PURPOSE:Bone remodeling depends on the coordinated balance between osteoclast-mediated resorption and osteoblast-mediated formation. Although Indian hedgehog (Ihh) is known to regulate skeletal development and bone homeostasis, its direct involvement in osteoclastogenesis remains unclear. METHODS:We generated a novel mouse model, Ctsk-CreERT2; Ihhfl/fl, to investigate the role of Ihh in osteoclast lineage cells. Skeletal phenotypes were assessed by radiography, micro-CT, histology, dynamic histomorphometry, and three-point bending tests. Bone marrow macrophages were isolated to assess osteoclast precursor viability, RANKL-induced osteoclast differentiation, F-actin ring formation, and bone resorptive activity using CCK-8 assays, TRAP staining, phalloidin staining, and resorption pit assays. Osteoclastogenic gene expression and signaling pathway activation were examined by RT-qPCR and Western blotting. RESULTS:IhhCKO mice exhibited reduced body weight and an osteosclerotic phenotype, characterized by increased metaphyseal trabecular bone mass, improved femoral peak load and stiffness, and reduced cortical bone parameters. Histological analyses revealed fewer TRAP-positive osteoclasts on trabecular surfaces, increased osteoblast-related parameters, and decreased cortical bone formation indices. In vitro, Ihh deficiency reduced osteoclast precursor viability, impaired RANKL-induced osteoclast formation, decreased F-actin ring number/size and nuclei per osteoclast, and markedly reduced resorption pit formation. Mechanistically, Ihh loss suppressed osteoclast marker and fusion-related genes and diminished RANKL-induced JNK phosphorylation, c-Fos, NFATc1, and CTSK expression. CONCLUSIONS:Osteoclast-lineage-derived Ihh is required for efficient RANKL-induced osteoclastogenesis and bone resorption, at least in part by sustaining the JNK/c-Fos/NFATc1 axis. These findings identify Ihh as an osteoclast-intrinsic regulator of postnatal bone remodeling.
PURPOSE:Amelogenesis imperfecta (AI) is a group of inherited diseases characterized by enamel defects. Mutation in multiple genes may cause AI. The objective of this study was to investigate the specific roles of Family with sequence similarity 83 member H (FAM83H) in AI and determine its effect on ameloblasts. METHODS:To investigate the impact of Fam83h on ameloblast gene expression, we utilized ameloblast line HAT-7 cells with knockdown of Fam83h gene for transcriptome sequencing. The experimental cell samples were undergone library preparation and RNA sequencing expreiments. Cell Adhesion test kit was employed to evaluate the influence of Fam83h on HAT-7 cell adhesion ability. RT-qPCR and western blot were conducted to analyze the expression levels of integrin and collagen proteins upon downregulation of Fam83h. RESULTS:RNA-seq analysis revealed differential expression of 572 genes in HAT-7 cells with knockdown of Fam83h gene, including 285 up-regulated genes and 287 down-regulated genes. GO and KEGG enrichment analysis indicated that Fam83h could modulate collagen synthesis in ameloblasts as well as affect the focal adhesion pathway. In the cell adhesion assay, we observed a decrease in adhesion ability due to downregulation of Fam83h in HAT-7 cell line. Furthermore, it was found that Fam83h can upregulated extracellular matrix collagen formation in ameloblasts. CONCLUSIONS:Fam83h may affect the adhesion ability and extracellular matrix collagen formation in ameloblasts, leading to AI.
PURPOSE:Neuronal senescence contributes to several age-related neurodegenerative diseases occurring with aging. Meanwhile, aging of our bodies is accompanied by the systemic dysregulation of type I collagen, the major component in the extracellular matrix. This study investigates whether type I collagen plays a protective role in neuronal senescence. METHODS:Cellular senescence was assessed by evaluating senescence-associated β-galactosidase staining, cell area, senescence-associated proteins, and senescence-associated secretory phenotypes (SASPs); ferroptosis was evaluated using C11-BODIPY 581/591 fluorescent probe, GSH, MDA, and total iron assay kits; fluorescently labeled phalloidin staining was employed to examine the changes in F-actin levels. RESULTS:Coating the cell plates with type I collagen attenuates the senescence of murine hippocampal neuronal HT22 cells and alleviates ferroptosis induced by tert-butyl hydroperoxide (tBHP), a donor of reactive oxygen species. Enhancing ferroptosis-associated signaling by inhibiting GPX4 or FSP1 pathways promotes senescence of HT22 cells, suggesting that the ferroptosis signaling accelerates senescence. Integrin β1, a major component of receptors for collagen, is downregulated in tBHP-treated cells but rescued by collagen. F-actin was markedly disrupted in tBHP-treated cells, while restored by collagen, it protects cells against tBHP-induced ferroptosis and senescence. CONCLUSIONS:Our study reveals an F-actin/ferroptosis axis for regulating senescence of HT22 neuronal cells by extracellular type I collagen. The findings here suggest new anti-senescent strategies targeting the F-actin and ferroptosis pathways.
