Volume 133 · Issue 18 · 2020

冠状病毒疾病2019（新冠肺炎）疫情已经成为一场全球健康危机。^[1,2]医护人员在疫情期间发挥着关键作用，但在高峰时段可能会出现人员严重短缺的情况。为了控制疫情的快速传播，需要足够的人员来管理受感染的患者，并防止周围的患者、工作人员以及当地社区受到感染。^[3]尽管组织和部署医务人员以应对迅速增加的新冠肺炎患者人数有多种模式，但来自中国武汉的成功经验可能有助于作为有效应对这一紧急情况的模式。^[4]

The peripheral perfusion index (PI), as a real-time bedside indicator of peripheral tissue perfusion, may be useful for determining mean arterial pressure (MAP) after early resuscitation of septic shock patients. The aim of this study was to explore the response of PI to norepinephrine (NE)-induced changes in MAP.

Twenty septic shock patients with pulse-induced contour cardiac output catheter, who had usual MAP under NE infusion after early resuscitation, were enrolled in this prospective, open-label study. Three MAP levels (usual MAP -10 mmHg, usual MAP, and usual MAP +10 mmHg) were obtained by NE titration, and the corresponding global hemodynamic parameters and PI were recorded. The general linear model with repeated measures was used for analysis of variance of related parameters at three MAP levels.

With increasing NE infusion, significant changes were found in MAP (F = 502.46, P < 0.001) and central venous pressure (F = 27.45, P < 0.001) during NE titration. However, there was not a significant and consistent change in continuous cardiac output (CO) (F = 0.41, P = 0.720) and PI (F = 0.73, P = 0.482) at different MAP levels. Of the 20 patients enrolled, seven reached the maximum PI value at usual MAP -10 mmHg, three reached the maximum PI value at usual MAP, and ten reached the maximum PI value at usual MAP +10 mmHg. The change in PI was not significantly correlated with the change in CO (r = 0.260, P = 0.269) from usual MAP -10 mmHg to usual MAP. There was also no significant correlation between the change in PI and change in CO (r = 0.084, P = 0.726) from usual MAP to usual MAP +10 mmHg.

Differing MAP levels by NE infusion induced diverse PI responses in septic shock patients, and these PI responses may be independent of the change in CO. PI may have potential applications for MAP optimization based on changes in peripheral tissue perfusion.

The relationship between macrocirculation and microcirculation remains controversial. The loss of coherence between microcirculation and macrocirculation has already been found in late-stage sepsis shock. The objective of this study was to determine the earliest possible time of detecting the loss of coherence between microcirculation and macrocirculation in early-stage endotoxemic shock.

We randomized 24 female New Zealand white rabbits into two groups: endotoxemic shock group (n = 14) and control group (n= 10). Rabbits in the endotoxemic shock group were equipped with arterial and venous catheters and received an intravenous infusion of Escherichia coli lipopolysaccharide (LPS, 2 mg/kg over 10 min). Rabbits in the control group received the same dose of saline infusion. Microcirculatory perfusion parameters were assessed in the sublingual mucosa using sidestream dark-field video microscopy. Systemic hemodynamics and blood lactate levels were measured at baseline and over a 120-min period.

Ninety minutes after completing LPS infusion, all animals in the endotoxemic shock group developed a hypodynamic septic condition, characterized by low cardiac output and increased systemic vascular resistance; 120 min after completing LPS infusion, the mean arterial pressure decreased by 25% (P = 0.01), confirming ongoing endotoxemic shock. However, significant decreases in sublingual microcirculatory parameters of small vessels (microvascular flow index, perfused vessel density, and proportion of small perfused vessels) were observed 30 min after completing LPS infusion (P = 0.01, for all), and threshold decreases of 30% were found 60 min after completing LPS infusion (P = 0.001, for all) in the endotoxemic shock group. Lactate levels significantly increased to more than 2 mm/L at 90 min and more than 4 mm/L at 120 min in the endotoxemic shock group (P = 0.02 and P = 0.01, respectively).

Changes in microcirculatory perfusion precede changes in macrocirculation and lactate levels in a rabbit model of endotoxemia shock. Microcirculation, macrocirculation, and oxygen metabolism are distinct in early-stage endotoxic shock.

