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Biomedical subjects

T J Moore

Publications and source records attributed to T J Moore.

At least 55 records · Page 3Linked to original sources
PubMed1992

Research in context (or if you want to study how fox and chickens relate, go to the hen house, not the zoo).

The context in which the research is carried out frequently is as important as the research question being investigated. The fact certainly is the etiology for many of the problems practicing physicians face when applying traditional research findings to clinical practice. The recent development of a family practice research network in South Dakota brought the investigators face to face with divergent views on this issue. This article provides some insight into different research philosophies.

Anti-Bacterial Agents↗
PubMed1992

Obstructive jaundice secondary to primary biliary involvement with Hodgkin's disease.

A 41-yr-old man presented with jaundice, night sweats, and weight loss. The patient had been on phenytoin for seizure disorder. The drug was discontinued, and a diminution of bilirubin and transaminases occurred over several weeks. Percutaneous liver biopsy revaled cholestasis at the time of maximal hyperbilirubinemia. Recurrent jaundice ensued several weeks later, and an ERCP revealed a common bile duct lesion. Laparotomy revealed Hodgkin's disease involving the common bile duct and periportal node. This cause represents the first report of extrahepatic biliary obstruction from Hodgkin's disease.

Adult↗
PubMed1991

Feasibility of outpatient electrolyte balance studies.

Clinical studies requiring controlled electrolyte balance have traditionally been conducted in an inpatient (IP), metabolic ward setting. The purpose of this study was to test the feasibility of performing such studies in an outpatient (OP) clinical research setting. Focusing on sodium (Na) and potassium (K) balance, we retrospectively compared 28 subjects studied as OP vs 25 studied as IP on our metabolic ward. We assessed their adherence to our metabolic diets and their compliance with serial 24-hr urine collections. Dietary compliance was assessed by checksheet and urinary Na excretion; urine collection accuracy was determined by serial 24-hr creatinine excretion. The diets for both studies contained a low Na phase (10 mEq) and a high Na phase (200 mEq for IP and 250 mEq for OP), each lasting 1 week. When in balance on the low Na diet, 24-hr Na excretion was 4.6 +/- 0.7 mEq for OP and 13.4 +/- 2.2 mEq for IP, indicating excellent compliance with the low salt diet. Na excretion on the high Na diet was 184.5 +/- 7.4 mEq for OP and 195.3 +/- 9.6 mEq for IP. These values were not significantly different from each other; however, the OP were significantly less than their diet of 250 mEq Na (p less than 0.05). This difference may have been due to dermal Na losses. K excretion was also similar in the two groups. There was no significant difference in the reproducibility of individual multiple urinary creatinine measurements in OP vs IP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Blood pressure and renal blood flow responses to dietary calcium and sodium intake in humans.

This study was designed to determine the interaction between salt and calcium intake on blood pressure (BP) and renal blood flow (RBF) in a predominantly white population. We measured BP and RBF (P-aminohippurate [PAH] clearance) in hypertensive patients after 7 days on a low salt/low calcium diet and again after either a high salt/high calcium diet (HS/HC) or a high salt/low calcium (HS/LC) diet for another 7 days. Compared to low salt BP, both high salt diets increased BP, but the increase with high salt/low calcium was significantly greater than with high salt/high calcium (+14.6 +/- 3.9/+8.2 +/- 1.7 mm Hg v +7.5 +/- 1.9/+2.5 +/- 1.4 mm Hg; systolic/diastolic, both P less than or equal to .05). PAH clearance increased 26 +/- 13 mL/min/1.73 m2 on the HS/HC diet but only 10 +/- 17 mL/min/1.73 m2 on HS/LC (P = .05 between groups). These data suggest that a low calcium diet may contribute to the phenomenon of salt sensitivity in a white population. The low calcium intake appears to affect both the systemic and renal vasculature.

Administration, Oral↗
PubMed1991

Salt restriction lowers resting blood pressure but not 24-h ambulatory blood pressure.

