眼部血管平滑肌瘤与平滑肌瘤

报告眼部血管平滑肌瘤１２例，平滑肌瘤２例，并作临床病理分析。本病临床特点是：①ＣＴ显示为圆或椭圆形边界清楚包块，部分病例有钙化斑存在。②手术时所见为一个圆或椭圆形、有包膜、紫红色肿块，与周围组织粘连及易出血。按组织病理学分类，血管平滑肌瘤可分为三个类型（海绵状型、静脉型、实体型），在部分病例标本中，三种类型可同时存在。     

Development of cyclosporin A-loaded hyaluronic microsphere with enhanced oral bioavailability

To develop a hyaluronic microsphere with the improved oral bioavailability of poorly water-soluble cyclosporin A (CsA), the microspheres were prepared with varying ratios of sodium hyaluronate (HA)/sodium lauryl sulfate (SLS)/CsA using a spray-drying technique. The effects of HA and SLS on the dissolution and solubility of CsA in microspheres were investigated. The CsA-microsphere prepared with HA/SLS/CsA at the ratio of 4/2/1 gave the highest solubility and dissolution rate of CsA among those formulae tested. As solubility and dissolution rate of CsA were increased about 17- and 2-fold compared to CsA powder, respectively, this CsA-microsphere was selected as an optimal formula for oral delivery in rats. The CsA-microsphere and Sandimmun neoral sol gave significantly higher blood levels compared with CsA powder alone. Moreover, the AUC, T(max) and C(max) values of CsA in CsA-microsphere were not significantly different from those in Sandimmun neoral sol in rats, indicating that CsA-microsphere was bioequivalent to the commercial product in rats. Our results demonstrated that the CsA-microsphere prepared with HA and SLS, with improved bioavailability of CsA, might have been useful to deliver a poorly water-soluble CsA.     

从正化膏脂论多囊卵巢综合征之防治思路

多囊卵巢综合征是以性激素、糖、脂等内分泌代谢紊乱为主要特点的育龄期女性常见疾病。中医学认为,膏脂为人体精微物质,具有润养、支持、滑利等作用,膏脂异常、不归正化则导致气液运行障碍,脏腑功能失常,百病丛生。基于此,本病病机可归纳为膏脂异常,不归正化,脾虚受损,三焦不利,气血津液失和,邪浊滋生胶着,冲任、胞宫壅滞,以膏脂异常为核心病机。防治本病当以健脾散膏、通利三焦为法,注重营养均衡,适当运动,对证选择半夏泻心汤、二陈汤、苍附导痰汤、三仁汤等,共同促进膏脂正化。附验案1则以佐证。     

Fatigue Cracking Evolution and Model of Cold Recycled Asphalt Mixtures during Different Curing Times

This paper aims to investigate the fatigue cracking evolution of cold recycled asphalt mixtures with asphalt emulsion (CRME) under different curing times. The fatigue cracking model of CRME based on damage mechanics and fracture mechanics was analyzed according to the fatigue loading curve. Firstly, the fatigue cracking evolution of CRME was studied through an SCB strength test and SCB fatigue test. Then, the fatigue damage mechanics were used to establish a nonlinear fatigue cracking model, and the damage degree of CRME at the initial cracking point was determined. The Paris formula was used to characterize the law of fatigue crack propagation. Finally, the microstructure of CRME was observed by scanning electron microscopy (SEM) with the backscattering method. The results indicate that the initial cracking point appears at around 60% of the fatigue life according to the SCB fatigue test by means of image analysis. The damage variable was obtained through the cracking model, and the value of the damage variable was determined as 0.06–0.17 at the initial cracking point. In addition, the Paris formula showed that the crack growth of CRME can be reflected by the stress intensity factor and correlative parameters. Moreover, cement hydration products were mixed with the asphalt membrane to form a denser spatial structure during the curing process, which may provide higher fatigue performance of CRME. This research may provide a theoretical reference for studying the fatigue cracking behavior of CRME.     

