Perspectives on osteoporosis research: its focus and some insights from a new paradigm.
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Adult↗
Biomedical subjects
C Jerome
Publications and source records attributed to C Jerome.
Self-analysis: structure, extension, and computerization.
In this article, a structure for self-analysis is described and the expanded applicability of self-analysis implied by the suggested structure is examined. Also, the stage of computer psychotherapy programs is reviewed, and an overview of a plan for merging self-analysis and computer psychotherapy is presented.
Affect↗
Failure to detect increases in brain dopamine metabolism in rats sham feeding sucrose and corn oil.
In a recent study we found that when rats sham fed 6% sucrose, 10% sucrose, and 100% corn oil, the rank order of inhibitory potency for D-1 and D-2 receptor antagonists was 6% sucrose greater than 10% sucrose greater than 100% corn oil. In a complementary study, sham-feeding rats preferred 100% corn oil greater than 10% sucrose greater than 6% sucrose as measured by two-bottle preference tests. The preferences are evidence for the rank order of reward value of these solutions. In the present study we tested the hypothesis that the relative antagonist potencies were due to differential release of DA, dependent on the reward value of the sham-fed solution. Dopamine metabolism, estimated by the ratio of dihydroxphenylacetic acid (DOPAC) to DA, was measured in forebrain-DA terminal fields during sham feeding of 100% corn oil, 6% sucrose, and 10% sucrose. The results did not support our hypothesis: no increase in DA metabolism was observed after the sham feeding of any solution.
3,4-Dihydroxyphenylacetic Acid↗
Unexpected frostbite in cynomolgus macaques after a short exposure to snow.
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Animals↗
Sham feeding of sucrose increases the ratio of 3,4-dihydroxyphenylacetic acid to dopamine in the hypothalamus.
Recent pharmacological experiments suggested that central dopaminergic (DA) mechanisms are necessary for the normal eating response to sweet stimuli. To test this hypothesis, we measured the ratio of dihydroxyphenylacetic acid (DOPAC) to dopamine (DA) in forebrain DA terminal fields during the sham feeding of sucrose (1-40%) by rats after 17 hr of food deprivation. After 9 min of sham feeding 10% or 40% sucrose, DOPAC/DA increased in the hypothalamus, but not in other forebrain regions including the n. accumbens, amygdala, and pyriform cortex. This increase in hypothalamic DOPAC/DA did not occur after 9 min of sham feeding 1%, 1.25%, or 2.5% sucrose. The increased DA metabolism required that sham feeding of 10% or 40% sucrose be maintained for longer than 3 min, because no increase of DOPAC/DA was observed in any forebrain region after 3 min of sham feeding. These results are strong evidence that hypothalamic DA mechanisms are activated by the sham feeding of sucrose solutions and they support the hypothesis that central DA mechanisms are necessary for the normal eating response to sweet stimuli.
3,4-Dihydroxyphenylacetic Acid↗
Specific postoperative syndromes after total and selective vagotomies in the rat.
Male Sprague-Dawley rats which survived bilateral subdiaphragmatic vagotomy (with hepatic branch intact) exhibited an acute syndrome of hypophagia, hypodipsia and severe loss of body weight when maintained on solid food and water for 14 days after vagotomy. This postvagotomy syndrome was attenuated when rats were maintained on a liquid diet (116EC) chosen to minimize postvagotomy dysphagia and abnormal gastric retention of food; vagotomized rats were hypophagic and lost body weight, but the degree of weight loss was not so severe as for vagotomized rats eating solid food. When rats with total subdiaphragramatic vagotomy were maintained on palatable sweet milk food, the acute postvagotomy syndrome was abolished; these vagotomized rats ate and drank as much as rats with sham vagotomy and they did not lose weight. When rats that underwent selective hepatic, gastric or coeliac vagotomy were maintained on the sweet milk diet, three different postoperative syndromes occurred: after selective hepatic vagotomy, rats were hyperphagic, hyperdipsic and gained body weight at a greater than normal rate; after selective gastric vagotomy, rats lost weight despite relatively normal food and water intakes; and after selective coeliac vagotomy, there was no change in food or water intakes or body weight. These results demonstrate that a sweet milk diet abolishes the anorexia, hypodipsia and weight loss that usually occur in vagotomized rats maintained on pellets and water. Use of this sweet milk diet revealed different acute syndromes after bilateral and selective vagotomies. The differences among the syndromes suggest that hepatic, gastric and coeliac vagal branches serve different functions in the control of food and water intake and body weight.
Animals↗
Afferent axons in abdominal vagus mediate satiety effect of cholecystokinin in rats.
Selective section of afferent vagal axons that reach below the diaphragm blocks the satiating effect of peripherally administered cholecystokinin in the rat. Section of the analogous efferent axons has no effect. After the behavioral tests, the selective axonal sections were confirmed with horseradish peroxidase histochemistry.
