Miracle-dz/UniFAR-FTUs huggingface dataset:
TIME‐COURSE REDUCTION OF RENAL FUNCTION IN RATS ON HIGH SODIUM INTAKE: ACUTE REVERSAL BY POTASSIUM CANRENOATE

1 Time course of renal alterations associated with long‐term (since weaning) administration of a high sodium (HS, 8% NaCl) diet was assessed in Sprague‐Dawley rats. Reversal by acute administration of the mineralocorticoid receptor antagonist, potassium canrenoate (40 mg/kg, i.p.) or the type 1 angiotensin II receptor antagonist, losartan (10 mg/kg, i.v.), was evaluated at the age of 5 months (i.e. after 21 weeks of HS feeding). 2 High sodium intake had no detectable effect on blood pressure; however, albuminuria was always higher in the HS than control group. Glomerular filtration rate, renal plasma flow and filtration fraction decreased significantly after 12 weeks of HS diet by approximately 50, 30 and 20%, respectively. Canrenoate was effective and markedly reversed the renal hypofiltration associated with HS feeding without change in systemic blood pressure. In contrast, losartan reduced blood pressure and it was devoid of a beneficial effect on renal function. 3 The present observations indicate that hypofiltration and hypoperfusion of the kidney occurred progressively and require a long period of exposure to a high sodium intake. Albuminuria, which increased before detectable changes in renal function, may represent an early marker of renal dysfunction. The beneficial effect of acute administration of potassium canrenoate favours the participation of aldosterone, at least partially, in the sustained deterioration of renal function after 21 weeks of high sodium feeding.
Análise histológica da viabilidade do transplante autólogo de hemi-ovário em retroperitônio de ratos

PURPOSE: To observe the indicative morphological signs of restorable ovarian function in retroperitoneal half-ovaries transplant autologous in Wistar rats. METHODS: 48 bilaterally oophorectomized female Wistar rats were used. Distributed by 6 groups, according to pos-operative timing, which was done after total removal, from the selftransplanted anatomical region (ovary and psoas muscle) The total ovaries were fixed in formalin during 24 hours, in 4o Celsius. The morphometric parameters useed in this work were the presence or absence of ovarian follicles, neovascularization, corpus luteum and granulation tissue. RESULTS: The results showed presence of ovarian follicles, corpus luteum and neovascularization in all groups. Observation of granulation tissue were more intense visualized in the early groups. CONCLUSION: The selftransplanted ovaries showed morphological signs of restorable of the ovarian function. Findings suggest that the implantation may allowed a higher survive of them in the retroperitoneum.
DEFECTIVE INTRACELLULAR Ca2+ HOMEOSTASIS CONTRIBUTES TO MYOCYTE DYSFUNCTION DURING VENTRICULAR REMODELLING INDUCED BY CHRONIC VOLUME OVERLOAD IN RATS

1 Previous studies have demonstrated progressive ventricular hypertrophy, dilatation and contractile depression in response to chronic volume overload. Whether this decompensation was related to intrinsic myocyte dysfunction was not clear. The present study evaluated ventricular myocyte function at critical times during the progression of ventricular remodelling induced by volume overload. 2 Chronic volume overload was induced with an infrarenal aortocaval fistula in rats. Myocyte contraction and intracellular Ca2+ concentrations ([Ca2+]i) were evaluated using a fura‐2 fluorescence and edge detection system. Protein levels of sarcoplasmic reticulum (SR) Ca2+ transporters were determined by western blots. Progressive ventricular dilatation developed following creation of the fistula. Although myocyte function in 5 week fistula rats was comparable to that of the control group, myocytes from rats 10 weeks post‐fistula demonstrated significant depression of cell shortening and peak [Ca2+]i. Application of isoproterenol (0.1 µmol/L) was not able to compensate for the functional deficiency in myocytes from 10 week fistula rats. Caffeine (10 mmol/L) induced SR Ca2+ release, as well as protein expression of SR Ca2+‐ATPase, and ryanodine receptors were reduced in myocytes obtained from the same group of 10 week fistula rats. 3 These data indicate that the transition to heart failure secondary to chronic volume overload is related to depressed myocyte contractility secondary to altered intracellular Ca2+ homeostasis.
SUBENDOCARDIAL VIABILITY RATIO ESTIMATED BY ARTERIAL TONOMETRY: A CRITICAL EVALUATION IN ELDERLY HYPERTENSIVE PATIENTS WITH INCREASED AORTIC STIFFNESS

