Objective To study the effect of sodium ferulate (SF) on the expressions of nuclear factor-?B (NF-?B) and inhibitory ?B? (I?B?) in rat brain microvascular endothelial cells (BMEC) injured by hypoxia. Methods Brain microvascular endothelial cells from Wistar rat cerebral cortex were isolated and cultured, and then cultivated in 95%N_2 and 5% CO_2 for 12 h to induce hypoxia injury. The cells were divided into normal group, hypoxia group, and SF group. BMEC activity was assayed by MTT assay. Endothelin-1(ET-1) concentration was evaluated by radioimmunoassay.The expression of NF-?B and I?B? of BMEC were assessed by immunocytochemistry. Results The content of ET-1 in BMEC media was increased after hypoxia, while sodium ferulate (100 ?g/ml) significantly decreased the content compared with hypoxia group. Immunocytochemistry indicated I?B? expression were significantly decreased in hypoxia BMEC in consistent with NF-?B expression. Conclusion Sodium ferulate may significantly reduce NF-?B of hypoxia BMEC and nuclear translocation, and increase I?B? expression and BMEC activity. It is a potent inhibitor of NF-?B in endothelial cells, which might explain its beneficial effect on injured BMEC by hypoxia.

Objective: Src homology phosphotyrosin phosphatase 2 (SHP2) has been implicated in the progression of several cancer types. However, its function in endometrial cancer (EC) remains unclear. Here, we report that the ten-eleven translocation 3 (TET3)-mediated DNA demethylation modification is responsible for the oncogenic role of SHP2 in EC and explore the detailed mechanism. Methods: The transcriptomic differences between EC tissues and control tissues were analyzed using bioinformatics tools, followed by protein-protein interaction network establishment. EC cells were treated with shRNA targeting SHP2 alone or in combination with isoprocurcumenol, an epidermal growth factor receptor (EGFR) signaling activator.The cell biological behavior was examined using cell counting kit-8, colony formation, flow cytometry, scratch assay, and transwell assays, and the median inhibition concentration values to medroxyprogesterone acetate/gefitinib were calculated. The binding of TET3 to the SHP2 promoter was verified. EC cells with TET3 knockdown and combined with SHP2 overexpression were selected to construct tumor xenografts in mice. Results: TET3 and SHP2 were overexpressed in EC cells. TET3 bound to the SHP2 promoter, thereby increasing the DNA hydroxymethylation modification and activating SHP2 to induce the EGFR/extracellular signal-regulated kinase (ERK) pathway. Knockdown of TET3 or SHP2 inhibited EC cell malignant aggressiveness and impaired the EGFR/ERK pathway. Silencing of TET3 inhibited the tumorigenic capacity of EC cells, and ectopic expression of SHP2 or isoprocurcumenol reversed the inhibitory effect of TET3 knockdown on the biological activity of EC cells. Conclusion TET3 promoted the DNA demethylation modification in the SHP2 promoter and activated SHP2, thus activating the EGFR/ERK pathway and leading to EC progression.

