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Objective To explore the effect and mechanism of ginsenoside Re on the intestinal mucosa of severe acute pancreatitis (SAP) mice by regulating the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/ STAT3) pathway. Methods Totally 48 mice were divided into : control group, SAP group, SAP + ginsenoside Re group and SAP + ginsenoside Re + LY2784544 group (n = 12). The mice were intraperitoneally injected with caerulein solution (after fasting for 12 hours, 100 μg/kg, 6 times, injection interval 60 minutes) to establish SAP models. Mice in the SAP+ ginsenoside Re group were intraperitoneally injected with ginsenoside Re (4 mg/kg, 1 time a day for 7 consecutive days). Intraperitoneal injection of 12.7 mg/kg LY2784544 was used to inhibit the JAK2/STAT3 pathway. Pancreatic and intestinal mucosal injury were detected in each group. The wet to dry weight ratio of pancreas, serum amylase and inflammatory factor levels were detected in each group. The intestinal mucosal barrier function was analyzed by detecting the levels of D-lactic acid and fluorescein isothiocyanate dextran (FITC-D). The damage of pancreatic tissue and intestinal mucosa tissue was observed by HE staining. Western blotting was used to detect the levels of apoptotic proteins Bax and Bcl-2 in the intestinal mucosa. The JAK2/STAT3 pathway expression levels in pancreatic tissue and intestinal mucosa tissue were detected by Realtime PCR and Western blotting. Results The pancreatic index, serum amylase, interieukin 6 (IL-6) and tumor necrosis factor a (TNF-a), FITC-D, D-lactic acid, Bax protein levels, JAK2 and STAT3 mRNA and protein levels in the SAP group were significantly higher than those in the control group, while Bcl-2 protein was significantly lower than that in the control group (P<0.05). The Bcl-2 protein of SAP+ginsenoside Re group was significantly higher than that of SAP group, and other indexes were significantly lower than those in SAP group (P<0.05). The Bcl-2 protein of SAP+ginsenoside Re+ LY2784544 group was significantly higher than that of SAP + ginsenoside Re group, and other indexes were significantly lower than those in the SAP+ginsenoside Re group (P<0.05). Conclusion Ginsenoside Re may reduce the pancreatic injury in SAP model mice by inhibiting the JAK/STAT pathway to alleviate the inflammatory response, and may protect the small intestinal mucosal barrier by alleviating pancreatitis and inhibiting the intestinal mucosal JAK/STAT pathway to inhibit cell apoptosis.
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Objective:To investigate the effect of a breathing pattern intervention (RPI) on the oral feeding of pre-term infants with suck-swallow-breath (SSwB) coordination disorder.Methods:Sixty pre-term infants with SSwB coordination disorder were divided into an observation group ( n=30) and a control group ( n=30) using a random number table. Both groups were given routine feeding training, including oral exercise intervention, non-nutritive sucking training, and swallowing induction training during nursing, while the observation group was additionally provided with 15 minutes of breathing pattern training once a day, including breathing pattern observation, resistive breathing training prior to eating and passive breathing pattern intervention during eating. Before and after the 7-day intervention, the Pre-term Infant Oral Feeding Readiness Assessment (PIOFRA) was used to evaluate each subject′s oral feeding ability. Rate of transfer (RT), proficiency (PRO), minimum oxygen partial pressure (SaO 2) and SaO 2 fluctuations were also recorded during the feeding process. Results:After 1 week of the intervention, significant improvement was observed in both groups. In the observation group the average RT (2.76±0.36ml/min), PRO, minimum SaO 2, the number of SaO 2 fluctuations, and PIOFRA score (33.28±0.58) were all significantly better than the control group′s averages. Conclusion:Breathing pattern intervention based on routine feeding training can enhance breathing coordination during swallowing and ultimately improve the oral feeding of pre-term infants with SSwB coordination disorders in a relatively short period of time.
