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Periodontitis is a multifactorial inflammatory disease. This chronic periodontal disease is caused by a bacterial infection in the gums, which triggers a host inflammatory response. To eliminate the bacterial infection, immune response mechanisms are activated, leading to inflammation and damage to the periodontal tissues. This process involves many cytokines, including IL-6, a cytokine with antibacterial properties. An ongoing bacterial infection in the periodontal tissues leads to its excessive production, which increases inflammation. In this study, we examined IL-6 receptor gene rs1800795 polymorphism in patients with periodontitis in comparison with healthy subjects, as well as the correlation between rs1800795 genotypes and clinical parameters. Additionally we examined the expression of IL-6 in gingival tissue in patients with periodontitis and control subjects, as well as the correlation between gingival expression of IL-6 and clinical parameters. This study included 200 patients with periodontitis and 158 healthy subjects as the control group. Biopsy specimens of gingival tissue in which IL-6 expression was detected were taken from 14 patients with periodontitis and 8 controls who had undergone minor surgery. There were no statistically significant differences in the distribution of IL-6 rs1800795 genotypes and alleles between patients with periodontitis and control subjects. There were also no statistically significant correlations between IL-6 rs1800795 genotypes and clinical parameters in patients with periodontitis. There were no differences in IL-6 expression in the gingival tissue between patients with periodontitis and controls. There was also no correlation between IL-6 expression in the gingival tissue of patients with periodontitis and clinical parameters. In the control group, IL-6 expression in gingival tissue correlated negatively with the approximal plaque index, which reflects the size of bacterial plaques. The results of our study suggest a protective role for IL-6 against bacterial growth in the periodontal tissue. However, it should be noted that several parameters directly or indirectly affect the accumulation of bacterial plaque. [ABSTRACT FROM AUTHOR]

Introduction: Sarcoidosis is a systemic inflammatory granulomatous disease most commonly found in the lungs, and less frequently in other organs such as the lymph nodes or the heart. Materials and methods: In this observational study, 62 adult patients with pulmonary sarcoidosis were enrolled. Their preexisting pulmonary diagnostics, including imaging and functional tests, were analyzed. Additionally, non-invasive cardiological diagnostics: electrocardiography (ECG), Holter electrocardiography (Holter ECG), transthoracic echocardiography (TTE) and laboratory tests were performed. Results: The most common findings were numerous ventricular arrhythmias (20.34%), pericardial effusion (40.32%), and left ventricular relaxation disorders (29.03%). A positive correlation was found between the duration of sarcoidosis and wall motion score index (WMSI; p = 0.026), as well as between the stage of sarcoidosis in chest X-ray/computed tomography (CXR/CT) and tricuspid regurgitation peak gradient – TRPG (p = 0.001). An inverse correlation was found between diffusion lung capacity for carbon monoxide (DLCO) and the stage of sarcoidosis (p = 0.037), forced vital capacity (FVC) and ventricular systolic asynchrony (p = 0.044), both forced expiratory volume in 1 s (FEV1) and FVC, and the width of the pulmonary trunk (p = 0.046 and p = 0.045), both FEV1 and FVC, and the width of the right ventricle (p = 0.036 and p = 0.04), and total lung capacity (TLC) and the width of the left atrium (p = 0.007). Conclusions: A longer duration of the disease was associated with more advanced heart involvement. Higher stages of sarcoidosis were associated with more frequent cardiac changes. [ABSTRACT FROM AUTHOR]

Introduction. Scientists are currently searching for new and improved diagnostic markers and treatment modalities for gastric cancer. One putative target are the cancer/testis genes (CTGs), whose expression is restricted to male germ cells, trophoblasts and ovaries. CTGs are also aberrantly expressed in several types of cancers. In healthy somatic tissues, CTGs expression is either not detected or present at low levels. About 270 CTGs have been described thus far. The aim of this study was to investigate the expression levels of CTGs in stomach tissue samples from patients with gastric neoplasm, in relation to selected clinical and pathomorphological parameters. Material and methods. 28 patients with histologically confirmed gastric neoplasms were included in this study. Total RNA was extracted from homogenates using the RNeasy Fibrous Tissue Mini Kit in accordance with the manufacturer’s protocol. A quantitative assessment of mRNA levels for 35 genes was performed using real-time RT-PCR. Results. We report that 11 out of 35 CTGs tested (ATAD2, FBXO39, HORMAD1, IGSF11, IL13RA2, KIF2C, LDHC, OIP5, PLU1, SPAG9 and TTK) were significantly (p≤0.05) overexpressed in tumour tissue compared with healthy stomach samples isolated from the same patients. Additionally, our results indicated that overexpression of OIP5 was associated with gastric adenocarcinoma in women. Moreover, two of the tested CTGs (HORMAD1, TTK) were significantly overexpressed in tubular gastric adenocarcinoma. Additional analysis showed a correlation between KU-CT-1 expression in gastric adenocarcinoma and patient age at diagnosis. Conclusions. Our results suggest that the overexpression of CTGs may be specific for gastric neoplasms, but it should be confirmed in larger numbers of patients. [ABSTRACT FROM AUTHOR]