Abdomen↗
Development of the drinking deficit to hypertonic saline in rats after abdominal vagotomy.
After abdominal vagotomy, rats drink significantly less water in response to hypertonic saline. The drinking deficit could be due to the disconnection of vagal afferent fibers from a peripheral receptor stimulated by hypertonic saline or the loss of a more complex, tonic, fascilitatory function. The loss of the phasic afferent fiber function should appear immediately after vagotomy, but the loss of the tonic function might take more time to develop. We attempted to distinguish between these two possibilities by preparing 5 different groups of vagotomized rats that were each tested with 1 M NaCl (1% BW) at one of five postoperative days--2, 4, 7, 14 or 21 days. The drinking response was significantly decreased from preoperative intake in the groups tested on postoperative days 7, 14, and 21, but not in the groups tested on postoperative days 2 and 4. Since the drinking deficit is not present 2 and 4 days after vagotomy, the effect of vagotomy is not the result of lesioning afferent fibers that mediate a peripheral phasic stimulation elicited by hypertonic saline. The postoperative delay of at least 7 days for the deficit to appear suggests that the effect of vagotomy is the loss of some more complex neurological function that is necessary for a normal drinking response. The nature of this lost function is unknown.
Angiotensin II↗
Effects of total and selective abdominal vagotomies on water intake in rats.
To determine if the decreased water intake of abdominal vagotomized rats in the presence and absence of food could be localized to a specific branch of the abdominal vagus, we measured the drinking response of rats that had undergone gastric vagotomy, hepatic vagotomy, coeliac vagotomy or a combined coeliac-hepatic vagotomy. The major results were: (1) gastric vagotomized rats drank less than rats that had had sham operations in the previous 24 h with and without food present; (2) hepatic vagotomized rats drank as much as sham operation rats in the presence or absence of food, but drank more than sham operation rats after 17 h water deprivation; (3) coeliac vagotomized rats drank normally in all tests; (4) combined coeliac and hepatic vagotomized rats drank normally except in a 2 h liquid food-related drinking test in which they drank more than sham operation rats; (5) no selective or total, abdominal vagotomized rat drank less than sham operation rats in response to 17 h water deprivation. Thus, gastric vagotomy was the selective vagotomy that most closely mimicked the effects of total abdominal vagotomy on drinking. In demonstrating that increases, decreases, or normal water intake depended on the specific vagal branch(es) disconnected and the specific dipsogenic test, these results refute the opinion that decreased drinking after abdominal vagotomy is simply the result of non-specific effects of vagal surgery. Finally, the normal water intake after water deprivation in total, gastric, and coeliac vagotomized rats in these experiments challenges the current theory that drinking after water deprivation is primarily due to osmotic thirst because previous experiments have shown that total, gastric, and coeliac vagotomized rats drink less than normal to the osmotic challenge produced by acute administration of hypertonic saline.
Abdomen↗
Chronic hypodipsia to intraperitoneal and subcutaneous hypertonic saline after vagotomy.
Recent studies suggest that the decreased drinking response to hypertonic saline produced by bilateral subdiaphragmatic vagotomy (VGX) is a function of the route of saline administration and the length of postoperative recovery. We determined the effects of VGX on drinking during the two hours after intraperitoneal and subcutaneous injections of 0.25, 0.5 and 1.0% body weight doses of 1 M NaCl 30 weeks after surgery. Regardless of the route of injection of saline, VGX rats took longer to initiate drinking and drank less water after the two highest doses than controls. Although VGX rats drank less than controls after both routes of injection, the decrease in water intake was greater after intraperitoneal administration. We conclude that, since both deficits were obtained regardless of the route of saline injection 30 weeks after surgery, route of administration and length of postoperative recovery are not important factors for demonstrating impairments in the drinking elicited by hypertonic saline after total abdominal vagotomy under our experimental conditions.
Animals↗
Gastric vagotomy inhibits drinking after hypertonic saline.
Rats with bilateral subdiaphragmatic vagotomy drank later and less in response to cellular dehydration produced by hypertonic saline. In an attempt to localize this deficit neurologically, we performed selective gastric, hepatic or coeliac vagotomies. The drinking responses of such selectively lesioned rats were compared with total bilateral vagotomized rats and sham operated rats after 0.15 M and 1 M NaCl (1% BW). Gastric vagotomy reproduced the drinking deficits that occurred after total vagotomy, but hepatic and coeliac vagotomies did not. These results demonstrate that disconnection of the gastric vagal fibers is the necessary and sufficient lesion of the abdominal vagal system for decreasing the drinking response to hypertonic saline.
Animals↗
Gastric or coeliac vagotomy decreases drinking after peripheral angiotensin II.
