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R A Davis

Publications and source records attributed to R A Davis.

At least 109 records · Page 6Linked to original sources
PubMed1984

Dietary carbohydrate induces lipogenesis and very-low-density lipoprotein synthesis.

Hepatocytes obtained from sucrose-fed rats secreted triacylglycerol at a rate that was about twice that of cells from control rats. The increased rate of triacylglycerol secretion by cells from sucrose-fed rats was accompanied by a twofold increase in its rate of synthesis as determined by 3H2O incorporation. In addition, cells from sucrose-fed rats had a two- to threefold increase in apolipoprotein synthesis. Differences between the two groups became even more marked when cells were challenged in vitro with glucose. Double-reciprocal analysis showed that compared with controls, cells from sucrose-fed rats had a fourfold increase in the Vmax that described the glucose stimulation of [3H]triacylglycerol secretion. In contrast to in vivo carbohydrate (sucrose) induction of apolipoprotein synthesis, glucose added in vitro did not affect apolipoprotein synthesis. These data suggest that in vivo induction by dietary carbohydrate requires factors in addition to increased hexose that are not contained within the isolated hepatocyte system. The coinduction by dietary carbohydrate of both lipogenesis and apolipoprotein synthesis is likely to play a role in the increased capacity of cells from sucrose-fed rats to both assemble and secrete triacylglycerol-rich lipoproteins.

Animals↗
PubMed1984

Prognostic factors in severe head injury.

Head injury is a significant economic, social and medical problem in the United States. For this reason, prognostic factors in head injury are of major importance to all surgeons who treat severely injured patients. Outcome of severe head injury is frequently determined at the time of impact, and surgical and medical treatment is often ineffective. Prediction of outcome of severe head injury should be based upon early neurologic signs, including degree of coma as measured by the Glasgow Coma Scale, brain stem reflexes, central nervous system lesion type, presence of increased intracranial pressure and multimodality evoked responses. The Glasgow Coma Scale is a standardized measurement of coma which numerically rates the response of eye opening, verbal response and motor response of the patient with head injury. The Glasgow coma score, the sum of the three response ratings, correlates with mortality of head injury, although the correlation between the coma score and morbidity has not been conclusively established. Because injury to the brain stem is generally irreversible, absence of oculocephalic reflexes, oculovestibular reflexes and pupillary response and the presence of decerebrate rigidity indicate an unfavorable outcome. Patients with focal brain injuries, especially subdural hematomas, generally have a higher mortality than patients who have diffuse brain injuries, regardless of the Glasgow coma score. Elevated intracranial pressure indicates an unfavorable outcome, especially if not reducible. Increased age and hypotension also subject patients with head injury to greater risk. Multiple injuries do not affect mortality of head injury. Multimodality evoked responses are a noninvasive prognostic technique which predicts outcome with a high degree of certainty. For optimal accuracy, prognosis should be based upon a combination of factors, including age, Glasgow coma score, pupillary response, eye movements, presence of surgical lesion, motor posturing and multimodality evoked responses. Decisions regarding surgical and medical treatment of patients with head injury should be based upon these prognostic factors.

Age Factors↗
PubMed1983

Bile acid synthesis by cultured hepatocytes. Inhibition by mevinolin, but not by bile acids.

The ability of cultured hepatocytes to maintain a constant rate of bile acid synthesis and secretion in a chemically defined serum-free culture medium allowed us to examine the direct effects of bile acids on their synthesis. Mass quantitation of bile acids by gas liquid chromatography showed that adding taurochenodeoxycholate at concentrations which were from 2 to 20 times the concentration of bile acids found in rat portal blood increased rather than decreased the secretion of cholic acid. Using a more direct approach to measure relative rates of bile acid synthesis and secretion, we determined the rate of de novo 14C-bile acid synthesis. Adding taurocholate at concentrations ranging from 2 to 60 times the concentration found in rat portal blood did not inhibit 14C-bile acid synthesis. Furthermore, free and conjugated di- and tri-hydroxy bile acids did not inhibit bile acid synthesis. In contrast, mevinolin, a potent inhibitor of cholesterol biosynthesis, inhibited 14C-bile acid synthesis by 63%. Since previous demonstration of bile acid negative feedback regulation was achieved in vivo by infusing taurocholate into the intestines of bile-diverted rats, we examined the possibility that bile acid synthesis must be induced in order for bile acids to inhibit their synthesis. Hepatocytes obtained from bile-diverted rats exhibited a 5-fold increase in the synthesis and secretion of 14C-bile acids. However, taurocholate did not inhibit bile acid synthesis by cells from bile-diverted rats. These data show that bile acids do not interact directly with the hepatocyte to inhibit their synthesis.

Animals↗
PubMed1983

Traumatic decerebrate rigidity and neurological recovery: a case report.

