Non-small cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC) figure prominently in the list of prevalent and resistant cancers that reveal significant differences in response to immunotherapy. Neoantigens, specific antigens resulting from tumor mutations, play an important role in provoking immune responses and the success of immunotherapy. This review scrutinizes the quantitative and qualitative differences in neoantigens in NSCLC and PDAC and their impact on the efficacy of immunotherapy. The evidence suggests that the higher mutational burden, greater diversity, and different quality of neoantigens in NSCLC compared with PDAC are among the key drivers contributing to the enhanced susceptibility to immunotherapy in this cancer. These differences could pave the way for the development of personalized therapies and novel strategies to improve treatment outcomes in resistant cancers.

Mannose-binding lectin (MBL) is a critical component of the innate immune system, serving a vital role in the body’s initial defense against pathogens. Sepsis, a severe condition triggered by an excessive immune response to infection, has been linked to variations in the MBL2 gene that affect MBL levels and functionality. Numerous studies across various populations have examined the role of MBL-2 promoter polymorphisms (H>L and Y>X), but their results have been conflicting. This study aims to investigate the genetic connection between MBL promoter polymorphisms and susceptibility to sepsis through a meta-analysis of previously published articles.
A thorough literature search was conducted using PubMed, Scopus, and ScienceDirect to locate relevant articles for the meta-analysis. Rigorous inclusion and exclusion criteria were implemented to ensure data accuracy. All analyses were performed using Comprehensive Meta-Analysis Software v4.
Seven studies were included, examining the role of MBL-2 promoter genetic variants in sepsis (H>L: n=3, sepsis cases: 449, control: 687; Y>X: n=6, sepsis cases: 1211, control: 1694). Egger’s regression analysis and funnel plots suggested no publication bias. Heterogeneity analysis indicated homogeneity among the data. The meta-analysis showed no association between MBL-2 promoter variants and susceptibility to sepsis. The trial sequential analysis highlighted the need for further studies on MBL-2 promoter variants in sepsis to draw a definitive conclusion.
The promoter variants of the MBL-2 gene (H>L and Y>X) do not appear to increase the risk of sepsis. Further investigation is needed to confirm this conclusion, including more participants from diverse populations and larger sample sizes.

Ataxia Telangiectasia (AT) is a rare autosomal recessive disease with features of progressive cerebellar atrophy, immunodeficiency, and enhanced cancer susceptibility due to mutations in the ataxia telangiectasia mutated (ATM) gene. However, despite evidence from patients with AT in consanguineous Iranian families, limited information is still available on the genotype-phenotype association. This paper presents a familial case series of AT in Yazd, Iran, with a novel homozygous ATM mutation.
This report examines a consanguine family in Yazd, Iran, with four members presenting with symptoms characteristic of AT, including progressive neurological decline, cerebellar atrophy, immunodeficiency, elevated alpha-fetoprotein, and recurrent infections.
Genetic analysis confirmed a novel homozygous mutation of the ATM gene (c.1834C>A; p.Leu612Ile), which is a non-conservative substitution. It is predicted to result in loss of function, and parents were carriers of the mutation. Treatment included intravenous immunoglobulin, prophylactic antibiotics, and supportive care. One of the patients died due to severe infection despite intervention.
This case series highlights the impact of consanguinity on the occurrence of AT and the supporting role of genetic testing in diagnosing ATM mutations. The results emphasize the need for improved genetic counseling, family planning, early immunological therapy, and culturally tailored public health strategies to effectively manage AT in consanguineous populations.

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.

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.

Alternaria alternata is one of the most potent fungal allergens associated with allergic respiratory diseases, particularly asthma. Sensitization to A alternata has been linked to poor asthma control and increased morbidity, yet its prevalence varies widely across populations due to environmental and methodological differences. This study aimed to determine the prevalence and demographic predictors of A alternata sensitization among patients with moderate to severe asthma.
A cross-sectional study was conducted from March to September 2024 among 80 patients with physician-diagnosed moderate or severe asthma in Shiraz, Iran. Participants underwent skin prick testing (SPT) for A. alternata. Demographic and clinical data were collected and analyzed using descriptive statistics, χ² tests, and logistic regression.
Among the 80 patients (mean age 29.03 ± 20.45 years; 53.8% male), 28.8% tested positive for Alternaria sensitization. Sensitization was significantly more prevalent in patients younger than 18 years (44.1%) compared to adults (17.4%). No significant difference was observed based on sex. Although sensitization was more frequent in patients with severe asthma (40.6%) than moderate asthma (20.8%), this trend was not statistically significant. Logistic regression identified younger age as the only independent predictor of sensitization.
Alternaria alternata sensitization is common among individuals with moderate to severe asthma, particularly in younger patients. These findings underscore the importance of routine fungal allergen screening in asthmatics, especially children, to inform targeted management strategies and potentially reduce asthma-related morbidity.

