Objective: To observe the clinical efficacy of acupuncture plus auricular point sticking for tension-type headache (TTH). Methods: A total of 90 TTH patients were divided into an acupuncture group, an auricular point sticking group and an observation group by random number table method, with 30 cases in each group. Patients in the observation group received acupuncture plus auricular point sticking for treatment, while those in the acupuncture group only received acupuncture and those in the auricular point sticking group only received auricular point sticking for treatment. The headache attack frequency and the scores of visual analog scale (VAS), self-rating anxiety scale (SAS) and self-rating depression scale (SDS) were observed before treatment, after treatment and 3 months after treatment. The clinical efficacy was evaluated at the follow-up of 3 months after treatment. Results: At follow-up, there were significant differences in clinical efficacy among the three groups (P<0.01 or P<0.05), and the clinical efficacy ranking from high to low was the observation group, the acupuncture group and the auricular point sticking group. After treatment and at follow-up, the VAS score, headache attack frequency, SAS and SDS scores in the three groups were significantly lower than those before treatment (all P<0.01). The above four results in the observation group were lower than those in the acupuncture group and the auricular point sticking group at the same time point (all P<0.01); VAS score in the acupuncture group was lower than that in the auricular point sticking group (both P<0.05). At follow-up, the headache frequency in the acupuncture group was lower than that in the auricular point sticking group (P<0.05). Conclusion: Either using acupuncture and auricular point sticking together or separately can reduce the headache degree of TTH patients, reduce the number of headache attacks, and relieve anxiety and depression. The efficacy of acupuncture plus auricular point sticking is most significant.

Objective To investigate the role of Gly82Ser polymorphism of receptor for advanced glycation end-products (RAGE) in the genesis and progression of colon cancer in Chinese population.Methods Using the method of PCR-restriction fragment length polymorphism (PCR-RFLP),the Gly82Ser genotype of RAGE were examined in 90 colon cancer patients and 78 control subjects age and sex matched.Analyses stratified by TNM and tumor differentiation were conducted to check the associations of the Gly82Ser gene polymorphisms in RAGE and development of colon cancer.Results The genotype distribution was in agreement with that predicted under Hardy-Weinberg equilibrium for both patients and controls (both P ＞ 0.05).With the GG genotype as reference,the odds ratio (OR) for heterozygous GG and carriers with S allele (GS and SS) were 2.037 (95％ CI:1.207-3.438) and 2.022 (95％ CI:1.275-3.208),respectively,which had a significantly higher risk of colon cancer.Moreover,the elevated colon cancer risk was especially evident in patients with TNM (Ⅲ + Ⅳ) and/or patients with poor differentiation by stratification analysis (OR,3.575,95％ CI:1.495-8.550 and OR,3.580,95％ CI:1.390-9.217,respectively).Conclusions The RAGE Gly82Ser polymorphism may confer not only an increased risk of colon cancer but also with invasion of colon cancer in the Chinese population.

Objective To study the effects of lead exposure on expression of nerve growth factor(NGF)gene in the rat hippocampus,and explore the molecular toxicological mechanism of the learning and damage induced by lead exposure. Methods Using the reverse transcription-polymerase chain reaction(RT-PCR)and in situ hybridization,NGF mRNA levels in the hippocampus of normal and lead exposure rats were investigated. Results NGF mRNA presented in the normal hippocampus of rats.NGF mRNA levels in the hippocampus were significantly decreased by lead exposure.There was a negative correlativity between the expression of nerve growth factor mRNA in the hippocampus and the time of lead exposure.Conclusion Lead can downregulate the expression of nerve growth factor gene in the rat hippocampus.

