Objective To obserVe the clinical efficacy and safety of yiqing caPsule in the treatment of acne with concomitant constiPation. Methods A randomized controlled method was used. One hundred and forty_fiVe Patients with acne and concomitant constiPation were randomized into treatment grouP (n=75) and control grouP (n=70). Patients in the treatment grouP receiVed yiqing caPsule orally and comPound tretinoin gel toPically, while Patients in the control grouP receiVed toPical comPound tretinoin gel only. Both grouPs were treated for 3 weeks. Results The theraPeutic effect of the treatment grouP was much better than that of control grouP (P<0. 01). No obVious adVerse reactions were obserVed in either grouP. In the treatment grouP,77.4%of Patients were relieVed from constiPation,the ratio being much higher than the control grouP (P<0.01). The chance of acne relief was remarkably higher in Patients whose constiPation were relieVed (P<0. 01). The SPearman correlation index between acne relief and constiPation imProVement was 0. 699 (P<0. 01). Conclusion Combination theraPy of yiqing caPsule and comPound tretinoin gel is effectiVe in the treatment of acne with no significant adVerse reactions. The constiPation imProVement from yiqing caPsule can contribute to the efficacy towards acne.

Objective To investigate the expression and methylation status of HOXA7 gene in human pancreatic cancer cell lines, and to explore the relationship between them.Methods HOXA7 mRNA expression of human pancreatic cancer cell lines BxPC3, CFPAC1, PANC1 and SW1990was detected by RT PCR.Bisulfite sequencing PCR (BSP) and combined bisulfite restriction analysis (COBRA) was used to test promoter methylation status.All the cell lines were treated by 5-aza-2-deoxycytidine (5-aza-dC), and HOXA7mRNA expression, methylation status was detected before and after this treatment.Results HOXA7 mRNA was expressed in BxPC3, CFPAC1 and SW1990, while there was no expression of HOXA7 mRNA in PANC1.HOXA7 promoter methylation rates of CFPAC1, BxPC3, PANC1 and SW1990 were 93.16%, 90.65%,90.09% ,52.30%.HOXA7 promoter methylation rate of SW1990 was significantly lower than those in other 3cell lines ( P ＜0.01 ).After 5-aza-dC treatment, HOXA7 mRNA of PANC1 was expressed again, and HOXA7mRNA of BxPC3 was increasingly expressed;while the expression of HOXA7 mRNA in CFPAC1 and SW1990was not significantly changed after 5-aza-dC treatment.Conclusions The expression of HOXA7 mRNA in BxPC3 and PANC1 was closely correlated with promoter hypermethylation, while there was no obvious relation in CFPAC 1 and SW1990.

Objective To determine the methylation status and expression of Ras association domain family 1A (RASSF1A), and the possible effect between promoter aberrant methylation and pathogenesis of pancreatic cancer. Methods The methylation status of RASSF1A promoter CpG island (CGI) pancreatic cancer cell line BxPC3 was detected in 5 cases of normal pancreatic tissue and 13 pairs of pancreatic cancer tissues (tumor and peri-tumor) by using COBRA (combined bisulfite restriction analysis) and the methylation rate was calculated. The RASSF1A mRNA expression of BxPC3 was compared between pre- and post-treatment of the inhibitor of DNA methyltransferase (5-Aza-2-deoxycitydine, 5-Aza-dC). Results The average methylation rate of RASSF1A promoter CGI was 62.90% in BXPC3, 9.14% in normal pancreas, 53.79% in peri-tumors (TP), and 55.82% in tumors. The methylation rates in port-tumors and tumors were significantly increased when compared with that of normal pancreas (P < 0.01), while there was no significant difference between in peri-tumors and tumors (P > 0.05). After 5-Aza-dC treatting BxPC3 cells, the methylation rates decreased to 42.5% (P < 0. 05) and RASSF1A mRNA expression was enhanced. Conclusions Aberrant hypermethylation of RASSF1A promoter CGI could be considered as an early event in the process of pancreatic cancer and participates in the pathogenesis of pancreatic cancer.

OBJECTIVETo explore the effect of half circle external fixation for the treatment of open tibial fractures.

METHODSFrom March 2005 to March 2011, 94 patients with open tibiofibula fractures were treated by closed manipulative or Kirschner-wire poking reduction with half circle groove external fixation including 63 males and 31 females with an average age of 39 years old ranging from 17 to 65 years old. Among these patients, 5 cases were cross shaped fractures, 19 were oblique form and spiral fractures, 70 cases were comminuted fractures. According to the fracture Gustilo classification, 49 cases were type IIIA, 45 were type IIIB. The incidence of wound infection, fracture healing time were observed. The function was evaluated according to the Johner-Wruhs standard.

