Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a prospective study, infants of high-risk mothers delivered over a 1-year period were evaluated by clinical, biochemical, and behavioral methods. Of 67 newborns whose mothers had oxytocin challenge tests (OCTs), 54 were delivered after negative tests, and 13 after positive tests. Infants with positive OCTs had poor state organization and reflexive performance when compared with negative-OCT babies. These infants also showed evidence of intrauterine malnutrition, but did not have any greater asphyxiation than the negative OCT group. These results are consistent with the hypothesis that a positive OCT implies pathological placental respiratory insufficiency, which may be superimposed, in many instances, on impairment in utero of the placenta's nutritional function. The clinical manifestation of such dysfunction is the alteration in subtle neonatal neurobehavior.
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PMID:A prospective study of the oxytocin challenge test and newborn neurobehavioral outcome. 45 Mar 65

Ewes carrying twin fetuses were maintained during late pregnancy on a uniformly high plane (n = 22), a uniformly low plane (LP) (n = 24) or a low plane increasing to a high plane (n = 14) of nutrition. Seven ewes at each nutritional level were killed at 142 days of gestation and the liver and muscle glycogen and body lipid concentrations of the fetuses were determined. The rest of the ewes lambed naturally at about 145 days and the colostrum yields were obtained by hand milking after oxytocin injections during the first 18 hours after birth. The lactose, lipid and protein concentrations of colostrum were determined. Undernutrition in the LP group did not apparently affect the body concentrations of available glycogen, reduced available body lipid by about 47 per cent and reduced the lactose, lipid and protein available in colostrum during the first 18 hours by about 50 per cent. Refeeding previously underfed ewes to a high plane during the last five to 10 days of pregnancy did not improve the available reserves of glycogen or lipid in the lambs but did increase the yields of colostral constituents by about 30 per cent. The relative contributions of body reserves and colostral constituents to the maintenance of high, medium and low metabolic rates in lambs from different groups was assessed. It was concluded that under normal field conditions refeeding undernourished ewes during the last weeks of pregnancy would improve only marginally the survival potential of the lambs and that most lambs would be compelled to draw on their body glycogen reserves in order to maintain heat production during the first 18 hours after birth, even when they consumed all the available colostrum.
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PMID:Effects of maternal nutrition on the availability of energy in the body reserves of fetuses at term and in colostrum from Scottish Blackface ewes with twin lambs. 407 Jul 90

Egg binding most often affects budgerigars, cockatiels, finches and canaries. Causes include oversized or malpositioned eggs, lack of exercise, nesting too early or late, excessive egg laying, uterine damage or infection, obesity, malnutrition, sudden drops in ambient temperature and genetic factors. Clinical signs are perching unsteadily with ruffled feathers and half-closed eyelids, frequent tail-wagging or straining, swelling over the tail base, and sitting on the cage bottom. Diagnosis is by physical examination and radiography. Treatment may involve increasing the ambient temperature to 85-90 F, lubricating the vent, IM injections of Ca solution and/or oxytocin, egg aspiration and laparotomy.
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PMID:Egg binding in caged and aviary birds. 673 18

Starvation-induced alterations of neuropeptide activity probably contribute to neuroendocrine dysfunctions in anorexia nervosa. For example, CRH alterations contribute to hypercortisolemia and NPY alterations may contribute to amenorrhea. Alterations of these peptides as well as opioids, vasopressin, and oxytocin activity could contribute to other characteristic psychophysiological disturbances, such as reduced feeding, in acutely ill anorexics. Such neuropeptide disturbances could contribute to the vicious cycle that has been hypothesized to occur in anorexia nervosa. That is, the consequences of malnutrition perpetuate pathological behavior.
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PMID:Neuropeptide abnormalities in anorexia nervosa. 873 16

Optic nerve formation in mouse involves interactions between netrin-1 at the optic disk and the netrin-1 receptor DCC (deleted in colorectal cancer) expressed on retinal ganglion cell (RGC) axons. Deficiency in either protein causes RGC pathfinding defects at the disk leading to optic nerve hypoplasia (). Here we show that further along the visual pathway, RGC axons in netrin-1- or DCC-deficient mice grow in unusually angular trajectories within the ventral hypothalamus. In heterozygous Sey(neu) mice that also have a small optic nerve, RGC axon trajectories appear normal, indicating that the altered RGC axon trajectories in netrin-1 and DCC mutants are not secondarily caused by optic nerve hypoplasia. Intrinsic hypothalamic patterning is also affected in netrin-1 and DCC mutants, including a severe reduction in the posterior axon projections of gonadotropin-releasing hormone neurons. In addition to axon pathway defects, antidiuretic hormone and oxytocin neurons are found ectopically in the ventromedial hypothalamus, apparently no longer confined to the supraoptic nucleus in mutants. In summary, netrin-1 and DCC, presumably via direct interactions, govern both axon pathway formation and neuronal position during hypothalamic development, and loss of netrin-1 or DCC function affects both visual and neuroendocrine systems. Netrin protein localization also indicates that unlike in more caudal CNS, guidance about the hypothalamic ventral midline does not require midline expression of netrin.
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PMID:Altered midline axon pathways and ectopic neurons in the developing hypothalamus of netrin-1- and DCC-deficient mice. 1055 99

