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OBJECTIVES@#To study the influence of umbilical cord milking versus delayed cord clamping on the early prognosis of preterm infants with a gestational age of <34 weeks.@*METHODS@#PubMed, Web of Science, Embase, the Cochrane Library, CINAHL, China National Knowledge Infrastructure, Wanfang Data, Weipu Database, and SinoMed were searched for randomized controlled trials on umbilical cord milking versus delayed cord clamping in preterm infants with a gestational age of <34 weeks published up to November 2021. According to the inclusion and exclusion criteria, two researchers independently performed literature screening, quality evaluation, and data extraction. Review Manger 5.4 was used for Meta analysis.@*RESULTS@#A total of 11 articles were included in the analysis, with 1 621 preterm infants in total, among whom there were 809 infants in the umbilical cord milking group and 812 in the delayed cord clamping group. The Meta analysis showed that compared with delayed cord clamping, umbilical cord milking increased the mean blood pressure after birth (weighted mean difference=3.61, 95%CI: 0.73-6.50, P=0.01), but it also increased the incidence rate of severe intraventricular hemorrhage (RR=1.83, 95%CI: 1.08-3.09, P=0.02). There were no significant differences between the two groups in hemoglobin, hematocrit, blood transfusion rate, proportion of infants undergoing phototherapy, bilirubin peak, and incidence rates of complications such as periventricular leukomalacia and necrotizing enterocolitis (P>0.05).@*CONCLUSIONS@#Compared with delayed cord clamping, umbilical cord milking may increase the risk of severe intraventricular hemorrhage in preterm infants with a gestational age of <34 weeks; however, more high-quality large-sample randomized controlled trials are needed for further confirmation.
Subject(s)
Female , Humans , Infant , Infant, Newborn , Pregnancy , Cerebral Hemorrhage , Constriction , Gestational Age , Infant, Premature , Prognosis , Umbilical Cord/physiology , Umbilical Cord ClampingABSTRACT
BACKGROUND@#Acitretin and matrine have been used in the treatment of psoriasis in China. This study was designed to investigate the role and related mechanisms of matrine alone and in combination with acitretin in the treatment of psoriasis in vitro and in vivo.@*METHODS@#HaCaT cells were treated with matrine at different concentrations of 0 (blank control), 0.2, 0.4, 0.8, and 1.6 mg/mL for 24, 48, 72 h, respectively. 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium cell viability assay was used to assess the growth and proliferation of HaCaT cells. Cell cycle and apoptosis were detected by flow cytometry. Expression of protein was detected by Western blotting. Autophagy was observed by transmission electron microscopy. Then HaCaT cells were assigned to normal saline (NS) control group, matrine (0.4 mg/mL) group, acitretin (10 μmol/L) group, and matrine plus acitretin group, and the above methods were repeated. In animal experiments, the cumulative score (erythema, scaling, thickening) as a measure of the severity of inflammation was used to measure the skin performance of mice after treated with matrine 50 mg/kg, acitretin 4.5 mg/kg or combination of the two drugs on the psoriasis-like mouse models, respectively. Pathological findings of the lesions were observed, and the protein expressions in the lesions were detected by immunohistochemistry.@*RESULTS@#Cell proliferation inhibition was seen in HaCaT cells with treatment of matrine in a dose- and time-dependent manner (P < 0.01, respectively). Cell cycle G0/G1 phase arrest was observed in a dose-dependent way (P < 0.01). The expression of p21 (P < 0.05), LC3II/I (P < 0.01), and Beclin 1 (P < 0.01) increased and the expression of cyclin D1 (P < 0.05) decreased with increasing doses of matrine. Compared with the blank control, more autophagosomes were seen in HaCaT cells treated with matrine at 0.4 mg/mL by transmission electron microscopy (2.667 ± 1.202 vs. 21.33 ± 1.453, t = 9.899, P < 0.01). Cell proliferation inhibition and degree of the G0/G1 phase arrest was significantly higher in matrine plus acitretin group than those in matrine, acitretin, or the NS control group (P < 0.01, respectively). Compared with matrine or acitretin group, the expression of p21 (P < 0.05, P < 0.05) and LC3II/I (P < 0.01, P < 0.05) in matrine plus acitretin group increased significantly and the expression of cyclin D1 (P < 0.01, P < 0.05) and p62 (P < 0.05, P < 0.05) was reduced significantly. Compared with matrine or acitretin, matrine plus acitretin significantly down-regulated the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway (P < 0.05) and its downstream p-p70S6K (P < 0.05). In addition, the cumulative score of mice in the matrine plus acitretin group was significantly better than that in the matrine or acitretin group (1.480 ± 0.230 vs. 2.370 ± 0.241, P < 0.01; 1.480 ± 0.230 vs. 2.888 ± 0.341, P < 0.01). The expression of LC3 protein in the matrine plus acitretin group was also higher than that in the matrine, acitretin, or the NS control group (P < 0.05, respectively).@*CONCLUSIONS@#Matrine has therapeutic potentials for psoriasis. Matrine and acitretin show synergistic effect via cell cycle arrest and autophagy induction by PI3K/Akt/mTOR pathway.
