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Relationship Between the Hip Flexion Angle and Sacral Interface Pressure Upon Lithotomy Position and Urethane Foam Utilization for its Mitigation
Get PDF手術室では術野の確保のため術式に合わせた体位固定が行われ、砕石位では仙骨部体圧の上昇により褥瘡につながる状況がある。そこで砕石位で下部消化管手術を受ける44名に対し、手術開始前に砕石位をとるための股関節外転角度、股関節屈曲角度、膝関節屈曲角度を測定し、それらの各角度と仙骨部体圧値との関連性を検討した。また、各患者に対し砕石位の各角度決定後の仙骨部下に体圧分散ウレタンフォームを挿入し体圧値の変化を検証した。結果は、仙骨部体圧値の平均値は94mmHgであった。分散分析と多重比較法から、BMI23以上の患者では、股関節屈曲角度を14～20度にすることで仙骨部体圧値が有意に低下していた(p<0.05)。さらに、仙骨部体圧値に影響を及ぼす項目に体圧分散ウレタンフォーム使用時が抽出された(p<O.OOl)。BMI23以上の患者に対し、股関節屈曲角度を14～20度にすることで仙骨部体圧値を低減する可能性があると考えられ、手術開始前に仙骨部に体圧分散ウレタンフォームの使用により、仙骨部体圧値を32mmHg低減することが示唆された。The lithotomy position may increase the sacral interface pressure，leading to decubitus ulcer formation postoperatively. We investigated the relationship between the hip and knee joint flexion angles and sacral interface pressure in 44 patients undergoing colon surgery in lithotomy position. Additionally，we determined the changes brought by the urethane foam on the sacral interface pressure. The hip and knee joint angles and sacral interface pressure were measured using the Todai Shiki Goniometer and Portable Interface Pressure Sensor (Palm Q) after induction of the lithotomy positioning. The mean sacral interface pressure was 94mmHg. The sacral interface pressure was significantly reduced after adjusting the hip flexion angle to 14-20 degrees in patients with a body mass index (BMI) of ≧23(p<0.05，one-way analysis of variance). The urethane foam significantly reduced the sacral interface pressure (p<0.001)to up to 32mmHg. Therefore，adjusting the hip flexion angle to 14-20 degrees in patients with a BMI of ≧23 is considered a potential method for keeping the sacral interface pressure to a minimum
小学5年生における運動器の健康状態と体力測定結果の関係
Get PDFBackground: Physical fitness tests determine the current state of physical fitness and athletic ability among children, and the results are widely used as basic administrative data. In 2016, Japan introduced locomotor examinations for elementary school children. In this study, we conducted physical fitness tests and locomotor examinations to assess whether physical fitness is
related to locomotor health. Methods: We conducted physical fitness tests (8 items) and surveys on locomotor health status (7 items) among 259 girls and 309 boys. Then, we counted the number of children who required consultation with an orthopedic surgeon for a secondary examination. Results: The physical fitness test results were normally distributed. According to the mean value, skewness, and kurtosis, we found no difference between these results and the distribution nationwide. The secondary examination was required in 39 (6.9%) children. A histogram of the physical fitness test results and the number of children requiring a secondary examination revealed no normal distribution, showing polarization between the peaks of the higher and lower parts of the physical fitness test results. Conclusions: Those with low physical fitness test results and impaired locomotor health may be affected by obesity, and those with high physical fitness test results and impaired locomotor health may be musculoskeletal overused. Therefore, it is necessary to consider appropriate interventions in the future
リファキシミンとルビプロストンの併用は脂肪性肝炎ラットの腸管バリア機能を修復し肝線維化を抑制する
Get PDFBackground: Although gut-derived lipopolysaccharide (LPS) affects the progression of non-alcoholic steatohepatitis (NASH) pathogenesis, few studies have focused on this relationship to develop treatments for NASH. Aims: To explore the effects of combination with rifaximin and lubiprostone on NASH liver fibrosis through the modulation of gut barrier function. Methods: To induce steatohepatitis, F344 rats were fed a choline-deficient l -amino acid-defined (CDAA) diet for 12 weeks and received oral administration of rifaximin and/or lubiprostone. Histological, molec- ular, and fecal microbial analyses were performed. Barrier function in Caco-2 cells were assessed by in vitro assays. Results: Combination rifaximin/lubiprostone treatment significantly suppressed macrophage expansion, proinflammatory responses, and liver fibrosis in CDAA-fed rats by blocking hepatic translocation of LPS and activation of toll-like