Distant skeletal muscle metastasis from intrahepatic cholangiocarcinoma presenting as Budd-Chiari syndrome

Intrahepatic cholangiocarcinoma is a malignant neoplasm arising from the biliary epithelium, which frequently invades adjacent organs or metastasizes to other visceral organs such as the lungs, bones, adrenals, and brain. However, distant skeletal muscle metastasis of cholangiocarcinoma has never been described before to the best of our knowledge and, furthermore, Budd-Chiari syndrome secondary to intrahepatic cholangiocarcinoma is also extremely rare. Here we present the first case overall of distant muscle metastasis from intrahepatic cholangiocarcinoma presenting as Budd-Chiari syndrome. A 44-year-old man admitted to the hospital with complaints of abdominal distension, edema of both legs, back pain and anorexia of 30 d' duration. Computed tomography and ultrasonography-guided percutaneous muscle biopsy established intrahepatic cholangiocarcinoma with disseminated thrombosis from inferior vena cava to bilateral iliac and femoral veins, and multiple skeletal muscle metastases in bilateral buttock and erector spinal muscle.     

Isolated facial myorhythmia

Myorhythmia, characterized by relatively rhythmic and regular 1- to 3-Hz muscle contractions, may involve isolated limbs or in combination with other various body regions. Isolated facial myorhythmia is rare. We highlight the clinical and electrophysiologic features of a unique case of isolated facial myorhythmia. Extensive investigations did not reveal any conclusive secondary causes. Dopaminergic dysfunction could be one of the etio-pathologic factors. However, the pathological basis why the facial region was selectively involved in our patient is unclear. Early recognition of the symptoms and signs would facilitate investigations for an underlying cause.     

预适应对肢体缺血再灌注后骨骼肌细胞凋亡的影响

目的观察大鼠肢体缺血再灌注（LIR）后骨骼肌细胞的凋亡情况及缺血顸适应（IPC）对其影响。方法实验用雄性Wistar大鼠24只,随机分为对照（Control）组、缺血再灌注（IR）组和缺血预适应（IPC＋IR）组,每组8只。分别测定血浆乳酸脱氢酶（LDH）、肌酸激酶（CK）、活性氧（ROS）、丙二醛（MDA）的含量;观察骨骼肌组织中谷胱甘肽过氧化物酶（GSH-P。）、还原型谷胱甘肽（GSH）、Ca^2＋、Na^＋-KtATP酶、Ca^2＋-Mg^2＋-ATP酶的含量变化及Caspase-3和骨骼肌凋亡指数（AI）。结果IPC＋IR组较IR组,血浆LDH、CK、ROS、MDA及骨骼肌组织中Ca^2＋含量下降,骨骼肌组织中GSH-Px、GSH、Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶水平升高,Caspase-3及骨骼肌AI下降。结论IPC可能通过减少自由基生成和提高自由基清除酶的活性、降低钙超载、抑制骨骼肌Caspase-3蛋白的表达,从而抑制大鼠LIR后骨骼肌细胞凋亡。     

高压氧结合中西医治疗脑梗塞肢体肌力障碍的疗效观察

目的探讨高压氧结合中西医治疗急性脑梗塞肢体肌力障碍的疗效。方法85例临床确诊的脑梗塞患者,随机分为治疗组和对照组。对照组45例,采用单纯中西医综合治疗。治疗组40例,在中西医综合治疗的同时进行高压氧治疗。分别于治疗前、后观察患者肢体肌力改变,14日为1个疗程,治疗2个疗程后判定临床疗效。结果治疗组治愈4例,显效24例,有效9例,无效3例,总有效率为92．50％。对照组治愈2例,显效17例,有效15例,无效11例,总有效率为75．56％。结论采用高压氧结合中西医综合治疗急性脑梗塞,可有效地缓解症状,减少肢体后遗症,改善患者生存质量。     

