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Biomedical subjects

R Boland

Publications and source records attributed to R Boland.

At least 91 records · Page 5Linked to original sources
PubMed1983

Effect of 1,25-dihydroxycholecalciferol on sarcoplasmic reticulum calcium transport in strontium-fed chicks.

Feeding of chicks with strontium, an inhibitor of 1,25-dihydroxycholecalciferol synthesis in kidney, during 7 days, significantly depressed the initial rate of calcium uptake and calcium storing capacity of sarcoplasmic reticulum membranes from skeletal muscle. Oral administration of 1,25(OH)2D3 to strontium-fed animals returned calcium transport values to normal. The changes observed could not be related to differences in the relative proportions of transport ATPase and calcium binding proteins. The results are consistent with a role of 1,25(OH)2D3 in muscle function.

Animals↗
PubMed1983

Reversal of decreased phosphorylation of sarcoplasmic reticulum calcium transport ATPase by 1,25-dihydroxycholecalciferol in experimental uremia.

When compared to that from sham-operated controls, sarcoplasmic reticulum isolated from skeletal muscle of uremic rabbits had a lower rate of calcium uptake and storing capacity. In vivo administration of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] restored the values in uremic animals toward normal. To obtain information about the mechanisms responsible for these differences, phosphorylation of the calcium transport ATPase was studied. The steady-state levels of phosphoprotein in uremic membranes were lower and returned to normal when the secosteroid was administered. Electrophoresis of the membranes phosphorylated with 32P-inosine triphosphate (32P-ITP) showed that the differences were related to a 100,000 dalton protein. The rate of phosphoprotein formation, determined with 32P-ITP and at 0 degrees C, was considerably lower in uremic than in control animals. Pretreatment with 1,25(OH)2D3 prevented this change. The hypothesis is advanced that the vitamin D metabolite affects the steady-state concentration and rate constant of formation of active sites in the Ca-ATPase. These results may partly explain the altered Ca transport function of the sarcoplasmic reticulum in experimental uremia.

Animals↗
PubMed1983

The effect of cholecalciferol in vivo on proteins and lipids of skeletal muscle from rachitic chicks.

The protein and lipid constituents of skeletal muscle subcellular fractions isolated from chicks fed a vitamin D-deficient diet for 3 weeks and chicks replated with cholecalciferol (vitamin D3) were analyzed. Administration of the sterol markedly altered the protein composition of mitochondria. The changes were localized in the inner membranes and consisted of a modification of the relative amounts of proteins of approximate mol wt of 83,000, 58,000, 42,000, and 34,000. In addition, treatment with vitamin D3 modified the distribution pattern of components of the actomyosin contractile complex. An increase in actin and troponin C was particularly noticeable. No differences between rachitic and treated animals were detected in the protein composition of sarcoplasmic reticulum membranes and postmicrosomal soluble fraction. A significant increase in the phospholipid content of sarcoplasmic reticulum (P less than 0.05), and to a lesser extent of mitochondria, was observed in repleted chicks. The relative proportions of individual phospholipids, however, were not changed. Injection of an acute dose of cholecalciferol to chicks less severely depleted in vitamin D significantly stimulated the incorporation of 32PO4 in vivo to muscle homogenates, mitochondria, and sarcoplasmic reticulum (P less than 0.05). As the increases in specific activities of sarcoplasmic inorganic P and membrane lipid P were similar whereas that of serum remained unchanged, the results are compatible with the idea that vitamin D3 stimulates phosphate fluxes across muscle membranes. The sterol produced minor modifications in the fatty acid composition of sarcoplasmic reticulum (P less than 0.05).

Animals↗
PubMed1980

Lack of involvement of sarcoplasmic reticulum in myopathy of acute phosphorous depletion.

