Search

The purpose of this study was to perform a comparative biochemical analysis between conventional spectrophotometry and Raman spectroscopy, techniques used for diagnoses, on the urine of healthy (CT) and diabetic and hypertensive patients (DM&HBP). Urine from 40 subjects (20 in the CT group and 20 in the DM&HBP group) was examined in a dispersive Raman spectrometer (an 830 nm excitation and a 350 mW power). The mean Raman spectra between both groups showed a significant difference in peaks of glucose; exploratory analysis by principal component analysis (PCA) identified spectral differences between the groups, with higher peaks of glucose and proteins in the DM&HBP group. A partial least squares (PLS) regression model estimated by the Raman data indicated the concentrations of urea, creatinine, glucose, phosphate, and total protein; creatinine and glucose were the biomarkers that presented the best correlation coefficient (r) between the two techniques analyzed (r = 0.68 and r = 0.98, respectively), both with eight latent variables (LVs) and a root mean square error of cross-validation (RMSecv) of 3.6 and 5.1 mmol/L (41 and 92 mg/dL), respectively. Discriminant analysis (PLS-DA) using the entire Raman spectra was able to differentiate the samples of the groups in the study, with a higher accuracy (81.5%) compared to the linear discriminant analysis (LDA) models using the concentration values of the spectrometric analysis (60.0%) and the concentrations predicted by the PLS regression (69.8%). Results indicated that spectral models based on PLS applied to Raman spectra may be used to distinguish subjects with diabetes and blood hypertension from healthy ones in urinalysis aimed at population screening. [ABSTRACT FROM AUTHOR]

Overconsumption of fructose leads to metabolic syndrome as a result of hypertension, insulin resistance, and hyperlipidemia. In this study, the renal function of animals submitted to high fructose intake was analyzed from weaning to adulthood using in vivo and ex vivo methods, being compared with a normal control group. We investigated in ex vivo model of the role of the renin Angiotensin system (RAS) in the kidney. The use of perfused kidney from animals submitted to 8-week fructose treatment showed that high fructose intake caused metabolic and cardiovascular alterations that were consistent with other studies. Moreover, the isolated perfused kidneys obtained from rats under high fructose diet showed a 33% increase in renal perfusion pressure throughout the experimental period due to increased renal vascular resistance and a progressive fall in the glomerular filtration rate, which reached a maximum of 64% decrease. Analysis of RAS peptides in the high fructose group showed a threefold increase in the renal concentrations of angiotensin I (Ang I) and a twofold increase in angiotensin II (Ang II) levels, whereas no change in angiotensin 1-7 (Ang 1-7) was observed when compared with the control animals. We did not detect changes in angiotensin converting enzyme (ACE) activity in renal tissues, but there is a tendency to decrease. These observations suggest that there are alternative ways of producing Ang II in this model. Chymase the enzyme responsible for Ang II formation direct from Ang I was increased in renal tissues in the fructose group, confirming the alternative pathway for the formation of this peptide. Neprilysin (NEP) the Ang 1-7 forming showed a significant decrease in activity in the fructose vs. control group, and a tendency of reduction in ACE2 activity. Thus, these results suggest that the Ang 1-7 vasodilator peptide formation is impaired in this model contributing with the increase of blood pressure. In summary, rats fed high fructose affect renal RAS, which may contribute to several deleterious effects of fructose on the kidneys and consequently an increase in blood pressure. [ABSTRACT FROM AUTHOR]

The acute effects of angiotensin-1–7 [ANG-(1–7)] on the reabsorptive bicarbonate flow (JHCO-3 ) were evaluated using stationary microperfusion in vivo in the proximal tubules of spontaneously hypertensive rats (SHR) and their normotensive controls, WistarKyoto (WKY) rats, using a microelectrode sensitive to H. In WKY rats, the control JHCO-3 was 2.40 ± 0.10 nmol·cm-2 ·s-1 (n =120); losartan (10-7 M) or A779 (10-6 M, a specific Mas antagonist), alone or in combination with losartan, decreased the JHCO-3 . ANG-(1–7) had biphasic effects on JHCO-3 : at 10-9 M, it inhibited, and at 10-6 , it stimulated the flow. S3226 [10-6 M, a specific Na-H exchanger 3 (NHE3) antagonist] decreased JHCO-3 and changed the stimulatory effect of ANG-(1–7) to an inhibitory one but did not alter the inhibitory action of ANG-(1–7). In SHR, the control JHCO-3 was 2.04 0.13 nmol·cm-2 ·s-1 (n = 56), and A779 and/or losartan reduced the flow. ANG-(1–7) at 10-9 M increased JJHCO-3 , and ANG-(1–7) at 10-6 M reduced it. The effects of A779, losartan, and S3226 on the JHCO-3were similar to those found in WKY rats, which indicated that in SHR, the ANG-(1–7) action on the NHE3 was via Mas and ANG II type 1. The cytosolic calcium in the WKY or SHR rats was ~100 nM and was increased by ANG-(1–7) at 10-9 or 10-6 M. In hypertensive animals, a high plasma level of ANG-(1–7) inhibited NHE3 in the proximal tubule, which mitigated the hypertension caused by the high plasma level of ANG II. [ABSTRACT FROM AUTHOR]

