Objective:To investigate the effects of different phototherapy intensities on the levels of malondialdehyde, a peroxidation product of intralipid, vitamin C and vitamin E in parenteral nutrition for premature infants.Methods:The parenteral nutrition for premature infants was prepared under strict aseptic condition and was divided into four groups based on different phototherapy intensities in simulated clinical settings, which were indoor light group, single-, double-, and three-sided phototherapy group. According to whether the nutrient solution shielded for light or not, each group was further divided into two subgroups: exposure or non-exposure group. The levels of malondialdehyde, vitamin C and vitamin E in all groups before phototherapy and 6, 12, 18, and 24 h after phototherapy were measured. Ten samples of parenteral nutrient solutions were prepared for each group, of which 2 ml were extracted for test at different time points. Repeated measurement analysis of variance was used for data analysis and the results were adjusted using Greenhouse-Geisser method if failed in Mauchly sphere test.Results:With the increase of phototherapy time, the malondialdehyde level increased in the exposure and the non-exposure subgroups in the one-sided phototherapy group [before phototherapy: (3.777±0.112) vs (3.746±0.141) nmol/ml; phototherapy for 6 h: (3.808±0.122) vs (3.715±0.145) nmol/ml; 12 h: (4.546±0.138) vs (4.507±0.136) nmol/ml; 18 h: (6.116±0.151) vs (5.239±0.156) nmol/ml; 24 h: (7.569±0.136) vs (5.300±0.200) nmol/ml; all P<0.05], but the level of vitamin C [before phototherapy: (62.507±0.205) vs (62.341±0.144)μg/ml; phototherapy for 6 h: (51.211±0.086) vs (58.128±0.076) μg/ml; 12 h: (43.288±0.084) vs (55.351±0.050) μg/ml; 18 h: (35.758±0.113) vs (51.215±0.093) μg/ml; 24 h: (33.473±0.075) vs (48.473±0.080)μg/ml] and vitamin E decreased [before phototherapy: (4.101±0.132) vs (4.084±0.141) μg/ml; phototherapy for 6 h: (3.761±0.119) vs (3.904±0.075) μg/ml; 12 h: (3.654±0.092) vs (3.729±0.087) μg/ml; 18 h: (3.385±0.102) vs (3.582±0.119) μg/ml; 24 h: (3.313±0.127) vs (3.438±0.113) μg/ml, all P<0.05]. The same situation was also observed in indoor light group, double-, and three-sided phototherapy groups. The malondialdehyde level at different time in the exposure subgroups were higher but the vitamin C and vitamin E levels were lower than those in the non-exposure subgroups, regardless of the phototherapy intensities (all P<0.001). (2) The analysis of all exposure phototherapy subgroups showed that the higher the intensity of light therapy, the higher the malondialdehyde level, and the lower the level of vitamin C and vitamin E, with statistical significance differences in any pairwise comparison. Analysis of all non-exposure subgroups showed statistically significant differences in the malondialdehyde level in any pairwise comparison (all P<0.05) except for the comparison between indoor light group and single-sided phototherapy group ( F=2.383. P=0.140). Moreover, the greater the phototherapy intensities, the lower vitamin C level, with statistically significant differences in any pairwise comparison. And statistical significance differences were observed in the vitamin E level in any pairwise comparison (all P<0.05) except for the comparison between double- and three-sided phototherapy groups ( F=1.358, P=0.259). Conclusions:Phototherapy can increase the malondialdehyde level in parenteral nutrient solution for premature infants and the degree of intralipid peroxidation, but can also lead to vitamin C and vitamin E loss in the parenteral nutrient and weaken its antioxidant capacity.

By participating in the national medical colleges and universities students' clinical skill competition and summarizing the experiences after the competition,we reflected on problems and weakness in the past clinical teaching including weak sterile concept and lack of clinical thinking,humanities,communication skills,teamwork awareness,etc.We should take methods to future improve medical students' clinical training capabilities including strengthening the concept of sterile and clinical skills,promoting training of comprehensive clinical thinking ability and problem-solving ability,emphasizing on humane care and communication between doctors and patients; cultivating teamwork awareness thus to comprehensively enhance the overall quality of medical students.