Background: Primary graft dysfunction (PGD) is a form of acute lung injury (ALI) that occurs within 72 h after lung transplantation (LuTx) and is the most common early complication of the procedure. PGD is diagnosed and graded based on the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen and chest X-ray results. PGD grade 3 increases recipient mortality and the chance of chronic lung allograft dysfunction (CLAD). Method: The aim of this retrospective study was to identify new PGD risk factors. The inclusion criteria were met by 59 patients, who all received transplants at the same center between 2010 and 2018. Donor data were taken from records provided by the Polish National Registry of Transplantation and analyzed in three variants: PGD 1–3 vs. PGD 0, PGD 3 vs. PGD 0 and PGD 3 vs. PGD 0–2. Results: A multiple-factor logistic regression model was used to identify decreasing recipient age; higher donor BMI and higher donor central venous pressure (CVP) for the PGD (of the 1–3 grade) risk factor. Conclusions: Longer cold ischemia time (CIT) and higher donor CVP proved to be independent risk factors of PGD 3. [ABSTRACT FROM AUTHOR]

Acute coronary heart disease (CHD) is mainly caused by the rupture of an unstable atherosclerotic plaque. Many different factors can cause stenosis or even occlusion of the coronary artery lumen, such as vasculitis and platelet aggregation. Our study was performed to assess the association between PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 polymorphisms and the risk of CHD, as well as the association between studied polymorphisms and selected clinical parameters affecting the risk of developing ischemic heart disease. A total of 232 patients with unstable angina were enrolled in this study. There were no statistically significant differences in the PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 polymorphism distributions between the total study and control groups. Total cholesterol plasma levels were significantly higher in patients with the PON1 rs662 TT genotype compared to those with the CC+TC genotypes, as well as in patients with the PON1 rs854560 TT genotype compared to those with the AA+AT genotypes. LDL plasma levels were significantly increased in patients with the PON1 rs854560 TT genotype compared to those with the AA+AT genotypes. Plasma levels of HDL were significantly decreased in patients with the TRIB1 rs17321515 AA+AG genotypes compared to those with the GG genotype, as well as in patients with the TRIB1 rs2954029 AA+AT genotypes compared to those with the TT genotype. Our results suggest that the analysed polymorphisms are not risk factors for unstable angina in the Polish population. However, the results of this study indicate an association between the PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 polymorphisms with lipid parameters in patients with coronary artery disease. [ABSTRACT FROM AUTHOR]

Background/Objectives: Gestational diabetes (GDM) is a metabolic disorder with altered glucose levels diagnosed in pregnant women. The pathogenesis of GDM is not fully known, but it is thought to be caused by impaired insulin production and insulin resistance induced by diabetogenic factors. The placenta may play an important role in the development of GDM. Glucose transporters (GLUTs) are responsible for the delivery of glucose into the foetal circulation. Placental zinc transporters regulate insulin and glucagon secretion, as well as gluconeogenesis and glycolysis. The aim of this study was to investigate the placental expression of GLUT3, GLUT4, GLUT7 and SLC30A8 in women with GDM. Furthermore, we evaluated whether the expression profiles of these transporters were correlated with clinical parameters. Methods: This study included 26 patients with GDM and 28 patients with normal glucose tolerance (NGT). Results: The placental expression of GLUT3 was significantly reduced in the GDM group, while the placental expression of GLUT4, GLUT7 and SLC30A8 was significantly upregulated in the GDM group. GLUT3 expression correlated significantly with body mass index (BMI) increase during pregnancy and body mass increase during pregnancy, while GLUT4 expression correlated negatively with BMI at birth. Conclusions: These results suggest the involvement of GLUT3 and GLUT4, GLUT7 and SLC30A8 in the pathogenesis of GDM. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy (DR) remains the leading cause of blindness in the working-age population. Its progression causes gradual damage to corneal nerves, resulting in decreased corneal sensitivity (CS) and disruption of anterior-eye-surface homeostasis, which is clinically manifested by increased ocular discomfort and dry eye disease (DED). This study included 52 DR patients and 52 sex- and age-matched controls. Ocular Surface Disease Index (OSDI) survey, tear film-related parameters, CS, and in vivo corneal confocal microscopy (IVCM) of the subbasal plexus were performed. Furthermore, all patients underwent tear sampling for neurotrophin and cytokine analysis. OSDI scores were greater in DR patients than in controls (p = 0.00020). No differences in the Schirmer test score, noninvasive tear film-break-up time (NIBUT), tear meniscus or interferometry values, bulbar redness, severity of blepharitis or meibomian gland loss were found. In the DR group, both the CS (p < 0.001), and the scotopic pupil diameter (p = 0.00008) decreased. IVCM revealed reduced corneal nerve parameters in DR patients. The stage of DR was positively correlated with the OSDI (Rs = +0.51, 95% CI: + 0.35–+0.64, p < 0.001) and negatively correlated with IVCM corneal nerve parameters and scotopic pupillometry (Rs = −0.26, 95% CI: −0.44–−0.06, p = 0.0097). We found negative correlations between the OSDI and IVCM corneal innervation parameters. The DR group showed lower tear film-brain-derived neurotrophic factor (BDNF) levels (p = 0.0001) and no differences in nerve growth factor (NGF)-β, neurotrophin (NT)-4, vascular endothelial growth factor (VEGF), interleukin (IL)-1β, IL-4, IL-5, IL-6, or IL-12 concentrations. Tumor necrosis factor (TNF)-α, IL-2, IL-8, IL-10, granulocyte macrophage colony-stimulating factor (GM-CSF), and interferon (IFN)-γ levels were decreased among patients with DR. Corneal innervation defects have a direct impact on patients' subjective feelings. The evolution of DR appears to be associated with corneal nerve alterations, emphasizing the importance of IVCM. [ABSTRACT FROM AUTHOR]

