In order to observe the therapeutic effect of azithromycin combined with IFN-γ on mouse toxoplasmosis and its impact on the cellular immune function of mouse, a total of 100 BALB/c mice were selected and divided into 5 groups, namely an infection control group (Group A) , azithromycin treatment group (Group B) , azithromycin combined with IFN-γ treatment group (Group C) , IFN-γ treatment group (Group D) and blank control group (Group E). The mice in Group A, B, C, D were infected by Toxoplasma tachyzoites through intraperitoneal injection and those in Group B, C, D were treated with relative drugs 24 h later for S days. The survival time of mice in each group and the levels of CD4 ~+ and CD8~+ T cells in blood were observed. The results showed that azithromycin combined with IFN-γ could improve the therapeutic effect of mouse toxoplasmosis and the cellular immune function of mice.

Objective To investigate the the treatment of class Ⅲ malocclusion by orthognathic surgery combined with postoperative orthodontics.Methods Nine patients with skeletal class Ⅲ malocclusion were treated by surgery-first approach without pre-surgical orthodontic from January 2012 to August 2014.The studied sample consisted of 7 women and 2 men (aged 15-28 years old, mean age 19.7 years), who had obvious mandibular protrusion.2 to 3 days after surgery, intermaxillary traction was used to made the maxilla and mandible together by board;we replaced a rubber band every 2 to 3 days and lasted for four weeks.We would dismantle board and performed conventional orthodontic treatment after patient's facial swelling subsided, and the positional relationship between the jaw stabilized.Results The face type of 9 patients were greatly improved after orthodontic treatment for 6.5 to 19.5 months.Patients and their family members felt satisfied, and their occlusal function returned to normal.At 3 to 32 months follow-up, the postoperative appearance and occlusion were becoming good without obvious signs of recurrence.Conclusions The surgery-first approach is an effective method to treat skeletal class Ⅲ malocclusion.

Objective To understand the clinical distribution and drug resistance of Acinetobacter baumannii during 2012-2013 to provides the theoretical basis for clinical rational drug uses and the prevention and control of hospital infection.Methods To un-derstand the clinical distribution and drug resistance of Acinetobacter baumannii during 2012-2013 to provides the theoretical basis for clinical rational drug uses and the prevention and control of hospital infection.Results The main sources of specimens were sputum(88.7%),followed by secretions (4.6%).Acinetobacter baumannii infection occurred mainly in emergency ICU,surgical ICU,nerve internal medicine department,etc.Acinetobacter baumannii had the high sensitivity to carbapenem.Multiple drug resist-ance was decreased from 47.2% in 2012 to 46.4% in 2013,pan-drug resistance was decreased from 33.3% in 2012 to 27.8% in 2013.Conclusion Multiple drug resistance of Acinetobacter baumannii is serious,there is an upward trend in resistance to common-ly used antibacterial drugs,clinic should reasonably use antibacterial drugs based on the results of drug susceptibility test.

BACKGROUND:n mandibular posterior dental implantation,injury to the inferior alveolar nerve sometimes occurs because of mandibular canal going across mandibular body.This restricts the use of dental implantation at this site.Therefore,it is essential to understand the anatomic structure of inferior alveolar nerve canal in mandibular posterior dental implantation.OBJECTIVE:To observe the intramandibular course of and anatomic structure of inferior alveolar nerve canal.METHODS:Fifteen adult complete mandible specimens with teeth and 4 fresh mandible arterial infusion specimens were researched.All the specimens had complete dentition and there were no obvious absorption in alveolar bone.The course of inferior alveolar nerve canal and its dimension including transverse and longitudinal diameters of mandibular canal and the distance between mandibular canal and mandible each side (superior,inferior,buccal and lingual side) were measured in 15 adult mandibles with teeth.The relationship between blood vessels and nerve of the canal was observed in 4 fresh arterial infusion specimens.RESULTS AND CONCLUSION:The distance between the medial border of the mandibular canal and the lingual wall was shorter than that of the lateral wall of the mandibular canal to the buccal wall (P < 0.01);The length from the upper wall of mandibiular canal to the top of the alveolar ridge was longer than that of the inferior border of the mandibular canal to the inferior border of the mandible (P < 0.01).The longitudinal diameter was smaller than the transverse diameter (P < 0.05),namely,the cross section of the mandibular canal was an ellipse with a longer longitudinal diameter.There was no significant difference between the transverse and longitudinal diameters of the canal in the anterior and posterior teeth region of the mandible.The inferior alveolar nerve and its associated blood vessels were located within a nervous vascular bunch in the mandibular canals.In every fresh specimen the blood vessels lay above the nerve.There were small branches of blood vessels surrounding thenerve.The mandibular canal ran towards the lingual side and was close to the inferior margin of the mandible.