Deficiency of CRH receptor 1 (CRHR1) severely impairs the stress response of the hypothalamic-pituitary-adrenocortical (HPA) system and reduces anxiety-related behavior in mice. Intriguingly, in mice deficient for the CRHR1 (Crhr1-/-), basal plasma levels of ACTH are normal, suggesting the presence of compensatory mechanisms for pituitary ACTH secretion. We therefore studied the impact of the hypothalamic neuropeptides arginine vasopressin (AVP) and oxytocin (OXT) on HPA system regulation in homozygous and heterozygous Crhr1 mutants under basal and different stress conditions. Basal plasma AVP concentrations were significantly elevated in Crhr1-/- mice. AVP messenger RNA expression was increased in the paraventricular nucleus of Crhr1-/- mutants together with a marked increase in AVP-like immunoreactivity in the median eminence. Administration of an AVP V1-receptor antagonist significantly decreased basal plasma ACTH levels in mutant mice. After continuous treatment with corticosterone, plasma AVP levels in homozygous Crhr1-/- mice were indistinguishable from those in wild-type littermates, thus providing evidence that glucocorticoid deficiency is the major driving force behind compensatory activation of the vasopressinergic system in Crhr1-/- mice. Neither plasma OXT levels under several different conditions nor OXT messenger RNA expression in the paraventricular nucleus were different between the genotypes. Taken together, our data reveal a selective compensatory activation of the hypothalamic vasopressinergic, but not the oxytocinergic system, to maintain basal ACTH secretion and HPA system activity in Crhr1-/- mutants.
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PMID:Selective activation of the hypothalamic vasopressinergic system in mice deficient for the corticotropin-releasing hormone receptor 1 is dependent on glucocorticoids. 1108 61

The majority of deaths associated with complex emergencies are attributed to infants and children under the age of five years. Most of these deaths are related to preventable diseases such as malnutrition, diarrhea, and malaria. Infant feeding emergencies have emerged as a major factor in complex emergencies. This paper reviews the current information relative to infant feeding, and uses four case studies as educational tools for the management of infant feeding emergencies. Child mortality rates in refugee population have been linked directly to protein-energy malnutrition (PEM). Breast feeding has many advantages over all other forms of feeding for children up to the age of two years of age. These advantages are discussed in detail in this paper. In addition, the appropriate and inappropriate uses of breast-milk substitutes (BMS) are discussed. Breast feeding also may play a role in the spread of HIV infections from the mother to the infant. However, in the setting of complex emergencies in the developing world, the risk of an infant dying of malnutrition and infection when not breastfed is likely to be greater than is the risk of death due to HIV acquisition through breastfeeding. The physiology of lactation is reviewed with particular reference to the roles of prolactin, oxytocin, and the feedback inhibitor of lactation (FIL) hormone. No medications have been demonstrated to augment milk production that can be used in a practical sense in complex emergencies. Lastly, the principles promulgated by the WHO and UNHCR for the feeding of infants and children in emergencies and for milk powder distribution are summarized.
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PMID:Infant feeding practices in complex emergencies: a case study approach. 1209 Feb 3

