Interleukin 6 and interleukin 17A serum levels and gene- polymorphisms in the development of early allograft rejection in living donor liver transplant recipients.

The aim of this study is to evaluate the role of serum level of Interleukin 6(IL-6) and Interleukin 17 (IL-17) in liver transplantation outcome for living recipients, Analyze the relation between the gene polymorphism and the occurrence of rejection after liver transplantation and Study the relation between the gene polymorphism and the occurrence of different infectious complications. The study was conducted in March 2023 and included 60 healthy volunteers from the National Liver Institute (NLI) blood bank at Menoufia University and 120 live donation liver recipient patients at NLI. During one month of liver transplantation, the cytokine levels (IL-17, IL-6 proteins, IL-6 G-174C, and IL-17 A rs2275913 gene polymorphism) and CD4 levels for 60 patients of 120 live donation liver recipient patients whom early reject transplanted tissue and the same parameters were measured after 6 months follow up for non-reject group. The main finding of this study was that the post-transplant rejection group and the post-transplant non-rejection and control groups differed significantly in the genotype frequency (CC, CG, and GG) or alleles of IL-6 G-174C (p = 0.011). On the other hand IL-17A rs2275913 gene polymorphism and its alleles (p = 0.71) showed no statistically significant difference. We also observed that serum IL-17 levels, with 100% specificity and 100% sensitivity threshold, will be more sensitive and specific than serum IL-6 and CD4 count in differentiating post-transplant rejection from non-rejection patients. The results showed that there was no significant relationship between the genotypes and serum levels of interleukins and the type and degree of rejection. Proinflammatory cytokines might be useful indicators for distinguishing and early identifying unfavorable outcomes after transplantation, allowing for prompt and effective treatment intervention. To evaluate these findings, prospective clinical trials are required.

Serum concentrations of levosimendan and its metabolites OR-1855 and OR-1896 in cardiac surgery patients with cardiopulmonary bypass.

Background: The inotropic drug levosimendan is often used as an individualized therapeutic approach perioperatively in cardiac surgery patients with cardiopulmonary bypass (CPB). Data regarding serum concentrations of levosimendan and its metabolites within this context is lacking. Methods: In this retrospective descriptive proof-of-concept study, total serum concentrations (TSC) and unbound fractions (UF) of levosimendan and its metabolites OR-1896 and OR-1855 in cardiac surgery patients with CPB were measured using LC-ESI-MS/MS. Simulation of expected levosimendan TSC was performed using Pharkin 4.0. Serum NT-proBNP was assessed with ELISA. Results: After levosimendan infusion (1.25 mg or 2.5 mg, respectively) after anaesthesia induction, a median TSC of 1.9 ng/ml and 10.4 ng/ml was determined in samples taken directly after surgery (T1). Median TSC of 7.6 ng/ml and 22.0 ng/ml, respectively, were simulated at T1. Whereas 1.1 ng/ml and 1.6 ng/ml TSC of OR-1896, respectively, was quantified the day after surgery (T2), TSC of the intermediate metabolite OR-1855 was mostly below the lower limit of quantification (LLOQ). The UF was 0.5% and 1.1% for levosimendan and 64.1% and 52.1% for OR-1896, respectively, with over half the samples being below LLOQ. NT-proBNP concentrations before surgery and T2 did not differ. Discussion: The low TSC, UF and unchanged NT-proBNP levels in combination with high variation of serum levels between patients suggest a need for optimized dosing regimen of levosimendan combined with therapeutic drug monitoring for such an individualized approach. In addition, the differences between the measured and estimated concentrations may suggest a possible influence of CPB on levosimendan serum concentrations.

Pituitary Adenoma: SSTR2 rs2236750, SSTR5 rs34037914, and AIP rs267606574 Genetic Variants, Serum Levels, and Ki-67 Labeling Index Associations.

