Objective:To study the clinical characteristics and etiological distribution characteristics of plastic bronchitis in children, analyze its early warning indicators, and evaluate the clinical diagnosis and treatment effect of flexible bronchoscopy.Methods:The clinical data of 232 children with severe pneumonia admitted to Guiyang Maternal and Child Health Hospital from January 2019 to February 2021 were retrospectively analyzed.The children were divided into the plastic bronchitis group and non-plastic bronchitis group according to bronchoscopic results.The gender, age, clinical manifestations, auxiliary examinations, imaging features, bronchoscopy findings and treatment of the children were collected, compared and analyzed, comparison between two groups by t test and χ2 test. Results:A total of 232 children were included in this study, including 98 cases in the plastic bronchitis group and 134 cases in the non-plastic bronchitis group.The main symptoms of both groups were fever, cough and shortness of breath.The age of onset in the plastic bronchitis group was (54.640±37.085) months, and the age of onset in the non-plastic bronchitis group was (14.870±19.813) months.The difference in the age of onset between the two groups was statistically significant ( t=9.656, P<0.001). The average hospitalization days of the plastic and non-plastic bronchitis groups were (16.133±6.227) d and (12.690±4.287) d, respectively.Significant difference was found in the average hospitalization days between the two groups ( t=4.721, P<0.001). The average fever days of the plastic bronchitis group were (10.090±3.473) d, and the average fever days of the non-plastic bronchitis group were (6.030±4.850) d. There was significant difference in the average fever days between the two groups ( t=5.654, P<0.001). The age of onset, hospitalization days, and fever days of the plastic bronchitis group were larger than those of the non-plastic bronchitis group (all P<0.001). The physical examination suggested that 40% (39/98) of patients in the plastic bronchitis group had reduced the breath sounds, and this percentage was significantly higher than that in the non-plastic bronchitis group[6%(8/134)]. The plastic bronchitis group had lower partial pressure of blood oxygen (PO 2) and oxygen saturation (SO 2) levels than the non-plastic bronchitis group (all P<0.01). The plastic bronchitis group had a higher percentage of neutrophils (N), C-reactive protein (CRP) level, procalcitonin (PCT) level, lactate dehydrogenase (LDH) level and D-dimer level than the non-plastic bronchitis group (all P<0.01). According to the imaging results, in the plastic bronchitis group, lung consolidation was found in 72 cases (73%, 72/98), atelectasis in 32 cases (33%, 32/98), and pleural effusion in 33 cases (34%, 33/98). In the non-plastic bronchitis group, 65%(87/134) cases had lung consolidation, 5%(7/134) cases had atelectasis, 3.7% (5/134) cases had pleural effusion.The first pathogen detected in 46.9% of the patients in the plastic bronchitis group was Mycoplasma pneumoniae (MP), and the percentage was significantly higher that in the non-plastic bronchitis group (11.1%). Flexible bronchoscopy was performed on both groups at their admission.The plastic bronchitis group received the flexible bronchoscopy check for (2.960±1.157) times on average, and the non-plastic bronchitis group was tested for (1.140±0.371) times on average.Of 98 children in the plastic bronchitis group, 95 cases were improved and discharged, 2 cases were transferred, and 1 case died.All 134 children in the non-plastic bronchitis group were improved and discharged. Conclusions:Preschool and school-age children, fever ≥10 d, PCT, CRP, LDH, D-dimer levels are early warning signs of plastic bronchitis clinically.MP is still the primary pathogen causing plastic bronchitis.Flexible bronchoscopy technique is a key measure for timely diagnosis and effective treatment of plastic bronchitis.

