In-hospital and mid-term adverse clinical outcomes of a direct stenting strategy versus stenting after predilatation for the treatment of coronary artery lesions

Background

Direct stenting without balloon dilatation may reduce procedural costs and duration, and hypothetically, the restenosis rate. This study was designed to compare the in-hospital and long-term outcomes of direct stenting (DS) versus stenting after pre-dilatation (PS) in our routine clinical practice.

Methods

The 1 603 patients treated with stenting for single coronary lesions were enrolled into a prospective registry. Patients with acute myocardial infarction (MI) within the preceding 48 hours, and those with highly calcified lesions, total occlusions, or a lesion in a saphenous graft were excluded. The baseline, angiographic and procedural data, inhospital outcomes and follow-up data were recorded in our database and analysed with appropriate statistical methods.

Results

Eight hundred and fifty-seven patients (53.5%) were treated with DS and 746 (46.5%) underwent PS. In the DS group, lesions were shorter in length, larger in diameter and had lower pre-procedural diameter stenosis. Type C and diffuse lesions and drug-eluting stents were found less often (p < 0.001). With univariate analysis, dissection and non-Q-wave MI occurred less frequently in this group (0.2 and 0.6% vs 3.9 and 2.1%, p < 0.001 and p = 0.01, respectively). However, the cumulative major adverse cardiac events (MACE) did not differ significantly (4.9 vs 4.6%, p = 0.79). With multivariate analysis, direct stenting reduced the risk of dissection (OR = 0.07, 95% CI: 0.01–0.33, but neither the cumulative endpoint of MACE (OR = 1.1, 95% CI = 0.58–2.11, p = 0.7) nor its constructing components were different between the groups.

Conclusions

Direct stenting in the real world has at least similar long-term outcomes in patients treated with stenting after pre-dilatation, and is associated with lower dissection rates.     

Comparison of the fertilizing capability of spermatozoa from ejaculates, epididymal aspirates and testicular biopsies using intracytoplasmic sperm injection

A prospective study was carried out to compare the fertilizing capability and pregnancy outcome following intracytoplasmic sperm injection (ICSI) using spermatozoa obtained from ejaculates, or surgically from epididymis or seminiferous tubules. A total of 77 ICSI cycles (one per patient) was included. In all, 28 patients had severe oligoasthenoteratozoospermia, 19 patients had obstructive azoospermia and 30 patients had non-obstructive azoospermia. The main outcome measures were fertilization rate per injected metaphase II oocyte and the clinical pregnancy rate per embryo transferred back to the female recipients. In patients with severe oligoasthenoteratozoospermia, the fertilization and pregnancy rates were 79 and 25 %. In patients with obstructive azoospermia, for whom epididymal spermatozoa were used, these were 75 and 28%, and in the non-obstructive group for which testicular spermatozoa were used for injection, they were 69 and 21% respectively. These rates were not significantly different in the three groups (P = 0.85 and P = 0.14 respectively), suggesting that spermatozoa from the ejaculates and epididymal or testicular biopsies are able to fertilize equally by using ICSI. Live birth per embryo transfer was significantly reduced in patients with non-obstructive azoospermia compared to the other two groups. The high abortion rate (50%) in the group in which testicular spermatozoa were used raises doubts about the developmental competence of such embryos.      

Entamoeba histolytica induces human neutrophils to form NETs

Entamoeba histolytica invades the intestine and other organs during the pathogenesis of amoebiasis. In the early stages, the host organism responds with an inflammatory infiltrate composed mostly of neutrophils. It has been reported that these immune cells, activated by E. histolytica, exert a protective role by releasing proteolytic enzymes and generating reactive oxygen/nitrogen species (ROS/RNS) and antimicrobial peptides. It is now known that neutrophils also produce neutrophil extracellular traps (NETs), which are able to damage and kill pathogens. Studies have shown that intracellular protozoan pathogens, including Toxoplasma gondi, Plasmodium falciparum and Leishmania spp, induce neutrophils to release NETs and are damaged by them. However, the action of this mechanism has not been explored in relation to E. histolytica trophozoites. Through scanning electron, epifluorescence microscopy and viability assays, we show for first time that during in vitro interaction with E. histolytica trophozoites, human neutrophils released NETs that covered amoebas and reduced amoebic viability. These NETs presented histones, myeloperoxidase and decondensed chromatin. The results suggest that NETs participate in the elimination of the parasite.     

