U.S. Hispanics: challenging issues for the 1990s.
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Biomedical subjects
Publications and source records attributed to C Davis.
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Several neuropsychiatric illnesses, including depression and Alzheimer's disease, are reported to be characterized by hypercortisolemia and by reduced levels of cerebrospinal fluid somatostatin-like immunoreactivity (CSF-SLI). To investigate a possible causal linkage between these abnormalities we administered prednisone, 80 mg orally per day for 5 days, to 9 healthy volunteers. We observed significant prednisone-induced reductions in CSF-SLI. Moreover, the magnitude of these reductions was inversely related to the magnitude of prednisone-induced reductions in plasma ACTH levels, suggesting a functional interaction between circulating corticosteroids, central somatostatin and pituitary ACTH release.
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A case of myelopathy with both intradural and extradural spinal arachnoid cysts is reported treated by cysto-peritoneal shunt, the spinal end of which was inserted percutaneously under fluoroscopic control. The site of drainage was determined by findings at computed myelography. The case illustrates the value of the latter in demonstrating the pathological bio-mechanics producing myelopathy in this condition.
We have assessed functional and structural evidence for sympathetic innervation of human tracheal and bronchial smooth muscles. In the bronchus, functional evidence for such innervation was shown by the following results: a leftward shift in the noradrenaline inhibitory dose-response curve by the neuronal uptake blocker imipramine; the inhibition of uptake of 3H-L-noradrenaline by the neuronal uptake blockers imipramine, cocaine and phenoxybenzamine; and the induced release of noradrenaline and its metabolites by tyramine and electrical field stimulation using nerve-specific parameters; and selective inhibition of field-stimulated contractions by isoprenaline. Structural evidence was shown by the presence of small dense-cored vesicles containing nerve varicosities, occasionally in close proximity to morphologically characteristic cholinergic nerve-endings. This suggests the possibility of presynaptic modulation of acetylcholine release by noradrenaline.
Fourteen patients with atrial fibrillation or flutter and a ventricular rate of greater than or equal to 120 beats/min occurring after cardiac surgery entered a double-blind placebo-controlled conditional crossover trial of intravenous propafenone. Patients randomly received either propafenone (2 mg/kg body weight) or placebo during a 10 minute intravenous infusion. If 20 minutes after the initiation of this infusion there was no conversion to sinus rhythm, the patient received a second intravenous infusion over 10 minutes (either propafenone or placebo, whichever was not given first). The electrocardiogram was recorded continuously throughout the study. Fourteen patients received propafenone and 10 received placebo. No patient's rhythm converted to sinus rhythm after placebo. In six patients (43%) (p less than 0.001), the arrhythmia converted to sinus rhythm between 5 and 10 minutes after the end of the propafenone infusion. After propafenone, the ventricular response to atrial fibrillation or flutter decreased significantly from 141.6 +/- 15.2 to 116.0 +/- 15.5 beats/min. Ventricular rate did not change after placebo. The mean propafenone plasma concentration was 3.46 +/- 2.17 mg/liter. The only side effect of propafenone noted was a decrease in systolic blood pressure of 9 +/- 9 mm Hg. Propafenone was useful for management of atrial fibrillation after cardiac surgery both for control of rapid ventricular response and for conversion to sinus rhythm.
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Biologically active molecular clones of avian sarcoma virus 17 (ASV 17) contain a replication-defective proviral genome of 3.5 kilobases (kb). The genome retains partial gag and env sequences, which flank a cell-derived putative oncogene of 0.93 kb, termed jun. The jun gene lacks preserved coding domains of tyrosine-specific protein kinases. It also shows no significant nucleic acid homology with other known oncogenes. The probable transformation-specific protein in ASV 17-transformed cells is a 55-kDa gag-jun fusion product.
The effect of PGE2 on neurotransmission in the canine tracheal strip dissected free of epithelium was studied in the single sucrose gap and organ bath. PGE2 was a potent inhibitor of the initiation of excitatory junction potentials (ejps) by just submaximal nerve stimulation. In a concentration of 10(-9) or 10(-8) M PGE2 nearly or completely abolished them. Contractile responses to field stimulation in the sucrose gap at 27 degrees C or in muscle baths at 37 degrees C were also reduced or abolished by PGE2 in the same dose range; reductions were greater at low frequency. Responses to acetylcholine were also depressed but significantly less than to field stimulation. These are consistent with major presynaptic as well as some postsynaptic inhibitory actions of PGE2. No evidence was obtained that endogenous PGE2 affected excitatory junction potentials and contractions; i.e. they were stable for hours and unaffected by indomethacin 10(-6) and 10(-5) M under our conditions. Post-stimulus potentiation of ejps amplitude, maximum at 10 s, was observed and became more marked after the first ejp had been markedly reduced or abolished by PGE2. This potentiation was unaffected by indomethacin. It was suggested that a presynaptic process inhibited by PGE2 might participate in this potentiation. The canine trachea is a useful preparation when studied under the experimental condition used here for study of effects of products of arachidonate on neurotransmission.
