Total cost minimization control scheme for biological wastewater treatment process and its evaluation based on the COST benchmark process.

This paper proposes a new cost minimisation control scheme for a predenitrification type of biological wastewater treatment process and evaluates the validity of the control scheme based on the benchmark process presented by Copp. The control scheme adopting a hierarchical control structure incorporates lower-level controllers that consist of a set of local dynamic controllers and a higher-level static optimiser that provides the set points of the lower-level controllers based on the total cost index of Vanrolleghem and Gillot. Prior to benchmarking, this paper derives a simplified process model used for the optimiser, which is able to approximate the benchmark process model effectively as well as is simplified sufficiently for faster set point optimisation for on-line purposes. Numerical experiments evaluate the effectiveness of the proposed control scheme from various viewpoints including process operational and optimisation viewpoints.

Low-dose tissue plasminogen activator followed by planned rescue angioplasty reduces time to reperfusion for acute myocardial infarction treated at community hospitals.

The time from admission to reperfusion in patients with acute myocardial infarction (AMI) was compared according to the type of hospital and treatment strategy. A total of 164 patients with a first AMI within 12h of onset were enrolled at one tertiary emergency center (TEC) and 6 community hospitals (CHs). The subjects were randomly assigned to receive either primary percutaneous transluminal coronary angioplasty (PTCA) (TEC-primary PTCA and CHs-primary PTCA groups) or 800,000 units of intravenous monteplase, half the standard dose of a mutant tissue plasminogen activator (t-PA), followed by rescue PTCA if the Thrombolysis in Myocardial Infarction (TIMI) flow grade was 2 or less (TEC-monteplase and CHs-monteplase groups) on the first coronary angiogram. Sixty minutes after admission, TIMI flow grade 3 rates of the study groups were as follows, in descending order: TEC-monteplase group, CHs-monteplase group, TEC-primary PTCA group, and CHs-primary PTCA group (56%, 41%, 36%, and 8%, respectively; p<0.01). However, there was no significant difference in the final TIMI flow grade 3 rate among the 4 groups. In the CHs, the peak creatine kinase tended to be lower in the monteplase group than in the primary PTCA group. The results suggest that low-dose monteplase followed by rescue PTCA is an effective strategy for promoting early reperfusion in patients with AMI, especially those who are treated at CHs.

Accumulation of latent transforming growth factor-beta binding protein-1 and TGF beta 1 in extracellular matrix of filtering bleb and of cultured human subconjunctival fibroblasts.

PURPOSE: To examine immunohistochemically whether extracellular matrix (ECM) of the filtering bleb and of cultured human subconjunctival fibroblasts contains latent TGF beta binding protein-1 (LTBP-1) and TGF beta. METHODS: An enucleated human eye that had undergone trabeculectomy and cultured human subconjunctival fibroblasts were processed for light microscopic immunohistochemistry. Antibodies against LTBP-1, collagen types, fibrillin-1 and TGF beta s were used. TGF beta 1 was located by detecting beta 1-latency associated peptide (LAP). RESULTS: LTBP-1, beta 1-LAP and fibrillin-1 were all located in the subepithelial ECM as well as in the basal epithelial cells of the conjunctiva over the filtering bleb. TGF beta 2 and beta 3 were immunolocated to epithelium and/or fibroblasts/keratocytes. ECM deposited in confluent fibroblast cultures was positive for beta 1-LAP, LTBP-1 and fibrillin-1, whereas sparse cells were negative. CONCLUSIONS: LTBP-1, beta 1-LAP and fibrillin-1 are co-localized to the ECM of the filtering bleb and of cultured conjunctival fibroblasts. Both conjunctival epithelium and fibroblasts are considered to be the source of TGF beta in healing bleb. ECM secreted by in vivo and in vitro subconjunctival fibroblasts may works as a scavenger or repository of TGF beta.

[Efficacy of low-dose mutant tissue-type plasminogen activator followed by planned rescue percutaneous transluminal coronary angioplasty as reperfusion therapy for acute myocardial infarction].

