Field-induced magnetic structures in the chiral polar antiferromagnet Ni2_2InSbO6_6

We have performed $^{115}$In-NMR spectroscopy for Ni$_{2}$InSbO$_6$ with corundum-related crystal structure to reveal magnetic structures that develop in high magnetic fields. At low fields Ni$_{2}$InSbO$_6$ shows a helical magnetic order with a long wavelength because of its chiral and polar crystal structure. The field-induced magnetic state was not investigated by microscopic experiment because an extremely high magnetic field is required to modify the antiferromagnetically coupled helical structure. From the analysis of our $^{115}$In-NMR spectra obtained at high magnetic fields, we confirm that the canted antiferromagnetic structure appears in fields applied in the $[110]$ direction and the propagation vector of magnetic helix is rotated toward the field direction for fields in the $[001]$ direction. We discuss the effect of magnetic field that modifies the magnetic structure of an antiferromagnetic chiral magnet.Comment: 9 pages, 8 figures, accepted for publication from Phys. Rev.

Latent heat in the chiral phase transition

The chiral phase transition at finite temperature and density is discussed in the framework of the QCD-like gauge field theory. The thermodynamical potential is investigated using a variational approach. Latent heat generated in the first-order phase transition is calculated. It is found that the latent heat is enhanced near the tricritical point and is more than several hundred MeV per quark.Comment: 6 pages, 3 figure

The Increased Burden of Morbidity Over the Life-Course Among Patients with COPD: A Register-Based Cohort Study in Sweden

Carolina Smith,1,2 Ayako Hiyoshi,1,3 Mikael Hasselgren,2,4 Hanna Sandelowsky,5– 7 Björn Ställberg,8 Scott Montgomery1,5,9 1Clinical Epidemiology and Biostatistics, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; 2Centre for Clinical Research and Education, Region Värmland, Karlstad, Sweden; 3Department of Public Health Sciences, Stockholm University, Stockholm, Sweden; 4School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; 5Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; 6Department of Neurobiology, Care Sciences and Society, Division of Family Medicine and Primary Care, Karolinska Institutet, Stockholm, Sweden; 7Academic Primary Health Care Center, Region Stockholm, Stockholm, Sweden; 8Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine, Uppsala University, Uppsala, Sweden; 9Department of Epidemiology and Public Health, University College, London, UKCorrespondence: Carolina Smith, School of Medical Sciences, Faculty of Medicine and HealthÖrebro University, Örebro, 701 82, Sweden, Email [email protected]: Patients with a diagnosis of chronic obstructive pulmonary disease (COPD) often have other chronic disorders. This study aims to describe the life-course pattern of morbidity in patients with COPD.Patients and Methods: Among all residents aged 50– 90 years in Sweden in 1997, people with a hospital COPD diagnosis were identified using Swedish national registers (1997– 2018). Each patient with COPD was matched by sex, birthyear and county of residency with up to five COPD-free controls. Other chronic disease diagnoses were identified during 1987– 2018. Conditional logistic regression calculated risk of diseases diagnosed prior to first COPD diagnosis, producing odds ratios (OR) and 95% confidence intervals (95% CI). Cox regression estimated risk of diagnoses after first COPD diagnosis, producing hazard ratios (HR) and 95% CI.Results: Among 2,706,814 individuals, 225,159 (8.3%) had COPD. The nested case–control sample included 223,945 COPD-cases with 1,062,731 controls. Prior to first COPD diagnosis, future COPD patients had higher risks than controls for most examined conditions. Highest risks were seen for chronic heart failure (OR = 3.25, 3.20– 3.30), peripheral arterial disease (OR = 3.12, 3.06– 3.18) and lung cancer (OR = 12.73, 12.12– 13.37). Following the COPD diagnosis, individuals with COPD had higher risks of most conditions than individuals without COPD. Chronic heart failure (HR = 3.50, 3.46– 3.53), osteoporosis (HR = 3.35, 3.30– 3.42), depression (HR = 2.58, 2.53– 2.64) and lung cancer (HR = 6.04, 5.90– 6.18) predominated. The risk of vascular dementia was increased after COPD diagnosis (HR = 1.53, 1.48– 1.58) but not Alzheimer’s disease.Conclusion: Accumulation of chronic morbidity may precede COPD. Following the diagnosis, an increased burden of cardiovascular disease and cancer is to be expected, but subsequent depression, osteoporosis, and vascular dementia should also be noted. Management strategies for patients with COPD should consider the higher-than-average risk of multimorbidity.Keywords: COPD, multimorbidity, register-stud

Correction: Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory

Correction to: International Journal of Obesity https://doi.org/10.1038/s41366-020-00735-9 The original version of this article unfortunately contained a mistake in the ESM. The original article has been corrected

Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory

BACKGROUND/OBJECTIVES: The mediating role of eating behaviors in genetic susceptibility to weight gain during mid-adult life is not fully understood. This longitudinal study aims to help us understand contributions of genetic susceptibility and appetite to weight gain. SUBJECTS/METHODS: We followed the body-mass index (BMI) trajectories of 2464 adults from 45 to 65 years of age by measuring weight and height on four occasions at 5-year intervals. Genetic risk of obesity (gene risk score: GRS) was ascertained, comprising 92 BMI-associated single-nucleotide polymorphisms and split at a median (=high and low risk). At the baseline, the Eating Inventory was used to assess appetite-related traits of 'disinhibition', indicative of opportunistic eating or overeating and 'hunger' which is susceptibility to/ability to cope with the sensation of hunger. Roles of the GRS and two appetite-related scores for BMI trajectories were examined using a mixed model adjusted for the cohort effect and sex. RESULTS: Disinhibition was associated with higher BMI (β = 2.96; 95% CI: 2.66-3.25 kg/m2), and accounted for 34% of the genetically-linked BMI difference at age 45. Hunger was also associated with higher BMI (β = 1.20; 0.82-1.59 kg/m2) during mid-life and slightly steeper weight gain, but did not attenuate the effect of disinhibition. CONCLUSIONS: Appetite disinhibition is most likely to be a defining characteristic of genetic susceptibility to obesity. High levels of appetite disinhibition, rather than hunger, may underlie genetic vulnerability to obesogenic environments in two-thirds of the population of European ancestry

Small Molecule Inhibition of HIV-1–Induced MHC-I Down-Regulation Identifies a Temporally Regulated Switch in Nef Action

Nef assembles a multi-kinase complex triggering MHC-I down-regulation. We identify an inhibitor that blocks MHC-I down-regulation, identifying a temporally regulated switch in Nef action from directing MHC-I endocytosis to blocking cell surface delivery. These findings challenge current dogma and reveal a regulated immune evasion program

Bile Acid-Induced Virulence Gene Expression of Vibrio parahaemolyticus Reveals a Novel Therapeutic Potential for Bile Acid Sequestrants

Vibrio parahaemolyticus, a bacterial pathogen, causes human gastroenteritis. A type III secretion system (T3SS2) encoded in pathogenicity island (Vp-PAI) is the main contributor to enterotoxicity and expression of Vp-PAI encoded genes is regulated by two transcriptional regulators, VtrA and VtrB. However, a host-derived inducer for the Vp-PAI genes has not been identified. Here, we demonstrate that bile induces production of T3SS2-related proteins under osmotic conditions equivalent to those in the intestinal lumen. We also show that bile induces vtrA-mediated vtrB transcription. Transcriptome analysis of bile-responsive genes revealed that bile strongly induces expression of Vp-PAI genes in a vtrA-dependent manner. The inducing activity of bile was diminished by treatment with bile acid sequestrant cholestyramine. Finally, we demonstrate an in vivo protective effect of cholestyramine on enterotoxicity and show that similar protection is observed in infection with a different type of V. parahaemolyticus or with non-O1/non-O139 V. cholerae strains of vibrios carrying the same kind of T3SS. In summary, these results provide an insight into how bacteria, through the ingenious action of Vp-PAI genes, can take advantage of an otherwise hostile host environment. The results also reveal a new therapeutic potential for widely used bile acid sequestrants in enteric bacterial infections

Renin, endothelial no synthase and endothelin gene expression in the 2Kidney-1clip goldblatt model of long-term renovascular hypertension

<p>Abstract</p> <p>Objective</p> <p>Numerous reports have shown the influence of renin, nitric oxide (NO) and the endothelin (ET) systems for regulation of blood pressure and renal function. Furthermore, interactions between these peptides have been reported. Aim of our study was to investigate the relative contribution of these compounds in long-term renovascular hypertension/renal ischemia.</p> <p>Methods</p> <p>Hypertension/left-sided renal ischemia was induced using the 2K1C-Goldblatt rat model. Renal renin, ET-1, ET-3 and endothelial NO synthase (eNOS) gene expression was measured by means of RNAse protection assay at different timepoints up to 10 weeks after induction of renal artery stenosis.</p> <p>Results</p> <p>Plasma renin activity and renal renin gene expression in the left kidney were increased in the clipped animals while eNOS expression was unchanged. Furthermore, an increase in ET-1 expression and a decrease of ET-3 expression was detected in early stenosis.</p> <p>Conclusions</p> <p>While renin is obviously involved in regulation of blood pressure and renal function in unilateral renal artery stenosis, ET-1, ET-3 and endothelium derived NO do not appear to play an important role in renal adaptation processes in long-term renal artery stenosis, although ET-1 and ET-3 might be involved in short-term adaptation processes.</p