Allergic disorders such as asthma, atopic dermatitis, and allergic rhinitis affect a large portion of the global population. The relationship between allergies and cancer has been studied extensively, but results remain inconsistent for head and neck cancer. The aim of this meta-analysis is to evaluate whether there is a negative association between allergic disorders and head and neck cancer. A systematic search of five databases was conducted based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Cohort- and case-control studies examining allergies and head and neck cancer were included. Random-effect and fixed-effect models were used to calculate pooled relative risk, with heterogeneity assessed via the I2 and Cochrane’s Q-test. Subgroup and sensitivity analyses were performed to explore variations by study design, allergy type, and cancer site. Twenty-five studies with 3.6 million participants were included. No significant overall association was found between allergic diseases and head and neck cancer (meta-RR: 0.89; 95% confidence intervals (CI): 0.76–1.05). Subgroup analyses revealed protective effects for asthma (meta-RR: 0.81; 95% CI: 0.70–0.95) and food allergies (meta-RR: 0.73; 95% CI: 0.54–0.99). Allergic rhinitis showed negative associations with oropharyngeal cancer (meta-RR: 0.76; 95% CI: 0.69–0.84) and hypopharyngeal cancer (meta-RR: 0.65; 95% CI: 0.55–0.78), but a positive association with nasopharyngeal cancer (meta-RR: 1.67; 95% CI: 1.15–2.43). These findings suggest complex relationships between allergies and head and neck cancer, with negative and positive associations varying by allergy type and cancer site. Further research is needed to clarify these associations.

Tumor microenvironment modulators have produced durable effects in cancer treatment. Targeting immune checkpoint receptors, such as PD-L1, has demonstrated efficacy in eliciting antitumor responses. However, resistance to immune checkpoint blockers (ICBs) has constrained the efficacy of these therapies. Previous studies showed a link between the expression of AXL receptor tyrosine kinase and resistance to ICBs. Therefore, designing combination treatments with synergistic mechanisms to overcome ICB-based resistance is needed. In addition to antibody-based therapies, gene silencing with siRNAs has recently been explored to alter the cancer environment to enhance the immune response.
In this study, we targeted PD-L1 using an siRNA and AXL using a blocker (R428) in OVACAR-3 and CaSki cells, ovarian and cervical cancer cell lines, respectively, in the following groups: Scramble-siRNA, PD-L1-siRNA, Scramble-siRNA in conjunction with R428, PD-L1-siRNA in conjunction with R428, R428 monotherapy and untreated controls. Cell viability was assessed by MTT assay after 48 hours of treatment, and cisplatin sensitization was evaluated in resistant OVACAR-3 cells. Gene expression was analyzed by qRT-PCR, while flow cytometry quantified CD44⁺PD-L1⁺ populations, apoptosis (Annexin V/PI), and cell cycle distribution.
The results showed a significant decrease in cell proliferation, suppression of EMT-regulating genes, reduction of stemness in cancer cells, increased apoptosis and disruption of the cell cycle in the studied cell lines.
These findings suggest that simultaneous blockade of PD-L1 and AXL could serve as a novel tumor-suppressive strategy, especially for cancer patients resistant to ICBs.

Sulfur mustard (SM) is a potent chemical warfare agent that causes severe cutaneous, ocular, and pulmonary injuries, with respiratory tract damage being the most life-threatening. Despite its well-documented toxicity, the cellular mechanisms driving SM-induced apoptosis remain poorly understood. This study seeks to elucidate the apoptotic pathways involved in SM-induced pulmonary injury using a rat model.
We induced acute lung injury through two delivery methods: intraperitoneal injection (8 mg/kg) and intratracheal instillation (2 mg/kg) of SM, with both doses representing 1 LD₅₀. We assessed apoptosis-related proteins and gene expression through TUNEL staining, immunohistochemistry, and quantitative real-time PCR analyses.
Intraperitoneal administration of SM resulted in significantly elevated expression of apoptotic markers including annexin A1, annexin A2, cytochrome C, caspase-12, and JNK3, in alveolar epithelial cells compared to intratracheal delivery. Both TUNEL assays and immunohistochemical staining confirmed these findings. These results indicate that intraperitoneal SM exposure triggers more severe apoptotic responses in alveolar epithelial cells than intratracheal exposure at equivalent doses.
These findings demonstrate that intraperitoneal models can effectively identify apoptosis-related molecular targets suitable for therapeutic development.

