cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29967837
title: Abnormal levels of miRNA in pancreatic cancer are linked to tumor progression by regulating the translation of tumor-associated mRNA

description: Pancreatic cancer remains one of the most malignant tumors, characterized by limited treatment efficacy. microRNAs (miRNAs) play a crucial role in regulating the proliferation, invasion, migration, drug resistance, apoptosis, and cell cycle progression of pancreatic cancer cells by inhibiting tumor-associated proteins. Metscape analysis revealed that miRNA-targeted proteins associated with pancreatic cancer are enriched in processes such as cell proliferation, mitosis, and cell migration, and participate in multiple signaling pathways. These proteins primarily localize to classical pathways, including JAK/STAT, PI3K/AKT, and Wnt/β-catenin. Furthermore, gene mutations or abnormal alternative poly(A)denylation (APA) within miRNA-targeted regions can disrupt base pairing to the 3’-Untranslated Region (3′-UTR), thereby enhancing the translation of oncogenic mRNA translation. Collectively, these findings indicate that multiple miRNAs act cooperatively to influence pancreatic cancer progression. Consequently, therapeutic strategies aimed at restoring the balance of the miRNA system are essential to disrupt the ‘mRNA-oncogene’ vicious cycle.
DOI: 10.6084/m9.figshare.29967837.v1
title: Abnormal levels of miRNA in pancreatic cancer are linked to tumor progression by regulating the translation of tumor-associated mRNA

description: Pancreatic cancer remains one of the most malignant tumors, characterized by limited treatment efficacy. microRNAs (miRNAs) play a crucial role in regulating the proliferation, invasion, migration, drug resistance, apoptosis, and cell cycle progression of pancreatic cancer cells by inhibiting tumor-associated proteins. Metscape analysis revealed that miRNA-targeted proteins associated with pancreatic cancer are enriched in processes such as cell proliferation, mitosis, and cell migration, and participate in multiple signaling pathways. These proteins primarily localize to classical pathways, including JAK/STAT, PI3K/AKT, and Wnt/β-catenin. Furthermore, gene mutations or abnormal alternative poly(A)denylation (APA) within miRNA-targeted regions can disrupt base pairing to the 3’-Untranslated Region (3′-UTR), thereby enhancing the translation of oncogenic mRNA translation. Collectively, these findings indicate that multiple miRNAs act cooperatively to influence pancreatic cancer progression. Consequently, therapeutic strategies aimed at restoring the balance of the miRNA system are essential to disrupt the ‘mRNA-oncogene’ vicious cycle.
DOI: 10.6084/m9.figshare.30856514
title: A comparison of allied healthcare versus no allied healthcare on participation, fatigue, physical functioning and health-related quality of life for patients with persistent complaints after a COVID-19 infection

