The effect of mesenchymal stem cells administration on DNA repair gene expressions in critically ill COVID-19 patients: prospective controlled study.

When the studies are evaluated, immunomodulatory effect of MSCs, administration in critically ill patients, obstacle situations in use and side effects, pulmonary fibrosis prevention, which stem cells and their products, regeneration effect, administration route, and dosage are listed under the main heading like. The effect of MSC administration on DNA repair genes in COVID-19 infection is unknown. Our aim is to determine the effect of mesenchymal stem cells (MSCs) therapy applied in critically ill patients with coronavirus infection on DNA repair pathways and genes associated with those pathways. Patients (n = 30) divided into two equal groups. Group-1: Patients in a critically ill condition, Group-2: Patients in critically ill condition and transplanted MSCs. The mechanism was investigated in eleven genes of five different pathways; Base excision repair: PARP1, Nucleotide excision repair (NER): RAD23B and ERCC1, Homologous recombinational repair (HR): ATM, RAD51, RAD52 and WRN, Mismatch repair (MMR): MLH1, MSH2, and MSH6, Direct reversal repair pathway: MGMT. It was found that MSCs application had a significant effect on 6 genes located in 3 different DNA damage response pathways. These are NER pathway genes; RAD23 and ERCC1, HR pathway genes; ATM and RAD51, MMR pathway genes; MSH2 and MSH6 (p < 0.05). Two main points were shown. First, as a result of cellular damage in critical patients with COVID-19, DNA damage occurs and then DNA repair pathways and genes are activated in reaction to this situation. Second, administration of MSC to patients with COVID-19 infection plays a positive role by increasing the expression of DNA repair genes located in DNA damage pathways.

IL2RA rs2104286 and IL2 rs2069762 polymorphisms may be associated with bipolar disorder and its clinical findings.

Study results supported that immuno-inflammatory pathways in the brain and environment contribute to the etiopathogenesis of bipolar disorder (BD), a chronic affective disease. Our study aimed to assess the relationship between BD risk and interleukin 2 (IL2) and interleukin 2 receptor subunit alpha (IL2RA) variants in a Turkish population. Genomic DNA from 86 diagnosed BD patients and 100 healthy blood donors was extracted. IL2RA rs2104286, IL2 rs2069762, and IL2 rs2069763 variants were genotyped using the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) method. It was compared to the relationship between the genotype distributions of these variants and clinical characteristics. Results were evaluated statistically. A statistically significant difference in the genotype distribution of the IL2RA rs2104286 variant was found between patients and controls. There was no GG genotype in the patient group. The IL2RA rs2104286 AA genotype was more common in the patient group than the controls, and the AG genotype was higher in the controls compared to the patients (p = 0.001, p = 0.001, respectively). The IL2 rs2069762 and IL2 rs2069763 genotype distributions did not differ between the patient and control groups (p > 0.05). We found that the clinical global impression severity (CGI-S) score was higher in those with IL2 rs2069762 TG and GG genotypes. In this study, we showed for the first time that the genotype distribution of IL2RA rs2104286 and IL2 rs2069762 is associated with BD susceptibility and CGI-S score in a Turkish population.

Effect of interleukin-2 (IL-2) polymorphisms on multiple myeloma: IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms.

Interleukin-2 (IL-2) is a cytokine secreted from T helper type 1 cells and released after induction of T helper cells with major histocompatibility complexes or antigens presented by antigen presenting cells. IL-2 activity and gene polymorphisms have been studied in both solid and hematological malignancies. In the present study, it was aimed to examine the effects of IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms on multiple myeloma (MM) susceptibility, progression-free survival (PFS) and overall survival (OS). A total of 300 patients diagnosed with MM in our clinic between January 2010 and January 2021, and 170 healthy individuals were included. In addition to the demographic data of the patients, MM subtypes, initial stages, prognostic index scores, laboratory results, treatment preferences, and survival data were recorded. The genotypes of the IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms were statistically compared between patients and healthy controls to reveal their effects on MM susceptibility and survival. In the statistical analysis performed to examine the effect of IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms on disease susceptibility, no significant difference was found between the patient and healthy control groups. Patients with the TG genotype of IL-2 rs2069762 had a significantly shorter median PFS and OS compared to others. Patients with the GG genotype of IL-2 rs2069763 had a significantly shorter median PFS compared to others. Having the TG genotype of IL-2 rs2069762 has been shown to be protective for short PFS and OS. Our study results will be guiding in terms of IL-2 based therapies, the future for MM and MM epigenetics.

Epigenetic and genetic investigation of SOCS-1 gene in patients with multiple myeloma.

Background: The suppressor of cytokine signaling-1 (SOCS-1) functions to induce an appropriate immune response and is an essential physiological regulator of interferon signaling. DNA methylation involves adding a methyl group to the carbon 5 position of cytosine. Besides comparing SOCS-1 gene methylation status between patients with multiple myeloma (MM) and healthy controls, this study also aimed to demonstrate the effect of SOCS-1 gene distribution and the effect of methylation of SOCS-1 on progression-free survival (PFS) and overall survival (OS). Methods: This study included 120 patients diagnosed with MM between January 2018 and 2020 and 80 healthy individuals. The distribution of the SOCS-1 genotypes was statistically compared between MM patients and healthy controls. Additionally, the statistically significant effects of these genotypes on survival were examined. Results: The CA/CA genotype of SOCS-1 was significantly higher in healthy controls (P=0.001), while the Del/Del genotype was significantly higher in patients with MM (P=0.034). The percent methylated reference (PMR) value of the SOCS-1 gene was significantly higher in the healthy controls (median, 43.48; range, 2.76‒247.75; P=0.001). Patients with a PMR value of ≥43.48 were 3.125 times more likely to develop progression than those with a PMR value of ＜43.48. Conclusion: The effects of SOCS-1 polymorphisms on the pathogenesis of.

Tumor Necrosis Factor-alpha (TNF-α) -238 G/A Polymorphism Is Associated with the Treatment Resistance and Attempted Suicide in Schizophrenia.

Abnormality of the immune system may play an important role in the pathogenesis of schizophrenia (SCZ). We aim to investigate the relationship between clinical features of SCZ and tumor necrosis factor-alpha (TNF-α) -238 G/A, -308 G/A polymorphisms in SCZ patients by comparing genotype distributions of TNF-α gene polymorphisms between patients and healthy controls. A sample of 113 patients with SCZ and 104 healthy volunteers was included in the study. SCID-I was used to confirming the diagnosis according to DSM-IV-TR criteria. We evaluated the patients with some scales and data forms in terms of clinical features, symptom severity, level of insight, suicidal behavior, and treatment response. PCR-RFLP was used to determine TNF-α gene polymorphisms from DNA material. The distributions of TNF-α - 238 G/A and TNF-α - 308 G/A polymorphisms of the patients diagnosed with SCZ were not significantly different from the control group. There was a significant difference in the TNF-α - 238 G/A genotype distributions between treatment-resistant and treatment-responsive SCZ patients. Again, the distributions of TNF-α - 238 G/A genotype of attempted suicide patients in SCZ were significantly different from the non-attempted suicide of SCZ patients. Whereas TNF-α - 238 G/A and -308 G/A polymorphisms were not associated with SCZ, TNF-α - 238 G/A polymorphism may be related to treatment resistance and attempted suicide in SCZ patients in the Turkish population.