Biomedical subjects

E Y Chi

Publications and source records attributed to E Y Chi.

At least 91 records · Page 5Linked to original sources

PubMed1985

Changes in lung volume and deflation stability in hyaline membrane disease.

Total lung capacity (TLC), inspiratory capacity, functional residual capacity, and deflation stability of prematurely delivered Macaca nemestrina primates were measured serially during development of, and recovery from, hyaline membrane disease (HMD) to relate changes in lung volumes to changes in deflation stability. Gestational age-matched primates that did not develop HMD served as controls. TLC, measured by N2 washout, fell at 2-12 h of age (P less than 0.0001) in animals with HMD and remained lower than controls for at least 48 h (P less than 0.005). However, deflation stability, defined as the fraction of TLC remaining upon deflation to 10 cm H2O, improved from 2 to 12 h of age (P less than 0.001). Postmortem studies confirm the measurements of TLC and deflation stability and provide evidence that interstitial thickening and obstruction of air spaces with debris may be partially responsible for the observed changes in TLC in primates that develop HMD. It has been assumed that TLC is reduced in HMD because of atelectasis from elevated alveolar surface tension, but the sequential measurements in these animals suggest that other mechanisms also contribute.

Animals↗

PubMed1985

Intermediate filaments in the developing type II cell of fetal monkey lung.

Anticytokeratin monoclonal antibody was used to study epithelial cell development in fetal monkey lungs taken from animals of different ages. It is well established that the overall maturity of fetal lung depends greatly on the maturation of type II epithelial cells in the alveolus. In this study, we have correlated the cytokeratin phenotype of mammalian epithelial cells with pneumocyte maturation. We show that differentiation and maturation of the type II cell is related to intermediate filament expression. Twenty-four fetal monkeys (Macaca nemestrina) were delivered by cesarean section at a gestational age of 135-140 days (term = 168 days) and divided into two groups. One group of animals was sacrificed during the first 3 hr of life, and the other group was maintained in incubators for 92-120 hr. Anticytokeratin monoclonal antibody recognizes only alveolar type I and type II epithelial cells. In the first 3 hr of life, the cytokeratin was localized only at the alveolar surface and at the cytoplasmic periphery of the type II cells of these premature animals. However, at the age of 92-120 hr, the epithelia in the lungs reacted more intensely than they did during the first 3 hr. Electron microscopy revealed and confirmed that the type II cells were matured and abundant intermediate filaments appeared in the cytoplasm. The filaments appeared to form either aggregates or parallel filament bundles and few were closely associated with the lamellar bodies. In the immature type II cells at 0-3 hr of life, few intermediate filaments could be localized in the cytoplasm, and no parallel filament bundle was observed, though many appeared in the 92-120 hr lungs. This suggests that the intermediate filaments have a functional significance in the development and maturation of the type II cell. The location and stability of keratin filaments in type II cells may confer the structural strength necessary for cells covering a free surface in the alveoli during lung maturation.

Animals↗

PubMed1985

Ultrastructural characterization and morphometric analysis of human eosinophil degranulation.

Human eosinophil degranulation induced by the calcium ionophore A23187 was examined by transmission and scanning electron microscopy, and morphometric analysis. After incubation with A23187, eosinophil degranulation was characterized by granule movement to the cell periphery and pentalaminar membrane fusion between perigranular and plasma membranes. As adjacent granules fused they became swollen and vesiculated; their contents were released into large cytoplasmic vacuoles, which communicated extracellulary through surface pores. Extracellular release of eosinophil peroxidase without release of lactate dehydrogenase occurred after treatment with the ionophore. Morphometric analysis of the transmission electron micrographs indicated a significant reduction of cytoplasmic granules in the degranulated cells. There was a loss primarily of larger granules and alternatively an increase in the smaller-sized granules (less than 0.1 micron2), suggesting the possibility that exocytosis of mature granules is accompanied by new cytoplasmic granule formation.

Calcimycin↗

PubMed1985

The ultrastructural study of glycogen and lamellar bodies in the development of fetal monkey lung.