Acinetobacter baumannii (A. baumannii) has become one of the most important opportunistic pathogens inducing nosocomial pneumonia and increasing mortality in critically ill patients recently. The interaction between A. baumannii infection and immune response can influence the prognosis of A. baumannii related pneumonia. The target of the present study was to investigate the role of immunodeficiency in A. baumannii induced pneumonia.

Male BALB/c mice were randomly divided into the normal immunity control (NIC) group, normal immunity infection (NIA) group, immune compromised control (CIC) group, and immune compromised infection (CIA) group (n = 15 for each group). Intraperitoneal injection of cyclophosphamide and intranasal instillation of A. baumannii solution were used to induce compromised immunity and murine pneumonia, respectively. The mice were sacrificed at 6 and 24 h later and the specimens were collected for further tests. Seven-day mortality of mice was also assessed.

After A. baumannii stimulation, the recruitment of neutrophils in mice with normal immunity increased sharply (P = 0.030 at 6 h), while there was no significant raise of neutrophil counts in mice with compromised immune condition (P = 0.092 at 6 h, P = 0.772 at 24 h). The Th cell polarization presented with pulmonary interleukin (IL)-4 and interferon (IFN)-γ level in response to the A. baumannii in CIA group were significantly depressed in comparison with in NIA group (IFN-γ: P = 0.003 at 6 h; P = 0.001 at 24 h; IL-4: P < 0.001 at 6 h; P < 0.001 at 24 h). The pulmonary conventional dendritic cell accumulation was even found to be inhibited after A. baumannii infection in immunocompromised mice (P= 0.033). Correspondingly, A. baumannii associated pneumonia in mice with compromised immunity caused more early stage death, more severe histopathological impairment in lung.

A. baumannii could frustrate the immune response in immunocompromised conditions, and this reduced immune response is related to more severe lung injury and worse outcome in A. baumannii induced pneumonia.

The association between free triiodothyronine (FT3) and long-term prognosis in dilated cardiomyopathy (DCM) patients has not been evaluated. The purpose of this study was to determine whether the level of FT3 could provide prognostic value in patients with DCM.

Data of consecutive patients diagnosed with DCM were collected from October 2009 to December 2014. FT3 was measured by fluoroimmunoassay. Other biochemical markers, such as free thyroxin (FT4), thyroid-stimulating hormone, red blood cell, hemoglobin, blood urea nitrogen, and serum creatinine, were tested at the same time. Follow-up was performed every 3 months. The primary endpoint was all-cause mortality. Pearson analysis was used to evaluate the correlation of FT3 and other lab metrics with DCM patients’ prognosis. The association of long-term mortality in DCM and FT3 was compared using Cox hazards model.

Data of 176 patients diagnosed with DCM were collected. Of them, 24 patients missed FT3 values and six patients were lost to follow-up. Altogether, data of 146 patients were analyzed. During the median follow-up time of 79.9 (53.5-159.6) months, nine patients lost, 61 patients died (non-survival group), and 85 patients survived (survival group). FT3 was significantly lower in non-survival group than that in survival group (3.65 ± 0.83 pmol/L vs. 4.36 ± 1.91 pmol/L; P = 0.003). FT3 also showed a significantly positive correlation with red blood cell and hemoglobin, negatively correlated with age, blood urea nitrogen and serum creatinine (P < 0.05), respectively. Patients in the group of lower FT3 levels (FT3 ≤ 3.49 pmol/L) suffered from a higher risk of all-cause mortality (P for log-rank = 0.001). In multivariate Cox regression analysis, FT3 level was significantly associated with all-cause mortality (hazard ratio: 0.70, 95% confidence interval 0.52-0.95, P for trend = 0.021).

Low levels of FT3 were associated with increased all-cause mortality in patients with DCM.

Developing effective spinal cord repair strategies for spinal cord injury (SCI) is of great importance. Emerging evidence suggests that microRNAs (miRNAs) are closely linked to SCI recovery. This study aimed to investigate the function of miR-34c in the neuronal recovery in rats with SCI.

A rat model with SCI was established. Differentially expressed miRNAs were identified by a microarray analysis. MiR-34c expression in rats was measured by reverse transcription quantitative polymerase chain reaction. Altered expression of miR-34c or C-X-C motif ligand 14 (CXCL14) was introduced in SCI rats to measure their roles in neuronal recovery. Western blot analysis was performed to determine the phosphorylation of Janus kinase 2 (JAK2) and signal transducer and activator of transcription-3 (STAT3). Neuronal apoptosis in rat spinal cord tissues was detected. The concentrations of SCI recovery-related proteins thyrotropin releasing hormone (TRH), prostacyclin (PGI2), and ganglioside (GM) were evaluated by enzyme-linked immunosorbent assay. Data were analyzed using a t-test with a one-way or two-way analysis of variance.

