The role of nutritional support with probiotics in outpatients with symptomatic acute respiratory tract infections: a multicenter, randomized, double-blind, placebo-controlled dietary study.

BACKGROUND: A number of laboratory data and clinical studies have shown that probiotic bacteria may be beneficial in respiratory viral diseases. We investigated the role of probiotics in coronavirus disease-19 (COVID -19), post-disease symptoms, and humoral immune responses to viral antigens. METHODS: This was a randomized, double-blind, placebo-controlled, prospective, multicenter study. We included symptomatic patients aged 18-65 years without risk of severe disease, and positive antigen/PCR test for SARS-CoV-2. Patients received (Bifidobacterium (B.) lactis BI040, B. longum BL020, Lactobacillus (L) rhamnosus LR110, L. casei LC130, L. acidophilus LA120, 5 billion CFU total) or placebo 1 capsule a day for 28 days and recorded symptoms. Three months later patients completed Post-COVID-19 Questionnaire (PCQ-19). On days 0-5 and 28-35, blood was sampled for IgG to nucleocapsid protein (NCP) and receptor binding domain (RBD)/spike 1 (S1) protein. The primary outcome measure was a patient global symptom score on day 10 of observation. The difference between groups was assessed using the Mann-Whitney U test. RESULTS: Seventy-three patients were assessed for clinical endpoints and 44 patients were evaluated for antibody production. At day 10, the median global symptom score (interquartile range) was lower in the probiotic group (0.0 (0.0-2.0) vs. 2.0 (1.0-5.0), P < 0.05). The probiotic group had a shorter duration of fatigue and anxiety after COVID -19 (P < 0.05) and a greater change in IgG concentration on RBD/S1 (225.9 vs. 105.6 binding antibody units/mL, P < 0.05). CONCLUSIONS: Use of probiotics alleviates acute and post-disease symptoms, and improves humoral immune response to viral antigens. TRIAL REGISTRATION: Registered at clinicaltrials.gov as NCT04907877, June 1, 2021.

Endothelium function biomarkers and carotid intima-media thickness changes in relation to NOS3 (rs2070744) and GNB3 (rs5443) genes polymorphism in the essential arterial hypertension.

Objective. The aim of the present study was to clarify the endothelial function biomarkers and carotid "intima media" thickness (IMT) changes in relation to GNB3 (rs5443) and NOS3 (rs2070744) genes polymorphism in the essential arterial hypertension (EAH). Methods. One-hundred EAH patients (48 - control) participated in the case-control study. Soluble vascular cell adhesion molecule (sVCAM-1), total NO metabolites (NO2 -+NO3 -), transcriptional activity of NOS3 gene, endothelium-dependent flow-mediated dilation of the brachial artery (FMD BA), and carotid IMT were studied. GNB3 (rs5443) and NOS3 (rs2070744) genotyping was performed by TaqMan probes (CFX96™Real-Time PCR). Results. The connection of NOS3 (rs2070744) with decreased total NO metabolites (F=71.11; p<0.001), reduced NOS3 genes transcription activity (F=8.71; p<0.001) and increased sVCAM-1 (F=6.96; p=0.002), especially in the C-allele carriers (particularly in CC-genotype patients with lower NO - 16.46% and 40.88%; p<0.001), lowered the transcription activity of NOS3 gene - 46.03% 7 times (p<0.001), and become higher sVCAM-1 - 35.48% and 89.48% (p<0.001), respectively. ANOVA did not confirm the association of GNB3 (rs5443) gene with endothelial function and carotid IMT. Severe EAH was associated with increased carotid IMT - 50.0% (p<0.001) and 57.14% (p=0.007), wider carotid arteries - 17.36% (p=0.012) and 21.79% (p=0.004), and decreased NOS3 genes transcription activity - 34.54% (p=0.003). Atherosclerotic plaques were unilateral - 24.77% (χ2=5.35; p=0.021) or bilateral - 27.62% (χ2=5.79; p=0.016). IMT---gt---0.9 mm was followed by a higher BP (p<0.001), FMD BA 11.80% decrease with compensatory increase in carotid arteries diameters - 17.38% and 21.99% (p<0.001) and sVCAM-1 by 20.49% (p=0.005). Conclusion. NOS3 (rs2070744), but not GNB3 (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and NOS3 genes reduced transcription activity.