Developing fetal monkey lung tissues were studied at the gestational period of 135-145 days. In general, glycogen is distributed throughout the cytoplasm of the type II pneumocytes at this gestational period. It is of interest that we found a structural relationship between glycogen particles and lamellar body formation in the type II pneumocytes. The glycogen particles were found inside the electron-dense pre-granules and the immature lamellar bodies. Some of the fully matured lamellar bodies also contained glycogen. This phenomenon has not been observed previously, and it supports the evidence that there is a close and direct structural relationship between glycogen and the development of lamellar bodies at this stage of lung development in the type II pneumocytes.

Animals↗

PubMed1984

Ultrastructure of mast cell degranulation induced by eosinophil peroxidase: Use of diaminobenzidine cytochemistry by scanning electron microscopy.

It has been previously demonstrated that eosinophil peroxidase (EPO) when supplemented with hydrogen peroxide and a halide induces noncytotoxic mast cell degranulation. Using a more highly purified EPO preparation, the ultrastructure of EPO-induced mast cell secretion has been studied using transmission and scanning electron microscopy and freeze-fracture techniques. At relatively low EPO concentrations, secretory changes were comparable to those caused by other mast cell secretagogues. Swollen and less electron-dense granules were seen in intracellular channels, some of which opened to the outside of the cell. EPO stimulation led to bulging of the surface membrane by submembranous granules and formation of pores in the cell surface that also contained fewer villous projections than control cells. During the secretory process, plasma membrane bulges were depleted of intramembranous particles in both the E and P faces of the apical regions of the perigranular and plasma membranes. Higher EPO concentrations caused a marked cytotoxic disruption of the mast cells. Diaminobenzidine cytochemistry was used to detect EPO reaction products on the mast cell surface by scanning electron microscopy; this technique should prove useful in detecting peroxidase reaction products on a variety of target cells.

Animals↗

PubMed1984

Human neutrophil-mediated killing of schistosomula of Schistosoma mansoni: augmentation by schistosomal binding of eosinophil peroxidase.

Eosinophil peroxidase (EPO) is a major component of the large cytoplasmic granules of eosinophils, and is released onto the surface of schistosomula when eosinophils adhere to antibody and complement coated organisms. EPO is a strongly cationic protein, which can bind to the surface of schistosomula with retention of peroxidatic activity. The binding per se was not toxic to the organisms under our conditions, but EPO-coated schistosomula were rapidly killed when H2O2 and halide were added, under conditions in which uncoated schistosomula were unaffected. The toxicity of the surface-bound EPO system was not significantly inhibited by albumin (20 mg/ml), in contrast to the complete inhibition by this concentration of protein when the EPO was free in solution. Purified polymorphonuclear leukocytes (PMNs) from normal donors were toxic to uncoated schistosomula in medium containing antischistosomal antibody and complement, and this toxicity was significantly increased when EPO was bound to the surface of the organisms. The toxicity of PMNs to EPO-coated schistosomula was inhibited but not abolished by the hemeprotein inhibitor azide. This is compatible with the involvement of surface-bound EPO in an enzymatic attack on the organism, utilizing H2O2 generated by PMNs stimulated by adherence to antibody and complement-coated schistosomula. PMN adherence to schistosomula is increased by surface-bound EPO, and this also may contribute to the enhancement of neutrophil-mediated toxicity by EPO. These findings indicate a mechanism by which two inflammatory cells, the eosinophil and neutrophil, may interact to enhance the destruction of a target organism.

Animals↗

PubMed1983

Preparation of multivesicular liposomes.

A novel type of liposome, named here multivesicular liposomes, was prepared by evaporation of organic solvents from chloroform-ether spherules suspended in water. Within each spherule were numerous water droplets that contained solutes to be trapped in liposomes upon solvent evaporation. Liposome preparations of different average diameters were made, varying from 29 +/- 10 microns to 5.6 +/- 1.7 microns. The liposomes were morphologically characterized by light microscopy and transmission electron microscopy. Materials successfully trapped within the liposomes ranged in molecular size from glucose to nucleic acids. Extremely high percentages of encapsulation (up to 89%) were achieved.

Chemical Phenomena↗

PubMed1983

Sequestration and release of polycyclic aromatic hydrocarbons by vertebrate cells in vitro.

