Indigenous people affected by cancer often encounter services that do not reflect their languages, relationships, knowledge systems, or community priorities. Survivor narratives are used in cancer education, yet the educational work undertaken by survivors has not been mapped. This scoping review examined the roles, formats, reported outcomes, and conditions shaping implementation when Indigenous cancer survivors participated in peer education and community knowledge exchange. Following Joanna Briggs Institute guidance and the reporting guideline for scoping reviews, six databases were searched from inception through July 2026. Twenty-one reports published between 2005 and 2026 were included. Survivor knowledge moved in three overlapping directions: between survivors through reciprocal support, outward to communities through education and storytelling, and toward organizations through co-design, navigation, advocacy, and service learning. Survivors served as peer educators, storytellers, advisors, advocates, resource co-creators, and knowledge stewards. Their activities produced peer sessions, performances, videos, digital stories, service priorities, navigation guidance, and community archives. Program evaluations reported cancer learning, greater comfort discussing cancer, reduced treatment anxiety, increased confidence sharing information, information seeking, and higher screening intention. Other reports described feeling less alone, healing and affirmation, culturally safer engagement, community-defined priorities, and survivor or community control over the representation and circulation of stories. Resourcing survivor leadership may strengthen cancer education while protecting reciprocity, cultural authority, and community control.

Long COVID is frequently associated with persistent exercise intolerance, although the relative contributions of peripheral vascular dysfunction and myocardial function remain unclear. We investigated whether persistent endothelial dysfunction and altered myocardial work (MW) contribute to exercise intolerance approximately 3 years after SARS-CoV-2 infection. This case-control study included adults with Long COVID (n = 10) and controls (n = 11) who underwent cardiopulmonary exercise testing (CPET), transthoracic echocardiography with global longitudinal strain (GLS) and MW analysis, and brachial artery flow-mediated dilation (FMD) with hyperemic shear assessment. Compared with controls, Long COVID participants exhibited lower peak V̇O₂ (19.6 ± 2.5 vs. 24.3 ± 6.5 mL·kg^-1·min^-1, p = 0.04), percent-predicted peak V̇O₂ (61.1 ± 8.3 vs. 77.0 ± 14.2%, p = 0.006), and V̇O₂ at first ventilatory threshold (11.0 ± 1.4 vs. 13.7 ± 3.8 mL·kg^-1·min^-1, p = 0.04). Conventional echocardiographic parameters and MW indices did not differ between groups (all p > 0.05). In contrast, endothelial function was impaired in the Long COVID group, with lower FMD (p < 0.001), peak shear rate (p = 0.01), AUCSR (p = 0.04), and AUCmax (p = 0.001). FMD correlated positively with exercise capacity in the Long COVID group (peak V̇O₂: r = 0.68, p = 0.03;percent-predicted peak V̇O₂: r = 0.64, p = 0.04). In conclusion, 3 years after infection, Long COVID remains characterized by endothelial dysfunction and blunted hyperemic shear despite preserved MW, supporting a predominantly peripheral vascular basis for persistent exercise intolerance.

Ventilator-associated pneumonia (VAP) is one of the infectious diseases with the highest mortality due to increasing bacterial resistance to antibiotics. Therefore, early diagnosis and targeted treatment against the etiologic agent are essential. The use of a pneumonia panel facilitates identification of the causative pathogen earlier than with conventional culture and may mitigate adverse events in patients.

To evaluate the association between the use of a pneumonia panel and clinical outcomes in patients with ventilator-associated pneumonia at a Peruvian hospital.

This retrospective cohort included patients diagnosed with severe COVID-19 and VAP between May 2021 and February 2022 in the intensive care unit (ICU) of a hospital in Lima, Peru. All patients diagnosed using panel + culture (n = 89) were included, and 89 controls diagnosed using culture only were randomly selected. Adjusted regression models were used to evaluate the association with clinical outcomes.

178 patients were included (mean age: 47.9 years; males: 72.5%). When comparing the panel + culture and culture-only groups, adjusted analyses found no statistically significant differences in mortality (aRR: 0.56, 95% CI: 0.25 to 1.27), days on mechanical ventilation (aMD: 4.74, 95% CI: -0.76 to 10.23), or ICU length of stay (aMD: 4.94, 95% CI: -1.09 to 10.97). However, the panel + culture group had more days of antibiotic therapy (aMD: 2.00, 95% CI: 0.45 to 3.55) and a higher number of isolated microorganisms.

