Grouse and ptarmigan nutrition in the wild and in captivity.
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Aging↗
Biomedical subjects
R Moss
Publications and source records attributed to R Moss.
Staff nurse job satisfaction and management style.
By using appropriate management styles, nurse managers can affect staff nurse job satisfaction. A study of 623 staff nurses in three Midwestern hospitals shows staff nurse job satisfaction clearly improves as the management style nears the participative management style.
Authoritarianism↗
Absence of the beta subunit (cchb1) of the skeletal muscle dihydropyridine receptor alters expression of the alpha 1 subunit and eliminates excitation-contraction coupling.
The multisubunit (alpha 1s, alpha 2/delta, beta 1, and gamma) skeletal muscle dihydropyridine receptor transduces transverse tubule membrane depolarization into release of Ca2+ from the sarcoplasmic reticulum, and also acts as an L-type Ca2+ channel. The alpha 1s subunit contains the voltage sensor and channel pore, the kinetics of which are modified by the other subunits. To determine the role of the beta 1 subunit in channel activity and excitation-contraction coupling we have used gene targeting to inactivate the beta 1 gene. beta 1-null mice die at birth from asphyxia. Electrical stimulation of beta 1-null muscle fails to induce twitches, however, contractures are induced by caffeine. In isolated beta 1-null myotubes, action potentials are normal, but fail to elicit a Ca2+ transient. L-type Ca2+ current is decreased 10- to 20-fold in the beta 1-null cells compared with littermate controls. Immunohistochemistry of cultured myotubes shows that not only is the beta 1 subunit absent, but the amount of alpha 1s in the membrane also is undetectable. In contrast, the beta 1 subunit is localized appropriately in dysgenic, mdg/mdg, (alpha 1s-null) cells. Therefore, the beta 1 subunit may not only play an important role in the transport/insertion of the alpha 1s subunit into the membrane, but may be vital for the targeting of the muscle dihydropyridine receptor complex to the transverse tubule/sarcoplasmic reticulum junction.
Action Potentials↗
Chloride-induced Ca2+ release from the sarcoplasmic reticulum of chemically skinned rabbit psoas fibers and isolated vesicles of terminal cisternae.
There is increasing evidence that Ca2+ release from sarcoplasmic reticulum (SR) of mammalian skeletal muscle is regulated or modified by several factors including ionic composition of the myoplasm. We have studied the effect of Cl- on the release of Ca2+ from the SR of rabbit skeletal muscle in both skinned psoas fibers and in isolated terminal cisternae vesicles. Ca2+ release from the SR in skinned fibers was inferred from increases in isometric tension and the amount of release was assessed by integrating the area under each tension transient. Ca2+ release from isolated SR was measured by rapid filtration of vesicles passively loaded with 45Ca2+. Ca2+ release from SR was stimulated in both preparations by exposure to a solution containing 191 mm choline-Cl, following pre-equilibration in Ca2+-loading solution that had propionate as the major anion. Controls using saponin (50 microg/ml), indicated that the release of Ca2+ was due to direct action of Cl- on the SR rather than via depolarization of T-tubules. Procaine (10 mM) totally blocked Cl-- and caffeine-elicited tension transients recorded using loading and release solutions having ([Na+] + [K+]) x [Cl-] product of 6487.69 mm2 and 12361.52 mm2, respectively, and blocked 60% of Ca2+ release in isolated SR vesicles. Surprisingly, procaine had only a minor effect on tension transients elicited by Cl- and caffeine together. The data from both preparations suggests that Cl- induces a relatively small amount of Ca2+ release from the SR by activating receptors other than RYR-1. In addition, Cl- may increase the Ca2+ sensitivity of RYR-1, which would then allow the small initial release of Ca2+ to facilitate further release of Ca2+ from the SR by Ca2+-induced Ca2+ release.
Animals↗
AORN sales professional course.
The sales professional course "Introduction to the Operating Room" offered by the AORN Center for Nursing Practice, Health Policy, and Research is an introductory program in OR etiquette. Its purpose is to provide sales professionals a working knowledge of OR protocol for them to function appropriately in OR settings. Sales professionals who have completed this course establish mutually beneficial perioperative partnerships with OR personnel. Sales professionals' effectiveness is strengthened as a result of their newly acquired knowledge of OR protocol, and patient safety is protected. An AORN Certificate of Recognition is awarded on completion of the course.
Commerce↗
Aerosolized recombinant human DNase in hospitalized cystic fibrosis patients with acute pulmonary exacerbations.
