To investigate ferroptosis-cuproptosis crosstalk in pulmonary arterial hypertension (PAH) and its potential association with pulmonary vascular immune microenvironment remodeling.

PAH-related bulk transcriptomic and single-cell RNA sequencing datasets were obtained from the GEO database. Differentially expressed genes between PAH(n=76) and normal lung tissues(n=42) were identified, and ferroptosis, cuproptosis and ferroptosis-cuproptosis crosstalk scores were calculated using ssGSEA/GSVA. Candidate crosstalk genes were screened by intersecting PAH differentially expressed genes, ferroptosis/cuproptosis-related genes and crosstalk score-related genes, followed by expression validation, correlation analysis and GO/KEGG functional enrichment analysis. Single-cell RNA sequencing data were further used for cell annotation, cell type-specific score evaluation and core gene distribution analysis. Cell Chat was applied to assess intercellular communication changes in PAH lung tissues. In addition, a PAH animal model(n=40) was used to validate hemodynamic alterations, key molecular expression by qRT-PCR and Western blot.

Ferroptosis-, cuproptosis- and crosstalk-related transcriptional features were markedly altered in PAH lung tissues: the ferroptosis, cuproptosis and crosstalk scores were all significantly lower in PAH than in normal lungs (P=5.3×10^5, 0.028 and 0.00029, respectively), and ferroptosis score was positively correlated with cuproptosis score (R=0.42, P=0.019). Sixteen candidate genes were obtained by intersection analysis, among which DLAT, SAT1, MTF1, SLC7A11, GCLM and NCOA4 were identified as core candidate genes involved in ferroptosis-cuproptosis crosstalk (DLAT was upregulated whereas the other five genes were downregulated in PAH; P=8.8×10^6, 2.0×10^4, 3.5×10^4, 0.0073, 6.7×10⁵ and 7.3×10^4, respectively). Functional enrichment analysis showed that these genes were mainly enriched in ferroptosis 7 genes, lipoic acid metabolism 4 genes, glutathione metabolism 3 genes, and cysteine and methionine metabolism 2 genes. Single-cell analysis (n=9) identified 16 cell types and revealed cell type-specific alterations of the crosstalk score in pulmonary vascular endothelial cells, smooth muscle cells and macrophages, all of which showed significantly lower crosstalk scores in PAH (P<0.05, P<0.01 and P<0.05, respectively). CellChat analysis showed increased interaction number (2 067 vs. 2 802) and interaction strength (32.759 vs. 58.673) in PAH, with enhanced macrophage communication with endothelial cells, fibroblasts and smooth muscle cells through signaling axes including THBS1-CD47, SELPLG-SELE, PECAM1-PECAM1 and FN1-(ITGA5+ ITGB1). Animal experiments showed significantly increased right ventricular systolic pressure (approximately 23 vs. 49 mmHg, P<0.01) and Fulton index (approximately 0.23 vs. 0.42, P<0.001) in the PAH group. Moreover, DLAT was upregulated at both mRNA and protein levels (P<0.0001 and P<0.001), whereas SAT1, MTF1, SLC7A11, GCLM and NCOA4 were downregulated (P<0.05).

Ferroptosis-cuproptosis crosstalk is dysregulated in PAH lung tissues and mainly involves pulmonary vascular endothelial cells, smooth muscle cells and macrophages. This dysregulation may participate in pulmonary vascular remodeling by regulating glutathione metabolism, lipoic acid metabolism and macrophage-vascular wall cell communication.

To investigate the regulatory effect of TGF-β activated kinase-1-binding protein 1 (TAB1) on immunoparalysisrelated phenotypes and to provide a potential biomarker for prognosis assessment in severe pneumonia.

Based on the GSE65682 dataset, 183 patients with severe pneumonia and 42 healthy controls were enrolled, and the differential expression of TAB1 was analyzed. Univariate Cox proportional hazards regression model was used to evaluate the association between TAB1 expression and patient prognosis. Human monocytederived macrophages (MDMs) were used as a model, and TAB1 was knocked down by RNA interference. Flow cytometry, Western blot, and realtime quantitative polymerase chain reaction (PCR) were employed to detect phagocytic capacity, human leukocyte antigen DR (HLADR) expression, macrophage polarization, and changes in the transcriptional levels of proinflammatory cytokine genes.

(1) The expression level of TAB1 in peripheral blood was significantly higher in healthy controls than in patients with severe pneumonia (P<0.05), and significantly higher in survivors than in nonsurvivors (P<0.01). Univariate Cox regression analysis showed that high TAB1 expression was significantly associated with favorable prognosis (HR=0.029, 95%CI: 0.004~0.214, P<0.001). (2) Compared with the control group, the siTAB1 group exhibited a decreased phagocytosis rate (56.2% vs. 16.8%, P<0.001), an increased proportion of M2 macrophages (CD80^- CD206⁺ ) (7.33% vs. 32.4%, P<0.05), and significantly reduced HLADR protein expression (P<0.001). The mRNA relative expression levels of proinflammatory cytokines interleukin1β (IL1β), IL6, and tumor necrosis factor (TNF) were significantly downregulated (P<0.01).

High TAB1 expression is associated with favorable prognosis in severe pneumonia. Knockdown of TAB1 induces typical immunoparalysis phenotypes in MDMs, including phagocytic dysfunction, low HLADR expression, M2 polarization, and suppression of proinflammatory cytokines. TAB1 holds promise as a potential molecular biomarker for prognosis and immune status monitoring in severe pneumonia.

To elucidate the molecular characteristics and core pathways of chronic obstructive pulmonary disease(COPD) in lung cancer patients, thereby providing a theoretical basis for precision diagnosis and treatment of this comorbidity.

Gene expression data and clinical information were obtained from The Cancer Genome Atlas (TCGA) database for a total of 375 patients with lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Of these, 65 patients with lung cancer and comorbid COPD constituted the COPD-comorbid group, and 310 patients with lung cancer without COPD constituted the non-COPD group. differentially expressed genes (DEGs) were identified using the Limma algorithm (FDR<0.05) after TPM normalization and log transformation. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were then performed to identify biological pathways related to COPD, and the inclusion of the DEGs in, and their overlap across, five immunological databases (IRIS, ImmPort, Immunome, InnateDB, and Reactome) were used to distinguish immunological-related DEGs.