No differences were found in mortality, ICU length of stay, or days on mechanical ventilation. However, a greater number of days of antibiotic therapy was observed in the cohort using the pneumonia panel.

Reliable estimation of sensitive public health outcomes, such as underreported COVID-19 cases and vaccine hesitancy, is frequently hindered by social stigma and nonresponse bias, particularly in culturally sensitive contexts like Pakistan. Traditional surveys often underestimate prevalence, limiting the effectiveness of public health interventions.

Multi-stage stratified paired response frameworks (MSPRFs) incorporating two and three-stage randomization with dual scrambling mechanisms under stratified simple random sampling were applied. A cross-sectional survey of 1,200 participants (600 urban, 600 rural) from Faisalabad, Lahore, Multan, and Rawalpindi (June-August 2021) was conducted using anonymous questionnaires to collect data on outbreak cases and vaccine hesitancy.

The MSPRFs demonstrated substantially enhanced estimation efficiency (PRE 290-399%) relative to conventional methods. MSPRF-I estimated COVID-19 prevalence at 16.8% (urban) and 20.8% (rural), compared with reported rates of 12.1% and 13.6%; MSPRF-II estimated 16.8% and 19.2% versus reported 12.6% and 14.6%. Vaccine hesitancy was estimated at 33.8% (MSPRF-I) and 29.5% (MSPRF-II), relative to 24.3% reported. Urban respondents exhibited higher reporting sensitivity ([Formula: see text]) than rural respondents ([Formula: see text]), indicating geographic disparities in disclosure behavior.

MSPRFs provide a robust, privacy-preserving methodology for accurately estimating underreported COVID-19 cases and vaccine hesitancy, supporting evidence-based public health decision-making. MSPRF-II offers marginally higher adjustment efficiency due to inclusion of a truthful-response component. These frameworks are appropriate for sensitive epidemiological surveys in contexts where conventional self-reporting underestimates prevalence.

Chronic rhinosinusitis (CRS) is a complex inflammatory condition affecting the sinonasal mucosa. The bitter taste receptor T2R38 (encoded by TAS2R38) is expressed on ciliated respiratory epithelial cells, detecting bacterial quorum-sensing acyl-homoserine lactones to stimulate nitric oxide production and accelerate mucociliary clearance. However, whether mucosal TAS2R38 transcript levels vary across distinct sinonasal anatomical niches remains unverified, raising concerns regarding potential sampling bias in translational airway research.

To determine whether sinonasal mucosal TAS2R38 gene expression differs across anatomical sub-sites in patients with CRS undergoing functional endoscopic sinus surgery (ESS) and evaluate variance contributions between individual host biology and biopsy sites.

In this prospective cross-sectional study, 337 mucosal specimens were harvested from up to six anatomical sites (inferior turbinate, maxillary, ethmoid, frontal, and sphenoid sinuses, and nasal polyps) in 67 surgical CRS patients (EPOS 2020 criteria), alongside 29 non-inflammatory septal control specimens. Relative TAS2R38 mRNA expression was quantified by MIQE-compliant RT-qPCR normalized to GAPDH. Clustered paired [Formula: see text]data were evaluated using linear mixed-effects modeling with patient-specific random intercepts as the principal analytical framework, alongside sensitivity analyses and fold-difference calculations ([Formula: see text]).

Following quality control (excluding 84 specimens due to strict cycle thresholds and minute fibrous tissue yield), 253 valid specimens across 55 patients were analyzed (inferior turbinate: n = 52; maxillary: n = 50; ethmoid: n = 49; polyps: n = 44; frontal: n = 43; sphenoid: n = 15). Mean [Formula: see text]values were comparable across subsites (range: 2.06 to 2.81; exploratory ANOVA F = 0.42, P = 0.834). In the principal linear mixed-effects model, anatomical sampling site was not associated with TAS2R38 expression ([Formula: see text]). Inter-individual biological variance ([Formula: see text]; ICC = 0.333) substantially exceeded intra-individual spatial variation. Robustness was verified across six sensitivity scenarios, including the exclusion of sphenoid tissues and multivariable adjustments for age and sex (P = 0.617). Diseased mucosa demonstrated an exploratory 2.48-fold upregulation relative to non-site-matched septal controls.

