Biomedical Journal最新文献

Lymphedema, a chronic lymphatic disorder characterized by swelling, fibrosis, and adipose tissue accumulation, requires precise, stage-specific imaging for effective diagnosis and management. This review evaluates conventional imaging modalities, including indocyanine green lymphography (ICG-L), lymphoscintigraphy, magnetic resonance imaging (MRI), and computed tomography (CT), alongside emerging artificial intelligence (AI) applications to enhance diagnostic accuracy and treatment planning. We analyze their capabilities in assessing lymphatic function and tissue changes through quantitative biomarkers, comparing their strengths across disease stages. ICG-L excels in detecting early lymphatic dysfunction, while MRI and CT provide detailed visualization of advanced fibrotic and adipose changes. AI-driven tools, such as automated segmentation and biomarker quantification, show promise in improving tissue characterization and supporting surgical planning. However, clinical integration of AI is hindered by data heterogeneity, lack of interpretability, and regulatory challenges. To address these, we propose a strategic framework incorporating federated learning for privacy-preserving model training, explainable AI for clinical transparency, and standardized imaging protocols. Future efforts should prioritize multicenter validation and harmonized guidelines to enhance reproducibility and ensure equitable, scalable adoption of advanced imaging technologies for lymphedema management worldwide.

Background: Psoriasis is a chronic inflammatory disease characterized by abnormal keratinocyte proliferation and dermal inflammation. TNF-α and IL-17/23 play significant roles in the pathophysiology of psoriasis. The immunomodulatory effect of extracorporeal shockwave therapy (ESWT) has been widely applied in the treatment of chronic inflammatory disorders.

Objective: This study aimed to investigate the effect of ESWT on imiquimod (IMQ)-induced psoriatic lesions and the mechanisms by which ESWT affects macrophages and T cell subsets.

Material and methods: Five groups of mouse models were included: wild type (WT) mice without treatment, mice receiving ESWT alone, mice treated with IMQ alone, mice treated with IMQ and ESWT (n=6), and mice treated with IMQ and adalimumab (anti- TNF-α). We measured epidermal thickness, inflammatory cell infiltration, and the levels of inflammatory cytokines in the skin.

Results: The increase in epidermal thickness caused by IMQ was substantially reduced by ESWT or adalimumab. In parallel, the increased number of IL17⁺ cells, along with the increased IL-23 and TNF-α induced by IMQ, decreased significantly after ESWT or adalimumab treatment. However, the IMQ-induced increase in the number of M1 and M2 macrophages was reduced selectively by ESWT, but not by adalimumab. Moreover, in vitro experiments revealed that ESWT decreased TNF-α production by M1 macrophages but increased IL-10 production by M2 macrophages.

Conclusions: ESWT significantly reduced epidermal thickness, macrophage and IL-17⁺ cell infiltration, and the expression of IL-23 and TNF-α in IMQ-induced psoriasis mice. These findings suggest that ESWT may ameliorate psoriatic skin lesions by modulating macrophage activity and IL-17⁺ cell-mediated inflammation.

This narrative review explores the transformative potential of Artificial Intelligence (AI) in addressing the limitations of traditional infection surveillance methods, which are often hindered by slow response times and restricted analytical capabilities. By integrating diverse data sources such as electronic health records, social media, spatiotemporal data, and wearable technologies, AI enables earlier detection of outbreaks, real-time monitoring, and improved disease transmission prediction. We reviewed peer-reviewed articles and reports to analyze AI's capacity to process heterogeneous datasets using machine learning. Specific applications, such as the use of social media for outbreak prediction, wearable sensors for early infection detection, and spatiotemporal data for tracking disease spread, were synthesized. AI-driven infection surveillance models improve the prediction of outbreaks and estimation of disease incidence. They also enhance risk assessment by identifying highly susceptible individuals and geographic hotspots, thereby strengthening public health strategies. For instance, integrating social media data improves influenza forecasting accuracy, while wearable technologies enable real-time monitoring of infection dynamics. However, these advancements face challenges such as data privacy concerns, model validation, and the need for external testing across diverse epidemiological settings. Despite these challenges, AI holds significant promise for revolutionizing infection surveillance. Future efforts should prioritize refining AI models to improve adaptability, ensuring robust validation processes, and developing integrative tools that merge diverse data sources for effective public health interventions.