The goal of this study was to evaluate the safety and efficacy of recombinant human DNase (rhDNase) in hospitalized patients with cystic fibrosis (CF) experiencing acute pulmonary exacerbations. Eighty patients with documented CF were enrolled at 11 CF centers when admitted for antibiotic therapy. Patients were at least 5 yr old with a forced vital capacity (FVC) > or = 35% of predicted and an oxygen saturation > or = 90% on a fraction of inspired oxygen (FIO2) < 0.5. Patients were randomized to receive rhDNase 2.5 mg in 2.5 ml excipient twice a day (n = 43) or 2.5 ml excipient alone twice daily (n = 37) along with conventional treatment for exacerbations. Administration of rhDNase was not associated with acute adverse events or deaths, and no patients experienced allergic or anaphylactic reactions. Although forced expiratory volume in one second (FEV1) and FVC improved in both treatment groups during the double-blind period, there were no statistically significant differences in the mean change from baseline in FEV1 or FVC between the two groups. rhDNase therapy is safe and well tolerated in CF patients with acute exacerbations requiring hospitalization, but the study did not demonstrate a statistically significant therapeutic effect of rhDNase when added to a regimen of antibiotics and chest physical therapy.
Acute Disease↗
Is there a future for the general hospital?
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England↗
Endothelial "stunning" following a brief exposure to endotoxin: a mechanism to link infection and infarction?
BACKGROUND: There is an association between infection, inflammation and acute cardiovascular events. In an attempt to explore the mechanism of this association we have developed a model to examine the effects on endothelial function of a brief exposure to endotoxin. METHODS AND RESULTS: Endotoxin was instilled into isolated superficial hand veins of healthy volunteers. The vein was isolated by means of two wedges and endotoxin instilled into the isolated segment. After 1 h the contents of the vein were aspirated and the wedges removed. Dose-response curves to bradykinin (a stimulator of nitric oxide synthesis), arachidonic acid (the precursor of prostanoid production) and GTN (a nitric oxide donor) were constructed before and 1 h after endotoxin. Endotoxin caused a glucocorticoid-inhibitable attenuation in the dose-response curves to bradykinin and arachidonic acid (P < 0.05). This effect persisted for 48 h and took 7 days to recover. Exposure of saphenous vein to endotoxin in vitro also caused selective impairment of endothelium-dependent relaxation (P < 0.05) yet microscopy of the vessels exposed to endotoxin showed no endothelial denudation or structural damage. CONCLUSION: The results demonstrate that a brief local exposure to endotoxin caused endothelial dysfunction that persists for 48 h and takes up to 7 days to recover. The endothelial dysfunction is not due to expression of the inducible isoform of nitric oxide synthase and persists for far longer than the effects of endotoxin on vascular smooth muscle function. We have coined the term endothelial "stunning" to describe the transient endothelial dysfunction and suggest it might provide a mechanism underpinning the association between infection or inflammation and increased cardiovascular risk. Endothelial stunning appears to provide a novel, transient, variable and modifiable potential cardiovascular risk factor.
Adult↗
Cell surface adrenergic receptor stimulation modifies the endothelial response to SIRS. Systemic Inflammatory Response Syndrome.
The complex pathway seen in patients with the systemic inflammatory response syndrome (SIRS) does not readily respond to mediator blockade. All such trials conducted in SIRS patients have shown no benefit in reducing mortality. We have shown experimentally that in sepsis, the administration of beta 2-adrenoceptor agonists reduces hepatic cellular injury, whereas administration of an alpha 1-adrenoceptor agonist increases hepatic cellular injury. Inflammatory mediators can cause a dose-related reversible change in target endothelial cells (ECs). There is a substantial body of literature describing the anti-inflammatory effects of beta 2-adrenoceptor agonists. They reduce both the increased permeability and the production of inflammatory mediators from ECs. Cellular transduction processes are involved when adrenergic receptor agonists modify either the anti-inflammatory or proinflammatory response to sepsis in ECs. Inflammatory mediators and alpha 1-adrenoceptor agonists stimulate their trimeric G protein-linked receptors to produce diacylglycerol (DAG) and increase the intracellular concentration of calcium. DAG is involved in the production of both inflammatory proteins and lipids. In addition, mitogen-activated protein kinase (MAPK) is activated which is also involved in the production of inflammatory proteins and lipids. beta 2-adrenoceptor agonists activate their trimeric G protein-linked receptors to produce the stimulatory G protein (Gs). Gs stimulates adenyl cyclase to form cyclic adenosine monophosphate (cAMP) and activate protein kinase A (PKA). PKA is involved in activating gene transcription agents to produce anti-inflammatory proteins such as interleukin-10. PKA also inhibits phospholipase C and MAPK. Although promising, the use of beta-adrenoceptor agonists or agonists that increase cellular cAMP to activate the cells' endogenous anti-inflammatory pathway requires further study.
