Background: Exercise is a well-accepted strategy to improve lipid and inflammatory profile in individuals with type 2 diabetes (T2DM). However, the exercise intensity having the most benefits on lipids and inflammatory markers in patients with T2DM remains unclear. We aimed to analyse the impact of a 1-year combined high-intensity interval training (HIIT) with resistance training (RT), and a moderate continuous training (MCT) with RT on inflammatory and lipid profile in individuals with T2DM.Methods: Individuals with T2DM (n=80, aged 59 years) performed a 1-year randomized controlled trial and were randomized into three groups (control, n= 27; HIIT with RT, n=25; MCT with RT, n=28). Exercise sessions were supervised with a frequency of 3 days per week. Inflammatory and lipid profiles were measured at baseline and at 1-year follow-up. Changes in inflammatory and lipid markers were assessed using generalized estimating equations. Results: After adjusting for sex, age and baseline moderate-to-vigorous physical activity (MVPA), we observed a time-by-group interaction for Interleukin-6 (IL-6) in both the MCT with RT (β=-0.70, p=0.034) and HIIT with RT (β=-0.62, p=0.049) groups, whereas, only the HIIT with RT group improved total cholesterol (β=-0.03, p=0.045) and LDL-C (β=-0.03, p=0.034), when compared to control. No effect was observed for C-reactive protein (CRP), cortisol, tumour necrosis factor-α (TNF-α), soluble form of the haptoglobin-hemoglobin receptor CD163 (sCD163), triglycerides and HDL-C in both groups (p>0.05).Conclusions: Favorable adaptations on IL-6 were observed in both the HIIT and MCT combined with RT groups following a long-term 1-year exercise intervention in individuals with T2DM. However, only the HIIT with RT prevented further derangement of total cholesterol and LDL-C, when compared to the control group. Therefore, in order to encourage exercise participation and improve inflammatory profile, either exercise protocols may be prescribed, however, HIIT with RT may have further benefits on the lipid profile.Trial registration: clinicaltrials.gov ID:NCT03144505

BACKGROUND The hepatitis C virus (HCV) is known to infect the brain, however findings on associated neuropsychiatric syndrome are controversial and the association itself remains unclear. Gender research in HCV infection is limited, failing to integrate the role of gender in neurocognitive syndrome. This study aimed to characterize psychological and neurocognitive profiles in HCV-infected patients before treatment and to describe gender differences in those profiles as well as the impact of disease severity. METHODS A total of 86 patients diagnosed with chronic hepatitis C were selected in the context of a multidisciplinary out-patient clinic. A semistructured interview was performed to collect social-demographic data and clinical characterization. Assessment was performed using the Hamilton anxiety scale (HAM-A), Hamilton depression scale (HAM-D), Beck depression inventory and a neuropsychological battery to measure attention, concentration, memory and executive functions components validated for the Portuguese population, before starting treatment. To identify the disease severity, platelet ratio index and FibroScan® were used. RESULTS A statistically significant gender effect was found on HAM-A (B = 0.64, confidence interval (CI): 0.17-1.11) and HAM-D, with women scoring higher (B = 0.62, CI: 0.14-1.09) compared to men. Regarding neuropsychological scores, significant differences between gender were identified in executive functions Trails Making Test (TMT)-B (B = 0.48, CI: 0.02-0.97), TMT B-A (B = 0.26, CI: -39.2 to -3.7) and in digit span total (B = -0.52, CI: -1.0 to -0.04), with women performing worse than men. Controlling for years of substance dependence, Digit Span Total was no longer significant; however, TMT-B and TMT B-A continued showing gender differences. Regarding the presence or absence of substance dependence, only HAM-A and HAM-D remained significant. For categorial variables, Digit Span Total was also influenced by gender, with women being more likely to be impaired (odds ratio (OR) = 7.07, CI: 2.04-24.45), and a trend was observed for Digit Span Backward (OR = 3.57, CI: 1.31-9.75). No significant differences were found between disease severity and neurocognitive performance. CONCLUSION Data suggest that gender has an influence on depression, anxiety and cognitive functions independently of the stage of infection. This effect seems influenced by substance dependence.