Objective:To investigate the role of modification level of lysine trimethylation at position 27 of histone 3 (H3K27me3) on expression of anti-apoptotic protein B lymphocyte tumor-2 gene (BCL2) during arsenic-induced hepatocyte apoptosis.Methods:Rat liver BRL-3A cells were cultured in vitro. According to the arsenic treatment factor, the experiment was divided into two parts, in the first part arsenic was not added, the experiment was divided into normal, transfection reagent, negative transfection, H3K27me3 specific demethylase (JMJD3) small interfering RNA (siRNA) transfection and H3K27me3 methyltransferase (EZH2) siRNA transfection groups. In the second part arsenic was added, the experiment was divided into control, arsenic treatment, arsenic + negative transfection, arsenic + JMJD3siRNA transfection and arsenic + EZH2siRNA transfection groups. When arsenic was not added, the corresponding siRNA and transfection reagent was used to transfect cells at a ratio of 100 pmol : 7.5 μl for 6 h [the normal group was treated with phosphate buffer solution (PBS) of the same volume as transfection reagent], then the medium was changed and the cells were incubated for a total of 48 h. After 24 h of treatment with the above transfection and culture method in arsenic added group, a final concentration of 30 μmol/L sodium arsenite (NaAsO 2) was added and the cells were incubated for 24 h (the control group was treated with PBS with the same volume of NaAsO 2 for 24 h). Real-time cell analysis (RTCA) was used to measure the proliferation of BRL-3A cells in arsenic added group. Apoptosis of BRL-3A cells was analyzed by flow cytometry in arsenic added group. Western blotting was used to detect JMJD3, EZH2, H3K27me3 and BCL2 in no-arsenic and arsenic-added BRL-3A cells. The modification levels of H3K27me3 in BCL2 gene promoter regions were detected by chromatin immunoprecipitation of the cells exposed to arsenic. Results:There were statistically significant differences of the proliferation rates [control, arsenic treatment, arsenic + negative transfection, arsenic + JMJD3siRNA transfection and arsenic + EZH2siRNA transfection groups: (100.00 ± 10.43)%, (12.19 ± 3.37)%, (31.86 ± 1.95)%, (24.58 ± 3.64)%, (11.53 ± 1.11)%] and the apoptosis rates [(1.15 ± 0.04)%, (13.06 ± 1.33)%, (17.39 ± 0.22)%, (23.90 ± 1.66)%, (15.07 ± 0.88)%] between groups ( F = 146.50, 194.30, P < 0.001), correspondingly. The protein expression level of H3K27me3 in JMJD3siRNA transfection group was higher than that of normal, transfection reagent and negative transfection groups, while EZH2siRNA transfection group had an opposite result ( P < 0.05). The protein expression level of BCL2 in JMJD3siRNA transfection group was lower than that of normal, transfection reagent and negative transfection groups, while EZH2siRNA transfection group had an opposite result ( P < 0.05). The protein expression levels of H3K27me3 and BCL2 were not statistically significant differences between normal, transfection reagent and negative transfection groups ( P > 0.05). The protein expression levels of JMJD3, EZH2, H3K27me3 and BCL2 among control, arsenic treatment, arsenic + negative transfection, arsenic + JMJD3siRNA transfection and arsenic + EZH2siRNA transfection groups were compared, and the differences were statistically significant ( F = 26.56, 7.82, 9.81, 31.19, P < 0.05). Compared with control group, the protein expression levels of JMJD3 and EZH2 in arsenic treatment group were significantly reduced ( P < 0.05), and the protein expression level of H3K27me3 was higher ( P < 0.05), meanwhile the protein expression level of BCL2 was lower ( P < 0.05). Compared with arsenic + negative transfection group, the protein expression level of JMJD3 was significantly reduced in arsenic + JMJD3siRNA group, and the protein expression level of EZH2 was significantly reduced in arsenic + EZH2siRNA group ( P < 0.05). In addition, arsenic + JMJD3siRNA increased the level of H3K27me3 modification while reducing the protein expression of BCL2, while arsenic + EZH2siRNA had an opposite result ( P < 0.05). Compared with control group, the enrichment levels of H3K27me3 in BCL2 gene promoter regions (CHIP1 and CHIP2) in arsenic treatment group were significantly higher ( P < 0.05). Conclusion:Arsenic may inhibit the expression of BCL2 by increasing the enrichment level of H3K27me3 in the promoter regions of BCL2 gene, and promoting hepatocyte apoptosis.

Objective:To investigate the current situation of students' academic procrastination behavior in medical colleges and universities and its influencing factors, and to put forward suggestions to reduce the academic procrastination of medical students.Methods:A total of 1 327 undergraduate students from three medical colleges and universities in Heilongjiang Province were randomly selected to receive questionnaire investigation on life satisfaction, anxiety, and academic procrastination. SPSS 23.0 was used for data analysis.Results:①The total procrastination scores of medical students were (35.00±8.92) points. ②There were statistical differences in the academic procrastination of medical students with different genders, whether the only children, the reasons for choosing the major, and the level of achievement ( P < 0.05). There was no statistical difference in academic procrastination among medical students of different ages and grades ( P > 0.05). ③Medical students' procrastination was positively correlated with their anxiety level ( r = 0.102, P < 0.01), and negatively correlated with life satisfaction ( r = -0.117, P < 0.01). ④Regression analysis showed that the following six predictive variables including the level of achievement, gender, life satisfaction, anxiety, reasons for choosing the major, and whether the only children could effectively explain the variance of 14.2% academic procrastination of medical students. Conclusion:The overall degree of academic procrastination of medical students is higher than that of non-medical students. And the students' achievement level, gender, life satisfaction, anxiety, the reasons for choosing this major and whether the only child are the influencing factors of academic procrastination.