Background and Objectives: This study explores the complex pathogenesis of pituitary adenomas (PAs), prevalent intracranial tumors in the pituitary gland. Despite their generally benign nature, PAs exhibit a diverse clinical spectrum involving hormone hypersecretion and varying invasiveness, hinting at multifaceted molecular mechanisms and abnormalities in tumorigenesis and gene regulation. Materials and Methods: The investigation focuses on the Ki-67 labeling index, SSTR2 rs2236750, SSTR5 rs34037914, and AIP rs267606574 polymorphisms, alongside serum levels of SSTR2, SSTR5, and AIP, to discern their association with PAs. The Ki-67 labeling index was assessed using immunohistochemical analysis with the monoclonal antibody clone SP6, representing the percentage of tumor cells showing positive staining. Genotyping was performed via real-time polymerase chain reaction, and serum levels were analyzed using ELISA. The study included 128 PA patients and 272 reference group subjects. Results: The results derived from binary logistic regression analysis revealed an intriguing correlation between the SSTR2 rs2236750 AG genotype and approximately a 1.6-fold increased likelihood of PA occurrence. When analyzing SSTR5 rs34037914, statistically significant differences were found between Micro-PA and the reference group (p = 0.022). Additionally, the SSTR5 rs34037914 TT genotype, compared with CC + CT, under the most robust genetic model (selected based on the lowest AIC value), was associated with a 12-fold increased odds of Micro-PA occurrence. However, it is noteworthy that after applying Bonferroni correction, these findings did not retain statistical significance. Conclusions: Consequently, while this study hinted at a potential link between SSTR2 rs2236750 and pituitary adenoma development, as well as a potential link between SSTR5 rs34037914 and Micro-PA development, it underscored the need for further analysis involving a larger cohort to robustly validate these findings.

Differences in Eotaxin Serum Levels between Polytraumatized Patients with and without Concomitant Traumatic Brain Injury-A Matched Pair Analysis.

Background/Objectives: Early detection of traumatic brain injury (TBI) is crucial for minimizing secondary neurological damage. Our study aimed to assess the potential of IL-4, IL-6, IL-7, IL-8, IL-10, TNF, and eotaxin serum levels-as a single clinical tool or combined into a panel-for diagnosing TBI in multiple injured patients. Methods: Out of 110 prospectively enrolled polytrauma victims (median age, 39 years; median ISS, 33; 70.9% male) admitted to our level I trauma center over four years, we matched 41 individuals with concomitant TBI (TBI cohort) to 41 individuals without TBI (non-TBI cohort) based on age, gender, Injury Severity Score (ISS), and mortality. Patients' protein levels were measured upon admission (day 0) and on days 1, 3, 5, 7, and 10 during routine blood withdrawal using one separation gel tube each time. Results: The median serum levels of IL-4, IL-6, IL-7, IL-8, IL-10, and TNF exhibited non-similar time courses in the two cohorts and showed no significant differences on days 0, 1, 3, 5, and 7. However, the median eotaxin levels had similar trend lines in both cohorts, with consistently higher levels in the TBI cohort, reaching significance on days 0, 3, and 5. In both cohorts, the median eotaxin level significantly decreased from day 0 to day 1, then significantly increased until day 10. We also found a significant positive association between day 0 eotaxin serum levels and the presence of TBI, indicating that for every 20 pg/mL increase in eotaxin level, the odds of a prevalent TBI rose by 10.5%. ROC analysis provided a cutoff value of 154 pg/mL for the diagnostic test (sensitivity, 0.707; specificity, 0.683; AUC = 0.718). Conclusions: Our findings identified the brain as a significant source, solely of eotaxin release in humans who have suffered a TBI. Nevertheless, the eotaxin serum level assessed upon admission has limited diagnostic value. IL-4, IL-6, IL-7, IL-8, IL-10, and TNF do not indicate TBI in polytraumatized patients.

Dietary patterns and micronutrients in respiratory infections including COVID-19: a narrative review.

