Notes

Barrier deep sea wellness in the Gulf associated with Honduras in relation to fluvial runoff, severe weather, along with fishing force.
Beta thalassemia (β-thalassemia) is a type of inherited blood disorder characterized by the impaired production of beta globin chains. β-Thalassemia can be categorized into three subtypes according to symptom severity β-thalassemia minor, β-thalassemia intermedia, and β-thalassemia major. Adipose tissue functions as an endocrine gland by synthesizing and secreting an array of bioactive peptides including leptin, adiponectin, and resistin.

We recruited 30 participants who were transfusion dependent β-thalassemia patients (major) and 30 participants who were non-transfusion dependent β-thalassemia patients (minor). The control group consisted of 20 healthy individuals. Analysis of the demographic profile, hematological profile, biochemical parameters, and serum adipokine concentrations (leptin, adiponectin and resistin) were performed for all participants.

Our results showed that leptin serum levels were significantly lower in the β-thalassemia major group compared with the β-thalassemia minor group or healthy individuals, while serum levels of adiponectin were significantly higher in β-thalassemic patients compared with healthy controls. Serum levels of resistin were significantly higher in β-thalassemic patients compared with the healthy control group. A significant negative correlation was noted between adiponectin and BMI in β-thalassemic patients, whereas leptin was observed to have a significant positive correlation with BMI in the control group. Leptin was observed to have a significant negative correlation with adiponectin and ferritin in the β-thalassemia major group.

The changes we observed in adipokine levels may play a role in the development of the complications related to β-Thalassemia and disease severity.
The changes we observed in adipokine levels may play a role in the development of the complications related to β-Thalassemia and disease severity.
Multiple sclerosis (MS) is a common demyelinating neurodegenerative disorder with significant heritability. Previous studies have associated genetic variants in human leukocyte antigen
complex,
, and
genes with the pathophysiology of MS.

In order to investigate the gene association in the Iranian population, we performed a genotyping study of 36 variants in the mentioned genes using Sanger sequencing in 102 MS patients and 113 healthy controls.

Our results identified significant associations as well as significant allele frequency differences in some of the studied single-nucleotide polymorphisms including rs4935356, rs3177928, and rs7197 from
gene, and rs12722489 and rs12722490 variants from
gene (p< 0.05). Moreover, the strong linkage disequilibrium of two common haplotypes was estimated from the
gene.

This association study may suggest the role of these polymorphisms in the genetic susceptibility of MS in the Iranian population and would facilitate the recognition of causative variants in this disease.
This association study may suggest the role of these polymorphisms in the genetic susceptibility of MS in the Iranian population and would facilitate the recognition of causative variants in this disease.
Autosomal dominant polycystic kidney disease (ADPKD), a multisystem disorder, is the most prevalent type of hereditary kidney disease. Here, we aimed to evaluate methylation of the
gene (
) promoter and its correlation with
expression in peripheral blood.

In this case-control study methylation of the
promoter was evaluated using methylation-sensitive high-resolution melt (MS-HRM) analysis.
expression was assessed by quantitative real-time PCR. The correlation was evaluated using the Pearson correlation test.

Twenty subjects from both the patient and control groups (n= 40 for each) were methylated at the
promoter to various levels (18.9% in patients and 62.5% in controls). This difference was statistically significant (p< 0.0001). CVT-313 molecular weight
expression in blood samples was significantly greater in ADPKD patients than in controls (p= 0.0081). Significant correlation was seen between
expression and its promoter methylation status in peripheral blood (r case= -0.5300, p= 0.0162, and r control = -0.6265, p= 0.0031).

Methylation of the
promoter in ADPKD patients was inversely correlated with
expression.
Methylation of the PKD1 promoter in ADPKD patients was inversely correlated with PKD1 expression.
Janus kinase 2 (
) is a tyrosine kinase located in the cytoplasm that plays a critical role in the signal transduction of cytokines and growth hormones. The conversion of valine to phenylalanine at the polypeptide position 617 results in the
(V617F) mutation, which often found in patients with myeloproliferative neoplasms (MPNs). As a result of this mutation,
is constitutively activated leading to uncontrolled cell growth. The present study aimed to investigate the frequency and relationship of the
(V617F) mutation in a population of patients with MPNs in Iran.

A total of 213 patients with myeloproliferative diseases (MPDs), were included in the study. Real-time PCR was used to detect the presence of the
(V617F) mutation in the genomic DNA isolated from patient peripheral blood samples.

Of the 213 patients with MPDs, approximately 60 (28%) patients were positive for the
(V617F) mutation. Polycythemia Vera (PV, 42.11%) was the most common MPD, followed by Essential Thrombocythemia (ET, 29.82%), Primary Myelofibrosis (MF, 12.28%), and Chronic Myeloid Leukemia (CML, 10.5%). A significant relationship between all types of MPDs and the clinical course (p< 0.05) was observed. The relationship between age and gender among all types of MPD disease was not significant (p> 0.05).

Of the examined cohort in North Eastern Iran, 28% of the patients with MPNs were found to have the
(V617F) mutation which determining the presence of the
(V617F) mutation helps to decide the correct form of treatment.
Of the examined cohort in North Eastern Iran, 28% of the patients with MPNs were found to have the JAK2 (V617F) mutation which determining the presence of the JAK2 (V617F) mutation helps to decide the correct form of treatment.
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