Objective: To probe into the antioxidation mechanism of lotus seedpod in vivo.Methods:Nineteen 4-month old rats were randomly divided into control group and procyanidins group. After feeding 100 mg/kg LSPC for 35 d, MDA and SOD in skin and serum, GSH-Px and Hyp in blood and skin were measured.Results: MDA levels in skin and serum in the procyanidins group were obviously lower than that of the control(P

Aims To study the effects of diterpenoid pekinenal of Euphorbia pekinensis Rupr. on cell prolif-eration, cell cycle phase and apoptosis of hepatoma SMMC-7721 cells and to probe into its anti-cancer mechanisms. Methods MTT assay was used to inves-tigate the effect of pekinenal on proliferation of SMMC-7721 cells; TUNEL method, Annexin V/PI staining and electron microscopy were employed to observe the cell apoptosis; Flow cytometry was applied to analyze the distribution of cell cycle. Results Proliferation of SMMC-7721 cells was markedly inhibited by pekinenal in a dose-dependent manner; Annexin V/PI staining showed that with the increase of pekinenal concentra-tion, apoptotic rate of SMMC-7721 cells increased sig-nificantly, compared with control group, the difference has significant statistical significance ( P < 0. 01 ) . TUNEL method test results showed that different con-centrations of pekinenal in SMMC-7721 cells could in-duce liver cancer cell apoptotic and apoptotic index ( AI) increased significantly ( P <0. 01 ) with the in-crease of drug concentration. Compared with control group, electron microscope found that after the treat-ment, hepatocyte mitochondrial swelling, endoplasmic reticulum expansion, cytoplasm inclusion body forma-tion, part of the nucleus apoptosis, and the more obvi-ous apoptosis appeared with the increase of drug con-centration. Flow cytometry analysis showed that differ-ent concentrations of pekinenal could all make the cell block in S phase. Conclusion Pekinenal has an obvi-ously inhibitory effect on the human liver cancer cells, and there is significant concentration dependence; Pe-kinenal probably inhibits cancer cell DNA synthesis for the human liver cell cycle arrest in S phase and inhibits the proliferation . It plays a role in liver cancer inhibi-tion by inducing liver cancer cells apoptosis, etc.

Objective To investigate the expression of LncRNA DLEU1 in ESCC tissues, and its effect on the proliferation and migration of ESCC cells. Methods We collected 58 cases of ESCC tissues and corresponding para-cancerous tissues. RT-qPCR was used to detect the relative expression levels of DLEU1 in ESCC tissues and cells. Log-rank test was used to analyze the relation between the expression of DLEU1 and clinicopathological features. Kaplan-Meier analysis was used to investigate the correlation between the expression of DLEU1 and the survival of ESCC patients. Multivariate Cox regression model was used to evaluate the effect of DLEU1 on the prognosis of ESCC patients. Effects of DLEU1 on the proliferation and migration of Eca9706 cells were evaluated by CCK-8 and wound healing assays, respectively. Results DLEU1 was highly expressed in ESCC tissues (P < 0.01) and significantly correlated with tumor size, TNM stage and lymph node metastasis (all P < 0.05). High expression of DLEU1 was negatively correlated with poor prognosis of ESCC patients (P < 0.01), and DLEU1 was also an independent prognostic risk factor (P < 0.05). Moreover, knockdown of DLEU1 significantly inhibited the proliferation and migration of Eca9706 cells, compared with the control group (P < 0.01). Conclusion DLEU1 is highly expressed in ESCC tissues. The expression of DLEU1 is an independent risk factor for the prognosis of ESCC patients and promotes ESCC cell proliferation and migration.