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ObjectiveTo analyze the relationship between the factors causing thoracolumbar burst fracture and the corresponding clinical manifestations, so as to improve the early warning and diagnosis of thoracolumbar burst fracture, reduce the misdiagnosis and missed diagnosis, and improve the success rate of first aid. MethodsThe clinical data of thoracolumbar burst fractures treated in the Intensive Care Unit of Depretment of Emergency of our hospital from Jan. 2009 to Dec. 2018 were retrospectively analyzed. The clinical data, including age, sex, hospital duration, causes, complications, discharge, and prognosis, were analyzed retrospectively. Results A total of 83 patients with thoracolumbar burst fracture, including 69 males (83.13%) and 14 females (16.87%), were selected for this study. The average age was (44.64±15.26) years. The causes of the injury included: High falling injury (53 cases, 63.86%), traffic accident injury (17 cases, 20.48%), and heavy object injury (12 cases, 14.46%). There were 31 cases (37.35%) of craniocerebral injury, 53 cases (63.86%) of chest injury, 37 cases (44.58%) of abdominal injury, 44 cases (53.01%) of other fracture. Among the 53 cases of chest injury, there were 19 cases (35.85%) with hemopneumothorax, 13 cases (13.21%) with simple hemothorax, 7 cases (24.53%) with simple pneumothorax, 8 cases (15.09%) with mediastinal hemorrhage, 7 cases (13.21%) with mediastinal emphysema, 11 cases (20.75%) with flail chest, and 5 cases (9.43%) with diaphragmatic hernia. Among 37 cases of abdominal injuries, there were 8 cases (21.62%) with rupture of spleen, 3 cases (8.11%) with subcapsule hematomas, and 4 cases (10.81%) with simultaneous injury of liver and spleen. The missed diagnoses at the initial diagnosis included: 5 cases (100.00%) of diaphragmatic hernia, 5 cases (62.50%) of mediastinal hemorrhage, 4 cases (57.14%) of mediastinal emphysema, 2 cases (18.18%) of flail chest, and 2 cases (15.38%) of simple hemothorax. Missed diagnosis rate of the other complications were all under 10.00%. The main complications were bronchopneumonia (37 cases, 44.58%) and traumatic hemorrhagic shock (17 cases, 20.48%). There were 8 cases (9.64%) complicated with multiple organ dysfunction syndrome (MODS), with more than 3 systems involved. There were 39 patients (46.99%) had paraplegia and 3 cases (3.61%) died at discharge. ConclusionThoracolumbar burst fractures are more common in young and middle-aged men, with high falling being the primary cause and hemopneumothorax being the main clinical manifestation. Diaphragmatic hernia, mediastinal hemorrhage and mediastinal emphysema are easy to have missed diagnosis. Nearly 50% patients have traumatic paraplegia, which is worthy of attention and in-depth study.
