Semi-automatic segmentation of myocardium at risk in T2-weighted cardiovascular magnetic resonance

Background

T2-weighted cardiovascular magnetic resonance (CMR) has been shown to be a promising technique for determination of ischemic myocardium, referred to as myocardium at risk (MaR), after an acute coronary event. Quantification of MaR in T2-weighted CMR has been proposed to be performed by manual delineation or the threshold methods of two standard deviations from remote (2SD), full width half maximum intensity (FWHM) or Otsu. However, manual delineation is subjective and threshold methods have inherent limitations related to threshold definition and lack of a priori information about cardiac anatomy and physiology. Therefore, the aim of this study was to develop an automatic segmentation algorithm for quantification of MaR using anatomical a priori information.

Methods

Forty-seven patients with first-time acute ST-elevation myocardial infarction underwent T2-weighted CMR within 1 week after admission. Endocardial and epicardial borders of the left ventricle, as well as the hyper enhanced MaR regions were manually delineated by experienced observers and used as reference method. A new automatic segmentation algorithm, called Segment MaR, defines the MaR region as the continuous region most probable of being MaR, by estimating the intensities of normal myocardium and MaR with an expectation maximization algorithm and restricting the MaR region by an a priori model of the maximal extent for the user defined culprit artery. The segmentation by Segment MaR was compared against inter observer variability of manual delineation and the threshold methods of 2SD, FWHM and Otsu.

Results

MaR was 32.9 ± 10.9% of left ventricular mass (LVM) when assessed by the reference observer and 31.0 ± 8.8% of LVM assessed by Segment MaR. The bias and correlation was, -1.9 ± 6.4% of LVM, R = 0.81 (p < 0.001) for Segment MaR, -2.3 ± 4.9%, R = 0.91 (p < 0.001) for inter observer variability of manual delineation, -7.7 ± 11.4%, R = 0.38 (p = 0.008) for 2SD, -21.0 ± 9.9%, R = 0.41 (p = 0.004) for FWHM, and 5.3 ± 9.6%, R = 0.47 (p < 0.001) for Otsu.

Conclusions

There is a good agreement between automatic Segment MaR and manually assessed MaR in T2-weighted CMR. Thus, the proposed algorithm seems to be a promising, objective method for standardized MaR quantification in T2-weighted CMR.     

青春期前型外阴纤维瘤临床病理分析

目的:探讨青春期前型外阴纤维瘤(prepubertal-type vulva fibroma,PVF)的临床病理特征。方法:分析2例PVF的临床特点,光镜观察组织病理学形态及免疫组织化学特征并复习相关文献。结果:2例分别为8岁和39岁女性,均以大阴唇肿块就诊。肿块均分布在一侧,4～5 cm大。组织学观察病变位于真皮层边界不清,由稀疏的梭形纤维母细胞样的细胞和大量胶原纤维组成,病变向皮下组织延伸,在邻近的脂肪组织及血管簇、神经周围穿插性生长;梭形细胞形态温和无异型、核分裂象未查见。免疫组织化学标记显示:瘤细胞表达波形蛋白、CD34,不表达SMA、desmin、CD99、S-100蛋白、bcl-2,成人局灶表达ER和PR。结论:PVF是一种好发于青春前期幼女或女童外阴的良性间叶性病变,偶可发生于成年人。其发生可能与激素有关并起源于外阴阴道间质细胞,表现为纤维母细胞分化特征。临床有少量病例如切除不净可局部复发,并见可自发性消退病例。     

