The poet as neurotic: the official biography of Robert Frost.
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Biomedical subjects
Publications and source records attributed to L Thompson.
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Eight hundred sixty-two postmyocardial infarction patients volunteered to be randomly selected and enrolled into: (1) a control section of 270 patients, who received group cardiologic counseling; and (2) an experimental section of 592 patients, who received group type A behavior counseling in addition to group cardiologic counseling. Reduction in type A behavior at the end of 3 years was observed in 43.8% of the 592 participants, who initially were enrolled to receive group cardiologic and type A behavioral counseling. This degree of behavioral reduction was significantly greater than that observed in participants who initially were enrolled to receive only group cardiologic counseling. The 3-year cumulative cardiac recurrence rate was 7.2% in participants who initially were enrolled to receive group cardiologic and type A behavioral counseling. This was significantly less (p less than 0.005) than that (13%) observed in participants who initially were enrolled to receive only cardiologic counseling. This difference in recurrence rates was due to a lesser incidence of nonfatal infarctions in the patients who had been enrolled in the section receiving type A behavioral as well as cardiologic counseling. These data suggest that type A behavior can be altered in a sizable fraction of postinfarction patients and that such alteration is associated with a significantly reduced rate of nonfatal myocardial infarctions.
The biochemical mechanism of lymphocyte dysfunction with adenosine deaminase deficiency has been investigated using cultured phytohemagglutinin stimulated normal peripheral blood lymphocytes and the adenosine deaminase (ADA) inhibitor 2'-deoxycoformycin. The addition of deoxyadenosine to ADA-inhibited (but not to uninhibited) cells generated increased dATP pools (up to 50-fold greater than controls) and depressed the mitogen response. dATP Accumulation was accompanied by depletion of the other three deoxynucleoside triphosphate (dNTP) pools (dTTP, dCTP, and dGTP). Suppression of the mitogen response could be prevented ("reversed") to 90% of control levels by the addition of deoxynucleoside precursors for the depleted dNTPs at the initiation of mitogen stimulation. "Reversal" restored the dTTP and possibly the dGTP pools. Thus the mechanism of toxicity in this model appears to be inhibition of ribonucleotide reductase by massive accumulation of dATP, resulting in starvation for the other three deoxyribonucleoside triphosphates. "Reversibility" of this toxicity by providing sources for the missing three deoxynucleoside triphosphates argues for ribonucleotide reductase inhibition rather than other mechanisms of deoxyadenosine toxicity in this model.
Two bioluminescence-measuring instruments, the Turner Design and Lumac systems, were compared with a standard plate culture method for their ability to rapidly screen 400 urine specimens. For cultures with less than 1,000 CFU/ml the Turner Design, with old and new evaluation formulas, gave 6.5 and 50.6% false-positive results, respectively, versus 17.6% at greater than or equal to 500 relative light units with the Lumac. For cultures which had greater than 10(5) CFU/ml the Turner Design gave 39% (old formula) and 14% (new formula) false-negative results compared with 4% at less than 200 relative units with the Lumac. The microorganisms most frequently isolated in the false-negative cultures from either system were gram-positive cocci. Predictive values for a positive test at greater than 10(5) CFU/ml were 77.4% (old formula) and 35.7% (new formula) for the Turner Design versus only 50% for the Lumac at greater than or equal to 500 relative light units. Predictive values for a negative test for both instruments were greater than 88% at greater than 10(5) CFU/ml. The Turner Design and Lumac systems were 4.0 and 3.7 times as expensive, respectively, as the plate culture method. Although both systems greatly reduce the time required to process urine specimens, their high costs as compared with that of plate culture, their failure to detect many specimens having greater than 10(5) CFU of gram-positive cocci per ml, and the numerous false-positives reported by both instruments suggest that additional improvements in the systems are warranted.
The effect of lithium administration on urine eletrolyte excretion is controversial with reports of increased, unaltered and reduced excretion rates of sodium, potassium, calcium, magnesium and inorganic phosphate. Therefore rats treated with daily intraperitoneal lithium chloride for 3 weeks were studied and were found to have marked fluctuations in electrolyte excretion when compared to untreated rats. Although lithium-treated rats were always polyuric, urinary sodium, potassium and calcium excretion was significantly elevated immediately following intraperitoneal lithium but their excretion rates then returned towards normal. Magnesium excretion was initially unaltered by lithium administration (6.8 +/- 1.3 compared with 7.3 +/- 1.7 mumol/100 g/8 h) but then decreased (2.5 +/- 0.5 with 7.8 +/- 1.1 mumol of magnesium/100 g/8 h; p less than 0.01) during the final collection period. A persistent phosphaturia also occurred with lithium treatment (122 +/- 5 compared with 92 +/- 6 mumol/100 g body weight/24 h). Despite these significant changes in renal electrolyte transport with lithium administration, similar changes were also noted in rats similarly treated with equimolar doses of sodium chloride although polyuria did not occur. Thus it is postulated that lithium ions exert their effect on renal electrolyte transport in a similar manner to that of sodium.
