Further studies on interactions between periaqueductal gray, nucleus accumbens and habenula in antinociception.

Previous findings from this laboratory with the intracerebral microinjection technique suggested that the periaqueductal gray (PAG), nucleus accumbens, and habenula might constitute a unidirectional loop to play their roles in pain modulation. In the present study we demonstrate that intra-habenular injection of naloxone antagonizes the analgesia elicited by morphine injected into the periaqueductal gray (PAG) and that intra-accumbens injection of naloxone is capable of attenuating the analgesic effects of morphine injected into the habenula. These results indicate that the relationships between these nuclei may be more complex than the putative unidirectional loop.     

Changes in malondialdehyde contents in serum and tissues after ischemia and reperfusion of the bowel in dogs]

The portal circulation was reduced to 50% for one hour by partially occluding the superior mesenteric artery, and the relationship between the changes in malondialdehyde (MDA) and multiple organ damage was studied. The results showed that there was a marked change in hepatic enzymology, with MDA values significantly elevated in serum and lung and liver tissues after the reperfusion when compared with controls. These results suggested that lipid peroxidation initiated by free oxygen radicals played an important role in the multiple organ damages, and the extent of organ damage was closely correlated with the contents of MDA in tissues.     

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.     

Expression of EGF receptors in cell lines derived from female genital cancers and enhancement of the therapeutic effect of anticancer drugs by EGF]

Manifestation of EGF receptors and enhancement of an anticancer agent by EGF were studied in cultured cells derived from female genital cancers. 1) The numbers of EGF-receptors of SKG-3a, RMUG-s, HUOA, A-431 and HEC-1 were 1.22 x 10(4), 6.94 x 10(4), 2.75 x 10(4), 5.25 x 10(5) and 0.92 x 10(4) sites per cell respectively. The values for the dissociation constant (Kd) of RMUG-s, SKG-3a, HUOA and HEC-1 were 340pM, 477pM, 989pM and 2,187pM, respectively. 2) All cell lines were stimulated by EGF at low concentrations and inhibited at higher concentrations. The growth stimulation rates for SKG-3a, HEC-1, HUOA and RMUG-s in the presence of 0.01 nM EGF at 48 hours were 8, 18, 21.1 and 3.7%, respectively. The growth inhibition rates for SKG-3a, A-431, HEC-1, HUOA and RMUG-s in the presence of 1.0 nM EGF at 48 hours were 32, 28, 25.8, 11.2 and 6.8%, respectively. 3) The antitumor effect of CDDP was enhanced by the presence of EGF at both a concentration of 0.01 nM (except for A-431) and a concentration of 1.0 nM, in all cell lines. 4) EGF receptors of RMUG-s and HUOA were decreased by CDDP. The values for RMUG-s and HUOA were 1.71 x 10(4), 0.52 x 10(4) (CDDP 0.4 microgram/ml) and 0.95 x 10(4), 0.29 x 10(4) sites per cell (CDDP 2.0 micrograms/ml), respectively. The effect of CDDP on EGF receptors was not recognized in SKG-3a and HEC-1. In brief, EGF receptors were significantly expressed in cell lines derived from female genital cancers.(ABSTRACT TRUNCATED AT 250 WORDS)     

卵巢恶性生殖细胞肿瘤患者保留生理功能的治疗

卵巢恶性生殖细胞肿瘤多发于青少年,在中国和亚洲其他地区,其发病率远高于西方国家,占全部卵巢恶性肿瘤的5%～20%.卵巢恶性生殖细胞肿瘤主要包括无性细胞瘤、未成熟畸胎瘤、内胚窦瘤、胚胎癌、原发性绒癌以及混合性生殖细胞肿瘤,前三者最常见.由于该疾病大多数生长迅速、恶性程度高、预后差且多发于年轻妇女甚至是幼女而受到临床医生的高度重视.在有效的化疗方法使用前,卵巢内胚窦瘤及未成熟畸胎瘤手术治疗后的存活率仅为7.1%和27%,而且过大的手术范围不仅使患者丧失了生育功能,更因为卵巢的切除而影响第二性征的发育,严重影响患者今后的生存质量.随着联合化疗的应用和不断改进,卵巢恶性生殖细胞肿瘤的存活率逐渐提高,达到87%～97.3%.与卵巢其他恶性肿瘤有所不同的是,该病的治疗方案需根据临床期别、病理组织学特征、患者年龄及生育要求等综合考虑.     

