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Phospholipase A and lysophosphatidyl choline (LPC) have been shown to induce significant changes in the lens permeability in vitro to cations and soluble proteins. During uveal inflammation, in various experimental models and in man as well, the levels of LPC in the aqueous humour have been shown to reach values which are harmful to the lens in vitro. In addition, a phospholipase is thought to be activated during the antigen + antibody + complement sequence. The possible significance of these findings is discussed in relation to the pathogenesis of complicated cataracts in uveitis and the possible role of the lens as a source of autoantigens in recurrent uveitis. [ABSTRACT FROM PUBLISHER]

Aim: To propose a new scoring system in the assessment of ocular surface epithelial damage in vernal keratoconjunctivitis (VKC)., Methods: 25 consecutive patients with VKC (50 eyes) were evaluated using the Quality of Life in children with VKC (QUICK) questionnaire and objective clinical measures: fluorescein and lissamine green staining and cornea confocal microscopy (Heidelberg Retina Tomography 3). Oxford, Van Bljsterweld and a new system, the VKC-Collaborative Longitudinal Evaluation of Keratoconus study (CLEK) (VKC-CLEK) scores, were used to evaluate the epithelial damage after staining., Results: Mean Oxford and VKC-CLEK scores were significantly different after fluorescein staining (P<0.001), but significantly correlated (P<0.001; r=0.649). The same data were obtained comparing Van Bljsterweld and VKC-CLEK after lissamine green staining (P<0.001; r=0.760). In patient with limbal VKC, a statistically significant difference was found comparing new VKC-CLEK scores and Oxford or Van Bljsterweld scores (P<0.001), but not in tarsal VKC. A statistically superior concordance was found between QUICK and VKC-CLEK scores compared with standard staining scores values (P<0.001)., Conclusions: Oxford and Van Bijsterveld scores are not adequate for the evaluation of the epithelial damage in patients with limbal VKC because the staining patterns considered for these tests do not correspond to the staining patterns in patients with VKC. We propose a new scoring system, VKC-CLEK, to better evaluate both limbal and tarsal epithelial damage in patients with VKC., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Purpose: To investigate the effects of various 5-fluorouracil (5-FU) concentrations, exposure times, and application techniques on in vitro-cultured human corneal cells., Methods: Human corneal epithelial cell (HCEC) and human corneal keratocyte (HCK) cultures were exposed to different 5-FU concentrations (0.025%-1%) and incubation durations (5 minutes to 2 hours). The cytostatic effect was evaluated as the percentage of inhibition of migration relative to the control. The evaluation of cytotoxic effect included both phase contrast microscopic observations and viability measures performed using an MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)] colorimetric assay. The results are expressed as ratio of optical density (OD) reduction 24 hours after exposure., Results: The cytostatic effect was time and dose dependent. The 50% inhibiting dose was 0.55% after 1 hour of incubation for HCECs and was 0.5% after 2 hours of incubation for HCKs. A 100% inhibitory effect was never observed at any concentration or incubation duration. No cytotoxic changes were observed using an 5-FU concentration of <1%; 1% 5-FU showed time-dependent cytotoxic changes in HCEC cultures only. MTT analysis showed no OD reduction at 5-FU concentrations of <1%, whereas 1% 5-FU showed OD reduction <50% at any tested exposure time. HCECs showed higher reduction in OD than HCKs., Conclusions: 5-FU formulations topically used in clinical practice showed limited toxicity in normal cultured corneal epithelial cells and keratocytes.

Purpose: To evaluate the ability of confocal scanning laser ophthalmoscope (cSLO) in the retromode imaging modality in detecting retinal changes secondary to exudative age-related macular degeneration (AMD)., Methods: Seventeen eyes of 13 consecutive patients affected by CNV secondary to AMD were evaluated with optical coherence tomography (OCT) to detect neuroretinal detachment (NRD), pigment epithelial detachment (PED), cystoid macular edema (CME), and epiretinal membranes (ERM). All eyes were examined with a cSLO equipped with infrared retromode (RM) imaging modality. Infrared and fundus autofluorescence images were also obtained (IR and FAF). The intermethod agreement between OCT and cSLO was evaluated considering single cSLO imaging modality separately (IR, FAF, and RM), and all imaging modalities together., Results: Eight eyes (47 %) had NRD at OCT; intermethod agreement was poor for any single cSLO imaging modality considered separately (k: 0.14, 0.01, and 0.29 for cSLO IR, FAF, and RM, respectively). Four eyes had PED at OCT (24 %); intermethod agreement was mild for cSLO RM, poor for IR and FAF (k: 0.51, 0.16, and 0.00, respectively). CME was present in eight eyes (47 %); intermethod agreement was excellent for cSLO RM, poor for IR and FAF (k: 0.88, 0.38, and 0.26, respectively). ERM was present in three eyes (18 %); intermethod agreement was mild for cSLO IR, poor for FAF, and excellent for RM (k: 0.59, 0.00, and 0.76, respectively)., Conclusions: cSLO RM imaging is a useful and reproducible technique in detecting retinal features associated with CNV, particularly CME.

