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Biomedical subjects

M Lieberman

Publications and source records attributed to M Lieberman.

At least 109 records · Page 6Linked to original sources
PubMed1986

Prevesical hematoma: a complication of prostatic biopsy.

Pelvic hematomas following prostatic biopsy are rare. We describe 2 cases of hematomas occurring in the prevesical space (space of Retzius) following transrectal biopsy. Computed tomography (CT) was useful in defining the extent of the hematoma and showing density changes related to the age and suppuration of the hematoma. While cystography has been used to diagnose prevesical hematomas, CT better assesses the size of the hematoma and changes that may occur over time.

Biopsy↗
PubMed1986

Na/H exchange in cultured chick heart cells: secondary stimulation of electrogenic transport during recovery from intracellular acidosis.

Intracellular acidosis is capable of stimulating a rapid amiloride-sensitive Na/H exchange mechanism in the cell membrane of cultured chick heart cells. The sequence of changes of intracellular sodium and potassium contents during recovery from an acid load in heart cells was determined by atomic absorption spectrophotometry and correlated with electrophysiological measurements. Induction of an intracellular acid load by removal of NH4Cl from the bathing solution caused a rapid rise in sodium content that was amiloride-sensitive. Following a peak, sodium content declined concomitant with a rise in potassium content; these changes were ouabain-sensitive and corresponded with a ouabain-sensitive membrane hyperpolarization beyond the calculated potassium equilibrium potential. These observations indicate that pHi regulation in cardiac muscle, following an intracellular acid load involves extrusion of H+ by electroneutral Na/H exchange with the consequent rise in Nai stimulating the electrogenic Na/K pump to return Nai to control level. In the presence of amiloride (10(-4) M), the hyperpolarization was slower although still present: this suggests the existence of another sodium uptake mechanism which contributes to stimulation of electrogenic transport.

Action Potentials↗
PubMed1986

Coupled sodium-calcium transport in cultured chick heart cells.

In cultured embryonic chick heart cells, alterations of extracellular Na (Nao) and Ca (Cao), intracellular Na (Nai) and Ca, extracellular pH, and membrane potential resulted in changes in Na and Ca contents that were consistent with sarcolemmal Na-Ca exchange. 24Na efflux measurements revealed a large ouabain-insensitive component, one-third of which was inhibited by removal of Cao. Incubating the cells in Na-free solution resulted in a rapid, 1.5- to 2-fold increase in total cell Ca that remained elevated for at least 15 min. Cells exposed for 15 min to Nao less than or equal to 20 mM became maximally loaded with Ca, whereas Ca loading fell off sharply at values of Nao greater than 20 mM. The movement of Na against its electrochemical gradient was shown to be associated with Ca accumulation. During Na-K pump inhibition (in 10(-4) M ouabain), Na initially rose 2- to 3-fold to a level below its equilibrium value; then, lowering Cao for 30 min from 1.25 to 0.75 mM caused a 26% elevation in Nai, whereas raising Cao from 1.25 to 2.7 mM resulted in a 25% fall in Nai against its electrochemical gradient. These data are consistent with Nai being maintained by a Na-Ca exchange during Na-K pump inhibition. In the presence of ouabain (10(-4) M), Ca uptake into intracellular organelles, e.g., mitochondria, was suggested by an increase in total cell Ca as well as the occurrence of mitochondrial matrix granules, which were shown qualitatively by X-ray analysis to contain Ca. Although matrix granules also occurred in mitochondria during Na-free incubation, they did not contain detectable amounts of Ca when examined under identical conditions of fixation and analysis.

Animals↗
PubMed1985

Patterns of thymocyte differentiation markers on virus and radiation induced lymphomas of C57BL/Ka mice.

To better understand the biology of tumorigenesis in virus and radiation lymphomas of C57Bl/Ka mice, we have examined the cell surface phenotypes of a large series of primary tumors induced by both agents. Data derived using flow cytometry and recently available monoclonal antibodies to thymocyte differentiation antigens supports three major conclusions. First, tumor cell populations are unimodal for staining with most antibodies and are probably of clonal origin. Second, many, but not all, tumor cells show surface phenotypes similar to those of previously defined subpopulations of normal thymocytes. Third, at the cell surface level, no major differences between virus- and radiation-induced lymphomas can be discerned. Our data thus further define the relationship between thymomas induced by these two agents.