Objective To explore the changes of programmed death receptor-1 (PD-1) in chronic hepatitis B (CHB) patients with different baseline of hepatitis B virus (HBV) DNA levels after treatment with adefovir dipivoxil (ADV).Methods One hundred CHB patients with positive hepatitis B e antigen (HBeAg),1 × 104 copy/mL≤HBV DNA≤1 × 107 copy/mL,and positive human leukocyte antigen-A2 were divided into two groups according to the baseline HBV DNA level:47 cases in low virus load group whose HBV DNA level was ≤1 × 105 copy/mL; 53 cases in high virus load group whose HBV DNA level was＞1 × 105 copy/mL.Both groups were treated with ADV 10 mg/d.Serum HBV DNA,HBeAg seroconversion rate,alanine aminotransferase (ALT) and total bilirubin (TBil) levels of both groups before treatment and 12 months after treatment were compared.Flow cytometry was used to test peripheral blood HBV-specific cytotoxic T lymphocyte (CTL) surface PD-1 and peripheral blood HBV-specific CTL level.Categorical data were tested by x2 test; quantitative data was compared with t-test.Results Peripheral blood HBV-specific CTL surface PD-1 of CHB patients in low virus load group was 20.17 ％±1.69％,which was lower than that in high virus load group (41.38％±2.30％,t =53.02,P＜0.01) ; peripheral blood HBV specific CTL levels in two groups were 0.37％±0.02％ and 0.17％± 0.02％,respectively (t=50.47,P＜0.01) ; ALT and TBil levels in low virus load group were both lower than those of high virus load group (t=13.07,P＜0.01; t=5.06,P＜0.01).Twelve months after treatment,HBV DNA of 25 cases (53.2％) in low virus load group and 10 cases (18.9％) in high virus load group were lower than the detectable level (HBV DNA＜500 copy/mL,x2 =12.89,P＜0.01);HBeAg seroconversion was achieved in 15 cases(31.9％) and 1 case (1.9％),respectively (x2 =16.72,P＜0.01) ; peripheral blood HBV-specific CTL surface PD-1 expression levels were 9.00 ％ ±1.38 ％ and 29.40 ％ ± 3.76 ％,respectively (t =36.80,P＜ 0.01) ; peripheral blood HBV-specific CTL levels were 0.65％±0.10％ and0.48％±0.07％,respectively (t=9.61,P＜0.01).Conclusions After treatment with ADV,along with the decrease of HBV DNA load,HBV-specific CTL surface PD-1 expression decreases,while HBV-specific CTL level increases.The changes in low virus load group are much more remarkable.

Cholelithiasis is a major health burden and is classified into two types of gallstones and bile duct stones. Biliary sludge is a special type of cholelithiasis and is often known as microlithiasis, microcrystal disease, and bile sand. It has complex clinical manifestations, with no symptoms or various clinical symptoms, and may also lead to serious complications. At present, major diagnostic methods for this disease include ultrasound, computed tomography, magnetic resonance, endoscopic retrograde cholangiopancreatography, intraductal ultrasound, and endoscopic ultrasound, and major treatment methods include traditional Chinese and Western medicine therapy, medical treatment, surgery, and minimally invasive treatment. This article reviews the advances in clinical diagnosis and treatment.

Objective To explore relationship between genotypes HBV C and B with HBV specific cytotoxic T lymphocyte (CTL) surface programmed death receptor-1 (PD-1) and its significance in patients with chronic hepatitis B (CHB).Methods A total of 71 CHB patients were studied,human leukocyte antigen(HLA)-A2 positive,HBV DNA ＞ 103 copies/ml,of which 34 cases(47.89％)had genotype C and 36 cases (50.70％) had genotype B.Peripheral blood HBV specific CTL surface PD-1 expression level,HBV specific CTL level,HBV DNA level,ALT and TBil levels of patients infected with genotype C and B were compared.Results HBV specific CTL surface PD-1 expression level of CHB patients infected with genotype C (37.30 ± 3.05％) was higher than that of patients infected with genotype B (26.19 ± 3.06％),t =15.47,P ＜ 0.001,HBV specific CTL level (0.25 ± 0.03％) was lower than that of patients infected with genotype B (0.45 ±0.13％),t =21.54,P ＜0.001,HBV DNA level (6.75 ±0.77 log10 copies/ml) was higher than that of patients infected with genotype B (4.96 ± 1.12 log10 copies/ml),t =7.93,P ＜ 0.001,ALT level (487.39 ± 87.36IU/L) was higher than that of patients infected with genotype B (235.25 ± 90.911U/L),t =12.32,P ＜ 0.001,TBil level (49.73 ± 6.45) was higher than that of patients infected with genotype B (28.48 ± 5.89％),t =9.01,P ＜ 0.001.Conclusion Peripheral blood HBV specific CTL surface PD-1 expression level of CHB patients infected with genotype C was higher than that of patients infected with genotype B,resulting in lower HBV specific CTL level and higher HBV DNA level of patients infected with genotype C than patients infected with genotype B,so damage to liver functions was more serious than patients infected with genotype B.

