Objective To investigate the results difference of the indirect immunofluorescence (IIF) and immunoblotting (LIA) for detecting ant-inuclear antibodies (ANA) and clinical value .Methods One hundred and forty-six ANA detection specimens of IIF negative and LIA positive were collected and performed the detection of HBV antibodies and anti-HCV antibodies .Results (1) In 146 specimens of IIF (-)LIA (+ ) ,the positive specimen numbers of single anti-Ro52 antibody ,anti-SSA antibody and anti-AMA-M2 antibody were 69 cases ,42 cases and 15 cases respectively ,which of anti-RNP antibody ,anti-PCNA antibody and PM-Scl antibody were 3 cases ,5 cases and 2 cases respectively ,the combined 2-item positive was in 8 cases .(2)Among positive specimens of single anti-Ro52 antibody ,HBsAg(+ ) ,anti-HBe(+ ) ,anti-HBc(+ ) model and HBsAg(+ ) ,HBeAg(+ ) ,HBcAb(+ ) model of hepatitis B ,and hepatitis C were 51 cases ,4 cases and 7 cases respectively ,7 cases were non-hepatitis patients .(3) Among positive specimens of single ant-SSA antibody ,6 cases were hepatitis B patients and 36 cases were the patients with non-hepatitis B .Conclu-sion Anti-Ro52 antibody and anti-SSA antibody are easier to be missed by the IIF detection .Anti-Ro52 antibody positive has a cer-tain relation with small three positive of hepatitis B .

Objective To investigate the composing characteristics and drug resistances of pathogens isolated from genital tracts in premature rupture of membranes of obstetrics from 2012 to 2014 ,for instructing clinical application of antibiotics reasonably . Methods A retrospective investigation analysis was made for all the isolated bacteria from genital tracts specimens as well as their drug resistances from 2012 to 2014 .Results The results shows that 598 strains of bacterial pathogens were isolated from 2000 detected samples ,The infection rate of bacterial pathogens was 29 .90% .The top four bacteria pathogens were E .coli(31 .44% ) ,Can . albicans(20 .90% ) ,Str .agalactiae(19 .23% ) and Sta .aureus(10 .03% ) .E .coli and Sta .aureus were highly resistant to commonly used antibiotics and demonstrated multi‐drug resistance .Str .agalactiae and Can .albicans were lowly resistant to commonly used antibiotics .Conclusion Inspecting pathogens and studying the composition of pathogens and the trend of their drug resistance are im ‐ portant to rationally select antibiotics ,decrease the occurrence of drug resistant strains in perinatal period ,and control the outbreak and prevalence of nosocomial infection .

Objective To explore the MRI findings of ovarian cancer peritoneal carcinomatosis (PC).Methods MRI findings of 34 cases with advanced ovarian cancer and PC confirmed by operation and pathology were reviewed retrospectively.MRI protocols included T1 WI,T2 WI,MRH,DWIBS,and gadolinium-enhanced 3D THRIVE sequences.The type of ovarian tumor and MRI manifestations of PC were analyzed.Results All of the ovarian tumors and PC lesions were high signal intensity in DWIBS.All of the ovarian tumors were shown as mixed cystic solid masses,including type Ⅱa in 12 cases,type Ⅱb in 7 cases,and type Ⅱc in 1 5 cases.The MR manifestations of PC were described as follow:linear thickening of the peritoneum (n=2),irregular linear thickening of the peritoneum (n=27);smudged thickening of the omentum (n=1 9),cake-like thickening of the omentum (n=1 1);fouling-appearance of the mesentery (n=4);plaque,nodule and mass in the abdominal cavity (n= 34),cystic mass (n=8).PC lesions were detected in the Douglas’space in 31 cases,paravesical interspace in 24 cases,omentum in 20 cases,paracolic gutter in 9 cases, right subdiaphragmatic / parahepatic space in 1 1 cases,and left subdiaphragmatic / parasplenic space in 10 cases.The primary and PC tumors invaded the rectum in 26 cases,sigmoid in 22 cases,and uterus in 1 6 cases.Ascites and lymphadenectasis in abdomen were seen in 33 and 7 cases,respectively.Conclusion Ovarian cancer PC can be diagnosed accurately by combing DWIBS and con-ventional MRI.

