418 research outputs found

    Magnetic ordering of the antiferromagnet Cu2MnSnS4 from magnetization and neutron-scattering measurements

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    Magnetization and neutron-diffraction measurements were performed on a single crystal of Cu2MnSnS4. This quartenary magnetic semiconductor has the stannite structure (derived from the zinc-blende structure which is common to many II-VI dilute magnetic semiconductors), and it orders antiferromagnetically at low temperature. The neutron data for the nuclear structure confirm that the space group is I42̄m. Both the neutron and magnetization data give TN=8.8 K for the Néel temperature. The neutron data show a collinear antiferromagnetic (AF) structure with a propagation vector k=[1/2,0,1/2], in agreement with earlier neutron data on a powder. However, the deduced angle θ between the spin axis and the crystallographic c direction is between 6° and 16°, in contrast to the earlier value of 40°. The magnetization curve at T≪TN shows the presence of a spin rotation (analogous to a spin flop), which indicates that the spin axis is indeed close to the c direction. The deduced magnetic anisotropy gives an anisotropy field HA≅2 kOe. At high magnetic fields the magnetization curve at T≪TN shows the transition between the canted (spin-flop) phase and the paramagnetic phase. The transition field, H=245.5 kOe, yields an intersublattice exchange field HE= 124 kOe. The exchange constants deduced from HE and the Curie-Weiss temperature Θ=-25 K show that the antiferromagnetic interactions are an order of magnitude smaller than in II-VI dilute magnetic semiconductors (DMS's). The much weaker antiferromagnetic interactions are expected from the difference in the crystal structures (stannite versus zincblende). A more surprising result is that the exchange constant which controls the AF order below TN is not between Mn ions with the smallest separation. This result contrasts with a prediction made for the related II-VI DMS, according to which the exchange constants decrease rapidly with distance.The work at Tufts University was partially supported by NSF Grant No. DMR-9219727. The research in Zaragoza was supported by CICYT Grant No. MAT94-0043. The work at Brown University was supported by NSF Grant No. DMR-9221141. The Francis Bitter National Magnet Laboratory was supported by NSF.Peer Reviewe

    Association of Childhood Psychosocial Environment With 30-Year Cardiovascular Disease Incidence and Mortality in Middle Age

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    Background Childhood adversity and trauma have been shown to be associated with poorer cardiovascular disease (CVD) outcomes in adulthood. However, longitudinal studies of this association are rare. Methods and Results Our study used the CARDIA (Coronary Artery Risk Development in Young Adults) Study, a longitudinal cohort that has followed participants from recruitment in 1985-1986 through 2018, to determine how childhood psychosocial environment relates to CVD incidence and all-cause mortality in middle age. Participants (n=3646) completed the Childhood Family Environment (CFE) questionnaire at the year 15 (2000-2001) CARDIA examination and were grouped by high, moderate, or low relative CFE adversity scores. We used sequential multivariable regression models to estimate hazard ratios of incident (CVD) and all-cause mortality. Participants were 25.1+/-3.6 years old, 47% black, and 56% female at baseline and 198 participants developed CVD (17.9 per 10 000 person-years) during follow-up. CVD incidence was \u3e 50% higher for those in the high CFE adversity group compared with those in the low CFE adversity group. In fully adjusted models, CVD hazard ratios (95% CI) for participants who reported high and moderate CFE adversity versus those reporting low CFE adversity were 1.40 (0.98-2.11) and 1.25 (0.89-1.75), respectively. The adjusted hazard ratios for all-cause mortality was 1.68 (1.17-2.41) for those with high CFE adversity scores and 1.55 (1.11-2.17) for those with moderate CFE adversity scores. Conclusions Adverse CFE was associated with CVD incidence and all-cause mortality later in life, even after controlling for CVD risk factors in young adulthood

    Earliest Triassic microbialites in the South China Block and other areas; controls on their growth and distribution

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    Earliest Triassic microbialites (ETMs) and inorganic carbonate crystal fans formed after the end-Permian mass extinction (ca. 251.4 Ma) within the basal Triassic Hindeodus parvus conodont zone. ETMs are distinguished from rarer, and more regional, subsequent Triassic microbialites. Large differences in ETMs between northern and southern areas of the South China block suggest geographic provinces, and ETMs are most abundant throughout the equatorial Tethys Ocean with further geographic variation. ETMs occur in shallow-marine shelves in a superanoxic stratified ocean and form the only widespread Phanerozoic microbialites with structures similar to those of the Cambro-Ordovician, and briefly after the latest Ordovician, Late Silurian and Late Devonian extinctions. ETMs disappeared long before the mid-Triassic biotic recovery, but it is not clear why, if they are interpreted as disaster taxa. In general, ETM occurrence suggests that microbially mediated calcification occurred where upwelled carbonate-rich anoxic waters mixed with warm aerated surface waters, forming regional dysoxia, so that extreme carbonate supersaturation and dysoxic conditions were both required for their growth. Long-term oceanic and atmospheric changes may have contributed to a trigger for ETM formation. In equatorial western Pangea, the earliest microbialites are late Early Triassic, but it is possible that ETMs could exist in western Pangea, if well-preserved earliest Triassic facies are discovered in future work