PURPOSE:The infrapatellar fat pad (IFP) is increasingly recognized as an active contributor to knee osteoarthritis (KOA) pathogenesis. However, age-related transcriptional changes in the IFP remain poorly understood, and whether observed differences are purely age-dependent or confounded by disease status is unclear. This study aimed to compare transcriptomic profiles of the IFP between young patients with traumatic knee injury and older patients with KOA. METHODS:IFP samples were obtained from three young trauma patients (21-28 years, KL grade 0) and three older patients with KOA (64-72 years, KL grade III-IV). Bulk RNA sequencing was performed to compare transcriptomes between groups. Differential expression was analyzed with DESeq2 (|log2FC| ≥1, unadjusted p < 0.05), followed by GO and KEGG pathway enrichment. Real-time PCR confirmed key expression changes. RESULTS:Compared with the young trauma group, the old KOA group exhibited 247 upregulated (CSN1S1, SCN9A, P2RY14, EIF3C, etc) and 334 downregulated genes (PI15, WISP3, DMKN, NUTM2G, etc). The old KOA group exhibited significantly reduced expression of extracellular matrix (ECM) genes, including COL1A1, COL2A1, and FN1. Additionally, core genes of the PI3K-Akt signaling pathway, such as AKT1, ITGA2B, and MYB, were also downregulated in the old KOA group. CONCLUSIONS:The IFP in old KOA exhibits a transcriptomic profile characterized by dampened ECM structural gene expression and suppressed PI3K-Akt signaling compared with young trauma patients. While confounded by injury status, these findings suggest that age-related loss of ECM integrity may contribute to IFP dysfunction in established KOA and warrant validation in healthy aging cohorts.
PURPOSE:To investigate the changes in synovial matrix stiffness in a mouse model of osteoarthritis (OA) and the expression of RAB27A, a key regulator of exosome biosynthesis, in synovial fibroblasts, and to validate the effect of matrix stiffness on RAB27A expression in vitro. METHODS:OA was induced in mouse knees by anterior cruciate ligament transection combined with medial meniscus destabilization (ACLT+DMM). Modeling efficacy was confirmed by Micro-CT, histology, and immunofluorescence. Synovial matrix stiffness was assessed by using nanoindentation. Mouse synovial fibroblasts were cultured on PEGDMA hydrogels with different stiffness, and RAB27A expression was detected by westernblot. RESULTS:Compared with the control group, the OA group exhibited a significant increase in synovial Young's modulus (~64%, p < 0.05), along with a ~ 1.53 fold increase in RAB27A-positive cells (p < 0.001). RAB27A expression showed a strong positive correlation with matrix stiffness (r = 0.671, p < 0.01). In vitro, the expression of RAB27A, MMP13, and COX2 was significantly upregulated in synovial fibroblasts cultured on stiff PEGDMA hydrogels, confirming a direct regulatory effect of matrix stiffness on exosome-related protein expression. CONCLUSIONS:Increased synovial matrix stiffness in OA may upregulate RAB27A expression, potentially regulating exosome secretion in synovial fibroblasts. This reveals a novel mechano-biological coupling mechanism in OA synovitis.
