轮匝肌切除术联合睫毛外翻褥式缝合对先天性下睑内翻的矫治效果

目的 探究轮匝肌切除术联合睫毛外翻褥式缝合对先天性下睑内翻的矫治效果。方法 选取2019年1月—2022年1月南通大学附属医院眼科收治的82例先天性下睑内翻患儿,采用随机数字表法分为切除术组和缝线组,每组41例,切除术组采用轮匝肌切除术联合睫毛外翻褥式缝合治疗,缝线组采用传统缝线法治疗。术后2个月,比较两组的临床疗效、角膜散光值、最佳矫正视力及泪膜破裂时间。结果 切除术组治疗有效率为98.75%,高于缝线组90.00%(P <0.05)。切除术组治疗前后柱镜度数、泪膜破裂时间的差值均高于缝线组（P <0.05）;两组治疗前后轴位、最佳矫正视力的差值比较,差异无统计学意义（P>0.05）。结论 轮匝肌切除术联合睫毛外翻褥式缝合应用于先天性下睑内翻患儿的治疗中,更有助于提升临床疗效,保护视力且安全性良好。     

Attachment and spreading of fibroblasts on an RGD peptide-modified injectable hyaluronan hydrogel

Hyaluronan (HA) hydrogels resist attachment and spreading of fibroblasts and most other mammalian cell types. A thiol-modified HA (3,3'-dithiobis(propanoic dihydrazide) [HA-DTPH]) was modified with peptides containing the Arg-Gly-Asp (RGD) sequence and then crosslinked with polyethylene glycol (PEG) diacrylate (PEGDA) to create a biomaterial that supported cell attachment, spreading, and proliferation. The hydrogels were evaluated in vitro and in vivo in three assay systems. First, the behavior of human and murine fibroblasts on the surface of the hydrogels was evaluated. The concentration and structure of the RGD peptides and the length of the PEG spacer influenced cell attachment and spreading. Second, murine fibroblasts were seeded into HA-DTPH solutions and encapsulated via in situ crosslinking with or without bound RGD peptides. Cells remained viable and proliferated within the hydrogel for 15 days in vitro. Although the RGD peptides significantly enhanced cell proliferation on the hydrogel surface, the cell proliferation inside the hydrogel in vitro was increased only modestly. Third, HA-DTPH/PEGDA/peptide hydrogels were evaluated as injectable tissue engineering materials in vivo. A suspension of murine fibroblasts in HA-DTPH was crosslinked using PEGDA plus PEGDA peptide, and the viscous, gelling mixture was injected subcutaneously into the flanks of nude mice; gels formed in vivo following injection. After 4 weeks, growth of new fibrous tissue had been accelerated by the sense RGD peptides. Thus, attachment, spreading, and proliferation of cells is dramatically enhanced on RGD-modified surfaces but only modestly accelerated in vivo tissue formation.     

幽门螺杆菌cagA菌株感染对IL-8蛋白在胃癌组织中表达的影响

目的 探讨胃癌组织中HpcagA菌株感染对IL-8蛋白表达的影响。方法 采用流式细胞技术，对27例胃癌及相应的癌旁正常组织中IL-8蛋白的表达进行定量检测，用PCR法，对27例胃癌组织中HpcagA基因进行扩增。结果 27例胃癌组织中中，有25例（92%）可明显表达IL-8蛋白；而相应的癌旁正常组织中，基本没有IL-8蛋白的表达或仅有弱相应的癌旁正常组织中，基本没有IL-8蛋白的表达或仅有弱表达，HpcagA感染的胃癌组织中，IL-8的表达水平为64.27%，高于未感染HpcagA的胃癌组织（39.86%)。结论 IL-8在胃癌组织中的高表达与HpcagA感染有关。即HpcagA菌株感染可上调IL-8在胃癌组织中的表达水平。     

利用密度的指数原理优化X射线中骨骼的边缘

利用指数衰减原理来抑制 x射线图像中小密度组织对骨骼边缘的影响 ,利用该方法很容易使用直方图原理提取出骨骼的边缘和内部结构变化的二值图 ,并有效地抑制了背景对骨骼边缘的影响 ,结合 canny算子的结果 ,可以有效地提取人体复杂结构中骨骼的边缘。     

Cyclin alterations in giant cell tumor of bone.

