Publications by authors named "Baer P"

Reduced renal 15-hydroxyprostaglandin dehydrogenase (PGDH) activity has been proposed as a cause, subsequent to elevation of intrarenal prostaglandin (PG) E2 levels, of the development or maintenance of high blood pressure (BP) in the New Zealand genetically hypertensive (NZGH) rat. To test this hypothesis, PGDH activity in homogenates of kidneys and lungs and in urine concentration and excretion of PGE2 were determined in male and female NZGH and normotensive control (NZNR) rats. Lung PGDH activities of the four groups were similar.

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A study was undertaken to evaluate the role of vasopressin in the pathogenesis of hypertension in New Zealand genetically hypertensive (NZGH) rats. During the course of development of hypertension in NZGH rats from 4 to 11 weeks of age, the 24 h urinary excretion of vasopressin did not differ from that of the New Zealand normotensive control rats (NZNR). Furthermore, at the conclusion of the study (rats 13 to 14 weeks old), the plasma vasopressin concentrations in NZGH and NZNR rats were not significantly different.

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To clarify the possible environmental mediation of familial aggregation of blood pressure (BP), we examined whether the behavior of family members differed between families with a hypertensive (n = 16) or a normotensive (n = 15) father. Three-member families consisting of a father, mother, and a boy or girl aged 8-13 years were videotaped as they interacted under standard conditions calling for disagreement or conflict. Their BPs were recorded before and after interactions.

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Mandel and Bridger (1967) found resistance to extinction of differentially conditioned skin conductance responses by subjects, who, according to a post-conditioning questionnaire, believed pre-extinction instructions that the shock-UCS would no longer be administered. The present study was intended to: (1) determine whether or not an extraordinarily noxious shock-UCS is required to produce such results; (2) eliminate possible retrospective falsification effects associated with the use of a post-conditioning questionnaire by monitoring subjects' UCS expectancies continuously throughout extinction as well as acquisition trials; (3) attempt to confirm that resistance to extinction is stronger with a 0.5 sec CS-UCS interval than with an 8 sec interval; and (4) test several predictions regarding UCS expectancies during the intertrial intervals of acquisition.

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In the first section of this two-part report human peripheral blood leukocytes were tested for reactivity to extracts of sclera. Absence of scleral antigenicity is suggested by the results which showed that the leukocytes reacted similarly in sclera stimulated cultures and in the controls. The second part of the report discusses the clinical aspects of sclera allografts and provides guidelines for their clinical use.

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Virus particles were detected within the nuclei and cytoplasm of odontogenic cells in the developing teeth of young hamsters infected with a small DNA virus (MVM). Disturbances of normal cytodifferentiation and organogenesis occurred as a result of viral multiplication. Virions were also observed in dense lysosome-like bodies of activated monocytes within the periodontal ligament and adjacent connective tissues.

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Severely fractured, hypoplastic, and carious mandibular anterior teeth in a 17-year-old patient precluded the ability to use adequate methods of control of plaque. With simple, inexpensive techniques, periodontal health was restored and a functional and esthetic occlusion was provided. This treatment plan was accomplished with minimal risk of injuring the pulps of the teeth.

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A 16-item self-report instrument was designed and cross-validated, comparing essential hypertensives with normotensives. After item selection using two sets of standardization groups, scores obtained from three additional sets of hypertensive and normotensive groups were significantly different. The scores were not significantly related to variables such as age, sex, socioeconomic status, hypochondriasis, social desirability or target organ involvement.

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Effects of PGE2 and PGI2 on renal vascular resistance (RVR) were compared in anesthetized rats. Renal blood flow and systemic blood pressure were measured before and during infusion of PGE2 (2--2 microgram/min) or PGI2 (1--5 microgram/min) into the aorta just proximal to the renal arteries. Both prostaglandins significantly decreased blood pressure and renal blood flow, but effects on RVR were dissimilar.

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Blood pressure, renal blood flow, glomerular filtration rate and urine composition and flow rate were measured, and renal vascular resistance was calculated, before and during infusion of prostacyclin (PGI2) i.v. or i.

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Earlier studies of renal transplantation and of sodium metabolism indicated that the cause of high blood pressure in the Milan strain of genetically hypertensive rats (MHS) was altered renal function. To pinpoint the active factors, we used micropuncture to study several indices of renal function in normal (NR) and MHS rats at three different ages: A) 26 to 30 days, before development of hypertension (pre-MHS); B) 35 to 40 days; and C) 75 to 90 days, after the development of hypertension. The indices studied and the important differences found between the two strains were: 1) Single nephron filtration rate (SNFR) and late proximal tubular fluid delivery to the distal nephron (LPF).

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