两种给药途径致痫大鼠海马神经元超微结构损伤及caspase-3的表达特征

为了观察两种给药途径致痫大鼠海马神经元超微结构的损伤及caspase-3的表达特征,本研究分别采用海人酸腹膜腔注射(A组)和尾静脉注射(B组)诱发大鼠癫痫持续状态(SE)。分别于SE终止后3、6、24、48和72h取海马,电镜观察神经元超微结构的变化,免疫组化方法检测caspase-3的表达。结果显示:两组大鼠均在SE后3h出现线粒体损伤,细胞核的改变出现于SE后24h。A组致痫的潜伏期为97min±11min,神经元以凋亡为主;B组为48min±13min,神经元以坏死为主。SE后6～24h,两组大鼠海马内caspase-3的表达由胞浆向胞核逐渐移位,且均在SE后6h明显增高,24h达顶峰;A组高表达持续至72h,B组在48h显著降低。上述结果提示,线粒体的损伤出现于SE的早期,且可能是神经元损伤的关键环节;致痫方法不同,神经元的死亡形式也不同;而caspase-3的激活是神经元凋亡和坏死的共同通路。     

选择性头部降温对胎羊缺血性脑损伤纹状体神经元凋亡和星形胶质细胞增殖的影响

目的研究选择性头部降温对缺血性脑损伤胎羊纹状体神经元凋亡和星形胶质细胞增殖的影响。方法胎羊于妊娠117~124d时通过双侧颈动脉阻塞30min造成双侧脑缺血损伤,损伤后将胎羊随机分为:损伤组(n=10)、2h低温组(损伤后2h开始亚低温治疗,n=7)和6h低温组(损伤后6h开始亚低温治疗,n=8),另设正常对照组(n=5)。通过冷循环水进行选择性头部降温,取脑组织用免疫组化法检测胎羊纹状体caspase-3(半胱天冬氨酸酶-3),GFAP(胶质纤维酸性蛋白)和PCNA(增殖细胞核抗原)的表达。结果①纹状体神经元凋亡:正常对照组中,caspase-3表达极少(11.00±13.77),损伤组caspase-3免疫阳性细胞为177.70±48.69,明显增加(P=0.000),损伤后2h治疗组(54.14±39.44,P=0.000)和损伤后6h治疗组(122.43±52.36,P=0.017)均能减少caspase-3免疫阳性细胞。②纹状体星形胶质细胞增殖:与正常对照组(163.40±21.98)相比,缺血性脑损伤组的GFAP免疫阳性细胞明显增多(433.25±66.69,P=0.000),损伤后2h开始亚低温治疗(219.50±35.31,P=0.000)和损伤后6h开始亚低温治疗(272.50±86.20,P=0.000)均能减少GFAP免疫阳性细胞。③纹状体PCNA阳性细胞的表达:在正常对照组中,PCNA免疫阳性细胞较少,为153.40±12.46,缺血性脑损伤组的PCNA免疫阳性细胞明显增多(353.70±45.60,P=0.000),损伤后2h开始亚低温治疗(187.14±26.26,P=0.000)和损伤后6h开始亚低温治疗(230.25±67.46,P=0.000)均能减少PCNA免疫阳性细胞。结论亚低温可以抑制纹状体神经元的凋亡和星形胶质细胞的增殖,该作用可能为选择性头部降温的脑保护作用机制之一。     

藏药独一味药理作用及临床应用新进展

简要综述了独一味及其制剂的药理作用和临床应用研究的最新进展,并对其今后的研究方向提出了建议。认为独一味有良好地利用价值和开发潜力,对其研究开发的前景广阔;对其药效的物质基础及作用机理的研究有待深入,尤其应重点关注其疗效确切的镇痛活性。     

Clinical course and outcomes of COVID-19 patients with chronic obstructive pulmonary disease: A retrospective observational study in Wuhan,China

