Double superconducting transition in the filled skutterudite PrOs4Sb12 and sample characterizations

A thorough characterization of many samples of the filled skutterudite compound PrOs4Sb12 is provided. We find that the double superconducting transition in the specific heat Tc1~1.89K and Tc2~1.72K tends to appear in samples with a large residual resistivity ratio, large specific heat jump at the superconducting transition and with the highest absolute value of the specific heat above Tc1. However, we present evidence which casts doubt on the intrinsic nature of the double superconducting transition. The ratio of the two specific heat jumps \Delta C(Tc1)/\Delta C(Tc2) shows a wide range of values on crystals from different batches but also within the same batch. This ratio was strongly reduced by polishing a sample down to 120um. Remarkably, three samples exhibit a single sharp transition of ~15mK in width at Tc~1.7K. The normalized specific heat jump (C-Cnormal)/Cnormal at Tc of two of them is higher than ~32% so larger than the sum of the two specific heat jumps when a double transition exists. As an evidence of better quality, the slope in the transition is at least two time steeper. We discuss the origins of the double transition; in particular we consider, based on X-ray diffraction results, a scenario involving Pr-vacancies. The superconducting phase diagram under magnetic field of a sample with a single transition is fitted with a two-band model taking into account the good values for the gap as deduced from thermal conductivity measurements.Comment: 10 pages, 9 figures, 2 tables, submitted to Physical review

Influence of myocardial infarction on changes in the expression of angiotensin type 1 receptor in the rat prostate

Angiotensin II (AngII) is the biologically active peptide of the renin-angiotensin system (RAS). Tissue- based, local RAS has been identified in the prostate, testis, epididymis and coagulating glands. Experimental and clinical studies have consistently shown that myocardial infarction (MI) is associated with activation of the systemic RAS with increased concentration of angiotensin peptides in the blood and changes in expression of angiotensin receptors (AT). Changes in angiotensin receptors in the renal and cardiovascular system after MI are well recognized, but the effects of MI influence on changes in other tissue like the prostate gland are unknown. In the present study, we investigated the effect of myocardial infarction on angiotensin receptor protein and mRNA expression in the rat prostate gland. MI model was established in Wistar rats by ligating the left coronary artery (modified Selye method). The levels of AT1a-b and AT2 receptor mRNAs and proteins were measured in the rat prostate. Our study demonstrates tissue-specific changes in AT1a-b and AT2 receptor expression after myocardial infarction. The results show that MI has a strong influence on the expression of angiotensin receptor type AT1 in the prostate at the protein and mRNA level. (Folia Histochemica et Cytobiologica 2011, Vol. 49, No. 3, 497–503

Association between the ACE I/D polymorphism and physical activity in Polish women

Angiotensin converting enzyme gene (ACE) is the most frequently investigated genetic marker in the context of genetic conditioning of athletic predispositions. However, the knowledge of ACE\u2019s potential modifying effect on changes in selected body traits achieved through a training programme is still limited. Therefore, we have decided to check whether selected body mass, body composition variables, oxygen uptake parameters as well as strength/speed parameters observed in physically active participants will be modulated by the ACE I/D polymorphism. The genotype distribution was examined in a group of 201 young healthy women measured for chosen traits before and after the completion of a 12-week moderate-intensive aerobic training programme. Our results revealed the significant genotype 7 training interactions for VEmax and power of countermovement jump, whereas training improvements were demonstrated for almost all parameters. In addition, main effects of the ACE I/D genotype on TGL, HDL, glucose and 10 m run were observed. A significant increase in VEmax was demonstrated for II and DD genotypes, but not for ID heterozygotes. The greatest gain in power of countermovement jump was observed in II homozygotes, although DD and ID were associated with a significant increase as well. Our study indicated that the polymorphism was associated with changes in VEmax and power of countermovement jump in response to a 12-week aerobic training programme in Caucasian women. However, more experimental studies are needed to establish the ACE gene 7 physical activity interaction

Differential regulation of wild-type and mutant alpha-synuclein binding to synaptic membranes by cytosolic factors

BACKGROUND: Alpha-Synuclein (alpha-syn), a 140 amino acid protein associated with presynaptic membranes in brain, is a major constituent of Lewy bodies in Parkinson's disease (PD). Three missense mutations (A30P, A53T and E46K) in the alpha-syn gene are associated with rare autosomal dominant forms of familial PD. However, the regulation of alpha-syn's cellular localization in neurons and the effects of the PD-linked mutations are poorly understood. RESULTS: In the present study, we analysed the ability of cytosolic factors to regulate alpha-syn binding to synaptic membranes. We show that co-incubation with brain cytosol significantly increases the membrane binding of normal and PD-linked mutant alpha-syn. To characterize cytosolic factor(s) that modulate alpha-syn binding properties, we investigated the ability of proteins, lipids, ATP and calcium to modulate alpha-syn membrane interactions. We report that lipids and ATP are two of the principal cytosolic components that modulate Wt and A53T alpha-syn binding to the synaptic membrane. We further show that 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (C16:0 PAF) is one of the principal lipids found in complex with cytosolic proteins and is required to enhance alpha-syn interaction with synaptic membrane. In addition, the impaired membrane binding observed for A30P alpha-syn was significantly mitigated by the presence of protease-sensitive factors in brain cytosol. CONCLUSION: These findings suggest that endogenous brain cytosolic factors regulate Wt and mutant alpha-syn membrane binding, and could represent potential targets to influence alpha-syn solubility in brain

ATP-binding cassette (ABC) transporters in normal and pathological lung

ATP-binding cassette (ABC) transporters are a family of transmembrane proteins that can transport a wide variety of substrates across biological membranes in an energy-dependent manner. Many ABC transporters such as P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1) and breast cancer resistance protein (BCRP) are highly expressed in bronchial epithelium. This review aims to give new insights in the possible functions of ABC molecules in the lung in view of their expression in different cell types. Furthermore, their role in protection against noxious compounds, e.g. air pollutants and cigarette smoke components, will be discussed as well as the (mal)function in normal and pathological lung. Several pulmonary drugs are substrates for ABC transporters and therefore, the delivery of these drugs to the site of action may be highly dependent on the presence and activity of many ABC transporters in several cell types. Three ABC transporters are known to play an important role in lung functioning. Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene can cause cystic fibrosis, and mutations in ABCA1 and ABCA3 are responsible for respectively Tangier disease and fatal surfactant deficiency. The role of altered function of ABC transporters in highly prevalent pulmonary diseases such as asthma or chronic obstructive pulmonary disease (COPD) have hardly been investigated so far. We especially focused on polymorphisms, knock-out mice models and in vitro results of pulmonary research. Insight in the function of ABC transporters in the lung may open new ways to facilitate treatment of lung diseases