receptor 4 signaling. Rifaximin and lubiprostone improved intestinal perme- ability via restoring tight junction proteins (TJPs) with the intestinal activation of pregnane X receptor and chloride channel-2, respectively. Moreover, this combination increased the abundance of Bacteroides, Lactobacillus, and Faecalibacterium as well as decreased that of Veillonella resulting in an increase of fecal short-chain fatty acids and a decrease of intestinal sialidase activity. Both agents also directly suppressed the LPS-induced barrier dysfunction and depletion of TJPs in Caco-2 cells. Conclusion: The combination of rifaximin and lubiprostone may provide a novel strategy for treating NASH-related fibrosis.博士（医学）・甲第860号・令和5年3月15
酢酸亜鉛とリファキシミンの併用療法による腸管バリアー機能維持によるエタノール誘発性肝線維化予防効果
Get PDFBACKGROUND
Hepatic overload of gut-derived lipopolysaccharide dictates the progression of
alcoholic liver disease (ALD) by inducing oxidative stress and activating Kupffer
cells and hepatic stellate cells through toll-like receptor 4 signaling. Therefore,
targeting the maintenance of intestinal barrier integrity has attracted attention for
the treatment of ALD. Zinc acetate and rifaximin, which is a nonabsorbable
antibiotic, had been clinically used for patients with cirrhosis, particularly those
with hepatic encephalopathy, and had been known to improve intestinal barrier
dysfunction. However, only few studies focused on their efficacies in preventing
the ALD-related fibrosis development.
AIM
To investigate the effects of a combined zinc acetate with rifaximin on liver
fibrosis in a mouse ALD model.
METHODS
To induce ALD-related liver fibrosis, female C57BL/6J mice were fed a 2.5% (v/v)
ethanol-containing Lieber-DeCarli liquid diet and received intraperitoneal carbon
tetrachloride (CCl4) injection twice weekly (1 mL/kg) for 8 wk. Zinc acetate (100
mg/L) and/or rifaximin (100 mg/L) were orally administered during experimental
period. Hepatic steatosis, inflammation and fibrosis as well as intestinal
barrier function were evaluated by histological and molecular analyses. Moreover,
the direct effects of both agents on Caco-2 barrier function were assessed by in
vitro assays.RESULTSIn the ethanol plus CCl4-treated mice, combination of zinc acetate and rifaximin
attenuated oxidative lipid peroxidation with downregulation of Nox2 and Nox4.
This combination significantly inhibited the Kupffer cells expansion and the
proinflammatory response with blunted hepatic exposure of lipopolysaccharide
and the toll-like receptor 4/nuclear factor kB pathway. Consequently, liver
fibrosis and hepatic stellate cells activation were efficiently suppressed with
downregulation of Mmp-2, -9, -13, and Timp1. Both agents improved the atrophic
changes and permeability in the ileum, with restoration of tight junction proteins
(TJPs) by decreasing the expressions of tumor necrosis factor α and myosin light
chain kinase. In the in vitro assay, both agents directly reinforced ethanol or
lipopolysaccharide-stimulated paracellular permeability and upregulated TJPs in
Caco-2 cells.
CONCLUSION
Dual therapy with zinc acetate and rifaximin may serve as a strategy to prevent
ALD-related fibrosis by maintaining intestinal barrier integrity.博士（医学）・甲第862号・令和5年3月15日©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial
交通外傷における救急隊の現場滞在時間に関連する要因とその地域差についての検討
Get PDFBackground: The outcome of road traffic injury (RTI) is determined by duration of prehospital time, patient’s demographics,
and the type of injury and its mechanism. During the emergency medical service (EMS) prehospital time
interval, on-scene time should be minimized for early treatment. This study aimed to examine the factors influencing
on-scene EMS time among RTI patients.
Methods: We evaluated 19,141 cases of traffic trauma recorded between April 2014 and March 2020 in the EMS
database of the Nara Wide Area Fire Department and the prehospital database of the emergency Medical Alliance
for Total Coordination of Healthcare (e-MATCH). To examine the association of the number of EMS phone calls until
hospital acceptance, age ≥65 years, high-risk injury, vital signs, holiday, and nighttime (0:00–8:00) with on-scene time,
a generalized linear mixed model with random effects for four study regions was conducted.
