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Gas exchange abnormalities is the pathophysiology characteristic of acute respiratory distress syndrome (ARDS). The severity of gas exchange abnormalities not only reflect the severity and outcome of the disease, but could also be an important index to guide individual mechanical ventilation settings and evaluate the therapeutic effects of inhaled vasodilator. The common techniques to measure gas exchange include multiple inert gas elimination technique, automatic lung parameter estimator, electrical impedance tomography, and single-photon emission CT. Nowadays, bedside techniques and measurements for improving gas exchange function in ARDS patients are still limited. Therefore, the improvement and promotion of bedside real-time gas exchange monitoring technology may achieve the goal of personalized medicine in ARDS. This article reviewed the common evaluation methods of gas exchange function in ARDS and their significance, in order to pay more attention to the evaluation of gas exchange function and further improve the prognosis of patients with ARDS.急性呼吸窘迫综合征（ARDS）的本质病理生理特征是气体交换功能障碍，评估气体交换功能可反映ARDS的严重程度，同时也是指导个体化机械通气治疗以及效果评估的重要指标。常用的气体交换功能评估方法主要包括多重惰性气体消除技术、自动肺参数估计系统、胸电阻抗断层成像技术和单光子发射计算机断层技术。但目前床旁可用的技术及改善ARDS患者气体交换功能的措施仍然有限，因此改进和推广床旁实时气体交换功能监测技术将有可能实现ARDS个体化医疗的目标。本文对目前常用的ARDS气体交换功能评估方式以及意义进行阐述，以期提高对评估ARDS气体交换功能的重视，进一步改善此类患者的预后。.

食管压在临床上可用于肺应力的监测及指导肺保护性通气策略的实施，主要包括呼气末正压的滴定、吸气末跨肺压的监测及自主呼吸的评价，但食管压对肺保护性通气策略的实施仅是其临床应用的一部分，基于食管压对胸腔内压的反应，其对呼吸功的监测、人机同步性的评价、血流动力学跨血管壁压力的校正等均是食管压在临床应用的指征，因此，对重症患者进行食管压的监测，可以达到临床精准治疗的目的。.

Lung cancer is one of the leading causes of death worldwide and non-small cell lung cancer (NSCLC) accounts for approximately 80% of lung cancer. Long noncoding RNAs (lncRNAs) are closely associated with the development and progression of various cancers, including lung cancer. The purpose of this study was to explore the potential role and molecular mechanism of lncRNA plasmacytoma variant translocation 1 (PVT1) in regulating the proliferation, apoptosis, migration, and invasion of NSCLC cells. The expressions of PVT1, integrin β-8 (ITGB8), and miR-145-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of ITGB8, MEK, p-MEK, ERK, and p-ERK were measured by western blot analysis. Cell proliferation, apoptosis, migration, and invasion were determined by MTT assay, flow cytometry, and transwell assay, respectively. The potential binding sites between miR-145-5p and PVT1 or ITGB8 were predicted by online software and verified by luciferase reporter assay. A xenograft tumor model was established to confirm the effect of PVT1 on NSCLC in vivo. We found out that the expression levels of PVT1 and ITGB8 were upregulated in NSCLC tissues and cells. Knockdown of PVT1 or ITGB8 suppressed cell proliferation, migration, invasion and promoted apoptosis in NSCLC cells, which could be reversed by ITGB8 overexpression in NSCLC cells. Moreover, PVT1 could regulate ITGB8 expression via direct binding to miR-145-5p. Furthermore, PVT1 regulated the MEK/ERK pathway by affecting ITGB8 expression. In addition, knockdown of PVT1 inhibited tumor growth, ITGB8 expression, MEK/ERK signaling pathway, and increased miR-145-5p expression in vivo. In conclusion, the knockdown of PVT1 inhibited proliferation, migration, and invasion but induced apoptosis of NSCLC cells by regulating miR-145-5p/ITGB8 axis and inhibiting MEK/ERK signaling pathway, providing a novel avenue for the treatment of NSCLC.

