cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.14317655.v1
title: miR-135a inhibits airway inflammatory response in asthmatic mice via regulating JAK/STAT signaling pathway

description: The objective of this study was to investigate the inhibitory effect of miR-135a in regulating JAK/STAT signaling pathway on airway inflammation in asthmatic mice. An asthma model was established by sensitization and stimulation with ovalbumin (OVA), and the corresponding drug intervention was given from the day of stimulation by means of nasal drops. Airway hyperresponsiveness was tested. The content of miR-135a in the lung tissue of mice was detected by RT-PCR. The pathological changes of lung tissue were evaluated by HE staining. Tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-5, and eotaxin in bronchoalveolar lavage fluid (BALF) and lung tissue were detected by ELISA and immunohistochemistry, respectively. The expression of JAK/STAT signaling pathway-related protein in lung tissue was detected by western blot. To further validate the effect of miR-135a overexpression on the JAK/STAT signaling pathway, pathway activators and inhibitors were added. Compared with the OVA group, the airway hyperresponsiveness of the mice was significantly decreased after treatment with the miR-135a agonist. The expression of miR-135a was significantly increased in the lung tissue and the pathological changes of the lung tissue were alleviated. The contents of TNF-α, IL-6, IL-5, and eotaxin in BALF and lung tissues were decreased. The expression of JAK/STAT signaling pathway-related proteins p-JAK3/JAK3, p-STAT1/STAT1, and p-STAT3/STAT3 were significantly reduced in lung tissue (P&lt;0.05). Addition of JAK inhibitor AG490 reduced airway inflammation in asthmatic mice. miR-135a agonists inhibit airway inflammation in asthmatic mice by regulating the JAK/STAT signaling pathway.
DOI: 10.6084/m9.figshare.14317655
title: miR-135a inhibits airway inflammatory response in asthmatic mice via regulating JAK/STAT signaling pathway

description: The objective of this study was to investigate the inhibitory effect of miR-135a in regulating JAK/STAT signaling pathway on airway inflammation in asthmatic mice. An asthma model was established by sensitization and stimulation with ovalbumin (OVA), and the corresponding drug intervention was given from the day of stimulation by means of nasal drops. Airway hyperresponsiveness was tested. The content of miR-135a in the lung tissue of mice was detected by RT-PCR. The pathological changes of lung tissue were evaluated by HE staining. Tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-5, and eotaxin in bronchoalveolar lavage fluid (BALF) and lung tissue were detected by ELISA and immunohistochemistry, respectively. The expression of JAK/STAT signaling pathway-related protein in lung tissue was detected by western blot. To further validate the effect of miR-135a overexpression on the JAK/STAT signaling pathway, pathway activators and inhibitors were added. Compared with the OVA group, the airway hyperresponsiveness of the mice was significantly decreased after treatment with the miR-135a agonist. The expression of miR-135a was significantly increased in the lung tissue and the pathological changes of the lung tissue were alleviated. The contents of TNF-α, IL-6, IL-5, and eotaxin in BALF and lung tissues were decreased. The expression of JAK/STAT signaling pathway-related proteins p-JAK3/JAK3, p-STAT1/STAT1, and p-STAT3/STAT3 were significantly reduced in lung tissue (P&lt;0.05). Addition of JAK inhibitor AG490 reduced airway inflammation in asthmatic mice. miR-135a agonists inhibit airway inflammation in asthmatic mice by regulating the JAK/STAT signaling pathway.
DOI: 10.6084/m9.figshare.14317657
title: Effects of transfusion load and suction pressure on renal function in intraoperative salvage autotransfusion

description: Although some investigations have been performed to determine the effects of transfusion load and suction pressure on renal function during intraoperative salvage autotransfusion, the precise threshold is still undetermined. A total of 625 patients undergoing surgery with the Continuous AutoTransfusion System (CATSplus) were enrolled and divided into groups according to the utilized suction pressure and transfusion volume. Plasma free hemoglobin (FHB) and creatinine clearance (CCr) were assayed to indicate the renal function. Both 0.03 MPa suction (≥4-unit load) and &gt;5 units transfusion changed the levels of FHB and CCr significantly when measured 24 h post-operation compared to pre-operation. Under 0.02 MPa suction (≥4-unit load), the alteration of FHB and CCr returned to normal after 24 h. Under 3 units transfusion, the levels of FHB and CCr at 6 and 12 h post-operation changed significantly compared to pre-operation (P&lt;0.05 or P&lt;0.01, respectively), and this alteration could be restored to normal at 72 h post-operation. After an exhaustive investigation, less than 4 units transfusion and less than 0.03 MPa suction pressure are recommended for intraoperative salvage autotransfusion.
DOI: 10.6084/m9.figshare.14317657.v1
title: Effects of transfusion load and suction pressure on renal function in intraoperative salvage autotransfusion

