Vulnerable plaques and patients: state-of-the-art

Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term 'vulnerable plaque' was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of 'vulnerability' of a specific lesion to the more comprehensive goal of identifying patient 'cardiovascular vulnerability'. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and 'local' diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of 'high-risk' plaques occurring in 'vulnerable' patients

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

Analysis of shared heritability in common disorders of the brain

Paroxysmal Cerebral Disorder

Identification and quantification of 16 inorganic ions in water by Gaussian curve fitting of near-infrared difference absorbance spectra

This study shows two novel fitting strategies applied to differential absorbance spectra for identification and quantification of electrolytes. The effects of 16 dissolved salts were investigated in the wavelength range from 14000 to 9091 wavenumbers (714–1100 nm) by linear fits of the differential absorbance values

Impact of the Anchoring Ligand on Electron Injection and Recombination Dynamics at the Interface of Novel Asymmetric Push-Pull Zinc Phthalocyanines and TiO2

Phthalocyanines are promising photosensitizers for dye-sensitized solar cells (DSSCs). A parameter that has been problematic for a long time involves electron injection (EI) into the TiO2. The development of push-pull phthalocyanines shows great potential to improve the ratio of EI to back electron transfer (BET). We have studied the impact of the anchoring ligand on EI and BET using transient absorption. The best performing derivative, which has a dicarboxylic acid anchoring ligand (TT15, DSSC efficiency of 3.96%), shows the fastest EI. The EI process occurs via an ultrafast component (~700 fs for all derivatives) and a slower component (5.8 ps for TT15). The ps component is considerably slower for the other derivatives studied. Also BET depends on the anchoring ligand and is the slowest for TT15. This knowledge is essential for the optimization of the EI/BET ratio and the efficiency of a phthalocyanine-based DSSC

Investigation of stressful life events in patients with systemic sclerosis*

Objective: To assess the occurrence of stressful life events in the year before the initiation of systemic sclerosis. Methods: A consecutive series of 40 patients with systemic sclerosis (mean age (56.3±11.9) years, mean disease duration (4.3±3.1) years; 32 females and 8 males), including 28 with diffuse cutaneous scleroderma and 12 with limited cutaneous scleroderma, were evaluated. A control group of 40 healthy subjects free of systemic sclerosis also was included. Socioeconomic status was investigated and Paykel’s interview for recent life events (a semi-structured research interview covering 64 life events) was conducted. Results: Patients with systemic sclerosis showed higher percentages of lower education (72.5%) and working class (82.5%), and reported more stressful life events (P<0.05), such as exits (P<0.05), undesirable events (P<0.01), and uncontrolled events (P<0.001), when compared with the control. More events that had an objective negative impact (P<0.001) were also reported in systemic sclerosis patients than in the control. These results are in accordance with a multifactorial model of pathogenesis in systemic sclerosis. Conclusion: We reported a strong relationship between stressful life events and the initiation of systemic sclerosis. Our findings are consistent with current understanding of the extensive links of behavioral responses to stress with neurophysiological and biochemical processes