This study aims to reveal the TWIST protein expression in the degenerated nucleus pulposus (NP), its effect on the TNF-α treated NP cells, and to explore its specific mechanism of anti-senescence.NP tissues from spine fracture patients without intervertebral disc degeneration (IDD) and the IDD patients were collected to detect the TWIST1/2 protein expression by Western blot (WB). NP cells isolated from the healthy tissue was treated with TNF-α to induce senescence, and the TWIST1/2 protein expression was also analyzed. We transfected NP cells with the plasmid coding TWIST to upregulate its expression, which was also cultured in the TNF-α condition. Besides, the TNF-α pretreated NP cells were further stimulated with the recombinant human TWIST1/2 protein. The collagen II and senescent marker β-galactosidase (β-gal) were determined by immunofluorescence (IF); the MMP-13, TIMP-3, IL-10, IL-1β mRNA expression level was detected by quantitative Real Time PCR; the cell proliferation was analyzed by CCK8 assay; the cell cycle was measured by flow cytometry.TWIST1/2 protein was decreased both in the degenerated NP tissue, and TNF-α treated NP cells. The overexpression of TWIST1/2 could prevent the p53, p21, β-gal, MMP-13, and IL-1β expression, moreover, it protected the collagen II, TIMP-3, and IL-10 expression in the TNF-α treated NP cells. Additionally, TWIST overexpression also promoted cell proliferation by ensuring the process of the cell cycle. Furthermore, the supplement of TWIST protein was functional to reverse these senescent phenotypes caused by TNF-α partly.TWIST alleviates the TNF-αinduced NP cells senescence via the inhibition of the p53/p21 pathway.

Gastrointestinal stromal tumor (GIST) is the most common soft tissue sarcoma in the gastrointestinal tract. Biological behavior of GIST is varied. It is very important to accurately assess the risk of recurrence and metastasis after resection of primary tumor in order to guide adjuvant therapy and predict prognosis. With increasing understanding of the biological behavior of GIST, the risk stratification criterion has undergone continuous reform and improvement since its introduction. In the early stage, clinical parameters such as tumor size and mitotic rate were formulated as risk stages, and then tumor site, tumor rupture and other factors were included to form a more accurate AFIP standard and modified NIH risk stratification. Recently, more researches have used new statistical methods such as nomogram and contour maps, which more accurately predict risk of recurrence and better guide adjuvant treatment. Thus, individualized treatment of GIST becomes possible.胃肠间质瘤（GIST）是胃肠道最常见的软组织肉瘤，它的生物学行为多种多样。制定准确的危险度分级、评估原发肿瘤切除术后的复发转移危险、指导辅助治疗以及预测患者预后，具有重要的临床意义。GIST危险度分级标准自面世以来，随着对GIST疾病逐渐深入地了解，不断地经历了变革和完善。初期主要是根据肿瘤大小、核分裂象计数等临床参数制定危险度分级；中期再把肿瘤部位、肿瘤破裂等因素纳入而形成较为完善的美军病理研究所（AFIP）标准以及改良美国国立卫生研究院（NIH）分级；近期更有研究使用新的统计学方法如列线图、等高线图等，使得预测患者复发风险更为精准，由此让GIST个体化治疗变成可能。.

对支援湖北省新型冠状病毒肺炎疫情的各医疗队来讲，正确防护是保证医护人员在工作中不被感染的重要前提。但由于多数医疗队员对防护流程不熟悉，加之各地制定的要求亦不一致，出现了过度防护与不正确防护的现象。国家卫生健康委员会医疗专家组和院感专家组的部分成员，就近期在武汉及周边城市巡查过程中发现的相关问题进行了汇总，提出了切实可行的建议。.

新型冠状病毒易导致急性呼吸窘迫综合征（ARDS），已对生命安全构成极大威胁。无创呼吸辅助治疗是新型冠状病毒肺炎引起ARDS的常规治疗手段，但在治疗过程中，往往存在过度使用无创呼吸功能支持治疗而导致气管插管延迟，进而影响患者的预后。因此，了解无创通气使用指征和禁忌，早期识别无创通气治疗失败的危险因素，适时终止无创通气转为有创通气是目前临床医师亟需关注的问题。.