液压扩张联合手法松解治疗粘连性肩关节囊炎的疗效观察

目的探讨液压扩张联合手法松解治疗粘连性肩关节囊炎（冻结肩）的疗效。方法78例冻结肩患者随机分为三组,单纯手法松解组28例行臂丛神经阻滞麻醉下手法松解,手法松解＋透明质酸钠组23例行手法松解后患侧肩关节腔内注射透明质酸钠,手法松解＋液压扩张组27例行手法松解后G臂机引导下患侧肩关节穿刺0．9％氯化钠注射液液压扩张。比较三组患者治疗前后及治疗6个月后随访评分、有效率、疼痛与肩功能评分情况。结果三组患者治疗后肩关节评分、疼痛缓解情况等与治疗前比较,差异均有统计学意义（均P〈0．05）;手法松解＋液压扩张组治疗有效率（92．6％）均优于单纯手法松解组（78．6％）和手法松解＋透明质酸钠组（82．6％）（均P〈0．05）,三组治疗后肩关节功能评分（83．6、71．8、74．5）之间差异无统计学意义（P〉0．05）,未发生严重并发症。结论臂丛神经阻滞麻醉下手法松解联合液压扩张治疗冻结肩有效、安全。     

Strength-Training Exercise in Dysphagia Rehabilitation: Principles,Procedures, and Directions for Future Research

Dysphagia rehabilitation, historically, has focused a great deal on various compensations during swallowing to prevent aspiration and/or improve safety and efficiency. Exercise, in general, has been a part of the dysphagia rehabilitation landscape. However, heightened discussions in the field regarding best practices for exercise training, particularly strengthening, raise more questions than answers. The intent of this paper is to (1) explore the overriding principles of neuromuscular plasticity with regard to strength training, (2) evaluate how current exercise-training interventions in dysphagia rehabilitation correspond to these principles, and (3) postulate directions for future study of normal and disordered swallowing and determine how to incorporate these principles into dysphagia rehabilitation.     

Dilinoleoyl-phosphatidic acid mediates reduced IRS-1 tyrosine phosphorylation in rat skeletal muscle cells and mouse muscle

Aims/hypothesis Insulin resistance in skeletal muscle is strongly associated with lipid oversupply, but the intracellular metabolites and underlying mechanisms are unclear. We therefore sought to identify the lipid intermediates through which the common unsaturated fatty acid linoleate causes defects in IRS-1 signalling in L6 myotubes and mouse skeletal muscle. Materials and methods Cells were pre-treated with 1 mmol/l linoleate for 24 h. Subsequent insulin-stimulated IRS-1 tyrosine phosphorylation and its association with the p85 subunit of phosphatidylinositol 3-kinase were determined by immunoblotting. Intracellular lipid species and protein kinase C activation were modulated by overexpression of diacylglycerol kinase ɛ, which preferentially converts unsaturated diacylglycerol into phosphatidic acid, or by inhibition of lysophosphatidic acid acyl transferase with lisofylline, which reduces phosphatidic acid synthesis. Phosphatidic acid species in linoleate-treated cells or muscle from insulin-resistant mice fed a safflower oil-based high-fat diet that was rich in linoleate were analysed by mass spectrometry. Results Linoleate pretreatment reduced IRS-1 tyrosine phosphorylation and p85 association. Overexpression of diacylglycerol kinase ɛ reversed the activation of protein kinase C isoforms by linoleate, but paradoxically further diminished IRS-1 tyrosine phosphorylation. Conversely, lisofylline treatment restored IRS-1 phosphorylation. Mass spectrometry indicated that the dilinoleoyl-phosphatidic acid content increased from undetectable levels to almost 20% of total phosphatidic acid in L6 cells and to 8% of total in the muscle of mice fed a high-fat diet. Micelles containing dilinoleoyl-phosphatidic acid specifically inhibited IRS-1 tyrosine phosphorylation and glycogen synthesis in L6 cells. Conclusions/interpretation These data indicate that linoleate-derived phosphatidic acid is a novel lipid species that contributes independently of protein kinase C to IRS-1 signalling defects in muscle cells in response to lipid oversupply. Electronic supplementary material The online version of this article (doi: ) contains supplementary material, which is available to authorised users.     