description: To assess the effectiveness of allied healthcare <i>versus</i> no allied healthcare. Data from the ParaCOV cohort (allied healthcare, <i>n</i> = 1,451) and the LongCOVID cohort (no allied healthcare/control, <i>n</i> = 1427) were analyzed. Average treatment effects (ATEs) between groups were estimated using Targeted Maximum Likelihood Estimation adjusted for age, sex, body mass index, smoking status, comorbidities, and effect outcomes’ baseline values. <i>A</i> ≥ 10% between-group difference in improvement from baseline (BTGD) was considered clinically relevant for participation, fatigue, and physical functioning, and ≥0.062 for health-related quality of life. Patients receiving allied healthcare were older (49.2 vs. 41.2 years), less often female (63.3% vs. 70.1%), had higher BMI (28.2 vs. 26.1), smoked less frequently (5.0% vs. 9.0%), had more comorbidities (49.2% vs. 41.9%), and lower baseline anxiety and depression scores compared to those not receiving allied healthcare. For participation, ATEs after 6 and 12 months were respectively −2.62 (95%CI: −4.39; −0.86) and −1.68 (95%CI: −4.81;1.45), with BTGDs of 4.7% and 1.8% favoring the control. For fatigue, ATEs were 1.72 (95%CI: −0.14; 3.58) and 0.97 (95%CI: −1.48; 3.41), with BTGDs of 6.5% and 3.7% favoring the control. For physical functioning, ATEs were 5.75 (95% CI: 4.42; 7.09) and 6.36 (95%CI: 4.84; 7.88), with BTGDs of 1.4% and 2.2% favoring allied healthcare. For health-related quality of life, ATEs were 0.017 (95%CI: −0.008; 0.0044) and 0.033 (95%CI: 0.011; 0.054). Patients with persistent complaints after a COVID-19 infection showed significantly lower participation after 6 months, higher health-related quality of life after 12 months, and better physical functioning after 6 and 12 months of allied healthcare, however, BTGDs were not clinically relevant. Study limitations warrant cautious results interpretation. Although health-related quality of life and physical functioning improved in Long COVID patients, this cannot be definitively attributed to allied healthcare.The observed outcome differences between Long COVID patients with and without allied healthcare were not clinically relevant.More research is needed for tailored rehabilitation treatments for these patients. Although health-related quality of life and physical functioning improved in Long COVID patients, this cannot be definitively attributed to allied healthcare. The observed outcome differences between Long COVID patients with and without allied healthcare were not clinically relevant. More research is needed for tailored rehabilitation treatments for these patients.
DOI: 10.6084/m9.figshare.30856514.v1
title: A comparison of allied healthcare versus no allied healthcare on participation, fatigue, physical functioning and health-related quality of life for patients with persistent complaints after a COVID-19 infection

description: To assess the effectiveness of allied healthcare <i>versus</i> no allied healthcare. Data from the ParaCOV cohort (allied healthcare, <i>n</i> = 1,451) and the LongCOVID cohort (no allied healthcare/control, <i>n</i> = 1427) were analyzed. Average treatment effects (ATEs) between groups were estimated using Targeted Maximum Likelihood Estimation adjusted for age, sex, body mass index, smoking status, comorbidities, and effect outcomes’ baseline values. <i>A</i> ≥ 10% between-group difference in improvement from baseline (BTGD) was considered clinically relevant for participation, fatigue, and physical functioning, and ≥0.062 for health-related quality of life. Patients receiving allied healthcare were older (49.2 vs. 41.2 years), less often female (63.3% vs. 70.1%), had higher BMI (28.2 vs. 26.1), smoked less frequently (5.0% vs. 9.0%), had more comorbidities (49.2% vs. 41.9%), and lower baseline anxiety and depression scores compared to those not receiving allied healthcare. For participation, ATEs after 6 and 12 months were respectively −2.62 (95%CI: −4.39; −0.86) and −1.68 (95%CI: −4.81;1.45), with BTGDs of 4.7% and 1.8% favoring the control. For fatigue, ATEs were 1.72 (95%CI: −0.14; 3.58) and 0.97 (95%CI: −1.48; 3.41), with BTGDs of 6.5% and 3.7% favoring the control. For physical functioning, ATEs were 5.75 (95% CI: 4.42; 7.09) and 6.36 (95%CI: 4.84; 7.88), with BTGDs of 1.4% and 2.2% favoring allied healthcare. For health-related quality of life, ATEs were 0.017 (95%CI: −0.008; 0.0044) and 0.033 (95%CI: 0.011; 0.054). Patients with persistent complaints after a COVID-19 infection showed significantly lower participation after 6 months, higher health-related quality of life after 12 months, and better physical functioning after 6 and 12 months of allied healthcare, however, BTGDs were not clinically relevant. Study limitations warrant cautious results interpretation. Although health-related quality of life and physical functioning improved in Long COVID patients, this cannot be definitively attributed to allied healthcare.The observed outcome differences between Long COVID patients with and without allied healthcare were not clinically relevant.More research is needed for tailored rehabilitation treatments for these patients. Although health-related quality of life and physical functioning improved in Long COVID patients, this cannot be definitively attributed to allied healthcare. The observed outcome differences between Long COVID patients with and without allied healthcare were not clinically relevant. More research is needed for tailored rehabilitation treatments for these patients.
DOI: 10.6084/m9.figshare.29625591
title: Efficacy of probiotics pretreatment in <i>Helicobacter pylori</i> eradication therapy: a systematic review and meta-analysis of clinical outcomes