近年来我国重症医学在学科规模和学科建设上飞速发展，取得了巨大成就。但作为临床医学二级学科，在致力于打造规范化同质化重症医学诊疗体系的同时，需构建和完善重症医学"预警—救治—长期预后"的大学科体系，以推进和完善重症医学的学科建设，更好地服务于人民健康。.

Coronavirus disease 2019 (COVID-19) has become a global public health emergency threatening people's lives around the world. Although the acute respiratory distress syndrome (ARDS) induced by COVID-19 is similar to the ARDS caused by other diseases in terms of pathophysiological basis and clinical manifestations, they are also different in many aspects, which lead to different clinical therapies. Therefore, understanding the differences and similarities of ARDS induced by COVID-19 and other diseases currently are the basis for clinicians to make decisions for the treatment of COVID-19 induced ARDS.新型冠状病毒肺炎(COVID－19)已成为全球公共卫生事件，对全球人民生命安全构成极大的威胁。而COVID－19导致的急性呼吸窘迫综合征(ARDS)与其他疾病导致的ARDS在病理生理基础、临床表现等方面有相同的地方，但也有很大的区别，从而导致临床治疗的差异。因此，了解COVID－19导致的ARDS与其他病因导致ARDS的异同，是目前临床医师对COVID－19导致的ARDS进行临床决策的基础。.

The treatment of critically ill patients with coronavirus disease 2019(COVID-19) faces compelling challenges. In this issue, we'd like to share our first-line treatment experience in treating COVID-19. Hemodynamics need be closely monitored and different types of shock should be distinguished. Vasoconstrictor drugs should be used rationally and alerting of complications is of the same importance. The risk of venous thromboembolism (VTE) needs to be assessed, and effective prevention should be carried out for high-risk patients. It is necessary to consider the possibility of pulmonary thromboembolism (PTE) in patients with sudden onset of oxygenation deterioration, respiratory distress, reduced blood pressure. However, comprehensive analysis of disease state should be taken into the interpretation of abnormally elevated D-Dimer. Nutritional support is the basis of treatment. It's important to establish individual therapy regimens and to evaluate, monitor and adjust dynamically. Under the current epidemic situation, convalescent plasma can only be used empirically, indications need to be strictly screened, the blood transfusion process should be closely monitored and the curative effect should be dynamically evaluated.新型冠状病毒肺炎（COVID-19）危重型患者的救治面临严峻挑战。循环状态需严密监测并鉴别不同类型的休克，合理应用血管收缩药物，警惕并发症。评估静脉血栓栓塞症（VTE）风险，高危者需实施有效预防，对突然出现氧合恶化、呼吸窘迫、血压下降等临床表现者需警惕肺血栓栓塞症（PTE）的发生，但对D-二聚体异常增高的解读需结合疾病的严重状态综合分析。营养支持作为基础治疗手段，应制定个体化营养方案，评估并动态调整。当前疫情下，恢复期血浆只能经验性应用，适应证需严格把控，输血过程中严密监测并动态评估疗效。.

新型冠状病毒肺炎所致的急性呼吸窘迫综合征是重型和危重型患者预后不良的主要病因，对常规肺保护和肺开放通气策略反应不佳者，俯卧位通气是治疗的重要措施，通过促进肺复张，改善低氧血症、高碳酸血症及急性右心功能衰竭。俯卧位通气同样对病情相对较轻的患者有效，可预防病情向重型和危重型进展。目前临床医师对俯卧位通气治疗新型冠状病毒肺炎仍存困惑，因此亟需在临床推广。.

新型冠状病毒易导致急性呼吸窘迫综合征(ARDS)，已对生命安全构成极大的威胁。无创呼吸辅助治疗是新型冠状病毒肺炎引起ARDS的常规治疗手段，但在新型冠状病毒肺炎治疗中，往往存在过度使用无创呼吸功能支持治疗而导致气管插管延迟进而影响患者的临床预后，因此，了解无创通气使用的指征和禁忌，早期识别无创通气治疗失败的危险因素，适时终止无创通气转为有创通气是目前临床医师治疗新型冠状病毒肺炎亟需关注的问题。.