Objective: Src homology phosphotyrosin phosphatase 2 (SHP2) has been implicated in the progression of several cancer types. However, its function in endometrial cancer (EC) remains unclear. Here, we report that the ten-eleven translocation 3 (TET3)-mediated DNA demethylation modification is responsible for the oncogenic role of SHP2 in EC and explore the detailed mechanism. Methods: The transcriptomic differences between EC tissues and control tissues were analyzed using bioinformatics tools, followed by protein-protein interaction network establishment. EC cells were treated with shRNA targeting SHP2 alone or in combination with isoprocurcumenol, an epidermal growth factor receptor (EGFR) signaling activator.The cell biological behavior was examined using cell counting kit-8, colony formation, flow cytometry, scratch assay, and transwell assays, and the median inhibition concentration values to medroxyprogesterone acetate/gefitinib were calculated. The binding of TET3 to the SHP2 promoter was verified. EC cells with TET3 knockdown and combined with SHP2 overexpression were selected to construct tumor xenografts in mice. Results: TET3 and SHP2 were overexpressed in EC cells. TET3 bound to the SHP2 promoter, thereby increasing the DNA hydroxymethylation modification and activating SHP2 to induce the EGFR/extracellular signal-regulated kinase (ERK) pathway. Knockdown of TET3 or SHP2 inhibited EC cell malignant aggressiveness and impaired the EGFR/ERK pathway. Silencing of TET3 inhibited the tumorigenic capacity of EC cells, and ectopic expression of SHP2 or isoprocurcumenol reversed the inhibitory effect of TET3 knockdown on the biological activity of EC cells. Conclusion TET3 promoted the DNA demethylation modification in the SHP2 promoter and activated SHP2, thus activating the EGFR/ERK pathway and leading to EC progression.

Objective: Src homology phosphotyrosin phosphatase 2 (SHP2) has been implicated in the progression of several cancer types. However, its function in endometrial cancer (EC) remains unclear. Here, we report that the ten-eleven translocation 3 (TET3)-mediated DNA demethylation modification is responsible for the oncogenic role of SHP2 in EC and explore the detailed mechanism. Methods: The transcriptomic differences between EC tissues and control tissues were analyzed using bioinformatics tools, followed by protein-protein interaction network establishment. EC cells were treated with shRNA targeting SHP2 alone or in combination with isoprocurcumenol, an epidermal growth factor receptor (EGFR) signaling activator.The cell biological behavior was examined using cell counting kit-8, colony formation, flow cytometry, scratch assay, and transwell assays, and the median inhibition concentration values to medroxyprogesterone acetate/gefitinib were calculated. The binding of TET3 to the SHP2 promoter was verified. EC cells with TET3 knockdown and combined with SHP2 overexpression were selected to construct tumor xenografts in mice. Results: TET3 and SHP2 were overexpressed in EC cells. TET3 bound to the SHP2 promoter, thereby increasing the DNA hydroxymethylation modification and activating SHP2 to induce the EGFR/extracellular signal-regulated kinase (ERK) pathway. Knockdown of TET3 or SHP2 inhibited EC cell malignant aggressiveness and impaired the EGFR/ERK pathway. Silencing of TET3 inhibited the tumorigenic capacity of EC cells, and ectopic expression of SHP2 or isoprocurcumenol reversed the inhibitory effect of TET3 knockdown on the biological activity of EC cells. Conclusion TET3 promoted the DNA demethylation modification in the SHP2 promoter and activated SHP2, thus activating the EGFR/ERK pathway and leading to EC progression.

Abnormal fatty acid metabolism is one of the unique metabolic ways in which malignant cells maintain their growth needs and plays a crucial role in tumor progression.Acetyl-CoA carboxylase (ACC) is the rate-limiting enzyme in fatty acid synthesis and oxidative metabolism.More and more researches confirm that ACC is highly expressed in many tumors,and is closely related to tumor progression and prognosis of patients,which makes ACC as a potential marker for clinical diagnosis and prognosis.Tumor cell fatty acid synthesis can be blocked and fatty acid β oxidation can be stimulated by inhibiting the activity of ACC,resulting in serious lipid consumption of tumor,and then inhibit tumor growth and proliferation.Investigating the effect and molecular mechanisms of ACC in the genesis and development of tumors can provide a new insight into cancer targeted molecular therapy.

