cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.28100533
title: COVID-19 vaccine acceptance and preference for future delivery among language minority, newcomer, and racialized peoples in Canada: a national cross-sectional and longitudinal study

description: Despite high COVID-19 vaccine coverage in Canada, vaccine acceptance and preferred delivery among newcomers, racialized persons, and those who primarily speak minority languages are not well understood. This national study explores COVID-19 vaccine acceptance, access to vaccines, and delivery preferences among ethnoculturally diverse population groups. We conducted two national cross-sectional surveys during the pandemic (Dec 2020 and Oct-Nov 2021). Binary logistic regression analysis investigated the association between newcomer, language, and racialized minority respondents’ perceptions and acceptance of COVID-19 vaccines, experiences of discrimination when accessing health services, and sociodemographic characteristics. McNemar-Bowker tests were used to assess changes in responses collected at two time points. Among 1630 respondents, 30.8% arrived in Canada within the last five years, 87.4% self-identified as a racialized minority, and 37.2% primarily spoke languages other than English or French. Although single dose COVID-19 vaccine uptake was at 92.7% among respondents, 14.8% experienced difficulty accessing vaccines, citing a need for translated resources or multi-lingual personnel. In longitudinal analysis, respondents were increasingly motivated over time to overcome barriers to accessing vaccines (61.4% to 69.6%, p = &lt;.001). Fifty-nine percent (59.9%) of respondents would accept annual vaccination and over half would accept co-administration with routine (56.2%) or influenza (52.3%) vaccines. Experiences of racism/discrimination upon health service access were reported by 12.3% of respondents, who recommended increasing culturally safe practices and community involvement at vaccination sites. Understanding how newcomers, racialized peoples, and minority language speakers perceive and access COVID-19 vaccines will support vaccination campaigns to optimize equitable access.
DOI: 10.6084/m9.figshare.28100533.v1
title: COVID-19 vaccine acceptance and preference for future delivery among language minority, newcomer, and racialized peoples in Canada: a national cross-sectional and longitudinal study

description: Despite high COVID-19 vaccine coverage in Canada, vaccine acceptance and preferred delivery among newcomers, racialized persons, and those who primarily speak minority languages are not well understood. This national study explores COVID-19 vaccine acceptance, access to vaccines, and delivery preferences among ethnoculturally diverse population groups. We conducted two national cross-sectional surveys during the pandemic (Dec 2020 and Oct-Nov 2021). Binary logistic regression analysis investigated the association between newcomer, language, and racialized minority respondents’ perceptions and acceptance of COVID-19 vaccines, experiences of discrimination when accessing health services, and sociodemographic characteristics. McNemar-Bowker tests were used to assess changes in responses collected at two time points. Among 1630 respondents, 30.8% arrived in Canada within the last five years, 87.4% self-identified as a racialized minority, and 37.2% primarily spoke languages other than English or French. Although single dose COVID-19 vaccine uptake was at 92.7% among respondents, 14.8% experienced difficulty accessing vaccines, citing a need for translated resources or multi-lingual personnel. In longitudinal analysis, respondents were increasingly motivated over time to overcome barriers to accessing vaccines (61.4% to 69.6%, p = &lt;.001). Fifty-nine percent (59.9%) of respondents would accept annual vaccination and over half would accept co-administration with routine (56.2%) or influenza (52.3%) vaccines. Experiences of racism/discrimination upon health service access were reported by 12.3% of respondents, who recommended increasing culturally safe practices and community involvement at vaccination sites. Understanding how newcomers, racialized peoples, and minority language speakers perceive and access COVID-19 vaccines will support vaccination campaigns to optimize equitable access.
DOI: 10.6084/m9.figshare.30876631
title: HDAC1 dysregulation promotes pro-inflammatory microglial activation and aggravates post-stroke neuroinflammation

