The purpose of this study was to systematically examine the association between bronchial asthma and lung cancer. Research on the correlation between bronchial asthma and lung cancer was retrieved from the database. Literature was screened based on inclusion and exclusion criteria, and the number of patients in the included studies was extracted and analyzed. This study used Stata statistical software version 16.0 and Cochrane Review Manager version 5.4 for meta-analysis. In our study, 19 articles were selected. Without considering other influencing factors, the risk of lung cancer in asthma patients was relative risk (RR)=1.40 (95% CI: 1.17-1.67, I2=55.7%), and after correcting for risk factors such as smoking and age, it was found that the risk of small-cell lung cancer in asthma patients was RR=2.11 (95% CI: 1.45-3.24). Asthma may increase the risk of developing lung cancer, with an even higher likelihood for small cell lung cancer.

To assess the impact of budesonide-formoterol on pulmonary ventilation function and prognosis in patients with mild-to-moderate acute exacerbations of bronchial asthma.
A retrospective analysis was conducted on clinical data from 232 patients with acute exacerbations of bronchial asthma. These patients were divided into 2 groups based on their treatment: a control group (n=104) receiving budesonide dry powder inhalation and an observation group (n=107) receiving budesonide-formoterol dry powder inhalation. Clinical efficacy and safety indicators were compared.
The results showed that the total treatment effectiveness rate in the observation group was significantly higher than that in the control group. Following treatment, the observation group exhibited significantly higher scores in the Asthma Quality of Life Questionnaire (AQLQ), as well as improved levels of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF), compared to the control group. Moreover, levels of tumor necrosis factor-alpha, interleukin-6, and C-reactive protein were significantly lower in the observation group. The incidence of adverse reactions between groups was comparable.
Based on these findings, the application of budesonide-formoterol demonstrated significant effectiveness in patients with mild-to-moderate acute exacerbations of bronchial asthma. The combination therapy led to improved clinical outcomes, including enhanced pulmonary ventilation function and reduced inflammatory markers. Importantly, the safety profile of budesonide-formoterol was comparable to that of budesonide monotherapy. These results highlight the potential benefits of using budesonide-formoterol as an alternative treatment option for patients experiencing acute exacerbations of mild-to-moderate bronchial asthma.

Allergic rhinitis is a common childhood disease. Although various drugs have been used to treat allergic rhinitis, including nasal corticosteroids, antileukotrienes, and antihistamines, there is still controversy about the optimal dose and the best combination with the highest efficacy. Higher doses of antihistamines are recommended for better control of urticaria, but there is insufficient evidence regarding the efficacy of increased doses of antihistamines in allergic rhinitis. The aim of the study was to evaluate the effectiveness of different drug combinations in the treatment of children with allergic rhinitis.
Sixty-four children with persistent moderate to severe allergic rhinitis were enrolled and randomly divided into 4 groups. All children received mometasone furoate nasal spray once daily. In addition to mometasone, each group received one of the following drugs or drug combinations: daily desloratadine, twice daily desloratadine, montelukast, or a combination of desloratadine and montelukast. The severity of symptoms before and after the intervention was evaluated based on the total nasal symptoms score, including sneezing, nasal congestion, nasal itching, and rhinorrhea.
Sixty patients completed the study. The reduction of nasal congestion score and total nasal symptoms score in the groups receiving desloratadine twice a day and desloratadine plus montelukast was superior to the daily desloratadine group and daily montelukast groups.
According to this work, the treatment of allergic rhinitis with mometasone nasal spray with desloratadine twice a day or with the combination of desloratadine and montelukast was more effective than other treatment regimens.

Mitochondrial missense mutations and pathogenic variants have been implicated in the pathogenesis of COVID‐19. This study evaluated the role of mitochondrial DNA (mtDNA) mutations and changes in gene expression in the progression of COVID-19 and their correlation with clinical characteristics.
Next‐generation sequencing with high throughput was used to identify mtDNA mutations in 30 COVID-19 patients compared to 20 healthy controls. The potential impact of identified mutations on protein structure and stability was predicted using bioinformatic tools. Quantitative real-time polymerase chain reaction was employed to assess the expression levels of mtDNA-encoded genes involved in oxidative phosphorylation in COVID-19 patients and healthy controls. Correlations between gene expression levels, clinical parameters, including leukocyte, lymphocyte, neutrophil, and platelet count, as well as creatinine, alanine transaminase (ALT), aspartate transaminase (AST), and blood urea nitrogen (BUN) levels, and disease severity were analyzed.
We found 8 different mtDNA mutations in ND1, ND5, CO3, ATP6, and CYB genes, which were predicted to alter amino acids and decrease protein stability. Two missense unique mutations, C9555T in CO3 and A12418T in ND5 were identified and correlated with Complexes I and IV, respectively. This downregulation was correlated with age, elevated levels of leukocytes, lymphocytes, neutrophils, platelets, creatinine, ALT, AST, and BUN, as well as disease severity.
These findings suggest that mtDNA mutations and altered expression of oxidative phosphorylation genes contribute to mitochondrial dysfunction in COVID-19. Targeting mitochondrial dysfunction may represent a promising therapeutic strategy for COVID-19 treatment.

The coronavirus disease 2019 (CVOID-19) has varied clinical manifestations including mild to severe acute respiratory symptoms. Inflammasome complex and mitochondria play an important role in initiating inflammatory responses and could potentially be affected by this infection. To study the inflammasome and mitochondrial fission and fusion gene expression levels in COVID-19 patients, we designed this experiment.
The inflammasome and mitochondrial gene expression profiles were determined by real-time polymerase chain reaction in the peripheral blood of 70 hospitalized CVOID-19 patients with mild to moderate symptoms (HOSP) and 30 ICU patients with severe symptoms (ICU) compared to 20 healthy controls (HC).
The results indicated that the expression of the dynamin-related protein-1 was extremely suppressed in HOSP while it came back to the normal range in the ICU group. However, the expression of fission 1 protein had a non-significant increase in HOSP and a decrease in the ICU group. The mitofusin-1 and dominant optic atrophy genes showed high expression levels (10-fold) and (70-fold), respectively, in the HOSP group. However, mitofusin-2 significantly decreased in both groups. Although leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase activating and recruitment domain genes dramatically increased in both groups (10 and 4-fold), other inflammasome genes declined in both groups. Finally, Nuclear factor kappa-light-chain-enhancer of activate d B cells (NF-κB) extremely decreased, and Intreleukine-1 showed high expression in ICU patients (3-fold).
CVOID-19 infection suppresses the fission genes and elevates the fusion gene expression in mitochondria, and it can cause activation of the inflammasome via the NLRP3 pathway.

Peripheral benign lung tumors are often asymptomatic and incidentally detected on chest radiographs. Surgical intervention is recommended when feasible. Single-port thoracoscopic resection has emerged as a promising technique for treating various chest diseases, including lung tumors. This study aimed to assess the clinical efficacy of single-port thoracoscopic resection for benign lung tumors and its impact on respiratory function and inflammatory factors.
A total of 128 eligible patients diagnosed with benign lung tumors were randomly assigned to either the observation group (undergoing single-port thoracoscopic resection) or the control group (undergoing conventional thoracic surgery). Surgical outcomes, complications, pulmonary and respiratory function, and inflammatory factors were compared between the two groups.
The observation group showed significantly lower intraoperative bleeding, shorter hospitalization time, and lower complication rates compared to the control group. Patients in the observation group exhibited higher vital capacity (VC), forced vital capacity (FVC), and total lung capacity (TLC) levels at 1/2 week and 1 month after surgery. Additionally, forced expiratory volume in one second (FEV1) and maximum ventilation volume per minute (MVV) levels were higher in the observation group post-surgery, with a lower Borg score. Levels of C-reactive protein (CRP), precalcitonin (PCT), and tumor necrosis factor (TNF-α) were lower in the observation group post-surgery.
Single-port thoracoscopic resection demonstrates favorable clinical efficacy for treating benign lung tumors, reducing bleeding, and shortening hospital stays. Furthermore, it improves lung and respiratory function while reducing inflammatory factors. This technique is safe, effective, and holds promise for wider application in managing benign lung tumors.

As the most common cause of bacillary dysentery or shigellosis, Shigella sonnei (S nonnei) has spread throughout the world. Invasion of the colorectal epithelial cells by this facultative intracellular bacterium occurs via various virulence factors. The increase in the resistance rate highlights the need for novel interventions, particularly increasing the urgency of the development of Shigella vaccines that may offer an effective solution.
A multiepitope protein vaccine (MEPV) construct previously designed using bioinformatics tools against Shigella species, was applied in vivo in BALB/C mice. The designed vaccine construct was expressed in a bacterial host, purified, and finally confirmed by Western blot analysis.
The immunogenicity of the purified MEPV was assessed against S sonnei via intranasal and subcutaneous administration routes, followed by evaluating its protective efficiency. We observed that interferon-gamma, interleukin-4, and immunoglobulin G levels were increased in all experimental groups.
Therefore, The MEPV effectively protected the mice against S sonnei.

Acellular pertussis vaccines (aPVs) have been developed as an alternative to whole-cell pertussis vaccines (wPVs) due to their similar efficacy but reduced reactogenicity. The aPV contains three or more immunogenic components of BP.  We aimed to evaluate the immunogenicity and protective potency of an aPV vaccine produced in our laboratory consisting of pertussis toxin (PT), filamentous hemagglutinin (FHA), and pertactin (PRN) in mice.

The aPV components were produced and purified from the supernatant and pellet of the bacterial culture. Two doses of formulated vaccine in parallel with two commercial vaccines, were administered intraperitoneally (IP) in mice at 3-week intervals. Antibody titers against aPV antigens were measured by ELISA after primary and booster vaccinations. To assess the protective efficacy, an intranasal challenge with a live pathogenic BP strain was conducted two weeks after the booster vaccination, and bacterial count (colony-forming unit, CFU) in the lungs was conducted two hours and ten days after the challenge.

The results demonstrated a significant increase in antibody titers against all pertussis antigens in the serum of vaccinated groups compared to the negative control group, following both the primary and booster doses. No significant differences were observed between our formulation and the commercial vaccines. Furthermore, the CFU results showed complete eradication of infection 10 days after the challenge in all immunized groups, in contrast to the control group.

Our aPV formulation, the first aPV candidate developed in Iran, exhibits immunogenicity and protective efficacy comparable to commercial vaccines. Further investigation in human subjects is warranted.

This study aimed to explore the effect of prednisone (PDN) combined with cyclophosphamide (CTX) on bleomycin-induced pulmonary fibrosis (PF) in rats via circular RNA mortality factor 4 like 1 (MORF4L1)/microRNA (miR)-29a-3p/Bromodomain protein 4 (BRD4) axis.
A rat model of PF was induced by bleomycin and treated with PDN combined with CTX, and the lentiviral vectors that interfered with MORF4L1, miR-29a-3p, or BRD4 expression were injected into the tail vein at the same time. The mRNA expressions of MORF4L1, miR-29a-3p, BRD4, and fibrosis-associated proteins including fibronectin, connective tissue growth factor, and collagen I were detected by real-time quantitative polymerase chain reaction. The expression level of BRD4 protein in rat lungs was detected by Western blot analysis. Lung pathology of rats was observed by hematoxylin and eosin and Masson’s trichrome staining. Apoptosis was observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The targeting relationship between miR-29a-3p and MORF4L1 or BRD4 was verified by the bioinformatics website and dual luciferase reporter experiment.
Bleomycin-induced PF enhanced MORF4L1 and BRD4 expression, inhibited miR-29a-3p expression, injured lung tissue, increased mRNA expression of fibrosis-related markers, and induced apoptosis in the lung tissue of rats. PDN combined with CTX had a therapeutic effect on PF in rats, which was further promoted by down-regulating MORF4L1 or up-regulating miR-29a-3p. After down-regulating miR-29a-3p or up-regulating BRD4, the effect of down-regulating MORF4L1 was reversed. MORF4L1 could bind to miR-29a-3p to target BRD4.
In short, PDN combined with CTX can effectively improve PF through downregulating MORF4L1 to enhance miR-29a-3p-targeted regulation of BRD4.

Agammaglobulinemia is a rare inherited immunodeficiency disorder characterized by low or absent B cells with absent immunoglobulins. While X-linked agammaglobulinemia (XLA) is the most common type other genetic forms of agammaglobulinemia have been identified. During early childhood, passively transferred maternal Immunoglobulin G protects against various infections. The depletion of these antibodies begins between 6 and 12 months of age, resulting in recurrent sinusitis, bronchitis, and pneumonia in children with X-linked agammaglobulinemia. However, less common autosomal recessive forms of agammaglobulinemia present with more severe clinical features, leading to earlier diagnosis. Herein we present the case of a two-month-old male with IGLL1 gene defect and different clinical findings of family members with the same mutation.

Patients with immunodeficiency are at higher risk of severe disease and death following SARS-CoV-2 infection compared to the general population. Here, we describe humoral and cellular immune responses in 5 patients with immunodeficiency, 2 patients with multiple sclerosis, 1 patient with chronic lymphocytic leukemia (CLL), 1 patient with Good’s syndrome, and 1Human Immunodeficiency Virus (HIV) positive with developed Acquired immunodeficiency syndrome (AIDS)- patient.
T-cell responses were evaluated using the QuantiFERON SARS-CoV-2 assay following incubation with the SARS-CoV-2 Ag1, Ag2, and Ag3 viral antigens. Immunophenotyping of CD4⁺ and CD8⁺ T cells and CD19⁺ and CD20⁺ B cells was determined by flow cytometry.
All studied immunocompromised patients or those with acquired immune dysregulation patients showed reduced cellular immune responses (release of interferon (IFN)-g) to SARS-CoV-2 antigens than healthy controls [patients; Ag1, Ag2 and Ag3 and Nil (Median 5-95% percentile) (12 (1-95), 12 (1.5-78), 13.5 (12-95) and 3 (1-98) U/mL)], controls; Ag1, Ag2 and Ag3 and Nil (Median 5-95% percentile) 24.5 (7-89), 65 (31-173), 53.5 (13-71.5) and 3 (1-14) U/mL)]. The frequency of peripheral blood B cells was also reduced in these patients compared to healthy control subjects.
T-cell-dependent antibody responses require the activation of B cells by helper T cells. Reduced B cell numbers in immunocompromised patients infected with SARS-CoV-2 indicate the need for these patients to take additional precautions to prevent COVID-19 infection.