Asthma is a chronic inflammatory disease characterized byimmune dysregulation. This study aimed to perform unbiased analysis of transcriptomic data to identify differentially expressed m6A-related genes in asthma, with a focus on exploring their potential as biomarkers and therapeutic targets.
Gene Expression Omnibus (GEO) (GSE134544) dataset was analyzed to identify differentially expressed m6A-related genes. Functional enrichment analysis was performed clusterProfiler, immune infiltration profiling was conducted with CIBERSORT, and a competing endogenous RNA (ceRNA, including microRNA [miR] and lncRNA) network was constructed. Drug enrichment analysis was carried out using DSigDB, and molecular docking was utilized to assess the interaction between dabigatran and the METTL3 protein.
From 192 differentially expressed genes, four m6A-related genes (METTL3, HNRNPC, IGFBP2, and RBMX) were identified as the intersecting genes between the m6A-related gene set and differentially expressed genes (DEGs) from the GSE134544 dataset. Gene Ontology (GO) analysis revealed significant enrichment in biological processes related to RNA metabolic processes and post-transcriptional regulation, while Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified important pathways such as spliceosome and p53 signaling pathways. METTL3 and HNRNPC were central in the ceRNA network, interacting with miRs such as hsa-miR-93-3p and lncRNAs like LINC01529. Drug enrichment analysis identified dabigatran as a potential METTL3 inhibitor, with molecular docking confirming a stable binding affinity (−5.9 kcal/mol).
This study emphasizes the critical role of m6A-related genes, particularly METTL3 and HNRNPC, as macromolecules in asthma pathophysiology, and provides insights into their potential as biomarkers and therapeutic targets for asthma treatment.

Idiopathic membranous nephropathy (IMN) presents a heterogeneous clinical course, with approximately 30% to 40% of patients experiencing spontaneous remission, while others respond poorly to treatment. This study aims to identify reliable biomarkers for risk stratification in IMN patients.
We conducted a prospective observational study involving 187 patients with IMN from February 2022 to February 2024. Patients were categorized into remission and non-remission groups based on clinical outcomes one year post-treatment. Comparative analyses revealed that the non-remission group exhibited significantly higher incidences of hypertension, elevated 24-hour urinary protein, higher serum creatinine levels, and increased inflammatory markers, including the systemic immune inflammation index (SII), systemic inflammation response index (SIRI), and pan-immune inflammation value (PIV). Conversely, the estimated glomerular filtration rate (eGFR) and lymphocyte-to-monocyte ratio (LMR) were lower in non-remission patients.
Spearman correlation identified hypertension, 24-hour urinary protein, and inflammatory indexes as positive correlates with non-remission, while eGFR showed a negative correlation.
Multivariate logistic regression confirmed hypertension, high 24-hour urinary protein, SII, SIRI, and PIV as independent risk factors for non-remission; eGFR was a protective factor. Receiver operating characteristic analysis revealed that SII and PIV effectively predicted non-remission (AUC=0.743 and 0.759, respectively). These findings underscore the potential of these indicators in assessing disease severity and guiding personalized treatment strategies.

Rigid nasopharyngoscopy is a valuable diagnostic method for immune-mediated allergy conditions, particularly for children aged≤6 years. In addition to evaluating the structural characteristics of the nasal cavity, the procedure also reveals inflammatory activity in the nasopharyngeal framework.

This study assessed 110 pediatric patients between 2 and 6 years old who presented with suspected allergic conditions. Rigid nasopharyngoscopy was performed, and its diagnostic performance was high with 85.45% sensitivity, 78.18% specificity, and an overall diagnostic accuracy of 83.00%, which supports its role in diagnosing and ruling out allergic disorders.