Animals↗
PubMed1985

Cytosolic free calcium in chick heart cells. Its role in cell injury.

The role of cytosolic free Ca2+ (Caf) in cell injury was investigated using two methods for measuring Caf in freshly disaggregated embryonic chick heart cells. The null-point method, using arsenazo III, is based on determining the extracellular Ca2+ concentration at which no net Ca2+ movement occurs when plasma membrane permeability is increased. With this technique, the null point Caf averaged 0.23 +/- 0.07 microM (n = 6) in the basal state. Using quin2, an intracellular fluorescent dye, to measure Caf a value of 0.05 +/- 0.01 microM (n = 5) was obtained. Elevation of Caf by various agents was associated with an increase in cell injury as measured by the release of the cytosolic enzyme, LDH. However, the relationship between Caf and LDH release was not a direct one under all experimental conditions, indicating that the level of Caf is not the sole determinant of cell injury.

Adenosine Triphosphate↗
PubMed1985

Na/H exchange in cultured chick heart cells. pHi regulation.

The purpose of this study was to establish the existence of Na/H exchange in cardiac muscle and to evaluate the contribution of Na/H exchange to pHi regulation. The kinetics of pHi changes in cultured chick heart cells were monitored microfluorometrically with 6-carboxyfluorescein and correlated with Nai content changes analyzed by atomic absorption spectrophotometry; transmembrane H+ movements were evaluated under pH stat conditions. After induction of an intracellular acid load by pretreatment with NH4Cl, a regulatory cytoplasmic alkalinization occurred with a t1/2 of 2.9 min. pHi regulation required external Na+ and was concomitant with transmembrane H+ extrusion as well as a rapid rise in Nai content in an Na/H ratio of 1:1. Microelectrode recordings of membrane potential demonstrated directly the electroneutral character of pHi regulation. Acid-induced net Na+ uptake could be either stimulated by further decreasing pHi or inhibited by decreasing pHo; Na+ uptake was unaffected by tetrodotoxin (10 micrograms/ml), quinidine (10(-3) M), DIDS (10(-4) M), Clo-free solution, or HCO3-free solution. Amiloride (10(-3) M) maximally inhibited both pHi regulation and Na+ uptake; the ID50 for amiloride inhibition of Na+ uptake was 3 microM. Nao-dependent H+ extrusion showed half-maximal activation at 15 mM Nao; Li+, but not K+ or choline+, could substitute for Na+ to support H+ extrusion. Cao-free solution also stimulated acid-induced Na+ uptake. We conclude that pHi regulation following an acid load in cardiac muscle cells is by an amiloride-sensitive, electroneutral Na/H exchange. Stimulation of Na/H exchange up to 54 pmol/cm2 X s indicates the rapidity of this exchange across cardiac cell membranes. Na/H exchange may also participate in steady state maintenance of pHi.

Amiloride↗
PubMed1985

Potassium-chloride cotransport in cultured chick heart cells.

The polystrand preparation of cultured chick heart cells has a unidirectional transmembrane Cl- efflux that is twice K+ efflux. However, Cl- conductance of this heart cell membrane is low [regardless of extracellular K+ (K+o)], suggesting the existence of electroneutral Cl--dependent transport mechanisms. Furosemide (10(-3) M) decreases the 36Cl tracer efflux rate constant from a control value of 0.67 to 0.33 min-1. Extracellular Na+--free solution, which depletes intracellular Na+ within 1 min, has no significant effect on 36Cl efflux. K+o-free solution plus 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 10(-4) M) promotes the loss of Cl- against the Cl- electrochemical gradient; Cl- loss is furosemide sensitive in a dose-dependent manner. Incubating polystrands in 133 mM K+o, normal extracellular Cl- (Cl-o) solution causes net K+ and Cl- uptake in a 1:1 stoichiometry as well as a furosemide-sensitive volume increase; 130 mM extracellular choline or Li+ cannot mimic this high-K+o-induced volume increase. Removal of Cl-o from 133 mM K+o solution prevents K+ uptake and causes a Cl- loss as well as a furosemide-sensitive volume decrease. Adjusting Cl-o concentrations in high-K+o solution plus DIDS, so that the Cl- chemical gradient equally opposes the K+ chemical gradient, prevents high-K+o-induced volume changes. These data suggest that the cardiac cell membrane contains a furosemide-sensitive K+-Cl- cotransport mechanism.

Animals↗
PubMed1984

Theoretical effects of transmembrane electroneutral exchange on membrane potential.