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.     

端粒酶在鳞状细胞癌和Bowen病组织中的表达

目的探讨端粒酶在皮肤鳞状细胞癌(SCC)及Bowen病(BD)病变组织中的表达及其临床意义。方法应用原位杂交方法检测30例皮肤SCC和30例BD病变组织中端粒酶基因hTR和hTERTmRNA的表达。结果在BD组织中hTR和hTERTmRNA呈弱表达,阳性率为23.33%和16.67%。在SCC中,hTR和hTERTmRNA的阳性率分别为86.67%和93.33%。其中Ⅰ、Ⅱ级SCC阳性率分别为82.35%和88.24%,无强阳性;Ⅲ、Ⅳ级SCC阳性率分别为92.31%和100%、强阳性表达率分别为69.23%和76.92%。SCC和BD两者比较差异有显著性(P<0.05)。SCCⅠ、Ⅱ级与Ⅲ、Ⅳ级比较差异有显著性(P<0.05)。结论端粒酶hTR和hTERTmRNA的表达增多是预测皮肤SCC的重要因素。     

Tardive dyskinesia in children treated with atypical antipsychotic medications.

Recent years have witnessed increased antipsychotic treatment of children despite limited long‐term safety data in children. In this study, motor side effects associated with the use of antipsychotic drugs in children were examined in a sample of pediatric psychiatric patients. Child and adolescent psychiatric patients receiving antipsychotics (most were on atypicals) for 6 months or longer (n = 118) were compared with antipsychotic‐naïve patients (n = 80) with similar age, sex ratio, and diagnoses. Only 19% of patients on antipsychotics had ever experienced psychotic symptoms. Eleven children (9%) on antipsychotics exhibited dyskinesia, when compared with 0 in the naïve group (P = 0.003, Fisher's exact test). Nine of 62 African–American children (15%) on antipsychotics exhibited dyskinesia, when compared with only 4% (2 of 52) of European–American children (P = 0.003, Fisher's exact test). Children treated with antipsychotic drugs might experience a significant risk of dyskinesia even when treated only with atypical antipsychotics. Ethnicity might also be a risk factor for dyskinesia in children. Side‐effect profile of the atypical antipsychotic drugs in children may be much different than that in adults. © 2007 Movement Disorder Society     

住院糖尿病病人病情分析

目的:通过对近年来我院住院糖尿病病人的资料分析,观察糖尿病转归、并发症的发生率及死亡原因.方法:查阅全院住院糖尿病病人病历,对患者的相关临床资料登记.结果:糖尿病患病率呈逐年增加的趋势,与1993年相比,1997年患病率增加0.5倍,1998年患病率增加1倍,2001年前半年增加2倍.2001年上半年住院糖尿病病人高血压、冠心病和心梗的患病率分别为39.1%,35.2%和6.7%,住院高血压病人糖尿病患病率由1998年的6%增至2001年的9%,住院冠心病病人糖尿病患病率增高约10%(P＜0.01).住院心梗病人糖尿病患病率增高约15%(P＜0.05).近3.5年,有2618例糖尿病病人住院(1.95%),与非糖尿病病人相比,病死率无显著性差异.糖尿病主要死亡原因为感染(41.2%),终末期肾病(39.2%)及癌症(31.4%).由于冠心病及脑血管意外死亡仅为15%及13%,而呼吸道感染(81%)及足感染(63%)为主要死因.结论:近8.5年中,在33 005病人中糖尿病病人逐年增多,特别是在近4年中,提高约2倍.高血压、冠心病及心梗病人糖尿病患病率逐年增高.近3.5年中住院糖尿病病人的死亡主要原因并非是心血管病变,而是感染.糖尿病病人癌症病死率有所增加.提倡早期诊断,早期预防,早期治疗糖尿病,采取健康的生活方式.