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Biomedical subjects

A R Mastri

Publications and source records attributed to A R Mastri.

At least 37 records · Page 2Linked to original sources
PubMed1982

Neural and vascular tissue reaction of cyanoacrylate adhesives: a further report.

The effect of a new tissue adhesive, carbohexoxymethyl 2-cyanoacrylate monomer (Ethicon CHC), was evaluated in six cats divided into two groups. With the cats under barbiturate anesthesia. Ethicon CHC was applied to the left cruciate cortex and the left femoral neurovascular bundle. Normal saline was applied to the right side for control. The first group (n = 4) and the second group (n = 2) were killed 4 and 7 days, respectively, after application of the adhesive. Neuropathological examination revealed meningeal astrocytosis, vascular wall degeneration, hemorrhage, and inflammatory reaction in both groups. This adhesive does not display the ideal property of inertness, which would permit its safe use. Focal tissue reactions caused by the adhesives in sensitive areas of the cortex can result in significant neurological deficit.

Animals↗
PubMed1981

Dementia of the Alzheimer type. Clinical genetics, natural history, and associated conditions.

Relatives of 125 probands, who had dementia of the Alzheimer type as proved by autopsy, were subjects of a genetic investigation. The relatives exhibited an excess of dementing illness consistent with genetic transmission. Risk to relatives decreased sharply as severity of the proband's illness decreased. Also, when compared with a control group and the general population, the relatives had excesses of Down's syndrome, lymphoma, and immune diatheses. These associated conditions also were more likely to be present when the proband had severe illness. Mortality at all ages was increased among the relatives.

Adult↗
PubMed1981

Aberrant peripheral nerves and neuromas in normal and injured spinal cords.

Spinal cords from 20 patients (13-78 years of age) were studied for the occurrence of peripheral nerve fibers within the cord. Peripheral nerve fibers were observed in all but two younger patients, 13 and 24 years old, respectively, but all the spinal cords were otherwise normal. The nerve fibers were thin and predominantly myelinated. They were seen in two forms, small parallel bundles resembling normal nerve fascicles and larger interlacing bundles or whorled masses indistinguishable from traumatic neuromas. They almost always occurred in the perivascular spaces of the major parenchymal branches of the anterior sulcal artery and/or in the anterior median sulcus. The neuromas in the otherwise normal cords were identical with those occurring in the cord with old traumatic injury in three patients studied, but they were few in the former, while numerous and widespread in the injured segments of the latter. Accumulating evidence suggests 1. that most, if not all, of the parallel nerve bundles about the anterior sulcal artery in otherwise normal spinal cords represent aberrant, regenerated nerve fibers originating from ventral spinal nerve roots which are severed by clinically occult injuries in adult life, and 2. that the regenerated nerve fibers continue to grow into the anterior median sulcus and perivascular spaces and may become entangled or return upon themselves, forming neuromas as their way is blocked by the pia-glial barrier.

Adolescent↗
PubMed1981

Axonal dystrophy in the gracile nucleus in children and young adults. Reappraisal of the incidence and associated diseases.

In 656 patients aged from one to 39 years, the incidence of axonal dystrophy in the gracile nucleus (ADG) is correlated with underlying diseases. The age-related incidence of ADG (minimal to severe) in these patients, 13, 53, 76 and 97% in the first, second, third, and fourth decades, respectively, is comparable to that observed by other investigators. The incidence drops to 8, 16, 31, and 60% when more than five spheroids in each gracile nucleus are taken into account. Diseases with which ADG is frequently associated vary according to the patient's age. Congenital biliary atresia and cystic fibrosis account for 71% of cases of ADG (mild to severe) in the first decade, while cystic fibrosis and malignancies account for 38 and 35% in the second decade, respectively. In the third decade, malignancies, renal diseases, cystic fibrosis, and heart diseases account for 30, 14, 12, and 12% of ADG cases, respectively, while malignancies, renal diseases, heart diseases, and diseases of digestive organs account for 30, 24, 15, and 11% in the fourth decade, respectively. The incidence of ADG also increases progressively with age, duration of the clinical course in the individual disease, or both, regardless of types of the diseases. This fact, when viewed together with the precocious development of severe ADG in patients with the malabsorption syndromes and in those with grave illnesses with protracted course leading to cachexia, seems to indicate that malnutrition represents a common factor correlated with severe ADG in the young patients. It seems to be premature at this time to disregard the hypothetical question that ADG in man is in some way related to deficiency or altered metabolism of vitamin E.

Adolescent↗
PubMed1980

An unusual degenerative disorder of neurons associated with a novel intranuclear hyaline inclusion (neuronal intranuclear hyaline inclusion disease). A clinicopathological study of a case.