BACKGROUND: COVID-19 is a pandemic caused by nCoV-2019, a new beta-coronavirus from Wuhan, China, that mainly affects the respiratory system and can be modulated by nutrition. METHODS: This review aims to summarize the current literature on the association between dietary intake and serum levels of micronutrients, malnutrition, and dietary patterns and respiratory infections, including flu, pneumonia, and acute respiratory syndrome, with a focus on COVID-19. We searched for relevant articles in various databases and selected those that met our inclusion criteria. RESULTS: Some studies suggest that dietary patterns, malnutrition, and certain nutrients such as vitamins D, E, A, iron, zinc, selenium, magnesium, omega-3 fatty acids, and fiber may have a significant role in preventing respiratory diseases, alleviating symptoms, and lowering mortality rates. However, the evidence is not consistent and conclusive, and more research is needed to clarify the mechanisms and the optimal doses of these dietary components. The impact of omega-3 and fiber on respiratory diseases has been mainly studied in children and adults, respectively, and few studies have examined the effect of dietary components on COVID-19 prevention, with a greater focus on vitamin D. CONCLUSION: This review highlights the potential of nutrition as a modifiable factor in the prevention and management of respiratory infections and suggests some directions for future research. However, it also acknowledges the limitations of the existing literature, such as the heterogeneity of the study designs, populations, interventions, and outcomes, and the difficulty of isolating the effects of single nutrients from the complex interactions of the whole diet.

Diagnostic Dilemma: IgG4-Related Sclerosing Mesenteritis Mimicking an Abdominal Malignancy Enveloping the Superior Mesenteric Artery.

Sclerosing mesenteritis, a rare fibroinflammatory disease affecting the mesentery, presents a diagnostic challenge due to its varied clinical manifestations and unknown etiology. We present a case of a 50-year-old female presenting with epigastric pain and weight loss, initially suspected of abdominal malignancy. Imaging revealed a mesenteric mass, and histopathological examination confirmed dense lymphoplasmacytic infiltrate with storiform fibrosis, along with elevated serum IgG4 levels, indicative of IgG4-related sclerosing mesenteritis. Treatment with thalidomide and prednisolone resulted in significant mass regression and symptom improvement. Our case highlights the importance of considering sclerosing mesenteritis in the differential diagnosis of abdominal masses and suggests a potential therapeutic approach for this rare condition. Further research is warranted to elucidate its pathogenesis and optimize management strategies.

Investigating the Potential Influence of TAS2R16 Genetic Variants and Protein Levels on Multiple Sclerosis Development.

The study aimed to investigate the association between the TAS2R16 gene (rs860170, rs978739, rs1357949), TAS2R16 serum levels, and multiple sclerosis (MS). A total of 265 healthy control subjects and 218 MS patients were included in the study. Single nucleotide polymorphisms (SNPs) were tested by real-time polymerase chain reaction (RT-PCR). The serum concentration of TAS2R16 was measured using the ELISA method. Analyses revealed that the TAS2R16 rs860170 TT genotype was statistically significantly less frequent in the MS group than in the control group (p = 0.041), and the CC genotype was statistically significantly more frequent in the MS group than in the control group (p < 0.001). In the most robust (codominant) model, the CC genotype was found to increase the odds of MS by ~27-fold (p = 0.002), and each C allele increased the odds of MS by 1.8-fold (p < 0.001). Haplotype analysis of the rs860170, rs978739, and rs1357949 polymorphisms showed that the C-C-A haplotype was associated with a ~12-fold increased odds of MS occurrence (p = 0.02). Serum TAS2R16 levels were elevated in the MS group compared to control subjects (p = 0.014). Conclusions: The rs860170, rs978739, and rs1357949 polymorphisms demonstrated that the C-C-A haplotype and elevated TAS2R16 serum levels can promote the development of MS. These preliminary findings underscore the importance of specific genetic variants, such as rs860170, rs978739, and rs1357949, in MS risk. Additionally, elevated TAS2R16 serum levels in MS patients suggest a potential role in MS pathogenesis. These findings provide insights into the genetic and molecular mechanisms underlying MS and pave the way for personalized diagnostic and therapeutic strategies. Integrating genetic and serum biomarker data in MS research offers promising avenues for improving clinical outcomes and advancing precision medicine approaches in the future.

The Association Between Epidermal Growth Factor rs3756261 A/G Gene Polymorphism and the Risk of Ankylosing Spondylitis in a Chinese Han Population.