BACKGROUND:This study aimed to investigate the effects of retinoic acid receptor responder 2 (RARRES2) on osteoclast differentiation in postmenopausal osteoporosis (PMOP) and to elucidate the underlying mechanisms. METHODS:A rat model of PMOP was induced by bilateral ovariectomy (OVX) method, and an in vitro osteoclast differentiation model was induced by treating RAW264.7 cells with nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). Femoral bone structure, biomechanical properties, histology, osteoclast activity, co‑localization of RARRES2/CMKLR1 with TRAP+ osteoclasts and Perilipin‑1+ bone marrow adipocytes, gene expression, Fe2+ levels, reactive oxygen species (ROS) level, and lipid peroxidation level were detected. RESULTS:OVX model rats exhibited significant trabecular bone loss, compromised bone biomechanical properties, increased osteoclast numbers, elevated osteoclast differentiation markers, and upregulated RARRES2 expression compared with Sham controls. Co‑localization immunofluorescence revealed that RARRES2 was predominantly co‑localized with TRAP+ osteoclasts and Perilipin‑1+ bone marrow adipocytes. In vitro, RARRES2 knockdown markedly suppressed osteoclast differentiation, as evidenced by decreased osteoclast-related markers (NFATc1, CTSK, c-Fos, and F-actin) and reduced TRAP activity. Mechanistically, RARRES2 knockdown increased ferroptosis in osteoclasts, manifesting by decreased Nrf2, GPX4, HO-1, NQO1, and FTH1, along with increased ACSL4, Fe2+ accumulation , ROS production, and lipid peroxidation. These findings were also confirmed in vivo. Activation of Nrf2 with DMF partially reversed the ferroptotic alterations and osteoclast‑inhibiting effects induced by RARRES2 knockdown both in vitro and in vivo. CONCLUSION:RARRES2 knockdown inhibits osteoclast differentiation and alleviates PMOP progression by suppressing the activation of Nrf2/GPX4 and promoting osteoclast ferroptosis.
PURPOSE:The surface of chondrocytes is covered with membrane ruffles. Chondrocytes sense mechanical signals through cell membrane stretching and unfolding, a process mediated by the pericellular matrix (PCM). PCM is known to be thicker on the bone-facing (bf) inferior side than the surface-facing (sf) superior side, a feature thought to minimize membrane strain. Previously, we studied chondrocyte membrane morphology and noticed that membrane ruffles of some cells are concentrated at specific surface regions. We hypothesized that PCM asymmetry drives this non-uniform ruffle distribution. METHODS:Fresh cartilage samples (n = 10) were harvested and histologically processed for electron microscopy. Cell membrane outline was tracked from micrographs. Cells were divided into bf inferior and sf superior halves and ruffle density was quantified as waviness and fractal dimension. The density and distribution of membrane ruffles were measured for chondrocytes in the superficial, middle, and deep zones of cartilage. RESULTS:We found that membrane ruffles almost double the surface area of chondrocytes. Ruffle density is tissue zone-dependent; deep zone cells have ~20% less ruffles than superficial and middle zone cells. Asymmetric membrane ruffles were observed for cells in the top 100 µm of the tissue; the extent of asymmetry decreased with tissue depth. CONCLUSIONS:Chondrocyte membrane morphology is likely adapted to their mechanical and osmotic surroundings. Asymmetric membrane ruffles may be a multi-purpose strategy to increase membrane reservoir size and to deposit thick PCM layers for strain attenuation. This study highlights the importance of studying cells in their native environment to provide insights into in-situ cell mechanobiology.
PURPOSE:Composite neuromuscular injuries involving damage to peripheral nerves and skeletal muscles result in poor functional recovery due to excessive scarring. Current therapies lack specificity or carry significant side effects. We investigated the efficacy of a recombinant anti-collagen antibody (ACA) designed to inhibit extracellular collagen fibril formation, thereby reducing scar formation without disrupting intracellular reparative pathways. MATERIALS AND METHODS:In a rabbit model of composite injury involving a peroneal nerve crush and volumetric muscle loss of the tibialis anterior muscle, animals received local injections of an ACA-loaded or control thermoresponsive hydrogel. We measured neuromuscular functional recovery after composite injury using biomechanical and electrophysiological assays. Tissue was analyzed using histology, immunohistochemistry, and Fourier transform infrared (FTIR) spectroscopy. RESULTS:While electrophysiological parameters of injured nerves declined in all injured groups, ACA treatment markedly improved biomechanical properties of the injured limbs at 4 weeks post-injury compared to controls. This functional benefit was sexually dimorphic; females, who exhibited a more robust fibrotic response and severe muscle atrophy compared to males, demonstrated the most pronounced therapeutic recovery with ACA treatment. FTIR spectroscopy and polarized light microscopy confirmed that ACA treatment modulated the scar architecture, showing a trend toward reduced collagen content and cross-link maturity. Notably, the uninjured contralateral limbs likely exhibited compensatory hypertrophy and electrophysiological changes, highlighting their active role in systemic adaptation. CONCLUSIONS:Together, these findings suggest that targeting extracellular collagen fibrillogenesis may modestly enhance early functional recovery in composite neuromuscular trauma, particularly in biological contexts prone to excessive fibrosis.