Background: Accumulated evidence shows that the ACE-AngII-AT1 axis of the renin-angiotensin system (RAS) is markedly activated in chronic heart failure (CHF). Recent studies provide information that Angiotensin (Ang)-(1–7), a metabolite of AngII, counteracts the effects of AngII. However, this balance between AngII and Ang-(1–7) is still little understood in CHF. We investigated the effects of exercise training on circulating and skeletal muscle RAS in the ischemic model of CHF. Methods/Main Results: Male Wistar rats underwent left coronary artery ligation or a Sham operation. They were divided into four groups: 1) Sedentary Sham (Sham-S), 2) exercise-trained Sham (Sham-Ex), sedentary CHF (CHF-S), and exercise-trained CHF (CHF-Ex). Angiotensin concentrations and ACE and ACE2 activity in the circulation and skeletal muscle (soleus and plantaris) were quantified. Skeletal muscle ACE and ACE2 protein expression, and AT1, AT2, and Mas receptor gene expression were also evaluated. CHF reduced ACE2 serum activity. Exercise training restored ACE2 and reduced ACE activity in CHF. Exercise training reduced plasma AngII concentration in both Sham and CHF rats and increased the Ang-(1–7)/AngII ratio in CHF rats. CHF and exercise training did not change skeletal muscle ACE and ACE2 activity and protein expression. CHF increased AngII levels in both soleus and plantaris muscle, and exercise training normalized them. Exercise training increased Ang-(1–7) in the plantaris muscle of CHF rats. The AT1 receptor was only increased in the soleus muscle of CHF rats, and exercise training normalized it. Exercise training increased the expression of the Mas receptor in the soleus muscle of both exercise-trained groups, and normalized it in plantaris muscle. Conclusions: Exercise training causes a shift in RAS towards the Ang-(1–7)-Mas axis in skeletal muscle, which can be influenced by skeletal muscle metabolic characteristics. The changes in RAS circulation do not necessarily reflect the changes occurring in the RAS of skeletal muscle. [ABSTRACT FROM AUTHOR]

Giardia spp. is a flagellate protozoan that presents two evolution forms, cysts and trophozoites. Cysts are resistant to chlorine, the most employed disinfectant agent in the treatment of water. For this reason, new techniques for the disinfection of waters that contain this parasite are necessary. This work evaluated the efficiency of the disinfection by ozone and ultrasound individually and simultaneously upon wastewater. The data obtained showed that after application, ozone, ultrasound, and combined techniques induced a significant elimination ofGiardia spp.cysts. Furthermore, this effect was more accentuated when the two techniques were applied simultaneously. [ABSTRACT FROM AUTHOR]

Abstract: Diabetes mellitus is a frequent cause of kidney function damage with diabetic nephropathy being predominantly related to glomerular dysfunction. Diabetes is capable of interfering with distinct hormonal systems, as well as catecholamine metabolism. Since mesangial cells, the major constituent of renal glomerulus, constitute a potential site for catecholamine production, the present study was carried out to investigate alterations in catecholamine metabolism in cultured mesangial cells from the nonobese diabetic mouse, a well-established model for type I diabetes. We evaluated mesangial cells from normoglycemic and hyperglycemic nonobese diabetic mice, as well as cells from normoglycemic Swiss mice as control. Mesangial cells from normoglycemic mice presented similar profiles concerning all determinations. However, cells isolated from hyperglycemic animals presented increased dopamine and norepinephrine production/secretion. Among the studied mechanisms, we observed an upregulation of tyrosine hydroxylase expression accompanied by increased tetrahydrobiopterin consumption, the tyrosine hydroxylase enzymatic cofactor. However, this increase in synthetic pathways was followed by decreased monoamine oxidase activity, which corresponds to the major metabolic pathway of catecholamines in mesangial cells. In addition, whole kidney homogenates from diabetic animals also presented increased dopamine and norepinephrine levels when compared to normoglycemic animals. Thus, our results suggest that diabetes alters catecholamine production by interfering with both synthesizing and degrading enzymes, suggesting a possible role of catecholamine in the pathogenesis of acute and chronic renal complications of diabetes mellitus. [Copyright &y& Elsevier]