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Background@#Acitretin and matrine have been used in the treatment of psoriasis in China. This study was designed to investigate the role and related mechanisms of matrine alone and in combination with acitretin in the treatment of psoriasis in vitro and in vivo.@*Methods@#HaCaT cells were treated with matrine at different concentrations of 0 (blank control), 0.2, 0.4, 0.8, and 1.6 mg/mL for 24, 48, 72 h, respectively. 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium cell viability assay was used to assess the growth and proliferation of HaCaT cells. Cell cycle and apoptosis were detected by flow cytometry. Expression of protein was detected by Western blotting. Autophagy was observed by transmission electron microscopy. Then HaCaT cells were assigned to normal saline (NS) control group, matrine (0.4 mg/mL) group, acitretin (10 μmol/L) group, and matrine plus acitretin group, and the above methods were repeated. In animal experiments, the cumulative score (erythema, scaling, thickening) as a measure of the severity of inflammation was used to measure the skin performance of mice after treated with matrine 50 mg/kg, acitretin 4.5 mg/kg or combination of the two drugs on the psoriasis-like mouse models, respectively. Pathological findings of the lesions were observed, and the protein expressions in the lesions were detected by immunohistochemistry.@*Results@#Cell proliferation inhibition was seen in HaCaT cells with treatment of matrine in a dose- and time-dependent manner (P < 0.01, respectively). Cell cycle G0/G1 phase arrest was observed in a dose-dependent way (P < 0.01). The expression of p21 (P < 0.05), LC3II/I (P < 0.01), and Beclin 1 (P < 0.01) increased and the expression of cyclin D1 (P < 0.05) decreased with increasing doses of matrine. Compared with the blank control, more autophagosomes were seen in HaCaT cells treated with matrine at 0.4 mg/mL by transmission electron microscopy (2.667 ± 1.202 vs. 21.33 ± 1.453, t = 9.899, P < 0.01). Cell proliferation inhibition and degree of the G0/G1 phase arrest was significantly higher in matrine plus acitretin group than those in matrine, acitretin, or the NS control group (P < 0.01, respectively). Compared with matrine or acitretin group, the expression of p21 (P < 0.05, P < 0.05) and LC3II/I (P < 0.01, P < 0.05) in matrine plus acitretin group increased significantly and the expression of cyclin D1 (P < 0.01, P < 0.05) and p62 (P < 0.05, P < 0.05) was reduced significantly. Compared with matrine or acitretin, matrine plus acitretin significantly down-regulated the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway (P < 0.05) and its downstream p-p70S6K (P < 0.05). In addition, the cumulative score of mice in the matrine plus acitretin group was significantly better than that in the matrine or acitretin group (1.480 ± 0.230 vs. 2.370 ± 0.241, P < 0.01; 1.480 ± 0.230 vs. 2.888 ± 0.341, P < 0.01). The expression of LC3 protein in the matrine plus acitretin group was also higher than that in the matrine, acitretin, or the NS control group (P < 0.05, respectively).@*Conclusions@#Matrine has therapeutic potentials for psoriasis. Matrine and acitretin show synergistic effect via cell cycle arrest and autophagy induction by PI3K/Akt/mTOR pathway.