Transmembrane electroneutral transport mechanisms [e.g., Na/H exchange, Cl/HCO3 exchange, (K + Cl) cotransport] have recently been identified in a wide variety of cell types. If these exchanges sum to give a net electroneutral Na/K exchange, they may hyperpolarize the membrane potential beyond the value calculated from the Mullins-Noda equation, provided the cell maintains steady state intracellular ionic concentrations. In extreme circumstances, the membrane potential could hyperpolarize beyond the potassium reversal potential. This effect is mediated by the electrogenic Na/K pump. If either Na or K exchanges electroneutrally against a third ion (e.g., Na/Ca exchange), then the exchange may depolarize the membrane potential.

Bicarbonates↗
PubMed1984

Prevalence of mandibular dysfunction in 10-18 year old Israeli schoolchildren.

The prevalence of mandibular dysfunction in a sample of 369 Israeli schoolchildren was found to be 56.4%, indicating that one or more of the cardinal symptoms were present. It increased with age from about 51% in the 10-13 year old group to 67.8% in the 16-18 year olds. The most common cardinal sign of dysfunction was joint sounds (35.8%), which increased with age from 28% in the youngest group to 44.3% in the oldest group. The second most common sign was joint sensitivity to palpation (30.4%), which showed a slight increase in the oldest group. Sensitivity of the superficial muscles was recorded third, with 20%. Joint pain and restriction of mandibular movement appeared infrequently. Two of the more common cardinal symptoms, namely joint sounds and muscle sensitivity, were statistically related to several possible aetiological factors and to age and sex. Analysis of association showed that the probability of muscle sensitivity increased in the presence of malocclusion and/or joint sensitivity to palpation. It also showed that age, occlusal wear, locking of the jaw and joint sensitivity to palpation increased the probability of joint sounds.

Adolescent↗
PubMed1984

Demonstration of uronic acid capsular material in the cerebrospinal fluid of a patient with meningitis caused by mucoid Pseudomonas aeruginosa.

A 39-year-old female with insulin-dependent diabetes mellitus developed Rhizopus infection of the maxillary sinus. Subsequent to successful treatment with amphotericin B and surgical debridement, she developed purulent meningitis due to a mucoid strain of Pseudomonas aeruginosa. Analysis of cerebrospinal fluid documented the presence of a uronic acid polymer at a concentration of 40 micrograms/ml. In spite of parenteral and intrathecal antibiotic therapy, the patient died. This case illustrates that mucoid strains of P. aeruginosa may result in fatal infection and that alginate capsule is produced in vivo in humans.

Adult↗
PubMed1984

Physiologic criteria for electrogenic transport in tissue-cultured heart cells.

A description of the physiologic criteria for electrogenic transport in cultured heart cells must consider the direct as well as the indirect contributions of the electrodiffusive and electroneutral transport mechanisms of the kind described in this chapter. It is important to recognize that fundamental transport processes whether active, passive, or coupled-passive, do not operate in isolation but function rather as an interrelated network represented by the example in Fig. 8. The results of our studies point to the importance of providing an accurate, quantitative description of the transmembrane movement of sodium, because this ion is intricately involved in the overall regulation of several transport mechanisms in cardiac muscle. Cultured heart cell preparations enable the rapid exchange of extracellular space essential to the study of complex transport mechanisms. These preparations have thus enhanced our understanding of the magnitude and interplay of exchange fluxes that may eventually be implicated in the repolarization phase of the cardiac action potential and genesis of pacemaker potentials.

Biological Transport↗
PubMed1983

Transmembrane chloride flux in tissue-cultured chick heart cells.

To evaluate the transmembrane movement of chloride in a preparation of cardiac muscle lacking the extracellular diffusion limitations of natural specimens, intracellular chloride concentration ( [Cl] i) and transmembrane 36Cl efflux have been determined in growth-oriented embryonic chick heart cells in tissue culture. Using the method of isotopic equilibrium, [Cl]i was 25.1 +/- 7.3 mmol x (liter cell water)-1, comparable to the value of 24.9 +/- 5.4 mmol x (liter cell water)-1 determined by coulometric titration. Two cellular 36Cl compartments were found; one exchanged with a rate constant of 0.67 +/- 0.12 min-1 and was associated with the cardiac muscle cells; the other, attributed to the fibroblasts, exchanged with a rate constant of 0.18 +/- 0.05 min-1. At 37 degrees C, transmembrane Cl flux of cardiac muscle under steady-state conditions was 30 pmol x cm-2 x s-1. In K-free, normal, or high-Ko solutions, the responses of the membrane potential to changes in external Cl concentration suggested that chloride conductance was low. These results indicate that Cl transport across the myocardial cell membrane is more rapid than K transport and is largely electrically silent.