Acute and chronic hypophosphatemia are known to cause metabolic myopathy. It has been proposed that impaired Ca transport in subcellular membranes is involved in its genesis. In the present study, calcium transport in the sarcoplasmic reticulum (SR), concentrations of ions or nucleotides and transmembrane potential were investigated in muscles of acutely hypophosphatemic rats, i.e. animals with chronic dietary phosphorous deprivation (PD) and superimposed acute hypophosphatemia resulting from the administration of insulin and glucose. Despite hypophosphatemia and low muscle phosphorous concentration, no significant change of the initial rate of Ca uptake or Ca concentrating ability was observed in the SR of PD rats. Storing capacity was decreased; this may result from altered vesicle geometry. Water content, Na concentration, the concentration of several nucleotides and transmembrane potential of muscle were unchanged in PD rats. The findings document that no intrinsic abnormality of vectorial Ca transport is present in the SR of acutely hypophosphatemic PD animals.

Animals↗
PubMed1980

The biosynthesis of sarcoplasmic reticulum.

Muscle differentiation provides a slow-motion picture of the assembly of highly specialized sarcoplasmic reticulum endowed with Ca2+ transport activity from its constituents. During development of chicken embryo pectoralis muscle, the sarcoplasmic reticulum evolves from the rough endoplasmic reticulum of myoblasts by insertion of Ca2+ transport ATPase molecules synthesized on membrane-bound polysomes into the phospholipid-rich endoplasmic reticulum membrane. The process continues until the Ca2+ ATPase content of the membrane approaches physical saturation. The rate of synthesis of Ca2+ ATPase sharply increases after fusion of myoblasts into multinucleated myotubes and the accumulation of sarcoplasmic reticulum and myofibrillar proteins follows a roughly similar time course. The regulation of Ca2+ ATPase synthesis during development involves myogenic as well as neurogenic mechanisms. There are indications that changes in intracellular free Ca2+ concentration may play a role in this regulation.

Animals↗
PubMed1980

[Phosphate-depletion (author's transl)].

The essential and critical role of inorganic phosphate has been known in veterinary medicine and experimental research on animals for decades. However, only recently has the phosphate depletion syndrome found widespread attention by clinicians. Hypophosphatemia is usually observed in the following clinical situations:chronic alcoholism, recovery phase of diabetic ketoacidosis, administration of phosphate-free solutions in parenteral nutrition, severe respiratory alkalosis, and infusion of fructose. Disturbed organ function in hypophosphatemia is the result of a depletion of inorganic phosphate in the cytoplasm of somatic cells. Such phosphate depletion may be due to either of the following mechanisms or a combination of both. (1) Negative external phosphate balance resulting from phosphate loss in urine or feces or (2) translocation of phosphate from the extracellular into the intracellular space with or without concomitant negative external phosphate balance. In principle, phosphate depletion interferes with the function of all somatic cells. In acute phosphate depletion, the clinically most important disturbances are observed in striated muscle (rhabdomyolysis with myoglobinuric acute renal failure), heart muscle (acute heart failure), and hematological systems (hemolysis, disturbed leukocyte and thrombocyte functions). In contrast, in chronic phosphate depletion skeletal abnormalities (osteomalacia) predominate. Organ disturbances are thought to result from diminished synthesis of ATP and other organic phosphate esters and/or from hypoxia secondary to changes in erythrocyte 2,3-DPG.

Acute Kidney Injury↗
PubMed1980

Phosphate, calcium and lipid metabolism.

Ca and Pi interact with lipid metabolism in several different ways. The enzymes of lipolysis and lipogenesis are sensitive to Ca. Ca and Pi concentrations affect insulin secretion and insulin action. Raising intestinal Ca lowers serum cholesterol and triglycerides presumably by sequestration of cholesterol and bile acids. Administration of vitamin D or increased sensitivity to vitamin D raise serum cholesterol levels. PTH acts primarily by activating adipose tissue lipase. Increased FFA delivery to the liver should increase hepatic lipoprotein synthesis. Experimental data in secondary hyperparathyroidism of renal insufficiency are consistent with this notion. Clinical observations in primary or renal secondary hyperparathyroidism, however, are not explicable by this simple schema.

Adipose Tissue↗
PubMed1980

Function of the sarcoplasmic reticulum (SR) in hypophosphatemic myopathy.