description: Although some investigations have been performed to determine the effects of transfusion load and suction pressure on renal function during intraoperative salvage autotransfusion, the precise threshold is still undetermined. A total of 625 patients undergoing surgery with the Continuous AutoTransfusion System (CATSplus) were enrolled and divided into groups according to the utilized suction pressure and transfusion volume. Plasma free hemoglobin (FHB) and creatinine clearance (CCr) were assayed to indicate the renal function. Both 0.03 MPa suction (≥4-unit load) and &gt;5 units transfusion changed the levels of FHB and CCr significantly when measured 24 h post-operation compared to pre-operation. Under 0.02 MPa suction (≥4-unit load), the alteration of FHB and CCr returned to normal after 24 h. Under 3 units transfusion, the levels of FHB and CCr at 6 and 12 h post-operation changed significantly compared to pre-operation (P&lt;0.05 or P&lt;0.01, respectively), and this alteration could be restored to normal at 72 h post-operation. After an exhaustive investigation, less than 4 units transfusion and less than 0.03 MPa suction pressure are recommended for intraoperative salvage autotransfusion.
DOI: 10.6084/m9.figshare.14268482
title: miR-92a-3p promotes ox-LDL induced-apoptosis in HUVECs via targeting SIRT6 and activating MAPK signaling pathway

description: Atherosclerosis could be induced by multiple factors, including hypertension, hyperlipidemia, and smoking, and its pathogenesis has not been fully elucidated. MicroRNAs have been shown to possess great anti-atherosclerotic potential, but the precise function of miR-92a-3p in atherosclerosis and its potential molecular mechanism have not been well clarified. Flow cytometry assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) assay were performed to evaluate effects of oxidized low-density lipoprotein (ox-LDL) on proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs), respectively. Malondialdehyde and superoxide dismutase levels in cell lysate were assessed with biochemical kits. The expression levels of miR-92a-3p and Sirtuin6 (SIRT6) in HUVECs exposed to ox-LDL were estimated by real-time quantitative polymerase chain reaction (RT-qPCR). In addition, the protein levels of SIRT6, c-Jun N-terminal kinase (JNK), phosphorylation JNK (p-JNK), p38 mitogen activated protein kinase (p38 MAPK), and phosphorylation p38 MAPK (p-p38 MAPK) were measured by western blot assays. The relationship between miR-92a-3p and SIRT6 was confirmed by dual-luciferase reporter assay. Ox-LDL induced apoptosis and oxidative stress in HUVECs in concentration- and time-dependent manners. Conversely, miR-92a-3p silencing inhibited apoptosis and SIRT6 expression in HUVECs. The overexpression of miR-92a-3p enhanced apoptosis and phosphorylation levels of JNK and p38 MAPK as well as inhibited proliferation in ox-LDL-induced HUVECs. In addition, SIRT6 was a target of miR-92a-3p. miR-92a-3p negatively regulated SIRT6 expression in ox-LDL-induced HUVECs to activate MAPK signaling pathway in vitro. In summary, miR-92a-3p promoted HUVECs apoptosis and suppressed proliferation in ox-LDL-induced HUVECs by targeting SIRT6 expression and activating MAPK signaling pathway.
DOI: 10.6084/m9.figshare.14268482.v1
title: miR-92a-3p promotes ox-LDL induced-apoptosis in HUVECs via targeting SIRT6 and activating MAPK signaling pathway

