bluuebunny/crossref_metadata_2025 huggingface dataset:
Protein Metabolism in Acute Renal Failure
Authors: Druml Wilfred
Published: April 2003

The hallmark of metabolic alterations in acute renal failure (ARF) is accelerated protein breakdown which, unfortunately, cannot be suppressed effectively by provision of exogenous nutritional substrates. Causes of excessive protein catabolism are manifold and present a combination of unspecific mechanisms induced by the acute disease process and underlying illness or associated complications, effects induced by the acute loss of renal function and, finally, the type and intensity of renal replacement therapy. Specific uremic toxic effects, insulin resistance, hormonal derangements, metabolic acidosis, circulating proteases, inflammatory mediators, and dialysis-related losses of nutritional substrates all contribute to the activation of protein degradation. Metabolism in ARF is also affected by an impairment of the multiple metabolic and endocrine functions of the kidney. Various amino acids are synthesized or interconverted by the kidneys and may become conditionally indispensable. The kidney is also an important organ in the degradation of peptides, such as peptide hormones. As a consequence of these metabolic aberrations, imbalances in amino acid pools in plasma and in the intracellular compartment occur in ARF and elimination and utilization of infused amino acids is altered. Protein or amino acids requirements are influenced more by the nature of the illness causing ARF, by the extent of hypercatabolism, by associated complications, and by the type and frequency of renal replacement therapy than by renal dysfunction per se. In noncatabolic patients, an intake of 1 g/kg body weight per day may be sufficient, while in critically ill hypercatabolic patients undergoing continuous renal replacement therapy, 1.5 g amino acids/kg body weight per day should be provided to minimize nitrogen losses. For the future, we need to identify safe methods to control the accelerated catabolism in order to improve the efficiency of nutritional interventions in patients with ARF.
Effects of a Supplemented Very Low Protein Diet in Predialysis Patients on the Serum Albumin Level, Proteinuria, and Subsequent Survival on Dialysis
Authors: Walser Mackenzie
Published: April 2003

A very low protein diet (0.3 g/kg ideal body weight) supplemented with essential amino acids (or ketoanalogues) is seldom employed at present in chronic renal failure for fear of inducing protein deficiency, especially in patients who also have the nephrotic syndrome. Nevertheless, we have used this dietary regimen in predialysis patients for a number of years. We have shown that when these patients reach the end stage, they rarely exhibit hypoalbuminemia, in contrast to the reported 25–50% hypoalbuminemia at the onset of dialysis nationwide. Furthermore, their survival for the first 2 years on dialysis is much improved, in comparison with the national experience, adjusted for age, sex, and cause of renal disease. When nephrotic patients are given this regimen, they exhibit some improvement in parameters of the nephrotic state, but nevertheless progress to dialysis, provided their initial glomerular filtration rate (GFR) is <30 ml/min. However, if their initial GFR is >30 ml/min, they may show gradual but complete remission of the nephrotic syndrome, even when the underlying disease is diabetic nephropathy or focal segmental glomerulosclerosis. We conclude that this dietary regimen is not only safe in patients with renal failure, with or without the nephrotic syndrome, but may be of substantial benefit. The mechanism remains to be explained.
Mechanisms of Insulin-Like Growth Factor-I-Induced Accelerated Recovery in Experimental Ischemic Acute Renal Failure
Authors: Hirschberg Raimund , Ding Hu
Published: April 2003

Exogenous administration of recombinant human insulin-like growth factor I (rhIGF-I) to normal rats or humans increases renal blood flow and glomerular filtration rate (GFR). In rats with ischemic acute renal failure (iARF) the peptide accelerates the recovery of renal function and tubular integrity. These latter effects may be caused by renal hemodynamic actions of IGF-I or may result from direct actions of IGF-I on injured tubular cells. To examine this hypothesis, in vivo studies were performed in rats with iARF and in vitro experiments were conducted using a model of anoxia/reoxygenation injury in primary cultures of rat proximal tubular cells. In rats with iARF, IGF-I ameliorates the rise in serum creatinine, improves GFR, increases the rate of bromodeoxyuridine (BrdU) incorporation and the mitosis score, and reduces the number of apoptotic bodies. In acutely injured proximal tubular cells, IGF-I receptor mRNA levels decrease, but the remaining receptors are functional as indicated by ligand-induced phosphorylation of the IGF-I receptor β-subunit. In anoxia/reoxygenation-injured cells, exogenous rhIGF-I improves ATP repletion, increases 3H-thymidine and BrdU incorporation and reduces the incidence of apoptosis as determined by the TUNEL method. We conclude that rhIGF-I accelerates the recovery of renal function in rats with iARF probably through hemodynamic effects, but in addition through direct metabolic, mitogenic and antiapoptotic actions on injured tubules.
High-Protein Diets Augment Albuminuria in Rats with Heymann Nephritis by Angiotensin II- Dependent and -Independent Mechanisms
Authors: Kaysen George A. , Webster Sarah , Al-Bander Hamoudi , Jones Jr. Hardin , Hutchison Florence N.
Published: April 2003

