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Biomedical subjects

U DeGirolami

Publications and source records attributed to U DeGirolami.

At least 37 records · Page 2Linked to original sources
PubMed1989

Medulloblastoma with cartilaginous differentiation.

We describe the histologic, immunocytochemical, and electron microscopic features of a medulloblastoma containing cartilage that occurred in the left cerebellar hemisphere of a 57-year-old man. By light microscopy, highly cellular areas of the tumor typical of medulloblastoma showed evidence of both glial and neuroblastic differentiation. The tumor also contained foci of mature and immature cartilage. Transitions were observed between the cartilaginous foci and the more densely cellular regions of the tumor. No frankly teratomatous features or mesenchymal components other than cartilage were present. We postulate that the production of cartilage within this neoplasm most likely resulted from the metaplastic transformation of preexisting mesenchymal elements within the tumor or from multipotential neural crest-derived ectomesenchymal cells. Alternatively, the cartilage could have been produced directly by the neuroectodermal cells themselves, possibly related to a capacity for the latter to produce a chondroid ground substance.

Cartilage↗
PubMed1988

Tissue plasminogen activator. Reduction of neurologic damage after experimental embolic stroke.

Tissue plasminogen activator (tPA) has become available for pharmacologic use, and it appears to produce relatively fewer hemorrhagic complications than the previously available, less specific thrombolytic agents. We tested the effects of tPA in several models of embolic stroke and found that neurologic damage was reduced when the drug was administered as late as 45 minutes after cerebral embolic occlusion. The mechanism of therapeutic efficacy of tPA was probably thrombolysis. Drug-induced hemorrhages did not occur when therapy was started within four hours after the onset of vascular occlusion. These results suggest that tPA may be useful for thrombolytic therapy of embolic stroke if the drug is administered rapidly after the onset of vascular occlusion.

Animals↗
PubMed1988

Fluosol and experimental spinal cord ischemia.

Spinal cord ischemia was produced by temporary aortic occlusion for 12.5 min in 27 rabbits. Animals were divided into three groups: Group A received Fluosol DA 20% and 100% oxygen; Group B Fluosol and room air only, and Group C Dextran 40 and 100% oxygen. There was no difference in neurological outcome or in the extent and severity of histologically documented infarction of the spinal cord in the three groups. There was also no difference between these groups and untreated controls previously studied by us.

Animals↗
PubMed1987

A model for quantitative evaluation of embolic stroke therapy.

We developed a small animal embolic stroke model for pharmacological screening trials. Microspheres are injected into the carotid circulations and group embolus dose-response relationships are calculated. Emboli quantity is related to neurologic injury, and small changes in neurologic function are detectable. Rabbits tolerated twice as many microspheres when cyproheptadine-treated after embolization. This demonstrated both the sensitivity of the model and the value of serotonin antagonists in reducing neurological injury.

Animals↗
PubMed1987

Vacuolar change in Alzheimer's disease.

A retrospective neuropathologic study of brains from 66 patients with Alzheimer's disease (AD) demonstrated the presence of a vacuolar change (VC) in 50 cases that was virtually indistinguishable histologically from the spongiform change characteristic of Creutzfeldt-Jakob disease (CJD). Indeed, in several instances, there was initial diagnostic confusion with CJD. Unlike the spongiform change in CJD, however, VC was almost entirely restricted to the medial temporal cortex and amygdala. Furthermore, the severity of VC was usually less intense than the spongiform change observed in cases of CJD with severe neurologic impairment. The VC could be readily distinguished from the fine microvacuolation of the upper layers of the isocortex reported in a number of different conditions, including AD. It also differed from the status spongiosus of the cerebral cortex that occurs in advanced AD and CJD as well as in other degenerative diseases. The artifactual rarefaction that occurs in improperly processed paraffin-embedded brain tissue was excluded as a contributory factor to the VC. Since VC does not invariably occur in AD, it conceivably could represent a subtype of this disorder or may represent a variant of the pathologic changes that can occur. Its relationship to CJD or other slow virus disorders is to date unknown but unlikely.

Aged↗
PubMed1986

Myxopapillary ependymoma of the filum terminale. A light and electron microscopic study.

The histology of a myxopapillary ependymoma of the filum terminale in a 15-year-old girl was studied by light and electron microscopy. The neoplasm contained both papillary and compact areas of cell growth. The papillary regions consisted of vacuolated cuboidal cells arranged around hyaline/vascular cores that were variably mucin-positive. In the compact regions, the tumor cells were intensely immunoreactive for glial fibrillary acidic protein and occasionally formed perivascular pseudorosettes. Ultrastructural examination revealed interdigitating cell processes, sometimes resting on a basement membrane. Surface specializations included numerous microvilli and occasional cilia. The cilia had an abnormal microtubular pattern (e.g., 8 + 1, 7 + 0). The cytoplasm of the tumor cells contained numerous 7-10 nm intermediate filaments and large numbers of abnormal microtubular aggregates, consisting of 4 to 50 single microtubules enclosed by a limiting membrane. These microtubular aggregates may represent a characteristic feature of myxopapillary ependymoma of the filum terminale.