Trauma is the most common cause of decerebrate rigidity (DR). DR has been incorrectly equated with extensor posturing alone, however, and the "classical" criteria of decerebration generally have not been incorporated in the neurological evaluation of head-injured patients. A high mortality rate is associated with extensor posturing in head injury, and there have been few reports detailing neurological recovery and the quality of survival of patients with traumatic DR. The criteria of Sherrington are applied to a case of DR caused by midbrain injury, accompanied by mild, diffuse, hemispheric white matter changes shown on computed tomographic scan. The neurological examination and recovery are discussed. The literature is reviewed and the potential of DR in the prognosis of head injury is suggested.

Adult↗
PubMed1983

A surgeon at war.

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General Surgery↗
PubMed1982

Evidence that reverse cholesterol transport occurs in vivo and requires lecithin-cholesterol acyltransferase.

The transport of cholesterol from extrahepatic tissues into plasma (reverse cholesterol transport) and the possible requirement for lecithin:cholesterol acyltransferase was examined in the rat. One hour after removal of the liver plasma cholesterol ester concentrations were significantly increased by 20%, whereas free cholesterol concentrations were unchanged. The lecithin:cholesterol acyltransferase inhibitor, 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) was administered to eviscerated rats. It inhibited plasma lecithin:cholesterol acyltransferase activity by 90% which in turn totally prevented the increase in plasma cholesterol ester concentrations. In addition, heat-inactivated plasma from DTNB-treated eviscerated rats was 50% more reactive toward a standard source of lecithin:cholesterol acyltransferase compared to plasma from control or untreated eviscerated rats. These data suggest that in the rat a reactive lecithin:cholesterol acyltransferase substrate is formed extrahepatically. Together with lecithin:cholesterol acyltransferase, this reactive substrate removes cholesterol from peripheral tissues.

Animals↗
PubMed1982

Ultrastructure of cultured hepatocytes from fat- and cholesterol-fed rats.

Hepatocytes were enzymatically dissociated from the livers of rats maintained for eight weeks on diets of (1) standard rat chow, (2) chow plus 20% olive oil, and (3) chow plus 20% olive oil and 2% cholesterol. Cells were cultured for up to one week and characterized by phase contrast light microscopy and transmission electron microscopy. Cultured hepatocytes derived from the cholesterol-fed rats (3) were distinguishable by phase contrast light microscopy from those derived from chow-or chow plus olive oil-fed (1 and 2) cells, since they contained numerous refractile cytoplasmic structures. Transmission electron microscopy demonstrated that these structures were lipid droplets. Hepatocytes were observed to accumulate non-membrane bound cytoplasmic lipid droplets in the order control-fed less than olive oil-fed less than cholesterol-fed. In addition to varying quantitatively among the feeding groups, lipid droplets also varied in size and osmiophilia as a function of the feeding regimen. Other than the differential accumulation of lipid droplets, the ultrastructure of the cultured hepatocytes was similar among cells derived from the various feeding groups.

Animals↗
PubMed1982

Decerebrate rigidity in humans.

Decerebrate rigidity (DR) in humans results from a midbrain lesion and is manifested by an exaggerated extensor posture of all extremities. It is characterized by shortening and lengthening reactions and can be modified by tonic neck, labyrinthine (Magnus-de Kleijn), and phasic spinal reflexes. These criteria, and not extensor posture alone, reflect the observations of Sherrington and should form the basis of the clinical examination; however, the experimental-anatomical lesion and physiological findings can never be reproduced exactly in humans. "Tonic and cerebellar fits" are not the equivalent of DR, but are forms of muscle spasm that result in an extensor attitude. They are caused by irritation and excitation of the brain stem. The most common cause of DR in humans is trauma. The incidence of DR in head-injured patients may be as high as 40%, resulting in an average mortality rate of 80%; the presence of an extensor posture increases the mortality from 20 to 70%. The surgical removal of an intracranial lesion does not improve the high mortality rate in patients with craniocerebral trauma who are decerebrate. Although the Glasgow coma scale (GCS) does not consider the specific type of central nervous system abnormality caused by trauma, it is an accurate and accepted assessment of outcome after coma lasting longer than 6 hours. DR is a factor in the best motor response of the GCS and should be assigned major importance in the prognosis of comatose head-injured patients.

Brain Injuries↗
PubMed1981

Metabolic fate of VLDL apolipoproteins B and E in hepatectomized rats.