COVID-19 has been prevalent in Wuhan and spread rapidly to all of our country. Some cases can develop into ARDS, or even death. We will share the treatment experience of severe COVID-19 with the first-line treatment experience. The best respiratory support mode should be selected, but the timing of intubation and protection during intubation are two difficulties; patients with high level peep and poor effect in prone position can be given ECMO support. For COVID-19 patients with mechanical ventilation, reasonable sedation and analgesia strategies should be formulated; delirium should not be ignored. In addition, there is up regulation of inflammatory factors in patients with severe COVID-19, but the effect of renal replacement therapy needs to be further confirmed by clinical research.新型冠状病毒肺炎（COVID-19）在武汉感染流行并迅速蔓延至全国，部分病例可发生急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS），甚至引起死亡。在此我们结合一线的救治体会，给大家分享危重型NCP的治疗经验。需选择最佳呼吸支持方式，但气管插管时机的把握及插管时的防护是两个难点；高水平呼气末正压通气（PEEP）、俯卧位效果不佳的患者可行体外膜氧合（ECMO）支持。对于机械通气的NCP患者，制定合理的镇静镇痛策略，谵妄不容忽视。此外，危重型COVID-19患者体内存在炎性因子的上调，但肾脏替代治疗的效果还需临床研究进一步证实。.

The new coronavirus pneumonia (NCP), also named as COVID-19 by WHO on Feb 11 2020, is now causing a severe public health emergency in China since. The number of diagnosed cases is more than 40,000 until the submission of this manuscript. Coronavirus has caused several epidemic situations world widely, but the present contagious disease caused by 2019 new coronavirus is unprecedentedly fulminating. The published cohorts of 2019 new coronavirus (n-Cov) are single-center studies, or retrospective studies. We here share the therapeutic experiences of NCP treatment with literature review. Combination of Ribavirin and interferon-α is recommended by the 5(th) edition National Health Commission's Regimen (Revised Edition) because of the effect on Middle East respiratory syndrome (MERS), and the effectiveness of Lopinavir/Ritonavir and Remdisivir needs to be confirmed by randomized controlled trial (RCT), given the situation of no specific antivirus drug on NCP is unavailable. Systemic glucocorticosteroid is recommended as a short term use (1~2 mg·kg(-1)·d(-1), 3~5 d) by the 5(th) edition National Health Commission's Regimen (Revised Edition) yet RCTs are expected to confirm the effectiveness. Inappropriate application of antibiotics should be avoided, especially the combination of broad-spectrum antibiotics, for the NCP is not often complicated with bacterial infection.新型冠状病毒肺炎（new coronavirus pneumonia，NCP）正在中国引起严重疫情，截至发稿之日，全国确诊人数已逾4万。冠状病毒已经在全世界范围内引起数次疫情，但此次疫情的来势之迅猛及传染性之强前所未有。我们对引起此次疫情的病原体——2019新型冠状病毒知之甚少，目前在国际上发表的临床研究文章或为单中心研究，或为回顾性分析。我们结合在新冠肺炎一线的救治体会及相关发表的研究成果，给大家分享新冠肺炎的治疗经验。抗病毒药物方面，目前仍无特效药物，利巴韦林和干扰素联合用药由于其治疗中东呼吸综合征（MERS）有效，仍被我国新冠肺炎诊疗方案推荐；洛匹那韦/利托那韦和瑞德西韦的疗效有待随机对照临床试验（randomized controlled trial，RCT）评价；糖皮质激素的短期应用（1~2 mg·kg(-1)·d(-1)，3~5 d）被我国诊疗方案推荐，但仍需RCT进一步证实；本次新冠肺炎合并细菌感染较少，应当避免盲目使用抗菌药物，尤其避免联用广谱抗菌药物。.

Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors in the world and its 5-year survival rate is very low. Long non-coding RNA X-inactive specific transcript (lncRNA XIST) has been demonstrated to play vital roles in NSCLC, but the exact molecular mechanisms underlying NSCLC still need to be further explored.Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of XIST, miR-212-3p and Casitas B-lineage proto-oncogene like 1 (CBLL1). Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to analyze the relationship among XIST, miR-212-3p and CBLL1. Cell Counting Kit-8 (CCK-8) assay and transwell invasion assay were carried out to evaluate cell proliferation, migration and invasion, respectively. Western blot analysis was conducted to examine the protein expression of CBLL1, E-cadherin, N-cadherin and Vimentin. Murine xenograft assay was conducted to explore the role of XIST in vivo.Expression levels of XIST and CBLL1 were markedly upregulated, while the miR-212-3p level was markedly downregulated in NSCLC tissues and cells. MiR-212-3p was identified as a direct target of XIST, and miR-212-3p was predicted to target CBLL1. XIST knockdown repressed NSCLC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro, and suppressed tumor growth in vivo, while miR-212-3p inhibition restored the effects. Furthermore, CBLL1 overexpression could abolish the effects of miR-212-3p overexpression on NSCLC cell proliferation, migration, invasion and EMT in vitro.XIST was significantly decreased in NSCLC tissues and cells, and XIST knockdown suppressed the proliferation, migration, invasion and EMT of NSCLC cells by miR-212-3p/CBLL1 axis. These findings facilitated our understanding of lncRNA regulation in NSCLC.

重症医学的快速发展使越来越多的患者得到救治，由于抢救的时效性与器官支持的重要性，容易忽视患者、家属及医生的心理感受，常使患者和社会对重症医学的认同度明显不高，重症医学医务人员的职业获得感也亟需改善。如何改变目前窘境，成为亟待解决的问题。本文就如何让重症患者和ICU医务人员都能回归"人"的本质，让社会切实感受重症医学的学科温度。.

急性呼吸窘迫综合征（ARDS）发病机制的核心是肺部促炎/抗炎失衡。巨噬细胞极化在早期ARDS炎症反应中发挥重要作用。ARDS初期，M1型巨噬细胞分泌促炎因子和趋化因子，发挥促炎作用。M2型巨噬细胞分泌抗炎因子并清除肺内中性粒细胞，发挥抗炎作用。因此，操控巨噬细胞极化可能是ARDS免疫调节治疗的新领域。.

近年来我国重症医学发展迅速，但发展不均衡，地区间、医院间、医生间的诊治水平差距明显，重症医学诊疗水平差异极大，严重影响重症患者的救治。互联网和重症信息化建设为"重症医学规范化-同质化管理平台"提供了基础和可能。我们率先在医联体内建立了基于互联网+的管理平台，进行区域内重症患者规范化-同质化救治，取得一定经验。为提高全国重症患者的救治水平，建立基于互联网+的"重症医学规范化-同质化管理平台"具有重要的临床和社会意义。.

Ganoderma lucidum extracts have shown antiepileptic effects in in vivo and in vitro studies. In this work, primary hippocampal neurons cultured in magnesium-free medium were used to study the neuroprotective effects of ganoderic acid A and B (GA-A and GA-B) on superoxide dismutase (SOD) activity and mitochondrial membrane potential, to improve our understanding of their antiepileptic effect. The activity of SOD was determined by the xanthine oxidase assay, the variations of mitochondrial membrane potential and cell apoptosis were measured by JC-1 fluorescent staining and flow cytometry. It was found that the SOD activity and mitochondrial membrane potential (118.84 U/mg protein and 244.08 Δψm) of the epileptic hippocampal neurons were significantly lower than control values (135.95 U/mg protein and 409.81 Δψm), associated with an increase of cell apoptosis (31.88% vs. 8.84%). These circumstances can be improved by treatment of GA-A/GA-B (for SOD, 127.15±3.82 / 120.52±4.30 U/mg protein; for membrane potential (Δψm), 372.35 / 347.28; and for cell apoptosis (%), 14.93 / 20.52). Results indicated that GA-A significantly improved SOD activity, while both GA-A/GA-B tranquillized the mitochondrial membrane potential of hippocampal neurons, and thereby protected these neurons by inhibiting apoptosis.