Objective To explore the value of static and dynamic MRI before and after operation of pelvic organ prolapse (POP). Methods 29 patients with POP (POP group)and 12 normal women (control group)underwent static and dynamic MRI.The morphologic changes of pelvic floor were observed on MR images.The measurements of bladder,uterus,Douglas pouch to pubococcygeal line (B-PCL,U-PCL,D-PCL),the puborectal hiatus line (H-line),muscular pelvic floor descent (M-line),the levator hiatus size (LHS),the levator plate angle (LPA),the iliococcygeus angle (ICA)and the urethral inclination angle (UA)were recorded on dynamic MR images.Results 19 cystoceles,28 uterine prolapses,4 rectoceles and 14 hernias of Douglas pouch were detected with MRI.29 cases of pelvic floor relaxation,27 cases of levator ani muscle defect and 24 cases of pubocervical fascial defect were found.The values of B-PCL,U-PCL, D-PCL,H-line,M-line,LHS,LPA,ICA and UA of POP group were larger than control group (P<0.01).The positions of pelvic organ returned to normal in 9 cases of 21 postoperative cases,while 12 cases remained prolapses.There was no displacement of mesh in 8 cases of mesh implant.The values of B-PCL,U-PCL,D-PCL,UA after operation were smaller than those before operation (P<0.05).Conclusion Static and dynamic MRI can evaluate morphological and functional changes of pelvic floor before and after operation of POP comprehensively,and may reveal those invisible pelvic floor dysfunction and postoperative remnant defects.

Objective:to investigate the therapeutic effect of low molecular weight heparin combined with average volumeassuredpressuresupport (AVAPS) on patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) complicated with type Ⅱ respiratory failure.Methods:A total of 82 patients with AECOPD combined with type Ⅱ respiratory failure in the Second People′s Hospital of Xindu District of Chengdu from February 2018 to April 2020 were selected as the research objects, and they were randomly divided into two groups with 41 cases in each group. The control group was given AVAPS mode, and the observation group was given low molecular weight heparin combined with AVAPS mode. The arterial partial pressure of oxygen (PaO 2), arterial carbon dioxide (PaCO 2), and forced vital capacity (FVC), forced expiratory volume in the first second (FEV 1), maximum peak expiratory flow rate (PEF), interleukin (IL)-6, IL-8, tumor necrosis factor-(TNF-α), 16 kDa Clara cell protein (CC16), surfactant protein D(SP-D), adiponectin (APN), superoxide dismutase (SOD), D-dimer, fibrinogen before and after treatment were compared between the two groups and the incidence of adverse reactions were observed. Results:After treatment, the levels of FEV 1, FVC, PEF, PaO 2 in the observation group were higher than those in the control group: (1.78 ± 0.29) L vs. (1.47 ± 0.25) L, (2.47 ± 0.29) L vs.(2.20 ± 0.25) L, (5.14 ± 0.37) ml/s vs. (4.69 ± 0.35) ml/s, (88.37 ± 10.52) mmHg (1 mmHg = 0.133 kPa) vs. (80.16 ± 9.87) mmHg; and the level of PaCO 2 was lower than that in the control group: (65.07 ± 6.71) mmHg vs. (70.84 ± 6.50) mmHg; and the differences were statistically significant ( P<0.05). After treatment, the levels of IL-6, IL-8 and TNF-α in the observation group were lower than those in the control group: (0.47 ± 0.09) ng/L vs. (0.58 ± 0.10) ng/L, (64.37 ± 7.25) ng/L vs. (88.24 ± 8.34) ng/L, (45.37 ± 4.63) ng/L vs. (66.31 ± 4.92) ng/L; and the levels of SOD and APN were higher than those in the control group: (92.37 ± 10.85) U/mg vs. (76.13 ± 9.84) U/mg, (13.94 ± 0.76) mg/L vs. (11.58 ± 1.21) mg/L; and the differences were statistically significant ( P<0.05). After treatment, the level of CC16 in the observation group was higher than that in the control group: (114.78 ± 12.15) μg/L vs. (107.41 ± 11.06) μg/L; while the levels of SP-D, D-dimer and FIB were lower than those in the control group: (93.24 ± 9.85) μg/L vs. (103.25 ± 10.78) μg/L, (0.58 ± 0.07) mg/L vs. (0.79 ± 0.11) mg/L, (1.98 ± 0.29) g/L vs. (2.56 ± 0.34) g/L; and the differences were statistically significant ( P<0.05). There was no significant difference in the incidence of adverse reactions between the two groups ( P>0.05). Conclusions:Low-molecular-weight heparin combined with AVAPS mode in the treatment of AECOPD complicated with type Ⅱ respiratory failure can significantly improve the lung inflammation and coagulation function in patients, adjust blood gas analysis and CC16, SP-D levels, and promote the recovery of patients′ lung function.