A 21-year-old woman with an unusual, progressive, degenerative neurological disorder is described. The disorder is characterized clinically by behavioral abnormality, peculiar involuntary movements, and ataxia starting in early childhood and subsequent development of dementia, choreoathetosis, rectal and bladder incontinence, bulbar and spinal muscular weakness, pes cavus, kyphoscoliosis, and generalized seizures. The clinical manifestations are correlated, with widespread pathological changes affecting almost all neuronal systems. The pathological changes are discussed in relation to the wide spectrum of "multisystem atrophies." Particular attention is directed to the ubiquitous occurrence of a novel intranuclear, eosinophilic, hyaline inclusion in almost all types of central, peripheral, and autonomic neurons. The ubiquitous neuronal involvement seems to explain the diffuse multiple system degeneration. The pathogenesis of the neuronal inclusions is unknown, but it is speculated that the disorder may represent a metabolic abnormality affecting the nuclear protein of neurons, rather than a viral infection. The pathological features, consisting of the neuronal intranuclear hyaline inclusions associated with multiple system atrophy, have not hitherto been described, and "neuronal intranuclear hyaline inclusion disease" is proposed as a name for the disorder. Rectal biopsy demonstrating the intranuclear hyaline inclusions in ganglion cells of the hyenteric plexuses may serve as a diagnostic procedure for the disorder.

Adult↗
PubMed1980

Spinal autonomic neurons in Werdnig-Hoffmann disease, mannosidosis, and Hurler's syndrome: distribution of autonomic neurons in the sacral spinal cord.

In Werdnig-Hoffman disease, mannosidosis, and Hurler's syndrome, two groups of neurons (the Onuf's and intermediomedial nuclei) in the ventral horn of the mid-sacral region are found to share common selective sparing or vulnerability with the intermediolateral nuclei of the thoracolumbar and sacral regions of the spinal cord. This finding confirms the previous observations on the characteristic involvement or sparing in Fabry's disease (14), Shy-Drager syndrome (17), amyotrophic lateral sclerosis, anterior poliomyelitis, and neuronal intranuclear hyaline inclusion disease (15), and supports the assumption that the Onuf's and intermediomedial nuclei in the ventral horn represent autonomic neurons much as the thoracolumbar and sacral intermediolateral nuclei.

Autonomic Nervous System↗
PubMed1980

Axonal dystrophy in the gracile nucleus in congenital biliary atresia and cystic fibrosis (mucoviscidosis): beneficial effect of vitamin E therapy.

In 63 patients with malabsorption syndromes, 16 with congenital biliary atresia (BA) and 47 with cystic fibrosis (CF), axonal dystrophy in the gracile nucleus (ADG) was studied. Of the 16 patients with BA, ADG of considerable severity was observed in all 10 over one year of age. Of the 47 patients with CF, it was observed in 32, 61 and 80% of the cases in the first, second, and third decades, respectively. Evidence is presented that there has been a substantial decrease in the incidence of ADG in CF patients in recent years and that the decreased incidence is attributable to vitamin E (Aquasol E) therapy. The beneficial effect of vitamin E supplementation in CF patients is proffered as strong evidence that ADG in BA and CF is related to vitamin E deficiency. The present study indicates that BA and CF patients require vitamin E supplementation to maintain a normal integrity of axons related to the gracile and perhaps other sensory nuclei. Critical neurological evaluation for possible dysfunction of the sensory nuclei in these patients with malabsorption syndromes is advised.

Adolescent↗
PubMed1980

Neuropathology of diabetic neurogenic bladder.

Disturbances of urinary bladder function are well-recognized problems in diabetic patients and are generally attributed to peripheral neuropathy. Because of the difficulties inherent in the histologic examination of the peripheral autonomic nerves, little is known about the pathology of these nerves. Recently, alterations have been observed in fine axons in the bladder wall in diabetic subjects. Pathologic changes have also been observed in ganglia of the bladder wall. Abnormalities previously described in the autonomic ganglia and nerve trunks of diabetic subjects may also be important in the development of urinary bladder dysfunction.

Autonomic Nervous System↗
PubMed1980

A trial of vidarabine for cytomegalovirus infection in renal transplant patients.

Vidarabine was evaluated in renal transplant patients as a potential therapeutic agent in cytomegalovirus (CMV) infection. Four patients received vidarabine on an open protocol, then ten additional patients were enrolled in a double-blind protocol. Among the nine patients who received vidarabine, no notable clinical improvement occurred in either the vidarabine- or placebo-treated groups. Thus, vidarabine showed no therapeutic effect in the treatment of CMV infections at the dosages used. Four patients showed dramatic CNS deterioration within several days of the onset of vidarabine therapy. Tremors and myoclonus were common, and one patient had unusual brain pathologic changes with widespread neuronal chromatolysis. The pathologic findings in the brain in the other three patients were complex and included intracerebral hemorrhage, Fabry's disease, coccidioidomycosis meningitis, and cerebral vascular occlusion. Thus, there was no conclusive proof that vidarabine contributed to the sudden neurologic deterioration of these patients.

