As a cross-disciplinary theory,euthanansia concerns the right of life and the dignity of death. In terms of law principles, according to the independent principle of life, the patient who is in extreme pain with an incurable disease should have the right of self-determination of euthanasia in order to safeguard his legitimate rights and dignity of death.

Objective To investigate and compare the actions of vecuronium and atracurium on adult and embryonic-type nicotinic acetylcholine receptors (?-and ?-nAChR) at skeletal muscle cell membrane. Methods The adult and embryonic nAChRs were heterologously expressed in HEK 293 cells. Peak currents induced by actions of vecuronium and atracurium at ?-and ?-nAChR were recorded in HEK 293 cells, using whole cell patch clamp technique. Results Vecuronium and atracurium competitively inhibited ?-and ?-nAChR in HEK 293 cells. The inhibitor concentrations for half-maximal response (IC50) for vecuronium and atracurium ate-nAChR were (8.3 ? 2.6) ?mol/L and (24.2 ? 10.5) ?mol/L respectively; The IC50 values for vecuronium and atracurium at e-nAChR were (55.0 44 28.4) ?mol/L and (183.2 ? 39.2) ?mol/L respectively.Conclusion According to IC50 values for both adult and embryonic type nAChR, vecuronium is more potent than atracurium on e-and 7-nAChR. Embryonic nAChR is less sensitive to vecuronium and atracurium than adult-type nAChR.

Objective To investigate the effects of pancuronium on nicotinic acetylcholine receptors (nAChRs) in pheochromocytoma cells (PC12 cells) and to determine if pancuronium has direct effects on PC cells.Methods PC12 cells (purchased from Institute of Cytology, Chinese Academy of Science) were cultured in DMEM containing penicillin and glutamine. nAChR in PC12 cells were stimulated with different concentrations of Ach ( 10, 30, 100, 300, 1 000 ?mol?L-1 ). Ach-mediated inward currents were recorded using whole-cell patch clamp technique with holding potential set at - 80 mV. To investigate the effects of pancuronium on nAChR in PC cells, the PC12 cells were perfused with different concentrations of pancuronium (0.01,0.1, 1, 10, 100, 1 000 ?mol ? L-1 ) before Ach 1 ?mol?L-1 was added. Results Inward currents were elicited by stimulation of nAChR with Ach in a concentration-dependent manner. 93.7% of nAChRs could be activated by 1 ?mol ? L1 Ach. Pancuronium reversibly suppressed the currents in a concentration-dependent manner compared to the control currents elicited by 1 ?mol?L-1 Ach. 1 ?mol?L-1 pancuronium could almost completely suppressed the currents elicited by 1 ?mol ? L-1 Ach.Conclusion Pancuronium could inhibit nAChR in PC12 cells and reduce catecholamine release.

Objective To investigate the effects of rocuronium and vecuronium on the adult-type (?-nAChR) and fetal-type (?-nAChR) muscle nicotinic acetylcholine receptors. Methods HEK293 cells were obtained from Institute of Cytology, Chinese Academy of Sciences.?- and ?-nAChRs were expressed heterologously in HEK293 cells using transfection technique. Whole cell patch clamp technique was used to determine the potencies of the two muscle relaxants alone or in combination in blocking the function of the two types of nAChRs. Results Both rocuronium and vecuronium could competitively inhibit the activation of ?- nAChR and ?-nAChR by Ach. The IC50 of rocuronium and vecuronium for ?-nAChR was 169.2 ? 12.5 and (8.3 ? 2.7) ?mol?L-1 and for ?-nAChR was 8.6 ? 2.7 and (55.0?10.4) ?mol?L-1 respectively. The IC50 of rocuronium in combination with vecuronium was (0.7 ? 0.3) ?mol ? L-1 for ?-nAChR and (36.3 ? 14.2) ?mol ? L-1 for ?-nAChR.Conclusion The two muscle relaxants have different blocking action on the two types of nAChRs. Rocuronium has stronger inhibitory effect on ?-nAChR than on ?-nAChR while vecuronium has stronger inhibitory effect on ?-nAChR than on ?-nAChR. The inhibitory effects of the two muscle relaxants in combination was synergistic on ?-nAChR and additive on ?-nAChR.

Objective:To investigate the impact on the level of serum IL-8 and IL-18 by Helicobacter pylori eradication therapy in patients with rheumatoid arthritis.Methods:Helicobacter pylori were assessed by 14-Curea breath test in patients with rheumatoid arthritis.All patients were divided into Hp positive group and Hp negative group on the basis of 14-C urea breath test results.The Hp positive group were divided into anti-helicobacter pylori group and control group.The level of ESR,serum C reactive protein (CRP), RF,IL-8 and IL-18 were measured in all patients before and after 12 weeks of treament.And the number of joint swelling,joint pain/tenderness,morning stiffness time, hands grip strength were recorded before and after 12 weeks treatment.Results: 12 weeks after treatment,the effective rate in the Hp negative group and the anti-helicobacter pylori group was higher than that in the control group (84.09%vs 62.50%,χ2=5.41,81.25% vs 62.50%,χ2=4.17,P<0.05).The clinical symptoms significantly improved and the levels of ESR, C-reactive protein, RF, IL-8 and IL-18 significantly reduced in the three groups ( P<0.05 ) .The clinical symptoms improved more obviously in the Hp negative group and the anti-helicobacter pylori group than that in the control group.The levels of ESR,C-reactive protein,IL-8 and IL-18 in the Hp negative group and the anti-helicobacter pylori group was lower than that in the control group.While there was no significantly difference in the level of RF in the three groups.Conclusion:From a certain extent ,Hp eradication therapy can improve the clinical curative effect of rheumatoid arthritis.