description: Probiotics inhibit <i>Helicobacter pylori (H. pylori)</i> growth and alter gut microbiome, in addition to alleviating the side effects of <i>H. pylori</i> eradication. It has also been reported that <i>H. pylori</i> be eradicated after fecal microbiota transplantation in some cases. However, whether probiotics used before <i>H. pylori</i> eradication improves the eradication rate remains unclear. This study evaluates their role through a systematic review and meta-analysis. We searched PubMed, EMBASE, the Cochrane Library, and the Conference Proceedings Citation Index up to January 31, 2024, to identify randomized controlled studies (RCTs) assessing the efficacy of probiotics used before <i>H. pylori</i> eradication. Meta-analyses of eradication rates were performed. Twelve eligible RCTs with 2,144 participants were included. The intention-to-treat analysis revealed that the overall eradication rate of <i>H. pylori</i> was higher in the probiotics pretreatment group compared to the control group (80.34% vs. 70.49%), with a risk ratio (RR) of 1.14 (95% CI: 1.08 to 1.19; <i>I<sup>2</sup></i> = 36%) and side effects were less (16.0% vs. 28.3%, RR = 0.59, 95% CI 0.41 to 0.84). The per-protocol analysis yielded similar results (86.43% vs. 76.88%, RR = 1.12, 95% CI: 1.08 to 1.17; <i>I<sup>2</sup></i> = 57%). Subgroup analyses, considering factors like geographic location, eradication regimens, and probiotic combinations, consistently confirmed the benefits. Finally, probiotics pretreatment durations of 14 days or more, as well as the study designs <i>pre vs. free</i> and <i>pre and combine vs. free</i>, demonstrated significant effects. Shorter durations and other study designs with fewer studies did not show significant effects. There is moderate to high evidence to suggest that probiotics pretreatment improves <i>H. pylori</i> eradication rate and reduces side effects. These findings highlight the potential value of gut microbiome modulation in <i>H. pylori</i> treatment and offer a new direction for addressing the challenges of antibiotic resistance and treatment failure.
DOI: 10.6084/m9.figshare.29625591.v1
title: Efficacy of probiotics pretreatment in <i>Helicobacter pylori</i> eradication therapy: a systematic review and meta-analysis of clinical outcomes

description: Probiotics inhibit <i>Helicobacter pylori (H. pylori)</i> growth and alter gut microbiome, in addition to alleviating the side effects of <i>H. pylori</i> eradication. It has also been reported that <i>H. pylori</i> be eradicated after fecal microbiota transplantation in some cases. However, whether probiotics used before <i>H. pylori</i> eradication improves the eradication rate remains unclear. This study evaluates their role through a systematic review and meta-analysis. We searched PubMed, EMBASE, the Cochrane Library, and the Conference Proceedings Citation Index up to January 31, 2024, to identify randomized controlled studies (RCTs) assessing the efficacy of probiotics used before <i>H. pylori</i> eradication. Meta-analyses of eradication rates were performed. Twelve eligible RCTs with 2,144 participants were included. The intention-to-treat analysis revealed that the overall eradication rate of <i>H. pylori</i> was higher in the probiotics pretreatment group compared to the control group (80.34% vs. 70.49%), with a risk ratio (RR) of 1.14 (95% CI: 1.08 to 1.19; <i>I<sup>2</sup></i> = 36%) and side effects were less (16.0% vs. 28.3%, RR = 0.59, 95% CI 0.41 to 0.84). The per-protocol analysis yielded similar results (86.43% vs. 76.88%, RR = 1.12, 95% CI: 1.08 to 1.17; <i>I<sup>2</sup></i> = 57%). Subgroup analyses, considering factors like geographic location, eradication regimens, and probiotic combinations, consistently confirmed the benefits. Finally, probiotics pretreatment durations of 14 days or more, as well as the study designs <i>pre vs. free</i> and <i>pre and combine vs. free</i>, demonstrated significant effects. Shorter durations and other study designs with fewer studies did not show significant effects. There is moderate to high evidence to suggest that probiotics pretreatment improves <i>H. pylori</i> eradication rate and reduces side effects. These findings highlight the potential value of gut microbiome modulation in <i>H. pylori</i> treatment and offer a new direction for addressing the challenges of antibiotic resistance and treatment failure.
DOI: 10.6084/m9.figshare.30796986
title: The impact of body mass index on the efficacy of CDK4/6 inhibitors in patients with metastatic breast cancer

