Biomedical subjects

J V Jester

Publications and source records attributed to J V Jester.

At least 109 records · Page 6Linked to original sources

PubMed1988

Return of human corneal sensitivity after penetrating keratoplasty.

To evaluate the reinnervation of corneal grafts, we studied 91 eyes of 79 patients for the return of sensitivity one month to ten years following penetrating keratoplasty for various corneal disorders including keratoconus, Fuchs' dystrophy, herpes simplex keratitis, aphakic and pseudophakic bullous keratopathy, glaucoma, trauma, and interstitial keratitis. Using the Cochet-Bonnet esthesiometer, a sensation was recorded in the center of the graft no earlier than 18 months. We found a progressive return of sensitivity from the periphery toward the center of the graft. Regression analysis indicated a rate of return of sensitivity that averaged 0.029 mm/mo for each diagnostic category except herpes simplex keratitis. The slope of the return of sensitivity in the group with herpes simplex keratitis was essentially flat, showing no central progression. None of the eight patients with herpes simplex keratitis had a sensation recorded further than 0.5 mm from the wound margin.

Cornea↗

PubMed1988

Essential iris atrophy. A clinical, immunohistologic, and electron microscopic study in an enucleated eye.

A 29-year-old woman had unilateral essential iris atrophy, corneal endothelial changes, and absolute glaucoma. The enucleated eye was examined by routine light microscopy. Separate portions of unfixed fresh frozen cornea were sectioned and reacted with monoclonal antibodies against keratins, vimentin, and inflammatory cell markers. Stains for filamentous actin (f-actin) were performed using the 7-nitro-benz-2-oxa-1,3-diazolylphallacidin (NBD phallacidin) probe. In addition, portions of cornea and iris were examined by scanning and transmission electron microscopy. Immunocytochemical stains with anti-keratin antibodies showed reactivity only in the corneal epithelium of the patient and normal control. Immunoreactivity with anti-vimentin antibodies was observed in corneal endothelium and keratocytes of the patient and control, but was negative in the epithelium. Staining for f-actin appeared more pronounced in the corneal endothelium of the patient. Scanning electron microscopy of the corneal endothelium showed irregularity in cell size and shape and filopodial processes characteristic of migrating cells. Transmission electron microscopy disclosed abnormalities of Descemet's membrane and endothelium with a posterior collagenous layer. The corneal endothelium displayed normal junctional complexes without desmosomal junctions or increased microvillus projections. Increased 10-nm cytoplasmic filaments were noted consistent with the expression of vimentin. Occasional chronic inflammatory cells perturbed the corneal endothelium and were detected within the endothelial layer. Alterations in the endothelium and Descemet's membrane suggest the acquired nature of this disease.

Actins↗

PubMed1988

Meibomian gland changes in the rhino (hrrhhrrh) mouse.

The rhino mouse, a single gene recessive mutation, is characterized by abnormal epidermal differentiation and maturation leading to the loss of hair at 1 month of age as well as follicular and epidermal hyperkeratoses. We evaluated the lids and corneas of nine rhino mice and their normal litter mates at various ages from 3 months to 1 year. Tissue specimens were studied by light microscopy, scanning and transmission electron microscopy as well as immunoperoxidase using a polyclonal rabbit anti-keratin antibody. At 3 months of age there was a thickening and hyperkeratinization of the palpebral epidermis which extended into and included the meibomian gland central duct. Whereas in the skin, hyperkeratinization is followed by follicular hyperkeratosis and dermal cyst formation, in the meibomian gland, ductal hyperkeratinization appeared to lead to loss of well developed acini followed by atrophy of the gland at 1 year as confirmed by immunostaining for keratin proteins. Scanning electron microscopy revealed marked plugging of the meibomian gland orifice with keratinized cells or debris in contrast to the patent orifice of the normal lid. Ocular surface changes included the presence of a whitish exudate covering the surface of the eye and increased numbers of preexfoliative corneal epithelial cells. These findings suggest that the rhino mouse may represents the first naturally occurring disorder of the meibomian gland.

Animals↗

PubMed1987

Immunopathology of acute experimental histoplasmic choroiditis in the primate.

