47; 95% confidence interval, 0.14-0.58; P < .01.).

Conclusion: Patients with AAAs have attenuated telomerase endothelial expression compared to controls, implying a protective role of telomerase against AAA formation. Further investigation of pathways involved in vascular aging may contribute to elucidation of AAA pathogenetic mechanisms. (J Vase Surg 2011;54:1778-83.)”
“Ideas of reference are considered hallmarks of schizophrenia-related psychopathology. However, the specificity of referential thinking to schizophrenia-related psychopathology has not been examined empirically. Schizotypy reflects the latent liability for Selleckchem GDC-0449 schizophrenia and is associated

with referential thinking. Referential thinking may occur in other forms of psychopatholoy, such as social anxiety, which is characterized by cognitive distortions in which the thoughts and judgments

of others are viewed as having reference to the self. Our primary aim was to examine Evofosfamide ic50 the specificity of referential thinking to schizotypy. A sample of 830 college students completed a psychometric screening, of which 102 met criteria for inclusion in one of three groups: schizotypy (n=30), social anxiety (n=28), non-nal controls (n=44). Participants completed the Referential Thinking Scale (REF), and other measures of schizotypy (Schizotypal Personality Questionnaire, Peters et al Delusion Index, Schizophrenia Proneness Scale, Social Anhedonia Scale), affect, and intellectual functioning. The schizotypy group exhibited higher REF scores than both comparison groups. REF scores were associated with other schizotypy measures and loaded onto a positive schizotypy factor, but not onto a negative schizotypy or negative affect factor. These findings Selleckchem Erastin support the specificity

of high levels of referential thinking to schizotypy and the construct validity of the REF. (C) 2007 Elsevier Ireland Ltd. All rights reserved.”
“Vascular calcification is an independent risk factor for cardiovascular disease. Arterial calcification of the aorta and coronary, carotid, and peripheral arteries becomes more prevalent with age. Genome-wide association studies have identified regions of the genome linked to vascular calcification, and these same regions are linked to myocardial infarction risk. The 9p21 region linked to vascular disease and inflammation also associates with vascular calcification. In addition to these common variants, rare genetic defects can serve as primary triggers of accelerated and premature calcification. Infancy-associated calcific disorders are caused by loss-of-function mutations in ENPP1, an enzyme that produces extracellular pyrophosphate. Adult-onset vascular calcification is linked to mutations in NTE5, another enzyme that regulates extracellular phosphate metabolism. Common conditions that secondarily enhance vascular calcification include atherosclerosis, metabolic dysfunction, diabetes, and impaired renal clearance.