description: Although Body Mass Index (BMI) has been reported to influence breast cancer prognosis, recent evidence challenges the traditional conclusion that high BMI consistently predicts poor prognosis. The aim of this study was to determine the impact of BMI on the efficacy of CDK4/6 inhibitors in patients with metastatic hormone receptor (HR)-positive breast cancer (BC). We performed a retrospective chart review of all female patients with metastatic HR-positive BC on a CDK4/6 inhibitor in first- or late-line settings and seen at our academic institution between 2016 and 2023. The primary endpoint was Overall Survival (OS), defined as the time from the start of CDK4/6 inhibitors to death due to any cause. We identified 212 patients who had received a CDK4/6 inhibitor in the first- or second-line settings for metastatic HR-positive BC. Of the 212 patients, 53.3% (113) had a low BMI (defined as &lt; 24 kg/m<sup>2</sup>) and 46.7% (99) had a high BMI (≥ 24 kg/m<sup>2</sup>). In the first-line setting, mean OS was 46.6 months (95% CI, 38.9 to 54.3) in the BMI-low group versus 78.9 months (95% CI, 69.2 to 88.5) in the BMI-high group (<i>p</i> = 0.047). The median PFS was 25 months (95% CI, 19.7 to 30.3) in the BMI-low group versus 33 months (95% CI, 21.4 to 44.6) in the BMI-high group, but the difference between the two groups was not statistically significant (<i>p</i> = 0.488). No statistically significant differences were observed in OS and PFS between the two groups in late-line settings (<i>p</i> = 0.83; <i>p</i> = 0.84). In HR positive advanced breast cancer patients treated with first-line CDK4/6 inhibitors, lower BMI is associated with poorer prognosis.
DOI: 10.6084/m9.figshare.30796986.v1
title: The impact of body mass index on the efficacy of CDK4/6 inhibitors in patients with metastatic breast cancer

description: Although Body Mass Index (BMI) has been reported to influence breast cancer prognosis, recent evidence challenges the traditional conclusion that high BMI consistently predicts poor prognosis. The aim of this study was to determine the impact of BMI on the efficacy of CDK4/6 inhibitors in patients with metastatic hormone receptor (HR)-positive breast cancer (BC). We performed a retrospective chart review of all female patients with metastatic HR-positive BC on a CDK4/6 inhibitor in first- or late-line settings and seen at our academic institution between 2016 and 2023. The primary endpoint was Overall Survival (OS), defined as the time from the start of CDK4/6 inhibitors to death due to any cause. We identified 212 patients who had received a CDK4/6 inhibitor in the first- or second-line settings for metastatic HR-positive BC. Of the 212 patients, 53.3% (113) had a low BMI (defined as &lt; 24 kg/m<sup>2</sup>) and 46.7% (99) had a high BMI (≥ 24 kg/m<sup>2</sup>). In the first-line setting, mean OS was 46.6 months (95% CI, 38.9 to 54.3) in the BMI-low group versus 78.9 months (95% CI, 69.2 to 88.5) in the BMI-high group (<i>p</i> = 0.047). The median PFS was 25 months (95% CI, 19.7 to 30.3) in the BMI-low group versus 33 months (95% CI, 21.4 to 44.6) in the BMI-high group, but the difference between the two groups was not statistically significant (<i>p</i> = 0.488). No statistically significant differences were observed in OS and PFS between the two groups in late-line settings (<i>p</i> = 0.83; <i>p</i> = 0.84). In HR positive advanced breast cancer patients treated with first-line CDK4/6 inhibitors, lower BMI is associated with poorer prognosis.
DOI: 10.6084/m9.figshare.29554320
title: TsR-0072 inhibits colorectal cancer progression through modulating lipid and vitamin D<sub>3</sub> metabolic reprogramming and inactivating the Wnt/β-catenin signalling pathway

