Anisotropic Structure of the Order Parameter in FeSe0.45Te0.55 Revealed by Angle Resolved Specific Heat

The symmetry and structure of the superconducting gap in the Fe-based superconductors are the central issue for understanding these novel materials. So far the experimental data and theoretical models have been highly controversial. Some experiments favor two or more constant or nearly-constant gaps, others indicate strong anisotropy and yet others suggest gap zeros ("nodes"). Theoretical models also vary, suggesting that the absence or presence of the nodes depends quantitatively on the model parameters. An opinion that has gained substantial currency is that the gap structure, unlike all other known superconductors, including cuprates, may be different in different compounds within the same family. A unique method for addressing this issue, one of the very few methods that are bulk and angle-resolved, calls for measuring the electronic specific heat in a rotating magnetic field, as a function of field orientation with respect to the crystallographic axes. In this Communication we present the first such measurement for an Fe-based high-Tc superconductor (FeBSC). We observed a fourfold oscillation of the specific heat as a function of the in-plane magnetic field direction, which allowed us to identify the locations of the gap minima (or nodes) on the Fermi surface. Our results are consistent with the expectations of an extended s-wave model with a significant gap anisotropy on the electron pockets and the gap minima along the \Gamma M (or Fe-Fe bond) direction.Comment: 32 pages, 7 figure

Studies of the Decay B+- -> D_CP K+-

We report studies of the decay B+- -> D_CP K+-, where D_CP denotes neutral D mesons that decay to CP eigenstates. The analysis is based on a 29.1/fb data sample of collected at the \Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e+ e- storage ring. Ratios of branching fractions of Cabibbo-suppressed to Cabibbo-favored processes involving D_CP are determined to be B(B- -> D_1 K-)/B(B- -> D_1 pi-)=0.125 +- 0.036 +- 0.010 and B(B- -> D_2 K-)/B(B- -> D_2 pi-)=0.119 +- 0.028 +- 0.006, where indices 1 and 2 represent the CP=+1 and CP=-1 eigenstates of the D0 - anti D0 system, respectively. We also extract the partial rate asymmetries for B+- -> D_CP K+-, finding A_1 = 0.29 +- 0.26 +- 0.05 and A_2 = -0.22 +- 0.24 +- 0.04.Comment: 10 pages, 2 figures, submitted to Physical Review Letter

Development of Korean Frailty Index for Primary Care (KFI-PC) and Its Criterion Validity

BACKGROUND: The objective of this study was to develop and validate the Korean Frailty Index for Primary Care (KFI-PC) based on a comprehensive geriatric assessment. METHODS: We developed a 54-item KFI-PC comprising 10 standard domains: cognitive status including delirium or dementia; mood; communication including vision, hearing, and speech; mobility; balance; bowel function; bladder function; ability to carry out activities of daily living; nutrition; and social resources. To test its validity, we applied KFI-PC to participants of the Korean Frailty Aging and Cohort Study (KFACS). We analyzed 1,242 participants (mean age, 77.9+/-3.9 years; 47.2% men) from the KFACS who visited 10 study centers in 2018, after excluding 32 participants with missing data required to assess Fried's physical frailty phenotype. RESULTS: The mean KFI-PC score was 0.17+/-0.08, ranging from 0.02 to 0.52. The median KFI-PC score was higher in women than in men, and there was a trend toward higher values in older age groups. The prevalence of frailty when applying a generally used frailty index cutoff point of >0.25 was 17.5% in the whole study sample. As a construct validation of KFI-PC, the area under the receiver operating characteristic curve for Fried's physical frailty was 0.921, and the optimal cutoff value to predict frailty phenotype was 0.23. The KFI-PC score also correlated well with physical, cognitive, and psychological functions; nutritional status; disability in activities of daily living; and instrumental activities of daily living. The Cronbach's alpha coefficient of the 54 total items was 0.737. CONCLUSION: We developed KFI-PC with 53 deficits, including comprehensive geriatric assessment components, and demonstrated the acceptable construct validity and internal consistency of KFI-PC

Prevalence of Physical Frailty and Its Multidimensional Risk Factors in Korean Community-Dwelling Older Adults: Findings from Korean Frailty and Aging Cohort Study