The findings revealed strong associations between mucosal erythema, cobblestoning, and mucosal secretions with symptoms like nasal obstruction and postnasal drip. These signs have proven to be reliable indicators of inflammation and chronic irritation in this age group. The procedure was well tolerated, and over 85% of children experienced no adverse effects.

Minor discomfort and nasal bleeding were reported in a small number of cases. Taken together, the results show that rigid nasopharyngoscopy is an essential diagnostic modality for early detection of allergy conditions in the pediatric population.

The aim of this research was to evaluate the diagnostic efficacy of integrating cervical length (CL), interleukin-6 (IL-6), placental alpha microglobulin-1 (PAMG-1), and fetal fibronectin (fFN) in predicting preterm birth among pregnant women with threatened preterm labor (TPL).
This study retrospectively analyzed clinical data from 150 pregnant women admitted for TPL between January 2021 and December 2024. Participants were divided into two groups based on pregnancy outcome: full-term delivery (n=85) and preterm birth (n=65). Additionally, 100 healthy pregnant women with no history of adverse pregnancy outcomes who underwent routine prenatal examinations during the same period were selected as the healthy control group. All participants underwent transvaginal ultrasound to measure CL, and venous blood samples were collected to assess serum IL-6 levels. PAMG-1 and fFN levels were measured in vaginal secretions.
There were no significant differences in baseline characteristics among the three groups. However, significant differences in CL, serum IL-6 levels, and positive rates of PAMG-1 and fFN were detected. Pearson correlation analysis showed significant associations between CL, IL-6, PAMG-1, fFN, and preterm birth. ROC curve analysis indicated that the AUC values for CL, IL-6, PAMG-1, and fFN alone were 0.798, 0.803, 0.753, and 0.754, respectively.
The combined application of these markers yielded an AUC of 0.920, significantly higher than any single marker. The combined use of CL, IL-6, PAMG-1, and fFN significantly enhances the diagnostic accuracy of preterm birth in patients with TPL.

Asthma is a common chronic respiratory disease in children, often leading to acute exacerbations marked by dyspnea, cough, and wheezing, which frequently necessitate emergency medical care. While standard therapies are effective, the exploration of novel drug delivery routes continues. Oral montelukast is a recognized treatment, but the efficacy of its intranasal formulation for acute attacks remains underexplored. This study aimed to evaluate the clinical effectiveness of intranasal montelukast as an adjunct therapy for pediatric asthma exacerbations.
A single-blinded, placebo-controlled, single-center trial was conducted involving children aged 2-12 years hospitalized with moderate to severe acute asthma. Participants were randomized to receive either intranasal montelukast or a placebo alongside standard care. Key outcomes, including the Pulmonary Index Score (PIS), respiratory rate, oxygen saturation, and length of hospital stay, were systematically assessed.
The analysis of 25 patients in each group revealed no significant baseline differences. The intranasal montelukast group demonstrated a statistically significant and sustained reduction in PIS scores at critical intervals (8, 12, and 24 hours) compared to the placebo group. Improvements in respiratory rate and oxygen saturation were also more pronounced with the active treatment. Notably, the mean hospital stay was significantly shorter for the montelukast group (2.16 days) than the placebo group (3.12 days).
In conclusion, intranasal montelukast shows significant promise as an effective adjunct therapy for acute pediatric asthma, correlating with accelerated clinical improvement and a reduced duration of hospitalization. These encouraging results justify further investigation through larger, multicenter trials to definitively establish its efficacy and safety profile.

Anti-recombinant human acid α-glucosidase (anti-rhGAA) antibody formation is a major challenge in patients with Pompe disease receiving enzyme replacement therapy (ERT). The clinical significance of these antibodies and their detection methods remain uncertain. This study aimed to evaluate the diagnostic and functional relevance of anti-rhGAA antibodies in late-onset Pompe disease (LOPD) and to compare the performance of ELISA and Western blot assays.
Fourteen patients with LOPD undergoing ERT and 14 age- and sex-matched healthy controls were studied. Serum anti-rhGAA antibodies and their IgG, IgM, and IgA isotypes were quantified using ELISA and verified by Western blot. Motor function was assessed using the Pompe Motor Function Levels Questionnaire, an adapted version of the GMFCS validated for Pompe disease.
Total and isotype-specific anti-rhGAA antibody levels were significantly higher in patients than in controls. ROC analysis showed excellent discrimination between groups. Strong agreement was observed between ELISA and Western blot results. However, antibody levels were not significantly correlated with motor function grade. Given the small sample size (n = 14), this non-significant result may reflect limited statistical power rather than a true lack of association.
Anti-rhGAA antibody detection effectively distinguishes LOPD patients from healthy individuals. Western blot provides a reliable, low-cost alternative to ELISA, particularly useful in resource-limited settings. Nevertheless, the prognostic utility of antibody titers for functional outcomes remains uncertain and warrants larger, multicenter validation studies.