description: Histone deacetylase 1 (HDAC1) is a key epigenetic regulator involved in DNA repair and neuronal survival. While HDAC1 downregulation has been implicated in ischemic brain injury, its role in regulating microglial functional shift and neuroinflammation remains unclear. This study aimed to investigate how HDAC1 dysfunction influences microglial activation states and contributes to neuroinflammatory processes in ischemic stroke. Using a rat model of endothelin-1–induced focal cerebral ischemia, HDAC1 knockdown was achieved <i>via</i> stereotactic co-injection of HDAC1 siRNA. Immunofluorescence, Western blotting, ELISA, and oxidative stress assays were performed to assess neuroinflammation, microglial polarization, and related signalling pathways. In parallel, HDAC1 was silenced in HMC3 human microglial cells, with or without IFN-γ stimulation, to evaluate transcriptional responses associated with pro-inflammatory activation. Finally, HDAC1 was selectively reactivated <i>in vivo</i> and <i>in vitro</i> using Compound 5104434 to assess behavioural, neuroinflammatory and mechanistic effects after ischaemic or inflammatory injury. HDAC1 knockdown <i>in vivo</i> led to a pronounced shift towards a pro-inflammatory microglial activation, evidenced by increased CD86 expression, along with elevated levels of IL-1β, IL-6, TNF-α, ROS, LDH and MMP activity. T-cell infiltration was also significantly enhanced. <i>In vitro</i>, HDAC1 deficiency sensitized microglia to IFN-γ, further amplifying the expression of pro-inflammatory genes. Mechanistically, HDAC1 knockdown activated the NF-κB pathway and its downstream effectors <i>MAP3K8, AP-1</i> and <i>SAT1,</i> while IFN-γ stimulation predominantly drove STAT3 phosphorylation. Notably, pNF-κB was upregulated even in the absence of exogenous stimulation, indicating that HDAC1 intrinsically suppresses pro-inflammatory signalling. HDAC1 enzymatic reactivation by compound 5104434 promotes functional recovery and suppresses NF-κB–driven microglial activation after stroke. HDAC1 acts as a key repressor of NF-κB–driven pro-inflammatory microglial activation and neuroinflammation in stroke. Its loss exacerbates inflammatory cascades, immune cell infiltration, and neuronal injury, underscoring HDAC1 as a potential therapeutic target for limiting secondary brain damage after ischaemic stroke.
DOI: 10.6084/m9.figshare.29348537
title: Da-Yuan-Yin decoction suppresses NETs formation, inhibits the IL-23/JAK2/STAT3 signalling pathway, and modulates metabolic profiles and gut microbiota composition in damp-heat syndrome

description: Da-Yuan-Yin Decoction (DYY), used since the early Qing Dynasty in China for damp-heat syndrome, was evaluated for its comprehensive protective effects. Rats received a high-fat/high-sugar diet for 14 days, then daily exposure to high temperature/humidity (31.0 ± 0.5°C, 85%-95%) for 10 hours over 14 days. Damp-heat syndrome was induced on day 29 via intraperitoneal lipopolysaccharide (LPS) injections (1 mg/kg and 0.5 mg/kg after 4 hours). Two hours post-modeling, rats received DYY (400 or 800 mg/kg/day) orally for 5 days. Symptoms were scored. On day 33, kidney, spleen, tongue, lung, liver, stomach, and colon tissues underwent histopathological and immunochemical/immunofluorescence analysis. Serum levels of inflammation factors, C-reactive protein (CRP), cell-free DNA (cfDNA), myeloperoxidase (MPO), and superoxide dismutase (SOD) were quantified. Complete blood count (CBC), blood biochemistry, short-chain fatty acids (SCFAs), gut microbiota composition in the colon, and metabolites in the cecum were analyzed. DYY significantly reduced symptom scores and decreased CRP level, while also regulating parameters in CBC and biochemical profiles. The treatment ameliorated tissue damage in the kidney, spleen, tongue, lung, liver, stomach, and colon. DYY downregulated citrullinated histone H3 (Cit H3), polyclonal peptidylarginine deiminase 4 (PADI4), and MPO expressions in the lung, stomach, and colon. Furthermore, it modulated inflammatory responses, suppressed the interleukin-23 (IL-23)/janus kinase-2 (JAK2)/signal transduction and transcription activator-3 (STAT3) signaling pathway and enhanced antioxidant activity. DYY administration significantly increased total SCFA content. The intervention restored gut microbiota diversity and abundance, while ameliorating metabolic dysregulation. Systemic pathophysiological alterations were observed in rats with damp-heat syndrome. The comprehensive protective effects of DYY involved suppression of neutrophil extracellular traps (NETs) formation through downregulation of PADI4 expression, modulation of inflammatory responses, inhibition of the IL-23/JAK2/STAT3 signaling pathway, restoration of intestinal microecological balance and metabolic homeostasis, and enhancement of antioxidant.
DOI: 10.6084/m9.figshare.29348537.v1
title: Da-Yuan-Yin decoction suppresses NETs formation, inhibits the IL-23/JAK2/STAT3 signalling pathway, and modulates metabolic profiles and gut microbiota composition in damp-heat syndrome