No statistically significant differences were observed between the two groups in age, sex, race, tumor stage, or history of other cancers, whereas smoking history and pathological type differed significantly (P<0.05). Survival analysis included 50 patients in the COPD-comorbid group and 286 patients in the non-COPD group; after exclusion of 25 patients with extreme values (≤0 d), the censoring rate was 17.33%. Both before and after adjustment for sex, smoking history, history of prior malignancy, and age, COPD status was not significantly associated with survival in patients with lung cancer (unadjusted: HR=1.069, P=0.826; adjusted: HR=0.826, P=0.560), and overall survival did not differ significantly (P=0.5598). Among the 375 patients, 42 deaths (13.55%) occurred in the non-COPD group and 15 deaths (23.08%) in the COPD-comorbid group (P=0.052), indicating a borderline statistical trend. DEG screening identified 140 differentially expressed transcripts. KEGG enrichment analysis showed significant enrichment in five pathways (P<0.05), namely the PI3K/AKT signaling pathway (9 genes), focal adhesion (7 genes), extracellular matrix (ECM)-receptor interaction (5 genes), human papillomavirus infection (9 genes), and regulation of the actin cytoskeleton (8 genes). FGF1 was uniquely and specifically enriched in the PI3K/AKT signaling pathway; PDGFC was enriched in two pathways, focal adhesion and the PI3K/AKT signaling pathway; PDGFRB was enriched in three pathways, human papillomavirus infection, focal adhesion, and the PI3K/AKT signaling pathway; and a total of seven genes-PDGFC, PDGFRB, LAMB2, ITGA10, COL6A2, COL9A2, and COMP -were simultaneously enriched in both focal adhesion and the PI3K/AKT signaling pathway. GO enrichment analysis showed no significant enrichment at the biological process (BP) level; at the cellular component (CC) level, significant enrichment was observed in the extracellular matrix (P=1.3×10^-6), collagen-containing extracellular matrix (P=2.6×10^-6), and extracellular region (P=2.0×10^-4, with 25 DEGs enriched, including CCL17 and PDGFC); and at the molecular function (MF) level, significant enrichment was observed in collagen binding (P=2.6×10^-5) and extracellular matrix structural constituent (P=3.2×10^-5). By checking immunological databases, a total of 46 DEGs were recorded: CCL17 was simultaneously recorded in four databases (IRIS, ImmPort, Immunome, and InnateDB); ETS1 was recorded in three databases; LITAF, PDGFRB, and ENTPD1 were each recorded in three databases; C1QTFN1 was recorded in two databases; and 40 genes were recorded in only a single database. FGF1 was significantly downregulated in the COPD-comorbid group; PDGFC/PDGFRB were significantly overexpressed; and CCL17 was differentially expressed (log2FC=-0.7862, P=0.0014).

The PI3K/AKT signaling pathway, together with FGF1, PDGFC/PDGFRB, and CCL17, may represent potential key targets in the development and progression of COPD comorbid with lung cancer, offering new insights for the precision diagnosis and treatment of this comorbidity.

To investigate the effect and molecular mechanism of long non-coding RNA EBLN3P (LncRNA EBLN3P) on the radiosensitivity and mitochondrial damage of non-small cell lung cancer (NSCLC) cells by targeting microRNA (miR)-144-3p to regulate the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-response element binding protein (CREB) signaling pathway.

Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of LncRNA EBLN3P and miR-144-3p in NSCLC cell lines (A549, H460, H1299, Calu-1) and normal lung epithelial cells BEAS-2B. A549 cells were selected, and a LncRNA EBLN3P overexpression vector was constructed. The cells were divided into the Control group (blank control), IR group (X-ray irradiation alone), IR+ oe-EBLN3P group (irradiation after LncRNA EBLN3P overexpression), and IR+ oe-EBLN3P+ miR-144-3p mimic group (irradiation after co-transfection with the LncRNA EBLN3P overexpression vector and miR-144-3p mimic). Techniques including the cell counting kit-8 (CCK-8) assay, Transwell assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, JC-1 staining, Western blot, and enzyme-linked immunosorbent assay (ELISA) were used to detect cell viability, invasion, apoptosis, mitochondrial membrane potential, DNA damage-related proteins [ataxia telangiectasia mutated (ATM), Nijmegen breakage syndrome protein 1 (NBS1), phosphorylated H2AX (γ-H2AX)], and the expression levels of key molecules in the cAMP/PKA/CREB pathway in each group. A dual-luciferase reporter gene assay was used to verify the targeting relationship between LncRNA EBLN3P and miR-144-3p.

Compared with the Control group, in the IR group, A549 cell viability [(100.00±2.47)% vs. (57.92±8.65)%] and invasion number [(93.86±15.02) vs. (25.31±4.19)] were decreased, apoptosis rate was increased [(3.16±0.54)% vs. (15.43±2.79)%], mitochondrial membrane potential [red/green fluorescence ratio: (1.00±0.16) vs. (0.27±0.05)] and cAMP/PKA/CREB pathway expression [cAMP: (18.25±2.67) mmol/L vs. (11.93±1.86) mmol/L; p-PKA/PKA: (1.00±0.18) vs. (0.17±0.03); p-CREB/CREB: (1.00±0.15) vs. (0.34±0.06)] were decreased (all P<0.001), and DNA damage was aggravated [ATM: (1.00±0.15) vs. (0.57±0.09); NBS1: (1.00±0.13) vs. (0.41±0.07); γ-H2AX: (1.00±0.16) vs. (2.74±0.49)]. Compared with the IR group, in the IR+ oe-EBLN3P group, cell viability [(57.92±8.65)% vs. (72.15±10.84)%], invasion [(25.31±4.19) vs. (78.63±12.76)], mitochondrial membrane potential [red/green fluorescence ratio: (0.27±0.05) vs. (0.79±0.14)], cAMP/PKA/CREB pathway activity [cAMP: (11.93±1.86) mmol/L vs. (16.47±2.58) mmol/L; p-PKA/PKA: (0.17±0.03) vs. (0.95±0.17); p-CREB/CREB: (0.34±0.06) vs. (0.71±0.13)] and ATM/NBS1 protein expression [ATM: (0.57±0.09) vs. (0.82±0.14); NBS1: (0.41±0.07) vs. (0.88±0.11)] were increased, while apoptosis [(15.43 ± 2.79)% vs. (6.27±1.08)%] and γ-H2AX levels [(2.74±0.49) vs. (1.69±0.28)] were decreased (P<0.01). The dual-luciferase reporter gene assay confirmed that LncRNA EBLN3P can target and bind miR-144-3p, and overexpression of LncRNA EBLN3P inhibited miR-144-3p expression. Compared with the IR+ oe-EBLN3P group, overexpression of miR-144-3p reversed the protective effect of LncRNA EBLN3P, manifested as increased apoptosis, decreased mitochondrial membrane potential, and inhibited cAMP/PKA/CREB pathway activity.

LncRNA EBLN3P is highly expressed in NSCLC and may reduce the radiosensitivity of tumor cells by competitively binding to miR-144-3p and affecting the activity of the cAMP/PKA/CREB signaling pathway; the mechanism is related to alleviating mitochondrial damage.

