心包横窦的范围、通连及其变异

目的：明确正常心包横窦的范围、通连及变异,为临床影像学及心脏外科疾病的诊断及治疗提供依据。方法：选用正常成人胸部连续断层标本４０例及心包完整的离体心脏１０例。对横窦的形态、通连关系、毗邻关系及变异进行观察。结果：５０例标本中,２例可见前垂中与主动脉上窦后部直接延续,未见中间水平部;４８例可见中间水平部或／及后垂直部,其中２４％（１２例）中间水平部延续到右肺动脉前下方,３０％（１５例）延续到右肺动脉     

山东省某些高危人群HIV-1感染者分子流行病学研究

目的 了解流行于山东境内ＨＩＶ－１毒株的亚型分布及变异情况,分析其来源并推测其流行趋势。方法 采集了２５份ＨＩＶ－１抗体阳性感染者的全血分离单核细胞（ＰＢＭＣ）,提取前病毒ＤＮＡ,经ｎｅｓｔｅｄ－ＰＣＲ扩增ＨＩＶ－１膜蛋白（ｅｎｖ）基因的Ｃ２－Ｖ３区并进行序列测定和亚型分析。结果 ２５例ＨＩＶ－１阳性感染者的ＰＢＭＣ样品中扩增到２４份可用于序列测定的ＨＩＶ－１ｅｎｖ基因片段,经序列测定和基因分析鉴     

Origin and incidence of xiphoid branch of the internal thoracic artery

The study presents the incidence of a variant terminal branch of the internal thoracic artery (ITA). The ITA’s were cannulated in situ, injected with coloured latex and dissected together with its branches in 62 cadavers. Unlike the usual termination of the ITA bifurcating into the musculophrenic and superior epigastric arteries, this third branch arose from the medial border of the ITA at the level of the 6th costal cartilage. As it descends it inclines medially towards the angle between the xiphoid process and the 7th costal cartilage, giving off 2 or 3 fine branches to the lower sternum. It then passes deep to this angle and can be observed on the anterior surface of the xiphoid process, terminating in fine branches distributed to the inferior aspect of the xiphoid cartilage. It is proposed that this branch at the “trifurcation” of the ITA be termed the xiphoid branch. This branch was noted in 61.3%. An incidence of 30.7% was seen on the right and 21% on the left with bilateral presence in 9.7%. The xiphoid branch contributes to the supply to the lower sternal region and may be of special importance when the collateral supply to the region is compromised in the event of the internal thoracic or superior epigastric artery damage or when used as a conduit in coronary artery by-pass grafts.     

Characterisation of the biochemical and biological variations from the venom of the death adder species (Acanthophis antarcticus, A. praelongus and A. pyrrhus)

We report on species variation in the venoms of the three species of death adder; the Common death adder (Acanthophis antarcticus), the Northern death adder (Acanthophis praelongus) and the Desert death adder (Acanthophis pyrrhus). The venoms were found to vary in their biochemical (chromatography) and biological (PLA₂ activity, anticoagulant activity and reactivity with commercial death adder antivenom) properties. Each species produced significant differences in the profile and distribution of PLA₂ activity, when whole venom was applied to a cation-exchange Mono-S column. PLA₂ enzymes were purified from each venom and termed acanthoxin B (from A. praelongus), acanthoxin C (from A. pyrrhus) and the previously characterised acanthoxin A (from A. antarcticus). Acanthoxin B and C showed lower enzymatic activities than acanthoxin A (4.0, 13.7 and 23.9 μmol of phospholipid hydrolyzed/min/mg protein, respectively). N-terminal sequencing revealed acanthoxin B to share highest homology with the numerous PLA₂ isozymes (Pa-12C, Pa-1G, Pa-12A) from the King brown snake (Pseudechis australis) and Acanthin I from the Common death adder. Similar to acanthoxin A, acanthoxin C showed highest homology with Acanthin I/II, and pseudexin A-chain from the Red-bellied black snake (Pseudechis porphyriacus). Whole venom from A. antarcticus, A. praelongus and A. pyrrhus each showed weak anticoagulant activity (being able to prolong coagulation of the plasma for 107, 220 and 195 s, respectively). By immunodiffusion, each venom produced precipitation bands against commercial death adder antivenom.     

