Obesity hypoventilation syndrome (OHS) includes morbid obesity (Body mass index>30 kilograms/m2), daytime hypercapnia (arterial carbon dioxide level >45 mm Hg) with features of sleep disordered breathing. Data are scarce in the management of acute-on-chronic hypercapnic failure with NIV, especially from developing countries like India. We set out to evaluate the demography of OHS patients presenting with acute on chronic hypercapnic failure and evaluate the effect of NIV in improvement of symptoms and correction of blood gas parameters.

This ambidirectional observational study included 30 patients who were confirmed cases of OHS and were admitted with hypercapnic respiratory failure and managed with NIV and discharged later on domiciliary NIV. The patients were evaluated for the complications of OHS and were followed up for improvement with domiciliary NIV.

Out of the 30 patients of OHS,16 (53%) were males while 14 (47%) were females. 17 patients (56.7%) had type II diabetes mellitus, while 25 (83%) patients were known cases of primary hypertension. The mean age was 61 years (SD-11.15), and the mean Body Mass Index (BMI) was 36.2 kilograms/meter2 (SD-6.19). On admission, the mean pH was 7.35 (SD-0.10), mean pCO2 was 55.33 mmHg (SD-17.56), and mean HCO3 was 31.31 (SD-5.23), suggestive of acute on chronic hypoventilation. 10 out of 30 patients were hypoxic at presentation, out of which 5 required (Non-Rebreathing Mask (NRBM on admission. All these patients were managed with NIV, and they showed significant clinical improvement in the form of improved sensorium, decreased oxygen requirement, and improved exercise tolerance. The mean improvement in pH after one week was 7.41, and the mean level of pCO2 was 48.10 mmHg after 1 week of NIV. Significant improvements were observed in arterial blood gases (pCO2 reduced from 55.33 ± 6.1 mmHg to 48.22; P<0.001) and Epworth Sleepiness Scale (ESS) scores. The decrease in pCO2 was statistically significant. These patients were discharged on domiciliary NIV and were followed up on an OPD basis.

All patients with OHS who presented with acute on chronic hypercapnic failure responded well to NIV therapy with significant improvement in exercise tolerance, weight loss, decreased symptom burden, and blood gase parameters. These findings reinforce the role of structured NIV therapy in OHS management.

Concerns about diabetic ketoacidosis (DKA) and euglycemic ketoacidosis (eKA) are balanced against possible organ-protective benefits in the debated perioperative management of sodium-glucose cotransporter-2 (SGLT2) inhibitors. This meta-analysis compared the perioperative clinical and laboratory outcomes associated with perioperative exposure to SGLT2i.

Through July 31, 2025, we searched PubMed, Web of Science, Scopus, and CENTRAL for observational studies and randomised controlled trials comparing the outcomes of preoperative use of SGLT2 inhibitors with non-use in patients undergoing cardiac or non-cardiac surgery. We pooled data using a random-effects model and investigated heterogeneity using leave-one-out sensitivity analyses.

CRD420251155809.

There were 10 studies comprising 246,242 patients. Due to considerable heterogeneity, the primary pooled analysis revealed no significant association between SGLT2 inhibitor use and either eKA (OR 4.86; p = 0.11) or DKA (OR 2.21; p = 0.11). However, a significant increase in the risk of eKA (OR 1.11; p < 0.001) and DKA (OR 5.33; p < 0.001) was observed using leave-one-out sensitivity analysis to identify outliers. On the other hand, the usage of SGLT2 inhibitors was associated with a statistically significant decrease in both mortality (OR 0.73; p = 0.006) and acute renal injury (OR 0.68; p < 0.0001). The SGLT2 inhibitor group had significantly lower perioperative pH, base excess, and blood glucose levels.

The use of perioperative SGLT2 inhibitors poses a clinical paradox between significant renoprotection and survival advantages and a latent risk of ketoacidosis concealed by considerable heterogeneity. While metabolic monitoring is essential, current surgeries requiring more prolonged withholding may need to weigh metabolic risk against the drug's significant benefit in reducing acute kidney injury and mortality.