Caenorhabditis elegans hid-1 gene was first identified in a screen for mutants with a high-temperature-induced dauer formation (Hid) phenotype. Despite the fact that the hid-1 gene encodes a novel protein (HID-1) which is highly conserved from Caenorhabditis elegans to mammals, the domain structure, subcellular localization, and exact function of HID-1 remain unknown. Previous studies and various bioinformatic softwares predicted that HID-1 contained many transmembrane domains but no known functional domain. In this study, we revealed that mammalian HID-1 localized to the medial- and trans- Golgi apparatus as well as the cytosol, and the localization was sensitive to brefeldin A treatment. Next, we demonstrated that HID-1 was a peripheral membrane protein and dynamically shuttled between the Golgi apparatus and the cytosol. Finally, we verified that a conserved N-terminal myristoylation site was required for HID-1 binding to the Golgi apparatus. We propose that HID-1 is probably involved in the intracellular trafficking within the Golgi region.
Animals ; Brefeldin A ; pharmacology ; Cell Line, Tumor ; Cytosol ; drug effects ; metabolism ; Humans ; Intracellular Space ; drug effects ; metabolism ; Membrane Proteins ; metabolism ; Protein Transport ; drug effects ; Rats ; Vesicular Transport Proteins ; metabolism ; trans-Golgi Network ; drug effects ; metabolism

Objective:To establish a prompt based feeding process for premature infants and explore its application effects.Methods:This study was a quasi-experimental research method. Firstly, the best evidence of prompt feeding for premature infants was systematically searched and summarized, and the expert consultation method and clinical practice were used to finally formulate a prompt feeding process for premature infants. The process was applied to clinical practice. A total of 82 hospitalized premature infants in the neonatal intensive care unit of Union Hospital, Tongji Medical College, Huazhong University of Science and Technology from October 2021 to March 2022 were selected as the control group, and routine feeding management was implemented. A total of 86 hospitalized premature infants from April to September 2022 were selected as the observation group. Feeding management for premature infants based on the prompt feeding process was followed, and the feeding efficiency, transition time of full oral feeding, and days of gastric tube retention, hospital stay and the incidence of feeding related complications in the two groups were compared.Results:The effective recovery rates of the two rounds of expert correspondence questionnaires were 100%, and the authoritative coefficients of expert opinions were 0.863 and 0.875, respectively. The Kendall harmony coefficients of expert opinions were 0.156 and 0.202, respectively, and the significance tests were all P<0.05. The total oral feeding rate of the observation group was 59.84%(5 256/8 784), the mixed feeding rate was 12.26%(1 077/8 784), and the tube feeding rate was 27.90%(2 451/8 784). Compared with the control group′s 52.20%(4 698/9 000), 14.68%(1 321/9 000), and 33.12%(2 981/9 000), the difference was statistically significant ( χ2 = 105.21, P<0.05). The transition time of full oral feeding, number of days of gastric tube retention, and hospitalization time in the observation group were (5.14 ± 1.67), (6.13 ± 1.62), and (12.77 ± 1.37) days, respectively. Compared with the control group′s (6.22 ± 1.59), (7.17 ± 1.55), and (13.72 ± 1.72) days, the differences were statistically significant ( t = 4.206, 4.26, 3.97, all P<0.05). The incidence of milk choking, hypoxia, and vomiting in the observation group were 9.30%(8/86), 6.98%(6/86), and 11.63%(10/86), respectively, which were lower than the 23.17%(19/82), 19.51%(16/82), and 34.15%(28/82) of the control group. The difference between the two groups was statistically significant ( χ2 = 5.99, 5.80, 12.16, all P<0.05). Conclusion:The application of prompt feeding process in premature infants can shorten the transition time of full oral feeding, promote the feeding process, reduce the complications caused by poor feeding, and ensure the feeding safety of premature infants.