OBJECTIVES: The efficacy of injection of a low-dose mutant tissue-type plasminogen activator (mt-PA), monteplase, followed by planned rescue percutaneous transluminal coronary angioplasty (PTCA) was compared with that of primary PTCA. METHODS: A total of 164 patients with acute myocardial infarction within 12 hr from onset were randomly assigned to a treatment with 80 x 10(4) U bolus of monteplase (Group M) or no administration (Group P) by the envelope method, followed by immediate angiography with angioplasty in patients with Thombolysis in Myocardial Infarction (TIMI) flow grade 0, 1 or 2. RESULTS: There were no differences in baseline characteristics between the two groups. Initial angiography showed a higher reperfusion rate (TIMI 2 + 3: 21% + 38% vs 13% + 9%, p < 0.001) and the median time to TIMI 3 was shorter (63 vs 78 min, p < 0.005) in Group M than in Group P, but the final TIMI 3 rate was similar (93% vs 96%). Peak creatine kinase was lower, and predischarge left ventricular ejection fraction measured in 70% of all patients was higher (59 +/- 9% vs 54 +/- 14%, p = 0.02) in Group M than in Group P. Recurrent ischemia with ST elevation occurred in three patients in Group M, but death, re-acute myocardial infarction or stroke did not occur in either group and the rate of bleeding complication was similar (4.9% vs 3.7%). PTCA was performed less frequently in Group M, but medical expenses were comparable in both groups. CONCLUSIONS: Low-dose mt-PA followed by rescue PTCA is effective for early recanalization and preservation of left ventricular function without increases in bleeding complications or medical expenses. These results suggest that low-dose mt-PA should be given to all patients with acute myocardial infarction who are scheduled to undergo primary PTCA.

Disappearance of desmosomal components in rat corneal epithelium during wound healing.

PURPOSE: Epithelial migration is essential for healing of the ablated corneal epithelium. To reveal the mechanism which enables the corneal epithelial cells to dissociate during migration, we investigated the immunolocalization of the components of the desmosome, which is the main constituent of the intercellular junction attaching the intermediate filaments to the cell surface, desmoplakin 1, desmoglein and plakoglobin, in the corneal epithelium during wound healing in rats. METHODS: Under general anesthesia with ether inhalation, Wistar rats (n = 48) underwent removal of the central corneal epithelium of one eye with a small trephine and a scalpel. After various intervals of healing (5 min; 1, 3, 6, 9, 12, 24, 48 h; 1 and 2 weeks), the animals were killed and the affected eye was excised. Cryosections of each anterior segment of the eye were fixed with cold acetone and treated with primary antibodies against desmoplakin 1, desmoglein and plakoglobin. Immunolocalization of these substances was visualized by the peroxidase-diaminobenzidine reaction. RESULTS: A marked immunoreactivity for these desmosome components was detected at the intercellular junction in the normal corneal and conjunctival epithelium. At 6-24 h after epithelial ablation, a weak immunoreactivity for desmoplakin 1 and plakoglobin was observed in the migrating epithelium. At 48 h after epithelial ablation, a marked immunoreactivity for these desmosome components was seen again. At 6-48 h after epithelial ablation, a weak immunoreactivity for desmoglein was observed in the migrating epithelium. At 1 week after epithelial ablation, a marked immunoreactivity for this desmosome component reappeared. The regenerated epithelium gradually exhibited normal immunolocalization of the proteins. CONCLUSIONS: The desmosome components were considered to be degraded or destroyed prior to epithelial migration and reconstructed during healing of the squamous epithelium.

Alterations in ultrastructure and c-met expression in a case of ocular epithelial dysplasia following topical mitomycin C treatment.

PURPOSE: Topical mitomycin C (MMC) administration is reportedly effective in treating ocular surface neoplasms such as squamous cell carcinoma. We treated a case of ocular epithelial dysplasia that had spread too diffusely to be completely removed. We examined the ultrastructure of and c-met (hepatocyte growth factor receptor) expression in dysplastic epithelial cells from this case to evaluate the efficacy of MMC treatment. METHODS: Specimens of dysplastic epithelial tissue from the corneo-limbal region of a 62-year-old man were obtained before and after topical application of MMC. Specimens were examined ultrastructurally and immunohistochemically with an antibody against human c-met. RESULTS: Following topical application of MMC, the dysplastic epithelium exhibited multilayered epithelial cells similar to those seen before treatment. However, ultrastructural examination showed tight interdigitation between neighboring cells, with no intercellular spaces. Also, the marked immunoreactivity to c-met in the dysplastic epithelial cells before MMC treatment was decreased after treatment. CONCLUSIONS: Ultrastructural observations indicated a restoration of epithelial cellular differentiation following MMC application. The expression of c-met protein was also reduced. Thus, topical MMC was effective in treating epithelial dysplasia of the ocular surface, with no recurrence 15 months post-therapy.

