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Biomedical subjects

W R Green

Publications and source records attributed to W R Green.

At least 55 records · Page 3Linked to original sources

Analysis of sex-mismatched human corneal transplants by fluorescence in situ hybridization of the sex-chromosomes.

The fate of the cells of corneal transplants has been controversial from the early days of keratoplasty. Various methods such as histological evaluation, radiolabeling of donor cells or Barr-body analysis have been applied to clarify the issue. However, the question whether the transplanted cells are replaced or survive, remains unsolved. In this study, we applied fluorescence in situ hybridization (FISH) of the X- and Y-chromosomes in paraffin sections of explanted sex-mismatched corneal transplants to distinguish between host and donor cells. Fourteen sex-mismatched cases with various reasons for explantation and different postoperative time intervals ranging from 11 months to 30 years were analysed. We found that all cell types, including epithelium, keratocytes and endothelial donor cells were replaced in most cases as early as 1 year after transplantation. In three cases, however, up to 26% of donor keratocytes were still detected up to 4.5 years after transplantation, demonstrating a certain individual variability in the process of replacement. Further studies must show if the extent and timing of donor cell replacement in clinically successful, totally clear transplants is different. Our results are in keeping with the phenomenon of recurrences of corneal dystrophies in the graft, the significant postoperative decline of the endothelial cell density, the fact that typical graft rejections usually take place within 1-2 years postoperatively and that relatively late rejections can occur in rare cases probably due to some surviving stromal keratocytes. Donor cell replacement is a special feature of corneal transplants when compared with other kinds of organ transplants and might be due to the presence of the same tissue type in the immediate neighbourhood of the graft.

Cornea↗

Efficacy of unilateral versus bilateral temporal artery biopsies for the diagnosis of giant cell arteritis.

PURPOSE: To determine the utility of unilateral versus bilateral temporal artery biopsies in detecting the pathologic changes of giant cell arteritis. METHODS: We performed a retrospective study to determine the utility of unilateral versus bilateral temporal artery biopsies in detecting the pathologic changes of giant cell arteritis. The pathologic reports of consecutive temporal artery biopsy specimens received at the Wilmer Ocular Pathology Laboratory over a 28-year period from 1968 to 1996 were reviewed. RESULTS: Of 908 specimens examined from 758 patients, 300 specimens were simultaneous bilateral biopsies from 150 patients, 72 specimens were bilateral sequential biopsies from 36 patients, and the remaining 536 specimens were unilateral biopsies from 536 patients. Of the 186 patients who had bilateral simultaneous or nonsimultaneous biopsies, 176 had identical diagnoses on both sides. In four patients, no artery was obtained on one side. In each of the remaining six patients, five of whom had bilateral simultaneous biopsies and one of whom had bilateral sequential biopsies performed 8 days apart, the biopsy specimen from one side was interpreted as showing only arteriosclerotic changes with no evidence of active or healed arteritis, whereas the other specimen was interpreted as showing either probable healed arteritis (three specimens) or possible early arteritis (three cases). In none of the six patients with differing diagnoses between the two sides was one side interpreted as showing definite, active giant cell arteritis. Five of the six patients were subsequently determined to have giant cell arteritis, based on a combination of clinical findings, erythrocyte sedimentation rate, and response to treatment with systemic corticosteroids. CONCLUSIONS: The results of this study indicate that performing a bilateral simultaneous or sequential temporal artery biopsy improves the diagnostic yield in at least 3% of cases of giant cell arteritis, whereas in 97% of cases, the two specimens show the same findings. Thus, in patients in whom only one artery can be biopsied, there is a high probability of obtaining the correct diagnosis. Nevertheless, although the improvement in diagnostic yield of bilateral temporal artery biopsies is low, the consequences of both delayed diagnosis and treatment of giant cell arteritis as well as the use of systemic corticosteroids in patients who do not have giant cell arteritis are of such potential severity that consideration should always be given to performing bilateral temporal artery biopsies in patients suspected of having the disease.