After bilateral subdiaphragmatic vagotomy, rats drank later and less in response to peripherally administered angiotensin II [13]. We attempted to localize this deficit neurologically by performing selective gastric, hepatic or coeliac vagotomies. The drinking responses of such selectively lesioned rats to 0.1 and 1.0 mg X kg-1 angiotensin II (SC) were compared to those of total bilateral vagotomized rats and sham vagotomized rats. Gastric or coeliac vagotomy produced drinking deficits that were similar to those produced by total abdominal vagotomy, but hepatic vagotomy did not. These results demonstrate the importance of abdominal vagal mechanisms in the drinking response to circulating angiotensin II.
Angiotensin II↗
Long-term venous access in rhesus monkeys.
Long-term, intermittent, intravenous infusion of substances, such as amphotericin B, with a high potential for causing peripheral vein thrombophlebitis was feasible by means of a subcutaneously implanted silastic reservoir catheter device, which gave access to the central venous compartment. The implanted reservoirs withstood at least 100 percutaneous entries with a 27-gauge needle; injections were carried out by using an infusion pump. With precautions taken to prevent infection, clotting, or the formation of precipitates in the catheter, the device permitted easy intravenous injection and was well tolerated.
Animals↗
Viral hepatitis (adenovirus) in a California sea lion.
A juvenile California sea lion (Zalophus californianus) died 28 days after admission to the California Marine Mammal Center. Necropsy revealed hemorrhagic fluid in the stomach and hepatomegaly. Histologically, there was evidence of multifocal necrotizing hepatitis and acute suppurative bronchopneumonia. Amphophilic intranuclear inclusions were found, and electron microscopy revealed virions morphologically classifiable as adenovirus.
Adenoviridae↗
Abdominal vagotomy blocks the satiety effect of cholecystokinin in the rat.
The site where peripherally administered cholecystokinin-8 elicits satiety was investigated by injecting rats with cholecystokinin-8 (1 to 8 micrograms per kilogram of body weight, intraperitoneally) after they had received bilateral lesions of the ventromedial hypothalamus or after they had undergone bilateral abdominal vagotomy or selective vagotomies. Abdominal vagotomy or gastric vagotomy abolished or reduced the satiety effect of cholecystokinin, but lesions of the ventromedial hypothalamus did not. These results demonstrate that peripherally administered cholecystokinin acts in the abdomen through gastric vagal fibers and not directly on the brain to produce satiety in the rat.
Afferent Pathways↗
The satiety effect of cholecystokinin: a progress report.
The satiety effect of cholecystokinin (CCK) that was first observed in rats has now been extended to chickens, rabbits, pigs, sheep, rhesus monkeys, lean mice, genetically obese mice and rats, neurologically obese rats, lean men and women, and obese men. The effect is specific and can be obtained in animals and humans without reports or signs of sickness. The mechanism of the effect is unknown, but the gastric vagal fibers are necessary for the effect. This has led to the hypothesis that the satiety effect is due to activation of vagal afferent fibers that inhibit the central control system of feeding by CCK acting directly on recently described vagal CCK receptors and/or indirectly through a gastric smooth muscle effect that vagal receptors are sensitive to.
Animals↗
Abdominal vagotomy does not block the satiety effect of bombesin in the rat.
Bombesin (2-16 microgram-kg-1, intraperitoneally) inhibited food intake in rats after abdominal vagotomy. Since the same vagotomized rats did not respond to the octapeptide of cholecystokinin (1-8 micrograms-kg-1, intraperitoneally), these data are decisive evidence (1) that bombesin does not produce satiety by releasing endogenous cholecystokinin and (2) that vagal afferents are not necessary for the satiety effect of bombesin.
Animals↗
Ceruletide acts in the abdomen, not in the brain, to produce satiety.
Ceruletide (caerulein), a decapeptide extracted from the skin of the frog, Hyla caerulea, is very similar in structure to the C-terminal octapeptide of cholecystokinin (CCK-8). Although ceruletide and CCK-8 act through similar or identical receptors to produce the same visceral effects, previous studies in the rat suggested that peripherally administered ceruletide acted directly on the ventromedial hypothalamic (VMH) area to decrease food intake, but peripherally administered CCK-8 acted at a vagally innervated abdominal site to decrease food intake. Since it is unprecedented for these two peptides to produce the same effect by acting at different sites, we investigated the site of action of ceruletide's satiety effect in the rat and compared it to the site of action of CCK-8. The major results were: (1) intraperitoneal administration of ceruletide and CCK-8 inhibited food intake, but intraventricular administration did not; (2) the satiety effect of ceruletide and CCK-8 was not changed by bilateral lesions of the VMH; and (3) the satiety effect of ceruletide and CCK-8 was abolished or markedly reduced by bilateral abdominal vagotomy. We conclude that ceruletide acts at the same vagally innervated abdominal site to produce satiety as CCK-8 does and that neither peptide acts directly on the VMH area.
Abdomen↗