Mucosal TAS2R38 mRNA expression shows no statistically significant association with anatomical sampling site in surgical CRS, with transcript variability driven predominantly by between-patient biological differences. These findings provide translational evidence supporting the potential utility of inferior turbinate biopsy as a pragmatic, accessible surrogate for investigating sinonasal chemosensory innate defense.

Cough is a prominent and often persistent manifestation of chronic bronchitis (CB) that is frequently difficult to resolve. While Qi Feng Gu Biao Granules (QFGBG) is a traditional Chinese medicine commonly used to treat CB, its pharmacological basis for CB-related cough remains unclear.This study characterized the chemical profile of QFGBG by UPLC-Q-TOF/MS, evaluated its antitussive and anti-inflammatory effects in a rat model induced by lipopolysaccharide instillation combined with cigarette smoke exposure, and integrated network pharmacology, molecular docking, Western blotting, and plasma metabolomics to explore the underlying mechanism.QFGBG reduced cough frequency, prolonged cough latency, improved body-weight gain, and decreased the lung index and wet-to-dry ratio. Histological analyses showed attenuation of lung and tracheal inflammatory injury and mucus hypersecretion. QFGBG also decreased the expression of inflammatory and cough-related factors. Network pharmacology identified 215 overlapping QFGBG-CB targets, with enrichment in inflammatory and metabolic pathways, including the AGEs/RAGE signaling pathway. Molecular docking suggested favorable binding of core components, including Formononetin, Acacetin, and Vanillin, to key targets. Western blotting confirmed that QFGBG downregulated AGEs, RAGE, p-STAT1/STAT1、p-STAT3/STAT3. Metabolomics indicated regulation of glycerophospholipid and arachidonic acid metabolism. These findings suggest that the active components of QFGBG may alleviate CB-related cough by inhibiting the AGEs/RAGE signaling pathway and regulating arachidonic acid and glycerophospholipid metabolism, thereby reducing pulmonary and neurogenic inflammation and the release of cough-related mediators.

Swine influenza A viruses (IAV-S) caused the 2009 H1N1 pandemic and pose a future zoonotic and pandemic threat. Vietnam represents a critical hotspot for IAV-S emergence within East and Southeast Asia, with dense swine and human populations and intensive livestock trade. We conducted genomic surveillance of IAV-S in Vietnam during 2020-2024, extending previous surveillance from 2013-2019. We identified multiple co-circulating H1 and H3 clades, including pandemic H1N1, Eurasian avian-like, and European lineages, by conducting phylogenetic analysis of 56 IAV-S isolates (21 H1N1, 31 H1N2, and 4 H3N2). Three H1 clades persisted exclusively in Vietnam, circulating up to 12 years. Phylogeographic analysis revealed multiple independent introduction events from North America, Europe, China, Thailand, and Cambodia. We detected extensive reassortment that frequently involved pandemic H1N1 virus internal genes. We identified several lineage-specific mutations associated with mammalian adaptation. Our findings underscore the ongoing IAV-S evolution and need for sustained surveillance in Vietnam.

To evaluate the diagnostic accuracy of the Arabic Composite Autonomic Symptom Score-31 (COMPASS-31) for detecting objectively confirmed autonomic neuropathy in patients with SLE.

In this cross-sectional diagnostic accuracy study, 45 patients with SLE, 23 patients with neurologically confirmed autonomic neuropathy (positive-control group), and 45 healthy controls completed the Arabic COMPASS-31 before undergoing cardiovascular autonomic reflex testing (CART) and sympathetic skin response (SSR). Objective autonomic neuropathy was defined as abnormal CART and/or absent SSR. Diagnostic accuracy analyses (receiver operating characteristic (ROC) curve analysis, optimal cut-off determination and multivariable logistic regression) were performed within the SLE cohort.