'Tako-Tsubo' transient ventricular dysfunction: a case report.

During admission for investigation of dysphagia, an 82-year-old woman suddenly complained of dyspnea, which was followed by cardiogenic shock. Her symptoms, electrocardiogram, echocardiogram and laboratory data were compatible with an extensive acute anterior myocardial infarction. Emergency cardiac catheterization showed no atheromatous narrowing in any coronary artery. However, the contractions of the left and right ventricles were diffusely and severely impaired, except for some hyperkinesis of the basal area. The asynergy, as well as the abnormalities on the ECG, improved almost to normal by the 35th hospital day. An endomyocardial biopsy from the right ventricle during the acute phase showed atypical myocardial damage with proliferation of fine collagen fibers and small round-cell infiltration including polymorphologic leukocytes. This type of transient cardiac disorder has recently been described in Japan, and is called 'Tako-tsubo cardiomyopathy' because of the characteristic appearance of the left ventricular asynergy. In the present case, ventricular asynergy was not limited to the left ventricle, but was also present in the right ventricle.

Transforming growth factor-beta isoform proteins in cell and matrix deposits on intraocular lenses.

PURPOSE: To determine whether the cells that adhere to poly(methyl methacrylate) (PMMA) posterior chamber intraocular lenses (PC IOLs) implanted in human eyes produce transforming growth factor-beta (TGF-beta) isoforms and whether the acellular proteinaceous deposits on these IOLs contain TGF-beta. SETTING: Department of Ophthalmology, Wakayama Medical College, Japan. METHODS: Thirty-two PMMA PC IOLs explanted from Japanese patients were immunostained for TGF-beta1, -beta2, or -beta3, and observed under light microscopy. RESULTS: Cell deposits were observed on 12 IOLs and proteinaceous deposits on 16. Components of the cell deposits were mainly of macrophage origin. The cell and matrix deposits tested positive for each isoform of TGF-beta. CONCLUSION: The cells that adhered to implanted PMMA PC IOLs produced TGF-beta, and the extracellular matrix that accumulated on the surface of the IOLs contained TGF-beta. Transforming growth factor-beta from the cells on IOLs may influence the healing process of residual lens capsules after cataract surgery with IOL implantation.

Immunolocalization of TGF-beta1, -beta2, and -beta3, and TGF-beta receptors in human lens capsules with lens implants.

PURPOSE: To establish the alteration in expression pattern of transforming growth factor (TGF)-betas and their receptors during repair of lens capsules after cataract surgery, we immunohistochemically located TGF-beta isoforms and their receptors in human lens capsules before and after cataract surgery. METHODS: Ten post-cataract surgery capsular specimens were obtained during vitrectomy. Three sections of the anterior capsules were obtained during cataract surgery. A whole lens capsular bag immediately after lens extraction was obtained during vitrectomy. Cryosections of these specimens were processed for immunohistochemical analysis for TGF-beta1, TGF-beta2, TGF-beta3, TGF-beta receptor type I (TbetaR-I), type II (TbetaR-II) and type III (TbetaR-III), and were observed under light micros-copy. RESULTS: Lens epithelial cells (LECs) lining the inner surface of the anterior capsules exhibited immunoreactivity for TGF-beta2 and TbetaR-II. Immunoreactivity for TGF-beta1, -beta3, TbetaR-I and TbetaR-III was negative. In the whole capsular bag specimen, equatorial LECs were positive for TGF-beta1 and -beta2, but not for -beta3. In post-cataract surgery specimens, antibodies for each TGF-beta isoform labelled either the LECs or ECM accumulated on the capsules. Post-surgical LECs expressed TbetaR-I and TbetaR-II, and had also TbetaR-III in seven of the nine specimens examined. CONCLUSION: Expression pattern of TGF-beta s in quiescent LECs showed regional heterogeneity. Anterior LECs exhibited TGF-beta2 immunoreactivity, while equatorial LECs were positive for TGF-beta1 and -beta2. Quiescent LECs expressed TbetaR-II. LECs proliferating around IOLs expressed proteins of each TGF-beta isoform and each TbetaR. TGF-beta s were also localized in the ECM on capsules undergoing repair. TGF-beta3, TbetaR-I and TbetaR-III are up-regulated in LECs after cataract surgery.

Ampulla cardiomyopathy ('Takotusbo' cardiomyopathy)--reversible left ventricular dysfunction: with ST segment elevation.

