Study on therapeutic mechanism of Neiyifang in treating endometriosis

Objective: To observe the clinical effect of Neiyifang (NYF) in treating endometriosis and to explore its therapeutic mechanism through observing its influence on plasma β-endorphin (β-EP) in different menstrual stages and levels of prostaglandins (PGs) in menstruation.Methods:NYF was administered to 104 patients with endometriosis one dose daily with 3 successive menstrual cycles as one therapeutic course. Peripheral blood β-EP level in follicular, luteal and menstrual stages, as well as PGF_2α, PGE2, thromboxane B₂ and 6-keto-PGFl α levels in menstrual stage were detected by RIA, and controlled with those in 15 healthy persons.Results: (1) The total effective rate of NYF was 81.3% and it showed significant effect in improving patients’ clinical symptoms and physical signs; (2) In menstrual stage, the levels of β-EP, 6-keto-PGF_α/ TXB₂ were lower(P <0.05) and levels of PGF_2α, PGE₂, TXB₂ and 6-keto-PGF_1α were higher (P< 0. 05) in patients than those in control, and the higher the level of PGE₂, the severer the menalgia, (3) NYF could increase levels of β-EP, 6-keto-PGF_1α, and reduce levels of PGF_2α, PGE_2α in menstrual stage of patients (all P<0.05).Conclusion: (1) NYF has good clinical effect in treating endometriosis; (2) Patients’ symptom of menalgia is closely related with the excessive high levels of PGF_2α and PGE₂, PGI₂/TXA₂ ratio disturbance, and excessive low level of β-EP; (3) NYF could significantly decrease the PGE₂, PGF_1α levels, increase the 6-keto-PGF_1α/TXB₂ ratio and the level of β-EP, so as to alleviate the menalgia in patients with endometriosis. This item was supported by National Funds of Natural Sciences(No. 30070942)     

C60的化学反应性和高分子化

综述了C_(60)化学研究的进展。C_(60)的化学反应性的研究展现了一个广阔的新领域,并使C_(60)作为一种新型的功能基团引入高分子成为现实。这些进展为进一步深入研究C_(60)尤其是C_(60)的材料化提供了前提。     

曲尼司特对豚鼠肺组织β肾上腺素受体向下调节的影响

用放射配体结合分析法分别测定了正常组、特布他林组、特布他林十曲尼司特组豚鼠的肺组织β受体最大结合力和解离常数,结果显示:给特布他林后豚鼠肺组织β受体发生明显的向下调节.曲尼司特可预防此向下调节的发生.     

国产rhGH的免疫原性及其对临床疗效的影响

目的　通过测定生长激素缺乏症 (GHD)患儿用国产重组人生长激素 (recom bined hum angrowth horm one,rh GH)治疗时血清生长激素抗体 (GH- Ab)水平及其结合特性 ,探讨 rh GH的免疫原性及其对疗效的影响。方法　对 6 1例 (男 49例 ,女 12例 ) GHD患儿用国产 rh GH治疗 ,每晚睡前皮下注射 rh GH 0 .1IU /kg共6个月 ;用放射免疫法测定治疗期间患儿血清 GH- Ab水平和滴度 ,并计算抗体结合容量、亲和常数 (Ka)。结果　48%患儿 (2 9/6 1)用药后 3个月血清 GH - Ab呈阳性至试验结束时仍未消失 ,其中 2 0例抗体为弱阳性 (结合率 <10 % ) ,9例呈强阳性 (结合率 >15 % ) ;5 2 %患儿 (32 /6 1)治疗期间抗体为阴性 ;血清 GH- Ab的结合容量、Ka及滴度均为低水平 ,分别为 (0 .1～ 4.8) pmol/L、(1.7× 10 7～ 6 .5× 10 8) L /mol和 1∶ 4～ 1∶ 8。GH- Ab阳性患儿治疗后的身高、身高增长速率及身高落后于正常 SD值的变化与同期阴性者比较无统计学差异 (P>0 .0 5 )。结论　本试验所用国产 rh GH对 GHD患儿身高增长具有确切的促进作用 ,其免疫原性所导致产生的 GH - Ab未对患儿体格线性增长产生负性影响     