RESULTSAll patients were followed up for 14 to 63 months (averaged 29 months). The wound healing time was from 16 to 39 weeks (means 21.4 weeks). No fracture nonunion, osteomyelitis and calf compartment syndrome occurred. The wounds of 81 cases were healed at the first period,deep wound infection occurred in 2 cases. According to the function Johner-Wruhs evaluation criteria:the result was excellent in 52 cases, good in 37 cases, fair in 5 cases.

CONCLUSIONClosed manipulative or Kirschner-wire poking reduction and half circle groove external fixation can reduce the infection rate of open tibiofibula fractures. For open tibiofibula comminuted fractures, after the half circle groove external fixation for 3 to 6 weeks, a middle Kirschner-wire was removed according to fracture end healing situation to make fixation dynamic and promote fracture healing.

Adolescent ; Adult ; Aged ; Bone Wires ; External Fixators ; Female ; Fracture Fixation ; instrumentation ; Fractures, Comminuted ; surgery ; Fractures, Open ; surgery ; Fractures, Ununited ; surgery ; Humans ; Male ; Middle Aged ; Tibial Fractures ; surgery ; Young Adult

Eleven C21 steroids were isolated from chloroform extract of roots of Cynanchum otophyllumby silica gel, MCI, ODS columns, and semi-preparative HPLC. Their structures were determined by spectroscopic data analysis as otophylloside B(1), caudatin-3-O-beta-D-cymaropyranosyl-(1-->4)-beta-D-oleandropyranosyl-(1-->4)-beta-D-cymaropyranosyl-(1-->4)-beta-D-cymaropyranoside (2), caudatin-3-O-beta-D-oleandropyranosyl-(1-->4)-beta-D-oleandropyranosyl-(1-->4)-beta-D-cymaropyranosyl-(1-->4)-beta-D-cymaropyranoside (3), caudatin-3-O-beta-D-oleandropyranosyl-(1-->4)-beta-D-digitoxopyranosyl-(1-->4)-beta-D-cymaropyranoside (4), otophylloside O (5), gagamine-3-O-beta-D-oleandropyranosyl-(1-->4)-beta-D-cymaropyranosyl-(1-->4)-beta-D-cymaropyranoside (6), sinomarinoside B (7), mucronatosides C (8), wallicoside J (9), stephanoside H (10), and qinyangshengenin-3-O-beta-D-oleandropyranosyl-(1-->4)-beta-D-cymaropyranosyl-(1-->4)-beta-D-digitoxopyranoside (11). Among them, compounds 2-3, and 6-11 were separated from the roots of this plant for the first time.
Cynanchum ; chemistry ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; Magnetic Resonance Spectroscopy ; Molecular Structure ; Plant Roots ; chemistry ; Steroids ; chemistry ; isolation & purification

Objective To measure the in vitro antibacterial activity of tigecycline against carbapenems-resistant Acinetobacter calcoacetcus-Acinetobacter baumannii complex.Methods The isolated strains of carbapenems-resistant Acinetobacter calcoacetcus-Acinetobacter baumannii complex were collected in our hospital from December 2013 to February 2014.The MIC test strip was a-dopted to measure the MIC value of tigecycline.The break point adopted the judgment criteria published by FDA.Results All 61 strains of carbapenems-resistant Acinetobacter calcoacetcus-Acinetobacter baumannii complex had extremely high drug resistant rate to the commonly used antimicrobial agents.The sensitive rate of tigecycline was 80.3%,intermediation was 19.7% and no re-sistant strain was found in this study.MIC50 and MIC90 were 2 μg/mL and 3 μg/mL respectively.Conclusion Tigecycline has bet-ter in vitro antibacterial activity to the carbapenems-resistant Acinetobacter calcoacetcus-Acinetobacter baumannii complex isolated in our hospital.

