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P Preisig

Publications and source records attributed to P Preisig.

11 recordsLinked to original sources
PubMed1999

A cell cycle-dependent mechanism of renal tubule epithelial cell hypertrophy.

The response of renal epithelial cells to injury can include hyperplasia (increase in cell number), apoptosis (cell death), antiproliferation (growth arrest), or hypertrophy (cells physically enlarge). Examining cell size and the protein:DNA ratio can differentiate between the growth response patterns, but it is proposed that the degree of activation of cyclin D kinase in the late G1 phase of the cell cycle differentiates between hyperplasia and hypertrophy.

Animals↗
PubMed1999

Introduction

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Journal Article↗
PubMed1999

TGF-beta1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase.

When renal epithelial cells are exposed to epidermal growth factor-transforming growth factor-beta1 (EGF-TGF-beta1) the typical EGF-mediated hyperplastic growth response is converted to a hypertrophic growth response. Hypertrophy in this setting involves cell entrance into G(1), but arrest of cell cycle progression at the G(1)/S interface. Late G(1) arrest is mediated by retaining retinoblastoma protein (pRB) in its active, hypophosphorylated state. The present studies examine the mechanism by which pRB is retained in its active state. The results demonstrate that TGF-beta1-mediated conversion of hyperplasia to hypertrophy involves preventing activation of cdk2/cyclin E kinase but has no effect on cdk4(6)/cyclin D kinase activity. Preventing activation of cyclin E kinase is associated with 1) decreased abundance of cdk2/cyclin E complexes and 2) retention of p57(Kip2) in formed cdk2/cyclin E complexes. The development of hypertrophy does not involve regulation of either cdk2, cyclin E, or cdc25A protein abundances, or the abundance of p27(Kip1) or p21 in formed complexes.

Animals↗
PubMed1998

Development of a patient classification system for chronic hemodialysis patients.

The purpose of this project was to develop a patient classification system that could indicate the caregiver time required by chronic hemodialysis patients during one dialysis treatment session. A patient acuity tool that used a condition indicator model was developed and validated. Initial indicator weights were established by an expert panel of 12 center directors. An experimental design was formulated that permitted evaluation of the influence of independent factors, such as type of ownership and cost-per-treatment environment on the acuity-time relationship. Acuity-time data were collected on more than 600 individual treatments performed in 12 different centers across the country. Results indicate that patient acuity, measured by The American Nephrology Nurses' Association (ANNA)/MECON acuity tool, is a strong predictor of the caregiver time that will be required by the patient during that treatment session (P < 0.0001) and that centers differ in the amount of time that caregivers spend with patients who are rated at the same level of acuity (P = 0.001). The overall average time spent by caregivers ranged from 61 minutes per treatment for level I patients to 97 minutes per treatment for level 5 patients. Ownership and cost-per-treatment effects were not significant as independent factors. However, some combinations of ownership and cost-per-treatment data may be significant.

Humans↗
PubMed1995

TmDOTP5- as a 23Na shift reagent for the in vivo rat kidney.

Since transmembrane sodium gradient is essential to many cell functions, there is continuing interest in methods that differentiate intracellular and extracellular Na+. In the kidney, shift reagent (SR) aided 23Na magnetic resonance spectroscopy (MRS) has been successfully used only in isolated cells, tubules, and the perfused organ. In this report, we demonstrate for the first time that TmDOTP5- can be used to distinguish Na+ compartments in kidneys in vivo. Infusion of 80 mM TmDOTP5- without added Ca2+ produced three resolved 23Na resonances, which we have assigned to intracellular Na+, vascular Na+, and intraluminal Na+. In comparison, infusion of 400 mM DyTTHA3- produced two broad and unresolved resonances. The 31P spectra of the cellular high energy phosphate metabolites indicate that TmDOTP5- is safe for in vivo applications. Washout studies suggest that this SR displays renal clearance similar to that of MR imaging contrast agents. However, the glomerular filtration rate (GFR) in animals infused with TmDOTP5- was reduced by 49% compared with the GFR in control animals, perhaps due to the hypotensive effects of the SR. We conclude that TmDOTP5- is effectively cleared from the blood of live animals but that a different formulation will be required for clinical application.

Animals↗
PubMed1994

Renal physiology series: part 7 of 8: renal acidification.

Maintenance of a normal body pH is essential to the efficient functioning of many physiologic processes. The body has a number of mechanisms for preventing fluctuations in body pH. Some of these are designed to prevent minute-to-minute pH fluctuations over the course of the day, and others are designed to maintain pH balance from day to day. The kidney plays a key role in both processes. The renal process of bicarbonate reclamation prevents the loss of bicarbonate in the urine, and thus, maintains plasma levels of one substrate that is instrumental to preventing minute-to-minute pH fluctuations. The other renal process, bicarbonate regeneration, replenishes the body's supply of bicarbonate, and thus, maintains pH balance on a day-to-day basis. This article will discuss basic principles of acid-base physiology, the mechanisms designed to prevent fluctuations in body pH, and the renal processes instrumental in maintaining a homeostatic pH environment.