The immunopathologic features of experimental acute histoplasmic choroiditis were studied in the nonhuman primate. Using an indirect immunoperoxidase technique, a panel of hybridoma-derived anti-human monoclonal antibodies, recognizing distinct lymphoid cell and macrophage surface antigens, have been adapted for use in the primate system. Twenty-two individual foci of histoplasmic choroiditis from five eyes were studied at time periods from 20 to 60 days post intracarotid injection of yeast phase Histoplasma capsulatum. A mononuclear and granulocytic cell infiltration was seen in all lesions. The predominant cell type was the CAPPEL+ T lymphocyte (suppressor/cytotoxic subset). Other cell types found in smaller numbers were OKT4+ T cells (helper/inducer subset), OK7+ (peripheral B lymphocytes), IgD+ (mantle B cells) and OKM1+ cells (macrophages and polymorphonuclear leukocytes). Herein, we present immunopathologic data on the acute phase of experimental ocular histoplasmosis.

Acute Disease↗

PubMed1987

Characterization of avascular corneal wound healing fibroblasts. New insights into the myofibroblast.

The characteristics and derivation of corneal wound healing fibroblasts (myofibroblasts) were evaluated by studying the temporal changes in the cellular actin distribution of corneal fibrocytes following full thickness 3-mm diameter central corneal wounds in the rabbit. Under certain conditions these wounds heal without neovascularization, allowing for the detailed analysis of invading fibroblasts with minimal contamination by other cell types. The authors employed transmission electron microscopy to localize microfilaments, fluorescent microscopy using NBD-phallacidin, a mushroom toxin which binds specifically to f-actin and oligomeres of g-actin, to localize actin filaments, and isoelectric focusing gels to characterize actin isotypes. During the early stages of wound healing (1-7 days) there is a gradual change in the corneal fibrocytes adjacent to the wound margin characterized by the development of extensive rough endoplasmic reticulum, microtubules, a prominent Golgi apparatus, and a cortical microfilament network. This is in contrast to the normal fibrocyte, which, for the most part, lacks these structures. The development of microfilaments correlated with increased NBD-phallacidin fluorescence of fibrocytes adjacent to the wound as compared with fibrocytes farther removed from the site of injury. Fibroblasts appearing within the wound from 7 days to 2 months after injury had ultrastructural characteristics similar to those of myofibroblasts, including parallel arrays of microfilaments, stress fibers and cell-cell, cell-matrix attachments. Furthermore, these cells stained intensely with NBD-phallacidin, supporting the ultrastructural findings. At 1 month after injury, cells contained within the wound possessed predominantly nonmuscle isoactins (gamma) as seen by silver staining of isoelectric focusing gels, but little or no (smooth muscle) isoactins could be detected. Moreover, no significant differences could be detected between electrophoretic profiles obtained from wounded versus normal corneas. These morphologic and biochemical data suggest that the corneal fibrocyte may develop into a fibroblastlike cell similar to the myofibroblast, and is characterized by a marked increase in filamentous actin.

Actins↗

PubMed1986

Immunofluorescent detection of Histoplasma capsulatum in primate experimental ocular histoplasmosis.

We have developed a polyclonal anti-Histoplasma capsulatum antibody to detect H. capsulatum antigens in ocular tissue. Antibodies were specific for H. capsulatum as determined by enzyme linked immunosorbent assay and immunoprecipitation. A total of 21 choroidal histoplasmic lesions in 4 primate eyes (Macaca speciosa and Macaca mulatta), taken at various times from 14 to 60 days after the internal carotid artery injection of yeast phase organisms, were evaluated. Using an indirect immunofluorescent technique, these antibodies stained yeast phase organisms within acute choroidal lesions at 14 days after infection. By 60 days intact organisms were no longer detected; occasional cells, however, contained intracellular inclusions that stained with these antibodies. Although yeast phase organisms are rapidly cleared from the primate choroid, these data indicate that residual H. capsulatum antigens may remain in choroidal lesions after the acute infectious stage. These findings are consistent with the hypothesis that H. capsulatum antigens play a role in the immunologic reactivation of atrophic choroidal scars in ocular histoplasmosis.

Animals↗

PubMed1985

Subretinal neovascularization after experimental ocular histoplasmosis in a subhuman primate.

