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Biomedical subjects

J W Harris

Publications and source records attributed to J W Harris.

At least 91 records · Page 5Linked to original sources
PubMed1982

Melanoma of the anorectal region.

Anorectal melanomas are more aggressive and behave differently from melanomas of the skin. Abdominoperineal amputation of the rectum is the favored procedure for potentially curable patients. Local recurrence in anorectal melanoma is less frequent in patients treated by local or wide excision of the tumor. Improvement in the primary anorectal melanoma survival rate appears to be dependent closely upon early diagnosis. Assessing the penetration of the tumor by the microstaging technique provides important prognostic information and serves for establishing indications for abdominoperineal amputation of the rectum in patients with primary anorectal melanoma. Two patients had a five year local and regional control of a primary anorectal melanoma achieved by abdominoperineal amputation of the rectum without groin dissection. One patient, free of disease, had an adenosquamous carcinoma of the lung develop with metastases to the skin. The carcinoma of the lung was considered as a secondary primary, which caused the death of the patient five years and nine months after the abdominoperineal amputation of the rectum.

Aged↗
PubMed1980

Polycythemia vera in childhood: case report and review of the literature.

A patient presented at 5 years of age with polycythemia vera. He subsequently developed splenic infarctions and died at 20 years of age following cerebral hemorrhage and infarctions. Two months before his death, he developed hypertension and had biochemical evidence of primary hyperparathyroidism and possibly pheochromocytoma. Only nine reported childhood cases of polycythemia vera fulfill the criteria of the Polycythemia Vera Study Group. These cases are summarized and the complications discussed. Although none have progressed to myeloid metaplasia or acute leukemia, these patients are at risk of developing thrombo-hemorrhagic complications; available evidence indicates that they should be managed to keep the hematocrit between 40 and 45%.

Bloodletting↗
PubMed1980

Optic atrophy in experimental vitamin B12 deficiency in monkeys.

The clinical findings and pathological changes of the visual pathway of vitamin B12 deficient monkeys have been described. The cellular morphology and counts of the peripheral blood and bone marrow remained normal during the study (nine deficient, three controls: one still alive in each group). Visual impairment was noted in all seven of the deficient animals that were evaluated by clinical observations. Ophthalmoscopic examination disclosed optic atrophy in six of the seven deficient monkeys. Degeneration of the visual pathway was demonstrated by pathological examination in eight of the deficient group of nine (one is still alive). Loss of ganglion cells was noted in the maculae of two of three deficient animals with completed studies. In the three control animals there were neither visual disturbances nor ophthalmoscopic changes and in two animals autopsies disclosed no lesions in the visual pathways. The third animal is still alive and well.

Animals↗
PubMed1980

Alpha globin gene number: population and restriction endonuclease studies.

Restriction endonuclease analysis was used to test a proposed genetic model using alpha-globin gene number to account for the observed distributions of the proportions of hemoglobin (Hb) S in sickle cell trait. In a subsample of specimens collected during a population survey in India, these studies confirmed that the postulated genotype was present in 22 of the 23 individuals examined. In the study population, the number of alpha-globin genes explains about 90% of the variance in the proportion of HbS in sickle cell trait (r2 = 0.895, p less than 10(-10)).

Anemia, Sickle Cell↗
PubMed1980

Studies in B12-deficient monkeys with combined system disease. I. B12-deficient patterns in bone marrow deoxyuridine suppression tests without morphologic or functional abnormalities.

A colony of rhesus monkeys made vitamin B12 deficient through dietary deprivation has been maintained since 1970. Deficient animals regularly develop neurologic lesions histologically, ultrastructurally, and topographically indistinguishable from those of human subacute combined degeneration but have failed to develop overt hematologic changes. No megaloblastic alterations, other evidence of impaired blood cell production, or subtle differences in mean red cell size are found. dU suppression tests on bone marrow were performed to determine whether functional B12 deficiency existed. All B12-deficient monkeys had markedly abnormal dU suppression test results after more than 10 months of B12 depviation, corrected by addition of B12 in vitro, whereas controls remained normal. Reasons for these disparate findings are considered, including species differences in metabolism of cobalamin analogues, cobalamin, and transcobalamins; the sensitivity of the dU test; the fact that ability to utilize preformed nucleotides may be greater in monkeys than in humans.

Animals↗
PubMed1979

Sickle cell anemia and trait in southern India: further studies.

Population surveys and family studies among 568 members of nine ethnic groups in southern India identified 15 homozygotes for sickle hemoglobin (HbS)who had mild clinical and hematological manifestations with high levels of fetal hemoglobin (mean=20%, range 8-36%) in a heterogeneous red cell distribution. In one family, the heterozygous mother had a hemoglobin pattern consistent with a form of the heterocellular hereditary persistence of fetal hemoglobin. Sickle cell trait was found in 153(27%) of those studied. Chromatographic quantitation of the hemoglobin fractions in these heterozygotes showed a trimodal distribution of the proportion of HB Sexplicable by a genetic model postulating the presence of genotypes with two (-alpha/-alpha), three (-alpha/alpha alpha) and four (alpha alpha/alpha alpha) active alpha-globin genes. Globin synthesis studies in four heterozygotes believed to have two active alpha-globin genes demonstrated an alpha/non-alpha total activity ratio (0.57) consistent with this model.

Anemia, Sickle Cell↗
PubMed1978

An ultrastructural study of subacute combined degeneration of the spinal cord in vitamin B12-deficient rhesus monkeys.

Prolonged deprivation of vitamin B12 in rhesus monkeys produced changes in the central nervous system that were indistinguishable topographically and histologically from those of human subacute combined degeneration. Ultrastructural studies of early lesions of the spinal cord disclosed a degeneration of myelin characterized by separation of myelin lamellae and formation of intramyelinic vacuoles, leading eventually to complete destruction of myelin sheaths. At a later stage, there was degeneration and loss of axons, and marked gliosis. The theories of pathogenesis of subacute combined degeneration are reviewed in the light of these observations.

Animals↗