Urinary albumin excretion (UalbV) increases following dietary protein augmentation (DPA) in nephrotic humans and rats. Angiotensin-converting enzyme inhibitors (ACEI) blunt, but do not entirely prevent, increased UalbV at doses that reduce blood pressure and entirely block the pressor effect of exogenously administered angiotensin I (Ang-I), suggesting that angiotensin II (Ang-II) might not mediate the effect of DPA on UalbV. We determined the effect of losartan (Los), a specific Ang-II receptor antagonist, and compared its effect to that of enalapril (En), an ACEI, on DPA-induced increase in UalbV in rats with passive Heymann nephritis (HN). When Los was administered to HN rats for 48 h prior to DPA from 8.5 to 40% casein. UalbV increased in an identical fashion in treated and untreated rats, even though Los caused hypotension and prevented the pressor effect of infused Ang-II. Only on day 6 after DPA did UalbV decrease. We then measured the effect of duration of pretreatment with Los on Ang-II binding to isolated glomeruli. Maximal inhibition of Ang-II binding required treatment with Los for 6 days. We then pretreated HN rats with either En or Los for 6 days prior to DPA. In contrast to administration of Los for 2 days prior to DPA, pretreatment with either Los or En for 6 days entirely prevented any increase in UalbV. We then increased dietary NaCl from 0.2% to 2% (HS) to determine whether En or Los would modulate UalbV after DPA when Ang-II activity was suppressed. En reduced the DPA-mediated increase in UalbV regardless of dietary NaCl, while Los was effective only in when dietary NaCl was reduced (0.2%), suggesting that under these conditions ACEI reduces UalbV by a mechanism that is independent of inhibition of Ang-II and that high protein diets augment UalbV by both Ang-II-independent and Ang-II-dependent mechanisms.
Nutritional Considerations in the Treatment of Patients with Chronic Uremia
Authors: Mitch William E. , Maroni Bradley J.
Published: April 2003

Low-protein diets ameliorate uremic symptoms and some of its metabolic complications. These diets can be used successfully to treat patients with chronic renal failure (CRF) because they are able to activate normal compensatory responses when protein intake is restricted and their protein and energy requirements are similar to healthy subjects. However, there has been concern that dietary therapy compromises the nutritional status of CRF patients and that initiating dialysis would be preferable to this type of therapy. Kopple and co-workers hade identified the requirements of CRF patients for protein and calories and available evidence indicates that when properly implemented, low-protein diets are safe and can maintain lean body mass even during long-term therapy. Based on the information published by Kopple and co-workers, the strategies for treating CRF patients should include careful analysis of the diet and the nutritional status of the patient.
Salt Intake and Renal Outcome in Patients with Progressive Renal Disease
Authors: Cianciaruso Bruno , Bellizzi Vincenzo , Minutolo Roberto , Tavera Antonello , Capuano Alfredo , Conte Giuseppe , De Nicola Luca
Published: April 2003

Experimental studies suggest that salt intake plays a critical role in the progressive glomerular filtration rate (GFR) loss of established renal disease; however, this issue has never been addressed in humans. To this aim, we have retrospectively analyzed the clinical data of patients with chronic renal failure (CRF), in whom a low-protein diet was prescribed, over a period of about 3 years. On the basis of the daily urinary sodium output, the patients were divided into two groups: a group of patients constantly ingesting >200 mEq NaCl/day (high sodium intake, HSD, n = 30) and a group in which salt intake was <100 mEq/day (low sodium intake, LSD, n = 27). Patients taking diuretics or ACE inhibitors were excluded. At baseline, the LSD group, as compared to the HSD group, was characterized by significantly lower creatinine clearance (24 ± 2 vs. 28 ± 2 ml/min) and higher proteinuria (2.9 ± 0.3 vs. 1.5 ± 0.2 g/day). Despite the presence of these risk factors for progression, and a similar control of blood pressure (the average of the mean arterial pressure during follow-up was 111 ± 2 mm Hg in LSD and 107 ± 2 mm Hg in HSD), the LSD patients showed a better renal outcome: in this group, as compared to HSD, the GFR decline was lower (0.25 ± 0.07 vs. 0.51 ± 0.09 ml/min/month, p < 0.05), and proteinuria did not change while it markedly increased in HSD. During follow-up, LSD patients also ingested a significantly lower amount of protein. This study therefore suggests that efficacious salt restriction in CRF patients improves the outcome of renal disease independent from its antihypertensive effects.
Hypophosphatemia in Acute-Phase Response Syndrome Patients
Authors: Ferreira da Cunha Daniel , Modesto dos Santos Vitorino , Pontes Monterio Jacqueline , Freire de Carvalho da Cunha Selma
Published: April 2003

Background: Hypophosphatemia is common in acutely ill patients and possibly may occur in the acute-phase response syndrome (APR), secondary to hyperglycemia and shifts of extracellular phosphorus into cells. Aim: To compare the frequency of hypophosphatemia in patients with or without APR. Methods: All plasma phosphorus results (n = 822) corresponding to a 6-month period were searched using an university hospital mainframe. Relevant laboratory and clinical details were also registered. All cases of alcohol withdrawal, diabetic ketoacidosis, parenteral nutrition, and chronic respiratory alkalosis and patients receiving antacids or intravenous dextrose (5%) in water at a rate higher than 50 g glucose/day were excluded. APR was defined on the basis of severe trauma or infection and at least two of the following: fever, leukopenia (WBC < 5,000/mm3), or leukocytosis (WBC >9,000/mm3). Hypophosphatemia was defined as a serum phosphorus concentration <2.0 mg/dl. Results: A total of 227 patients were studied. Thirty-five (15.4%) patients fulfilled the criteria for APR. Hypophosphatemia was observed in 11.4% of the APR-positive patients, in contrast to 0.5% in the APR-negative group. Hyperglycemia was more common in APR-positive patients (60.0 vs. 36.8%). Conclusion: Our results suggest that hypophosphatemia may be attributed to increased serum glucose levels secondary to tissue injury and infection in APR-positive patients.
Action of Angiotensin Receptor Subtypes on the Renal Tubules and Vasculature: Implications for Volume Homeostasis and Atherosclerosis
Authors: Zitnay Christopher , Siragy Helmy
Published: April 2003