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Because mammalian distal nephron segments with both calcitonin- and antidiuretic hormone- (ADH) sensitive adenylate cyclase activity have been described, in vivo and in vitro experiments were performed to study the effect of calcitonin on rat distal nephron water permeability. Calcitonin 1 and 0.1 U/ml, but not 0.01 U/ml, significantly increased the diffusional water permeability in the isolated papillary collecting duct by 15 and 11%, respectively. However, this effect was small when compared with a 68% increase with a supramaximal concentration of ADH (from 4.0 +/- 0.3 to 6.7 +/- 0.9 microns/s; n = 6, P less than 0.01). The normal increase in water permeability with increasing concentration of ADH (0.02 and 0.2 mU/ml) was depressed by the previous addition of calcitonin (1 U/ml) to the bath but was unaltered with the supramaximal ADH concentration (2 mU/ml). Verapamil, a compound that antagonizes cellular calcium entry, did not alter the effect of calcitonin on diffusional water permeability. Calcitonin in concentrations of 0.05, 0.5, and 5 U/ml produced a significant reduction in urine flow and free water clearance. Pretreatment with calcitonin in these concentrations inhibited the antidiuretic action of ADH. These studies suggest that calcitonin acts as a partial agonist to ADH within the distal nephron. It is unclear whether such an action represents a physiological or a pharmacological effect.
Two experiments investigated the effects of novelty and familiarity on illness-induced aversions to taste and place cues in coyotes (Canis latrans). Coyotes were made ill on familiar food laced with lithium chloride in a novel place and then received preference tests. In Experiment 1, coyotes avoided the previously poisoned familiar food in the novel treatment place but readily ate the same familiar food in a familiar safe place. In Experiment 2, the results of Experiment 1 were replicated, and it was found that coyotes would eat a different familiar food in the novel treatment place. On the basis of the results of this and other studies, a model for averting animals from places where they are not wanted is presented.
Monoclonal antibody T305, prepared by immunizing mice with the T-ALL derived cell line RPMI-8402, immunoprecipitates a single chain glycoprotein with m.w. 160,000 daltons (under reducing conditions) or 180,000 daltons (under nonreducing conditions). In immunofluorescence assays, antibody T305 reacted with a subpopulation of T cells in normal blood (22 +/- 6%), thymus (28 +/- 11%), and lymph node (24 +/- 6%). Increased frequency of T cells reactive with antibody T305 was found in peripheral blood of patients with infectious mononucleosis (greater than 80%), graft-vs-host disease after bone marrow transplantation (65 +/- 11%), acquired immunodeficiency syndrome (53 +/- 12%). The T cells in synovial fluid of patients with rheumatoid arthritis had increased frequency of antibody T305 reactive cells (59 +/- 8%) as compared to their peripheral blood (18 +/- 7%). Two color immunofluorescent studies demonstrated that the T305+ T cells predominantly co-stained with antibody Leu 2a (suppressor/cytotoxic subset) in both normals and disease state blood. After cell sorting to obtain T305+ and T305- subpopulations, we demonstrated that a) natural killer and antibody-dependent cellular cytotoxicity activity in normal blood was in the T305+ but not T305- T cells; b) cytotoxic T cells induced by mixed lymphocyte reaction were predominantly T305+; c) T305- T cells could be induced in vitro to express T305 antigen by mitogens or allogeneic B cells; d) the DNA content of T305+ and T305- T cells in normal blood was similar (greater 95% of cells with G0/G1 level); e) after mitogen stimulation, T305 antigen induction on previously T305- cells occurs before S-phase; and f) significantly more [3H]-thymidine after mitogen stimulation was incorporated by originally T305- cells than by originally T305+ cells (p less than 0.001). The T305 antigen was not restricted to T cells because it was also found on myeloid precursors in bone marrow but was not present on polymorphonuclear leukocytes, red blood cells, platelets, muscle, liver, skin, kidney, lung, or brain. Antibody T305 was found on 24/25 cases of acute leukemia (6 T-ALL, 10/11 cALL, 7 AML, and 1 AMOL) but not on 18 cases of chronic leukemia (B-CLL, T-CLL, null CLL, CML). The importance of the T305 antigen is that it is present on a high number of T cells in certain autoimmune diseases and on virtually all acute leukemia cells. Its distribution on immature and in vitro activated cells suggests that it may represent a receptor for signals related to cellular replication or differentiation.
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One hundred seventeen unselected women with symptoms of acute cystitis were randomized to groups for immediate therapy with one of the following four single-dose regimens: (1) 1 g of sulfisoxazole; (2) 2 g of sulfisoxazole; (3) a combination of trimethoprim, 160 mg, and sulfamethoxazole, 800 mg; and (4) a combination of trimethoprim, 320 mg, and sulfamethoxazole, 1,600 mg. Forty-one women were excluded, 13 did not return for follow-up, and 28 did not have significant bacteriuria in the pretherapy culture. Escherichia coli was isolated in 81% of infections. Antibacterial activity was significantly greater in urine collected during the 24 hours after therapy in those who received trimethoprim-sulfamethoxazole. However, overall cure varied from 85% to 95%, without any great differences between the regimens. The rate of cure of 69% in the 13 patients with presumptive evidence of renal infection (antibody-coated bacteria present) was significantly lower than the rate of cure of 95% in women without evidence of renal infection. Single-dose therapy with these regimens was safe and effective in adult women with symptoms of acute cystitis, regardless of the localization of the site of infection.