1 Increased aortic stiffness predisposes to myocardial ischaemia by increasing the systolic tension–time index and by decreasing aortic pressure throughout diastole. The tonometric subendocardial viability ratio (SEVR) is a non‐invasive estimate of myocardial perfusion relative to cardiac workload. The hypothesis that SEVR is impaired in elderly hypertensives with high aortic pulse pressure (PP) was tested in the present study. 2 The SEVR was calculated by radial applanation tonometry in 203 subjects. In addition, diastolic time (DT), systolic time (ST) and mean diastolic and systolic aortic pressures (Pd and Ps, respectively) were calculated. First, 60 subjects matched for age and gender were analysed (20 controls, 20 hypertensives with pulse pressure (PP) ≤ 60 mmHg, 20 hypertensives with PP > 60 mmHg; mean (±SD) age 64 ± 9 years; 24 women, 36 men). The remaining 143 subjects, aged 53 ± 10 years, were analysed subsequently. 3 The SEVR was similar in the three elderly groups (1.39 ± 0.34, 1.39 ± 0.28 and 1.35 ± 0.25, in controls and hypertensive patients with PP ≤ 60 and > 60 mmHg, respectively). The SEVR was positively related to DT/ST (r2 = 0.89) and to DT (r2 = 0.73) and was negatively related to heart rate (r2 = 0.56; P < 0.001 each). However, SEVR was not related to ST, PP, mean Pd or mean Ps. At a given DT/ST, SEVR tended to be lower in hypertensives with PP > 60 mmHg than in hypertensives with normal PP. The positive linear relationship between SEVR and DT/ST was confirmed in the remaining 143 subjects (r2 = 0.90), with no influence of aortic pressure. 4 The tonometric SEVR was not impaired in elderly hypertensive patients with increased aortic stiffness. In resting elderly and middle‐aged individuals, the tonometric SEVR was mainly related to DT/ST ratio, not to aortic pressure.
EVIDENCE THAT INHIBITION OF SPINAL NITRIC OXIDE PRODUCTION CONTRIBUTES TO THE ANTINOCICEPTIVE EFFECTS OF EMULSIFIED ISOFLURANE ON FORMALIN‐INDUCED PAIN IN RATS

1 The aim of the present study was to investigate the contribution of spinal nitric oxide (NO) to the antinociceptive effects of emulsified isofluane in rats. 2 The formalin test was used to assess nociceptive responses. Immunocytochemistry and histochemistry were performed to determine the effects of emulsified isoflurane on formalin‐induced changes in Fos‐like immunoreactive (Fos‐LI)‐ and nicotinamide adenine dinucleotide phosphatediaphorase (NADPH‐d)‐positive neurons, respectively. 3 The results showed that emulsified isofluane, administered intraperitoneally, significantly decreased the formalin‐induced paw licking time and that this was attenuated by pretreatment with intrathecal injection of the NO precursor l‐arginine. Furthermore, Fos‐LI‐ and NADPH‐d‐positive neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were Fos‐LI/NADPH‐d double‐labelled neurons. 4 Administration of emulsified isofluane significantly decreased Fos‐LI‐ and NADPH‐d‐positive, as well as Fos‐LI/NADPH‐d double‐labelled, neurons. Finally, emulsified isofluane produced a significant reduction of NOS activity and a decrease of NO production in the spinal cord of formalin‐treated rats. 5 In conclusion, the results suggest that inhibition of spinal NO production contributes to the antinociceptive effects of emulsified isofluane on formalin‐induced pain in rats.
Mortality and Morbidity of Acute Cerebral Infarction Related to Temperature and Basal Analytic Parameters