OBJECTIVETo investigate the relationship between the expression of hepatitis B virus (HBV) core antigen and viral replication and liver tissue inflammation damage in chronic hepatitis B (CHB) patients, and to analyze the relationship of core antigen expression differences with clinical and pathological features in e antigen-negative and e antigen-positive CHB patients.

METHODSSixty-three treatment-naive patients diagnosed with CHB who underwent liver biopsy were included in this retrospective analysis. Liver pathology was assessed, and the karyotype, pulp type, and pulp karyotype were determined. Core and e antigen expression was quantitatively determined by automated immunoassay. Blood samples were used to determine the amount of peripheral lymphocytes or monocytes and HBV DNA load. Results The median titer of HBV DNA was significantly higher in the CHB patients with e antigen positivity (n = 48) than those with e antigen negativity (n = 15) (5.4 * 106 copies/ml vs. 5.4 * 104 copies/ml, P = 0.003). The core antigen positive expression rate was significantly higher in the e antigen-positive CHB patients than in the e antigen-negative CHB patients (80.33% vs. 53.33%, P = 0.042). For the e antigen-positive CHB patients, the HBV DNA titer in karyotype core antigen cases was higher than that in the pulp karyotype mixed-type cases (P = 0.008) and in the negative cases (P = 0.013); in addition, the karyotype patients showed higher titer than the plasma patients (P = 0.019). Also for the e antigen-positive CHB patients, the HBV DNA titer was positively correlated with the rank level of pulp karyotype in core antigen expression (r = 0.589, P = 0.003) but negatively correlated with lobular inflammation, interface inflammation, and fibrosis level (r = -0.552, P = 0.000; r = -0.381, P = 0.008; r = -0.555, P = 0.000); in addition, the level of peripheral blood lymphocytes was negatively correlated with lobular inflammation and fibrosis level (r = -0.361, P = 0.012; r = -0.356, P = 0.013). For the e antigen-negative CHB patients, the level of peripheral blood lymphocytes was negatively correlated with lobular inflammation and interface inflammation (r = -0.702, P = 0.004; r = -0.578, P = 0.024), while the level of peripheral blood mononuclear cells was negatively correlated with lobular inflammation, interface inflammation, and fibrosis level (r = -0.682, P = 0.005; r = -0.620, P = 0.014; r = -0.527, P = 0.044); in addition, age positively correlated with interface inflammation (r = 0.690, P = 0.004).

CONCLUSIONThe pulp karyotype mixed-type of core antigen expression may reflect the level of HBV replication. Negative expression of core antigen may be associated with variation in pre-C or C zone. The monocyte-macrophage system may be involved in the pathogenesis of e antigen-negative CHB, while the mechanism of immune escape may play an important role in increasing HBV DNA titer in an e-antigen-negative CHB condition.

Adult ; Aged ; DNA, Viral ; blood ; Female ; Hepatitis B Core Antigens ; blood ; Hepatitis B virus ; physiology ; Hepatitis B, Chronic ; blood ; pathology ; virology ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Viral Load ; Virus Replication ; Young Adult