宫颈癌组织Raf激酶抑制蛋白和NF—κBp65表达及其临床意义

目的研究宫颈癌组织中Raf激酶抑制蛋白（RKIP）和核因子xBp65（NF-κBp65）的表达,探讨二者表达之间的相关性及其与宫颈癌各临床病理因素之间的关系。方法用免疫组织化学方法检测69例宫颈癌组织、37例宫颈上皮内瘤变组织和18例正常宫颈组织的RKIP和NF-κBp65表达,并分析其与宫颈癌临床病理学特征的关系。结果宫颈癌组织中RKIP的表达低于宫颈上皮内瘤变及正常宫颈组织,而NF-κBp65的表达高于宫颈上皮内瘤变及正常宫颈组织,差异有统计学意义（Hc=45．124、38．107,Z=4．309～5．159,P〈O．01）;RKIP和NF—κBp65在宫颈癌组织中的表达均与临床分期、有无淋巴结转移及肿瘤分化程度有关（χ^2=5．150～11．917,P〈0．05）。宫颈癌组织中RKIP与NF-κBp65的表达呈显著负相关（r=-0．464,P〈O．01）。结论RKIP表达的减少或缺失与宫颈癌的发生、发展密切相关,RKIP表达的减少或缺失可能通过上调NF—κBp65的表达促进宫颈癌的侵袭和转移。     

肠缺血再灌流时肠内给予葡萄糖能增加肠粘膜血流量

目的探讨肠缺血再灌流损伤时肠内营养与肠粘膜血流改变的关系.方法SD大鼠分为三组,先制作空肠袋,然后将激光多谱勒探头和肠粘膜张力计放置在空肠袋两端,分别向袋内注射丙氨酸、葡萄糖及甘露醇.用动脉夹阻断肠系膜上动脉血流60分后,再恢复灌流60分.分别测定肠粘膜血流量和局部PCO2张力(PrCO2).结果缺血再灌流过程中,与甘露醇组比较,葡萄糖组粘膜血流量显著增加,PrCO2降低.结论缺血再灌流过程中,肠内给予葡萄糖能增加肠粘膜血流量,对缺血再灌流损伤的肠道提供保护作用.     

BH3 mimetic ABT-737 potentiates TRAIL-mediated apoptotic signaling by unsequestering Bim and Bak in human pancreatic cancer cells

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to induce mitochondrial apoptotic signaling that can be negatively regulated by prosurvival Bcl-2 proteins. ABT-737 is a small-molecule BH3 mimetic that binds to and antagonizes Bcl-2/Bcl-x(L) but not Mcl-1. We show that ABT-737 can synergistically enhance TRAIL-mediated cytotoxicity in human pancreatic cancer cell lines. ABT-737 was shown to enhance TRAIL-induced apoptosis as shown by DNA fragmentation, activation of caspase-8 and Bid, and cleavage of caspase-3 and poly(ADP-ribose) polymerase. A Bax conformational change induced by TRAIL was enhanced by ABT-737. ABT-737 disrupted the interaction of Bak with Bcl-x(L) in both cell lines. Furthermore, ABT-737 untethered the proapoptotic BH3-only protein Bim from its sequestration by Bcl-x(L) or Bcl-2. Bim small hairpin RNA (shRNA) was shown to attenuate caspase-3 cleavage and to reduce the cytotoxic effects of TRAIL plus ABT-737 compared with shRNA control cells. Finally, Mcl-1 shRNA potentiated caspase-3 cleavage by ABT-737 and enhanced its cytotoxic effects. Taken together, ABT-737 augments TRAIL-induced cell killing by unsequestering Bim and Bak and enhancing a Bax conformational change induced by TRAIL. These findings suggest a novel strategy to enhance cross-talk between the extrinsic and intrinsic apoptotic pathways to improve therapeutic efficacy against pancreatic cancer.     

