从培养的香菇菌丝中提取抗病毒及诱导干扰素的新多肽甘露聚糖:KS-2

具有抗肿瘤活性的免疫增效剂KS-2是由香菇菌丝培养物中提取而得,含有α-甘露糖与小肽相连,分子量为6×10~4～9.5×10~4,小鼠口服急性毒性LD_(50)大于12,500mg/kg。小鼠或大鼠口服或腹腔注射KS-2,通过宿主机体免疫功能的提高可抑制各种转移瘤的生长。DDI小鼠口服或腹腔注射KS-2200mg/kg,16小     

195例绝经后出血的临床与病理分析

目的讨论绝经后出血（PMB）的部位、年龄、绝经年限和病理的关系.方法通过对195例PMB的临床资料和病理资料进行分析.结果PMB大多数来源于子宫腔和子宫颈,病理诊断良性疾病占82.05%、恶性肿瘤占17.95%;PMB多发生在绝经后1～5年.结论PMB出血部位主要来自子宫腔,并且大多数是良性疾病;随着PMB绝经年限的增长,患者年龄的增长,恶性肿瘤的发生率亦愈高.     

雷公藤甲素的免疫抑制机理

雷公藤甲素(Triptolide,TL)为雷公藤主要有效对大剂量环磷酰胺所致DTH反应增高模型亦具显成分之一。在体外,0.5～10μg·L~(-1)的TL可抑制单向著抑制作用“0.25 mg·kg~(-1)的TL还可明显降低小鼠混合淋巴细胞培养(MLC).TL5和10μg·L~(-1)所诱导胸腺Th/Ts细胞比值.这些资料显示TL对小鼠细胞出的混合淋巴细胞经~(60)Co照射后可抑制第二次免疫功能具有显著抑制作用,其机理可能与抑制ThMLC.表明TL可以诱导抑制性T细胞(Ts)。体内给细胞和IL—2分泌活性及诱导Ts细胞有关。药.0.12～0.5 mg·kg~(-1)的TL可以显著抑制DNFB所致小鼠迟发性超敏反应(DTH).0.25和0.5 mg·kg~(-1)时,小鼠脾细胞的IL—2分泌活性亦明显受抑,     

多黏菌素B对于耐碳青霉烯类鲍曼不动杆菌感染重症患者的疗效和安全性分析

目的: 围绕耐碳青霉烯类鲍曼不动杆菌(carbapenem-resistant Acinetobacter baumannii,CRAB)感染的重症患者,探索影响多黏菌素B(polymyxin B,PMB)疗效与安全性的相关因素。方法: 收集南京大学医学院附属鼓楼医院重症监护室2020年1月至2021年12月感染CRAB患者的基本特征、感染情况、治疗方案等信息,首先以细菌清除率和感染缓解率作为主要结局指标开展单因素分析,而后以28 d全因死亡率为次要结局指标开展单因素分析及Logistic回归,并比较部分患者的治疗药物监测结果。结果: 共纳入68例以PMB治疗的患者,其细菌清除率、感染缓解率分别为39.7%,44.1%,而28 d全因死亡率为41.2%。围绕主要结局指标,使用PMB疗程＞7 d的患者相较于疗程3~7 d患者,有更高的细菌清除率与感染缓解率。对于次要结局指标,PMB疗程以及PMB治疗过程中采用的连续性肾脏替代治疗,是患者28 d全因死亡的主要相关因素。结合治疗药物监测结果的单因素分析结果显示,CRAB清除患者的PMB峰浓度以及平均稳态血药浓度更高,同时发生肾毒性患者具有更高的PMB谷浓度,差异均具有统计学意义(P＜0.05)。结论: PMB治疗中,患者疗程应大于7 d以保证疗效,同时应重点关注采用连续性肾脏替代治疗患者的治疗结局;安全性方面PMB引起的肾毒性则可通过测定PMB谷浓度进行监测。     