Progesterone impairs cell respiration and suppresses a compensatory increase in glucose transport in isolated rat skeletal muscle: a non-genomic mechanism contributing to metabolic adaptation to late pregnancy?

Aims/hypothesis The aim of the study was to gain better insight into the mechanisms responsible for impaired glucose metabolism during late pregnancy. We explored the direct effects of progesterone on glucose metabolism of skeletal muscle. Methods Specimens of skeletal muscle from untreated rats were incubated with progesterone and rates of substrate fluxes through the various pathways of glucose metabolism were analysed. Results Progesterone dose-dependently reduced the rates of glucose and pyruvate oxidation (insulin-stimulated rates after 5 h of exposure to 1 and 10 μmol/l progesterone: glucose oxidation, −6 ± 4%, NS, and −39 ± 4%, p < 0.001; pyruvate oxidation, −28 ± 2% and −55 ± 4%, p < 0.001 each) and increased lactate release (+28 ± 4% and +58 ± 9%, p < 0.005 each), which indicated inhibition of mitochondrial respiratory function. Impairment of cell respiration, e.g. by the specific inhibitor rotenone, is known to trigger a compensatory increase in glucose transport, but this response was blunted in the case of progesterone (change of glucose transport in response to 10 μmol/l progesterone vs 60 nmol/l rotenone, both causing a reduction in glucose oxidation by −39%: progesterone, +14 ± 8% vs rotenone, +84 ± 23%, p < 0.03). Further experiments dealt with the underlying mechanisms and revealed a rapid mode of action (50 μmol/l progesterone, reduction in insulin-stimulated glucose oxidation after 30 min: −29 ± 7%, p < 0.01) not affected by blockers of gene expression or the nuclear progesterone receptor. Conclusions/interpretation Progesterone inhibits cell respiration and at the same time suppresses a compensatory increase in glucose transport, causing cellular carbohydrate deficiency in isolated rat skeletal muscle. This effect is mediated by a direct, rapid and non-genomic mechanism and could contribute to pregnancy-associated changes in glucose homeostasis. Electronic supplementary material The online version of this article (doi: ) contains supplementary material, which is available to authorised users.     

Comparison of the effect of multiple short-duration with single long-duration exercise sessions on glucose homeostasis in type 2 diabetes mellitus

Aims/hypothesis We evaluated and compared the effects on glycaemic control of two different exercise protocols in elderly men with type 2 diabetes mellitus. Methods Eighteen patients with type 2 diabetes mellitus carried out home-based bicycle training for 5 weeks. Patients were randomly assigned to one of two training programmes at 60% of maximal oxygen uptake: three 10 min sessions per day (3 × 10) or one 30 min session per day (1 × 30). Plasma insulin, C-peptide and glucose concentrations were measured during a 3 h oral glucose tolerance test (OGTT). Insulin sensitivity index (ISI_composite), pre-hepatic insulin secretion rates (ISR) and change in insulin secretion per unit change in glucose concentrations (B_total) were calculated. Results Cardiorespiratory fitness increased in response to training in both groups. In group 3 × 10 (n = 9) fasting plasma glucose (p = 0.01), 120 min glucose OGTT (p = 0.04) and plasma glucose concentration areas under the curve at 120 min (p < 0.04) and 180 min (p = 0.07) decreased. These parameters remained unchanged in group 1 × 30 (n = 9). No significant changes were found in ISI_composite, ISR and B_total in either of the exercise groups. In a matched time-control group (n = 10), glycaemic control did not change. Conclusions/interpretation Moderate to high-intensity training performed at 3 × 10 min/day is preferable to 1 × 30 min/day with regard to effects on glycaemic control. This is in spite of the fact that cardiorespiratory fitness increased similarly in both exercise groups. A possible explanation is that the energy expenditure associated with multiple short daily sessions may be greater than that in a single daily session.