Angiotensin-II (ANG-II) is a potent endocrine and paracrine hormone that functions in humans through two distinct G-protein-coupled transmembrane receptor subtypes (AT-1 and AT-2). ANG-II is found in nearly all tissues of the body including the brain, heart, kidneys, gonads, and gastrointestinal tract. Just as it is found in nearly every organ system of the body, so is it involved in an array of physiologic processes from fetal development to blood pressure control. ANG-II regulates blood pressure by controlling sodium reabsorption in the proximal tubule, altering the glomerular filtration rate and renal blood flow, and by modifying the production and release of aldosterone in the adrenal gland. Additionally, ANG-II is involved in several pathologic processes including the development of hypertension, cardiomyopathy, atherosclerosis, and diabetic nephropathy. It is able to exert influences in these widely varying processes by working together with multiple different second messenger systems including the MAP kinase pathway, nitric oxide production, and phospholipase C and D, and several arachidonic acid metabolites. This paper is a review of the current knowledge of ANG-II and its receptors in health and disease.
The Renin-Angiotensin System in Diabetic Nephropathy: The Endothelial Connection
Authors: Rabelink Ton , Bakris George
Published: April 2003

In recent years endothelial function has been forwarded a modulator in the pathogenesis of diabetic nephropathy. This review summarizes how an imbalance between endothelium-derived reactive nitrogen species and reactive oxygen species as well as increased expression of the endothelium-derived peptide endothelin-1 may contribute to loss of renal function in diabetes. In addition, the potentially beneficial effects of blockade of the renin-angiotensin system on this endothelial dysbalance is discussed.
Interaction of the Renal Amylin and Renin-Angiotensin Systems in Animal Models of Diabetes and Hypertension
Authors: Wookey P.J. , Cao Z. , Cooper M.E.
Published: April 2003

The range of known actions of amylin are reviewed together with the proposal that an important role for amylin may be the hormonal integration of diverse physiological systems activated with feeding. Major targets for the action of amylin are found within the kidney. Components of the amylin system (AS) have been shown to influence the activity of components of the renin-angiotensin system (RAS), and vice versa, in normal, hypertensive and diabetic models. For instance, amylin injected into humans and rats elicits a rapid rise in plasma renin activity. Furthermore, in two models of hypertension (the spontaneously hypertensive rat (SHR) and the model with subtotal nephrectomy (STNx)), the density of amylin-binding sites in the renal cortex associated with the proximal tubules, was associated with elevation of blood pressure. In normotensive controls and in the STNx model, but not in the SHR model, treatment with angiotensin-converting enzyme (ACE) inhibitors reduced blood pressure and the density of amylin binding in the renal cortex. In Sprague-Dawley rats, angiotensin II (Ang II) infusion was associated with increased density of amylin-binding sites as well as elevated blood pressure. Thus, there appears to be a direct relationship between the activity of Ang II and the binding sites for amylin in the renal cortex. From these studies it has been postulated that the activation of the AS in the kidney may play a role in the genesis and/or development of hypertension in certain contexts. The transient expression of amylin mRNA has been detected perinatally, using in situ hybridization, in the subnephrogenic zone of the metanephros and is associated with proximal tubules of the developing nephron. These cells situated close to the glomeruli, represent a subset of brush border epithelial cells. Amylin immunoreactivity (IR) is also found in these cells and colocalizes with angiotensinogen IR. Thus a second important role for amylin is described in which it plays a role as a growth factor in the developing kidney and in renal regrowth in the adult kidney. In a model of IDDM (streptozotocin diabetes), amylin and angiotensinogen IR are both restricted to a subset of brush border epithelial cells close to glomeruli which, in the developing kidney, expressed amylin mRNA. Thus in this IDDM model, we hypothesize that amylin mRNA transcription which is normally downregulated in the adult, is upregulated in this subset of these brush border epithelial cells, and that it stimulates the activity of a local RAS by an intracellular mechanism, leading to the biosynthesis of Ang II. It remains to be determined that if amylin is playing a role in stimulating local Ang II production at these sites, this provides a mechanism for activation of TGF-β, ultimately leading to interstitial fibrosis.
A Potential Role for Angiotensin II-Induced Vascular Endothelial Growth Factor Expression in the Pathogenesis of Diabetic Nephropathy?
Authors: Williams Bryan
Published: April 2003