Objective To investigate the effect of MACC1 on RSL3-induced ferroptosis in colorectal cancer cells and explore its molecular mechanism.Methods MACC1 expression was detected in SW620,HCT116,LOVO and RKO cells using Western blotting.The effects of different concentrations of RSL3(an inducer of ferroptosis)or Fer-1(an inhibitor of ferroptosis)alone,or 10 μmol/L RLS3 combined with 10 μmol/L Fer-1,on viability of SW620 cells were examined using MTT assay.The survival of SW620 cells with mRNA interference of MACC1 was analyzed following treatment with RSL3,and RT-qPCR and Western blotting were performed to detect the changes in MACC1 expressions after RSL3 treatment at different concentrations and the changes in GPX4 expression after MACC1 knockdown.Flow cytometry and laser confocal microscopy were used to analyze the changes in ROS-induced lipid peroxidation in SW620 cells after MACC1 knockdown.Results SW620 cells had the highest MACC1 expression among the 4 colorectal cancer cell lines.Treatment with RSL3 significantly inhibited the viability of SW620 cells in a dose-dependent manner,while Fer-1 did not significantly affect the survival of SW620 cells.RSL3 alone reduced SW620 cell survival by 50%(P<0.01),and the combined treatment with RSL3 and Fer-1 caused no significant changes in cell survival(P>0.05).Treatment with RSL3 concentration-dependently suppressed MACC1 expressions at both the mRNA and protein levels in SW620 cells(P<0.01).MACC1 knockdown obviously enhanced the cytotoxic effect of RSL3,inhibited the expression of GPX4,and increased ROS-induced lipid peroxidation in SW620 cells(P<0.05).Conclusion MACC1 knockdown enhances RSL3-induced ferroptosis in cultured colorectal cancer cells by inhibiting the expression of GPX4.

Objective To investigate the effect of MACC1 on RSL3-induced ferroptosis in colorectal cancer cells and explore its molecular mechanism.Methods MACC1 expression was detected in SW620,HCT116,LOVO and RKO cells using Western blotting.The effects of different concentrations of RSL3(an inducer of ferroptosis)or Fer-1(an inhibitor of ferroptosis)alone,or 10 μmol/L RLS3 combined with 10 μmol/L Fer-1,on viability of SW620 cells were examined using MTT assay.The survival of SW620 cells with mRNA interference of MACC1 was analyzed following treatment with RSL3,and RT-qPCR and Western blotting were performed to detect the changes in MACC1 expressions after RSL3 treatment at different concentrations and the changes in GPX4 expression after MACC1 knockdown.Flow cytometry and laser confocal microscopy were used to analyze the changes in ROS-induced lipid peroxidation in SW620 cells after MACC1 knockdown.Results SW620 cells had the highest MACC1 expression among the 4 colorectal cancer cell lines.Treatment with RSL3 significantly inhibited the viability of SW620 cells in a dose-dependent manner,while Fer-1 did not significantly affect the survival of SW620 cells.RSL3 alone reduced SW620 cell survival by 50%(P<0.01),and the combined treatment with RSL3 and Fer-1 caused no significant changes in cell survival(P>0.05).Treatment with RSL3 concentration-dependently suppressed MACC1 expressions at both the mRNA and protein levels in SW620 cells(P<0.01).MACC1 knockdown obviously enhanced the cytotoxic effect of RSL3,inhibited the expression of GPX4,and increased ROS-induced lipid peroxidation in SW620 cells(P<0.05).Conclusion MACC1 knockdown enhances RSL3-induced ferroptosis in cultured colorectal cancer cells by inhibiting the expression of GPX4.

