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Biomedical subjects

R A Levy

Publications and source records attributed to R A Levy.

At least 73 records · Page 4Linked to original sources
PubMed1984

Enhanced virus isolation by use of the transporter for a regional laboratory.

Transporter tubes with fibroblast monolayers were compared with sucrose-phosphate-glutamate buffer for transport of 385 specimens to a regional laboratory for virus culture. Ninety-two (91%) of 101 viral isolates were recovered in cell culture from the Transporter, as compared with 82 (81%) from sucrose-phosphate-glutamate buffer. Twenty-five (24.7%) of the viral isolates were detected by cytopathic effect from 1 to 11 days earlier from the Transporter than from the sucrose-phosphate-glutamate buffer. The Transporter also permitted the use of ambient temperature for transport.

Cytopathogenic Effect, Viral↗
PubMed1984

Evaluation of a commercial enzyme-linked immunosorbent assay for detection of herpes simplex virus antigen.

A commercial enzyme-linked immunosorbent assay (ELISA) for detection of herpes simplex virus (HSV) antigen in clinical specimens and culture lysates was evaluated. A total of 1,155 specimens and an additional 335 cell culture lysates were tested by ELISA, and results were compared to those obtained by cell culture in primary rabbit kidney, human foreskin, and MRC-5. The sensitivity and specificity of the direct test were 52.5 and 96.9% and those of the culture lysate test were 98.7 and 96.9%, respectively. The sensitivity of the direct ELISA correlated with early cytopathic effect in cell culture and varied with specimen source, ranging from 100% with skin lesions to 40.9% with cervical swabs. Of 60 cervical specimens from asymptomatic individuals, 22 (36.6%) yielded false-positives, which may be due to noninfectious HSV. No reproducible cross-reactions were found with other viruses isolated. The Ortho HSV ELISA was found to be rapid, sensitive, and specific for detection of HSV from cell culture lysates, but it needs reevaluation for direct specimen testing, in particular for screening of asymptomatic obstetrical patients.

Antigens, Viral↗
PubMed1984

Blood pressure response to thyrotropin-releasing hormone in euthyroid subjects.

The iv administration of TRH has been associated with side effects, such as nausea, flushing, and urinary urgency. However, few reports mention changes in blood pressure. This study defines the mean and range of the blood pressure responses in 70 euthyroid patients subjected to iv administered TRH. The mean increase was 21.0 +/- 1.4 mm Hg for systolic and 13.9 +/- 1.0 mm Hg for diastolic blood pressure; however, individual peak values increased as much as 56 and 42 mm Hg, respectively. Thus, the hemodynamic response to iv administered TRH can be quite severe in some subjects, and caution is suggested in selecting patients for testing.

Blood Pressure↗
PubMed1983

Antinociception following microinjection of dibutyryl cyclic nucleotides into the caudal reticular formation and periaqueductal gray of the rat brain.

The tail flick, paw pinch, and hot plate tests were used to assess changes in nociceptive threshold following microinjection of dibutyryl derivatives of cyclic nucleotides into areas of the central nervous system previously shown to be involved in modulation of nociceptive threshold and mediation of morphine analgesia. An elevation in the nociceptive threshold was observed on all three tests following administration of 10 micrograms dibutyryl cyclic 3':5' adenosine monophosphate (db cAMP) into the caudal brainstem reticular formation (CRF) and periaqueductal gray (PAG). Two micrograms db cAMP produced the same magnitude of analgesia but had a shorter duration of action. Twenty micrograms dibutyryl cyclic 3':5' guanosine monophosphate (db cGMP) produced analgesia on all three tests following microinjection at CRF sites but not at PAG sites. These data indicate that morphine analgesia and the antinociception produced by cyclic nucleotides may involve, at least in part, common neuronal substrates. However, the observed capacity of db cAMP to elevate nociceptive threshold does not support the hypothesis that the mechanism of morphine's analgesic action involves inhibition of adenylate cyclase.

Analgesia↗
PubMed1982

Low density lipoprotein receptor activity in homozygous familial hypercholesterolemia fibroblasts.