Rats with SCI presented decreased grip strength (112.03 ± 10.64 vs. 17.32 ± 1.49 g, P < 0.01), decreased miR-34c expression (7 days: 3.78 ± 0.44 vs. 0.95 ± 0.10, P < 0.05), and increased CXCL14 expression (7 days: 0.61 ± 0.06 vs. 2.91 ± 0.27, P < 0.01). MiR-34c was found to directly bind to CXCL14. Overexpression of miR-34c increased grip strength (11.23 ± 1.08 vs. 31.26 ± 2.99 g, P < 0.01) and reduced neuronal apoptosis in spinal cord tissues (53.61% ± 6.07% vs. 24.59% ± 3.32%, P < 0.01), and silencing of CXCL14 also increased the grip strength (12.76 ± 1.13 vs. 29.77 ± 2.75 g, P < 0.01) and reduced apoptosis in spinal cord tissues (55.74% ± 6.24% vs. 26.75% ± 2.84%, P < 0.01). In addition, miR-34c upregulation or CXCL14 downregulation increased the concentrations of TRH, PGI2, and GM, and reduced phosphorylation of JAK2 and STAT3 in rats with SCI (all P < 0.01).

The study provided evidence that miR-34c could promote neuronal recovery in rats with SCI through inhibiting CXCL14 expression and inactivating the JAK2/STAT3 pathway. This study may offer new insights into SCI treatment.

冠状病毒疾病2019（新冠肺炎）已被宣布为全球疫情，是全球范围内的重大公共卫生问题。新冠肺炎是一种损害多器官的全身性疾病，其中以肺为主要靶器官。

The predictive value of hemoglobin A1c (HbA1c) levels in non-diabetic patients with myocardial infarction undergoing percutaneous coronary intervention (PCI) is still controversial. This study aimed to evaluate whether HbA1c levels were independently associated with adverse clinical outcomes in non-diabetic patients with coronary artery disease (CAD) who had undergone PCI by performing a meta-analysis of cohort studies.

This meta-analysis included non-diabetic patients with CAD who had undergone PCI. A systematic search for publications listed in the PubMed, Embase, and Cochrane Library databases from commencement to December 2018 was conducted. Studies evaluating the adverse clinical outcomes according to abnormal HbA1c levels in non-diabetic patients diagnosed with CAD who had undergone PCI were eligible. The primary outcomes were long-term all-cause deaths and long-term major adverse cardiac events, and the secondary outcome was short-term all-cause deaths. The meta-analysis was conducted with RevMan 5.3 and Stata software 14.0. Odds ratios (ORs) were pooled using a random or fixed-effects model, depending on the heterogeneity of the included studies. Sub-group analysis or sensitivity analysis was conducted to explore potential sources of heterogeneity, when necessary.

Six prospective cohort studies involving 10,721 patients met the inclusion criteria. From the pooled analysis, abnormal HbA1c levels were associated with increased risk for long-term all-cause death (OR 1.39, 95% confidence interval [CI] 1.16-1.68, P = 0.001, I² = 45%). Sub-group analysis suggested that abnormal HbA1c levels between 6.0% and 6.5% predicted higher long-term major adverse cardiac event (including all-cause deaths, non-fatal myocardial infarction, target lesion revascularization, target vessel revascularization, recurrent acute myocardial infarction, heart failure requiring hospitalization, and stent thrombosis) risk (OR 2.05, 95% CI 1.46-2.87, P < 0.001, I² = 0). Contrarily, elevated HbA1c levels were not associated with increased risk of short-term all-cause death (OR 1.16, 95% CI 0.88-1.54, P = 0.300, I²= 0).

An abnormal HbA1c level is an independent risk factor for long-term adverse clinical events in non-diabetic patients with CAD after PCI. Strict control of HbA1c levels may improve patient survival. Further studies in different countries and prospective cohort studies with a large sample size are required to verify the association.