氯化稀土抑制氨基甲酸乙酯诱发肺癌的研究

本研究通过每日给小鼠喂饲内含稀土（０．０６２５％，０．２５％，１．０％）饮水１０ｄ后，经腹腔一次注射诱癌剂氨基甲酸乙酯后，再继续喂饲同样含稀土饮水共１１０ｄ。观察稀土对小鼠肺癌发生抑制率以及小鼠抗肿瘤免疫功能和抗氧化功能的变化。结果发现，稀土处理组小鼠肺癌发生率比阳性组降低１１．６％～３１．３％，每只小鼠平均发生肿瘤数降低了３５．７％～５８．０％。同时还发现，促进小鼠ＮＫ细胞活力增加达４６％～８５％，并增加ＳＯＤ活性，以及降低脂质过氧化物的含量。由此可见，轻稀土处理不仅可抑制小鼠肺癌发生率，还可提高小鼠免疫功能和抗氧化能力。     

经阴道对绝经后阴道出血的超声诊断价值

目的 :探讨TVU对PMB病因的超声诊断价值。方法 :通过 2 0 8例PMB患者的TVU检查结果与诊刮后 (或 /和手术后 )病理进行对照分析。结果 :PMB绝大多数病因是子宫内膜的良性病变 ( 93.75 % ) ,其中内膜厚度 <5mm占 46.16% ;而恶性病变其内膜厚度增厚最明显 ,均≥ 5mm。结论 :TVU检查对PMB病因诊断有一定的帮助 ,可作为内膜活检前的一种筛查方法 ,当内膜厚 <5mm ,可免于诊刮。     

华泽兰清热解毒作用研究

目的研究华泽兰清热解毒作用。方法通过二甲苯致小鼠耳廓肿胀、糖皮质激素诱导小鼠免疫功能低下、干酵母致大鼠发热等实验,研究华泽兰的清热解毒作用。结果华泽兰可抑制二甲苯所致小鼠耳廓肿胀,并随剂量的增加作用增强;华泽兰能提高糖皮质激素诱导的免疫功能低下小鼠的免疫功能,且华泽兰1 g·kg-1药效作用显著;华泽兰1.5 g·kg-1能对抗干酵母所致大鼠发热。结论华泽兰具有清热解毒作用。     

黄蛭口服液对血小板聚集功能的影响研究

目的:研究黄蛭口服液对血小板聚集功能的影响。方法:以比浊法测量家兔血小板聚集功能;并测量小鼠出血时间。结果:黄蛭口服液可分别抑制由二磷酸腺苷、花生四烯酸、血小板聚集蛇毒试剂引起的血小板聚集(P<0·01);且能延长小鼠出血时间。结论:黄蛭口服液可抑制血小板聚集功能。     

雷公藤甲素对小鼠免疫功能的抑制作用

研究了雷公藤甲素对小鼠免疫功能的影响。分别用碳粒廓清实验、DNFB诱导小鼠迟发型变态反应实验、T淋巴细胞转化实验和血清溶血素测定方法,观察雷公藤甲素对小鼠免疫功能的影响。发现雷公藤甲素25μg/kg能抑制小鼠的血清溶血素水平;100μg/kg抑制小鼠迟发型变态反应;雷公藤甲素0.3～25μg/ml处理小鼠T淋巴细胞,其受刺激后增殖情况显著差于正常小鼠;以25、50、100μg/kg雷公藤甲素处理的小鼠,吞噬系数α与正常小鼠比较,有免疫抑制的趋势,但无统计学意义。     

妇炎栓抗炎、镇痛与刺激性研究

目的:研究妇炎栓抗炎、镇痛、刺激性。方法:以小鼠耳肿胀实验(妇炎栓剂量为4.5、3.0、1.5 g/kg)、小鼠足跖肿胀实验(测定时间点为5 min与0.5、1、4、6 h)研究妇炎栓的抗炎作用;以小鼠扭体反应实验(妇炎栓剂量为4.5、3.0、1.5 g/kg)研究妇炎栓止痛作用;以家兔阴道黏膜刺激实验研究妇炎栓的阴道刺激性(妇炎栓剂量为1.0 g/只,每天1次,连续1周)。结果:4.5、3.0、1.5 g/kg剂量下,妇炎栓可抑制小鼠的耳肿胀、减少小鼠扭体反应次数;3.0 g/kg剂量下,给药0.5~6 h时妇炎栓可抑制小鼠足跖肿胀;对家兔阴道无刺激性。结论:妇炎栓具有较好的抗炎和止痛作用;对家兔阴道无刺激性,理论上可认为阴道给予妇炎栓较安全。     