Aged↗

Giant cell angiofibroma of the orbit and eyelid.

PURPOSE: To report the clinicopathologic features of a newly recognized tumor, giant cell angiofibroma. DESIGN: Observational case series. MAIN OUTCOME MEASURES: Clinical and histopathologic features of giant cell angiofibroma. METHODS: Light and electron microscopy and immunohistochemistry of five cases of giant cell angiofibroma. RESULTS: A total of five patients (4 women and 1 man) are described: two presented with a painless mass in the eyelid, two with a mass in the orbit, and one presented with a conjunctival lesion. All lesions were well demarcated with no capsule and were composed of blood vessels, a patternless spindle-shaped cell proliferation with a solid and pseudovascular appearance, and multinucleated giant cells. Both spindle-shaped and giant tumor cells were intensely positive for CD34 and vimentin. CONCLUSION: Giant cell angiofibroma resembles solitary fibrous tumor and giant cell fibroblastoma and should be considered in the differential diagnosis of spindle-cell tumors in the eyelid, orbit, and conjunctiva.

Aged↗

Ocular explosions from periocular anesthetic injections: a clinical, histopathologic, experimental, and biophysical study.

OBJECTIVES: An increasing number of cases are being recognized in which a periocular anesthetic for cataract surgery has been inadvertently injected directly into the globe under high pressure until the globe ruptures or "explodes." The objectives of the current study were to (1) analyze this injury clinically and histopathologically through a series of seven case reports; (2) reproduce the injury experimentally in human eyebank eyes, live anesthetized rabbit eyes, and human cadaveric eyes; (3) investigate the biophysical basis of the injury; and (4) outline recommendations to help decrease the risk of ocular rupture with periocular injections. DESIGNS/PARTICIPANTS: Clinical, histopathologic, experimental animal, autopsy eye, and theoretical biophysical study. METHODS: The clinical and histopathologic findings of the patients' eyes were documented. Human eyebank eyes, live anesthetized rabbit eyes, and human cadaveric eyes were exploded via direct intraocular saline injection. The laws of Bernoulli, LaPlace, Friedenwald, and Pascal were used to investigate theoretically the biophysics of the injury. RESULTS: The findings of anterior and posterior scleral rupture, retinal detachment, vitreous hemorrhage, and lens extrusion were observed clinically and experimentally. In some clinical and experimental cases, the anterior segment appeared entirely normal despite a posterior rupture. The surgeon proceeded with and completed the cataract surgery in two of the seven clinical cases without knowledge of the rupture. The pressure required to produce such an injury is in the range of 2800 to 6400 mmHg, and this pressure is more easily attained with a 3-ml syringe than with a 12-ml syringe. CONCLUSIONS: Explosion of an eyeball during the injection of anesthesia for ocular surgery is a devastating injury that may go unrecognized. The probability of an ocular explosion can be minimized by (1) the use of a blunt needle and a 12-ml syringe, (2) aspirating the plunger and wiggling the syringe before injection, (3) discontinuing the injection if corneal edema or resistance to injection is noted, and (4) inspecting the globe for evidence of intraocular injection before ocular massage or placement of a Honan balloon. On recognition of an ocular explosion, immediate referral to and intervention by a vitreoretinal surgeon is optimal.

Aged↗

Provision of anesthesia with single application of lidocaine 2% gel.