In elderly patients with chronic obstructive pulmonary disease (COPD), lung function progressively declines, exercise tolerance decreases, and recurrent acute exacerbations are common. Non-invasive ventilation (NIV) alone is difficult to improve skeletal muscle function and long-term quality of life. To investigate the clinical effects of precision pulmonary rehabilitation training combined with non-invasive ventilation (NIV) on the prognosis of elderly patients with COPD, clarify the application value of this combined regimen in elderly COPD, and explore individualized pulmonary rehabilitation models, thereby providing a clinical reference for optimizing comprehensive management of elderly COPD, reducing readmissions, and improving patients′quality of life.

A total of 138 elderly patients with COPD admitted to our hospital from July 1, 2023, to June 30, 2025, were selected and randomly divided into a control group 68 cases and an observation group 70 cases. Pulmonary function, respiratory rate, exercise endurance, laboratory indicators, quality of life-related scales, and mental health scales were recorded for both groups before treatment (H₀) and at 5 days (H₁), 30 days (H₂), and 90 days (H₃) of treatment.

The observation group showed better improvements than the control group in the following parameters: forced expiratory volume in the first second (FEV₁) percentage (11.00% vs. 9.00%, P=0.009), FEV₁/forced vital capacity ratio (FVC) (9.00% vs. 5.00%, P<0.001), respiratory rate (-7.00 breaths/min vs. -4.00 breaths/min, P<0.001), 6-minute walking distance(6MWD) (P<0.001), Borg score(P<0.001), modified British Medical Research Council dyspnea scale score(mMRC) (P<0.001), body mass index-obstruction-dyspnea-exercise index(BODE) (-2.10 points vs. -1.20 points, P<0.001), COPD assessment test score(CAT) (-9.00 points vs. -4.00 points, P<0.001), Epworth Sleepiness Scale score(CAT)(-9.00 points vs. -5.00 points, P<0.001), and sleep apnea clinical score(SACS) (-7.00 points vs. -4.00 points, P<0.001). At H₁-H₃, the observation group exhibited greater reductions in procalcitonin(PCT) and arterial partial pressure of carbon dioxide(PaCO₂), as well as greater increases in arterial partial pressure of oxygen(PaO₂) compared with the control group, with significant group × time interaction effects (F=42.208, 413.330, 81.261, all P<0.001). At H3, the observation group′s Self-Rating Anxiety Scale and Geriatric Depression Scale scores were lower than those of the control group[ (52.17±5.29) vs. (54.29±5.90) points, P=0.028; (7.55±2.79) points vs. (10.64±3.34) points, P<0.001].

Precision pulmonary rehabilitation training combined with NIV can improve pulmonary function, quality of life, and mental health in elderly patients with COPD, and has clinical significance.

Prone position ventilation (PPV) is an important lungprotective therapeutic measure for patients with respiratory failure in the intensive care unit (ICU). When conventional auxiliary cushions are used for prone position ventilation in clinical practice, complications such as impaired circulatory status caused by compression of the chest and abdomen, pressure injuries to the skin, displacement or dislodgement of pipelines, vomiting and aspiration tend to occur. Meanwhile, traditional manual back percussion for sputum clearance has limited efficiency, which compromises the safety and clinical efficacy of prone position ventilation therapy. To investigate the effects of the multiangle PPV auxiliary device combined with a vibration sputum expectoration instrument on hemodynamics, arterial blood gas parameters and related complications in ICU patients with respiratory failure, so as to provide clinical reference for the standardized and safe implementation of prone position ventilation for such patients.

Fifty-one patients with respiratory failure admitted to our hospital from October 2024 to February 2026 were selected and randomly divided into a control group (26 cases) and an observation group (25 cases). The control group received an auxiliary cushion combined with manual back percussion for sputum expectoration, while the observation group received multi-angle PPV combined with a vibration sputum expectoration instrument for postural drainage management. Central venous pressure (CVP), cardiac output (CO), stroke volume variation (SVV), and cardiac index (CI); arterial oxygen saturation (SaO₂), partial pressure of oxygen in arterial blood (PaO₂), oxygenation index (PaO₂/FiO₂), and the incidence of complications were compared between the two groups.

At 6 h of prone position ventilation, the hemodynamic parameters in the observation group, including CO[(4.11 ± 0.62) L/min vs. (3.42±0.95)L/min], SVV[(9.55±2.25)% vs. (11.11±2.08)%], and CI[(3.47±0.27)L/(min·m²) vs. (3.03±0.26)L/(min·m²)], were superior to those in the control group (P<0.05). On day 3, there were no statistically significant differences in SaO₂, PaO₂, or PaO₂/FiO₂ between the observation group and the control group (P>0.05). On day 7, SaO₂[(92.39±2.10)% vs. (90.93±1.93)%], PaO₂[(90.12±1.93) mmHg vs. (88.59±2.75)mmHg], and PaO₂/FiO₂[(364.07±21.02) vs. (351.77±17.92)] in the observation group were higher than those in the control group (P<0.05). The observation group had lower incidences of pressure skin injury (1 case vs. 5 cases), tube dislodgement (0 cases vs. 3 cases), vomiting (1 case vs. 4 cases), and aspiration (0 cases vs. 4 cases) than the control group. The single sputum suctioning operation time in the observation group [(56.76±8.22)s vs. (86.16±7.65)s] was shorter than that in the control group (P<0.05). In the observation group, 18 patients survived (72.00%) and 7 died (28.00%); in the control group, 18 patients survived (69.23%) and 8 died (30.77%).

The multi-angle prone position assistive device combined with a vibration sputum expectoration instrument can improve hemodynamic and arterial blood gas parameters, the incidence of related complications, shorten sputum suctioning time of ICU patients with respiratory failure.

To investigate the effects of Sanzi Yangqin Decoction combined with Xiaoqinglong Decoction on lung tissue and peripheral blood CD4⁺ T lymphocytes in ovalbumin (OVA)-induced asthmatic rats.

Fifty SD rats were randomly divided into blank control group, asthma model group, dexamethasone group, Sanzi Yangqin Decoction + Xiaoqinglong Decoction group (double-drug combination), and dexamethasone + Sanzi Yangqin Decoction + Xiaoqinglong Decoction group (triple-drug combination), with 10 rats in each group (half male and half female). Except for the blank control group, asthma models were established by OVA sensitization and challenge in all other groups. After successful modeling, the treatment groups received corresponding drugs via intragastric administration for 2 weeks, while the blank control and model groups received equal volumes of normal saline. At the end of the experiment, resting minute ventilation (VE) and peak expiratory flow (PEF) were measured; the proportions of peripheral blood T helper 17 cells (Th17), regulatory T cells (Treg), T helper 1 cells (Th1), and T helper 2 cells (Th2) were detected by flow cytometry; serum levels of interferon-γ(IFN-γ), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-10 (IL-10), and interleukin-17 (IL-17) were measured by ELISA; and the mRNA and protein expressions of epidermal growth factor receptor (EGFR), phosphorylated EGFR (p-EGFR), phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (AKT), and phosphorylated AKT (p-AKT) in lung tissues were determined by qRT-PCR and Western blot.