Subretinal neovascularization was demonstrated in a subhuman primate eye (Macaca speciosa) one year after the internal carotid injection of yeast-phase Histoplasma capsulatum. In this animal model of ocular histoplasmosis, initial injection of viable H. capsulatum results in the development of self-limiting acute multifocal choroiditis. Acute lesions resolve within six months, forming chorioretinal scars that are clinically similar to human histo spots. Detailed ultrastructural study of a peripapillary scar 30 months after the injection showed the presence of subretinal neovascularization located between Bruch's membrane and degenerated retinal inner segments. These vessels appeared to be continuous, had tight junctional complexes, and a well-developed basal lamina with occasional pericytes. Failure of fluorescein angiography to demonstrate the presence of this neovascular net may be explained by the presence of tight junctions within the subretinal capillaries.

Animals↗

PubMed1985

In vivo transillumination biomicroscopy and photography of meibomian gland dysfunction. A clinical study.

Meibomian gland transillumination biomicroscopy and infrared photography were performed on 18 patients with clinically evident meibomian gland dysfunction (MGD) and dermatologic rosacea, 22 patients having MGD without evidence of dermatologic rosacea, and 15 unaffected individuals who served as controls. All patients having clinical signs of MGD demonstrated morphologic abnormalities of their meibomian glands by transilluminated biomicroscopy. Patients without dermatologic rosacea were noted to have varying degrees of gland distortion. Moreover, infrared photography documented a loss of the normal grape-like clusters of dark spots that represent the gland, suggesting a loss of glandular acini. Patients with dermatologic rosacea had more severe alterations, including marked distortion and loss of normal gland anatomy. There were no such abnormalities in clinically unaffected individuals. These data demonstrate that transilluminated biomicroscopy and infrared photography have the ability to identify a spectrum of morphologic alterations of the meibomian glands in MGD patients. The authors suggest that these techniques could be used to classify clinical MGD based upon the presence or absence of identifiable meibomian gland abnormalities.

Eyelid Diseases↗

PubMed1985

Change in epithelial keratin expression during healing of rabbit corneal wounds.

Corneal epithelial wound healing following full-thickness trephination and transcorneal freeze injury was studied by electron microscopy and immunofluorescent microscopy using monoclonal antibodies AE1, AE2, and AE3 to human epithelial keratin. Wounds were evaluated at various time intervals between 4 hr and 2 mo after injury. By scanning and transmission electron microscopy, epithelial migration was evident 4 hr after injury and was characterized by thinning of the epithelium and extension of filopodial processes. AE1 monoclonal antibody, which stains specifically the superficial cells of normal corneal epithelium, reacted to cells at the leading edge of the migrating epithelium. By 24 hr, all cells migrating over the wound displayed positive fluorescence with AE1 while the epithelium over the undamaged cornea exhibited normal fluorescence limited to the superficial epithelial cells. In full-thickness corneal wounds, reepithelialization was complete by 1-2 wk; however, all epithelial cells covering the wound remained positive for the AE1 antikeratin antibody. By 2 mo, the AE1 fluorescence returned to normal. In transcorneal freeze injuries, reepithelialization was complete by 4 to 7 days after injury, with all cells overlying the wound reacting with the AE1 antibody. By 2 wk after freeze injury, all epithelial cells appeared to express a normal AE1 staining pattern. No change was noted in the fluorescent distribution of either AE2 antibody, which did not react with the corneal epithelium, or AE3, which reacts with all corneal epithelial cells. These results suggest that healing of corneal epithelial wounds involves changes in keratin expression of the corneal epithelium.

Animals↗

PubMed1985

Photodynamic therapy of intraocular tumors: examination of hematoporphyrin derivative distribution and long-term damage in rabbit ocular tissue.

Studies were performed to determine the distribution of hematoporphyrin derivative (HPD) in ocular structures and to characterize long-term damage associated with ocular HPD photodynamic therapy. Pigmented rabbits with an amelanotic melanoma heterotransplanted to the iris were used to obtain quantitative tissue levels of HPD as well as to document HPD localization by fluorescence microscopy. HPD was administered i.v., and tissue concentrations of HPD were determined by spectrofluorometry following porphyrin extraction. Vascular structures such as the tumor, iris, and choroid-retina as well as the aqueous fluid from eyes containing tumors demonstrated rapid HPD localization. The sclera had minimal HPD uptake, and the drug was not detected in avascular structures such as the lens or cornea. HPD was cleared from all ocular structures except the tumor and choroid-retina by 24 h following injection. Fluorescence microscopy data indicate that HPD remained in the avascular photoreceptor cell outer segments of the retina. Long-term damage was documented in rabbits which received HPD photodynamic therapy to a 1-sq cm area of retina via transpupillary light delivery. Acute damage to the exposed area of retina (in the form of a chorioretinal scar) could be induced. This damage was permanent but not progressive. Lens opacities were not observed, and the cornea, aqueous, and vitreous remained clear on all test eyes. The results from these studies suggest that HPD photodynamic therapy may provide a selective and safe approach to the treatment of ocular tumors.