Adolescent↗
PubMed1986

Motor fibers in the sural nerve.

In an ischemia-induced model of an acute motor neuron disorder, there is anterior horn cell damage with Wallerian degeneration in ventral roots; dorsal root ganglia and dorsal roots are unaffected. In a mixed nerve there is axonal degeneration reflecting loss of motor fibers. The sural nerve is normal showing that it does not contain motor fibers. This observation is relevant to the neuropathology of motor neuron disease where axonal degeneration found in the sural nerve suggests involvement of sensory fibers.

Animals↗
PubMed1986

Perineuritis and ulcerative colitis.

We describe the association of chronic polyneuropathy with ulcerative colitis. Electrophysiologic studies disclosed a severe neuropathy with both axonal and demyelinating features. The CSF protein content was 875 mg/dl. Sural nerve biopsy revealed perineuritis. Peripheral neuropathy with perineuritis may be an immunologically mediated extraintestinal manifestation of ulcerative colitis.

Colitis, Ulcerative↗
PubMed1986

Spontaneous hemorrhage in a mixed glioma of the cerebellum: case report.

An 8-year-old boy presented in coma and was found to have a massive posterior fossa hemorrhage on computed tomographic scan. Autopsy disclosed a large cerebellar hematoma within a mixed glioma containing both juvenile pilocytic astrocytoma and oligodendroglioma. It is postulated that the hemorrhage originated from the oligodendroglial component of the tumor.

Astrocytoma↗
PubMed1985

Tissue plasminogen activator reduces neurological damage after cerebral embolism.

Intravenous administration of tissue plasminogen activator immediately after the injection of numerous small blood clots into the carotid circulation in rabbit embolic stroke model animals caused a significant reduction in neurological damage. In vitro studies indicate that tissue plasminogen activator produced substantial lysis of clots at concentrations comparable to those expected in vivo, suggesting that this may be the mechanism of action of this drug. Drug-induced hemorrhages were not demonstrable. Tissue plasminogen activator may be of value for the immediate treatment of embolic stroke.

Animals↗
PubMed1985

Neuropathological changes related to the transorbital application of ethyl 2-cyanoacrylate adhesive to the basal cerebral arteries of cats.

The long-term toxic effects of ethyl 2-cyanoacrylate adhesive were evaluated histologically in 25 cats. Fresh medical- or commercial-grade adhesive was introduced transorbitally into the subarachnoid space in the vicinity of the right middle cerebral artery. Three sham-operated animals served as controls. The animals were sacrificed at intervals ranging from 2 days to 6 months. For both medical- and commercial-grade adhesive, neuropathological examination disclosed acute and chronic granulomatous inflammation of the meninges and evidence of severe vascular damage, including vessel wall necrosis, inflammation, thrombosis, and occasionally hemorrhage. Most animals showed cerebral infarcts of variable size in the territories of distribution of the basal arteries which were in contact with adhesive. The results of this study show that ethyl 2-cyanoacrylate is capable of producing severe arterial and parenchymal damage. The risk of its deleterious effects should be weighed against its potential benefits. Clinical experience would suggest that ethyl 2-cyanoacrylate can be used in difficult situations as long as care is taken to protect the brain and local blood vessels.

Animals↗
PubMed1984

Selective necrosis and total necrosis in focal cerebral ischemia. Neuropathologic observations on experimental middle cerebral artery occlusion in the macaque monkey.

Temporary (15 minutes to 24 hours) or permanent focal cerebral ischemia was induced in 87 awake monkeys (Macaca mulatta and Macaca fasicularis) by transorbital snare ligation of the middle cerebral artery (MCA) and neuropathological evaluation was carried out two weeks later. The size, location and histology of lesions varied within each time-period of MCA occlusion. However, most animals that underwent long-term ischemia (eight hours to permanent) had a single, confluent infarct involving deep and sometimes cortical structures. These animals had total necrosis chracterized by: 1. indiscriminate involvement of white and gray matter, 2. relatively sharp margins containing astrocytic and mononuclear cells, 3. an inner zone of liquefaction, infiltrated with fat-laden macrophages and newly formed blood vessels. Animals that underwent moderate to short-term ischemia (30 minutes to four hours) showed multiple, non-confluent deep infarcts. These animals had selective necrosis characterized by: 1. involvement of gray matter and relative sparing of white matter, 2. poorly circumscribed, multiple and often perivascular lesions with incomplete tissue destruction, 3. preferential loss of neurons and proliferation of reactive astrocytes and microglia.

Animals↗
PubMed1984

Beneficial effects of induced hypertension on experimental stroke in awake monkeys.

