cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.6026735
title: Maternal genetic backgrounds contribute to the genetic susceptibility of tongue cancer patients in Hunan, central of China

description: Mitochondrial DNA (mtDNA) mutations played crucial roles on affecting the susceptibility to cancer. In this study, to investigate whether mitochondrial DNA mutations contributed to the genetic susceptibility of Chinese tongue cancer patients, mtDNA control regions of 105 Chinese tongue cancer patients were amplified and sequenced, the mutations were recorded by comparing with the revised Cambridge Reference Sequence (rCRS), which were attributed to certain mtDNA haplogroups based on the specific variations motif of each patients. The Miao Chinese group (a Chinese ethnic minority) from surrounding region has no essential difference with tongue cancer group, which was taken as the matched control group with principal component analysis by taking the haplogroups frequency of 105 tongue cancer individuals and 354 healthy individuals of eight groups from the similar geographic regions as input factors. This was supported by the smallest genetic distance between tongue cancer and Miao_2 groups. Further, the statistical analysis based on mtDNA variations of hypervariable sequence I (HVSI) indicated that 13 variations including 16,124, 16,148, 16,182C, 16,183C, 16,227, 16,266A, 16,249, 16,272, 16,291, 16,327, 16,335, 16,497, and 16,519 have significant differences between tongue cancer group and matched control group. Comparison of mtDNA haplogroups between tongue cancer and control groups indicated that mtDNA haplogroups C, F2*, and M10 have significant differences. It’s worth noting that 16,327 and 16,291 was the defining variation of haplogroups C and F2*, respectively. Our results suggested that mitochondrial DNA may play a crucial role for the maternal genetic susceptibility of tongue cancer patients from Hunan, central of China.
DOI: 10.25582/data.2023-02.2732349/2305105
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.21755418
title: Protection of intestinal immune barrier against ischemia/reperfusion injury in a swine model using anisodamine hydrobromide

description: Abstract Intestinal ischemia/reperfusion (I/R) causes barrier impairment and bacterial influx. This study explored the protective effects of anisodamine hydrobromide (AH) on intestinal I/R injury caused by cardiopulmonary resuscitation (CPR) after cardiac arrest (CA). After successful CPR, minipigs were randomly divided into two groups (n = 8): saline and AH (4 mg/kg), and then treated with saline or AH via central venous injection, respectively. The same procedures without ventricular fibrillation initiation were conducted in the Sham group (n = 8). Levels of interferon gamma (IFN-γ) and interleukin 4 (IL-4) were measured at different time points (0, 0.5, 1, 2, 4, and 6 h) in serum and 6 h in gut associated lymphoid tissues (GALTs) after the return of spontaneous circulation (ROSC) to evaluate changes in the proportion of T-helper type 1 (Th1) and T-helper type 2 (Th2). Moreover, the positive culture rates of GALTs were examined to evaluate bacterial translocation. AH treatment markedly alleviated aberrant arterial blood gas and hemodynamics as well as intestinal macroscopic and morphological changes after CPR. Moreover, AH treatment significantly increased IFN-γ and decreased IL-4 in both serum and GALTs. Furthermore, AH treatment dramatically decreased positive bacterial growth in GALTs. AH treatment mitigated immunosuppression caused by intestinal I/R and protected the intestinal immune barrier against bacterial translocation, thereby reducing the risk of secondary intestinal infection.
DOI: 10.6084/m9.figshare.21755418.v1
title: Protection of intestinal immune barrier against ischemia/reperfusion injury in a swine model using anisodamine hydrobromide