We evaluated the mortality and morbidity of acute cerebral infarction as related to modifiable factors: glucose level, temperature, hematocrit, hemoglobin and platelet count. We studied 177 patients with acute cerebral infarction in the territory of the middle cerebral artery, admitted within 24 h of stroke onset. Blood was drawn on admission and temperature was recorded every 2 h, selecting the highest during the 1st day. Patient follow-up lasted 6 months. Barthel Index and Neurological Score of patients were evaluated at admission and on days 1, 4, 7, 14, 21 and at 3 and 6 months. A Glasgow Scale was administered at 6 months. Forty-five of 177 patients died within this period. These patients reached a temperature of 38.3 ± 0.76 °C, while temperature in those surviving was 36.9 ± 0.46°C ( p
EFFECT OF CHRONIC ASPIRIN ADMINISTRATION ON AN EXPERIMENTAL MODEL OF METABOLIC SYNDROME

1 The aim of the present study was to examine the effect of chronic administration of aspirin on metabolic and cardiovascular parameters in fructose‐fed rats (FFR), an experimental model of metabolic syndrome. 2 Chronic treatment of FFR with aspirin (10 mg/kg per day for 6 weeks) partially reversed the increment in systolic blood pressure. In addition, chronic aspirin treatment normalized relative heart weight and vascular remodelling of renal and carotid arteries, measured as lumen diameter : medial thickness ratio. 3 Furthermore, chronic aspirin administration completely reversed glucose intolerance and decreased the oxidative status that characterizes the FFR model, as indicated by decreased plasma levels of thiobarbituric acid‐reactive substances and aortic NAD(P)H oxidase activity. 4 Prevention of oxidative stress and vascular remodelling in FFR may contribute to the protective actions attributed to aspirin in the treatment of metabolic syndrome.
Risk factors for local recurrence in patients with pTa/pT1 urinary bladder cancer

Objective. This study evaluated risk factors for local tumour recurrence, defined as recurrence at the same location in the bladder within 18 months after primary resection in patients with newly diagnosed pTa or pT1 bladder cancer. Patients and methods. The study included 472 patients with newly diagnosed pTa/T1 bladder cancer between 1992 and 2001. The patients were followed prospectively in accordance with a control programme and possible risk factors for tumour recurrence were registered. Results. Local tumour recurrence was observed in 164 (35%) patients, another 117 (25%) patients had recurrence at other locations in the bladder (non-local recurrence) and 191 (40%) had no recurrence at all. Tumour size and multiple tumours were significantly associated with a higher risk for developing local recurrence as opposed to non-local recurrence. Tumour category was of borderline statistical significance. Gender and tumour grade were not found to be risk factors for developing local recurrence. Conclusion. Tumour size and multiplicity are risk factors for development of recurrence at the same location in the bladder as the primary tumour. Local tumour recurrence may be a result of non-radical primary transurethral resection. One may consider recommending standard re-resection within 6–8 weeks in patients with tumours >3 cm or those with multiple primary tumours.
METHODS FOR STUDYING THE PHYSIOLOGY OF KIDNEY OXYGENATION

1 An improved understanding of the regulation of kidney oxygenation has the potential to advance preventative, diagnostic and therapeutic strategies for kidney disease. Here, we review the strengths and limitations of available and emerging methods for studying kidney oxygen status. 2 To fully characterize kidney oxygen handling, we must quantify multiple parameters, including renal oxygen delivery (DO2) and consumption (VO2), as well as oxygen tension (Po2). Ideally, these parameters should be quantified both at the whole‐organ level and within specific vascular, tubular and interstitial compartments. 3 Much of our current knowledge of kidney oxygen physiology comes from established techniques that allow measurement of global kidney DO2 and VO2, or local tissue Po2. When used in tandem, these techniques can help us understand oxygen mass balance in the kidney. Po2 can be resolved to specific tissue compartments in the superficial cortex, but not deep below the kidney surface. We have limited ability to measure local kidney tissue DO2 and VO2. 4 Mathematical modelling has the potential to provide new insights into the physiology of kidney oxygenation, but is limited by the quality of the information such models are based on. 5 Various imaging techniques and other emerging technologies have the potential to allow Po2 mapping throughout the kidney and/or spatial resolution of Po2 in specific renal tissues, even in humans. All currently available methods have serious limitations, but with further refinement should provide a pathway through which data obtained from experimental animal models can be related to humans in the clinical setting.
Clinical usefulness of ambulatory urodynamics in the diagnosis and treatment of lower urinary tract dysfunction

