Bilateral spontaneous pigment epithelial detachments in a premature neonate.
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Biomedical subjects
Publications and source records attributed to J A Deutsch.
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The hypothesis that pregnancy sickness has evolved to expel dietary toxins (PROFET, 1988; 1992; HOOK, 1976) is critically reviewed. Instead it is proposed that pregnancy sickness and mastalgia have evolved to reduce frequency of sexual intercourse in early pregnancy. Reduction in coital frequency during the first trimester has often been documented. Uterine motility during sexual excitement contrasts with lack of spontaneous myometrial activity in the first trimester, except when uterine cramping sometimes occurs as a result of intercourse. Such cramping would be expected to increase the chances of spontaneous abortion.
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Immunohistochemistry was used to map c-fos expression in rats to investigate the neural substrates that mediate the emetic action of lithium chloride and the effect of osmotic pressure. Solutions of 3% lithium chloride or 4.14% saline, isotonic to each other, as well as 0.65% lithium chloride or 0.9% saline, also isotonic to each other, were administered intraperitoneally (3 ml/kg) in rats. Both lithium chloride and osmotic pressure enhanced c-fos expression in the nuclei of the solitary tract, the paraventricular nuclei and supraoptic nuclei of the hypothalamus, and in the amygdala. This suggests that these brain structures might be the sites where the autonomic, neuroendocrine and behavioral responses elicited by lithium chloride and osmotic pressure are integrated.
Immunohistochemical techniques were used to map c-fos expression in the rat brain after the i.p. administration of CCK-8 (8 micrograms/kg). C-fos expression was observed in the rostral and the caudal parts of the nuclei of the solitary tract (NTS), and the paraventricular nuclei (PVN) in the hypothalamus. The c-fos expression in these areas was suppressed by the administration of L364,718 (120 micrograms/kg). Since L364,718 is known to be a powerful selective antagonist to the peripheral CCK-A receptors, these data suggest that the effects produced by exogenous CCK are due to peripheral receptors that project to the NTS.
The effect of treatment with the cholecystokinin antagonist L364,718 on intake of different dilutions of corn oil emulsion was tested under two levels of familiarity with the oil emulsion. No increase in intake was observed. To see if the CCK antagonist was effective under our conditions, exogenous CCK was administered under the same conditions. A complete suppression of the large reduction produced by CCK on intake was found.
Thirty patients with moderate angle exotropia of 15 to 20PD were treated with a unilateral lateral rectus recession of 7.0 or 7.5mm. All 30 patients improved postoperatively to orthophoria, small angle exophoria, or small angle tropia of 10PD or less. Alignment was stable during an average follow-up of 21 months.
We prospectively studied 76 patients to analyze the effectiveness of peribulbar anesthesia during strabismus surgery. The patients, ranging in age from 14 to 77 years, were given anesthesia with standard preoperative medication and a peribulbar injection of a mixture of 2% mepivacaine hydrochloride and hyaluronidase. Only one of the 76 patients required an additional injection of anesthetic to achieve adequate anesthesia. No morbidity was associated with the peribulbar anesthesia. Local anesthesia, particularly retrobulbar anesthesia, has been used as an alternative technique in an attempt to reduce the morbidity and mortality associated with general anesthesia in ocular surgery, particularly in those patients with high-risk characteristics. Even with retrobulbar anesthesia, however, there is a risk of morbidity and, in rare cases, mortality. Our results suggest that the use of peribulbar anesthesia is a safe and effective means of anesthesia in strabismus surgery because of minimal associated morbidity.
When one unflavored, nonprotein diet was available in two differently scented bins, rats fed a protein-free diet over four days ate more from the bin smelling of gluten, ovalbumin, yeast or fibrin, but not soy, casein or lactalbumin, than from the bin smelling of butter. Rats fed a protein-containing diet over the same four-day period had no such preference. This result demonstrates that protein-deprived rats can use odor cues in making their selection of certain proteins. Since the direction, speed, and size of preference for these protein odors, excepting soy, are remarkably similar to those previously observed when rats actually consumed the proteins, olfactory stimuli appear to elicit appropriate protein selection responses independently of other protein quality variables such as taste, texture or nutrient composition.