We have identified specific low affinity low density lipoprotein (LDL) receptors in skin fibroblasts from two patients previously classified as having LDL receptor-negative homozygous familial hypercholesterolemia (FHC). Km and maximum capacity for cell-associated and degraded 125I-LDL were determined by two independent methods, a traditional technique in which increasing amounts of 125I-LDL were added until receptor saturation was achieved and a new technique in which the displacement of a small amount of 125I-LDL tracer was observed during the addition of variable amounts of unlabeled LDL. The Km for specific cell-associated 125I-LDL in FHC cells was 3.5-7.3 times that of normal cells and the maximum specific capacity was reduced to 11% of normal. Thus, some FHC cells have reduced affinity as well as reduced capacity for LDL. The FHC cell receptors share many but not all properties of the normal skin fibroblast LDL receptor. Specific degradation of bound 125I-LDL occurred concomitantly with LDL binding and was greatly reduced by the addition of chloroquine, an inhibitor of lysosomal function. Preincubation of FHC cells with cholesterol or LDL resulted in significant suppression of receptor function. Modification of lysine residues of LDL abolished receptor activity in both normal and FHC cells. Treatment of FHC cells with compactin, a cholesterol synthesis inhibitor, resulted in significant increases in specific 125I-LDL binding and degradation compared to FHC cells without compactin treatment. Normal cells also showed increases in 125I-LDL binding and degradation with compactin treatment, but the mean percentage increase in specific 125I-LDL degradation was significantly greater in FHC cells (strain GM 2000, 160 +/- 18%) than in normal cells (29 +/- 8%).

Binding, Competitive↗
PubMed1982

Feasibility of altering type A behavior pattern after myocardial infarction. Recurrent Coronary Prevention Project Study: methods, baseline results and preliminary findings.

We studied 1035 consecutive postinfarction patients to determine the feasibility of altering type A behavior and the effect such alteration might have on subsequent rates of infarction and cardiovascular death. Approximately 300 subjects were enrolled in small groups and primarily received cardiologic counseling on the usually accepted coronary risk factors. Six hundred subjects received, in addition to cardiologic counseling, advice and instructions designed to diminish the intensity of their type A behavior. The remaining subjects, serving as controls, received no counseling, but were examined and interviewed annually, as were those who dropped out of counseling groups. More than 98% of the 1035 subjects exhibited moderate-to-severe type A behavior during a videotaped structured interview. After the first year of this 5-year study, the rates of infarction and cardiovascular death were lower (p less than 0.01 and p less than 0.05, respectively) among subjects who received both cardiologic and behavioral counseling than among the control subjects. The rate of nonfatal infarction was lower (p less than 0.05) among subjects who received behavioral counseling than among those who received only cardiologic counseling or those who dropped out of either counseling group. The circumstances that most often preceded recurrent infarction or cardiovascular death were emotional crisis, excess physical activity, ingestion of a single fatty meal or a combination of these phenomena.

Adult↗
PubMed1982

Familial hypercholesterolemia. Evidence for a newly recognized mutation determining increased fibroblast receptor affinity but decreased capacity for low density lipoprotein in two siblings.

Cultured skin fibroblasts were obtained from two siblings with classic clinical features of homozygous familial hypercholesterolemia. Plasma cholesterol values were 970 and 802 mg/100 ml in the siblings, 332 mg/100 ml in the mother, and 426 mg/100 ml in the father. Fibroblast receptor-specific capacity for binding and degradation of (125)I-low density lipoprotein (LDL) at 37 degrees C was 11% of normal, consistent with the diagnosis of "homozygous LDL receptor-defective" hypercholesterolemia, a disorder in which LDL binding activity is low but detectable. The residual LDL receptor activity was clearly qualitatively abnormal. The Michaelis constant (K(m)) for (125)I-LDL was reduced to 20-40% of normal, indicating a substantially increased affinity for LDL. Increased affinity and reduced capacity for (125)I-LDL are also found when normal fibroblasts are assayed at 4 degrees C. As the temperature is raised to 37 degrees C surface LDL binding affinity decreases while capacity increases. At 4 degrees C the fibroblasts of our subjects had an affinity for LDL indistinguishable from normal cells assayed at that temperature and a binding capacity 23% of normal. However, only small changes in affinity and capacity occurred upon increasing the temperature to 37 degrees C. When (125)I-apoprotein E-phospholipid vesicles were bound at 37 degrees C the receptor deficiency appeared only half as severe as when (125)I-LDL was used as ligand.A family study suggests that the siblings are genetic compounds rather than homozygotes, having inherited a mutant maternal gene causing absent or silent LDL receptors and a mutant paternal gene resulting in qualitatively altered LDL receptors. It is not clear whether these defects are present at the same or different genetic loci. The altered receptors are characterized by increased affinity and moderately reduced capacity for LDL at 37 degrees C and are accompanied by hypercholesterolemia at least as severe as that associated with familial hypercholesterolemia with absent or nonfunctional LDL receptors.