This study aimed to investigate whether propofol-remifentanil anesthesia offers superior perioperative outcomes compared to propofol-fentanyl in pancreatic cancer surgery patients, with a focus on its effects on apoptotic molecules, plasma CXCL10/CXCL13 levels, and postoperative recovery.
A total of 150 pancreatic cancer patients were divided into 2 cohorts receiving either propofol-fentanyl (control group, n=75) or propofol-remifentanil (study group, n=75) anesthesia. We measured perioperative hemodynamics (cardiac index [CI], mean arterial pressure [MAP], heart rate [HR]), T-cell subsets, postoperative recovery indices (eye-opening time, extubation time, spontaneous respiration recovery time), sedation and analgesia levels (via Ramsay sedation score [RSS] and visual analog scale [VAS]), plasma CXCL10/CXCL13 levels, and apoptosis-related proteins (Survivin, Bax, Caspase-4, Bcl-2) using enzyme-linked immunosorbent assays (ELISAs). Adverse reactions were also recorded.
The study group exhibited significant advantages in hemodynamic stability and immune preservation. Despite similar baseline cardiovascular parameters, the remifentanil group maintained better CI, MAP, and HR stability during and after surgery. Flow cytometry analysis revealed better preservation of T-cell immunity (CD4⁺, CD3⁺, CD4⁺/CD8⁺ T cells) at 24 hours post-surgery. The intervention group also demonstrated accelerated postoperative recovery with significantly reduced emergence times (eye-opening, extubation, spontaneous respiration). Notably, the study group had more favorable inflammatory profiles (lower CXCL10/CXCL13 levels) and enhanced apoptotic responses (modulated Bax, Caspase-4, Survivin, and Bcl-2 expression). Clinical outcomes were superior in the study group, with significantly fewer adverse events (2 vs. 9 patients).
Propofol-remifentanil anesthesia provides effective sedation and analgesia in pancreatic cancer surgery, modulates key biological pathways related to apoptosis and inflammation, and improves postoperative recovery. These findings suggest that the choice of anesthesia regimen may have significant implications for perioperative outcomes and potentially long-term prognosis in pancreatic cancer patients. Future research should further explore the underlying mechanisms and long-term clinical benefits of this anesthesia strategy.

Background: Bronchial asthma (BA) involves immune imbalance and airway remodeling (AR), with CB2 receptors playing a role in inflammation regulation. This study explores the therapeutic potential of a CB2 receptor inverse agonist in BA rats and its mechanisms via the TLR4/NF-κB pathway.

Methods: Twenty-seven rats were divided into control (CG), model (MG), and intervention (IG) groups. BA models were induced in MG and IG via ovalbumin sensitization. IG received a CB2 receptor inverse agonist, while CG and MG received saline. Th1/Th2 cytokines, Th1/Th2 cell subpopulations, AR parameters, and TLR4/NF-κB expression in lung tissue were analyzed.

Results: Compared to CG, MG showed Th1/Th2 imbalance, increased AR indices, upregulated TLR4/NF-κB expression, shorter asthma latency, and prolonged total asthma attack duration (tAAD). IG exhibited restored Th1/Th2 balance, decreased TLR4/NF-κB expression, prolonged asthma latency, and reduced tAAD (P < 0.05).

Conclusion: CB2 receptor inverse agonist shows potential for BA prevention and treatment by regulating Th1/Th2 balance, inhibiting AR, and modulating the TLR4/NF-κB pathway.

Intervertebral Disc Degeneration (IVDD) is a complex biological process marked by changes in gene expression that final result in structural and functional problems in the intervertebral disc. This study was undertaken to obtain a thorough comprehension of the molecular mechanisms that drive IVDD.

The present work incorporated and examined two sets of gene expression data related to IVDD, obtained from the Gene Expression Omnibus database. An investigation of functional enrichment was conducted utilizing gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to clarify the biological processes and signaling pathways linked to these differentially expressed genes (DEGs). A protein-protein interaction (PPI) network was constructed, and Biomarkers were identified by selecting 13 hub genes using LASSO and SVM-RFE algorithms. An analysis of immune infiltration was conducted using ssGSEA, and the identification of transcription factor targets and medicines was investigated. The expression of ADM, ITGB5, RTN4, SLPI, and CSNK1E was validated using qPCR and Western blot approaches in an IL-1β-induced HNPCs model.

A profound correlation between IVDD and 112 DEGs was observed. The functional enrichment analysis demonstrated their participation in the organization of the extracellular matrix, translation in the cytoplasm, and the PI3K-Akt signaling pathway. An immunological infiltration examination revealed reduced infiltration of suppressor cells and monocytes derived from myeloid cells in the IVDD group. A total of thirteen hub genes were identified as promising indicators. An in vitro validation showed a notable decrease in the expression of ADM, ITGB5, RTN4, SLPI, and CSNK1E in the IVDD group as compared to the control group.

This thorough investigation provides deep understanding of the molecular processes that cause IVDD and reveals possible targets for treatment. The confirmation of important genes and their interactions with drugs in a laboratory setting strongly supports the results and lays the groundwork for future drug development and therapy approaches targeting IVDD.

Allergy and lung cancer are two distinct health concerns. While allergies are typically associated with heightened immune activity, such immune responses may also influence the tumor microenvironment. This study aimed to investigate a potential link between allergic conditions and the risk of lung cancer.
We conducted a case-control study analyzing 82 histologically confirmed lung cancer patients and 82 healthy controls from 2019 to 2022. Data were collected through structured questionnaires assessing asthma, allergic rhinitis (AR), food/drug allergies, and chronic urticaria. Statistical analyses included independent samples t-tests and chi-square tests, with significance set at a predetermined threshold.
We observed a significant inverse association between AR and lung cancer (8.54% vs 47.56% in controls; OR=0.14, 95% CI: 0.06–0.32). No significant associations were found for asthma (7.32% vs 3.66%), chronic urticaria (3.66% vs 3.66%), drug allergy (4.88% vs 1.22%), or food allergy (2.44% vs 6.10%). The association between AR and lung cancer remained robust after adjustment for demographic factors.
AR demonstrated a strong negative association with lung cancer, suggesting potential protective mechanisms distinct from other allergic conditions. These findings support the growing evidence for allergy-cancer immunomodulatory interactions and highlight the need for mechanistic studies on AR-specific pathways in oncogenesis.