description: Atherosclerosis could be induced by multiple factors, including hypertension, hyperlipidemia, and smoking, and its pathogenesis has not been fully elucidated. MicroRNAs have been shown to possess great anti-atherosclerotic potential, but the precise function of miR-92a-3p in atherosclerosis and its potential molecular mechanism have not been well clarified. Flow cytometry assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) assay were performed to evaluate effects of oxidized low-density lipoprotein (ox-LDL) on proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs), respectively. Malondialdehyde and superoxide dismutase levels in cell lysate were assessed with biochemical kits. The expression levels of miR-92a-3p and Sirtuin6 (SIRT6) in HUVECs exposed to ox-LDL were estimated by real-time quantitative polymerase chain reaction (RT-qPCR). In addition, the protein levels of SIRT6, c-Jun N-terminal kinase (JNK), phosphorylation JNK (p-JNK), p38 mitogen activated protein kinase (p38 MAPK), and phosphorylation p38 MAPK (p-p38 MAPK) were measured by western blot assays. The relationship between miR-92a-3p and SIRT6 was confirmed by dual-luciferase reporter assay. Ox-LDL induced apoptosis and oxidative stress in HUVECs in concentration- and time-dependent manners. Conversely, miR-92a-3p silencing inhibited apoptosis and SIRT6 expression in HUVECs. The overexpression of miR-92a-3p enhanced apoptosis and phosphorylation levels of JNK and p38 MAPK as well as inhibited proliferation in ox-LDL-induced HUVECs. In addition, SIRT6 was a target of miR-92a-3p. miR-92a-3p negatively regulated SIRT6 expression in ox-LDL-induced HUVECs to activate MAPK signaling pathway in vitro. In summary, miR-92a-3p promoted HUVECs apoptosis and suppressed proliferation in ox-LDL-induced HUVECs by targeting SIRT6 expression and activating MAPK signaling pathway.
DOI: 10.6084/m9.figshare.14317661.v1
title: Suppressive effect of platycodin D on bladder cancer through microRNA-129-5p-mediated PABPC1/PI3K/AKT axis inactivation

description: Platycodin D (PD) is a major constituent of Platycodon grandiflorum and has multiple functions in disease control. This study focused on the function of PD in bladder cancer cell behaviors and the molecules involved. First, we administered PD to the bladder cancer cell lines T24 and 5637 and the human uroepithelial cell line SV-HUC-1. Cell viability and growth were evaluated using MTT, EdU, and colony formation assays, and cell apoptosis was determined using Hoechst 33342 staining and flow cytometry. The microRNAs (miRNAs) showing differential expression in cells before and after PD treatment were screened. Moreover, we altered the expression of miR-129-5p and PABPC1 to identify their functions in bladder cancer progression. We found that PD specifically inhibited the proliferation and promoted the apoptosis of bladder cancer cells; miR-129-5p was found to be partially responsible for the cancer-inhibiting properties of PD. PABPC1, a direct target of miR-129-5p, was abundantly expressed in T24 and 5637 cell lines and promoted cell proliferation and suppressed cell apoptosis. In addition, PABPC1 promoted the phosphorylation of PI3K and AKT in bladder cancer cells. Altogether, PD had a concentration-dependent suppressive effect on bladder cancer cell growth and was involved in the upregulation of miR-129-5p and the subsequent inhibition of PABPC1 and inactivation of PI3K/AKT signaling.
DOI: 10.6084/m9.figshare.14317661
title: Suppressive effect of platycodin D on bladder cancer through microRNA-129-5p-mediated PABPC1/PI3K/AKT axis inactivation

description: Platycodin D (PD) is a major constituent of Platycodon grandiflorum and has multiple functions in disease control. This study focused on the function of PD in bladder cancer cell behaviors and the molecules involved. First, we administered PD to the bladder cancer cell lines T24 and 5637 and the human uroepithelial cell line SV-HUC-1. Cell viability and growth were evaluated using MTT, EdU, and colony formation assays, and cell apoptosis was determined using Hoechst 33342 staining and flow cytometry. The microRNAs (miRNAs) showing differential expression in cells before and after PD treatment were screened. Moreover, we altered the expression of miR-129-5p and PABPC1 to identify their functions in bladder cancer progression. We found that PD specifically inhibited the proliferation and promoted the apoptosis of bladder cancer cells; miR-129-5p was found to be partially responsible for the cancer-inhibiting properties of PD. PABPC1, a direct target of miR-129-5p, was abundantly expressed in T24 and 5637 cell lines and promoted cell proliferation and suppressed cell apoptosis. In addition, PABPC1 promoted the phosphorylation of PI3K and AKT in bladder cancer cells. Altogether, PD had a concentration-dependent suppressive effect on bladder cancer cell growth and was involved in the upregulation of miR-129-5p and the subsequent inhibition of PABPC1 and inactivation of PI3K/AKT signaling.
DOI: 10.6084/m9.figshare.14317667.v1
title: The essential oil of Hyptis crenata Pohl ex Benth. presents an antiedematogenic effect in mice

