BACKGROUND: Artificial intelligence (AI) offers significant potential to drive advancements in healthcare; however, the development and implementation of AI models present complex ethical, legal, social, and technical challenges, as data practices often undermine regulatory frameworks in various regions worldwide. This study explores stakeholder perspectives on the development and deployment of AI algorithms for diabetic retinopathy (DR) screening, with a focus on ethical risks, data practices, governance, and emerging shortcomings in the Global South AI discourse. METHODS: Fifteen semi-structured interviews were conducted with ophthalmologists, program officers, AI developers, bioethics experts, and legal professionals. Thematic analysis was guided by OECD principles for responsible AI stewardship. Interviews were analyzed using MAXQDA software to identify themes related to AI trustworthiness and ethical governance. RESULTS: Six key themes emerged regarding the perceived trustworthiness of AI: algorithmic effectiveness, responsible data collection, ethical approval processes, explainability, implementation challenges, and accountability. Participants reported critical shortcomings in AI companies' data collection practices, including a lack of transparency, inadequate consent processes, and limited patient awareness about data ownership. These findings highlight how unchecked data collection and curation practices may reinforce data colonialism in low and middle-income healthcare systems. CONCLUSION: Ensuring trustworthy AI requires transparent and accountable data practices, robust patient consent mechanisms, and regulatory frameworks aligned with ethical and privacy standards. Addressing these issues is vital to safeguarding patient rights, preventing data misuse, and fostering responsible AI ecosystems in the Global South.

Alpha-lipoic acid (α-LA), an endogenous antioxidant co-factor of important enzymatic complexes, is rapidly catabolised in dihydrolipoic acid becoming an even stronger antioxidant for strengthening the activity of endogenous antioxidants (vitamin C, E, glutathione). AIM. To evaluate the effects of an oral use liquid formulation containing the natural and more active α-lipoic acid (R-αLA) enantiomer on 20 subjects oxidative status: 10 apparently healthy subjects and 10 affected by risk factors (such as excess weight, hypertension) and/or diseases (such as diabetes, polyneuropathy). The subjects’ oxidative status was assessed by measuring blood concentrations of: reactive oxygen species (ROS), total antioxidant capacity (TAC), glutathione, Vitamin C and Vitamin E at baseline (T0) and after 1-month’ supplementation (T1) with R-αLA. Moreover, cysteine and homocysteine levels, well-known cardiovascular risk factors, were measured. Results. Interesting findings on the cellular antioxidant regeneration cycle: a significant decrease in reduced glutathione (GSH) levels and GSH/GSSG ratio, a slight downward trend in oxidised glutathione (GSSG) and vitamin C and E concentrations. Due to the brief treatment period, the study did not however show any significant differences in the oxidative “status” balancing parameters (ROS and TAC) and on homocysteine and cysteine levels. Remarkable were the findings regarding patients who reported a lessening, or even the disappearance, of pain symptoms. Comment. After 1-month’ treatment, the R-αLA oral use liquid formulation seemed to reinforce endogenous antioxidant activity and, notably, helped mitigate the pain symptoms typical of several stress oxidative-dependent diseases. This effect could probably depend on greater bioavailability of the liquid formulation.

BACKGROUND: Platelet-derived growth factor-BB (PDGF-BB) is a profibrotic factor in liver fibrosis through its ability to stimulate hepatic stellate cells (HSC). The liver-derived serine protease factor VII activating protease (FSAP) regulates the activities of PDGF-BB in a cell-specific manner. AIMS: Our aim was to determine the influence of FSAP on the activation of HSC and to analyse the regulation of FSAP in hepatic fibrogenesis. METHODS: The effect of FSAP on PDGF-stimulated p42/p44 mitogen-activated protein kinase (MAPK) activation in primary rat HSC was determined by Western blotting. Migration and proliferation of HSC was evaluated in Boyden chamber experiments and (3)H-thymidine incorporation assays respectively. Expression of FSAP was analysed in a CCl(4) mouse model of liver fibrosis by Western blot, quantitative real-time polymerase chain reaction and immunohistochemistry. RESULTS: FSAP inhibited PDGF-BB-stimulated p42/p44 MAPK phosphorylation, proliferation and migration of HSC. FSAP mRNA expression level was increased 3 h after CCl(4) application and decreased after 18 h and, in established fibrosis, after chronic CCl(4) administration. In parallel, there was a decrease in the circulating FSAP protein in chronic fibrosis. Concurrently, the homogenous hepatic expression pattern of FSAP was disturbed. Immunohistochemistry revealed a decrease of FSAP in hepatocytes in inflammatory and fibrotic lesions. CONCLUSIONS: Our results demonstrate an inhibitory effect of FSAP on PDGF-mediated activation of HSC. In addition, FSAP expression is transiently increased in acute-phase reaction but decreased during chronic fibrogenesis, which in turn may influence PDGF-BB availability and myofibroblast activity.

The administrative burden in healthcare, particularly documentation-related tasks, poses a critical challenge for oncology nurses in the Asia-Pacific region. This diverts valuable time from direct patient care and contributes significantly to cognitive overload, burnout, and workforce attrition.1-7 Empirical studies from India2,3 and South Korea4,5 highlight the mental health toll on oncology nurses, identifying clinical documentation as a consistent and substantial source of stress.6,7 Addressing this pressing issue demands innovative, evidence-based interventions.

