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Biomedical subjects

L M Reid

Publications and source records attributed to L M Reid.

At least 109 records · Page 6Linked to original sources
PubMed1984

Congenital pulmonary vein stenosis: structural changes in a patient with normal pulmonary artery wedge pressure.

A male infant is described who died at 13 months of age with stenosis of all extrapulmonary veins except the left upper vein. The pulmonary artery wedge pressure was normal, the first time this is reported in this condition. At autopsy, there were structural changes of the pulmonary arteries and veins in all lobes with or without pulmonary vein stenosis. Arterial changes-muscle extension, medial hypertrophy and decreased arterial size--analyzed quantitatively were found to be similar in all lobes. Venous medial hypertrophy was more marked in obstructed lobes. These anatomic changes are presumably due to fixed venous obstruction in the pulmonary lobes drained by stenotic veins and to high flow in the left upper lobe.

Cardiac Catheterization↗
PubMed1984

Hepatocyte proliferation in vitro: its dependence on the use of serum-free hormonally defined medium and substrata of extracellular matrix.

The culture conditions found to result in stable proliferation of normal rat hepatocytes are: (i) subconfluent cell densities; (ii) serum-free medium; (iii) hormonally defined medium containing epidermal growth factor, insulin, glucagon, prolactin, and other growth factors; and (iv) substrata of liver extracellular matrix depleted of growth inhibitors. Serum was found deleterious to parenchymal cells: it was inhibitory to the expression of liver-specific functions, cytostatic to parenchymal cells at all seeding densities, and cytotoxic to them at low seeding densities. These studies emphasize the relevance of synergies in the influences of hormones and extracellular matrix in regulating hepatocellular physiology.

Animals↗
PubMed1984

Posttranscriptional modulation of gene expression in cultured rat hepatocytes.

The maintenance of high levels of two liver-specific mRNAs in cultured hepatocytes was achieved in a serum-free hormonally defined cell culture medium. However, this maintenance of liver-specific mRNA levels did not correlate with the level of transcription of the genes but was apparently due to increased stabilization of the tissue-specific mRNAs. The mRNA stabilization did not occur in serum-supplemented medium. In both defined and serum-supplemented medium, actin and tubulin mRNAs were also greatly increased, in both cases predominantly if not entirely due to increased mRNA stability.

Actins↗
PubMed1984

Extracellular calcium ion depletion induces release of glycoproteins by canine trachea.

The effect of depletion of extracellular Ca2+ on the release by canine trachea in vitro of [14C]glucosamine-labeled trichloroacetic-phosphotungstic acid-precipitable glycoproteins was evaluated. Incubation in Ca2+,Mg2+-free medium containing ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA, 10(-3) to 10(-5) M) induced a time-dependent increase in base-line release of high molecular weight, radiolabeled glycoprotein that was not blocked by 10(-5) M atropine, propranolol, or phentolamine. Maximal increase was proportional to EGTA concentration and was augmented by preincubation with methacholine chloride. The secretory response was reversed by reincubation of explants in medium containing Ca2+, Sr2+, or Ba2+ but not Mg2+. Assessment of explants denuded of epithelium or cartilage indicated that the secretory response to depletion of Ca2+ originated in the tracheal submucosa, probably the submucosal glands. Quantitative autoradiographic analyses showed, however, that incubation in Ca2+,Mg2+-free medium had no effect on radiolabel release from mucous or serous cells in the tracheal submucosal glands. Increased radiolabeled glycoprotein release in Ca2+,Mg2+-free medium was accompanied by exfoliation of the surface epithelium, though the two effects were apparently unrelated. The secretory response was not due to cell lysis or increased release of radiolabeled glycosaminoglycans, and the finding that the specific activity (ratio of bound radiolabel to protein content) of the glycoprotein released was not changed in Ca2+,Mg2+-free medium showed that it was not due to a change in the rate of glycoprotein synthesis. A model is proposed in which depletion of Ca2+ increases the rate of flow of mucus from the duct lumens of the tracheal glands.

Animals↗
PubMed1984

Early recovery from hypoxic pulmonary hypertension: a structural and functional study.

This study follows the recovery during 1 mo in ambient air from the hemodynamic and structural changes found in Sprague-Dawley rats after 2 wk of hypobaric hypoxia. In the time studied there is some degree of recovery for all features analyzed. The only features that completely return to normal are hematocrit level, new muscle in arteries at alveolar wall level, medial thickness of intra-acinar arteries, and density of filled arteries. For some features much of the recovery is early or rapid; for other features the recovery is late or slow. The rapid changes, occurring within two days of removal from hypoxia, include a fall in pulmonary arterial pressure (36.6 +/- 1.5 to 30.1 +/- 1.1 mmHg), a drop in hematocrit (61.1 +/- 1.3 to 53.0 +/- 1.0%), and the disappearance of new muscle, as judged by light microscopy from many arteries at alveolar wall (39.5 +/- 4.9 to 17.7 +/- 4.0%) and alveolar duct (85.9 +/- 2.5 to 68.2 +/- 3.4%) levels. The slow recovery includes the decrease in right ventricular and arterial medial hypertrophy, disappearance of muscle from respiratory bronchiolar arteries, reduction in lung volume, and increased density of filled arteries. These slow changes are probably the response to a fall in pulmonary arterial pressure.