description: Da-Yuan-Yin Decoction (DYY), used since the early Qing Dynasty in China for damp-heat syndrome, was evaluated for its comprehensive protective effects. Rats received a high-fat/high-sugar diet for 14 days, then daily exposure to high temperature/humidity (31.0 ± 0.5°C, 85%-95%) for 10 hours over 14 days. Damp-heat syndrome was induced on day 29 via intraperitoneal lipopolysaccharide (LPS) injections (1 mg/kg and 0.5 mg/kg after 4 hours). Two hours post-modeling, rats received DYY (400 or 800 mg/kg/day) orally for 5 days. Symptoms were scored. On day 33, kidney, spleen, tongue, lung, liver, stomach, and colon tissues underwent histopathological and immunochemical/immunofluorescence analysis. Serum levels of inflammation factors, C-reactive protein (CRP), cell-free DNA (cfDNA), myeloperoxidase (MPO), and superoxide dismutase (SOD) were quantified. Complete blood count (CBC), blood biochemistry, short-chain fatty acids (SCFAs), gut microbiota composition in the colon, and metabolites in the cecum were analyzed. DYY significantly reduced symptom scores and decreased CRP level, while also regulating parameters in CBC and biochemical profiles. The treatment ameliorated tissue damage in the kidney, spleen, tongue, lung, liver, stomach, and colon. DYY downregulated citrullinated histone H3 (Cit H3), polyclonal peptidylarginine deiminase 4 (PADI4), and MPO expressions in the lung, stomach, and colon. Furthermore, it modulated inflammatory responses, suppressed the interleukin-23 (IL-23)/janus kinase-2 (JAK2)/signal transduction and transcription activator-3 (STAT3) signaling pathway and enhanced antioxidant activity. DYY administration significantly increased total SCFA content. The intervention restored gut microbiota diversity and abundance, while ameliorating metabolic dysregulation. Systemic pathophysiological alterations were observed in rats with damp-heat syndrome. The comprehensive protective effects of DYY involved suppression of neutrophil extracellular traps (NETs) formation through downregulation of PADI4 expression, modulation of inflammatory responses, inhibition of the IL-23/JAK2/STAT3 signaling pathway, restoration of intestinal microecological balance and metabolic homeostasis, and enhancement of antioxidant.
DOI: 10.6084/m9.figshare.30327543
title: Estimating global prevalence of gallbladder stones in general population from 2000 to 2024: systematic review and meta-analysis

description: Gallbladder stones (GS), is one of the most common and costly of all the gastrointestinal diseases. However, global prevalence estimates of GS remain heterogeneous due to methodological variations across studies, and consensus on risk factor hierarchies is still evolving. Therefore, we performed current study in order to estimate the global prevalence of GS. The quality of included studies was assessed using the Newcastle-Ottawa Scale. Data were analysed <i>via</i> the DerSimonian-Laird random-effects model with Logit transformations, and sensitivity analysis was performed using a ‘Leave-one-out’ approach. Of 18,277 identified records, 139 studies were included in the final analysis. The overall global prevalence of GS in the general population was 5.86% (95% CI 5.28–6.47). Marked geographical disparities were observed, with the highest prevalence in Uganda (21.92%, 95% CI 18.43–25.61) and the lowest in Australia (0.18%, 95% CI 0.17–0.18) – a 122-fold difference. Multivariable meta-regression showed that study size was the strongest predictor (importance: 97.79%). Regarding risk factors, female gender, age &gt; 50 years, increased body mass index, and family history of GS were significantly associated with higher GS prevalence. In contrast, factors such as education level, smoking, alcohol consumption, lifestyle, vegetarian diet, and serum lipid levels had no significant impact. Comorbidities including hypertension, diabetes mellitus, and metabolic-associated fatty liver disease (MAFLD) were strongly correlated with elevated GS prevalence. This meta-analysis showed that the GS was a common disease and affected the health of one in twenty people worldwide. Accurate estimates of the global and population-based prevalence of GS are helpful for healthcare improvements.
DOI: 10.6084/m9.figshare.30327543.v1
title: Estimating global prevalence of gallbladder stones in general population from 2000 to 2024: systematic review and meta-analysis