Acute calculous cholecystitis (ACC) often triggers transient perioperative elevations in liver enzymes and systemic inflammation, yet existing complication-prediction tools seldom incorporate dynamic biomarker changes. Our goal was to establish and develop, using internal validation, a multivariable risk model that incorporates perioperative variations in liver function tests (LFTs) and the Systemic Immune-Inflammation Index (SII) in order to predict Clavien–Dindo grade ≥II complications following cholecystectomy for ACC. In this retrospective cohort study at a tertiary academic center (January 2022–December 2024), we analyzed 260 adult patients undergoing laparoscopic or open cholecystectomy for ACC.
We calculated Δ-values (day 1 minus baseline) for alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin, and SII (platelet × neutrophil/lymphocyte). Multivariable logistic regression with backward stepwise selection was used to derive the final model, which included ΔALT, ΔAST, Δbilirubin, ΔSII, age, American Society of Anesthesiologists (ASA) status, and operative duration. Internal validation employed 1 000 bootstrap replications.
The model demonstrated good discrimination (optimism-corrected area under the curve, 0.82; 95% CI, 0.77–0.87) and excellent calibration (slope, 0.95; intercept, –0.02). Significant predictors included ΔALT, ΔAST, Δbilirubin, and ΔSII, along with age, ASA III status, and longer operative duration. The decision-curve analysis demonstrated net benefit across threshold probabilities of 5% to 40%, with 15 additional true positives per 1 000 at the 20% threshold.
Integrating dynamic perioperative changes in LFTs and SII with key clinical factors yields a robust risk prediction model for postoperative complications after ACC surgery.

This study aimed to explore the effects of different dexmedetomidine (DEX) administration routes on anesthesia quality in pediatric patients undergoing endoscopic low-temperature plasma adenotonsillar ablation.
We selected 120 children with obstructive sleep apnea hypopnea syndrome scheduled for surgery between May and December 2023. Participants were divided into four groups (n=30 each): a control group (Group S) receiving standard anesthesia without DEX; a local anesthesia group (Group L) receiving ropivacaine infiltration with 0.3 µg·kg⁻¹ DEX; an intravenous group (Group T) receiving 0.6 µg·kg⁻¹ DEX infusion post-induction; and a nasal drip group (Group N) receiving 0.6 µg·kg⁻¹ DEX intranasally upon room entry. We compared operation/extubation/recovery times, and scores from the Observer Assessment of Alertness and Sedation (OAA/S), Objective Pain Scale (OPS), and Pediatric Anesthesia Emergence Delirium (PAED) scales. Rescue sedation and safety were also assessed.
Group T showed lower heart rates at specific timepoints, while Group L had lower blood pressures. Recovery time (Steward score ≥4) was longer in Groups L and T compared to Group S, but not in Group N. Groups T and N showed increased OAA/S scores post-awakening, with Group N having the highest scores. OPS and PAED scores decreased in all DEX groups, with Group N demonstrating the lowest scores, followed by Group L and then Group T. No significant differences were found in operation time, extubation time, or the incidence of rescue sedation/complications among groups.
Intranasal DEX emerged as the optimal route, providing effective analgesia and sedation without prolonging recovery time.

