BACKGROUND & AIMS: :An understanding of the time course and correlation with injury of heat shock proteins (HSPs) released during brain and/or spinal cord cellular stress (ischemia) is critical in understanding the role of the HSPs in cellular survival, and may provide a clinically useful biomarker of severe cellular stress. We have analyzed the levels of HSPs in the cerebrospinal fluid (CSF) from patients who are undergoing thoracic aneurysm repair. Blood and CSF samples were collected at regular intervals, and CSF was analyzed by enzyme-linked immunosorbent assay for HSP70 and HSP27. These results were correlated with intraoperative somatosensory-evoked potentials measurements and postoperative paralysis. We find that the levels of these proteins in many patients are elevated and that the degree of elevation correlates with the risk of permanent paralysis. We hypothesize that sequential measurement intraoperatively of the levels of the heat shock proteins HSP70 and HSP27 in the CSF can predict those patients who are at greatest risk for paralysis during thoracic aneurysm surgery and will allow us to develop means of preventing or attenuating this severe and often fatal complication.

背景与目标： ：了解时间过程及其与脑和/或脊髓细胞应激（缺血）过程中释放的热休克蛋白（HSP）损伤的相关性对于了解HSP在细胞存活中的作用至关重要，并且可能提供临床上的帮助严重细胞应激的生物标志物。我们已经分析了正在接受胸动脉瘤修复的患者的脑脊液（CSF）中的HSPs水平。定期采集血液和脑脊液样本，并通过酶联免疫吸附法对脑脊液中的HSP70和HSP27进行分析。这些结果与术中体感诱发电位的测量和术后瘫痪有关。我们发现许多患者中这些蛋白质的水平升高，并且升高的程度与永久性麻痹的风险相关。我们假设在术中连续测量脑脊液中热休克蛋白HSP70和HSP27的水平可以预测那些在胸动脉瘤手术期间最有可能瘫痪的患者，这将使我们能够开发出预防或减轻这种严重且经常致命的并发症。

BACKGROUND & AIMS: :The purpose of this study was to examine whether selective iNOS inhibition can restore the hemodynamic changes and reduce the nitrotyrosine levels in the cerebral cortex of rats with streptozotocin-induced diabetes during endotoxin-induced shock. The study was designed to include three sets of experiments: (1) measurement of changes in systemic hemodynamics, (2) measurement of biochemical variables, including iNOS activity and nitrotyrosine formation in the brain, and (3) assessment of mortality rate. Rats were randomly divided into four groups: group 1, control; group 2, LPS: Escherichia coli endotoxin, 10.0 mg/kg (i.v.) bolus; group 3 (i.v.) LPS and L-N6-(1-iminoethyl)-lysine (L-NIL), 4mg/kg (i.p.); and group 4, LPS and NG-nitro-L-arginine methyl ester (L-NAME), 5 mg/kg (i.p.). In nondiabetic rats, administration of L-NIL prevented the hemodynamic and biochemical changes, and increases in plasma nitrite and cerebral nitrotyrosine levels induced by LPS. Administration of L-NAME partially prevented these LPS-induced changes. On the other hand, in diabetic rats, administration of L-NIL only partially prevented the hemodynamic and biochemical changes, and increases in plasma nitrite and cerebral nitrotyrosine levels associated with LPS. Administration of L-NAME, however, had no effects on these LPS-induced changes in diabetic rats. There was a significant difference in nitrotyrosine levels between nondiabetic and diabetic rats in groups 2, 3, and 4 at 2 and 3 h after the treatment (at 3 h; nondiabetic--control, 4.6 +/- 0.4; LPS (i.v.), 8.9 +/- 1.0, LPS (i.v.) + L-NIL, 4.7 +/- 0.5; LPS (i.v.) + L-NAME, 7.1 +/- 0.9; diabetic--control, 5.5 +/- 0.4; LPS (i.v.), 13.6 +/- 1.2; LPS (i.v.) + L-NIL, 9.0 +/- 0.9; LPS (i.v.) + L-NAME, 13.0 +/- 1.0; densitometric units). Insulin therapy resulted in a decrease in iNOS activity (at 3 h: 1.0 +/- 0.5 fmol mg min), nitrotyrosine formation (at 3 h; 5.0 +/- 0.5, densitometric units), and mortality rates (30% at 6 h, 50% at 12 h) in the LPS (i.v.) + L-NIL group of diabetic rats. Selective iNOS inhibition in diabetic rats could not improve hemodynamic instability, chemical changes, iNOS activity, and nitrotyrosine formation during septic shock compared with the improvements observed in nondiabetic rats. Tight glucose control along with administration of L-NIL can result in more effective restoration of the biochemical changes of septicemia in diabetic rats. Thus, hyperglycemia may be one of the mechanisms related to the aggravation of endotoxin-induced shock.

