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Biomedical subjects

M L Grunnet

Publications and source records attributed to M L Grunnet.

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

Effects of fetal insulin secretory deficiency on metabolism in fetal lamb.

Fetal insulin secretion may be of importance in determining both fetal metabolic rate and glucose homeostasis in the resting state. To investigate this question, streptozocin (STZ) was injected into 10 late-gestation fetal lambs, and the effects of STZ on fetal pancreatic insulin storage and secretion, fetal metabolic rate, and umbilical glucose uptake were then studied. Fetal STZ injection caused a relative fetal hyperglycemia by 24 h after injection. Fetal hyperglycemia reached a maximum by 72 h and persisted for at least 10 days after injection. Neonates delivered after fetal injection were frankly diabetic. Fetal STZ injection was associated with complete suppression of both glucose- and tolbutamide-stimulated insulin release, although no changes in peripheral insulin concentration were observed when compared with controls. Fetal pancreatic insulin content was only 13% of that expected on the basis of gestational age. In a subgroup of 7 STZ-treated fetal lambs, fetal hyperglycemia was related to decrements in umbilical venoarterial difference of glucose, umbilical glucose uptake, and glucose-O2 quotient. No changes in maternal glucose homeostasis or in fetal O2 consumption were noted. The data suggest that deficient fetal insulin storage and secretion are associated with a decrement in exogenous fetal glucose entry but not in fetal metabolic rate. Whether the observed fetal changes relate to enhanced endogenous fetal glucose production with a passive decrease in maternofetal glucose transfer or are simply due to a decrease in overall fetal glucose utilization is not known. It is speculated that a quantitative decrease in pancreatic insulin secretion is responsible for the observed changes.

Animals↗
PubMed1985

Juvenile multisystem degeneration with motor neuron involvement and eosinophilic intracytoplasmic inclusions.

A case of juvenile multisystem degeneration with motor neuron involvement, possibly of familial type, showing many unusual clinical and pathologic features is reported. Eosinophilic intracytoplasmic inclusions were present in some remaining anterior horn cells and motor nerve nuclei of the brain stem as well as in a few neurons of the reticular activating system, the dorsal vagus nuclei, and the intermediolateral cell column. Smaller eosinophilic inclusions were seen in large neurons of the caudate nucleus and putamen, substantia nigra, and subthalamic nucleus.

Adult↗
PubMed1983

Ultrastructure and electrodiagnosis of peripheral neuropathy in Cockayne's syndrome.

Cockayne's syndrome is a multisystem disease that begins in infancy and is inherited as an autosomal recessive. We studied a 4-year-old girl with nystagmus, ataxia, motor weakness, peripheral neuropathy, deficient growth, and developmental delay. Nerve biopsy revealed segmental demyelination and granular lysosomal inclusions on ultrastructural examination.

Child, Preschool↗
PubMed1983

Granulomatous angiitis presenting as chronic meningitis and ventriculitis.

A 35-year-old woman had a diffuse encephalopathy with increased intracranial pressure and chronic lymphocytic meningitis. Hypoglycorrhachia and ventricular accumulation of tracer on radionuclide brain scanning suggested an infection. Cerebral cortical and leptomeningeal biopsies were done when she failed to improve with antituberculous therapy, but were not diagnostic. Granulomatous angiitis of the nervous system was diagnosed at postmortem examination and should be considered in the differential diagnosis of culture-negative chronic meningitis.

Adult↗
PubMed1982

Cockayne syndrome.

The diagnosis of Cockayne syndrome was established with the aid of cranial computed tomography (CT) in a child with growth deficiency, mental retardation, and neurologic findings which are typical for this rare childhood disorder. Calcification of basal ganglia and hydrocephalus ex vacuo are neuropathologic characteristics of Cockayne syndrome which may be present on CT as early as 3 years of age.

Child, Preschool↗
PubMed1981

Brain abnormalities in infants with Potter syndrome (oligohydramnios tetrad).

We examined the brains of seven unrelated infants with Potter syndrome (oligohydramnios tetrad), a lethal neonatal disorder characterized by abnormal facies, lung hypoplasia, limb deformities, and classically, renal agenesis. All infants had defects of neuronal migration. The brains were small for gestational age in five of seven infants, and in four infants, the middle and inferior temporal gyri were incompletely demarcated. Cerebellar heterotopia occurred in five infants. All had abnormal hippocampi and abnormal lamination of the cerebral cortex. These neuropathologic abnormalities suggest that Potter syndrome may not be the result of a single toxic or infectious insult but may represent a polygenic inherited disorder.

