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Biomedical subjects

E A Barker

Publications and source records attributed to E A Barker.

17 recordsLinked to original sources

c-myc, c-erbB-2, and Ki-67 expression in normal breast tissue and in invasive and noninvasive breast carcinoma.

c-myc, c-erbB-2, and Ki-67 expression was examined by immunohistochemistry in 11 normal breast tissues and 42 invasive and 14 noninvasive breast carcinomas. The c-myc product was detected in all breast carcinoma specimens and in 7 of 11 normal breast tissues. Invasive tumors stained more frequently with the anti-myc monoclonal antibody than did noninvasive tumors, while the level of expression in normal breast tissue was much less than that in breast cancer. Membrane staining of the c-erbB-2 protein was demonstrated in 29% (4 of 14) of noninvasive ductal carcinomas and in 45% (19 of 42) of invasive breast carcinomas. None of the 11 normal breast tissue samples was positive. The mean value of Ki-67-positive cells was 0.91 +/- 0.31% for normal breast tissue, 4.57 +/- 1.36% for noninvasive ductal carcinoma, and 12.76 +/- 2.18% for invasive breast cancer. In 42 invasive breast carcinomas, the expression of c-myc, c-erbB-2, and Ki-67 proliferation marker were compared with lymph node status, estrogen receptor status, progesterone receptor status, and age of patients at diagnosis. c-erbB-2 overexpression and Ki-67 overexpression were identified as the only factors associated with lymph node status. We concluded that they might be additional prognostic factors for breast carcinoma.

Breast

Chronic cutaneous graft-versus-host disease in man.

This clinicopathologic study of patients with chronic graft-versus-host disease (GVHD) after allogeneic marrow transplantation emphasizes the most prominent feature of the syndrome, the cutaneous aspects, and describes the ophthalmic-oral sicca syndrome with sialoadenitis and the neurologic findings. Chronic cutaneous GVHD affected 19 of 92 recipients surviving 150 days or more. In 6 patients chronic GVHD presented as a continuation of acute GVHD; in 8 it occurred after the resolution of acute GVHD; and in 5 it arose without preceding acute GVHD, ie, de novo late onset. Two cutaneous types were distinguished. The generalized type affected 16 patients and ran a progressive course resulting in late complications of poikiloderma, diffuse dermal and subcutaneous fibrosis, and contractures. Microscopically, it resembled generalized morphea and lupus erythermatosus hypertrophicus et profundus. The local type affected 3 patients with a more variable picture of poikiloderma, dermal sclerosis, and contractures. Microscopically, it resembled lupus of erythematosus profundus and scleroderma. Guidelines for defining and subclassifying chronic cutaneous GVHD are proposed.

Adolescent

The skin biopsy in the diagnosis of acute graft-versus-host disease in man.

Criteria for diagnosis of acute graft-versus-host disease (GVHD) using skin biopsies were derived from a) general experience with more than 300 human marrow grafts and b) the results of "blind" studies of skin biopsy specimens of patients grafted with either allogeneic or syngeneic marrow. Large doses of cytotoxic drugs and irradiation given before grafting can produce transient skin changes interfering significantly with the diagnosis of GVHD. Artifacts can also cause difficulty. Epidermal cytologic atypia, dyskeratosis, and satellitosis were present both in allografted patients with acute clinical GVHD of multiple systems and in patients given autologous or syngeneic marrow. Due to the marked overlap in histopathologic findings between these two types of skin injury, frequent serial skin biopsies must be combined with all other available clinical and biopsy data to provide reliable diagnosis of acute GVHD in man.

Acute Disease

Prevention of folate deficiency by food fortification. III. Effect in pregnant subjects of varying amounts of added folic acid.

Maise meal fortified with folic acid was administered to subjects in late pregnancy in a daily dose of either 500 or 300 mug of folic acid. Changes in hematological and folate nutritonal status were compared to those in subjects receiving 300 mug folic acid/day in tablet form, and also in subjects in a previous study who received unfortified maize meal (control group) or meal containing 1,000 mug folic acid/day. In all groups receiving folic acid, red cell and serum folate levels rose progressively, and the rate of rise increased with increasing doses of folic acid. Maize meal containing a daily dose of 500 mug folic acid produced an effect similar to that of 300 mug daily in tablet form. Maize containing 300 mug added folic acid daily was effective in preventing the progression of folate depletion in late pregnancy.

Dose-Response Relationship, Drug

Prevention of folate deficiency by food fortification. IV. Identification of target groups in addition to pregnant women in an adult rural population.

In a rural Negro population subsisting on a predominantly maize meal diet, the incidence of folate deficiency was 43.8% in nonanaemic women in late pregnancy, 32.1% in nonpregnant women, and 18.6% in adult males. More than one-third of all subjects older than 60 were deficient. No instance of unequivocal vitamin B12 deficiency was revealed in 431 subjects sampled, and it is considered that the hazards of giving a small daily dose of folic acid in this population are negligible. These findings warrant food fortification with folic acid in this and similar population groups.

Adolescent

Lipid content in the liver of fatty metamorphosis of pregnancy.

Lipid analyses were performed on the liver of a patient who died during an episode of acute fatty liver of pregnancy, and on livers from normal subjects and from subjects suffering from nutritional fatty livers. Comparison of these data indicates that in fatty liver of pregnancy the increased hepatic lipids consist primarily of free fatty acids. The recognized toxicity of fatty acids suggests a pathogenic mechanism for the disease. Nutritional fatty liver is associated predominantly with an increase in triglyceride. These changes are not the result of postmortem change, and they confirm and extend the previous data concerning the fat accumulation in human hepatic illness.

Adult

Nonhepatic thioacetamide injury. II. The morphologic features of proximal renal tubular injury.

Thioacetamide given orally to rats produces centrolobular hepatic necrosis and also causes death of the cells in the terminal portion of the proximal renal tubule. The morphologic changes observed during the course of the renal toxicity include the early and transient appearance of apical dense bodies, which appear to fuse to form large lysosomes, and the appearance of nucleolar hypertrophy, reminiscent of the same change seen in the hepatocytes. In addition a variety of changes described in lethally injured tubular cells in other toxicities appear. A diuresis, which lasts for 5 days, coincides with the appearance of tubular cell destruction. The mechanism of cell injury due to thioacetamide is not identified, but the temporal sequence of morphologic and physiologic change is consistent with both a relative concentration of the thioacetamide in the proximal tubule and its potential conversion to a putative proximate toxin.

Acetamides

Nonhepatic thioacetamide injury. I. Thymic cortical necrosis.

Normal and adrenalectomized rats were given a single oral dose of thioacetamide (5, 10 or 20 mg/100 g body weight). The size, weight and histology of the thymus were observed for 3 weeks following intoxication. An initial rapid loss of thymic weight and size occurred during the first 3 days of intoxication; there was no significant recovery. This loss was associated with decreased cortical mass without significant change in medullary size or histology. The decrease of the cortex was associated with significant cortical cell death and the formation of a "starry sky" pattern. This response occurred in both adrenalectomized and nonadrenalectomized rats, suggesting that this phenomenon is not the adrenal-mediated stress response. Measurement of circulating mononuclear cells indicated that thymocyte release did not play a significant role in depletion changes. The basis for this prompt, at least temporarily irreversible, chemically induced thymic atrophy is not apparent.

Acetamides