The Kaohsiung journal of medical sciences最新文献

Radiofrequency ablation is an effective treatment for benign thyroid nodules. Since initial nodule volume may impact the efficacy of radiofrequency ablation, this study evaluated its long-term outcomes across varying nodule sizes, focusing on regrowth, new growth, and clinical management implications. This retrospective study included 160 patients who underwent thyroid radiofrequency ablation for benign thyroid nodules at a Taiwanese tertiary center between July 2016 and April 2018. Patients were classified into three groups based on nodule size: small (< 10 mL), medium (10-30 mL), and large (> 30 mL). Treatment efficacy was assessed over a period of up to 5 years, focusing on volume reduction rate, regrowth, residual volume, and new growth. The initial ablation rate of all benign thyroid nodules was 99.46%. After the 5-year follow-up, the volume reduction rate was 92.96%. The small nodule group demonstrated the highest volume reduction rate. The incidence of increased residual vital volume was 3.57%. The overall regrowth rate was 9.82%, with a mean time to regrowth of 2.8 years. No nodules required retreatment due to regrowth. New growth was observed in 22.32% of patients, with the highest incidence in the large nodule group (34.29%). Radiofrequency ablation is effective in the long-term management of benign thyroid nodules across various sizes, achieving substantial volume reduction rate with minimal complications. For larger nodules, monitoring for new growth warrants increased attention and may serve as a critical parameter indicative of recurrence and the potential need for retreatment.

Inflammation is a common mediator of pancreatic cancer and depression. This study investigated the predictive value and clinical associations of inflammatory markers and depression in cancer patients using machine learning (ML) and statistical modeling. Pancreatic cancer patients (n = 328; mean age, 65 years; majority with stage IV disease) were assessed using the Patient Health Questionnaire-9 (PHQ-9; depression defined as PHQ-9 ≥ 10). Clinically significant depression was present in 35% of subjects at baseline, and the rate declined at follow-up. Four ML models (logistic regression, random forest, support vector machine, and extreme gradient boosting; XGBoost) were trained using routinely collected clinical data and showed comparable performances with moderate but consistent discriminative capacity (AUC: 0.70-0.72). Permutation importance analysis revealed C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), and albumin as key predictors of depression. Generalized estimating equations further confirmed that elevated CRP (OR = 1.32, p = 0.001) and NLR (OR = 1.55, p = 0.001) were independently associated with depression. These findings suggest that inflammatory markers can not only help to identify patients at risk for depression but also underscore the linkage between inflammation and depression. ML models incorporating these markers may therefore support early detection and intervention in pancreatic cancer care.

Stress causes depression and cognitive decline. With limitations in pharmacotherapy, sciatic nerve stimulation (SNS) offers a promising nondrug alternative. This study aimed to explore the therapeutic efficacy of SNS in mitigating stress-induced depressive behaviors and memory deficits by focusing on astrocytic dysfunction and cellular senescence in the hippocampus. C57BL/6 mice were subjected to the water immersion restraint stress (WIRS) paradigm to induce stress-related behavioral deficits. Behavioral tests assessed locomotion, anxiety, depression-like behavior, and memory. Astrocytic disruption and cellular senescence in the hippocampus were assessed using glial fibrillary acidic protein (GFAP) immunostaining and senescence-associated β-galactosidase (SA-β-gal) staining. SNS at 20 Hz significantly improved cognitive function and reduced depression-like behavior in WIRS-treated mice. It also restored hippocampal GFAP expression and decreased both SA-β-gal-positive cell accumulation and the expression of senescence markers p16 and p21, suggesting an attenuation of cellular senescence. To further explore the link between cellular senescence and SNS-mediated effects, we administered the anti-senescence agent vitamin C to WIRS mice. While vitamin C alleviated stress-induced hippocampal senescence and depressive behavior, it failed to reverse memory deficits or restore GFAP expression, indicating that the benefits of SNS extend beyond its anti-senescent actions. In summary, SNS effectively counteracts the neurobehavioral consequences of chronic stress by targeting astrocytic dysfunction and cellular senescence. These findings support SNS as a promising, nonpharmacological strategy for treating stress-related depression and cognitive decline. Future studies should explore its clinical translation and broader therapeutic potential.