description: tRNA-derived small RNAs (tsRNAs), newly developed non-coding RNAs with specialized biological features, are aberrantly expressed in the majority of malignancies. However, whether tsRNAs are involved in metabolic reprogramming of colorectal cancer (CRC) remains to be elucidated. A novel tsRNA, tsRNA-Ser-3-0072 (tsR-0072), was screened from the tsRFun database and its expression was characterized by real-time quantitative PCR (qRT-PCR). CCK8, 5-ethynyl-2′-deoxyuridine (EdU), colony formation, transwell experiments and nude mice transplantation models were performed to assess CRC cell proliferation and metastasis <i>in vitro</i> and <i>in vivo</i>. The target genes of tsR-0072 were verified using a dual luciferase reporter assay, and enzyme-linked immunosorbent assay (ELISA), Western blotting, and qRT-PCR were employed to analyse the potential mechanisms of CRC. TsR-0072 was downregulated in CRC and was found to be associated with TNM stage, T stage, lymph node metastasis and the prognosis of CRC patients. Functional experiments revealed that tsR-0072 inhibited CRC growth and metastasis both <i>in vivo</i> and <i>in vitro</i>. Moreover, sterol O-acyltransferase 1 (SOAT1) and 25-hydroxyvitamin D<sub>3</sub>-24-hydroxylase (CYP24A1) were identified as direct targets of tsR-0072. Mechanistic studies revealed that tsR-0072 arrested lipid metabolism by downregulating the expression of SOAT1, which inhibited the activity of sterol regulatory element-binding protein 1 (SREBP1), sterol regulatory element-binding protein 2 (SREBP2) and fatty acid synthase (FASN). In addition, tsR-0072 promoted vitamin D<sub>3</sub> metabolism by decreasing the expression of CYP24A1, thereby increasing 1α,25-dihydroxyvitamin D<sub>3</sub> (1,25(OH)<sub>2</sub>D<sub>3</sub>) secretion and vitamin D receptor (VDR) expression. Both lipid and vitamin D<sub>3</sub> metabolic reprogramming induced by tsR-0072 resulted in inhibition of CRC progression through inactivation of the Wnt/β-catenin signalling pathway. TsR-0072 acted as an anti-oncogene to modulate lipid and vitamin D<sub>3</sub> metabolic reprogramming, thereby impeding CRC progression. Consequently, it might be a potential therapeutic target to overcome metabolic disorders in tumours. This study provided a promising transfer RNA (tRNA)-oriented strategy for the treatment of CRC treatment.
DOI: 10.6084/m9.figshare.29554320.v1
title: TsR-0072 inhibits colorectal cancer progression through modulating lipid and vitamin D<sub>3</sub> metabolic reprogramming and inactivating the Wnt/β-catenin signalling pathway

