Metabolic reprogramming towards enhanced glycolysis contributes to cervical cancer progression and radioresistance, but its upstream regulatory mechanisms remain poorly understood. Here, we investigated the role and underlying mechanisms of kinesin family member C1 (KIFC1) in glycolytic reprogramming and radiosensitivity in cervical cancer. KIFC1 expression and clinical relevance were analysed using public datasets and cervical cancer tissue microarrays. In vitro and in vivo assays were performed to evaluate the effects of KIFC1 on tumour growth, glycolysis and radiosensitivity. Transcriptomic and molecular interaction analyses were performed to define the KIFC1-SRSF3-PKM regulatory axis. KIFC1 was upregulated in cervical cancer tissues and associated with poor clinical outcomes. KIFC1 depletion inhibited tumour growth, reduced glycolytic activity and enhanced radiosensitivity both in vitro and in vivo. Mechanistically, KIFC1 may facilitate the nuclear localization of the splicing factor SRSF3, thereby influencing PKM alternative splicing. Loss of KIFC1 resulted in cytoplasmic retention of SRSF3 and a switch from the pro-glycolytic PKM2 isoform to PKM1, leading to impaired glycolysis. This splicing-mediated metabolic reprogramming was a key determinant of radiosensitization and could be partially reversed by pharmacological activation of PKM2. These findings identify the KIFC1-SRSF3-PKM axis as a novel splicing-metabolic checkpoint governing radiosensitivity in cervical cancer and highlight KIFC1 as a promising therapeutic target for improving radiotherapy efficacy in cervical cancer.

Myxoma is the most common benign cardiac tumor. We reported a rare variant of balloon-like cystic cardiac myxoma.

A 54-year-old woman presented with exertional dyspnea, chest tightness, and intermittent dizziness. Electrocardiogram and laboratory studies were unremarkable. Transthoracic echocardiography(TTE) revealed a balloon-like cystic mass in the left atrium mimicking a blood-filled cyst. Contrast echocardiography demonstrated a contrast-filled lesion with iso-myocardial enhancement. Transesophageal echocardiography(TEE) identified a distinct arterial inflow at the cyst base and an outflow orifice, which was further confirmed during surgery by the administration of cardioplegic solution. The mass was successfully resected and confirmed a cystic cardiac myxoma.

Cystic myxoma is a rare variant with only few cases reported. The presented balloon-like variant of myxoma exhibited unique anatomical and hemodynamic features that elucidate its formation mechanism.

Acquired radioresistance limits effective radiotherapy. Cuproptosis is a copper-dependent form of cell death driven by mitochondrial copper accumulation and lipoylated protein aggregation. Building on evidence that radioresistant cancer cells exhibit increased cuproptosis susceptibility, here we combine a radiation-responsive, copper-incorporated covalent organic framework (COF‑Tpy‑Se‑Cu) with an oncolytic adenovirus to target this vulnerability. X-ray irradiation triggers copper release from COF‑Tpy‑Se‑Cu and induces FDX1-dependent cuproptosis, while the oncolytic adenovirus depletes intracellular glutathione and stabilizes FDX1 by limiting its mitochondrial protease-mediated degradation. The combination enhances tumor cell death and remodels the immunosuppressive tumor microenvironment into a T-cell-inflamed state. In models of radioresistant tumors in female mice, this regimen improves tumor control and elicits CD8⁺ T cell-dependent systemic antitumor immunity and durable immunological memory. These findings support the combined use of radiation-responsive copper delivery and oncolytic virotherapy as a strategy for exploiting cuproptosis susceptibility and improving radiotherapy responses.

The phase III ADVANCE study prospectively assessed a chemotherapy-free strategy combining aumolertinib with definitive radiotherapy (RT) in patients with unresectable stage III non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations (ChiCTR.org: ChiCTR2000040590). Participants were assigned in a 1:1 ratio to either the experimental arm (110 mg daily aulomertinib plus RT) or the control arm (cisplatin/pemetrexed with RT). The primary endpoint was progression-free survival (PFS). Planned enrollment was 98 patients to detect a hazard ratio (HR) of 0.5. A protocol-prespecified real-world cohort (n = 125) was used for validation. 43 eligible patients were randomized (24 experimental, 19 control). The trial was terminated early following the prespecified interim analysis because of loss of equipoise in an open-label setting, slow accrual, and a large observed PFS difference. At a median follow-up of 25.5 months, the experimental arm had significantly longer PFS (median 34.0 vs. 7.4 months; HR 0.15; P < 0.001). Median overall survival (OS) was not reached vs. 30.5 months (HR = 0.32; P = 0.09). Neutropenia and nausea were more frequent in the control arm; quality of life favored the experimental arm. These findings were supported by real-world validation (n = 125, median follow-up 32.7 months), in which EGFR tyrosine kinase inhibitors (TKIs) + RT and TKIs+cCRT showed similar outcomes, both superior to cCRT (P < 0.001) (ClinicalTrials.gov: NCT04304638). The ADVANCE trial establishes a novel chemo-free strategy incorporating TKI and RT, which prolongs PFS and demonstrates promising OS in unresectable stage III EGFR-mutant NSCLC versus cCRT.