Purpose: To compare corneal morphologic features using in vivo confocal microscopy in vernal keratoconjunctivitis (VKC) patients compared with normal subjects., Design: Prospective, comparative study., Participants: Thirty-two VKC patients (26 males, 6 females; mean age, 17.1 years) and 40 normal subjects (20 males, 20 females; mean age, 19.3 years) were included., Methods: All subjects underwent a full ophthalmologic examination. Confoscan CS4 (Nidek, Gamagori, Japan) images of the central cornea were obtained with a ×40 noncontact lens and Z-ring device., Main Outcome Measures: The superficial and basal epithelium, subbasal nerve plexus, anterior stroma, stromal nerves, and endothelium of the central cornea were studied., Results: The VKC patients had increased diameter, reflectivity, and presence of nuclear activation of superficial epithelial cells; reduced density of the basal membrane; lower density of keratocytes, increased presence of activated keratocytes, and inflammatory cells in the anterior stroma; and lower density and number of fibers, lower number of beadings, and higher grade of tortuosity of fibers in the subbasal nerve plexus. Increased alterations in thickness, deflections, and tortuosity were observed in stromal corneal nerves. An increased number of inflammatory cells in close proximity to the subbasal and stromal nerve fibers also was observed in VKC subjects., Conclusions: Corneal involvement in VKC is associated with alterations of the epithelium and subbasal and stromal corneal nerves. These changes may relate to the tear dysfunction and nonspecific hyperreactivity typical of these patients. Corneal confocal microscopy is a useful tool for studying in vivo pathologic corneal changes in VKC., (Copyright © 2012 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.)

Purpose: The purpose of this study was to assess the cytotoxic effects of the fluoquinolone ofloxacin and the aminoglycoside netilmicin on stromal human keratocytes in vitro., Methods: Cultured human keratocytes were exposed to various concentrations of ofloxacin or netilmicin (0.16-5.0 mg/mL). Both cell proliferation (MTT assay) and cell morphology (phase-contrast microscopy) were evaluated after 1, 4, 12, and 24 hours of incubation. Measurement of annexin V binding performed in association with the dye exclusion test using propidium iodide (PI) was also performed by FACS analysis after 4 hours of exposure., Results: Both antimicrobials induced dose- and time-dependent morphologic changes in keratocytes, yet the effects of netilmicin were minimal. After 24 hours of exposure, both drugs induced a dose-dependent inhibition of cell proliferation; however, ofloxacin demonstrated significantly more toxic effects than netilmicin (t test for ED50 values, P < 0.0001). Statistical differences between 2 antibiotics start at concentrations above 1.25 mg/mL (ANOVA with post-hoc test, P < 0.01). Expression of the apoptotic marker annexin V was unaffected by antibiotic exposure, whereas the uptake of the necrotic marker PI was increased by ofloxacin (5 mg/mL) but not by netilmicin (ofloxacin versus netilmicin, ANOVA, P < 0.05)., Conclusions: Relative effects of aminoglycosides and fluoroquinolones on stromal keratocytes appear to be different: netilmicin was shown to be significantly less toxic than ofloxacin. This finding is particularly relevant in deciding the optimal antibiotic to be applied in clinical situations in which the epithelium is absent or compromised, as after photorefractive keratectomy, alkali burns, or ulcerative keratitis.