Dietary salt restriction is the most common therapeutic recommendation given to hypertensives, but past studies have assessed the effect of salt restriction using resting blood pressure (BP) measurements not with the newer technique of 24-h ambulatory BP monitoring. We compared the effect of high (250 mEq Na/day) and low (10 mEq Na/day) salt diets on resting versus ambulatory BP in 12 normal and 15 hypertensive subjects. Each diet was given for 7 days. Ambulatory BP was monitored from day 6 to day 7 of each diet; resting supine BP was measured on the morning of day 8. In normal subjects, neither resting nor ambulatory BP changed with sodium restriction. In hypertensives, resting BP fell 14 +/- 3/6 +/- 2 mm Hg (systolic/diastolic; P less than .01 for both) with sodium restriction while ambulatory BP fell only 4 +/- 2/2 +/- 2 (P = NS). The resting BP fall was significantly greater than the ambulatory BP fall (P less than .05) for both systolic and diastolic pressure. Ambulatory heart rates were also significantly greater during sodium restriction, suggesting that the low salt diet activated the sympathetic nervous system. This may, in turn, have partially offset the hypotensive effect of sodium restriction. We conclude that using resting BP to assess the effect of sodium restriction may overestimate the efficacy of this therapy. Ambulatory BP monitoring should be employed in future studies of sodium restriction.

Ambulatory Care↗
PubMed1991

Train versus pedestrian accidents.

Railroad-related trauma has been associated with injuries causing considerable morbidity. This is a retrospective study of 15 consecutive patients who were run over by trains. The initial injury produced a traumatic amputation of 10 extremities in eight patients. Limb salvage in two other patients with severe fractures failed, and subsequent lower extremity amputation was required. Despite efforts to salvage the most distal tissue possible, 8 of 12 extremities amputated in the acute traumatic period required revision to a more proximal level. Alcohol ingestion was involved in 13 of the 15 incidents in the study. No patient received posthospitalization alcohol rehabilitation. In addition, despite the young age of the patients in this series, only one patient was rehabilitated to a prosthetic ambulator.

Accidents↗
PubMed1991

Kinetic abnormalities of the red blood cell sodium-proton exchange in hypertensive patients.

The present study was designed to examine the kinetics of Na(+)-H+ exchange in red blood cells of normotensive and hypertensive subjects and its relation to the previously reported abnormalities in Na(+)-Li+ exchange. The Na(+)-H+ antiporter activation kinetics were studied by varying cell pH and measuring net Na+ influx (mmol/l cell x hr = units) driven by an outward H+ gradient. The Na(+)-Li+ exchange was determined at pH 7.4 as sodium-stimulated Li+ efflux. Untreated hypertensive patients (n = 30) had a higher maximal rate of Na(+)-Li+ exchange (0.43 +/- 0.05 versus 0.26 +/- 0.02 units, p less than 0.0003), a higher maximal rate of Na(+)-H+ exchange (62.3 +/- 6.2 versus 47 +/- 4 units; p less than 0.02), but a similar affinity for cell pH compared with normotensive subjects (n = 46). The cell pH activation of the Na(+)-H+ antiporter exhibited a lower Hill coefficient than that of normotensive subjects (1.61 +/- 0.12 versus 2.56 +/- 0.14; p less than 0.0001). This index of occupancy of internal H+ regulatory sites was found reduced in most of the hypertensive patients (73%) whether their hypertension was untreated or treated. Hypertensive patients with Na(+)-Li+ exchange above 0.35 units (0.68 +/- 0.057 units, n = 16) did not exhibit elevated maximal rates of Na(+)-H+ exchange (57.3 +/- 10 units, NS) in comparison with those with Na(+)-Li+ exchange below 0.35 units (66.4 +/- 7.6 units, n = 26), but both groups exhibited reduced Hill coefficients. Hypertensive patients with enhanced Na(+)-H+ exchange activity (more than 90 units) had normal maximal rates of Na(+)-Li+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Renal and endocrine responses to a renin inhibitor, enalkiren, in normal humans.