Breast cancer (BC) and Thyroid cancer (TC) are prevalent malignancies in women that share epidemiological and molecular features. Emerging evidence indicates that non-coding RNAs are key regulators of cancer associated gene expression. Long non-coding RNA (lncRNA) drive tumor progression by acting as competing endogenous RNAs (ceRNAs), sponging microRNA (miRNA) to deregulate oncogenic messenger RNA (mRNA). The influence of functional genetic polymorphisms of lncRNAs on their expression, as well as the expression of their ceRNA components RNA in a direct comparative context of BC and TC, remains unexplored.

60 breast cancer and 60 thyroid cancer tissue samples, alongside matched adjacent healthy controls from a Pakistani female patient, were used. Genotyping of lncRNA H19 SNPs (rs3741219 and rs2839698) was performed using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) followed by quantitative real-time PCR (qRT-PCR) to assess the expression of lncRNA H19, miR-152, and DNMT1. Expression and genotype associations, association with clinical parameters, and diagnostic and prognostic utility of the studied RNA were statistically evaluated.

Genotyping revealed that rs3741219 showed significant tumor-control differences in breast cancer (p < 0.05). Expression analysis revealed upregulation of lncRNA H19 and DNMT1, and downregulation of miR-152, in tumor samples compared with adjacent healthy controls in both cancers. In genotype-expression analysis, rs3741219 influenced lncRNA H19 expression in both cancer types. Receiver Operating Characteristic (ROC) analysis confirmed the strong diagnostic potential of H19 and DNMT1 (AUC 0.98-1.00). Correlation and regression analyses validated the proposed ceRNA interactions and their significant association with advanced cancer stage. A high-risk score from the H19/miR-152/DNMT1 axis was prognostic only in thyroid cancer (HR = 2.97).

De novo metastatic breast cancer (dnMBC), defined as stage IV disease at initial diagnosis, comprises 6-10% of all metastatic breast cancer cases. Despite therapeutic advances, the unique clinical course of dnMBC remains underexplored, particularly with regard to patterns of first treatment failure and the potential role of metastasis-directed therapy (MDT). This study investigated patterns of treatment failure in patients with dnMBC treated with first line systemic therapy to understand how to better direct local therapies.

A prospective single-institution database was used to examine patient and tumor characteristics, treatment response, and outcome among 326 patients with dnMBC diagnosed between 2011 and 2022. Anatomic site of first disease progression was categorized as occurring at a pre-existing site only (in breast and/or pre-existing metastatic sites only) vs other (including any combination involving a new metastatic site). Progression patterns were analyzed overall and stratified by clinical subtype. Cumulative incidence functions were used to evaluate time to first treatment failure by site and subtype.

Among the full cohort, progression-free survival at 2 years was 32.7% (95% CI [27.3, 38.0]) and at 5 years, 7.8% (95% CI [4.5, 11.2]). In total, 40.8% experienced first progression at pre-existing sites only, while 46.5% progressed at new sites. The cumulative incidence of first progression at a pre-existing site only at 5 years by clinical subtype was: 45.4% for HR + /HER2-, 43.8% for HR-/HER2 + , 39.3% for HR-/HER2-, and 34.5% for HR + /HER2 +.

A substantial proportion (approximately 40%) of dnMBC patients experience initial progression at pre-existing sites, highlighting a potential role for locoregional and MDT in delaying progression and extending time on first-line systemic therapy. These findings support further prospective evaluation of MDT in dnMBC, with an emphasis on subtype-specific strategies and quality-of-life outcomes.

Although each patient has their own unique needs and preferences, healthcare practitioners may not know the type of support the patient needs. The aim of the present study was to assess the unmet informational needs in patients with cancer and to explore their association with clinicians' beliefs about information given to them about diagnosis, prognosis, and treatment.

In six Italian oncology departments, 980 consecutive patients were invited to participate in the study. Eight hundred three patients accepted to take part in the research. Patients were administered the Needs Evaluation Questionnaire, a sense of coherence scale, and a scale on psychological distress.