To establish the experts consensus on the right heart function management in critically ill patients. The panel of consensus was composed of 30 experts in critical care medicine who are all members of Critical Hemodynamic Therapy Collaboration Group (CHTC Group). Each statement was assessed based on the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) principle. Then the Delphi method was adopted by 52 experts to reassess all the statements. (1) Right heart function is prone to be affected in critically illness, which will result in a auto-exaggerated vicious cycle. (2) Right heart function management is a key step of the hemodynamic therapy in critically ill patients. (3) Fluid resuscitation means the process of fluid therapy through rapid adjustment of intravascular volume aiming to improve tissue perfusion. Reversed fluid resuscitation means reducing volume. (4) The right ventricle afterload should be taken into consideration when using stroke volume variation (SVV) or pulse pressure variation (PPV) to assess fluid responsiveness.(5)Volume overload alone could lead to septal displacement and damage the diastolic function of the left ventricle. (6) The Starling curve of the right ventricle is not the same as the one applied to the left ventricle,the judgement of the different states for the right ventricle is the key of volume management. (7) The alteration of right heart function has its own characteristics, volume assessment and adjustment is an important part of the treatment of right ventricular dysfunction (8) Right ventricular enlargement is the prerequisite for increased cardiac output during reversed fluid resuscitation; Nonetheless, right heart enlargement does not mandate reversed fluid resuscitation.(9)Increased pulmonary vascular resistance induced by a variety of factors could affect right heart function by obstructing the blood flow. (10) When pulmonary hypertension was detected in clinical scenario, the differentiation of critical care-related pulmonary hypertension should be a priority. (11) Attention should be paid to the change of right heart function before and after implementation of mechanical ventilation and adjustment of ventilator parameter. (12) The pulmonary arterial pressure should be monitored timingly when dealing with critical care-related pulmonary hypertension accompanied with circulatory failure.(13) The elevation of pulmonary aterial pressure should be taken into account in critical patients with acute right heart dysfunction. (14) Prone position ventilation is an important measure to reduce pulmonary vascular resistance when treating acute respiratory distress syndrome patients accompanied with acute cor pulmonale. (15) Attention should be paid to right ventricle-pulmonary artery coupling during the management of right heart function. (16) Right ventricular diastolic function is more prone to be affected in critically ill patients, the application of critical ultrasound is more conducive to quantitative assessment of right ventricular diastolic function. (17) As one of the parameters to assess the filling pressure of right heart, central venous pressure can be used to assess right heart diastolic function. (18). The early and prominent manifestation of non-focal cardiac tamponade is right ventricular diastolic involvement, the elevated right atrial pressure should be noticed. (19) The effect of increased intrathoracic pressure on right heart diastolic function should be valued. (20) Ttricuspid annular plane systolic excursion (TAPSE) is an important parameter that reflects right ventricular systolic function, and it is recommended as a general indicator of critically ill patient. (21) Circulation management with right heart protection as the core strategy is the key point of the treatment of acute respiratory distress syndrome. (22) Right heart function involvement after cardiac surgery is very common and should be highly valued. (23) Right ventricular dysfunction should not be considered as a routine excuse for maintaining higher central venous pressure. (24) When left ventricular dilation, attention should be paid to the effect of left ventricle on right ventricular diastolic function. (25) The impact of left ventricular function should be excluded when the contractility of the right ventricle is decreased. (26) When the right heart load increases acutely, the shunt between the left and right heart should be monitored. (27) Attention should be paid to the increase of central venous pressure caused by right ventricular dysfunction and its influence on microcirculation blood flow. (28) When the vasoactive drugs was used to reduce the pressure of pulmonary circulation, different effects on pulmonary and systemic circulation should be evaluated. (29) Right atrial pressure is an important factor affecting venous return. Attention should be paid to the influence of the pressure composition of the right atrium on the venous return. (30) Attention should be paid to the role of the right ventricle in the acute pulmonary edema. (31) Monitoring the difference between the mean systemic filling pressure and the right atrial pressure is helpful to determine whether the infusion increases the venous return. (32) Venous return resistance is often considered to be a insignificant factor that affects venous return, but attention should be paid to the effect of the specific pathophysiological status, such as intrathoracic hypertension, intra-abdominal hypertension and so on. Consensus can promote right heart function management in critically ill patients, optimize hemodynamic therapy, and even affect prognosis.