Background: Epidermal growth factor (EGF) is a potent pro-angiogenic molecule promoting the angiogenic phenotype of ankylosing spondylitis (AS). Studies demonstrated that EGF rs3756261 polymorphism was associated with the risk of inflammatory diseases, but not including AS. Methods: To investigate the association between EGF rs3756261 polymorphism and the risk of AS, we genotyped the EGF rs3756261 polymorphism in 208 patients with AS and 412 controls in a Chinese Han population using a custom-by-design 48-Plex SNP scanTM Kit. The serum EGF levels were measured using an enzyme-linked immunosorbent assay in 208 AS patients and 412 controls. Results: Our data indicated that EGF rs3756261 polymorphism was associated with an increased risk of AS in the Chinese Han population. Stratified analyses indicated that the EGF rs3756261 polymorphism elevated the risk of AS among the males, smokers, drinkers and those aged <30 years. In addition, the EGF rs3756261 polymorphism was related to increased CRP and HLA-B27 levels in AS patients. Next, we found that the average serum levels of EGF were significantly higher in AS patients compared with controls. Meanwhile, EGF serum levels were significantly higher in AG genotype carriers when compared with AA genotype carriers in AS patients. Conclusion: In conclusion, this study indicated that EGF rs3756261 polymorphism was associated with the risk of AS and EGF serum levels in a Chinese Han population.

Influence of STAT4 Genetic Variants and Serum Levels on Multiple Sclerosis Occurrence in the Lithuanian Population.

Background: Multiple sclerosis (MS) is an autoimmune disease involving demyelination, inflammation, gliosis, and the loss of neurons. MS is a growing global health problem most likely caused by genetic, immunological, and environmental factors. However, the exact etiology of the disease is still unknown. Since MS is related to a dysregulation of the immune system, it could be linked to signal transducer and activator of transcription 4 (STAT4). To fully comprehend the significance of the STAT4 gene and STAT4 serum levels in MS, further research is required. Methods: A total of 200 MS patients and 200 healthy controls participated in the study. Deoxyribonucleic acid (DNA) was extracted using silica-based membrane technology. Polymerase chain reaction was used in real time for genotyping. Using the ELISA technique, serum levels were measured. Results:STAT4 rs7601754 AA genotype and the A allele were statistically significantly less frequent in MS patients (p = 0.003). Also, rs7601754 was associated with 1.9-fold increased odds of MS occurrence (p = 0.004). The rs7601754 AG genotype was more common in males with MS (p = 0.011) and was associated with 2.5-fold increased odds of MS occurrence in males (p = 0.012). STAT4 serum levels were statistically significantly lower in MS patients compared to the control group (p = 0.007). Conclusions:STAT4 rs7601754 increases the odds of MS occurrence. STAT4 serum levels were statistically significantly lower in MS patients compared to the control group.

Exploring the Potential of IL-4 and IL-13 Plasma Levels as Biomarkers in Atopic Dermatitis.

Atopic dermatitis (AD) is a persistent inflammatory skin condition that impacts individuals of various age groups, including both children and adults. Its pathophysiology involves allergens penetrating a disrupted epidermal barrier, triggering the dermal cells to produce pro-inflammatory cytokines and eliciting a T-cell-mediated immune response. Notably, interleukins (ILs), particularly interleukin 4 (IL-4) and interleukin 13 (IL-13), play a key role in AD pathogenesis. Therapies directed at inflammatory mechanisms, including Dupilumab, have demonstrated notable effectiveness in enhancing skin lesions, alleviating subjective symptoms, and improving the overall quality of life for individuals with AD. Despite therapeutic advances, assessing AD severity remains challenging. The commonly used tools, such as the SCORAD and DLQI scores, rely on subjective patient responses. Paraclinically, the search for universal biomarkers continues, with efforts to identify reliable indicators reflecting disease severity and treatment response. Various biomarkers, including Th2-related chemokines and cytokines, have been explored, but none have gained universal recognition for routine clinical use. This study aims to investigate the dynamics of the plasma levels of IL-4 and IL-13 during Dupilumab treatment and establish correlations between these ILs and disease severity, as measured using the SCORAD and DLQI scores. The ultimate endpoint is to determine whether IL-4 and IL-13 can serve as reliable biomarkers, assessing their correlation with patient-reported feelings and disease activity and potentially influencing their inclusion or exclusion as diagnostic elements in routine clinical practice.