The final sample employed in the current study included 782 patients with approximately 40% showing significant distress and 54% of patients expressing the need for more information on their prognosis. Informational needs score was higher for patients admitted in ward, patients with higher distress, and patients with lower sense of coherence (p < 0.001). Patients with low levels of trust in conventional treatment expressed higher informational needs (p < 0.05). Clinicians' judgment of the levels of information received by the patients about diagnosis, prognosis, and treatment and their judgment of patients' awareness on those same dimensions were not associated with the informational needs expressed by the patients. Hierarchical regression showed a significant amount of additional explained variance in distress when informational needs expressed by patients were entered in the analysis.

Most patients with cancer reported greater need for information in Italy. The lack of association between informational needs explicitly expressed by the patient and the clinician's judgment of the patient's needs suggests that for clinicians it is difficult to accurately predict which patients are expressing greater or lesser needs. These results suggest that self-report assessment tools are necessary to assess the patient's information needs during the process of care.

It is widely acknowledged that B-cell lymphoma represent a significant threat to human health, and Bruton Tyrosine Kinase inhibitors (BTKi) have been shown to exhibit superior clinical efficacy and safety in comparison to conventional chemotherapy and immunotherapy modalities. However, as patients continue to use BTKi over a time, they will inevitably encounter the drug resistance. This resistance renders the therapeutic efficacy of BTKi, thereby significantly constraining its clinical benefits. Drug resistance of tumor is a multifaceted process influenced by numerous factors, mainly including individual genetic variations, tumor stem cells, drug inactivation, reduced drug absorption, and altered metabolism of anti-tumor drugs. The tumor microenvironment (TME) has been demonstrated to exert an important influence on the process of therapy resistance. It is evident that non-cellular components (e.g. the extracellular matrix, hypoxia, an acidified microenvironment, exosome, and cytokines) modulate the drug resistance through different mechanisms. These mechanisms include physical barriers that impede drug delivery, the formation of an immunosuppressive microenvironment, metabolic reprogramming and the activation of bypass signal moueculars. Furthermore, the presence of mutations of moleculars involved in the BCR signaling pathways (e.g. BTK and PLCG2 mutations) and the aberrant activation of key pathways such as PI3K-AKT-mTOR, NF-κB, Wnt/β-catenin and MAPK/ERK signaling further weakened the efficacy of BTKi. This review focus on the mechanism of BTKi resistance, the role of the TME and its components in drug resistance. It emphasized that targeting TME remodeling and combined the inhibition of multiple pathways may provide a new strategy for overcoming drug resistance, optimizing the treatment paradigm of B-cell lymphoma.

Diffuse large B-cell lymphoma (DLBCL) is an aggressive and common subtype of non-Hodgkin lymphoma (NHL). Despite the availability of several risk stratification tools, substantial room for improvement in personalized prognostic prediction still exists. Furthermore, considering the heterogeneity of DLBCL, how to select an appropriate treatment in a personalized manner remains a clinical challenge. In this study, we developed a random survival forests model by integrating clinical and gene expression data from 677 DLBCL case in Gene Expression Omnibus (GEO) database. Our model predicted overall survival with high concordance between training and validation datasets (C-index: 0.832 and 0.758, respectively), outperforming the consistency predicted by common prognostic markers such as Cell-Of-Origin Subtype, IPI score and Ann Arbor stage. Time-dependent ROC curves also showed good predictive performance for 1-year, 3-year, and 5-year survival in training and validation cohorts, the models are accessible via an open-access website. Survival analysis demonstrated that the group receiving the optimal treatment showed a more favorable survival association. Furthermore, we also used Kaplan-Meier curves, multivariate analysis and penalized Cox regression model to identify six genes (C2CD5, CD163, JADE3, BIRC3, TMEM200A, and LINC00877) related to the prognosis of DLBCL. In conclusion, we developed a machine learning model integrating clinical characteristics and gene expression profiles, providing a reliable decision-support tool for DLBCL prognosis and treatment selection.