Adult↗
PubMed1982

An alternative approach to teaching statistics to dental students.

From a review of the literature, instruction in statistics appears to be common in dental schools but beset with problems. Based, in part, on several surveys of the statistics content of dental literature, there is some general agreement that dentists-in-training need to acquire a working knowledge of statistics. Content guidelines developed for health science statistics courses are available and are considered entirely appropriate for dental education. Several authors have suggested that computer-assisted instruction is ideally suited to minimize the problems encountered in teaching statistics to dental students. Computer-assisted instruction is expensive, however, and self-instruction using a programmed text was found, on the basis of preliminary evaluation, to be an effective and inexpensive alternative.

Curriculum↗
PubMed1981

Analgesia following local injection of dibutyryl cyclic nucleotides at sites in the rat CNS.

Tail flick latency (TFL) was elevated following microinjection of both dibutyryl cyclic AMP (dbcAMP) was dibutyryl cyclic GMP (dbcGMP) at sites in the caudal reticular formation. TFL was also elevated following injection of dbcAMP but not dbcGMP into the periaqueductal gray. TFL was unaltered following administration of either agent into the lumbar intrathecal space. These actions are discussed with respect to the possible involvement of cyclic nucleotides in the analgesic action of morphine.

Analgesia↗
PubMed1981

The contribution of increases in extracellular potassium to primary afferent depolarization in the bullfrog spinal cord.

To assess the extent to which depolarization by accumulated K+ contributes to the generation of primary afferent depolarization (PAD), the isolated bullfrog spinal cord was superfused with K+-rich Ringer solutions and the resultant dorsal root depolarizations were recorded extracellularly. Action potential blockade (with tetrodotoxin) did not reduce the K+-induced depolarization of primary afferents, indicating that the depolarization was generated locally in the region around the afferents. In this respect superfusion with K+-rich solutions adequately models the localized K+ accumulation which occurs physiologically during afferent activity. K+-induced depolarizations were decreased in the presence of 20 mM Mg2+; this effect was due to a direct decrease in the membrane response to K+ and not to blockade of K+-induced transmitter release onto primary afferents. The depolarization caused by a K+ concentration comparable to a maximum estimate of the K+ accumulating around afferent terminals following a single afferent volley was found to account for no more than about one-third of the DRP height. However, higher K+ levels, comparable to those resulting from high frequency afferent stimulation, caused large depolarizations of primary afferents, sometimes greater than the DRP amplitude. Therefore, K+-induced depolarization may contribute more significantly to PAD evoked by high frequency afferent activity.

Afferent Pathways↗
PubMed1981

Analysis of lipids and endothelial and smooth muscle cells of umbilical cord in familial homozygous hypercholesterolemia.

Umbilical cord lipids from a familial hypercholesterolemia homozygote were extracted and quantitated. Free cholesterol was increased 26% and esterified cholesterol was increased 379% compared to normal, whereas phospholipid content was not altered. Analysis of homozygote umbilical artery revealed no excess cholesterol and the vessels were histologically normal. Thus, in the homozygote cord, accumulation of cholesterol occurs first in Wharton's jelly, the hypocellular glycosaminoglycan-enriched cord matrix. Skin fibroblasts, umbilical vein endothelial cells, and umbilical vein smooth muscle cells were cultured from the homozygote. Low density lipoprotein receptor activity was reduced to 9%-38% of normal in all cell types from the homozygote, demonstrating that vessel cells express the LDL, receptor defect seen in skin fibroblasts.