Modification of immune response by cinnarizine

Effects of cinnarizine on immune response in mice were investigated. Mice were orally administered with cinnarizine and were immunized with sheep red blood cells (SRBC) intravenously. Numbers of plaque forming cells (PFC) to SRBC in spleen of these mice were assayed and delayed-type hypersensitivity (DTH) response to SRBC was measured. 1) PFC response in immunization with 5 X 10(6) cells/mouse of SRBC was enhanced by administration of 25 mg/kg of cinnarizine, while the response in immunization with 5 X 10(8) cells/mouse was suppressed by 25 to 200 mg/kg of cinnarizine. 2) From study on timing of administration, suppression of PFC response by 6.25 to 200 mg/kg of cinnarizine was observed at 24 hr. after the immunization. 3) 12.5 to 200 mg/kg of cinnarizine suppressed polyclonal B cell activation induced by lipopolysaccharide (LPS). 4) Colchicine induced suppressor T cell inactivation was prevented by administration of 50 mg/kg of cinnarizine and it was suggested that cinnarizine may induce suppressor T cells from the study of adoptive cell transfer system. 5) 50 mg/kg of cinnarizine showed the suppression of DTH response in expression phase, but not in induction phase. It was concluded that immune responses in mice were modified by cinnarizine.     

Cytochrome P450 1B1 is required for 7,12-dimethylbenz(a)-anthracene (DMBA) induced spleen cell immunotoxicity.

7,12-Dimethylbenz(a)anthracene (DMBA) is a potent carcinogen that induces immunosuppression of both humoral and cell-mediated immunity in mice and other species. Previous studies have shown that CYP1B1 is required for bone marrow toxicity produced by DMBA in mice. Therefore, the purpose of these studies was to determine whether CYP1B1 was required for spleen cell immunotoxicity. Female C57BL/6N wild-type (WT) and CYP1B1 knockout (-/-) mice were treated with 0, 17, 50, or 150 mg/kg (cumulative dose) DMBA in corn oil by oral gavage once a day for five days. Several immunotoxicological assays were used to assess the effects of DMBA on systemic immunity. These included the in vitro T-dependent antibody response to sheep red blood cells (SRBC) measured using a direct plaque forming cell (PFC) assay, T- and B-cell mitogenesis induced by Con A and LPS, and nonspecific cell-mediated immunity was evaluated using an NK cytotoxicity assay. In addition, lymphocyte subpopulations were measured by flow cytometry using specific cell surface markers. Following five days of DMBA treatment, the body weights and spleen cell surface markers of the WT and CYP1B1 (-/-) mice showed no significant changes. A decrease in NK activity was found at the 50 mg/kg DMBA dose in WT mice, but not in the CYP1B1 (-/-) mice. Interestingly, at the 150 mg/kg dose of DMBA, CYP1B1 null mice had decreased NK activity, whereas WT mice did not. The SRBC PFC response demonstrated that the IgM antibody response was suppressed by DMBA in WT mice in a dose-dependent manner (significant at 50 and 150 mg/kg). However, there were no changes in the SRBC PFC responses in any DMBA test group in the CYP1B1 (-/-) mice. Similarly, while DMBA suppressed B- and T-cell mitogenesis at the 50 and 150 mg/kg dose levels in C57BL/6N WT mice, no effect was seen in CYP1B1 (-/-) mice. Thus, CYP1B1 appears to be critical for the immunosuppression of DMBA in mice, suggesting a role for bioreactive metabolites in the spleen cell immunotoxicity produced by DMBA.     