Diabetic nephropathy often co-exists with other manifestations of microangiopathy, in particular retinopathy. Recent clinical evidence suggests that inhibition of the renin-angiotensin system in humans can delay the development and/or progression of diabetic nephropathy and perhaps also retinopathy. The benefits of this therapeutic strategy may in part be explained by inhibition of the nonhaemodynamic actions of angiotensin II (Ang II). The recognized nonhaemodynamic actions of Ang II include the augmented release of many growth factors. Ang II can stimulate the release of vascular endothelial growth factor (VEGF) from human vascular tissues. VEGF is a family of potent cytokines which act to induce angiogenesis and markedly increase microvascular permeability. VEGF is abundantly expressed in the renal glomerulus, specifically within the podocyte, where its function is unknown. VEGF is also expressed in the retina and increased retinal VEGF expression occurs in diabetes and has been implicated in the pathogenesis of diabetic retinopathy. This review considers the potential clinical significance of Ang II-induced VEGF expression, if any, in the pathogenesis of diabetic nephropathy and retinopathy.
Pathophysiology of Heart Failure
Authors: Chiariello Massimo , Perrone-Filardi Pasquale
Published: April 2003

Heart failure is a leading cause of mortality and morbidity in Western countries. Common etiology is mostly represented by ischemic and hypertensive heart disease. Clinically, heart failure can be defined as an impaired cardiac performance, unable to meet the energy requirements of the periphery. Pathophysiologically, the clinical onset of heart failure symptoms already represents an advanced stage of disease when compensatory mechanisms triggered by the underlying decrease in contractility are no longer capable of maintaining adequate cardiac performance during exercise and, subsequently, under resting conditions. Independent of its underlying etiology, cardiac failure is always characterized by an impairment in the intrinsic contractility of myocytes. As a consequence of reduced contractility, a number of central and peripheral compensatory mechanisms take place that are capable of effectively counteracting reduced intravascular intrinsic performance for a long period of time. Among them, recruitment of preload reserve, enhanced neurohormonal stimulation and cardiac hypertrophy are the most important. All of them, however, also carry unfavorable effects that contribute to further deterioration of cardiac function. In fact, increased end-diastolic volume determines increased wall stress that further reduces systolic performance; sympathetic and angiotensin stimulation increases peripheral resistance and contributes to increase volume expansion; hypertrophic myocytes demonstrate impaired intrinsic contractility and relaxation, and hypertrophy causes a clinically relevant deterioration of ventricular relaxation and compliance that substantially participates in increased end-diastolic pressure, and, therefore, to limited exercise performance. Diastolic dysfunction usually accompanies systolic dysfunction, although in some cases it may represent the prevalent mechanism of congestive heart failure in patients in whom systolic performance is preserved. Biological causes of reduced contractility in heart failure are not completely elucidated. Changes in myosin composition and in sarcoplasmic ATPase activity, causing reduced Ca2+ availability during contraction, have been reported, although their exact contribution is not clear. Recently, impaired endothelial function has also been described in heart failure, and new appealing hypotheses have been made regarding the causative role of circulating cytokines like tumor necrosis factor in the pathogenesis of heart failure.
Pathogenesis of Renal Sodium Retention in Congestive Heart Failure
Authors: Andreoli Thomas
Published: April 2003

This article summarizes briefly some factors responsible for edema in chronic congestive heart failure. It is now generally thought that so-called ‘backward failure’ is a manifestation of diastolic dysfunction, while systolic ‘pump failure’ is a disease that depends on two key factors: an inadequate cardiac output, and renal salt and water retention. The key elements involved in what might be termed the ‘integrated volume response’ are hemodynamic and renal factors. The hemodynamic factors include vasoconstriction, tachycardia and a reduced venous capacitance. These responses occur within minutes, while salt and water retention occurs over days to weeks. The key renal elements modulating sodium retention in congestive heart failure include, at a minimum, four variables. First, there is a reduction in renal blood flow produced by the almost simultaneous operation of α- and β-catecholamines, antidiuretic hormone, the endothelins, and angiotensin II. Second, activation of the tubuloglomerular feedback system enhances intrarenal angiotensin II release, which augments proximal sodium absorption. In addition, β-catechols also enhance proximal sodium absorption. A third key element involved in renal sodium retention is activation of apical sodium channels, ENaC, of principal cells in the cortical collecting tubule by aldosterone and by vasopressin. Finally, the inner medullary collecting duct becomes resistant to the action of atrial natriuretic peptide, thus adding a final dimension to the syndrome of sodium retention in underfilling.
Body Impedance Studies in End-Stage Heart Failure
Authors: Stellato Davide , Cirillo Massimo , De Santo Luca , Maiello Ciro , Marra Claudio , De Vivo Fabrizio , Anastasio Pietro , Frangiosa Annamaria , Cotrufo Maurizio , De Santo Natale Gaspare , Di Iorio Biagio
Published: April 2003

This study adds another category of patients to those amenable to body impedance analysis (BIA). BIA measurements were obtained for the first time in 23 male patients with end-stage heart failure who were waiting for heart transplantation, and the data were compared with those obtained in 69 healthy controls matched for age, sex, height and weight. The data indicate that in end-stage heart failure there is an increased reactance (p<0.01) and an altered intracellular water/extracellular water ratio (p<0.03) due to the increased intracellular water (p<0.01) and decreased extracellular water (p<0.01).
Daily Hemofiltration in Severe Heart Failure
Authors: Iorio Luigi , Nacca Remo Giuseppe , Simonelli Roberto , Saltarelli Giuseppe , Violi Fabio
Published: April 2003