Information about coronavirus disease 2019 (COVID-19) patients with pre-existing chronic obstructive pulmonary disease (COPD) is still lacking. The aim of this study is to describe the clinical course and the outcome of COVID-19 patients with comorbid COPD.This retrospective study was performed at Wuhan Huoshenshan Hospital in China. Patients with a clear diagnosis of COVID-19 who had comorbid COPD (N = 78) were identified. COVID-19 patients without COPD were randomly selected and matched by age and sex to those with COPD. Clinical data were analyzed and compared between the two groups. The composite outcome was the onset of intensive care unit admission, use of mechanical ventilation, or death during hospitalization. Multivariable Cox regression analyses controlling for comorbidities were performed to explore the relationship between comorbid COPD and clinical outcome of COVID-19.Compared to age- and sex-matched COVID-19 patients without pre-existing COPD, patients with pre-existing COPD were more likely to present with dyspnea, necessitate expectorants, sedatives, and mechanical ventilation, suggesting the existence of acute exacerbations of COPD (AECOPD). Greater proportions of patients with COPD developed respiratory failure and yielded poor clinical outcomes. However, laboratory tests did not show severer infection, over-activated inflammatory responses, and multi-organ injury in patients with COPD. Kaplan–Meier analyses showed patients with COPD exhibited longer viral clearance time in the respiratory tract. Multifactor regression analysis showed COPD was independently correlated with poor clinical outcomes.COVID-19 patients with pre-existing COPD are more vulnerable to AECOPD and subsequent respiratory failure, which is the main culprit for unfavorable clinical outcomes. However, COPD pathophysiology itself is not associated with over-activated inflammation status seen in severe COVID-19.     

Distinct histopathological phenotypes of severe alcoholic hepatitis suggest different mechanisms driving liver injury and failure

Intrahepatic neutrophil infiltration has been implicated in severe alcoholic hepatitis (SAH) pathogenesis; however, the mechanism underlying neutrophil-induced injury in SAH remains obscure. This translational study aims to describe the patterns of intrahepatic neutrophil infiltration and its involvement in SAH pathogenesis. Immunohistochemistry analyses of explanted livers identified two SAH phenotypes despite a similar clinical presentation, one with high intrahepatic neutrophils (Neu^hi), but low levels of CD8⁺ T cells, and vice versa. RNA-Seq analyses demonstrated that neutrophil cytosolic factor 1 (NCF1), a key factor in controlling neutrophilic ROS production, was upregulated and correlated with hepatic inflammation and disease progression. To study specifically the mechanisms related to Neu^hi in AH patients and liver injury, we used the mouse model of chronic-plus-binge ethanol feeding and found that myeloid-specific deletion of the Ncf1 gene abolished ethanol-induced hepatic inflammation and steatosis. RNA-Seq analysis and the data from experimental models revealed that neutrophilic NCF1-dependent ROS promoted alcoholic hepatitis (AH) by inhibiting AMP-activated protein kinase (a key regulator of lipid metabolism) and microRNA-223 (a key antiinflammatory and antifibrotic microRNA). In conclusion, two distinct histopathological phenotypes based on liver immune phenotyping are observed in SAH patients, suggesting a separate mechanism driving liver injury and/or failure in these patients.     

Effect of Bi,Sb, and Ti on Microstructure and Mechanical Properties of SAC105 Alloys

The Sn-Ag-Cu (SAC) solder alloys with a low Ag (Ag < 3 wt.%) content have attracted great attention owing to their low cost, increased ability in bulk compliance, and plastic energy dissipation. However, some of their mechanical properties are generally lower than the SAC alloys with a higher Ag content. Adding alloying elements is an effective approach for improving the mechanical properties of the SAC alloys. In this study, the effect of Bi, Sb, and Ti on Sn-1 wt.%Ag-0.5 wt.%Cu (SAC105) solder alloys was investigated. The SAC solders with four compositions: SAC105-1 wt.%Bi, SAC105-1 wt.%Sb, SAC105-1 wt.%Bi-1 wt.%Sb, SAC105-1 wt.%Bi-1 wt.%Sb-0.4 wt.%Ti were prepared. The microstructure and phase compositions were characterized using electron scanning microscopy, and X-ray diffraction. The thermal properties and wettability were also examined. Uniaxial tensile tests and nano-indentation tests were conducted to evaluate the mechanical properties. The results show that adding Bi or Sb could increase the strength of SAC105 alloys mainly due to the solid solution strengthening effect. The creep resistance of SAC105 alloys was also improved with the additions of Bi and Sb. The co-additions of Bi and Sb into SAC105 alloys exhibit an enhanced creep resistance than that calculated by the theoretical calculation. The further addition of Ti into SAC105-1Bi-1Sb alloys demonstrated a much-improved creep resistance, which could be attributed to the synergistic effects of both solid solution strengthening and the precipitation hardening effects.