Animals↗
PubMed1984

Potent stimulation of glycoprotein secretion in canine trachea by substance P.

The effects have been investigated of the regulatory peptides, substance P (SP) and bombesin, on the secretion of [14C]glucosamine-labeled trichloroacetic acid-phosphotungstic acid precipitable glycoproteins by canine tracheal explants. SP (10(10) to 10(-7) M) induced a dose-dependent increase in secretion of high-molecular-weight (greater than 2 X 10(6) radiolabeled glycoproteins predominantly from the submucosal glands. On a molar basis, SP [median effective concentration (EC50) = 8.2 X 10(-10) M] was about 1,000-fold more potent than methacholine (EC50 = 6.3 X 10(-7) M). Bombesin (10(-10) to 10(-4) M) had no effect on glycoprotein secretion. The time course of SP effect was characterized by an initial stimulation of glycoprotein secretion followed by a period of inhibition, suggesting that it rapidly exhausts a pool of glycoprotein, possibly that present within the duct lumen of the submucosal gland. Consistent with this are the findings that SP-induced secretion of glycoprotein was augmented by preincubation with methacholine while methacholine-induced secretion was diminished by preincubation with SP. Our findings show that SP is a potent stimulant of airway glycoprotein secretion in vitro and suggest that it acts by increasing the rate of clearance of mucus from the ducts of the submucosal gland, possibly by induced constriction of the secretory tubules and collecting duct. A role is discussed for SP in mucus hypersecretion induced by local axonal reflexes in the airway mucosa.

Animals↗
PubMed1984

Mapping of beta-adrenergic receptors in rat lung: effect of isoproterenol.

beta-Adrenergic receptors were mapped in the rat lung using a light microscopic technique that identifies binding sites for 3H-labeled dihydroalprenolol in intact slide-mounted tissue sections, which were also used for biochemical analysis of ligand binding. Grain density measurements were combined with morphometric data. These results indicate that, although over 97% of the specific binding is to cells of alveolar walls, beta-adrenergic receptors are present and can be quantified in tissues that represent a small fraction of total lung mass, such as bronchial epithelium and smooth muscle of bronchial walls and pulmonary vessels. Repeated administration of isoproterenol decreased the receptor number, as determined biochemically and from grain density measurements, in all anatomic regions studied, but did not alter the distribution of binding.

Animals↗
PubMed1984

Bronchopulmonary dysplasia: a morphometric study with emphasis on the pulmonary vasculature.

Using morphometry, the pulmonary vasculature in lungs obtained at autopsy from 8 patients with bronchopulmonary dysplasia (BPD) was studied. In these specimens the axial arterial pathway was similar in length to those of equivalently aged fetuses and increased with lengthening survival. The internal diameter of axial arteries was variable--excessively wide in 2 patients and diffusely narrow in 3. Microscopically, the percent medial thickness of muscular pulmonary arteries was reduced compared to fetal values and tended to be less in older patients. Compared to normal fetuses, there were more muscularized intraacinar arteries, suggesting peripheral extension of smooth muscle. Arterial concentrations were elevated in 2 long-term survivors. The weight of the cardiac right ventricle was reduced in 4 patients. These findings indicate that in patients with BPD there is a complex dual process of pathological remodeling and an attempt at normal anatomic adaptation of the pulmonary vasculature to extrauterine life.

Bronchial Arteries↗
PubMed1984

The structural basis of PPHN.

Discussed in this article are the three main anatomic types of persistent pulmonary hypertension of the newborn; (1) maladaptation of the pulmonary vascular bed; (2) excessive muscularization of the pulmonary vascular bed; and (3) underdevelopment of the pulmonary vascular bed.

Amniotic Fluid↗
PubMed1984

Characterization of a human, sex steroid-responsive transitional cell carcinoma maintained as a tumor line (R198) in athymic nude mice.