Objective To investigate the effects of alantolactone on cell proliferation,cell-cycle and cell cycle-related proteins in human chronic myelogenous leukemia drug-resistant cell line K562/ADR.Methods K562/ADR cells were treated with 0,1.0,2.0,4.0,6.0,8.0,and 10.0 μmol/L of alantolactone for 12,24 and 48 h,with its cell viability analyzed by MTT assay.Flow cytometry was used to examine the effect of alantolactone on the cell-cycle of K562/ADR cells.The cell cycle-related proteins were analyzed by using Western blot after treatment with alantolactone.Results The results of MTT showed that alantolactone effectively inhibited the proliferation of K562/ADR cells in dose and time-dependent way,and the IC50 value of alantolactone in K562/ADR cells was about 5 μmol/L.Flow cytometric analysis displayed that alantolactone could arrest cell cycle at G2/M phase.The percentage of accumulated cells in the G2/M phase was increased from (15.8±1.7) ％ in the control group to (21.0±2.4) ％,(26.4±2.7) ％,and (30.1±3.9) ％ in cells treated with 2.5,5.0,and 7.5 μmol/L of alantolactone for 24 h,respectively (P ＜ 0.05).Alantolactone significantly decreased the expression of CDK1 and CyclinB1 and increased the expression of cyclin-dependent kinase inhibitor p21.Meanwhile,the treatment of K562/ADR with alantolactone led to a dose-dependent decrease in bcr-abl protein levels.Conclusion Alantolactone can significantly inhibit the proliferation and cell-cycle arrest in G2/M phase of K562/ADR cells,in which mechanism may be associated with the regulation of cell cycle-related proteins and downregulation of bcr-abl protein.

By taking the course of laboratory hematology in Curtin University in Australia as an ex-ample, this paper introduced the characteristics of its teaching mode, teaching contents, teaching methods, assessment methods and laboratory practice. The advantages and disadvantages of education characteristics between Australia and China were compared and analyzed on the training methods and the training objec-tives, respectively. The education characteristics of laboratory hematology in Curtin University provided an important inspiration for our education reform in the field of medical laboratory in the future.

In the process of teaching international students laboratory diagnostics,teaching mode has been actively explored. The management of teaching,the foundation of teaching team,the selection of teaching materials and reformation of teaching mode are the key points that affect the teaching quality directly.

A total of 118 patients with type 2 diabetes mellitus were divided into acarbose treatment group ( A group,n =58 ) and no acarbose treatment group ( B group,n =60),and 57 healthy subjects were used as control group (C group).The quantification of fecal bifidobacteria and enterococcus faecalis in these subjects was made by realtime PCR.The results showed that fecal bifidobacteria contents in A and B groups were lower and enterococcus faecalis contents were higher compared with C group.After four weeks of intervention,fecal bifidobacteria contents in A and B groups increased ( P＜0.01 ),especially in A group,while enterococcus faecalis contents decreased ( P＜0.05 )compared with the baseline.Univariate correlation analysis showed that bifidobacteria content was negatively associated with lipopolysaccharides(LPS),advanced glycation index,high sensitive C reactive protein ( hs-CRP),and body mass index ( BMI ) at baseline ( P＜0.05 or P＜0.01 ).The enterococcus faecalis content was positively associated with levels of monocyte chemoattractant protein-1,LPS,tumor necrosis factor-α,hs-CRP,plasminogen activator inhibitor-1,BMI,and HbA1c (P ＜0.01 ).After four weeks of intervention,the above associations disappeared.Stepwise multivariate regression showed that basal BMI,HbA1c,and age contributed to the increase in the number of enterococcus faecalis,and BMI negatively contributed to the decrease in number of bifidobacteria.

Background and purpose:The human oncogene B-cell-speciifc moloney murine leukemia virus integration site 1 (Bmi-1) is an important member of the polycomb group family, and it regulates cell proliferation and senescence via INK4a/ARF locus. This study investigated the effects of Bmi-1-siRNA on the proliferation of lung adenocarcinoma cell line SPC-A1 cells with INK4a/ARF locus and clarify the mechanism of Bmi-1-mediated effect on proliferation of lung adenocarcinoma cells. Methods:In this study, we chose the most efifcient siRNA chain the pGeneshl-2-Bmi-1 sense-1 and inserted into a pSUPER-retro-neo retroviral vector. The packaged si-Bmi-1 pSUPERret-ro-neo retroviral vector was stably transfected into lung adenocarcinoma SPC-A1 cell line. The stably transfected cells were cultured and passed. After transfection, the levels of Bmi-1 mRNA and protein expression of SPC-A1 cells were analyzed by RT-PCR and Western blot respectively. Trypan blue, MTT and plate colony forming assay were performed to observe the proliferation capibility of SPC-A1 cells and evaluate the cloning forming ability in vitro. The potency of tumorigenesis was observed in nude mouse through hypodermic inoculation of SPC-A1 cells. Cell cycle distribu-tion was analyzed by lfow cytometry (FCM) in SPC-A1 cells. The expression levels of proliferation proteins including p16INK4a, p53, Cyclin D1, PTEN, Akt and Ser473p-Akt were analyzed by Western blot. Results:The mRNA and protein expression levels of Bmi-1 were signiifcantly reduced in SPC-A1-Bmi-1-siRNA cells transfected with pSUPER-retro-neo retroviral vector. Knockdown of Bmi-1 could inhibit the growth, colony formation in vitro and tumorigenesis in vivo of SPC-A1 cells (P<0.01). The transfected SPC-A1 cells were arrested in G1 phase [(64.6±1.2)%, P<0.05]. Compared with two control groups, p16INK4a, p53 and Akt were not affected (P>0.05), while Cyclin D1 and Ser473p-Akt were downregulated (P<0.01) and PTEN was up-regulated (P<0.01) in the SPC-A1-Bmi-1-siRNA cells. SPC-A1-Bmi-1-siRNA cells were treated with various concentrations of PTEN inhibitor to determine expression levels of PTEN, Bmi-1 and Ser473p-Akt protein. Ablation of PTEN rescued Bmi-1 and Ser473p-Akt expression in SPC-A1-Bmi-1-siRNA cells. Conclusion:Knockdown of Bmi-1 gene can arrest the proliferation of SPC-A1 cells through G0/G1 phase arrest by inhibiting Cyclin D1 expression indirectly, which may be not associated with p16INK4a signaling pathway.