Pediatric rhinitis is a common recurrent disorder that may progress to asthma or sinusitis in severe cases. This study aimed to compare the efficacy of different doses of glucocorticoid nasal spray combined with loratadine for rhinitis in children, and provide evidence for optimizing clinical treatment.
A total of 150 children with rhinitis admitted from June 2022 to June 2024 were divided into three groups: group I (low-dose group, n=50), group II (medium-dose group, n=50), and group III (high-dose group, n=50). Patients in all three groups were treated with a glucocorticoid nasal spray with loratadine combined with antihistamines. The immune function, serum inflammatory factor level, quantitative Lund-Kennedy score by nasal endoscopy, nasal symptom score, Quality of Life Questionnaire (RQLQ) scores, clinical efficacy, incidence of adverse events, and treatment compliance were assessed.
Post-treatment, all indices improved in the three groups. The percentages of CD4⁺ and CD8⁺ T cells, IL-10 content, and clinical efficacy in groups II and III were significantly higher than those in group I, while the immunoglobulin E (IgE), IL-6 and IL-17 content, the quantitative Lund-Kennedy score of nasal endoscopy, the children’s nasal symptom scores, the RQLQ scores, and the incidence rate of adverse events were below in group I. No significant differences were found between groups II and III in all indices, nor in treatment compliance across the three groups.
Loratadine combined with a glucocorticoid nasal spray therapy effectively improves clinical outcomes, inflammation, immune function, symptoms, and quality of life in rhinitis in children, with high clinical application value.

Osteoarthritis (OA) is the most common form of arthritis, characterized by pathological changes in joint components. Increasing evidence suggests that helper T (T_H) lymphocytes play a pivotal role in the inflammatory processes associated with OA. Curcumin, the primary polyphenolic compound found in Curcuma longa, exhibits potent antioxidant and anti-inflammatory properties. This study aimed to evaluate the effects of curcumin on the gene expression of key transcription factors of T_H1 and T_H2 cells and to explore their associations with clinical and immunological parameters in patients with knee OA.
This mechanistic sub-study presents a secondary molecular analysis of RNA biospecimens from a previously completed double-blind, placebo-controlled clinical trial involving 30 patients with knee OA. Participants were randomly assigned to receive either 80 mg/day of nano-micelle curcumin or a placebo for 3 months. Expression levels of T-box transcription factor 21 (T-bet) and GATA binding protein 3 (GATA3), the key transcription factors of T_H1 and T_H2 cells, respectively, were quantified using SYBR Green-based real-time PCR. Their associations with changes in visual analogue scale (VAS) score, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and percentages of CD4⁺ and CD8⁺ T cells were analyzed.
Curcumin administration significantly reduced T-bet gene expression compared to baseline and showed a positive correlation with the frequency of CD8⁺ T cells, while GATA3 expression remained unchanged.
These findings may provide a novel molecular perspective on curcumin's potential to influence CD8⁺ T cell dynamics by modulating T_H1-associated transcriptional programs.

Non-alcoholic fatty liver disease (NAFLD) is a major hepatic manifestation of metabolic syndrome and encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). This study aimed to evaluate the contribution of immunological, inflammatory, and metabolic parameters-including cytokine levels, immune cell profiles, and microRNA (miR) expression-in the progression from NAFLD to NASH among individuals with features of metabolic syndrome.
An observational study was conducted between January 2022 and December 2024, enrolling 300 adult patients with radiologically or histologically confirmed NAFLD. Patients underwent comprehensive anthropometric, biochemical, and immunological assessments, including cytokine profiling (interleukin [IL]-6, IL-17, tumor necrosis factor-α [TNF-α], transforming growth factor-β1 [TGF-β1]), immune cell phenotyping (T helper 17 [T_H17], regulatory T cells [Tregs], monocytes), and miR quantification (miR-122, miR-34a). Liver biopsy was performed in 95 selected cases.. The nursing team also assists in coordinating multidisciplinary care and ensuring follow-up compliance, which are vital for long-term disease management and reducing progression to NASH.
Significant elevations were observed in metabolic parameters (body mass index [BMI], homeostatic model assessment for insulin resistance [HOMA-IR]), hepatic enzymes (alanine aminotransferase [ALT], aspartate aminotransferase [AST]), inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], ferritin), and oxidative stress markers (malondialdehyde [MDA]). Adipokines (↑leptin, ↓adiponectin), hepatokines (↑fibroblast growth factor 21 [FGF21], ↑fetuin-A), and cytokines (↑IL-6, ↑TNF-α, ↑IL-17) were markedly altered in patients with biopsy-proven NASH.
This study reinforces that pro-inflammatory cytokines, altered immune cell profiles, and dysregulated miRs serve as promising biomarkers for early identification and potential therapeutic targeting in metabolic syndrome-associated steatohepatitis.

Anaphylaxis is a severe, rapidly progressing, and potentially life-threatening emergency requiring prompt, evidence-based intervention. This study assessed pre-hospital emergency healthcare professionals’ knowledge of anaphylaxis diagnosis, acute management, and treatment protocols in line with current clinical guidelines.
A descriptive cross-sectional study was conducted between February and April 2025 among physicians, paramedics, and emergency medical technicians (EMTs) working in Emergency Medical Services (EMS) stations. Data were collected via a 21-item Google Forms survey covering demographics and key knowledge domains based on established pediatric anaphylaxis guidelines.
A total of 322 professionals participated: paramedics (n = 214, 66.5%), EMTs (n = 73, 22.7%), and physicians (n = 35, 10.9%). Although most reported prior anaphylaxis training (90.0%) and clinical encounters (87.6%), only 52.2% correctly identified all three diagnostic criteria. Regarding pharmacologic management, 81.7% recognized epinephrine as first-line treatment, with physicians performing best (94.3%) compared to paramedics (81.8%) and EMTs (75.3%). Similarly, 81.1% correctly identified the intramuscular route, with physicians again demonstrating superior knowledge (95.5%). However, major deficiencies were noted in appropriate patient positioning (52.2%) and epinephrine auto-injector use (50.6%), with significant inter-professional differences across both domains.
Substantial knowledge gaps exist among pre-hospital emergency providers regarding anaphylaxis diagnosis, patient positioning, and auto-injector administration. Targeted training and standardized protocols are urgently needed to enhance competency and improve patient safety in pre-hospital anaphylaxis management.

