Anterior chamber crystals following hyphema.
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Biomedical subjects
Publications and source records attributed to C S Foster.
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The effects on corneal wound healing of two topical nonsteroidal anti-inflammatory agents, flurbiprofen sodium (0.03%) and diclofenac sodium (0.1%), and the topical corticosteroid, prednisolone sodium phosphate (1%), were evaluated in masked, controlled rabbit studies. Healing of epithelial scrape wounds was significantly retarded in all three treatment groups for the first 3 days after wounding. There was no difference in the epithelial healing rate between the two nonsteroidal or corticosteroid treatment groups. Clinical grading of epithelial quality, conjunctival hyperemia, keratitis, stromal edema, and corneal haze were similar in all groups. There was a significant early decrease in the iritis score in the diclofenac treatment group. The strength of 2-mm central penetrating corneal trephination wounds and the collagen content of these wounds were similar in all groups. Both the topical nonsteroidal anti-inflammatory agents and the corticosteroid used in the preparations and dosages investigated in this study decreased early epithelialization of scrape wounds but had no apparent effect on corneal stromal healing. No toxic effects of the various drugs were found.
Normal prostates from Copenhagen/Fischer F1 hybrid rats were removed at 14 month of age. After routine formalin fixation and paraffin embedding, the expression of seven oligosaccharide structures by prostatic epithelial cells was assessed by an examination of lectin binding sites before and after neuraminidase digestion. Con-A bound to plasma membranes as well as the cytoplasm of all cells, thus confirming the presence of complex-type glycoconjugates. However, only two other oligosaccharides, apart from Con-A, were freely expressed on epithelial luminal plasma membranes. These were the Type I structure (Gal beta 1----3GalNAc-) identified by PNA-binding and (GlcNAc beta 1----4GlcNAc beta 1----4-)n identified by WGA. PNA, WGA, UEA-1 and SBA bound to the cytoplasm of almost all epithelial cells, although their intracellular distribution was not identical. DBF binding was not identified. ECG bound to only a very few cells and then only after digestion with neuraminidase when it was localised to the cytoplasm. Following removal of sialic acid groups by neuraminidase digestion, PNA-binding became more prominent, SBA-binding appeared localized to paranuclear intracellular vesicles and WGA binding sites were abolished. This study has now characterized the major oligosaccharide determinants expressed by rat normal prostatic epithelial cells and provides a baseline against which alterations occurring during ontogenesis and oncogenesis may be compared.
Oligosaccharides expressed by the 3327-H and 3327-MAT LyLu sublines of the Dunning rat prostate cancer model have been compared in formalin-fixed and routinely paraffin-embedded tumour tissues. Binding by lectins of defined specificity has been employed to identify expression of seven oligosaccharide structures by primary and metastatic prostatic carcinoma cells. Neuraminidase digestion was employed to reveal determinants masked by sialic acid. The presence of core Man alpha 1----3(Man alpha 1----6)Man beta 1----4GlcNAc beta 1----4 determinants recognised by Con-A (Canavalia ensiformis) confirmed expression of complex-type glycoconjugates by plasma membrane and cytoplasmic components of the 3327-H tumour but only by cytoplasmic determinants within 3327 MAT LyLu variant tumour-cells. The only other oligosaccharide freely expressed by either tumour-subline was (GlcNAc beta 1----4GlcNAc beta 1----4-)n, recognised by WGA (Triticum vulgaris). Prior to neuraminidase digestion, PNA (Arachis hypogaea) (which identifies Type I oligosaccharides: Gal beta 1----3GalNAc-) bound to pseudoluminal membranes of the 3327-H tumour. However, ECG (Erythrina cristagalli) (which identifies type II oligosaccharides: Gal beta 1----4GlcNAc-) did not bind to this tumour. Unmasked Type I (Gal beta 1----3GalNAc-) and Type II (Gal beta 1----4GlcNAc-) oligosaccharides were not identified in the MAT-LyLu variant. After neuraminidase digestion, PNA-binding was identified along pseudoluminal plasma membranes within 3327-H tumours but only within the cytoplasm of 3327-MAT LyLu primary and metastatic tumour cells. Following neuraminidase digestion, ECG-binding was observed along pseudoluminal plasma membranes of 3327-H tumours and heterogeneously within the cytoplasm of