不同类型基底动脉闭塞机械取栓的疗效观察

目的评价机械取栓治疗不同类型基底动脉(BA)闭塞的疗效。方法回顾性分析2013年9月至2019年9月海军军医大学附属长海医院脑血管病中心连续收治的95例行机械取栓治疗的BA闭塞患者的临床资料。根据BA闭塞是否为串联病变,分为非串联病变组(67例)和串联病变组(28例)。比较两组血管成功再通(改良脑梗死溶栓分级2b~3级)的比例、90 d预后良好(改良Rankin量表评分为0~3分)的比例、术中挽救措施及不良事件发生率等的差异。结果与非串联病变组相比,串联病变组的年龄偏低(P=0.002),而男性(P=0.009)、有吸烟史(P=0.014)、缺血性卒中TOAST分型为大动脉粥样硬化型(P=0.001)以及存在一侧椎动脉发育不良(P=0.036)的比例更高。两组患者在术前及术后24 h的美国国立卫生院卒中量表评分、股动脉穿刺至BA再灌注时间、血管成功再通比例及90 d预后良好比例方面的差异均无统计学意义(均P>0.05)。串联病变组的发病至就诊时间(P=0.049)、发病至BA再灌注时间(P=0.046)均较非串联病变组延长,且术中挽救措施(包括单纯球囊扩张、急诊支架置入、静脉应用替罗非班)的使用比例均更高(均P<0.05)。两组在手术相关的不良事件及病死率方面的差异均无统计学意义(均P>0.05)。结论对于不同类型的BA闭塞患者,应用机械取栓治疗的临床结局及不良事件的发生率无明显差异,但该结论仍需进一步扩大样本量或进行随机对照试验加以证实。     

A recombined protein (rSj16) derived from Schistosoma japonicum induces cell cycle arrest and apoptosis of murine myeloid leukemia cells

rSj16, a recombined protein from Schistosoma japonicum, has been identified as an anti-inflammatory molecule. In this study, we demonstrated that rSj16 strongly suppressed the growth of murine myeloid leukemia WEHI-3B JCS cells in a dose- and time-dependent manner. rSj16 induced apoptosis by increasing the proportion of sub-G1 apoptotic cells as well as causing cell cycle arrest at the G0/G1 phase. The expressions of cyclin D1, D2, D3, and E, and Cdk 2, 4, and 6 genes in WEHI-3B JCS cells were significantly down-regulated at 24 h as measured by real-time PCR. Furthermore, apoptosis induced by rSj16 was confirmed by 4,6-diamidino-2-phenylindole nuclear staining assay and annexin V/propidium iodide double staining. A reduction of the mitochondrial membrane potential indicated an active involvement of mitochondria in the apoptosis process. rSj16 treatment induced an increase in the activity of caspase 3, 6, and 9, and expression of pro-apoptotic Bax. Meanwhile, the decreased expression of anti-apoptotic Bcl-2 was observed after rSj16 treatment. Taken together, our results implied that rSj16 can inhibit proliferation by inducing G0/G1 cell cycle arrest and apoptosis of murine myeloid leukemia cells via activation of the caspase-mediated mechanism by regulating the expression of Bcl-2 family.     

Reducing False-Positive Biopsies using Deep Neural Networks that Utilize both Local and Global Image Context of Screening Mammograms

Journal of Digital Imaging - Breast cancer is the most common cancer in women, and hundreds of thousands of unnecessary biopsies are done around the world at a tremendous cost. It is crucial to...     

新鲜标本的下胫腓联合韧带解剖特点及临床意义

目的： 研究新鲜标本下胫腓联合韧带的解剖学特点,为下胫腓联合韧带相关损伤及韧带重建提供解剖学依 据。方法： 选取新鲜胫腓下联合标本,剥离新鲜标本的下胫腓联合的肌、血管及筋膜组织,对下胫腓联合前、后、 横韧带进行解剖学测量,包括胫腓下联合前、后、横韧带的近端长度、远端长度、平均宽度、与水平面的夹角、 冠状面的夹角等相关解剖学数据。结果： 下胫腓联合前韧带近、远端平均长度为（8.51±0.70）mm、（19.03±1.35） mm,平均宽度（15.98±1.17） mm,与水平面、冠状面夹角分别为（42.27±3.43）°、（20.50±4.69）° ;下胫腓联 合后韧带近、远端平均长度为（9.32±0.62）mm、（16.92±1.76）mm,平均宽度（14.36±0.88）mm,与水平 面、冠状面夹角分别为（40.96±3.16）°、（13.10±1.99）°;下胫腓联合横韧带近、远端平均长度为（18.46±2.48） mm、（21.87±2.52）mm,平均宽度（4.56±0.17）mm,与水平面、冠状面夹角分别为（30.60±3.65）°、（13.48±1.60）°。 对左右、男女的下胫腓联合前、后、横韧带的解剖学数据进行对比,差异均无统计学意义。结论： 了解下胫腓联 合韧带各解剖结构及其特点,有助于指导下胫腓联合韧带损伤的修复和重建,帮助外科医生制定手术方案,改善 预后。     