Chemokines and their receptors play a central role in mediating the migration of pathogenic T cells into the central nervous system of patients with multiple sclerosis (MS). Vitamin D and curcumin are known to possess anti-inflammatory and immunomodulatory properties; however, their combined effects on T-cell chemokine receptor expression in MS remain poorly defined.
In this study, we investigated the in vitro effects of vitamin D, curcumin, and their combination on CD4⁺ and CD8⁺ T cells expressing CXCR3, CCR6, and CCR4 in patients with relapsing-remitting MS (RRMS). Peripheral blood mononuclear cells were collected from patients in relapse (n=10), remission (n=14), and healthy controls (n=15) and analyzed using flow cytometry.
Relapse patients exhibited elevated frequencies of CXCR3⁺CD4⁺ T cells compared to healthy controls, which normalized following treatment. Increased CCR6⁺CD4⁺ T cells and CXCR3⁺CD8⁺ T cells were also observed in patients, with a significant reduction achieved only after combined treatment with vitamin D and curcumin. The combined treatment further decreased the mean fluorescence intensity of CXCR3 and CCR6 on T cells in relapse patients, while vitamin D alone specifically reduced CCR4⁺CCR6⁺CD4⁺ T cells, a T_H17-like subset enriched during relapse.
These findings indicate that vitamin D and curcumin, particularly in combination, modulate T-cell activity by downregulating chemokine receptor expression and may represent a promising adjunctive approach for controlling immune cell migration in MS.

Autoimmune hepatitis (AIH) is a chronic immune-mediated liver disease that can progress to cirrhosis and liver failure if untreated. Current therapies, mainly corticosteroids, are effective but limited by adverse effects and incomplete responses, prompting the search for safer alternatives. Peiminine, an alkaloid derived from Fritillaria species, has demonstrated anti-inflammatory and antioxidant properties in several disease models. This study evaluated its efficacy in a concanavalin A (ConA)–induced mouse model of AIH.
Male C57BL/6 mice were divided into six groups, including ConA-injured animals, and treatment groups receiving peiminine (3 mg/kg, i.p.), prednisolone (10 mg/kg, i.p.), or their combination.
ConA injection caused sharp increases in ALT (↑ 5.4-fold), AST (↑ 4.8-fold), and ALP (↑ 3.9-fold), alongside marked elevations in MPO activity, nitric oxide, and pro-inflammatory cytokines (TNF-α, IL-6, IFN-γ). Peiminine significantly reversed these alterations—reducing ALT, AST, and ALP by 65% to 75% and restoring IL-4, TGF-β, and SOD activity toward normal values. Pre-treatment provided stronger protection than post-treatment, and outcomes were comparable to those of prednisolone, with combination therapy yielding the greatest improvement across all indices.
These findings indicate that peiminine mitigates immune-mediated hepatic injury by modulating cytokines, reducing oxidative stress, and maintaining liver integrity. Peiminine may represent a promising preventive or adjunct therapy for AIH, warranting further mechanistic and long-term investigations.

Exhausted T cells are phenotypically and functionally heterogeneous, from progenitor- to terminally-exhausted T cells. We evaluated gene expression profile of CD8⁺ T cells in acute leukemia to characterize the phenotype of exhausted T cells.
Blood samples were collected from acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) patients prior to treatment and from control subjects. Additionally, samples were obtained from ALL patients after induction therapy. TCF7, NFATc1, IRF4, and BATF gene expression was then evaluated in isolated CD8⁺ T cells.
CD8⁺ T cells from ALL patients showed higher expression of TCF7 and NFATc1 compared to the control group. The two study groups did not have a significant difference in the expression of BATF and IRF4. When compared to the control group, CD8⁺ T cells of AML patients showed an elevated expression level of NAFTc1 and IRF4. Significant differences were not found between the two study groups in AML when it came to the expression of BATF and TCF7.
To our findings, the majority of CD8⁺ T cells found in ALL patients consist of progenitor-exhausted T cells.

Chédiak-Higashi syndrome (CHS) is a rare autosomal recessive disorder characterized by severe immunodeficiency, partial albinism, recurrent infections, and progressive neurologic dysfunction. Unless patients undergo successful hematopoietic cell transplantation (HCT), a majority of them die during childhood because of an accelerated phase of immune dysfunction and hemophagocytic lymphohistiocytosis (HLH). Herein, we aim to describe the laboratory diagnosis, clinical manifestations, and genetic findings in three patients with CHS.
Three patients with partial albinism associated with CHS were included in this study. Immunological screening tests were done. Leukocyte granules in peripheral blood smear (PBS) and hair shafts were examined. Subsequently, genetic analyses were performed by Whole Exome Sequencing (WES) followed by Sanger sequencing for all patients and their parents.
Initial immunology screening tests were within normal limits. Light microscopy studies of patients’ PBS showed giant granules in the leukocyte cytoplasm. Furthermore, there were evenly distributed melanin granules in the patients' hair shafts. Variant analysis of the LYST gene identified three splicing site defects: one known variant, c.7060-1G>A in intron 24, and two novel variants, c.2363+2T>C in intron 5, and c.10702-3A>G in intron 47.
Hair shaft assay and PBS are rapid and suitable tests in early diagnosis and differentiation in CHS patients. WES results revealed 2 novel splice site variants that might contribute to earlier and more accurate diagnosis. This facilitates early enrolment of CHS patients in the HCT protocol-the optimal treatment path-and enables prenatal diagnosis for affected families.