背景与目标： ：本研究的目的是研究选择性内源性iNOS抑制能否在内毒素诱导的休克期间恢复链脲佐菌素诱发的糖尿病大鼠的血流动力学变化并降低其大脑皮质的硝基酪氨酸水平。该研究设计为包括三组实验：（1）测量全身血流动力学的变化，（2）测量生化变量，包括iNOS活性和脑中硝基酪氨酸的形成，以及（3）死亡率评估。将大鼠随机分为四组：第1组，对照组；和第2组。第2组，LPS：大肠埃希菌内毒素，每次推注10.0 mg / kg（i.v.）；第3组（静脉）LPS和L-N6-（1-亚氨基乙基）-赖氨酸（L-NIL），4mg / kg（腹膜）;第4组，LPS和NG-硝基-L-精氨酸甲酯（L-NAME），5 mg / kg（腹膜内）。在非糖尿病大鼠中，L-NIL的给药阻止了血流动力学和生化变化，并增加了LPS诱导的血浆亚硝酸盐和脑硝基酪氨酸水平。 L-NAME的管理部分阻止了这些LPS引起的变化。另一方面，在糖尿病大鼠中，L-NIL的施用仅部分阻止了血流动力学和生化变化，并增加了与LPS相关的血浆亚硝酸盐和脑硝基酪氨酸水平。但是，在糖尿病大鼠中，L-NAME的给药对这些LPS诱导的变化没有影响。第2、3和4组的非糖尿病和糖尿病大鼠在治疗后2和3小时的硝酸酪氨酸水平存在显着差异（3小时;非糖尿病对照组为4.6 /-0.4; LPS（iv）为8.9） /-1.0，LPS（iv）L-NIL，4.7 /-0.5； LPS（iv）L-NAME，7.1 /-0.9；糖尿病对照，5.5 /-0.4； LPS（iv），13.6 /-1.2； LPS（iv）L-NIL，9.0 /-0.9； LPS（iv）L-NAME，13.0 /-1.0；光密度单位）。胰岛素治疗导致iNOS活性（3 h：1.0 /-0.5 fmol mg min），硝基酪氨酸形成（3 h; 5.0 /-0.5，光密度单位）和死亡率（6h，50时30％）降低LPS（iv）L-NIL组的糖尿病大鼠在12 h时的％）。与非糖尿病大鼠相比，对糖尿病大鼠的选择性iNOS抑制不能改善败血性休克期间的血流动力学不稳定，化学变化，iNOS活性和硝基酪氨酸形成。严格的葡萄糖控制以及L-NIL的使用可以使糖尿病大鼠败血病的生化变化更有效地恢复。因此，高血糖症可能是与内毒素诱发的休克加重有关的机制之一。

BACKGROUND & AIMS: PURPOSE OF REVIEW:The conventional view in severe sepsis or septic shock is that most of the lactate that accumulates in the circulation is due to cellular hypoxia and the onset of anaerobic glycolysis. A number of papers have suggested that lactate formation during sepsis is not due to hypoxia. I discuss this hypothesis and outline the recent advances in the understanding of lactate metabolism in shock. RECENT FINDINGS:Numerous experimental data have demonstrated that stimulation of aerobic glycolysis - that is, glycolysis not attributable to oxygen deficiency - and glycogenolysis occurs not only in resting, well-oxygenated skeletal muscles but also during experimental haemorrhagic shock and experimental sepsis, and is closely linked to stimulation of sarcolemmal Na+/K+ -ATPase under epinephrine stimulation. A human study of hyperkinetic septic shock demonstrated that skeletal muscle is a leading source of lactate production by exaggerated aerobic glycolysis through Na+/K+ -ATPase stimulation. SUMMARY:There is increasing evidence that sepsis is accompanied by a hypermetabolic state, with enhanced glycolysis and hyperlactataemia. This should not be rigorously interpreted as an indication of hypoxia. It now appears, at least in the hyperkinetic state, that increased lactate production and concentration as a result of hypoxia are often the exception rather than the rule.

背景与目标： 审查的目的：严重败血症或败血性休克的传统观点是，循环中积累的大多数乳酸是由于细胞缺氧和厌氧糖酵解的开始所致。许多论文表明败血症期间乳酸的形成不是由于缺氧引起的。我讨论了这一假设，并概述了休克中乳酸代谢的最新研究进展。
最近的发现：大量的实验数据表明，有氧糖酵解的刺激-即不是由于缺氧引起的糖酵解-糖原分解不仅发生在静息的，充氧的骨骼肌中，而且发生在实验性失血性休克和实验性败血症中，并且密切相关与肾上腺素刺激下肌膜Na / K -ATPase的刺激有关。一项针对运动过度性败血性休克的人体研究表明，骨骼肌是通过Na / K -ATPase刺激导致的过度有氧糖酵解产生乳酸的主要来源。
摘要：有越来越多的证据表明败血症伴有代谢亢进状态，并伴有糖酵解和高乳酸血症。不应将其严格解释为缺氧的征兆。现在看来，至少在运动亢进状态下，缺氧导致的乳酸产生和浓度增加通常是例外而不是规则。

BACKGROUND & AIMS: :For comparative examination of the pathological findings in burn shock and hemorrhagic shock, histological and immunohistochemical investigations of the lungs were performed. Histological specimens of 30 cases each were examined by means of immunohistological staining with P-selectin, von Willebrand factor (vWF) and PECAM-1. The results showed statistically significant differences between the two groups. There was strong staining for P-selectin (especially in the lumina of the blood vessels) and vWF (especially in the endothelium of medium-sized blood vessels) in the specimens of burn shock fatalities. In cases of rapid death after exposure to fire the strong expression of adhesion molecules, which are mainly responsible for the initial inflammatory reaction of leucocytes and platelets in burn shock, suggests prompt activation of inflammatory cells in the lung tissue. In cases of hemorrhagic shock, this reaction was much less distinct in the early stages. The same is true of the expression of PECAM-1, which was lower in lungs from burn shock fatalities than in those from hemorrhagic shock fatalities. The low expression of PECAM-1 in burn shock is a clue to the migration/diapedesis of leucocytes into the areas of burn damage. In total, the results of the investigation indicate different pathophysiological processes even in the very early stages of burn shock and hemorrhagic shock.

