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Biomedical subjects

J S Davis

Publications and source records attributed to J S Davis.

At least 127 records · Page 7Linked to original sources
PubMed1984

Angiotensin II rapidly increases phosphatidate-phosphoinositide synthesis and phosphoinositide hydrolysis and mobilizes intracellular calcium in cultured arterial muscle cells.

Smooth muscle cells were cultured from rat thoracic aorta and labeled to a stable specific activity with 45Ca2+, myo-[2-3H]inositol, or 32Pi. The efflux of 45Ca2+ was monitored over 10-sec intervals. Angiotensin II (AII) increased the amount of 45Ca2+ lost by 5-fold in the first 10-sec interval after the addition of AII and by 10-fold in the second 10-sec interval. AII-stimulated 45Ca2+ release was blocked by the angiotensin antagonist [1-sarcosine, 8-leucine]AII and by La3+. The removal of external Ca2+ had no effect on AII-stimulated 45Ca2+ release. Depolarization with high external K+ only slightly increased 45Ca2+ efflux and had no effect on AII-induced 45Ca2+ release. AII had no effect on the initial rate of 45Ca2+ influx. These results indicate that the rapid 45Ca2+ efflux evoked by AII is probably due to the release of 45Ca2+ sequestered intracellularly rather than to an increase in the Ca2+ permeability of the plasma membrane. AII provoked rapid increases in the levels of phosphatidic acid and phosphoinositides in the cells. These increases in phospholipids were associated with increases in phospholipase C-generated inositol phosphates (tri-, di-, and mono-). It appears that AII simultaneously increases phosphoinositide hydrolysis and synthesis in vascular smooth muscle, and both phospholipid effects may contribute to inositol triphosphate generation, which was sufficiently rapid to have a role in intracellular Ca2+ mobilization.

Angiotensin II↗
PubMed1984

Rapid effects of angiotensin-II on polyphosphoinositide metabolism in the rat adrenal glomerulosa.

Angiotensin-II (A-II) provoked a rapid decrease in 32p in triphosphoinositide (TPI) in 32p-prelabeled rat adrenal glomerulosa cells. This effect (presumably reflecting TPI hydrolysis) of A-II was nearly maximal at 5 sec of incubation and appeared to precede increases in labeling of phosphatidic acid and phosphatidylinositol. Other aldosterone-stimulating agents (ACTH, K+ and serotonin) did not provoke this effect. Since this effect appeared to be independent of Ca++, it is possible that TPI hydrolysis may be important for Ca++ mobilization during A-II action in glomerulosa tissue.

Adrenal Glands↗
PubMed1983

Activation of protein kinase in the bovine corpus luteum by phospholipid and Ca2+.

A new species of protein kinase has been identified in cytosol preparations from bovine corpora lutea. Enzyme activity required the simultaneous presence of Ca2+ and phospholipid, and was also enhanced by glyceryl dioleate. Phosphatidylserine was the most effective phospholipid for stimulating histone phosphorylation. Other phospholipids capable of supporting enzymic activity were, in order of decreasing activity, phosphatidylinositol, phosphatidic acid, cardiolipin and phosphatidylglycerol. Several other phospholipids tested were ineffective. A cyclic AMP-dependent protein kinase was also present in the luteal cytosol. This enzyme activity was eliminated by protein kinase inhibitor without affecting the Ca2+- and phospholipid-stimulated activity. Lysine-rich histone (IIIS) was a much better substrate than type-IIA histone for Ca2+- and phospholipid-dependent phosphorylation. Ca2+ and phospholipid also enhanced phosphorylation of endogenous luteal cytosol protein. Calmodulin, alone or in the presence of Ca2+, was unable to increase phosphorylation. Trifluoperazine inhibited protein kinase activity stimulated by Ca2+ and phospholipid. These data suggest that a phospholipid-sensitive, Ca2+-dependent protein kinase may provide an important link between hormonally-induced changes in phospholipid metabolism and corpus-luteum function.

Animals↗
PubMed1983

Acute effects of steroids on immune complex profile of patients with systemic lupus erythematosus. Correlation of profile with development of target organ involvement.