Purpose: To determine whether cytokines involved in chronic allergic conjunctival disorders may affect formation of giant papillae and tissue remodeling., Methods: Conjunctival fibroblast cultures were challenged with different concentrations of human recombinant interleukin (IL)-4, IL-13, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha. Procollagens I (PIP) and III (PIIIP), matrix metalloproteinase (MMP)-1 and -9, and tissue inhibitor of metalloproteinase (TIMP)-1 were measured in supernatants, and their respective mRNAs were evaluated by RT-PCR., Results: IL-4 and -13 (10 ng/mL) significantly increased production and expression of PIP compared with nonstimulated cells, whereas IFN-gamma elicited the opposite effect, at both the protein and mRNA levels. Both IL-4 and -13 significantly decreased production of MMP-1 and increased that of TIMP-1, whereas TNF-alpha increased production of MMP-1 and -9. Expression of MMP-1 was reduced by IL-4 and increased by the other tested cytokines, whereas expression of TIMP-1 was increased by all tested cytokines., Conclusions: IL-4 and -13 increased production of collagen and modified the equilibrium between MMP-1 and its inhibitor, TIMP-1. These effects were partially opposed by IFN-gamma and TNF-alpha.

Purpose: Conjunctival fibroblasts stimulated with histamine (H) may be directly involved in the inflammatory and remodeling processes of chronic allergic conjunctival diseases., Methods: Proinflammatory cytokine and growth factor production, and the expression of intercellular adhesion molecule-1 (ICAM-1) were studied in conjunctival fibroblast cultures challenged with different concentrations of H (from 10(-9) M to 10(-) (4) M). Interleukin (IL)-1, IL-4, IL-6, IL-8, tumor necrosis factor-alfa (TNF-alpha), fibroblast growth factor (FGF), epidermal growth factor (EGF) and transforming growth factor-beta (TGFbeta-1) were measured in supernatants. ICAM-1 expression was evaluated by a fluorescence activated cell sorter (FACS). Inhibitory effects of the H-1 antagonists (antiH): emedastine, levocabastine, and azelastine, and of the antiH-2, cimetidine, on H-stimulated fibroblasts were evaluated by measuring both cytokines in supernatants and the cellular expression of ICAM-1., Results: Histamine increased the production of IL-1, IL-6 and IL-8, and ICAM-1 expression. TNF-alpha, IL-4 and growth factor production were not modified by histamine. The antiH-1, emedastine, significantly reduced H-induced production of IL-1, IL-6 and IL-8, while azelastine reduced only IL-1. Levocabastine and cimetidine were less effective. The histamine-induced increase in ICAM-1 expression was inhibited by emedastine but not by azelastine and levocabastine., Conclusions: Histamine has pro-inflammatory effects on conjunctival fibroblasts, inducing the production of cytokines and the expression of ICAM-1. Emedastine significantly reduced cytokine and ICAM-1 expression from H-stimulated fibroblasts. Conjunctival fibroblasts may contribute to the maintenance of inflammation in chronic allergic diseases.

Objective: To evaluate the effects of cyclosporin A (CsA) on cytokine and/or collagen production, cell growth, and apoptosis in conjunctival fibroblast cultures., Methods: Fibroblast cultures derived from normal subjects and patients with vernal keratoconjunctivitis and pemphigoid were exposed to different concentrations of CsA for either 24 hours or 30 days. The effects were evaluated by the colorimetric MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) test to assess cell proliferation, and by the measurement of procollagen I (PIP) and procollagen III (PIIIP) cytokines and total protein in culture medium. CsA-induced apoptosis was assessed by fluorescence-activated cell sorter analysis., Results: After 24 hours of exposure to doses of CsA of more than 10 microg/mL, cell proliferation and migration were significantly reduced. Cyclosporin A reduced PIP and interleukin 1 (IL-1) production in a dose-dependent manner. Interleukin 6 and IL-8 were increased by 10 microg/mL of CsA, whereas transforming growth factor beta, PIIIP, and total protein were unaffected. Cyclosporin A exposure induced apoptosis in a time- and dose-dependent manner. Long-term exposure to CsA reduced IL-6 but did not modify PIIIP production., Conclusion: Exposure to CsA directly modified fibroblast behavior., Clinical Relevance: Cyclosporin A ability to accelerate apoptosis in clinically fibrotic tissues may prove to be therapeutic and useful in hyperproliferative conjunctival disorders.