(1) Pulmonary function: VE and PEF in the model group were significantly lower than those in the blank control group [ (85.32±10.25) ml vs. (165.25±26.36) ml, (2.87±0.13) ml/s vs. (5.30±0.39) ml/s, P<0.05]; all treatment groups showed increased VE and PEF (P<0.05), with the triple-drug combination group increasing VE and PEF to (150.32±18.42) ml and (4.64±0.25)ml/s, respectively. (2)Pulmonary fibrosis: The lung collagen fiber area in the model group was significantly higher than that in the blank control group [(49.55±5.65)% vs. (3.26±0.25)%, P<0.05]; the triple-drug combination group reduced it to (19.25±2.05)%. (3) T cell subsets: The model group showed imbalances in Th17/Treg and Th1/Th2 ratios (P<0.05); compared with the model group, the triple-drug combination group decreased Th17/Treg [ (1.90±0.19) vs. (0.45±0.04)] and increased Th1/Th2 [(0.89±0.11) vs. (6.29±0.57)] (P<0.05). (4) Cytokines: The model group had elevated IL-4, IL-10, and IL-17, and decreased IFN-γ and IL-2 (P<0.05); the triple-drug combination group reversed these changes (P<0.05). (5) Pathway molecules: The mRNA and protein expressions of EGFR, p-EGFR, PI3K, p-PI3K, AKT, and p-AKT in the model group were significantly increased (P<0.05); the triple-drug combination group reduced these expressions and decreased the p-EGFR/EGFR ratio compared with the model group. The improvements in all above indicators in the double-drug and triple-drug combination groups were superior to those in the dexamethasone group, and the triple-drug combination group was superior to the double-drug combination group (P<0.05).

Sanzi Yangqin Decoction combined with Xiaoqinglong Decoction ameliorates airway inflammation and pulmonary function abnormalities and restores Th1/Th2 and Th17/Treg immune balance in CD4⁺ T cells in asthmatic rats by inhibiting the aberrant activation of the EGFR-PI3K-AKT signaling pathway.

This real-world study aimed to evaluate medication adherence and treatment persistence in chronic obstructive pulmonary disease (COPD) patients receiving dupilumab, and to identify key determinants influencing long-term treatment continuation.

A retrospective analysis was conducted using clinical records of COPD patients. Participants were stratified into adherent and non-adherent groups based on medication regularity. Clinical improvement was measured by the COPD Assessment Test (CAT), with a reduction ≥2 points defined as meaningful benefit. Multivariable logistic regression (illustrated via forest plot) was applied to identify independent predictors of adherence. Kaplan-Meier survival analysis was performed to compare treatment persistence across different response subgroups.

Baseline demographic and lung function characteristics were comparable between groups, with no statistically significant differences in age, sex, or baseline pulmonary function (all P>0.05). Follow-up data indicated that higher adherence was associated with greater symptomatic relief, evidenced by larger reductions in CAT scores, and adherence status positively correlated with CAT improvement (P=0.003). After adjusting for confounders in logistic regression, CAT improvement (≥2 points) remained the only independent protective factor for high adherence (OR=0.28, 95%CI: 0.10~0.72, P=0.011). Kaplan-Meier curves further revealed significantly longer treatment persistence in the clinically improved group compared to the non-improved group (Log-rank P=0.0012). The median treatment duration was only 28 days in the non-improved group, whereas the improved group demonstrated stronger willingness to continue treatment, with markedly prolonged persistence.

In the real-world self-pay healthcare setting, continued use of dupilumab in COPD patients largely depends on early perceived symptomatic benefit. Early improvement in CAT score serves as a critical predictor for treatment persistence. Clinical practice should emphasize close monitoring of initial treatment response and proactive communication with patients regarding efficacy and cost-effectiveness, in order to tailor individualized therapy and avoid prolonged low-benefit treatment.

To systematically evaluate the expression characteristics, diagnostic and prognostic value of stratifin in lung adenocarcinoma based on bioinformatics methods, and to analyze its correlation with immune cell infiltration.

RNAseq data from 538 lung adenocarcinoma tissues and 58 adjacent normal tissues were obtained from the TCGA database, and immunohistochemical data for SFN protein were retrieved from the HPA database. The Kruskal Wallis test and paired sample ttest were used to compare the differential expression of SFN mRNA between tumour and normal tissues. Diagnostic performance was assessed using receiver operating characteristic (ROC) curves. Prognostic value was evaluated by Kaplan-Meier survival analysis and Cox regression analysis. The ssGSEA algorithm and Spearman correlation analysis were employed to assess the correlations between SFN expression and the infiltration levels of 24 immune cell types.

SFN mRNA was significantly overexpressed in lung adenocarcinoma tissues (unpaired comparison P<0.001; paired comparison P<0.001), and the immunohistochemical results from HPA were consistent. SFN expression levels were significantly associated with T stage (P=0.012), N stage (P=0.008), pathological stage (P=0.015), and overall survival (OS)(P=0.021), but not with age, sex, race, smoking status, or treatment outcome (P>0.05). The area under the ROC curve (AUC) was 0.755, indicating moderate diagnostic capability. Kaplan-Meier analysis showed that the high SFN expression group had significantly shorter progressionfree survival (PFS)(P=0.004) and OS (P=0.009) than the low expression group. Multivariate Cox regression identified residual tumour, T stage, N stage, M stage, and primary therapy outcome as independent risk factors (all P<0.05). Immune infiltration analysis revealed that SFN expression was significantly positively correlated with NK cells (R=0.157, P<0.001), immature dendritic cells (iDC, R=0.155, P<0.001), and Th17 cells (R=0.135, P<0.001), while it was significantly negatively correlated with central memory T cells (Tcm, R=0.306, P<0.001) and helper T cells (Th, R=0.250, P<0.001).

SFN is significantly overexpressed in lung adenocarcinoma and shows good diagnostic efficacy. Its high expression is closely associated with poor prognosis and a specific pattern of immune cell infiltration. SFN may participate in lung adenocarcinoma progression through immune regulation and holds promise as a potential target for early diagnosis and personalised treatment.

To analyze the association between a disintegrin and metalloproteinase 33 (ADAM33) gene polymorphisms and asthma susceptibility, explore the molecular mechanism by which they mediate airway remodeling, and evaluate the impact of these polymorphisms on the efficacy of allergen immunotherapy (AIT).