Objective. Ambulatory urodynamics is reported to be useful for the detection of detrusor overactivity. However, the procedure is time-consuming, technically challenging and expensive. Its clinical usefulness for the detection and treatment of bladder dysfunction has not been studied in detail. Material and methods. Twenty-five patients (17 men, eight women, median age 59 years) with lower urinary tract symptoms underwent ambulatory urodynamic examination. Results. In six out of 25 patients (24%), ambulatory urodynamics was not evaluable. Where the procedure was technically feasible, diagnosis was possible in 72%. Treatment was modified in 63%, leading to satisfactory results in 42% of the patients. Conclusions. Ambulatory urodynamics is the most sensitive tool for the detection or exclusion of detrusor overactivity. Therefore, the method is valuable when all other diagnostic means have failed to detect the underlying lower urinary tract dysfunction. In these cases, treatment decisions can safely be based on the results of ambulatory urodynamics.
Effects of Cardiopulmonary Bypass on Renal Perfusion, Filtration, and Oxygenation in Patients Undergoing Cardiac Surgery

Background: Acute kidney injury is a common complication after cardiac surgery with cardiopulmonary bypass. The authors evaluated the effects of normothermic cardiopulmonary bypass on renal blood flow, glomerular filtration rate, renal oxygen consumption, and renal oxygen supply/demand relationship, i.e., renal oxygenation (primary outcome) in patients undergoing cardiac surgery. Methods: Eighteen patients with a normal preoperative serum creatinine undergoing cardiac surgery procedures with normothermic cardiopulmonary bypass (2.5 l · min−1 · m−2) were included after informed consent. Systemic and renal hemodynamic variables were measured by pulmonary artery and renal vein catheters before, during, and after cardiopulmonary bypass. Arterial and renal vein blood samples were taken for measurements of renal oxygen delivery and consumption. Renal oxygenation was estimated from the renal oxygen extraction. Urinary N-acetyl-&bgr;-D-glucosaminidase was measured before, during, and after cardiopulmonary bypass. Results: Cardiopulmonary bypass induced a renal vasoconstriction and redistribution of blood flow away from the kidneys, which in combination with hemodilution decreased renal oxygen delivery by 20%, while glomerular filtration rate and renal oxygen consumption were unchanged. Thus, renal oxygen extraction increased by 39 to 45%, indicating a renal oxygen supply/demand mismatch during cardiopulmonary bypass. After weaning from cardiopulmonary bypass, renal oxygenation was further impaired due to hemodilution and an increase in renal oxygen consumption, accompanied by a seven-fold increase in the urinary N-acetyl-&bgr;-D-glucosaminidase/creatinine ratio. Conclusions: Cardiopulmonary bypass impairs renal oxygenation due to renal vasoconstriction and hemodilution during and after cardiopulmonary bypass, accompanied by increased release of a tubular injury marker.
Pediatric Immune Dysfunction and Health Risks Following Early-Life Immune Insult

Chronic pediatric diseases arising from early-life immune insult and postnatal immune dysfunction are among the most prevalent health challenges for children. Diseases such as childhood asthma and allergies, chronic otitis media, type 1 diabetes, childhood leukemia and pediatric celiac disease all feature dysfunctional immune responses and/or inappropriately skewed immune capacities. Additionally, these disorders have been increasing in incidence in recent years with previously identified risk factors unable to fully account for the change. Still, some treatment approaches target the initial health complaint and its symptoms without fully addressing either the underlying immune dysfunction of the initial disease or the likelihood for additional associated health risks in later life. Therefore, it is useful to understand both the nature of the immune dysfunction as well as the reported associated health risks. This review characterizes those pediatric immune dysfunctions produced by well-studied immunotoxicants and provides a matrix of those health risks that appear to be linked together via the underlying pediatric immune dysfunction. This information could lead to: 1) improved identification and treatment of underlying immune dysfunction, 2) long-term approaches to health management, and 3) improved prenatal and neonatal prevention strategies to avoid environmentally-induced immune insult and developmental immunotoxicity.
Do changes in the coupling between respiratory and sympathetic activities contribute to neurogenic hypertension?