PURPOSE: To compare the efficacy of a single application of lidocaine 2% gel with tetracaine 0.5% drops for topical anesthesia in clear corneal cataract surgery. SETTING: The Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. METHODS: A preliminary toxicity study applied lidocaine 2% gel in the conjunctival fornices of rabbit eyes (n = 9). Biomicroscopic examination was performed and then enucleation at sequential intervals after the application. Intentional intracameral injection of lidocaine gel was performed (n = 3), followed by enucleation. Histopathological analysis was performed on all eyes. A randomized clinical trial comparing topical anesthesia in clear corneal cataract surgery was performed in 25 eyes of 25 patients (12 eyes randomly assigned to lidocaine gel, 13 eyes to tetracaine drops). Corneal sensation was measured with the Cochet-Bonnet aesthesiometer before application of the topical anesthesia, 5 minutes after application, and at the conclusion of surgery. Additional intraoperative local anesthesia and systemic sedation were recorded. Patients' subjective level of comfort was reported 20 minutes after surgery, and the surgeon's perception of patients' comfort was also noted. RESULTS: In rabbits, lidocaine gel did not cause clinical or histopathological alteration of the ocular tissues. In the clinical study, median corneal sensitivity before application, after 5 minutes, and postoperatively was 6, 0, 0 (maximum sensitivity = 6), respectively, in the lidocaine gel group and 5, 0, 0, respectively, in the tetracaine drops group. Additional local anesthesia was administered in 17% and 31% of patients, respectively. Satisfactory comfort was reported by 58% in the lidocaine gel group and 62% in the tetracaine drops group. CONCLUSIONS: A single application of lidocaine 2% gel was a safe and effective alternative to multiple topical anesthetic drops for clear corneal cataract surgery. Lidocaine 2% gel was similar to tetracaine drops in provision of corneal anesthesia and patient comfort, while causing no significant toxicity to the ocular surface.

Aged↗

Remarkable case of early Aspergillus endophthalmitis.

BACKGROUND: This case demonstrates the early stage of Aspergillus endophthalmitis and is the second ultrastructural study of endogenous Aspergillus endophthalmitis. It is the first description of phagocytosis of Aspergillus fungi by retinal pigment epithelium (RPE). METHODS: A case report and detailed light- and electron microscopic findings are presented. RESULTS: Histopathological examination of serial sections of the affected right eye displayed a spread of Aspergillus fumigatus fungi along two separate paths: via the retinal and choroidal vessels. The retinal and choroidal lesions were not contiguous. The organisms penetrated blood vessel walls, Bruch's membrane and the internal limiting membrane, but not the RPE layer. A curious accumulation of the Aspergillus fungi was present on the internal aspect of Bruch's membrane, where the RPE acted as a barrier and the subretinal space was not invaded. Phagocytosis of fungi by the RPE was observed. No inflammatory cells were present between Bruch's membrane and the RPE. CONCLUSIONS: This report describes a remarkable barrier function, possible local immunosuppression and phagocytosis by the RPE cells in a case of early Aspergillus endophthalmitis.

Aspergillosis↗

Histopathologic study of presumed parafoveal telangiectasis.

PURPOSE: To report the postmortem histopathologic features that closely resemble the clinical features of parafoveal telangiectasis. METHODS: Light and electron microscopy. RESULTS: Histopathologic features included macular edema; telangiectatic vessels; retinal, subretinal, and superficial retinal neovascularization; retinal pigment epithelial hyperplasia around neovascular aggregates; retinal-choroidal vascular anastomosis; and superficial pigmented cells with lipofuscin. CONCLUSION: The postmortem histopathologic findings in a 36-year-old woman with Down syndrome and other systemic conditions correlate with features noted in previous reports of presumed parafoveal telangiectasis.

Adult↗

Cytotoxic T lymphocytes to endogenous mouse retroviruses and mechanisms of retroviral escape.