PubMed, Embase, Web of Science, Cochrane Library, CNKI, Wanfang, SinoMed, and ClinicalTrials.gov were searched from inception to December 31, 2025, supplemented by manual reference tracing. Inclusion criteria were established according to the PICOS principle: asthma patients and healthy controls, with reported ADAM33 genotype frequencies, airway remodeling phenotypes, or AIT efficacy. Data were extracted, risk of bias was assessed, and case-control matching and genotype quality control were performed. Random-effects model analyses were conducted using Stata 17 (metan, metareg, metainf) and R 4.3 (metafor, forestplot); heterogeneity was assessed by Cochran Q, I^2, tau2, and H^2; leave-one-out sensitivity analysis was performed; and mixed-effects meta-regression was used to explore sources of heterogeneity, reporting regression coefficient beta (95%CI), R^2, and residual I². Bioinformatics annotation (HaploReg, RegulomeDB, GTEx, STRING, miRBase) and eQTL/chromatin interaction analyses were also performed.

A total of 2 847 records were initially retrieved, with 1926 remaining after deduplication; 1 523 reviews and irrelevant studies were excluded, leaving 403, and after full-text screening, 47 studies (43 case-control, 4 prospective) were finally included, comprising 23, 816 asthma cases and 28, 942 healthy controls, including 28 from Asia, 14 from Europe, 4 from North America, and 1 from South America. The pooled OR of the rs3918396 (S1) allele model (A vs. G) was 1.18 (95%CI 1.09~1.28, I²=38%); after removing any single study, the OR ranged from 1.14 to 1.22, with I² decreasing to 19%~29%. rs2280090 (T2), rs2280091 (T1), and rs511898 (F+ 1) were significant in Asian populations and childhood asthma. rs2280090 was associated with annual FEV₁ decline and airway wall thickening. Meta-regression suggested that ethnicity (Asian vs. others) was the main source of heterogeneity (beta=0.21, 95%CI 0.04~0.38, partial R²=31.2%, residual I²=19%). Carriers of ADAM33 risk alleles showed a smaller reduction in asthma exacerbation risk during house dust mite sublingual immunotherapy (P<0.05); risk genotypes were associated with poorer asthma control, lower FEV₁%, and higher sADAM33 levels.

ADAM33 gene polymorphisms, especially the highly linked rs3918396-rs2280090-rs2280091, participate in airway remodeling through soluble ADAM33(sADAM33)-mediated protease activity, airway smooth muscle/fibroblast proliferation, and Th2 inflammation, and represent potential genetic markers for asthma susceptibility and differential AIT efficacy, providing potential molecular targets for personalized asthma treatment.

To examine the association between individualized anticoagulation management guided by dynamic Caprini scoring and in-hospital clinical outcomes in patients with pulmonary embolism (PE).

This was a retrospective cohort study. A total of 179 hospitalized patients with PE (Caprini score ≥5 on admission) admitted to our hospital between May 2022 and May 2024 were analyzed, including 102 men and 77 women. According to the anticoagulation management strategy used during hospitalization, patients were divided into an observation group (n=87, dynamic Caprini monitoring combined with individualized anticoagulation) and a control group (n=92, routine anticoagulation management). The study endpoint was restricted to the in-hospital period. The incidence of new-onset PE and deep venous thrombosis (DVT), coagulation indices, D-dimer, arterial blood gas parameters, echocardiographically estimated pulmonary arterial systolic pressure, bleeding events and all-cause mortality were compared between the two groups. Multivariable logistic regression and inverse probability of treatment weighting (IPTW) were used to control for confounding.

Baseline characteristics were comparable between the two groups (all P>0.05). The incidence of new-onset PE was lower in the observation group than in the control group [3.45%(3/87) vs. 13.04% (12/92); χ²=4.185, P=0.041], as were the incidences of new-onset DVT (6.90% vs. 17.39%, P=0.040) and the repeat CTPA positivity rate (3.45% vs. 14.13%, P=0.017). After treatment, D-dimer and fibrinogen were lower, PaO₂ and the oxygenation index were higher, and pulmonary arterial systolic pressure was lower in the observation group (all P<0.001). PT, APTT and INR also differed significantly between groups, with lower values in the observation group that remained within or close to the normal reference range. No significant differences were found in bleeding events (4.60% vs. 3.26%, P=0.715), in-hospital all-cause mortality (1.15% vs. 5.43%, P=0.212) or the overall response rate (87.37% vs. 81.52%, P=0.05). Multivariable logistic regression and IPTW-weighted analyses were consistent in direction with the primary analysis.

This retrospective study suggests that individualized anticoagulation management guided by dynamic Caprini monitoring is associated with a lower incidence of in-hospital thromboembolic events and with improvement in multiple clinical indicators, without an increase in bleeding risk. Given the retrospective design, these findings are associative rather than causal and require confirmation in prospective studies.

To identify key genes associated with colorectal cancer lung metastasis and explore their potential molecular mechanisms, thereby providing references for the early diagnosis and targeted therapy of colorectal cancer lung metastasis.

The GSE41258 dataset was obtained from the Gene Expression Omnibus (GEO) database. Differential expression analysis was performed between primary colorectal cancer samples and lung metastatic samples to identify differentially expressed genes (DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to investigate the biological functions of DEGs, and candidate genes were screened using a Protein-Protein Interaction (PPI) network. Subsequently, Random Forest (RF), Logistic Regression (LR), and Light Gradient Boosting Machine (LightGBM) algorithms combined with Shapley Additive Explanations (SHAP) analysis were employed to identify key genes. The Human Protein Atlas (HPA) database and Gene Set Enrichment Analysis (GSEA) were further used for validation and functional characterization.

A total of 196 differentially expressed genes (DEGs) associated with colorectal cancer lung metastasis were identified. GO and KEGG enrichment analyses revealed that these genes were mainly enriched in biological processes and signaling pathways related to extracellular matrix (ECM) remodeling, cell adhesion regulation, and energy metabolism, suggesting their potential roles in colorectal cancer lung metastasis and metastatic microenvironment remodeling. The area under the curve (AUC) values of the RF, LR, and LightGBM models in the testing set were 0.830, 0.852, and 0.942, respectively, with LightGBM showing the best predictive performance. Integrated machine learning and SHAP analyses identified ATP citrate lyase (ACLY) and aggrecan (ACAN) as the key genes associated with colorectal cancer lung metastasis. Validation using the HPA database demonstrated that ACLY and ACAN proteins were expressed at higher levels in colorectal cancer tissues than in normal tissues, further supporting their potential roles in colorectal cancer progression. GSEA revealed that the ACAN high-expression group was mainly enriched in extracellular matrix (ECM) receptor interaction and integrin-related pathways, whereas the ACLY high-expression group was primarily enriched in complement and coagulation cascades, ribosome biogenesis, and spliceosome-related pathways, suggesting potential roles for these genes in colorectal cancer lung metastasis through the regulation of tumor metabolic reprogramming and extracellular matrix remodeling.