description: Abstract Intestinal ischemia/reperfusion (I/R) causes barrier impairment and bacterial influx. This study explored the protective effects of anisodamine hydrobromide (AH) on intestinal I/R injury caused by cardiopulmonary resuscitation (CPR) after cardiac arrest (CA). After successful CPR, minipigs were randomly divided into two groups (n = 8): saline and AH (4 mg/kg), and then treated with saline or AH via central venous injection, respectively. The same procedures without ventricular fibrillation initiation were conducted in the Sham group (n = 8). Levels of interferon gamma (IFN-γ) and interleukin 4 (IL-4) were measured at different time points (0, 0.5, 1, 2, 4, and 6 h) in serum and 6 h in gut associated lymphoid tissues (GALTs) after the return of spontaneous circulation (ROSC) to evaluate changes in the proportion of T-helper type 1 (Th1) and T-helper type 2 (Th2). Moreover, the positive culture rates of GALTs were examined to evaluate bacterial translocation. AH treatment markedly alleviated aberrant arterial blood gas and hemodynamics as well as intestinal macroscopic and morphological changes after CPR. Moreover, AH treatment significantly increased IFN-γ and decreased IL-4 in both serum and GALTs. Furthermore, AH treatment dramatically decreased positive bacterial growth in GALTs. AH treatment mitigated immunosuppression caused by intestinal I/R and protected the intestinal immune barrier against bacterial translocation, thereby reducing the risk of secondary intestinal infection.
DOI: 10.6084/m9.figshare.6026735.v1
title: Maternal genetic backgrounds contribute to the genetic susceptibility of tongue cancer patients in Hunan, central of China

description: Mitochondrial DNA (mtDNA) mutations played crucial roles on affecting the susceptibility to cancer. In this study, to investigate whether mitochondrial DNA mutations contributed to the genetic susceptibility of Chinese tongue cancer patients, mtDNA control regions of 105 Chinese tongue cancer patients were amplified and sequenced, the mutations were recorded by comparing with the revised Cambridge Reference Sequence (rCRS), which were attributed to certain mtDNA haplogroups based on the specific variations motif of each patients. The Miao Chinese group (a Chinese ethnic minority) from surrounding region has no essential difference with tongue cancer group, which was taken as the matched control group with principal component analysis by taking the haplogroups frequency of 105 tongue cancer individuals and 354 healthy individuals of eight groups from the similar geographic regions as input factors. This was supported by the smallest genetic distance between tongue cancer and Miao_2 groups. Further, the statistical analysis based on mtDNA variations of hypervariable sequence I (HVSI) indicated that 13 variations including 16,124, 16,148, 16,182C, 16,183C, 16,227, 16,266A, 16,249, 16,272, 16,291, 16,327, 16,335, 16,497, and 16,519 have significant differences between tongue cancer group and matched control group. Comparison of mtDNA haplogroups between tongue cancer and control groups indicated that mtDNA haplogroups C, F2*, and M10 have significant differences. It’s worth noting that 16,327 and 16,291 was the defining variation of haplogroups C and F2*, respectively. Our results suggested that mitochondrial DNA may play a crucial role for the maternal genetic susceptibility of tongue cancer patients from Hunan, central of China.
DOI: 10.25582/data.2023-01.2708298/2305106
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2708337/2305107
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.7075361
title: Decreased serum PON1 arylesterase activity in familial hypercholesterolemia patients with a mutated LDLR gene

description: Abstract Paraoxonase 1 (PON1) is a serum enzyme associated with high density lipoprotein (HDL) regulation through its paraoxonase and arylesterase activity. PON1 inhibits the oxidation of HDL and low density lipoprotein (LDL), and is involved in the pathogenesis of a variety of diseases including atherosclerosis. Conversely, mutations in the low density lipoprotein receptor (LDLR) result in failure of receptor mediated endocytosis of LDL leading to its elevated plasma levels and onset of familial hypercholesterolemia (FH). In the current study we investigated the role of PON1 polymorphisms rs662; c.575A &gt; G (p.Gln192Arg) and rs854560; c.163T &gt; A (p.Leu55Met) in a large family having FH patients harboring a functional mutation in LDLR. Genotypes were revealed by RFLP, followed by confirmation through Sanger sequencing. PON1 activity was measure by spectrophotometry. Our results show significantly reduced serum paraoxonase and arylesterase activities in FH patients compared with the healthy individuals of the family (p &lt; 0.05). PON1 QQ192 genotype showed a significantly higher association with FH (p=0.0002). PON1 Q192 isoform was associated with reduced serum paraoxonase activity by in silico analysis and PON1 R192 exhibited higher serum paraoxonase and arylesterase activity than the other polymorphs. Our results highlight that the combination of LDLR mutations and PON1 MMQQ genotypes may lead to severe cardiac events.
DOI: 10.6084/m9.figshare.7075361.v1
title: Decreased serum PON1 arylesterase activity in familial hypercholesterolemia patients with a mutated LDLR gene