背景与目标： ：为了比较检查烧伤休克和出血性休克的病理结果，进行了肺的组织学和免疫组化研究。用P-选择蛋白，von Willebrand因子（vWF）和PECAM-1进行免疫组织染色，检查30例患者的组织学标本。结果显示两组之间在统计学上有显着差异。烧伤休克死亡标本中的P-选择蛋白（特别是在血管腔中）和vWF（特别是在中型血管内皮中）有很强的染色。在着火后迅速死亡的情况下，粘附分子的强表达主要是烧伤休克中白细胞和血小板的初始炎症反应，提示肺组织中的炎症细胞会迅速活化。在失血性休克的情况下，早期反应不明显。 PECAM-1的表达也是如此，其在烧伤性休克死亡中的肺低于在出血性休克死亡中的肺。 PECAM-1在烧伤休克中的低表达是白细胞向烧伤部位迁移/渗血的线索。总体而言，研究结果表明，即使在烧伤休克和失血性休克的早期，病理生理过程也不同。

BACKGROUND & AIMS: :A cDNA clone (Tgzy85d11.r1) obtained from the Toxoplasma Expressed Sequence Tag project was chosen due to its homology with proteins of the heat shock 90 family. The cDNA encodes 137 amino acids of the C-terminal portion of the Toxoplasma Hsp90 protein (TgHsp90). Serum samples obtained from orally infected BALB/c and C57BL/6 mice showed reactivity against a recombinant TgHsp90 (rTgHsp90) after 8 weeks postinfection. Isotype analysis showed an anti-rTgHsp90 IgG2a/IgG3 response in infected BALB/c and anti-rTgHsp90 IgG1/IgG2a/IgG2b response in infected C57BL/6 mice. Serum samples from individuals chronically and putative acutely infected with T. gondii showed a similar anti-rTgHsp90 IgG response. Our work identifies TgHsp90 as a novel parasite antigen that seems to elicit a higher relation of anti-TgHsp90/anti-T. gondii IgGs during chronic infection in comparison with the acute stage.

背景与目标： ：选择从弓形虫表达序列标签项目获得的cDNA克隆（Tgzy85d11.r1），因为它与热休克90家族蛋白同源。 cDNA编码弓形虫Hsp90蛋白（TgHsp90）C端部分的137个氨基酸。从口腔感染的BALB / c和C57BL / 6小鼠获得的血清样品在感染后8周后显示出对重组TgHsp90（rTgHsp90）的反应性。同型分析表明，在感染的BALB / c中存在抗rTgHsp90 IgG2a / IgG3反应，在感染的C57BL / 6小鼠中具有抗rTgHsp90 IgG1 / IgG2a / IgG2b反应。弓形虫被慢性和假定急性感染的个体的血清样品显示出相似的抗rTgHsp90 IgG反应。我们的工作将TgHsp90鉴定为一种新型的寄生虫抗原，似乎引起了更高的抗TgHsp90 / anti-T关系。与急性期相比，在慢性感染期间感染了刚地IgG。

BACKGROUND & AIMS: :Sepsis and its sequelae of multiple organ failure is one of the leading causes of death in the industrial countries. Several studies have shown that patients who are treated with low-dose acetyl salicylic acid (ASA) for secondary prevention of atherothrombosis may have a lower risk to develop organ failure in the case of critical illness. The benefit of ASA is probably due to an inhibition of platelet activation as well as an increase in the formation of anti-inflammatory lipoxin A4. On the other hand, the effect of ASA could be - at least partially - an indirect one, caused by atherosclerotic vascular diseases as the cause of ASA treatment. Atherosclerosis is considered as a moderate systemic inflammation and we hypothesise that this chronic condition could have an impact on the outcome in sepsis. To get more information on the benefit of ASA in critically ill patients and on possible interference with atherosclerotic vascular diseases, we analysed the medical records of 886 septic patients who were admitted to the surgical intensive care unit (ICU) of a university hospital. Logistic regression analysis indicated that patients who were treated during the ICU stay with ASA (100 mg/d) had a significantly lower mortality. Odds ratios (ORs; with 95% confidential intervals) of 0.56 (0.37-0.84) and 0.57 (0.39-0.83) were calculated for ICU and hospital mortality, respectively. In contrast, statin treatment did not have significant effect on mortality. Diagnosis of atherosclerotic vascular diseases according to ICD classification did not influence ICU mortality but lowered hospital mortality (OR = 0.71 (0.52-0.99)). Subgroup analysis provided preliminary evidence that clopidogrel when given as only anti-platelet drug may have a similar benefit as ASA, but the combination of ASA and clopidogrel failed to improve the outcome. The time course of plasma fibrinogen and procalcitonin levels indicate that ASA seems to reduce the activation of haemostasis and increase the resolution of inflammation. It is concluded that prospective interventional studies should be done to test the use of ASA as novel therapeutic approach in critically ill patients.