Frailty is defined as a state of increased vulnerability to stressors, and it predicts disability and mortality in the older population. This study aimed to investigate the standardized prevalence and multidimensional risk factors associated with frailty among Korean community-dwelling older adults. We analyzed the baseline data of 2907 adults aged 70-84 years (mean age 75.8 +/- 3.9 years, 57.8% women) in the Korean Frailty and Aging Cohort Study. The Fried frailty phenotype was used to define frailty. Analyzed data included sociodemographic, physical, physical function, biological, lifestyle, health condition, medical condition, psychological, and social domains. Data were standardized using the national standard population composition ratio based on the Korean Population and Housing Census. The standardized prevalence of frailty and prefrailty was 7.9% (95% confidence interval (CI) 6.8-8.9%) and 47.0% (95% CI, 45.1-48.8%), respectively. The following 14 risk factors were significantly associated with frailty: at risk of malnutrition, sarcopenia, severe mobility limitation, poor social capital, rural dwellers, depressive symptoms, poor self-perceived health, polypharmacy, elevated high-sensitivity C-reactive protein, elevated glycosylated hemoglobin, low 25-hydroxy vitamin D level, longer Timed Up and Go, and low Short Physical Performance Battery score (p < 0.05). Physiconutritional, psychological, sociodemographic, and medical factors are strongly associated with frailty

Induction of interleukin-8 preserves the angiogenic response in HIF-1 alpha-deficient colon cancer cells

authorHypoxia inducible factor-1 (HIF-1) is considered a crucial mediator of the cellular response to hypoxia through its regulation of genes that control angiogenesis^1, ^2, ^3, ^4. It represents an attractive therapeutic target^5, ^6 in colon cancer, one of the few tumor types that shows a clinical response to antiangiogenic therapy^7. But it is unclear whether inhibition of HIF-1 alone is sufficient to block tumor angiogenesis^8, ^9. In HIF-1_α knockdown DLD-1 colon cancer cells (DLD-1^HIF-kd), the hypoxic induction of vascular endothelial growth factor (VEGF) was only partially blocked. Xenografts remained highly vascularized with microvessel densities identical to DLD-1 tumors that had wild-type HIF-1_α (DLD-1^HIF-wt). In addition to the preserved expression of VEGF, the proangiogenic cytokine interleukin (IL)-8 was induced by hypoxia in DLD-1^HIF-kd but not DLD-1^HIF-wt cells. This induction was mediated by the production of hydrogen peroxide and subsequent activation of NF-_KB. Furthermore, the KRAS oncogene, which is commonly mutated in colon cancer, enhanced the hypoxic induction of IL-8. A neutralizing antibody to IL-8 substantially inhibited angiogenesis and tumor growth in DLD-1^HIF-kd but not DLD-1^HIF-wt xenografts, verifying the functional significance of this IL-8 response. Thus, compensatory pathways can be activated to preserve the tumor angiogenic response, and strategies that inhibit HIF-1α may be most effective when IL-8 is simultaneously targeted

Observation of Ds+K- and evidence for D-s(+)pi(-) final states in neutral B decays

We report the first observation of a B meson decay that is not accessible by a direct spectator process. The channel (B) over bar (0)-->Ds+K- is found in a sample of 85x10(6) B (B) over bar events, collected with the Belle detector at KEKB, with a branching fraction B((B) over bar (0)-->Ds+K-)=(4.6(-1.1)(+1.2)+/-1.3)x10(-5). We also obtain evidence for the B-0-->D(s)(+)pi(-) decay with branching fraction B(B-0-->D(s)(+)pi(-))=(2.4(-0.8)(+1.0)+/-0.7)x10(-5). This value may be used to extract a model-dependent value of \V-ub\

TRPM2 channel deficiency prevents delayed cytosolic Zn²⁺ accumulation and CA1 pyramidal neuronal death after transient global ischemia

Transient ischemia is a leading cause of cognitive dysfunction. Postischemic ROS generation and an increase in the cytosolic Zn²⁺ level ([Zn²⁺]c) are critical in delayed CA1 pyramidal neuronal death, but the underlying mechanisms are not fully understood. Here we investigated the role of ROS-sensitive TRPM2 (transient receptor potential melastatin-related 2) channel. Using in vivo and in vitro models of ischemia-reperfusion, we showed that genetic knockout of TRPM2 strongly prohibited the delayed increase in the [Zn²⁺]c, ROS generation, CA1 pyramidal neuronal death and postischemic memory impairment. Time-lapse imaging revealed that TRPM2 deficiency had no effect on the ischemia-induced increase in the [Zn²⁺]c but abolished the cytosolic Zn²⁺ accumulation during reperfusion as well as ROS-elicited increases in the [Zn²⁺]c. These results provide the first evidence to show a critical role for TRPM2 channel activation during reperfusion in the delayed increase in the [Zn²⁺]c and CA1 pyramidal neuronal death and identify TRPM2 as a key molecule signaling ROS generation to postischemic brain injury