The metabolic fate of VLDL apolipoproteins B and E was examined in functionally hepatectomized rats. 1 h after hepatectomy, there was almost complete absence of ultracentrifugally isolated VLDL lipid and protein, including apolipoproteins B and E. Analysis of apolipoprotein concentrations by electroimmunoassay showed hepatectomy did not affect the total serum concentrations of apolipoproteins B and E; thus, hepatectomy caused a redistribution of these apolipoproteins from VLDL to higher density lipoproteins. In the LDL (d = 1.03--1.063 g/ml) fraction, hepatectomy, increased the concentrations of free cholesterol (40%), esterified cholesterol (57%) and protein (18--67%), due to an increase in apolipoproteins B (22--48%) and E (250--300%). After hepatectomy, the HDL fraction accumulated the greatest total amount of apolipoprotein E. Since the majority of apolipoprotein E was isolated in the d greater than 1.21 g/ml fraction after sequential ultracentrifugation, the redistribution of apolipoproteins B and E was further defined by fractionation of serum on 5 M agarose columns. Electroimmunoassay of the column fractions showed that the apolipoprotein B peak eluted before the apolipoprotein E peak. Although a considerable portion of apolipoprotein E eluted with A-I, the peak of apolipoprotein E eluted before the A-I peak in both groups. These data suggest that a portion of apolipoprotein E is associated with particles which are similar than LDL but are larger than A-I-rich HDL. Hepatectomy caused an accumulation of apolipoprotein B in LDL, and apolipoprotein E and cholesterol in particles which were smaller than LDL and may represent LDL1. It is likely that under normal physiological conditions the liver plays a role in the removal of these apolipoprotein E-rich particles which are derived, at least in part, from the metabolism of VLDL.

Animals↗
PubMed1981

Female labor force participation, status integration and suicide, 1950-1969.

Using Census data covering the 29 year period starting in 1950 this study tests the hypothesis that (1)#female labor force participation may result in more married women committing suicide due to the strain of household and outside working responsibilities and the (2) female labor force participation may also be associated with higher rates of male suicide due to the fact that it represents apparent failure of the husband as sole breadwinner (Stack, 1978). Results show that during the 1950's male suicide was not associated with growth in the female labor force, but female suicide was. During the 1960s male suicide was negatively associated with female labor force participation, but the opposite was true for females. It is argued that working women represented a weakening of norms concerning sex roles. Apparently as more and more women entered the labor force, role conflict did ensue, but contrary to the above hypothesis it only increased female suicide potential. These results are discussed in terms of different normative sex role contexts of the 1950s and the 1960s.

Employment↗
PubMed1981

Decerebrate rigidity in animals.

Decerebrate rigidity (DR) in animals is caused by a release of spinal neurons from supraspinal inhibition, which results in a caricature of reflex standing and includes tonic neck and labyrinthine reflexes. The reticular formation, cerebellum, vestibular complex, spinal cord, and muscle spindle system and their neurophysiological interaction are critical to DR. Its discovery and investigation were essential to Sherrington's concept of the integrative action of the nervous system. There are two types of DR with different anatomical and physiological bases. Intercollicular decerebration yields rigidity in extensor muscles that results from bilateral destruction of the central tegmental tracts, is abolished by posterior root section, and is due to a facilitation of gamma motoneuron discharge (gamma animal). Anemic decerebration is characterized by excessive extensor rigidity, depends upon the release of tonic labryinthine reflexes from cerebellar inhibition, is independent of posterior root section, and is caused by excessive alpha motoneuron discharge (alpha animal). DR has provided an insight into the mechanisms of posture and standing, but the correlation of laboratory observations and results from animals to humans must be made with caution.

Animals↗
PubMed1980

Reversal of ethinyl estradiol-induced bile secretory failure with Triton WR-1339.

The effects of Triton WR-1339 and phenobarbital on ethinyl estradiol bile secretory failure were examined to determine the mechanism responsible for decreased bile salt excretion. When administered to ethinyl estradiol-treated rats, Triton WR-1339 restored bile salt independent bile flow and maximum taurocholate transport, whereas phenobarbital corrected bile flow only. Ethinyl estradiol decreased the activities of Na(+)-K(+)-ATPase, 5'-nucleotidase, while increasing the activities of Mg(++)-ATPase and alkaline phosphatase. In contrast to these heterogeneous changes in surface membrane enzyme activities, the number and affinity of [(14)C]cholic acid carriers were not altered. When administered in vivo or added directly to surface membrane fractions Triton WR-1339 restored the activities of Na(+)-K(+)-ATPase and Mg(++)-ATPase of rats treated with ethinyl estradiol through a process that did not require protein synthesis (unaffected by cycloheximide). Phenobarbital also restored the activity of Na(+)-K(+)-ATPase to control levels, but, unlike Triton WR-1339 it did not correct the defect responsible for reduced bile salt secretion. Ethinyl estradiol increased the concentration of cholesterol esters in surface membrane fractions. When administered to ethinyl estradiol-treated rats, Triton WR-1339 restored cholesterol ester concentrations to normal, whereas phenobarbital did not. These combined data suggest that decreased or altered bile salt carriers or reduced sodium driving forces resulting from impaired activity of Na(+)-K(+)-ATPase are not responsible for decreased bile salt excretion in ethinyl estradiol-treated rats. It is proposed that the diverse changes in surface membrane function, which are associated with ethinyl estradiol bile secretory failure, may be the result of a generalized alteration in membrane lipid structure.

Animals↗