    Manganese [III] tetrakis [5,10,15,20]-benzoic acid porphyrin reduces adiposity and improves insulin action in mice with pre-existing obesity

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    The superoxide dismutase mimetic manganese [III] tetrakis [5,10,15,20]-benzoic acid porphyrin (MnTBAP) is a potent antioxidant compound that has been shown to limit weight gain during short-term high fat feeding without preventing insulin resistance. However, whether MnTBAP has therapeutic potential to treat pre-existing obesity and insulin resistance remains unknown. To investigate this, mice were treated with MnTBAP or vehicle during the last five weeks of a 24-week high fat diet (HFD) regimen. MnTBAP treatment significantly decreased body weight and reduced white adipose tissue (WAT) mass in mice fed a HFD and a low fat diet (LFD). The reduction in adiposity was associated with decreased caloric intake without significantly altering energy expenditure, indicating that MnTBAP decreases adiposity in part by modulating energy balance. MnTBAP treatment also improved insulin action in HFD-fed mice, a physiologic response that was associated with increased protein kinase B (PKB) phosphorylation and expression in muscle and WAT. Since MnTBAP is a metalloporphyrin molecule, we hypothesized that its ability to promote weight loss and improve insulin sensitivity was regulated by heme oxygenase-1 (HO-1), in a similar fashion as cobalt protoporphyrins. Despite MnTBAP treatment increasing HO-1 expression, administration of the potent HO-1 inhibitor tin mesoporphyrin (SnMP) did not block the ability of MnTBAP to alter caloric intake, adiposity, or insulin action, suggesting that MnTBAP influences these metabolic processes independent of HO-1. These data demonstrate that MnTBAP can ameliorate pre-existing obesity and improve insulin action by reducing caloric intake and increasing PKB phosphorylation and expression

    Ribosomal oxygenases are structurally conserved from prokaryotes to humans

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    2-Oxoglutarate (2OG)-dependent oxygenases have important roles in the regulation of gene expression via demethylation of N-methylated chromatin components1,2 and in the hydroxylation of transcription factors3 and splicing factor proteins4. Recently, 2OG-dependent oxygenases that catalyse hydroxylation of transfer RNA5,6,7 and ribosomal proteins8 have been shown to be important in translation relating to cellular growth, TH17-cell differentiation and translational accuracy9,10,11,12. The finding that ribosomal oxygenases (ROXs) occur in organisms ranging from prokaryotes to humans8 raises questions as to their structural and evolutionary relationships. In Escherichia coli, YcfD catalyses arginine hydroxylation in the ribosomal protein L16; in humans, MYC-induced nuclear antigen (MINA53; also known as MINA) and nucleolar protein 66 (NO66) catalyse histidine hydroxylation in the ribosomal proteins RPL27A and RPL8, respectively. The functional assignments of ROXs open therapeutic possibilities via either ROX inhibition or targeting of differentially modified ribosomes. Despite differences in the residue and protein selectivities of prokaryotic and eukaryotic ROXs, comparison of the crystal structures of E. coli YcfD and Rhodothermus marinus YcfD with those of human MINA53 and NO66 reveals highly conserved folds and novel dimerization modes defining a new structural subfamily of 2OG-dependent oxygenases. ROX structures with and without their substrates support their functional assignments as hydroxylases but not demethylases, and reveal how the subfamily has evolved to catalyse the hydroxylation of different residue side chains of ribosomal proteins. Comparison of ROX crystal structures with those of other JmjC-domain-containing hydroxylases, including the hypoxia-inducible factor asparaginyl hydroxylase FIH and histone Nε-methyl lysine demethylases, identifies branch points in 2OG-dependent oxygenase evolution and distinguishes between JmjC-containing hydroxylases and demethylases catalysing modifications of translational and transcriptional machinery. The structures reveal that new protein hydroxylation activities can evolve by changing the coordination position from which the iron-bound substrate-oxidizing species reacts. This coordination flexibility has probably contributed to the evolution of the wide range of reactions catalysed by oxygenases

