辨证分期治疗慢性盆腔炎合并免疫性不孕症18例疗效观察

目的：探讨辨证分期治疗慢性盆腔炎合并免疫性不孕症的临床疗效。方法：选择慢性盆腔炎合并免疫性不孕症(血清抗精子抗体阳性)患者18例，采用辨证分期治疗。月经干净后，治以活血化瘀、理气祛湿为主；在(或相当于)排卵期或排卵后，治以补肾养血，活血化瘀为主；在经前期，治以理气活血调经为主；在月经干净后至经前期，加用小剂量阿司匹林。结果：盆腔炎临床症状及体征痊愈7例，显效6例，有效5例；全部患者获得妊娠，宫内妊娠者17例(观察至妊娠3月，均正常)，输卵管妊娠1例；结论：中医辨病辨证结合的周期疗法加小剂量阿司匹林治疗慢性盆腔灸合并免疫性不孕症有一定的疗效。     

LHRH拮抗剂Cetrorelix对子宫内膜癌细胞生长周期的影响及其机理

目的 :研究LHRH拮抗剂Cetrorelix对子宫内膜癌细胞生长周期及周期相关蛋白的影响 ,探讨其抑制内膜癌细胞生长的机理。方法 :用流式细胞仪细胞周期分析及Westernblotting蛋白分析法 ,研究在Cetrorelix的作用下子宫内膜癌细胞系HEC 1A细胞生长周期及相关周期蛋白的改变。结果 :1 0 -5mol/LCetrorelix可导致HEC 1A细胞生长停滞于G2 /M期 ,而与G2 /M期停滞相关的p5 3 ,磷酸化p5 3 (phospho p5 3 ) (丝氨酸 3 92 )及磷酸化cdc2 (phospho cdc2 ) (酪氨酸 1 5 )蛋白水平均显著增高。结论 :Cetrorelix抑制内膜癌细胞增殖作用的机理是结合细胞表面受体后引起一系列抑制性信号传递 ,导致细胞周期停滞于G2 /M期 ,主要表现为G2 期停滞。其中p5 3激活及cdc2磷酸化失活是引起细胞周期停滞的重要因素     

Exposure to 1-bromopropane causes ovarian dysfunction in rats.

Although 1-bromopropane has been used in chemical and electronic industries as an alternative to ozone layer-depleting solvents, its toxicity on female reproductive organs has not been fully elucidated. The aim of this experiment was to determine the effect of 1-bromopropane on female reproductive function in rats. Forty female Wistar rats were divided into four equal groups. Each group was exposed daily to 0, 200, 400, or 800 ppm of 1-bromopropane for eight h a day. After exposure for 7 weeks, all rats in the 800-ppm group became seriously ill and were sacrificed during the 8th week. The other dose groups were exposed for 12 weeks. In the 800-ppm group, but not in the other two exposed groups, body weight was significantly less than the control at each time point from 2 to 7 weeks after the beginning of exposure. Tests of vaginal smears showed a significant increase in the number of irregular estrous cycles with extended diestrus in the 400- and 800-ppm groups. Histopathological examination of the ovary showed a significant dose-dependent reduction of the number of normal antral follicles and a decrease in the number of normal growing follicles in the 400-ppm group. No significant change was found in plasma concentrations of LH or FSH in any group when compared with the control. Our results indicate that 1-bromopropane can induce a dose-dependent ovarian dysfunction in nonpregnant female rats associated with disruption in follicular growth process.     

调肝益肾法在治疗妇科病中的运用

在妇科病的治疗中，以调肝益肾之法多获良效，例举月经失调、绝经期综合征及带下病验案三则以佐证。     

PDGF-B链基因三链形成寡核苷酸对C6胶质瘤细胞增殖和细胞周期的影响

目的观察PDGF-B链基因三链形成寡核苷酸(triplex-forming oligonucleotide,TFO)对C6胶质瘤细胞增殖和细胞周期的影响.方法应用免疫荧光流式细胞技术观察PDGF-B链基因TFO对C6胶质瘤细胞PDGF-B、PCNA表达的影响.应用流式细胞技术观察PDGF-B链基因TFO对C6胶质瘤细胞细胞周期的影响.结果 PDGF-B链基因TFO对C6胶质瘤细胞PDGF-B链基因、PCNA的表达有明显抑制作用,而且抑制作用存在浓度依赖性.PDGF-B链基因TFO能使C6胶质瘤细胞S期的百分率明显降低,阻止细胞由静止期(G0-G1期)进入(S期).结论 PDGF-B链基因TFO能够抑制C6胶质瘤细胞PDGF-B链基因的表达,阻碍细胞进入S期,降低细胞增殖能力.     

