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Biomedical subjects

M Miller

Publications and source records attributed to M Miller.

At least 739 records · Page 41Linked to original sources
PubMed1982

Altered osmotic threshold for vasopressin release and impaired thirst sensation: additional abnormalities in Kallmann's syndrome.

Seven subjects with Kallmann's syndrome were studied to determine whether they had disturbances of fluid homeostasis. Simultaneous measurements of urine and plasma osmolality (Uosm and Posm, respectively) were made during free access to fluids. The Uosm-Posm relationship was abnormal in five patients on at least one occasion. Patient 2 was frequently overhydrated (Posm less than or equal to 280 mosmol/kg) and patient 5 excreted a dilute urine when his Posm was 290 mosmol/kg. The three subjects (1, 5, and 7) tending to have an increased Psom (greater than or equal to 300 mosmol/kg) were able to concentrate their urine (Uosm greater than 800 mosmol/kg) and denied polyuria and polydipsia. Their elevated Posms could be explained by impairment of thirst, rather than increased excretion of water, because the patients concentrated their urines at normal Posms during fluid deprivation. The osmotic threshold for vasopressin release was decreased (Posm = 270.6 mosmol/kg) in one patient and increased (Posm greater than or equal to 295 mosmol/kg) in two others of the seven patients. The elevated osmotic threshold was not due to chronic hyperosmolality or a generalized defect in vasopressin secretion. In the patient with the highest osmotic threshold (Posm = 296 mosmol/kg) and Posms between 289--301 mosmol/kg during free access to fluid, the osmotic threshold decreased to only 293 mosmol/kg after 6 weeks of adequate hydration and desmopressin acetate. However, in response to hypotension induced by trimethaphan, he increased his plasma vasopressin from 1--26 microU/ml. In conclusion, some patients with Kallmann's syndrome may have osmoreceptor dysfunction and abnormal thirst regulation, indicating more extensive hypothalamic involvement than previously appreciated.

Adolescent↗
PubMed1982

Immunochemical determination of CK-MB isoenzyme in human serum. II. An enzymic approach.

A novel immunochemical technique for a specific enzymic determination of the myocardial isoenzyme of creatine kinase, CK-MB, involves determination of B-subunit activity of a specimen in which the M-subunit activity has been inhibited by specific antibodies to the M-subunit. Interfering activities from CK-BB isoenzyme, atypical forms of creatine kinase, and adenylate kinase are eliminated by using a blank tube in which all the M-subunit-containing isoenzymes have been removed by a specific immunoprecipitation step. The assay is convenient, linear, and reproducible, and results compare well with those by agarose electrophoresis.

Creatine Kinase↗
PubMed1981

Maturation of rat visual cortex. II. A combined Golgi-electron microscope study of pyramidal neurons.

Tissue removed from 3, 6, 9, 12, 15, and 21-day-old rats has been prepared for correlative light and electron microscopy to examine the maturation of cell bodies, dendrites, and axons of pyramidal neurons in layer V of rat visual cortex. As the size of the cell body increases steadily during the first 3 postnatal weeks there is an equivalent growth in nuclear volume. By day 15, there are infoldings in the nuclear envelope which may be induced by eye opening on day 14. Nucleoli increase in size until day 9, after which they appear to condense. Within the perikarya, the most conspicuous change is the amount and organization of the rough endoplasmic reticulum. Symmetric axosomatic synapses are evident by day 6. The ultrastructure of dendrites does not change substantially with age. Dendrites form synapses with symmetric densities as early as day 3 and asymmetric ones by day 9. It seems that dendritic spines begin as low, broad protrusions having symmetric junctions with smaller diameter axonal processes. With time they become taller stumps, before acquiring their mature lollipop shape and participating in asymmetric synapses with axonal varicosities. Other dendritic appendages, filopodia, and growth cones are transient structures, being conspicuous only between days 3 and 12. "Terminal" growth cones are essential for extension of dendritic processes, whereas "en passant" growth cones and filopodia seem important for dendritic branching. Boutons of mature pyramidal cell axons form asymmetric synapses with dendritic shafts and spines, but the developing synapses formed by these axons have more symmetric junctions. The maturation of pyramidal cell features progresses in concert with such extrinsic determinants as afferent input and is probably influenced by the competency of synaptic connections.

Animals↗
PubMed1981

Maturation of rat visual cortex. I. A quantitative study of Golgi-impregnated pyramidal neurons.