description: Hyptis crenata, commonly known as “salva-do-Marajó”, “hortelã-do-campo”, and “hortelãzinha”, is used in folk medicine in Northeast Brazil as tea or infusion to treat inflammatory diseases. Due to the pharmacological efficacy and the low toxicity of the essential oil of Hyptis crenata (EOHc), we decided to investigate the EOHc antiedematogenic effect in experimental models of inflammation. EOHc was administrated orally at doses of 10-300 mg/kg to male Swiss albino mice. Paw edema was induced by subcutaneous injection in the right hind paw of inflammatory stimuli (carrageenan, dextran, histamine, serotonin, and bradykinin) 60 min after administration of EOHc. EOHc significantly inhibited the induced edema. The inhibitory effect of EOHc on dextran-induced edema extended throughout the experimental time. For the 30, 100, and 300 mg/kg doses of EOHc, the inhibition was of 40.28±1.70, 51.18±2.69, and 59.24±2.13%, respectively. The EOHc inhibitory effect on carrageenan-induced edema started at 10 mg/kg at the second hour (h) and was maintained throughout the observation period. At 30, 100, and 300 mg/kg doses the inhibition started earlier, from 30 min. At the edema peak of 180 min, 56, 76, and 82% inhibition was observed for 30, 100, and 300 mg/kg doses, respectively. Additionally, the effect of EOHc on carrageenan-induced paw edema was influenced by the time of administration. The EOHc also inhibited myeloperoxidase activity. In conclusion, the EOHc showed a potent effect, both preventing and reversing the edema, consistent with its anti-inflammatory use in folk medicine.
DOI: 10.6084/m9.figshare.14317667
title: The essential oil of Hyptis crenata Pohl ex Benth. presents an antiedematogenic effect in mice

description: Hyptis crenata, commonly known as “salva-do-Marajó”, “hortelã-do-campo”, and “hortelãzinha”, is used in folk medicine in Northeast Brazil as tea or infusion to treat inflammatory diseases. Due to the pharmacological efficacy and the low toxicity of the essential oil of Hyptis crenata (EOHc), we decided to investigate the EOHc antiedematogenic effect in experimental models of inflammation. EOHc was administrated orally at doses of 10-300 mg/kg to male Swiss albino mice. Paw edema was induced by subcutaneous injection in the right hind paw of inflammatory stimuli (carrageenan, dextran, histamine, serotonin, and bradykinin) 60 min after administration of EOHc. EOHc significantly inhibited the induced edema. The inhibitory effect of EOHc on dextran-induced edema extended throughout the experimental time. For the 30, 100, and 300 mg/kg doses of EOHc, the inhibition was of 40.28±1.70, 51.18±2.69, and 59.24±2.13%, respectively. The EOHc inhibitory effect on carrageenan-induced edema started at 10 mg/kg at the second hour (h) and was maintained throughout the observation period. At 30, 100, and 300 mg/kg doses the inhibition started earlier, from 30 min. At the edema peak of 180 min, 56, 76, and 82% inhibition was observed for 30, 100, and 300 mg/kg doses, respectively. Additionally, the effect of EOHc on carrageenan-induced paw edema was influenced by the time of administration. The EOHc also inhibited myeloperoxidase activity. In conclusion, the EOHc showed a potent effect, both preventing and reversing the edema, consistent with its anti-inflammatory use in folk medicine.
DOI: 10.6084/m9.figshare.14317669.v1
title: Obesity as a predictive factor for chronic kidney disease in adults: systematic review and meta-analysis

description: Chronic kidney disease (CKD) is one of the main chronic diseases affecting the world population due to its high prevalence and increasing morbidity. Similarly, obesity gained the interest of the scientific community as it directly or indirectly increases mortality from cardiovascular causes, and its prevalence characterizes a pandemic. The objective of this study was to investigate obesity measured by body mass index as a predictor for end-stage renal disease in the general adult population. A systematic review and meta-analysis was carried out by searching 10 databases for prospective or retrospective cohort studies, with no restrictions on the language of publication, including adults with obesity without previous renal disease and who evolved to CKD (diagnosed by estimated glomerular filtration rate below 60 mL&mac_middot;min-1&mac_middot;(1.73 m2)-1 over the follow-up period. The R software and Meta package were used for data analysis. After removing duplicates, 5431 studies were submitted to the steps of the systematic review, and 21 articles were included in the data analysis. In total, 3,504,303 patients, 521,216 with obesity, and an average follow-up time of 9.86 years were included. The relative risk of obese people for developing CKD in the random effects model was 1.81 (95%CI: 1.52-2.16). The evidence found in this meta-analysis confirmed that obese people are at higher risk of developing CKD that the non-obese population (1.81 times higher), with obesity being a priority risk factor in preventive actions.
DOI: 10.6084/m9.figshare.14317669
title: Obesity as a predictive factor for chronic kidney disease in adults: systematic review and meta-analysis

