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Biomedical subjects

B Rose

Publications and source records attributed to B Rose.

At least 55 records · Page 3Linked to original sources
PubMed1988

Neural differentiation, NCAM-mediated adhesion, and gap junctional communication in neuroectoderm. A study in vitro.

We studied the development of NCAM and gap junctional communication, and their mutual relationship in chick neuroectoderm in vitro. Expression of NCAM, as detected by monoclonal and polyclonal antibodies, and development of junctional communication, as detected by extensive cell-to-cell transfer of 400-500-D fluorescent tracers, occurred in cultures from stage-2 embryos onward. Both expressions presumably required primary induction. The differentiating cells formed discrete fields of expression on the second to third day in culture, with the NCAM fields coinciding with the junctional communication fields delineated by the tracers. Other neural differentiations developed in the following order: tetanus toxin receptors, neurofilament protein, and neurite outgrowth. Chronic treatment with antibody Fab fragments against NCAM interfered with the development of communication, suggesting that NCAM-mediated adhesion promotes formation of cell-to-cell channels. Temperature-sensitive mutant Rous sarcoma virus blocked (reversibly) communication and the subsequent development of neurofilament protein and neurites, but expression of NCAM continued.

Animals↗
PubMed1988

Restenosis following coronary artery angioplasty: patterns, recognition, and results of repeat angioplasty.

Restenosis is an important problem confronting PTCA. Controversy relative to the long-term outcome of PTCA continues to be fueled by this important problem. At present, certain patterns related to clinical, anatomic, and procedural considerations can be identified as related to restenosis. No interventions based on data from controlled trials offer conclusive treatment to substantially prevent restenosis risk.

Angioplasty, Balloon↗
PubMed1986

Downregulation of cell-to-cell communication by the viral src gene is blocked by TMB-8 and recovery of communication is blocked by vanadate.

The viral src gene downregulates junctional communication, closing cell-to-cell membrane channels presumably by way of the phosphoinositide signal route. We show that TMB-8 [8-N, N-(diethylamino) octyl-3,4,5-trimethoxybenzoate] counteracts this downregulation in cells transformed by temperature-sensitive mutant Rous sarcoma virus: TMB-8 (36-72 microM) raises junctional permeability when applied during activity of src protein kinase, i.e., at steady permissive temperature; and TMB-8 inhibits the fall of junctional permeability, when the activity of src protein kinase gets turned on. TMB-8 also (reversibly) inhibits the growth of the cells at permissive temperature and reverses the morphological changes associated with transformation. The morphological reversal lags several hours behind the junctional-permeability reversal. Communication recovers within a few minutes when the activity of the src protein kinase is turned off (in absence of TMB-8). Sodium orthovanadate (20 microM) prevents this recovery, but it has no major effect on junctional permeability on its own. We discuss possible modes of action of these agents on critical stages of the signal route, related to intracellular Ca2+ and protein kinase C.

Animals↗
PubMed1986

Expression of blood group antigens by cultured human epidermal cells.

The presence of blood group antigens on the surface of cultured human epidermal cells has been demonstrated using monoclonal antibody supernatants in indirect immunoperoxidase and immunofluorescence tests. An isoantigen pattern, consistent with the blood group of the donor infant, was detected in cultures derived from 10 different foreskin specimens, and in sections of the epidermis of 5 of these specimens. The A, B, and H antigens were found on the surface of cultured keratinocytes which resembled those of the spinous and granular cell layers of the in vivo epidermis. These antigens were readily detectable throughout the majority of the lifespan of the cells in vitro. This finding may be of relevance to those contemplating allograft transplantation of cultured human epidermis.

ABO Blood-Group System↗
PubMed1985

Diacylglycerol downregulates junctional membrane permeability. TMB-8 blocks this effect.

