The effect of paracervical block in 30 nulliparas undergoing artificial abortion were com- pared. An electric stimulation was given to the cervix five minutes before anesthesia, three and twenty minutes after anesthesia. The value of stimulant voltages was recorded when patients felt pain. The pain threshold increased from 63.63 ? 18.26 volts of preanesthesia to 110.80? 17.27 volts of 3 minutes after paracervical block (P

We describe a modification of retrograde guided intubation. With the help of transcricothyroid high-frequence jet ventilation, we used the epidural catheter to pull and guide the tracheal tube down the larynx and trachea, The tests of blood gas of six patients were done at the time of preanaesthesia, intubation and ten minutes after intubation. PaO_2of preanaesthesia, intubation and ten minutes after intubation were 77.72?21.17mmHg; 207.4 ?96.24mmHg ( P

Objective To determine the role of adenosine A1 receptor system in the delayed protective effects of ischemic preconditioning(IPC) in brain ischemia.Methods Thirty-five rabbits weighing 2-2.5kg were randomly divided into 7 groups: control (group Ⅰ), 3-min ischemia (group Ⅱ), 10-min ischemia (group Ⅲ), IPC (group Ⅳ), N6-cyclopentyladenosine (CPA)(group V), 8-cyclopentyl-1,3-dipropylxanthine (DPCPX)+ IPC(group Ⅵ), and DPCPX+3-min ischemia (group Ⅶ).Cerebral ischemia was produced by occlusion of both carotid arteries in combination withdrawing blood to maintain MAP at 35-40 mmHg.After 3-min IPC and 3 days of recovery , cerebral ischemia was induced and lasted 10 min (model of delayed protective effects of IPC). Adenosine A1 receptor agonist CPA or antagonist DPCPX was used instead of IPC to evaluate the role of adenosine A1 receptor in the delayed protective effects of IPC.The expression of heat shock protein 70 (HSP70) was analyzed by immunohistochemistry.Neurons density and expression of HSP70 in the hippocampal CA1 region were examined and measured 3 days later.Results (1) CPA could reduce cerebral ischemic injury, but the effects of CPA were not as good as those of IPC (about 70% of IPC).After adenosine A1 receptors being blocked by DPCPX the delayed protective effects of IPC disappeared.(2) 3-min ischemia alone did not cause neuronal injury but induced obvious expression of HSP70.DPCPX not only could make 3-min ischemia cause injury but also reduce the expression of HSP70.Conclusions (1) The delayed protective effects of IPC is related with activation of adenosine A1 receptor system.(2) One of the mechanisms of the blocking effects of DPCPX may be due to the reduction in expression of HSP70 .

To investigate the relationship between the effects of arecoline hydrobromide on contraction of the smooth muscles in oncomelania foot, and explore the mechanism of arecoline hydrobromide in decreasing climbing adhesion and increasing snail－killing. 　Method: The in vitro experiment was used to observe the effects of arecoline hydrobromide on contraction activitive of foot smooth muscles of oncomelania. 　Results: With a concentration of 3×10-6mol*L-1, arecoline hydrobromide strengthened the contraction and increased the frequency of the contraction of the foot smooth muscles of oncomelania, which was antagonized by verapamil. The same concentration of arecoline hydrobromide enhanced the contraction of smooth muscles in Ringer's solution with ECTA but Ca2+, and this effect was antagonized by caffeine. The concentrations of 10－5 and 3×10－5mol*L-1 of arecolin hydrobromide blocked the effect of Bay K8644 in enhancing foot smooth muscle contraction, with a characteristic of concentration－dependence. 　Conclusion:Arecoline hydrobromide may block the calcium channel of the smooth muscles in oncomelania foot. This could provide an explanation why arecoline hydrobromide decreases the rate of oncomelania climbing adhesion and enhances snail－killing.

Objective To investigate the levels of immunoglobulins and complement in children with cerebral palsy. Methods 59 children with cerebral palsy were assessed with Gross Motor Function Classification System (GMFCS), and the serum levels of immunoglobulin (Ig)G, IgA, lgM, complements C3 and C4 were measured in the children with cerebral palsy and other 61 children without cerebral palsy (controls). Results The serum levels of IgG, IgA, lgM, complement C3 and C4 decreased significantly in the children with cerebral palsy compared with the controls (P<0.001). There was significant difference in the levels of IgG, IgM, and complement C4 among cerebral palsy children of different grades of GMFCS (P<0.05), but not in the levels of IgA and complement C3 (P>0.05). Conclusion There is humoral immune dysfunction in some children with cerebral palsy, which may associated with the severity of the disease.

