Cases reported "Disease Models, Animal"

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1/4. Treatment of sialocele: an experimental study in dogs.

    A patient had a delayed complication of parotid trauma, namely a sialocele. He was successfully treated by repeated needle aspiration of the fluid. An experiment using 30 dogs was then done. On each dog, one parotid gland was used as a control, the other parotid was treated by one of three methods that the author felt would be most satisfactory. Needle aspiration was found to be the simplest and the most effective manner of treatment, because the proximal duct quickly becomes obstructed with the cessation of salivary flow, disappearance of the sialocele, and later parotid atrophy. One patient and 30 dogs are surely not conclusive proof of what would be proper treatment, but the author hopes that this paper will stimulate otolaryngologists to try this method if confronted with a similar problem.
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2/4. Central hypothyroidism.

    Central hypothyroidism is an uncommon condition characterized by insufficient thyroid gland stimulation by TSH, owing to hypothalamic and/or pituitary dysfunction. It is rarely isolated but more often occurs in conjunction with deficiencies of other pituitary hormones, as well as with neurologic symptoms and signs owing to hypothalamic/pituitary lesions. The diagnosis rests on documentation of clinical and biochemical hypothyroidism with an inappropriately low or nonelevated serum TSH level. Recent studies suggest that the temporal pattern of TSH secretion, as well as TSH structure, is altered in central hypothyroidism, providing a mechanism for the induction of the hypothyroid state in this condition.
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3/4. Primary cortisol resistance: a familial syndrome and an animal model.

    Primary cortisol resistance in man is a familial disease. It is characterized by increased plasma cortisol concentrations, high urinary free cortisol excretion, a normal circadian pattern of cortisol secretion, resistance to adrenal suppression by dexamethasone and absence of clinical stigmata of Cushing's syndrome. In its severe form, hypertension and hypokalemic alkalosis are present, owing to increased secretion of the sodium-retaining corticoids, corticosterone and deoxycorticosterone. In subjects with a less severe resistance to cortisol, there are no clinical abnormalities and the disease is revealed only by detailed examination of several parameters of cortisol metabolism. In the whole-cell assay (peripheral mononuclear leukocytes or fibroblasts) the glucocorticoid receptor shows a low affinity for dexamethasone. The receptor may be unsaturable as suggested by decreased receptor concentrations in broken-cell systems. Thus, generalized target-tissue resistance to cortisol, including the pituitary gland and the hypothalamus, is accompanied by a decreased negative feedback of the cortisol-ACTH feedback system resulting in increased ACTH secretion. This causes higher plasma cortisol to compensate for the end-organ resistance and also increases the production of adrenal mineralocorticoids, as by-products. Thus hypertension and hypokalemic alkalosis depends on the degree of the resistance. Cortisol resistance in many New World primate species is characterized by greatly increased plasma cortisol concentrations, decreased cortisol binding globulin capacity and affinity, high levels of plasma and urinary free cortisol, marked resistance of ACTH suppression by dexamethasone, and no physiologic evidence of glucocorticoid hormone excess. Target tissues have normal concentrations of glucocorticoid receptors with decreased affinity for dexamethasone. The New World primates, unlike man, have compensated for this cortisol resistance with intra-adrenal adaptations over the 50 million years of their evolutionary development. These primates also have abnormalities of other steroid hormone-receptor systems such as progesterone, estrogen, androgen and mineralocorticoid. In contrast, the human syndrome appears to be a recent mutation with pathophysiologic consequences.
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4/4. Studies on a primaquine-tolerant strain of plasmodium vivax from brazil in Aotus and saimiri monkeys.

    A nonimmune American acquired an infection of plasmodium vivax Type 1 malaria in brazil in 1994. After returning to the U.S.A., he had a primary attack followed by 3 relapses. The primary attack and first 2 relapses were treated with a standard regimen of chloroquine, followed by 14 days of primaquine (15 mg/day). Following the third relapse, the primaquine treatment was extended to 28 days. No further relapses occurred. The lack of response to primaquine by this strain may recommend it as a suitable candidate for chemotherapeutic study if it can be adapted to an animal model. Anopheles quadrimaculatus mosquitoes infected by feeding on the patient during the first relapse were used to establish the strain in Aotus and saimiri monkeys. Monkeys supported well the development of long-lasting parasitemia. Anopheles freeborni, Anopheles stephensi, and anopheles gambiae mosquitoes were readily infected by feeding on the monkeys and by membrane feeding on diluted blood. Monkey-to-monkey transmission was obtained via the bites of infected mosquitoes and the intravenous injection of sporozoites dissected from salivary glands. This parasite is designated as the brazil I/CDC strain of P. vivax.
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