The clinicopathologic findings of reversible ampulla-like ventriculogram of the left ventricle were studied in 8 elderly women and one middle-aged man. Their coronary arteriograms were normal, even in the 7 patients who had ST elevation on electrocardiogram. Coronary spasm was positive in only 2 of the 7 patients who received provocation tests. Biopsy specimens revealed focal myocyte injury. Normal coronary arteriograms during ST elevation and the presence of pathologic myocardial lesions were not consistent with a concept of stunned myocardium. The presence of myocardial lesions suggested that focal and disseminated myocardial damage had occurred.

[Calcification in culprit lesions of coronary artery disease].

Coronary calcification, a type of coronary atherosclerosis, has recently been closely examined in clinical cardiology because its presence may influence the selection of interventional therapy. In addition, plaque instability is one of the most important factors in the mechanism of acute coronary syndrome, and calcium deposit is frequently detected in advanced lesions. However, little is known about the clinical significance of coronary calcification. The incidence of calcium deposits was investigated in the culprit lesions (culprit coronary calcification) of patients with serious coronary artery disease to discover any cardioprotective effect. Initial coronary angiography was performed in 179 consecutive patients with acute myocardial infarction with Q wave on electrocardiography (AMI group; male 139, female 40, mean age 60.2 +/- 10 yr) and in 119 consecutive patients with stable effort angina pectoris (SAP group; male 78, female 41, mean age 63.8 +/- 8 yr) for which balloon plasty or bypass surgery was necessary from 1990 to 1997. Culprit coronary calcification was defined positive if the calcification deposit was present cinefluoroscopically within 5 mm from the culprit point. The culprit point was defined as the narrowest point after successful intracoronary thrombolytic therapy or the latest point to be dilated during a balloon inflation in direct or rescue percutaneous transluminal coronary angioplasty in the AMI group, and the narrowest point of the culprit lesion in the SAP group. There was no statistical difference in clinical background between the 2 groups other than male dominance in the AMI group and high incidence of family history of ischemic heart disease in the SAP group (p < 0.05). Culprit coronary calcification in patients over 50 years old was less frequently positive in the AMI group than the SAP group (26% vs 66%, p < 0.005, respectively). In younger patients under 50 years old, the incidence of culprit coronary calcification was low (14-15%) in both groups. Culprit coronary calcification was frequently positive in the right or the left anterior descending coronary artery in the SAP group (p < 0.005). There was no incidental sex difference of culprit coronary calcification. This comparison suggests that if a plaque contains cinefluoroscopically visible calcification, it may be regarded as less vulnerable or having a history of chronic process of atherosclerosis which results in protecting plaque rupture.

Immunolocalization of c-Fos and c-Jun in rat ocular surface epithelium.

We immunohistochemically located c-Fos and c-Jun, the major components of transcription factor activator protein 1 (AP1), in normal epithelia of rat cornea and conjunctiva to determine the expression of these genes in the ocular surface epithelia. Immunoreactivity for c-Fos was detected in the nuclei of basal cells of the limbal and conjunctival epithelia, while that for c-Jun was detected in the cytoplasm of the cells of these epithelia. The corneal epithelium lacked immunoreactivity for either protein. AP1 may have an important role in the maintenance of homeostasis of limbal and conjunctival epithelia.

Matrix metalloproteinases and tissue inhibitors of metalloproteinases of fibrous humans lens capsules with intraocular lenses.

PURPOSE: We located immunohistochemically the matrix metalloproteinases (MMP) -1, -2, -3 and -9 and the tissue inhibitors of matrix metalloproteinases (TIMP) -1 and -2 in the fibrous capsule of patients with intraocular lenses (IOLs). METHODS: During vitreoretinal surgery in 10 patients we obtained post-cataract surgery lens capsules with or without an IOL. The mean interval between the previous cataract operation and the extraction of the specimens was 35.2 months (range: 2-120 months). Circular sections of the anterior capsule with lens epithelial cells (LECs) were also obtained during cataract surgery. Specimens were processed for immunohistochemical identification of MMPs and TIMPs by light microscopy. RESULTS: While all the members of MMPs and TIMPs were not detected in the normal anterior capsules, they were detected in the ECM and/or LECs on the lens capsules extracted within 18 months after IOL implantations in all of the 4 patients, but were not observed in specimens obtained 18 months or longer postoperatively. In LECs of 1 capsule specimen 10 years postoperatively, MMP-1, but not other MMPs and TIMPs, was detected. CONCLUSIONS: MMPs and TIMPs were detected in the ECM and/or LECs on post-cataract surgery capsules. These proteins may be remodeling the newly deposited ECM and regulating LEC behavior on residual lens capsules in the early phase of healing after cataract surgery.

