Background: Taurine has an active role in providing glucose homeostasis and diabetes causes a decline in taurine levels. This paper investigates the relationship between taurine and diabetic complications, patients’ demographic features, and biochemical parameters. Methods: Fifty-nine patients with type 2 diabetes mellitus (T2DM), and 28 healthy control subjects between the ages of 32 and 82 were included in the study. The mean age of subjects was 55.6 ± 10.3 and mean diabetes duration was 10.2 ± 6.0 years. The most commonly accompanying comorbidity was hypertension (HT) (64.5%, n = 38), and the most frequent diabetic complication was neuropathy (50.8%, n = 30). Plasma taurine concentrations were measured by an enzyme-linked immunoassay (ELISA) kit. Results: Plasma taurine concentrations were significantly lower in diabetic patients (0.6 ± 0.1 mmol/L) than controls (0.8 ± 0.2 mmol/L) and in hypertensive (0. 6 ± 0.1 mmol/L) patients (p = 0.000, p = 0.027 respectively). Conclusion: Plasma taurine levels were decreased in patients with T2DM and this was not related to FBG, HbA1c, and microalbuminuria. With regard to complications, we only found a correlation with neuropathy. We suggest that taurine levels may be more important in the development of diabetes; however, it may also have importance for the progression of the disease and the subsequent complications. We further assert that taurine measurement at different times may highlight whether there is a causal relationship in the development of complications.

The aims of this study were to describe the clinical, radiological and immunological features of a population of sarcoidosis patients and to analyse chitinase-3-like protein 1 (YKL-40), soluble interleukin-2 receptor (sIL-2R), neopterin concentrations and adenosine deaminase (ADA) activity in serum of these patients in order to understand their potential as disease markers. Fifty-nine patients affected by chronic sarcoidosis, in active (20 patients) and inactive (39 patients) phase according to the clinical, radiological and laboratory criteria were studied. Serum YKL-40, sIL-2R, high-sensitive C-reactive protein (hs-CRP), neopterin levels and ADA activities were evaluated and compared with those of 25 healthy controls. Individuals with chronic sarcoidosis were significantly higher serum YKL-40, sIL-2R, neopterin, hs-CRP concentrations, angiotensin converting enzyme (ACE) and ADA activity than those of control subjects. Sarcoidosis patients in the active phase of the disease were significantly higher YKL-40, sIL-2R, hs-CRP levels and ACE activity than those in the inactive phase, while ADA activities and neopterin levels did not display any significant difference between the active and inactive disease groups. In comparison to the other parameters, as panel measurement of the serum YKL-40, sIL-2R, ACE and hs-CRP indicate a greater discrimination between active and inactive disease. The results indicate that serum YKL-40, sIL-2R, ACE and hs-CRP concentrations may be useful marker for monitoring sarcoidosis disease activity.

To investigate whether the circulating miR-1 (microRNA-1) and miR-21 expression might be used in the diagnosis of heart failure (HF) and silent coronary artery disease (SCAD) in asymptomatic type 2 diabetes mellitus (T2DM) patients and to explore the relationship of these miRs with N-terminal pro-brain natriuretic peptide (NT-proBNP) and galectin-3. One hundred thirty-five consecutive patients with T2DM and 45 matched control subjects were enrolled in the study. This study consisted of the following four groups: control group (mean age: 60.23 ± 6.27 years, female/male (F/M): 23/22); diabetic group (DM) (mean age: 61.50 ± 5.08, F/M: 23/22); DM + SCAD group (mean age: 61.61 ± 6.02, F/M: 20/25); and DM + acute HF group (mean age: 62.07 ± 5.26 years, F/M: 20/25). miR-1 was downregulated in the DM, CAD + DM and HF + DM groups by 0.54, 0.54, and 0.12 fold as compared with controls, respectively. The miR-1 levels were significantly lower in HF + DM than DM with 0.22 fold changes (p < 0.001); and in patients with CAD + DM group with 0.22 fold changes (p < 0.001). Similarly, miR-21 was overexpressed in patients with DM, CAD + DM, and HF + DM with 1.30, 1.79 and 2.21 fold changes as compared with controls, respectively. An interesting finding is that the miR-21 expression was significantly higher in the HF + DM group as compared with the CAD + DM group; miR-1 was negatively correlated with NT-proBNP (r = −0.891, p < 0.001) and galectin-3 (r = −0.886, p < 0.001) in the HF + DM group; and miR-21 showed a strongly positive correlation with (r = 0.734, p < 0.001) and galectin-3 (r = 0.764. p < 0.001) in the HF + DM group. These results suggest that the circulating decreased miR-1 and increased miR-21 expression are associated with NT-proBNP and galectin-3 levels in acute HF + DM. Especially the miR-21 expression might be useful in predicting the onset of acute HF in asymptomatic T2DM patients. The miR-21 expression is more valuable than the miR-1 expression in predicting cardiovascular events of acute HF and the combined analysis of miR-21 expression, galectin-3, and NT-proBNP can increase the predictive value of miR-21 expression.

Background: Antimicrobial peptides are effectors of host defence against infection and inflammation and can encourage wound repair. Objectives: The objectives of this study were to investigate the plasma antimicrobial peptide LL-37 and nuclear factor-kappaB (NF-κB) levels in patients with stable COPD compared with a control group and to highlight their importance in immune inflammation. Methods: One hundred and thirty-eight stable COPD patients and 33 control subjects were enrolled in the study. The COPD patients were classified into four groups based on FEV₁ (groups I–IV) and also divided into “low-risk and high-risk” groups (groups A–B [low risk], C–D [high risk]). Results: Plasma LL-37 levels were significantly lower while plasma NF-κB levels of the COPD patients were significantly higher than those of the control subjects (P<0.001, both). LL-37 levels were significantly lower in group IV than in groups I, II, and III (P<0.01, all). NF-κB levels were significantly higher in groups III and IV than in groups I and II (P<0.05, both). There was a positive correlation between FEV₁ and FEV₁/FVC in all COPD patients (r=0.742, P<0.001) and in group D (r=0.741, P<0.001). Furthermore, there was an inverse correlation between LL-37 and NF-κB in both the groups C (r=-0.566, P<0.001) and D (r=-0.694, P<0.001) and group C+D combined (r=-0.593, P<0.001). Furthermore, in group C, LL-37 and FEV₁ were positively correlated (r=0.633, P<0.001). Conclusion: Our study indicated that plasma LL-37 and NF-κB may play an important role in chronic immune inflammation. Decreased LL-37 levels may be particularly high risk for patients in stage IV disease. The role of LL-37 as a target for treatment of the immune system and COPD must be widely evaluated.