Adrenergic beta-Agonists↗
Ethics committees across a continuum of care.
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Continuity of Patient Care↗
Goal-directed therapy with dopexamine, dobutamine, and volume expansion: effects of systemic oxygen transport on hepatic ultrastructure in porcine sepsis.
OBJECTIVES: Can the hepatic structural deterioration that occurs during peritonitis be attenuated by increasing cardiac output and oxygen consumption (VO2)? Do the agents used to achieve these increases have any characteristic affects on these hepatic structural changes? DESIGN: Randomized, prospective, observational animal study. SETTING: Research laboratory of a university medical school. SUBJECTS: Twenty-five Middle White adolescent pigs, weighing 25 to 30 kg, divided into five groups. INTERVENTIONS: A thermodilution flotation catheter was advanced into the pulmonary artery. Additional catheters were inserted into the jugular, portal, and hepatic veins, and into the femoral artery. Ultrasound flow probes were placed around the portal vein and the hepatic artery. A metabolic cart was attached to the ventilator. Baseline measurements were made and cardiac output was increased by > 25% by administering either dobutamine (10 micrograms/min), dopexamine (10 micrograms/kg/min), or colloid. A control group had its cardiac output maintained at its baseline value. Peritonitis was induced in the four groups by contamination with cecal content and maintained for 6 hrs. Hepatic tissue was then removed for ultrastructural analysis and the animals were killed. MEASUREMENTS AND MAIN RESULTS: Before infection, cardiac output, VO2, and hepatic blood flow were increased in the three treatment groups. In the dobutamine and dopexamine groups, oxygen delivery increased, but decreased in the volume group. Mean arterial pressure increased in the dobutamine and dopexamine groups, but in the volume group, mean arterial pressure was maintained. Six hours after infection, cardiac output and VO2 had further increased in the dobutamine and volume groups, but both variables had decreased in the dopexamine group. After infection in the control group, cardiac output had decreased, although oxygen delivery and VO2 increased. There were no significant differences between hepatic hemodynamic or oxygen transport variables in any of the groups during the infection period. Hepatic ultrastructure was well maintained in the dopexamine group, while considerable deterioration was seen in the volume and control groups. In the dobutamine group, hepatic deterioration was greater than in the other three groups. CONCLUSIONS: Increasing cardiac output and VO2 before and during infection was only protective when dopexamine was administered. Dobutamine infusion was associated with greater hepatic deterioration than that effect seen in either the control or volume groups.
Adrenergic beta-Agonists↗
Injury surveillance at the USTA Boys' Tennis Championships: a 6-yr study.
Injuries that required physical or medical assistance were recorded for participants at the United States Tennis Association National Boys' Tennis Championships from 1986-1988, 1990-1992 (N = 1440, 240 athletes per year). Over the 6-yr period, a total of 304 athletes (or 21.1%) sustained new or recurrent injuries that required evaluation by the medical team. New injuries alone numbered 145 (incidence rate of 9.9 per 100 athletes). The analysis of injuries showed a higher rate of lower than upper extremity injuries. When evaluated by anatomic regions, back injuries were most common followed by thigh, shoulder, and ankle injuries, respectively. When evaluated by injury type, strains and sprains were most common (71% of all injuries) with fractures and dislocations being rare (1.3% of all injuries). The lower extremity provided the majority of sprain type injuries with 87.5% of ligament sprains coming from the knee and ankle. Injuries with tennis eponyms (i.e., tennis toe, tennis leg, tennis elbow, and tennis shoulder) were rare (0%-5% of all injuries). It would appear that these young elite athletes are at significant risk of injury.
Adolescent↗
Decreased glucose transporter protein (GLUT4) in skeletal muscle of hypertriglyceridaemic insulin-resistant rat.