Heart failure of class IV NYHA has a very severe prognosis. Its most frequent electrolytic alterations are hyponatremia, hypokalemia, and hypomagnesemia which can cause serious arrhythmias and sudden death. The regulation of the electrolytic equilibrium by means of pharmacological therapy becomes impossible in patients with severe heart failure resistant to strong doses of diuretics in the oligo-anuric phase. This study focused on the use of daily hemofiltration in a group of patients suffering from cardiac insufficiency of class IV NYHA. The results have been evaluated over 1 year.
Early Dialysis in Heart Insufficiency of Patients with Chronic Renal Failure
Authors: Iorio Luigi , Simonelli Roberto , Saltarelli Giuseppe , Nacca Remo Giuseppe , Violi Fabio , Lamberti Franco , Rossi Giovanni
Published: April 2003

In patients with severe heart failure life expectancy is short, the quality of life is affected, and the service costs are very high. Drug therapies remain restricted despite continuous clinical research. Therefore new therapeutic approaches have been attempted to improve the signs and symptoms of the disorder. In our study we followed patients suffering from class-IV cardiac failure concomitant with chronic renal failure. The patients were initially treated by means of hemofiltration, and subsequently they underwent a personalized dialysis program. The survival rate after 2 years was 62.5%. In 7 of the 8 patients the results revealed a drop to a class-III condition. The hospitalization period was limited to a few days. Early dialytic therapy represents a reality for such patients.
Heart Transplantation in Patients with Diuretic Resistant Heart Failure
Authors: De Vivo Fabrizio , De Santo Luca , Maiello Ciro , Marra Claudio , Marmo Joseph , Cotrufo Maurizio
Published: April 2003

Advanced heart failure is becoming an increasing cause of mortality and morbidity in a large number of patients. Heart transplantation is the treatment of choice for many selected patients in this group. According to the clinical status at the time of transplant, patients may have a different outcome related to the early survival, while the late results are similar and not affected by the patient’s initial clinical status. All surviving patients showed recovery of kidney function as soon the cardiac output was restored to normal values. High urine output was present in a large number of patients in the early postoperative period. However, in severely ill patients with cardiac index <2.5 l/min/m2, diuretic resistance and mortality were higher.
Homocysteine, a New Crucial Element in the Pathogenesis of Uremic Cardiovascular Complications
Authors: Perna Alessandra , Ingrosso Diego , Castaldo Pasquale , De Santo Natale , Galletti Patrizia , Zappia Vincenzo
Published: April 2003

Most large observational studies available today establish that moderate hyperhomocysteinemia, either genetically or nutritionally determined, is an independent risk factor for myocardial infarction, stroke, and thromboembolic disease. This is also true for chronic renal failure patients, who exhibit a high prevalence of hyperhomocysteinemia (85–100%), which reaches high plasma concentrations (20–40 µM, while control values range between 8 and 12 µM−). After a renal transplant, homocysteine levels decrease, but tend to be higher than normal. The cause of hyperhomocysteinemia in renal failure is still obscure, since recent data have questioned the previous notion that a net homocysteine renal extraction and/or excretion take place in man. No matter the cause of its increase, the sulfur amino acid homocysteine is thought to induce an increment in cardiovascular risk through three basic biochemical mechanisms: (1) homocysteine oxidation, with H2O2 generation; (2) hypomethylation through S-adenosylhomocysteine accumulation, and (3) protein acylation by homocysteine thiolactone. The final result is membrane protein damage, endothelial damage, and endothelial cell growth inhibition, among other effects. Hyperhomocysteinemia, in general, is susceptible of therapeutic intervention with the vitamins involved in its metabolism. Depending on the cause, vitamin B6, vitamin B12, betaine, and/or folic acid can be effectively utilized. Chronic renal failure patients benefit from folic acid in high dosage: 1–2 mg are usually not effective (‘relative folate resistance’), while 5–15 mg reduce homocysteine levels to a ‘normative’ range (<15 µM) in a substantial group of patients. Good results are also obtained in transplant patients, best with a combination of folic and vitamin B6. The results of the interventional trials focusing on the possible reduction in cardiovascular risk after homocysteine-lowering therapy, both in the general population and in end-stage renal disease, are expected soon, as well as the genetic and biochemical studies in suitable models, with the aim to clarify the cause-effect link suggested by the numerous observational and basic science studies.
Fighting from the Right Side of the Brain: Left Visual Field Preference during Aggression in Free-Ranging Male Tree Lizards (Urosaurus ornatus)
Authors: Hews Diana K. , Worthington R. Andrew
Published: April 2003