Background: Mitochondrial autophagy is linked to neuropathic pain. This study explores how Fu's subcutaneous needling (FSN) affects sciatica via mitochondrial autophagy modulation.

Methods: 40 male SD rats were divided into four groups. Except for the control group (COT), the other three groups were utilized to establish a chronic sciatic nerve injury model. Mechanical pain thresholds were measured. FSN and acupuncture (ACP) groups received treatments every other day for four sessions. Mitochondrial quantity and morphology were examined under a transmission electron microscope, and the expression levels of PINK1, Parkin, and P62 proteins in the rat pyriform were analyzed through immunohistochemistry and immunofluorescence. Furthermore, the levels of TNF-α and IL-6 inflammatory factors in the serum of all groups were measured using ELISA, and the expression levels of midbrain opioid receptors κ and μ mRNA in each group of rats were determined via qPCR.

Results: FSN and ACP groups showed higher pain thresholds than the model group from the second intervention. FSN outperformed ACP after the fourth intervention. Transmission electron microscope showed improved mitochondrial morphology in FSN and ACP groups, with FSN showing better morphology. FSN upregulated PINK1/Parkin and downregulated P62. FSN also reduced TNF-α and IL-6 levels.

Conclusions: FSN alleviates neuropathic pain by enhancing mitochondrial autophagy, restoring mitochondrial dynamics, and reducing inflammation. It shows promise as a therapeutic strategy for neuropathic pain.

Background /objectives: Although the underlying cause of ischemic stroke is vascular occlusion, the post-stroke pathophysiology remains unclear. Therefore, numerous biomarkers have been investigated for both diagnostic and prognostic purposes. In our study, the diagnostic value of the parameters NLR, PLR, RDW-CV, RDW-SD, HIF-1, and DEC-1 was comprehensively evaluated.

Methods: NLR, Blood samples from patients with ischemic stroke and healthy controls were analyzed for NLR, PLR, RDW-CV, RDW-SD, HIF-1, and DEC-1 levels. Demographic and clinical characteristics of both patient and control groups were recorded. The relationship between HIF-DEC measurements and laboratory parameters was subsequently assessed. For statistical analysis, the Mann-Whitney U test was used for comparisons between groups, and the Chi-Square test was applied for categorical variables.

Results: RDW-SD values were found to be higher in patients diagnosed with cerebrovascular accident (CVA) while DEC levels were lower in the stroke group. Although no significant correlation was observed between HIF levels and other parameters in either the CVA or control groups, there was a weak inverse correlation found between DEC and NLR (r:-0.258), and between DEC and RDW-CV (r:-0.268), and a weak linear correlation between DEC and RDW (r:0.319) in the whole group. No significant correlations were found between DEC and other measurements within either the control or CVA groups individually.

Conclusions: Our study may indicate that pathways increasing the levels of DEC-1, which acts on the PI3K/Akt pathway, could lead the development of new therapeutic strategies for ischemic stroke.

Background: Non-communicable diseases (NCD) are the major silent contributors to mortality and morbidity globally. In Malaysia, 2.5% of adults live with up to four NCD. However, long-term trend analyses and state-specific data on the NCD burden remain limited. This study assessed the burden of disease (BoD) trend of selected NCD in two northern states in Peninsular Malaysia.

Method: This was a descriptive observational study. Mortality data for cardiovascular disease (CVD), respiratory disease (RD), and diabetes mellitus (DM) were obtained from the Department of Statistics Malaysia. Hospital admission data were obtained from the Ministry of Health Malaysia, covering 2005-2021 for the states of Kedah and Kelantan. The BoD was estimated using Global Burden of Disease study methodology, which included the estimation of years of life lost (YLL), years lived with disability (YLD), and disability-adjusted life years (DALY). The descriptive findings were presented as the total DALY, DALY %, and DALY per 100,000 population, and stratified by sex and age.