Eleven patients with active systemic lupus erythematosus, previously untreated, were studied to 1) determine the acute effect of corticosteroids on circulating immune complex (CIC) levels and 2) correlate the initial CIC profile with the development of organ system involvement. Using serial measurements of CIC as detected by assays for cryoglobulins and binding to C1q, Raji cells, and rheumatoid factor, we found that levels of CIC change little during the first month of high dose daily steroid therapy, but they uniformly decrease to near normal by 6 to 12 months. High levels of CIC detected by Raji cell assay early in the course of systemic lupus erythematosus and before steroid therapy appear to be predictive of the development of chronic lupus nephritis (P less than 0.005).

Adult↗
PubMed1983

The effects of IgM rheumatoid factor on EAM and EAG rosette formation with Fc receptor-bearing lymphoid cells.

IgM rheumatoid factors (IgM-RF) and IgM from normal donors (IgM-C) were tested for their effects on rosette formation of Fc receptor (FcR)-bearing lymphoid cells with IgM- or IgG-coated bovine red blood cells (EAM or EAG). All cell populations tested bearing FcR for IgG (FcRG) showed reduced numbers of EAG rosettes formed in the presence of IgM-RF; IgM-C had no effect on EAG rosette formation with FcRG-bearing cells. T cells or L cells bearing FcRM showed reduced numbers of EAM rosettes in the presence of any IgM preparation. In addition, IgM-RF facilitated EAG-rosette formation with TM cells. These studies confirm that native IgM can bind to FcRM, blocking EAM rosettes, and that IgM-RF can modulate the binding of an IgG-containing immune complex to FcR-bearing cells.

Humans↗
PubMed1983

Gonadotropin-releasing hormone (GnRH) stimulates phosphatidylinositol metabolism in rat granulosa cells: mechanism of action of GnRH.

This report describes the effects of gonadotropin-releasing hormone (GnRH; gonadoliberin) and an agonist, [D-Ala6, des-Gly10]GnRH ethyl amide (GnRHa), on phospholipid metabolism in rat granulosa cells isolated from mature Graafian follicles. As indicated by the incorporation of 32PO4, GnRHa rapidly (less than 2 min) stimulated the labeling of phosphatidic acid and phosphatidylinositol but had no effect on the labeling of other phospholipids. Increased phosphatidylinositol labeling was also observed when myo-[2-3H]inositol was incubated with granulosa cells in the presence of GnRHa. Increases in labeling were dependent on the dose of GnRH and time of incubation. Thyrotropin-releasing hormone and a specific GnRH antagonist had no effect on labeling, but a GnRH antagonist prevented the stimulatory action of GnRH. In addition, treatment with GnRHa slightly increased the levels of phosphatidylinositol (15%) in 60-min incubations but had no effect on the levels of other phospholipids. Significant increases in progesterone accumulation were observed after 30 min of incubation with GnRHa, and further increases were correlated with the time of incubation. The stimulatory action of GnRH on phospholipid metabolism and progesterone accumulation was not related to increases in cyclic nucleotide accumulation. In incubations lasting up to 30 min, GnRHa had no effect on cAMP accumulation. However, a transient decrease in cGMP levels was observed in response to GnRHa. These studies suggest that the rapid and specific effects of GnRH on phospholipid metabolism in rat granulosa cells represent early events in the action of GnRH.

Animals↗
PubMed1983

Stimulation of phospholipid synthesis by luteinizing hormone in isolated rat granulosa cells.

This report describes the effect of LH on phospholipid metabolism in rat granulosa cells isolated from mature Graafian follicles. As indicated by the incorporation of radioactive phosphate, LH specifically stimulated the labeling of phosphatidic acid (PA) and phosphatidylinositol (PI). This effect was observed after 2 min and was more pronounced with further incubation with LH. Increases in PI labeling were correlated with increases in LH-induced progesterone accumulation. LH also increased the tissue concentrations of PI. Addition of exogenous PA or PI, but not other phospholipids, increased progesterone accumulation by granulosa cells. These results indicate that LH has selective effects on phospholipid metabolism in rat granulosa cells which may play a role in ovarian steroidogenesis.