We have established a transplantable tumor line, R198, derived from a papillary (transitional cell) carcinoma of the human urinary bladder. In nude mice, the tumor line exhibits properties attributable to both prostatic and transitional epithelia. In tumor-bearing animals given androgens, the neoplasm has a rapid growth rate, possesses low levels of measurable androgen receptors, produces tartrate-inhibitable acid phosphatase, and forms well-encapsulated, cystic tumors composed of transitional, glandular, and squamous cells. The administration of estrogens or transplantation of the tumor into female mice causes regression of the tumor. In a small percentage of the transplants placed into females or estrogenized animals, selection occurs for tumor cells which can grow under these conditions. The resulting tumors are infiltrating scirrhous carcinomas that closely resemble squamous cell carcinomas of the urinary bladder. These neoplasms grow slowly and do not possess androgen receptors or secretory material. They are composed of a homogeneous population of squamous cells which are locally invasive. The paradox of a bladder tumor with some prostatic characteristics may be explained by the fact that the tumor was derived from the trigone region of the bladder, which embryologically is formed by an admixture of tissue from the wolffian duct and the urogenital sinus. Some trigone-derived neoplasms have characteristics of both bladder and prostate. We hypothesize that sex steroid-sensitive R198, with characteristics of both bladder transitional cells and prostatic epithelia, is a tumor which phenotypically expresses the embryological origins of these tissues. As such, the tumor line will serve as a useful model for studying sex steroid-responsive cells of the urogenital epithelium.

Aged↗
PubMed1984

Lung structure in asphyxiating thoracic dystrophy.

It has been assumed that asphyxiating thoracic dystrophy (ATD) is always associated with abnormal lung development due to the small thoracic cage. Applying precise quantitative morphometric techniques to the injected and inflated lung from an infant with ATD who died at 4 months of age, normal lung growth was demonstrated. The number of bronchial generations and preacinar arteries was normal, indicating normal development in the first 16 weeks of intrauterine life. Alveolar number and acinar complexity suggested that alveolar growth was normal at birth and had continued with only minor impairment after birth. Arterial changes compatible with hypoxic pulmonary hypertension were also present.

Bronchi↗
PubMed1983

Effects of leukotrienes C4 and D4 on glycoprotein and lysozyme secretion by human bronchial mucosa.

The effects of leukotrienes C4 (LTC4) and D4 (LTD4) on the secretion by human bronchial mucosa of [14C]glucosamine-labeled, trichloro-acetic acid/phosphotungstic acid-precipitable glycoprotein and lysozyme were evaluated in vitro. LTC4 and LTD4, in the concentration range of 0.16 to 1600 nM, induced a dose-related increase in the release of radiolabeled glycoprotein, but not of lysozyme. This secretagogue effect was selective for high molecular weight glycoproteins of about 2-5 x 10(6) daltons, and the median effective concentrations (EC50) of LTC4 of 9.4 x 10(-9) M and of LTD4 of 2.44 x 10(-8) M, indicate that these leukotrienes are approximately 100-fold more potent than the cholinergic agonist methacholine. Incubation of [14C]glucosamine-labeled bronchial mucosal explants with LTC4 or LTD4 for six sequential 15-min periods revealed a rapid, progressive decrement in glycoprotein release, compatible with stimulatory action on secretion rather than augmentation of the rate of glycoprotein synthesis. This interpretation is also consistent with the finding that the specific activity (ratio of bound radiolabel: protein content) of the macromolecular glycoprotein secreted by the explants is not changed with stimulation of release by the leukotrienes. Based upon the activity of synthetic leukotriene analogs, the specific C-6 chirality of the sulfidopeptide of LTD4, the presence of a hydroxyl at C-5 and the presence of eicosanoid carbons 9-20 were of no importance for secretagogue activity. These findings contrast with the stereochemical requirements for the spasmogenic response to sulfidopeptide leukotrienes and suggest that leukotriene-induced secretion is not likely to be mediated via a specific receptor.

Bronchi↗
PubMed1983

Regulation of growth and differentiation of a rat hepatoma cell line by the synergistic interactions of hormones and collagenous substrata.

Serum-free, hormonally defined media have been developed for optimal growth of a rat hepatoma cell line. The cells' hormonal requirements for growth are dramatically altered both qualitatively and quantitatively by whether they were plated onto tissue culture plastic or collagenous substrata. On collagenous substrata, the cells required insulin, glucagon, growth hormone, prolactin, and linoleic acid (bound to BSA), and zinc, copper, and selenium. For growth on tissue culture plastic, the cells required the above factors at higher concentrations plus several additional factors: transferrin, hydrocortisone, and triiodothyronine. To ascertain the relative influence of hormones versus substratum on the growth and differentiation of rat hepatoma cells, various parameters of growth and of liver-specific and housekeeping functions were compared in cells grown in serum-free, hormonally supplemented, or serum-supplemented medium and on either tissue culture plastic or type I collagen gels. The substratum was found to be the primary determinant of attachment and survival of the cells. Even in serum-free media, the cells showed attachment and survival efficiencies of 40-50% at low seeding densities and even higher efficiencies at high seeding densities when the cells were plated onto collagenous substrata. However, optimal attachment and survival efficiencies of the cells on collagenous substrata still required either serum or hormonal supplements. On tissue culture plastic, there was no survival of the cells at any seeding density without either serum or hormonal supplements added to the medium. A defined medium designed for cells plated on tissue culture plastic, containing increased levels of hormones plus additional factors over those in the defined medium designed for cells on collagenous substrata, was found to permit attachment and survival of the cells plated into serum-free medium and onto tissue culture plastic. Growth of the cells was influenced by both substrata and hormones. When plated onto collagen gel substrata as compared with tissue culture plastic, the cells required fewer hormones and growth factors in the serum-free, hormone-supplemented media to achieve optimal growth rates. Growth rates of the cells at low and high seeding densities were equivalent in the hormonally and serum-supplemented media as long as comparisons were made on the same substratum and the hormonally supplemented medium used was the one designed for that substratum. For a given medium, either serum or hormonally supplemented, the saturation densities were highest for tissue culture plastic as compared with collagen gels.(ABSTRACT TRUNCATED AT 400 WORDS)