Histamine, an important mast cell mediator in allergic disorders, may affect extracellular matrix production and cell growth in vernal keratoconjunctivitis (VKC). In the present study, the histamine reactivity of conjunctival fibroblasts derived from VKC patients was investigated in vitro. Conjunctival fibroblast cultures were derived from biopses of 8 tarsal VKC patients and 5 normal subjects. These cells were maintained in vitro and stimulated with different concentrations of histamine with and without H1 (clorpheniramine) and H2 (cimetidine) receptor antagonists. Comparisons were made to fibroblasts grown in the same media without histamine and to fibroblasts stimulated with just antihistamine. The effects of histamine were evaluated by: (1) the MTT test to assess cell proliferation; (2) an in vitro wound model for cell migration and (3) the measurement of procollagen I (PIP) and procollagen III (PIIIP) in supernatants for collagen production. Results showed: (1) While VKC-derived fibroblasts proliferated at a faster rate than normal cells in unstimulated media, after histamine stimulation, VKC and normal cells grew at a similar rate. Both H1 and H2 antagonists significantly inhibited (P<0.05) histamine-induced cell proliferation. (2) Histamine enhanced cell migration after wounding; this effect was inhibited only by H2 antagonism. (3) When stimulated with histamine, VKC fibroblasts produced significantly more PIP than those in control media. Furthermore, VKC-derived fibroblasts were more sensitive to histamine challenge, producing significantly more PIP than normal fibroblasts. H1 and H2 antagonists did not modify histamine-stimulated PIP production. The enhanced proliferative and productive capacity of VKC fibroblasts may be the result of a selective overgrowth of one or more fibroblast subpopulations in a chronically inflamed tissue. Histamine increased proliferation, migration and collagen production in both normal and VKC fibroblasts. Since H2 antagonism modulated both cell growth and migration, but not histamine-induced collagen production, the latter may be mediated by a different receptor. These results showed that histamine is at least partially responsible for fibroblast stimulation., (Copyright 1999 Academic Press.)

The objectives of this study were two-fold: to identify tear histamine content and its relationship to changes in tear histaminase activity during the early (EPR) and late phases (LPR) of the allergic reaction induced by a conjunctival provocation test (CPT) and to evaluate the effects of lodoxamide on histamine release and allergic signs and symptoms during EPR and LPR. A baseline CPT was administered to 20 allergic patients with no baseline signs or symptoms of allergy. Clinical signs and symptoms were evaluated after 20 minutes and 6 hours. Tear samples were taken after 5-10 minutes and after 6 hours for subsequent analyses of cytology and histamine content (ELISA). Patients were then randomly assigned to receive lodoxamide or placebo four times daily for one week in a double-masked fashion. A second CPT was done after this therapy and the same parameters were re-evaluated. During EPR, tear histamine increased significantly with respect to baseline values (p < 0.05). During LPR, tear histamine increased significantly (p < 0.05) only in histamine inactivated samples. Histaminase enzymes were also significantly less active during the EPR (5.5 +/- 0.7) than the LPR (9.9 +/- 2.3) and at baseline. Histamine levels significantly correlated with allergic signs and symptoms (p < 0.05) only during the EPR. Lodoxamide significantly reduced histamine release during EPR (p < 0.05), allergic signs and symptoms during both EPR (p < 0.001) and LPR (p < 0.005), and tear cytology counts during LPR. In conclusion, greater histaminase activity may account for the smaller amount of tear histamine generally found during LPR, while these enzymes seem to play less of a role during the surge of histamine release and activity in the EPR. Lodoxamide was shown to ideally inhibit various aspects of the allergic reaction: clinical signs and symptoms in both the early and late phases, the primarily EPR-related peak of histamine release, and the primarily LPR-related changes in tear cytology.