primary, but not metastatic 3327-MAT LyLu tumours. Terminal alpha/beta GalNAc- residues recognised by SBA (Glycine max) were not freely expressed by either subline. These structures were readily detected along luminal membranes of 3327-H cells and weakly detected within the cytoplasm of primary but not metastatic MAT 3327-LyLu tumour cells following neuraminidase digestion. Fucosylated Type II structures Fuc alpha 1----2Gal(GalNAc)-), recognised by UEA-1 (Ulex europaeus-1) and GalNAc alpha 1----3GalNAc- structures recognised by DBF (Dolichos biflorus) were not identified as a component of either tumour subline. The different patterns of oligosaccharide expression, identified by lectin-binding, clearly differentiated between the two tumour sublines and distinguished them from normal prostatic epithelium. The Dunning 3327 rat prostatic cancer sublines offer a useful model with which to examine the relationship between cell-surface oligosaccharide structures and phenotypic variants within a defined tumour-cell population.(ABSTRACT TRUNCATED AT 400 WORDS)
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Conjunctival biopsy specimens from 13 patients with cicatricial pemphigoid and from 13 age-matched healthy individuals undergoing cataract surgery were analyzed by light microscopy and immunohistochemical techniques, including a panel of monoclonal antibodies used to characterize inflammatory mononuclear cell phenotypes. Results of histologic examination of cicatricial pemphigoid specimens showed typical squamous metaplasia, vasculopathy, increased numbers of mast cells, and abundant plasma cells. All cicatricial pemphigoid specimens demonstrated immunoreactants at the epithelial basement membrane zone (BMZ). Epithelium of cicatricial pemphigoid conjunctiva showed significantly more T-helper cells (CD4+), dendritic cells (CD1+), and macrophages (CD14+), and a significantly higher helper/suppressor ratio than did controls. In the substantia propria, pemphigoid specimens showed dramatically increased inflammatory infiltrate with significantly more cells staining, in order of frequency, for T cells (CD3+, CD5+), T-helper cells (CD4+), T-suppressor cells (CD8+), macrophages (CD14+, Mac-1+), and dendritic cells (CD1+, HLA-DR+). Ten percent of these cells expressed interleukin-2 receptor protein (CD25+), indicating T-cell activation.
Acne rosacea is an idiopathic dermatologic disease that frequently produces conjunctival inflammation. The authors studied the histology and immunopathology of epibulbar conjunctival biopsy specimens from eight patients with ocular rosacea and compared the findings with those from conjunctiva from 13 normal individuals. The conjunctival epithelium in ocular rosacea was attenuated and infiltrated by inflammatory cells, mainly T-helper/inducer (CD4) cells, phagocytic cells, and antigen-presenting (CD14, Mac-1) cells. The difference between the normal control group and the rosacea group in the number of mononuclear cells forming these populations was statistically significant (P less than 0.01). The substantia propria of the rosacea specimens contained large subepithelial infiltrates of chronic inflammatory cells, and in some cases frank granuloma formation was evident. There was an overall mean increase of nearly all cell types, but especially of T-helper cells in the rosacea specimens compared with the controls. Interestingly, T-helper/inducer (CD4) cells, which were outnumbered by the T-suppressor (CD8) cells in the normal conjunctival epithelium (CD4/CD8 = 0.85), outnumbered the CD8-positive cells in the rosacea specimens (CD4/CD8 = 1.6). There also was a 3.5-fold increase of the CD4/CD8 ratio in the rosacea conjunctival stroma compared with the normal specimens. The mechanism involved in rosacea conjunctival inflammation resembles a type IV hypersensitivity reaction.
The ability of syphilis to mimic different ocular disorders can lead to misdiagnosis and delay in appropriate antimicrobial therapy. The authors describe their experience over the past 5 years with the ocular manifestations of syphilis in 25 patients who comprised 2.45% of 1020 new patients. Uveitis was the most common ocular manifestation seen. All patients had positive results from FTA-ABS tests, whereas only 68% had reactive serum VDRLs. Two of five patients tested for human immunodeficiency virus (HIV) antibody were reactive. The authors recommend routine FTA-ABS and VDRL screening in patients with uveitis or unexplained ocular inflammation. They also recommend testing for HIV antibody in luetics and aggressive treatment with high-dose aqueous penicillin for syphilis.