Adult↗
PubMed1979

Pathology of Shy-Drager syndrome.

In four patients with the Shy-Drager syndrome, detailed pathological findings in the central nervous system are described. All four patients had striatonigral degeneration, olivopontocerebellar atrophy, pyramidal tract degeneration and ventral horn cell loss. Along with the multisystem degeneration, there was widespread loss of thoracolumbar autonomic neurons, which was demonstrated by comparative cell counts of the intermediolateral horns in two of the four patients. In all four patients, autonomic nuclei of the sacral cord, particularly the Onuf's and intermediolateral nuclei, were severely affected and diffuse cell loss in the nuclei seems to account for disordered bladder, rectal and sexual functions in Shy-Drager syndrome.

Aged↗
PubMed1979

Acute cerebral revascularization after regional cerebral ischemia in the dog. Part 2: Clinicopathological correlation.

The efficacy of cerebral revascularization by anastomosis of the superficial temporal artery (STA) to the middle cerebral artery (MCA), performed 4 and 24 hours after a regional MCA infarction had been produced by combined occlusion of the MCA and internal carotid artery, was tested in 12 dogs. To control possible intercurrent variables, seven other dogs remained untreated and five had a sham operation. Clinical and pathological changes were recorded and analyzed. An incidence of 85% infarction was obtained in the untreated control group. The severity of the clinical deficits and pathological changes for the anastomosed groups were greater than those seen in the untreated control group. The extent of the infarction was significantly greater (p less than 0.05) in the anastomosed groups than in the sham-operated and control groups. Hemorrhagic infarcts occurred in most of the dogs in the anastomosed groups, but were not present in either control group (p less than 0.05). Two dogs in the 4-hour and one in the 24-hour group improved more than any control dog, but the difference was not statistically significant (p greater than 0.05). In two dogs with occluded anastomosis the clinical deficits and the pathological changes were less than those seen in animals with patent anastomosis. The severity of the pathological and clinical changes correlated well with the reestablishment of flow in the MCA territory. It is proposed that cerebral revascularization at 4 and 24 hours following a regional MCA infarct in the dog is followed by an exacerbation of the microcirculatory obstruction, cerebral edema, and infarction. From improvement noted in three animals the authors suggest that under special conditions the revascularization could benefit some cases following acute cerebral infarction.

Animals↗
PubMed1979

Acute cerebral revascularization: part I. Cerebral ischemia experimental animal model.

Thirty-two mongrel dogs divided into two groups were subjected to a transorbital occlusion of the middle cerebral artery (MCA) or a combined transorbital MCA and cervical internal carotid artery (ICA) occlusion. Clinically apparent deficits were present in the MCA group in 18% of cases and in 73% of MCA/ICA cases. Pathologically, 55% of MCA cases and 73% of MCA/ICA cases had demonstrable areas of infarction. The incidence and severity of clinical deficits as well as the location and extent of pathological infarction were significantly greater (p less than 0.05) with the MCA/ICA group than in the MCA group. The mortality rate and frequency of pathologically apparent infarcts were not statistically different p greater than 0.05. No hemorrhagic infarctions were seen in any case.

Animals↗
PubMed1978

Aluminum levels in brain in Alzheimer's disease.

In both human Alzheimer's disease and aluminum encephalopathy of animals, changes are observed in neurofibrillary structures. We have found that brains from Alzheimer patients contain approximately 1.4 times the aluminum level found in a control series. Some possible methodological problems are discussed. We have proposed a plausible chemical mechanism for the changes of aluminum encephalopathy.

Aged↗
PubMed1977

The genetics of Alzheimer's disease: associations with hematologic malignancy and Down's syndrome.

Relatives of probands with histologically confirmed Alzheimer's disease had excessive morbidity from Alzheimer's disease, Down's syndrome, and hematologic malignancies. These associations coupled with two previously reported ones, the indistinguishable histopathological changes in brain in Alzheimer's disease and Down's syndrome, and the 20-fold increased incidence of leukemia among persons with Down's syndrome, are evidence that some instances of those disorders are associated with a unitary genetic etiology. The genetic defect may be expressed through disorganization of microtubules. Other evidence suggests that the same process may be involved in aging and in other chromosomal aberrations.

Adolescent↗