Outcomes of Damage Control Surgery for Abdominal Trauma Evaluated Using the Trauma and Injury Severity Score and Lethal Triad in a Single Institution

In trauma management, damage control surgery is an effective approach to decrease the incidence of preventable trauma death. In this study, we aimed to investigate the survival outcomes and clinical factors in patients undergoing damage control surgery for severe abdominal trauma, in relation to trauma severity based on the trauma and injury severity score and lethal triad (hypothermia, metabolic acidosis, and coagulopathy), to assess the indicators of mortality and criteria for performing damage control surgery. Fifteen patients with severe abdominal trauma underwent damage control surgery from January 2011 to September 2017. We compared the short-term outcomes and perioperative factors associated with the trauma and injury severity score and the lethal triad between survivors and non-survivors. Of the 15 included patients, eight (53.3%) survived and seven (46.7%) died. No preventable deaths occurred. The patient characteristics, including age, sex, and mechanism of injury were not related to survival. The injury severity score (p = 0.035) and abbreviated injury scale score of the head (p = 0.005) were significantly higher among the nonsurvivors than among the survivors. Of the lethal triad, the incidence of metabolic acidosis was significantly higher in the non-survivors (p < 0.050). This study found that head injury and metabolic acidosis are predictors of mortality. These indications provide a practical basis for determining whether to use damage control surgery and postoperative management

RANKL expression in chondrocytes and its promotion by lymphotoxin-alpha in the course of cartilage destruction during rheumatoid arthritis

We investigated the expression and localization of the receptor activator nuclear factor kappa B ligand (RANKL) in cartilage from patients with rheumatoid arthritis (RA) of relevance to cartilage degeneration. We also examined the role of exogenous lymphotoxin (LT)-alpha on RANKL expression in human chondrocytes and its effect on in vitro osteoclast differentiation. Cartilage and synovial fluid samples were obtained from 45 patients undergoing total joint replacement surgery or joint puncture, including 24 patients with osteoarthritis (OA) and 21 patients with RA. RANKL expression in articular cartilage was examined by immunohistochemistry. LT-alpha concentrations in synovial fluid were measured using an enzyme-linked immunosorbent assay (ELISA). Normal human chondrocytes were stimulated with LT-alpha, and the relative mRNA levels of RANKL, osteoprotegerin (OPG), matrix metalloproteinase-9, and vascular endothelial growth factor were examined by real-time polymerase chain reaction. Soluble RANKL protein in culture media was measured using ELISA, and membrane-bound RANKL protein in cells was examined by western blotting. Co-cultures of human chondrocytes with peripheral blood mononuclear cells (PBMCs) were stimulated with macrophage-colony stimulating factor and LT-alpha, and osteoclast differentiation was evaluated by staining for tartrate-resistant acid phosphatase. LT-alpha concentrations were higher in RA synovial fluid than in OA samples. The population of RANKL-positive chondrocytes of RA cartilage was higher than that of OA cartilage, and correlated with cartilage degeneration. Stimulation of cultured human chondrocytes by LT-alpha increased RANKL expression, the RANKL/OPG ratio, and angiogenic factors. Membrane-bound RANKL in chondrocytes was up-regulated after stimulation of LT-alpha, whereas soluble RANKL in culture medium did not increase. Co-cultures of human chondrocytes and PBMCs demonstrated that LT-alpha stimulated human chondrocytes to produce RANKL and induced osteoclastic differentiation of PBMCs. RANKL produced by chondrocytes may contribute to cartilage destruction during RA and LT-alpha could promote the expression of RANKL in human chondrocytes

A Novel Radiographic Measurement Method for the Evaluation of Metatarsophalangeal Joint Dislocation of the Lesser Toe in Patients with Rheumatoid Arthritis

Dorsal dislocation of metatarsophalangeal (MTP) joints of the lesser toe frequently occurs in patients with rheumatoid arthritis (RA), and may cause painful and uncomfortable plantar callosities and ulceration. The current study examined the reliability and clinical relevance of a novel radiographic parameter (the MTP overlap distance [MOD]) in evaluating the severity of MTP joint dislocation. The subjects of the current study were 147 RA patients (276 feet; 1104 toes). MOD, defined as the overlap distance of the metatarsal head and the proximal end of the phalanx, was measured on plain radiographs. The relationship between the MOD and clinical complaints (forefoot pain and/or callosity formation) was analyzed to create a severity grading system. As a result, toes with callosities had a significantly larger MOD. ROC analysis revealed that the MOD had a high AUC for predicting an asymptomatic foot (-0.70) and callosities (0.89). MOD grades were defined as follows: grade 1, 0 = 10 mm. The intra- and inter-observer reliability of the MOD grade had high reproducibility. Furthermore, the MOD and MOD grade improved significantly after joint-preserving surgeries for lesser toe deformities. Our results suggest that MOD and MOD grade might be useful tools for the evaluation of deformities of the lesser toe and the effect of surgical intervention for MTP joints in patients with RA

Light activates the adrenal gland: Timing of gene expression and glucocorticoid release