The clinical presentation and severe complications of atopic keratoconjunctivitis, a potentially blinding disorder, were characterized in a 9-year retrospective study of 45 patients seen at a large referral center. Twenty-six patients had subepithelial fibrosis, 13 with symblepharon and/or fornix fore-shortening. Thirty-four patients had severe keratopathy, which included neovascularization in 17 patients. Persistent epithelial defect was another major complication, occurring in 21 eyes and causing severe loss of vision. These patients required interdisciplinary therapeutic strategies; systemic antihistamine therapy and strict environmental controls were the keys to success in most cases.
The authors reviewed the records of 11 patients with relapsing polychondritis associated with active scleritis and analyzed the immunopathologic characteristics of ocular tissue from three of these. Seven patients (63%) required cytotoxic drugs, alone or in combination with low-dose oral corticosteroids. Only one patient was treated successfully with systemic corticosteroids alone. Two patients were controlled with dapsone and one with an oral nonsteroidal anti-inflammatory drug. Dapsone, which has been reported to be effective in the treatment of relapsing polychondritis, did not control the destructive scleral inflammation in six (75%) of eight patients; two (50%) of four patients with diffuse anterior scleritis were controlled with this drug. Patients with nodular and necrotizing scleritis were controlled with azathioprine and cyclophosphamide, respectively. These data suggest that the ocular manifestations of relapsing polychondritis, especially nodular and necrotizing scleritis, are less amenable to treatment with systemic corticosteroids and/or dapsone and that more potent immunosuppressants (azathioprine and cyclophosphamide) may be required to treat these lesions successfully. Results of histologic and immunofluorescent examination of conjunctival and/or scleral biopsy specimens from three patients confirmed the vasculitic nature of the eye lesions in this disease.
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We reviewed the charts of 10 patients who were admitted to the Massachusetts Eye and Ear Infirmary over a 10-year period with the diagnosis of Bacillus species endophthalmitis. To our knowledge this is the largest single series in the literature and includes the first two reported cases of Bacillus endophthalmitis following glaucoma filtering procedures. Seven cases developed following penetrating ocular trauma. One occurred in an intravenous drug abuser. Five eyes ultimately underwent enucleation; only the two eyes that developed endophthalmitis after elective surgery retained useful vision. Review of the literature indicates that parenteral and intravitreal antibiotic prophylaxis against endophthalmitis after penetrating ocular trauma should include gentamicin, in combination with vancomycin or clindamycin, to provide adequate coverage against infection with Bacillus spp., as prognosis is poor once infection is established. Bacillus spp. cultured from ocular tissues or fluids should not be dismissed as contaminants.
Susceptibility to Herpes simplex virus type 1 (HSV-1) stromal keratitis (HSK) in the mouse has previously been linked to the Igh-1 locus. The role of natural killer cells (NK) in resistance to viral infections is controversial. The authors studied the influence of the Igh-1 locus on in vitro murine NK activity against HSV-1 infected cell lines. The HSV-1 infected targets were lysed better than uninfected cells by murine splenic lymphocytes. Strain had no influence on virus-augmented cell lysis. Spleen cells from naive HSK-susceptible CAL-20 (Igh-1d) and BALB/c (Igh-1a) mice lysed YAC-1 targets better than HSK-resistant C.B-17 (Igh-1b) mice. The reverse was seen 24 hours after in vivo infection intraperitoneally with HSV-1. In contrast, CAL-20 splenocytes lysed PU5-1R targets better than BALB/c and C.B-17 splenocytes 24 hours after intraperitoneal (IP) infection. No significant differences were detected in interferon (IFN) levels after IP challenge with HSV-1 among the Igh-1 congenics. The data show that differences in NK activity were determined by both the Igh-1 genotype and the uninfected target cell. Susceptibility to HSK in these Igh-1-disparate congenics thus cannot be explained simply by differences in NK activity against HSV-1-infected targets.
We observed 48 patients for 7-21 months (mean, 18 months) after pterygium excision and 2 weeks of placebo or mitomycin topical therapy to evaluate whether or not the short-term efficacy of mitomycin in preventing pterygium recurrence would be reflected in long-lasting efficacy as well. Placebo-treated pterygia showed a 73% recurrence rate. One of 58 (1.7%) mitomycin-treated pterygia recurred (p less than 0.05). We also performed a pilot study comparing pterygia treated with excision followed by 0.4 mg/ml of mitomycin to pterygia treated with excision coupled with conjunctival autograft transplantation to estimate the number of patients required for a randomized clinical trial comparing these two treatment modalities and thereby to decide whether or not such a study would be justified. Thirteen primary and two recurrent pterygia were treated with mitomycin, while 14 primary and one recurrent pterygia were treated with conjunctival autograft transplantation. With mean follow-up times of 4 and 6 months, respectively, no recurrences were noted in the mitomycin-treated group, while the conjunctival autograft transplantation group had one recurrence (6.6%). We estimate that 400 patients would be required for a properly designed clinical trial comparing these two effective therapies for prevention of recurrent pterygia. We conclude that such a study is unjustified, and further conclude that the vastly less expensive, simple therapy of mitomycin eye drops is the more appropriate treatment.