Mouse retrovirus-induced lymphoma/leukemia and immunodeficiency are useful models for analogous human diseases. Both ecotropic (mouse tropic) and recombinant retroviruses, including the polytropic mink cytopathic focus-inducing type, have been studied for disease pathogenesis and as targets for humoral and cellular immunity, particularly cytotoxic T-lymphocyte (CTL) responses. For AKR/Gross murine leukemia viruses (MuLV) we have defined an immunodominant CTL epitope in the p 15E transmembrane anchor envelope protein and three minor/subdominant epitopes. Evidence is presented for retroviral escape from CTL by selection following genetic recombination and point mutation both within and outside CTL epitope sequences, and via endogenous retrovirus-infected cell downregulation of the generation of anti-AKR/Gross MuLV CTL. As demonstrated in vivo in naturally occurring non-responder strains by adoptive transfer, and in vitro by cell-mixing experiments, a central non-responsiveness mechanism appears to be peripheral inhibition mediated by infected cells expressing MHC-presented viral peptides. Such inhibition requires Fas expression by antiviral T cells; occurs upon TCR-mediated recognition of virus-infected, Fas ligand-expressing "veto" cells; and apparently leads to an antigen-specific form of activation-induced cell death of T cells. In the LP-BM5 MuLV isolate that causes murine AIDS (MAIDS) retroviral variation also leads to CTL escape--the BM5-helper virus has altered forms of the immunodominant and two minor/subdominant epitopes. In contrast, a novel immunodominant CTL epitope is recognized by MAIDS resistant, but not MAIDS-susceptible, strains. This epitope is uniquely encoded in an alternative translational reading frame of the viral gag gene. It also appears that the LP-BM5 MuLV have co-opted the cells of the immune system for retroviral pathogenesis--CD40/CD40L (CD154) interactions are required both for the initiation and progression of MAIDS.

Animals↗

Immune CD8(+) T cells prevent reactivation of Toxoplasma gondii infection in the immunocompromised host.

Toxoplasma gondii remains a serious cause of morbidity and mortality in individuals that are immunosuppressed, patients with AIDS in particular. The cellular immune response, especially by gamma interferon (IFN-gamma)-producing CD8(+) T cells, is an essential component of protective immunity against the parasite. In the present study the role of CD8(+) T cells during the reactivation of Toxoplasma infection in an immunocompromised murine model was evaluated. Chronically infected mice were challenged with LP-BM5 virus, and the kinetics of CD8(+) T-cell function was studied. At 10 weeks after viral infection, mice showed obvious signs of systemic illness and began to die. At this stage, CD8(+) T cells were unresponsive to antigenic stimulation and unable to kill Toxoplasma-infected targets. IFN-gamma production by the CD8(+) T cells from dual-infected animals reached background levels, and a dramatic fall in the frequency of precursor cytotoxic T lymphocytes was observed. Histopathological analysis of the tissues demonstrated signs of disseminated toxoplasmosis as a result of reactivation of infection. However, treatment of the dual-infected animals with immune CD8(+) T cells at 5 weeks post-LP-BM5 challenge prevented the reactivation of toxoplasmosis, and mice continued to live. Our study for the first time demonstrates a therapeutic role for CD8(+) T cells against an opportunistic infection in an immunocompromised state.

Animals↗

Antiretroviral cytolytic T-lymphocyte nonresponsiveness: FasL/Fas-mediated inhibition of CD4(+) and CD8(+) antiviral T cells by viral antigen-positive veto cells.