In a field study on male tree lizards (Urosaurus ornatus), we tested the hypothesis that aggression is lateralized, and predicted that resident males should preferentially use the left-visual field (LVF)/right hemisphere in aggressive interactions with other males. This prediction was based on results for a small but taxonomically diverse number of vertebrates indicating a left-eye preference/ right hemisphere specialization for aggression. Many lizards use postural displays to signal aggression and lateral eye placement prevents binocular vision of such displays. The fullshow is an aggressive display that is typically performed with the body held perpendicular to that of the opponent. We staged male-male encounters by introducing stimulus males to free-ranging males (hereafter called focal males), and then recorded both the focal male’s behavior and the visual field that he used to view the intruder while performing fullshow displays. When intruders were introduced in the right visual field (RVF), focal males were equally likely to use either the LVF or RVF to perform their first fullshow. However, in these RVF introductions focal males were more likely to turn and use the LVF if the intruder was smaller. In contrast to RVF introductions, in LVF introductions focal males were significantly more likely than expected by chance to continue to use the LVF to view the intruder when performing the first fullshow. Furthermore, if focal males performed their first fullshow with the intruder in their LVF, they subsequently gave more aggressive displays than focal males that performed their first display with the intruder in their RVF. Additionally, charge (a highly aggressive behavior that usually leads to direct physical contact and a bite) was significantly more likely to occur while the LVF was being used to view the opponent. These results are consistent with the hypothesis that aggression is lateralized to the right hemisphere. This study is one of only a few examples of laterality of brain function demonstrated in a free-ranging vertebrate.
Caries Incidence in Young Type 1 Diabetes mellitus Patients in Relation to Metabolic Control and Caries-Associated Risk Factors
Authors: Twetman S. , Johansson I. , Birkhed D. , Nederfors T.
Published: April 2003

The aim of this study was to evaluate the caries incidence in a group of young patients with type 1 diabetes mellitus over a 3-year period from the onset of the disease in relation to metabolic control and to caries-associated risk factors. Sixty-four children and adolescents (8–15 years of age) had their diabetes treated and monitored according to a standard medical protocol and received extensive preventive oral health care based on individual needs. Data on blood glucose and glycosylated haemoglobin (Hb AIc) were collected from the medical records. Whole saliva was collected every 3rd month and secretion rate, buffer capacity, glucose concentration, mutans streptococci and lactobacilli counts were determined. Dental examinations, including radiographs, were carried out once a year. Patients with less good metabolic control (>8.0% Hb AIc) exhibited higher glucose levels in resting saliva (p < 0.05) and a significantly higher caries incidence (p < 0.05) compared to those with good metabolic control. The most influential determinants for high caries development during the 3-year follow-up period were metabolic control (odds ratio, OR = 5.7), poor oral hygiene (OR = 6.5), previous caries experience (OR = 5.3) and high levels of salivary lactobacilli (OR = 5.0). The findings suggest that the level of metabolic control and traditional caries risk markers are important factors for caries development in children and adolescents with type 1 diabetes mellitus.
Fluoride Concentrations in Saliva and Dental Plaque in Young Children after Intake of Fluoridated Milk
Authors: Petersson L.G. , Arvidsson I. , Lynch E. , Engström K. , Twetman S.
Published: April 2003

This study determined fluoride (F) concentrations in whole saliva and dental plaque after intake of fluoridated milk using a randomised crossover experimental design. Eighteen healthy children (6–8 years) were subjected to each of four different 3-day drinking regimens: (a) 200 ml F-free tap water; (b) 200 ml tap water with 1.0 mg F; (c) 200 ml standard milk, and (d) 200 ml standard milk with 1.0 mg F. A washout period of 7 days was organised between the different drinking regimens. All children used F-free toothpaste prior to and during the trial and were instructed to avoid F-rich food and drinks. F concentration in unstimulated whole saliva was determined at baseline and after 15 and 120 min and in plaque samples at baseline and after 2 h. The mean baseline values ranged from 0.01 to 0.02 mg F/l in saliva and between 10.4 and 14.2 mg F/l in dental plaque. A statistically significant (p < 0.05) increase of F was disclosed in saliva 15 min after drinking F-containing milk and water (0.052 and 0.058 mg F/l, respectively). After 2 h, the salivary F– concentrations were back to baseline values. In the plaque, however, a statistically significant (p < 0.01) twofold increase was found at 2 h after the intake of fluoridated milk and water, respectively. The results indicate that consumption of fluoridated milk contributes to a F storing process with significantly elevated F concentrations in dental plaque up to 2 h after intake. Further studies are required to determine the ‘therapeutic concentration’ of F in dental plaque after intake of fluoridated milk.
Acidogenicity of Buccal Plaque after a Single Rinse with Amine Fluoride – Stannous Fluoride Mouthrinse Solution
Authors: Damen J.J.M. , Buijs M.J. , ten Cate J.M.
Published: April 2003

Caries and gingivitis prevention may benefit from chemotherapeutic plaque control, therefore we compared in a cross–over study with 5 subjects the anti–acidogenic effects of a single use of AmF–SnF2 mouthrinse solutions (Meridol® with and without 5% alcohol) with baseline and with the effects of a placebo and a chlorhexidine mouthrinse (CHX). Buccal plaque was collected 0.5, 3 and 8 h after the subjects used one of the mouthrinses, each time before and after a rinse with 10% sucrose to induce lactic acid production. Samples were analysed for acid anions by capillary electrophoresis and for protein. At 0.5 h after the use of AmF–SnF2 or CHX, the concentration of acetate in resting plaque was 70% lower than at baseline or after using the placebo. Average post–sucrose acetate and lactate concentrations in the placebo group were 30–80% higher than at baseline; up to 3 h this difference was significant. 8 h after using AmF–SnF2 or CHX, the post–sucrose acetate and lactate concentrations were still 30–50% lower than after the placebo, and up to 40% lower than at baseline. To conclude, AmF–SnF2 in both Meridol formulations and CHX were shown to have a similar potency to inhibit acid production after a single rinse.
Prognosis of Asymptomatic Hematuria and/or Proteinuria in Men
Authors: Yamagata Kunihiro , Takahashi Hideto , Tomida Chie , Yamagata Yoh , Koyama Akio
Published: April 2003