背景与目标： 败血症及其多器官功能衰竭的后遗症是工业化国家死亡的主要原因之一。几项研究表明，用低剂量乙酰水杨酸（ASA）进行动脉粥样硬化血栓形成二级预防的患者在危重病情况下发生器官衰竭的风险可能较低。 ASA的好处可能是由于抑制了血小板活化以及增加了抗炎脂蛋白A4的形成。另一方面，ASA的作用可能（至少部分是）由动脉粥样硬化性血管疾病（作为ASA治疗的原因）引起的间接作用。动脉粥样硬化被认为​​是中度的全身性炎症，我们假设这种慢性病可能会对败血症的预后产生影响。为了获得更多有关ASA对重症患者的益处以及对动脉粥样硬化性血管疾病可能产生的干扰的信息，我们分析了886例脓毒症患者的病历，这些患者被大学医院的外科重症监护病房（ICU）收治。 Logistic回归分析表明，在ICU期间接受ASA（100μmg/ d）治疗的患者死亡率显着降低。 ICU和医院死亡率分别计算为0.56（0.37-0.84）和0.57（0.39-0.83）的赔率（OR）。相反，他汀类药物治疗对死亡率没有显着影响。根据ICD分类诊断动脉粥样硬化性血管疾病并不影响ICU死亡率，但可以降低医院死亡率（OR = 0.71（0.52-0.99））。亚组分析提供了初步证据，表明氯吡格雷仅作为抗血小板药物使用可能具有与ASA相似的益处，但是ASA和氯吡格雷的组合未能改善结局。血浆纤维蛋白原和降钙素原水平的时间变化表明，ASA似乎减少了止血的激活并增加了炎症的缓解。结论是，应该进行前瞻性干预研究，以测试ASA在危重患者中作为新型治疗方法的应用。

BACKGROUND & AIMS: :Chronic obesity imposes an organismal state of low-grade inflammation because the physiological resolution of inflammation is progressively repressed giving rise to cellular senescence and its accompanying Senescence-Associated Secretory Phenotype (SASP), which avoids apoptosis but perpetuates the relay of inflammatory signals from adipose tissue toward the rest of the body. Conversely, resolution of inflammation depends on the integrity of heat shock response (HSR) pathway that leads to the expression of cytoprotective and anti-inflammatory protein chaperones of the 70 kDa family (HSP70). However, chronic exposure to the aforementioned injuring factors leads to SASP, which, in turn, suppresses the HSR. A main metabolic tissue severely jeopardized by obesity-related dysfunctions is the endocrine pancreas, particularly β-cells of the islets of Langerhans. Because exercise is a powerful inducer of HSR and predicted to alleviate negative health outcomes of obesity, we sought whether obesity influence HSP70 expression in pancreatic islets and other metabolic tissues (adipose tissue and skeletal muscle) of adult B6.129SF2/J mice fed on a high-fat diet (HFD) for 13 weeks since the weaning and whether acute exercise as well as moderate-intensity exercise training (8 weeks) could interfere with this scenario. We showed that acute exercise of moderate intensity protects pancreatic islets against cytokine-induced cell death. In addition, acute exercise challenge time-dependently increased islet HSP70 that peaked at 12 h post-exercise in both trained and untrained mice fed on a control diet, suggesting an adequate HSR to exercise training. Unexpectedly, however, neither exercise training nor acute exercise challenges were able to increase islet HSP70 contents in trained mice submitted to HFD, but only in untrained HFD animals. In parallel, HFD disrupted glycemic status which is accompanied by loss of muscular mass resembling sarcopenic obesity that could not be rescued by exercise training. These results suggest that exercise influences HSR in pancreatic islets but obesity undermines islet, muscle and adipose tissue HSR, which is associated with metabolic abnormalities observed in such tissues.

背景与目标： ：慢性肥胖会导致机体处于低度炎症状态，因为炎症的生理学分辨率会逐渐受到抑制，从而引起细胞衰老及其伴随的衰老相关分泌表型（SASP），从而避免了细胞凋亡，但使脂肪中的炎症信号得以延续组织朝向身体的其余部分。相反，炎症的解决取决于热休克反应（HSR）途径的完整性，该途径导致70kDa家族（HSP70）的细胞保护性和抗炎性蛋白伴侣的表达。但是，长期暴露于上述伤害因素会导致SASP，进而抑制HSR。肥胖相关功能障碍严重危害的主要代谢组织是内分泌胰腺，特别是朗格罕氏岛的β细胞。由于运动是HSR的有力诱因，并且预计可减轻肥胖对健康的负面影响，因此我们寻求肥胖是否会影响以B6,129SF2 / J成年小鼠喂养的成年B6.129SF2 / J小鼠的胰岛和其他代谢组织（脂肪组织和骨骼肌）中HSP70的表达。断奶后连续13周进行高脂饮食（HFD），以及急性运动以及中等强度的运动训练（8周）是否会干扰这种情况。我们表明中等强度的急性运动可以保护胰岛免受细胞因子诱导的细胞死亡。此外，急性运动挑战随时间增加的胰岛HSP70随时间增加，在接受对照饮食喂养的训练和未训练小鼠中均在运动后12h达到峰值，表明有足够的HSR进行运动训练。但是，出乎意料的是，运动训练和急性运动挑战均无法增加接受HFD训练的小鼠的胰岛HSP70含量，而仅在未经训练的HFD动物中增加。同时，HFD破坏了血糖状态，伴随着肌肉减少，类似于肌肉减少症，运动训练无法挽救。这些结果表明，运动会影响胰岛的HSR，但肥胖会破坏胰岛，肌肉和脂肪组织的HSR，这与在此类组织中观察到的代谢异常有关。