Strabismus is one of the most common ocular disorders encountered in children. The misalignment may be manifest in any field of gaze, may be constant or intermittent, and may occur at near or distant fixation or both. Early detection of strabismus is essential for restoration of proper alignment of the visual axes and the establishment of binocular vision. The proper assessment and management of a child with strabismus requires knowledge of the various clinical types, methods of detection and principles of treatment.
Appetite for most protein appears to be unlearned. Protein-depleted rats, in the first half hour of a test, chose a significantly larger proportion of soybean, gluten, zein, fibrin, yeast torula and ovalbumin than protein replete controls, but not of casein or lactalbumin. There had been no opportunity to learn such dietary preference before the test. The preference for the protein in protein-depleted rats manifested itself significantly from the first minute, and also in females in which protein need was induced by pregnancy rather than a diet different from the controls.
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Stomach balloons were inflated with 20 ml of warm water in anesthetized rats who had a left cervical vagotomy. This increased [14C]2-deoxyglucose (2-DG) uptake in the commissural and medial portions of the right nucleus solitarius. This effect was not present in controls which received 2 ml of water in their stomach balloons.
Bilateral section of the greater splanchnic nerve in the rat abolishes the compensatory ingestion for nutrient removed from the stomach that occurs in normal animals. However, such section leaves normal ingestion unaffected. These results suggest that this nerve participates in food intake regulation.
Rats were trained to ingest corn oil emulsion. Such ingestion was accompanied by intragastric injection either of dilute amino acid (e.g., 4.3 mM L-tryptophan) in one group or saline in a second. No significant difference between the two groups was observed at the end of training. However sudden omission of the amino acid led to a large increase in intake, whereas sudden introduction of the amino acid produced no significant change. It seems that signals for the amount of nutrient ingested can be arbitrarily associated with different nutrients and that the value of such satiety signals is not innately fixed in the amount of feeding inhibition exerted.
The 30 min intake of a 50% corn oil emulsion was measured in 12 hr fasted Sprague-Dawley rats equipped with gastric tubes. When the subjects were given 5 ml intragastric injections of normal saline or of the same oil emulsion they drank by mouth their voluntary intake was unaffected. However, when they were injected with oil emulsion that had been previously ingested by donor subjects, they decreased their feeding significantly. These results suggest that the putative satiety receptors are not stimulated by undigested corn oil triglycerides but by a product of their digestion. This factor appears to be present in the oily rather than the aqueous fraction of the digested oil because when these fractions were given separately only the oily fraction induced inhibition of feeding. Finally, intragastric injections of predigested oil failed to act as an unconditioned stimulus in the development of taste aversions to neutral flavors. This suggests that the reductions in eating observed were not the product of malaise or discomfort.
The paper is concerned with the locus of provenance of satiety signals, what these are generated by, and pathways by which they reach the brain. Satiety signals are generated by the stomach and are of two kinds: distention at high volume and nutrient content. The former, but not the latter, are relayed to the brain via the vagus. Receptors that signal nutrient respond to digestive breakdown product of such nutrient. Further experiments are summarized to show that the gastric nutrient signals are calibrated through learning by association with various flavors. Previous to such learning, when food is novel, gastric controls do not operate, but regulation occurs through oropharyngeal metering.
Rats were given access to small quantities of a 50% oil/water mixture on each of 7 baseline days. On the eighth day, a 30 min compensation test was conducted during which control rats had access to the 50% oil/water mixture and experimental rats had access to either a more concentrated or a more dilute oil/water mixture. Experimental rats given the more concentrated mixture consumed significantly less than controls, while rats given the dilute mixture consumed significantly more than controls. These results suggested that rats can immediately adjust their food intake in response to changes in the caloric density of their diets. In a second experiment, immediate adjustment for caloric change was inhibited by giving rats a supplementary meal directly after access to the 50% oil/water mixture during the baseline phase. These results were discussed in terms of a hypothetical "calibration" mechanism which allows rats to estimate the density of novel caloric concentrations on the basis of a standard concentration.