Aim: To elucidate prognosis and prevalence of chronic renal diseases among proteinuric and/or hematuric subjects found in mass screening, a long-term follow-up study (6.35 years, range 1.03–14.6 years) was conducted on Japanese working men. Methods: A total of 772 subjects selected from 50,501 Japanese men aged 15–62 years were found to have asymptomatic hematuria (n = 404), concomitant hematuria and proteinuria (n = 155), and proteinuria (n = 213) during their annual urine examination and five consecutive urinalyses. Results: Hematuria patients showed significant improvements in urinary abnormalities as compared with both hematuria/proteinuria and proteinuria patients. Both hematuria/proteinuria patients with normotension and hematuria/proteinuria patients aged under 40 years showed significant improvements. During the follow-up period, 9.5% of the hematuria patients became hematuric/proteinuric. Hematuria/proteinuria patients had the highest risk of developing renal insufficiency. The presence of hypertension at detection of urinary abnormalities did not affect the renal function; however, if proteinuria appeared after the age of 40 years, these patients had a higher risk of developing renal insufficiency. The incidence of IgA nephropathy in the present subjects was as high as 143 cases per 1 million per year. Conclusion: Detailed follow-up and definitive diagnosis of asymptomatic urinary abnormalities may raise the prevalence of IgA nephropathy worldwide.
Plasma Pentosidine Levels Measured by a Newly Developed Method Using ELISA in Patients with Chronic Renal Failure
Authors: Sanaka Tsutomu , Funaki Takenori , Tanaka Toshihisa , Hoshi Sayako , Niwayama Jyun , Taitoh Takashi , Nishimura Hideki , Higuchi Chieko
Published: April 2003

The plasma pentosidine levels in patients with renal disease were measured by a simple method which was established for plasma and urinary pentosidine determinations. The method, which can be completed within a few hours, involves pretreating plasma with proteolytic enzyme (pronase) and measuring the concentration of pentosidine in the sample by ELISA using antipentosidine antibodies. The prepared antibodies showed no cross-reaction with the raw materials for pentosidine synthesis or with compounds having similar structures. SDS-PAGE indicated that the antibodies had a high purity. The reaction of the antibodies and keyhole limpet hemocyanin-pentosidine in the competitive ELISA system was inhibited by free pentosidine. Excellent standard curves for pentosidine determination were obtained. In actual measurements of clinical samples from patients, a good correlation (r = 0.9356) was obtained between the values measured by ELISA and HPLC. The plasma pentosidine level in patients with renal disease correlated significantly with plasma creatinine, urea nitrogen, β2-microglobulin, and creatinine clearance, indicating its usefulness in evaluating the severity of renal disease. A significant elevation in plasma pentosidine levels was observed in mild renal dysfunction, whereas no significant increases in creatinine and urea nitrogen levels were detected, suggesting that the plasma pentosidine level is useful in the early diagnosis of beginning renal failure. In patients with chronic renal failure, no difference in plasma pentosidine levels was observed between diabetic nephropathy and chronic glomerulonephritis, while a significant correlation was observed with phosphatidylcholine hydroperoxide, suggesting the possibility that the plasma pentosidine level reflects injury due to oxidation. From these results, the quantitative measurement method developed by us is judged to be a superior innovation for measuring pentosidine in body fluids. The plasma pentosidine level may be useful for the early diagnosis of mild renal failure and to estimate the degree of the severity of renal diseases.
How Glomerular Extracapillary Proliferation Might Lead to Loss of Renal Function: Light Microscopic and Immunohistochemical Investigation
Authors: Bertani Tullio , Mazzucco Gianna , Monga Guido
Published: April 2003

Although there has been extensive research into the mechanisms involved in glomerular crescent formation, it is not yet fully understood how this change may cause renal function impairment. The aim of this study is to identify morphologic changes which may be responsible for this phenomenon. Thirty-eight renal biopsies showing glomerulonephritis with extracapillary proliferation (20 vasculitis-related, 6 idiopathic, 9 due to immune-complex deposition and 3 superimposed on diabetic nephropathy) were considered, and 146 glomeruli in which both crescents and the urinary pole were found at the same time, were studied. The involvement of the urinary pole by cellular crescents was observed in 93.1 and 100% of the glomeruli with segmental or circumferential crescents, respectively. A tridimensional study, for the evaluation of the glomeruli as a whole, was performed on 8 biopsies by means of the step-section technique and disclosed the involvement of the urinary space and a close contact between crescent and tubular cells in all 54 investigated glomeruli. The reported features do not seem to be related to the type of cells which formed the crescent. Indeed, as shown by immunohistochemical study on 10 cases with anti-cytokeratin and anti-CD68 antisera, the crescent localization at the urinary pole had no correlation with the prevalence of epithelial or macrophagic cells. These findings suggest that crescents, due to epithelial proliferation or macrophage clustering, tend to localize at the urinary pole and thus come into close contact with cells of the proximal convoluted tubule: the formation of a sort of plug or a ‘glomerular stone’ could well explain the block in the urine flow and the consequent impairment of renal function in the acute phase of the disease, even in those cases where crescents are segmental.
Is Platelet-Activating Factor Produced during Hemodialysis with AN-69 Polyacrylonitrile Membrane?
Authors: Iatrou Christos , Afentakis Nicolaos , Nomikos Tzortzis , Dinas Christos , Stavropoulos-Giokas Catherine , Antonopoulou Smaragdi
Published: April 2003