CD4⁺CD25⁺FOXP3⁺ regulatory T cells (Treg) are highly activated in tumors and promote disease progression. Specific, universal targeting of these effector Treg cells is limited by the lack of a conserved signature across human cancers and information on their origin. Here we combine analysis of single-cell RNA-sequencing datasets with spectral flow cytometry and identify a core signature of 88 genes consistently upregulated in intratumoral Treg cells among 9 epithelial cancers. We describe 4 Treg cell subsets - CCR7⁺ quiescent, CCR8⁺ effector, CD161⁺ and intermediate, with distinct tissue distribution, function, differentiation trajectories and molecular drivers. By single-cell T cell receptor sequencing, we observe that protumoral, effector CCR8⁺ Treg cells exhibit little clonal relationship with other Treg cell subsets inside tumors, but are clonally related to Treg cells in tumor-draining lymph nodes, as well as conventional T cells in tumors. This resource provides insights for development and fine-tuning of CCR8⁺ Treg cell-targeting therapies in cancer.

The Regulator of Cullins 1 (ROC1) or RING box protein-1 (RBX1) is an essential component of the largest multiunit Cullin-RING ubiquitin ligase (CRL). Previous studies demonstrated that ROC1 is frequently overexpressed in multiple malignancies, which predicts advanced cancer stages and poor prognosis. However, the molecular mechanisms driving ROC1 overexpression in cancers remain largely unknown. Herein, we reveal that HSP90 binds to ROC1 with its N-Terminus, thus promoting ROC1 stabilization. HSP90 inhibition with the N-Terminal, but not the C-Terminal inhibitors accelerate ROC1 destabilization by facilitating its ubiquitination and subsequent degradation by CHIP E3 ligase. CHIP specifically interacts with ROC1 at its CC domain, thus promoting the K48-linked-ubiquitin-mediated degradation of ROC1 at the K26 residue. Indeed, deletion of CHIP markedly blocks HSP90-inactivation-induced ROC1 reduction. Function exploration reveals that HSP90 inhibition suppresses lung adenocarcinoma (LUAD) cell growth substantially by decreasing ROC1 abundance. In clinic, HSP90β and ROC1 are overexpressed in LUAD samples, which have positive correlation and predict poor prognosis of LUAD patients. LUAD organoids analysis reveals that HSP90 blockage promotes ROC1 destabilization and inhibits the growth of organoid cells. Taken together, the present results demonstrate the regulatory mechanism of ROC1 in malignancies and suggest a novel mechanism of the oncogenic role of HSP90 to promote lung tumorigenesis.

To evaluate short-term changes in electrocardiographic (ECG) parameters after tocilizumab administration in COVID-19 patients, considering the drug's role in treating severe cases and the involvement of IL-6 in cardiovascular effects and ECG alterations.

In this retrospective study, we assessed cardiovascular and electrocardiographic parameters in PCR-confirmed COVID-19 patients who received tocilizumab. ECG variables were evaluated at two time points: 24 h before and 24 h after drug administration. All ECGs were verified by a supervisor, and demographic information was extracted from patient records.

33 patients were included, of whom 36.4% were men. The patients' ages ranged from 37 to 79 years. The corrected QT interval (QTc) measured 24 h before (QTc1) and 24 h after (QTc2) tocilizumab administration showed no significant difference (QTc1: 390.3 ± 31.67 ms; QTc2: 392.73 ± 36.68 ms). No significant ECG changes were observed in the ST segment, ventricular fibrillation (VF), ventricular tachycardia (VT), or atrial fibrillation (AF). Four patients experienced cardiorespiratory arrest within 24 h after receiving tocilizumab.

Tocilizumab administration in critically ill COVID-19 patients was not associated with significant short-term ECG changes or specific cardiovascular complications. Although previous studies in inflammatory diseases such as rheumatoid arthritis have reported QTc shortening following tocilizumab treatment, likely through suppression of IL-6-mediated systemic inflammation, no significant QTc reduction was observed in our cohort during the 24-h follow-up period. A few cases of cardiorespiratory arrest occurred; a causal relationship with tocilizumab could not be established due to the severity of illness and limited clinical data.

To estimate the prevalence of diagnosed chronic obstructive pulmonary disease (COPD) and characterize the frequency and distribution of multimorbidity among individuals with and without COPD in Colombia's contributory health system.

We conducted a cross-sectional study using administrative healthcare data from the Capitation Unit Sufficiency Database (Unidad de Pago por Capitación, UPC) and the Unique Enrollees Database (Base de Datos Única de Afiliados, BDUA). An electronic algorithm was used to identify individuals with a COPD diagnosis and to estimate diagnosed COPD prevalence among all affiliates during 2018-2019. We also estimated the prevalence of selected health conditions among individuals with and without COPD. Differences between groups were assessed in two steps. First, standardized mean differences (SMDs) were calculated for prevalence estimates. Second, conditions with SMDs of approximately 0.1 or greater were further evaluated using prevalence ratios (PRs) adjusted for sex, region, age, insurer, and prior healthcare service utilization estimated with Poisson regression with robust variance and 95% confidence intervals.