To investigate the utility of optomap panoramic 200Tx in screening fundus disease among the patients after cataract surgery.
●METHODS: From November 18 th to December 31st , 2013 all 146 post- cataract surgery patients were recruited. All non - mydriatic fundus images were taken with the optomap panoramic 200Tx and were diagnosed by one masked retinal specialist. Non - mydriatic direct ophthalmoscope exam and mydriatic slit-lamp lens exam were also done by other two masked specialists. Comparisons of the three methods were made.
●RESULTS: Among 146 patients ( 161 eyes), 40 eyes (24. 8%) of retinal lesions was detected by non-mydriatic direct ophthalmoscope exam, 59 ( 36. 7%) by non -mydriatic optomap 200Tx exam, and 61 (37. 9%) by slit-lamp lens exam. Nine eyes ( 5. 6%) needed medical intervention immediately. Results of optomap 200Tx exams and slit - lamp lens exams were similar without statistically significant difference ( P > 0. 05), better than direct ophthalmoscope exam ( P < 0. 05) with statistically significant difference.
● CONCLUSlON: Opacification of the refractive medium makes thorough fundus examination impossible. So post-operative fundus examination is highly necessary and should be a routine. Optomap panoramic 200Tx, which shows no statistically difference from mydriatc slit- lamp lens exam, is a convenient and feasible method in discovering fundus pathological changes.

ObjectiveTo investigate the methylation of the promoter region in miRNA in pancreatic cancer cell line PANC1 and normal pancreatic tissue,to discover the miRNA with hypermethylation associated with pancreatic cancer.MethodsThe genomic DNA of PANC1 and normal pancreatic tissue was extracted,and fractured by ultrasound.Methylation DNA fragments were obtained by 5-methyl of pyrimidine nucleoside antibodies and immunomagnetic beads.The hypermethylation miRNA differentially expressed between PANC1 and normal pancreatic tissue was selected by using methylation DNA chip.BSP ( bisulfite genomic sequencing PCR) and TA clone sequencing was performed for further validation.The genomic DNA of pancreatic cancer cell lines BXPC3,CFPAC1,PANC1 and SW1990 was extracted.The COBRA (combined bisulfite restriction analysis) was used to validate differentially expressed hypermethylation miRNA.ResultsEight differentially expressed hypermethylation miRNAs were screened from the DNA methylation chips,then five of them were selected for sequencing.The methylation status of miRNA-615,-663,-663b was significantly higher in the PANC1 than in normal tissues (60.6％ vs 7.6％,88.8％ vs 22.2％,94.4％ vs 13.0％ ) ; the methylation status of miRNA-675 was not significantly different between PANC1 and normal pancreatic tissue (76.0％ vs 100％ ).Due to large error in sequencing,miRNA1826 was excluded.The results of COBRA confirmed all the 4 miRNAs were highly methylated in PANC1 ; except for miRNA-675,other 3 miRNAs were highly methylated in BxPC,miRNA-663,miRNA-663b were highly methylated in CFPAC1,while miRNA-615,miRNA-663 were highly methylated in SW1990.ConclusionsHypermethylation miRNAs were differentially expressed between pancreatic cancer cell lines and normal pancreatic tissue,among them,highly methylated miRNA-663 was possibly associated with pancreatic cancer.