We tested the question whether junctional cell-to-cell communication is regulated by the diacylglycerol branch of the phosphoinositide transmembrane signal pathway. Cultured epithelial rat liver cells were treated with the synthetic diacylglycerol 1-oleoyl-2-acetyl glycerol, while their junctional permeability was probed with the microinjected 443-dalton fluorescent tracer Lucifer Yellow. The treatment reduced junctional permeability (without affecting Lucifer permeability of nonjunctional cell membrane). The effect was dose dependent, with a threshold of about 25 micrograms diacylglycerol/ml in sparse cultures and about 50 micrograms/ml in confluent cultures. The reduction of junctional permeability began within 3 min of diacylglycerol application, peaked within 20 min, and reversed spontaneously within 90 min. The phorbol ester TPA mimicked the diacylglycerol effect, but the (spontaneous) reversal was slower. We propose that cell-to-cell communication is under dual physiological control: an up-regulatory one, as exerted by the cyclic AMP signal route (Loewenstein, W.R., 1985, Biochem. Soc. Symp. London, 50: 43-58), and a downregulatory one, by the diacylglycerol signal route. TMB-8 (54-70 microM)--a blocker of intracellular Ca2+ mobilization--impeded the diacylglycerol action on junctional permeability. It prevented the effect of low diacylglycerol doses completely and it markedly reduced the effect of high doses. (It also counteracted the effect of TPA.) Ca2+ thus emerges as a possible candidate for a role in the junctional downregulation by the diacylglycerol signal route. We tentatively advance two models. In one, leaning closely on the Calcium Hypothesis of cell-to-cell channel regulation (Loewenstein, W.R., 1966, Ann. N.Y. Acad. Sci. 137:441-472), Ca2+ mediates the action of the route on the channel. In the other, Ca2+ acts farther removed from the channel, on protein kinase C. Calmidazolium (5-10 microM)--an inhibitor of calmodulinactivated proteins--did not prevent the diacylglycerol-induced reduction of junctional permeability. Nor did sodium orthovanadate (25 or 50 microM)--an inhibitor of tyrosyl phosphatase--prevent the reversal of diacylglycerol-induced (or TPA-induced) reduction of junctional permeability.

Animals↗
PubMed1985

Permeability properties of cell-to-cell channels: kinetics of fluorescent tracer diffusion through a cell junction.

We have analyzed the intracellular and cell-to-cell diffusion kinetics of fluorescent tracers in the Chironomus salivary gland. We use this analysis to investigate whether membrane potential-induced changes in junctional permeability are accompanied by changes in cell-to-cell channel selectivity. Tracers of different size and fluorescence wavelength were coinjected into a cell, and the fluorescence was monitored in this cell and an adjacent one. Rate constants, kj, for cell-to-cell diffusion were derived by compartment model analysis, taking into account (i) cell-to-cell diffusion of the tracers; (ii) their loss from the cells; (iii) their binding (sequestration) to cytoplasmic components; and (iv) their relative mobility to cytoplasm, as determined separately on isolated cells. In cell pairs, we compared a tracer's kj with the electrical cell-to-cell conductance, gj. At cell membrane resting potential, the kj's ranged 3.8-9.2 X 10(-3) sec-1 for the small carboxyfluorescein (mol wt 376) to about 0.4 X 10(-3) sec-1 for a large fluorescein-labeled sugar (mol wt 2327). Cell membrane depolarization reversibly reduced gj and kj for a large and a small tracer, all in the same proportion. This suggests that membrane potential controls the number of open channels, rather than their effective pore diameter or selectivity. From the inverse relation between tracer mean diameter and relative kj we calculate an effective, permeation-limiting diameter of approximately 29 A for the insect cell-to-cell channel. Intracellular diffusion was faster than cell-to-cell diffusion, and it was not solely dependent on tracer size. Rate constants for intracellular sequestration and loss through nonjunctional membrane were large enough to become rate-limiting for cell-to-cell tracer diffusion at low junctional permeabilities.

Animals↗
PubMed1983

Cell-to-cell channels with two independently regulated gates in series: analysis of junctional conductance modulation by membrane potential, calcium, and pH.

We study cell-to-cell channels, in cell pairs isolated from Chironomus salivary gland, by investigating the dependence of junctional conductance (gj) on membrane potentials (E1, E2), on Ca2+, and on H+, and we explore the interrelations among these dependencies; we use two separate voltage clamps to set the membrane potentials and to measure gj. We find gj to depend on membrane potentials whether or not a transjunctional potential is present. The pattern of gj dependence on membrane potentials suggests that each channel has two closure mechanisms (gates) in series. These gates pertain, respectively, to the two cell faces of the junction. By treating the steady-state gj as the resultant of two simultaneous but independent voltage-sensitive open/closed equilibria, one within each population of gates (i.e., one on either face of the junction), we develop a model to account for the steady-state gj vs. E relationship. Elevation of cytosolic Ca2+ or H+ at fixed E lowers gj, but at moderate concentrations of these ions this effect can be completely reversed by clamping to more negative E. Overall, the effect of a change in pCai or pHi takes the form of a parallel shift of the gj vs. E curve along the E axis, without change in slope. We conclude (1) that the patency of a cell-to-cell channel is determined by the states of patency of its two gates; (2) that the patency of the gates depends on membrane potentials (not on transjunctional potential), on pCai, and on pHi; (3) that pCai and pHi determine the position of the gj vs. E curve on the E axis; and (4) that neither Ca2+ nor H+ at moderate concentrations alters the voltage sensitivity of gj.

Animals↗
PubMed1982

Compensatory hypoventilation in metabolic alkalosis.

