Two cases of primary splenic hydatid cyst in Greece

Cystic disease of the spleen is an uncommon entity in general population. Most cases result from parasitic infection by Echinococcus granulosus, a form called splenic hydatid disease (SHD), with a reported frequency of 0.5-6.0% within abdominal hydatidosis. On the contrary, an isolated splenic involvement of hydatid disease is very uncommon even in endemic regions. Two cases of primary SHD managed with open and laparoscopic radical surgery in our department are reported herein. Primary SHD is a rare entity with non-specific symptoms underlying clinical suspicion by the physician for prompt diagnosis. Surgical treatment is the mainstay therapy, while laparoscopic approach when feasible is safe, offering the advantages of laparoscopic surgery.     

腹腔镜与阴式子宫肌瘤剔除术临床疗效比较

目的观察比较腹腔镜与阴式子宫肌瘤剔除术的临床疗效。方法符合手术指征的90例子宫肌瘤患者分为腹腔镜组和阴式组（每组45例）,比较疗效。结果二组疗效相似,且术后无并发症发生,住院时问相当。阴式组手术时间、术中出血量、术后排气时间、住院费用明显低于腹腔镜组。结论与腹腔镜手术相比,经阴道手术直视下操作精确、快捷,价格低廉,适应症宽。但由于阴道空间狭窄,易损伤邻近脏器。临床应根据不同情况选择不同的手术方法,达到满意的治疗效果。     

Proteomics of ischemia and reperfusion injuries in rabbit myocardium with and without intervention by an oxygen-free radical scavenger

A brief period of ischemia followed by timely reperfusion may lead to prolonged, yet reversible, contractile dysfunction (myocardial stunning). Damage to the myocardium occurs not only during ischemia, but also during reperfusion, where a massive release of oxygen-free radicals (OFR) occurs. We have previously utilized 2-DE and MS to define 57 protein spot changes during brief ischemia/reperfusion (15 min ischemia, 60 min reperfusion; 15I/60R) injury in a rabbit model (White, M. Y., Cordwell, S. J., McCarron, H. C. K., Prasan, A. M. et al., Proteomics 2005, 5, 1395-1410) and shown that the majority of these occur because of physical and/or chemical PTMs. In this study, we subjected rabbit myocardium to 15I/60R in the presence of the OFR scavenger N-(2-mercaptopropionyl) glycine (MPG). Thirty-seven of 57 protein spots altered during 15I/60R remained at control levels in the presence of MPG (15I/60R + MPG). Changes to contractile proteins, including myosin light chain 2 (MLC-2) and troponin C (TnC), were prevented by the addition of MPG. To further investigate the individual effects of ischemia and reperfusion, we generated 2-DE gels from rabbit myocardium subjected to brief ischemia alone (15I/0R), and observed alterations of 33 protein spots, including 18/20 seen in both 15I/60R-treated and 15I/60R + MPG-treated tissue. The tissue was also subjected to ischemia in the presence of MPG (15I/0R + MPG), and 21 spot changes, representing 14 protein variants, remained altered despite the presence of the OFR scavenger. These ischemia-specific proteins comprised those involved in energy metabolism (lactate dehydrogenase and ATP synthase alpha), redox regulation (NADH ubiquinone oxidoreductase 51 kDa and GST Mu), and stress response (Hsp27 and 70, and deamidated alpha B-crystallin). We conclude that contractile dysfunction associated with myocardial stunning is predominantly caused by OFR damage at the onset of reperfusion, but that OFR-independent damage also occurs during ischemia. These ischemia-specific protein modifications may be indicative of early myocardial injury.     

Intracellular transport of vitellogenin in Xenopus oocytes: An autoradiographic study

The role of primordial yolk platelets (PYPs) in the transport of the yolk precursor vitellogenin to the yolk platelets in Xenopus laevis oocytes has been demonstrated by electron microscopic autoradiography. Within 20 min after exposure of the oocyte to ³H-labeled-vitellogenin, silver grains are associated with small PYPs which are formed by the fusion of endosomes. At 40 min after incorporation of ³H-labeled vitellogenin, autoradiographic silver grains are associated with larger PYPs and with the superficial layer of yolk platelets. Thus, the results demonstrate that PYPs are an intermediate in the transport of vitellogenin from endosomes to yolk platelets. These observations are consonant with the general hypothesis that vitellogenin first associates (binds?) with the plasma membrane, then is incorporated by endocytosis into endosomes which fuse to form PYPs, and finally the contents of the PYPs are eventually deposited into yolk platelets.     

