P235Relation between myocardial deformation by three-dimensional speckle tracking analysis , control of the hypertension and functional capacity in patients with systemic hypertension.

The purpose of this study was to investigate left ventricular (LV) function in hypertensive patients by 3-dimensional (3D) speckle tracking imaging, and determine the relation between the LV mechanics and functional capacity in this population. This cross-sectional study included 20 treated subjects with well-controlled arterial hypertension (group B) and 20 treated participants with uncontrolled hypertension (group A), adjusted by gender and age. All the subjects underwent 24-hour blood pressure monitoring, complete 2-dimensional and 3D examination, and exercise testing. Patients had similar 3D LV ejection fraction. LV mass was higher in group of uncontrolled hypertension (154.71 ± 49.7 g/m2 versus 147.12±44.8 g/m2 p < 0.01), as well as E/E'ratio (11.4 versus 8.9, p =0.02). 3D global longitudinal and circumferential strain and strain rate were significantly decreased in patients with inadequately controlled hypertension (LS 16.25% versus -19.24%, p=0.007, L-SR -0.97/sec versus -1.48/sec, p=0.04, CS -17.89%versus -21.76%, p=0.04, respectively), while the difference of radial strain and strain rate did not reach statistical significance. Group A of patients had also a significantly lower functional capacity (mean duration of test 13,3 min. versus 17,4 min, nr. of METS 9.4 versus 13.7). Duration of exercise was independently associated with LV mass , mean BP at daytime , E/E' ratio and 3D global longitudinal strain (ß = 0.34, p = 0.02) in the whole hypertensive population in our study. In conclusion, LV longitudinal strain and functional capacity are significantly impaired in the patients with uncontrolled hypertension in comparison with the well-controlled hypertensive patients and are independently associated.

The study of the rs9939609 FTO gene polymorphism in association with obesity and the management of obesity in a Romanian cohort.

The incidence of obesity especially in Romanian population is presently escalating as a major nutrition and health problem. Clinicians aided by scientists are engaged in research approaches that include heredity aspects linked with behavior, education, applied nutrition studies and clinical therapies in order to prevent, control and reverse obesity. The common goal is to identify areas of basic and clinical research to understand aspects of human biology that may be considered as obesogenic. Regarding these approaches, recent discoveries in genetics, epigenetics and functional genomics, based on advancing technologies, are tools employed to prevent and treat obesity. The purpose of this article is to present the current knowledge of key components of the FTO gene role in the obesogenic system that links genetic, epigenetic and environmental, lifestyle/ diet nutritional and behavioral components and to describe the results obtained by genotyping and interviewing relevant selected groups of Romanian population. FTO rs9939609 genotyping was performed on a Romanian study group of 53 subjects (30 obese, 23 normal). Results have been analyzed in association with obesity parameters and comorbidities in order to identify this polymorphism's effect on body mass in our Caucasian cohort. At the same time, personal history of the subjects in correlation with the FTO genotypes provided important information on the FTO gene's influence on the feeding behavior and food selection of these individuals. In conclusion, the FTO rs9939609 polymorphism has been identified as a common gene variant in our Romanian Caucasian cohort, proving a high association with all the parameters of obesity and obesity comorbidities. The adherence to a Mediterranean diet is benefic for subjects with genetic predisposition for this disorder as long as it is kept for a long period of time along with sustained physical exercise. Association studies are an extremely important tool in understanding the hunger-satiety pathway, providing information on the relation between obesity-related genes, gene expression and behavior.

Effects of adenosine and gamma-aminobutyric acid A receptor antagonists on N-methyl-D-aspartate induced neurotoxicity in the rat hippocampus.

This study investigated the modulatory actions of adenosine and gamma-aminobutyric acid (GABA) on several aspects of N-methyl-D-aspartate (NMDA)-induced neurotoxicity, including neuronal loss, atrophy, necrosis, and calcium accumulation in the hippocampus. For this purpose, we combined unilateral intrahippocampal injections of NMDA (24 nmoles) with acute injections of the selective A1 adenosine receptor antagonist DPCPX (0.03 pmoles), the selective adenosine A2a receptor antagonist CSC (1.5 pmoles), a combination of these two antagonists, and injections of the selective GABA A receptor antagonist bicuculline (60 pmoles). Fifteen days after NMDA injection, neuronal loss with preservation of architecture was observed in stratum oriens, pyramidale, radiatum, lacunosum-moleculare, and stratum moleculare of Ammon's horn, and in radial and granular layers of the dentate gyrus. NMDA plus vehicle also produced a small degree of brain tissue necrosis (holes in the structure) in four of five brains. Acute injections of CSC, but not DPCPX or bicuculline, significantly increased the extent of neuronal loss produced by NMDA plus vehicle. CSC in combination with NMDA induced significantly more necrosis than NMDA plus vehicle. A significant degree of atrophy was observed in the hippocampus after treatment with NMDA plus vehicle, and bicuculline significantly increased the magnitude of this atrophy. NMDA-induced calcium deposits were detected within the radiatum and lacunosum-moleculare layers of the hippocampus and in the hilus of the dentate, but not in the stratum oriens, stratum pyramidale, or in the granular layer of the dentate gyrus. However, treatment with the different antagonists did not significantly modify the magnitude of the NMDA-induced calcium deposits. These results reveal a selective vulnerability of certain areas of the hippocampus to the accumulation of calcium deposits, and a selective interaction between adenosine receptors and NMDA-induced neurotoxicity in the hippocampus.

Perinatal human hypoxia-ischemia vulnerability correlates with brain calcification.

Deregulation of intracellular calcium homeostasis is widely considered as one of the underlying pathophysiological mechanisms of hypoxic-ischemic brain injury. Whether this alteration can result in cerebral calcification was investigated in basal ganglia, cerebral cortex, and hippocampus of human premature and term neonates together with glial reaction. In all samples nonarteriosclerotic calcifications were observed, their number and size were area-specific and increased in term neonates. Basal ganglia always presented the highest degree of calcification and hippocampus the lowest, located mainly in the CA1 subfield. In all cases, neuronal damage was associated with astroglial reaction and calcium precipitates, with microglial reaction only in basal ganglia and cerebral cortex, and argues for the participation of excitatory amino acid receptors in hypoxia-ischemia damage. These data correlate with hypoxia-ischemia vulnerability in the perinatal period. The clinical relevance of these precipitates and the neuroprotective interest of non-NMDA receptor manipulation are discussed in the light of our results.