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Objective Angiotensin Ⅱ (Ang Ⅱ)-induced vascular damage is a major risk of hypertension. However, the underlying molecular mechanism of AngⅡ-induced vascular damage is still unclear. In this study, we explored the novel mechanism associated with Ang II-induced hypertension. Methods We treated 8- to 12-week-old C57BL/6J male mice with saline and Ang Ⅱ(0.72 mg/kg·d) for 28 days, respectively. Then the RNA of the media from the collected mice aortas was extracted for transcriptome sequencing. Principal component analysis was applied to show a clear separation of different samples and the distribution of differentially expressed genes was manifested by Volcano plot. Functional annotations including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were performed to reveal the molecular mechanism of Ang Ⅱ-induced hypertension. Finally, the differentially expressed genes were validated by using quantitative real-time PCR. Results The result revealed that a total of 773 genes, including 599 up-regulated genes and 174 down-regulated genes, were differentially expressed in the aorta of Ang Ⅱ-induced hypertension mice model. Functional analysis of differentially expressed genes manifested that various cellular processes may be involved in the Ang Ⅱ-induced hypertension, including some pathways associated with hypertension such as extracellular matrix, inflammation and immune response. Interestingly, we also found that the differentially expressed genes were enriched in vascular aging pathway, and further validated that the expression levels of insulin-like growth factor 1 and adiponectin were significantly increased (P<0.05). Conclusion We identify that vascular aging is involved in Ang Ⅱ-induced hypertension, and insulin-like growth factor 1 and adiponectin may be important candidate genes leading to vascular aging.
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Animais , Masculino , Envelhecimento , Angiotensina II , Aorta/fisiopatologia , Pressão Sanguínea/genética , Perfilação da Expressão Gênica/métodos , Ontologia Genética , Hipertensão/genética , Camundongos Endogâmicos C57BL , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
Background@#Trocar-site hernia (TSH) is a serious complication after laparoscopic procedures. Although it is a rare entity, it can have life-threatening consequences. This study aimed to retrospectively analyze the potential associated factors for TSH following gynecologic laparoscopy and summarize prevention strategies based on our experience.@*Methods@#We searched for gynecological laparoscopic surgeries in the medical records system of Peking Union Medical College Hospital (PUMCH) from August 1998 to July 2018 and further sifted through the results for cases involving TSH. All included patients were divided into different groups according to patient characteristics, and the rate of TSH was compared among groups. Moreover, the detailed information of all patients with TSH was recorded and analyzed. Statistical analyses were performed with GraphPad Prism 6.@*Results@#The approximate total rate of post-operative TSH among gynecologic laparoscopy procedures performed at PUMCH in the last 20 years was 0.016% (9/55,244). The rate of TSH was significant higher in elder patients (≥60 years old; 3/2686, 0.112%) than in younger patients (<60 years old, 6/52,558; 0.011%, P = 0.008). Moreover, the approximate rate of TSH was significantly higher after single-incision laparoscopic surgery (SILS, 2/534, 0.357%) than conventional laparoscopic surgery (7/54,710, 0.013%, P = 0.003). The average age of patients with TSH was 53.4 years (range, 35.0-79.0 years). Two of the nine patients had late-onset TSH following SILS; the other seven had early-onset TSH following conventional laparoscopy. Five TSH cases occurred at right lateral port sites, and the remaining three occurred at the umbilical port site. All patients underwent repair surgery, and one required small bowel resection.@*Conclusion@#Older age and SILS are potential associated factors for TSH development, while reducing excessive manipulation and improving suturing skills, especially at the umbilical trocar site following SILS and the right lateral trocar site, can avoid herniation.
