Objective To prepare a nano drug(PFOB@Lip-MMC)with liposome as the carrier,liquid perfluorooc-tyl bromide(PFOB)as core and mitomycin C(MMC)loading on the liposome shell and study its inhibitory effect on the proliferation of human pterygium fibroblasts(HPFs).Methods The thin film dispersion-hydration ultrasonic method was used to prepare PFOB@Lip-MMC and detect its physical and chemical properties.Cell Counting Kit-8,Cam-PI cell viability staining and flow cytometry were employed to detect the impact of different concentrations of PFOB@Lip-MMC on the via-bility of HPFs.DiI fluorescence labeled PFOB@Lip-MMC was used to observe the permeability of the nano drug to HPFs under a laser confocal microscope.After establishing HPF inflammatory cell models,they were divided into the control group(with sterile phosphate-buffered saline solution added),PFOB@Lip group(with PFOB@Lip added),MMC group(with MMC added),PFOB@Lip-MMC group(with PFOB@Lip-MMC added)and normal group(with fresh culture medi-um added)according to the experimental requirements.After co-incubation for 24 h,flow cytometer was used to detect the apoptosis rate of inflammatory cells,and the gene expression levels of interleukin(IL)-1β,prostaglandin E2(PGE2),tumor necrosis factor(TNF)-α and vascular endothelial growth factor(VEGF)in cells were analyzed by PCR.Results The average particle size and Zeta potential of PFOB@Lip-MMC were(103.45±2.17)nm and(27.34±1.03)mV,respec-tively,and its entrapped efficiency and drug loading rate were(72.85±3.28)％and(34.27±2.04)％,respectively.The sustained-release MMC of drug-loaded nanospheres reached(78.34±2.92)％in vitro in a 24-hour ocular surface environ-ment.The biological safety of PFOB@Lip-MMC significantly improved compared to MMC.In terms of the DiI fluorescence labeled PFOB@Lip-MMC,after co-incubation with inflammatory HPFs for 2 h,DiI fluorescence labeling was diffusely dis-tributed in the cytoplasm of inflammatory HPFs.The apoptosis rate of inflammatory HPFs in the PFOB@Lip-MMC group[(77.23±4.93)％]was significantly higher than that in the MMC group[(51.62±3.28)％].The PCR examination results showed that the gene transcription levels of IL-1 β,PGE2,TNF-α and VEGF in other groups were significantly reduced com-pared to the control group and PFOB@Lip group,with the most significant decrease in the PFOB@Lip-MMC group(all P＜0.05).Conclusion In this study,a novel nano drug(PFOB@LIP-MMC)that inhibited the proliferation of HPFs was successfully synthesized,and its cytotoxicity was significantly reduced compared to the original drugs.It has good bio-compatibility and anti-inflammatory effects,providing a new treatment approach for reducing the recurrence rate after pte-rygium surgery.

Objective:To explore the influencing factors of postoperative infection in patients undergoing thoracoscopic lung cancer resection, and provide the basis for formulating nursing strategies and reducing the infection rate.Method:Using the convenient sampling method, a total of 83 patients who underwent thoracoscopic lung cancer resection in Henan Provincial People's Hospital from March 2017 to March 2021 were selected as the research objects. A self-made questionnaire was used to investigate the influencing factors. Patients were divided into the infection group ( n=7) and the non-infection group ( n=76) according to whether postoperative infection occurred. Univariate analysis was used to investigate influencing factors of postoperative infection in patients undergoing thoracoscopic lung cancer resection. And targeted nursing interventions were proposed. Results:The incidence of postoperative infection in 83 patients with thoracoscopic lung cancer resection was 8.43% (7/83) . There were statistically significant differences in age, smoking, diabetes, postoperative bed rest time between the infected group and the non-infected group ( P<0.05) . Conclusions:Age, smoking, diabetes, postoperative bed rest time are the influencing factors of postoperative infection in patients undergoing thoracoscopic lung cancer resection. Nursing staff should formulate targeted nursing interventions according to the influencing factors of infection.