BACKGROUND & AIMS: :Implantable cardioverter defibrillators (ICDs) are indicated in patients with Brugada syndrome with resuscitated ventricular arrhythmias. When these patients have atrial septal defects, they also need closure to prevent paradoxic embolism of thrombus from the defibrillator leads. A 15-year-old boy with Brugada syndrome had transvenous ICD placement along with device closure of a large atrial septal defect. When the defibrillation threshold was checked during device testing, a shock was delivered to terminate the induced ventricular fibrillation. The sudden jerk during this shock resulted in device embolization into the left atrium. The device was successfully retrieved and the defect closed with a larger device. This report discusses this extremely rare association of Brugada syndrome with atrial septal defect, unreported complications after device closure, and successful management of the problem.

背景与目标： ：植入性心脏复律除颤器（ICD）适用于Brugada综合征伴有复苏性室性心律失常的患者。当这些患者患有房间隔缺损时，他们还需要关闭以防止除颤器导线产生血栓的矛盾性栓塞。一名患有Brugada综合征的15岁男孩经静脉ICD植入并关闭了一个较大的房间隔缺损。在设备测试期间检查除颤阈值时，会发出电击以终止诱发的心室纤颤。在这种电击过程中突然的急动导致装置栓塞入左心房。已成功检索设备，并使用较大的设备关闭了缺陷。本报告讨论了Brugada综合征与房间隔缺损，装置闭合后未报告的并发症以及成功解决该问题的这种极为罕见的关联。

BACKGROUND & AIMS: :1. An earlier study had demonstrated that indomethacin, administered before E. coli endotoxin, abolished the initial pulmonary vasoconstriction and delayed the onset of the secondary shock phase that results from the intravenous injection of this agent in cats. The object of the present study was to determine whether indomethacin modified the shock phase when administered after endotoxin. 2. All the cats (whether or not they received indomethacin, 10 mg/kg) exhibited the characteristic features of the delayed shock phase that result from the administration of endotoxin (2 mg/kg). These included systemic hypotension, hypoglycaemia, reductions in arterial pH, cardiac output and systolic ejection time and an increase in arterial lactate. Five out of the ten animals given indomethacin survived 4 h compared with four out of twelve in the control (endotoxin along) group. 3. These results do not support the suggestion that antipyretic-analgesic drugs like indomethacin may be of benefit when given during bacteraemic or septic shock. They do support the suggestion that the acute pulmonary changes (hypertension and decreased compliance) that occur in this species within a few minutes of endotin administration ultimately contribute to the severity of the shock phase.

背景与目标： ：1。较早的一项研究表明，吲哚美辛在大肠杆菌内毒素之前使用，可消除最初的肺血管收缩，并延迟了在猫中静脉注射该药后引起的继发性休克期的发作。本研究的目的是确定内毒素治疗后消炎痛是否能改变休克期。 2.所有猫（无论是否接受吲哚美辛10 mg / kg）均表现出因施用内毒素（2 mg / kg）而导致的延迟休克期的特征。这些包括全身性低血压，低血糖症，动脉pH值降低，心输出量和收缩期射血时间以及动脉乳酸的增加。给予吲哚美辛的十只动物中有五只存活4小时，而对照组（沿内毒素）组的十二只中有四只存活。 3.这些结果不支持这样的建议，即在细菌性或败血性休克期间给予消炎痛镇痛药（如消炎痛）可能会有所帮助。他们确实支持这样的建议，即在服用内毒素后几分钟内，该物种发生的急性肺部变化（高血压和顺应性下降）最终会导致休克期的严重性。

BACKGROUND & AIMS: OBJECTIVE:Coccydynia is a disorder that decreases quality of life with significant functional failure. Extra-corporeal shock wave therapy (ESWT) is used to treat several painful musculoskeletal disorders. SUBJECTS AND METHODS:The medical records of 34 patients (29 females, 5 males) who had been treated with ESWT between 2017 and 2018 for chronic coccydynia were evaluated. Visual analog scale (VAS) scores were noted at the initial consultation, at each session, and during the initial and follow-up (at 6 months) examinations after the treatment. The 36-item short form (SF-36) quality of life scale survey was conducted at the beginning and end of the treatment. MRI was performed before the start of the procedure and 1 month after the end of the treatment. RESULTS:The mean VAS score was 9.6 (9-10) before the treatment and 3.4 (0-2) after the treatment (p < 0.05). The VAS score decreased to ≤3 in 79.4% of patients. Bone marrow edema regressed in 6% of patients. Significant improvement was observed in all of the SF-36 parameters, except for two. CONCLUSION:In our patient group, ESWT provided effective pain control. In order to evaluate the efficacy of ESWT more accurately and sensitively, prospective randomized studies with longer follow-up periods, in which ESWT is compared with different energy doses and different treatment methods, are needed.