In order to characterize the local ocular immunologic milieu of Igh-1-restricted herpes simplex keratitis (HSK), we investigated histologic and immunohistologic correlates of disease over a 21-day time course. Clinically observable keratitis began 10 days postinoculation in susceptible C.AL-20 (Igh-1d) and moderately susceptible BALB/c (Igh-1a) mice, whereas HSV-1-resistant C.B-17 (Igh-1b) mice rarely developed disease. Igh-1-restricted histologic differences were observed by day 11 postinoculation; C.AL-20 and BALB/c mice showed augmented recruitment of neutrophils and mononuclear cells in conjunctival, limbal, and corneal tissues compared to C.B-17 mice. On immunohistologic study, Lyt-1 to Lyt-2 cell ratios by day 11 postinoculation were 7:1, 2:1, and 1:8 in corneas from C.AL-20, BALB/c, and C.B-17 mice, respectively. Macrophages and neutrophils were absent in corneas from C.B-17 mice at this time, but could be found in large numbers in the corneas of susceptible mouse strains through day 21. These data demonstrate a strong relationship between Igh-1 phenotype and inflammatory cell recruitment in response to corneal infection with HSV-1, and support a role for T cell subpopulations in mediating Igh-1-restricted HSK.
Igh-1-disparate congenic murine strains differ in their susceptibility to develop contralateral chorioretinitis after intracameral (AC) inoculation with Herpes simplex virus type 1 (HSV-1): 75% of BALB/cByJ (Igh-1a) and 5% of C.B-17 (Igh-1b) develop necrotizing chorioretinitis. To determine the mechanism of influence of host genetics on development of contralateral chorioretinitis, the authors did viral isolation studies in contralateral eyes, determined in vivo and in vitro T-cell responses, and HSV-antibody levels at various times after AC inoculation of BALB/cByJ and C.B-17 mice with HSV-1. Viral isolation was similar in both mouse strains (P less than 0.2). Similarities in systemic immune responses included suppressed delayed-type hypersensitivity responses 5 days, cytotoxic T-lymphocyte and lymphocyte proliferation responses 8 days, and viral neutralizing antibody titers 5 days postinoculation (PI). Differences in systemic immune responses included: (1) delayed-type hypersensitivity responses were not suppressed in C.B-17 mice (P greater than 0.1) and were hyperactive in BALB/cByJ mice (P less than 0.025) 10 days PI and (2) HSV-neutralizing antibody production was higher in C.B-17 mice 10 days PI. These data suggest that the mere presence of HSV-1 in the uninoculated eye is insufficient for the development of chorioretinitis. Virus-specific delayed-type hypersensitivity reactions might be involved in the pathogenesis of retinitis in BALB/cByJ mice; and virus-neutralizing antibodies and suppressed HSV-specific delayed-type hypersensitivity reactions might be instrumental in the protection enjoyed by C.B-17 mice.
A potent cytolytic pore-forming protein (PFP, perforin, or cytolysin) is associated with the cytoplasmic granules of cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. The role of PFP/perforin in cytolytic reactions carried out in vivo is still unclear. Here, the authors performed immunohistochemical analysis using antibodies monospecific for perforin and made use of a murine uveitis model produced by intracameral inoculation of herpes simplex virus I (HSV-I). The main cell infiltrate found in the anterior segment of virus-inoculated eyes consisted of Thy-1+/asialo GM1+/CD8-/CD4- cells, presumably representing NK cells. Perforin staining was detected mainly in cells bearing this phenotype. Perforin was only detected in cells displaying the large granular lymphocyte morphology. A small number of perforin-positive cells (less than 5%) colabeled as CD8+, indicating that these cells could have belonged to the CTL lineage. These observations show for the first time the presence of perforin-containing NK cells in tissues of animals undergoing acute viral infections.