Background: Platelet-activating factor (PAF) production during hemodialysis (HD) with cuprophane (CU) membrane has previously been demonstrated, while the results regarding PAF production during HD with AN-69 polyacrylonitrile membrane are dubious. In this study an attempt is made to show that PAF is produced during HD using AN-69 membrane while comparing this production with the corresponding one from HD with CU. Since previous studies have indicated that PAF, like the complement system, could also be implicated in HD-related leukopenia and thrombocytopenia (especially when CU membrane is used), the circulating leukocyte and platelet counts as well as the C3a-desArg and SC5b-9 (soluble, nonlytic form of the terminal complement complex) levels were measured. Methods: Ten hemodialyzed patients were subjected to HD with CU and AN-69 membranes for 2 consecutive weeks (first week with CU and second with AN-69). During the third HD session of each week and at different times (0, 2, 5, 15, 30, 60, 180 and 240 min), the PAF levels in the blood as well as the leukocyte and platelet counts were measured, while the circulating levels of the C3a-desArg and SC5b-9 were measured at 0, 5, 15, 60 and 240 min. PAF was detected by ethanol extraction, followed by purification by column chromatography and high-pressure liquid chromatography and finally quantified by bioassay. The C3a-desArg and SC5b-9 fractions of the complement were measured by immunoassay while an autoanalyzer gave the leukocyte and platelet counts. Results: Circulating PAF levels were detected at all time intervals during HD with AN-69 (PAFAN-69) and CU (PAFCU) membranes. At all time intervals PAFAN-69 < PAFCU, however, statistically significant differences (s) between the two membranes existed only at 15, 30, 60, 180 and 240 min. The highest PAFAN-69 and PAFCU occurred at 5 and 15 min into dialysis, respectively. The same observations were made for circulating C3a-desArg levels (s existed additionally at 5 min as well). The reduction of the circulating leukocytes had almost a mirror image with the C3a-desArg as well as PAF levels while the maximal reduction of platelets was observed after 2 min into dialysis with both membranes (i.e., simultaneously with the first increase in PAF secretion). Conclusions: PAF is indeed produced during HD with AN-69 membrane, as it is during HD with CU. At all time intervals during the HD procedure, PAFAN-69 < PAFCU. PAF seems to contribute to HD-related leukopenia and thrombocytopenia with both membranes.
Vitamin E Protects Renal Antioxidant Enzymes and Attenuates Glomerulosclerosis in Adriamycin-Treated Rats
Authors: van den Branden Christiane , Deman An , Ceyssens Bart , Pauwels Marina , Empsen Christophe , Verbeelen Dierik
Published: April 2003

Background/Aims: In the rat Adriamycin model of chronic renal failure, the development of glomerulosclerosis and tubulointerstitial lesions is accompanied by decreased activities and mRNA levels of the antioxidant enzymes. In this study, we investigated the effect of oral vitamin E supplementation on antioxidant enzyme activities in both the cortex and isolated glomeruli from Adriamycin-treated rats. Methods: Glomerulosclerosis, tubulointerstitial lesions and ferric iron deposits were evaluated by histochemical staining methods, and antioxidant enzyme activities were measured by spectrophotometry. Results: Vitamin E supplementation of the normal diet attenuates Adriamycin-induced glomerulosclerosis and tubulointerstitial lesions, but not proteinuria and serum total cholesterol, low-density lipoprotein cholesterol, triglycerides and total protein concentrations. In the cortex, vitamin E completely prevented a decrease in enzyme activity for Cu/Zn superoxide dismutase and catalase, and partly for Mn superoxide dismutase and glutathione peroxidase. In the glomeruli, vitamin E completely prevented a decrease in activity for Cu/Zn superoxide dismutase, catalase and glutathione peroxidase, and partly for Mn superoxide dismutase. Conclusion: Dietary supplementation of vitamin E protects the activities of antioxidant enzymes in the kidney cortex and glomeruli, and attenuates the evolution towards terminal renal failure in rats treated with Adriamycin.
Metabolic Profile of Pre-Pregnancy, Pregnancy and Early Lactation in Multiple Lambing Sakız Ewes
Authors: Fırat Ayşen , Özpınar Aysel
Published: April 2003

Twenty synchronized Sakiz ewes aged 3–4 years were used in the study. Blood samples were taken once in pre-pregnancy and at the 100th day of pregnancy. At the 120th day of pregnancy and on the 10th day of lactation, blood samples were collected every 2 h for 24 h from only 10 ewes. Plasma cortisol levels were analyzed by radioimmunoassay. Plasma glucose and 3-hydroxybutyrate levels were determined spectrophotometrically. Plasma cortisol level slightly increased at the 100th day of pregnancy, decreased during late pregnancy and continued to decrease during lactation. Plasma glucose and 3-hydroxybutyrate levels were not significantly different during pre-pregnancy, pregnancy and the early lactation periods. In conclusion, the results showed that metabolic disorders such as pregnancy toxaemia did not occur in ewes fed a balanced ration sufficient in energy and protein levels even in a multiple lambing breed of ewes.