Objective To investigate the effects of different duration of sevoflurane anesthesia in the neonatal period on the long?term cognitive function and hippocampal synaptic plasticity in rats. Methods Twenty?four pathogen?free healthy Sprague?Dawley rats of both sexes, aged 7 days, weighing 12-16 g, were divided into 3 groups ( n=8 each) using a random number table: control group ( group C) , sevoflu?rane anesthesia for 2 h group ( group S1 ) , and sevoflurane anesthesia for 6 h group ( group S2 ) . Group S1 and group S2 inhaled 2% sevoflurane for 2 and 6 h, respectively. Morris water maze test was performed at 30 days after the end of anesthesia ( postnatal day 37) to assess the cognitive function. After the end of the test, the rats were sacrificed, and hippocampi were isolated for determination of the expression of brain?de?rived neurotrophic factor ( BDNF) , postsynaptic density?95 ( PSD?95) and synapsin 1 in hippocampal tis?sues by Western blot. Results Compared with group C, the escape latency on 4th and 5th days of the test in group S1 and on 2nd-5th days of the test in group S2 was significantly prolonged, and the frequency of crossing the original platform was significantly decreased, and the time of staying at the platform quadrant was significantly shortened in S1 and S2 groups, the expression of BDNF, PSD?95 and synapsin 1 in hipp?ocampal tissues was significantly down?regulated in group S2 (P<0?05), and no significant change was found in the expression of BDNF, PSD?95 and synapsin 1 in hippocampal tissues in group S1 ( P>0?05) . Compared with group S1 , no significant change was found in the escape latency and frequency of crossing
the original platform (P>0?05), the time of staying at the platform quadrant was significantly shortened, and the expression of BDNF, PSD?95 and synapsin 1 in hippocampal tissues was significantly down?regula?ted in group S2 ( P<0?05) . Conclusion Short?time and long?time sevoflurane anesthesia both can induce long?term cognitive dysfunction in the neonatal period, and the severity is aggravated with prolonged anes?thesia; the partial mechanism is related to inhibition of the synaptic plasticity of hippocampal neurons of rats.

Objectives To explore the clinical features and diagnosis of LMNA-associated congenital muscular dystrophy. Methods The clinical data from a case of muscular dystrophy caused by LMNA gene mutation were retrospectively analyzed. The related literatures were reviewed. Results A 8-month-old female infant suffered from weakness of raising head, eyelid droop, and motor development retardtion. LMNA gene was sequenced for the infant, her parents and the older sister. Heterozygous mutation of c. 94_96 del AAG (p. K 32 del) was found in the infant leading to the diagnosis of LMNA- associated congenital muscular dystrophy. No mutation was found in the infant’s parents and her older sister. The literature review showed that all ofLMNA- associated congenital muscular dystrophy patients had LMNA gene mutation, more than 80% patients mainly presented with weakness of raising head and may accompany with weakness of proximal limb, motor development retardation, and weakness of axial muscle. Conclusions Mutation analysis of LMNA gene is conducive to the diagnosis of congenital muscular dystrophy.

Aim Expressing muscle acetylcholin e receptors in mammallian cells using receptor clone technique.Methods The cDNA coding for the ?,?,?, ?,?-subunits of the mouse muscle nAC hR in pSP65, pSP64,pBS SK(-) are subcloned into pcDNA3.1+ by gene recobinant technique and then transfect HEK293 cells using lipofection technique.The ?-n AChR and ?-nAChR are transiently expressed in HEK293 cells membrane. Recording the response of transfected HEK293 cells to acetylcholine by using the whole- cell clamp technique.Results Transfected HEK293 cells may produ ce a inward current as appling acetylcholine.The current values are acctylcholin e-concentration-dependent.Conclusion ?-nAChR or ?-nAChR i s expressed successfully in HEK293 cells.

YKL-40 (human cartilage glycoprotein 39) is a newly discovered inflammatory cytokine, which belongs to the member of 18 glycosyl hydrolase of mammal family. Previous studies have indicated that YKL-40 is associated with the acute or chronic inflammatory diseases and tumors. Studies in recent years have suggested that YKL-40 may be involved in the occurrence and development of atherosclerotic plaques, and it is correlated with the plaque instability. The physiological function and the mechanisms of YKL-40 are not fully understood. It may have the roes of promoting vascular smooth muscle migration and proliferation, promoting cell adhesion and proliferation, as well as regulating extracellular matrix remodeling The detection of YKL-40 may have some significance in the aided diagnosis, predicting prognosis, prevention of cardiocerebrovascular diseases, and even the establishment of new therapeutic strategies.

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) can be induced in ischemia and other pathological states and mediate neuronal apoptosis after cerebral ischemia.Understanding the upregulation mechanism of TRAIL in ischemic brain tissue is promising to develop new treatment for stroke.