Animals↗
PubMed1983

Calcium- and lipid-dependent protein phosphorylation in the human ovary.

The cytosol of human ovarian tissues was observed to promote protein phosphorylation in the combined presence of Ca2+, 1,2-diolein, and phosphatidylserine. Ca2+ alone or lipid alone did not produce full activation of this protein kinase(s). The addition of human erythrocyte calmodulin to the assay mixture, in the presence or absence of Ca2+, had no effect on protein kinase activity. Phosphorylation of cytosol proteins ranging in mol wt from 10,000 to 200,000 was selectively increased by Ca2+ plus lipid. This protein kinase activity may play a crucial role in the intracellular transmission of the action of hormones affecting cellular Ca2+ flux and/or phospholipid metabolism.

Calcium↗
PubMed1983

Coronary bypass operation following acute complicated myocardial infarction.

The indications for operation to correct acute mechanical defects after myocardial infarction are clearly established. Less clear is the use of surgical procedures for nonmechanical complications such as persistent ischemia or circulatory collapse. Between 1974 and 1981, 80 patients underwent coronary artery bypass grafting (CABG) within 2 weeks of infarction. Continued pain was the indication in 83% and cardiogenic shock in 17%. Seventeen patients were operated upon within 24 hours of infarction, 35 from 1 to 7 days, and 28 from 8 to 14 days. Eighty-one percent were men; mean age was 58 years. In 39% of patients the infarction was the premier symptom of coronary artery disease. Sixty-two percent had impaired left ventricular function as judged by left ventricular end-diastolic pressure greater than 15 mm Hg or abnormal wall motion seen on ventriculogram. Overall operative mortality was 5.0%; early mortality by indication was 3.0% for pain and 14.3% for shock. Operation for pain carried a 7.7% mortality if done within 48 hours of infarction and was 0% for those patients operated upon after that time. The status of 90% of all patients was known as of December, 1981, with a mean follow-up of 2.9 years. Life-table analysis demonstrates a 5 year survival rate of 85% +/- 6% in the group operated upon for pain. CABG in the immediate postinfarction period can be done safely with a 5 year survival in patients without hemodynamic compromise comparable to that of patients with chronic angina undergoing elective operation. These results should encourage the application of early postinfarction CABG in other high-risk subgroups of patients.

Angina Pectoris↗
PubMed1982

Rheumatoid factor inhibition of in vitro binding of IgG complexes in the human glomerulus.

We studied the effects of rheumatoid factor (RF) on binding of immune complexes to activated C3 (C3b) receptors in vitro. IgM fraction of serum containing RF activity (IgM-RF), IgM isolated from pooled normal human serum and have no RF activity (IgM-control), bovine serum albumin, and Veronal buffered saline solutions were used in a C3b assay system consisting of aggregated human IgG (AggHuIgG) coupled to sheep erythrocytes (SRBC) with guinea pig and normal human serum complement. The number of glomerular bound AggHuIgG-SRBC with IgM-control and bovine serum albumin or Veronal buffered saline was similar, while the number of bound cells with IgM-RF was reduced significantly, This effect was seen with both guinea pig and normal human serum complements. Supernatant hemolytic complement activity was maintained with IgM-RF, but reduced with control solutions. The blocking factor was shown to be RF by serial dilutions of IgM-RF resulting in inverse correlations with latex flocculation and inhibition of SRBC binding, absorption of blocking from IgM-RF with insolubilized AggHuIgG, and failure of IgM-control to block binding. IgM-RF did not directly interfere with activation of complement, but blocked attachment of C3 to AggHuIgG and formation of C3b capable of reacting with glomerular receptors. These results showed that IgM-RF can inhibit binding of AggHuIgG complexes to human glomeruli. This in vitro phenomenon may represent a possible protective mechanism of RF in vivo in diseases with immuno complexes.

Antigen-Antibody Complex↗
PubMed1982

The design and use of a hydraulically operated upward pressure-jump.