Imatinib-induced ophthalmological side-effects, including conjunctiva hemorrhage and periorbital oedema, although very common and still remain relatively little understood. The present study investigated the effects of genetic polymorphisms of drug targets and membrane transporters on these side effects. We found that the minor allele of EGFR rs10258429 and SLC22A1 rs683369 were significant risk determinants of conjunctival hemorrhage with OR of 7.061 (95%CI=1.791-27.837, P=0.005 for EGFR rs10258429 CT+TT vs CC), and 4.809 (95%CI=1.267–18.431, P=0.021 for SLC22A1 rs683369 GG+CG vs CC). The minor allele of SLC22A5 rs274558 and ABCB1 rs2235040 were protective factors to periorbital oedema with OR of 0.313 (95%CI=0.149–0.656, P=0.002 for SLC22A5 rs274558 AA+AG vs GG), and 0.253 (95%CI=0.079–0.805, P=0.020 for ABCB1 rs2235040 CT vs CC). These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.

On August 2nd, 2014, a massive dust explosion occurred in a factory of Kunshan, resulting in a mass casualty involving 185 burn patients. They were transported to 20 medical institutions in Jiangsu province and Shanghai. More than one thousand of medical personnel of our country participated in this emergency rescue, and satisfactory results were achieved. In this paper, the characteristics of this accident were analyzed, the positive effects of interdisciplinary cooperation were affirmed, and the contingency plan, rescue process and pattern, and reserve, organization and management of talents during this rescue process were reviewed retrospectively.

There are some discussions concerning the admissibility of estimated regression coefficients under the balanced loss function in the general linear model. We study this issue for the generalized linear regression model. First, we propose a generalized weighted balance loss function for the generalized linear model. For the proposed loss function, we study sufficient and necessary conditions for the admissibility of the estimated regression coefficients in two interesting linear estimation classes. Ведуться дєякі дискусії щодо допустимості оцінєних коєфіцієнтів регресії для збалансованої функції втрат у загальній лінійній моделі. В роботі вивчається ця проблема для узагальненої лінійної моделі регресії. Так, запропоновано узагальнену зважену функцію втрати балансу для узагальненої лінійної моделі. Для вказаної функції втрат ми вивчаємо необхідні та достатні умови допустимості оцінених коефіцієнтів регресії для двох цікавих лінійних випадків оцінювання.

To evaluate the prognostic effect of dobutamine stress test in patients with septic shock.Patients with septic shock received intravenous infusion of dobutamine at 10 microg . kg-1 . min-1 for 1 h. Hemodynamics and oxygen metabolism was observed. A patient who was able to increase oxygen consumption index (VO2) by15 % was designated as a responder to the test.In 47 patients with septic shock, twenty one responders and twenty six nonresponders were identified, and mortality was 33.3 % and 76.9 % respectively. After the dobutamine infusion, the responders showed increases in cardiac index (18.1 %), oxygen delivery index (12.7 %), VO2 (38.6 %), and oxygen extraction ratio (18.0 %), and reductions in systemic vascular resistance index (18.5 %). The nonresponders demonstrated increases in cardiac index (11.5 %), but no change in oxygen delivery, VO2, and oxygen extraction ratio.Dobutamine stress test might be a good predictor of outcome in patients with septic shock.