Cells, Cultured↗
PubMed1981

Analgesia following microinjection of phosphodiesterase inhibitors at brainstem sites.

Microinjection of RO 20-1724 (0.60 micrograms) at sites in the caudal reticular formation of the rat brainstem resulted in analgesia as measured in the tail flick, paw pinch and hot plate tests. Microinjection of theophylline (0.45 micrograms) at sites in the caudal reticular formation also produced analgesia in the tail flick and hot plate tests, but not in the paw pinch test. Since these agents inhibit phosphodiesterase and elevate cyclic nucleotides in rat brain homogenates, these data suggest that cyclic nucleotides have a functional role in brainstem structures involved in modulation of nociceptive threshold.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1981

Biofeedback rehabilitation of airsick aircrew.

The biofeedback treatment of 20 aircrew, disabled by chronic severe airsickness, is reported. The USAF School of Aerospace Medicine (SAM) Airsick Rehabilitation Program requires careful selection to insure high motivation and thorough medical screening to rule out intercurrent medically disqualifying conditions. Patients are trained in relaxation techniques and placed in a modified Barany chair, capable of tilting as well as rotating. Psychological responses to motion stimulation are constantly monitored by both patient and investigators. Motion sickness is provoked, which the patient learns to control and abort through exercising autonomic control. Of 19 eligible, 16 have been returned to fully flying duties.

Aerospace Medicine↗
PubMed1980

Hypoalgesia induced by microinjection of a norepinephrine antagonist in the raphe magnus: reversal by intrathecal administration of a serotonin antagonist.

Microinjection of phentolamine in the nucleus raphe magnus produces hypoalgesia as assessed by both the tail flick and hot plate tests. The elevation of tail flick latency appears to result from activation of serotonergic raphe-spinal projections, while the elevation of hot plate latency appears to be mediated by activation of non-serotonergic raphe-spinal neurons and/or by activation of raphe neurons which project to supraspinal nuclei.

Animals↗
PubMed1980

Interaction between amino acid induced and K+-induced depolarization of primary afferents in the bullfrog spinal cord.

In view of the possible contribution of both gamma-aminobutyric acid (GABA) and K+ to primary afferent depolarization (PAD) it was of interest to study the way in which depolarizations caused by administration of these agents combine at the primary afferent membrane. GABA (and glutamate) depolarizations of bullfrog afferents were found to be reduced if they were superimposed on ongoing K+-induced depolarizations. The extent of reduction was greater with K+ depolarizations of increasing size. The contribution of GABA to PAD should therefore be greatest when extracellular K+ is low, such as during single volleys or low frequency afferent activity. The effect of temporal order of administration on the summation of amino acid and K+ responses was tested by reversing the order of their application. GABA could not be used in this test because GABA depolarizations rapidly desensitize. However, when K+ depolarization was superimposed on maintained glutamate depolarization, the total depolarization was equal to the sum of depolarizations observed when glutamate and K+ were given alone (linear summation). Therefore, the temporal order of administration of amino acid and K+ affects the size of the total depolarization. No evidence was found for a superadditive effect when amino acid and K+ were applied together.

Amino Acids↗
PubMed1979

Analgesia produced by microinjection of baclofen and morphine at brain stem sites.

Microinjection of either baclofen (1.5 microgram) or morphine (2.5 microgram), in equimolar doses (14 mM), at sites located in the caudal periaqueductal gray (PAG) resulted in a delay in tail flick latency (analgesia). The relative analgesic potency of baclofen among caudal PAG sites, however, did not correlate with that of morphine. Application of either drug into the caudal aspect of the cerebral aqueduct also produced analgesia, but neither agent caused analgesia when applied at PAG sites rostral to the interaural line. Baclofen also produced analgesia when microinjected in the lower brain stem at sites lateral to the midline in or near the nucleus gigantocellularis, but did not produce analgesia when applied on the midline at sites located within or near the raphe magnus. Conversely, morphine produced analgesia when applied locally at midline sites but not at sites located lateral to the midline. These data suggest that the analgesia produced by systemic administration of baclofen and morphine involves activation of different neuronal substrates.

Analgesics↗