T helper 1 (T_H1) and T helper 2 (T_H2) cells can secrete various proinflammatory and anti-inflammatory factors, which can serve as indicators for predicting the severity of pneumonia. However, they are rarely used in combination with procalcitonin (PCT) and high-sensitivity C-reactive protein (hsCRP) detection to predict the severity of pneumonia. The purpose of this study is to investigate the combination of serum T_H1/T_H2 cytokines, PCT, and hsCRP for predicting the severity of community-acquired pneumonia (CAP).
This study observed 58 inpatients with CAP. Analyses were conducted on the serum levels of T_H1/T_H2 cytokines, PCT, and hsCRP; imaging examination results; underlying diseases; pathogens; and the pneumonia severity index (PSI).
The severe pneumonia group showed significantly higher PSI scores, age, and complication rates. Serum IL-2 was notably elevated in severe cases, while a combination of PCT, IL-4, TNF-α, and IFN-γ effectively predicted severe pneumonia, with an AUC of 0.712. Specific alterations in cytokines and biomarkers were identified as risk factors for higher PSI, complications, and prolonged hospitalization.
The combined detection of PCT, IL-4, TNF-α, and IFN-γ provides a potential tool for predicting severe CAP, and distinct biomarker profiles are associated with different clinical outcomes.

Allergic rhinitis (AR), as a chronic disease, seriously affects the quality of life of patients while concurrently exerting a significant economic and healthcare burden on the medical system. However, the existing treatment methods have certain limitations, and more effective treatment strategies are needed. To this end, we proposed an ovalbumin-induced guinea pig model of AR to investigate the potential impact of activated polyethylene glycol (PEG) with varying molecular weights and concentrations in local nasal treatment.
The therapeutic effect was evaluated by behavioral score, serological detection, and histopathological observation.
The behavioral assessment demonstrated significant alleviation of sneezing frequency, nasal pruritus, and clear nasal discharge in the activated PEG-600 treatment groups relative to the sham group. However, statistical analysis revealed no appreciable intergroup differences between the activated PEG-3400 treatment groups and the sham group. Histopathological evaluation disclosed a marked reduction in eosinophilic infiltration in the activated PEG-600 group, accompanied by preservation of nasal mucosal structural integrity and notable attenuation of inflammatory infiltration. In contrast, the activated PEG-3400 group exhibited comparatively limited therapeutic efficacy, demonstrating only a subtle reduction in inflammatory cell counts and more pronounced disorganization of mucosal epithelial architecture compared to the PEG-600-treated group. Serum immunological profiling indicated that while local inflammatory markers showed evidence of mitigation, systemic immune parameters remained unaffected by either activated PEG formulation.
These findings underscore the differential efficacy profile between PEG-600 and PEG-3400 derivatives in ameliorating AR symptoms, among which PEG-600 exhibits superior anti-inflammatory effects.

Ulcerative colitis (UC) is a chronic immune-mediated disease with a growing global burden. In this study, bioinformatics analysis and machine learning methods were employed to screen the potential immune microenvironment-related feature genes.
We identified 4 immune-related genes that are consistently dysregulated in UC and correlate with immune infiltration, including APOBEC3B (Apolipoprotein B mRNA Editing Enzyme Catalytic Subunit 3B), CXCL11, PLA2G2A, and TMEM173. Their diagnostic performance was verified in an external cohort and in our clinical samples.
Then, the proportion of ambiguous clustering (PAC) successfully classified UC patients into 2 molecular subtypes, including subtype 1 (metabolism-related subtype) and subtype 2 (immune-related subtype). The single sample gene set enrichment analysis (ssGSEA) algorithm revealed that subtype 2, with a higher score, of the majority of immune cells presented a worse inflammatory response.
In addition, we assessed scores of partial novel drugs querying the cMAP database and found that the efficacy of clinical small-molecule compounds presented different results across UC subtypes. These findings identify biomarkers, establish a concise immune-based classification of UC, and support subtype-guided therapy.