Immunolocalization of transcription factor AP1 in human ocular surface epithelia.

PURPOSE: The present study examined whether normal human ocular surfcae epithelia express AP1 components. Changes in expression patterns of these components in a case of ocular surface epithelial dysplasia was also evaluated before and after topical mitomycin C treatment. METHODS: Specimens of normal corneas (n = 2) and conjunctiva (n = 4) were obtained from 4 patients during cataract surgery or post mortem, while specimens of dysplastic epithelial tissue from the limbus were obtained from one patient. Specimens were immunohistochemically studied using antibodies against components of AP1. RESULTS: The normal corneal epithelium showed no staining with antibodies against c-Fos, Fra-2, FosB, c-Jun or JunB, whereas the limbal and bulbar conjunctival epithelia were positive for c-Fos, Fra-2, and c-Jun. Anti-FosB and -JunB antibodies reacted weakly with the conjunctival epithelium. JunD was absent in normal corneal and conjunctival epithelia. The dsyplastic epithelium showed positive labelling for c-Fos, Fra-2, c-Jun, and JunD throughout its thickness. Fra-1 was present in all specimens of epithelia examined. The dysplastic epithelium treated with mitomycin C was not labeled by anti-c-Fos or -Fra-2 antibody. CONCLUSION: Individual AP1 components show specific expression patterns in normal ocular surface epithelia and a case of dysplastic epithelium before and after topical MMC treatment, implying that these factors may play important roles in modulating epithelial cell function, e.g., proliferation and differentiation.

Immunohistochemical and ultrastructural analysis of dysplastic epithelium of human ocular surface: basement membrane and intermediate filament.

PURPOSE: The dysplastic corneal epithelium is characterized by the abnormal proliferation of epithelial cells. The phenotypes of these cells have not been elucidated. We investigated whether such epithelium expresses the phenotypes of corneal or conjunctival epithelial cells. METHODS: The corneas and conjunctivae from four normal subjects and from one patient with epithelial dysplasia of the central cornea were immunostained for IV and VII collagens and for cytokeratins. Monoclonal antibodies against collagen IV reacted to the [alpha1(IV)]2alpha2(IV) or alpha5(IV) molecule. Anti-cytokeratin antibodies were used to define epithelial cell types. The ultrastructure of the basement membrane (BM) of each specimen also was examined. RESULTS: Type VII collagen immunoreactivity was detected in all the specimens of epithelial BM. The anti-collagen IV [alpha1(IV)]2alpha2(IV) antibody labeled the conjunctival BMs, not the BMs of the corneal epithelia, of each subject. The normal corneal epithelial BM, not the BM of the conjunctival or dysplastic corneal epithelium, was immunolabeled with anti-alpha5(IV) antibody. The pattern of cytokeratin expression in the corneal epithelial dysplasia resembled that seen in the normal conjunctivae. Small breaks in the BM of dysplastic corneal epithelium were ultrastructurally revealed. The number of hemidesmosomes in the dysplastic corneal epithelium was decreased as compared with that in the normal BM. CONCLUSION: The composition of collagen types within the BM and the cellular phenotype of the dysplastic epithelium in the cornea resembled those of conjunctival epithelium, not of the cornea.

Immunohistochemical evaluation of cellular deposits on posterior chamber intraocular lenses.

PURPOSE: We used immunohistochemistry to characterize cellular and proteinaceous deposits on the surfaces of explanted posterior chamber intraocular lenses (PC-IOLs). METHODS: A total of 30 PC-IOLs were immunostained for the alpha- or beta-subunits of prolyl 4-hydroxylase, which is involved in collagen biosynthesis; cellular fibronectin; alpha B crystalline; and CD68, a macrophage marker, to characterize the cellular deposits that adhere to the IOL surfaces and to evaluate the distribution of cells involved in the deposition of extracellular matrix on IOLs. RESULTS: Cellular or proteinaceous deposits were observed on all 30 PC-IOLs. Cells that showed positive staining for alpha B crystallin were classified as lens epithelial cells; CD68-positive cells were considered to be of macrophagic origin. Positivity for cellular fibronectin, including the macrophages and related cells, appeared to be responsible for the accumulation of fibronectin on the surfaces of PC-IOLs. Prolyl 4-hydroxylase-positive cells were involved in the deposition of collagen on PC-IOLs. CONCLUSION: Immunohistochemical study revealed that macrophages, foreign-body giant cells, and lens epithelial cells adhered to explanted PC-IOLs. Such adherent cells are responsible for the deposition of extracellular matrix on the surfaces of PC-IOLs and may regulate the assembly of the extracellular matrix, influencing the biocompatibility of PC-IOLs.