This review evaluates the effectiveness and safety of acupuncture and moxibustion for CRF management and provides evidence-informed clinical recommendations. The review intends to answer the questions: (1) How effective and safe are acupuncture and moxibustion in managing CRF? (2) What clinical recommendations can be provided from the evidence?

A systematic literature search across seven English and Chinese databases, identifying 13 randomized controlled trials (RCTs) published between 2015 and 2025, involving 919 participants with various cancer types.

Acupuncture and/or moxibustion significantly alleviated CRF with p-values ranging from < 0.001 to 0.050. In contrast, control groups demonstrated either no statistically significant change or a significantly lower magnitude of improvement, with clinical response rates (34.60%-66.67%) consistently inferior to those observed in the intervention groups (68.00% to 86.67%). Commonly selected acupoints included Zusanli (ST36), Qihai (CV6), and Guanyuan (CV4). Treatment protocols were categorized into short-term (≤ 3 weeks), cycle-based (synchronized with chemotherapy cycles), and long-term (up to 6 months), with needle retention times of 10 to 30 min. All studies reported high safety profiles, with no adverse events. CRF was measured using validated instruments such as the Cancer Fatigue Scale (CFS), Brief Fatigue Inventory (BFI), Piper Fatigue Scale (PFS), and the Functional Assessment of Cancer Therapy-Fatigue (FACT-F), showing consistent improvements.

Acupuncture and moxibustion are safe and effective for CRF and may be integrated into supportive oncology care alongside exercise, mind-body intervention, and cognitive behavioural therapy (CBT) to enhance quality of life in oncology populations. However, limited sample sizes and methodological heterogeneity highlight the need for larger and well-designed studies to strengthen the evidence.

The pretemporal anteromedial interdural approach provides direct extradural access to Meckel's cave by exploiting the natural plane between the temporal dura propria and the meningeal layer of the lateral wall of the cavernous sinus. After a pretemporal craniotomy, the foramen rotundum guides interdural dissection along V2 toward the corridor between V1 and V2, enabling controlled exposure of the Gasserian ganglion and proximal trigeminal rootlets. Tumor resection proceeds through internal debulking and circumferential dissection, with extension into the posterior fossa when necessary.

In this How I Do It article, we present the key technical steps of the pretemporal anteromedial interdural approach to Meckel's cave, emphasizing anatomical landmarks and operative nuances.

This approach allows safe and effective removal of trigeminal schwannomas while limiting cavernous sinus manipulation and reducing morbidity.

Esophageal squamous cell carcinoma (ESCC) remains treatment-resistant; we explored Elbasvir, an NS5A inhibitor, as a ferroptosis inducer. Cell viability was assessed by CCK-8 assays. Apoptosis and cell cycle were analyzed via flow cytometry, and key markers via Western blotting. In vivo efficacy was evaluated using BALB/c nude mouse xenografts. Proteomic analysis was conducted by mass spectrometry. Ferroptosis induction was verified via TEM, JC-1, FerroOrange, DCFH-DA, MDA assays, and Western blotting of NCOA4, Ferritin, and FTH1. Binding to NCOA4 was confirmed by surface plasmon resonance (SPR) and drug affinity responsive target stability (DARTS) assays. Elbasvir (40 µM, 48 h) suppressed KYSE150/TE1 viability, induced apoptosis/G0/G1 arrest, and inhibited xenograft growth without toxicity. Proteomics identified ferroptosis as the top pathway. SPR/DARTS confirmed NCOA4 binding. NCOA4 knockdown reduced ferroptosis; overexpression enhanced it. Elbasvir triggered NCOA4-mediated ferritinophagy, FTH1 degradation, iron accumulation, and lipid peroxidation. Elbasvir targets NCOA4-FTH1 to induce ferroptosis, offering a repurpose strategy for ESCC. Its safety profile supports clinical translation, with potential applications in iron metabolism-dependent cancers.