Interpretation of renin-angiotensin blockade with angiotensin converting enzyme inhibitors is potentially confounded by their multiple effects. We used a selective renin inhibitor (enalkiren, A-64662) to explore the renal and endocrine effects of angiotensin II in healthy men. Each received 90-minute enalkiren infusions at 2-day intervals, on a low (10 mmol, 16 subjects) and high (200 mmol, 12 subjects) salt diet. Plasma renin activity, immunoreactive plasma angiotensin II and aldosterone concentrations, inulin, and p-aminohippurate clearance were measured by standard methods. Plasma renin activity fell at 0.1 micrograms/kg, but the threshold for biologic effect was 256 micrograms/kg, where plasma immunoreactive angiotensin II and aldosterone concentration fell, and renal plasma flow rose (p less than 0.01). The maximal renal vascular response (+152 +/- 23 ml/min/1.73 m2) occurred at 512 micrograms/kg (p less than 0.01). Diastolic and mean blood pressure fell modestly but significantly (p less than 0.05). Responses were limited on a high salt diet. We confirm that conventional plasma renin activity measurement is misleading in humans receiving a renin inhibitor. The renal vascular response to renin inhibition in this study appeared to substantially exceed reported responses to angiotensin converting enzyme inhibition, perhaps reflecting a crucial and relatively inaccessible intrarenal locus.

Adult↗
PubMed1991

Salt loads raise plasma fatty acids and lower insulin.

Some fatty acids are potent inhibitors of angiotensin binding and aldosterone production in adrenal glomerulosa cells and thereby may be involved in regulating salt and water balance. To study the possible regulation of fatty acids by salt, we measured the levels of unesterified fatty acids in plasma from patients subjected to extremes of dietary salt intake and saline infusion. Insulin and catecholamines, two known regulators of plasma fatty acids, also were measured. Infusion of 2 l saline over 4 hours caused the levels of most unesterified fatty acids to rise. Total unesterified fatty acids rose 60-100%. A high salt diet caused a smaller rise in total unesterified fatty acids (approximately 33%). In both instances, oleic and palmitoleic acids showed the greatest proportionate increases, whereas stearic acid was relatively unaffected. When salt loads were administered by either intravenous or dietary routes, plasma insulin levels fell by approximately 50%. Plasma norepinephrine increased after saline infusion but not during a high salt diet. Postsaline levels of fatty acids correlated inversely with postsaline levels of aldosterone, supporting a possible role for fatty acids as physiological regulators of the adrenal glomerulosa. A rise in plasma fatty acids and fall in insulin in response to salt loads could act in concert to increase sodium excretion, constituting a physiological mechanism contributing to salt and water balance.

Chromatography, High Pressure Liquid↗
PubMed1991

The use of open phenol blocks to the motor branches of the tibial nerve in adult acquired spasticity.

Spasticity of the posterior calf muscles often occurs following head injury or spinal cord injury. If left untreated, equinovarus contractures of the foot and ankle may occur in a relatively short time period. This paper retrospectively reviews nine patients with either closed head injury (six patients) or spinal cord injury (three patients) who underwent open phenol injections into the motor branches of the tibial nerve in 16 limbs. Spasticity was decreased in all patients. No significant equinus contractures had occurred at final follow-up. Five of the patients were subsequently able to ambulate. One patient had recurrence of spasticity requiring a second surgical procedure (split anterior tibial tendon transfer), and two patients had significant toe clawing at final follow-up. Open phenol injections to the motor branches of the tibial nerve safely and effectively prevent foot and ankle contractures following spinal cord injury or head injury.

Adult↗
PubMed1991

Utility of breath ethane as a noninvasive biomarker of vitamin E status in children.