Purpose: To investigate the activity of histamine-degradating enzymes in tears and plasma of patients with vernal keratoconjunctivitis (VKC)., Method: Tear and plasma samples were collected from patients with VKC and from age-matched control subjects. Histamine was measured by enzyme-linked immunosorbent assay in acid samples treated with perchloric to deactivate histaminase and in untreated samples. Tear cytology, skin test reactivity to histamine, and the sum clinical score of allergic signs and symptoms in patients with VKC also were evaluated. Nineteen patients with active VKC and six age-matched control subjects participated in this study., Results: In untreated samples, tear histamine (mean +/- standard error of the mean) was 11.15 +/- 2.16 ng/ml in patients with VKC and 0.855 +/- 0.225 ng/ml in control tears (P < 0.001). In treated samples, mean tear histamine was 22.25 +/- 4.17 ng/ml in patients with VKC versus 10.64 +/- 2.85 ng/ml in control subjects (not statistically different). The ratio of histamine in treated to untreated samples (indicating histaminase activity) was significantly lower in patients with VKC (2.30 +/- 0.263) than in control subjects (17.57 +/- 5.97; P = 0.0001). Plasma histamine levels in untreated and treated samples were significantly higher in patients with VKC (untreated, 2.23 +/- 0.334 ng/ml; treated, 4.37 +/- 0.357 ng/ml) than in control subjects (untreated, 0.254 +/- 0.068, P = 0.0002; treated, 2.96 +/- 0.171 ng/ml, P = 0.0082). The enzymatic breakdown of histamine (treated/ untreated) in plasma was significantly decreased in patients with VKC (2.54 +/- 0.447) compared with control subjects (14.78 +/- 4.86; P = 0.0012). Skin reactivity to histamine was not increased in VKC. Tear histamine levels were significantly correlated to tear lymphocyte content in the general population and to tear basophils in the patients with tarsal-vernal VKC only. An increased number of tear eosinophils were correlated with elevated enzyme activity only in patients with tarsal-vernal VKC and to the clinical score only in limbal-vernal patients., Conclusion: The enzymatic degradation of histamine was significantly decreased in patients with VKC compared with control subjects in both tears and plasma, suggesting that this dysfunction may be a primary factor in the pathophysiology of VKC.

To assess the diagnostic efficiency and direct costs of electrophysiologic tests, times and clinical data (admittance, diagnosis, final diagnosis and clinical reports) of 144 patients were recorded and statistically analyzed. Capital outlay on equipment and personnel costs were also evaluated to determine the economic impact of the tests. Electrophysiologic tests were found to play an important role in diagnosis and choice of therapy. It is important to improve collaboration between the referring ophthalmologist and the electrophysiology staff to inform patients better and to optimize the cost-benefit standards of the service. The current reimbursement by the Regional Public Health Service underestimates the costs of electrophysiologic tests.

Allergic mechanisms have been shown to induce gastric and intestinal damage in animal models. It has been demonstrated that people allergic to food may complain of gastrointestinal disorders. Furthermore food allergens can induce gastric mucosal damage in sensitized people. Little is known as regards allergic mechanisms underlying "peptic" ulcers although there are reports suggesting that some forms of gastric and duodenal ulcer may be caused by allergy. AIM. Of the study was to evidence if IgE specific to food and inhalants are localized in gastric and duodenal mucosa and if the in vitro incubation of gastric and duodenal biopsies with specific allergens, stimulate mast-cell mediators. MATERIALS AND METHODS. Twenty-one patients affected by gastric/duodenal ulcers (14 with high total IgE serum levels) and 16 controls were studied. All patients were submitted to upper digestive endoscopy and biopsies were taken from gastric fundus, body and antrum and duodenal bulb. Specific IgE to food and inhalant allergens were tested after homogenization of biopsies, using commercial kits. In 3 selected patients, 3 biopsies from gastric fundus and 3 from duodenal bulb were taken. After incubation of mucosal of mucosal biopsies with allergens (wheat, lactoalbumin, Parietaria J. pollen), the release of histamine and tryptase was measured. The release of Pepsinogen A was measured in the same conditions, as control. RESULTS. Specific IgE to food and inhalants allergens have been found in 164/586 tests (27.9%) of "peptic" ulcer patients and in 17/430 tests (4%) of controls. The duodenal bulb resulted the site in which most frequently IgE have been found. The release of histamine and tryptase has been stimulated only in 1/6 tests by incubation of biopsies with specific allergens in patients with specific IgE. PG-A release has been always stimulated by incubation of gastric biopsies, but not duodenal biopsies, with all tested allergens. DISCUSSION AND CONCLUSION. Specific IgE may be localized in gastric and duodenal mucosa of patients with "peptic" ulcer and/or food allergy. This event is linked to high total IgE serum levels and in a lesser extent, intestinal parasitosis, it is not strictly correlated with specific IgE in the serum and it regards both food and inhalant allergens. No relevant effects were observed after incubation of specific allergens with gastric or duodenal mucosa biopsies containing specific IgE. The possibility that higher allergens concentration stimulate mediator release from mast cells should be investigated. A defect of the gastric or duodenal epithelial barrier which permit a passage way for proteins with subsequent IgE production in the submucosa, appears to be the cause of localization of specific IgE in stomach and duodenum.