Results: CVD and RD were notably increased in both states in Q4 (2017-2021). The CVD DALY % was highest in 2021 in Kelantan (14.4%) and in 2020 in Kedah (14.5%). The RD DALY % was highest in Kelantan in 2019 (6.2%) and in Kedah in 2020 (8.2%). The DM burden fluctuated over the years. The YLL component consistently exceeded the YLD for CVD and RD, while DM was YLD-driven. Males experienced a higher CVD and RD burden, while DM affected both sexes. The CVD and RD burden was highest in the elderly (>60 years), while DM affected the elderly and young adults.

Conclusion: The CVD and RD DALY increased in Q4 in both states, whereas the DM burden fluctuated across the years. These results emphasize the pressing need for sex- and age-specific interventions to mitigate the long-term effects of NCD.

Background: Falls are a leading cause of injury and premature death in older adults, and cataract surgery reduces fall risk. Concerns existed that blue-light filtering (BF) intraocular lenses (IOLs) might impair light transmittance and increase fall risk. We aimed to compare fall incidence and injury diagnoses among patients who received bilateral cataract surgery with premium BF, premium non-BF, and standard non-BF IOLs.

Material and methods: We emulated a target trial by enrolling 26,730 well-matched patients per IOL cohort who underwent bilateral cataract surgeries between 2011 and 2017 from the Taiwan National Health Insurance Research Database. They were followed until a fall, death, withdrawal, or December 31, 2022. Propensity score matching minimized baseline differences across groups.

Results: Fall incidence increased over time, from 9.07 to 21.13 per 1,000 person-years. The premium BF-IOL (12.94) and premium non-BF-IOL (13.12) groups had lower fall rates than the standard non-BF-IOL group (14.85). Both Cox and Fine-Gray models showed significantly lower fall risks for premium BF-IOL (HR 0.86, SHR 0.92) and premium non-BF-IOL (HR 0.88, SHR 0.91) compared to standard IOLs. There was no significant difference in fall risk between premium BF-IOL and premium non-BF-IOL (HR/SHR 0.99). While hospitalization rates post-fall (68.6%) and 30-day fatal fall rate (1.29%) were comparable, standard IOLs were associated with significantly higher fracture rates.

Conclusions: We found no evidence that BF-IOLs increase fall incidence. Both premium IOL groups consistently had lower fall rates than standard non-BF-IOLs, suggesting that socioeconomic factors, in addition to IOL type, may contribute to this reduction.

Background: Lipid peroxidation and 4-hydroxynonenal (4-HNE) contribute to oxidative stress-related tissue damage, but their roles in pulmonary fibrosis remain unclear. We examined their involvement in bleomycin-induced pulmonary fibrosis.

Materials and methods: Lung fibrosis model mice were used to assess collagen deposition, lipid peroxidation markers, and oxidative stress. Ferroptosis inhibitors ferrostatin-1 (Fer-1) and deferoxamine (DFO) were administered to the mice. In vitro, murine lung epithelial (MLE-12) cells were treated with bleomycin, with or without lipid peroxidation inhibitors, and analyzed for oxidative stress and apoptosis. 4-HNE expression in idiopathic pulmonary fibrosis lung tissues was assessed using immunohistochemistry.

Results: Bleomycin increased deposition of collagen and levels of 4-HNE and malondialdehyde levels while decreasing the glutathione/glutathione disulfide ratio. Fer-1 and DFO improved pulmonary function, reduced fibrosis, and restored the glutathione/glutathione disulfide ratio. In vitro, lipid peroxidation inhibition suppressed bleomycin-induced cell death and oxidative stress. Direct 4-HNE treatment induced apoptosis and lipid peroxidation, implicating 4-HNE in epithelial injury. 4-HNE upregulation was linked to increased transforming growth factor-β expression via c-Jun amino-terminal kinase/c-Jun signaling. Fer-1 and DFO mitigated these effects. Human idiopathic pulmonary fibrosis tissues exhibited elevated 4-HNE, correlating with fibrosis severity.

Conclusions: Lipid peroxidation and 4-HNE play key roles in pulmonary fibrosis progression. Their regulation of transforming growth factor-β expression suggests targeting lipid peroxidation as a potential therapeutic strategy.