In summary, based on transcriptomic data from the GEO database, this study identified ACLY and ACAN as candidate genes associated with colorectal cancer lung metastasis through differential expression analysis, functional enrichment analysis, PPI network analysis, and machine learning screening. The expression features of ACLY and ACAN may reflect the molecular phenotype of colorectal cancer lung metastasis and may potentially serve as auxiliary markers for histological diagnosis of lung metastasis or as candidate molecules for targeted intervention.

To investigate the expression level of cystatin 4 (CST4) in lung adenocarcinoma tissues and cells and its effect on the malignant behaviors of H1650 cells, as well as the underlying mechanism.

The TCGA database was used to analyze CST4 expression in lung adenocarcinoma and its diagnostic value. qRT-PCR and Western blot were performed to detect CST4 expression in normal lung epithelial cells BEAS2B and lung adenocarcinoma cell lines A549, PC9, and H1650. CST4 knockdown and overexpression models were established in H1650 cells. Cell proliferation, apoptosis, migration, and invasion were assessed by CCK8 assay, flow cytometry, wound healing assay, and Transwell invasion assay, respectively. epithelial-mesenchymal transition (EMT)related protein expression was detected by Western blot. Rescue experiments were conducted by coknockdown of Ecadherin.

CST4 was highly expressed in lung adenocarcinoma tissues, and ROC curve analysis showed high diagnostic efficacy. Compared with BEAS2B cells, the protein (P=0.011, 0.009, 0.001) and mRNA (P=0.005, 0.002, 0.001) levels of CST4 were significantly upregulated in A549, PC9, and H1650 cells. Functional assays revealed that CST4 knockdown inhibited cell proliferation, increased the apoptosis rate [(22.68±1.89)% vs. (38.23±3.62)%, P=0.007], decreased wound healing ability [(59.16±4.31)% vs. (42.45±3.87)%, P=0.022], and reduced the number of invading cells [(51.93±4.76) vs. (31.28±3.07), P=0.007]. Conversely, CST4 overexpression showed opposite effects: apoptosis rate decreased [(24.51±1.89)% vs. (14.26±1.29)%, P=0.004], wound healing increased [(56.61±5.03)% vs. (75.47±6.28)%, P=0.034], and invading cells increased [(46.39±4.23) vs. (67.11±6.36), P=0.016]. Mechanistically, CST4 knockdown upregulated Ecadherin and downregulated Ncadherin and Vimentin (P=0.003, 0.027, 0.016), while overexpression produced the opposite effects (P=0.006, 0.039, 0.011). Rescue experiments showed that simultaneous knockdown of Ecadherin reversed the CST4deficiencyinduced inhibition of invasion and promotion of apoptosis.

CST4 is highly expressed in lung adenocarcinoma and promotes proliferation, migration, and invasion while inhibiting apoptosis in H1650 cells through regulation of the EMT pathway. CST4 may serve as a potential diagnostic and therapeutic target for lung adenocarcinoma.

To investigate the relationship between cytokine levels and the lesion degree, clinical significance and prognosis of patients with chronic obstructive pulmonary disease(COPD) complicated lung cancer by liquid chip technology.

A series of 130 patients with simple COPD(control group) and 57 patients with COPD combined with lung cancer( observation group)treated in our hospital from January 2020 to January 2025 were selected as study objects. According to the 2015 GOLD guidelines, patients in the combined group were divided into mild 53 cases, moderate 48 cases, severe 28 cases and extremely severe 16 cases. Serum interleukin (IL)-22, IL-17, IL-6, IL-8 and tumor necrosis factor (TNF)α were expressed by liquid chip technology. The relationship between the levels of IL-22, IL-17, IL-6, IL-8 and clinical features was analyzed. The median value of IL-22, IL-17, IL-6, IL-8 and TNF-α was used as the standard, higher than this value was the high expression group, otherwise the low expression group, and the prognostic difference was analyzed.

In observation group IL-22(0.42±0.10)pg/ml, IL-17(8.28±1.32)pg/ml, IL-6(63.22±9.15)ng/L、IL-8(25.44±4.10)ng/L, TNF-α(0.86±0.12)pg/ml higher than control group(0.37±0.05)pg/ml, (5.90±0.60)pg/ml, (39.67±5.08)ng/L, (60.08±5.99)ng/L, (0.51±0.07)pg/ml(P<0.05). The levels of IL-22, IL-17, IL-6, IL-8 and TNF-α were correlated with TNM stage (P<0.05). The expression levels of IL-22 and IL-17 were correlated with lymph node metastasis and distant metastasis in patients (P<0.05). Compared with mild COPD patients with lung cancer, the levels of IL-22, IL-17, IL-6, IL-8 and TNF-α were increased (P<0.05). Compared with moderate patients, the level of IL-6 was higher in severe patients (P<0.05). The 2-year overall survival rate of patients with high expression of IL-17, IL-6, IL-8 and TNF-α was lower than that of patients with low expression (P<0.05).

The detection of IL-22, IL-17, IL-6, IL-8 and TNF-α by liquid chip technology in patients with COPD complicated with lung cancer can better reflect the severity of the patient′s disease, and the expression level of some cytokines is related to clinical stage and prognosis.

To analyze the independent influencing factors for short-term prognosis in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and to construct a nomogram prediction model based on the neutrophil-to-lymphocyte ratio/albumin ratio (NLR/ALB).

A total of 220 patients with AECOPD admitted to our hospital from July 2023 to January 2026 were enrolled as the research subjects, and they were divided into a critical illness group and a stable condition group according to their short-term prognosis outcomes. The clinical data of the patients were collected, univariate and multivariate Logistic regression analyses were adopted to screen out the independent influencing factors for short-term prognosis, and a nomogram prediction model was constructed by using R software. The predictive performance and clinical utility of the model were evaluated via the receiver operating characteristic (ROC) curve, calibration curve and decision curve.

The observation group had a mean age of (69.47±8.25) years, Charlson Comorbidity Index (CCI) score of (3.21±1.02), procalcitonin (PCT) of (0.82±0.31) μg/L, red blood cell distribution width (RDW) of (14.82±2.45)%, and NLR/ALB of (3.62±1.25), compared with (65.29±9.76) years, (2.54±1.00), (0.62±0.33) μg/L, (13.19±2.32)%, and (2.76±1.02) in the control group, with statistically significant differences (P<0.05). Multivariate logistic regression analysis showed that age (OR=1.083, 95%CI: 1.029~1.141, P=0.002), CCI score (OR=1.613, 95%CI: 1.131~2.300, P=0.008), PCT(OR=3.819, 95%CI: 1.237~11.792, P=0.020), RDW (OR=1.318, 95%CI: 1.136~1.531, P<0.001), and NLR/ALB (OR=1.940, 95%CI: 1.401~2.687, P<0.001) were independent influencing factors for short-term prognosis in AECOPD patients. The constructed nomogram model achieved an AUC of 0.838(95%CI: 0.780~0.896), with a sensitivity of 72.31% and a specificity of 83.23%. The calibration curve showed good agreement with the ideal diagonal line (Hosmer-Lemeshow test: χ²=3.280, P=0.772). Within the threshold probability range of 5% to 89%, the model demonstrated a high clinical net benefit.