Background and Objectives: The effective treatment of chronic myeloid leukemia leads to the restoration of proper immune system function. We aimed to investigate fluctuations in circulating cytokines, angiogenic factors and complement components in patients with CML during the first year of treatment with TKI and correlate them with the degree of achieved molecular response. Material and Methods: We recruited 31 patients with newly diagnosed CML. Peripheral blood and bone marrow samples were obtained, and concentrations of serum proteins were measured using an immunology multiplex assay. Results: The study cohort was divided into two groups of optimal or non-optimal in accordance with the European Leukemia Net (ELN) guidelines. We found significantly higher concentrations of C1q, C4 and C5a in serum after 3 months of TKI treatment in patients who achieved optimal responses in the 6 months after diagnosis. The most alterations were observed during 12 months of therapy. Patients in the optimal response group were characterized by higher serum concentrations of TGF-β, EGF, VEGF, Angiopoietin 1, IFN-γ and IL-8. Conclusions: The later plasma concentrations of complement components were significantly increased in patients with optimal responses. The changes after 12 months of treatment were particularly significant. Similar changes in bone marrow samples were observed. [ABSTRACT FROM AUTHOR]

Objectives: Osteoprotegerin (OPG) is a member of the tumor necrosis factor receptor family involved in processes in many inflammatory states. OPG concentration is enhanced in the majority of chronic kidney disease (CKD) patients and those undergoing renal replacement therapy. The aim of the study was to assess the relation of OPG and chronic inflammation in peritoneal dialysis (PD) patients and to evaluate whether OPG concentrations in plasma and dialysate were related to plasma and dialysate levels of proinflammatory mediators (interleukin 6 (IL-6), high-sensitivity C-reactive protein (hsCRP), interleukin 33 (IL-33) and interleukin 1 receptor-like 1IL-1RL1 (IL-1RL1, sST2)). Methods: The study included 37 patients of the Peritoneal Dialysis Center, Department of Nephrology, Transplantology and Internal Medicine, Szczecin, Poland, 4–6 weeks after the onset of peritoneal dialysis therapy. During a peritoneal equilibration test, plasma (at 2 h) and dialysate (at 4 h) OPG, IL-33, 1IL-1RL1 (sST2), IL-6 and hsCRP concentrations were determined. Results: Plasma concentration of OPG did not correlate with dialysate OPG level (Rs = 0.04, p = 0.8). There was a strong positive correlation between plasma OPG concentrations and plasma IL-1RL1 (sST2) (Rs = 0.41; p = 0.01), plasma IL-6 (Rs = 0.38; p = 0.01) and plasma hsCRP (Rs = 0.35; p = 0.02). Dialysate OPG concentrations were positively associated with dialysate IL-1RL1 (sST2) (Rs = 0.37; p = 0.02) and dialysate IL-6 levels (Rs = 0.44; p = 0.005). Multivariate analysis showed that higher IL-1RL1 (sST2) (ß = +0.38, p = 0.006), higher plasma hsCRP (ß = +0.32, p = 0.02) and older age (ß = +0.35, p = 0.01) were independent determinants of higher plasma OPG concentration and that higher concentrations of dialysate IL-6 (ß = +0.37, p = 0.02) were independent determinants of higher dialysate OPG concentration. Conclusions: Both plasma and dialysate OPG levels are associated with the severity of systemic and local inflammation illustrated by the plasma and dialysate concentrations of IL-1RL1 (sST2), hsCRP and IL-6, suggesting that OPG might have a pivotal role in explaining the milieu of systemic and intraperitoneal inflammation. [ABSTRACT FROM AUTHOR]