成人型胆管囊肿及其合并症的超声与核磁及胰胆管水成像诊断

目的　探讨成人胆管囊肿及其合并症的超声、核磁及胰胆管水成像 (MR/ MRCP)的影像表现。方法　选取胆管扩张病例进行超声及核磁检查 ,观察胆胰管内径、胆管扩张形态、管壁厚度、回声 ,并进行彩色多普勒血流检测及核磁胰胆管水成像 (MR/ MRCP)检查 ,两者结果与术后病理对照。结果　经手术证实胆管囊肿 2 0例 ,包括 :Caroli's病 2例 , 型胆总管囊肿 14例 ,呈囊性、梭形、圆柱形扩张 ;肝门部胆管囊肿 (囊肿型 ) 3例 ,胆总管上段憩室 1例 ( 型 )。合并胆囊结石 10例 ,肝内胆管、胆总管结石 8例 ;合并肝局灶性炎 3例 ,肝脓肿 1例 ;合并癌变 5例 (高、低分化腺癌 3例 ,黏液腺癌 1例 ,类癌 1例 ) ;共同管过长 (>1.5 cm) 6例。超声与 MRCP对胆管囊肿全部诊断。合并症中超声对炎变、结石、癌变诊断分别为 95 % ,10 0 % ,95 % ,而 MRCP/MR为 10 0 % ,90 % ,95 %。超声对结石、癌变及管壁的微细结构观察优于 MRCP,MRCP对胆管全程显示优于超声 ,结合平扫及增强扫描诊断炎变符合率 10 0 %。结论　超声与 MR成像在成人胆管囊肿及其合并症中的诊断意义重大 ,联合应用有利于对该病的全面认识 ,便于指导临床。     

Nonprogression of coronary artery atherosclerosis in homozygous familial hypercholesterolemia after 31 months of repetitive plasma exchange

The effects of plasma exchange performed every two weeks for 31 months in combination with diet and drug therapy were studied in a patient with receptor-defective homozygous familial hypercholesterolemia. Coronary angiography performed three years prior to commencing plasma exchange was compared to angiography 31 months after starting the program. Comparison of the angiograms taken six years apart showed no progression of coronary atheroma in the main left coronary artery in which a 30% narrowing was originally seen. An internal mammary artery-coronary artery bypass remained widely patent and showed no development of atherosclerosis. Plasma cholesterol levels were reduced 46% by plasma exchange, diet and drug compared to diet and drug alone. Achilles tendon xanthoma diminished significantly. It appears that plasma exchange combined with diet and drug therapy, while not producing regression of existing atheromatous lesions, does retard or prevent further progression.     

Identification of MEN1 gene mutations in sporadic carcinoid tumors of the lung

Lung carcinoids occur sporadically and rarely in association with multiple endocrine neoplasia type 1 (MEN1). There are no well defined genetic abnormalities known to occur in these tumors. We studied 11 sporadic lung carcinoids for loss of heterozygosity (LOH) at the locus of the MEN1 gene on chromosome 11q13, and for mutations of the MEN1 gene using dideoxy fingerprinting. Additionally, a lung carcinoid from a MEN1 patient was studied. In four of 11 (36%) sporadic tumors, both copies of the MEN1 gene were inactivated. All four tumors showed the presence of a MEN1 gene mutation and loss of the other allele. Observed mutations included a 1 bp insertion, a 1 bp deletion, a 13 bp deletion and a single nucleotide substitution affecting a donor splice site. Each mutation predicts truncation or potentially complete loss of menin. The remaining seven tumors showed neither the presence of a MEN1 gene mutation nor 11q13 LOH. The tumor from the MEN1 patient showed LOH at chromosome 11q13 and a complex germline MEN1 gene mutation. The data implicate the MEN1 gene in the pathogenesis of sporadic lung carcinoids, representing the first defined genetic alteration in these tumors.      