Five years after the onset of the COVID-19 pandemic, health workers worldwide continue to endure significant, ongoing strain. The World Health Organization’s (WHO) 2025 global assessment reported that 63% of country offices observed job-related impacts on health workers1. Initially an acute crisis characterized by equipment shortages, overcrowded facilities, and rapidly evolving protocols, the pandemic has evolved into a protracted systemic challenge. Complementary analyses from the Organization for Economic Co-operation and Development (OECD) indicate that nearly 40% of physicians under the age of 55 report burnout, with over 10% intending to leave clinical practice2.

UNLABELLED: In addition to liver-resident Kupffer cells, infiltrating immune cells have recently been linked to the development of liver fibrosis. Blood monocytes are circulating precursors of tissue macrophages and can be divided into two functionally distinct subpopulations in mice: Gr1(hi) (Ly6C(hi)) and Gr1(lo) (Ly6C(lo)) monocytes. The role of these monocyte subsets in hepatic fibrosis and the mechanisms of their differential recruitment into the injured liver are unknown. We therefore characterized subpopulations of infiltrating monocytes in acute and chronic carbon tetrachloride (CCl(4))-induced liver injury in mice using flow cytometry and immunohistochemistry. Inflammatory Gr1(hi) but not Gr1(lo) monocytes are massively recruited into the liver upon toxic injury constituting an up to 10-fold increase in CD11b(+)F4/80(+) intrahepatic macrophages. Comparing wild-type with C-C chemokine receptor (CCR2)-deficient and CCR2/CCR6-deficient mice revealed that CCR2 critically controls intrahepatic Gr1(hi) monocyte accumulation by mediating their egress from bone marrow. During chronic liver damage, intrahepatic CD11b(+)F4/80(+)Gr1(+) monocyte-derived cells differentiate preferentially into inducible nitric oxide synthase-producing macrophages exerting proinflammatory and profibrogenic actions, such as promoting hepatic stellate cell (HSC) activation, T helper 1-T cell differentiation and transforming growth factor beta (TGF-beta) release. Impaired monocyte subset recruitment in Ccr2(-/-) and Ccr2(-/-)Ccr6(-/-) mice results in reduced HSC activation and diminished liver fibrosis. Moreover, adoptively transferred Gr1(hi) monocytes traffic into the injured liver and promote fibrosis progression in wild-type and Ccr2(-/-)Ccr6(-/-) mice, which are otherwise protected from hepatic fibrosis. Intrahepatic CD11b(+)F4/80(+)Gr1(+) monocyte-derived macrophages purified from CCl(4)-treated animals, but not naïve bone marrow monocytes or control lymphocytes, directly activate HSCs in a TGF-beta-dependent manner in vitro. CONCLUSION: Inflammatory Gr1(+) monocytes, recruited into the injured liver via CCR2-dependent bone marrow egress, promote the progression of liver fibrosis. Thus, they may represent an interesting novel target for antifibrotic strategies.

NOV/CCN3 is a matricellular protein of the CCN family, comprising CCN1 (CYR61), CCN2 (CTGF), CCN4 (WISP-1), CCN5 (WISP-2), and CCN6 (WISP-3). CCN proteins are involved in mitosis, adhesion, apoptosis, extracellular matrix production, growth arrest and migration of multiple cell types. Compared with CTGF, NOV has been studied to a lesser degree and its biological role in liver fibrosis remains primarily unknown. We therefore investigated hepatic expression of NOV in chronic liver injury upon long term CCl4 treatment and bile duct ligation (BDL) rat models. NOV gene expression was quantified by TaqMan RT-PCR, immunohistochemistry and ELISA. In both models of chronic liver injury, NOV mRNA showed significant and sustained upregulation. Specifically in BDL models, immunohistochemistry revealed clear expression of NOV protein in portal myofibroblasts, HSC and proliferative bile ducts along the fibrotic septa. Additionally, CCL4 models showed positive staining in particular regenerative hepatocytes. By contrast, TaqMan RT-PCR demonstrated no NOV expression in cultured hepatocytes isolated from naive and CCl4 treated rats. Culture-activated HSC however showed significant upregulation of NOV, reaching the highest levels in MFB.

BACKGROUND: The aim of this study was to assess work system factors and nurse and physician well-being across professionals (nurse vs. physician) and geographic locations (rural vs. urban) during COVID-19 pandemic. METHODS: This study invited nurses and physicians within four hospitals from one large healthcare system to participate: one urban academic medical center and three rural hospitals. We measured work systems factors using the National Academy of Medicine (NAM) framework and the National Institute for Occupational Safety and Health (NIOSH) survey. Wellbeing was measured using the 2-question summative burnout score, Patient Health Questionnaire (PHQ-9) to measure depression, and post-traumatic stress disorder (PTSD) checklist (PCL) to measure PTSD symptoms. Statistical analyses were conducted using Chi-square (for Likert-scale items) and <em>t</em>-tests (for continuous scales) as appropriate. Statistical significance was set at the .05 level, two-tailed. RESULTS: Overall, our results suggested that nurses and physicians working in the urban settings experience more impeding work system factors and are more burned out, depressed, exhibit more PTSD symptoms, and face greater overall well-being issues, when compared to nurses and physicians working in the rural settings.Conclusions/Applications to Practice:This study examined a comprehensive set of work system factors and well-being measures to better understand differences between rural and urban settings, and nurses compared to physicians. By examining this entire set of measures, we were able to provide a greater insight into the key differences, highlighting opportunities for policy-level contributions to prevent work related impairments from reaching the healthcare workforce.

Detailed reports from four working session and a workshop on preclinical models in personalized medicine. The working sessions were dedicated to 1. Industry, 2. In silico models, 3. In vivo models and 4. In vitro models. The main workshop discussed the outline of recommendations for robust and reproducible preclinical research in personalised medicine.