C57BL/6 (H-2(b)) mice generate type-specific cytolytic T-lymphocyte (CTL) responses to an immunodominant Kb-restricted epitope, KSPWFTTL located in the membrane-spanning domain of p15TM of AKR/Gross murine leukemia viruses (MuLV). AKR.H-2(b) congenic mice, although carrying the responder H-2(b) major histocompatibility complex (MHC) haplotype, are low responders or nonresponders for AKR/Gross MuLV-specific CTL, apparently due to the presence of inhibitory AKR. H-2(b) cells. Despite their expression of viral antigens and Kb, untreated viable AKR.H-2(b) spleen cells cause dramatic inhibition of the C57BL/6 (B6) antiviral CTL response to in vitro stimulation with AKR/Gross MuLV-induced tumor cells. This inhibition is specific (AKR.H-2(b) modulator spleen cells do not inhibit allogeneic MHC or minor histocompatibility antigen-specific CTL production), dependent on direct contact of AKR.H-2(b) cells in a dose-dependent manner with the responder cell population, and not due to soluble factors. Here, the mechanism of inhibition of the antiviral CTL response is shown to depend on Fas/Fas-ligand interactions, implying an apoptotic effect on B6 responder cells. Although B6.gld (FasL-) responders were as sensitive to inhibition by AKR.H-2(b) modulator cells as were B6 responders, B6.lpr (Fas-) responders were largely insensitive to inhibition, indicating that the responder cells needed to express Fas. A Fas-Ig fusion protein, when added to the in vitro CTL stimulation cultures, relieved the inhibition caused by the AKR.H-2(b) cells if the primed responders were from either B6 or B6.gld mice, indicating that the inhibitory AKR.H-2(b) cells express FasL. Because of the antigen specificity of the inhibition, these results collectively implicate a FasL/Fas interaction mechanism: viral antigen-positive AKR.H-2(b) cells expressing FasL inhibit antiviral T cells ("veto" them) when the AKR.H-2(b) cells are recognized. Consistent with this model, inhibition by AKR.H-2(b) modulator cells was MHC restricted, and resulted in approximately a 10- to 70-fold decrease in the in vitro expansion of pCTL/CTL. Both CD8(+) CTL and CD4(+) Th responder cells were susceptible to inhibition by FasL+ AKR.H-2(b) inhibitory cells as the basis for inhibition. The CTL response in the presence of inhibitory cells could be restored by several cytokines or agents that have been shown by others to interfere with activation-induced cell death (e.g. , interleukin-2 [IL-2], IL-15, transforming growth factor beta, lipopolysaccharide, 9-cis-retinoic acid) but not others (e.g., tumor necrosis factor alpha). These results raise the possibility that this type of inhibitory mechanism is generalized as a common strategy for retrovirus infected cells to evade immune T-cell recognition.

AKR murine leukemia virus↗

Core-binding factor influences the disease specificity of Moloney murine leukemia virus.

The core site in the Moloney murine leukemia virus (Moloney MLV) enhancer was previously shown to be an important determinant of the T-cell disease specificity of the virus. Mutation of the core site resulted in a significant shift in disease specificity of the Moloney virus from T-cell leukemia to erythroleukemia. We and others have since determined that a protein that binds the core site, one of the core-binding factors (CBF) is highly expressed in thymus and is essential for hematopoiesis. Here we test the hypothesis that CBF plays a critical role in mediating pathogenesis of Moloney MLV in vivo. We measured the affinity of CBF for most core sites found in MLV enhancers, introduced sites with different affinities for CBF into the Moloney MLV genome, and determined the effects of these sites on viral pathogenesis. We found a correlation between CBF affinity and the latent period of disease onset, in that Moloney MLVs with high-affinity CBF binding sites induced leukemia following a shorter latent period than viruses with lower-affinity sites. The T-cell disease specificity of Moloney MLV also appeared to correlate with the affinity of CBF for its binding site. The data support a role for CBF in determining the pathogenic properties of Moloney MLV.

3T3 Cells↗

Absence of ocular effects after either single or repeated exposure to 10 mW/cm(2) from a 60 GHz CW source.

This study was designed to examine ocular effects associated with exposure to millimeter waves (60 GHz). Rabbits served as the primary experimental subjects. To confirm the results of the rabbit experiments in a higher species, the second phase of the study used nonhuman primates (Macaca mulatta). First, this study used time-resolved infrared radiometry to assess the field distribution patterns produced by different antennas operating at 60 GHz. These results allowed us to select an antenna that produced a uniform energy distribution and the best distance at which to expose our experimental subjects. The study then examined ocular changes after exposure at an incident power density of 10 mW/cm(2). Acute exposure of both rabbits and nonhuman primates consisted of a single 8 h exposure, and the repeated exposure protocol consisted of five separate 4 h exposures on consecutive days. One eye in each animal was exposed and the contralateral eye served as the sham-exposed control. After postexposure diagnostic examinations, animals were euthanized and the eyes were removed. Ocular tissue was examined by both light and transmission electron microscopy. Neither microscopic examinations nor the diagnostic procedures performed on the eyes of acute and repeatedly exposed rabbits found any ocular changes that could be attributed to millimeter-wave exposure at 10 mW/cm(2). Examination of the primates after comparable exposures also failed to detect any ocular changes due to exposure. On the basis of our results, we conclude that single or repeated exposure to 60 GHz CW radiation at 10 mW/cm(2) does not result in any detectable ocular damage.