Objective:To investigate the trademark registration situation of grade-A tertiary hospitals in China, so as to analyze the current situation of hospital brand protection and explore suggestions for hospital brand protection.Methods:The top 50 hospitals ranked in the 2021 National Hospital Comprehensive Ranking by the Hospital Management Research Institute of Fudan University, excluding military hospitals, were selected as the sample hospitals. The trademark registration information of the 50 sample hospitals was queried through the China Trademark Website of the Trademark Office of China National Intellectual Property Administration on March 15, 2023, and the registration of the full name, abbreviation, hospital emblem and other trademarks of the hospitals was counted. Results:Among the 50 sample hospitals, 26 hospitals already held hospital brand trademarks, which meant that at least one of the hospital′s full name, abbreviation, and emblem was registered as a trademark, accounting for 52%; 7 hospitals did not hold any trademarks, accounting for 14%; 17 hospitals held other trademarks but did not hold hospital brand trademarks, accounting for 34%. Among the 26 hospitals that already held brand trademarks, 11 hospitals only registered in one category. There were 3 hospitals with expired registered trademarks.Conclusions:Nearly half of the sample hospitals did not hold hospital brand trademarks, indicating that the trademark registration and brand protection of tertiary hospitals in China need to be strengthened. It is suggested to establish a hospital brand protection system, clarify the trademark management department, standardize the responsibilities of trademark management, and improve the use of trademarks, so as to do a good job in hospital trademark registration and brand protection.

AIM:To investigate the effects of cannabinoid receptor agonist WIN55212-2(WIN)on acute lung injury(ALI)in septic mice,and to explore its potential mechanisms through glycolysis.METHODS:A mouse model of septic ALI was established by intraperitoneal injections of lipopolysaccharide(LPS).Male C57BL/6J mice were randomly divided into 4 groups(n=6):(1)control group;(2)LPS group,receiving intraperitoneal injections of LPS at 10 mg/kg;(3)LPS+WIN group,receiving 1 mg/kg WIN intraperitoneally 30 min prior to LPS injection;(4)LPS+WIN+MHY1485[mammalian target of rapamycin(mTOR)activator]group,receiving 10 mg/kg MHY1485 intraperitoneally 1 d before LPS injection and 1 mg/kg WIN plus 10 mg/kg MHY1485 30 min before LPS injection.Tissues were collected 24 h after modeling for analysis.Lung indexes were calculated,and histopathological changes of lung tissues were observed via he-matoxylin-eosin(HE)staining.Inflammatory cytokines interleukin-1β(IL-1β)and IL-10 in lung tissues,and lactic acid and lactate dehydrogenase A(LDHA)in serum were quantified using ELISA.The levels of mTOR/hypoxia-inducible fac-tor-1α(HIF-1α)/6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3(PFKFB3)signaling pathway-related proteins were assessed by Western blot.RESULTS:Compared with control group,the LPS group exhibited an increased lung in-dex,significant lung tissue damage,an increase in IL-1β levels(P＜0.05),a decrease in IL-10 levels(P＜0.05),and el-evated expressions of lactate and LDHA(P＜0.05),along with increased levels of phosphorylated mTOR(p-mTOR),HIF-1α and PFKFB3 proteins(P＜0.05).The LPS+WIN group showed improvements with a reduced lung index(P＜0.05),lessened lung injury,decreased IL-1β levels(P＜0.05),increased IL-10 levels(P＜0.05),and lower levels of lactic acid,LDHA,p-mTOR,HIF-1α,and PFKFB3(P＜0.05).Conversely,the LPS+WIN+MHY1485 group displayed increased lung indexes and lung tissue damage,elevated IL-1β levels(P＜0.05),reduced IL-10 levels(P＜0.05),and higher expressions of lactic acid,LDHA,p-mTOR,HIF-1α and PFKFB3(P＜0.05)compared to the LPS+WIN group.CONCLUSION:WIN55212-2 mitigates sepsis-induced ALI,potentially by modulating the mTOR/HIF-1α/PFKFB3 sig-naling pathway,thereby inhibiting glycolysis and alleviating inflammatory responses.

[Abstract] Objective: To investigate the expression of long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) in esophageal squamous cell carcinoma (ESCC) tissues, and to analyze its relationship with clinicopathological features and prognosis of ESCC patients. Methods: The expression of DGCR5 in ESCC data set from TCGA database was analyzed by bioinformatics method. Sixty pairs of ESCC tissues and para-cancerous tissues resected at the Fourth Hospital of Hebei Medical University from August 2016 to March 2017 were collected for this study. The expression of DGCR5 in ESCC tissues was detected by qPCR. The correlation between the expression of DGCR5 and the clinicopathological features and prognosis of ESCC patients was analyzed. Results: TCGAdatabase analysis showed that the expression of DGCR5 in ESCC tissues was significantly higher than that in normal esophageal tissues (P<0.01). The expression of DGCR5 in ESCC tissues was significantly higher than that in para-cancerous tissues (P<0.01). The expression level of DGCR5 was significantly correlated with TNM staging and lymph node metastasis in ESCC patients (all P<0.05). Kaplan-Meier univariate analysis showed that the 2-year survival rate of ESCC patients with high DGCR5 expression was significantly lower than that of patients with low expression (P<0.05). Conclusion: DGCR5 is highly expressed in ESCC tissues and is closely related to TNM staging, lymph node metastasis and poor prognosis, which may serve as a molecular marker for early diagnosis and prognosis prediction of ESCC.