家兔静注水杨醛-N'-(2-呋喃硫羰基)腙铜配合物的药物动力学

目的：研究水杨醛－Ｎ′－（２－呋喃硫羰基）腙铜配合物（ＣＳＦＣ）在兔体内的药物动力学。方法：１０只家兔静脉注射ＣＳＦＣ５ｍｇ·ｋｇ－１，用反相ＨＰＬＣ法测定血清药物浓度。结果：ＣＳＦＣ的血药浓度－时间曲线符合二室开放模型，主要药动学参数为：Ｔ１２α＝３．４±１．７ｍｉｎ，Ｔ１２β＝６５．５±１４．６ｍｉｎ，Ｋ１２＝０．１１８３±０．０６６９ｍｉｎ－１，Ｋ２１＝０．０２２８±０．００６５ｍｉｎ－１，Ｋ１０＝０．１２０２±０．０４０７ｍｉｎ－１，Ｖ０＝０．３０５±０．１８４Ｌ·ｋｇ－１，ＣＬ＝１．８９６±０．４７０Ｌ·ｋｇ－１·ｈ－１，ＡＵＣ＝１７０．１±５７．０ｍｇ·ｍｉｎ－１·Ｌ－１。结论：ＣＳＦＣ在兔体内分布迅速而广泛，消除也较快。家兔静注５ｍｇ·ｋｇ－１，可维持抗结核杆菌有效血浓度６ｈ。     

大鼠感染性脑损伤中神经细胞内游离钙的变化

采用荧光法测定负载Ｆｕｒａ－２／ＡＭ大脑皮层突触体内游离钙「Ｃａ＾２＋」ｉ浓度大鼠感染性脑损伤中的变化及其意义。     

Transneuronal degeneration of thalamic neurons following deafferentation: quantitative studies using [3H]thymidine autoradiography.

Transneuronal degeneration of thalamic neurons following partial deafferentation was studied using [3H]thymidine autoradiography. Timed-pregnant female Sprague-Dawley rats received systemic injections of [3H]thymidine on embryonic day (E) 13, 14 and/or 15. On the day of birth, pups were anesthetized by hypothermia and subjected to unilateral enucleation, unilateral removal of the inferior colliculus or sham lesion. Animals were sacrificed on postnatal day 10 or 30 and the brains processed for autoradiography. Material from sham-lesioned animals demonstrates that neurons destined for the dorsal lateral geniculate nucleus (LGd) undergo final mitoses on E13, 14 and 15. Neurons in the ventral medial geniculate nucleus (MGv) undergo final mitoses on E13 and 14. Thirty days following neonatal unilateral eye removal, the contralateral LGd displays a loss of approximately 30-35% of [3H]thymidine labeled neurons. Neonatal unilateral removal of the inferior colliculus results in a loss of approximately 30-40% of labeled neurons in MGv. For both LGd and MGv, shorter survival times reveal less severe cell loss. Late generated (E15) LGd neurons show less severe loss following enucleation than do earlier generated neurons. These results document the degree of cell loss in sensory thalamic nuclei following deafferentation and demonstrate that [3H]thymidine autoradiography provides a useful quantitative method for assessing anterograde transneuronal cell loss in targeted populations of neurons in the developing central nervous system.     

Calcium, network activity, and the role of NMDA channels in synaptic plasticity in vitro.

Functionally effective neuronal circuits are constructed through a competitive process that requires patterned neuronal activity elicited by structured input from the environment. To explore the mechanisms of this activity-dependent synaptic restructuring, we have developed an in vitro preparation of mouse spinal cord neurons maintained in a 3-chambered cell-culture system. Sensory afferents that received chronic electrical stimulation for 3-5 d developed stronger synaptic connections than unstimulated afferents converging onto the same postsynaptic spinal cord neuron. Exposure to 100 microM DL-2-amino-5-phosphonovaleric acid (APV), an antagonist of the NMDA channel, during the stimulation period prevented the competitive advantage associated with electric stimulation. However, when APV was applied with a higher concentration of calcium (3 mM), activity-dependent synaptic plasticity was no longer inhibited by the NMDA receptor antagonist. This reversal of APV block of the plasticity was not impaired by reducing transmitter release with 3 mM magnesium (in addition to 3 mM calcium and APV). A suppressant effect of APV on spontaneous activity was observed, which was attributed to loss of the NMDA component of the EPSP. Activity-dependent plasticity was also blocked if spontaneous activity was suppressed with dilute tetrodotoxin (TTX; 5-10 nM), a dosage that reduces excitability of neurons but is insufficient to block sodium-dependent action potentials. These experiments bring into question how NMDA channel activation is involved in the processes of synaptic remodeling during development. The data suggest that postsynaptic activity is required for synaptic remodeling, but this activity need not involve NMDA receptor activation specifically for activity-evoked synaptic plasticity. Instead, the mechanism for plasticity appears to operate through calcium-dependent processes in general.