Crystal structure, electronic, and magnetic properties of the bilayered rhodium oxide Sr3Rh2O7

The bilayered rhodium oxide Sr3Rh2O7 was synthesized by high-pressure and high-temperature heating techniques. The single-phase polycrystalline sample of Sr3Rh2O7 was characterized by measurements of magnetic susceptibility, electrical resistivity, specific heat, and thermopower. The structural characteristics were investigated by powder neutron diffraction study. The rhodium oxide Sr3Rh2O7 [Bbcb, a = 5.4744(8) A, b = 5.4716(9) A, c = 20.875(2) A] is isostructural to the metamagnetic metal Sr3Ru2O7, with five 4d electrons per Rh, which is electronically equivalent to the hypothetic bilayered ruthenium oxide, where one electron per Ru is doped into the Ru-327 unit. The present data show the rhodium oxide Sr3Rh2O7 to be metallic with enhanced paramagnetism, similar to Sr3Ru2O7. However, neither manifest contributions from spin fluctuations nor any traces of a metamagnetic transition were found within the studied range from 2 K to 390 K below 70 kOe.Comment: To be published in PR

Destruction of the Mott Insulating Ground State of Ca_2RuO_4 by a Structural Transition

We report a first-order phase transition at T_M=357 K in single crystal Ca_2RuO_4, an isomorph to the superconductor Sr_2RuO_4. The discontinuous decrease in electrical resistivity signals the near destruction of the Mott insulating phase and is triggered by a structural transition from the low temperature orthorhombic to a high temperature tetragonal phase. The magnetic susceptibility, which is temperature dependent but not Curie-like decreases abruptly at TM and becomes less temperature dependent. Unlike most insulator to metal transitions, the system is not magnetically ordered in either phase, though the Mott insulator phase is antiferromagnetic below T_N=110 K.Comment: Accepted for publication in Phys. Rev. B (Rapid Communications

World Health Organization cardiovascular disease risk charts: revised models to estimate risk in 21 global regions

BACKGROUND: To help adapt cardiovascular disease risk prediction approaches to low-income and middle-income countries, WHO has convened an effort to develop, evaluate, and illustrate revised risk models. Here, we report the derivation, validation, and illustration of the revised WHO cardiovascular disease risk prediction charts that have been adapted to the circumstances of 21 global regions. METHODS: In this model revision initiative, we derived 10-year risk prediction models for fatal and non-fatal cardiovascular disease (ie, myocardial infarction and stroke) using individual participant data from the Emerging Risk Factors Collaboration. Models included information on age, smoking status, systolic blood pressure, history of diabetes, and total cholesterol. For derivation, we included participants aged 40-80 years without a known baseline history of cardiovascular disease, who were followed up until the first myocardial infarction, fatal coronary heart disease, or stroke event. We recalibrated models using age-specific and sex-specific incidences and risk factor values available from 21 global regions. For external validation, we analysed individual participant data from studies distinct from those used in model derivation. We illustrated models by analysing data on a further 123 743 individuals from surveys in 79 countries collected with the WHO STEPwise Approach to Surveillance. FINDINGS: Our risk model derivation involved 376 177 individuals from 85 cohorts, and 19 333 incident cardiovascular events recorded during 10 years of follow-up. The derived risk prediction models discriminated well in external validation cohorts (19 cohorts, 1 096 061 individuals, 25 950 cardiovascular disease events), with Harrell's C indices ranging from 0·685 (95% CI 0·629-0·741) to 0·833 (0·783-0·882). For a given risk factor profile, we found substantial variation across global regions in the estimated 10-year predicted risk. For example, estimated cardiovascular disease risk for a 60-year-old male smoker without diabetes and with systolic blood pressure of 140 mm Hg and total cholesterol of 5 mmol/L ranged from 11% in Andean Latin America to 30% in central Asia. When applied to data from 79 countries (mostly low-income and middle-income countries), the proportion of individuals aged 40-64 years estimated to be at greater than 20% risk ranged from less than 1% in Uganda to more than 16% in Egypt. INTERPRETATION: We have derived, calibrated, and validated new WHO risk prediction models to estimate cardiovascular disease risk in 21 Global Burden of Disease regions. The widespread use of these models could enhance the accuracy, practicability, and sustainability of efforts to reduce the burden of cardiovascular disease worldwide. FUNDING: World Health Organization, British Heart Foundation (BHF), BHF Cambridge Centre for Research Excellence, UK Medical Research Council, and National Institute for Health Research

Mutant loricrin is not crosslinked into the cornified cell envelope but is translocated into the nucleus in loricrin keratoderma

BLACKWELL SCIENCE INC, Ishida-Yamamoto, A; Kato, H; Kiyama, H; Armstrong, DKB; Munro, CS; Eady, RAJ; Nakamura, S; Kinouchi, M; Takahashi, H; Iizuka, H, JOURNAL OF INVESTIGATIVE DERMATOLOGY, 115(6), 2000, 1088-1094. authorLoricrin is a major constituent of the epidermal cornified cell envelope (CE). We have recently identified heterozygous loricrin gene mutations in two dominantly inherited skin diseases, the ichthyotic variant of Vohwinkel syndrome (IVS) and progressive symmetric erythrokeratoderma with palmoplantar keratoderma (PSEK-PPK), collectively termed loricrin keratoderma (LK). In order to see whether the mutant loricrin molecules predicted by DNA sequencing are expressed in vivo and to define their pathological effects, we raised antibodies against synthetic peptides corresponding to the mutated sequences of loricrin. Immunoblotting of horny cell extracts from LK patients showed specific bands for mutant loricrin. Immunohistochemistry of LK skin biopsies showed positive immunoreactivity to the mutant loricrin antibodies in the nuclei of differentiated epidermal keratinocytes. The immunostaining was localized to the nucleoli of the middle epidermal layer. As keratinocyte differentiation progressed the immunoreactivity moved gradually into the nucleoplasm leaving nucleoli mostly non-immunoreactive. No substantial staining was observed along the CE. The present study confirmed that mutant loricrin was expressed in the LK skin. Mutant loricrin, as a dominant negative disrupter, is not likely to affect CE crosslinking directly, but seems to interfere with nuclear/nucleolar functions of differentiating keratinocytes. In addition, detection of the mutant loricrin in scraped horny layer could provide a simple non-invasive screening test for LK