Neuropeptides play an important role in the regulation of feeding behavior and obesity. The mechanisms for controlling food intake involve a complicated interplay between peripheral systems (including gustatory stimulation, gastrointestinal peptide secretion, and vagal afferent nerve responses) and central nervous system (CNS) neuropeptides and/or monoamines. These neuronal systems include neuropeptides (CRH, opioids, neuropeptide-Y (NPY) and peptide YY (PYY), vasopressin and oxytocin, CCK, and leptin) and monamines (serotonin, dopamine, norepinephrine). In addition to regulating eating behavior, a number of CNS neuropeptides participate in the regulation of neuroendocrine pathways. Thus, clinical studies have evaluated the possibility that CNS neuropeptide alterations may contribute to dysregulated secretion of the gonadal hormones, cortisol, thyroid hormones and growth hormone in the eating disorders. Most of the neuroendocrine and neuropeptide alterations apparent during symptomatic episodes of AN and BN tend to normalize after recovery. This observation suggests that most of the disturbances are consequences rather than causes of malnutrition, weight loss and/or altered meal patterns. Still, an understanding of these neuropeptide disturbances may shed light on why many people with AN or BN cannot easily "reverse" their illness and even after weight gain and normalized eating patterns, many individuals who have recovered from AN or BN have physiological, behavioral and psychological symptoms that persist for extended periods of time.
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PMID:A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa. 1276 12

Anorexia and Bulimia Nervosa are disorders of unknown etiology that invariably begin during adolescence and near in time to puberty in young women. These disorders are associated with aberrant eating behaviors, body image distortions, impulse and mood disturbances, as well as characteristic temperament and personality traits. It is well known that malnutrition produces changes in neuroendocrine function. More recently, disturbances in neuronal systems have been found to play a role in the modulation of feeding, mood, and impulse control. These neuronal systems include neuropeptides (CRH, opioids, neuropeptide-Y (NPY) and peptide YY (PYY), vasopressin and oxytocin, CCK, and leptin) and monoamines (serotonin, dopamine, norepinephrine). Disturbances of most of these neuronal systems have been found when people are ill with an eating disorder, but it was not certain whether they were a cause or consequence of symptoms. In order to address these questions, a growing number of studies have investigated whether neuromodulatory disturbances persist after recovery. Studies from several centers tend to show altered serotonin activity persists after prolonged normalization of weight, nutrition, and menstrual function, as do anxiety, obsessionality, and perfectionism. While there are fewer data, there may be persistent alterations of dopamine or some neuropeptides in some subjects in a recovered state. The inaccessibility of the central nervous system has made it difficult to understand brain and behavior. In the past decade, new tools, such as brain imaging, have offered the possibility of better characterization of complex neuronal function and behavior. Such studies have tended to consistently find that alterations of brain regions, such as the temporal lobe, occur in people who are ill with anorexia nervosa and appear to persist after some degree of weight gain and recovery. New imaging technology, that marries Positron Emission Tomography (PET) imaging with selective neurotransmitter radioligands, confirms that altered serotonin neuronal pathway activity persists after recovery from an eating disorder and supports the possibility that these psychobiological alterations might contribute to traits, such as increased anxiety or extremes of impulse control, that, in turn, may contribute to a vulnerability to the development of an eating disorder. In summary, studies of pathophysiology are starting to nominate new candidates for treatment leading to the possibility of finding effective treatments for this often chronic or fatal disorder.
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PMID:Neurotransmitter and imaging studies in anorexia nervosa: new targets for treatment. 1276 13

Lactation deficiency may have important consequences on infant health, particularly in populations of low socioeconomic status. The OFA hr/hr (OFA) strain of rats, derived from Sprague-Dawley (SD) rats, has deficient lactation and is a good model of lactation failure. We examined the reproductive performance and hormonal profiles in OFA and SD strains to determine the cause(s) of the lactation failure of the OFA strain. We measured hormonal (PRL, GH, gonadotropins, oxytocin, and progesterone) levels by RIA in cycling, pregnant, and lactating rats and in response to suckling. Dopaminergic metabolism was assessed by determination of mediobasal hypothalamic dopamine and dihydroxyphenylacetic acid (DOPAC) concentrations by HPLC and tyrosine hydroxylase expression by immunocytochemistry and western blot. OFA rats have normal fertility but 50% of the litters die of malnutrition on early lactation; only 6% of the mothers show normal lactation. The OFA rats showed lower circulating PRL during lactation, increased hypothalamic dopamine and DOPAC, and impaired milk ejection with decreased PRL and oxytocin response to suckling. Before parturition, PRL release and lactogenesis were normal, but dopaminergic metabolism was altered, suggesting activation of the dopaminergic system in OFA but not in SD rats. The number of arcuate and periventricular neurons expressing tyrosine hydroxylase was higher in SD rats, but hypothalamic expression of TH was higher in OFA rats at the end of pregnancy and early lactation. These results suggest that the OFA rats have impaired PRL release linked with an augmented dopaminergic tone which could be partially responsible for the lactational failure.
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PMID:Hormonal profile and reproductive performance in lactation deficient (OFA hr/hr) and normal (Sprague-Dawley) female rats. 1750 26


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