孕妇妊娠晚期疲乏特征的潜在类别分析

目的 探讨孕妇妊娠晚期疲乏特征的潜在类别,比较不同类别孕妇在人口学特征及睡眠质量、心理韧性上的差异。方法 于2022年4—7月便利选取郑州市某三级甲等医院产科门诊就诊的251例孕妇为研究对象,采用一般资料调查表、疲劳自评量表、匹兹堡睡眠质量指数量表及心理韧性量表进行调查。结果 孕妇妊娠晚期疲乏特征可分为2个潜在类别,即高情境性-广泛疲乏型（29.08%）和积极情境性-疲乏低发型（70.92%）;Logistic回归分析结果显示：孕周、不良妊娠史、睡眠质量及心理韧性是孕妇妊娠晚期疲乏特征的潜在类别的影响因素（P<0.05）。结论 孕妇妊娠晚期疲乏特征存在群体异质性,可分为2个潜在类别,妊娠周数较大、既往有不良妊娠史、睡眠质量差的孕妇妊娠晚期疲乏症状较重,应对该类别孕妇给予更多关注。     

Platelet-agglutinating protein P37 from a thrombotic thrombocytopenic purpura plasma forms a complex with human immunoglobulin G

We have previously reported the purification of a 37-kd platelet- agglutinating protein (PAP p37) from the plasma of a patient with thrombotic thrombocytopenic purpura (TTP) that was shown to be present in a subset of TTP patients. The platelet agglutination induced by PAP p37 has been shown to be inhibited by IgG from normal human adults and the same TTP patient after recovery. To elucidate the mechanism of inhibition of IgG, the interaction between PAP p37 and IgG was studied. The complex formation was demonstrated by the binding of fluid-phase IgG from normal adults and the same TTP patient after recovery to adsorbed PAP by using an enzyme-linked immunosorbent assay. The binding was specific, concentration dependent, and saturable. IgG purified from a 5-month-old baby and the same TTP patient during active disease did not form complex with PAP p37. The IgG covalently cross-linked to Sepharose 4B bound 125I-PAP p37 but not 125I-fibrinogen. Sucrose density gradient ultracentrifugation of a mixture of 125I-PAP p37 and IgG also revealed the fluid-phase complex formation with a sedimentation value of 19S. Complexes of molecular weight ranging from 180,000 to over 350,000 daltons were also detected by molecular sieve chromatography. The IgG that was bound to PAP p37 conjugated to Sepharose 4B inhibited the agglutination of washed platelets induced by TTP plasma containing PAP p37, whereas the IgG that was not bound to PAP p37 did not have a significant inhibitory effect. The complex formation between PAP p37 and specific IgG is likely to account for the in vitro inhibition of TTP plasma-induced agglutination and, at least partly, the in vivo successful treatment with specific IgG-containing normal plasma.     

Post-study aspirin intake and factors motivating participation in a colorectal cancer chemoprevention trial.

We conducted an exploratory, cross-sectional study examining motivators for study participation and post-study aspirin intake in a chemoprevention trial. The parent clinical trial aimed to determine the optimal aspirin dose for colorectal cancer chemoprevention using prostaglandin E(2) as a mucosal biomarker. This trial was randomized and double-blinded in 60 subjects with prior sporadic colorectal adenoma(s) and evaluated three aspirin doses or placebo taken once daily for 4 weeks. A cross-section of 55 evaluable participants who completed the chemoprevention trial were mailed a 16-item, self-administered questionnaire evaluating subject demographics, motivational factors, and health-related behaviors within the framework of Pender's Health Promotion Model (HPM). Forty-three (78%) of 55 participants returned the questionnaire. The most important motivators for study participation were altruistic, i.e., a desire to help future generations at risk of colorectal cancer and personal factors including a desire to reduce one's own risk. Nineteen (44%) of 43 respondents reported that they chose to take daily aspirin post-study without knowledge of study results. At a mean follow-up of 17.3 months, 18 of these 19 subjects continued to take aspirin regularly. Regular use of vitamin supplements pre-study was found to correlate with post-study aspirin use (Mann-Whitney U test, U = 154.0; P = 0.04). We demonstrate, for the first time, that participation in a chemoprevention study can influence the decision to continue the study drug, if available, to reduce perceived cancer risk. Continued post-study aspirin intake indicates an impact of study participation on a health-related behavior and underscores the importance of patient education to guide such decision-making.