Objective To evaluate the targeted killing of malignant melanoma cells by aclarubicin liposomes conjugated with vascular endothelial growth factor(ADM-VEGF-SSL)in vitro.Metheds To detect the binding abilitv of liposomes to malignant melanoma(MM)cells,the human malignant melanoma cell line A375 was cultured in the presence of ADM-VEGF-3H-SSL or ADM-3H-SSL for 2 days followed by the detection of radioactivity of these cells.Then.A375 cells were cultured with various concentrations(0.01,0.1,1,10,100 mol/L)of ADM-VEGF-SSL,ADM-SSL or free ADM for 48 hours in the 48-hour cytotoxity test,or for 0.5 hour followed by another 48-hour culture in drug-free medium in the 0.5-hour cytotoxity test.After that,MTT assay was used to detect the survival rate of these cells.Results ADM-VEGF-SSL could specifically bind to and kill A375 cells.The binding rate of ADM-VEGF-SSL was 2.15 folds as high as that of ADM-SSL.The survival rate of A375 cells after being treated with ADM-VEGF-SSL for 48 hour was similar to that with flee ADM(P＞0.05).but lower than that with ADM-SSL(P＜0.05),while the survival rate of melanocytes treated with ADM-VEGF-SSL was higher than that with free ADM or ADM-SSL(both P＜0.05).As shown by the 0.5-hour cytotoxity test.shortening the treatment course did not attenuate the effect of ADM-VEGF-SSL on A375 cells.Conclusions ADM-VEGF-SSL can specifically recognize A375 cells.efficiently deliver adriamycin into tumor cells,markedly inhibit the proliferation of A375 cells,and eventually,a targeted kill of these cells is realized.

Objective To investigate the action and mechanism of NF-κB pathway in up-regulating B cell-activating factor receptor (BAFF-R) expression in multiple myeloma cells induced by IFN-γ.Methods Activated NF-κB were detected with Western blot, while the expression of BAFF-R were measured with RT-PCR and ELISA, and investigated the effect of BAY11-7082 on transcription of BAFF-R mRNA and translation of protein in multiple myeloma cells stimulated by IFN-γ. Results IFN-γ can induce the degradation of IκB-α in time-dependent and dosage-dependent manner, and up-regulated BAFF-R expression in multiple myeloma cells. BAY11-7082, an NF-κB inhibitor, inhibited not only the transcription of BAFF-R mRNA but also the protein of regulated by IFN-γin dosage-dependent manner. Conclusion NFκB may play an important role in high expression of BAFF-R in multiple myeloma cells induced by IFN-γ.

Progesterone has nongenomic effects on inducible nitric oxide synthase (iNOS), which is mediated by mitogen activated protein kinase (MAPK) pathways. This effect is supposed to have some potential association with asymptomatic gonococcal infections in women by immunological depression. In this study, polymorphonuclear leukocytes (PMNs) challenged by gonococci were used to study the nongenomic effects of progesterone. The activation of iNOS was assessed by measuring [(3)H] L-arginine converses to [(3)H] L-citrulline, and the activity of MAPK was detected by Western blot. It was found that the activity of iNOS and the yields of NO were enhanced significantly in gonococci-challenged PMNs compared with the controls (P<0.01). Progesterone could repress the activation of iNOS through P38MAPK pathway within PMNs (P<0.05), which could be blocked by SB203580 (P<0.01), but not by actinomycin D (P>0.05). It was also found subsequently that in the serum specimens collected from gonococci-infected but asymptomatic women, the progesterone level was higher than that in women with severe symptoms (P<0.01). Moreover, the yield of NO had an inverse correlation with progesterone. With these results it suggested that the rapid nongenomic effects of progesterone may inhibit iNOS activation and NO yields mediated by P38MAPK pathways, which were supposed to be concerned with asymptomatic women infected with gonococci.

The expression of the interferon regulatory factor 4 (IRF-4) and the IRF-4-binding protein (IBP) in psoriatic skin lesions was investigated. The expression of IRF-4 and IBP in skin lesions of 20 patients with psoriasis vulgaris were immunohistochemically dectected. Normal skin from 10 healthy people was used as normal control. The study showed that expression of IRF-4 was increased significantly in keratinocytes and inflammatory cells in the lesions of psoriasis vulgaris than that in the normal control. The detection revealed that IBP expression in keratinocytes, lymphocytes, hair follicles, and sebaceous glands in normal skin was significantly lower than that in the lesions of psoriasis vulgaris (P<0.05). Both IRF-4 and IBP might be involved in the pathogenesis of psoriasis vulgaris.

Objective To evaluate the effects of progesterone on polymorphonuclear leukocyte (PMN)-mediated inflammatory responses to gonococcal infection. Methods Peripheral neutrophils were isolated from heparinized peripheral blood obtained from normal individuals, then divided into 4 groups: progesterone group (pretreated with progesterone only), gonococcus group (stimulated with gonococcal suspension), intervention group (pretreated with progesterone followed by stimuation with gonococcal suspension), and control group (receiving no pretreatment or stimulation). Real-time RT-PCR was conducted to detect the mRNA expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)in neutrophils from all groups at 0, 3, 8, 12 and 24 hours after the last treatment, and iNOS protein levels were measured by Western-blot in gonococcus group and intervention group. Results Real-time RT-PCR indicated that the expression levels of iNOS, TNF-α and IL-1β mRNA increased in gonococcus group and intervention group, and reached their peak at 8 hours in gonococcus group, while no significant changes were noted in the above parameters in progesterone group or control group. Also, the level of iNOS, TNF-α and IL-1β mRNA was lower in intervention group than that in the gonococcus group (P ＜ 0.05). Western blot showed an elevation in iNOS protein expression in both gonococcus group and intervention group, and the former group was higher than the latter group in the parameter (P ＜ 0.05). Conclusions Progesterone can downregulate the expressions of iNOS, TNF-α and IL-1 β by PMNs, inhibit the PMN-induced inflammatory responses induced by gonococcal infection, which is likely to be associated with the asymptomatic gonococcal infection in women.