Acid-Base Equilibrium↗
PubMed1993

Cyclic adenosine monophosphate acutely inhibits and chronically stimulates Na/H antiporter in OKP cells.

Parathyroid hormone, dopamine, alpha-adrenergic catecholamines, and angiotensin II regulate renal Na excretion, at least in part through modulation of acute cyclic (c)AMP-induced proximal tubule Na/H antiporter inhibition. The present studies examined the effect of chronic increases in cell cAMP on Na/H antiporter activity in OKP cells. Whereas 8-bromo cAMP acutely inhibited Na/H antiporter activity, chronic application for 6 h led to a 24% increase in Na/H antiporter activity measured 16-20 h after cAMP removal. This chronic persistent activation of the Na/H antiporter required > 2 h exposure. This effect was not a nonspecific effect of 8-bromo cAMP, in that addition of forskolin or forskolin + 3-isobutyl-1-methylxanthine for 6 h also led to a chronic persistent increase in Na/H antiporter activity. Inhibition of protein synthesis with cycloheximide prevented 8-bromo cAMP-induced Na/H antiporter stimulation. Although 8-bromo cAMP addition decreased cell pH by 0.15-0.20 pH U, Na/H antiporter stimulation could be dissociated from cell acidification. In summary, while cAMP acutely inhibits Na/H antiporter activity, it chronically increases antiporter activity. This chronic activation occurs with exogenous addition or endogenous generation of cAMP. These results imply that for hormones that modulate renal Na excretion and proximal tubule Na/H antiporter activity via cAMP and protein kinase A, acute effects may not predict chronic effects.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Renal physiology series: Part 3 of 8. Urinary concentration and dilution.

The maintenance of extracellular volume depends on the appropriate excretion of both salt and water. When extracellular volume is expanded, the excretion of a dilute urine facilitates the return of extracellular volume to normal. When extracellular volume is contracted, the retention of both salt and water and the excretion of a small amount of concentrated urine contributes to the reexpansion of extracellular volume. The formation of either a dilute or concentrated urine is dependent on the physical arrangement of the loops of Henle, collecting tubules, and vasa recta within the kidney medulla, the transport properties of each segment; and the appropriate presence or absence of antidiuretic hormone (ADH), a hormone synthesized in the hypothalamus and secreted from the posterior pituitary gland.

Humans↗
PubMed1990

Crystalloid versus colloid fluid therapy after cardiac surgery.

Differences in hemodynamic stability and fluid requirements were examined in patients randomly assigned to receive either normal saline crystalloid solution (N = 10) or hetastarch colloid solution (N = 11) after coronary artery bypass or valve operation. Both solutions were administered in the same manner for 8 hours after surgery, with hourly assessment of hemodynamic parameters and intake/output data. Infusion rates and 8-hour intake were higher for the group receiving normal saline solution (p less than 0.001), as was postoperative weight gain (p less than 0.01), although urine and chest tube outputs did not differ. Despite lower filling pressures, subjects receiving hetastarch exhibited higher systolic blood pressures and cardiac outputs (p less than 0.05). Hematocrits on postoperative day 1 were lower in the group given hetastarch (p less than 0.001), suggesting prolonged intravascular expansion. The subjects given hetastarch also required significantly less time in the intensive care unit (p less than 0.001). Thus, cardiac surgical patients receiving colloids exhibited reduced fluid requirements, superior hemodynamic performance, and shortened intensive care stay when compared with those given crystalloid resuscitation.

Cardiac Surgical Procedures↗
PubMedDate not supplied

What makes cells grow larger and how do they do it? Renal hypertrophy revisited.

Hypertrophy, defined as an increase in cell size without an increase in cell number, occurs in a number of conditions, including compensatory renal growth, diabetes mellitus, protein feeding, chronic metabolic acidosis, and chronic potassium deficiency. In vitro cell culture studies have been used to characterize the mechanisms involved in the development of hypertrophy. Two mechanisms have been identified and characterized. One mechanism involves regulation of processes that are also associated with the initial events of the hyperplastic growth process, and is referred as a cell cycle-dependent mechanism. The other mechanism occurs independently of these particular cell cycle processes, but involves regulation of protein degradation by lysosomal enzymes. This latter mechanism is referred to as a cell cycle-independent mechanism. In vivo studies suggest that both compensatory renal hypertrophy following uninephrectomy and diabetes mellitus-induced hypertrophy involve the cell cycle-dependent mechanism.

Animals↗