皮肤是最外层的保护性器官，容易受到外部损伤的损害，并且在伤口愈合后保留不希望的疤痕，这通常会降低生活质量并导致经济负担。骨膜素是一种细胞外基质成分，据报道与皮肤伤口愈合和病理性瘢痕形成密切相关。它在各种正常组织中表达，通常与成纤维细胞相关，并参与细胞外基质环境的重塑。^[1,2]在一些疾病状态，如心肌梗塞、癌症、肝纤维化和皮肤的病理性瘢痕形成中，骨膜素据报道是疾病进展的重要调节因子并且显著过表达。^[3]本文就骨膜素在皮肤创伤愈合和病理性瘢痕形成中的作用的研究进展作一综述。

2019冠状病毒病（新冠肺炎）已引起全球爆发，并成为全球重大公共卫生问题。研究发现，新冠肺炎患者普遍并发凝血异常，凝血异常与患者的严重程度和预后密切相关。全面了解新冠肺炎患者凝血病的患病率和凝血参数异常的潜在原因，对于临床医生规范新冠肺炎相关凝血病的诊断和管理至关重要。

心源性休克（CS）是重症监护室中一种危及生命的疾病，导致许多危重患者死亡。尽管CS患者的存活率似乎有所提高，但其预后仍然较差，死亡率在60%至80%之间。^[1]

症状发作4.5 h内溶栓治疗是公认的急性缺血性卒中（AIS）有效且标准的治疗方法，但仍有部分患者临床结局较差。评估和控制AIS不良临床结局的预测因素对于实现最佳治疗是不可或缺的，但入院血糖（ABG）对此的预后价值尚不清楚，仍在争论中。在无糖尿病（DM）患者中评估的ABG常提示急性应激性高血糖，而ABG可能与DM患者的长期血糖控制有密切关系。然而，在大多数关于ABG对AIS后重组组织型纤溶酶原激活剂（rtPA）治疗预后影响的研究中，患者没有被分为有和没有DM的患者。本研究旨在根据中国人群的DM状态调查ABG对溶栓后AIS临床结局的预后价值。

胱硫醚-β-合酶（CBS）缺乏引起的同型胱氨酸尿症是一种罕见的遗传性疾病，最常在儿童期诊断，可导致多系统损伤。^[1,2]的继承模式哥伦比亚广播公司基因缺乏通常为常染色体隐性遗传。已鉴定出160多个突变哥伦比亚广播公司基因到目前为止（http://cbs.lf1.cuni.cz/index.php），最常见的突变之一是c.833T>C点突变，其次是c.572C>T、c.919G>A和c.1006C>T点突变。2018年，李等人^[2]在中国CBS缺乏症患者中发现了8个全新的突变位点，指出哥伦比亚广播公司中国人的突变位点谱与其他种族有显著差异。在本文中，我们进一步对7例同型胱氨酸尿症患者进行了回顾性分析哥伦比亚广播公司我们研究所承认的缺陷。

由于其发病率、死亡率和相关的医疗费用不断增加，血流感染（BSIs）已成为全球关注的问题。ESKAPE中的菌株包括屎肠球菌(屎肠球菌),金黄色葡萄球菌(金黄色葡萄球菌),肺炎克雷伯菌(K.肺炎),鲍曼不动杆菌(鲍曼不动杆菌),铜绿假单胞菌(铜绿假单胞菌），以及肠杆菌spp.，以及大肠杆菌(大肠杆菌），占BSI致病病原体的一半以上。^[1]此外，ESKAPE和大肠杆菌近年来发生了变化。罗马的一项研究发现大肠杆菌，其次是金黄色葡萄球菌、是最常鉴定的微生物；此外，该研究显示，无论在医院还是社区发病，产生超广谱β-内酰胺酶的数量大肠杆菌正在增加，并产生碳青霉烯酶肺炎克雷伯菌在研究期间变得更加普遍。^[1]最近的一项研究表明ESKAPE和大肠杆菌2014年至2018年在意大利一家医院从血液培养物中分离出的微生物。^[2]ESKAPE的频率和阻力率大肠杆菌很可能与疾病谱、地理位置、抗菌药物管理和手部卫生相关。2012年以来，我院逐步执行《抗菌药物临床应用管理办法》（卫生部令第84号）、《抗菌药物临床应用指导原则（2015年版）》、《关于抗菌药物临床应用持续管理的通知》（国家卫健委办公厅，2018年）的部分要求。然而，尚不清楚这些措施是否有效地将抗生素耐药率降至最低。本研究调查了ESKAPE和大肠杆菌从我院血样中分离出来，旨在为ESKAPE和大肠杆菌以及抗生素给药方法的可用性。