description: Abstract Paraoxonase 1 (PON1) is a serum enzyme associated with high density lipoprotein (HDL) regulation through its paraoxonase and arylesterase activity. PON1 inhibits the oxidation of HDL and low density lipoprotein (LDL), and is involved in the pathogenesis of a variety of diseases including atherosclerosis. Conversely, mutations in the low density lipoprotein receptor (LDLR) result in failure of receptor mediated endocytosis of LDL leading to its elevated plasma levels and onset of familial hypercholesterolemia (FH). In the current study we investigated the role of PON1 polymorphisms rs662; c.575A &gt; G (p.Gln192Arg) and rs854560; c.163T &gt; A (p.Leu55Met) in a large family having FH patients harboring a functional mutation in LDLR. Genotypes were revealed by RFLP, followed by confirmation through Sanger sequencing. PON1 activity was measure by spectrophotometry. Our results show significantly reduced serum paraoxonase and arylesterase activities in FH patients compared with the healthy individuals of the family (p &lt; 0.05). PON1 QQ192 genotype showed a significantly higher association with FH (p=0.0002). PON1 Q192 isoform was associated with reduced serum paraoxonase activity by in silico analysis and PON1 R192 exhibited higher serum paraoxonase and arylesterase activity than the other polymorphs. Our results highlight that the combination of LDLR mutations and PON1 MMQQ genotypes may lead to severe cardiac events.
DOI: 10.25582/data.2023-01.2709608/2305108
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2708972/2305109
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2705702/2305110
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2710294/2305111
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2715693/2305112
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-02.2732644/2305113
title: Data for EMSL Project 51287 from February 2023
DOI: 10.25582/data.2023-01.2710170/2305114
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.8123978
title: Silibinin’s regulation of proliferation and collagen gene expressions of rat pancreatic β-cells cultured on types I and V collagen involves β-catenin nuclear translocation

description: Extracellular matrix (ECM) molecules have multiple functions; prevention of cytotoxicity, provision of mechanical support, cell adhesive substrates and structural integrity in addition to mediation of cellular signaling. In this study, we report that the proliferation of INS-1 cells cultured on collagen I-coated dishes is enhanced, but it is inhibited on collagen V-coated dishes. Inhibitory proliferation on collagen V-coated is not due to apoptosis induction. Silibinin decreases hepatic glucose production and protects pancreatic β-cells, as a potential medicine for type II diabetes. Silibinin up-regulates the proliferation of cells cultured on both collagen I- and V-coated dishes. Collagen-coating regulates gene expression of collagen in a collagen type-related manner. Silibinin increases mRNA expression of collagen I in the cells on collagen I- and V-coated dishes; however, silibinin decreases collagen V mRNA expression on collagen I- and V-coated dishes. Collagen I-coating significantly enhances nuclear translocation of β-catenin, while collagen V-coating reduces it. Differential effects of silibinin on collagen I mRNA and collagen V mRNA can be accounted for by the finding that silibinin enhances nuclear translocation of β-catenin on both collagen I- and V-coated dishes, since phenomenologically nuclear translocation of β-catenin enhances collagen I mRNA but represses collagen V mRNA. These results demonstrate that nuclear translocation of β-catenin up-regulates proliferation and collagen I gene expression, whereas it down-regulates collagen V gene expression of INS-1 cells. Differential gene expressions of collagen I and V by nuclear β-catenin could be important for understanding fibrosis where collagen I and V may have differential effects.
DOI: 10.6084/m9.figshare.8123978.v1
title: Silibinin’s regulation of proliferation and collagen gene expressions of rat pancreatic β-cells cultured on types I and V collagen involves β-catenin nuclear translocation