Vertebrate fibroblasts grown in vitro and exposed to various concentrations of the mutagen/carcinogen benzo(a)pyrene (B(a)P) internalized the compound and recrystallized it in lysosomes by 6-18 h postexposure. This phenomenon occurred when B(a)P at or above 10 micrograms/ml was introduced to the culture medium in a solvent such as DMSO or acetone but not when introduced dissolved in serum. Likewise, high fetal bovine serum concentrations in the culture medium (greater than 20%) as well as human serum (10%) inhibited crystal formation, presumably owing to lipid competition for the compound. Electron-microscopic observations of the cells during the uptake and crystal forming periods revealed that the cell membrane became altered within 3 h of exposure to B(a)P. This was followed by a return to normal of the membrane and the appearance of vesicles within the cell by 6-8 h. The vesicles then became filled with crystals which continued to grow while in the presence of B(a)P and disappeared when the cells were exposed to B(a)P-free culture medium or serum lipids. Introduction of B(a)P into culture medium containing delipidated serum resulted in crystal formation indistinguishable from that which occurred when whole serum was present. Crystals were not formed when total lipoprotein and the lipoprotein components VLDL, LDL, HDL2, and HDL3 were used as solvents for B(a)P. The process of crystal formation was inhibited by the addition of 10(-3) M KCN, and removal of the crystals was dependent on the concentration of lipoprotein in the culture medium.

Acid Phosphatase↗

PubMed1983

Ventilation-perfusion relationships after hemorrhage and resuscitation: an inert gas analysis.

Previous investigations suggest that ventilation-perfusion (VA/Q) relationships after hemorrhagic shock are primarily dependent on regional distribution of pulmonary blood flow and implicated early VA/Q heterogeneity secondary to disproportionate redistribution of pulmonary blood flow to dependent lung regions. Multiple inert gas elimination analysis, as described by Wagner et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 36: 588-599, 1974), was applied to a standard hemorrhagic shock preparation to test this hypothesis. Soon after hemorrhage, VA/Q distributions shifted homogeneously into high VA/Q compartments, preserving base-line VA/Q relationships around a new mean VA/Q ratio. Although the mean VA/Q and VA/Q distribution returned to base line after resuscitation with autologous blood, absolute dead space ventilation persisted. Gas exchange defects included increased Bohr dead space ventilation, which could be attributed to 1) a homogeneous shift of VA/Q distributions into high VA/Q compartments, and 2) new absolute dead space ventilation associated with observed intravascular leukostasis and vascular occlusion. In contrast to previous investigations, these data suggest that VA/Q heterogeneity does not occur after hemorrhage, but rather pulmonary blood flow decreases proportionately throughout all lung regions, preserving base-line VA/Q patterns around a new mean VA/Q ratio.

Animals↗

PubMed1983

Comparative effects of inhaled volcanic ash and quartz in rats.

To investigate the relative toxicities of inhaled volcanic ash and quartz, we exposed matched groups of rats to either respirable volcanic ash (100 mg/m3), quartz (100 mg/m3), or clean air only for 6 h daily for 10 days. Thereafter, we examined animals sequentially for as long as 9 months, and measured changes in lung histopathologic aspects, air-space cells and lipids, and lung density. Neutron activation studies demonstrated that 3.3% of the inhaled daily dose of volcanic ash was detectable in the lung parenchyma. Volcanic ash was less toxic to the lung than quartz. Immediately after exposure, the lungs of animals treated with volcanic ash had ultrastructural evidence of damage to type I pneumocytes and early alveolar edema formation. By contrast, quartz-treated animals had an intense acute injury, with intraalveolar accumulation of lipid, protein, macrophages, and granulocytes. Six months after exposure, animals treated with volcanic ash had moderate interstitial thickening and fibrosis, whereas the quartz-treated animals had severe pulmonary fibrosis. Quartz, but not volcanic ash, caused a marked increase in lavage granulocytes, protein, and phospholipids. Lung density increased in quartz-exposed, but not in volcanic-ash-exposed animals. These data indicate that volcanic ash is less harmful to the lung parenchyma than is quartz. Persons exposed to volcanic ash for short periods are at much less risk of subsequent lung damage than are those who are exposed to similar amounts of quartz in the workplace.