Protein levels (Western blot) of the major glucose transporter isoform (GLUT4) were measured in skeletal muscles (quadriceps femoris) of an animal model of human metabolic syndrome X, i.e. the hereditary hypertriglyceridaemic (HTG) insulin-resistant rats fed various diets. The results were compared with the data obtained in normal Wistar rats which underwent the identical protocol. In HTG rats fed the basal diet (B) or high-sucrose diet (HS) (known to induce hypertriglyceridaemia and to impair insulin action), a decrease of GLUT4 protein levels (B: Control 100 +/- 3 vs HTG 46 +/- 5%, p < 0.005; HS: Control 80 +/- 9 vs HTG 49 +/- 3%, p < 0.005) was observed. Furthermore, marine fish oil (FO) rich in n-3 polyunsaturated fatty acids (PUFA), added to the basal diet (30 wt % of n-3 PUFA) reduced the GLUT4 protein levels (B: 100 +/- 3 vs B+FO: 42 +/- 4%, p < 0.005) in control rats to values similar to those found in HTG rats (B: 46 +/- 4%). However, dietary FO did not have any effect in HTG rats (49 +/- 3%). Feeding the high-sucrose diet supplemented with FO to both the control and HTG rats was followed by a further decrement of GLUT4 protein (Control 15 +/- 5 vs HTG 14 +/- 4%). In conclusions, a) the hereditary HTG rats had by about 50% lower GLUT4 protein levels in the quadriceps femoris muscle in comparison to normal Wistar rats; b) high-sucrose diet or raised dietary intake of n-3 PUFA did not further alter the number of glucose carriers in quadriceps femoris muscle in HTG rats and c) feeding the high-sucrose diet with higher proportion of n-3 PUFA was associated with an additional reduction of the GLUT4 protein level in this muscle.
Animals↗
Free, cytoskeletal-bound and membrane-bound polysomes isolated from MPC-11 and Krebs II ascites cells differ in their complement of poly(A) binding proteins.
A three-step detergent/salt extraction procedure (Vedeler et al., Mol Cell Biochem 100: 183-193, 1991) was used to isolate free polysomes (FP), cytoskeletal-bound polysomes (CBP) and membrane-bound polysomes (MBP) from MPC-11 and Krebs II ascites cells. Polysomes were pelleted, washed with high salt buffer and re-pelleted. Proteins in the dialysed high-salt extracts were subjected to poly(A) Sepharose chromatography and poly(A) binding and non-binding proteins were separated by SDS-PAGE. In MPC-11 cells the FP fraction contains thirteen poly(A) binding proteins and four non-poly(A) binding proteins while the corresponding fraction in Krebs II ascites cells has four poly(A) binding proteins and six proteins which do not bind poly(A). The CBP fraction isolated from MPC-11 cells has a complement of ten poly(A) binding proteins, four which are non-poly(A) binding, and a protein of 105 kDa which has both poly(A) binding and non-poly(A) binding properties. In the CBP fraction prepared from Krebs II ascites cells a protein band at 32 kDa exhibits both poly(A) binding and non-poly(A) binding properties. In this fraction there are six poly(A) binding proteins and an additional eight which do not bind poly(A). Of the total number of proteins eight of these have a molecular weight below 40 kDa. The MBP fraction in MPC-11 cells contains three poly(A) binding proteins and eleven with non-poly(A) binding properties. In contrast this fraction in Krebs II ascites cells has a complement of thirteen poly(A) binding and ten non-poly(A) binding proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
3T3 Cells↗
Transformation techniques for Drosophila cell lines.
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Animals↗
International transport of animals: problems relating to disease, welfare and stress.
The author examines reports received by the Office International des Epizooties (OIE) from OIE Member Countries, and presents details and analysis of some of the regulations which currently govern international transport of animals. An examination follows of two of the more comprehensive reports on the subject, prepared on the initiative of the European Commission. The conclusions drawn from the above sources highlight the need to ensure the following: a) only healthy animals are transported, b) precautions are taken to prevent the spread of disease during transport, c) satisfactory environments, feed, watering and rest are provided to animals before, during and after transport, d) only qualified attendants, handlers and drivers are used.
Animal Diseases↗
Macrophage colony-stimulating factor stimulates survival and chemotactic behavior in isolated osteoclasts.
Macrophage colony-stimulating factor (M-CSF) is known to play an important role in osteoclast formation. However, its actions on mature cells have not been fully characterized. We now report that M-CSF dramatically stimulates osteoclastic motility and spreading; osteoclasts responded to a gradient of M-CSF with orientation, and random cell polarization occurred after isotropic exposure. M-CSF also supported the survival of osteoclasts by preventing apoptosis. Paradoxically, M-CSF inhibits bone resorption by isolated osteoclasts. We found that this was effected predominantly by reduction in the number of excavations. Thus, M-CSF showed a propensity to suppress resorption through a reduction in the proportion of cells that were resorbing bone. Our data suggest that apart from the established role of M-CSF in the provision of precursors for osteoclastic induction, a major role for M-CSF in bone resorption is to enhance osteoclastic survival, migration, and chemotaxis. It seems appropriate that during these processes resorptive functions should be suppressed. We suggest that M-CSF continues to modulate osteoclastic activity once osteoclasts are on resorptive sites, through regulation of the balance between resorption and migration, such that not only the quantity, but the spatial pattern of resorption can be controlled by adjacent M-CSF-secreting cells of osteoblastic lineage.
Animals↗