description: Extracellular matrix (ECM) molecules have multiple functions; prevention of cytotoxicity, provision of mechanical support, cell adhesive substrates and structural integrity in addition to mediation of cellular signaling. In this study, we report that the proliferation of INS-1 cells cultured on collagen I-coated dishes is enhanced, but it is inhibited on collagen V-coated dishes. Inhibitory proliferation on collagen V-coated is not due to apoptosis induction. Silibinin decreases hepatic glucose production and protects pancreatic β-cells, as a potential medicine for type II diabetes. Silibinin up-regulates the proliferation of cells cultured on both collagen I- and V-coated dishes. Collagen-coating regulates gene expression of collagen in a collagen type-related manner. Silibinin increases mRNA expression of collagen I in the cells on collagen I- and V-coated dishes; however, silibinin decreases collagen V mRNA expression on collagen I- and V-coated dishes. Collagen I-coating significantly enhances nuclear translocation of β-catenin, while collagen V-coating reduces it. Differential effects of silibinin on collagen I mRNA and collagen V mRNA can be accounted for by the finding that silibinin enhances nuclear translocation of β-catenin on both collagen I- and V-coated dishes, since phenomenologically nuclear translocation of β-catenin enhances collagen I mRNA but represses collagen V mRNA. These results demonstrate that nuclear translocation of β-catenin up-regulates proliferation and collagen I gene expression, whereas it down-regulates collagen V gene expression of INS-1 cells. Differential gene expressions of collagen I and V by nuclear β-catenin could be important for understanding fibrosis where collagen I and V may have differential effects.
DOI: 10.25582/data.2023-01.2710474/2305115
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2706843/2305116
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2710119/2305117
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.7075418
title: Network analysis of ABA-dependent and ABA-independent drought responsive genes in Arabidopsis thaliana

description: Abstract Drought is one of the most severe abiotic factors restricting plant growth and yield. Numerous genes functioning in drought response are regulated by abscisic acid (ABA) dependent and independent pathways, but knowledge of interplay between the two pathways is still limited. Here, we integrated transcriptome sequencing and network analyses to explore interplays between ABA-dependent and ABA-independent pathways responding to drought stress in Arabidopsis thaliana. We identified 211 ABA-dependent differentially expressed genes (DEGs) and 1,118 ABA-independent DEGs under drought stress. Functional analysis showed that ABA-dependent DEGs were significantly enriched in expected biological processes in response to water deprivation and ABA stimulus, while ABA-independent DEGs were preferentially enriched in response to jasmonic acid (JA), salicylic acid (SA) and gibberellin (GA) stimuli. We found significantly enriched interactions between ABA-dependent and ABA-independent pathways with 94 genes acting as core interacting components by combining network analyses. A link between ABA and JA signaling mediated through a direct interaction of the ABA responsive elements-binding factor ABF3 with the basic helix-loop-helix transcription factor MYC2 was validated by yeast two-hybrid and bimolecular fluorescence complementation (BiFC) assays. Our study provides a systematic view of the interplay between ABA-dependent and ABA-independent pathways in response to drought stress.
DOI: 10.6084/m9.figshare.7075418.v1
title: Network analysis of ABA-dependent and ABA-independent drought responsive genes in Arabidopsis thaliana

description: Abstract Drought is one of the most severe abiotic factors restricting plant growth and yield. Numerous genes functioning in drought response are regulated by abscisic acid (ABA) dependent and independent pathways, but knowledge of interplay between the two pathways is still limited. Here, we integrated transcriptome sequencing and network analyses to explore interplays between ABA-dependent and ABA-independent pathways responding to drought stress in Arabidopsis thaliana. We identified 211 ABA-dependent differentially expressed genes (DEGs) and 1,118 ABA-independent DEGs under drought stress. Functional analysis showed that ABA-dependent DEGs were significantly enriched in expected biological processes in response to water deprivation and ABA stimulus, while ABA-independent DEGs were preferentially enriched in response to jasmonic acid (JA), salicylic acid (SA) and gibberellin (GA) stimuli. We found significantly enriched interactions between ABA-dependent and ABA-independent pathways with 94 genes acting as core interacting components by combining network analyses. A link between ABA and JA signaling mediated through a direct interaction of the ABA responsive elements-binding factor ABF3 with the basic helix-loop-helix transcription factor MYC2 was validated by yeast two-hybrid and bimolecular fluorescence complementation (BiFC) assays. Our study provides a systematic view of the interplay between ABA-dependent and ABA-independent pathways in response to drought stress.
DOI: 10.25582/data.2023-01.2706079/2305118
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2706911/2305119
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.9696872
title: Glycogen synthase kinase-3 beta inhibitors protectagainst the acute lung injuries resulting from acute necrotizing pancreatitis

