地西泮的肠胃循环对中枢抑制作用的影响

研究了小鼠ig不同酸度溶液和活性碳对地西泮肠胃循环的干扰,是否影响其中枢抑制作用。HPLC法测定证实,酸性液体(pH1)ig可使小鼠iv地西泮后1h胃中地西泮排泌量显著增加。以iv地西泮后睡眠持续时间、自主活动抑制及转棒试验跌落率的恢复速度和死亡率为指标,比较了酸性活性碳(2g·kg^-1)、中性活性碳和生理盐水对地西泮中枢抑制作用的影响。结果表明,酸性碳组动物其地西泮所致中枢抑制状态的恢复速度明显加快,死亡率降低。     

The combined contraceptive vaginal device (NuvaRing®): A comprehensive review

Objectives?The aim of this study is to review the development of NuvaRing® over the past decade to illustrate its use-effectiveness and acceptance as an alternative contraceptive option for women.

Methods?The data were extracted from the literature using computerised MEDLINE system. NuvaRing® is a new combined hormonal contraceptive vaginal ring made of ethylene-vinyl-acetate copolymer, releasing 120?μg etonorgestrel and 15?μg ethinyloestradiol per day. This ring is inserted on any day from day 1 to day 5 of a menstrual cycle for 21 days, thereafter removed for 7 days ring-free period and discarded.

Results?Complete inhibition of ovulation is observed during treatment with this device. Clinical exposure to NuvaRing® for 1786 women-years has resulted in 21 pregnancies, giving a Pearl Index of 1.18. Withdrawal bleeding (4.7–5.3 days) is regular (97–99% of cycles) with rare incidence of irregular bleeding (2.6–6.4%). The cycle control is good with the use of this combined contraceptive vaginal ring. NuvaRing® is well tolerated and accepted by women as compared to oral pill.

Conclusions?NuvaRing® is an effective vaginal contraceptive option for women. However, further study is needed for monitoring its long-term effectiveness and impact on patient's quality of life since the NuvaRing^R is marketed in many countries.     

Gene amplification, mutation, and protein expression of EGFR and mutations of ERBB2 in serous ovarian carcinoma

EGFR and erbB-2 are targets for specific cancer therapy. The purpose of this study was to examine the frequency and clinicopathological correlations of gene amplification, protein expression, and mutations of EGFR and ERBB2 in serous carcinoma, the most common and aggressive type of ovarian cancer. Tissue microarray constructed of 398 carcinomas was examined by chromogenic in situ hybridization (CISH) and by immunohistochemistry. Cases with amplification of EGFR by CISH were further analyzed by fluorescence in situ hybridization. One hundred ninety-eight samples were analyzed for mutations in exons 18, 19, or 21 of EGFR and in exon 20 of ERBB2 using denaturating high-performance liquid chromatography and direct sequencing. Amplification of EGFR was present in 12% (41/333), low-level gain in 43% (144/333), and protein overexpression in 17% (66/379) of the tumors. Both increased copy number and overexpression of EGFR were associated with high tumor grade, greater patient age, large residual tumor size, high proliferation index, aberrant p53, and poor patient outcome. Furthermore, increased copy number of EGFR was associated with increased copy number of ERBB2. No mutations were identified in EGFR, whereas one tumor had an insertion mutation in exon 20 of ERBB2. Both amplification and protein overexpression of EGFR occur in serous ovarian carcinoma, but EGFR copy number has a stronger prognostic value. This makes EGFR amplification a potentially useful criterion for selecting patients in clinical trials testing the effect of EGFR inhibitors in serous ovarian carcinoma.     

Platelets lacking functional CD36 (glycoprotein IV) show reduced adhesion to collagen in flowing whole blood

A parallel-plate perfusion chamber has been used to evaluate the contribution of the adhesive membrane glycoprotein CD36 (GPIV) to platelet adhesion on type I collagen in flowing whole blood at a shear rate of 800 s-1. In one series of experiments, reconstituted normal blood (hematocrit 0.4; platelet count 1.5 x 10(5)/microL) was prepared from washed red blood cells, plasma, and washed platelets that had been incubated with Fab fragments of a monospecific polyclonal anti-CD36 antibody (50 micrograms/mL, 30 minutes, 37 degrees C). Percent surface coverage of collagen-coated coverslips using reconstituted blood with antibody-blocked platelets, as compared with paired reconstituted controls (100%), was 50% at 2 minutes, 87% at 5 minutes, and 90% at 10 minutes. Further studies were performed by perfusion of whole blood from a healthy donor of the Naka-negative phenotype, whose platelets constitutively lack CD36, over collagen-coated coverslips. In this case, percent surface coverage was 55% of normal controls at 2 minutes, 76% of controls at 5 minutes, and 72% of controls at 10 minutes. In both preparations, platelets lacking functional CD36 had a statistically significant decrease (P < .005) in adhesion after 2 minutes and 10 minutes perfusion but not at 5 minutes. These results show that functional CD36 facilitates the rapid adhesion of platelets to collagen and that this effect is seen at the earliest time points of their interaction.     