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<p><b>OBJECTIVE</b>To study the protective effect of lipoxin A4 (LXA4) against sepsis induced by lipopolysaccharide (LPS) in rats with obesity and its effect on the expression of Toll-like receptor 4 (TLR4) and TNF receptor-associated factor 6 (TRAF6) in the liver.</p><p><b>METHODS</b>A total of 60 male Sprague-Dawley rats aged three weeks were randomly divided into a normal group and an obesity group, with 30 rats in each group. A rat model of obesity was established by high-fat diet. Each of the two groups was further randomly divided into control group, sepsis group, and LXA4 group, and 8 rats were selected from each group. The rats in the control, sepsis, and LXA4 groups were treated with intraperitoneal injection of normal saline, LPS, and LXA4+LPS respectively. Twelve hours later, blood samples were collected from the heart and liver tissue samples were also collected. ELISA was used to measure the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Western blot was used to measure the protein expression of TLR4 and TRAF6 in liver tissue. Quantitative real-time PCR was used to measure the mRNA expression of TLR4 and TRAF6.</p><p><b>RESULTS</b>After being fed with high-fat diet for 6 weeks, the obesity group had significantly higher average weight and Lee's index than the normal group (P<0.05). Compared with the normal group, the obesity group had significant increases in the serum levels of IL-6 and TNF-α (P<0.05). In the normal group or the obesity group, the sepsis subgroup had significant increases in the serum levels of IL-6 and TNF-α compared with the control subgroup (P<0.05), while the LXA4 subgroup had significant reductions in the two indices compared with the sepsis subgroup (P<0.05). Compared with the normal group, the obesity group had significant increases in the protein and mRNA expression of TLR4 and TRAF6 (P<0.05). In the normal group or the obesity group, the sepsis subgroup had significant increases in the protein and mRNA expression of TLR4 and TRAF6 compared with the control subgroup (P<0.05). Compared with the sepsis subgroup, the LXA4 subgroup had significant reductions in the protein and mRNA expression of TLR4 and TRAF6 (P<0.05).</p><p><b>CONCLUSIONS</b>LXA4 can reduce the serum levels of IL-6 and TNF-α and alleviate inflammatory response. LXA4 can inhibit the expression of TLR4 and TRAF6 in the liver of septic rats, possibly by inhibiting the TLR4 signaling pathway.</p>
Subject(s)
Animals , Humans , Male , Rats , Interleukin-6 , Genetics , Metabolism , Lipoxins , Liver , Metabolism , Obesity , Drug Therapy , Genetics , Metabolism , Rats, Sprague-Dawley , Sepsis , Drug Therapy , Genetics , Metabolism , Signal Transduction , TNF Receptor-Associated Factor 6 , Genetics , Metabolism , Toll-Like Receptor 4 , Genetics , Metabolism , Tumor Necrosis Factor-alpha , Genetics , MetabolismABSTRACT
Chemical constituents of the roots of Ficus stenophylla were isolated and purified by repeated column chromatography on silica gel and Sephadex LH-20. Their structures were elucidated based on physicochemical and spectral data. Five compounds were identified as methyl 3-(6-hydroxy-4-methoxybenzofuran-5-yl) propanoate (1), kaemferol (2), kampferol 3-O-beta-D-glucoside (3), quercetin (4) and tricin (5), separately. Compound 1 is a new phenylpropionic acid derivatives. All compounds were obtained from this plant for the first time.
Subject(s)
Benzofurans , Chemistry , Ficus , Chemistry , Flavonoids , Magnetic Resonance Spectroscopy , Methods , Plant Extracts , Plant Roots , Chemistry , Plants, Medicinal , Chemistry , Propionates , Chemistry , QuercetinABSTRACT
<p><b>OBJECTIVE</b>To explore the role of hepatitis C virus core protein on the infiltration and metastasis of cholangiocarcinoma tissues.</p><p><b>METHODS</b>From January 2001 to November 2006, 34 patients with cholangiocarcinoma who had intact follow-up data randomly were chosen. The expression of HCVc protein, epithelium markers and mesenchymal markers in cholangiocarcinoma tissues were examined by SP methods of immunohistochemistry, clinical-pathological data were recorded and analyzed.</p><p><b>RESULTS</b>The positive expression rate was observed in 47.1% for HCVc protein, 50% for N-cadherin, 44.1% for Vimentin, 55.9% for Fibronectin and the decreased expression rate was E-cadherin for 55.9%, alpha-catenin for 70.6%, beta-catenin for 55.9%. The positive expression of HCVc protein was associated with the decreased expression of E-cadherin, alpha-catenin and the positive expression of N-cadherin, Vimentin, Fibronectin (chi(2) = 4.480, 4.163, 4.250, 7.438, 12.260, P < 0.05). A positive-correlation between the expression of HCVc protein and metastasis of lymph nodes and other organs were found (chi(2) = 5.708, 4.163, P < 0.05).</p><p><b>CONCLUSION</b>HCVc protein might promote cholangiocarcinoma tissues' infiltration and metastasis by inducing it's epithelial-mesenchymal transition.</p>