Immunohistochemical identification of proteoglycan types in fibrotic human capsules with intraocular lens implants.

Lens capsules become fibrotic after cataract extraction. A variety of extracellular matrix (ECM) components accumulate on these capsules in association with the proliferation of lens epithelial cells. To provide a better understanding of the process of capsular fibrosis, we assessed the types of proteoglycans (PG) in human lens capsules with intraocular lenses (IOL). Lens capsules containing IOLs were removed from 1 patient with proliferative vitreoretinopathy and 1 patient with proliferative diabetic retinopathy. After treatment with chondroitinase ABC, tissue sections were processed for immunohistochemical detection of the proteoglycans including chondroitin, large PG, chondroitin 4-sulfate PG, chondroitin 6-sulfate PG, dermatan sulfate PG, and keratan sulfate PG. Extracellular matrix was found on the inner surface of the capsular bag. In association with what appeared to be proliferating lens epithelial cells, each of the six types of PG was present in the ECM on the capsules. All six types of PG might be involved in the fibrosis and opacification of lens capsules after extraction of the cataract and implantation of the IOL.

Immunolocalization of proto-oncogene products in keratocytes after epithelial ablation, alkali burn and penetrating injury of the cornea in rats.

BACKGROUND: We examined the immunolocalization of proto-oncogene products, including c-Fos and c-Jun, in the rat cornea during epithelial and stromal wound healing after simple epithelial ablation, penetrating injury or alkali burn. METHODS: Eighty-four male Wistar rats were divided into three groups and subjected to treatments as follows: (a) ablation of central corneal epithelium leaving basement membrane intact, (b) alkali burn in the central cornea with 1 N NaOH and (c) penetrating injury at the central cornea. The affected eyes were then enucleated after various intervals of healing. The frozen sections were immunohistochemically stained with the antibodies against proto-oncogene products. RESULTS: c-Fos- and c-Jun-immunoreactive cells were detected in the epithelium around the epithelial defect from 60 to 120 min after these treatments. The distribution of these cells were varied in these three types of injury. The immunoreactivities for these proteins were also detected in keratocytes after epithelial ablation. In the corneas with alkali burn, the immunoreactivities were detected in the keratocytes in the whole corneal stroma, and these immunoreactions were stronger than those observed in simple epithelial ablation. In the corneas with penetrating injury, such immunoreaction was seen only in keratocytes around the wound. CONCLUSION: These findings indicate that activator protein 1-mediated transcriptional activation for epithelial migration is initiated in the early phase after each injury, and that stromal keratocytes are also transcriptionally activated not only by alkali burn or penetrating injury but also by simple epithelial ablation in which basement membrane was not affected.

Immunolocalization of prolyl 4-hydroxylase in rabbit lens epithelial cells.

PURPOSE: To localize the enzyme prolyl 4-hydroxylase in the crystalline lens and determine the ability of lens epithelial cells (LECs) to synthesize procollagen. SETTING: Research laboratory, Department of Ophthalmology, Wakayama Medical College, Wakayama, Japan. METHODS: Phacoemulsification and aspiration of the crystalline lens followed by implantation of a poly(methyl methacrylate) intraocular lens (IOL) were performed in 1 eye each of 6 albino rabbits; the eye was enucleated 1 or 2 months later. Crystalline lenses were also extracted from the eyes of 2 rabbits. These samples were processed for immunohistochemical detection of the alpha- and beta-subunits of prolyl 4-hydroxylase. RESULTS: A monolayer of LECs was detected on the inner surface of the intact anterior capsule. Antibodies directed against both subunits of prolyl 4-hydroxylase reacted strongly to LECs proliferating on capsules with IOLs, whereas little or no reaction was observed in quiescent LECs or in the regenerated lenticular structure. CONCLUSION: The presence of prolyl 4-hydroxylase in LECs proliferating on the inner surface of the lens capsule suggests that these cells are involved in the production of procollagen and fibrosis during capsular injury and repair. Suppression of prolyl 4-hydroxylase activity may prevent the capsule opacification that results from cataract removal and IOL implantation.