 Atopic dermatitis (AD) is a chronic inflammatory skin disease with heterogeneous immune dysregulation. Although interleukin-17 (IL-17) signaling is implicated in AD, IL-17-related diagnostic biomarkers and molecular subtypes remain unclear. This study aimed to identify IL-17-associated biomarkers, characterize immune infiltration and subtypes, and explore upstream regulatory mechanisms.
Gene expression datasets (GSE121212, GSE6012) were acquired from the Gene Expression Omnibus database, and an IL-17-related gene set was collected from the Gene Set Enrichment Analysis website (GSEA)(http://www.gsea-msigdb.org/gsea/msigdb/search.jsp). Differential expression (limma) and Weighted Gene Co-expression Network Analysis were integrated to identify candidate genes, followed by feature selection using Least Absolute Shrinkage and Selection Operator and random forest. We evaluated immune cell infiltration by applying the CIBERSORT algorithm alongside single-sample Gene Set Enrichment Analysis. GSEA was applied to investigate underlying biological processes. AD patients were clustered into subtypes relying on IL-17 scores using ssGSEA.
Our integrated analysis identified IL4R and PRSS22 as key IL-17-related diagnostic biomarkers for AD, demonstrating excellent diagnostic accuracy across both training and validation cohorts. Immune-infiltration analyses revealed altered immune-cell composition and correlations observed between the identified biomarkers and specific immune cells. Two distinct AD subtypes were identified based on IL-17 scores, exhibiting immune infiltration patterns and enriched biological pathways. A ceRNA network highlighted potential regulatory mechanisms involving these biomarkers.
IL4R and PRSS22 are robust IL-17-related diagnostic biomarkers for AD, with high predictive power across cohorts. Immune infiltration profiling and IL-17 score-based subtyping reveal AD heterogeneity. These findings provide a foundation for improved diagnosis, molecular stratification, and potential therapeutic targeting in AD.

Cognitive dysfunction (CD) is a common neuropsychiatric manifestation of systemic lupus erythematosus (SLE), but its early identification lacks objective serological markers. This study aimed to explore the predictive value of combined serum interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and neurofilament light chain (NfL) for CD in SLE patients.
A total of 108 SLE patients (January 2018–December 2019) and 50 healthy controls were enrolled. SLE patients were divided into CD group (MoCA score <26, n=49) and non-CD group (MoCA score ≥26, n=59). Serum IL-6, ICAM-1, and NfL levels were detected by ELISA. Logistic regression and ROC curve analyses were performed to evaluate risk factors and predictive efficacy.
Serum IL-6, ICAM-1, and NfL levels were significantly higher in SLE patients than in controls (p<0.05), and further elevated in the CD group. These three markers were independent risk factors for SLE-related CD. The AUC of combined detection (0.852) was significantly higher than individual markers (0.734, 0.712, 0.677).
Serum IL-6, ICAM-1, and NfL have certain predictive value for CD in SLE patients, and the combined detection of these three indicators offers higher predictive value.

Immune and inflammatory factors influence endometrial cancer outcomes, the pan-immune inflammation value (PIV) shows potential but remains underexplored.
This study aims to evaluate the relationship between preoperative PIV, T cell subtypes, and surgical prognosis in endometrial cancer patients, providing insights for prognostic markers and predictive models. We conducted a prospective observational study involving 101 endometrial cancer patients from August 2022 to August 2024. Based on prognosis within 6 months post-surgery, patients were divided into good and poor prognosis groups. We compared clinical characteristics, inflammatory indices, and T cell immune profiles between the groups.
The mean age of participants was 50.12 years, with 23 patients experiencing a poor prognosis. The poor prognosis group exhibited significantly higher proportions of advanced International Federation of Gynecology and Obstetrics (FIGO) stage, larger tumor diameter, elevated neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), systemic inflammatory response index (SIRI), and PIV. Conversely, this group showed lower proportions receiving neoadjuvant chemotherapy, CD4⁺ T cells, and CD4⁺CD8⁺ T cell ratios. Notably, elevated PIV emerged as an independent risk factor for poor prognosis, while increased CD4+ T cell proportion and CD4⁺CD8⁺ ratio were protective.
PIV is significantly associated with poor prognosis in endometrial cancer, serving as an independent risk factor. Higher CD4+ T cell counts and CD4+:CD8+ ratios provide protective benefits. The constructed logistic regression model demonstrates strong predictive capability for post-surgical outcomes. However, limitations, including sample size and short follow-up, necessitate further investigation in larger cohorts.

Hepatocellular carcinoma (HCC) is the predominant type of primary liver cancer.
This study aimed to elucidate the involvement of genes associated with 25 cell-death modalities in HCC development and progression. HCC transcriptomic datasets were integrated with curated cell death-related genes. Candidate genes were screened by differential expression analysis and protein–protein interaction network construction. Prognostic genes were identified using univariate Cox regression, proportional hazards assumption testing, and stepwise multivariate Cox regression. A risk score model and a nomogram were established, followed by risk stratification and analyses of immune infiltration, immune checkpoints, somatic mutations, and in silico drug sensitivity. Single-cell RNA sequencing was used to identify key cell types, infer temporal dynamics, and characterize intercellular communication, and findings were validated by quantitative real-time PCR (qRT-PCR).
MAPT, CDKN2A, NQO1, CHGA, SERPINE1, and RET were identified as prognostic genes, and the risk model and nomogram showed good prognostic performance. Immune profiling revealed significant differences in multiple immune cell subsets between risk groups, including activated CD4+ T cells. Notably, CDKN2A correlated with activated CD4+ T cells, NQO1 with natural killer cells, RET with CD4+ central memory cells, and SERPINE1 with activated dendritic cells; RET also showed the strongest positive correlation with HAVCR2. Mutation spectra differed across risk groups, and ten drugs displayed significant predicted IC50 differences; all six genes were negatively correlated with KIN001.135.
Single-cell analyses highlighted hepatocytes as a key cell type with strong hepatocyte–epithelial communication. qRT-PCR confirmed higher MAPT, CDKN2A, NQO1, and SERPINE1 expression in HCC tissues than in normal tissues.