糖尿病伴抑郁患者囊泡单胺转运蛋白2基因的多态性

目的:探讨囊泡单胺转运蛋白2基因(VMAT2)多态性与糖尿病患者抑郁状态相关性。方法:糖尿病患者106例,其中合并抑郁(HAMD评分>20分)的患者50例。分析患者的VMAT2基因多态性分布。用logistic回归分析筛选影响抑郁发生的独立危险因素。比较不同基因型的糖尿病合并抑郁患者基线HAMD评分。结果:伴抑郁组rs363371基因位点的GG基因型比率均高于不伴抑郁组(24.0%vs.8.9%,P<0.05)。家庭人均月收入≤3000元、并发症≥2种、rs363371(GG基因型)为糖尿病合并抑郁的独立危险因素(OR=1.86、2.40、1.87,均P<0.001)。rs363371(GG基因型)患者的HAMD评分高于AA基因型、AG基因型[(27.6±3.0)vs.(22.2±2.2),(23.7±2.7),P<0.05]。结论:VMAT2上的rs363371(GG基因型)是糖尿病患者伴发抑郁的危险因素。     

MIR210HG Aggravates Sepsis-Induced Inflammatory Response of Proximal Tubular Epithelial Cell via the NF-κB Signaling Pathway

PurposeAcute kidney injury (AKI) is a serious complication of sepsis and is characterized by inflammatory response. MicroRNA-210 host gene (MIR210HG) is upregulated in human proximal tubular epithelial cells under treatment of inflammatory cytokines. This study aimed to explore the role of MIR210HG in sepsis-induced AKI.Materials and MethodsCell viability was detected by a cell counting kit 8 assay. The levels of proinflammatory cytokines were detected by enzyme-linked immunosorbent assay kits. The protein levels of p65, IκBα, and p-IκBα were examined by western blot analysis. The nuclear translocation of nuclear factor kappa B (NF-κB) was detected by immunofluorescence assay. The histological changes of kidneys were analyzed by hematoxylin and eosin staining assay.ResultsLipopolysaccharide (LPS) treatment significantly inhibited cell viability and increased productions of proinflammatory cytokines in proximal tubular epithelial cells (HKC-8). Additionally, MIR210HG levels in HKC-8 cells were increased by LPS treatment. MIR210HG silencing inhibited the LPS-induced cell inflammatory response. MIR210HG activated the NF-κB signaling pathway by promoting the phosphorylation of IκBα and nuclear translocation of p65. Rescue assays revealed that the MIR210HG-induced increase of cytokines levels and decline of cell viability were rescued by QNZ treatment. Knockdown of MIR210HG decreased blood urea nitrogen, serum creatinine, and proinflammatory cytokine levels in AKI rats. Moreover, the knockdown of MIR210HG protected against AKI-induced histological changes of kidneys in rats.ConclusionMIR210HG promotes sepsis-induced inflammatory response of HKC-8 cells by activating the NF-κB signaling pathway. This novel discovery may be helpful for the improvement of sepsis-induced AKI.     

Dalbavancin exposure in vitro selects for dalbavancin-non-susceptible and vancomycin-intermediate strains of methicillin-resistant Staphylococcus aureus

ObjectivesDalbavancin is a lipoglycopeptide active against methicillin-resistant Staphylococcus aureus (MRSA). Its long half-life (8.5–16 days) allows for once-weekly or single-dose treatments but could prolong the mutant selection window, promoting resistance and cross-resistance to related antimicrobials such as vancomycin. The objective of this study was to evaluate the capacity of post-distributional pharmacokinetic exposures of dalbavancin to select for resistance and cross-resistance in MRSA.MethodsWe simulated average, post-distributional exposures of single-dose (1500 mg) dalbavancin (fCmax 9.9 μg/mL, β-elimination t_1/2 204 h) in an in vitro pharmacokinetic/pharmacodynamic (PK/PD) model for 28 days (672 h) against five MRSA strains and one methicillin-susceptible strain (MSSA). Samples were collected at least daily, and surviving colonies were enumerated and screened for resistance on drug-free and dalbavancin-supplemented medium respectively. Isolates from resistance screening plates were subjected to whole-genome sequencing (WGS) and susceptibly testing against dalbavancin, vancomycin, daptomycin, and six β-lactams with varying penicillin-binding protein (PBP) affinities.ResultsDalbavancin was bactericidal against most strains for days 1–4 before regrowth of less susceptible subpopulations occurred. Isolates with eight-fold increases in dalbavancin MIC were detected as early as day 4 but increased 64–128-fold in all models by day 28. Vancomycin and daptomycin MICs increased 4–16-fold, exceeding the susceptibly breakpoints for both antibiotics; β-lactam MICs generally decreased by two-to eight-fold, suggesting a dalbavancin–β-lactam seesaw effect, but increased by eight-fold or more in certain isolates. Resistant isolates carried mutations in a variety of genes, most commonly walKR, apt, stp1, and atl.ConclusionsIn our in vitro system, post-distributional dalbavancin exposures selected for stable mutants with reduced susceptibility to dalbavancin, vancomycin, and daptomycin, and generally increased susceptibility to β-lactams in all strains of MRSA tested. The clinical significance of these findings remains unclear, but created an opportunity to genotype a unique collection of dalbavancin-resistant strains for the first time. Mutations involved genes previously associated with vancomycin intermediate susceptibility and daptomycin non-susceptibility, most commonly walKR-associated genes.