背景与目标： 目的：球囊痛是一种会导致生活质量下降并伴有严重功能衰竭的疾病。体外冲击波疗法（ESWT）用于治疗几种痛苦的肌肉骨骼疾病。
研究对象和方法：评估了2017年至2018年期间接受ESWT治疗的慢性球虫病的34例患者的病历（女性29例，男性5例）。在初次会诊时，每次疗程中以及治疗后的初次和随访（6个月）检查中均记录有视觉模拟量表（VAS）评分。在治疗的开始和结束时进行了36项简短表格（SF-36）的生活质量量表调查。在手术开始之前和治疗结束后1个月进行MRI检查。
结果：VAS平均评分在治疗前为9.6（9-10），治疗后为3.4（0-2）（p <0.05）。在79.4％的患者中，VAS评分降至≤3。 6％的患者骨髓水肿消退。除了两个参数外，其他所有SF-36参数都得到了显着改善。
结论：在我们的患者组中，ESWT提供了有效的疼痛控制。为了更准确，更敏感地评估ESWT的疗效，需要对随访期较长的前瞻性随机研究，其中将ESWT与不同的能量剂量和不同的治疗方法进行比较。

BACKGROUND & AIMS: :Sixteen monoclonal antibodies (MAbs) directed against toxic shock syndrome toxin-1 (TSST-1) were generated by immunization of mice with purified TSST-1 and subsequent fusion of spleen cells with myeloma cells. Antibody-producing clones, identified by an enzyme-linked immunosorbent assay, were maintained as ascites tumors, and MAbs were purified by protein A chromatography. High-titered clones were further characterized and tested for the ability to neutralize several biological activities of TSST-1. The MAbs, which are of several immunoglobulin subtypes, reacted specifically with purified TSST-1 and TSST-1 present in Staphylococcus aureus culture supernatants. Three MAbs neutralized TSST-1-induced mitogenesis in a dose-dependent manner. Three of eight MAbs tested were able to neutralize induction by TSST-1 of interleukin-1 production by human monocytes. One neutralizing MAb, 8-5-7, was tested for the ability to protect rabbits from a constant infusion of TSST-1. Rabbits given the MAb had an attenuated clinical illness and were protected from the hypocalcemia, lipemia, and hepatic and renal insufficiency seen in control rabbits. Six of seven control rabbits died, compared with only one of seven rabbits treated with MAb 8-5-7. These experiments suggest that MAb 8-5-7 is directed against an antigenic determinant critical to the toxicity of TSST-1 and that the MAbs should be useful as probes in structure-function analyses of the TSST-1 molecule.

背景与目标： ：通过用纯化的TSST-1免疫小鼠，然后将脾细胞与骨髓瘤细胞融合，产生了针对中毒性休克综合症毒素1（TSST-1）的16种单克隆抗体（MAb）。通过酶联免疫吸附测定法鉴定的产生抗体的克隆被保留为腹水肿瘤，并通过蛋白A色谱法纯化单克隆抗体。进一步鉴定了高滴度克隆，并测试了中和TSST-1几种生物学活性的能力。具有几种免疫球蛋白亚型的单克隆抗体与金黄色葡萄球菌培养上清液中存在的纯化的TSST-1和TSST-1特异性反应。三个单克隆抗体以剂量依赖的方式中和TSST-1诱导的有丝分裂。测试的八个单克隆抗体中的三个能够中和人单核细胞产生白介素-1的TSST-1诱导作用。测试了一种中和的单克隆抗体8-5-7，具有保护兔子免于持续输注TSST-1的能力。接受单克隆抗体的兔子临床疾病减弱，并受到保护，免受对照兔子看到的血钙过低，血脂过多以及肝肾功能不全的困扰。七只对照兔中有六只死亡，而接受单抗8-5-7处理的七只兔中只有一只。这些实验表明，MAb 8-5-7针对针对TSST-1毒性至关重要的抗原决定簇，并且该MAbs可用作TSST-1分子结构功能分析的探针。

BACKGROUND & AIMS: :Cold shock proteins (CSP) belong to the family of single-stranded nucleic acid binding proteins with OB-fold. CSP are believed to function as 'RNA chaperones' and during anti-termination. We determined the solution structure of Bs-CspB bound to the single-stranded DNA (ssDNA) fragment heptathymidine (dT7) by NMR spectroscopy. Bs-CspB reveals an almost invariant conformation when bound to dT7 with only minor reorientations in loop beta1-beta2 and beta3-beta4 and of few aromatic side chains involved in base stacking. Binding studies of protein variants and mutated ssDNA demonstrated that Bs-CspB associates with ssDNA at almost diffusion controlled rates and low sequence specificity consistent with its biological function. A variation of the ssDNA affinity is accomplished solely by changes of the dissociation rate. 15N NMR relaxation and H/D exchange experiments revealed that binding of dT7 increases the stability of Bs-CspB and reduces the sub-nanosecond dynamics of the entire protein and especially of loop beta3-beta4.