description: Chronic kidney disease (CKD) is one of the main chronic diseases affecting the world population due to its high prevalence and increasing morbidity. Similarly, obesity gained the interest of the scientific community as it directly or indirectly increases mortality from cardiovascular causes, and its prevalence characterizes a pandemic. The objective of this study was to investigate obesity measured by body mass index as a predictor for end-stage renal disease in the general adult population. A systematic review and meta-analysis was carried out by searching 10 databases for prospective or retrospective cohort studies, with no restrictions on the language of publication, including adults with obesity without previous renal disease and who evolved to CKD (diagnosed by estimated glomerular filtration rate below 60 mL&mac_middot;min-1&mac_middot;(1.73 m2)-1 over the follow-up period. The R software and Meta package were used for data analysis. After removing duplicates, 5431 studies were submitted to the steps of the systematic review, and 21 articles were included in the data analysis. In total, 3,504,303 patients, 521,216 with obesity, and an average follow-up time of 9.86 years were included. The relative risk of obese people for developing CKD in the random effects model was 1.81 (95%CI: 1.52-2.16). The evidence found in this meta-analysis confirmed that obese people are at higher risk of developing CKD that the non-obese population (1.81 times higher), with obesity being a priority risk factor in preventive actions.
DOI: 10.6084/m9.figshare.14317670
title: The value of preoperative systemic immune-inflammation index in predicting vascular invasion of hepatocellular carcinoma: a meta-analysis

description: Vascular invasion and systemic immune-inflammation index (SII) are risk factors for the prognosis of patients with hepatocellular carcinoma. At present, the correlation between the two is not clear. This meta-analysis explored the relationship between preoperative SII and vascular invasion in patients with hepatocellular carcinoma. According to the search formula, the Pubmed, Embase, Cochrane, Web of Science, and CNKI databases were searched for the relevant research until March 2020. After the quality evaluation of the included literature, the odds ratio (OR) and its corresponding 95% confidence interval (CI) were used as the effect measure. Stata 15. 0 software was used for statistical analysis. The meta-analysis eventually included seven retrospective cohort studies of 3583 patients with hepatocellular carcinoma. The results showed that the choice of SII cut-off value affects SII's efficiency in predicting the risk of vascular invasion. In the cohort of studies with appropriate SII cut-off value, the high SII preoperative group had a higher risk of vascular invasion (OR=2.62; 95%CI: 2.07-3.32; P=0.000) and microvascular invasion (OR=1.82; 95%CI: 1.01-3.25; P=0.045) than the low SII group. The tumor diameter (OR=2.88; 95%CI: 1.73-4. 80; P=0.000) of the high SII group was larger than that of the low SII group. There was no publication bias in this study (Begg's test, P=0.368). As a routine, cheap, and easily available index, SII can provide a certain reference value for clinicians to evaluate vascular invasion before operation.
DOI: 10.6084/m9.figshare.14317670.v1
title: The value of preoperative systemic immune-inflammation index in predicting vascular invasion of hepatocellular carcinoma: a meta-analysis

description: Vascular invasion and systemic immune-inflammation index (SII) are risk factors for the prognosis of patients with hepatocellular carcinoma. At present, the correlation between the two is not clear. This meta-analysis explored the relationship between preoperative SII and vascular invasion in patients with hepatocellular carcinoma. According to the search formula, the Pubmed, Embase, Cochrane, Web of Science, and CNKI databases were searched for the relevant research until March 2020. After the quality evaluation of the included literature, the odds ratio (OR) and its corresponding 95% confidence interval (CI) were used as the effect measure. Stata 15. 0 software was used for statistical analysis. The meta-analysis eventually included seven retrospective cohort studies of 3583 patients with hepatocellular carcinoma. The results showed that the choice of SII cut-off value affects SII's efficiency in predicting the risk of vascular invasion. In the cohort of studies with appropriate SII cut-off value, the high SII preoperative group had a higher risk of vascular invasion (OR=2.62; 95%CI: 2.07-3.32; P=0.000) and microvascular invasion (OR=1.82; 95%CI: 1.01-3.25; P=0.045) than the low SII group. The tumor diameter (OR=2.88; 95%CI: 1.73-4. 80; P=0.000) of the high SII group was larger than that of the low SII group. There was no publication bias in this study (Begg's test, P=0.368). As a routine, cheap, and easily available index, SII can provide a certain reference value for clinicians to evaluate vascular invasion before operation.