Hydrophidae, one of the precious traditional Chinese medicines, is generally drily preserved to prevent corruption, but it is hard to identify the species of Hydrophidae through the appearance because of the change due to the drying process. The identification through analysis on gene barcode, a new technique in species identification, can avoid the problem. The gene barcodes of the 6 species of Hydrophidae like Lapemis hardwickii were aquired through DNA extraction and gene sequencing. These barcodes were then in sequence alignment and test the identification efficency by BLAST. Our results revealed that the barcode sequences performed high identification efficiency, and had obvious difference between intra- and inter-species. These all indicated that Cyt b DNA barcoding can confirm the Hydrophidae identification.
Animals ; Base Sequence ; China ; Cytochromes b ; genetics ; DNA Barcoding, Taxonomic ; Elapidae ; classification ; genetics ; Molecular Sequence Data ; Phylogeny ; Reptilian Proteins ; genetics ; Sequence Analysis, DNA

Dental Bonding ; methods ; Dentin ; Dentin-Bonding Agents ; chemistry ; Electricity ; Humans

Objective To observe the inhibition of amikacin in vitro on platelet aggregation and blood coagulation tests, and to study its effects on hemostasis and the related mechanisms.Methods Plateletrich plasma and platelet-poor plasma from donors were mixed with different concentration of amikacin, which was divided into four groups:0 mg/L, 30 mg/L, 91 mg/L and 910 mg/L group.The maximial ratio of platelet aggregation induced by ADP were measured with Platelet Aggregation Analyzer.The expression levels of P-selectin, GP Ⅱ b/Ⅲ a and Fg-R were determined with Flow Cytometer.The PT, APTT, TT and Fg of platelet-poor plasma were detected with Blood Coagulation Analyzer. The four concentration of amikacin mentioned above and two anticoagulants (62.5 U/ml of sodium heparin and 109 mmol/L of sodium citrate)were interacted with fresh whole blood, in which the blood CT and plasma Ca2+ were detected. Blood samples were collected from 10 patients with acute lower respiratory tract infection before and 30 minutes after routine amikcin treatment respectively.The maximial ratio of platelet aggregation, the expression levels of P-selectin, GPⅡ b/Ⅲa and Fg-R induced by ADP were measured; while PT, APTT, CT and plasma Ca2+ were determined.Results At 30 mg/L of amikacin group, the maximal ratios of platelet aggregation (65.8±3.9)%, the expression levels of P-selectin (9.2 ± 1.0)% and Fg-R (12.6 ± 1.7)% were statistically lower than those [(88.0 ±4.6%, (16.1 ± 1.3)% and (31.0 ±2.5)%]at 0 mg/L of amikacin group ( t = 9.442,8.432,9.993,P ＜ 0.01 ).At 30 mg/L of amikacin group, the APTT (80.5 ±6.8) s and CT ( 857 ± 66) s were significantly higher than those [(33.0 ± 3.6) s and (447 ± 35 ) s] at 0 mg/L of amikacin group ( t = 11.312, 13.211, P ＜ 0.01 ). There was a negative correlation between amikacin concentration and maximial ratio of platelet aggregation ( r = - 0.832, P ＜ 0.05 ), but a positive correlation between amikacin concentration and inhibitory rates of platelet aggregation ( r = 0.939, P ＜0.05) was observed, as well as APTT (r ＞0.870, P＜0.05).At 30 mg/L, 91 mg/L, and 910 mg/L of amikacin groups, the P-selectin and Fg-R expression were remarkably inhibited with a dose-dependent manner, the CT was notably enhanced [Fwithin subjects =21.44, 26.24, ( ＞29.81 ), P ＜0.01].At 0 mg/L,30 mg/L, 91 mg/L and 910 mg/L of amikacin groups, the PT values were ( 14.7 ± 1.9) s, ( 15.2 ± 1.7) s,(15.6±1.5) s and (22.1 ±2.1) s, respectively (F=8.21,P＜0.05), but there was no markeddifference for the levels of GP Ⅱ b/Ⅲ a, TT, Fg and plasma Ca2+ among the four groups ( P ＞ 0.05 ).After 30 minutes of amikacin treatment, the maximial ratio of platelet aggregation (51.6 ± 10.1)%, the expression levels of P-selectin (6.8 ± 1.8) % and Fg-R ( 20.1 ± 5.8 ) % were significantly lower than those [(66.8 ± 11.4)%, ( 10.9 ±3.1 )% and (28.5 ±7.4)%] before amikacin treatment, but APTT (49.8 ±5.9) s and CT (660 ±59) s were remarkably higher than those [(26.9 ±3.8) s and (410 ±45) s] before amikacin treatment, respectively ( t = 5.456,8.875,7.423,10.012,11.322, P ＜ 0.01 ), while the GP Ⅱ b/Ⅲ a expression, PT and Ca2+ concentration had no significant changes ( P ＞ 0.05).Conclusions There are inhibitory effects of amikacin on platelet aggregation mainly through the inhibition of both fibrinogen receptor activation and secretion reaction of activated platelet. Amikacin may also inhibit pathway of coagulation system factor to prevent blood coagulation.Therefore, risk of hemorrhage may be investigated in the patients with amikacin for anti-infection treatment.