BDNF blood serum linkage with BDNF gene polymorphism (rs6265) in thyroid pathology patients in the West-Ukrainian population.

Objective. Brain-derived neurotrophic factor (BDNF) is identified as an important growth factor involved in learning and memory. Patients with Hashimoto's thyroiditis can suffer from cognitive dysfunction, whereas BDNF is directly regulated by thyroid hormones. It seems reasonable to propose that changes in BDNF expression underlie some of the persistent neurological impairments associated with hypothyroidism. Methods. The study involved a total of 153 patients with various forms of thyroid pathology. BDNF levels in the sera of the patients and healthy individuals were quantified using enzyme-linked immunosorbent assay with highly sensitive Human BDNF ELISA Kit. Genotyping of the BDNF (rs6265) gene polymorphism using TaqMan probes and TaqMan Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System. Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions. Results. Distribution rs6265 variants in the patients depending on the different types of thyroid pathology showed no significant difference in the relative frequency of BDNF polymorphic variants. Presence of hypothyroidism, regardless of its cause (autoimmune or postoperative), there was a decrease in the serum BDNF levels in all genotypes carriers compared with the control group. The analysis of the correlation between BDNF levels and the levels of thyroid-stimulating hormone (TSH), thyroxine (T4), anti-thyroglobulin (anti-Tg), and anti-thyroid peroxidase (anti-TPO) antibodies showed a significant inverse relationship between BDNF and TSH levels (p<0.001), a direct correlation between BDNF and T4 levels in the blood (p<0.001), and a weak direct relationship between anti-Tg and BDNF levels (p=0.0157). Conclusion. The C allele presence is protective and associates with the lowest chances for reduced serum BDNF levels in thyroid pathology patients in the West-Ukrainian population. However, the T-allele increases the risk of low BDNF levels almost 10 times in observed subjects.

The parameters of liver functional state as a risk factor of edematous pancreatitis development providing of genetic determination of il-4 production.

OBJECTIVE: Introduction: One of the main pathophysiological mechanisms of acute pancreatitis development is the damage of pancreas cells and hepatocytes with enzymes activation. Recently, a powerful mechanism of the immune system involvement in the acute pancreatitis pathogenesis, in particular, from the position of genes polymorphism influence attracts more attention. The aim: To study the parameters of liver functional state as risk factors for the development of edematous pancreatitis under the conditions of genetic determination of IL-4 production. PATIENTS AND METHODS: Materials and methods: The study involved 101 patients with acute and the exacerbation of chronic pancreatitis in whom the polymorphic variants of gene IL-4 (C-590T), the activity of ALT, AST, GGTP, LDG and bilirubin fractions levels were determined. RESULTS: Results: Among the patients with T-allele of IL-4 gene was more commonly encountered the excess of the activity of AST and ALT standarts than those with CC-genotype - by 27.94% and 24.33% respectively. The increase of the GGTP concentration was recorded in 79.21% of patients. The serum GGTP level was significantly higher in the TT-genotype owners than in those with C-allele. Hyperbilirubinemia by the total bilirubin, indirect and direct fractions was diagnosed more often in TT-genotype carriers than in CC-homozygotes. CONCLUSION: Conclusions: The dysfunction of hepatopancreatobiliary system is more significant in the TT-genotype carriers of IL-4 gene by the AST, ALT, bilirubin and its fractions high levels, however, were found to be risk factors the high levels of total bilirubin and its direct fraction.