Objective:To retrieve relevant evidence on exercise assessment and exercise training for children with congenital heart disease at home and abroad, and to summarize the best evidence to provide reference for clinical medical staff.Methods:UpToDate, National Guidelines Clearinghouse (NGC), Registered Nurses Association of Ontario (RNAO), Scottish Intercollegiate Guidelines Network (SIGN), National Institute for Health and Care Excellence (NICE), BMJ Best Practice, American Heart Association (AHA), Cochrane Library, Joanna Briggs Institute(JBI) Evidence-Based Health Care Center Database, PubMed, CINAHL, China Biomedical Literature Database, Yimaitong, Wangfang Database, CNKI were searched, related evidence on exercise assessment and exercise training for children with congenital heart disease. The search period was from the establishment of the database to March 2021. Clinical decision-making and recommended practice used retrospective evaluation methods for quality evaluation; guidelines used the 2012 version of the clinical guideline research and evaluation system (AGREE Ⅱ) for evaluation; systematic reviews used the systematic evaluation tool (AMSTAR) for evaluation; expert consensus used JBI (2016 version) evaluate the authenticity evaluation tools of opinions and consensus articles. Two researchers independently evaluated the literature, combined with the judgment of professionals, and extracted the literature data that met the standards.Results:A total of 15 documents were included, including 2 clinical decisions, 4 guidelines, 1 recommended practice, 5 systematic reviews, 3 expert consensus, and 22 best evidences. Including related personnel, exercise evaluation, exercise monitoring, exercise classification, exercise training, and exercise follow-up.Conclusions:This study summarizes the best evidence of exercise assessment and exercise training for children with congenital heart disease, and provides evidence-based evidence for clinical practice. It is recommended that children with congenital heart disease undergo exercise assessment and formulate a personalized exercise training program to promote the transformation of the best evidence into clinical practice.

Objective:To evaluate the efficacy and safety of linaclotide with polyethylene glycol in bowel preparation.Methods:From September 2021 to February 2022, 240 patients who visited the Department of Gastroenterology, Third People′s Hospital of Hubei Province, Jianghan University and underwent colonoscopy were selected. According to the random number table, in the ratio of 1 to 1, the patients were divided into the linaclotide with polyethylene glycol group and the simple polyethylene glycol group, with 120 cases in each group. The patients in the linaclotide with polyethylene glycol group took 580 μg linaclotide and 2 L polyethylene glycol electrolyte powder solution, and the patients in the simple polyethylene glycol group took 3 L polyethylene glycol electrolyte powder solution. The Boston bowel preparation scale(BBPS) score, the detection rate of polyps or adenomas, the insertion time of colonoscopy, the withdrawal time of colonoscopy, the time of the first defecation, the frequency of defecations, the success rate of cecal intubation, the occurrence of adverse effects and the satisfaction rate of patients were compared between the 2 groups. Independent sample t test and chi-square test were used for statistical analysis. Results:A total of 235 patients completed bowel preparation and accepted colonoscopy. There were no statistically significant differences in the BBPS score, the detection rate of polyps or adenomas, the insertion time of colonoscopy, the withdrawal time of colonoscopy, the success rate of cecal intubation and the frequency of defecations between the linaclotide with polyethylene glycol group and simple polyethylene glycol group(7.3±1.1 vs. 7.0±1.2; 58.1%, 68/117 vs. 60.2%, 71/118; 38.5%, 45/117 vs. 39.8%, 47/118; (4.2±1.9) min vs.(4.3±1.6) min; (5.9±2.7) min vs.(6.2±2.4) min; 100.0%, 117/117 vs. 100.0%, 118/118; 5.3±2.3 vs. 5.1±2.7; all P>0.05). The rate of adverse effects of the linaclotide with polyethylene glycol group was lower than that of simple polyethylene glycol group(25.6%, 30/117 vs. 39.8%, 47/118), the satisfaction rate of patients was higher than that of the simple polyethylene glycol group (93.2%, 109/117 vs. 76.3%, 90/118), and the differences were statistically significant( χ2=0.24 and 0.64, P=0.018 and 0.031). Conclusion:Compared with the 3 L polyethylene glycol regimen, 580 g linaclotide with 2 L polyethylene glycol regimen can achieve the same bowel preparation effect with higher safety and patient satisfaction, which is worthy of clinical application.