Mutational analysis of susceptibility genes RNASEL/HPC1, ELAC2/HPC2, and MSR1 in sporadic prostate cancer

Three putative prostate cancer-susceptibility genes, RNASEL/HPC1 at 1q24, MSR1 at 8p22, and ELAC2/HPC2 at 17p11, have recently been identified. Our objective was to investigate somatic mutations in these genes in sporadic prostate cancer. We analyzed 39 clinical prostate cancer specimens, 10 prostate cancer xenografts (LuCaP series), and 4 prostate cancer cell lines (LNCaP, DU145, PC-3, and MPC-3) for genetic changes using denaturing high-performance liquid chromatography and direct sequencing in order to screen the whole coding regions of RNASEL and MSR1, as well as exons 7 and 17 of ELAC2. The known 471delAAAG truncating mutation was found in the RNASEL gene in cell line LNCaP. The only new missense variation in RNASEL, Gly296Val, was found in cell line DU145, but not in any other samples. RNASEL and ELAC2 also showed the common missense polymorphic changes. A previously reported truncating mutation (Arg293X) was found in MSR1 in the germ line of one individual. Our results indicate that inactivation of the RNASEL, ELAC2, or MSR1 genes by somatic mutation is a rare phenomenon in sporadic prostate cancer.     

应用诱导缓解及干细胞疗法治疗急性早幼粒细胞白血病的治疗策略特点

目的:全反式维甲酸、砷剂(三氧化二砷、复方黄黛片)、化疗治疗的联合应用明显提高了急性早幼粒细胞白血病的完全缓解率,缓解后治疗则进一步提高了长期生存率,但治疗方案及治疗时间仍存在争议,本文对此进行综述。资料来源:应用计算机检索Medline和CNKI 1992-01/2007-02期间的相关文献,检索词为"白血病、早幼粒细胞、急性、治疗、干细胞、移植,leukemia,promyelocytic,acute,therapy,stem cells,transplantation"。资料选择:对资料进行初审,并查看每篇文献后的引文。纳入标准:与急性早幼粒细胞治疗相关。排除标准:重复研究。资料提炼:共收集到361篇相关文献,41篇文献符合纳入标准,排除的320篇文献为内容陈旧或重复的文献。资料综合:临床分别采用全反式维甲酸、三氧化二砷、复方黄黛片或化疗治疗急性早幼粒细胞白血病,全反式维甲酸、三氧化二砷、复方黄黛片完全缓解率达60%～98%,联合化疗可提高具有高危因素患者的缓解率达90%。联合用药进行完全缓解后治疗可降低复发率,提高无病生存率,但治疗时间短者,其复发率较高,以采用长程治疗(时间大于6年)者5年无病生存率高达48%,而造血干细胞移植者5年无病生存率更可达100%。结论:全反式维甲酸或砷剂单独应用及其联合化疗治疗急性早幼粒细胞白血病均可获得较高的完全缓解率,全反式维甲酸或砷剂联合化疗和造血干细胞移植可进一步降低复发率,提高完全缓解率,以长程治疗和干细胞移植疗效较好。     

Internal podalic version for neglected shoulder presentation with fetal demise

In modern obstetrics, the role of internal podalic version (IPV) is limited to delivery of the second twin. A retrospective study was conducted to assess the efficacy of IPV in singleton neglected shoulder presentation with fetal demise. Women with live fetuses, previous CS or contracted pelvis were excluded. The procedure involved repositioning the prolapsed hand under anaesthetic followed by breech extraction. 12 women were identified over a 19 month period and all underwent successful IPV. One woman had a postpartum haemorrhage. We conclude that, in singleton pregnancies with a transverse lie, IPV has a role to play in the delivery of dead fetuses.     

通信兵智力水平与专业水平的关系

0　引言　智力在很大程度上决定着个体的作业绩效水平 [1 - 3] ,同时也是预测个体职业成就的一个重要指标 .因此 ,我们试图通过对通信兵智力的测量与分析 ,揭示通信兵智力与专业技术水平的关系以及通信兵重要岗位人员智力与专业技术水平的关系 ,为最终科学地建立通信兵职业适宜性测评体系奠定必要的工作基础 .1　对象和方法1.1　对象　某集团军通信团在岗专业技术人员 ,其中技术难度高的报、话务专业人员 6 3名 ,载波、接力等仅对仪器进行操作的专业人员 5 1名 ,外线、架设等一般专业人员 43名 ,共 15 7名 .工作 1a以上 ,年龄在 18～ 32岁之…     

Prostate cancer susceptibility genes: many studies,many results,no answers

Since the first report of a genome-wide scan for hereditary prostate cancer (HPCA hereinafter) in 1996, several publications have presented data implicating various chromosomal regions by linkage analysis without any consequential identifications of the target genes. The most intensive attention has been focused on chromosome 1, and it has been proposed to contain at least three sub-chromosomal regions (HPC1, PCAP, CAPB) harboring putative prostate cancer susceptibility genes. Nevertheless, one susceptibility gene, ELAC2/HPC2 at chromosome 17, has now been identified. Yet it seems to have a questionable role in prostate cancer predisposition. HPCA susceptibility loci have become undeniable archenemies of prostate cancer investigators, as the results of candidate gene analyses have been bewilderingly inconclusive. Predisposition to prostate cancer is most likely to be caused by several genes, different models of Mendelian inheritance, incomplete penetrance and varying population ethnicity frequencies. We will review the current state of the HPCA field and discuss the difficulties associated with identifying prostate cancer susceptibility genes.