Objective:To study the influence of different feeding patterns on mother-to-child transmission (MTCT) of hepatitis B virus (HBV) in pregnant women with high viral loads who received antiviral medication during pregnancy to the day of delivery.Methods:This prospective cohort study was conducted in Beijing You'an Hospital. From January 1, 2019, to March 31, 2020, and 574 pregnant women with positive hepatitis B surface antigen (HBsAg) and HBV DNA>2×10 5 IU/ml were enrolled. All participants received tenofovir, telbivudine, lamivudine, or propofol tenofovir from 24-28 weeks of gestation and discontinued on the day of delivery, and their neonates were postnatally given routine passive-active immunoprophylaxis. Based on the feeding patterns, the subjects were divided into three groups: breastfeeding ( n=257), bottle-feeding ( n=241) and mixed feeding groups ( n=76). The follow-up data were obtained from liver functions and HBV DNA level of the mothers at 6-8 weeks postpartum and HBV serological markers of infants at 7-12 months. One-way ANOVA, Student-Newman-Keuls, Chi-square test or Fisher exact test, and repeated measures ANOVA were used to analyze the data. Results:The average maternal HBV DNA levels before antiviral treatment did not differ significantly between the three groups [(7.90±0.67), (7.82±0.70), (7.83±0.70) log 10 IU/ml, F=0.912, P>0.05]. HBV DNA level before delivery in the mixed feeding group was slightly lower than that in the breastfeeding and bottle-feeding group [(3.87 ±1.08) vs (4.21±1.17) and (4.30±1.28) log 10 IU/ml, q= 3.052 and 3.831, both P<0.05], while the comparison between the latter two groups showed no significant differences ( P>0.05). After delivery, HBV DNA level in the bottle-feeding group was slightly lower than that in the breastfeeding group [(7.42±0.93) vs (7.69±0.90) log 10 IU/ml, q=4.583, P<0.05]. Among 580 infants (including six pairs of twins), only one bottle-fed infant (0.4%, 1/243) was infected with HBV through MTCT, and none in the breastfeeding or mixed feeding group ( P=0.553). Conclusions:For pregnant women with high viral loads of HBV who have received antiviral medication during pregnancy, although HBV DNA level will rebound after discontinuation upon delivery, breastfeeding is recommended considering it does not increase the risk of MTCT.

Objective:To explore the consistency of peripheral whole blood and venous serum procalcitonin (PCT) levels, and the value of peripheral whole blood PCT in evaluating pediatric bacterial infection.Methods:This multicenter cross-sectional parallel control study was conducted in 11 children′s hospital. All the 1 898 patients older than 28 days admitted to these hospitals from March 2018 to February 2019 had their peripheral whole blood and venous serum PCT detected simultaneously with unified equipment, reagent and method. According to the venous serum PCT level, the patients were stratified to subgroups. Analysis of variance and chi-square test were used to compare the demographic characteristics among groups. And the correlation between the peripheral blood and venous serum PCT level was investigated by quantitative Pearson correlation analysis.The PCT resultes were also converted into ranked data to further test the consistency between the two sampling methods by Spearman′s rank correlation test. Furthermore, the ranked data were converted into binary data to evaluate the consistency and investigate the best cut-off of peripheral blood PCT level in predicting bacterial infection.Results:A total of 1 898 valid samples were included (1 098 males, 800 females),age 27.4(12.2,56.7) months. There was a good correlation between PCT values of peripheral whole blood and venous serum ( r=0.97 , P<0.01). The linear regression equation was PCT?venous serum=0.135+0.929×PCT peripheral whole blood. However, when stratified to 5 levels, PCT results showed diverse and unsatisfied consistency between the two sampling methods ( r=0.51-0.92, all P<0.01). But after PCT was converted to ordinal categorical variables, the stratified analysis showed that the coincidence rate of the measured values by the two sampling methods in each boundary area was 84.9%-97.1%. The dichotomous variables also showed a good consistency (coincidence rate 96.8%-99.3%, Youden index 0.82-0.89). According to the severity of disease, the serum PCT value was classified into 4 intervals（<0.5、0.5-<2.0、2.0-<10.0、≥10.0 μg/L）, and the peripheral blood PCT value also showed a good predictive value (AUC value was 0.991 2-0.997 9). The optimal cut points of peripheral whole blood PCT value 0.5、1.0、2.0、10.0 μg/L corresponding to venous serum PCT values were 0.395, 0.595, 1.175 and 3.545 μg/L, respectively. Conclusions:There is a good correlation between peripheral whole blood PCT value and the venous serum PCT value, which means that the peripheral whole blood PCT could facilitate the identification of infection and clinical severity. Besides, the sampling of peripheral whole blood is simple and easy to repeat.