Permeability changes which take place in the lens in the course of uveitis are probably due to 'Lens Permeability Factors' present in the inflammatory aqueous. One of these 'factors', lysophosphatidyl-choline (LPC), has been shown to damage the lens in vitro: a leakage of Rb(86) and proteins, and an increase of Na(+) and water content indicate a dose-related membrane lytic effect. Damaging levels of LPC (up to 10μg/ml of aqueous humor) were found in the anterior chamber of inflamed eyes in the course of experimental uveitis in rabbits, and also in humans during uveitis. This report deals with an ultrastructural investigation on the damaging effect of different concentrations of LPC on rabbit lenses in culture. Concentrations of LPC higher than 12μg/ml caused signs of degeneration immediately below the capsule. Scanning electron microscopy revealed grossly enlarged lens fibers, globular structures of different size and widespread water vacuoles. Transmission electron microscopy showed inter- and intracellular changes in the epithelium and the outer cortex, swollen lens epithelial cells, fiber cells separation, vacuoles, and areas of decreased electron density. The overall structure of the lens fibers in the inner cortex and in the nucleus was always intact.

The benefit of focal and grid-laser photocoagulation in reducing the risk of visual loss from diabetic macular edema has been established. In order to investigate the effect of this treatment on macular function, 30 diabetics with macular edema and 1.0 visual acuity were tested before and after laser treatment at intervals of 1 week, and 1 and 3 months, respectively. The test was carried out by means of nyctometry, contrast sensitivity, hue discrimination and critical flicker frequency of blue cones. All patients had abnormal results in macular tests before treatment. During the follow-up, visual acuity remained stable and the macular tests did not statistically modify, except for nyctometry, which deteriorated at the 1-week follow-up (P = 0.02) and then increased to the basal values, and contrast sensitivity [improved at the last control (P = 0.006)]. Clinical regression of macular edema was observed, but macular function tests never normalized. Patients with diabetic macular edema and good visual acuity should be monitored with many functional methods, and laser treatment should be performed before macular function deteriorates irreversibly.

T lymphocyte subsets from inflammatory aqueous humor (n = 34) have shown one of three different patterns: group 1 = lower CD4+/CD8+ ratio in aqueous as compared to peripheral blood (0.43 +/- 0.25 vs. 1.96 +/- 0.82; n = 9); group 2 = similar CD4+/CD8+ ratio in aqueous and peripheral blood (1.76 +/- 0.60 vs. 1.60 +/- 0.62; n = 22); and group 3 = higher CD4+/CD8+ ratio in aqueous as compared to peripheral blood (7.53 +/- 0.47 vs. 2.13 +/- 0.55; n = 3). DR+ T lymphocytes were significantly higher, and natural killer cells significantly lower, in inflammatory aqueous as compared to peripheral blood.

At 5 or more years after renal transplantation, 42 patients were studied for their lymphocyte subsets to Leu-1, Leu-2, Leu-3, and Leu-7. It was found that, in this group of patients who ranged from 25 to 60 years of age, there was a significant decrease in the number of T helper cells and a decrease in the absolute level of T lymphocytes, with no significant change in the number of T suppressor cells. On a relative basis, the helper/suppressor ratio was decreased in patients when compared with normal persons. This was due to an increase in the relative numbers of suppressor cells. It was demonstrated that the Leu-7+ subset, which marks the NK population, was significantly elevated, in relative proportion, in peripheral blood when compared with controls. This was not seen on an absolute basis. The age-dependence of the relative numbers of Leu-7+ cells was seen in the normal control population and in the transplant cohort. There was no significant correlation between lymphocyte subset measurements and delayed-type hypersensitivity skin tests in the transplant population. A finding of interest is that 6 of the patients who had been treated for malignant disease during their posttransplant course had significantly higher numbers of Leu-7+ cells on a relative basis. In 5 of these patients, for whom data was available on absolute numbers, there was also a highly significant difference in the absolute numbers of Leu-7+ cells in these treated and surviving allograft recipients. It is speculated that this finding may suggest that an increase in Leu-7+ cells marks posttransplant patients who have a successful outcome following the treatment of malignancy, for which they are at increased risk.

Normal rabbit lenses exposed in vitro to heterologous antibody (Ab)--antigen (Ag) interactions lose control of the intracellular 86Rb; this membrane damage, which seems to be related to the quantitative ratio Ab/Ag, is relatively complement independent and is followed by a subsequent leakage of lenticular proteins. A possible implication of these findings in the development of complicated cataracts in uveitis (as 'permeability cataracts') and in the self-maintenance of recurrent uveal inflammation is shortly discussed.