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Biomedical subjects

C Gillies

Publications and source records attributed to C Gillies.

28 records · Page 2Linked to original sources
PubMed1985

An in vitro model of leukocyte mediated injury to the corneal epithelium.

To enhance efforts directed at unraveling the role and mechanisms of leukocytes in mediating injury to corneal epithelium, an isolated bovine corneal cup was developed and evaluated. Bovine peripheral leukocytes and lysates were added to the corneal epithelial surface of isolated cornea for various periods after which the degree of morphologic changes and cell damage were assessed using light and electron microscopy. Results of these studies indicate that leukocyte/epithelial cell interactions are characterized by five successive stages: (1) leukocyte adhesion to superficial layer of the epithelium, (2) leukocyte penetration beneath the superficial epithelium, (3) epithelial cell injury, (4) leukocyte phagocytosis of killed epithelial cells and (5) ulceration and total destruction of the full thickness of the epithelial layer. The above sequence appears to be both time and dose dependent; that is epithelial cells exposed to leukocytes for short periods (5-60 minutes) or to low dose levels (10(5) - 10(7) cells/ml) shows leukocyte adhesion and penetration beneath the superficial layer of the epithelium, (stage 1 and 2), while longer exposures (2-3 hours) or higher numbers of leukocytes (10(7) - 10(8) cells/ml), leads to deeper penetration of epithelium by leukocytes and epithelial injury (Stages 3,4,and 5). We also observed that direct contact of intact leukocytes with epithelial cells is apparently necessary to induce this type of injury. These findings demonstrate the ability of leukocytes to destroy corneal epithelial cells and the value of this new ocular model for studies of the basic immunology of ocular inflammation.

Animals↗
PubMed1985

Fibrin: mediator of in vivo and in vitro injury and inflammation.

We examined the role that fibrin deposition and fibrin-associated factors (FAF) play in acute anterior segment inflammatory responses in the rabbit eye. It was demonstrated by immunofluorescence that fibrin represented a major component of the exudative meshwork deposited within the anterior chamber and on leukocyte surfaces therein. Using our in vivo model of endocular inflammation we next demonstrated that fibrin and fibrinogen-derived peptides, but not thrombin, induced inflammatory responses characterized by both leukocyte influx and endothelial cell injury. Fibrin formation within the anterior chamber induced a leukocyte influx consisting primarily of PMN's. Fibrinogen-derived peptides induced primarily a monocyte influx. This dichotomy suggests that multiple inflammatory mediators are elaborated or released during endocular fibrinogenesis and fibrinolysis. To investigate direct effects of fibrin deposition on the corneal endothelial cells (CEC) an in vitro "corneal cup" organ culture model was next developed. Studies comparing various types of mediators demonstrated that only fibrin- derived preparations directly induced CEC injury. Fibrin deposition may thus play multiple roles in endocular inflammation, including the modulation of leukocyte influx, and the direct mediation of corneal endothelial cell injury.

Animals↗
PubMed1985

Congenital alveolar capillary dysplasia: a developmental vascular anomaly causing persistent pulmonary hypertension of the newborn.

The clinical course and histologic findings are presented of an infant with an unusual form of pulmonary dysplasia. Characteristic sonographic findings and progressive hypoxemia led to the diagnosis of persistence of the fetal circulation. The patient expired despite ventilatory and pharmacologic intervention. Postmortem findings of severe pulmonary capillary hypoplasia, despite normal anatomical and biochemical parenchymal maturation, were observed. It is suggested that factors controlling pulmonary capillary maturation may be significantly different from those involved in airway and pulmonary parenchymal development.

Capillaries↗
PubMed1984

Leukocyte-mediated injury to corneal endothelial cells. A model of tissue injury.

Although leukocyte-mediated cell injury has long been suggested as a major mechanism of general tissue injury in acute and chronic inflammation, only limited data have been developed to directly implicate leukocytes in ocular tissue injury. In an effort to unravel the role and mechanisms of leukocyte-mediated injury to the cornea, an isolated corneal cup model was developed. For this model, peripheral bovine leukocytes were added to isolated bovine corneal cultures (corneal cup) in vitro, after which endothelial cell damage and death were evaluated morphologically. In general, corneal endothelial cell swelling was observed within 5-10 minutes after leukocyte exposure, followed by detachment of the corneal endothelium at a 30-75-minute interval. Grossly, the detached endothelium appeared as a floating sheet. Using trypan blue dye exclusion, cells in the sheet were found to be nonviable. When examined ultrastructurally, the sheet was found to consist of leukocytes and endothelial cell debris. Light-microscopic examination of the corneal cup at 5-10 minutes after leukocyte action demonstrated extensive endothelial cell damage, as indicated by cell membrane thickening, cytoplasmic vacuolization, and changes in nuclear shape. These changes in the endothelial cells were confirmed by electron microscopy. Vacuolization and swelling of the endothelium appeared as the first changes, induced by leukocyte interactions with the endothelial cell layer. In general, the endothelial cell nucleus became convoluted, mitochondria swelled, and the endoplasmic reticulum became dilated. These changes become more pronounced as the endothelial cells become detached from the underlying Descemet's membrane. Leukocyte interaction with corneal epithelium, on the other hand, did not result in cell detachment, but only cell damage. These studies demonstrate the ability of leukocytes to denude Descemet's membrane of endothelial cells and destroy corneal endothelial cells in vitro. They also suggest that the corneal cup model system will enhance both morphologic and biochemical evaluation of the mechanisms and consequences of leukocyte-mediated injury to the cornea, and thereby provide new insights into the mechanisms of endocular inflammation and tissue injury in vivo.

Animals↗
PubMed1979

Nemaline (rod) myopathy: a possible cause of rapidly fatal infantile hypotonia.

Two infant siblings (male and female) manifested extreme hypotonia and flaccidity at birth and had a rapidly fatal course. In each, rod-like structures were demonstrated within a variety of skeletal muscles, and accumulations of thin filaments were seen in numerous muscle fibers. The possibility exists that this represents a severe and rapidly fatal form of nemaline myopathy that should be included in the differential diagnosis of infantile hypotonias.

Biopsy↗
PubMedDate not supplied

Nonsurgical management of the infant with gastroesophageal reflux and respiratory problems.

Gastroesophageal reflux (GER), which is associated with respiratory problems such as choking, aspiration, apnea, and chronic respiratory disorders, is a source of significant concern to parents and health care providers. An understanding of the physiologic basis for the association between GER and these disorders enables the nurse practitioner (NP) to act as case manager for these patients. Knowledge of diagnostic procedures and components of management such as positional therapy, feeding techniques, pharmacologic therapy, home monitoring, and social support strategies enables the NP to collaborate effectively with other members of the health care team in providing nonsurgical treatment for these infants.

Continuity of Patient Care↗