Experimental Evidence of t_{2g} Electron-Gas Rashba Interaction Induced by Asymmetric Orbital Hybridization.

We report the control of Rashba spin-orbit interaction by tuning asymmetric hybridization between Ti orbitals at the LaAlO_{3}/SrTiO_{3} interface. This asymmetric orbital hybridization is modulated by introducing a LaFeO_{3} layer between LaAlO_{3} and SrTiO_{3}, which alters the Ti-O lattice polarization and traps interfacial charge carriers, resulting in a large Rashba spin-orbit effect at the interface in the absence of an external bias. This observation is verified through high-resolution electron microscopy, magnetotransport and first-principles calculations. Our results open hitherto unexplored avenues of controlling Rashba interaction to design next-generation spin orbitronics.

[Screening of hot-spot deafness gene mutations among 277 cochlear implantation patients in Sichuan province].

Objective:To investigate the spectrum and incidence of the hot-spot deafness gene mutations of 277 patients with cochlear implantation in Sichuan province, and to provide information of the prevention and treatment for clinical application. Method: The data of the hotspot deafness gene mutations screening of 277 patients with cochlear implantation was analyzed retrospectively. A deafness related gene mutations detection kit was used to detect 9 mutation sites in four deafness-associated genes,including GJB2(35delG,176del16,235delC,299delAT), GJB3(538C＞T),SLC26A4(2168A＞G, IVS7-2A＞G), Mitochondrial 12SrRNA(1494C＞T, 1555A＞G). Result: ① A total of 122 patients with hot-spot Deafness Gene Mutations were detected in 277 cochlear implantation patients(44.04%),among which there were 39 patients were GJB2235delC homozygous mutation(14.08%), 23 patients were GJB2 235delC heterozygous mutation(8.30%), 1 patient was GJB2 299delAT homozygous mutation(0.36%), 2 patients were GJB2 176del16& 235delC compound heterozygous mutation(0.72%), 13 patients were GJB2 235delC& 299delAT compound heterozygous mutation(4.69%), 2 patients were SLC26A4 2168A＞G heterozygous mutation(0.72%), 16 patients were SLC26A4 IVS7-2A＞G homozygous mutation(5.78%), 22 patient were SLC26A4 IVS7-2A＞G heterozygous mutation(7.94%), 1 patients was SLC26A4 2168A＞G& IVS7-2A＞G compound heterozygous mutation(0.36%), 2 patients were mitochondrial 12SrRNA gene 1555A＞G homogenous mutation(0.72%), 1 patient carried both GJB2 235delC homozygous mutation and SLC26A4 IVS7-2A＞G heterozygous mutation(0.36%). ②A total of 49 patients with LVAS were found in 277 cochlear implantation patients: including 15 patients with IVS7-2A＞G homozygous mutation(30.61%), 22 patients with IVS7-2A＞G heterozygous mutation(44.90%), 1 patient with 2168A＞G heterozygous mutation(2.04%), 1 patient with complex heterozygosis mutations of 2168A＞G and IVS7-2A＞G(2.04%), 1 patient with GJB2 235delC homozygous mutation(2.04%) and 1 patient with GJB2 235delC&299delAT compound heterozygous mutation(2.04%), and no hotspot deafness gene mutations were found in 8 patients. ③There were 40 out of 277 cochlear implantation patients with definite family history.There was no statistic difference of the detection rate of hot-spot deafness gene mutations between in patients with family deafness history (57.50%) and in patients without family deafness history (41.77%). ④A total of 273 patients with profound binaural deafness were found among 277 cochlear implantation patients. Three patients with profound deafness in right ear and severe deafness in left ear were found among 277 cochlear implantation patients.Two patients of three were SLC26A4 IVS7-2A＞G heterozygosis mutations, and one patient of three was GJB2 235delC heterozygosis mutations; 1 patient with profound deafness in left ear and severe deafness in right ear was found among 277 cochlear implantation patients,and was GJB2 235delC heterozygosis mutations. Conclusion:① The detection rate of hotspot deafness gene mutations in 277 cochlear implantation patients is 44.04%(122/277). GJB2 Mutation is the most common, SLC26A4 mutation takes the second place, mitochondrial 12SrRNAgene mutation is not common and GJB3 mutation is not found in this study.② SLC26A4 mutation may not be the sole pathogenic factor of LVAS. ③ The results of this study suggest that the genetic background of cochlear implants patients has little effect on the data of the hotspot deafness gene mutations screening.

Associations of intra-renal arterial resistance index with chronic kidney disease and carotid intima-media thickness in type 2 diabetes mellitus.