Objective autonomic neuropathy was present in 28 of 45 patients with SLE (62%). Total COMPASS-31 score discriminated autonomic neuropathy status with an area under the ROC curve (AUC) of 0.81 (95% CI 0.68 to 0.94) at a cut-off of ≥5 (sensitivity 89% and specificity 59%), increasing to 0.89 (95% CI 0.79 to 0.98) when restricted to definite/severe autonomic neuropathy. The orthostatic intolerance (AUC 0.78, 95% CI 0.64 to 0.91) and pupillomotor (AUC 0.77, 95% CI 0.64 to 0.90) domains performed similarly to the total score (DeLong's test, both p>0.4), while the vasomotor, secretomotor, gastrointestinal and bladder domains performed significantly worse. The COMPASS-31 total score remained independently associated with autonomic neuropathy after adjustment for age, disease duration and disease activity (adjusted OR 1.29, 95% CI 1.06 to 1.57). Internal consistency of the Arabic COMPASS-31 was good (Cronbach's α=0.83, McDonald's ω=0.857).

The Arabic COMPASS-31 demonstrates good discrimination for objectively confirmed autonomic neuropathy in SLE, with the orthostatic intolerance and pupillomotor domains contributing most of its discriminative value. It can be used as a screening tool to identify patients who warrant confirmatory autonomic testing. Disease-specific validation should precede recommending COMPASS-31 as an autonomic neuropathy screening tool in other rheumatic diseases.

Interleukin-22 (IL-22), a member of the IL-10 cytokine family, primarily targets non-haematopoietic epithelial and stromal cells, contributing to maintenance of epithelial barrier integrity, antimicrobial immunity and tissue regeneration. In this study, we sought to evaluate the association between serum levels of IL-22, measured by an ultrasensitive assay, and disease characteristics in patients with SLE.

In this cross-sectional study, we thoroughly assessed 313 patients with SLE, collecting data on autoantibody status as well as disease activity indices (SLE Disease Activity Index-2000 and Lupus Low Disease Activity State), damage accrual (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SLICC-DI)) and remission status (Definitions of Remission in SLE). The cohort was also characterised in terms of haematological parameters, lipid profile, insulin resistance markers and measures of subclinical carotid atherosclerosis and arterial stiffness. Serum IL-22 concentrations were quantified using the Simoa (Single Molecule Array) platform. We then used multivariable linear regression to explore the associations between these clinical characteristics and circulating IL-22 levels.

After multivariable adjustment, serum IL-22 levels were independently linked to longer disease duration, cumulative damage (SLICC-DI >1) and inversely to methotrexate use. However, these associations did not remain significant after multiple comparison correction. Disease activity, autoantibody profile or complement and interferon levels did not show significant associations with IL-22 levels. Similarly, haematological parameters were not related to circulating IL-22. Regarding cardiovascular risk factors, IL-22 was inversely related to high-density lipoprotein-cholesterol and apolipoprotein A1 suggesting an adverse lipid profile. In addition, serum C-peptide levels were independently related to higher circulating IL-22 concentrations whereas the presence of metabolic syndrome was associated with increased IL-22 levels. Besides, carotid intima-media thickness was significantly correlated with superior IL-22 levels after adjustment for covariates although in this case this association did not withstand adjustment for multiple testing.

In patients with SLE, IL-22 identifies a phenotype of increased cardiovascular risk despite showing little relationship with current disease activity.

Pesticides have been widely used in agricultural practices, as well as in the prevention of vector-borne and other communicable diseases. Although the ecotoxicology and adverse effects on human health are known, recent studies have shown that some types of pesticides may interact with therapeutic drugs, a fact that should be recognized by public health authorities as a new public health issue. The current review was intended to provide an overview of the present knowledge of different groups of pesticides (insecticides, herbicides, and fungicides), as well as their mechanisms of action, which could influence both human health and the action of therapeutic drugs. These mechanisms affect ADME processes and share similar pharmacodynamic targets with drugs acting at the level of the central nervous system, cardiovascular system, endocrine glands, or Parkinson's disease. Importantly, these mechanisms of action of pesticides are also relevant for drug pharmacokinetics and pharmacodynamics and may result in interactions between pesticides and therapeutic drugs, very much like typical drug-drug interactions. However, vulnerable groups such as farmers, pregnant women, children, and people suffering from chronic conditions are especially vulnerable. Oxidative stress turns out to be a common pathology that ties exposure to pesticides to brain cell degeneration, infertility, and reduced pharmacodynamics. Despite the availability of safer substitutes, such as biopesticides, human-based research is vital in terms of mixtures and modulators. It is imperative to acknowledge pesticides as environmental factors influencing drug responsiveness for optimal pharmacological treatment.