Objective:To investigate the changes of microRNA-153 (miR-153) expression and the mechanism of regulating histone H3 lysine 4 (H3K4) methyltransferase (SET7/9) and histone H3K4 methylation (H3K4me1) in the process of arsenic-induced endoplasmic reticulum stress-related hepatocytes apoptosis.Methods:Human normal hepatocytes (L-02 cells) were cultured in vitro and divided into control, arsenic treatment, arsenic + negative transfection, arsenic + miR-153 up-regulation and arsenic+ miR-153 down-regulation groups according to different treatment methods. Arsenic+ negative transfection, arsenic+ miR-153 up-regulation and arsenic+ miR-153 down-regulation groups were transfected with transfection plasmid and transfection reagent according to a certain proportion (3 μg: 8 μl). After 24 h, arsenic treatment, arsenic+ negative transfection, arsenic+ miR-153 up-regulation and arsenic+ miR-153 down-regulation groups were all treated with 100 μmol/L sodium arsenite (NaAsO 2) as the final concentration for 24 h. The control group was treated with phosphate buffer solution (PBS) of the same volume as NaAsO 2 for 24 h. The expression of miR-153 was detected by real-time quantitative polymerase chain reaction (RT-qPCR); cell apoptosis and cell cycle were detected by flow cytometry; real-time cell dynamic analyzer (RTCA) was used to detect cell proliferation; Western blotting was used to detect the expression of endoplasmic reticulum marker proteins glucose regulatory protein 78 (GRP78), SET7/9 and H3K4me1. Results:The expression levels of miR-153 in each group were significantly different ( F = 10.73, P < 0.05). Compared with the control group [(41.10 ± 6.08)%], the expression level of miR-153 in arsenic treatment group [(4.35 ± 0.20)%] was significantly decreased ( P < 0.05); compared with the arsenic+ negative transfection group [(10.00 ± 2.40)%], the expression level of miR-153 in arsenic+ miR-153 up-regulation group [(157.70 ± 42.70)%] was significantly increased ( P < 0.05), and that in arsenic+ miR-153 down-regulation group [(4.20 ± 0.28)%] was significantly decreased ( P < 0.05). There were significant differences in the total cell apoptosis rate and G1 phase cell proportion among the five groups ( F = 29.69, 104.32, P < 0.05). Compared with the control group, the total cell apoptosis rates and G1 phase cell proportions in arsenic treatment, arsenic+ miR-153 up-regulation and arsenic+ miR-153 down-regulation groups were significantly increased ( P < 0.05); compared with the arsenic+ negative transfection group, the total cell apoptosis rate and G1 phase cell proportion in arsenic+ miR-153 up-regulation group were significantly decreased ( P < 0.05), and those in arsenic+ miR-153 down-regulation group were significantly increased ( P < 0.05). The difference of cell proliferation rate in each group was statistically significant ( F = 799.35, P < 0.05). Compared with the control group, the cell proliferation rates in arsenic treatment, arsenic+ miR-153 up-regulation and arsenic+ miR-153 down-regulation groups were significantly decreased ( P < 0.05); compared with the arsenic+ negative transfection group, the cell proliferation rate in arsenic+ miR-153 up-regulation group was significantly increased ( P < 0.05), and that in arsenic+ miR-153 down-regulation group was significantly decreased ( P < 0.05). The protein expression levels of SET7/9, GRP78 and H3K4me1 in each group were significantly different ( F = 78.52, 52.13, 54.32, P < 0.05). Compared with the control group, the protein expression levels of SET7/9, GRP78 and H3K4me1 in arsenic treatment group were significantly increased ( P < 0.05); compared with the arsenic+ negative transfection group, the protein expression levels of SET7/9, GRP78 and H3K4me1 in arsenic+ miR-153 up-regulation group were significantly decreased ( P < 0.05), and those in arsenic + miR-153 down-regulation group were significantly increased ( P < 0.05). Conclusion:miR-153 plays an important role in arsenic-induced endoplasmic reticulum stress-related hepatocytes apoptosis, the expression and regulation are related to the changes of SET7/9 and H3K4me1 levels.