Background Platelet-derived growth facto(PDGF) affectthe proliferation of human lenepithelial cell(LECs),and human LECexpresPDGF-α recepto(PDGFR-α) throughoutheilifetime.The binding of activated PDGF-α receptowith PDGF promotethe synthesiof DNA.Othestudiedemonstrated thasilencing of PDGFR-α by antisense oligodeoxynucleotide(ASODN) inhibitthe growth of RPE cellin proliferative vitreoretinopathy (PVR),buwhethethitechnique ifeasible foLECiunclear.Objective Thistudy wato investigate the effecof the knockdown of the PDGFR-α on the proliferation of human LECin vitro,and to offean experimental basifothe gene therapy of posteriocapsule opacification.MethodHuman LECstrain SRA01/ 04 wacultured in α-MEM containing fetal bovine serum.The cellwere incubated in 6-well platea5 × 104 cells/ well and transfection of ASODN-containing liposome waperformed.The cellwere divided into the blank control group (with blank liposome),PDGFR-α missense oligodeoxynucleotide(MSODN) group (with PDGFR-α MSODN + liposome),0.5 μmol/L PDGFR-α ASODN group (with 0.5 μmol/L PDGFR-α ASODN+liposome) and 1.0 μmol/L PDGFR-α ASODN group (with 1.0 μ mol/L PDGFR-α ASODN+liposome).The morphology of LECwaexamined undean inverse microscope 24 houraftetransfection.The expression of PDGFR-α mRNin the cellwadetected by reverse transcription-PC(RT-PCR).The rate of proliferation (A490) of the cellwaassayed using Mtand the inhibitory rate of PDGFR-α ASODN on proliferation wameasured.The percentage of LECin G1 phase waanalyzed by flow cytometer.ResultThe LECgrew well and exhibited polygonal shape in the blank control group and PDGFR-α MSODN group 24 houraftetransfection.Buin the 0.5 μmol/L and 1.0 μmol/L PDGFR-α ASODN groups,the cellappeared round in shape and the numberof cellwere obviously decreased.The expression of PDGFR-α mRNdetected by RT-Pcdemonstrated highelevel in the blank control group and PDGFR-α MSODN group;however,the PDGFR-α mRNexpression waobviously lowein the 0.5 μmol/L and 1.0 μmol/L PDGFR-α ASODN groups.The A490 value wa0.661 ± 0.036,0.655 ± 0.016,0.529 ± 0.030 and 0.441 ± 0.039 in the blank control group,PDGFR-α MSODN group,0.5 μmol/L PDGFR-α ASODN group and 1.0 μmol/L PDGFR-α ASODN group,respectively,showing significandecline in the 0.5 μmol/L PDGFR-α ASODN group and 1.0 μ mol/L PDGFR-α ASODN group in comparison with the blank control group (F=34.08,P＜0.01).The percentageof LECin G1 phase were (47.73±1.18)％,(49.48±1.09)％,(53.31±1.30)％ and (59.98±0.95) ％ in the blank control group,PDGFR-α MSODN group,0.5 μmol/L PDGFR-α ASODN group and 1.0 μmol/L PDGFR-α ASODN group,showing significandifference among them (F =68.41,P＜0.01),and thain the 0.5 μmol/L PDGFR-α ASODN group o1.0 μmol/L PDGFR-α ASODN group showed significantly increase in comparison with the blank control group (P＜0.05).ConclusionPDGFR-α silencing could inhibithe proliferation of human LECin vitro.

BackgroundRetinal pigment epithelial(RPE) cells can secrete platelet-derived growth factor (PDGF) and PDGF receptor(PDGFR).Studies have shown that PDGF plays a key role in the formation of proliferative vitreous retinopathy(PVR). ObjectiveThis study was to investigate the proliferation and apoptosis changes of RPE after blockage of the PDGFR-α expression by antisense oligonucleotide ( ASODN ) in vitro. Methods Human RPE cells strain was cultured in low glucose DMEM with 10％ fetal bovine serum.Logarithmic phase cells were collected and incubated in 96-well plate at the density of 5 × 105 cells/hole.PDGFR-α ASODN was transfected into RPE cells at different concentrations for 48 hours.The cells of the blank control group were regularly cultured without any transfection.The changes of PDGFR-α expression were detected by reverse transcription-polymerase chain reaction(RT-PCR),and the proliferation of RPE was detected by MTT as the A490 value.Hoechst 33258 fluorescence staining was used to determine the apoptosis of RPE.Flow cytometry method (FCM) was applied to detect the change of cell cycle and apoptosis rate of RPE cells. ResultsThe A490 values of RPE cells were 1.45±0.12,1.07±0.06,0.65±0.05 in blank control group,1.0 μmol/L Lipo-ASODN group and 2.0 μmol/L Lipo-ASODN group with the significant difference(P=0.00 ),and that of 1.0 μmol/L Lipo-ASODN group and 2.0 μ mol/L Lipo-ASODN group were significantly lower than the blank control group ( P =0.00,0.00).Hoechst 33258 staining showed that the apoptosis cells were obviously more in Lipo-ASODN group compared with blank control group.PDGFR-α ASODN transfection induced an increase of percentage of RPE cells in G0/G1 phase( F =206.70,P =0.00),and the apoptosis rates in 1.0 μmol/L Lipo-ASODN group and 2.0 μmol/L Lipo-ASODN group were significantly enhanced in comparison with blank control group ( 37.8 ± 1.3 vs 10.5 ± 0.1,61.2 ± 1.9 vs 10.5 ± 0.1 ) ( F =1808.90,P =0.00 ).Expression intensity of PDGFR-α mRNA in RPE cells in Lipo-ASODN groups was lower. ConclusionsBlocking the PDGFR-α expression with ASODN technology can suppress proliferation and induce apoptosis of RPE cells.Intensity of PDGFR-α mRNA expression in RPE cells is ASODN dose-dependent.ASODN targeted to PDGFR-α offers an experimental basis of the gene therapy for PVR.