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Biomedical subjects

R J Joynt

Publications and source records attributed to R J Joynt.

At least 37 records · Page 2Linked to original sources
PubMed1986

Amitotic neuroblastoma cells used for neural implants in monkeys.

The potential utility of cultured neuroblastoma cells as donor tissue for neutral implants into the mammalian brain has been examined. Cells from a human neuroblastoma cell line, IMR-32, were labeled with [3H]thymidine and chemically rendered amitotic. These differentiated IMR-32 cells were grafted into the hippocampi of five adult African Green monkeys, and graft survival was evaluated for up to 270 days after transplantation. Autoradiographically labeled grafted cells were identified in four animals. Processes from grafted cells could be followed for distances of up to 150 micrometers into the host brain. No evidence for neoplastic growth of the transplant was found. Thus, grafted neuroblastoma cells can survive for prolonged periods in the primate brain and may serve as a practical source of donor tissue for neural implants.

Animals↗
PubMed1985

Cerebral dominance.

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Dominance, Cerebral↗
PubMed1984

Neuropeptides in aging and dementia.

Although senile dementia of the Alzheimer's type (SDAT) is a common disease associated with advancing age, recent studies have suggested that SDAT should not be considered synonymous with old age but a disease process separate from normal aging. This study examined the morphology of two neurochemically-defined neuronal populations (i.e., neurophysin, somatostatin) in the cortex and hypothalamus to determine if structural changes in these neuropeptide systems associated with advancing age are similar to those seen with SDAT. Our findings suggest that morphological changes consistent with neuronal degeneration occur in somatostatin but not neurophysin-containing neurons in cases diagnosed to have SDAT, and these structural changes are different from those seen in aged brain without central nervous system disease. These data support the concept that senile dementia of the Alzheimer's type is not a single neurochemical related disease, but may be associated with anatomical lesions and biochemical imbalances among a number of neuropeptide and neurotransmitter systems.

Aged↗
PubMed1981

Antidiuretic hormone levels in stroke patients.

Serum osmolality and antidiuretic hormone (ADH) levels were determined for 17 patients with cerebral infarction, 4 with subarachnoid hemorrhage, and 12 controls. The ADH levels were elevated significantly in the stroke patients. Hyponatremia was not observed. Stroke patients are at risk for developing electrolyte disturbances; thus, fluid intake and electrolyte levels should be closely observed.

Cerebral Infarction↗
PubMed1981

Catecholamine-associated refractory hypertension following acute intracranial hemorrhage: control with propranolol.

Seven patients (4 with subarachnoid hemorrhage, 2 with intracerebral hemorrhage, and 1 with massive cerebral infarction) had acute arterial hypertension refractory to control by several antihypertensive drugs (hydralazine, sodium nitroprusside, alpha-methyldopa, and trimethaphan camsylate) used singly or in combination. In each case, catecholamine excretion--measured by urinary norepinephrine plus epinephrine--was markedly elevated, averaging 218 microgram/day. Patients without the acute refractory hypertension had normal or only slightly elevated urinary catecholamine levels (mean, 72 microgram/day). The beta-adrenergic blocking agent propranolol, in doses between 20 and 40 mg every 6 hours, successfully controlled blood pressure, while other agents failed. The intense sympathetic nervous system discharge resulting in acute refractory hypertension may be due to injury to the diencephalon or brainstem (or both) or to diffuse brain dysfunction from increased intracranial pressure or intracranial blood.

Adult↗
PubMed1980

Role of angiotensin in the osmotic control of vasopressin release by the organ-cultured rat hypothalamo-neurohypophyseal system.

Angiotensin II (AII) appears to either mediate or modulate osmotically stimulated vasopressin (VP) release by the organ-cultured rat hypothalamo-neurohypophyseal system. Saralasin, an AII antagonist, blocked VP release in response to a 10-mosmol increment in culture medium osmolality achieved by the addition of NaCl. This was observed at all concentrations tested (10(-7), 10(-6), 10(-4) M). Saralasin (10(-4) M) also blocked VP release in response to a comparable mannitol-induced increase in osmolality. Since nicotinic-cholinergic antagonists previously were shown to inhibit osmotically stimulated VP release, the effect of hexamthonium, a nicotinic, a nicotinic-cholinergic antagonist, on AII-stimulated VP release was examined. Hexamethonium (10(-5)-10(-3) M) was ineffective in blocking AII stimulation of VP release. This finding coupled with the previous observation that saralasin does not block acetylcholine stimulation of VP release suggests independent AII and cholinergic mechanisms controlling VP release; however, the effectiveness of both types of antagonists in blocking osmotically stimulated VP release indicates some interaction between these regulators of VP release.

Angiotensin II↗