Genetic variants in cell cycle control pathway confer susceptibility to lung cancer.

PURPOSE: To test the hypothesis that common sequence variants of cell cycle control genes may affect lung cancer predisposition. EXPERIMENTAL DESIGN: We explored lung cancer risk associations of 11 polymorphisms in seven cell cycle genes in a large case-control study including 1,518 Caucasian lung cancer patients and 1,518 controls. RESULTS: When individuals with variant-containing genotypes were compared with homozygous wild-type carriers, a significantly increased lung cancer risk was identified for polymorphisms in p53 intron 6 [rs1625895; odds ratio (OR), 1.29; 95% confidence interval (95% CI), 1.08-1.55] and in p27 5' untranslated region (UTR; rs34330; OR, 1.27; 95% CI, 1.01-1.60). Compared with homozygous wild-types, the homozygous variant genotypes of STK15 F31I and CCND1 G870A were associated with a significantly altered lung cancer risk with ORs of 0.58 (95% CI, 0.37-0.90) and 1.26 (95% CI, 1.03-1.53), respectively. To assess the cumulative effects of all the investigated polymorphisms on lung carcinogenesis, we conducted a combined analysis and found that compared with low-risk individuals with few adverse alleles, individuals with more adverse alleles had an increased risk in a significant dose-dependent manner (P(trend) = 0.041). This pattern was more evident in ever smokers (P(trend) = 0.037), heavy smokers (P(trend) = 0.020), and older subjects (P(trend) = 0.011). Higher-order gene-gene interactions were evaluated using the classification and regression tree analysis, which indicated that STK15 F31I and p53 intron 6 polymorphisms might be associated with lung carcinogenesis in never/light-smokers and heavy smokers, respectively. CONCLUSIONS: Our results suggest that cell cycle gene polymorphisms and smoking may function collectively to modulate the risk of lung cancer.     

Differential induction in telomerase activity among bladder cancer patients and controls on gamma-radiation.

Expression of telomerase is one of the hallmarks of tumor cells and has been used as a diagnostic biomarker and a therapeutic target in cancer. Novel findings have shown that telomerase activation in normal human epithelial cells may affect expression of several cancer-related genes, such as growth-related genes and c-myc gene, suggesting a possible role of telomerase in tumor initiation. Therefore, we hypothesized that individuals who are sensitive to mutagen challenge in terms of induced telomerase activity might have increased cancer risk. We tested this hypothesis in a bladder cancer case-control study (51 cases and 51 matched controls) by measuring baseline and gamma-radiation-induced telomerase activities in peripheral blood lymphocytes. We found a significantly higher gamma-radiation-induced telomerase activity in bladder cancer cases compared with the controls (1.34 versus 1.23; P = 0.044). A similar finding was also observed using the normalized telomerase activity (ratio of gamma-radiation induced versus baseline; 1.49 versus 1.19; P < 0.001). In further categorizing the telomerase activity using 75% of the normalized value in the controls as a cutoff point, we found a significantly increased risk for bladder cancer associated with higher induced telomerase activity (adjusted odds ratio, 3.62; 95% confidence interval, 1.38-9.51). In quartile analysis, a dose-response association was noted between the induced telomerase activity and increased bladder cancer risk (P(trend) = 0.005). Our findings provide the first evidence linking the mutagen-induced telomerase activity in peripheral blood lymphocytes to the risk of bladder cancer, which warrants further investigation in large-sized studies and other cancer types.