description: Gallbladder stones (GS), is one of the most common and costly of all the gastrointestinal diseases. However, global prevalence estimates of GS remain heterogeneous due to methodological variations across studies, and consensus on risk factor hierarchies is still evolving. Therefore, we performed current study in order to estimate the global prevalence of GS. The quality of included studies was assessed using the Newcastle-Ottawa Scale. Data were analysed <i>via</i> the DerSimonian-Laird random-effects model with Logit transformations, and sensitivity analysis was performed using a ‘Leave-one-out’ approach. Of 18,277 identified records, 139 studies were included in the final analysis. The overall global prevalence of GS in the general population was 5.86% (95% CI 5.28–6.47). Marked geographical disparities were observed, with the highest prevalence in Uganda (21.92%, 95% CI 18.43–25.61) and the lowest in Australia (0.18%, 95% CI 0.17–0.18) – a 122-fold difference. Multivariable meta-regression showed that study size was the strongest predictor (importance: 97.79%). Regarding risk factors, female gender, age &gt; 50 years, increased body mass index, and family history of GS were significantly associated with higher GS prevalence. In contrast, factors such as education level, smoking, alcohol consumption, lifestyle, vegetarian diet, and serum lipid levels had no significant impact. Comorbidities including hypertension, diabetes mellitus, and metabolic-associated fatty liver disease (MAFLD) were strongly correlated with elevated GS prevalence. This meta-analysis showed that the GS was a common disease and affected the health of one in twenty people worldwide. Accurate estimates of the global and population-based prevalence of GS are helpful for healthcare improvements.
DOI: 10.6084/m9.figshare.30876631.v1
title: HDAC1 dysregulation promotes pro-inflammatory microglial activation and aggravates post-stroke neuroinflammation

description: Histone deacetylase 1 (HDAC1) is a key epigenetic regulator involved in DNA repair and neuronal survival. While HDAC1 downregulation has been implicated in ischemic brain injury, its role in regulating microglial functional shift and neuroinflammation remains unclear. This study aimed to investigate how HDAC1 dysfunction influences microglial activation states and contributes to neuroinflammatory processes in ischemic stroke. Using a rat model of endothelin-1–induced focal cerebral ischemia, HDAC1 knockdown was achieved <i>via</i> stereotactic co-injection of HDAC1 siRNA. Immunofluorescence, Western blotting, ELISA, and oxidative stress assays were performed to assess neuroinflammation, microglial polarization, and related signalling pathways. In parallel, HDAC1 was silenced in HMC3 human microglial cells, with or without IFN-γ stimulation, to evaluate transcriptional responses associated with pro-inflammatory activation. Finally, HDAC1 was selectively reactivated <i>in vivo</i> and <i>in vitro</i> using Compound 5104434 to assess behavioural, neuroinflammatory and mechanistic effects after ischaemic or inflammatory injury. HDAC1 knockdown <i>in vivo</i> led to a pronounced shift towards a pro-inflammatory microglial activation, evidenced by increased CD86 expression, along with elevated levels of IL-1β, IL-6, TNF-α, ROS, LDH and MMP activity. T-cell infiltration was also significantly enhanced. <i>In vitro</i>, HDAC1 deficiency sensitized microglia to IFN-γ, further amplifying the expression of pro-inflammatory genes. Mechanistically, HDAC1 knockdown activated the NF-κB pathway and its downstream effectors <i>MAP3K8, AP-1</i> and <i>SAT1,</i> while IFN-γ stimulation predominantly drove STAT3 phosphorylation. Notably, pNF-κB was upregulated even in the absence of exogenous stimulation, indicating that HDAC1 intrinsically suppresses pro-inflammatory signalling. HDAC1 enzymatic reactivation by compound 5104434 promotes functional recovery and suppresses NF-κB–driven microglial activation after stroke. HDAC1 acts as a key repressor of NF-κB–driven pro-inflammatory microglial activation and neuroinflammation in stroke. Its loss exacerbates inflammatory cascades, immune cell infiltration, and neuronal injury, underscoring HDAC1 as a potential therapeutic target for limiting secondary brain damage after ischaemic stroke.
DOI: 10.6084/m9.figshare.30206725
title: Efficacy and toxicity of treatment of smoldering multiple myeloma: a systematic review and meta-analysis

description: Smoldering multiple myeloma (SMM) is a slowly progressive, asymptomatic plasma cell disorder. This meta-analysis evaluated the efficacy and safety of novel agent-based therapies for SMM, particularly high-risk patients. PubMed, Embase, Web of Science, Ovid MEDLINE, Scopus and ClinicalTrials.gov were searched for randomized controlled trials (RCTs) and non-randomized studies from 2003 to 2024. Nineteen studies were included, comprising 5 RCTs and 14 non-randomized, single-arm trials. These studies involved a total of 1217 patients. Pooled analysis of intervention groups showed progression-free survival (PFS) and overall survival (OS) rate at 12 months of 94% (95% CI, 89%–98%) and 99% (95% CI, 97%–100%), respectively. The overall response rate (ORR) was 64% (95% CI, 50%–77%), and the complete response rate (CRR) was 12% (95% CI, 3%–25%). Minimal residual disease (MRD) negativity rate was 62% (95% CI, 42%–81%), and grade 3–4 adverse events (AEs) rate was 36% (95% CI, 30%–43%). As a comparison, we pooled data from the control groups of 5 RCTs, showing that PFS and OS rate-12m were 76% and 97%, respectively, with 0% CRR, 0% ORR and 25% grade 3–4 AEs. Subgroup analysis revealed high-risk SMM patients achieved higher PFS rate −12 m (97% vs. 91%), ORR (77% vs. 53%) and CRR (24% vs. 5%) compared to all SMM patients, with similar OS rate-12m (99% vs. 99%) and AEs rates (38% vs. 34%). Early intervention may delay progression and improve clinical responses, especially in high-risk SMM. However, adverse events (AEs) warrant caution. More well-designed RCTs are needed to confirm our findings.
DOI: 10.6084/m9.figshare.30206725.v1
title: Efficacy and toxicity of treatment of smoldering multiple myeloma: a systematic review and meta-analysis