The purpose of our study was to determine if the ethane content of expired air could be a useful index of vitamin E status in children. Eight children with vitamin E deficiency secondary to chronic severe liver disease were studied: six of these children were treated with parenteral vitamin E (2-5 mg/kg/dose every 4-7 d). Measures of vitamin E status pre- and posttherapy were: serum vitamin E, 2 +/- 1 versus 7 +/- 1 micrograms/mL (p less than 0.001); serum vitamin E:total lipids, 0.3 +/- 0.1 versus 1.0 +/- 0.1 mg/g (p less than 0.001); and erythrocyte peroxide hemolysis test, 80 +/- 10 versus 6 +/- 12% (p less than 0.001). Fasting breath ethane in the patients pre- and posttherapy was 78 +/- 10 versus 31 +/- 11 pmol/kg/min (p less than 0.001). Breath ethane correlated negatively with serum vitamin E (p less than 0.042) and serum E:total lipids (p less than 0.004) and positively with the erythrocyte peroxide hemolysis test (p less than 0.003). Values for treated patients did not differ from those for fasted sibling controls (34 +/- 12 pmol/kg/min), postprandial sibling controls (31 +/- 12 pmol/kg/min), and healthy children sampled randomly, in the nonfasted state (21 +/- 14 pmol/kg/min). Breath ethane production in one patient (up to 168 pmol/kg/min) did not normalize after treatment of vitamin E deficiency until her selenium deficiency was corrected as well. We conclude that this noninvasive test can be useful as a screen for vitamin E deficiency in children and for ascertaining response to therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

The effect of sodium intake on angiotensin content of the rat adrenal gland.

To determine whether dietary sodium intake modifies the generation of adrenal-produced angiotensins and/or their relative proportions, Sprague-Dawley rats were maintained on a low (0.02%), normal (0.4%), or high (1.5%) sodium intake for 5 days. The animals were then killed by decapitation at 0900 h, and their adrenal glands were removed and dissected into two parts: capsular tissue, containing the zona glomerulosa (ZG), and the decapsulated adrenal gland. The tissue was frozen in liquid nitrogen and extracted, and the individual angiotensins [angiotensin-II (AII), angiotensin-III (AIII), angiotensin-I (AI), and Des-Asp-angiotensin-I (Des-Asp-AI)] were separated by HPLC and quantitated by RIA. On a normal sodium intake, the molar contents of the four angiotensins were similar in ZG, ranging from 3.1-6.6 pmol/g, although AII was present in a 60-70% higher concentration than AIII. In the decapsulated adrenal, the concentrations of the various angiotensins were again similar, but the absolute levels (per g tissue) were significantly (P less than 0.02) less than those in the ZG layer. With sodium restriction, the AII content increased more than 2-fold in the ZG, but not in the decapsulated adrenal tissue. In contrast, both AI and Des-Asp-AI significantly (P less than 0.01) decreased with sodium restriction, so that their contents on the low salt diet were only 15-20% of those observed on the high sodium diet. Thus, there was an inverse correlation (P less than 0.001) between the salt content of rat chow and the AII content of the ZG. The correlation between salt intake and AI as well as Des-Asp-AI levels was direct and significant (P less than 0.02). The AIII level in the ZG was similar on all diets. After a lag period, ZG AII increased sharply between 16-48 h of sodium restriction. These data document that sodium intake has a profound effect on the angiotensin content of the ZG, with sodium restriction substantially increasing the levels of AII while reducing the level of its substrate, AI. This also appears to be unique for glomerulosa cells, as in the decapsulated adrenal gland there is little if any change with sodium restriction. We conclude that these sodium-mediated changes in tissue AII production may be involved in the increased responsiveness of glomerulosa cells to aldosterone secretagogues during sodium restriction.

Adrenal Glands↗
PubMed1991

Potassium-stimulated angiotensin release from superfused adrenal capsules and enzymatically dispersed cells of the zona glomerulosa.