SummaryLight is a powerful synchronizer of the circadian rhythms, and bright light therapy is known to improve metabolic and hormonal status of circadian rhythm sleep disorders, although its mechanism is poorly understood. In the present study, we revealed that light induces gene expression in the adrenal gland via the suprachiasmatic nucleus (SCN)-sympathetic nervous system. Moreover, this gene expression accompanies the surge of plasma and brain corticosterone levels without accompanying activation of the hypothalamo-adenohypophysial axis. The abolishment after SCN lesioning, and the day-night difference of light-induced adrenal gene expression and corticosterone release, clearly indicate that this phenomenon is closely linked to the circadian clock. The magnitude of corticostereone response is dose dependently correlated with the light intensity. The light-induced clock-dependent secretion of glucocorticoids adjusts cellular metabolisms to the new light-on environment

Adipose-Derived Extract Suppresses IL-1 beta-Induced Inflammatory Signaling Pathways in Human Chondrocytes and Ameliorates the Cartilage Destruction of Experimental Osteoarthritis in Rats

We investigated the effects of adipose-derived extract (AE) on cultured chondrocytes and in vivo cartilage destruction. AE was prepared from human adipose tissues using a nonenzymatic approach. Cultured human chondrocytes were stimulated with interleukin-1 beta (IL-1 beta) with or without different concentrations of AE. The effects of co-treatment with AE on intracellular signaling pathways and their downstream gene and protein expressions were examined using real-time PCR, Western blotting, and immunofluorescence staining. Rat AE prepared from inguinal adipose tissues was intra-articularly delivered to the knee joints of rats with experimental osteoarthritis (OA), and the effect of AE on cartilage destruction was evaluated histologically. In vitro, co-treatment with IL-1 beta combined with AE reduced activation of the p38 and ERK mitogen-activated protein kinase (MAPK) pathway and nuclear translocation of the p65 subunit of nuclear factor-kappa B (NF-kappa B), and subsequently downregulated the expressions of matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, IL-6, and IL-8, whereas it markedly upregulated the expression of IL-1 receptor type 2 (IL-1R2) in chondrocytes. Intra-articular injection of homologous AE significantly ameliorated cartilage destruction six weeks postoperatively in the rat OA model. These results suggested that AE may exert a chondroprotective effect, at least in part, through modulation of the IL-1 beta-induced inflammatory signaling pathway by upregulation of IL-1R2 expression

Research on Pupils' Progress of Mathematical Ability at Lower Secondary School Level (4) : Considering the "Number" of Test Points

Kassel-Exeter Projectによって開発された共通問題を用いて, 日本の中学生の数学的能力の発達・変容を調査し, その検討を通して, よりよい数学教育に向けての示唆を得ることが本研究の目的である。「数」調査問題をもとに1019名の公立中学校2, 3年生を対象とする調査を行ったところ, 日本の中学生の「数」得点は1年次からすでに高いレベルにあり, そのレベルを維持したままで, イギリス・ドイツなどと比して遜色のない程度の伸びを示していることがわかった。さらに, 問題ごとの正答率の変容に着目すると同時に, 被験者を3つの群に層化することによって, 正答率の変容の要因を分析した。その結果, 数学学習に対する「潜在力」の高い生徒および「潜在力」の低い生徒の「数」得点の変容に関する特徴が洗い出され, 個に応じた数学指導を考慮していく際の示唆が得られた。, The authors administered the "number" of test composed of 50 problems developed by Kassel-Exeter Project to students in Tokyo, Nara, Hiroshima, Fukuoka and Nagasaki prefectures a year earlier to identify the students' progress in mathematical ability at lower secondary school level. Analysis of the test shows that Japanese students' progress is almost comparable with the students from other countries like England and Germany, which can be attributed to the effective teaching of Mathematics.Aside from the overall analysis of the test scores, a longitudinal analysis of each problem was made. The analysis showed that Japanese pupils made remarkable progress in many problems but they showed corresponding regression on estimation of problems. Based on their points in a "potential" test, students were grouped as potentially high (PH), potentailly medium (PM) or potentially low (PL). PH students exhibited high points in comparatively difficult problem items while PL students' showed progress in comparatively easy problem items. The observed regression could be attributed to the same kind of problem items. Important implications for the improvement of the teaching of Mathematics were identified

MicroRNA-125b regulates the expression of aggrecanase-1 (ADAMTS-4) in human osteoarthritic chondrocytes

INTRODUCTION: Increased expression of aggrecanase-1 (ADAMTS-4) has emerged as an important factor in osteoarthritis (OA) and other joint diseases. This study aimed to determine whether the expression of ADAMTS-4 in human chondrocytes is regulated by miRNA. METHODS: MiRNA targets were identified using bioinformatics. Chondrocytes were isolated from knee cartilage and treated with interleukin-1 beta (IL-1β). Gene expression was quantified using TaqMan assays and protein production was determined by immunoblotting. Luciferase reporter assay was used to verify interaction between miRNA and target messenger RNA (mRNA). RESULTS: In silico analysis predicted putative target sequence of miR-125b on ADAMTS-4. MiR-125b was expressed in both normal and OA chondrocytes, with significantly lower expression in OA chondrocytes than in normal chondrocytes. Furthermore, IL-1β-induced upregulation of ADAMTS-4 was suppressed by overexpression of miR-125b in human OA chondrocytes. In the luciferase reporter assay, mutation of the putative miR-125b binding site in the ADAMTS-4 3'UTR abrogated the suppressive effect of miR125. CONCLUSIONS: Our results indicate that miR-125b plays an important role in regulating the expression of ADAMTS-4 in human chondrocytes and this identifies miR-125b as a novel therapeutic target in OA