Suppression of luteal phase, but not midcycle, prolactin levels by chronic follicular phase opiate antagonism

Objective: To investigate whether establishment and maintenance of chronic opioid blockade throughout the follicular phase of the menstrual cycle influences midcycle and luteal phase prolactin levels.Design: Randomized, double-blind, crossover study.Setting: Academic research environment.Patient(s): Volunteers, aged 21–35 years, with regular menstrual cycles.Intervention(s): Naltrexone (50 mg) or placebo were administered on cycle days 2–14. Blood samples were obtained in the early follicular phase and in the periovulatory and midluteal phases of the menstrual cycle.Main Outcome Measure(s): Serum prolactin levels.Result(s): In the early follicular phase, serum prolactin levels were equivalent in naltrexone (12.0 ± 2.7 μg/L; mean ± SE) and placebo (12.1 ± 2.9 ug/L) cycles. A statistically significant increase in serum prolactin was observed on the day of the LH surge (naltrexone: 22.6 ± 3.7 μg/L; placebo: 21.7 ± 2.7 μg/L; P < 0.05 versus early follicular phase), but no difference between treatments was observed. However, midluteal prolactin levels were statistically significantly lower in naltrexone cycles compared with placebo cycles (12.6 ± 3.3 versus 15.4 ± 3.0 )ug/L; P < 0.05).Conclusion(s): Chronic blockade of opioid activities during the follicular phase does not affect midcycle prolactin increments, but withdrawal of opioid blockade may enhance opioid effects on prolactin levels in the luteal phase.     

Cell cycle effects of antifolate antimetabolites: implications for cytotoxicity and cytostasis

 Purpose: Cell cycle-related events in CCRF-CEM lymphocytic leukemia cells were examined subsequent to inhibition of thymidylate synthase (TS) or GAR formyltransferase (GARFT) and prior to cell death or stasis. Methods: Cell populations were treated with the GARFT inhibitors 6R-5,10-dideazatetrahydrofolate (lometrexol) or LY309887, the TS inhibitor ZD1694, or the multitargeted antifolate LY231514. DNA content, nucleoside precursor incorporation and proliferating cell nuclear antigen (PCNA) expression as functions of drug treatment were assessed by multiparameter flow cytometry. Cellular respiration was measured by MTT analysis and apoptosis was detected by extraction of DNA fragments. Results: Cell populations treated for up to 96 h with lometrexol or LY309887 did not replicate and maintained a cell cycle distribution with distinct G₁, S and G₂/M regions. The number of S phase cells in treated populations was slightly elevated relative to control as measured by DNA content and PCNA. However, these cells were unable to incorporate 5-bromodeoxyuridine (BrdU). Throughout treatment, cells incubated with GARFT inhibitors maintained intact membranes and respired at a level comparable to untreated cells. In contrast, ZD1694 as well as LY231514, induced synchronization of the treatment population at the G₁/S interface within 12 h of drug addition. This was followed by synchronous entry of the population into S phase. After 24 h of treatment, more than 90% of the cells were capable of incorporating BrdU and stained positive for PCNA. DNA fragmentation occurred in cells treated with ZD1694 or LY231514 but not in those treated with GARFT inhibitors. In addition, the viable cells remaining after 24–48 h of treatment with ZD1694 or LY231514 were respiring at twice the level of untreated cells. Conclusion: These results demonstrate that the distinct endpoints of GARFT and TS inhibition are preceded by distinct cell cycle and metabolic alterations. Received: 1 April 1996 / Accepted: 5 September 1996     

Enhancement of Radiation Response by Paclitaxel in Mice According to Different Treatment Schedules

Purpose: The aim of our study was to determine if paclitaxel could be used as a radiosensitizer in vivo.