The early postnatal maturation of pyramidal neurons in layers II/III and V of the rat visual cortex has been examined in an attempt to elucidate some determinants of their mature morphology. Three indices have been quantified using Golgi-impregnated pyramidal cells; densities of spines along apical dendrites, numbers of primary based dendrites and volumes of cell bodies. The mean density of spines on the apical dendrites of all pyramidal neurones increases in a stepwise fashion. The first significant increase occurs between days 6 and 9 and the second, between days 12 and 15; these increases may correlate with the arrival of geniculate afferents and with the opening of the eyes, respectively. In younger animals, the distribution of spines along the apical shafts is relatively even, whereas in older animals, spine density increases significantly over the proximal 125 micrometers portion and is relatively constant over the remaining distal portion. By day 21, layer V pyramidal cells have acquired more primary basal dendrites and larger somatic volumes than layer II/III cells. Furthermore, as the cells mature the rate of change in these characteristics are significantly different for neurons in layer II/III and in layer V. For both cell populations, the mean number of primary basal dendrites increases to a maximum before falling to a steady level, but for neurons in layer V, the maximum is higher and attained three days earlier than for layer II/III cells. Moreover, the increase in volume of cell bodies of layer V neurons begins three days before that of layer II/III cells. This three day phase difference in maturation may reflect the cell birth dates, since autoradiographic evidence indicates that layer V pyramidal neurons reach the cortical plate about three days prior to those which occupy layer II/III in the adult visual cortex.

Aging↗
PubMed1981

Pacemaker syndrome: a non-invasive means to its diagnosis and treatment.

Vertigo, lightheadedness, syncope, and hypotension occurring after implantation of a ventricular pacemaker has become known as pacemaker syndrome. In one patient with this syndrome we have demonstrated an associated decrease in the pulse amplitude of the ophthalmic arteries during ventricular pacing by utilizing ocular pneumoplethysmography (O.P.G.). This non-invasive technique was subsequently used intra-operatively to test the presence of ophthalmic artery pulse amplitude changes after implantation of the ventricular electrode. An A-V sequential pacemaker was then implanted and eliminated all symptoms of pacemaker syndrome.

Bradycardia↗
PubMed1981

Ocular abnormalities in the amniogenic band syndrome.

Craniofacial and limb abnormalities are characteristic of amniogenic band syndrome. We present the ocular findings of a patient with this syndrome and compare these abnormalities with those in 20 previously reported cases.

Abnormalities, Multiple↗
PubMed1981

Role of thromboxane and prostacyclin in pulmonary vasomotor changes after endotoxin in dogs.

Cyclooxygenase inhibitors prevent the pulmonary vasomotor changes in response to low-dose endotoxin. We, therefore, explored the role of two highly vasoactive prostanoids, thromboxane A(2), a vasoconstrictor, and prostacyclin, a vasodilator, in the transient pulmonary vasoconstriction and subsequent loss of alveolar hypoxis vasoconstriction (AHPV) that follows endotoxin. AHPV was tested in the dog with a double-lumened endotracheal tube allowing ventilation of one lung with nitrogen as a hypoxic challenge while the other lung was ventilated with oxygen to maintain systemic oxygenation. Relative distribution of perfusion to the two lungs was assessed with intravenous (133)Xe and external scintillation detectors. The stable metabolites of thromboxane and prostacyclin, i.e., thromboxane B(2) and 6-keto-prostaglandin F(1alpha) were measured in plasma with radioimmunoassay. 15 mug/kg i.v. of endotoxin induced no rise in pulmonary vascular resistance (PVR), but prevented AHPV so that the initial 33% (+/-2 SEM) decrease in perfusion to the hypoxic lung became only a 2% (+/-1) decrease. Circulating levels of thromboxane and prostacyclin concurrently rose (P < 0.01) from nondetectable levels to 380 pg/ml (+/-40) and 360 pg/ml (+/-130). 150 mug/kg of endotoxin induced a transient rise in PVR from 4.09 to 9.00 mm Hg/liter per min in association (r = 0.89, P < 0.01) with a sharp rise in thromboxane levels to 4,460 pg/ml (+/-1,350) whereas prostacyclin levels were elevated less markedly to 550 pg/ml (+/-400). Prostaglandin F(2alpha), another vasoconstrictor, was not elevated. 30 min after endotoxin when PVR was again base line and AHPV lost, thromboxane fell significantly (P < 0.01) to 2,200 pg/ml (+/-1,100) whereas prostacyclin remained elevated at 360 pg/ml (+/-135), a level similar to that seen when 15 mug/kg of endotoxin induced loss of AHPV. Indomethacin prevented the rise in thromboxane and prostacyclin after endotoxin as well as the changes in pulmonary vasomotor tone. Thus, a complex interaction between thromboxane and prostacyclin is involved in the pulmonary vasomotor response to low-dose endotoxin.

6-Ketoprostaglandin F1 alpha↗