AIM:To investigate the molecular mechanism underlying ferroptosis induced by celastrol(Cel)in huamn pancreatic cancer cell line PANC-1.METHODS:The viability of PANC-1 cells was analyzed by MTT assay,and the effects of Cel on cell proliferation were analyzed using EdU and colony formation assays.Flow cytometry and fluores-cence microscopy were used to assess and observe changes in lipid reactive oxygen species(ROS)levels,respectively,while the levels of malondialdehyde(MDA),glutathione(GSH)and Fe2+were measured using specific kits.The protein expression of glutathione peroxidase 4(GPX4)was evaluated by Western blot,and GPX4 ubiquitination was measured by immunoprecipitation.RESULTS:It was found that the viability,proliferation and colony formation in PANC-1 cells de-creased gradually as the concentration of Cel increased.Addition of Cel alone to the cells reduced both cell rounding and viability,while treatment with ferrostatin-1(Fer-1)alone or in combination with Cel had no effect on either cell morpholo-gy or viability.Fluorescence staining of lipid ROS with BODIPYTM 581/591 C11 followed by flow cytometry analysis showed significantly increased levels of green fluorescence indicative of oxidized lipid ROS,which were further increased after treatment of the cells with Cel.Treatment of the cells with both Cel and Fer-1 reduced the green fluorescence and lip-id ROS levels.Treatment with Cel also increased the levels of MDA and Fe2+,relative to the controls,which reducing the levels of GSH,while addition of both Cel and Fer-1 to the cells restored the levels of MDA,Fe2+,and GSH to those of the control group.CONCLUSION:Treatment with Cel reduces the proliferation of pancreatic cancer cells by inducing fer-roptosis through promoting the ubiquitination and degradation of GPX4.

Objective:To investigate the effect of tocilizumab (TCZ) on ventricular arrhythmias (VAs) after myocardial infarction (MI) in Sprague-Dawley rats and explore its potential mechanism.Methods:The random number table method was used to divide 32 adult male Sprague-Dawley rats into 4 groups: Sham group, TCZ group, MI group and MI+TCZ group, with 8 rats in each group. The MI model was established by ligation of the left anterior descending branch of the coronary artery in the MI and MI+TCZ groups, and only sutured without ligation in the Sham and TCZ groups. TCZ was injected into the left superior cervical ganglion (SCG) of rats in the TCZ and MI+TCZ groups after successful modeling or sham operation, and the same amount of normal saline was injected in the Sham and MI groups. 24 h after successful modeling, ECG of rats in each group was recorded, heart rate variability (HRV, including low frequency power (LF), high frequency power (HF), LF/HF ratio), QT interval, QTc interval were calculated, and left ventricular effective refractory period (ERP) and VA inducibility were measured. Myocardial infarct size and tissue changes were observed with triphenyl tetrazolium chloride staining and HE staining. Real-time PCR analysis was used to detect the messager RNA (mRNA) expression of interleukin-6 (IL-6) and signal transducer and activator of transcription (STAT) 3 in SCG and potassium voltage-gated channel subfamily D member 2 (Kcnd2) in myocardial infarction periphery. The expression of c-fos in SCG was detected by immunofluorescence staining.Results:Compared with Sham group and MI+TCZ group, rats in MI group had higher LF and LF/HF ratio, longer QT interval and QTc interval, more VAs induced, lower HF and shorter ERP ( P all<0.05). Triphenyl tetrazolium chloride staining and HE staining showed that rats in the Sham and TCZ groups had normal myocardial tissue structure, those in the MI group had severe myocardial injury, and those in the MI+TCZ group had less myocardial injury than those in the MI group. Real-ime PCR analysis showed that compared with Sham group and MI+TCZ group, mRNA expression levels of IL-6 and STAT3 in SCG of rats in MI group were higher, and mRNA expression level of myocardial Kcnd2 was lower ( P all<0.05). Immunofluorescence staining showed that the content of c-fos in SCG of rats in MI group was higher than that of Sham group and MI+TCZ group ( P all<0.05). Conclusions:TCZ may reduce neural activity of the SCG after MI by inhibiting the IL-6/STAT3 signaling pathway, thereby alleviating myocardial injury and inhibiting VAs.