Oogenesis in Fundulus heteroclitus: I. Preliminary observations on oocyte maturation in vivo and in vitro

During the breeding season, the ovary of Fundulus heteroclitus contains follicles of all sizes up to around 1.8 mm in diameter and continuously ovulates eggs (1.7 mm) into the ovarian lumen. Vitellogenic follicles appear to extend up to 1.3 mm, while those larger than 1.4 mm are undergoing hydration concomitant with maturation. If feeding ceases, vitellogenesis appears to stop and maturational stages flush out of the ovary. Refeeding causes reappearance of maturational stages. A culture procedure was developed for dissected F. heteroclitus follicles and a size range (1.3–1.4 mm) was defined which responded to added hormones by undergoing the same maturational changes (germinal vesicle breakdown, fusion, and peripheral detachment of oil droplets, appearance of activability) as occurs in vivo, although the extent of hydration was not quite as extensive. Ovulation, however, did not consistently occur in vitro. Both 11-deoxycorticosterone and progesterone are potent inducers of maturation in vitro, with median effective doses being 10–20 ng/ml. Hydrocortisone is about one-tenth as active. Human chorionic gonadotropin promotes maturational changes in about 25% of the follicles over a broad concentration range (1–100 IU/ml). The environmental and hormonal mechanisms which influence oocyte maturation in teleosts are discussed in relation to our findings for F. heteroclitus.     

Gel-to-gel phase transition may occur in mammalian cells: Mechanism of formation of "dark" (compacted) neurons

In the course of many diseases, individual non-apoptotic cells that are randomly distributed among undamaged cells in various mammalian tissues become shrunken and hyperbasophilic ("dark"). The light microscopic shrinkage is caused by a potentially reversible, dramatic compaction of all ultrastructural elements inside the affected cells, and escape of the excess water through apparently intact plasma membrane. In the case of neurons, the ultrastructural compaction rapidly involves the soma-dendrite domains in an all-or-nothing manner, and also mm-long axon segments. The present paper demonstrates that such ultrastructural compaction in neurons, which affects the whole soma-dendrite domain or long axon segments, can take place both immediately after an in vivo head injury and in rat brains perfusion-fixed for 30 min., and then chilled to just above the freezing point before the same kind of head injury was inflicted. This argues strongly against any enzyme-mediated compaction mechanism. On the analogy of gel-to-gel phase transitions in polymer chemistry, we hypothesize a pure physico-chemical compaction mechanism. Specifically, after initiation at a single site in each affected cell, the ultrastructural compaction is propelled throughout the whole cell on the domino principle by the free energy stored in the form of non-covalent interactions among the constituents of some cytoplasmic gel structure.     

1 July 1858: what Wallace knew; what Lyell thought he knew; what both he and Hooker took on trust; and what Charles Darwin never told them

At the Linnean Society on 1 July 1858, Charles Lyell and Joseph Hooker, using only an extract from Charles Darwin's unpublished essay of 1844, and a copy of a recent letter to Asa Gray in Boston, argued successfully that Darwin understood how species originate long before a letter from Alfred Russel Wallace outlining his own version of the theory of evolution arrived at Darwin's home. That letter from Ternate in the Malay Archipelago, however, was not the first letter Darwin received from Wallace. This article will contend that two of the three letters Wallace sent Darwin between 10 October 1856 and 9 March 1858 arrived much earlier than Darwin recorded, thereby allowing him time to assess Wallace's ideas and claim an independent understanding of how the operation of divergence and extinction in the natural world leads strongly marked varieties to be identified as new species. By the time of the Linnean meeting Darwin's new ideas had filtered into his letters and ‘big’ species book, despite the absence of any independent evidence from the natural world to justify his constant insistence to have been guided only by inductive reasoning. © 2013 The Linnean Society of London, Biological Journal of the Linnean Society, 2013, 109 , 725–736.     

后腹腔镜下保留肾单位肾部分切除术后肾功能的影响因素分析

目的:分析后腹腔镜下保留肾单位肾部分切除术后患肾肾功能的影响因素。方法:回顾性分析2011年5月~2013年10月本院收治的45例行后腹腔镜下肾部分切除术肾癌患者的临床资料,采用99mTc-DTPA肾核素扫描评估术前及术后3月术侧肾的肾小球滤过率(GFR)。结果:手术时间100~240min,平均(135±33.21)min。肾动脉阻断时间(20.01±7.35)min,肿瘤大小(3.05±1.24)cm。术前及术后3月术肾GFR分别是(46.53±6.35)、(32.22±4.65)ml/min。术侧肾术后GFR下降(15.36±2.36)ml/min,与术前相比下降约34%。经随访1月-2年,无复发及转移病例,患者全部无瘤生存。影响手术前后血肌酐水平变化的相关因素主要为手术时间、阻断时间、气流量、术中失血量(P0.05);影响手术前后GFR水平变化的相关因素主要为阻断时间、气流量、手术时间(P0.01)。术前肾功能情况、缺血时间和肿瘤最大径是术侧肾功能下降程度的独立预测因子;术前肾功能情况和肿瘤最大径是总体肾功能下降程度的独立预测因子。结论:后腹腔镜下保留肾单位肾部分切除术后患肾肾功能的影响因素包括术前肾功能、手术时间、肾动脉阻断时间、气流量、术中失血量、肿瘤大小等。