Cyclins play an important role in regulating the passage of dividing cells through critical checkpoints in the cell cycle. Because alterations of several cyclins, especially cyclin D1, have been implicated in the development of many human neoplasms, we examined 32 cases of giant cell tumor of long bones for cyclin D1 gene amplification and protein overexpression using differential polymerase chain reaction and immunohistochemistry, respectively. In addition, the expression of cyclin D3, cyclin B1, and the proliferation-associated antigen Ki-67 (MIB-1) was assessed immunohistochemically. Low-level cyclin D1 gene amplification was detected in 61% of giant cell tumor cases. All tumors showed cyclin D1, cyclin D3, cyclin B1, and Ki-67 (MIB-1) staining; however, the distribution was very characteristic. Cyclin D1 protein expression was seen predominantly in the nuclei of the giant cells, with occasional mononuclear cells staining. There was no correlation between cyclin D1 gene amplification and protein overexpression. Cyclin D3 staining showed a similar distribution, with 88% of cases showing protein overexpression. Cyclin D1 and/or D3 staining in the giant cells was never associated with staining for either cyclin B1 or Ki-67 (MIB-1), as the expression of the latter two proteins was restricted to the mononuclear cells. Cyclin B1 overexpression was seen in 44% of cases. Ki-67 (MIB-1) staining was present in all cases, and between 10 to 50% of the mononuclear cells were positive. These results suggest that alterations in cyclin D1 and/or D3 might play a role in the pathogenesis of giant cell tumor of bone.     

Changes in ultrastructure and Ca2+ distribution in the isolated working rabbit heart after ischemia. A time-related study.

Ultrastructural changes in cardiac muscle of isolated working rabbit hearts after various periods of ischemia are described and compared with distributional changes in calcium. The effects of reperfusion on these structural parameters were also investigated. The purposes of this study were to relate the role of calcium in the degeneration of cardiac muscle; to determine whether Ca2+ localizations could serve as additional criteria to determine more closely the point of no return; and to investigate the contributory role of reoxygenation to the development of myocardial damage. This study shows the existence of topographic differences in the tolerance to ischemia in the mid area, subendocardium, and subepicardium; that the sequestration of Ca2+ by mitochondria is an energy-requiring (active) process that occurs only during reperfusion; the loss of the sarcolemma's ability to bind Ca2+ during ischemia to coincide with increased Ca2+ entry during postischemic reperfusion (this Ca2+ is scavenged by mitochondria as long as sufficient energy remains available; these changes are interpreted as being at the edge of irreversibility); and the lack of additional damage and and lack of Ca2+ accumulation in mitochondria during reperfusion in cells that are damaged to such an extent that mitochondria possess flocculent densities already at the end of the ischemic insult.     

Somatic mitochondrial mutation in gastric cancer.

Likely hot spots for mutations are mitochondrial sequences as there is less repair and more damage by carcinogens compared with nuclear sequences. A somatic 50-bp mitochondrial D-loop deletion was detected in four gastric adenocarcinomas. The deletion included the CSB2 region and was flanked by 9-bp direct repeats. The deletion was more frequent in adenocarcinomas arising from the gastroesophageal junction (4/32, 12.5%) compared with more distal tumors (0/45). Topographical analysis revealed the absence of the deletion from normal tissues except in focal portions of smooth muscle in one case. In two cases, apparent mutant homoplasmy was present throughout two tumors, including their metastases. In the two other cases, the mutation was present in only minor focal portions ( < 5%) of their primary tumors. These findings document the presence of somatic mitochondrial alterations in gastric cancer, which may reflect the environmental and genetic influences operative during tumor progression.