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Biomedical subjects

D A Baron

Publications and source records attributed to D A Baron.

45 records · Page 3Linked to original sources
PubMed1979

Mitoses in peripheral pulmonary epithelium: the effect of colchicine.

Injury in the periphery of the lung was studied in rats given intratracheal trypsin. Mitotic figures were noted in the alveolar epithelium, and colchicine enhanced the yield. Of 65 mitotic figures examined in detail, 46 were present in the alveolar epithelium. Epithelial mitoses were confined to type II cells, many of which contained lamellar inclusions, abundant rough endoplasmic reticulum, and luminal microvilli. Mitoses were not seen in type I cells or in less well differentiated epithelial cells, but they were noted in occasional endothelial and interstitial cells. Colchicine-arrested type II cells were distinguished by radially disposed chromosomes surrounding pairs of centrioles and randomly oriented microtubules. In addition, many of these cells showed a pronounced cortical zone, devoid of microvilli, and others showed cytotoxic degenerative changes. These observations indicate that the alveolar epithelium is renewed exclusively by division of differentiated type II cells.

Animals↗
PubMed1975

Histochemical demonstration of lysosomal hydrolase activity in endometrial mononuclear cells. I. Normal endometrium.

Interstitial cell reactivity for lysosomal hydrolases was demonstrated in 67 endometrial specimens with histochemical techniques. Cyclic changes in the number of reactive cells corresponded to the stage of the menstrual cycle. Techniques for galactosidase and glucuronidase showed increasing numbers of reactive cells through the late secretory stage. Staining for glucosaminidase and nonspecific esterase also increased in late secretory endometrium. In contrast, acid phophatase activity was biphasic, and that of leucine aminopeptidase remained relatively constant. Only minimal interstitial staining was seen in prepubertal and postmenopausal specimens.

Acid Phosphatase↗
PubMed1975

Histochemical demonstration of lysosomal hydrolase activity in endometrial mononuclear cells. II. Abnormal endometrium.

The mononuclear cells in the endometrial stoma change in reactivity for lysosomal hydrolases during the menstrual cycle. Lymphoid follicles may occur in the stroma in any phase of the cycle and have been found in gestational endometrium. However, these cells have no significant lysosomal activity. Alterations in the endometrium are reflected in modified patterns of activity. Endometritis, association with an intrauterine contraceptive device, pregnancy, and adenocarcinoma result in increased numbers and staining intensity of mononuclear cells. In contrast, no consistent changes were apparent in foci of glandular hyperplasia, and decreased staining was seen in atrophic areas of endometrium. These data suggest that interstitial mononuclear cells are a sensitive monitor of morphologic changes in the endometrium.

Acid Phosphatase↗
PubMedDate not supplied

Cyclooxygenase-2 expression in the developing human kidney.

Cyclooxygenase (COX) exists in two related but unique isoforms, COX-1 and COX-2, and is suggested to have specific functions in different segments of the nephron. COX-2 knockout mice develop fatal nephropathy, which implies that this isoform is important during nephrogenesis. The histologic changes seen in the COX-2 knockout mice are similar to those observed in the kidneys of human fetuses exposed to non-steroidal anti-inflammatory drugs (NSAIDs) in the third trimester of pregnancy. However, only minimal amounts of COX-2 mRNA or protein have been reported in the adult human kidney. We hypothesized that expression of COX-2 is significant in the fetal human kidney and that it is involved in the development of the nephron. To characterize the presence of COX-2 in the human fetal kidney, we used immunohistochemistry to evaluate its expression in 23 fetal kidneys ranging between 15 and 23 weeks of gestational age. Strong expression of COX-2 was localized primarily in the macula densa and the thick ascending limb of the loop of Henle, and in rare glomerular podocytes and vascular endothelial cells. There was a progressive decrease in COX-2 immunoreactivity from the most immature nephrons adjacent to the metanephric regions to the well-developed nephrons in the middle to inner cortex. In contrast to the adult human kidney, this temporal and spatial expression of COX-2 in the fetal kidney suggests that this enzyme may be involved in nephrogenesis, and its inhibition by NSAIDs during the third trimester may be responsible for fetal renal syndromes.

