MRI顺磁性造影剂增强及护理

目的 :进一步探讨 MRI增强前后的准备与护理方法。材料与方法 :共增强 833例 ,男 5 85例 ,女 2 4 8例。使用顺磁性造影剂 Gd- DTPA,按 0 .2 m L/kg体重给药。其中双倍量增强 110例 ,增强前认真履行告知义务和签署同意书。发生造影剂外漏者给予鲜马铃薯片外敷。结果 :增强效果达良好以上共 82 5例 ,占 99% ,未发生严重负反应。 3例造影剂外漏 ,鲜马铃薯片外敷后 3h痊愈。结论 :增强前充分细致的准备是保证增强效果的重要因素。认真履行告知义务和签置同意书 ,不仅尊重了病人的权利 ,也是依法行医 ,保证医疗安全的需要     

环氧合酶-2和血管内皮生长因子共表达与肝细胞癌血管形成的关系

目的　探讨环氧合酶 (COX) 2与肝细胞癌血管形成的关系。方法　利用免疫组织化学、Westernblot方法检测 48例肝癌组织中COX 2和血管内皮生长因子 (VEGF)蛋白及逆转录 聚合酶链反应法 (RT PCR)检测COX 2和VEGFmRNA的共表达 ,对共表达COX 2和VEGF蛋白和mRNA的肝癌组织进行微血管记数。结果　免疫组织化学检测中 ,48例肝癌组织 3 6例共表达COX 2和VEGF蛋白。类似结果见于蛋白电泳分析。RT PCR显示 ,48例肝癌组织 3 6例共表达COX 2mRNA和VEGFmRNA。两者之间的表达明显相关 (γ =0 .845 )。共表达COX 2和VEGF蛋白和mRNA的肝癌组织中 ,平均微血管数 (5 6.8± 17.5 )个 ,明显高于阴性表达组。结论　COX 2可能与肝细胞癌的血管形成有关 ,且其作用之一可能是通过上调VEGF通道来发挥的     

椎管内原发性孤立性纤维性肿瘤临床病理观察(附2例报告)

目的探讨椎管内孤立性纤维性肿瘤的临床病理特征、诊断和鉴别诊断,以期提高对该肿瘤的诊断水平。方法复习2例椎管内原发性孤立性纤维性肿瘤的临床资料,并观察其组织学特征和免疫组化标记。结果2例患者男、女各1例,年龄分别为23岁和32岁,临床表现为局部神经压迫症状。MRI示椎管内髓外硬膜内占位。组织学特征为梭形、卵圆形细胞呈束状、波浪状或旋涡状排列,富于胶原纤维及伴有分支状薄壁血管。细胞未见异型性和核分裂像。免疫组化示瘤细胞Vimentin( ),CD34( ),CD99( ),Bcl-2( ),AACT(-),Actin(-),S-100(-),EMA(-),GFAP(-),CD68(-),CD117(-),SMA(-),NF(-)。结论椎管内原发性孤立性纤维性肿瘤是一种罕见的肿瘤,诊断主要依靠病理形态学及免疫组化,并应与椎管内的其他梭形细胞肿瘤鉴别。     

自信，男人成长的催化剂

人的成长要经历不同的阶段，每个阶段的跨越，都是在“高压”、“高温”、“催化剂”的作用下，经过所有的物质、精神、社会的转换而完成。自信——则是男人成长的最好催化剂。[编者按]     

Effect of tacrolimus and partial hepatectomy on transthyretin metabolism in rats

Liver transplantation, which serves as treatment of familial amyloidotic polyneuropathy (FAP), and domino liver transplantation, which utilizes resected livers from patients with FAP for treatment of liver diseases, may induce changes in transthyretin (TTR), a pathogenic FAP-related protein. To evaluate this possibility, we performed a 70% hepatectomy or administered tacrolimus to Dark Agouti (DA) rats for 7 days and then measured changes in liver TTR mRNA levels and changes in serum TTR concentrations. After hepatectomy, TTR mRNA levels decreased by 77%; at day 3, they returned to preoperative levels. Except for slightly elevated serum TTR concentrations 12 h after operation, serum TTR levels remained unchanged. Thus, partial hepatectomy did not influence serum TTR concentrations. After tacrolimus administration, TTR mRNA declined by 56% 12 h after the experiment started; however, after day 3, a rebound phenomenon occurred until day 7. Tacrolimus may facilitate serum TTR degradation, although production of TTR in the liver also increased. This finding -- that TTR, the source of FAP-inducing amyloid, did not increase after transplantation -- may help post-transplantation treatment of patients who have FAP and other liver diseases.     

Anti-ulcer activity and mode of action of the polysaccharide fraction from the leaves of Panax ginseng.