急性肺栓塞（APE）是一种具有挑战性的疾病，经常漏诊或延迟诊断，因此可能是致命的。在有冠心病病史的急诊患者中，心电图（ECG）结果往往不具有特异性，APE难以诊断。因此，患者倾向于被诊断为急性冠状动脉综合征（ACS），并且要么在急诊科接受心肌酶观察的复查，要么入院进行冠状动脉造影。2008年欧洲心脏病学会（ESC）急性肺栓塞诊断和处理指南指出，APE的临床风险评估应以Wells评分为依据。^[1]然而，尽管有这一官方建议，Wells评分在急诊医学中并没有广泛使用，尤其是对于冠心病和伴随APE的患者。本研究分析了Wells评分联合D-二聚体水平在识别冠心病患者APE中的预测价值。

颞下窝入路设计用于切除位于颞骨和侧颅底的大肿瘤。^[1]这种方法有几种亚型，包括A型、B型、C型和D型。颞下窝B型（ITFB）入路暴露颈内动脉（ICA）的岩尖、斜坡和水平段，用于切除该区域的肿瘤。^[2]完全暴露ICA水平段的经典ITFB入路包括岩骨次全切除、外耳道前壁和颧弓切除、下颌骨关节盘和髁突切除、下颌骨向下牵引、三叉神经下颌支和脑膜中动脉横断。^[3]

非隔离肺的异常全身动脉（ASANSL）是一种罕见的先天性异常，以前被归类为Pryce I型隔离；它包括通往正常肺的异常全身动脉（ASA）。^[1]为了更清楚地确定ASANSL的特征，我们收集了15例病例的数据并复习了相关文献。已经得出结论，多层计算机断层扫描（MSCT）可以作为一种高度可靠和微创的工具来诊断ASANSL和规划治疗计划。

致编辑：踝关节扭伤约占所有运动损伤的40%，20%~33%的踝关节扭伤会导致踝关节不稳定。^[1]功能性踝关节不稳定（FAI）还没有一个准确和广泛接受的可测量定义，尽管许多外科医生多年来一直在治疗它合并距腓前韧带损伤、跟腓韧带损伤或两者兼而有之。在中国，可能仅仅因为韧带损伤的影像学证据和可能（但不确定）的FAI，就进行一些不必要的韧带修复手术，导致一些不理想的结果。已经开发了几份自我报告问卷来帮助定义FAI，但没有经过验证的中文版本，尽管中国的FAI患者数量最多。国际踝关节联盟推荐了踝关节不稳定仪器、坎伯兰踝关节不稳定工具和基于前两份问卷的功能性踝关节不稳定识别（IdFAI）问卷来评估FAI。^[2]IdFAI在三份问卷中准确率最高。^[3]IdFAI的英文原版已被翻译成多种语言，日语、韩语、巴西语和波斯语版本已得到验证。我们开发了IdFAI中文版（IdFAI-C），并通过评估其区分效度、内部一致性、准确性和重测信度来确定其效度。

致编辑：Kasabach-Merritt综合征（KMS）是一种非常罕见的危及生命的侵袭性血管肿瘤，与Kaposiform血管内皮瘤和簇状血管瘤有关。以血小板减少和血管内凝血为特征，偶尔发展为弥散性血管内凝血。^[1,2]弥漫性浸润性胰腺血管瘤的罕见发病率和KMS的高漏诊可能性使其成为一种致命疾病。在这里，我们描述了一例诊断为胰腺弥漫性浸润性血管瘤（DIH）伴有KMS的病例，并为早期和准确的诊断提供了超声数据，以及西罗莫司的成功治疗经验。

致编辑：广泛使用的他汀类药物降低了心血管疾病的死亡风险。然而，他汀类药物相关的骨骼肌主诉在一定程度上阻碍了其临床应用。杨新石中药配方片（YXST）与常规药物合用，可有效改善心血管疾病患者的临床症状。然而，YXST与他汀类药物联合使用的协同作用和潜在机制仍然未知。因此，探讨YXST改善他汀类药物诱导的肌肉损伤的作用和机制可能有利于心血管疾病患者的运动康复和预后。