Trans,trans,trans-Diethanoldiquinaldinatoiron(II)

金沢大学理学部金沢大学大学院自然科学研究科物質創成The title complex, trans,trans,trans-[FeII(C10H 6NO2)2-(C2H6O) 2], is centrosymmetric and the quinaldinate ligands form five-membered chelate rings. The geometry of the complex is distorted octahedral, with a trans-FeN2O4 chromophore. The hydroxy H atom forms an intermolecular hydrogen bond with the carbonyl O atom of the quinaldinate ligand. © 2003 International Union of Crystallography Printed in Great Britain - all rights reserved

Essential and Instructive Roles of GATA Factors in Eosinophil Development

GATA transcription factors are major regulators of hematopoietic and immune system. Among GATA factors, GATA-1, GATA-2, and GATA-3 play crucial roles in the development of erythroid cells, hematopoietic stem, and progenitor cells, and T helper type 2 (Th2) cells, respectively. A high level of GATA-1 and GATA-2 expression has been observed in eosinophils, but their roles in eosinophil development remain uncertain both in vitro and in vivo. Here we show that enforced expression of GATA-1 in human primary myeloid progenitor cells completely switches myeloid cell fate into eosinophils. Expression of GATA-1 exclusively promotes development and terminal maturation of eosinophils. Functional domain analyses revealed that the COOH-terminal finger is essential for this capacity while the other domains are dispensable. Importantly, GATA-1–deficient mice failed to develop eosinophil progenitors in the fetal liver. On the other hand, GATA-2 also showed instructive capacity comparable to GATA-1 in vitro and efficiently compensated for GATA-1 deficiency in terms of eosinophil development in vivo, indicating that proper accumulation of GATA factors is critical for eosinophil development. Taken together, our findings establish essential and instructive roles of GATA factors in eosinophil development. GATA-1 and GATA-2 could be novel molecular targets for therapeutic approaches to allergic inflammation

Effects of muscle cooling on kinetics of pulmonary oxygen uptake and muscle deoxygenation at the onset of exercise

This study investigated effects of skeletal muscle cooling on the metabolic response and kinetics of pulmonary oxygen uptake (urn:x-wiley:2051817X:media:phy213910:phy213910-math-0001O2) and skeletal muscle deoxygenation during submaximal exercise. In the cooling condition (C), after immersion of the lower body into 12°C water for 30 min, eight healthy males performed 30‐min cycling exercise at the lactate threshold while undergoing thigh cooling by a water‐circulating pad. In the normal condition (N) as control, they conducted the same exercise protocol without cooling. Blood lactate concentration was significantly higher in C than N at 10 min after onset of exercise (4.0 ± 1.7 and 2.4 ± 1.2 mmol/L in C and N, P < 0.05). The percent change in the tissue oxygen saturation of the vastus lateralis, measured by a near‐infrared spectroscopy, was significantly lower in C at 2, 8, 10, and 20 min after the exercise onset compared with N (P < 0.05). The percent change in deoxy hemoglobin+myoglobin concentration (Deoxy[Hb+Mb]) showed a transient peak at the onset of exercise and significantly higher value in C at 10, 20, and 30 min after the exercise onset (P < 0.05). Compared to N, slower urn:x-wiley:2051817X:media:phy213910:phy213910-math-0002O2 kinetics (mean response time) was observed in C (45.6 ± 7.8 and 36.1 ± 7.7 sec in C and N, P < 0.05). The mean response time in C relative to N was significantly correlated with the transient peak of Deoxy[Hb+Mb] in C (r = 0.84, P < 0.05). These results suggest that lower oxygen delivery to the hypothermic skeletal muscle might induce greater glycolytic metabolism during exercise and slower urn:x-wiley:2051817X:media:phy213910:phy213910-math-0003O2 kinetics at the onset of exercise

Fatal case of subdural empyema caused by Campylobacter rectus and Slackia exigua

We report a fatal subdural empyema caused by Campylobacter rectus in a 66-year-old female who developed acute onset of confusion, dysarthria, and paresis in her left extremities. A CT scan showed hypodensity in a crescentic formation with a mild mid-line shift. She had a bruise on her forehead caused by a fall several days before admission, which initially raised subdural hematoma (SDH) diagnosis, and a burr hole procedure was planned. However, her condition deteriorated on the admission night, and she died before dawn. An autopsy revealed that she had subdural empyema (SDE) caused by Campylobacter rectus and Slackia exigua. Both microorganisms are oral microorganisms that rarely cause extra-oral infection. In our case, head trauma caused a skull bone fracture, and sinus infection might have expanded to the subdural space causing SDE. CT/MRI findings were not typical for either SDH or SDE. Early recognition of subdural empyema and prompt initiation of treatment with antibiotics and surgical drainage is essential for cases of SDE. We present our case and a review of four reported cases