Lipid composition and Ca2+ transport properties were examined in the isolated sarcoplasmic reticulum of non-exercised muscles of markedly phosphorus depleted rats. Phosphorous depletion with a fall of plasma Pi from 8.04 +/- 0.85 to 2.56 +/- 0.48 mg/dl was accompanied by a decrease in muscle Pi and ATP content and by a significant decrease in the phospholipid/protein ratio of sarcoplasmic reticulum. The phosphatidyl -choline/phosphatidyl-ethanolamine ration in sarcoplasmic membranes was increased. Storing capacity for Ca2+ was significantly diminished. In contrast, there was no significant change of kinetic parameters of Ca2+ transport, i.e. of the initial rate of uptake and concentrating ability. These findings do not necessarily exclude changes of cytosolic Ca2+ concentration in phosphate depletion, but they exclude alterations of intrinsic kinetic properties of the sarcoplasmic reticulum as a cause of any such potential changes.

Animals↗
PubMed1979

[Vitamin D metabolism in kidney insufficiency: disorders of an endocrine regulatory zone].

The vitamin metabolite 25(OH)D is transformed into the active secosterole 1.25(OH)2D3 in the proximal tubular epithelium of the kidney. This transformation is disturbed in patients with renal insufficiency. However, this review shows that presumably not all vitamin D dependent disturbances in patients with renal insufficiency are explicable merely as the consequence of reduced renal synthesis of 1.25(OH)2D3 secondary to nephronal loss. In incipient renal failure, vitamin D dependent functions (calcemic action of PTH, intestinal absorption of Ca) are disturbed. Yet, circulating 1.25(OH)2D3 levels are slightly elevated. This finding is compatible with an inadequate response of the renal 1-alpha-hydroxylase system to activating stimuli (hyperparathyroidism, hypocalcemia, fasting hypophosphatemia) and/or end-organ resistance to the action of 1.25(OH)2D3. Osteomalacia in renal insufficiency cannot entirely be explained as the consequence of a reduction of the serum-concentration of any of the known vitamin D metabolites [25(OH)D3; 1.25(OH)2D3; 24.25(OH)2D3]. The relatively poor response of osteomalacia of uremic patients to the administration of 1.25(OH)2D3 leads to the question of whether other vitamin D metabolites or non-vitamin D related factors are important in its genesis. Critical information is lacking with respect to 1.25(OH)2D3 receptors, post receptor events and interaction between vitamin D metabolites and PTH in bone cells of such patients. A specific action of 1.25(OH)2D3 on longitudinal growth of uremic children has been described. However, several clinical and experimental studies failed to provide evidence of normalization of growth by 1.25(OH)2D3 and failed to show differences in this respect between vitamin D and 1.25(OH)2D3. Currently, it remains undecided whether vitamin D metabolites affect PTH secretion, and if so which vitamin D metabolite is involved. Clarification of this problem is of paramount importance for the therapeutic suppression of the parathyroids of uremic patients. Vitamin D metabolites play an important role in some organ functions unrelated to homeostasis of Ca-Pi-metabolism (e.g. muscle, testis, pancreas, etc). The loss of such function is of potential importance in the genesis of the uremic syndrome and its imcomplete reversal by hemodialysis.

Absorption↗
PubMed1979

Synthesis of the calcium transport ATPase of sarcoplasmic reticulum and other muscle proteins during development of muscles cells in vivo and in vitro.

The effect of medium Ca2+ concentration upon the concentration and the rate of synthesis of muscle proteins was investigated in chicken pectoralis muscle cultures. There is an easily identifiable class of muscle protein which includes the Ca2+-ATPase of sarcoplasmic reticulum, myosin, troponin C, ATP : creatine phosphotransferase, muscle specific actin, tropomysin 1 and 2, and muscle hemagglutinin, which show a large increase in concentration during normal development. The increased synthesis of these proteins was inhibited, without inhibition of cell proliferation, in culture media of relatively low Ca2+ concentration, 0.05--0.3 mM, where fusion was prevented. Similar medium Ca2+ concentration was required for the expression of all these proteins, suggesting their coordinate regulation. The proteins are denoted as 'calcium-modulated proteins'. The increased Ca2+ transport activity of sarcoplasmic reticulum in cultured chicken pectoralis muscle cells during development at 1.8 mM medium calcium concentration represents de novo synthesis of the Ca2+ transport ATPase, as shown by immunoprecipitation, active site labeling and direct identification of the Ca2+ transport ATPase on two-dimensional gel electropherograms of whole muscle homogenates. The concentration and the turnover rate of the majority of the muscle proteins is not affected significantly by medium Ca2+ concentration between 0.06 and 1.8 mM. It is proposed that increase in cytoplasmic free Ca2+ concentration during fusion plays a central role in the regulation of the synthesis of calcium-modulated proteins.