The effects of a weakly acidic polysaccharide fraction, GL-4, from the leaves of Panax ginseng C. A. Meyer on various experimental gastric ulcer models in mice and rats have been studied. Oral administration of GL-4 at doses of 50 to 200 mg/kg inhibited the formation of the gastric lesions induced by necrotizing agents such as HCl/ethanol and ethanol in a dose-dependent manner. This protective effect was observed not only upon oral but also upon subcutaneous administration of GL-4 (50-100 mg/kg). GL-4 also inhibited the formation of gastric ulcers which were induced by water immersion stress, indomethacin, or pylorus-ligation. The contents of prostaglandin E2 in the gastric juice from rats were not influenced by oral administration of GL-4. The protective action of GL-4 against HCl/ethanol-induced gastric lesions was not abolished by pretreatment with indomethacin. When GL-4 (100 mg/kg, p.o.) was administered into pylorus-ligated rats, both gastric acidity and pepsin activity in the gastric juice decreased significantly.     

Inhibition of a dihydropyridine, omega-conotoxin insensitive Ca2+ channel in rat synaptosomes by venom of the spider Hololena curta.

Inhibition of the N and L type Ca2+ channels with omega conotoxin GVIA (omega-CgTx) together with the dihydropyridine (-)-202-791 produces slight reduction (congruent to 25%) of K(+)-evoked Ca2+ influx in mammalian synaptosomes. These results and others suggest the existence of a third high threshold voltage sensitive calcium channel (VSCC) responsible for the majority of influx. Venom from the funnel web spider Hololena curta potently and persistently inhibited Ca2+ influx in rat cortical synaptosomes (IC50 1:10,000 or 4.21 micrograms/venom protein/ml of synaptosomes). Also Ca2+ influx in cerebellar synaptosomes was inhibited in a similar manner. K(+)-evoked tritium release from synaptosomes labeled with [3H]noradrenaline was inhibited by Hololena venom (congruent to 60% reduction at 10 micrograms/venom protein). Inhibition of Ca2+ influx by venom was unaffected by combined omega-CgTx and (-)-202-791 pretreatment (both 1 microM). Hololena venom and its active constituent should provide useful tools to investigate the role of this novel Ca2+ channel in neuronal function.     

Microencapsulated pancreatic islets: a pathologic study.

Dog pancreatic islets isolated by an enzymatic digestion method were encapsulated in an alginate-poly L-lysine-alginate membrane. These microencapsulated pancreatic islets were cultured in vitro to study their ability of insulin secretion. Portions of these in vitro-cultured microencapsulated pancreatic islets were taken out for a viability dye exclusion study as well as for pathologic studies to correlate them with insulin secretion ability. We found that there was a strong correlation between them. Good insulin-secreting microcapsules showed well-preserved cell membranes and beta-cell granules. An in vitro culture for one to two days in RPMI-1640 made the islets more stable, the cellular surface became smoother and the beta-granules were in better shape. The microencapsulated pancreatic islets were also injected into the peritoneum of streptozotocin-induced diabetic CDF1 mice. Blood glucose levels dropped and stayed low for up to 60 days. But, when non-encapsulated dog pancreatic islets were used, the blood glucose levels remained low for only about 14 days. A small portion of the injected microcapsules were washed out at specific times for pathologic study. Up to 28 days after injection, only a few of the injected microcapsules showed pericapsular cellular infiltrate. However, after 56 days, most of the microcapsules showed dense pericapsular cellular infiltrate. Immunohistochemical analysis of these infiltrates showed that the majority of cells were fibroblasts and macrophages. Most of the cells located in the inner portion of the infiltrate were fibroblasts, while the macrophages were located mainly on the outer portion. Both scanning and transmission electron microscopy showed that the surface of the microcapsule outer wall was much smoother than the inner wall. The size of the microcapsules was approximately 0.6-0.8 mm and the thickness of the wall measured around 10 nm. The smaller the microcapsule is, the less chance there is of rupture with release of the xenographic islets. Once the wall of the transplanted microcapsules was ruptured, the inner surface showed more increased inflammatory cell and fibroblast infiltration than the outer surface.     

Macrophages are activated by 17beta-estradiol: possible permission role in endometriosis.

On the basis of the common occurrence of high concentration of estrogen and activated macrophages in patients with endometriosis, we postulate that interaction between 17beta-estradiol and macrophage may be an important affair in endometriosis. So our study was focused on the effect of 17beta-estradiol on macrophage. First morphology of macrophages was examined with environmental scanning electron microscopy. Increased size, extension of more microvilli, expression of retraction fibers and elaboration of membrane ruffles were detected in 17beta-estradiol treated macrophages. Then Nitrate and nitrite level in the supernatant was measured by the method of Griess and iNOS expression was analyzed using immunohistochemical staining. It showed that 17beta-estradiol could induce NO release from peritoneal macrophages and expression of iNOS was increased. Also more TNF-alpha in supernatant that was measured by MTT via L929 cell was produced by macrophages under the inducing of 17beta-estradiol. Furthermore, [Ca2+]i, which was viewed by microscope in a laser scanning confocal unit, elevated 39.8% in peritoneal macrophages after 17beta-estradiol 100 nmol/L treated. The results above demonstrated that peritoneal macrophage had been activated in both morphology and cytokine line when interaction with 17beta-estradiol, which indicated that macrophage activated by 17beta-estradiol might play a permission role in development of endometriosis.