Cholera remains a major public health concern in Ethiopia, particularly in conflict-affected agro-pastoral regions where access to healthcare, clean water and vaccination is limited. The main objective was to identify predictors of time to recovery from cholera among patients in a conflict-affected agro-pastoral area of Ethiopia using survival analysis models. Understanding the clinical and epidemiological factors influencing recovery time is critical for improving outcomes and guiding outbreak responses. A retrospective cohort study was conducted using data from cholera treatment centers in a conflict-affected agro-pastoral region. Time to recovery was analyzed using Kaplan-Meier recovery curves, Cox proportional hazards, and Accelerated Failure Time (AFT) models. Variables included clinical signs, demographic factors, vaccination status, and exposure history. Severe dehydration (HR = 0.49, p < 0.0001; TR = 1.49), low pulse rate (HR = 0.69, p = 0.005), and lack of vaccination (HR = 0.56, p < 0.0001) were associated with significantly longer recovery times. Notably, patients with known contact with cholera cases showed slower improvement (HR = 0.63, p = 0.0003), suggesting higher exposure or delayed care-seeking. Vaccinated individuals and those with mild dehydration recovered significantly faster. The log-Normal AFT model confirmed these findings, showing prolonged recovery among high-risk groups. In conflict-affected agro-pastoral settings, clinical severity, vaccination status, and exposure history are key determinants of cholera recovery time. These findings underscore the importance of early case detection, aggressive rehydration, and targeted vaccination, especially among known contacts and high-risk individuals. Public health interventions should prioritize rapid response strategies and contact-based follow-up to reduce disease burden and improve recovery outcomes.
Shelter and settlement are critical determinants of health in humanitarian crises, yet their impacts on health outcomes remain underexplored. This review synthesizes published evidence on how shelter and settlement interventions impact health outcomes in humanitarian crises. A systematic review of peer-reviewed literature was conducted to identify studies examining the association between shelter and settlement interventions and health outcomes in humanitarian crises. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines a protocol was developed and three databases were searched for studies published between 2005 and 2025. Relevant data were extracted and thematically analysed. A total of 138 articles were found. Thematic analysis identified six themes (living conditions, accommodation type, camp and site planning, displacement status, essential household items and cash-based interventions). Three cross cutting themes of gender, climate change and vulnerability were also identified. Two themes (living conditions and accommodation type) are presented here. Poor living conditions including damaged shelters, poor housing design and materials were associated with increased risks of communicable diseases such as malaria, diarrhoea, and soil-transmitted helminth infections while overcrowding heightened injury risk and psychological distress. Accommodation type influenced health outcomes with short-term shelters linked to acute mental health challenges and increased injuries; medium-term shelters with increased risk of non-communicable disease; and long-term housing with deteriorations in chronic disease management. This systematic review synthesises the evidence base showing how shelter and settlement interventions play a role in influencing health outcomes in humanitarian crises. It shows that shelter is a critical yet often under recognised determinant of health in these settings. Health outcomes are influenced by housing quality, accommodation type and duration, camp and settlement planning, displacement dynamics including frequency and length of displacement, and access to essential household items. Poor shelter conditions are likely to increase the risk of communicable diseases and mental health issues and have the potential to worsen chronic disease outcomes and risk. A key contribution of this review is the identification of shelter as a core entry point for public health action, highlighting the need for clearer operational guidance on shelter typologies, minimum standards, and their integration with health, protection and social services.