Acetylcholinesterase↗
PubMed1977

The lipid composition of muscle cells during development.

Developmental changes in the phospholipid, cholesterol, and fatty acid composition of chicken pectoralis muscle cells were analyzed during development in vivo and in tissue culture. The phospholipid composition of muscle cells showed only minor changes during in vivo or in vitro development but there were significant alterations in fatty acid composition. During in vivo development between the 12th and 22nd days the concentration of palmitate and arachidonate decreased with increase in linoleate. In cultured muscle cells the fatty acid composition changes with surprising plasticity depending on the fatty acid supply. Compensatory changes were observed in the chain length and unsaturation of several fatty acids, aimed presumably at maintaining the physical properties of the lipid phase relatively constant.

Animals↗
PubMed1977

Development of sarcoplasmic reticulum in cultured chicken muscle.

The development of sarcoplasmic reticulum membranes was studied in vivo and in tissue culture in chicken pectoralis muscle cells. The concentration of the calcium- and magnesium-activated ATPase measured by selective labeling of the enzyme with [32P]ATP in whole muscle homogenates was found to increase in developing chicken pectoralis muscle in vivo from 0.01 nmol/mg of protein in 12-day embryos to 0.3 to 0.4 nmol/mg of protein in 1-month-old chicks, where it constitutes about 3% of the total protein content of muscle. In cultured muscle cells the concentration of calcium-sensitive phosphoprotein increased from 0.015 nmol/mg of protein at 2 days to 0.04 to 0.05 nmol/mg of protein after 5 days of culture. This amount represents about 0.5% of the protein content of the muscle cells. The accumulation of Ca2+ transport ATPase began during fusion and continued with a linear rate during 8 days of culture. The density of 75 A intramembranous particles seen by freeze-etch electron microscopy on fracture faces of sarcoplasmic reticulum membranes is about 4,000/mum2 in adult chick pectoralis muscle but only 400/mum2 in cultured muscle cells in rough proportion to the concentration of Ca2+-sensitive phosphoprotein. The Ca2+, Na+, and K+ concentration of the medium and addition of ouabain, caffeine, or the calcium ionophores A23187 and X537A sharply influence the concentration of calcium transport ATPase in cultured muscle cells, parallel with their effect upon cell fusion and growth. These observations are consistent with the proposition that the gene expression leading to the accumulation of Ca2+ transport ATPase during development in culture may be regulated by intracellular ion concentrations.

Aging↗
PubMed1976

Mechanism of ATP hydrolysis by sarcoplasmic reticulum and the role of phospholipids.

Exchange of sarcoplasmic reticulum phospholipids with dipalmitoyllecithin inhibits the (Mg2+ + Ca2+)-activated ATPase activity below 40 degrees by inhibition of the decomposition of phosphoprotein intermediate. The rate of phosphoprotein formation and the steady state concentration of phosphoprotein measured by rapid kinetic techniques are affected to a lesser extent. The inhibitory effect of dipalmitoyllecithin on ATPase activity is probably related to the viscosity of the hydrocarbon region of the membrane which inhibits the conformational change leading to calcium translocation and the eventual cleavage of phosphoprotein.

Adenosine Triphosphatases↗
PubMedDate not supplied

What, why, and how of consultation-liaison psychiatry. An analysis of the consultation process in the 1990s at five urban teaching hospitals.

There is controversy about the role and function of a consultation-liaison (C-L) psychiatrist, as reflected in the ongoing debate about what to call ourselves. To clarify the essential elements of our function, the authors analyzed the process and content of the entire consultation experience from the time of initial consultation to the time of discharge in 50 patients across 5 urban teaching hospitals. The common components of the C-L process, in this pilot study, were identified to be facilitative, consensus-seeking, and interpretative. Implications of these findings for the C-L psychiatrist's role in the general hospital are discussed.

Hospitals, Teaching↗