Objective:To evaluate the biosafety of medical injectable carboxymethyl glycosaminoglycan gel.Methods:Ames test, chromosome aberration test in vitro and gene mutation test in vitro were used to detect the genotoxicity of the medical carboxymethyl glycosaminoglycan gel. The gel saline extract (50 ml/kg) was injected slowly through the marginal vein of the ear into Japanese big-eared rabbits. The body temperature was measured and the temperature rise was calculated. The gel saline extract (50 ml/kg) and normal saline (control) were injected intraperitoneally and intravenously into the Kunming mice, respectively. The toxicity response in mice was observed after injection, and bodyweight change was valued. The gel saline extract, normal saline and distilled water were added into the rabbit anti-clotting, to detect the rate of hemolysis.Results:Under active and inactive conditions, the number of spontaneous revertants of the 4 strains of gel saline extract group and gel DMSO extract group did not reach 2 times of that of the corresponding negative control group. The rate of chromosome aberration of the three dose groups were 0. There was no significant increase in the large colony mutation frequency, small colony mutation frequency and total mutation frequency in three dose groups (all P>0.05). After injection of gel saline extract for 24, 48 and 72 h, no toxic reaction was found in each group of mice. With the extension of time after injection, the body weight of mice in the sample group and the control group increased, but the difference was not statistically significant ( P>0.05). After injection of gel saline extract, the temperature rise of 3 Japanese big-eared rabbits were 0.0, 0.3 and 0.2 ℃ respectively. The results of hemolysis test showed that the hemolysis rate of the polycarboxymethyl glucosamine gel was 0.1%. Conclusions:No genetic toxicity changes were found in carboxymethyl glycosaminoglycan to induce gene mutation or chromosome damage in bacteria and cells, and no pyrogenicity, acute systemic toxicity and hemolysis were observed. These results indicate that thecarboxymethyl glycosaminoglycan gel has good biosafety.

Objective: To investigate the effect of intestinal flora in children with functional constipation (FC) on expression of acid-sensitive Ion channel 3(ASIC3) in rats and their regulation in intestinal motility. Methods: Faeces of FC children identified according to RomeⅣ criteria and healthy children from the First Affiliated Hospital of Anhui Medical University from December 2017 to June 2018 were collected, and then made into fecal microbiota solution.A pseudo - sterile rat model was established, according to the random number table method, and the rats were randomly divided into the treatment group and the control group, with 12 rats in each group, then the treatment group was given fecal microbiota solution of the children with FC and the control group was given fecal microbiota solution of the healthy children.The visceral sensitivity and intestinal propulsion rate of rats were determined by means of abdominal withdrawal reflex (AWR), while the intestinal microorganism of rats and children with FC were determined by 16SrDNA high-throughput sequencing, and the expressions of ASIC3 of intestinal in mRNA and protein were determined by adopting fluorescence quantitative PCR and Western blot. Results: The species and quantity of intestinal flora of the children with FC and rats implanted with FC faecal bacteria were reduced(all P<0.05), and firmicutes and bacteroidetes were the main bacteria; compared to the control group, the small intestine propulsion rate(52% vs.74%) and visceral sensitivity(78 mmHg vs.63 mmHg) of the treated group were significantly decreased compared with those in the control group (all P<0.05); the mRNA (0.003 1±0.000 8 vs.0.012 4±0.002 5) and protein levels of ASIC3 (0.013 2±0.001 9 vs.0.072 1±0.008 7) in the small intestine were down-regulated significantly(all P<0.05); and the mRNA (0.002 8±0.000 7 vs.0.009 4±0.001 1) and protein levels of ASIC3(0.038 2±0.004 5 vs.0.089 7±0.009 4) in the colon were down-regulated significantly(all P<0.05). Conclusions Children with FC have intestinal flora disorder, and intestinal flora of FC children may affect intestinal motility by down-regulating the expression of intestinal ASIC3 in rats.