Absorptiometry, Photon↗

PubMed1983

Horse eosinophil degranulation induced by the ionophore A23187. Ultrastructure and role of phospholipase A2.

Horse eosinophils stimulated with the calcium ionophore A23187 were examined by transmission and scanning electron microscopy. Secretion was characterized by granule movement to the cell periphery and fusion of adjacent granules. The granules became swollen and less electron-dense as their contents were released into large intracellular vacuoles, which opened to the outside of the cell through surface pores. A23187-induced eosinophil peroxidase (EPO) release, as measured by guaiacol oxidation, was blocked by eicosa-5,8,11,14-tetraynoic acid (ETYA) (which inhibits both the cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism) but not by indomethacin (which inhibits only the cyclooxygenase pathway). Highly purified porcine phospholipase A2 induced noncytotoxic eosinophil degranulation (as measured by the release of EPO without the concomitant release of the cytoplasmic marker lactate dehydrogenase), which was blocked by pretreatment of the enzyme with the phospholipase A2 inhibitor 4-bromophenacyl bromide. These results suggest that calcium-dependent activation of phospholipase A2 and generation of lipoxygenase products of arachidonic acid metabolism are important in the initiation of eosinophil degranulation.

Acetophenones↗

PubMed1982

Phospholipase A2-induced rat mast cell secretion. Role of arachidonic acid metabolites.

Highly purified porcine phospholipase A2 induced noncytotoxic rat cell degranulation, as indicated by release of histamine without release of the cytoplasmic marker lactate dehydrogenase. Ultrastructural studies using transmission, scanning, and freeze fracture electron microscopic techniques indicated that phospholipase A2-induced degranulation was comparable to that caused by other mast cell secretagogues. Secretory changes noted were fusion of perigranular and plasma membranes, formation of vacuoles containing less electron-dense granules, and exocytosis of the altered granules through pores in the plasma membrane, without alteration in other intracellular organelles. The earliest consistent feature of the exocytotic process (within 1 minute) was the formation of plasma membrane bulges overlying cytoplasmic granules, with depletion of intramembranous particles from the bulges and a reduction in surface microridges. Phospholipase A2-induced mast cell degranulation was blocked by the phospholipase inhibitor 4-bromophenacyl bromide and by eicosa-5,8,11,14-tetraynoic acid (ETYA) but not by indomethacin. Since ETYA inhibits both the cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism and indomethacin only the cyclooxygenase pathway, these findings are compatible with the mediation of phospholipase A2-induced mast cell degranulation by a lipoxygenase product of the released arachidonic acid ETYA, however, may inhibit phospholipase activity directly and thus affect degranulation by phospholipase A2 in this way. These studies indicate that phospholipase A2 can induce mast cell degranulation and provides evidence that is compatible with, but not proof of, mediation of this process by a lipoxygenase product of arachidonic acid metabolism.

Animals↗

PubMed1981

Mast cell-mediated tumor-cell cytotoxicity. Role of the peroxidase system.

Mast cells, when supplemented with H2O2 and iodide, are cytotoxic to mammalian tumor cells as determined by 51Cr release, and transmission and scanning electron microscopy. H2O2 at the concentration employed (10(-4) M) initiates mast cell degranulation, and mast cell granules (MCG), which contain a small amount of endogenous peroxidase activity, are toxic to tumor cells when combined with H2O2 and iodide. This toxicity is greatly increased by binding eosinophil peroxidase (EPO) to the MCG surface. Each component of the mast cell, MCG, or MCG-EPO system was required and toxicity was inhibited by the addition of the hemeprotein inhibitors azide or aminotriazole, which is compatible with a requirement for peroxidase in the cytotoxic reaction. A sequence of reactions is proposed in which mast cells, stimulated to release their granules by H2O2 generated by adjacent phagocytes, react with H2O2 and a halide to damage tumor cells. EPO release from eosinophils may contribute to this sequence of reactions, both by stimulation of H2O2-induced mast cell secretion and by combination with MCG to form a complex with augmented tumoricidal activity. These rections may play a role in the host defense against neoplasms.