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BACKGROUND@#Trocar-site hernia (TSH) is a serious complication after laparoscopic procedures. Although it is a rare entity, it can have life-threatening consequences. This study aimed to retrospectively analyze the potential associated factors for TSH following gynecologic laparoscopy and summarize prevention strategies based on our experience.@*METHODS@#We searched for gynecological laparoscopic surgeries in the medical records system of Peking Union Medical College Hospital (PUMCH) from August 1998 to July 2018 and further sifted through the results for cases involving TSH. All included patients were divided into different groups according to patient characteristics, and the rate of TSH was compared among groups. Moreover, the detailed information of all patients with TSH was recorded and analyzed. Statistical analyses were performed with GraphPad Prism 6.@*RESULTS@#The approximate total rate of post-operative TSH among gynecologic laparoscopy procedures performed at PUMCH in the last 20 years was 0.016% (9/55,244). The rate of TSH was significant higher in elder patients (≥60 years old; 3/2686, 0.112%) than in younger patients (<60 years old, 6/52,558; 0.011%, P = 0.008). Moreover, the approximate rate of TSH was significantly higher after single-incision laparoscopic surgery (SILS, 2/534, 0.357%) than conventional laparoscopic surgery (7/54,710, 0.013%, P = 0.003). The average age of patients with TSH was 53.4 years (range, 35.0-79.0 years). Two of the nine patients had late-onset TSH following SILS; the other seven had early-onset TSH following conventional laparoscopy. Five TSH cases occurred at right lateral port sites, and the remaining three occurred at the umbilical port site. All patients underwent repair surgery, and one required small bowel resection.@*CONCLUSION@#Older age and SILS are potential associated factors for TSH development, while reducing excessive manipulation and improving suturing skills, especially at the umbilical trocar site following SILS and the right lateral trocar site, can avoid herniation.
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<p><b>Background</b>Estrogen receptor (ER) and progesterone receptor (PR) are involved in endometriosis, but the involvement of microRNAs (miRNAs) is unknown. The aim of the study was to explore the correlation between miRNA and ER/PR in uterine tissues of rats with endometriosis during the implantation window.</p><p><b>Methods</b>Twenty female Sprague-Dawley rats were randomized in three groups: endometriosis (n = 7), fat tissue control (n = 6), and normal (n = 7) groups. The female rats were mated and sacrificed on day 5 (implantation). Uterine tissues were obtained for hematoxylin-eosin staining, immunohistochemistry, and miRNA expression. Reverse transcription polymerase chain reaction (RT-PCR) was used to validate the expression of rno-miR-29c-3p, rno-miR-34c-5p, rno-miR-141-5p, rno-miR-24-1-5p, and rno-miR-490-5p.</p><p><b>Results</b>The 475 miRNAs were found to differentially express between the endometriosis and normal control groups, with 127 being upregulated and 348 being downregulated. Expression of five miRNAs (rno-miR-29c-3p, rno-miR-34c-5p, rno-miR-141-5p, rno-miR-24-1-5p, and rno-miR-490-5p) were validated by RT-PCR and found to be differentially expressed among the three groups. Expression of ER and PR proteins (immunohistochemistry) in the glandular epithelium and endometrial stroma was significantly different among the three groups (all P < 0.05). Five miRNAs were involved in pathways probably taking part in implantation and fertility.</p><p><b>Conclusions</b>The results suggested that miRNAs, ER, and PR could play important roles in the embryo implantation period of rats with endometriosis. These miRNAs might play a role in endometrial receptivity in endometriosis.</p>
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Animais , Feminino , Humanos , Masculino , Gravidez , Ratos , China , Modelos Animais de Doenças , Endometriose , Metabolismo , MicroRNAs , Distribuição Aleatória , Ratos Sprague-Dawley , Receptores de Estrogênio , Metabolismo , Receptores de Progesterona , Metabolismo , Motilidade dos EspermatozoidesRESUMO
Objective To quantify the validity and reliability of the Hong Kong version of the functional test for the Hemiplegic Upper Extremity (FTHUE-HK).Methods Forty-two stroke patients were studied.Patients were assessed twice within one week using the FTHUE-HK,the upper extremity component of Fugl-Meyer movement assessment (FMA) and the modified Barthel index (MBI).The test-retest reliability and inter-rater reliability of the FTHUE-HK were thus quantified.The FTHUE-HK's validity was evaluated according to the correlation between the FTHUE-HK,FMA and MBI results.Results Significant correlations between the three assessments were demonstrated(P≤0.01).The intra-and inter-class correlation coefficients were 0.983 and 0.985 respectively.Conclusion The FTHUE-HK is a simple and useful assessment of the upper extremity function of stroke patients with good validity and reliability.