We studied the functionally discrete calcium sources used by acetylcholine, 5-hydroxytryptamine, histamine and high K+ in the dog tracheal smooth muscle. The extracellular calcium dependence of their responses was assessed by altering the calcium and by pretreatment with the calcium antagonist, nifedipine. The intracellular calcium pool was assessed by studying the interactions between caffeine and the agonists in both skinned and unskinned preparations. The extent of overlap for the different calcium pools between the various agonists was determined by studying the dose-response relationships of these agents before and after pretreatment with another agonist, i.e., the conditioning agonist, in zero calcium conditions. The rank order of sensitivity to calcium removal and to nifedipine was histamine greater than KCl greater than 5-hydroxytryptamine greater than acetylcholine. Caffeine-induced atenuation of the agonist responses was predominantly through physiological antagonism. However, the caffeine responses in unskinned fibres were augmented by pretreatment with the agonists through both nifedipine-sensitive (as with KCl) and -insensitive (as with acetylcholine) mechanisms. The responses to acetylcholine and caffeine were inhibited by theophylline and forskolin. In the skinned muscle fibres, the pCa-tension relationship suggested high calcium sensitivity, a significant caffeine-sensitive calcium pool, and no evidence of calcium release by exogenous inositol trisphosphate. The results are consistent with multiple extracellular and intracellular calcium sources for the agonist responses. We observed considerable overlap of the calcium sources used by these agonists. Of the four agonists studied, histamine appeared to inhibit the release and sequestration of calcium utilized by the other agonists most effectively.
The plasma steroid-binding proteins play a fundamental role in the modification and delivery of the steroid "signal" to its target tissue. While their precise function requires further evaluation, the measurement of these proteins, particularly of SHBG, provides clinically useful information. This article reviews the current theories of sex steroid transport and uptake, and documents the changes in SHBG status relevant to health, disease and drug therapy.
Compression of the anterior aspect of the thoracic cord is a common neurosurgical emergency. Treatment is generally unrewarding. Decompression by the anterior and antero-lateral approach is difficult and time consuming, and decompressive laminectomy offers poor results. It is suggested that in selected cases the removal of a small part posterior of the vertebral body via a posterolateral approach is an appropriate alternative treatment.
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In our previous work, two-dimensional gel electrophoretic analysis of the translational products from mRNA of lens from rats maintained on 50% galactose up to 45 days has suggested that synthesis of mRNA was not arrested by the disease process, but it decreased significantly relative to the control. The loss in mRNA number was due mainly to loss in cell population. Specifically, the gamma-crystallin mRNA product decreased to very low levels at onset of the disease. However, this mRNA was resynthesized in the surviving cells as the cataracts matured. Therefore, it became of interest to explore whether reversal or inhibition of cataracts would lead to some measurable changes in mRNA population in the experimental lens. The results show that the percentage (relative to the total mRNA population) of the in vitro [35S]-labeled translational products from alpha-, beta- and gamma-crystallin mRNAs combined, remained unchanged irrespective of the state of the lens. The severity of the cataracts was examined by indirect immunofluorescence with polyclonal MP26 antibody. Reversal of cataracts led to partial recovery of normal fiber cell morphology. Treatment with sorbinil in combination with galactose led to inhibition of cataracts with indication of appearance of vacuoles at longer periods of exposure to the drug. The translational products profile reflected the expected variation in non-crystallin and crystallin mRNA synthesis. It is concluded that there appears to be a combined fixed level of synthesis for the crystallins, such that inhibition in synthesis of gamma-crystallin mRNAs appears to lead to an increase in synthesis of alpha-crystallin mRNAs, while synthesis of beta-crystallin mRNAs showed insignificant fluctuation. A similar conclusion may also be drawn relative to the combined synthesis for the non-crystallin mRNAs.
We studied neutrophil activation in patients with burns by serial immunofluorescent measurement of neutrophil expression of the complement opsonin receptors CR1 and CR3. CR1-dependent fluorescence was initially (days 0 through 5 after the burn) elevated (mean +/- SEM, 294 +/- 42 vs. 63 +/- 6 in the controls; P less than 0.001) and gradually returned to normal (days 6 through 8, 270 +/- 62, P less than 0.001; days 9 through 13, 185 +/- 38, P less than 0.001; days 14 through 19, 143 +/- 27, P less than 0.001; and days 20 through 50, 93 +/- 5, P less than 0.04). CR3-dependent fluorescence paralleled that of CR1. Neutrophil chemotaxis in response to zymosan-activated serum, a source of C5a, was depressed (days 0 through 5, 77 +/- 4 percent of control, P less than 0.001; days 6 through 8, 70 +/- 4 percent, P less than 0.001; days 9 through 13, 74 +/- 3 percent, P less than 0.001; days 14 through 19, 90 +/- 4 percent, P less than 0.01; and days 20 through 50, 97 +/- 3 percent, P not significant) and inversely correlated with CR1- and CR3-dependent fluorescence (r = -0.559, P less than 0.001; and r = -0.709, P less than 0.001, respectively). Plasma C3a desArg levels were above normal (100 +/- 5 ng per milliliter) throughout (days 0 through 5, 305 +/- 42; days 6 through 8, 546 +/- 69; days 9 through 13, 490 +/- 72; days 14 through 19, 409 +/- 54; and days 20 through 50, 260 +/- 36; all P less than 0.005). Thus, neutrophils in burned patients were activated as indicated by increased expression of complement receptors. The correlation between this increase and the depression of chemotaxis in response to zymosan-activated serum suggests that C5a is responsible for systemic neutrophil activation, which may contribute to the increased susceptibility to infection of patients with burns.