Background and purpose:The pro-oncogene Bmi-1 is a member of the polycomb-group family, can regulation of the proliferation and self-renewal of normal and tumor stem cells. In recent years, Bmi-1 has been found that it is overexpressed in varieties of human malignant tumors. The study aimed to observe the effects of Bmi-1-siRNA on the growth capacity of lung cancer cell line A549 in vivo and in vivo, and explore its mechanism. Methods:The most effective one as a target sequence was chosen from four Bmi-1 siRNA sequences which were designed by our lab, and one random sequence was chosen as a negative control. In short, the chemically synthesized siRNA and control sequences were connected to a retrovirus expressing vector, pSUPERretro-Neo plasmid, and then transfected into A549 cells. The stably transfected cells were cultured and passed. The level of mRNA and protein of Bmi-1 in A549 cells were assessed by RT-PCR and Western blot respectively. The proliferations of A549 cells in vivo was analyzed with MTT, trypan blue exclusion and plate colony forming methods. Flow cytometry was used for cell cycle analysis. The potency of tumorigenesis was observed in nude mouse through hypodermic inoculation of A549 cells. The expressions of cyclin D, p21/27, p-AKT and PTEN were analyzed by Western blot. Results:Compared to A549-ctr and A549-wt cells, Bmi-1 mRNA and protein levels all signiifcantly reduced in A549-Bmi-1-siRNA cells. Bmi-1-siRNA inhibited the growth, colony formation in vitro and tumorigenesis in vitro of A549 cells, and the interference cells cell cycle arrested in G1 phase. In A549-Bmi-1-siRNA cells, p-AKT and cyclinD1 expression were down-regulated while p21/p27 and PTEN were up-regulated. Conclusion:Silencing Bmi-1 gene inhibits the proliferation of A549 cells through G1 phase arrest, which involves the downregulation of cyclin D/p-AKT and upregulation of p21/p27/PTEN.