Animals↗

Evidence for a continued requirement for CD40/CD40 ligand (CD154) interactions in the progression of LP-BM5 retrovirus-induced murine AIDS.

In genetically susceptible C57BL/6 mice the LP-BM5 isolate of murine retroviruses causes profound splenomegaly, lymphadenopathy, hypergammaglobulinemia, and an immunodeficiency syndrome bearing many similarities to the pathologies seen in AIDS. Because of these similarities, which also include terminal B cell lymphoma formation, this syndrome has been called murine AIDS or MAIDS. Prompted by previous reports showing that the onset of MAIDS is dependent on the presence of both CD4+ T and B cells, we have previously shown that anti-gp39/CD40 ligand mAb (anti-CD40L mAb) treatment of LP-BM5-infected mice is effective in inhibiting the induction of MAIDS when a short course of anti-CD40L mAb treatment was started on the same day as LP-BM5 administration. The success of anti-CD40L mAb therapy, as indicated by a much reduced degree of splenomegaly, hypergammaglobulinemia, and mitogen and allogeneic CTL unresponsiveness, demonstrated that CD40L/CD40 interactions were critical to the establishment of MAIDS. Here we extend these findings through the use of delayed anti-CD40L mAb treatment of mice, beginning 3-4 weeks after LP-BM5 infection, by showing that interruption of CD40L/CD40 interactions also interferes with the progression of MAIDS. About 60% of LP-BM5-preinfected mice were affected by delayed anti-CD40L mAb treatment, with substantially reduced spleen weights and serum hypergammaglobulinemia and normal or greatly restored proliferative responses to Con A stimulation and CTL responses to allogeneic stimulation. The other LP-BM5-infected mice that did not respond to anti-CD40L therapy were found to have made antibodies to the anti-CD40L mAb. Thus, in a majority of mice anti-CD40L mAb therapy was very effective in interfering with MAIDS pathogenesis well after the establishment of the virus infection and MAIDS symptomatology, indicating that CD40L/CD40 interactions are crucial to the maintenance and progression of the disease, as well as its initiation.

Animals↗

An alternative translational reading frame encodes an immunodominant retroviral CTL determinant expressed by an immunodeficiency-causing retrovirus.

Recognition of virus-infected or transformed cells by CD8+ CTL requires a trimolecular complex composed of MHC class I, beta2-microglobulin, and a specific foreign peptide composed of 8 to 10 linear amino acids. The generation of such CTL epitopes has traditionally been thought to be from the primary open reading frame encoding the viral or tumor-associated proteins. In this report it is demonstrated that a viral CTL epitope can also be generated from an alternative reading frame. Using a combination of synthetic peptides and Sindbis or vaccinia expression systems, MHC class I Kd-restricted BALB/cByJ CTL directed against defective gag gene constructs of the LP-BM5 virus complex that causes murine AIDS were shown to have specificity for the antigenic peptide SYNTGRFPPL. This epitope is generated in a novel fashion from the second open reading frame (ORF2) of both the defective and ecotropic helper virus components of LP-BM5. Importantly, lysis of target cells expressing BM5 ecotropic helper, and/or defective viral gag, demonstrated that the SYNTGRFPPL epitope is generated during the course of a normal retroviral infection. Furthermore, MAIDS-resistant BALB/cByJ mice also generated secondary restimulated CTL specific for SYNTGRFPPL following in vivo priming with the LP-BM5 retroviral complex. These data suggest that retroviruses, and potentially other viruses and foreign genes, are capable of expressing T cell epitopes from alternative open reading frames. If one considers the influence of self peptides on T cell development, these "alternative reading frame-derived" peptides could provide an important additional influence on the functional T cell repertoire.

Amino Acid Sequence↗

Familial Axenfeld-Rieger anomaly, atrial septal defect, and sensorineural hearing loss: a possible new genetic syndrome.