Skin cancer, encompassing melanoma and non-melanoma types, remains a significant public health concern globally. Conventional therapies-such as surgery, radiotherapy, chemotherapy, and immunotherapy-are constrained by poor skin penetration, systemic toxicity, and high recurrence rates. Nanotechnology has emerged as a promising strategy to address these limitations through enhanced drug delivery, targeted tumor accumulation, and reduced off-target effects. This review summarizes recent advances in nanocarrier-based approaches for skin cancer therapy. Key platforms include liposomes, polymeric nanoparticles, dendrimers, metallic nanoparticles, and biomimetic systems. These nanocarriers facilitate passive, active, and stimuli-responsive targeting, thereby improving drug distribution within tumors and enhancing therapeutic precision. Applications include chemotherapy, photothermal and photodynamic therapy, gene and RNA delivery, and immunotherapy. Despite substantial preclinical success, challenges persist in translating findings to the clinic. These include limited dermal penetration, tumor heterogeneity, immune clearance, and regulatory barriers. Innovative solutions-such as multifunctional nanocarriers, personalized formulations, and non-invasive delivery devices-are being investigated to address these issues. In conclusion, nanotechnology holds considerable potential to transform skin cancer treatment. Continued interdisciplinary efforts are crucial for translating laboratory innovations into clinically viable therapies, ensuring safer and more effective outcomes for patients.

Osimertinib (OSI) resistance in non-small cell lung cancer (NSCLC) remains a significant challenge. This report explored the precise role of USP28 on OSI resistance in NSCLC and identified a functional downstream effector. OSI-resistant H1975 cells (H1975/OSI) were established by long-term OSI exposure. USP28 and SIRT1 expression levels were analyzed by quantitative PCR, immunoblotting, and immunohistochemistry. Functional assays included cell viability, colony formation, EdU incorporation, apoptosis analysis, and glycolysis assays. The interaction between USP28 and SIRT1 was confirmed by co-immunoprecipitation (Co-IP) assay and SIRT1 protein stability analysis. In vivo validation was performed using H1975/OSI xenograft models. USP28 and SIRT1 were upregulated in H1975/OSI cells and OSI-resistant NSCLC tissues. USP28 overexpression enhanced cell proliferation and glycolysis, suppressed apoptosis, and conferred OSI resistance in H1975 cells, while its depletion exerted opposite effects in H1975/OSI cells. Mechanistically, USP28 stabilized SIRT1 by deubiquitination. SIRT1 knockdown attenuated the effects of USP28 overexpression, while SIRT1 restoration reversed the phenotype alterations upon USP28 depletion. In vivo, USP28 depletion sensitized H1975/OSI xenografts to OSI treatment. Our study indicates that USP28 promotes OSI resistance in NSCLC by deubiquitinating SIRT1. Targeting the USP28/SIRT1 axis may represent a novel therapeutic approach to overcome OSI resistance in EGFR-mutant NSCLC.

Spontaneous pneumomediastinum (SPM) with pneumorrhachis is rare but generally benign and self-limiting. However, the impact of environmental and seasonal factors on SPM remains unclear. This study investigated their association with SPM onset and clinical outcomes. We conducted a 12-year retrospective review of SPM cases, comparing clinical characteristics and outcomes between patients with and without pneumorrhachis. A case-crossover design was used to assess short-term associations between environmental exposures and SPM incidence, analyzed via conditional logistic regression. A total of 70 consecutive patients were identified, with 9 classified as SPM with pneumorrhachis and 61 as SPM without pneumorrhachis. While both groups were predominantly managed with hospitalization, those with pneumorrhachis had longer hospital stays (median: 7 vs. 3 days, p = 0.002) and were more often associated with severe-grade SPM and identifiable triggers (p < 0.001 and p = 0.009, respectively). No significant environmental exposure differences were observed between groups. Seasonally, SPM incidence was significantly higher in autumn and winter (p < 0.001), consistent with elevated air pollutant levels. Linear regression showed that standardized β coefficients for PM_2.5 were higher in autumn and winter (β = 1.15 and β = 1.18), indicating a seasonal association between PM_2.5 and SPM onset. Despite experiencing more triggers and longer hospitalization, patients with pneumorrhachis had similarly favorable clinical courses. The seasonal clustering of SPM and its association with elevated PM_2.5 levels suggest that air pollution may be a contributing factor, warranting further investigation.