement. In recent years the role of angiogenesis has been investigated in physiologic and pathologic conditions. However, it is known that angiogenetic factors, especially vascular endothelial growth factor (VEGF), cause differentiation of the hemangioblast. The role of angiogenesis has been investigated in different kinds of anemia, such as malignancy related anemia and sickle cell anemia. However, the role of angiogenesis has not been investigated in thalassemia major (TM) patients. In this study the angiogenesis was researched in thalassemic patients by serum VEGF measurement. Material and method: Forty-four consecutive patients with TM were included in this prospective study. TM patients’ findings were compared with those of a healthy control group (n=12). Blood samples were analyzed using commercially available ELISA kits for VEGF Results: VEGF levels were not affected by hemoglobin levels, ferritin levels, or chelation type (p&gt;0.05). However, VEGF was positively affected by chelation starting age and negatively affected by yearly blood transfusion rate (p&lt;0.05). In addition, VEGF of patients who underwent splenectomy was higher than those who didn’t undergo splenectomy (p&lt;0.05). In conclusion, VEGF causes differentiation of hemangioblasts, however, early starting transfusion age and regular blood transfusion decrease angiogenesis in thalassemic patients. The besides regular blood transfusion and effective chelation therapy, splenectomy decreases angiogenesis in this group of patients.