Results: EMS phone calls were the biggest factor, accounting for 5.69 minutes per call, and high-risk injury
accounted for an additional 2.78 minutes. Holiday, nighttime, and age ≥65 years were also associated with increased
on-scene time, but there were no significant vital sign variables for on-scene time, except for the level of consciousness.
Regional differences were also noted based on random effects, with a maximum difference of 2 minutes among
regions.
Conclusions: The number of EMS phone calls until hospital acceptance was the most significant influencing factor
in reducing on-scene time, and high-risk injury accounted for up to an additional 2.78 minutes. Considering these factors,
including regional differences, can help improve the regional EMS policies and outcomes of RTI patients.博士（医学）・甲第880号・令和5年3月15日© The Author(s) 2022.
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data
急性呼吸促迫症候群の病態におけるヒストン修飾酵素Setdb2の重要な役割
Get PDFIntroduction: Acute respiratory distress syndrome (ARDS) is a severe hypoxemic respiratory failure with a high in-hospital mortality. However, themolecular mechanisms underlying ARDS remain unclear. Recent findings have indicated that the onset of severe inflammatory diseases, such as sepsis, is regulated by epigenetic changes. We investigated the role of epigenetic changes in ARDS pathogenesis using mouse models and human samples. Methods: Acute respiratory distress syndrome was induced in a mouse model (C57BL/6 mice, myeloid cell or vascular endothelial cell [VEC]–specific SET domain bifurcated 2 [Setdb2]–deficient mice [Setdb2ffLyz2Cre+ or Setdb2ffTie2Cre+], and Cre− littermates) by intratracheal administration of lipopolysaccharide (LPS). Analyses were performed at 6 and 72 h after LPS administration. Sera and lung autopsy specimens from ARDS patients were examined. Results: In the murine ARDS model, we observed high expression of the histone modification enzyme SET domain bifurcated 2 (Setdb2) in the lungs. In situ hybridization examination of the lungs revealed Setdb2 expression in macrophages and VECs. The histological score and albumin level of bronchoalveolar lavage fluid were significantly increased in Setdb2ffTie2Cre+ mice following LPS administration compared with Setdb2ffTie2Cre- mice, whereas there was no significant difference between the control and Setdb2ffLyz2Cre+ mice. Apoptosis of VECs was enhanced in Setdb2ffTie2Cre+ mice. Among the 84 apoptosis-related genes, the expression of TNF receptor superfamily member 10b (Tnfrsf10b) was significantly higher in Setdb2ffTie2Cre+ mice than in control mice. Acute respiratory distress syndrome
patients' serum showed higher SETDB2 levels than those of healthy volunteers. SETDB2 levels were negatively correlated with the partial pressure of oxygen in arterial blood/fraction of inspiratory oxygen concentration ratio. Conclusion: Acute respiratory distress syndrome elevates Setdb2, apoptosis of VECs, and vascular permeability. Elevation of histone methyltransferase Setdb2 suggests the possibility to histone change and epigenetic modification. Thus, Setdb2 may be a novel therapeutic target for controlling the pathogenesis of ARDS.権利情報：© 2023 The Author(s). Published byWolters Kluwer Health, Inc. on behalf of the American College of Sports Medicine. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal
GRK2を血管平滑筋で過剰発現させることで過度な血圧上昇ひいてはCS1急性心不全様の病態を呈した
Get PDFClinical scenario 1 (CS1) is acute heart failure (HF) characterized by transient systolic blood pressure (SBP) elevation and pulmonary congestion. Although it is managed by vasodilators, the molecular mechanism remains unclear. The sympathetic nervous system plays a key role in HF, and desensitization of cardiac β-adrenergic receptor (AR) signaling due to G protein-coupled receptor kinase 2 (GRK2) upregulation is known. However, vascular β-AR signaling that regulates cardiac afterload remains unelucidated in HF. We hypothesized that upregulation of vascular GRK2 leads to pathological conditions similar to CS1. GRK2 was overexpressed in vascular smooth muscle (VSM) of normal adult male mice by peritoneally injected adeno-associated viral vectors driven by the myosin heavy chain 11 promoter. Upregulation of GRK2 in VSM of GRK2 overexpressing mice augmented the absolute increase in SBP (+ 22.5 ± 4.3 mmHg vs. + 36.0 ± 4.0 mmHg, P < 0.01) and lung wet weight (4.28 ± 0.05 mg/g vs. 4.76 ± 0.15 mg/g, P < 0.01) by epinephrine as compared to those in control mice. Additionally, the expression of brain natriuretic peptide mRNA was doubled in GRK2 overexpressing mice as compared to that in control mice (P < 0.05). These findings were similar to CS1. GRK2 overexpression in VSM may cause inappropriate hypertension and HF, as in CS1.権利情報：© The Author(s) 2023. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The version of record of this article, first published in Scientific Reports, is available online at Publisher’s website: https://doi.org/10.1038/s41598-023-34209-
慢性閉塞性肺疾患患者における血清フリーラジカル消去活性能の評価
Get PDFBackground: Oxidative stress is an important mechanism for the development and progression of chronic obstructive pulmonary disease (COPD). It may also contribute to systemic manifestation in patients with COPD. Reactive oxygen species (ROS) including free radicals play a crucial role in oxidative stress in COPD. The aims of this study were to determine serum scavenging capacity profile against multiple free radicals and to evaluate its correlation with pathophysiology, exacerbations, and prognosis in patients with COPD.