OBJECTIVE: To describe the clinical and ocular histopathological findings in multiple members of a family with congenital Axenfeld-Rieger anomaly, atrial septal defect, and sensorineural hearing loss. METHODS: We performed a retrospective review of the medical charts and the ocular histopathological material of multiple members of a family. RESULTS: Congenital Axenfeld-Rieger anomaly and glaucoma were inherited by both the proband and her male half-sibling from a phenotypically positive father and 2 different phenotypically negative mothers, suggesting an autosomal dominant inheritance. The proband's male half-sibling and her father also had atrial septal defects and sensorineural hearing loss. The proband's paternal grandmother had severe glaucoma. Histopathological analysis of blind, painful eyes removed from the proband's father and paternal grandmother showed incomplete development of the anterior chamber angle with iris stromal hypoplasia, prominent posterior embryotoxon with iris adhesions, and abnormal position and insertion of the ciliary muscles. CONCLUSIONS: This is the first description of coexisting Axenfeld-Rieger anomaly, atrial septal defect, and sensorineural hearing loss in multiple members of a single family. The iris, trabecular meshwork, and large portions of the cardiac intraventricular septum all arise from neural crest anlagen, thus supporting the notion that anterior segment dysgenesis represents a developmental disorder of the neural crest.

Abnormalities, Multiple↗

Histopathologic and ultrastructural findings of surgically excised choroidal neovascularization. Submacular Surgery Trials Research Group.

OBJECTIVE: To study the histologic and ultrastructural features of surgically excised choroidal neovascularization (CNV) from patients who had undergone submacular surgery. MATERIALS AND METHODS: Voluntarily submitted surgically excised CNV specimens from a subset of specimens obtained by the Submacular Surgery Trials Research Group between January 1, 1994, and December 31, 1996, were available for this study. The specimens were routinely processed for transmission electron microscopic examination. The largest horizontal and vertical dimensions, cellular and extracellular constituents, and relationship of the CNV to the neurosensory retina and retinal pigment epithelium (RPE) were recorded. RESULTS: Seventy-eight surgical specimens were obtained from 160 patients treated surgically in Submacular Surgery Trials centers. Sixty-one (78%) were from patients with age-related macular degeneration (ARMD) and 17 (22%) were from patients with ocular histoplasmosis syndrome or idiopathic causes (hereafter referred to as the non-ARMD group). The histologic diagnosis was fibrovascular tissue, fibrocellular tissue, or hemorrhage in all cases. Vascular endothelium and RPE were the most common constituents of the CNV. Basal laminar deposit was only present in CNV from patients with ARMD. Age-related macular degeneration specimens were larger (mean +/- SD, 2042 [+/- 1175] x 320 [+/- 185] microm vs 1498 [+/- 792] x 227 [+/- 166] microm) and were more likely to have a sub-RPE (beneath the RPE) component than non-ARMD specimens. CONCLUSIONS: All evaluated surgically excised CNV specimens in this study from patients enrolled in the Submacular Surgery Trials consisted of fibrovascular tissue, fibrocellular tissue, or hemorrhage. Surgically excised CNV associated with ARMD in this series was larger and often was located beneath the RPE compared with non-ARMD CNV, although fewer than half of all the specimens could be oriented by topographic relationship to the RPE.

Choroid↗

Tick infestation of the eyelid.

PURPOSE: To report the rare occurrence of tick infestation of the eyelid margin. METHODS: A 58-year-old woman was initially examined with a small yellow lesion of the left upper eyelid margin that appeared after she felt a sting near her eye. Close examination disclosed an insect body attached to the eyelid margin. En bloc excision of the insect with part of the eyelid was performed. RESULT: Gross examination of the specimen identified the organism as the nymph stage of a bloated tick of the genus Hyalomma but of an uncertain species. CONCLUSION: Ticks (Hyalomma) can become embedded in the meibomian gland orifice and manifest as a mass at the eyelid margin.

Animals↗