Predictors of Plasma Levels of Direct Oral Anticoagulants Among Patients with Atrial Fibrillation in Need of Elective Cardiac Procedures.

BACKGROUND: The withdrawal timing of direct oral anticoagulants (DOACs) among patients in need of elective invasive surgery is based on DOAC pharmacokinetics in order to perform the procedure out of the DOAC peak plasma concentration. We aimed to investigate the prevalence and predictors of plasma levels of DOACs out of trough range in patients with atrial fibrillation (AF) in need of elective cardiac procedure. MATERIALS AND METHODS: We evaluated all consecutive AF patients on DOAC therapy in need of elective cardiac procedure, admitted to our division from January 2022 to March 2022. All patients underwent DOAC plasma dosing the morning of procedure day. They were categorized as in range, above range, and below range, according to the DOAC reference range at the downstream point. The timing of discontinuation of DOAC therapy was considered as appropriate or not, according to the current recommendations. The clinical predictors of out-of-range DOAC plasma levels have been evaluated. RESULTS: We included 90 consecutive AF patients (56.6% male, mean age 72.95 ± 10.12 years); 74 patients (82.22%) showed DOAC concentration out of the expected reference range. In half of them (n, 37), the DOAC plasma concentration was below the trough reference range. Of the study population, 17.7% received inappropriate DOAC dosages (10% overdosing, 7% underdosing), and 35.5% had incorrect timing of DOAC withdrawal (26% prolonged, 9.5% shortened). At multivariable analysis, inappropriate longer DOAC withdrawal period (OR 10.13; P ≤ 0.0001) and increased creatinine clearance (OR 1.01; P = 0.0095) were the independent predictors of plasma DOAC levels below the therapeutic trough range. In contrast, diabetes mellitus (OR 4.57; P = 0.001) was the only independent predictor of DOAC plasma level above the therapeutic trough range. CONCLUSION: Increased creatinine clearance and inappropriate longer drug withdrawal period are the only independent predictors of DOAC plasma levels below the reference range; in contrast, diabetes is significantly correlated with DOAC plasma levels above the reference.

Malondialdehyde Serum Levels in a Full Characterized Series of 430 Rheumatoid Arthritis Patients.

Background. Oxidative stress has been involved in the pathogenesis of rheumatoid arthritis (RA). The serum malondialdehyde (MDA) level is a reliable biomarker of oxidative stress status. In the present work, we aimed to analyze how a comprehensive characterization of the disease characteristics in RA, including a lipid profile, insulin resistance, and subclinical atherosclerosis, relates to serum MDA levels. Methods. In a cross-sectional study that included 430 RA patients, serum MDA levels were evaluated. Multivariable analysis was performed to examine the relationship of MDA with disease activity scores and disease characteristics, including subclinical carotid atherosclerosis, a comprehensive lipid molecule profile, and indices of insulin resistance and beta cell function indices. Results. The erythrocyte sedimentation rate (ESR) showed a significant and positive relationship with MDA. However, this did not occur for other acute phase reactants such as C-reactive protein or interleukin-6. Although the DAS28-ESR score (Disease Activity Score in 28 joints) had a positive and significant association with MDA serum levels, other disease activity scores that do not use the erythrocyte sedimentation rate in their formula did not show a significant relationship with MDA. Other disease characteristics, such as disease duration and the existence of rheumatoid factor and antibodies against citrullinated protein, were not related to serum MDA levels. This also occurred for lipid profiles, insulin resistance indices, and subclinical carotid atherosclerosis, for which no associations with circulating MDA were found. Conclusions. The disease characteristics are not related to circulating MDA levels in patients with RA.

Generalised Periodontitis: Examining TAS2R16 Serum Levels and Common Gene Polymorphisms (rs860170, rs978739, rs1357949).

