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 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.

Objective To observe the effects of low frequency electromagnetic fields (LFEMFs) on the proliferation of human epidermal stem cells (hESCs) cultured in a three dimensional environment so as to provide an experimental basis for applying LFEMF in skin tissue engineering.Methods hESCs from human prepuces were isolated and purified by the method of rapid adherence to collagen type ⅣV. They were grafted into a type-I collagen sponge or chitosan scaffold in vitro, and then stimulated with different frequencies of LFEMF ( 1 Hz, 10 Hz or 50 Hz) at a magnetic field intensity of 5 mT for 30 min/d. The cells' growth and proliferation were tracked using hematoxylin and eosin (HE) and diamine pheny1 indole (DAPI) staining and observed under the scanning electron microscope at different time points ( on 2nd, 7th, 10th and 14th days of LFEMF intervention). The amounts of cell proliferation at every time point were analyzed and compared.Results LFEMFs of different frequencies showed significantly different efficacy in promoting hESC proliferation. The two scaffolds also showed significantly different effects.By the 10th day, hESCs had grown significantly better on collagen sponge scaffolds than on the chitosan ones. All LFEMF frequencies could promote proliferation of hESCs, but the differences in their effects were statistically significant.Conclusion Collagen sponge may be a preferable scaffold for hESCs cultured in vitro. Rapid proliferation of ESCs in three-dimensional settings can be promoted by LFEMF intervention. LFEMF has relatively great potential in skin tissue engineering.

Objective To observe the effects of low intensity electromagnetic fields (LIEMFs) in promoting the reconstruction of full skin loss wounds grafted with human epidermal stem cells (ESCs). Methods Fifty nude mice aged 7 to 8 weeks with full skin loss wounds were equally divided into 3 experimental subgroups ( 1 Hz, 10Hz and 50Hz) and two control groups (a cell suspension control group and a blank control group) , with ten mice each. In the 3 experimental subgroups and the cell suspension control group, ESCs separated from human foreskin and cultured in vitro were grafted to the wounds using collagen sponge scaffolds. The experimental subgroups were then stimulated with an LIEMF (magnetic field intensity 5mT) at the appropriate frequency for 30min/day for 15 days. The blank control group was put under the same conditions without the cell suspension and LIEMF. The healing rates of the wounds were observed, and tissue slices were stained and observed under a light microscope. The inner structure of the regenerating skin was observed using transmission electron microscopy. Results The ESCs were successfully grafted. A few human integrin β1 positive stained cells appeared in the regenerating skin. The average healing rates in the experimental subgroups were significantly superior to those of the control groups. Well differentiated epidermis and dermis could be seen in the regenerating skin in all of the experimental groups. The epidermis had more cell layers and was thicker than in the control groups. More desmosome, hemidesmosome and keratin filaments were seen among the epidemic cells of the experimental groups. Conclusions LIEMF promotes the healing of full skin loss wounds grafted with ESCs in nude mice, and can promote complete repair of skin defects and the regeneration of skin function.

Objective To investigate the effects of geraniin on platelet aggregation and platelet-neutrophil interactions.Methods Platelet aggregation,in vitro and ex vivo,was determined by use of Born's method,and the binding of thrombin-stimulated platelets to neutrophils was observed based on the rosette assay.Intracellular calcium concentration of platelets was measured by using Fura-2-AM.Results Geraniin in vitro significantly inhibited arachidonic acid (AA)-,adenosine diphosphate (ADP)-,or platelet activating factor (PAF)-induced platelet aggregation,in a concentration-dependent manner.The medium inhibitory concentrations (IC50) were 2.4,0.4 and 1.1 μmol/L,respectively.Intragastric geraniin at 5 mg/kg markedly suppressed platelet aggregation induced by AA,ADP,or PAF.Geraniin decreased the total rise of [Ca2+]i,Ca2+ release,and Ca2+ influx,in a concentration-dependant manner.The IC50 values were 71.9,84.9,and 62.9 μmol/L,respectively.Geraniin decreased the binding of thrombin-stimulated platelets to neutrophils,and significantly inhibited washed platelet aggregation stimulated by fMLP-activated neutrophils.The IC50 values were 3.2 and 10.2 μmol/L,respectively.Conclusion It is suggested that geraniin inhibited platelet aggregation in vitro and ex vivo,decreased the calcium mobilization of platelets,and suppressed the interactions between platelets and neutrophils.