Access to essential medicines is a fundamental human right and a critical pillar of effective healthcare. In Africa, armed conflicts severely weaken health systems, disrupting the availability of essential medicine, leading to gaps in patients’ treatment and, in turn, posing a serious risk to overall public health. Therefore, this study aimed to identify the impact of armed conflicts on the availability of essential medicines as a cornerstone of healthcare across African regions, and quantify the extent of this disruption over time and by country. In this systematic review and meta-analysis, data were retrieved from published articles accessible in PubMed, Semantic Scholar, and grey literature covering the period from 1985 to 2025 and 2001 to 2024 for system impact and medicines availability studies, respectively. The literature search was conducted from January to May 2025. Following the Preferred Reporting Items for Systematic Reviews and Meta-analysis guidelines, studies were independently screened by two reviewers and included if they contained information on medicine availability or its relation to health systems in conflict zones and were published in English. The quality of studies was evaluated using the Joanna Briggs Institute criteria. Pooled estimates of medicine availability and their 95
Abstract Background Armed conflicts severely disrupt cancer care delivery, destroying infrastructure and limiting access to essential diagnostics and treatments. Evidence on service challenges, adaptations, and policy implications remains fragmented. Methods This scoping review of four databases (Scopus, PubMed, ScienceDirect, and CINAHL) was conducted for original peer-reviewed studies published between January 2020 and August 2025. The search focused on the effect of wars on cancer service delivery in conflict zones, and its impact on cancer care. Results Wars in conflict-affected countries like Palestine, Sudan, Syria, Iraq, Ukraine, and Afghanistan caused widespread destruction of cancer infrastructure, unsafe hospitals, and interruptions in chemotherapy, radiotherapy, and surgery. Countries faced shortages of specialized centers, technicians/radiologists, and medical records, alongside high costs and supply chain disruptions. Despite these challenges, healthcare systems demonstrated resilience through adaptations including Ukraine’s MedEvac program for EU treatment evacuation, cross-border referrals (Iraq→Lebanon, Afghanistan→Pakistan), telemedicine, mobile diagnostic units, and community-based care models. Policy responses emphasized international aid coordination, conflict-sensitive health planning, and supply chain restoration. Conclusion Conflicts cause infrastructure destruction, workforce depletion/migration, treatment barriers/delays, drug supply disruptions, and psychosocial/economic impacts, which in turn create urgent policy/governance challenges. Although humanitarian aid may provide temporary relief, sustainable solutions require peace and global commitment, grounded in equity and the fundamental right to health.
PURPOSE:Discitis is a severe suppurative infection of the intervertebral disc (IVD) posing significant clinical challenges. This study evaluated the therapeutic efficacy of ozonated water (OW) in a rat model of Staphylococcus aureus-induced discitis and elucidated its underlying mechanisms, focusing on NF-κB signaling, extracellular matrix homeostasis, and nucleus pulposus (NP) cell apoptosis. METHODS:A rat tail coccygeal IVD discitis model was established by injecting S. aureus (102 cfu) into the disc space. From day 3 post-infection, animals received transdiscal lavage with normal saline, levofloxacin (5 mg/mL), or OW (30 μg/mL) three times daily until day 9. In vitro, NP cells were stimulated with S. aureus Protein A (SpA, 1 μg/mL). Antibacterial activity, extracellular matrix metabolism, inflammatory cytokine expression, NF-κB p65 signaling, and apoptosis were evaluated by bacterial culture, Western blotting, immunohistochemistry, TUNEL assay, and flow cytometry. RESULTS:OW significantly alleviated tail swelling and IVD structural damage. OW demonstrated potent antibacterial activity against S. aureus, disrupting bacterial membrane integrity. OW attenuated extracellular matrix degradation by upregulating collagen II and aggrecan while downregulating MMP3 and MMP9, and suppressed inflammatory responses (IL-1β, IL-6, TNF-α, Cox2) by inhibiting NF-κB p65 phosphorylation and nuclear translocation. OW also reduced NP cell apoptosis, evidenced by decreased TUNEL-positive rate, elevated Bcl-2/Bax ratio, and reduced Cleaved caspase-3. CONCLUSIONS:OW attenuates S. aureus-induced discitis through direct antibacterial action, suppression of NF-κB-mediated inflammation, protection against NP cell apoptosis, and preservation of extracellular matrix integrity, highlighting its promise as a novel lavage strategy for discitis management.