The objective of this study was to evaluate and compare the associations between TAS2R16 serum levels and common gene rs860170, rs978739, and rs1357949 polymorphisms in patients affected by generalized periodontitis. The study enrolled 590 patients: 280 patients with periodontitis and 310 healthy controls as a reference group. Patients underwent periodontal examination and radiographic analysis to confirm the periodontitis diagnosis. Blood samples were collected, and the DNA salting-out method was used for DNA extraction from peripheral venous blood. Genotyping of TAS2R16 (rs860170, rs978739, and rs1357949) was performed using real-time polymerase chain reaction (RT-PCR), and serum level analysis was performed for both periodontitis-affected patients and reference group subjects. The analysis of TAS2R16 rs860170 (TT, CT, and CC) showed a statistically significant difference between generalized periodontitis and the reference group (41.8%, 58.2%, and 0% vs. 38.7%, 56.1%, and 5.2%, p < 0.001). TAS2R16 rs860170 (TT, CT, and CC) showed a statistically significant difference between males in generalized periodontitis and reference groups (38.4%, 61.6%, and 0% vs. 32.9%, 56.6%, and 10.5%, p = 0.002). Female-specific analysis showed that the TAS2R16 rs978739 C allele was more frequent in generalized periodontitis compared to the reference group (37.5% vs. 28.7%, p = 0.016). Subjects aged 70 years and older demonstrated a statistically significant difference in TAS2R16 rs860170 (TT, CT, and CC) between generalized periodontitis and the reference group (42.8%, 57.2%, and 0% vs. 38.6%, 53.8%, and 7.6%, p = 0.003). TAS2R16 serum levels were elevated in generalized periodontitis compared to the reference group (0.112 (0.06) ng/mL vs. 0.075 (0.03) ng/mL, p = 0.002). Females carrying the TAS2R16 rs978739 C allele were more prone to generalized periodontitis development. Associations were found between TAS2R16 rs860170 polymorphisms, elevated TAS2R16 serum levels, and generalized periodontitis development.

Maternal serum angiopoietins levels in pre-eclampsia and pregnancy outcomes.

Background and Aims: Although the understanding of pre-eclampsia (PE) has improved, there is still insufficient knowledge on the exact etiology and pathophysiological mechanisms. Dysregulation of angiogenic factors has emerged as a significant contributing factor. Among these factors, angiopoietins (Ang-1 and Ang-2) have gained considerable attention due to their crucial role in regulating vascular development and endothelial function. This study explored the maternal serum levels of angiopoietins and perinatal outcomes in PE. Methods: A case-control study involving women with PE (cases) and normotensive pregnancies (controls) was conducted at the Maternity unit of the Korle-Bu Teaching Hospital. Descriptive analysis was performed and the Mann-Whitney U test (two-sided) was used to compare maternal serum levels of angiopoietins between the cases and controls. Results: We included 188 participants comprising 94 cases (women with PE) and 94 controls (normotensive pregnancies) with an average maternal age of 29.76 ± 5.56 and 28.43 ± 5.57 years, respectively. Maternal serum levels of Ang-2 were significantly lower among the PE cases compared to the normotensive controls (1.25 [0.90, 2.15] vs. 2.14 [1.18, 5.73] ng/mL, p = 0.001) but no significant difference in Ang-1 levels (92.61 [80.92, 114.92] vs. 99.26 [81.76, 113.12] ng/mL, p = 0.429) was observed between the groups. The Ang-1/Ang-2 ratio was significantly elevated among women with PE compared to normotensive controls (74.47 [37.69, 110.59] vs. 45.98 [16.11, 88.22] ng/mL, p = 0.014). Also, women who delivered vaginally had significantly high maternal serum levels of Ang-1 compared to women who had cesarean section delivery (107.98 ± 27.79 vs. 89.02 ± 32.62 ng/mL). Conclusion: Maternal serum levels of Ang-2 but not Ang-1 were significantly depressed in women with PE compared to the pregnant normotensive controls. No significant associations were observed between Ang-1, Ang-2 levels, or the Ang-1/Ang-2 ratio and pregnancy outcomes such as preterm birth, birth weight, and severity of hypertension.

Vascular Endothelial Growth Factor A serum levels and common gene polymorphisms in generalized periodontitis affected patients.