Materials and methods: Paclitaxel was tested as a single agent and combined with an X-ray treatment. Paclitaxel was administered i.p. in doses from 30 to 120 mg/kg b.w. to (C3D2F1) mice bearing spontaneous mammary carcinoma. Tumor growth delay (TGD) or tumor control dose (TCD₅₀, radiation dose needed to induce local tumor control in 50% of irradiated animals) and moist desquamation dose (MDD₅₀, radiation dose needed to induce serious moist desquamation in 50% of the non-tumor-bearing feet) were the endpoints. DNA flow cytometric analysis was performed.

Results: DNA analysis demonstrated a G2/M block of tumor cells and a depletion of cells in S phase, with a maximum at 24 h from paclitaxel administration. Administering paclitaxel, in graded doses, 15 min before a 10-Gy X-ray treatment resulted in a linear regression line, almost parallel to that with paclitaxel alone, with a growth delay of about 6 days. In contrast, varying the X-ray dose with a constant paclitaxel injection (45 mg/kg b.w.) treatment showed some degree of synergism as the linear regression curves diverged. Interval time and sequence between paclitaxel administration and a 10 Gy X-ray treatment did not influence TGD. Protocols with paclitaxel at 30, 45, or 60 mg/kg were combined with radiation treatments at various doses (from 10 to 65 Gy). Values of TCD50 varied from 50.8 Gy for X-ray alone to 31.8 Gy for paclitaxel 60 mg/kg + X-ray. No differences were observed among MDD of different protocols.

Conclusions: These results suggest that, under some conditions, paclitaxel combined with radiation can show superadditive effects and this result combined with the lack of severe normal tissue damage indicate that a favorable therapeutic gain can be obtained.     

丹酚酸B对PDGF及MDA诱导的人鼠原代肝星状细胞增殖的影响

目的：探讨丹酚酸B（SAB）对血小板生长因子（PDGF）和丙二醛（MDA）刺激的大鼠原代肝星状细胞（HSC）增殖的影响。方法：采用原位灌注法消化大鼠肝脏，108g／L Nycodenz密度梯度离心，分离HSC，以MTT法观察细胞的增殖能力。免疫组化法检测血小板生长因子受体（PDGFR）含量。结果：MDA组与正常组相比可明显增加MTT吸光度（P〈0．05），PDGF组亦较正常组明显增加MTT吸光度（P〈0．01）；1μmol／LSAB和10μmol／L SAB不仅可显著抑制MDA刺激的HSC吸光度增加（P均〈0．01），也可抑制PDGF—BB刺激的HSC吸光度增加（P均〈0．01）。PDGF及MDA作用后细胞PDGFR的表达均明显增加，而10μmol／L SAB则可抑制PDGFR的表达。结论：SAB可通过抑制PDGFR的表达而抑制体外培养HSC的增殖．这种抑制作用与SAB的抗氧化作用有一定的关系。     

冷冻应激对Wistar雌性大鼠生殖周期与生育能力的影响

目的为观察低温应激对大鼠生殖周期与生育能力的影响及人参多糖对其调节,本实验研究了Wistar雌性大鼠生殖周期与生育能力的变化规律及人参多糖的生物学效应。方法将Wistar大鼠分16℃对照组、4℃低温应激实验组与4℃低温应激人参多糖实验组,生殖器官的发育和生殖周期变化采用称重法与观察法。LH与FSH水平检测采用放免分析法。结果对照组、4℃低温应激实验组与4℃低温应激人参多糖实验组的卵巢重量分别为(36±1.20)g、(24±1.31)g和(27±1.14)g;子宫重量为(0.64±0.03)g、(0.45±0.01)g和(0.49±0.02)g;开口率为68%、39%和43%;LH和FSH为(0.28±0.04)ng/ml、(0.11±0.07)ng/ml和(0.14±0.05)ng/ml与(0.35±0.01)ng/ml、(0.17±0.03)ng/ml和(0.21±0.02)ng/ml;与对照组比较P<0.05。动情周期、怀孕率及生仔数,与对照组比较P<0.05。结论低温应激抑制大鼠生殖器官发育,使动情期延长,怀孕率降,LH与FSH分泌水平降低,人参多糖对其有上调作用。