Relationship of symptoms to cardiac arrhythmias during 24 hours continuous ambulatory electrocardiography.
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Biomedical subjects
Publications and source records attributed to J Mann.
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The current status of Geriatric Dentistry Educational Activities (GDEA) in U.S. dental schools is reported in this survey. Data were collected regarding faculty involvement in geriatric programs, didactic and clinical academic curricula, and other aspects of the ongoing activities in schools. Data were reported by 50 (88 percent) of the nation's 57 dental schools in continuing operation. Forty-two schools reported discrete GDEA at the time of the study. Seven of these schools had a formal division or department of geriatric dentistry. The survey indicated that educational qualification of GDEA coordinators had risen significantly in recent years. The mean number of didactic hours (29) of instruction in geriatric education available to students has also risen. Curriculum time and financial considerations were the primary obstacles to expansion of clinical geriatric activities. With the current economic constraints in dental education, present GDEA levels are unlikely to expand in the foreseeable future, unless governmental or private agencies recognize the importance of developing GDEA and increase their support.
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Large numbers of functional mast cells were obtained by bronchoalveolar lavage (BAL) of Macaca arctoides monkeys that had been infected with the nematode Ascaris suum. These lavage cells, of which 21% were mast cells, released histamine, LTC4, and PGD2 in a concentration-dependent fashion when challenged with ascaris antigen or antibody to human IgE. However, there was no release of histamine when these cells were challenged with compound 48/80. The amount of mediator released was highly dependent on the sensitivity of the cells to immunologic challenge, but was generally in the range of 2 to 5 micrograms histamine (30 to 70% of total), 20 to 80 ng LTC4, and 100 to 300 ng PGD2 per 10(6) mast cells when maximally challenged. Other eicosanoids measured were released only in much smaller quantities. Maximal values were 4 ng LTB4, 2 ng PGE2, and approximately 10 to 20 ng PGF2 alpha per 10(6) mast cells. The amount of LTC4 and PGD2 released correlated with the release of histamine, the calculated regression line indicating that 18 ng LTC4 and 50 ng PGD2 were released per microgram of histamine released. This correlation suggests that the majority of the LTC4 and PGD2 released was probably mast cell-derived. Further support for this conclusion was given by the observation that when lavage cells were fractioned on continuous Percoll gradients, the ability to release LTC4 and PGD2 on immunologic challenge coincided with the peak of mast cells.
As described in the preceding companion paper, bronchoalveolar lavage (BAL) of the primate Macaca arctoides infected with the nematode Ascaris suum yields a population of cells containing a high proportion of mast cells (21%). Nedocromil sodium, a new drug undergoing clinical evaluation for the treatment of reversible obstructive airways disease, inhibited the release of histamine, LTC4, and PGD2 from these cells challenged with antigen (with IC30 values of 2.1 X 10(-6) M, 2.3 X 10(-6) M, and 1.9 X 10(-6) M, respectively) and with anti-human IgE (IC30 values of 4.7 X 10(-6) M, 1.3 X 10(-6) M, and 1.3 X 10(-6) M, respectively). Cromolyn sodium was essentially inactive. Histamine release from rat peritoneal mast cells induced by anti-rat IgE was, however, inhibited by both nedocromil sodium and cromolyn sodium with IC30 values of 1.1 X 10(-6) M and 5.5 X 10(-7) M, respectively. Both compounds induce phosphorylation of a 78,000 m.w. protein in the rat peritoneal mast cell in the absence of any stimulus at the same concentrations as those required to inhibit histamine release stimulated by anti-IgE. This event may be part of a feedback mechanism to limit degranulation. Nedocromil sodium and cromolyn sodium were equipotent in their ability to inhibit anti-IgE-induced histamine release from rat peritoneal mast cells, but differed markedly in their ability to inhibit histamine release from macaque BAL cells.
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Renal failure as a consequence of manifest lead intoxication (nephropathia saturnina) has almost completely disappeared in the FRG. However, there has been rising concern that increased lead burden, primarily as a result of environmental pollution, may adversely affect blood pressure and renal function even in the absence of extrarenal signs of lead intoxication. Such concern is based on epidemiological studies which demonstrated a relation between blood lead level and blood pressure and on experimental studies which showed that lead activates several pressor mechanisms. Furthermore, increased body lead burden is found in a substantial proportion of patients with renal failure, particularly when concomitant gout is present. Unfortunately, none of the above findings constitute irrefutable evidence and further studies are clearly necessary.
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Four experimental models of myocardial hypertrophy were investigated in rats: 1. Mild hypertrophy induced by physical exercise, 2. mild hypertrophy induced by chronic pressure overload (24 weeks), 3. moderate hypertrophy induced by chronic pressure overload (8 weeks), 4. moderate hypertrophy in diabetes induced by chronic pressure overload (8 weeks). Stereological investigations on left ventricular papillary muscles disclosed different morphological reaction patterns: 1. The capillary bed of the myocardium responded differently in mild hypertrophy:physical training, but not mild chronic pressure overload, evoked neoformation of capillaries. 2. Mild hypertrophy and moderate hypertrophy induced by chronic pressure overload were not associated with quantitative structural reactions of myofibrils and mitochondria. Those alterations appeared, however, in hypertensive-diabetic rats with moderate hypertrophy. Our data provide further experimental evidence for the existence of a hypertensive-diabetic cardiomyopathy.
4-[14C]HAD was rapidly metabolized (99% after 5 min) by hepatocytes from phenobarbital-treated rats. An array of phase I metabolites was formed, variously involving one and two reductions, hydroxylation, hydration and hydroxylation plus one or two reductions. Some of the metabolites were identified by synthesis and others tentatively by mass spectrometry. After 10 min, approximately 30% of the original radioactivity was present in HAD glucuronide and, after 15 min, approximately 60% was present in the total glucuronide fraction which contained several components. Only one of the phase I metabolites (2-hydroxy-HAD) exhibited significant aromatase inhibitory activity (45% of that of HAD).
HL-60 human leukaemic cell line a suitable homogeneous target population for the selective endogenous inhibitor of myelopoiesis, isolated in our laboratory, was submitted to multiparameter analysis of cell proliferation in suspension cultures. As detected by 3H-TdR incorporation, a single dose of the regulator elicited a 6 to 8 hours arrest of DNA synthesis. The inhibition could be prolonged by repeated applications. As affected by the factor, alteration of population kinetics is characterized, revealed by flow cytofluorometric analysis, in G1 arrest of a fraction of cells, and diminishing those in hyperdiploid and tetraploid stage. 51Cr-release detection of vitality proved, that the endogenous factor, chemically determined as nucleopeptide, affected non-toxically and reversibly HL-60 cell proliferation.
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In order to correlate the percent of coronary lumen reduction measured by cineangiography and by pathology, we reviewed the coronary trees of 12 patients who died of coronary heart disease. The 36 arterial segments were divided in two groups: group I showing a good correlation in its 24 segments (less than 15% difference between both methods, r = 0.90), and group II (12 segments) with a poor correlation. No significant differences were found every time there was a greater than 70% stenosis. Milder lesions have a higher rate of discrepancies, due to pathology overestimation because of collapse of the vessel and tissue shrinkage, and to the angiographic underestimation that appears when comparing the stenotic segment with a remaining presumably normal artery.
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