To investigate the feasibility and effectiveness of targeted lung recruitment and the titration of optimal positive end-expiratory pressure (PEEP) in neonates under the guidance of lung ultrasound.
The atelectasis neonates from June 2022 to June 2024 in the Neonatology Department of People's Hospital of Pidu were collected and randomly divided into a lung ultrasound scoring (LUS) group and an oxygen (OXY) group, both of which were given mechanical ventilation treatment. The lung recruitment and optimal PEEP were performed by the LUS and OXY methods, respectively. The optimal PEEP and the respiratory and hemodynamic indexes of the two groups were compared before and after lung recruitment and after the optimal PEEP was titrated.
After the intervention, the dynamic lung compliance (Cdyn) in the LUS group increased by 38.2% compared with the baseline (from 30.6 ± 4.3 to 42.3 ± 5.1 mL/cmH₂O), which was significantly higher than the 21.4% increase in the OXY group (from 29.8 ± 4.1 to 35.6 ± 4.8 mL/cmH₂O). The improvement in PaO2/FiO2 in the LUS group was 22.5% higher than in the OXY group. There was no statistically significant difference in the incidence of complications between the two groups.
Lung ultrasound can guide neonatal lung recruitment and optimal PEEP titration, improving lung compliance and oxygenation without affecting the safety of treatment.

Natural killer (NK) cells contribute to the development of Rheumatoid Arthritis (RA). Increased expression of programmed cell death protein 1 (PD-1), encoded by the PDCD1 gene, indicates NK cell exhaustion, a process that may be influenced by microRNAs (miRNAs). In this study, we examined PD-1 expression on NK cells from RA patients and evaluated whether miRNAs modulate this pathway.
Although antibiotics are critical for treating infections, they can provoke harmful immune responses by releasing bacterial components that overstimulate the immune system. Such responses may lead to excessive inflammation or cytokine storms. To address this risk, we assessed the immune safety of a newly designed chimeric endolysin, ZAM-MSC, and compared its effects with traditional antibiotics using transcriptomic, proteomic, and computational analyses.
We analyzed public gene and protein expression datasets from antibiotic-treated human cells and performed in silico studies on ZAM-MSC. Differential expression analysis and pathway enrichment were conducted, alongside structural modeling of the endolysin and its predicted interactions with immune receptors.
Antibiotic treatment strongly activated inflammatory genes and pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). In contrast, ZAM-MSC minimally affected immune-related gene expression, with downregulation of interleukin-6 receptor (IL6R) and tumor necrosis factor receptor 1A (TNFRSF1A). Structural modeling showed weak interactions with Toll-like receptors, and epitope analysis predicted low immunogenicity. These results suggest ZAM-MSC may offer a safer antimicrobial alternative, though all protein-level findings are based on computational predictions and require experimental validation. 

Volatile anesthetics, particularly sevoflurane, have demonstrated cardioprotective properties during cardiac surgery. However, their immunomodulatory mechanisms at the molecular level remain unclear. Given the close relationship between cardiac injury and immune responses, understanding how anesthetic agents influence immune-related pathways may provide new insights into perioperative myocardial protection.
This study aimed to explore the immunological and molecular mechanisms underlying the effects of sevoflurane anesthesia on cardiomyocytes in patients undergoing coronary artery bypass grafting (CABG).
Gene expression data (GSE4386) from myocardial tissues of CABG patients anesthetized with sevoflurane or propofol were analyzed. Differentially expressed genes (DEGs) were identified using R software, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Protein–protein interaction networks were constructed to identify key immune-associated hub genes. A total of 211 DEGs were identified. Functional enrichment revealed that these genes were predominantly associated with immune and inflammatory processes, including leukocyte activation, cytokine–cytokine receptor interaction, neutrophil extracellular trap formation, and chemokine signaling pathways. Hub genes such as ITGAM, PTPRC, TYROBP, TLR2, and TLR4 were identified as central immune regulators potentially mediating the cardioprotective and immunomodulatory effects of sevoflurane.
Sevoflurane anesthesia may confer myocardial protection after CABG by modulating immune-related signaling pathways and inflammatory gene expression. These findings highlight the immunoregulatory potential of volatile anesthetics, providing novel perspectives for immune-targeted strategies in perioperative cardiac management.

Type 2 diabetes (T2D) is defined by persistent inflammatory processes. This study evaluated the anti-inflammatory properties of empagliflozin in combination with metformin therapy in patients with T2D.
In this prospective cohort study, 50 individuals with type 2 diabetes were non-randomly assigned to receive metformin (MTF, n = 25) or empagliflozin (10 mg/day) and metformin (EMPA+MTF, n = 25) and followed for 6 months. Fasting blood glucose (FPG), HbA1c, body mass index (BMI), glomerular filtration rate (GFR), and urinary albumin were measured at baseline and then 6 months later. Interleukin-1beta (IL-1β) and interleukin-6 (IL-6) secretion from isolated and stimulated peripheral blood mononuclear cells were measured using ELISA and compared in the different study groups.
The MTF+EMPA group showed significantly decreased levels of FPG, HbA1C, and body mass index compared to the baseline. FPG and HbA1c in the MTF+EMPA group showed a significant decrease six months after treatment versus the MTF group. A significant reduction in IL-1β levels was observed at the six months post-treatment compared to baseline and in relation to the MTF group after six months. The levels of IL-6 exhibited no significant differences, both within and between the study groups. Significant direct correlations were observed between IL-1β levels and FPG as well as HbA1c within the MTF+EMPA group following six months of treatment.
Incorporating empagliflozin (10 mg/day) into metformin treatment markedly enhanced glycemic regulation and lowered IL-1β secretions, indicating a possible anti-inflammatory benefit in overweight individuals with T2D following six months of treatment.