Objective: To investigate the interventional effect of bicyclol on isoniazid-induced liver injury in rats and the expression of endoplasmic reticulum stress (ERS) protein, glucose regulatory protein 78 (GRP78), and growth arrest and DNA-damage-inducible gene 153(CHOP). Methods: Eighty Wistar rats were randomly divided into control group (8 rats) and model group (72 rats). After 10 days of intragastric administration of isoniazid, the model group rats were randomly divided into treatment group (A), natural recovery group (B), etiological persistence group (C) and etiological persistence plus treatment group (D). Sixteen rats from each group were sacrificed after 1 and 2 weeks of intervention with different methods. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected. Liver pathological morphology was observed. Apoptotic cells were detected by TUNEL assay. ERS protein expression was detected by Western blot. A t-test or randomized block analysis of variance, K-S test and Levene’s test were used to analyze the normality and homogeneity of variance. Kruskal-Wallis rank sum test was used for data that did not suit the conditions of t-test and variance analysis. Results: ALT and AST were elevated in the model group, and liver pathological examination showed liver tissue damage. Apoptotic index was higher than control group (7.13% ± 1.55% vs. 0.75% ± 0.71%, Z = -3.411, P < 0.01), and the expression value of ERS protein in model group was significantly higher than control group (GRP78: 1.16 ± 0.30 vs. 0.23 ± 0.05, t = -6.008, P < 0.01; CHOP: 0.98±0.23 vs. 0.20 ± 0.10, t = -6.378, P < 0.01). Serum enzymes, apoptotic index and ERS protein expressions of rats were decreased after treatment with bicyclol, and the pathological damage was eased. Rats in natural recovery group recovered less than the treatment group. Conclusion Isoniazid-induced liver injury is associated to ERS-related excessive apoptosis and the therapeutic effect of bicyclol on drug-induced liver injury may minimize ERS-induced apoptosis.

Objective To examine the current situation of the career plateau among anesthesiologists and analyze the impact of occupational stressors on it. Methods A questionnaire survey was conducted on the anesthesiologists. A total of 300 questionnaires were distributed and 278 questionnaires were effectively collected. Statistical analysis using SPSS 19.0 was performed to assess the status quo of career plateau among anesthesiologists. Pearson correlation analysis and stepwise regression analysis were used to analyze the influence of occupational stressors on career plateau . Results The average value of occupational stressors among anesthesiologists was (3.22±0.55), and the average value of career plateau was (3.90±0.70). Occupational interest in the occupational stressors of anesthesiologists is negatively correlated with the occupational plateau (r=-0.552, P<0.01), and career development is negatively correlated with occupational plateau (r=-0.541, P<0.01) as well. Both occupational interest and career development show a negative predictive effect on the career plateau (β=-0.359, P<0.01 andβ=-0.334, P<0.01, respectively). Conclusion Career plateau among anesthesiologists is at a medium-to-high level. Occupational interest and occupational development in occupational stressors have a negative predictive effect on occupational plateaus, so hospital managers should pay attention to them.

Objective To explore the impact of work-family conflict on job satisfaction and turnover intention of anesthesiologists in Heilongjiang Province.Methods Questionnaire survey was used for data collection.Descriptive statistics,Pearson correlation analysis and multivariate linear hierarchy regression analysis were performed to analyze the impact of work-family conflict on job satisfaction and turnover intention of anesthesiologists.Results The average value of work-family conflict among anesthesiologists was (2.99 ± 0.57).The finding indicated that work-family conflict of anesthesiologists had a significant negative effect on job satisfaction (β=-0.248,P＜0.01) and a positive effect on turnover intention (β=0.329,P＜0.01).Conclusion Anesthesiologists' work-family conflict is above the middle level in Heilongjiang Province.The work-family conflict of anesthesiologists can reduce job satisfaction and increase turnover intention.