Age, CCI score, PCT, RDW, and NLR/ALB are independent influencing factors for short-term prognosis in AECOPD patients. The nomogram prediction model constructed in this study has good predictive performance and clinical utility, providing a reference for early identification of high-risk patients with poor short-term prognosis in AECOPD and for optimizing clinical intervention strategies.

To investigate the safety and accuracy of robotassisted CTguided hookwire localization before videoassisted thoracoscopic surgery (VATS) for pulmonary groundglass nodules (GGNs), and to construct a decision tree algorithm (DTA) prediction model.

A total of 378 patients with GGNs who underwent robotassisted CTguided hookwire localization followed by VATS in our hospital from January 2022 to April 2025 were enrolled. Among them, 345 cases with successful localization were assigned as the control group, and 33 cases with unsuccessful localization as the observation group. The clinical data, localization accuracy, and puncturerelated complications were compared between the two groups. A DTA prediction model was constructed, and its predictive performance was evaluated using receiver operating characteristic (ROC) curves, calibration curves, and 5fold crossvalidation.

Localization failed in 33 cases (8.73%), including 9 cases of hookwire dislodgement from lung tissue with ectopic placement into the pleural cavity and 24 cases of hookwire displacement. Localizationrelated complications included pneumothorax in 27 cases (7.14%), selflimiting pulmonary hemorrhage in 46 cases (12.17%), and mild pleural reactions in 2 cases. No critical complications such as hemothorax or air embolism occurred. The incidence of pulmonary hemorrhage in the observation group was significantly higher than that in the control group [10 cases (30.30%) vs. 36 cases (10.43%), P=0.001]. Univariate analysis showed that nodule size, distance from nodule to pleura, total depth, smoking history, and lesion location were associated with poor localization (P<0.05). In the DTA model, the feature weights were: distance from nodule to pleura 0.454, total depth 0.245, nodule size 0.217, smoking history 0.076, and lesion location 0.007. The ROC analysis yielded an area under the curve (AUC) of 0.909 (95%CI: 0.716~0.996) for the training set and 0.950 (95%CI: 0.901~1.000) for the validation set. After 5fold crossvalidation, the model accuracy was 83.2%. The calibration curve showed good consistency between the predicted probability and the actual incidence. During postoperative followup, tumor recurrence/metastasis occurred in 45 cases, and 19 patients died.

Robotassisted CTguided hookwire localization is safe and reliable for preoperative localization of GGNs. Distance from nodule to pleura, nodule size, total depth, smoking history, and lesion location are influencing factors for localization failure. The DTA model can effectively predict the risk of preoperative localization failure.

Through bibliometric statistical analysis and visual analysis of studies related to brain metastasis of lung cancer, this study aims to explore the research hotspots and development trends in this field over the past 10 years.

A total of 1, 349 Chinese-language articles and 3, 352 English-language articles were retrieved, of which 376 were related to immunotherapy for brain metastases from lung cancer. An overall analysis of the WOS database showed that the annual growth rate of English-language publications was 15.15%, involving 17, 814 authors and 53, 537 references. Based on the core database of CNKI and Web of Science, Citespace was used to explore the research hotspot and development trend of brain metastases related to lung cancer in recent 10 years through bibliometric statistics and visual analysis VOS viewer and R software conducted bibliometrics statistics and visual analysis of the published articles from 2014 to 2024, conducted visual analysis of the annual distribution and citation of the published articles, national and regional institutions and keywords, and conducted co-occurrence analysis of the keywords cluster analysis and emergence analysis.

Through the visual analysis of 1 349 CNKI and 3 352 WOS core database literature in the field of lung cancer brain metastasis, the number of papers published in this field showed an increasing trend year by year, China and United States ranked the top two in English, published 1, 224 and 887 articles, respectively, accounting for approximately 60% of the total publications of all countries in the past decade. Zhengzhou University and Hanvard University were the institutions with the largest number of Chinese and English articles, and the authors with the most Chinese and English literature output were Wu Yilong, Ahn and Myung-Ju, respectively, and keyword analysis suggested targeted therapy and chemotherapy, radiotherapy, immunotherapy and combination therapy are hot spots.

In the past 10 years, the field of lung cancer brain metastases has continued to develop, the change of treatment protocols has extended the survival time, and immunization and combination therapy have become the mainstream to break the therapeutic barrier. In the future, multidisciplinary integration will realize the precision treatment of lung cancer brain metastases.

Pulmonary Cryptococcosis (PC) lacks specificity in clinical manifestations and imaging features, making it highly prone to being confused with pulmonary tuberculosis, lung cancer, and other pulmonary infectious diseases. To a relatively high rate of misdiagnosis and missed diagnosis and delays the optimal timing of treatment. This study aims to investigate the clinical, imaging, and pathological characteristics of PC with chronic granulomatous inflammation as the main pathological manifestation, so as to provide a reference for early clinical identification of pulmonary cryptococcosis, rational selection of auxiliary examinations, reduction of unnecessary invasive procedures and antibiotic misuse, and improvement in the diagnosis and treatment of pulmonary fungal diseases.

A total of 20 patients with pathologically confirmed PC and histological manifestations of chronic granulomatous inflammation, admitted to our hospital from January 2023 to June 2025, were enrolled. Their clinical and pathological data were analyzed, and relevant literature was reviewed.

Among the 20 patients, there were 6 males and 14 females. Eight patients were asymptomatic; symptomatic presentations included cough in 8 cases, sputum production in 3, chest pain in 3, fever in 2, dyspnea in 3, and fatigue in 2. A definite history of pigeon exposure was noted in 2 cases. Lesions were located in the right lung in 12 cases (60.00%), left lung in 5 (25.00%), and both lungs in 3 (15.00%); lower lobe involvement was observed in 10 cases (50.00%). Imaging revealed solitary nodules in 11 cases (55.00%) and lesions adjacent to the pleura in 13 cases (65.00%). The lesion diameter ranged from 0.4 to 5.6 cm, with 15 cases (75.00%) having a diameter <3 cm. CT scans predominantly showed highdensity solid nodules, accompanied by groundglass halo sign in 3 cases (15.00%), spiculation sign in 4 cases (20.00%), vacuole sign in 2 cases (10.00%), air bronchogram sign in 2 cases(10.00%), and patchy consolidation in 9 cases (45.00%); cavity and a small amount of pleural effusion were observed in 1 case (5.00%). Histopathologically, all cases exhibited chronic granulomatous inflammation or chronic inflammation with aggregates of multinucleated giant cells and epithelioid cells; among them, 14 cases (70.00%) were of epithelioid granulomatous type, 3 (15.00%) with necrosis, and 3 (15.00%) with organization, without obvious caseous necrosis. PAS and GMS special staining were positive in all 20 cases, clearly revealing cryptococcal organisms and spores. Concurrent PC and lung adenocarcinoma were diagnosed in 2 cases; metagenomic nextgeneration sequencing (mNGS) indicated Cryptococcus infection in 4 cases, sputum culture was positive in 1 case, and bronchoscopy was positive in 1 case.