Objective To investigate the genetic stability, immunogenicity and protective efficacy of AdC68-rab. gp, a novel rabies vaccine based on the replication-defective chimpanzee adenoviral vector AdC68-ept. Methods The recombinant adenovirus AdC68-rab. gp expressing the glycoprotein of rabies vi-rus ERA strain was constructed. Genomes of the AdC68-rab. gp of different generations were extracted and analyzed. HEK293 and Huh7 cells were infected with the AdC68-rab. gp of different generations. ICR mice were immunized with the AdC68-rab. gp and blood samples were collected 4 weeks or 6 months after immuni-zation. Rapid fluorescent focus inhibition test ( RFFIT) was performed to detect the neutralizing antibody against rabies virus in mice serum samples. ICR mice were challenged with lethal dose of rabies virus 4 weeks after the immunization with AdC68-rab. gp to evaluate the protective efficacy of AdC68-rab. gp. Re-sults The genome of AdC68-rab. gp was stable after 15 passages, which was identical to that of the 5th and 1st generations. High levels of neutralizing antibody against rabies virus in serum samples were detected in mice immunized with AdC68-rab. gp and maintained for a long period of time. Immunization mice with one dose of AdC68-rab. gp could protect all mice from the lethal dose challenge of rabies virus. Conclusion The novel AdC68-rab. gp was characterized by good genetic stability and ideal protective effi-cacy. The adenoviral vector based vaccine could be further developed as a potential candidate for the substi-tute of current rabies vaccine.

Objective To evaluate the effects of nerve growth factor-beta (NGF-β) pretreatment on cell apoptosis induced by endoplasmic reticulum stress during ischemia-reperfusion in isolated rat hearts.Methods Male Sprague-Dawley rats,weighing 180-220 g,were anesthetized with intraperitoneal 10％ chloral hydrate 300 mg/kg.The hearts were excised and perfused in a Langendorff apparatus with K-H solution aerated with 95％ O2 and 5％ CO2 at 37 ℃.Thirty-two isolated rat hearts were randomly divided into 4 groups (n =8 each) using a random number table:control group (group C),I/R group,NGF-β pretreatment group (group N) and NGF-β combined with K252a (trkA receptor antagonist) pretreatment group (group N + K).In group C,the hearts were continuously perfused with K-H solution for 195 min.The hearts were perfused with K-H solution for 45 min in group I/R.In N and N + K groups,the hearts were perfused with K-H solution for 15 min,and then with K-H solution containing 0.1 μg/ml NGF-β and 0.1 μg/ml NGF-β mixed with 100 nmol/L K252a,respectively,for 30 min.The perfusion was suspended for 30 min followed by 120 min of reperfusion with K-H solution in I/R,N and N + K groups.HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and + dp/dtmax were measured at the end of 15 min equilibration (baseline) and at 5,30,60 and 120 min of reperfusion.Myocardial specimens were obtained at 120 min of reperfusion for detection of myocardial apoptosis (by TUNEL) and expression of glucose-related protein 78 (GRP78),CCAAT/enhancer-binding protein homologous protein (CHOP),and caspase-12 (by Western blot analysis).Apoptosis index was calculated.Results Compared with group C,HR,LVDP and + dp/dtmax were significantly decreased,and LVEDP,apoptosis index and expression of GRP78 and CHOP were increased in I/R and N groups,and the expression of caspase-12 was upregulated in I/R group.Compared with group I/R,HR,LVDP,and + dp/dtmax were significantly increased,and LVEDP,apoptosis index and expression of GRP78,CHOP and caspase-12 were decreased in group N,and the expression of GRP78 was down-regulated in group N + K.There was no significant difference in cardiac function indexes between group I/R and N + K.Compared with group N,HR,LVDP and + dp/dtmax were significantly decreased,and LVEDP,apoptosis index,and expression of GRP78,CHOP and caspase-12 were increased in group N + K.Conclusion NGF-β pretreatment can protect the isolated rat hearts against ischemia-reperfusion injury,and inhibition of the endoplasmic reticulum stress-triggered cell apoptosis after activating trkA receptors is involved in the mechanism.