Teacher Expectancy Effects on Pupils\u27 Scholastic Achievement

I We discussed the implications and limitations of Pygmalion in the classroom and other investigations on teacher expectancy effects, and emphasized the importance of naturalistic studies. II We investigated the inflnence of prior experiences with an older sibling upon teacher expectations and student achievement by younger siblings. We identified 124 pairs of siblings who were taught by the same teacher (experimental group) and 488 pairs of siblings who were taught by different teachers (control group). We compaired the grade point average data of each sibling and found that the discrepancies of the grade point average between experimental siblings were smaller than that between control ones. It is interpreted that teacher expectations formed through prior experiences with an older sibling produced this difference

Cardiomyocyte Formation by Skeletal Muscle-Derived Multi-Myogenic Stem Cells after Transplantation into Infarcted Myocardium

BACKGROUND: Cellular cardiomyoplasty for myocardial infarction has been developed using various cell types. However, complete differentiation and/or trans-differentiation into cardiomyocytes have never occurred in these transplant studies, whereas functional contributions were reported. METHODS AND RESULTS: Skeletal muscle interstitium-derived CD34(+)/CD45(-) (Sk-34) cells were purified from green fluorescent protein transgenic mice by flowcytometory. Cardiac differentiation of Sk-34 cells was examined by in vitro clonal culture and co-culture with embryonic cardiomyocytes, and in vivo transplantation into a nude rat myocardial infarction (MI) model (left ventricle). Lower relative expression of cardiomyogenic transcription factors, such as GATA-4, Nkx2-5, Isl-1, Mef2 and Hand2, was seen in clonal cell culture. However, vigorous expression of these factors was seen on co-culture with embryonic cardiomyocytes, together with formation of gap-junctions and synchronous contraction following sphere-like colony formation. At 4 weeks after transplantation of freshly isolated Sk-34 cells, donor cells exhibited typical cardiomyocyte structure with formation of gap-junctions, as well as intercalated discs and desmosomes, between donor and recipient and/or donor and donor cells. Fluorescence in situ hybridization (FISH) analysis detecting the rat and mouse genomic DNA and immunoelectron microscopy using anti-GFP revealed donor-derived cells. Transplanted Sk-34 cells were incorporated into infarcted portions of recipient muscles and contributed to cardiac reconstitution. Significant improvement in left ventricular function, as evaluated by transthoracic echocardiography and micro-tip conductance catheter, was also observed. CONCLUSIONS AND SIGNIFICANCE: Skeletal muscle-derived multipotent Sk-34 cells that can give rise to skeletal and smooth muscle cells as reported previously, also give rise to cardiac muscle cells as multi-myogenic stem cells, and thus are a potential source for practical cellular cardiomyoplasty

Protective role of podocyte autophagy against glomerular endothelial dysfunction in diabetes.

To examine the cell-protective role of podocyte autophagy against glomerular endothelial dysfunction in diabetes, we analyzed the renal phenotype of tamoxifen (TM)-inducible podocyte-specific Atg5-deficient (iPodo-Atg5-/-) mice with experimental endothelial dysfunction. In both control and iPodo-Atg5-/- mice, high fat diet (HFD) feeding induced glomerular endothelial damage characterized by decreased urinary nitric oxide (NO) excretion, collapsed endothelial fenestrae, and reduced endothelial glycocalyx. HFD-fed control mice showed slight albuminuria and nearly normal podocyte morphology. In contrast, HFD-fed iPodo-Atg5-/- mice developed massive albuminuria accompanied by severe podocyte injury that was observed predominantly in podocytes adjacent to damaged endothelial cells by scanning electron microscopy. Although podocyte-specific autophagy deficiency did not affect endothelial NO synthase deficiency-associated albuminuria, it markedly exacerbated albuminuria and severe podocyte morphological damage when the damage was induced by intravenous neuraminidase injection to remove glycocalyx from the endothelial surface. Furthermore, endoplasmic reticulum stress was accelerated in podocytes of iPodo-Atg5-/- mice stimulated with neuraminidase, and treatment with molecular chaperone tauroursodeoxycholic acid improved neuraminidase-induced severe albuminuria and podocyte injury. In conclusion, podocyte autophagy plays a renoprotective role against diabetes-related structural endothelial damage, providing an additional insight into the pathogenesis of massive proteinuria in diabetic nephropathy

The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection