Evaluating the Serum Levels of CCL17, CCL22, and CCL28 Chemokines and the Gene Expression of α4β1 and α4β7 Integrins in Patients With Allergic Rhinitis

Allergic rhinitis (AR) is a chronic inflammatory disease involving the nasal mucosa. Leukocytes recruitment to the inflammation sites is controlled by chemokines, cytokines, and adhesion molecules. Retinoic acid (RA), a vitamin A metabolite, plays an essential role in mucosal immunity and the production of inflammatory cytokines and chemokines. This study intended to evaluate the serum levels of RA, CCL17, CCL22, CCL28, and the mRNA expression levels of α4, β1, and β7 integrins in AR patients compared to healthy subjects. Peripheral blood was collected from 37 patients with AR and 30 age- and gender-matched healthy individuals. Serum levels of RA, CCL17, CCL22, and CCL28 were measured by the enzyme-linked immunosorbent assay (ELISA) technique, and the mRNA expression levels for α4, β1, and β7 integrins were assessed using the quantitative real-time PCR method. Our results showed that the serum levels of CCL22 and CCL28 chemokines are significantly higher in the AR group compared to the healthy controls (P<0.01). However, the gene expression of the β1 integrin in the AR group was significantly lower than that of the control group (P<0.001). Besides, there was a positive association between serum RA and CCL17 levels in patients (P<0.0001, r=0.6). In conclusion, increased serum levels of CCL22 and CCL28 chemokines, as well as decreased gene expression of β1 integrin in AR patients, may contribute to the pathogenesis and/or exacerbation of AR

Epidemiology and Causes of Poisoning in Patients Referred to Loqman Hospital, Tehran, Iran during Summer 2010

Background: Poisoning is a serious health problem in the world. In the intentional type, the person may attempt suicide by self-poisoning or may be poisoned by others in a criminal act. The present study was designed to investigate the causes and the frequency of poisoning cases referring to Loqman Hospital, Tehran, Iran, during summer 2010. Methods: In this descriptive-analytical study, age, gender, educational level, daily sleep duration, history of physical illness, and type of substance used for poisoning were analyzed by SPSS software. Results: Of the 200 poisoned patients, 51% were male and 49% female. 60% of the patients were single. The patients’mean of age was 26.82 years. Minimum age was 14 years and maximum age was 77 years. Most of the patients were graduated from high school and 95.5% of them were living in large cities. Their parents were alive in most cases (92.2%) and 70.5% of them were the first to third child of their family. The person in charge of them was their parents in most cases. The mean daily sleep duration was 7 hours and 72% of the subjects did not have any physical illnesss. Also, 42% of the patients had history of cigarette smoking. Overall, 57% of the patients were poisoned by antidepressant drugs, 31% by narcotic compounds, and remaining 12% by unknown substances. Conclusion: Most poisoned cases by antidepressant drugs can be explained by a various of reasons such as availability of the drugs. The findings of this study necessitate more vigilance from physicians in prescribing drugs and community in educating people about drugs

Cell Therapy Based SARS-cov 2-2019 Managements: A Literature Review

In early December 2019, an outbreak of coronavirus disease 2019 (COVID-19) occurred in Wuhan City, Hubei Province, China, affirmed to be the result of a novel coronavirus (later named Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)). Coronavirus disease-19, a kind of viral pneumonia, is caused by SARS-COV2. This virus infects angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) positive cells and causes influenza like symptoms ranging from mild disease to severe type with multi-organ involvement. In patients with more sever conditions, dysregulation of immune system, due to either virus activity or immune-based issues, leads to cytokine storm and unwanted inflammatory changes further followed by tissue damage. COVID-19 has spread rapidly by human-to-human transmission, caused an outbreak worldwide with considerable morbidity rates and mortality, which forced WHO to officially classified it as pandemic and a global concern on March 11. Without any signs of amelioration and with confirmed cases that are expected to increase further as they are updated daily as of May 8, the outbreak has stressed global socioeconomic and health systems and posed governments to clinical management challenges. Finding appropriate clinical strategy to control and even prevent is nowadays top priority issues globally. Recent studies and investigation considerably improve our understanding of disease pattern of distribution, pathology and immune-related changes in both mild and sever cases. Thus, many promising therapeutic approaches for clinical intervention and treatment of the disease are now under further investigations and their safety and efficiency are yet to be proved in clinical trials. One of these therapeutic approaches is cell therapy based interventions. Mesenchymal stem cells (MSCs) have commonly applied clinical trials and possess two positive roles, immunomodulatory effect and differentiation ability. MSCs immunomodulatory effects which mediated by anti-inflammatory cytokine release prevent or reduce the overactivation of the immune system and cytokine storm. So, MSCs therapy and other immune-based cell therapies can be promising in severe COVID-19 management and treatment. In this review the aim is investigation the impact of these kind of interventions in treatment of COVID-19 patients

Decreased Gene Expression of Lipoxin A4 Receptor May Contribute to Nonallergic Rhinitis Pathogenesis

Background: Rhinitis is a prevalent chronic inflammatory illness of the nasal mucosa. Arachidonic acid-derived lipoxin A4 (LXA4) has long been recognized to exert crucial antiinflammatory and pro-resolving effects on inflammatory responses through a specific receptor named LXA4 receptor/formyl peptide receptor-2 (ALX/FPR2). This study aimed to determine the serum level of LXA4 and the relative mRNA expression level of FPR2 in peripheral blood cells of patients with rhinitis (allergic and nonallergic) compared to healthy individuals. Materials And Methods: The study groups consisted of 37 patients with Allergic Rhinitis (AR), 16 patients with Nonallergic Rhinitis (NAR), and 20 sex- and age-matched healthy individuals. The measurement of LXA4 serum level was performed by the Enzyme-Linked Immunosorbent Assay (ELISA) technique, and the analysis of FPR2 mRNA expression level was performed by quantitative real-time PCR method. Results: The serum concentrations of LXA4 decreased in AR and NAR patients compared to healthy controls; however, this difference was not statistically significant (P>0.05). Besides, the mRNA expression level of FPR2 in peripheral blood cells of patients with nonallergic rhinitis was significantly lower than that in allergic rhinitis (P<0.05). Conclusion: Our results suggest that reduced gene expression of FPR2 may contribute to developing persistent and chronic nasal mucosa inflammation seen in NAR patients. Therefore, stable analogs of LXA4 and its receptor agonist may help develop new therapeutic approaches for rhinitis

Downregulation of E-cadherin expression in breast cancer by promoter hypermethylation and its relation with progression and prognosis of tumor

Breast cancer is the most common cancer in women around the world, and novel prognosis strategies is needed to control more accurate and effective of this malignant disease. Among the latest prognostic markers is E-cadherin, which mediates cell-cell adhesion by associating with catenins. Loss of E-cadherin gene (CDH1) function by genetic or epigenetic alteration leads to tumorigenesis. The aim of our study was to investigate E-cadherin gene promoter methylation in breast cancer, and its correlation with E-cadherin protein expression. Fifty primary breast cancers tissue with ductal type and 50 normal breast sample from the same patients that was located adjacent to tumor region as controls were provided by Imam Reza-based referral and teaching hospital affiliated to Tabriz University of Medical Sciences, Tabriz, Iran. CDH1 promoter region CpG sites methylation and E-cadherin protein expression were determined by bisulfitespecific polymerase chain reaction and Western blot analysis, and the resulting products were sequenced on an ABI automated sequencer for firm conclusion. CDH1 hypermethylation in breast tumor specimen (ductal type) was observed in 94 % (47 of 50) comparing with normal samples methylation, and the significant difference was (p = 0.000). Protein expression in tumor samples tends to diminish with the CDH1 promoter region methylation. In the group of 50 ductal carcinomas cases, most of the cases showing CDH1 hypermethylation correlated inversely with the reduced levels of expression of E-cadherin proteins (95 % of full-methylated tumor samples had no protein expression, and 4.5 % of them had weak expression levels). Possible association was observed between CDH1 methylation and its protein expression (p = 0.000). The results of methylation analysis in promoter region in ten CpG sites (863, 865, 873, 879, 887, 892, 901, 918, 920, and 940) suggested that abnormal CDH1 methylation occurs in high frequencies in ductal breast tumors probably sounds the process of carcinogenesis progression

Downregulation of E-cadherin expression in breast cancer by promoter hypermethylation and its relation with progression and prognosis of tumor

Breast cancer is the most common cancer in women around the world, and novel prognosis strategies is needed to control more accurate and effective of this malignant disease. Among the latest prognostic markers is E-cadherin, which mediates cell-cell adhesion by associating with catenins. Loss of E-cadherin gene (CDH1) function by genetic or epigenetic alteration leads to tumorigenesis. The aim of our study was to investigate E-cadherin gene promoter methylation in breast cancer, and its correlation with E-cadherin protein expression. Fifty primary breast cancers tissue with ductal type and 50 normal breast sample from the same patients that was located adjacent to tumor region as controls were provided by Imam Reza-based referral and teaching hospital affiliated to Tabriz University of Medical Sciences, Tabriz, Iran. CDH1 promoter region CpG sites methylation and E-cadherin protein expression were determined by bisulfitespecific polymerase chain reaction and Western blot analysis, and the resulting products were sequenced on an ABI automated sequencer for firm conclusion. CDH1 hypermethylation in breast tumor specimen (ductal type) was observed in 94 % (47 of 50) comparing with normal samples methylation, and the significant difference was (p = 0.000). Protein expression in tumor samples tends to diminish with the CDH1 promoter region methylation. In the group of 50 ductal carcinomas cases, most of the cases showing CDH1 hypermethylation correlated inversely with the reduced levels of expression of E-cadherin proteins (95 % of full-methylated tumor samples had no protein expression, and 4.5 % of them had weak expression levels). Possible association was observed between CDH1 methylation and its protein expression (p = 0.000). The results of methylation analysis in promoter region in ten CpG sites (863, 865, 873, 879, 887, 892, 901, 918, 920, and 940) suggested that abnormal CDH1 methylation occurs in high frequencies in ductal breast tumors probably sounds the process of carcinogenesis progression

Comparison of Common Monogenic Defects in a Large Predominantly Antibody Deficiency Cohort

Background: Predominantly antibody deficiencies (PADs) are the most common primary immunodeficiencies, characterized by hypogammaglobulinemia and inability to generate effective antibody responses. Objective: We intended to report most common monogenic PADs and to investigate how patients with PAD who were primarily diagnosed as suffering from agammaglobulinemia, hyper-IgM (HIgM) syndrome, and common variable immunodeficiency (CVID) have different clinical and immunological findings. Methods: Stepwise next-generation sequencing and Sanger sequencing were performed for confirmation of the mutations in the patients clinically diagnosed as suffering from agammaglobulinemia, HIgM syndrome, and CVID. Results: Among 550 registered patients, the predominant genetic defects associated with agammaglobulinemia (48 Bruton's tyrosine kinase [BTK] and 6 μ heavy chain deficiencies), HIgM syndrome (21 CD40 ligand and 7 activation-induced cytidine deaminase deficiencies), and CVID (17 lipopolysaccharides-responsive beige-like anchor deficiency and 12 atypical Immunodeficiency, Centromeric instability, and Facial dysmorphism syndromes) were identified. Clinical disease severity was significantly higher in patients with μ heavy chain and CD40 ligand mutations compared with patients with BTK (P = .003) and activation-induced cytidine deaminase (P = .009) mutations. Paralysis following live polio vaccination was considerably higher in patients with μ heavy chain deficiency compared with BTK deficiency (P < .001). We found a genotype-phenotype correlation among patients with BTK mutations regarding clinical manifestation of meningitis and chronic diarrhea. Surprisingly, we noticed that first presentations in most patients with Immunodeficiency, Centromeric instability, and Facial dysmorphism were respiratory complications (P = .008), whereas first presentations in patients with lipopolysaccharides-responsive beige-like anchor deficiency were nonrespiratory complications (P = .008). Conclusions: This study highlights similarities and differences in the clinical and genetic spectrum of the most common PAD-associated gene defects. This comprehensive comparison will facilitate clinical decision making, and improve prognosis and targeted treatment