Climate change presents more dire impacts on food security and health in Africa than any other region worldwide. These impacts are expectedly more pronounced in predominantly agrarian refugee settings like Uganda, which is also the largest refugee host in Africa. However, there is limited contextual evidence regarding the effects of climate change-related hazards in Uganda to guide context-relevant interventions amidst the ongoing aid cuts. We assessed the impact of climate change-related hazards on food security and the health of refugees in three settlements in Uganda. We conducted a cross-sectional study using concurrent mixed methods in Kiryandongo, Nakivale, and Rhino Camp refugee settlements. We collected data from 600 heads of refugee households using a structured questionnaire, conducted 45 in-depth interviews with refugees, and held 14 key informant interviews with program implementers. Quantitative data were analysed using STATA v16, and a modified Poisson regression model was employed to determine significant associations. Qualitative data were analysed inductively using thematic analysis to complement the quantitative findings. Of the 600 respondents, 60.6
Adolescence is a critical developmental stage marked by physical, psychological, and cognitive growth, increasing autonomy, social exploration, and risk-taking behaviors. However, these natural transitions in displacement settings are overshadowed by heightened vulnerabilities such as gender-based violence. In many displacement settings, recurrent exposure to violence leads to its acceptance as an unavoidable part of daily life. Sometimes, violence is normalized, leading to further exacerbation of the crisis. Our study explored the in-depth experiences and normalization of abuse and existing barriers to reporting within the internally displaced persons settlement in Cross River State, Nigeria. Our qualitative study included adolescents and young people aged 15–24 years residing in the Bakassi Internally Displaced Persons camp within the Bakassi Local Government Area. Participants were selected via purposive sampling. Data were collected through 12 individual interviews and 3 focus group discussions. Data were transcribed verbatim, and thematic analysis was conducted using NVivo 14 to identify key themes. Findings from the study reveal participants’ experiences with sexual exploitation, abuse, harassment, and gender-based violence, as well as their perceptions of abuse and how it is normalized. Contextual factors such as self-blame, societal pressure to accept advances from men, and limited accountability contribute to heightened vulnerability within the camps, which result in emotional and psychological impacts. Barriers to reporting and seeking help included fear of repercussions, lack of trust in authorities or services, and stigma associated with victimhood. Our study demonstrates that normalization of abuse, alongside systemic barriers such as fear of repercussions, stigma, and limited trust in authorities, significantly constrains reporting and help-seeking behaviors. Furthermore, our study identifies weak and largely absent accountability mechanisms as a key structural factor enabling continued abuse. To enhance accountability and safeguard vulnerable populations, appropriate legal penalties and enforcement measures should be applied to all forms of abuse. Additionally, future interventions should also address the underlying vulnerabilities that predispose individuals to abuse, ensuring a more comprehensive approach to prevention and protection.
International humanitarian organizations providing surgical care in conflict-affected settings have an ethical obligation to adopt practices that promote sustainable surgical services. Our objective was to evaluate the prevalence of sustainable surgical practices and policies implemented by humanitarian organizations in conflict-afflicted settings, as well as to document instances where surgical services were disrupted or discontinued due to the outbreak of conflict. A review of primary literature was conducted using Medline. Articles were included if they described sustainable surgical practices or policies in conflict-affected settings. Sustainability was defined according to a previously published modified Delphi consensus framework, which outlined key pillars of sustainability in global surgery partnerships. A grey literature review was also performed to identify sustainable policies published by international humanitarian organizations on their online platforms. Of 1,057 articles screened, 29 articles met inclusion criteria, describing 54 surgical programs implemented by 17 international humanitarian organizations —most commonly Médecins Sans Frontières (n = 27) and International Committee of the Red Cross (n = 5). These programs were implemented in 36 conflicts between 1946 and 2023, most commonly in Sub-Saharan Africa (n = 20), the Middle East (n = 11), and Southeast Asia (n = 9). The following six sustainability pillars were explicitly described: context-relevant education (94.4