Renal dysfunction can be evaluated by increased intra-renal arterial resistance index (RI). We evaluated 113 Chinese men with type 2 diabetes on their RI. Results suggest that RI is associated with chronic kidney disease and subclinical arteriosclerosis. RI may help monitoring the deterioration of intra-renal hemodynamics.

Mesenteric fat thickness as an independent determinant of fatty liver.

OBJECTIVE: Mesenteric fat is drained by the portal circulation and has been suggested to be a key component in obesity-related health risk, notably the metabolic syndrome. There are increasing epidemiological and experimental data showing that fatty liver is another component of this multifaceted syndrome. Given their intimate anatomical and physiological relationships, we hypothesized that mesenteric fat thickness may be independently associated with the risk of fatty liver. To test this hypothesis, we examined the predictive role of various fat deposits including mesenteric fat thickness, and various metabolic variables on the risk of fatty liver. SUBJECTS AND METHODS: A total of 291 Chinese subjects (134 men and 157 women with a mean BMI of 23.7 kg/m2, range: 16.5-33.4 kg/m2) underwent ultrasound examination for measurement of mesenteric, subcutaneous and preperitoneal fat thickness, and for diagnosis of fatty liver. Body mass index, waist circumference, and waist-hip ratio were recorded. Blood pressure was measured. Fasting plasma glucose, insulin resistance, high-density lipoprotein cholesterol (HDL-C), triglycerides, low-density lipoprotein cholesterol (LDL-C), liver enzymes were determined by common methods. RESULTS: The subjects with fatty liver had greater abdominal fat thickness and higher anthropometric indexes than those without fatty liver. The subjects with fatty liver also showed higher blood pressure, worse lipid and glycaemic profile compared with those without fatty liver. Using multiple logistic regression analysis, mesenteric fat thickness was a risk factor of fatty liver, independent of body mass index, age, sex, insulin resistance, fasting plasma glucose, lipid and blood pressure. The odds ratio was 1.5 (95% confidence interval: 1.27-1.77) for every 1 mm increase in the mesenteric fat thickness. Measurement of preperitoneal and subcutaneous fat deposits did not show significant associations with fatty liver. CONCLUSION: Mesenteric fat thickness measured on ultrasound is an independent determinant of fatty liver.

Sonographic measurement of mesenteric fat thickness is a good correlate with cardiovascular risk factors: comparison with subcutaneous and preperitoneal fat thickness, magnetic resonance imaging and anthropometric indexes.

OBJECTIVE: Visceral fat, notably mesenteric fat, which is drained by the portal circulation, plays a critical role in the pathogenesis of metabolic syndrome through increased production of free fatty acids, cytokines and vasoactive peptides. We hypothesize that mesenteric fat thickness as measured by ultrasound scan could explain most of the obesity-related health risk. We explored the relationships between cardiovascular risk factors and abdominal fat as determined by sonographic measurements of thickness of mesenteric, preperitoneal and subcutaneous fat deposits, total abdominal and visceral fat measurement by magnetic resonance imaging (MRI) and anthropometric indexes. DESIGN: A cross-sectional study. SUBJECTS: Subjects included 18 healthy men and 19 women (age: 27-61 y, BMI: 19-33.4 kg/m(2)). MEASUREMENTS: The maximum thickness of mesenteric, preperitoneal and subcutaneous fat was measured by abdominal ultrasound examination. MRI examinations of whole abdomen and pelvis were performed and the amount of total abdominal and visceral fat was quantified. The body mass index, waist circumference and waist-hip ratio were recorded. Cardiovascular risk factors were assessed by physical examination and blood taking. RESULTS: Men had more adverse cardiovascular risk profile, higher visceral fat volume and thicker mesenteric fat deposits than women. Among all the investigated obesity indexes, the mesenteric fat thickness showed the highest correlations with total cholesterol, LDL-C, triglycerides, fasting plasma glucose, HbA(1c) and systolic blood pressure in men, and with triglycerides and HbA(1c) in women. On stepwise multiple regression analysis with different obesity indexes as independent variables, 30-65% of the variances of triglycerides, total cholesterol, LDL-C and HbA(1c) in men, and triglycerides in women were explained by the mesenteric fat thickness. CONCLUSION: Compared with sonographic measurement of subcutaneous and preperitoneal fat thickness, MRI measurement of total abdominal and visceral fat and anthropometric indexes, sonographic measurement of mesenteric fat thickness showed better associations with some of the cardiovascular risk factors. It may potentially be a useful tool to evaluate regional distribution of obesity in the assessment of cardiovascular risk.