BACKGROUND AND AIMS Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease characterized by the formation and growth of renal cysts, affecting the decrease of renal function, which may lead to end-stage renal disease (ESRD). Due to the enormous intrafamilial phenotypic variability of ADPKD and since serum creatinine and glomerular filtration rate (GFR) have a limited ability to assess the disease and predict its progression at earlier stages, there is a need to find new biomarkers to predict disease progression. The α-glutathione s-transferase (GST-α) and haptoglobin (Hp) are produced mainly by the proximal convoluted tubule, and these enzymes are released into the urinary lumen in direct response to tubular damage. This study aims to evaluate the urine concentration of α-GST and Hp biomarkers at different stages of ADPKD progression and correlate the levels of urinary biomarkers α-GST and Hp with traditional markers of renal dysfunction. METHOD Twenty-five patients with ADPKD, mean age of 41.57 ± 14.43 years, mostly female (56.0%), diagnosed according to the Ravine criteria and with a follow-up of at least 60 months. Demographic, hemodynamic, urinary creatinine (UCr) and serum creatinine (SCr) data were collected in baseline (T0) and at the end of the follow-up period (T1). GFR was determined using the CKD-EPI formula, grouping patients into early stages (CKD1 and CKD2) and advanced stages (CKD3 to CKD5). Biomarkers were determined by the ELISA method and indexed to UCr in T1. In addition, α-GST was determinate in a control sample composed of 17 individuals without diagnosed kidney disease. Statistical analysis was performed by SPSS version 26 with a significant value of P < 0.05. RESULTS Comparing the means of SCr and GFR between T0 and T1 were observed a decrease of renal function during the follow-up period (P = 0.013 and P = .017, respectively). About 14.4% of patients were in an advanced stage of kidney disease in T1, compared with 4.8% in T0. ADPKD patients had increased values of α-GST in relation to the control group (P < 0.001), but no difference in the SCr was found. We also found a trend for higher levels of HP in advanced stages of CKD (P = 0.071). In ADPKD patients, direct correlations were observed between the variation of SCr during the follow-up with α-GST and Hp (r = 0.606, P = 0.048 and r = 0.738, P = 0.037, respectively). A trend to correlation was found between the levels of Hp and the Scr in T1 (r = P = 0.058). CONCLUSION The levels of α-GST and Hp are associated with renal damage and may be helpful in the early identification of the decline in renal function in ADPKD patients.

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Objective:Psoriasis is a chronic inflammatory disease associated with cardiovascular risk factors. Aquaporins(AQP) are a family of channels, which can transport: water, urea, hydrogen peroxide and/or glycerol, essential for redox signalling and metabolic skin homeostasis.Heparanase(HPSE) is an endo--glucuronidase that cleaves heparan sulfate chains of proteoglycans from the extracellular matrix(ECM), an essential step in the neovascularization and cell growth process.Vascular endothelial growth factor-C(VEGF-C) is an important growth factor regulating lymphatic neovascularization and pathological processes associated with sodium accumulation in ECM in the skin. The VEGF soluble receptors(s-flt1) are decoy receptors present in endothelial cells, hematopoietic stem cells, monocytes, macrophages, and platelets.This study aims to evaluate the impact of AQP3, AQP7 and HPSE genetic polymorphisms in biomarkers related to cardiovascular risk in patients with psoriasis and their clinical severity determined by Psoriasis Area and Severity Index(PASI).Design and method:Sixty-three psoriasis patients with a mean age of 52.50 ± 12.81years. Sociodemographic, hemodynamic and routine blood laboratory data were collected. Biochemical parameters were determined in serum according to standardized methods. Genetic polymorphisms were determined by endpoint analysis and s-flt1 and VEGF-C by ELISA. Patients were stratified based on PASI:< 5(G1) and > or equal to 5(G2). For statistical analysis, SPSS program was used with a p-value < 0.05.Results:Comparing the genotypic and allelic frequencies of the studied polymorphisms, no differences were found between G1 and G2.In general, patients with genotype AA of AQP3 had higher levels of s-flt1(p = 0.005) and VEGF-C(p = 0.048). For AQP7, genotype TT was associated with higher levels of mean platelet volume(p = 0.049) and lower levels of creatinine(Cr)(p = 0.023).Elevated levels of neutrophils(N)(p = 0.017) and potassium(p = 0.001) was observed in genotype AA of HPSE.For G1 was observed an increased level of: s-flt1(p = 0.022) and VEGF-C(p = 0.044) associated with genotype AA of AQP3; Cr in allele C of AQP7(p = 0.018), N in genotype CC of AQP7(p = 0.017). For G2 was observed: higher levels of leucocytes in allele C of AQP3(p = 0.016) and angiotensin-converting enzyme activity(ACE1) in allele T of AQP7(p = 0.033).Conclusions:AQP3, AQP7 and HPSE polymorphisms appear to modulate some biochemical parameters relevant to lymphangiogenesis associated with cardiovascular risk in a sample of patients with psoriasis.