Animals↗

PubMed1980

Eosinophil peroxidase-induced mast cell secretion.

Eosinophil peroxidase (EPO) at relatively low levels (4-30 mU), when supplemented with H2O2 and a halide, induced mast cell degranulation. Histamine release occurred without concomitant release of the cytoplasmic marker lactic dehydrogenase (LDH), and this, together with ultrastructural studies, indicated a noncytotoxic effect comparable with that induced by other mast cell secretagogues. At pH 7.4, iodide was effective at concentrations down to 10(-5) M, and although chloride alone was ineffective at 0.1 M, a combination of 0.1 M chloride and 10(-6) iodide could meet the halide requirement. Chloride alone was effective at pH 6.5 and 6.0. EPO could be replaced by myeloperoxidase. When the EPO level was increased to 100 mU, combination with H2O2- and iodide-induced cytotoxic histamine release as indicated by concomitant LDH release and ultrastructural evidence of cell disruption. This cytotoxic response reverted to a secretory one on the addition of albumin. Peroxidase was detected on the surface of extruded granules by diaminobenzidine cytochemistry. The mast cell granule (MCG)/EPO complex when supplemented with H2O2 and iodide was more effective than free EPO in the stimulation of mast cell secretion. The stimulation of mast cell mediator release by the EPO-H2O2-halide system and the formation of MCG/EPO complexes with augmented cytotoxic activity may influence the adjacent inflammatory response.

Animals↗

PubMed1980

Ultrastructural and histochemical studies of conjunctival concretions.

Ultrastructural and histochemical studies were performed on conjunctival concretions (yellow spots in the tarsal conjunctiva) from two patients who had associated atopic keratoconjunctivitis and posttrachomatous degeneration. By electron microscopy, these concretions were composed of finely granular material and membranous debris accumulating in the conjunctival subepithelium. Histochemically, concretions stained strongly positive for phospholipid and elastin, weakly positive for neutral polysaccharides and lipid, and were negative for amyloid, collagen, glycogen, iron, mucopolysaccharides, RNA, and DNA. In view of the absence of both calcium and phosphate in the accumulated material, the use of the term "lithiasis" is misleading and should be avoided. These findings support a hypothesis that concretions that follow chronic conjunctivitis represent products of cellular degeneration.

Aged↗

PubMed1980

Surface replicas of aortic endothelium.

Relief casting of critical point-dried aortic endothelium provides high resolution images of the cell surface, revealing details not readily apparent by scanning electron microscopy or conventional transmission electron microscopy. These surface replicas show the cell junction to be highly interfolded. Caveoli are present, although some cells have many while others have few. Moreover, the caveoli appear as shallow pits, suggesting that the opening of the caveolus is filled or covered. Finally, the replicas show other surface details including microvilli and distinct cell surface textures.

Animals↗

PubMed1978

Linear arrays of intramembranous particles in pulmonary tubular myelin.

Freeze-fracture preparations of tubular myelin in edematous rat lungs reveal the presence of linear arrays of intramembranous particles. The lines of particles are approximately 50 nm apart and appear to correspond to the intersections of sheets of bilayer membranes. Particles are not seen in lamellar bodies but become evident first in membranes transitional between lamellar bodies and tubular myelin. It is proposed that the particles represent a hydrophobic protein that plays a significant role in the organization of tubular myelin.

Animals↗

PubMed1978

Mast cell secretion: membrane events.

Stimulation of secretion with A23187 circumvents the usual mechanism of stimulation of secretion by direct mediation of an increase in cytoplasmic Ca++ and thereby permits study of the terminal components of the secretory process in which granules are externalized by membrane fusion events. Two alterations in the plasma membrane precede fusion: the formation of bulges and the aggregation of intramembranous particles. These changes require a permissive level of ATP and are sensitive to reagents that bind to intracellular protein sulfhydryl groups. They seem not to be attributable to a direct effect of Ca++ on membrane phospholipids. The cell components responsive to Ca++ and responsible for the alterations in the membrane are not known; neither microtubules nor actin filaments seem to qualify.

Adenosine Triphosphate↗