异丙肌苷对小鼠免疫功能的增强作用

在正常小鼠和注射环磷酰胺所致的免疫功能抑制的小鼠,异丙肌苷)25,50,100mg/kg,ip)能显著促进溶血素生成;增加空斑形成细胞数;增强二硝基氯苯所致迟发型皮肤超敏反应。在16月龄老年小鼠,异丙肌苷(2.5mg/kg,ip)可使减少的空斑形成细胞数增加至接近3月龄小鼠的水平,加大剂量作用反减弱或使空斑形成细胞数显著减少。体外试验,异丙肌苷(5,10,20mg/L)可显著增强刀豆素A诱导的C57 BL/6J小鼠的淋巴细胞增殖反应,并使16月龄老年小鼠低下的刀豆素A诱导的淋巴细胞增殖反应明显恢复。     

Behavioral effects of HR-592, a new derivative of indole

Effects of HR-592 on various behaviors were investigated in rats and mice. 1) HR-592 at doses of 10-100 mg/kg, p.o., and chlorpromazine at doses of 2.5-20 mg/kg, p.o., suppressed dose-dependently spontaneous activities of mice. 2) In the mice treated with HR-592, 10 and 30 mg/kg, p.o., and with chlorpromazine, 1.25-5 mg/kg, p.o., the durations of loss of the righting reflex induced by thiopental-Na were extended in a dose-dependent manner. 3) In the mice and rats when HR-592 was administered at doses of 3-100 mg/kg, p.o., catalepsy was induced in a dose-dependent manner. 4) The incidence of catalepsy induced by haloperidol in mice was reduced dose-dependently after HR-592 administration (10-100 mg/kg, p.o.). 5) Dose-dependent suppressions of the slant of screen at which the mice slipped down were observed by HR-592 at 3-100 mg/kg, p.o., and chlorpromazine at 5-20 mg/kg, p.o. 6) The rotarod performance in mice was suppressed dose-dependently by HR-592, 3-100 mg/kg, p.o., and chlorpromazine, 5-20 mg/kg, p.o. 7) HR-592 at doses of 0.3-3 mg/kg, i.p., suppressed dose-dependently the turning behavior induced by methamphetamine in unilateral substantia nigra-lesioned rats. From these results and our previous data, it is considered that HR-592 has pharmacological properties as a major tranquilizer, although its behavioral effect is slightly weaker than that of chlorpromazine. Furthermore, these results imply that HR-592 has anti-cataleptogenic activity and might thereby alleviate the adverse effect of neuroleptics such as haloperidol.     

北沙参多糖的免疫抑制活性

北沙参为伞形科珊瑚属植物珊瑚菜(Glehnia littoralis F.Schmidt ex Mig.)的根,是一种常用中药,具有养阴清肺功能。据报道北沙参可延长家兔抗甲胎球蛋白抗体的存在时间。不少植物多糖,如人参、黄芪、刺五加和当归等的多糖成分,对机体的免疫功能有促进作用。为此我们观察了北沙参的多糖成分对机体免疫功能的影响。     

Suppression by bepotastine besilate of substance P-induced itch-associated responses through the inhibition of the leukotriene B4 action in mice

Anti-pruritic effects of the antihistamine bepotastine besilate were studied in mice. Bepotastine besilate (10 mg/kg) inhibited scratching induced by an intradermal injection of histamine (100 nmol/site), but not serotonin (100 nmol/site). Bepotastine besilate (1-10 mg/kg, oral) dose-dependently suppressed scratching induced by substance P (100 nmol/site) and leukotriene B(4) (0.03 nmol/site). An intradermal injection of substance P (100 nmol/site) increased the cutaneous concentration of leukotriene B(4), which was not affected by bepotastine besilate (10 mg/kg, oral). Leukotriene B(4) increased Ca(2+) concentration in cultured neutrophils, which was suppressed by bepotastine besilate (1-100 microM). Leukotriene B(4) increased Ca(2+) concentration in cultured dorsal root ganglion neurons, which was also suppressed by bepotastine besilate (100 microM). The results suggest that the inhibition of the actions of leukotriene B(4) as well as histamine is involved in the anti-pruritic effect of bepotastine besilate.     