1 It is well known that respiration markedly modulates the sympathetic nervous system. Interactions between pontine and medullary neurons involved in the control of sympathetic and respiratory functions are the main mechanism underlying the respiratory related oscillations in sympathetic nerve activity. 2 Recently, in rats treated with chronic intermittent hypoxia, we demonstrated that alterations in respiratory pattern may drive increased sympathetic outflow and hence the development of systemic hypertension. These experiments, performed in the in situ working heart–brain stem preparation, raise the possibility that enhanced central coupling between respiratory and sympathetic activities could be a potential mechanism underpinning the development and/or the maintenance of neurogenic hypertension. 3 In the present review, we discuss the neural basis of the enhanced entrainment between respiratory and sympathetic neurons in the brain stem that can be induced by chronic intermittent hypoxia and the possible implications of these mechanisms in the genesis of sympathetic overactivity and, consequently, hypertension.
Carotid body potentiation induced by intermittent hypoxia: Implications for cardiorespiratory changes induced by sleep apnoea

1 The most usual form of chronic hypoxia in humans is the intermittent hypoxia resulting from obstructive sleep apnoea (OSA). The OSA syndrome is a highly prevalent sleep breathing disorder that is considered an independent risk factor for hypertension and cardiovascular diseases. Endothelial dysfunction, oxidative stress, inflammation and sympathetic activation have been proposed as potential mechanisms involved in the onset of the hypertension. However, evidence for a unique pathogenic mechanism has been difficult to establish in OSA patients because of concomitant comorbidities. Thus, animal models have been developed to study the pathological consequences of exposure to chronic intermittent hypoxia (CIH). 2 Because OSA patients and animals exposed to CIH show augmented ventilatory, sympathetic and cardiovascular responses to acute hypoxia, it has been proposed that enhanced carotid body responsiveness to hypoxia is involved in the autonomic changes induced by OSA and in the development of the hypertension. Recently, this proposal has received further support from recordings of carotid body chemosensory neural discharges in situ and in vitro showing that exposure of animals to CIH increases basal carotid body chemosensory discharges and enhances the chemosensory response to hypoxia. 3 In the present brief review, we discuss the evidence supporting an important role for the carotid body in the progression of cardiorespiratory changes induced by OSA and the contribution of oxidative stress, endothelin‐1 and pro‐inflammatory molecules in the potentiation of the carotid body chemosensory function induced by CIH.
Dissecting the mechanism of Ca2+‐triggered membrane fusion: Probing protein function using thiol reactivity

1. Ca2+‐triggered membrane fusion involves the coordinated actions of both lipids and proteins, but the specific mechanisms remain poorly understood. The urchin cortical vesicle model is a stage‐specific native preparation fully enabling the directly coupled functional–molecular analyses necessary to identify critical components of fast triggered membrane fusion.
(Pro)renin receptor contributes to diabetic nephropathy by enhancing renal inflammation

1. (Pro)renin receptor (PRR) binding to renin or prorenin mediates angiotensin (Ang) II‐dependent and ‐independent effects. Expression of the PRR is increased in kidneys of diabetic rats, but its role in diabetic nephropathy is unknown. In the present study, we investigated the contribution of the PRR to the development of diabetic nephropathy through enhancement of renal production of tumour necrosis factor (TNF)‐α and interleukin (IL)‐1β.
Linear Mixed Models in Practice: A SAS-Oriented Approach

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Anionic peroxidase production by Arnebia euchroma callus

Arnebia euchroma callus, obtained from the root cell culture of an Iranian native specimen, has gained a doubling time of 63 H after regular subculturing on Linsmaier–Skoog (LS) medium containing sugar (50 g/L), 2,4‐dichlorophenoxyacetic acid (10−6 M), and kinetin (10−5 M) under darkness at 25°C. Despite the observed somaclonal variations, peroxidase production by the A. euchroma calli has been stable over 4 years under the aforementioned conditions. Isoelectric focusing experiments revealed that the partially purified A. euchroma peroxidases (AePoxs) are mainly anionic with pI values of about 5.5 and 6.6. AePox reaches its optimal activity at 55°C and pH 7.5. Results of the various kinetic studies suggest that AePox belongs to the type III plant peroxidases with no activity for the oxidation of 3‐indoleacetic acid, but seems to play a role in the lignin biosynthesis and H2O2 regulation during the proliferation of the A. euchroma cells on LS medium. Comparing the biochemical properties of AePox with horseradish peroxidase and in view of the ease of solid cell culture, the A. euchroma callus could be considered as a source of plant peroxidase for some biotechnological applications.