Amniotic Fluid↗
PubMed1981

Fulminant amebic meningoencephalitis due to Acanthamoeba.

A 57-year-old chronically immunosuppressed woman with systemic lupus erythematosus developed fulminant meningoencephalitis due to Acanthamoeba castellanii. Amebic trophozoites were also found in the lungs, suggesting a primary pulmonary focus of infection. This case illustrates that Acanthamoeba can cause a fulminant, rapidly fatal meningoencephalitis, as well as the previously reported chronic granulomatous meningoencephalitis. X

Amebiasis↗
PubMed1979

Periventricular leukomalacia complex.

At autopsy in the past three years, a new complex of CNS lesions has appeared in 54% (50/93) of the brains of premature infant cadavers that have come from our neonatal intensive care unit. This complex consists of necrotizing lesions in the periventricular white matter and in the gray nuclei of the cerebral hemispheres, the hippocampus and subiculum, cerebellar folia and white matter, and basis pontis. This entity is called the periventricular leukomalacia complex, since the distribution of lesions is similar, yet much more severe, than that described by Banker and Larroche in 1962. Clinical studies have indicated that these lesions may be related to long periods of time at high blood oxygen or prolonged periods in which PO2 and pH fluctuated widely.

Cerebellum↗
PubMed1978

Gomori's trichrome stain. Its use with myelin sheaths.

We report the use of Gomori's one-step trichrome stain as a method for staining myelin sheaths of peripheral nerves. The stain is simple to perform and allows myelin sheaths to be easily detected and evaluated.

Connective Tissue Cells↗
PubMed1976

Carbon monoxide-induced neuropathy in the rat. Ultrastructural changes.

The peroneal and ventral caudal nerves of rats exposed to 2,500 ppm CO until loss of nerve conduction occurred were studied by electron microscopy. Loss of normal axonal and Schwann cell structure was seen at the node of Ranvier. This loss was more prominent in large myelinated fibers, but was also seen in small myelinated fibers at seven and ten days postexposure. At this time, ventral caudal nerve conduction velocity decreased following a transient period of recovery lasting 9 to 13 days. Repair of the node began at 14 to 21 days postexposure, when maximal nerve conduction velocity had returned to normal. Complete normalization of node structure was not seen even 60 days after exposure, in many instances.

Animals↗
PubMed1976

Cerebellar hemorrhage in the premature infant.

Lesions of the central nervous system were reviewed in 144 premature neonates without anomalies or infections coming to autopsy from the Intermountain Regional Neonatal Intensive Care Unit. Twelve neonates were found to have had cerebellar hemorrhages. Eleven of the 12 with cerebellar hemorrhage also had germinal plate hemorrhages at postmortem examination. Some hemorrhages destroyed one or both cerebellar hemispheres. Three of 19 (16%) infants between 20 to 24 weeks' gestation, six of 26 (25%) infants between 26 to 28 weeks' gestation, two of 24 (8%) infants between 28 to 30 weeks' gestation, and one of 19 (5%) infants between 20 to 32 weeks' gestation had cerebellar hemorrhage. No premature neonate after 32 weeks' gestation had cerebellar hemorrhage. It is probable that trauma does not play a role in the pathogenesis of the cerebellar hemorrhage.

Birth Injuries↗
PubMed1975

Extreme toxicity from combustion products of a fire-retarded polyurethane foam.

The products from nonflaming combustion of wood and a trimethylol-propane-based rigid-urethane foam that was not fire-retarded produced elevated carboxyhemoglobin levels but no abnormal neurological effects. However, when this type of foam contained a reactive phosphate fire retardant, the combustion products caused grand mal seizures and death in rats. The toxic combustion product responsible for the seizures has been identified as 4-ethyl-1-phospha-2,6,7-trioxabicyclo(2.2.2.)octane-1-oxide.

Animals↗
PubMed1975

Nuclear bodies in Creutzfeldt-Jakob and Alzheimer's diseases.

Nuclear bodies types I, II, III, and IV, as described by Bouteille, Kalifat, and Delarue, have been found in one case of Creutzfeldt-Jakob disease and one case of Alzheimer's disease. The relationship of nuclear bodies to viral disease in the central nervous system is not clear.

Adult↗
PubMed1975

Teratoma of the spinal cord. Report of a case and review of the literature.

A 6-week-old infant had a teratoma that involved the entire spinal cord. No reports of another such extensive teratoma of the spinal cord can be found in the literature. We postulate that an embryonic rest was incorporated into the spinal canal and, when removed from its normal inducer tissue, grew haphazardly throughout the spinal cord.

Female↗