Actins↗
PubMed1983

Role in nude mice of interferon and natural killer cells in inhibiting the tumorigenicity of human hepatocellular carcinoma cells infected with hepatitis B virus.

The human hepatoma cell line, PLC/PRF/5, which is persistently infected with hepatitis B virus (HBV), has integrated HBV-DNA, secretes HBV surface antigen (HBsAg), and does not grow readily in congenitally athymic (nu/nu) mice. The present investigation was undertaken to ascertain whether the low tumorigenicity of this cell line was governed by a host immune response and/or was related to expression of HBsAg. Subcutaneous injection of 4-5 X 10(6) cells into BALB/c nude mice produced localized encapsulated tumors with morphologic features of primary hepatocellular carcinoma in 25% of the animals within 29-40 d. No tumor growth was observed at lower cell inocula. In contrast, SK-HEP-1, an HBV-negative human hepatoma cell line, produced tumors at 1-5 X 10(6) cells inocula in 66% of the animals. Immunosuppression of mice with antilymphocyte serum (ALS) or irradiation increased tumor incidence in mice inoculated with 1 X 10(6) PLC/PRF/5 cells to almost 100% and produced local invasiveness. Immunosuppression also reduced the latency, i.e., time to tumor appearance, and increased mean tumor weight. These results suggest that tumorigenicity was limited by the host immune response. The nature of the response was delineated by treating nude mice challenged with tumor cells with sheep anti-mouse interferon globulin (anti-IFN). When 2 X 10(6) cells were injected, tumor growth occurred in 75% of anti-IFN-treated mice, whereas controls injected with the same number of cells, but not receiving anti-IFN, failed to develop tumors. The tumors in the anti-IFN-treated mice were highly invasive and the latency period until tumor appearance was reduced to 3-5 d. An inverse correlation was found between susceptibility of the hepatoma cells to natural killer (NK) activity in vitro and resistance to tumor growth in vivo. In vitro cytotoxicity for PLC/PRF/5 cells was eliminated by anti-NK 1.1 and complement, establishing the effector cell as an NK cell. NK cell activity 14 d after inoculation of mice with PLC/PRF/5 cells was augmented against PLC/PRF/5 target cells but not against SK-HEP-1 cells. Treatment of mice with ALS, irradiation, or anti-IFN abolished NK activity against PLC/PRF/5 cells. Co-cultivation of nude mouse spleen cells with PLC/PRF/5 but not with HBsAg or SK-HEP-1 cells induced secretion of murine IFNalpha. These results suggest that the IFN/NK cell system may play a role in limiting tumorigenicity and invasiveness of HBV-infected human hepatocellular carcinoma cells by a mechanism similar to that found for other cells persistently infected with viruses.

Animals↗
PubMed1983

The pulmonary vascular lesions of the adult respiratory distress syndrome.

Specimen arteriography, morphometry, and light and electron microscopy were used for examination of the pulmonary vasculature of 22 patients who died with the adult respiratory distress syndrome (ARDS), for the purpose of defining the lesions that contribute to pulmonary hypertension in this setting. The different lesions correlated with the duration rather than the cause of ARDS. Thromboemboli occurred in 21 patients, and macrothrombi found at autopsy correlated with the number of filling defects on antemortem angiography. Acute endothelial injury was documented ultrastructurally even in intermediate and late-stage patients. Fibrocellular intimal obliteration of arteries, veins, and lymphatics and infective vasculitis were prominent in those surviving beyond 10 days. In long-term survivors, tortuous arteries and irregularly dilated capillaries were striking features. Peripheral extension of vascular smooth muscle and a significant increase in the percentage of medial thickness of muscular arteries with duration of ARDS were noted. The pathogenesis and clinical significance of these lesions is discussed.

Angiography↗