Objective To evaluate the correlation between three-dimensional histogram vascular indexes of ovarian tumors and microvessel density (MVD).Methods Fifty-seven patients with ovarian cystic-solid or solid masses from Beijing Obstetrics and Gynecology Hospital,Capital Medical University were evaluated by three-dimensional (3D) power ultrasound within one week before surgery from January 2008 to December 2009.We captured 3D power imaging in the interested and solid areas of tumors,and used three-dimensional histogram from virtual organ computer-aid analysis (VOCAL) to calculate vascularization index (Ⅵ),flow index (FI) and vascularization-flow index (VFI).After operation the specimens underwent immunohistochemistry staining and MVD and vascular endothelial growth factor (VEGF) were calculated.Two independent-samples t tests were used to compare MVD between ovarian benign and malignant tumors.Rank sum test was used to compare VEGF.Spearman was used to analyze the relationship between 3D PD vascular indices and MVD.Results Sixty-two ovarian masses in 57 patients were confirmed by pathology (5 cases were bilateral tumors),including 22 benign and forty malignant messes (including eight borderline tumors).Fifty-four tumors underwent immunohistochemistry staining.MVD and VEGF were calculated.Both of MVD and VEGF in ovarian malignant tumors were obviously higher than those in benign ones (t=-5.255,Z=-3.868,both P ＜ 0.01).Both of Ⅵ and VFI were positive correlative to MVD (r=0.295,0.280,both P ＜ 0.05).Conclusions There was a positive correlation between vascular indexes and microvessel density.The vascular indexes could reflect the density of angiogenesis in ovarian tumors before surgery,and they could provide valuable information for early-stage diagnosis of ovarian cancer.

Objective: To study the expression of miR-142-5p in lung adenocarcinoma tissues, and to explore its effect on proliferation, invasion, migration and epithelieal-mesenchymal transition (EMT) of H1650 cells and the potential mechanisms. Methods:Atotal of 107 pairs of lung adenocarcinoma tissues and corresponding para-cancerous tissues from patients, who underwent tumor resection and were pathologically confirmed at the Department of Thoracic Surgery, the Fourth Hospital of Hebei Medical University between Jan. 2014 and Jan. 2015, were collected for this study; in addition, human lung adenocarcinoma cell lines (H1650, HCC827, A549, H1975, PC9) and human bronchial epithelial BEAS-2B cells were also used in this study. qPCR was used to detect the expression of miR-142-5p in lung adenocarcinoma tissues and cell lines. The correlation between expression of miR-142-5p and clinical features was analyzed.After transfection with miR-142-5p mimics or miR-negative control (miR-NC) plasmid, the proliferation, invasion and migration of H1650 cells were detected with CCK-8, Transwell invasion assay and Wound healing assay, respectively. The bioinforamtics tool was used to predict the target genes of miR-142-5p, and Luciferase reporter gene assay was performed to validate the regulation of miR-142-5p on target gene. Western blotting (WB) was used to detect the expressions of cyclin-dependent kinase 5 (CDK5) and EMTrelated protein. Results: Compared to Para-cancerous tissues and BEAS-2B cells, the expression of miR-142-5p was lower in lung adenocarcinoma tissues and cell lines (all P<0.01). Of the 107 cases of lung adenocarcinoma tissues, 61 cases (57.01%) showed decreased miR-142-5 expression, which was correlated with the TNM stage and lymph node metastasis (both P<0.01). Transfection of miR-142-5p mimics significantly up-regulated the expression of miR-142-5p and decreased the proliferation, invasion and migration of H1650 cells (all P<0.05 or P<0.01). Bioinformatics showed that CDK5 was a target gene of miR-142-5p. Luciferase reporter gene assay and WB validated that miR-142-5p could significantly down-regulate CDK5 expression in H1650 cells, up-regulate the expression of E-cadherin and down-regulate the expressions of N-cadherin, Twist and Snail in H1650 cells (all P<0.01). Conclusion: miR-142-5p is low expressed in lung adenocarcinoma tissues and cell lines; it suppresses the EMT process to inhibit, invasion and migration of H1650 cells via down-regulating the expression of CDK5.