背景与目标： ：冷休克蛋白（CSP）属于OB折叠的单链核酸结合蛋白家族。据信CSP在抗终止过程中起“ RNA伴侣”的作用。我们通过NMR光谱法确定了结合到单链DNA（ssDNA）片段庚啶（dT7）上的Bs-CspB的溶液结构。当与dT7结合时，Bs-CspB几乎显示出不变的构象，在环beta1-beta2和beta3-beta4中只有很小的重新定向，并且参与碱基堆积的芳香族侧链很少。对蛋白质变体和突变的ssDNA的结合研究表明，Bs-CspB与ssDNA的结合几乎以扩散控制的速率进行，且序列特异性低，与生物学功能一致。 ssDNA亲和力的变化仅通过解离速率的变化来实现。 15N NMR弛豫和H / D交换实验表明，dT7的结合增加了Bs-CspB的稳定性，并降低了整个蛋白质（尤其是环beta3-beta4）的亚纳秒级动力学。

BACKGROUND & AIMS: INTRODUCTION:While the efficacy of focused Extracorporeal Shock Wave Therapy (ESWT) in the treatment of Dupuytren's disease (DD) is supported by one positive trial, the effects of radial ESWT is unclear. PATIENT CONCERNS:A 79-year-old man with a 4-year history of impairment of left-hand function and pain due to DD with weakness and flexion deformities of middle and ring fingers. He has not been treated before for this impairment. DIAGNOSIS:The diagnosis of DD was based on clinical features and ultrasound images. INTERVENTIONS:Four weekly sessions of radial ESWT with 1400 impulses 3 bar each, 12 Hz. OUTCOMES:The limitations in activities of daily living were analyzed through the Disabilities of Arm Shoulder and Hand Questionnaire (DASH) and Michigan Hand Outcome Questionnaire (MHQ) at baseline, after four sessions of radial ESWT and at 4-months follow-up. Data analysis showed a significant reduction of hand deformities and an improvement of daily living performance. The effects continued at the 4-months follow-up. CONCLUSION:This case report demonstrates the feasibility of radial ESWT. Radial ESWT sessions may be carried out by a physiotherapist in outpatient clinics with cost reduction compared with surgical treatment and focused ESWT. Radial ESWT is a non-invasive, well tolerated therapy, so it should be considered in the DD treatment.

背景与目标： 引言：虽然一项体外试验证实了聚焦体外冲击波疗法（ESWT）治疗Dupuytren病（DD）的疗效，但radial动脉ESWT的疗效尚不清楚。
患者担忧：一位79岁的男性，有4年的DD左手功能受损和疼痛病史，中指和无名指无力和屈曲畸形。之前他没有得到过这种损伤的治疗。
诊断：DD的诊断基于临床特征和超声图像。
干预：每周进行四次of声ESWT训练，每次1400脉冲，压力3 bar，12 Hz。
结果：在基线ESWT，四次radial动脉ESWT治疗后以及4个月的随访中，通过手臂肩膀和手问卷（DASH）和密歇根州手结果问卷（MHQ）分析了日常生活活动中的局限性。数据分析显示手畸形显着减少，日常生活能力得到改善。在四个月的随访中，效果持续。
结论：本病例报告证明了放射状ESWT的可行性。 out理ESWT可以由物理治疗师在门诊诊所进行，与手术治疗和重点ESWT相比，其成本降​​低了。放射状ESWT是一种无创，耐受性良好的疗法，因此在DD治疗中应予以考虑。

BACKGROUND & AIMS: OBJECTIVE:To compare lung injury induced by a hemorrhagic shock resuscitated with normal saline or with small volumes of a hypertonic/hyperoncotic solution. DESIGN AND SETTING:Randomized, controlled, laboratory study in an animal research laboratory. SUBJECTS:Nineteen pigs (43 +/- 4 kg). INTERVENTIONS:After anesthesia and mechanical ventilation animals were bled to induce a 2-h deep shock and resuscitated for 2 h using normal saline (NS, 2 ml/kg per minute, n = 7) or the association of 7.2% NaCl with 6% hydroxyethylstarch 200/0.5 (HSHES, 4 ml/kg in 10 min followed by 0.2 ml/kg per minute, n = 7) to reach cardiac index and mixed venous oxygen saturation goals. Lungs were removed 6[Symbol: see text]h after the initiation of hemorrhage. Five animals were used as controls without hemorrhage. MEASUREMENTS AND RESULTS:Resuscitation goals were achieved using 90 +/- 17 ml/kg NS or 6.8 +/- 1.9 ml/kg HSHES. Lung injury was noted in both hemorrhage groups but was not influenced by the type of resuscitation. Extravascular lung water was measured at 9.6 +/- 1.8 ml/kg in the NS group, 9.2 +/- 1.6 ml/kg in the HSHES, group and 6.4 +/- 1 m/kg in the control group. The degree of histological alveolar membrane focal thickening and interstitial neutrophil infiltration were significantly more pronounced in the hemorrhage groups with no difference between the two types of fluid loading. Finally, pulmonary levels of IL-8 were higher after hemorrhage regardless of the type of resuscitation. CONCLUSIONS:When included in an optimized and goal directed resuscitation, the use of normal saline or a small volume of hypertonic/hyperoncotic solution does not result in a different early hemorrhage-induced lung injury.