猪蛔虫雌雄个体蛋白质与酶变异初步研究

本文以聚丙烯酰胺梯度凝胶电泳分析了猪蛔虫酶与蛋白质的群体内变异。初步结果表明:在雌雄虫各10个个体的样本中,依据某些区带的增减或迁移率改变,可以将梯度胶蛋白质电泳图谱分为4型;将非特异性脂酶同工酶谱分为4型;但苹果酸脱氢酶谱则无任何个体变异。而且,没有检测到任何与雌雄性别有关的蛋白质或酶的差异。     

Managed Clinical Network for esophageal cancer enables reduction of variation between hospitals trends in treatment strategies,lead time,and 2-year survival

IntroductionDespite evidence-based guidelines, variation in esophageal cancer care exists in daily practice. Many oncology networks deployed regional agreements to standardize the patient care pathway and reduce unwarranted clinical variation. The aim of this study was to explore the trends in variation of esophageal cancer care between participating hospitals of the Managed Clinical Network (MCN) in the Netherlands.Materials and methodsPatients with esophageal cancer diagnosed from 2012 to 2016 were selected from the Netherlands Cancer Registry. Variation on treatment strategies, lead time to start of treatment, and 2-year survival, were calculated and compared between five clusters of hospitals within the network.ResultsA total of 1763 patients, diagnosed in 17 hospitals, were included. 71% of all patients received treatment with a curative intent, which ranged from 69% to 77% between the clusters of hospitals in 2015–2016. Although variation in treatment modalities between the clusters was observed in 2012–2014, no significant variation existed in 2015–2016, except for patients receiving no treatment at all. The 2-year overall survival of patients receiving treatment with a curative intent did not vary significantly between the clusters of hospitals (range: 56%–63%). Nevertheless, the median lead time before patients started treatment with a curative intent varied between clusters of hospitals in 2015–2016 (range: 34–47 days; p < 0.001).ConclusionLimited variation in esophageal cancer treatment between clusters of hospitals in the MCN existed. This study shows that oncology networks can promote standardization of cancer care and reduce variation between hospitals through insight into variation.     

Unraveling a case of 46,XY DSD due to 17ß-Hydroxysteroid Dehydrogenase type 3 mutations at the age of 49

17-ß Hydroxysteroid dehydrogenase type 3 (17β-HSD3) is an enzyme transforming Delta 4 androstenedione into testosterone. It is involved in the early development of the male genital tract. In this case report, we describe a 46,XY Difference of Sexual Development (DSD) individual with a female phenotype, primary amenorrhea, facial dysmorphia and mental retardation. Gene sequencing using a panel of genes involved in DSD revealed two heterozygous loss-of-function mutations in the HSD17B3 enzyme. Furthermore, a microarray analysis revealed a 37Mb segmental 3p duplication and a recurrent 16p13.11 microduplication. The large 3p duplication is responsible for her mental retardation and her facial dysmorphia. Interestingly, HSD17B3 mutations were identified only in adulthood, at the age of 49. Furthermore, the patient's severe mental retardation and facial dysmorphia are due to genetic abnormalities different from the ones involved in her DSD.     

Variability of in vivo potency assays of whole-cell pertussis,inactivated polio,and meningococcal B vaccines

For the batch release of vaccines, potency release assays are required. Non-animal in vitro tests have numerous advantages and are preferred; however, several vaccines are still released using in vivo assays. Their major drawback is the inherent variability with its practical implications. We quantified the variability of in vivo potency release assays for whole-cell pertussis, inactivated polio and meningococcal B (MenB) vaccines which showed large CV (Coefficient of Variation) ranging from 34% to 125%. As inherent variability might potentially be attributed to the highly variable immune system between individual animals, we evaluated the antibody titres to four MenB antigens in 344 individual outbred mice. These varied strongly, with more than 100-fold differences in antibody titres in responsive mice. Furthermore, within individual mice there was generally no correlation between the strengths of the responses to the four antigens. A mouse with a very low or no response to one antigen in many cases exhibited a strong response to another antigen. The large differences between individual animals is likely a considerable contributor to the inherent variability of in vivo potency assays. Our data again support the notion that it is preferred to move away from in vivo potency assays for monitoring batch to batch consistency as part of vaccine batch release testing.     

Self-paced treadmills do not allow for valid observation of linear and nonlinear gait variability outcomes in patients with Parkinson’s disease

BackgroundDue to the imposed constant belt speed, motorized treadmills are known to affect linear and nonlinear gait variability outcomes. This is particularly true of patients with Parkinson’s Disease where the treadmill can act as an external pacemaker. Self-paced treadmills update the belt speed in response to the subject's walking speed and might, therefore, be a useful tool for measurement of gait variability in this patient population. This study aimed to compare gait variability during walking at self-paced and constant treadmill speeds with overground walking in individuals with PD and individuals with unimpaired gait.MethodsThirteen patients with Parkinson’s Disease and thirteen healthy controls walked under three conditions: overground, on a treadmill at a constant speed, and using three self-paced treadmill modes. Gait variability was assessed with coefficient of variation (CV), sample entropy (SampEn), and detrended fluctuation analysis (DFA) of stride time and length. Systematic and random error between the conditions was quantified.ResultsFor individuals with PD, error in variability measurement was less during self-paced modes compared with constant treadmill speed for stride time but not for stride length. However, there was substantial error for stride time and length variability for all treadmill conditions. For healthy controls the error in measurement associated with treadmill walking was substantially less.SignificanceThe large systematic and random errors between overground and treadmill walking prohibit meaningful gait variability observations in patients with Parkinson’s Disease using self-paced or constant-speed treadmills.