description: tRNA-derived small RNAs (tsRNAs), newly developed non-coding RNAs with specialized biological features, are aberrantly expressed in the majority of malignancies. However, whether tsRNAs are involved in metabolic reprogramming of colorectal cancer (CRC) remains to be elucidated. A novel tsRNA, tsRNA-Ser-3-0072 (tsR-0072), was screened from the tsRFun database and its expression was characterized by real-time quantitative PCR (qRT-PCR). CCK8, 5-ethynyl-2′-deoxyuridine (EdU), colony formation, transwell experiments and nude mice transplantation models were performed to assess CRC cell proliferation and metastasis <i>in vitro</i> and <i>in vivo</i>. The target genes of tsR-0072 were verified using a dual luciferase reporter assay, and enzyme-linked immunosorbent assay (ELISA), Western blotting, and qRT-PCR were employed to analyse the potential mechanisms of CRC. TsR-0072 was downregulated in CRC and was found to be associated with TNM stage, T stage, lymph node metastasis and the prognosis of CRC patients. Functional experiments revealed that tsR-0072 inhibited CRC growth and metastasis both <i>in vivo</i> and <i>in vitro</i>. Moreover, sterol O-acyltransferase 1 (SOAT1) and 25-hydroxyvitamin D<sub>3</sub>-24-hydroxylase (CYP24A1) were identified as direct targets of tsR-0072. Mechanistic studies revealed that tsR-0072 arrested lipid metabolism by downregulating the expression of SOAT1, which inhibited the activity of sterol regulatory element-binding protein 1 (SREBP1), sterol regulatory element-binding protein 2 (SREBP2) and fatty acid synthase (FASN). In addition, tsR-0072 promoted vitamin D<sub>3</sub> metabolism by decreasing the expression of CYP24A1, thereby increasing 1α,25-dihydroxyvitamin D<sub>3</sub> (1,25(OH)<sub>2</sub>D<sub>3</sub>) secretion and vitamin D receptor (VDR) expression. Both lipid and vitamin D<sub>3</sub> metabolic reprogramming induced by tsR-0072 resulted in inhibition of CRC progression through inactivation of the Wnt/β-catenin signalling pathway. TsR-0072 acted as an anti-oncogene to modulate lipid and vitamin D<sub>3</sub> metabolic reprogramming, thereby impeding CRC progression. Consequently, it might be a potential therapeutic target to overcome metabolic disorders in tumours. This study provided a promising transfer RNA (tRNA)-oriented strategy for the treatment of CRC treatment.
DOI: 10.6084/m9.figshare.28613748
title: Lipid profile and non-alcoholic fatty liver disease detected by ultrasonography: is systemic inflammation a necessary mediator?

description: To examine the relationship between lipid profile and non-alcoholic fatty liver (NAFL), compare the predictive strengths of different lipid indicators to NAFL, and explore the possible mechanisms. Male workers from a baseline survey of a cohort of workers in southern China were included. Basic information was collected through face-to-face interviews. Plasma concentrations of fasting plasma glucose (FPG), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were determined using a blood biochemical analyzer. Liver sonography was used to identify NAFL cases. Regression models were used to calculate ORs, and examine the association between C-reactive protein (CRP) levels and lipid profiles. Restricted cubic spline regression with four knots was used to examine the dose-response relationship, and mediation analysis was employed to examine the mediation effect. h Among the 4016 male workers, 829 (20.64%) were diagnosed with NAFL. Compared with normal lipid profile, individuals with abnormal lipid profile had higher prevalence of NAFL (OR=2.27, 95%CI: 1.85-2.79 for TG; OR=1.45, 95%CI: 1.03-2.04 for TC; OR=1.56, 95%CI: 1.21-2.02 for HDL; OR=1.65, 95%CI: 1.25-2.18 for LDL; OR=2.28, 95%CI: 1.87-2.77 for dyslipidaemia) after adjusting for potential confounders. Dose-response relationships were observed among TG, HDL, and NAFL. In addition, no significant mediation effect of C-reactive protein (CRP) was found in the association between lipid profiles and NAFL. Abnormal TG, TC, HDL, and LDL levels were all positively associated with NAFL, while CRP has no mediating effect, and TG tended to be a better predictor of NAFL.