The authors performed a controlled study of induced hypertension therapy for treatment of experimental stroke in unanesthetized monkeys. Ten control and 10 treated animals were subjected to a 4-hour occlusion of the middle cerebral artery (MCA) by an implanted tourniquet. Neurological status and local cerebral blood flow (CBF) were monitored serially. Local CBF was determined by hydrogen clearance in and around the elevated 20% to 40% by intravenous infusion of phenylephrine hydrochloride. Neuropathological evaluation was performed after about 2 weeks. A 4-hour occlusion of the MCA in control animals caused moderate stable neurological deficits, moderate stable decreases in local CBF, and medium-sized infarcts. With induced hypertension, five of 10 treated animals showed neurological improvement, and eight exhibited increased CBF in the ischemic zone. Average infarct size tended to be smaller in the treated group, although the difference did not reach statistical significance. Hemorrhagic infarcts were not observed. In four animals, phenylephrine caused cardiac dysrhythmias and hypotension which were reversed by appropriate measures. In this unanesthetized primate model of moderate experimental stroke, induced hypertension had beneficial effects on neurological status, local CBF, and infarct size without causing hemorrhagic infarction. Induced hypertension may be beneficial for some clinical cases of focal cerebral ischemia.

Anesthesia, General↗
PubMed1983

The intracerebral microcirculation of the rat in hemorrhagic shock.

The intracerebral microcirculation of the isocortex was studied in unanesthetized rats under hemorrhagic shock. To observe the microvessels, three markers were separately injected intravenously during the shock period: (a) Evans blue for fluorescence microscopic visualization of the vessels. (b) India ink for gross and light microscopic evidence of retention of carbon. (c) Horseradish peroxidase (HRP) for light and electron microscopic study. Lack of spontaneous recovery from shock was associated with: (a) 55-65% blood loss, a low blood pressure (30-40 mm Hg), and a dramatic increase in pulse rate; (b) marked Evans blue fluorescence along the vessels; (c) no retention of India ink in the microcirculation; (d) peroxidase activity on the luminal surface of the endothelium. Absence of India ink in the microcirculation of the isocortex during the shock period, as shown by light and electron microscopy, suggests that there is sufficient cerebral blood flow to clear the carbon particles from the blood stream and that there are no openings greater than 30 nm in the endothelial layer allowing seepage of carbon particles through or between endothelial cells. Vascular Evans blue fluorescence and peroxidase activity were both demonstrated on the luminal surface of the endothelial cells, by light microscopy, indicating that these markers are abnormally retained. Ultrastructural demonstration of increased HRP uptake and adherence onto the endothelial cells confirms these observations. These results show that regional endothelial alterations occur in this model of hemorrhagic shock.

Anesthesia, Inhalation↗
PubMed1982

Spectrum of neurological deficits in experimental CNS ischemia. A quantitative study.

The sequence of events in focal cerebral ischemia has been difficult to study quantitatively in humans. Experimental investigation of these phenomena has been impeded because reproducible animals models that simulate human stroke are lacking. We have developed a rabbit spinal cord ischemia model that resembles human stroke patterns in many respects. Using this model, we have found that (1) brief ischemia produces completely reversible neurological deficits; (2) intermediate ischemic periods may produce transiently reversible deficits that later progress without further manipulation; (3) prolonged ischemia produces irreversible lesions in all animals. The model should be useful for studies of the pathophysiological mechanisms of CNS ischemia.

Animals↗
PubMed1982

Neuropathology of experimental spinal cord ischemia in the rabbit.

We studied a highly reproducible spinal cord model of focal central nervous system ischemia produced by occlusion of the abdominal aorta in the rabbit just below the renal arteries. The neuropathology of the lesion at one week or longer is characterized by: 1. Necrosis of gray matter and relative sparing of white matter throughout the lumbar and sacral cord with periods of ischemia between 45 minutes and 2 hours; and 2. Selective necrosis of elements within the anterior horns of the gray matter (neurons) in the lumbar cord with periods of ischemia between 15 and 30 minutes and in the transition zone between normal and infarcted gray matter with periods of ischemia between 45 minutes and 2 hours. Within the time period that causes irreversible damage (15 minutes to 1 hour), the distribution, size, and severity of infarcts is proportional to the duration of ischemia. The degree of functional impairment correlated closely with the extent of tissue damage. Previous work on ischemia of the spinal cord in experimental animals is critically reviewed. The segmental topographic distribution of the lesion and its histologic characteristics are discussed in relation to two important pathophysiological mechanisms of injury in central nervous system ischemia: the microcirculatory network, which in turn governs the adequacy of collateral flow, and the differential susceptibility of cells in nervous tissue. Sequential regional spinal cord blood flow determinations will be necessary to establish the precise relationship between levels of blood flow over time and space and neuropathology.

Animals↗
PubMed1982

Vascular labelling with monastral blue B.

Vascular labelling is an established technique of experimental pathology whereby leaky vessels can be identified in vivo. A suspension of a suitable colloidal pigment is injected intravenously; the pigment is then trapped in the wall of the leaky vessels. The colloidal preparation of carbon black, which has been used for many years for this purpose, is no longer commercially available. This communication introduces a substitute: Monastral blue B which gives beautiful preparations in whole mounts, is readily visible in paraffin and plastic embedded histologic sections, has a distinctive appearance in electron micrographs, and is nontoxic in the required dosage.

Animals↗