Pulmonary cryptococcosis presents with insidious clinical manifestations and nonspecific imaging features, and is easily confused with lung cancer and pulmonary tuberculosis. For peripheral subpleural highdensity nodules, especially those with groundglass halo sign and without calcification, PC should be suspected. The combination of HE morphology, fungal special staining (PAS/GMS), and mNGS detection can improve the pathogen detection rate and diagnostic accuracy for PC presenting as chronic granulomatous inflammation.

To investigate the clinical efficacy and safety of the novel β-lactam/β-lactamase inhibitor combination, sulbactam-durlobactam, in the salvage treatment of severe pneumonia caused by Hypervirulent Klebsiella pneumoniae (hvKP) complicated by a secondary infection of Carbapenem-Resistant Acinetobacter baumannii (CRAB). This study also reviews relevant literature to enhance the clinical understanding, diagnosis, and management of such complex, life-threatening co-infections.

A comprehensive retrospective analysis was conducted on the clinical data of a critically ill 37-year-old male patient admitted to our hospital in 2025. The patient suffered from severe hvKP pneumonia complicated by a secondary CRAB infection. We systematically collected and evaluated the patient′s epidemiological history, dynamic clinical manifestations, and comprehensive laboratory tests (including detailed inflammatory markers, blood gas analysis, and metagenomic next-generation sequencing [mNGS]). High-resolution chest computed tomography (CT) imaging and the complete clinical treatment course-encompassing multidisciplinary antimicrobial regimen adjustments, surgical debridement, and mechanical ventilation-were thoroughly reviewed. Furthermore, a rigorous literature review was performed to summarize the pathogenic mechanisms, infection control measures, and salvage treatment strategies for this dual critical infection.

The patient initially presented with a perianal soft tissue infection that rapidly progressed to septic shock, acute respiratory failure, and diabetic ketoacidosis. Initial vital signs showed a temperature of 39.2 ℃. Laboratory findings revealed a white blood cell count of 6.8×10⁹/L (86.4% neutrophils), C-reactive protein of 284.49 mg/L, procalcitonin of 26.3 ng/mL and IL-6>5 000 pg/ml. On day 2, mNGS of blood and deep sputum identified hvKP (454 and 154, 161 sequences, respectively). By day 7, chest CT demonstrated new bilateral pneumothoraces and multiple cavitary consolidations, while bronchoalveolar lavage fluid confirmed a secondary CRAB infection (colony count 4+ ). Despite an initial 12-day aggressive empirical regimen of meropenem combined with omadacycline and polymyxin B, the patient maintained a high fever and copious pink frothy sputum; cultures persistently grew CRAB (3+ ) and hvKP (2+ ). The treatment regimen was subsequently adjusted to meropenem (1 g q 6 h) combined with sulbactam-durlobactam (2 g q 6 h). Following this targeted intervention, the patient′s temperature normalized rapidly, sputum volume decreased, and oxygenation improved significantly. After sequential therapy with polymyxin B and sulbactam, mechanical ventilation was successfully discontinued on day 41, and sputum cultures converted to negative for CRAB. By day 55, chest CT showed substantial absorption of the bilateral pneumothoraces and pulmonary exudates, allowing for discharge. No significant hepatic, renal, or neurological toxicities were observed during the extended treatment period.

hvKP infections are characterized by acute onset and aggressive systemic dissemination. Patients with prolonged exposure to broad-spectrum antibiotics and invasive procedures are highly susceptible to secondary CRAB infections, which significantly increase mortality. Early diagnostic integration of mNGS and aggressive surgical source control for primary foci are indispensable. Sulbactam-durlobactam demonstrated qualified microbiological clearance and clinical efficacy with a favorable safety profile in this refractory CRAB infection, succeeding where traditional multidrug regimens failed. It represents a vital salvage therapeutic strategy for critical drug-resistant infections.

Influenza A is a common respiratory infectious disease, and its clinical manifestations and prognosis are influenced by multiple factors. To analyze the characteristics of peripheral blood leukocyte and lymphocyte counts in patients with influenza A, and to explore their clinical significance in the assessment of influenza A severity. Early symptoms of influenza A lack specificity and are easily confused with other respiratory infections; as a simple, rapid, and basic laboratory test, the complete blood count can provide clues for early identification.

We retrospectively analyzed 159 patients with influenza A who were admitted to our hospital between January 2023 and February 2025, categorizing them into a non-severe group (mild and moderate) and a critical group (severe and critical). We compared the gender, age, duration of illness, and leukocyte and lymphocyte counts at admission and discharge between the two groups to investigate their clinical characteristics.

In the observation group, there were 39 males (81.25%), and in the control group, there were 71 males (63.96%); males accounted for the majority in both groups. The time to onset (4.33±4.18) d, length of hospital stay (17.21±9.91) d, and total disease duration (21.54±11.16) d in the observation group were compared with those in the control group (1.88±1.81) d, (10.23±4.11) d, and (12.11±4.68) d, and the differences were statistically significant (P<0.05). The white blood cell count in the observation group was 7.56(4.78, 11.30)×10⁹/L at admission and 7.32(5.82, 9.48)×10⁹/L at discharge, which were significantly higher than those in the non critical group [5.64(4.20, 7.48)×10⁹/L at admission and 5.46(4.34, 7.57)×10⁹/L at discharge] (P<0.005); The lymphocyte count in the observation group was 0.50(0.29, 0.75)×10⁹/L at admission and 0.86 (0.60, 1.46)×10⁹/L at discharge, which were significantly lower than those in the non critical group [0.92(0.63, 1.40)×10⁹/L at admission and 1.34(1.01, 1.73)×10⁹/L at discharge] (P<0.005). ROC curve analysis indicated that the leukocyte and lymphocyte counts at discharge were good predictors of patient survival. Further COX regression analysis showed that the lymphocyte levels at discharge significantly affected the risk of death in patients, while the impact of leukocyte count was less significant. Kaplan-Meier survival analysis indicated that leukocyte and lymphocyte counts within the normal range were associated with better prognosis.

The leukocyte and lymphocyte counts in patients with influenza A are important for clinical classification and prognosis, which means these indicators should be taken seriously in clinical management to improve patient prognosis and survival rates. Future research could look into the clinical value and potential mechanisms of these indicators.