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 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 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 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 compare the effects of fentanyl,sufentanil and remifentanil on the immune function of dendritic cells in human umbilical cord blood.Methods Human umbilical cord blood mononuclear cells were obtained by density gradient centrifugation and seeded in 24-well plates with a density of 1 × 106/ml (2ml/hole).The cells were randomly divided into 7 groups (n =15 each):control group (group C),fentanyl 1.0 ng/ml group (group F1),fentanyl 5.0 ng/ml group (group F5),sufentanil 0.1 ng/ml group (group S1),sufentanil 0.5 ng/ml group (group S5),remifentanil 1.0 ng/ml group (group R1),and remifentanil 5.0 ng/ml group (group R5).The cells were incubated for 10 days in serum-free culture medium containing 50 ng/ml recombinant human granulocyte colony stimulating factor,10 ng/ml recombinant human interleukin-4 or the corresponding concentration of fentanyl,sufentanil or remifentanil,and then 50 ng/ml recombinant human tumor necrosis factor alpha was added to the culture medium and the cells were incubated for another 4 days in the seven groups.Three holes in each group were chosen and the cell morphology was examined with inverted microscope.Six holes in each group were chosen for determination of the concentration of IL-12 in the supernatant and expression of CD80/CD86.Six holes in each group were chosen for measurement of the cell viability.Results Compared with group C,the concentration of IL-12 and cell viability were significantly decreased and the expression of CD80/CD86 was down-regulated in groups F5,S1,S5,R1 and R5 (P ＜ 0.05).The concentration of IL-12,cell viability and expression of CD80/CD86 were significantly lower in groups S1 and R1 than in group F1 (P ＜ 0.05).Compared with group F5,the concentration of IL-12 was significantly decreased in group S5,and the concentration of IL-12 and cell viability were significantly decreased and the expression of CD80/CD86 was down-regulated in group R5 (P ＜ 0.05).The concentration of IL-12 and cell viability were significantly lower in group R1 than in group S1 (P ＜ 0.05).The concentration of IL-12,cell viability and expression of CD80/CD86 were significantly lower in group R5 than in group S5 (P ＜ 0.05).Conclusion Remifentanil has stronger inhibitory effect on the immunological function of dendritic cells in human umbilical cord blood than sufentanil,and the inhibitory effect of sufentanil is stronger than that of fentanyl.

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.

Objective To investigate the clinical features and genetic basis of cryopyrin-associated periodic syndrome (CAPS). Methods The clinical manifestations, laboratory tests, and genetic tests of one case of CAPS were retrospectively analyzed. The related literatures were reviewed. Results A 7 year and eight month old male patient had recurrent fever for 7 years and his whole body was covered with patchy red rash which was itchy and faded with pressure. The limbs and joints were normal. The levels of high-sensitivity C-reactive protein, erythrocyte sedimentation rate, rheumatoid factors were increased. The patient had fundus arteriosclerosis, double conjunctival lesions and nerve deafness on both sides. There was no mutation found in NLRP3 gene coding region, but a heterozygous mutation (-2667G>T) had been found in 5 ' untranslated region. Compared with normal control, the mRNA level of NLRP3 increased 4.2 times and the expressions of IL-1βand IL-18 gene increased 2.2 (P=0.002) and 1.2 times (P>0.05). Conclusions The clinical features of CAPS can be recurrent fever, rash, and joint involved. The oph-thalmologic abnormalities and varying degrees of deafness may occur during the progression. The test of NLRP3 gene may help diagnosis.

Objective To explore the clinical features of lissencephaly and the detection ofLISI gene.MethodsThe characteristic of clinical features, laboratory examination and gene detection in one case of lissencephaly was retrospectively analyzed. Meanwhile, the related literatures were reviewed.ResultsA 5-month-old female child diagnosed with epilepsy 20 days ago was hospitalized for convulsive seizure more than 30 times in 3 days. The manifestations were eyes staring, and turning upward, cyanosis of lips and face, froth at the mouth, extremities rigidity and loss of consciousness, and the symptoms can spontaneously remitted in 2-3 minutes. Laboratory examination showed that peripheral blood white cell count was 13.67×109/L, hemoglobin 108 g/L, red blood cell count 3.90×1012/L, lymphocyte 10.26×109/L; maocardial enzyme and hepatic and renal function were normal; blood ammonia was 23 μmol/L and lactic acid 2.11 mmol/L. Long-range video EEG showed highly arrhythmia, and frequent partial epilepsy, and sometimes secondary generalized epilepsy. Head MRI showed lissencephaly. The child was treated with oral administration of Keppra 27 mg/(kg·day), Topiramate 6.5 mg/(kg·day), currently no seizure. The detection ofLIS1 gene found that heterozygous mutation of c.232delG, which lead to protein shift mutation (p.E78NfsX25). No mutation was found in her parents.ConclusionsChild with lissencephaly may combine with epilepsy which may cause by mutation inLIS1 gene. And there was no information about point mutation of c.232delG inLIS1 gene being reported at home and abroad so far.

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.