Objective: To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down-regulating miR-29. Methods: The expression levels of HULC and miR-29 in HCC tissues and cells were detected by real-time quantitative PCR (RT-qPCR), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR-29 and its target gene SETDB1 were determinate by RT-qPCR. According to the bioinformatic prediction of the miR-29 binding site in the HULC sequence, the report gene plasmids were constructed. The HCC cells were co-transfected with miR-29 mimics or miR-29 inhibitor, and the HULC targeted regulation of miR-29 was verified by dual luciferase reporter assay. The effect of miR-29 on the HULC-mediated proliferation in HCC cells was detected by cell count kit 8 (CCK-8) experiment. Expression of tumor proliferation antigen Ki-67 was detected by RT-qPCR.The Hep3B cells were inoculated in mice and miR-29 mimics and miR-29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki-67 in tumor tissues were detected by immunohistochemical staining. Results: The expression of HULC was significantly up-regulated while the expression of miR-29 was significantly down-regulated in HCC tissues and cells (P<0.01). The level of HULC was negatively correlated with miR-29 in tumor tissues (r=-0.754, P<0.01) and HCC cells (r=-0.865, P<0.05). The in vitro experiments showed that, compared with the blank control group, the expression of miR-29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR-29 target gene SETDB1 was increased (P<0.01). The expression of miR-29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P<0.01). Double luciferase reporter gene assay showed that miR-29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type (psi-HULC-WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid (psi-HULC-Mut). However, the miR-29 inhibitor antagonized the inhibitory effect of miR-29 mimics on luciferase activity of psi-HULC-WT (P<0.01). Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR-29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87±3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P<0.05). After treatment for 48 and 72 hours, the proliferation rates of miR-29 mimics transfected Huh7 cells were (57.10±1.94)% and (73.76±3.46)%, respectively, significantly lower than (83.45±7.46)% and (123.34±8.67)% of control group (P<0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR-29 mimics and miR-29 inhibitor group were (76.45±3.24)% and (89.37±4.37)%, respectively, significant higher than (57.10%±1.94)% and (73.76±3.46)% of the control group (P<0.05). After 48 h transfection, the expression of Ki-67 in Huh7 transfected with miR-29 mimics was significantly inhibited compared with the control group (P<0.01). However, the expression of Ki-67 mRNA was increased in Huh7 cells transfected with miR-29 inhibitor (P<0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR-29 mimics group and miR-29 mimics + miR-29 inhibitors group were (504.0±19.6) mm³, (310.0±24.3) mm³ and (483.7±21.2) mm³, respectively. Injection of miR-29 mimics reduced while miR-29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P<0.01). The immunohistochemical staining showed that the average optical density values of Ki-67 protein in tumor tissues of the control group, miR-29 mimics group and miR-29 analogue+ miR-29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki-67 protein in miR-29 mimics group was significantly reduced (P<0.01) while increased in the miR-29 mimics+ miR-29 inhibitor group (P<0.01). Conclusion LncRNA HULC promotes HCC growth by down-regulating miR-29.