Methods: Serum scavenging capacity profile against multiple free radicals comprising hydroxyl radical (•OH), superoxide radical (O2−•), alkoxy radical (RO•), methyl radical (•CH3), alkylperoxyl radical (ROO•), and singlet oxygen (1O2) was assessed using the multiple free-radical scavenging method in 37 patients with COPD (mean age, 71 years; mean forced expiratory volume in 1 s, 55.2% predicted). The severity of emphysema was evaluated by Goddard classification on chest computed tomography. Exacerbations were recorded prospectively for 1 year and the overall mortality was assessed 5 years after the initial assessment.
Results: •OH scavenging capacity was significantly decreased (p < 0.05) and O2−• and •CH3 scavenging capacity tended to decrease in patients with COPD compared to that in healthy controls. On the other hand, ROO• scavenging capacity tended to increase. In addition, RO• scavenging capacity was associated with severity of emphysema (p < 0.05) and exacerbation frequency (p < 0.02). There was a difference in the profile of the scavenging capacity between survived and deceased patients with COPD for 5 years after initial assessment.
Conclusion: Characteristic profile of free radical scavenging capacity can provide insight into the pathophysiology and prognosis of patients with COPD.権利情報：© 2023 Sakaguchi et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php)
脳皮質静脈梗塞ラットモデルを用いた脳静脈虚血におけるプラバスタチンの神経保護効果
Get PDFObjectives: Pravastatin sodium is reported to have multiple beneficial effects in cerebral atherosclerosis and neuronal injury; however, the preventive effects on cerebral venous ischemia are still unknown. Herein, we aimed to examine the neuroprotective effects of transoral prior administration of pravastatin sodium against cerebral cortical venous ischemia with suppression of apoptosis.
Methods: Thirty 8-week-old male Wistar rats were divided equally into two study groups (n = 15 vs. n = 15); the pravastatin group was fed 1% pravastatin sodium with their usual diet for 2 weeks, while the control group only received the usual diet. Two-vein occlusion (2VO) model was applied for this study, and two adjacent cortical veins in each animal were permanently occluded photochemically with rose bengal dye. During photothrombosis, regional changes of the cerebral blood flow (CBF) in area of the venous ischemia were recorded. At 48-h after 2VO, animals were euthanized using perfusion fixation, and we histologically measured ratios of infarcted area to contralateral hemisphere, and counted Bax- and Bcl-2-positive cells in the penumbra to investigate the implications for apoptosis.
Results: The ratio of infarcted area was significantly decreased in the pravastatin group compared to the control group (P < 0.01). The number of Bax-positive cells also decreased significantly in the pravastatin group (P < 0.01). In contrast, immunolabeling for Bcl-2 was essentially negative in all areas in both groups. There were also no significant differences in regional CBF changes after 2VO between the two groups (P = 0.13).
Conclusions: Pre-emptive administration of pravastatin sodium mixed in the food has neuroprotective effects against cerebral cortical venous ischemia with suppression of apoptosis associated with inhibition of Bax expression but has little influence on regional CBF.権利情報：© 2023 The Authors. Published by Elsevier Ltd on behalf of International Brain Research Organization. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)