Objective To evaluate the role of 1-phosphatidylinositol 3-kinase (PI3K) signaling pathway in nerve growth factor-beta (NGF-β)-produced mitigation of cell apoptosis induced by endoplasmic reticulum stress during hypoxia-reoxygenation (H/R) in rat cardiomyocytes.Methods H9c2 cells were seeded in 96-well plates at a density of 5× 105 cells/ml (100 μl/well).The wells were randomly divided into 5 groups (n =15 each) using a random number table: control group (group C);group H/R;NGF-β group (group N);NGF-β+NGF receptor trkA antagonist K252a group (group N+K);NGF-β+ PI3K inhibitor LY294002 group (group N+L).The cells were exposed to 95％ N2-5％ CO2 for 4 h in an anaerobic incubator, followed by reoxygenation in a standard incubator for 4 h in H/R, N, N+K and N+L groups.In addition, the cells in N, N + K and N + L groups were incubated in a standard incubator containing NGF-β, the mixture of NGF-β and K252a and the mixture of NGF-β and LY294002, respectively, during reoxygenation, and the final concentrations of NGF-β , K252a and LY294002 were 50 ng/ml, 100 nmol/L and 50 μmol/L, respectively.The cell viability was detected by using CCK-8 assay, and the cell survival rate was calculated.The cell apoptosis was examined by flow cytometry, and apoptosis rate was calculated.The expression of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), caspase-12, Akt and phosphorylated Akt (p-Akt) was detected by Western blot.The ratio of p-Akt to Akt was calculated.Results Compared with group C, the cell survival rate was significantly decreased, and the apoptosis rate was increased in H/R and N groups, and the expression of GRP78, CHOP and caspase-12 was significantly up-regulated in group H/R, and p-Akt/Akt was significantly increased in group N (P＜0.05).Compared with group H/R, the cell survival rate was significantly increased, the apoptosis rate was decreased, the expression of GRP78, CHOP and caspase-12 was up-regulated, and p-Akt/Akt was increased in group N (P＜0.05), and no significant change was found in the parameters mentioned above in N+K and N+L groups (P＞0.05).Compared with group N, the cell survival rate was significantly decreased, the apoptosis rate was increased, the expression of GRP78, CHOP and caspase-12 was up-regulated, and p-Akt/Akt was decreased in N+K and N+L groups (P＜0.05).Conclusion NGF-β can mitigate the cell apoptosis induced by endoplasmic reticulum stress during H/R, and activation of PI3K signaling pathway is involved in the mechanism.

Objective To analyse the clinical characteristics,treatments and prognosis of the chemotheray-induced lung injury in malignant hematological diseases patients.Methods 26 malignant hematological diseasespatients with chemotheray-induced lung injury were collected.The clinical characteristics,chemotherapy regimen,treatments and prognosis of the patiants were retrospectively analyzed.Results Among 26 patients,10 patients were male and 16 patients were famale.The dignosis were nonHodgkin's lymphoma (16 cases),leukemia (9 cases) and multiple myeloma (1 case).The chemotherapy regimens inducing lung injure probably were R-CHOP,R-BEACOP and BEACOP in lymphoma,while they were HA,AA,DA and IA in leukemia.The symptoms of lung injury in these patients were fever,cough,hemoptysis,dyspnea,fatigue,or asymptomatic radiological examination revealed.Pulmonary diffuse infiltration and shadows were showed in CT scan.21 cases were cured by hormone therapy,5 cases died of lung injury,2 cases died of tumor recurrence after lung injury cured.There was no effect on the quality of life in most cured patients.Conclusion The lung injury induced by chemotherapy has no specific clinical characteristics and diagnostic criteria,and it could progress rapidly to cause death.But early dignosis and early hormonal treatment can obtain good therapeutic effect.The occurrence regularity and clinical characteristics should be studied furtherly.