Animals↗

PubMed1985

In vitro contractility of avascular corneal wounds in rabbit eyes.

Contraction of corneal wounds has been the topic of recent speculation, particularly in reference to regression of corneal flattening following radial keratotomy. In an animal model of corneal wound fibroplasia, we offer the first demonstration of in vitro contractility by avascular corneal wound tissue. Three millimeter diameter full-thickness corneal trephine wounds were made in 17 New Zealand white rabbit eyes. The animals were killed and specimens were extracted 3-4 wk postinjury. Contractile responses of corneal wounds were measured on a microdynagauge force transducer. When exposed to serotonin, epinephrine or norepinephrine corneal wounds showed contractions reaching maximum force of 20-100 mg with a peak response obtained within 5-10 min and persisting several hours. Normal corneas did not respond to any agent. All normal iris muscle specimens contracted to acetylcholine exhibiting peak responses of 30-60 mg of force within 5 sec decaying over the following 10-20 min. This is different from corneal wounds which fail to respond to acetylcholine (P less than 0.005). These data suggest that avascular corneal wounds possess contractile properties.

Animals↗

PubMed1984

Endothelial cell loss following radial keratotomy in a primate model.

The effect of radial keratotomy on the corneal endothelium of subhuman primates was studied by serial specular microscopy and histopathology. Fixed-frame analysis of specular micrographs of 13 operated eyes at one month after surgery revealed an endothelial cell loss of 13% (+/- 4%). Follow-up of all 13 eyes for six months disclosed no statistically significant progressive endothelial cell loss. Similarly, no significant loss could be demonstrated in five eyes followed up for 18 months and two eyes followed up four years after surgery. Variable frame analyses of specular micrographs of all 13 unoperated eyes followed up for six months also did not suggest progressive endothelial cell loss following radial keratotomy. Histopathology and ultrastructural studies of corneas undergoing radial keratotomy disclosed no abnormalities suggesting ongoing endothelial cell damage. These findings suggest that radial keratotomy produces an acute postoperative endothelial cell loss that is nonprogressive. Much longer term follow-up with larger numbers of subjects is necessary before the ultimate delayed effects of radial keratotomy on the endothelium can be determined.

Animals↗

PubMed1984

Keratophakia and keratomileusis: histopathologic, ultrastructural, and experimental studies.

We present ultrastructural findings in two cases, one of keratophakia (9 months postoperatively) and one of keratomileusis (1 year, 7 months post-operatively), which best demonstrate the pathologic changes we observed in six cases of cryorefractive surgery. In addition, we studied a rabbit model of keratophakia which appears to exhibit similar features to that of human keratophakia. In the keratomileusis cases, there were marked abnormalities, including deposition of redundant basal lamina, loss of Bowman's membrane and deposition of a 6 nm fibrillar material in areas devoid of Bowman's membrane. In keratophakia lenticule we noted the absence of keratocyte regeneration, abnormal deposition of long-spacing collagen, and the presence of necrotic cellular debris. In experimental keratophakia, little to no evidence of keratocyte regeneration was evident 4 months after surgery. Keratophakia lenticules implanted into actively regenerating corneas induced by freeze injury exhibit only a slight increase in the number of keratocytes migrating into the donor tissue, suggesting that implants lack a primary factor necessary for keratocyte regeneration. Immunofluorescent localization of fibronectin and fibrinogen demonstrated absence of these factors in normal host stroma, implanted lenticules and freeze injured corneal stroma. Actively migrating fibroblasts, however, did react positively for fibronectin, suggesting that these cells synthesize and secrete fibronectin during regeneration. These results do not support a role for soluble fibronectin or fibrinogen in keratocyte repopulation.

Adult↗

PubMed1984

Hematoporphyrin derivative photoradiation induced damage to normal and tumor tissue of the pigmented rabbit eye.