TC-1 is a recognized cancer cell line derived from lung epithelial cells that have been altered using the oncogenic E6 and E7 genes of human papillomavirus (HPV). These TC-1 cells are frequently utilized in preclinical research focused on lung cancer and HPV-associated tumors. The incidence of lung cancer and HPV-related cancers is significantly increasing. Drug resistance and the lack of selectivity in current treatments reduce their effectiveness. Researchers are seeking new therapeutic methods, including targeted therapies, immunotherapy, and oncolytic virus and bacterial therapies, to improve treatment outcomes and decrease mortality associated with these diseases. In this context, the present original study aimed to evaluate the potency of wild-type Newcastle disease virus (NDV-WTS) on lactate dehydrogenase (LDH) secretion and the induction of apoptosis in TC-1 cells.
In this experimental study, the TC-1 cell lines were cultured under laboratory conditions. Subsequently, they were treated with different multiplicities of infection (MOIs) of NDV-WTS (1, 2, and 4). Finally, the oncolytic effects of the virus were evaluated using laboratory assays, including MTT (cell viability), reactive oxygen species (ROS), LDH, survival rates, and the activities of Caspases 8 and 9.
The results indicated that NDV-WTS significantly decreased cell viability while increasing apoptosis, ROS levels, LDH release, and Caspase 8 and 9 activities compared to the control group. Molecular analyses further revealed that treatment of TC-1 cells with NDV significantly increased the expression of Bax, Casp8, and Casp9, while significantly decreasing Bcl2 expression relative to the control group.
NDV-WTS demonstrated remarkable efficacy in treating lung cancer and HPV-associated tumors. Based on the results of the present study, the use of Newcastle disease virus in the treatment of lung cancer and HPV-associated tumors may be beneficial, which requires further studies and clinical trials.

Traditional radical cystectomy has a high recurrence rate, a high probability of metastasis, and a reduced quality of life for patients. This study aimed to explore the efficacy of combining immunotherapy and surgical resection for high-risk muscle-invasive bladder cancer.
In a retrospective study, 231 patients with high-risk muscle-invasive bladder cancer admitted to Yueyang People’s Hospital between January 2019 and May 2024 were selected. After exclusions, 200 cases were analyzed and divided into two groups according to the treatment modality: the control group (surgical resection alone, n=100) and the intervention group (combination of immunotherapy and surgical resection, n=100). The cellular immune function indexes (CD3⁺, CD4⁺/CD8⁺, and natural killer cell levels), tumor markers (carcinoembryonic antigen, carbohydrate antigen 125, cytokeratin 21-1, and neuron-specific enolase), serum cytokines (basic fibroblast growth factor, vascular endothelial growth factor, and tumor necrosis factor-α), pathological complete remission (pCR), 1-year survival, and Functional Assessment of Cancer Therapy-Bladder (FACT-BL) quality-of-life scores were assessed in the two groups.
After 1 year of treatment, the indicators of the two groups of patients were statistically significant in comparison with each other. Patients in the intervention group had substantial improvements in immune function indexes, pCR, 1-year survival rate, and FACT-BL scores in comparison with the control group. Tumor markers and serum cytokines were lower than those in the control group.
The combination of immunotherapy and surgical resection can enhance clinical efficacy, providing a scientific basis for optimizing the clinical treatment plan.

Lung cancer remains a major cause of cancer-related mortality worldwide, with current treatments such as surgery, chemotherapy, and immunotherapy facing limitations, including severe side effects and high costs. Hyperthermia (H) has emerged as a promising strategy to enhance tumor sensitivity to treatments and reduce toxicity. This study investigates the effects of H in enhancing the anti-tumor efficacy of pemetrexed (PEM) and altering the expression profile of hsa-MiR-548c-3p (tumor suppressor) in the A549 cell line.
A549 cells were cultured in DMEM medium and divided into four groups: Control, and treatment with H, PEM, and a combination of H and PEM. Subsequently, cell viability, apoptosis percentage, release rate of LDH, production of ROS, and the expression level of hsa-MiR-548c-3p, CASP 8 and 9, and TYMS genes were measured.
Results revealed that the combination of H and PEM treatment had greater antitumor effects compared to the other groups. The combination of H and PEM significantly reduced cell viability, increased the percentage of apoptosis, LDH release, and ROS production, and upregulated hsa-MiR-548c-3p, CASP 8, and 9, while downregulating TYMS.
The findings suggest that H enhances the chemotherapeutic efficacy of PEM by upregulating hsa-MiR-548c-3p expression and promoting apoptosis in lung cancer cells, making it a promising complementary approach for overcoming drug resistance.