Objective To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down?regulating miR?29. Methods The expression levels of HULC and miR?29 in HCC tissues and cells were detected by real?time quantitative PCR ( RT?qPCR ), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR?29 and its target gene SETDB1 were determinate by RT?qPCR. According to the bioinformatic prediction of the miR?29 binding site in the HULC sequence, the report gene plasmids were constructed.The HCC cells were co?transfected with miR?29 mimics or miR?29 inhibitor, and the HULC targeted regulation of miR?29 was verified by dual luciferase reporter assay. The effect of miR?29 on the HULC?mediated proliferation in HCC cells was detected by cell count kit 8 ( CCK?8) experiment. Expression of tumor proliferation antigen Ki?67 was detected by RT?qPCR.The Hep3B cells were inoculated in mice and miR?29 mimics and miR?29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki?67 in tumor tissues were detected by immunohistochemical staining. Results The expression of HULC was significantly up?regulated while the expression of miR?29 was significantly down?regulated in HCC tissues and cells (P＜0.01). The level of HULC was negatively correlated with miR?29 in tumor tissues (r＝－0.754, P＜0.01) and HCC cells ( r＝－0.865, P＜0.05).The in vitro experiments showed that, compared with the blank control group, the expression of miR?29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR?29 target gene SETDB1 was increased ( P＜0.01). The expression of miR?29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P＜0.01). Double luciferase reporter gene assay showed that miR?29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type ( psi?HULC?WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid ( psi?HULC?Mut). However, the miR?29 inhibitor antagonized the inhibitory effect of miR?29 mimics on luciferase activity of psi?HULC?WT (P＜0.01).Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR?29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87± 3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P＜0.05).After treatment for 48 and 72 hours, the proliferation rates of miR?29 mimics transfected Huh7 cells were ( 57.10 ± 1.94)% and ( 73.76± 3.46)%, respectively, significantly lower than (83.45±7.46)% and ( 123.34±8.67)% of control group ( P＜0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR?29 mimics and miR?29 inhibitor group were (76.45± 3.24)% and ( 89.37± 4.37)%, respectively, significant higher than (57.10%±1.94)% and ( 73.76 ± 3.46)% of the control group ( P＜0.05). After 48 h transfection, the expression of Ki?67 in Huh7 transfected with miR?29 mimics was significantly inhibited compared with the control group (P＜0.01). However, the expression of Ki?67 mRNA was increased in Huh7 cells transfected with miR?29 inhibitor (P＜0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR?29 mimics group and miR?29 mimics + miR?29 inhibitors group were ( 504.0± 19.6) mm3, (310.0±24.3) mm3 and (483.7±21.2) mm3, respectively. Injection of miR?29 mimics reduced while miR?29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P＜0.01). The immunohistochemical staining showed that the average optical density values of Ki?67 protein in tumor tissues of the control group, miR?29 mimics group and miR?29 analogue+miR?29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki?67 protein in miR?29 mimics group was significantly reduced ( P＜0.01) while increased in the miR?29 mimics+miR?29 inhibitor group ( P＜0.01). Conclusion LncRNA HULC promotes HCC growth by down?regulating miR?29.

Objective To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down?regulating miR?29. Methods The expression levels of HULC and miR?29 in HCC tissues and cells were detected by real?time quantitative PCR ( RT?qPCR ), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR?29 and its target gene SETDB1 were determinate by RT?qPCR. According to the bioinformatic prediction of the miR?29 binding site in the HULC sequence, the report gene plasmids were constructed.The HCC cells were co?transfected with miR?29 mimics or miR?29 inhibitor, and the HULC targeted regulation of miR?29 was verified by dual luciferase reporter assay. The effect of miR?29 on the HULC?mediated proliferation in HCC cells was detected by cell count kit 8 ( CCK?8) experiment. Expression of tumor proliferation antigen Ki?67 was detected by RT?qPCR.The Hep3B cells were inoculated in mice and miR?29 mimics and miR?29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki?67 in tumor tissues were detected by immunohistochemical staining. Results The expression of HULC was significantly up?regulated while the