OBJECTIVE: To evaluate and compare the associations of VEGFA serum levels and SNPs (rs1570360, rs699947, rs3025033, and rs2146323) with periodontitis in study participants grouped by gender. METHODS: The study enrolled 261 patients with periodontitis and 441 healthy controls as a reference group. Patients underwent periodontal examination and radiographic analysis to confirm the periodontitis diagnosis. Blood samples were collected, and the DNA salting-out method was used for DNA extraction from peripheral venous blood. Genotyping of VEGFA (rs1570360, rs699947, rs3025033, and rs2146323) was performed using real-time polymerase chain reaction (RT-PCR) and serum level analysis was done for 80 individuals - 40 periodontitis-affected patients and 40 reference group subjects. RESULTS: The analysis of VEGFA (rs1570360, rs699947, rs3025033, and rs2146323) showed that the rs3025033 GG genotype was less frequent in the periodontitis group than in the reference group (1.6% vs. 5.7%,p = 0.008). VEGFA serum levels were not statistically significantly different between periodontitis patients and reference group subjects (554.29 (522.38) ng/ml vs. 581.32 (348.16) ng/ml, p = 0.786). Individuals carrying rs1570360, rs699947, rs3025033, and rs2146323 haplotype A-A-G-A had decreased risks of periodontitis, while rare haplotype of VEGFA (rs1570360, rs699947, rs3025033, and rs2146323) was associated with increased odds of periodontitis (OR= 0.42; 95% CI: 0.20-0.85; p < 0.017; OR= 4.08; 95% CI: 1.86-8.94; p < 0.0001, respectively). CONCLUSION: The rs3025033 GG genotype and the rs1570360, rs699947, rs3025033, and rs2146323 A-A-G-A haplotypes may play a protective role in the development of periodontitis, but a less common haplotype of the same VEGFA polymorphism may be associated with the risk of developing periodontitis.

Association of KDR (rs2071559, rs1870377), CFH (rs1061170, rs1410996) genes variants and serum levels with pituitary adenoma.

INTRODUCTION: Pituitary adenomas (PA) are slow-growing, benign tumors that usually do not metastasize to other body organs. Although they are referred to as benign, tumor growth can eventually put pressure on nearby structures, spread to surrounding tissues, and cause symptoms. The exact cause of PA is unknown, and the pathogenesis is multifactorial. METHODS: Our study included PA patients and healthy volunteers. Genomic DNA was extracted using the DNA salting-out method. All participants were genotyped for the KDR rs2071559, rs1870377, CFH rs1061170, and rs1410996 polymorphisms. Serum levels of KDR and CFH were examined using the ELISA method. RESULTS: The results of the present study showed that KDR rs2071559 A allele was associated with the occurrence of PA, hormonally active PA, invasive PA, and PA without recurrence development. KDR rs1870377 increased the probability of invasive PA and PA recurrence. CFH rs1061170 C allele was associated with hormonally active PA and the T allele was associated with non-invasive PA development. CONCLUSION: KDR rs2071559, rs1870377, and CFH rs1061170 could be potential biomarkers associated with PA.

Serum Western Blot for the Detection of a c-Myc Protein Tag in Non-human Primates and Mice.

This protocol allows for the detection of a c-Myc tag on alpha-1 antitrypsin (AAT) delivered to species that already have endogenous AAT such as non-human primates allowing reliable and repeatable semi-quantitation of serum levels of AAT.

Association of TAS2R16 gene (rs860170, rs978739, rs1357949) polymorphisms and TAS2R16 serum levels in patients with age-related macular degeneration.