背景与目标： 目的：比较生理盐水或少量高渗/高渗溶液复苏的失血性休克引起的肺损伤。
设计与设置：在动物研究实验室中进行随机，受控的实验室研究。
受试者：19头猪（43 /-4公斤）。
干预措施：麻醉和机械通气后，将动物放血以引起2小时的深度休克，并使用生理盐水（NS，2 ml / kg每分钟，n = 7）或7.2％NaCl和6％的联合复苏2 h羟乙基淀粉200 / 0.5（HSHES，每10分钟4 ml / kg，然后每分钟0.2 ml / kg，n = 7）达到心脏指数和混合静脉血氧饱和度目标。出血开始后6 h切除肺。五只动物用作无出血的对照。
测量和结果：使用90 /-17 ml / kg NS或6.8 /-1.9 ml / kg HSHES达到了复苏目标。两个出血组均注意到肺损伤，但不受复苏类型的影响。 NS组测得的血管外肺水为9.6 /-1.8 ml / kg，HSHES组测得为9.2 /-1.6 ml / kg，而对照组则为6.4 /-1 m / kg。出血组的组织学肺泡膜局灶性增厚和间质中性粒细胞浸润的程度更为明显，而两种液体负荷量之间没有差异。最后，不管复苏的类型如何，出血后肺中的IL-8水平都较高。
结论：当包括在优化的，目标明确的复苏中时，使用生理盐水或少量高渗/高渗溶液不会导致早期出血引起的肺损伤。

BACKGROUND & AIMS: :Heat shock proteins (HSPs) are synthesized by cells under metabolic stress and are known to enhance a cell's ability to survive life-threatening stress. The authors have begun to examine HSPs in the context of human atherosclerosis. This study demonstrated immunohistochemically the presence of HSP-70 in human and rabbit arteries, and its distribution in relation to necrosis and lipid accumulation, as well as vascular smooth muscle cells and macrophages, in human atherosclerotic plaques. Advanced lesions from 10 human carotid endarterectomy specimens were compared with 11 human aortic specimens from autopsy and 8 rabbit aortas. The immunostaining procedure used a mouse monoclonal antibody specific for the inducible form of HSP-70. Normal rabbit aortas were tested for changes in HSP-70 up to 24 hours after removal, and were used as controls for the human aortas. Representative plaques were examined for lipid content by osmium staining, and for smooth muscle cell and macrophage components using cell-specific monoclonal antibodies followed by immunostaining. The results indicated that HSP-70 was present in human and rabbit arteries and remained unchanged in distribution or concentration up to 15 hours after death. HSP-70 was present weakly throughout the media of normal-appearing arterial specimens. In contrast, HSP-70 was concentrated in the central portions of more thickened atheromas around sites of necrosis and lipid accumulation. Macrophages were coincident with these areas and were observed to be lipid-loaded. In contrast, patches of smooth muscle cells were observed in very complicated plaques, but without consistent association with necrosis or increased HSP-70; plaque smooth muscle cells also were observed to contain lipid. Large, relatively avascular and collagenous areas of plaque also were occasionally positive for HSP-70 staining. The results support the hypothesis that elevated HSPs indicate which plaque cells, particularly macrophages, are more stressed in the depth of atheroma, especially in association with necrosis, and should prompt further investigation of the significance of HSP accumulation to the evolution of atherosclerotic plaques.

背景与目标： 热休克蛋白（HSP）由细胞在新陈代谢压力下合成，并已知能增强细胞抵抗威胁生命的压力的能力。作者已经开始在人类动脉粥样硬化的背景下研究HSP。这项研究通过免疫组织化学方法证明了人和兔动脉中HSP-70的存在及其在人的动脉粥样硬化斑块中与坏死和脂质蓄积以及血管平滑肌细胞和巨噬细胞有关的分布。将来自10个人类颈动脉内膜切除术标本的晚期病变与来自尸体解剖的11个人类主动脉标本以及8个兔主动脉进行了比较。免疫染色程序使用了对HSP-70的可诱导形式具有特异性的小鼠单克隆抗体。正常兔子的主动脉在取出后24小时内测试HSP-70的变化，并用作人主动脉的对照。通过cell染色检查代表性噬斑的脂质含量，并使用细胞特异性单克隆抗体随后进行免疫染色检查平滑肌细胞和巨噬细胞成分。结果表明，HSP-70存在于人和兔子的动脉中，并且在死亡后15小时内其分布或浓度均保持不变。在正常出现的动脉标本中，HSP-70几乎不存在于整个介质中。相反，HSP-70集中在坏死和脂质堆积部位周围更增厚的动脉粥样硬化的中央部分。巨噬细胞与这些区域重合，并观察到脂质装载。相反，在非常复杂的斑块中观察到了平滑肌细胞的斑块，但是与坏死或HSP-70升高没有一致的联系。还观察到斑块平滑肌细胞含有脂质。斑块较大，相对无血管和胶原的区域有时也对HSP-70染色呈阳性。该结果支持以下假设：HSP升高表明哪些斑块细胞（尤其是巨噬细胞）在动脉粥样硬化的深度（尤其是与坏死相关）受到更大的压力，并应促使人们进一步研究HSP积累对动脉粥样硬化斑块演变的重要性。