Cyclooxygenase 2↗
PubMedDate not supplied

Expression of cyclooxygenase-2 in the macula densa of human kidney in hypertension, congestive heart failure, and diabetic nephropathy.

Cyclooxygenase-2 (COX-2) is constitutively expressed in the macula densa of several laboratory animal species where it is considered to play a physiologic role in the regulation of basal renal function. Pertubations to normal homeostasis is shown to be associated with the upregulation of COX-2 in the macula densa of rats and dogs. In contrast, COX-2 has not been detected in the macula densa of normal adult human and non-human primate kidneys, suggesting a less prominent role of this isoform in normal renal function in these species. In this study, we characterized COX-2 expression in human kidneys collected from subjects with a clinical history indicative of compromised renal function associated with diabetic nephropathy (DN), hypertension, and congestive heart failure (CHF). COX-2 expression was evaluated by immunohistochemistry using isoform-specific antibodies and in situ hybridization. No COX-2 protein or mRNA was observed in the macula densa of normal kidneys (n= 11), whereas slight to moderate COX-2 expression was present in the macula densa of 7/15 subjects (46%) with DN, 5/11 (46%) subjects with hypertension, and 3/10 subjects (30%) with CHF. These results indicate that COX-2 is variably induced in the macula densa of the human kidney in compromised renal conditions and that COX-2-mediated prostaglandins may be involved in maintaining adequate renal functions in some patients with DN, hypertension, and CHF. This variability may be related to individual clinical status or synthesis of vasodilatory prostaglandins by cyclooxygenase-1 (COX-1).

Cyclooxygenase 2↗
PubMedDate not supplied

Pathology of perbutylated-N-butyl-1-deoxynojiromycin (an alpha-glucosidase-1 inhibitor) in Sprague-Dawley rats.

Perbutylated-N-butyl-1-deoxynojiromycin (p-N-butyl-DNJ, SC-49483), an alpha-glucosidase-1 inhibitor, is a candidate anti-HIV agent targeted against viral glycoprotein processing in host cell endoplasmic reticulum. The potential toxicity of this compound was evaluated in Sprague-Dawley rats after 4, 13, or 26 wk of oral administration at doses ranging from 300 to 3,670 mg/kg/day. In these studies, the target organs of p-N-butyl-DNJ effects were thyroid gland, salivary gland, stomach, and pancreas. The most prominent histologic change in these organs was the presence of clear or lightly eosinophilic vacuoles in the cytoplasm of thyroid follicular cells, gastric chief cells, salivary gland acinar cells, and exocrine pancreatic acinar cells. Ultrastructurally, these vacuoles were consistent with dilated rough endoplasmic reticulum, which sometimes contained homogeneously stained, moderately electron-dense material. The vacuoles in thyroid follicular cells contained pale eosinophilic colloidlike material consistent with accumulated thyroglobulin, as shown by immunohistochemical staining methods. The biological functions of these organs were not adversely affected as evidenced by the absence of clinical signs and the results of selected hormonal analyses. The morphologic changes were completely reversed after a 4-wk recovery period. The incidence and severity of histologic changes were decreased after 13 and 26 wk of treatment compared to 4 wk of treatment, indicating an attenuation of the host response or adaptation to the prolonged p-N-butyl-DNJ administration. We believe that morphologic changes in thyroid follicular cells, salivary gland acinar cells, pancreatic acinar cells, and gastric chief cells were the result of nonspecific inhibition of host alpha-glucosidase(s) by p-N-butyl-DNJ, causing clinically silent perturbation in host cell glycoprotein processing and/or glycoprotein transport.

Animals↗