BACKGROUND: The aim of this study is to determine the association of TAS2R16 (rs860170, rs978739, rs1357949) gene polymorphisms and TAS2R16 serum levels in patients with the occurrence of age-related macular degeneration (AMD). METHODS: Subjects with early AMD, subjects with exudative AMD, and healthy controls participated in the study. DNA was isolated by salting out leukocytes from peripheral venous blood. Single nucleotide polymorphisms (SNPs) were analysed by RT-PCR. TAS2R16 levels were determined by enzyme-linked immunosorbent assay (ELISA) using the Abbexa Human Taste Receptor Type 2 Member 16 (TAS2R16) ELISA kit. Statistical data analysis was performed using "IBM SPSS Statistics 27.0" and SNPstats statistical data analysis programmes. RESULTS: The TAS2R16 rs860170 TT genotype is statistically significantly less frequent in the exudative AMD group than in the control group, whereas the TAS2R16 rs860170 C allele gene is statistically significantly more frequent in the exudative AMD group. Each C allele of TAS2R16 rs860170 is associated with a 2.8-fold increased probability of occurrence of exudative AMD. The C allele of TAS2R16 rs860170 is statistically significantly more frequent in men and women with exudative AMD than in the control group. The C allele of TAS2R16 rs860170 is associated with a 2.8-fold increased odds of occurrence of exudative AMD in women and a 2.9-fold increased odds of occurrence of exudative AMD in men. In TAS2R16 (rs860170, rs978739, and rs1357949), the T-T-A haplotype is associated with a 2.6-fold decreased likelihood of developing early AMD and the T-T-A haplotype is associated with a 3.2-fold decreased likelihood of developing early AMD in women. For TAS2R16 (rs860170, rs978739, and rs1357949), carriers of the T-T-G and T-T-A haplotypes are associated with a 2.2- and 3.2-fold decreased probability of exudative AMD, respectively. Individuals with the C-C-A haplotype are 9.2-fold more likely to develop exudative AMD. Specifically, the C-C-A haplotype is associated with a 9.3-fold increased likelihood of exudative AMD in men. In contrast, women with the T-T-A haplotype are 5.6-fold less likely to develop exudative AMD. CONCLUSION: TAS2R16 plays an important role in the development of AMD.

Evaluation of SOCS5 mRNA and its association with serum IL-12 levels and rs41379147 SNP in various subsets of allergic disorders: A case control study.

BACKGROUND: The SOCS proteins act as suppressors of cytokine signaling by impeding certain signaling pathways. SOCS5, a constituent of the SOCS family, has been associated with the management of allergic reactions, primarily by impeding the signaling of interleukin-4 (IL-4), which is known to have a cardinal function in accelerating the development of an allergic reaction. The key goal of our research was to explore the probable ramifications of the SOCS5 single nucleotide polymorphism (SNP) namely rs41379147 on the expression of SOCS5 mRNA and serum IL-12 levels, as well as to analyze the interaction between SOCS5 genotypes and various clinicopathological parameters in atopic diseases. METHODS: The study involved the enrollment of 314 subjects comprising 154 atopic individuals and 160 healthy controls. PCR-RFLP was employed to conduct SNP analysis. Real-Time PCR was employed to quantify SOCS5 mRNA. The enzyme-linked immunosorbent assay (ELISA) technique was used for the quantification of interleukin-12 and total IgE levels in the serum while as chemiluminescence was used to determine Vitamin D levels. RESULTS: The PCR-RFLP analysis indicated a lack of statistically significant variation in genotypic and allelic frequencies between the cases and controls (p > 0.05) for - 9147 C/T SNP either in total atopy (OR-0.70, 95% CI=0.43-1.12, p =0.15), and on subgroup stratifications of chronic urticaria (OR-0.81, 95 % CI = 0.42-1.59, p = 0.61), allergic rhinitis (OR-0.63, 95 % CI = 0.33-1.19, p = 0.16) and bronchial asthma (OR-0.66,95% CI = 0.29-1.4, p=0.32). There was reduced mRNA expression of SOCS5 in total atopic cases, allergic rhinitis, bronchial asthma and chronic urticaria in comparison to controls which advocates the fact that SOCS5 has a protective role in allergic disease development. Despite the reduced amounts of IL-12 in total atopic cases and different allergic disorders in comparison to controls, IL-12 showed significant positive correlation with SOCS5 mRNA expression (p < 0.05). CONCLUSION: SOCS5 SNP rs41379147(C/T) does not pose any significant risk towards the development of any allergic disorder and has no impact on the expression of SOCS5 and IL-12. Our study has shown the reduced mRNA expression of SOCS5 among individuals diagnosed with chronic urticaria, allergic rhinitis and bronchial asthma and the expression of SOCS5 showed complete dependence on the cytokine milieu of IL12. The modulation of SOCS5 and IL-12 may represent potential curative targets for treating the menace of allergic diseases and present promising avenues for future investigation.