[Abstract] Objective: To investigate the effects and mechanisms of long non-coding RNA (lncRNA) non-coding RNA-activated by DNA damage (NORAD) on the proliferation and migration of esophageal squamous cell carcinoma (ESCC) EC9706 cells. Methods: RT-PCR was used to detect the mRNA expression level of NORAD in different ESCC cells (EC9706, TE1, YES-2, KYSE150). Small interfering RNA (siRNA) targeting NORAD gene was transfected into EC9706 cells (as si-NORAD group) with RNA interference technique to knockdown NORAD expression; in addition, blank control group (as Ctrl group, without any transfection) as well as negative control group (as NC group, transfected with siRNAnegative control sequence)werealsoestablished. qPCR was used to verify the transfection efficiency. MTT, Colony formation assay and Wound-healing test were used to detect the abilities of proliferation and migration of EC9706 cells before and after NORAD knockdown. Western blotting was used to detect the expressions of E-cadherin, N-cadherin and Snail in EC9706 cells before and after NORAD knockdown. Results: NORAD mRNAwas highly expressed in 4 ESCC cell lines. Comparing with TE1, YES-2 and KYSE150 cells, the expression of NORAD mRNA was significantly higher in EC9706 cells (P<0.01). After transfection of NORAD-siRNA into EC9706 cells, the expression of NORAD was down-regulated significantly as comparing with Ctrl group and NC group (all P<0.01), in the meanwhile, the proliferation and migration abilities of EC9706 cells were also significantly suppressed (P<0.05).After NORAD knockdown, the expression of E-cadherin was up-regulated while the expressions of N-cadherin and Snail were down-regulated in EC9706 cells (all P<0.05). Conclusion: NORAD is highly expressed in EC9706 cells;knockdown of NORAD expression can inhibit the proliferation and migration ability of EC9706 probably through up-regulating E-cadherin and down-regulating N-cadherin and Snail.

BACKGROUND:Ischemic stroke is a highly prevalent disease associated with apoptosis.Neuronal death occurs after cerebral ischemia,including necrosis and apoptosis.The ischemic core region is dominated by necrosis,while delayed neuronal death in the penumbra is dominated by apoptosis.The penumbra has become a target for the treatment of ischemic stroke.This bibliometric analysis was used to identify the characteristics,hotspots,and frontiers of global scientific output related to apoptosis in ischemic stroke over the past 5 years. OBJECTIVE:To analyze the role of apoptosis and its mechanisms in the pathological process of ischemic stroke through a bibliometric approach. METHODS:A total of 927 relevant literature records from 2018 to 2022 were retrieved from Science Citation Index Expanded(SCI-Expanded)and Social Science Citation Index Expanded(SSCI-Expanded)of the Web of Science Core Collection.Research trends and hotspots of apoptosis in ischemic stroke were visualized using Citespace,VOSviewer and Bibliometrix. RESULTS AND CONCLUSION:From 2018 to 2020,the number of papers on the role of apoptosis in ischemic stroke showed an upward trend,but in 2020,the number of papers began to reduce.China had the largest number of publications,and the United States ranked the second.Capital Medical University and BRAIN RESEARCH BULLETIN were the institutions and journals with the most articles,respectively.In recent years,the two keywords"expression"and"oxidative stress"have appeared more frequently.The bibliometric study showed that in the past 5 years,most of the studies focused on basic research,in which research on the role of apoptosis in ischemic stroke has gradually decreased in the last 3 years,showing a downward trend.On the contrary,nerve regeneration has gradually become a research hotspot,especially the regulation of neurotrophic factors under the influence of different mechanisms,and the research on angiogenesis and glial cell repair is on the rise.At the same time,apoptosis in nerve regeneration is a potential point of discovery.