Common variable immunodeficiency disease (CVID) is the most prevalent symptomatic inborn errors of immunity, determined by defective B cell function, impaired antibody production, and susceptibility to frequent respiratory infections, enteropathy, autoimmunity, and malignancy. Due to the importance of autoimmunity in CVID and the probable role of regulatory B lymphocytes, we aimed to determine the frequency of B10 cells in CVID patients with and without autoimmunity.
A total of 24 CVID patients and 12 healthy controls were enrolled in the study. Patients were divided into two equal groups, with and without autoimmunity. Peripheral blood cells were stained with monoclonal antibodies (mAbs) to identify CD24^hiCD38^hi B cells, CD27^int CD38⁺ (plasmablasts), and CD24^hiCD27⁺ B cells by flow cytometry.
The percentages of B10, CD24^hiCD27⁺ and CD27^int CD38⁺ cells were significantly lower in total CVID patients, CVID patients with autoimmunity and CVID patients without autoimmunity compared to healthy controls (mean±standard deviation (SD) percentage of B10 cells: 6.36±9.21(total CVID), 2.81±5.00 (CVID with autoimmunity), and 3.25±3.5 (CVID without autoimmunity) vs. 13.02±12.45 (healthy controls); CD24^hiCD27⁺ cells: 2.39±3.89, 3±5.20 and 1.78±1.94 vs. 20.38±14.27; CD27^int CD38⁺ cells: 6.80±18.49, 7.40±20.24 and 6.20±17.45 vs. 11.84±5.71). CVID patients without autoimmunity had a higher percentage of CD24^hiCD38^hi cells than CVID patients with autoimmunity (4.73±4.14 vs. 2.62±5.02).
The defect of regulatory B cells plays a significant role in the pathogenesis of autoimmunity in CVID. Further multicenter studies with higher sample sizes are suggested to determine the role of Breg cells in the clinical course of autoimmunity. 

Childhood asthma and eczema are common chronic diseases that significantly affect the health of children and parents. These children experience physical and psychosocial problems, including behavioral and emotional disturbances. This study was conducted to identify the psychological issues such as children's attachment, maternal emotion regulation, and child-parent relationship in children with autoimmune disorders, especially asthma and eczema.
This cross-sectional study included80 mother-child pairs (40 with asthma and 40 with eczema) recruited from Yazd autoimmune clinics between 2022 and 2023. Exclusion criteria included additional physical or psychiatric illnesses in parents and parental drug addiction. Participants completed a demographic questionnaire and three validated questionnaires: Children's Attachment Questionnaire, Gross Emotion Regulation Strategies Questionnaire, and Pianta Mother-Child Relationship Questionnaire.
Results analysis and comparison showed that both the asthma and eczema groups have moderate levels of secure attachment with a 25% achieving favorable score. Emotion regulation showed very low desirability (up to 25% for its subscales). Geographical location had a slight but significant effect on attachment and emotion regulation. Scores of the Pianta mother-child relationship scale were generally positive. No significant effects were observed in relation to the child's gender, occupation, and educational status of the mothers.
This study found moderate levels of children's secure attachment and maternal emotion regulation in both groups and favorable mother-child relationships in children aged 5 to 12 years with asthma and eczema. Only a small percentage of children demonstrated secure attachment, reflecting existing research linking childhood illness to parental distress and impaired child development.

Human cytomegalovirus (HCMV) is a frequent complication in kidney transplant recipients (KTRs), often impacting immune regulation. T_H9 cells, a subset of CD4⁺ T cells, are characterized by their secretion of interleukin-9 (IL-9). This study aimed to analyze the phenotypic profile of T_H9 cells and their associated cytokine expression in KTRs, and to evaluate mRNA levels of IL-4 and transforming growth factor-β (TGF-β), key cytokines involved in T_H9 differentiation.
Ten HCMV⁺ and 10 HCMV⁻ KTRs, along with 10 age- and sex-matched healthy controls, were enrolled. HCMV viral load was quantified using TaqMan real-time polymerase chain reaction. Flow cytometry was used to assess surface markers (CCR6⁺CCR4⁻IL-4Rα⁺CD4⁺) and intracellular IL-9 expression in T_H9 cells. Gene expression levels of IL-4 and TGF-β were also assessed.
Surface staining revealed a significantly higher frequency of CD4⁺CCR4⁻ and CD4⁺CCR6⁺ T cells in HCMV⁻ KTRs compared to HCMV⁺ patients. Conversely, the overall frequency of CD4⁺ T_H9 cells was elevated in HCMV⁺ KTRs. Intracellular staining demonstrated a significant increase in CD4⁺IL-9⁺ and CD4⁺IL-4Rα⁺ T cells in the HCMV⁺ group. Additionally, mRNA expression levels of IL-4 and TGF-β were markedly higher in HCMV⁺ KTRs than in HCMV⁻ counterparts.
These findings suggest a potential role for T_H9 cells and their signature cytokine IL-9 in the antiviral immune response in KTRs. While T_H9 cells may contribute to HCMV-related immune modulation, further research is needed to fully elucidate their protective mechanisms against viral infections.

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Chronic Spontaneous Urticaria (CSU) patients’ responses to regular therapeutic options are different. While some of the patients are treated by these methods but many of they do not respond successfully. Despite several studies that have been conducted to find out which immunologic and inflammatory biomarkers of the patients could be used to predict responding patients but our knowledge are not sufficient. The present study aimed to determine the effective biomarkers that may contribute in predicting of the therapeutic response.

The present interventional study evaluated 61 moderate to severe CSU patients aged 20 to 50 years who presented to our clinic from January 2024 and January 2025. A peripheral blood sample, serum and plasma were collected for measuring inflammatory and immunological parameters and were analyzed at a reference laboratory. Subsequently, patients were treated with Cetirizine 10 mg every 12 hours and Famotidine 40 mg every night and after one month, urticarial severity was reassessed using the same questionnaire. Severity scores were compared between patients with elevated biomarkers and those with normal levels.

Sixty-one patients with chronic spontaneous urticaria were enrolled; 77% were female and 23% were male. Forty-two patients had a good response to treatment, while 20 patients did not have a response. The average UAS7 scores before and after treatment were 27.72 and 12.67, respectively. Among the serum biomarkers evaluated, only the Neutrophil-to-Lymphocyte Ratio (NLR) and serum eosinophil count showed a significant relationship with treatment response. 

To conclude, a high Eosinophil count and NLR may serve as predictors of a poor clinical response to antihistamine therapy. However, further clinical trials are needed to confirm these findings.

MicroRNAs (miRs) play a crucial role in the pathogenesis, progression, and prognosis of cancer, including non-small-cell lung cancer. The purpose of this present study was to investigate the correlation between ‎MIR141‎ expression in peripheral blood mononuclear cells and serum levels of interleukins (IL-6 and IL-8) and CXCL10 in non-small-cell lung cancer patients.
Forty-six patients diagnosed with primary non-small-cell lung cancer and 30 age- and gender-matched healthy controls were recruited in this prospective cohort study. Two 3-mL samples of systemic blood were collected into tubes either containing or without an anticoagulant from all patients before treatment and from healthy controls. PBMCs were isolated, total RNA extracted, and microRNA expression measured using real-time quantitative polymerase chain reaction. Serum cytokine levels were measured by enzyme-linked immunosorbent assay.
MIR141‎ expression in peripheral blood mononuclear cells was significantly higher in non-small-cell lung cancer patients (4.124 [3.259–4.944]) compared to healthy controls (2.181 [1.036–2.946]). The area under the Receiver operating characteristic (ROC) curve, AUC for MIR141,‎ was 0.695 (95% CI, 0.603–0.787), indicating statistically significant diagnostic performance. Serum levels of IL-6, IL-8, and CXCL10 were also markedly elevated in non-small-cell lung cancer patients compared to healthy controls.
Increased expression of MIR141 in peripheral blood mononuclear cells is associated with non-small-cell lung cancer and elevated systemic inflammatory mediators. These findings suggest that peripheral blood MIR141 may serve as a promising non-invasive biomarker for the diagnosis of non-small-cell lung cancer.

This study aimed to identify a novel microRNA (miRNA)-related circulating biomarker that is easily accessible for clinical use and can dynamically monitor the biological characteristics of diffuse large B-cell lymphoma (DLBCL).
We analyzed miRNA expression profiles in DLBCL from the Gene Expression Omnibus (GEO) (GSE171272 and GSE173080) and The Cancer Genome Atlas (TCGA). The immune microenvironment and immune-related gene differences associated with hsa-miR-23a-5p were assessed through the single-sample gene set enrichment analysis and CIBERSORT. Gene set enrichment analysis identified expression trends related to hsa-miR-23a-5p. The 50% inhibitory concentration of chemotherapy agents was estimated for hsa-miR-23a-5p. Potential miRNA targets were identified using TargetScan, miRWalk, and RNA22, and validated with miRTarBase, DIANA-TarBase, and NPInter. Gene functions and associated pathways were analyzed through Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes. Protein-Protein Interaction networks were built using Cytoscape. SNRPD1-related analysis was conducted using TCGA and GEO data.
Hsa-miR-23a-5p was significantly overexpressed in the tumor tissues and serum exosomes of patients with DLBCL. The expression levels of hsa-miR-23a-5p were associated with distinct prognostic outcomes, immune landscapes, chemoresistance, and biological processes, serving as potential risk factors. The target gene SNRPD1 was an independent prognostic factor significantly associated with patient survival.
This study identifies hsa-miR-23a-5p and its target SNRPD1 as potential prognostic factors for DLBCL. Specifically, the overexpression of hsa-miR-23a-5p in serum exosomes of patients with DLBCL suggests that it could serve as a convenient, non-invasive biomarker for clinical evaluation of DLBCL. However, further research and validation are necessary to confirm these findings.

The Warburg effect is one of the most important metabolic alterations in tumor cells. Hypoxia-inducible factor 1-alpha (HIF-1α) targets a broad range of gene promoters in normoxic and hypoxic conditions in cancers. Herein, we investigate the effects of HIF-1α inhibition on cell viability and messenger RNA (mRNA) expression of immune checkpoint receptors (ICRs) in acute myeloid leukemia cell lines.
K-562 and HL-60 cells were treated with silibinin as an HIF-1α inhibitor. Cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, followed by quantification of V-domain immunoglobulin suppressor of T-cell activation (VISTA), T-cell immunoglobulin and mucin domain 3 (TIM3), and Galectin-9 mRNA expression via quantitative reverse-transcription polymerase chain reaction (qRT-PCR).
The expression levels of VISTA, TIM3, and Galectin-9 decreased after silibinin treatment within both K-562 and HL-60 cells; however, there were some disparities in gene expression levels between the two cell lines. VISTA and TIM3 expression were reduced by approximately 70% in K-562 at the 40% inhibitory concentration (IC40), while no significant changes were observed in HL-60 cells. Conversely, Galectin-9 expression was decreased significantly at both the IC30 and IC40 in HL-60, whereas it was almost consistent in K-562 cells.
 Collectively, we have shown that silibinin could serve as a cytotoxic small-molecule inhibitor and regulate the expression of ICRs, potentially counteracting T-cell exhaustion.

Iran has an extensive governmental network of primary health care facilities and hospitals. In 2019, the integration of asthma-related services into this network was designed and pilot-tested. Primary health care providers (PHCPs) and family physicians (FPs) are the main members of the care provision team and are responsible for case identification and management.
The pilot was conducted from November 2019 through April 2020 in seven areas-Kerman, Maragheh, Ahvaz, Kashan, Urmia, Karun, and Qazvin-covering both urban and rural locations and a population of approximately one million people. Our objective was to report indicators related to the integration of asthma identification, referral, and management within the existing primary health care system.
In total, 350,894 individuals were screened for asthma by PHCPs. The observed proportion of positive (probable) cases among those screened was 2.48%. Key process indicators included screening uptake (34%), attendance of referred cases at physician visits (83%), and follow-up adherence (49% of confirmed cases).
We conclude that improving screening uptake and the accuracy of asthma case detection by PHCPs are the most effective strategies for enhancing care provision efficiency. The findings of the pilot project have significant implications for understanding efficient integration of asthma-related services. The results indicate that integrating asthma care into primary health services is feasible and can improve early detection and care coordination, informing policy decisions for broader implementation and resource planning.

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.