    Geographic variation in hypertension prevalence among blacks and whites: the multi-ethnic study of atherosclerosis

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    BACKGROUND: Many studies have examined differences in hypertension across race/ethnic groups but few have evaluated differences within groups. METHODS: We investigated within-group geographic variations in hypertension prevalence among 3,322 black and white participants of the Multi-Ethnic Study of Atherosclerosis (MESA). Place of birth and place of residence were included in multivariate Poisson regression analyses. RESULTS: Blacks born in southern states were 1.11 (95% confidence interval (CI): 1.02, 1.23) times more likely to be hypertensive than non-southern states after adjusting for age and sex. Findings were similar, though not statistically significant, for whites (prevalence ratio (PR): 1.15, 95% CI: 0.98, 1.35). Blacks and whites living in Forsyth (blacks, PR: 1.23, 95% CI: 1.07, 1.42; whites, PR: 1.32, 95% CI: 1.09, 1.60) and Baltimore (blacks, PR: 1.14, 95% CI: 1.00, 1.31; whites, PR: 1.24, 95% CI: 1.05, 1.47) were also significantly more likely to be hypertensive than those living in Chicago after adjusting for age and sex. Among blacks, those living in New York were also significantly more likely to be hypertensive. Geographic heterogeneity was partially explained by socioeconomic indicators, neighborhood characteristics or hypertension risk factors. There was also evidence of substantial heterogeneity in black-white differences depending on which geographic groups were compared (ranging from 82 to 13% higher prevalence in blacks compared with whites).http://deepblue.lib.umich.edu/bitstream/2027.42/78514/1/KershawDiezRoux2010_AmJHTN.pd

    Time spent with cats is never wasted: Lessons learned from feline acromegalic cardiomyopathy, a naturally occurring animal model of the human disease

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    <div><p>Background</p><p>In humans, acromegaly due to a pituitary somatotrophic adenoma is a recognized cause of increased left ventricular (LV) mass. Acromegalic cardiomyopathy is incompletely understood, and represents a major cause of morbidity and mortality. We describe the clinical, echocardiographic and histopathologic features of naturally occurring feline acromegalic cardiomyopathy, an emerging disease among domestic cats.</p><p>Methods</p><p>Cats with confirmed hypersomatotropism (IGF-1>1000ng/ml and pituitary mass; n = 67) were prospectively recruited, as were two control groups: diabetics (IGF-1<800ng/ml; n = 24) and healthy cats without known endocrinopathy or cardiovascular disease (n = 16). Echocardiography was performed in all cases, including after hypersomatotropism treatment where applicable. Additionally, tissue samples from deceased cats with hypersomatotropism, hypertrophic cardiomyopathy and age-matched controls (n = 21 each) were collected and systematically histopathologically reviewed and compared.</p><p>Results</p><p>By echocardiography, cats with hypersomatotropism had a greater maximum LV wall thickness (6.5mm, 4.1–10.1mm) than diabetic (5.9mm, 4.2–9.1mm; Mann Whitney, p<0.001) or control cats (5.2mm, 4.1–6.5mm; Mann Whitney, p<0.001). Left atrial diameter was also greater in cats with hypersomatotropism (16.6mm, 13.0–29.5mm) than in diabetic (15.4mm, 11.2–20.3mm; Mann Whitney, p<0.001) and control cats (14.0mm, 12.6–17.4mm; Mann Whitney, p<0.001). After hypophysectomy and normalization of IGF-1 concentration (n = 20), echocardiographic changes proved mostly reversible. As in humans, histopathology of the feline acromegalic heart was dominated by myocyte hypertrophy with interstitial fibrosis and minimal myofiber disarray.</p><p>Conclusions</p><p>These results demonstrate cats could be considered a naturally occurring model of acromegalic cardiomyopathy, and as such help elucidate mechanisms driving cardiovascular remodeling in this disease.</p></div

    Infection-Associated Nuclear Degeneration in the Rice Blast Fungus Magnaporthe oryzae Requires Non-Selective Macro-Autophagy

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    addresses: School of Biosciences, University of Exeter, Exeter, Devon, United Kingdom.notes: PMCID: PMC3308974Freely-available open access article.The rice blast fungus Magnaporthe oryzae elaborates a specialized infection structure called an appressorium to breach the rice leaf surface and gain access to plant tissue. Appressorium development is controlled by cell cycle progression, and a single round of nuclear division occurs prior to appressorium formation. Mitosis is always followed by programmed cell death of the spore from which the appressorium develops. Nuclear degeneration in the spore is known to be essential for plant infection, but the precise mechanism by which it occurs is not known
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