Objective:To investigate the perinatal risk factors and correlation between bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP).Methods:A retrospective analysis was performed on 173 preterm infants born at less than 32 weeks' gestation with BPD who were admitted to the neonatal intensive care unit (NICU) of the Women and Children's Hospital of Qingdao University from June 2017 to July 2022. According to the diagnostic criteria for ROP, these preterm infants were divided into the ROP group ( n=64) and the non-ROP group ( n=109). Chi-square test, two independent samples t-test, and Mann-Whitney U test were used to compare the general data, treatment, and the incidence of complications between the two groups. Multivariate logistic stepwise regression analysis was used to analyze the independent risk factors of ROP in preterm infants with BPD and the receiver operating characteristic (ROC) curve was drawn to analyze the predictive value of independent risk factors on ROP. The correlation between the severity of BPD and the incidence of ROP was analyzed. Results:The gestational age at birth [(28.0±1.1) vs. (28.8±1.2) weeks, t=4.01], the birth weight [(1 075.9±141.4) vs. (1 143.2±168.6) g, t=2.68], the partial pressure of carbon dioxide [42.5 mmHg (1 mmHg=0.133 kPa) (34.0-51.0 mmHg) vs. 47.0 mmHg (39.0-54.0 mmHg), Z=－2.31], and the total fluid intake on the first day of birth [80.0 ml (72.3-88.7 ml) vs. 83.6 ml (76.6-92.8 ml), Z=－2.28] in the ROP group were all lower than those in the non-ROP group (all P<0.05). While the prothrombin time [15.7 s (14.1-17.7 s) vs. 14.6 s (13.1-16.7 s), Z=－2.17], activated partial thromboplastin time [64.7 s (52.9-77.9 s) vs. 55.8 s (48.4-68.9 s), Z=－2.12], the proportion of patients treated with pulmonary surfactant [71.9% (46/64) vs. 49.5% (54/109), χ 2=8.25], the total duration of oxygen supplementation [50.5 d (40.0-64.0 d) vs. 45.0 d (37.0-52.0 d), Z=－2.77], the duration of invasive ventilation [5.0 d (1.0-11.0 d) vs. 1.0 d (0.0-5.0 d), Z=－4.03], the duration of noninvasive ventilation or high-flow oxygen therapy [(31.7±12.7) vs. (26.4±13.1) d, t=－2.59], and the incidence of neonatal respiratory distress syndrome [76.6% (49/64) vs. 57.8% (63/109), χ 2=6.22] were increased in the ROP group (all P<0.05). There was no significant difference in the proportion of BPD treated with corticosteroids between the ROP and non-ROP groups [60.3% (38/63) vs. 74.3% (81/109), χ 2=3.67, P=0.055]. Multivariate logistic stepwise regression analysis showed that smaller gestational age ( OR=1.599, 95% CI: 1.126-2.272, P=0.009), less fluid intake on the first day ( OR=1.033, 95% CI: 1.004-1.062, P=0.024), and longer duration of invasive ventilation ( OR=1.076, 95% CI:1.017-1.138, P=0.011) were independent risk factors for ROP in BPD infants, while glucocorticoid treatment was an independent protective factor ( OR=0.378, 95% CI:0.173-0.827, P=0.015). Most patients with mild or moderate BPD did not develop ROP [64.6% (73/113) and 66.7% (34/51)], while those with severe BPD were more likely to be complicated by ROP (7/9) ( χ 2=6.84, P=0.033). Conclusions:BPD infants with smaller gestational age, longer duration of invasive ventilation, and less fluid intake on the first day of birth are more likely to develop ROP, while glucocorticoid therapy can reduce the incidence of ROP in this population. Severe BPD may increase the risk of ROP in infants.

Objective To evaluate the effect of acarbose on the circulating concentration of inflammatory factors in patients with type 2 diabetes mellitus(T2DM). Methods Total 118 patients with T2DM who did not take acarbose before enrollment within 4 weeks were recruited by a randomizing formula into 2 groups ( group A and B). 57 healthy subjects were included into group C as control. After excluding those of inadequate samples, 57 patients with T2DM were enrolled into group A in which acarbose was prescribed 50 mg three times a day, 59 patients with T2DM were enrolled into group B in which acarbose was not given and other hypoglycemic approaches were similar to group A. Serum samples at the time of enrollment and at the end of 4 weeks intervention were collected and stored in refrigerator at -80℃ until analysis. Analysis of biochemical indexes was performed in central lab of the institution,inflammatory factors were determined with commercial ELISA kits. Results (1) The metabolic indexes were significantly decreased after intervention in two diabetic groups. (2) The baseline levels of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α( TNF-α), prothrombin activator inhibitor-1 (PAI-1), lipopolysaccharide (LPS), high sensitive C reactive protein ( hs-CRP), and advanced glycation index (AGI) in diabetic patients were significantly higher than in group C MCP-1 [( 463.4± 187.1 vs 267.1 ± 158.3 ) pg/ml, TNF-α( 12.07 ± 19.59 vs 4.18 ±3.03 ) pg/ml, PAI-1 ( 2.47 ± 1.87 vs 1.38 ± 2.37 )ng/ ml, LPS ( 130.6 ± 128.5 vs 29.39 ± 17.93 ) pg/ml, hsCRP(4.25 ±2.29 vs 2.11 ± 1.07 ) μg/ml, AGI (3.78 ± 2.61 vs 0. 74 ± 0. 15 ) AU, all P ＜ 0. 05]. (3) Repeated measurement ANOVA analysis showed that after four weeks of intervention, MCP-1 [F( 1,106 ) = 19. 830, P＜0.001],LPS[F(1,106)=7.815, P＜0.01], PAI-1 [F(1,106)= 7.792, P＜0.01], TNF-α[F(1,106=24. 656, P=0.001 )] ,AGI[F( 1,106)= 12. 971 ,P=0. 01] decreased significantly in group A than in group B. Although hsCRP decreased in both group A and group B, but the trend was not different [F( 1,102 )= 0. 915, P = 0. 342].Conclusion The levels of inflammatory factors were elevated in patients with type 2 diabetes mellitus, which could be mostly reduced by acarbose.