Background: The analysis of the complete blood count (CBC) of patients with community-acquired pneumonia (CAP) is an essential practice both for diagnosing the disease and for evaluating the patient's clinical evolution. It is proposed in the present study to analyze the hematological alterations resulting from photobiostimulation using near-infrared light-emitting diodes (LEDs) in patients with CAP. Methods: This was a clinical, prospective, blinded, and descriptive longitudinal study that involved 21 patients undergoing CAP treatment who were divided into two groups: LED, 11 patients who were treated with infrared LED and conventional treatment; and CON (control), 10 patients who received only conventional treatment (antibiotic therapy and physiotherapy). Physiotherapy was applied before LED irradiation in the LED group. The patients' CBCs were obtained before and after treatment, and erythrocyte counts, hemoglobin and hematocrit concentrations, and leukocyte and platelet counts were assessed. The phototherapy was performed with a vest with an array of 300 LEDs (940 nm) mounted on an area of 36 × 58 cm and positioned in the patient's anterior thoracic and abdominal regions. The total power was 6 W, with 15 min of irradiation time. The patients were treated daily for seven consecutive days. Statistical analyses of the intra- and intergroups of CBC data were done using Student's t -test and one-way ANOVA (analysis of variance), respectively, both at the significance level of α = 0.05. Results: There was a statistically significant recovery difference after treatment in the LED group compared with the CON group for erythrocytes, hemoglobin, leukocytes, segmented and band neutrophils, lymphocytes, and monocytes ( p  < 0.05). The greatest differences between the LED and CON groups were lymphocyte count reduction (60% vs. 16%), erythrocyte increase (86% vs. 35%), and leukocyte reduction (28% vs. 15%). Conclusions: The hematologic components of CAP patients recovered their normal values faster with conventional treatment associated with infrared LED therapy, thus indicating greater treatment efficiency when compared with the conventional therapy. This study was registered with the Brazilian Registry of Clinical Trials (ReBeC) under Universal Trial Number (UTN) U1111-1229-1296 (2019/06/05).

The acute effects of angiotensin-1-7 [ANG-(1-7)] on the reabsorptive bicarbonate flow (J[Formula: see text]) were evaluated using stationary microperfusion in vivo in the proximal tubules of spontaneously hypertensive rats (SHR) and their normotensive controls, Wistar-Kyoto (WKY) rats, using a microelectrode sensitive to H + In WKY rats, the control J[Formula: see text] was 2.40 ± 0.10 nmol·cm -2 ·s -1 ( n = 120); losartan (10 -7 M) or A779 (10 -6 M, a specific Mas antagonist), alone or in combination with losartan, decreased the J[Formula: see text] ANG-(1-7) had biphasic effects on J[Formula: see text]: at 10 -9 M, it inhibited, and at 10 -6 , it stimulated the flow. S3226 [10 -6 M, a specific Na + -H + exchanger 3 (NHE3) antagonist] decreased J[Formula: see text] and changed the stimulatory effect of ANG-(1-7) to an inhibitory one but did not alter the inhibitory action of ANG-(1-7). In SHR, the control J[Formula: see text] was 2.04 ± 0.13 nmol·cm -2 ·s -1 ( n = 56), and A779 and/or losartan reduced the flow. ANG-(1-7) at 10 -9 M increased J[Formula: see text], and ANG-(1-7) at 10 -6 M reduced it. The effects of A779, losartan, and S3226 on the J[Formula: see text] were similar to those found in WKY rats, which indicated that in SHR, the ANG-(1-7) action on the NHE3 was via Mas and ANG II type 1. The cytosolic calcium in the WKY or SHR rats was ~100 nM and was increased by ANG-(1-7) at 10 -9 or 10 -6 M. In hypertensive animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated the hypertension caused by the high plasma level of ANG II., (Copyright © 2017 the American Physiological Society.)

Chronic angiotensin II (ANG II) infusion for 1 or 2 wk leads to progressive hypertension and induces inward hypertrophic remodeling in preglomerular vessels, which is associated with increased renal vascular resistance (RVR) and decreased glomerular perfusion. Considering the ability of preglomerular vessels to exhibit adaptive responses, the present study was performed to evaluate glomerular perfusion and renal function after 6 wk of ANG II infusion. To address this study, male Wistar rats were submitted to sham surgery (control) or osmotic minipump insertion (ANG II 200 ng·kg(-1)·min(-1), 42 days). A group of animals was treated or cotreated with losartan (10 mg·kg(-1)·day(-1)), an AT1 receptor antagonist, between days 28 and 42 Chronic ANG II infusion increased systolic blood pressure to 185 ± 4 compared with 108 ± 2 mmHg in control rats. Concomitantly, ANG II-induced hypertension increased intrarenal ANG II level and consequently, preglomerular and glomerular injury. Under this condition, ANG II enhanced the total renal plasma flow (RPF), glomerular filtration rate (GFR), urine flow and induced pressure natriuresis. These changes were accompanied by lower RVR and enlargement of the lumen of interlobular arteries and afferent arterioles, consistent with impairment of renal autoregulatory capability and outward preglomerular remodeling. The glomerular injury culminated with podocyte effacement, albuminuria, tubulointerstitial macrophage infiltration and intrarenal extracellular matrix accumulation. Losartan attenuated most of the effects of ANG II. Our findings provide new information regarding the contribution of ANG II infusion over 2 wk to renal hemodynamics and function via the AT1 receptor., (Copyright © 2016 the American Physiological Society.)