Objective To determine the effects of histone deacetylase inhibitor suberoylanilide hydroxamic acid(SAHA) on the cell proliferation and apoptosis of the human hepatic stellate cell line LX-2.The possible underlying mechanisms were also investigated.Methods The LX-2 cells were treated with SAHA in vitro.The morphology of LX-2 cells in different concentrations groups was observed by inverted microscope;the proliferation of LX-2 cells was measured by MTT assay;the Annexin V-FITC and PI staining was used to detect the apoptosis of LX-2 cells by flow cytometry and fluorescence microscope;the expression of α-SMA,collagen Ⅰ,acH3K9,acH3K14 and acH3K18 were detected by Western blot.Results The morphology change of LX-2 cells showed that SAHA inhibited the proliferation rate of LX-2 cells and in a dose dependent manner(P<0.05).The LX-2 cells were sensitive to SAHA along with time increasing,and in a time-dependent manner(P<0.05).Western blot showed that the expression levels of α-SMA and collagen-Ⅰ were significantly lower(P<0.05),on the contrary,the acetylation levels of acH3K9,acH3K14 and acH3K18 were significantly higher (P<0.05).Conclusions The increased acetylation of the histone acH3K9,acH3K14,acH3K18 and the lower expressed α-SMA and collagen-Ⅰ in LX-2 cells may be one of the mechanisms of SAHA.

AIM:To study the effects of suberoylanilide hydroxamic acid (SAHA) on the apoptosis of hepatic stellate cells (HSCs) and expression of associated proteins, and to investigate the mechanisms of SAHA to induce apoptosis.METHODS:The rat HSCs were isolated by OptiPrep gradient centrifugation method.The effect of SAHA on HSC proliferation was detected by real-time cell analyzer.The morphological changes of HSCs treated with SAHA at different concentrations were observed under inverted microscope.The apoptotic rates of HSCs were analyzed by flow cytometry with Annexin V-FITC/PI staining and fluorescence microscopy.The protein expression of α-smooth muscle actin (α-SMA), collagen I, tissue inhibitor of metalloproteinase 1 (TIMP1), glucose-regulated protein 78 (GRP78) and histone deacetylase 6 (HDAC6) was detected by Western blotting.The interaction of GRP78 with HDAC6 in the HSCs was determined by co-immunoprecipitation.RESULTS:HSCs were successfully isolated and cultured for 14 d, during which the HSCs changed gradually from rest state to active state.SAHA significantly inhibited the proliferation of HSCs in a time-and dose-dependent manner (P<0.05).The results of Western blotting showed that the protein expression levels of α-SMA, TIMP1, collagen-I and HDAC6 were significantly decreased (P<0.05), while GRP78 was significantly increased (P<0.05).Compared with activated HSCs, GRP78 and total acetyl-lysine protein were significantly increased in the co-immunoprecipitated HSCs treated with SAHA, while HDAC6 protein was significantly decreased, indicting that GRP78 formed a complex with HDAC6.CONCLUSION:The anti-hepatic fibrosis effect of SAHA may be related to down-regulation of HDAC6 and up-regulation of acetylated GRP78, thus inducing endoplasmic reticulum stress of HSCs and promoting the apoptosis of HSCs.

AIM:To investigate the changes of histone modifications during the activation of primarily cultured rat hepatic stellate cells ( HSCs) and the relationship between histone modification patterns andα-smooth muscle actin (α-SMA) expression, and to explore the roles of histone modifications in the activation of HSCs.METHODS:The rat HSCs were isolated by in situ perfusion of collagenase combined with density gradient centrifugation, cultured in vitro and identi-fied by immunofluorescence staining.The morphological features of the cells were observed under inverted microscope.The changes of desmin and α-SMA during the activation of HSCs were detected by immunofluorescence staining and Western blotting.The levels of histone 3 lysine 4 dimethylation (H3K4me2), histone 3 lysine 9 dimethylation (H3K9me2), his-tone 3 lysine 9 acetylation (acH3K9) and histone 4 lysine 12 acetylation (acH4K12) in quiescent HSCs and activated HSCs were determined by Western blotting.RESULTS: The morphology of HSCs shifted from a quiescent phenotype to highly activated myofibroblast during the culture.Immunofluorescence staining and Western blotting showed that the expres-sion levels of α-SMA and desmin were increased over time and reached maximum at 15 d.According to the results of cell morphology and immunofluorescence staining, the cells cultured for 24 h and 15 d were quiescent and activated HSCs, re-spectively.Compared with quiescent HSCs, there were higher H3K4me2 and lower H3K9me2, acH3K9 and acH4K12 modification levels in activated HSCs ( P<0.01 ) .CONCLUSION: Histone modifications show anomalous expression during the activation of primarily cultured rat HSCs.Histone modifications may contribute to the transdifferentiation of HSCs and the development of hepatic fibrosis.