Cytotoxicity induced by hematoporphyrin derivative (HpD) photoradiation in both normal and experimental tumor tissue of pigmented rabbit eyes has been examined. In addition, documentation of HpD induced fluorescence in ocular structures has also been obtained. Acute normal ocular tissue toxicity studies demonstrated that HpD (1-10 mg HpD/kg) followed 48 hours later by a transpupil irradiation of red light (635 nm, 36-90 J/cm2) resulted in demarcated areas of retinal damage. Long term (chronic) toxicity studies have shown that the initial damage to the retina was permanent but that no damage to the cornea, lens or vitreous could be observed during a 16 month follow-up. Visual and histological documentation have been obtained, following HpD photoradiation therapy (PRT), in rabbit eyes having heterotransplanted single nodule amelanotic melanomas. A toxic effect characterized by tumor blanching, edema and hemorrhage was observed within 24 hours of treatment. Histological examination obtained 24 hours following HpD PRT illustrated massive tumor tissue necrosis and vascular disruption. HpD PRT at clinically relevant doses was also shown to be effective in selectively curing the highly malignant amelanotic iris melanoma. It is concluded that HpD PRT may prove to be an effective modality for treating certain ocular tumors.

Animals↗

PubMed1984

Actin filament localization in normal and migrating rabbit corneal epithelium.

The molecular probe NBD phallacidin (7-nitro-benz-2-oxa-1, 3-diazolylphallacidin), which reacts specifically with filamentous actin (f-actin), was used to study the distribution of polymerized actin oligmers in normal and migrating rabbit corneal epithelial cells. In the normal cornea, the majority of the NBD phallacidin fluorescence was localized to the cortical or sub-plasma membrane area of the superficial and wing epithelial cells. Following full thickness corneal trephination injury, migrating corneal epithelial cell exhibited a marked increase in the cortical NBD phallacidin fluorescence. Transmission electron microscopy, using fixation techniques which revealed bundles of fine filaments (6nm underlying the plasma membrane of migrating epithelial cells, thus supporting the fluorescent results. These findings suggest that corneal re-epithelialization is characterized by a marked increase in the amount of filamentous actin within the migrating epithelial cells. We conclude that NBD phallacidin may be of value in analyzing changes in actin polymerization during wound healing.

Actins↗

PubMed1984

Effect of monensin on secretion of basement membrane collagen by cultured rabbit corneal endothelial cells in comparison with rabbit tendon fibroblasts.

Monensin, a monovalent ionophore, affects differently the secretion of basement membrane collagen and interstitial procollagen. At 1 X 10(-8) M, monensin inhibited only slightly the secretion of procollagen synthesized by tendon cells while secretion of basement membrane collagen synthesized by endothelial cells was inhibited by 43% after 2 hours of labelling. At higher concentration (1 X 10(-6) M), the secretion of type I procollagen by tendon cells was inhibited after two h (36%) or 24 h (24%) of labelling. The pattern of basement membrane collagen secretion varied from inhibition to stimulation depending on the labeling time. No changes in the phenotypic expression of collagen were observed in either the monensin-treated tendon cultures or endothelial cells. Phase-contrast microscopy revealed differential responses of cells to monensin: tendon cells appeared spindle-shaped or rounded-up, in contrast to the enlarged shape displayed by endothelial cells.

Animals↗

PubMed1984

Natural history of experimental histoplasmic choroiditis in the primate. I. Clinical features.

The clinical features of the long-term (3-year) natural history of experimental histoplasmic choroiditis in primates are documented in this report. The acute choroiditis resolved into four types of lesions: chorioretinal adhesions (atrophic scars) (2%); retinal pigment epithelial window defects (21%); subclinical lesions (19%); and "disappearing" lesions (58%). It was noted that the most obvious, acute lesions tend to disappear by clinical examination with long-term follow up. No subretinal neovascularization or spontaneous "reactivation" was observed.

Animals↗

PubMed1984

Natural history of experimental histoplasmic choroiditis in the primate. II. Histopathologic features.

The histopathologic features of experimental multifocal histoplasmic choroiditis in the primate are presented. Eyes were studied at various time periods from 30 days to 3 years after intracarotid injection with live Histoplasma capsulatum organisms. The acute lesions produced resolved into four distinct resolution patterns (chorioretinal scars, retinal pigment epithelial defects, subclinical lesions, and "disappearing" lesions) whose histopathologic features were studied. Organisms could not be demonstrated by culture or special stains in lesions present more than 6 weeks. A feature common to all eyes studied, including those whose lesions were clinically inactive or had clinically "disappeared," was the persistence of small foci of lymphocytes in the choroid. Damage to Bruch's membrane was observed in some specimens.

Animals↗