Objective:To investigate the effect of vincristine on the proliferation of ovarian cancer cells by regulating RASSF2A demethylation.Methods:SKOV3 cells were infected with control (LV-NC) and RASSF2A lentivirus (LV-RASSF2A) and treated with or without vincristine. Cell counting kit-8 (CCK-8) was used to detect the activity of ovarian cancer cells (SKOV3) treated with different doses of vincristine. Colony formation assay was used to detect the proliferation of SKOV3 cells. Flow cytometry was used to detect the apoptosis of SKOV3 cells. Real time polymerase chain reaction (RT-PCR) was used to examine the mRNA expression of RASSF2A in IOSE-29 and SKOV3 cells. Western blot was used to examine the protein expression of RASSF2A in IOSE-29 and SKOV3 cells. Methylation-specific PCR was used to detect methylation and demethylation levels of RASSF2A gene in IOSE-29 and SKOV3 cells.Results:The cell viabilities of SKOV3 cell treated with 6.25 nmol/L, 12.5 nmol/L, 25 nmol/L, 50 nmol/L and 100 nmol/L vincristine were (87.19±4.49)%, (73.67±8.62)%, (66.35±6.04)%, (50.32±6.00)% and (34.92±6.11)%, respectively, lower than (100.46±4.69)% of control group ( P<0.05). The half maximal inhibitory concentration of vincristine at 48 hours was 50.02 nmol/L. The proliferation abilities of SKOV3 cells in vincristine 12.5 nmol/L group, 25 nmol/L group and 50 nmol/L group were (41.70±2.21)%, (32.15±1.80)% and (23.00±2.01)%, respectively, significantly lower than (100.78±5.66)% in the control group (all P<0.05). The apoptotic rates of SKOV3 cells in vincristine 12.5 nmol/L group, 25 nmol/L group and 50 nmol/L group were (3.65±0.27)%, (5.21±0.76)% and (10.46±1.00)%, respectively, significantly higher than (2.12±0.23)% in the control group (all P<0.05). Compared with the IOSE-29 group (1.00±0.07 and 0.68±0.04), the mRNA expression (0.32±0.04) and protein expression (0.24±0.02) of RASSF2A were down-regulated in SKOV3 cells ( P<0.05). Compared with the LV-NC group [(101.60±4.39)%, (100.73±3.29)%, (4.06±0.30)%], over-expression of RASSF2A down-requlated cell viability (68.92±3.94)%, inhibited proliferation (16.38±2.16)%, and promoted apoptosis (8.65±0.56)%, ( P<0.05). Conclusion:Vincristine can increase RASSF2A expression and inhibit ovarian cancer cell proliferation by promoting the demethylation of RASSF2A promoter.

Objective:To investigate the effect of vincristine on the proliferation of ovarian cancer cells by regulating RASSF2A demethylation.Methods:SKOV3 cells were infected with control (LV-NC) and RASSF2A lentivirus (LV-RASSF2A) and treated with or without vincristine. Cell counting kit-8 (CCK-8) was used to detect the activity of ovarian cancer cells (SKOV3) treated with different doses of vincristine. Colony formation assay was used to detect the proliferation of SKOV3 cells. Flow cytometry was used to detect the apoptosis of SKOV3 cells. Real time polymerase chain reaction (RT-PCR) was used to examine the mRNA expression of RASSF2A in IOSE-29 and SKOV3 cells. Western blot was used to examine the protein expression of RASSF2A in IOSE-29 and SKOV3 cells. Methylation-specific PCR was used to detect methylation and demethylation levels of RASSF2A gene in IOSE-29 and SKOV3 cells.Results:The cell viabilities of SKOV3 cell treated with 6.25 nmol/L, 12.5 nmol/L, 25 nmol/L, 50 nmol/L and 100 nmol/L vincristine were (87.19±4.49)%, (73.67±8.62)%, (66.35±6.04)%, (50.32±6.00)% and (34.92±6.11)%, respectively, lower than (100.46±4.69)% of control group ( P<0.05). The half maximal inhibitory concentration of vincristine at 48 hours was 50.02 nmol/L. The proliferation abilities of SKOV3 cells in vincristine 12.5 nmol/L group, 25 nmol/L group and 50 nmol/L group were (41.70±2.21)%, (32.15±1.80)% and (23.00±2.01)%, respectively, significantly lower than (100.78±5.66)% in the control group (all P<0.05). The apoptotic rates of SKOV3 cells in vincristine 12.5 nmol/L group, 25 nmol/L group and 50 nmol/L group were (3.65±0.27)%, (5.21±0.76)% and (10.46±1.00)%, respectively, significantly higher than (2.12±0.23)% in the control group (all P<0.05). Compared with the IOSE-29 group (1.00±0.07 and 0.68±0.04), the mRNA expression (0.32±0.04) and protein expression (0.24±0.02) of RASSF2A were down-regulated in SKOV3 cells ( P<0.05). Compared with the LV-NC group [(101.60±4.39)%, (100.73±3.29)%, (4.06±0.30)%], over-expression of RASSF2A down-requlated cell viability (68.92±3.94)%, inhibited proliferation (16.38±2.16)%, and promoted apoptosis (8.65±0.56)%, ( P<0.05). Conclusion:Vincristine can increase RASSF2A expression and inhibit ovarian cancer cell proliferation by promoting the demethylation of RASSF2A promoter.