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Abstract?AIM:To evaluate the pupil light reflex in patients with primary open angle glaucoma, and to investigate the relation between pupil and visual field defect.?METHODS:From July 2014 to October 2015, 115 eyes in 86 patients with primary open angle glaucoma and 23 eyes in 16 healthy individuals were continuously enrolled in this study.All the subjects received comprehensive eye examination, visual field examination ( Humphrey, SITA Standard 24-2 ) and dynamic pupil measurement ( MonCV3 Metrovision) .According to the visual field and the Glaucoma Staging System, the patients with glaucoma were divided into 5 subgroups: stage 1, stage 2, stage 3, stage 4 and stage 5. The parameters of pupillary light reflex were as follows: pupil diameter ( minimum, maximum ) , latency and duration of contraction, latency and duration of dilatation, contraction amplitude, contraction and dilatation speed, and percent of pupil contraction ( PPC ). SPSS 19.0 statistical software was used to analyze the measurement results.?RESULTS:The control group significantly differed from the stage 4 subgroup ( P=0.032 ) and stage 5 subgroup (P=0.014) in terms of minimum pupil diameter; there was significant difference in the pupil contraction speed between groups ( F =648.675, P <0.01 ), and the contraction speed in stage 5 subgroup was significantly lower than those in the other subgroups and control group (P<0.05); the control group significantly differed from the stage 3, stage 4, and stage 5 subgroup in terms of PPC ( P<0.05 ).Pupil contraction speed, PPC and minimum diameter showed correlation with the stages of glaucoma.?CONCLUSION:Pupil contraction ability in patients with primary open angle glaucoma was impaired, and the degree of impairment is related with the degree of visual field defect.
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<p><b>OBJECTIVE</b>To assess the value of color Doppler ultrasound in evaluating the mesenteric lymph nodes in healthy children.</p><p><b>METHODS</b>The mesenteric lymph nodes were examined with color Doppler ultrasonography for 730 randomly selected healthy children under 14 years of age, including 410 boys and 298 girls who did not report any recent medical conditions.</p><p><b>RESULTS</b>Abdominal lymph node detection rate was higher in boys than in girls. Abdominal lymph nodes were detected most often in children between the ages of 1 and 4 years, and the lymph node size decreased gradually with age.</p><p><b>CONCLUSION</b>Color Doppler ultrasonography is valuable for evaluating abdominal lymph nodes in children.</p>
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Criança , Feminino , Humanos , Masculino , Linfonodos , Diagnóstico por Imagem , Mesentério , Diagnóstico por Imagem , Ultrassonografia Doppler em CoresRESUMO
<p><b>OBJECTIVE</b>To compare the enlarged mesenteric lymph nodes in healthy children with those children with mesenteric lymphadenitis.</p><p><b>METHODS</b>According to the diagnostic criteria defining lymph node enlargement as a 5-mm enlargement or greater in the short diameter, 137 healthy children and 148 children with mesenteric lymphadenitis were retrospectively analyzed for mesenteric lymph node enlargement based on the ultrasonographic data.</p><p><b>RESULTS</b>The distribution of enlarged mesenteric lymph nodes was detected in the right lower quadrant (RLQ) in 46.3%, in the para-aortic areas in 19.2%, and in the left lower quadrant (LLQ) in 13.6% of the children. The clusters of lymph nodes between the two groups showed no significant difference in the distribution, age, L/W, longitudinal diameter or clusters, only the short diameter differed significantly between them.</p><p><b>CONCLUSION</b>Enlarged mesenteric lymph nodes are present in many healthy children, which does not necessarily suggests any abnormalities. The mesenteric lymph nodes increase with the age until 6 years and then decrease. The lymph nodes with a short diameter larger than 8 mm may indicate the condition of mesenteric lymphadenitis.</p>