This study explored the diagnostic value of peripheral blood indices for acute pyelonephritis (APN) and the factors influencing poor prognosis.
A total of 118 patients with APN admitted to our hospital from January 2022 to June 2024 were retrospectively included as the observation group. Another 62 healthy volunteers were selected as the control group. Clinical data from the two groups were collected, and the diagnostic value of peripheral blood indices for APN was analyzed. The patients were divided according to their prognoses into good-prognosis group and poor-prognosis group, and the influencing factors of poor prognosis were identified by multivariate logistic regression analysis.
Compared to the control group, the white blood cell count (WBC) and C-reactive protein (CRP) were higher in the observation group, while IgG and C3 were lower. The areas under the curves (AUCs) of WBC, CRP, IgG, and C3 in the diagnosis of APN were 0.857, 0.846, 0.902, and 0.893, respectively, and their combined AUC was 0.981. After 3 months of follow-up, there were 43 cases of recurrence (36.44%). The multivariate logistic analysis showed that serum albumin< 35 g/L and a decrease of the IgG level were the influencing factors of poor prognosis in patients with APN.
In conclusion, WBC, CRP, IgG, and C3 had high value for the diagnosis of APN, and serum albumin< 35 g/L and the decrease of IgG level were the i factors influencing prognosis.

Common variable immunodeficiency disorder (CVID) is the most prevalent primary immunodeficiency in adults. Pathogenic mutations of the TNFRSF13B gene were identified in CVID patients and associated with autoimmunity and lymphoproliferation. A study on Swedish children unaffected by CVID has shown that rare variants in the TNFRSF13B gene increase the risk of asthma. To the best of our knowledge, asthma has not been reported in CVID patients with TNFRSF13B gene mutations. We described a patient suffering from asthma and CVID with a heterozygous mutation in the TNFRSF13B gene. According to our findings and previous studies, mutations in the TNFRSF13B gene seem to be possibly associated with the occurrence of asthma in CVID patients. 

Good’s syndrome (GS), a rare immunodeficiency disorder characterized by thymoma and hypogammaglobulinemia, presents diagnostic and therapeutic challenges due to recurrent infections.
We report a 53-year-old male farmer with GS complicated by recurrent pulmonary infections and COVID-19. Initial management focused on antiviral/anti-infective therapy and corticosteroids, but persistent hypogammaglobulinemia, B-cell depletion, and thymoma history were overlooked.
Diagnosis was confirmed upon integrating the thymoma history, immunological profiling, and bronchial alveolar lavage-next generation sequencing, revealing Pneumocystis jirovecii and Herpes Simplex Virus-1 coinfections. Treatment with intravenous immunoglobulin loading dose (2 g/kg), pathogen-targeted therapy (voriconazole, cotrimoxazole), and tapered corticosteroids achieved clinical remission, with immunoglobulin G (IgG) elevating to 6.35 g/L.
This case underscores the necessity of a "four-dimensional early warning system" integrating thymoma history, immune, imaging, and pathogen for timely GS diagnosis. Multidisciplinary collaboration and personalized regimens combining immunoglobulin replacement, precision anti-infectives, and immunomodulation are pivotal for optimizing outcomes in GS patients with complex infections.

Chronic Granulomatous Disease (CGD) is a defect or abnormality in the immune system that produces severe and persistent signs and symptoms in affected individuals.
Phenotypic diversity and genetic heterogeneity exist among patients with inborn errors of immunity (IEI). Symptoms may vary even when the mutations are identical; conversely, patients with different mutations may have similar clinical features. The expression of phenotype may be determined by the gene sequence, epigenetic changes, and sometimes environmental factors. Some of these outcomes are influenced by the individual’s past immunological exposure.
This study discusses two CGD cases, a father and son; after the diagnosis of CGD in the child and confirmation of the genetic mutation, the same mutation was also identified in the father.
Therefore, physicians should have more awareness that a single genetic mutation can have different clinical manifestations.