description: Smoldering multiple myeloma (SMM) is a slowly progressive, asymptomatic plasma cell disorder. This meta-analysis evaluated the efficacy and safety of novel agent-based therapies for SMM, particularly high-risk patients. PubMed, Embase, Web of Science, Ovid MEDLINE, Scopus and ClinicalTrials.gov were searched for randomized controlled trials (RCTs) and non-randomized studies from 2003 to 2024. Nineteen studies were included, comprising 5 RCTs and 14 non-randomized, single-arm trials. These studies involved a total of 1217 patients. Pooled analysis of intervention groups showed progression-free survival (PFS) and overall survival (OS) rate at 12 months of 94% (95% CI, 89%–98%) and 99% (95% CI, 97%–100%), respectively. The overall response rate (ORR) was 64% (95% CI, 50%–77%), and the complete response rate (CRR) was 12% (95% CI, 3%–25%). Minimal residual disease (MRD) negativity rate was 62% (95% CI, 42%–81%), and grade 3–4 adverse events (AEs) rate was 36% (95% CI, 30%–43%). As a comparison, we pooled data from the control groups of 5 RCTs, showing that PFS and OS rate-12m were 76% and 97%, respectively, with 0% CRR, 0% ORR and 25% grade 3–4 AEs. Subgroup analysis revealed high-risk SMM patients achieved higher PFS rate −12 m (97% vs. 91%), ORR (77% vs. 53%) and CRR (24% vs. 5%) compared to all SMM patients, with similar OS rate-12m (99% vs. 99%) and AEs rates (38% vs. 34%). Early intervention may delay progression and improve clinical responses, especially in high-risk SMM. However, adverse events (AEs) warrant caution. More well-designed RCTs are needed to confirm our findings.
DOI: 10.6084/m9.figshare.28524541
title: Sodium butyrate alleviates DSS-induced inflammatory bowel disease by inhibiting ferroptosis and modulating ERK/STAT3 signaling and intestinal flora

description: Inflammatory bowel disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), can seriously impact patients’ quality of life. Sodium butyrate (NaB), a product of dietary fiber fermentation, has been shown to alleviate IBD symptoms. Some studies have shown that it is related to ferroptosis. However, the precise mechanism linking NaB, IBD, and ferroptosis is not clear. This study aimed to demonstrate that NaB suppresses ferroptosis, thereby alleviating inflammatory bowel disease (IBD) through modulation of the extracellular regulated protein kinases/signal transducer and activator of transcription 3 (ERK/STAT3) signaling pathway and intestinal flora. An IBD model was established using 2.5% (<i>w/v</i>) dextran sulfate sodium (DSS). Mice were orally administered low-dose NaB, high-dose NaB , or 5-aminosalicylic acid (5-ASA). Ferroptosis-related molecules were measured using specific kits, and western blotting (WB) and real-time polymerase chain reaction (RT-qPCR) were used to determine the levels of the target molecules. NaB alleviated symptoms in IBD mice, including reduced weight loss, prolonged colon length, reduced disease activity index (DAI), and reduced spleen index and mRNA expression of inflammatory factors. Additionally, NaB reduced the content of Fe<sup>2+</sup> and myeloperoxidase (MPO) and increased the content of GSH and the activity of superoxide dismutase (SOD), which reflected NaB-inhibited ferroptosis. Moreover, western blotting showed that NaB enhanced STAT3 and ERK phosphorylation. In addition, NaB regulates the composition and functions of flora related to IBD. NaB alleviates IBD by inhibiting ferroptosis and modulating ERK/STAT3 signaling and the intestinal flora. Sodium butyrate; IBD; ferroptosis; STAT3; ERK; gut microbiota