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Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Abdome , Estudos de Casos e Controles , Hipertrofia , Linfonodos , Patologia , Doenças Linfáticas , Diagnóstico , Patologia , Linfadenite Mesentérica , Diagnóstico , Patologia , Mesentério , Estudos RetrospectivosRESUMO
<p><b>BACKGROUND</b>Tumstatin is a novel endogenous angiogenesis inhibitor which is widely studied using purified protein. The current study evaluates the antiangiogenic effects of tumstatin-overexpression plasmid in vitro, reveals the mechanism underlying the vascular endothelial cell growth inhibition and searches for a novel method administering tumstatin persistently.</p><p><b>METHODS</b>The eukaryotic expression plasmid pcDNA-tumstatin encoding tumstatin gene was constructed and transfected to human umbilical vein endothelial cell ECV304 and human renal carcinoma cell ACHN. Expression of tumstatin in the two cell lines was determined by RT-PCR and Western blotting. Vascular endothelial cell proliferation was assessed by CCK-8 assay and cell cycle was analyzed by flow cytometry. To investigate the mechanism by which pcDNA-tumstatin inhibited vascular endothelial cell proliferation in vitro, cyclin D1 protein was detected by Western blotting.</p><p><b>RESULTS</b>DNA sequence confirmed that pcDNA-tumstatin was successfully constructed. RT-PCR and Western blotting indicated that tumstatin could express in the two cell lines effectively. After tumstatin gene transfer, ECV304 cell growth was significantly inhibited and the cell cycle was arrested in G1 phase. And Western blotting showed that pcDNA-tumstatin decreased the level of cyclin D1 protein.</p><p><b>CONCLUSIONS</b>Overexpression of tumstatin mediated by pcDNA 3.1 (+) specially inhibited vascular endothelial cells by arresting vascular endothelial cell in G1 phase resulting from downregulation of cyclin D1 and administration of tumstatin using a gene therapy might be a novel strategy for cancer therapy.</p>
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Humanos , Autoantígenos , Genética , Metabolismo , Western Blotting , Ciclo Celular , Genética , Fisiologia , Linhagem Celular , Linhagem Celular Tumoral , Proliferação de Células , Colágeno Tipo IV , Genética , Metabolismo , Células Endoteliais , Biologia Celular , Metabolismo , Citometria de Fluxo , Plasmídeos , Genética , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
<p><b>OBJECTIVE</b>Angiotensin converting enzyme 2 (ACE2) efficiently hydrolyses the potent vasoconstrictor angiotensin II to vasodilative angiotensin (1-7). We hypothesized that ACE2 overexpression may inhibit inflammation response in atherosclerotic plaque by degrading Ang II into Ang-(1-7).</p><p><b>METHODS</b>Atherosclerosis (AS) plaques were induced in the abdominal aorta of 38 rabbits by endothelial injury and atherogenic diet for 3 months. Rabbits were then underwent injection of a recombinant adenovirus (2.5 x 10(9) pfu/ml) carrying a murine ACE2 gene (Ad-ACE2) through a catheter into the abdominal aortic segments rich in plaques (n = 19) or injection of a control vector Ad-EGFP (n = 19). One month later, all rabbits were sacrificed and plaques from aortic segments were analyzed.</p><p><b>RESULTS</b>ACE2 expression in aortic tissues of the Ad-ACE2 group were confirmed by immunohistochemistry. Macrophage infiltration (13.6% +/- 4.2% vs. 23.6% +/- 6.9%, P < 0.01) and MCP-1 expression (13.2% +/- 0.4% vs. 25.0% +/- 7.4%, P < 0.01) were significantly reduced in Ad-ACE2 group compared to Ad-EGFP group.</p><p><b>CONCLUSIONS</b>Overexpression of ACE2 inhibited atherosclerotic plaque inflammation response in hypercholesterolemic rabbits.</p>