description: Abstract Purpose The research is intended for clarification of the efficacy as well as the underlying mechanism of GSK-3β inhibitors on the advancement of acute lung injuries in acute necrotizing pancreatitis (ANP) in rats. Methods Seventy-two rats were randomly divided into 6 groups: (1)ANP-vehicle; (2)ANP-TDZD-8;(3)ANP-SB216763;(4)Sham-vehicle;(5)Sham-TDZD-8;(6)Sham-SB216763; Blood biochemical test, histopathological examination and immunohistochemical analysis of rats pancreas and lung tissues were performed. The protein expression of GSK-3β, phospho-GSK-3β (Ser9), iNOS, ICAM-1, TNF-α, and IL-10 were detected in lung tissues by Western-blot. Results The outcomes revealed that the intervention of GSK-3β inhibitors alleviated the pathological damage of pancreas and lung (P&lt;0.01), reduced serum amylase, lipase, hydrothorax and lung Wet-to-Dry Ratio, attenuated serum concentrations of IL-1β and IL-6 (P&lt;0.01), inhibited the activation of NF-κB, and abated expression of iNOS, ICAM-1 and TNF-α protein, but up-regulated IL-10 expression in lung of ANP rats (P&lt;0.01). The inflammatory response and various indicators in ANP-TDZD-8 groups were lower than those in ANP-SB216763 groups. Conclusions Inhibition of GSK-3β weakens acute lung injury related to ANP via the inhibitory function of NF-κB signaling pathway. Different kinds of GSK-3β inhibitors have different effects to ANP acute lung injury.
DOI: 10.6084/m9.figshare.9696872.v1
title: Glycogen synthase kinase-3 beta inhibitors protectagainst the acute lung injuries resulting from acute necrotizing pancreatitis

description: Abstract Purpose The research is intended for clarification of the efficacy as well as the underlying mechanism of GSK-3β inhibitors on the advancement of acute lung injuries in acute necrotizing pancreatitis (ANP) in rats. Methods Seventy-two rats were randomly divided into 6 groups: (1)ANP-vehicle; (2)ANP-TDZD-8;(3)ANP-SB216763;(4)Sham-vehicle;(5)Sham-TDZD-8;(6)Sham-SB216763; Blood biochemical test, histopathological examination and immunohistochemical analysis of rats pancreas and lung tissues were performed. The protein expression of GSK-3β, phospho-GSK-3β (Ser9), iNOS, ICAM-1, TNF-α, and IL-10 were detected in lung tissues by Western-blot. Results The outcomes revealed that the intervention of GSK-3β inhibitors alleviated the pathological damage of pancreas and lung (P&lt;0.01), reduced serum amylase, lipase, hydrothorax and lung Wet-to-Dry Ratio, attenuated serum concentrations of IL-1β and IL-6 (P&lt;0.01), inhibited the activation of NF-κB, and abated expression of iNOS, ICAM-1 and TNF-α protein, but up-regulated IL-10 expression in lung of ANP rats (P&lt;0.01). The inflammatory response and various indicators in ANP-TDZD-8 groups were lower than those in ANP-SB216763 groups. Conclusions Inhibition of GSK-3β weakens acute lung injury related to ANP via the inhibitory function of NF-κB signaling pathway. Different kinds of GSK-3β inhibitors have different effects to ANP acute lung injury.
DOI: 10.25582/data.2023-01.2710108/2305120
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2710878/2305121
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.9696875
title: MiR-106a aggravates sepsis-induced acute kidney injury by targeting THBS2 in mice model

description: Abstract Purpose To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. Methods Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfected with THBS2-small interfering RNA (siTHBS2), miR-106a inhibitor, miR-106a mimics and their negative controls (NCs). The expression of miR-106a, thrombospondin 2 (THBS2), Bax, cleaved caspase-3 and Bcl-2, cell viability, relative caspase-3 activity and TNF-α, IL-1β, IL-6 content were respectively detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Cell Counting Kit-8 (CCK-8) and enzyme linked immunosorbent assay (ELISA). The relationship between miR-106a and THBS2 was confirmed by dual luciferase reporter assay. Results MiR-106a was up-regulated in serum of sepsis patients, CLP-induced mice models and LPS-induced TCMK-1 cells. LPS reduced cell viability and Bcl-2 expression, and increased caspase-3 activity, Bax expression, the content of TNF-α, IL-1β, IL-6. THBS2 was a target of miR-106a. The decreases of caspase-3 activity, TNF-α, IL-1β, IL-6, Bax expression and the increases of cell viability, Bcl-2 expression caused by miR-106a knockdown were reversed when THBS2 silencing in LPS-stimulated TCMK-1 cells. Conclusion MiR-106a aggravated LPS-induced inflammation and apoptosis of TCMK-1 cells via regulating THBS2 expression.