Expression of cartilage-specific markers in calcified and non-calcified atherosclerotic lesions

Recently, molecular mechanisms resembling endochondral ossification were suggested to be important for atherosclerotic vessel calcification. The aim of this study was to investigate in a series of human atherosclerotic (non-diabetic) lesions of the crural arteries the distribution and expression of classical marker genes of the endochondral ossification pathway. Immunostaining for marker proteins S-100 protein and collagen types II and X were performed on atherosclerotic lesions of different grades (according to Stary). Quantitative real-time PCR for human COL1A1, COL2A1, COL10A1, SOX9, and BMP-2 was applied on RNA isolated from atherosclerotic arteries. In most samples, no expression of collagen type II and S-100 protein was found. Exceptionally, S-100 protein and type II collagen expression was observed very focally within advanced atherosclerotic plaques. Type X collagen was not detected in any of the lesions investigated. Overall, in our study we found no evidence that chondrogenic differentiation pathways are generally active in atherosclerotic plaque formation. In particular type X collagen, one important molecule in cartilage calcification, was not expressed in any of the investigated specimens. Occasionally, however, chondrocytic differentiation markers occur within atherosclerotic lesions. This most likely represents a metaplastic event associated, but not causative for atherosclerotic vessel degeneration and calcification.     

Integration of PET-imaging into radiotherapy treatment planning for low-grade meningiomas improves outcome

European Journal of Nuclear Medicine and Molecular Imaging - Meningiomas have an excellent survival prognosis, and radiotherapy (RT) is a central component of interdisciplinary treatment. During...     

Nordic OCD & Related Disorders Consortium: Rationale,design, and methods

Obsessive‐compulsive disorder (OCD) is a debilitating psychiatric disorder, yet its etiology is unknown and treatment outcomes could be improved if biological targets could be identified. Unfortunately, genetic findings for OCD are lagging behind other psychiatric disorders. Thus, there is a pressing need to understand the causal mechanisms implicated in OCD in order to improve clinical outcomes and to reduce morbidity and societal costs. Specifically, there is a need for a large‐scale, etiologically informative genetic study integrating genetic and environmental factors that presumably interact to cause the condition. The Nordic countries provide fertile ground for such a study, given their detailed population registers, national healthcare systems and active specialist clinics for OCD. We thus formed the Nordic OCD and Related Disorders Consortium (NORDiC, www.crowleylab.org/nordic ), and with the support of NIMH and the Swedish Research Council, have begun to collect a large, richly phenotyped and genotyped sample of OCD cases. Our specific aims are geared toward answering a number of key questions regarding the biology, etiology, and treatment of OCD. This article describes and discusses the rationale, design, and methodology of NORDiC, including details on clinical measures and planned genomic analyses.     

Adolescent self-control predicts joint trajectories of marijuana use and depressive mood into young adulthood among urban African Americans and Puerto Ricans

Previous studies have identified an association between depressive mood and marijuana use. We examined adolescent self-control as a predictor of membership in joint developmental trajectories of depressive mood and marijuana use from adolescence to young adulthood. Urban African Americans and Puerto Ricans (N = 838) were sampled when participants were on average 14, 19, 24, and 29 years old. Using growth mixture modeling, four joint trajectory groups of depressive mood and marijuana use were established: low marijuana use/low depressive mood, low marijuana use/intermediate depressive mood, high marijuana use/low depressive mood, and high marijuana use/high depressive mood. Weighted logistic regression analysis showed that self-control at age 14 distinguished the high marijuana use/high depressive mood group and the low marijuana use/low depressive mood group from each of the other groups. Findings show that the co-occurrence of high levels of marijuana use and depressive mood from adolescence into young adulthood is predicted by low levels of self-control in adolescence. On the other hand, high selfcontrol is associated with low marijuana use and low levels of depression over time. Thus, while deficits in self-control in adolescence constitute a significant risk for maladjustment over time, high self-control exerts a protective factor with regard to marijuana use and depressive mood into young adulthood.     

Superior temporal metabolic changes related to auditory hallucinations: a 31P-MR spectroscopy study in antipsychotic-free schizophrenia patients

Structural deficits in the superior temporal cortex and transverse temporal gyri appear to be related to auditory hallucinations in schizophrenia, which are a key symptom of this disorder. However, the cellular and neurochemical underpinnings are poorly understood and hardly studied in vivo. We used ³¹P-MRS (magnetic resonance spectroscopy) with chemical shift imaging to assess the association between left superior temporal cortex metabolism and severity of auditory hallucinations in 29 schizophrenia patients off antipsychotics. Hallucinations scores derived from the Scale for the Assessment of Positive Symptoms showed significant positive correlations with both measures of phospholipids (phosphomonoesters and phosphodiesters), and energy (inorganic phosphate and phosphocreatine, but not adenosine tri-phosphate) metabolism in left superior temporal gyrus/Heschl gyrus voxels. There was no correlation of metabolites in these regions with formal thought disorder, a symptom also linked to superior temporal pathology, thus suggesting symptom specificity. Our findings provide a link between established structural deficits and neurochemical pathology related to membrane pathology and markers of general metabolic turnover.