To observe the effects of tripcholorolide (T4) on inflammatory reaction of mouse alveolar macrophages.RT-PCR was used to investigate tumor necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), IL-6, IL-10, and inducible nitric-oxide synthase (iNOS) mRNA expression in alveolar macrophages after LPS 10 mg/L and T4 500 micrograms/L treatment. ELISA was used to detect TNF alpha, IL-1 beta, IL-6, and IL-10 protein expression. Nitrite was measured by Griess reaction.TNF alpha, IL-1 beta, IL-6, IL-10, and nitrite increased in supernatants, when alveolar macrophages were stimulated by LPS 10 mg/L at 24 h. Both T4 500 micrograms/L and dexamethasone 100 mumol/L had inhibitory effects on the production of TNF alpha, IL-1 beta, IL-6, IL-10, and nitric oxide. The mRNA expression of TNF alpha, IL-6, IL-10, and iNOS increased at 5 h after LPS stimulation which was decreased on addition of T4 500 micrograms/L or dexamethasone 100 mumol/L. T4 had no effect on stability of LPS-induced mRNA expression in TNF alpha, IL-6, and IL-10.T4 had inhibitory effects on the expression of proinflammatory and antiinflammatory mediators.

To observe the effects of nitric oxide and interleukin-10 (IL-10) on inflammatory reaction in mouse alveolar macrophages (AM).AM from mice were stimulated by lipopolysaccharides (LPS) 10 mg.L-1 and nitric-oxide synthase inhibitor, S-methylisothiorea sulfate (SMT) or nitric-oxide donor, S-nitroso-N-acetyl-D, L-penicillamine (SNAP). The production of tumor necrosis factor alpha (TNF alpha), IL-1 beta, IL-6, and IL-10 by AM were measured by ELISA.After LPS-stimulation, TNF alpha, IL-1 beta, and IL-6 peaked at 6, 12, and 24 h, respectively by AM. SMT inhibited LPS-induced nitric oxide release and increased IL-1 beta and IL-6 secretions in AM, but the TNF alpha levels remained unchanged. SNAP had inhibitory effects on IL-1 beta and IL-6 secretions in a concentration-dependent manner, but exerted no effect on TNF alpha release. TNF alpha, IL-1 beta, and IL-6 secretions were inhibited by recombinant IL-10, but the cytokines release was upregulated by anti-IL-10 monoclonal antibody.Both endogenous and exogenous nitric oxide and IL-10 had inhibitory effects on the LPS-induced TNF alpha, IL-1 beta, and IL-6 secretions in mouse AM.

To study the kinetics of tumor necrosis factor alpha (TNF alpha), interleukine-1 (IL-1 beta), and macrophage inflammatory protein-1 alpha (MIP-1 alpha) gene expression in rat lung after i.p. lipopolysaccharides (LPS) and the effect of dexamethasone (Dex) and ibuprofen (Ibu) on the cytokines gene expression.The amount of Evans blue in lung was measured by fluorescence method. The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung were assessed by slot blot analysis.The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung after i.p. LPS increased in a dose-dependent manner, and peaked at 2, 6, and 12 h, respectively. Both Dex 50 mg.kg-1 and Ibu 90 mg.kg-1 injected at 1 h before i.p. LPS markedly decreased the content of Evans blue in lung at 1 h after i.p. LPS. After Dex or Ibu pretreatment, the peak levels of TNF alpha, IL-1 beta, and MIP-1 alpha mRNA decreased markedly compared with LPS alone.The gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung increased after i.p. LPS. Dex and Ibu prevented LPS-induced lung injury through inhibiting the cytokines gene expression.

To study the influence of dexamethasone (Dex), ibuprofen (Ibu), and ligustrazini (Lig) on lipopolysaccharides (LPS)-induced tumor necrosis factor alpha (TNF alpha) gene expression (both mRNA and protein).TNF alpha in supernatants of human whole blood was measured by ELISA; The TNF alpha mRNA was assessed by slot blot analysis.LPS-induced TNF alpha production was in a dose-dependent manner. TNF alpha levels in the whole blood increased markedly at 3 h and peaked at 6 h. The induction of TNF alpha mRNA was very rapid, peaking at 2 h after LPS challenge. Dex exerted inhibitory effects on TNF alpha production in a dose-dependent manner. Ibu and Lig had 2-phase effects on TNF alpha release.Dex, Ibu, and Lig affected TNF alpha gene expression, so they may be new approaches of anti-TNF alpha for treatment of sepsis.