Anemia remains a significant public health issue, especially in emergency areas and refugee camps. This study was conducted to determine the prevalence of anemia and its associated factors among children aged 6 to 59 months in Qoloji internally displaced people camp site, Somali Region, eastern Ethiopia. A community-based cross-sectional study was conducted among 401 children aged 6 to 59 months. Capillary blood was collected and hemoglobin level was determined using HemoCue Hb 301. Data was analyzed using SPSS version 26. Bivariable and multivariable logistic regression were used to identify determinants of anemia. The overall prevalence of anemia was found to be 51.4
Abstract Background High infant mortality rate (IMR) is a critical public health indicator. Understanding its trajectory is vital for policymaking, particularly in Somalia, where rates remain elevated. This study aimed to model and forecast Somalia’s IMR to identify the most accurate method, providing data-driven insights for public health strategy. Objectives The study aimed to formulate time series models, propose hybrid models, and rigorously compare their performance in forecasting IMR. Methods This quantitative time-series analysis utilized annual World Bank data for Somalia from 1950 to 2022. Three models were developed: Autoregressive Integrated Moving Average (ARIMA), Artificial Neural Network (ANN), and a hybrid ARIMA-ANN model. Performance was evaluated using Root Mean Square Error (RMSE) and Symmetric Mean Absolute Percentage Error (sMAPE) on a test set spanning 2013 to 2022. Results Upon achieving stationarity via first-order differencing, the ARIMA (1, 1, 3) model proved most effective. It demonstrated superior accuracy with an RMSE of 0.85, significantly outperforming the ANN (RMSE 1.04) and hybrid models (RMSE 3.01). Validated ARIMA forecasts project a continued, gradual decline in IMR from 59.02 deaths per 1,000 live births in 2023 to 40.37 in 2032. Conclusion The ARIMA model offers the most reliable framework for forecasting Somalia’s infant mortality rate based on historical data.
Patients receiving maintenance hemodialysis are highly vulnerable during armed conflict, particularly when healthcare systems are disrupted. However, factors associated with survival under prolonged disruption remain poorly understood. This study examined survival and key associated factors among hemodialysis patients during the armed conflict in Sudan. We conducted a retrospective cohort study of 158 adults receiving maintenance hemodialysis in Khartoum, Sudan, at the onset of the April 2023 conflict, with follow-up extending up to 18 months. Outcomes were confirmed for 122 patients, while 36 were untraceable and censored at their last verified contact. Participants were categorized according to displacement trajectory within the first three months. The primary outcome was survival. Key variables included displacement trajectory, dialysis frequency during follow-up, and out-of-pocket costs. Risk ratios and time-to-event approaches were used to examine associations, with sensitivity analyses conducted to assess the impact of loss to follow-up. Of the 122 patients with confirmed outcomes, 53.3
PURPOSE:Dupuytren's contracture (DC) is a common fibroproliferative disorder with strong genetic predisposition. This study aimed to investigate the association between genetic variants in key fibrotic pathways and DC susceptibility in a Lithuanian population. MATERIALS AND METHODS:We conducted a case-control study including 116 patients with DC and 103 healthy controls. Genotyping of four single nucleotide polymorphisms (SNPs) involved in fibrotic pathway regulation was performed: COL1A1 rs1800012, TAB2 rs2179367, SFRP4 rs1668357, and SFRP4 rs1668347. RESULTS:The COL1A1 rs1800012 A allele demonstrated a significant protective effect against DC (OR = 0.584; 95% CI: 0.350-0.973; p = 0.039), with the strongest association observed in the dominant model (CA + AA vs. CC: OR = 0.521; 95% CI: 0.286-0.951; p = 0.034). Conversely, the SFRP4 rs1668347 C allele was associated with increased DC risk (OR = 1.831; 95% CI: 1.126-2.976; p = 0.015), with significant associations in codominant (AC vs. AA: OR = 2.203; p = 0.007), dominant (AC + CC vs. AA: OR = 2.162; p = 0.007), and overdominant (AC vs. AA + CC: OR = 2.105; p = 0.010) models. No significant associations were found for the other investigated SNPs. CONCLUSIONS:Our findings support the involvement of collagen metabolism and Wnt signaling in DC pathogenesis. The protective effect of COL1A1 rs1800012 and the risk-enhancing effect of SFRP4 rs1668347 provide additional insights into the genetic basis of DC and may contribute to the development of predictive tools and targeted therapies for this debilitating condition.