The cells of the adrenal cortex contain angiotensin-II (AII), but whether this peptide is synthesized there (vs. internalized from the systemic circulation), whether it is secreted, and whether it is important in aldosterone production remain uncertain. To address these issues, we studied AI and AII release from superfused rat adrenal capsules and dispersed glomerulosa cells. Superfused adrenal capsules released 7-fold more AII in 270 min than the capsules originally contained (495 +/- 101 fmol AII/rat released vs. 66 +/- 8 fmol AII/rat tissue content). The amount of AI released in the same period only slightly exceeded the tissue content. In response to higher potassium concentrations in the medium (9 vs. 3.6 mM K+), adrenal capsules and dispersed glomerulosa cells both released significantly more AI and AII into the superfusate. This release of AI and AII was oscillatory. The oscillations occurred in each of 15 experiments, with a period of 45-90 min. Decapsulated adrenal glands (the zona faciculata/reticularis plus medulla) also contained and released AII, but did not respond to potassium stimulation. There was a highly significant correlation between AII and aldosterone release. This was especially apparent if aldosterone secretion was examined during oscillations of AII release (r = 0.97; P less than 0.0001). We conclude that AII is synthesized in the zona glomerulosa and can be released in response to stimuli. The close correlation between AII and aldosterone secretion suggests that locally produced AII may play an important role in aldosterone biosynthesis.

Adrenal Glands↗
PubMed1991

Dysregulation of aldosterone secretion and its relationship to the pathogenesis of essential hypertension.

The level of sodium intake has a reciprocal influence on the vascular and adrenal responses to angiotensin II, with sodium restriction enhancing the adrenal responses and reducing vascular, and particularly renal vascular, responses. In two subgroups of the essential hypertensive population, this relationship is abnormal. Both subgroups have sodium-sensitive hypertension. One is a subset of the low renin essential hypertensive subgroup and its abnormality is an enhanced aldosterone response to angiotensin II with sodium loading, ie, a failure to down-regulate the aldosterone response. The other subgroup, termed nonmodulators, is a subset of the normal-high renin essential hypertensive subgroup. In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Of clinical importance, the nonmodulator's abnormality is corrected by the administration of converting enzyme inhibitors--this class of drugs therefore being a specific form of therapy in these patients.

Aldosterone↗
PubMed1990

Effect of angiotensin II on collagen-induced platelet activation in normotensive subjects.

We examined the effect of angiotensin II (AII) on platelet activation in 15 normotensive volunteers. By measuring the initial phase of platelet aggregation on the optical density aggregation tracing and generation of thromboxane production, we demonstrated that AII enhances collagen-induced platelet activation. This enhancement in platelet activation is significantly greater when subjects are on a high salt than on a low salt diet. Furthermore, the increase in platelet activation parallels an increase in platelet AII receptor number. These parallel changes in platelet activation and platelet AII receptors provide a possible mechanism through which AII may affect platelet function.

Adult↗
PubMed1990

Growth of group A rotaviruses in a human liver cell line.

Recent observations in children with rotavirus gastroenteritis and in infant mice given rotavirus vaccine by oral administration suggest that this well-known gastrointestinal pathogen may infect the liver. To examine this possibility, the susceptibility of Hep G2 cells to infection with a variety of rotavirus strains was tested. These cells were used because they are considered to be well differentiated and exhibit many liver-specific functions. The Hep G2 cells supported the growth of the simian strain rhesus rotavirus (MMU 18006), a strain currently being used in vaccine trails, but did not support the growth of any human strain (D, DS1, Price or ST3). The rhesus rotavirus infection was cytopathic and resulted in release of lactate dehydrogenase. Rhesus rotavirus growth in Hep G2 cells displayed trypsin-enhanced infectivity and was inhibited by pretreatment of cells with Arthrobacter ureafaciens neuraminidase but not with neuraminidase from Clostridium perfringens. Hep G2 cells were also permissive for another simian strain (SA11), a bovine strain (UK) and single gene substitution reassortants containing VP7 (the major outer capsid neutralization protein) from a human rotavirus strain and the remaining 10 genes from either rhesus rotavirus or UK. In general, UK and its reassortants produced lower levels of antigen than did rhesus rotavirus and its reassortants. Hep G2 cells and other hepatic cell lines may prove to be useful tools to explore the hepatotropic potential of wild-type rotaviruses and candidate vaccine strains.

Antigens, Viral↗