Although hyperventilation is a well-known compensatory mechanism in metabolic acidosis, compensatory hypoventilation has been inconsistent and controversial in metabolic alkalosis. Six healthy subjects were studied under baseline conditions and during steady-state metabolic acidosis (seven episodes) and alkalosis (14 episodes). Minute ventilation (VE) fell in metabolic alkalosis and rose in metabolic acidosis. These changes in ventilation were entirely due to reduction and elevation of tidal volume (VT) respectively, while respiratory frequency (f) remained unchanged. Alveolar ventilation fell during metabolic alkalosis and resulted in elevation of arterial PCO2 in all subjects. The ventilatory response to arterial PCO2 in all subjects. The ventilatory response to CO2 breathing was also diminished. There was a linear relationship between PaCO2 and plasma [HCO-3] in metabolic acidosis and alkalosis which was defined as PaCO2 (mm Hg = 0.7 [HCO-a] + 20 (+/- SEM), r = 0.95. Although arterial PO2 and plasma [K+] fell during metabolic alkalosis, minute ventilation did not change upon breathing oxygen and there was no correlation between changes in plasma [K+] and plasma H+ regulation.

Acidosis↗
PubMed1981

Diameter of the cell-to-cell junctional membrane channels as probed with neutral molecules.

The cell-to-cell channels in the junctions of an insect salivary gland and of insect and mammalian cells in culture were probed with fluorescent molecules-neutral linear oligosaccharides, neutral branched glycopeptides, and charged linear peptides. From the molecular dimensions of the largest permeants and smallest impermeants the permeation-limiting channel diameter was obtained: 16 to 20 angstroms for the mammalian cells and 20 to 30 angstroms for the insect cells.

Animals↗
PubMed1980

Permeability of the cell-to-cell membrane channel and its regulation in an insect cell junction.

Cells of organs and tissues commonly communicate directly with one another via permeable membrane junctions. Cell-to-cell channels, spanning the width of both membranes of a junction, are thought to provide the pathways between the cytoplasms of adjacent cells for the immediate exchange of ions and small molecules. We study these cell-to-cell channels in a cell model system, the salivary gland of Chironomus. Using intracellularly injected fluorescent labelled peptides and oligosaccharides of various molecular dimensions as channel permeability probes we find the channels to have a bore of about 2 nm. The channel permeability can be modulated and, in the extreme, the channels can be closed under various experimental conditions. With the aid of the Ca2+-sensitive photoprotein aequorin as monitor of cytoplasmic free Ca2+ concentration, we show that a determining factor in this modulation of channel permeability is the cytoplasmic free Ca2+ concentration. Moreover, results obtained by injection of different-sized and different-labelled channel permeability probes together with Ca2+ indicate that closure of the individual channels may occur in more than one step, i.e., by a graded reduction of channel bore.

Animals↗
PubMed1980

Monocyte chemotaxis in leukemia patients.

Monocyte chemotaxis was studied in 35 patients with ALL, six with CLL, six with AML, and 10 with CML before beginning chemotherapy. Function was contrasted to age-matched control groups. Significant inhibition of chemotaxis was seen in patients with ALL (p less than 0.001) and CLL (p less than 0.01), whereas function in CML and AML patients was not significantly depressed. The deficient monocyte chemotaxis was not due merely to decreased percentages of peripheral blood monocytes. Thus, in addition to numerical deficiencies in monocyte numbers, qualitative deficiencies in monocyte function exist in patients with ALL and CLL.

Acute Disease↗
PubMed1979

Acute nonlymphoblastic leukemia in childhood.

Cytogenetic studies have been done on a group of childhood patients over a period of 3 1/2 years in which time Giemsa trypsin banding was applied to all specimens. Fifteen of the 107 patients (14%) were diagnosed as having acute nonlymphoblastic leukemia (ANLL). Twelve of the 15 had chromosomal abnormalities. The most common was an involvement of the No. 7 chromosome which occurred in five patients. Three patients had trisomy 19. No correlation could be found between the disease subgroup and the karyotypic aberration in patients with anomalies involving a common chromosome.

Adolescent↗
PubMed1979

Cytogenetic studies of chronic myelocytic leukemia in children and adolescents.

In a 3 1/2 year cytogenetic study of 107 leukemia patients diagnosed in childhood and adloescence, 8 presented with chronic myelogenous leukemia (CML). Seven of the 8 had chromosomal abnormalities. Six had the Ph1 chromosome; 5 had the usual 9;22 translocation. Two patients had involvement with chromosome 15; one had a 9;15 translocation in Ph1 positive cells during remission while a second had a 1;15 translocation during blastic crisis. The 2 patients who did not have a Ph1 chromosome survived 13 and 30 months, respectively, considerably less time than the 4+ year survival in most of those with Ph1 positive CML.

Adolescent↗