Animals↗
PubMed1983

Microfluorometric monitoring of pHi in cultured heart cells: Na+-H+ exchange.

Continuous measurement of intracellular pH (pHi) should enhance the likelihood of defining the mechanisms of pHi regulation in actively contracting preparations of cardiac muscle. A filter microfluorometric technique was adapted for use with growth-oriented embryonic chick heart cells to continuously monitor changes in the fluorescence intensity of the pH-sensitive chromophore 6-carboxyfluorescein, generated in situ. Data pertaining to the direction and the rate of pHi changes assisted in thermodynamically characterizing and ascertaining net kinetic parameters of a Na+-H+ exchange mechanism. Imposing an outward Na+ gradient across the cardiac cell membrane rapidly (t 1/2 = 44 s) induced cytosolic acidification, whereas an inward Na+ gradient produced cytosolic alkalinization (t 1/2 = 40 s). Amiloride (10(-3) M) caused the cytoplasm to acidify (t 1/2 = 46 s) and also reversibly blocked the acidification induced by low extracellular Na+. These results are consistent with the presence of a rapid Na+-H+ exchange mechanism in the cardiac cell membrane. Further investigations are required to characterize the involvement of Na+-H+ exchange in pHi regulation and to differentiate the effects of Na+-H+ exchange from other ion gradient-coupled mechanisms, e.g., Na+-Ca2+ exchange.

Amiloride↗
PubMed1983

Calcium elevation in cultured heart cells: its role in cell injury.

Inhibition of the Na+-K+ pump in cultured embryonic chick heart cells promotes the elevation of intracellular Ca2+ and is a useful manipulation to study the relationship between Ca2+ and myocardial cell injury. One hour of Na+-K+ pump inhibition resulted in a fourfold increase in cell Na+, a 50% decline in cell K+, and a 5- to 10-fold increase in cell Ca2+, 45% of which is mitochondrial. The degree of cell injury induced by Ca2+ loading was evaluated by monitoring the content of adenosine 5'-triphosphate (ATP) and the release of the intracellular enzyme lactate dehydrogenase (LDH). Under these conditions ATP content declined by 25-30% and LDH release increased from 1 to 1.4% of the total LDH. Furthermore, cells subjected to 1 h of Na+-K+ pump inhibition and returned to control solution for 5 h showed that Ca2+ decreased to near control levels and ATP content was restored. Although inhibition of Na+-K+ transport caused a large increase in cell Ca2+, neither Na+-K+ pump inhibition nor elevation in total cell Ca2+ per se resulted in irreversible myocardial cell injury.

Adenosine Triphosphate↗
PubMed1983

Pool size of pluripotential hematopoietic stem cells increased in continuous bone marrow culture by Friend spleen focus-forming virus.

Continuous mouse bone marrow cultures were infected with Friend murine leukemia virus. Production of nonadherent (NA) and adherent cells, granulocyte-macrophage colony-forming unit(s) of progenitor cells (GM-CFUc), pluripotential hematopoietic stem cells (CFUs), the self-renewal potential (Rs) of CFUs, and generation of factor-dependent (FD) multipotential and committed permanent stem cell cloned lines were measured. Uninfected marrow cultures from C57BL/6J, C57BL/6JUt, B6.S, C3H/HeJ, (C57BL/6J x DBA/2J)F1, CD- 1 Swiss, or N:NIH(S) mice generated NA cells, GM-CFUc, and CFUs for 20-41 weeks; cultures infected with Rauscher or other helper viruses generated them for 35-45 weeks. GM-CFUc and CFUs production in SFFV-positive cultures persisted for over 65 weeks and exceeded control levels by twentyfold to fiftyfold. The Rs of CFUs in SFFV-positive cultures was not detectably increased above control cultures. Multipotential (erythroid-neutrophil-mast cell-basophil-eosinophil) permanent FD cell clones were derived from control and SFFV-positive cultures. Thus SFFV amplifies the stem cell pool in vitro without detectably increasing the Rs capacity of CFUs.

Animals↗