The study included 6,865,420 individuals. The nationwide prevalence of diagnosed COPD was 2.21% (95% CI, 2.20-2.22), with the highest prevalence observed in the Central region (2.77%; 95% CI, 2.74-2.79). In adjusted analyses, several conditions were more prevalent among individuals with COPD, including asthma (PR = 3.88; 95% CI, 2.88-5.23), sleep apnea (PR = 2.62; 95% CI, 2.05-3.35), heart failure (PR = 1.89; 95% CI, 1.29-2.78), ischemic heart disease (PR = 1.60; 95% CI, 1.26-2.03), hypertension (PR = 1.08; 95% CI, 1.02-1.15), and osteoporosis (PR = 2.34; 95% CI, 1.52-3.58), among others, were more prevalent among individuals with COPD. Lung cancer (PR = 6.41; 95% CI, 5.89-6.97) and breast cancer (PR = 1.17; 95% CI, 1.08-1.25) were also more prevalent in this population.

Individuals with diagnosed COPD in Colombia's contributory health system had a substantial burden of multimorbidity, particularly respiratory and cardiovascular conditions. These findings support interdisciplinary care models and locally tailored strategies to address regional differences in diagnosed COPD.

Human respiratory syncytial virus (HRSV) is a major cause of respiratory disease. It is classified into two antigenic subgroups. While several authors have studied the potential link between HRSV infection and later development of recurrent wheezing (RW) or asthma, no previous studies have assessed the role of HRSV subtypes. The aim of this study was to assess the medium-term respiratory morbidity in children and adolescents with prior severe bronchiolitis due to HRSV-A or HRSV-B infection.

From September 2023 to June 2025 an observational, prospective, cross-sectional follow-up study was conducted, including children and adolescents (5-18 years) with a history of hospital admission due to single HRSV infection. Patients underwent a structured questionnaire, measurement of exhaled nitric oxide, spirometry and skin prick testing for allergic sensitization.

A total of 185 patients were recruited (129 HRSV-A, 56 HRSV-B). No differences in the variables regarding hospital admission for bronchiolitis were detected. The prevalence of current asthma in both groups was similar (HRSV-A 17.2% vs. 25.5%, p = 0.190). Patients with prior HRSV-B bronchiolitis reported more severe respiratory symptoms, particularly speech-limiting wheezing (HRSV-A 1.5% vs. HRSV-B: 8.9%, p = 0.039, OR 2.62 (95% CI: 1.3-5.4)) and more frequent nocturnal dry cough not associated with infections (HRSV-A: 7.7% vs. HRSV-B 16.9%, p = 0.044, OR: 1.78, (95% CI: 1.78-2.9)). Multivariate analysis revealed HRSV-B prior bronchiolitis to be an independent risk factor for medical diagnoses of asthma and nocturnal cough.

Schoolchildren and adolescents with prior severe bronchiolitis due to HRSV-B have poorer respiratory outcome compared to those with HRSV-A, with more frequent intercrisis symptoms.

Live bird markets (LBMs) are high-risk environments for the amplification and transmission of avian influenza viruses (AIVs). In Cambodia, limited data exist on knowledge, attitudes, and practices (KAP) among poultry workers, who represent a key occupational risk group. This study assessed KAP related to avian influenza (AI) among poultry workers in three major Cambodian LBMs, with a focus on changes before and during the COVID-19 pandemic.

A cross-sectional survey of 100 poultry workers was conducted using a structured questionnaire covering socio-demographics, AI awareness, personal protective equipment (PPE) use, training participation, and preventive behaviors. Comparisons were made between the pre-COVID-19 pandemic and COVID-19 pandemic periods using McNemar's test for dichotomous variables, and the symmetry chi-square and marginal homogeneity tests for variables with more than two categories, to determine whether response distributions changed significantly over time.

The proportion of workers earning below USD 350 per month increased from 41% before the pandemic to 52% during the pandemic (p < 0.001). PPE use declined significantly: Face mask use dropped from 58% to 40% (p = 0.003), while reports of no PPE use rose from 21% to 49% (p < 0.001). Awareness of avian influenza decreased from 81% to 59% (p < 0.001), and participation in influenza-related training fell from 30% to 10% (p < 0.001). Workers primarily relied on informal information channels, with veterinary officers identified as trusted but underutilized sources.

Despite moderate baseline awareness of avian influenza, preventive practices among Cambodian poultry workers were limited and further declined during the COVID-19 pandemic, reflecting broader economic and structural challenges. Supporting affordable access to PPE, strengthening market-based training, and expanding culturally adapted, multiplatform risk communication strategies will be essential. Integrated interventions, combined with enhanced surveillance during peak poultry trade periods, can help reduce occupational exposure and interrupt zoonotic transmission pathways in LBMs.