绞股兰总皂甙对鼠免疫功能的影响

绞股兰总皂甙对环磷酰胺所致小鼠血清溶血素减少、对皮质激素地塞米松所致大鼠脾脏空斑形成细胞(PFC),特异玫瑰花形成细胞(SRFC)和脾细胞抗体分泌量(QHS)减少及对荷S-180实体瘤小鼠PFC、SRFC和QHS减少均有明显保护作用。并能减轻环磷酰胺所致小鼠免疫器官的萎缩。这些结果表明绞股兰总皂甙对免疫反应低下动物有显著的免疫增强作用。     

Effect of traxanox on antibody formation in BALB/c mice

The production of spleen- and thymus-rosette forming cells (RFC) in BALB/c mice 4 days after immunization with 5 X 10(8) sheep red blood cells (SRBC) was inhibited by traxanox at doses of 10-30 mg/kg, p.o. This agent (100 mg/kg, p.o.) suppressed the 19S hemagglutinin titer and elevated the 7S hemagglutinin titer. The transfer of spleen-RFC of thymus-RFC into syngeneic recipient mice 4 days after immunization with SRBC increased the production of spleen hemolytic plaque forming cells (HPFC). This increase was abolished by the transfer of spleen-RFC obtained from mice treated with traxanox (30 mg/kg, p.o.), but not by the transfer of spleen-RFC treated with anti-Lyt 2.2 antiserum and complement. The viability of the spleen-RFC in mice treated with traxanox was decreased by treatment with anti-Lyt 2.2 antiserum and complement. Traxanox (3-30 mg/kg, p.o) significantly increased the inhibition of HPFC, spleen-RFC and thymus-RFC production by Concanavalin A at a dose of 50 micrograms/mouse. This agent (3-30 mg/kg, p.o) inhibited the production of HPFC, spleen-RFC and thymus-RFC in mice 4 days after the secondary immunization. These results suggest that traxanox may inhibit antibody production via the induction of Lyt 2.2 positive cells (suppressor T cells).     

Effects of immunoagents on circulating serum hemolysin formation in bone marrow and spleen

The bone marrow as a source of serum hemolysin to sheep red blood cells (SRBC) was studied in splenectomized mice. Splenectomy prevented the hemolysin formation in the primary response, but not in the secondary response. Cyclophosphamide 100 mg/kg and dexamethasone 10 mg/kg decreased hemolysin formation in the bone marrow as well as in the spleen. Levamisole 50 mg/kg increased its formation in both organs. Prednisolone 10 mg/kg significantly suppressed its formation in the spleen, but not in the bone marrow. Hydroxyurea 50 mg/kg suppressed its formation in the bone marrow, but not in the spleen. These results suggest that the bone marrow is the major source of serum hemolysin to SRBC during the secondary response and drug has different effects on antibody production in the bone marrow and in the spleen.     

Non-amphetaminic mechanism of stimulant locomotor effect of modafinil in mice

Previously established dose-response curves indicated that modafinil 20–40 mg/kg i.p. elicited in mice an obvious stimulation of locomotor activity roughly similar to that induced by (+)amphetamine 2–4 mg/kg. The effects of various agents modifying dopamine transmission were compared on the locomotor response to both drugs. The preferential D2 dopamine receptor antagonist haloperidol 37.5–150 μg/kg i.p. suppressed the stimulant effect of (+)amphetamine in a dose dependent manner, but not that of modafinil. The D1 dopamine receptor antagonist SCH 23390 (7.5–30 μg/kg s.c.) reversed the (+)amphetamine but not the modafinil induced hyperactivity. The tyrosine hydroxylase inhibitor -methyl-para-tyrosine (200 mg/kg) suppressed the hyperactivity induced by 4 mg/kg dexamphetamine but not that induced by 20 mg/kg modafinil. Associating L-DOPA 150 mg/kg and benserazide 37.5 mg/kg with (+)amphetamine 2 mg/kg resulted in stereotyped climbing behavior, that was not observed with modafinil 10–80 mg/kg. The profound akinesia induced by reserpine (4 mg/kg s.c.; 5 h before testing) was reversed by (+)amphetamine 2 mg/kg but not by modafinil 40 mg/kg. Finally, on synaptosomes prepared from mouse striata preloaded with [³H]dopamine, modafinil 10⁻⁵ M did not increase the spontaneous [³H]dopamine release whereas (+)amphetamine, at the same concentration, doubled it. From all these differences between the two drugs, it is concluded that the mechanism underlying the modafinil induced stimulant locomotor effect differs completely from that of (+)amphetamine.