expression of miR?29 was significantly down?regulated in HCC tissues and cells (P＜0.01). The level of HULC was negatively correlated with miR?29 in tumor tissues (r＝－0.754, P＜0.01) and HCC cells ( r＝－0.865, P＜0.05).The in vitro experiments showed that, compared with the blank control group, the expression of miR?29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR?29 target gene SETDB1 was increased ( P＜0.01). The expression of miR?29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P＜0.01). Double luciferase reporter gene assay showed that miR?29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type ( psi?HULC?WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid ( psi?HULC?Mut). However, the miR?29 inhibitor antagonized the inhibitory effect of miR?29 mimics on luciferase activity of psi?HULC?WT (P＜0.01).Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR?29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87± 3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P＜0.05).After treatment for 48 and 72 hours, the proliferation rates of miR?29 mimics transfected Huh7 cells were ( 57.10 ± 1.94)% and ( 73.76± 3.46)%, respectively, significantly lower than (83.45±7.46)% and ( 123.34±8.67)% of control group ( P＜0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR?29 mimics and miR?29 inhibitor group were (76.45± 3.24)% and ( 89.37± 4.37)%, respectively, significant higher than (57.10%±1.94)% and ( 73.76 ± 3.46)% of the control group ( P＜0.05). After 48 h transfection, the expression of Ki?67 in Huh7 transfected with miR?29 mimics was significantly inhibited compared with the control group (P＜0.01). However, the expression of Ki?67 mRNA was increased in Huh7 cells transfected with miR?29 inhibitor (P＜0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR?29 mimics group and miR?29 mimics + miR?29 inhibitors group were ( 504.0± 19.6) mm3, (310.0±24.3) mm3 and (483.7±21.2) mm3, respectively. Injection of miR?29 mimics reduced while miR?29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P＜0.01). The immunohistochemical staining showed that the average optical density values of Ki?67 protein in tumor tissues of the control group, miR?29 mimics group and miR?29 analogue+miR?29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki?67 protein in miR?29 mimics group was significantly reduced ( P＜0.01) while increased in the miR?29 mimics+miR?29 inhibitor group ( P＜0.01). Conclusion LncRNA HULC promotes HCC growth by down?regulating miR?29.

Objective The aim of this study was to evaluate the value of pleural effusion heparin-binding protein ( HBP) in differential diagnosis of parapneumonic effusion .Methods Case-control study. The pleural effusion of 189 patients with pleural effusion admitted to Quzhou People's Hospital from February to July 2018, including parapneumonic effusion (n=72), tuberculous pleural effusion (n=24), cases of malignant pleural effusion ( n=46 ) and transudative pleural effusion ( n=47 ) were collected.Routine analysis,lactate dehydrogenase(LDH),adenosine deaminase (ADA) and total protein(TP)examination of all pleural effusions were performed .The levels of heparin-binding protein in the patients'pleural fluid were measured by ELISA.The difference in the overall level of each group was determined by One-way ANOVA or LSD test followed by Kruskal-Wallis H test dependence on the homogeneity of variances .The categorical data was analyzed by chi-square test.Receiver operating characteristic ( ROC) curve was plotted to evaluate the diagnostic value of heparin-binding protein for parapneumonic effusion . Results The concentration of heparin-binding protein was low in malignant pleural effusion [15.2(8.4, 33.3) ng/ml] and transudative effusion[14.1(6.5, 23.0)ng/ml], but high in parapneumonic effusion[316.1(99.5,399.8)ng/ml]and tuberculous pleurisy [64.7 (18.6, 96.8) ng/ml] .The heparin-binding protein level in parapneumonic effusion was significantly different from the other three groups (H=120.3,P<0.05).The receiver operating characteristic curve analysis for an optimal discrimination between parapneumonic effusion from non -parapneumonic effusion could be performed at a cut-off point of 64.2 ng/ml with area under the curve of 0.953[sensitivity:88.9％(64/72), specificity:89.7％(105/117),positive predictive value:84.2％(64/76), negative predictive value:92.9％(105/113)].Conclusions Heparin-binding proteinin pleural fluid is effective to be used to classify parapneumonic effusion samples .The detection of heparin-binding protein in pleural effusion has good sensitivity and specificity .It could be a biomarker for differential diagnosis of parapneumonic effusion .