The construction of a hydraulically operated upward pressure-jump is described. Previous instruments with a comparable rate of pressurization used helium gas to pressurize an observation cell to approximately half of the operating pressure reached with the present design. The above instrument, which can pressurize the observation cell in 1.8-3.8 ms, is safe to use and has a maximum working pressure of 30 MPa (300 atm). The device is compact in design and can easily be fitted to any observation cell capable of withstanding the transient change in pressure and of effectively damping cell resonances. The instrument finds specific application in the study of macromolecular equilibria with a large difference in volume between the equilibrium partners. This allows the system to be perturbed far from the equilibrium position at atmospheric pressure; the relaxations obtained can be analysed as essentially unidirectional processes. Kinetic data for the reverse reaction would be obtained from experiments in a conventional downward pressure-jump. A study on the kinetics of the self-assembly of the myosin thick-filament is presented as a practical example.

Animals↗
PubMed1981

The influence of pressure on the self-assembly of the thick filament from the myosin of vertebrate skeletal muscle.

The thick-filament-monomeric-myosin equilibrium was prepared from pure myosin at pH 8.1. The application of hydrostatic pressure to the self-assembly equilibrium resulted in a biphasic dissociation curve in which a linear decrease in turbidity (a measure of weight added to or lost from the filament) was followed by a transition to a second pressure-insensitive phase. The first phase represents the effect of hydrostatic pressure on the growth or propagation phase of filament assembly. Here is was shown that hydrostatic pressure served to shorten the filaments in concert towards the bare zone whilst maintaining the narrow length distribution seen at atmospheric pressure; the filament concentration remained constant during the experiment. A more precise definition of the delta-v for the assembly of monomer into filament was obtained than had hitherto been possible. The positioning of the bare zone at the centre of the filament seems to be one of the more obvious functions of the length-regulation mechanism. It also appears that all the basic structural elements of the native thick filament are potentially present in the pH 8.1 homopolymer; its length can be increased by physiological concentrations of MgCl2 and decreased by pressure. The monodisperse native filament could then be formed by a fine tuning of the basic length-regulation mechanism of the homopolymer by the co-polymerization of the other thick-filament proteins.

Animals↗
PubMed1981

Pressure-jump studies on the length-regulation kinetics of the self-assembly of myosin from vertebrate skeletal muscle into thick filament.

The self-assembly of myosin monomer into thick filament occurs via a two-step mechanism. At first a pair of myosin monomers reacts to form a parallel dimer; the dimer in turn adds to the filament ends at a rate that is independent of filament length. The rate of the dissociation reaction on the other hand is length-dependent. The 'off' rate constant has been shown to increase exponentially by a factor of 500 as the filament grows from the bare-zone out to its full length. The length of the filament is thus kinetically controlled; myosin is added to the filament at a fixed rate, whereas the dissociation rate increases to a point where equilibrium is established and the filament ceases to grow. The structural implications implicit in the mechanism are discussed.

Animals↗
PubMed1981

Energy coupling to K+ transport in Paracoccus denitrificans.

Paracoccus denitrificans requires potassium for normal growth and transports this cation by at least two systems, one with low (Km approximately 1 to 2 mM) and another with high (Km approximately 0.1 microM) affinity. Neither of the two systems seems to be dependent on periplasmic components since each retains full activity in cells subjected to an osmotic shock. P. denitrificans accumulates potassium at high velocity (270 nmol of K+/min/mg dry weight of cells) and against a large concentration gradient. The intracellular concentration of K+ in media of high osmolarity (about 320 mosmol) is 0.4 M; this gives a concentration gradient [K+]i/[K+]e of greater than or equal to 2 X 10(4). The uptake of potassium against its concentration gradient requires a source of energy and is eliminated by the addition of uncouplers. The increased rate of energy usage for potassium transport results in an increased rate of ATP synthesis by the respiratory chain and is expressed in enhanced rates of respiration and substrate utilization. The stimulation of respiration is accompanied by increased steady state reduction level of the components of the respiratory chain. The calculations show that two K+ are most likely to be transported per one ATP hydrolyzed.

Adenine Nucleotides↗