Loss of TRPV4 Cation Channel Inhibition of Macrophage Infiltration and Neovascularization in a Mouse Cornea.

Corneal injury-associated inflammation could induce inward-growing neovascularization from the periphery of the tissue. Such neovascularization could cause stromal opacification and curvature disturbance, and both potentially impair visual function. In this study, we determined the effects of the loss of transient receptor potential vanilloid 4 (TRPV4) expression on the development of neovascularization in the corneal stroma in mice by producing a cauterization injury in the central area of the cornea. New vessels were immunohistochemically labeled with anti-TRPV4 antibodies. TRPV4 gene knockout suppressed the growth of such CD31-labeled neovascularization in association with the suppression of infiltration of macrophages and tissue messenger RNA expression of the vascular endothelial cell growth factor A level. Treatment of cultured vascular endothelial cells with supplementation of HC-067047 (0.1 µM, 1 µM, or 10 µM), a TRPV4 antagonist, attenuated the formation of a tube-like structure with sulforaphane (15 µM, for positive control) that modeled the new vessel formation. Therefore, the TRPV4 signal is involved in injury-induced macrophagic inflammation and neovascularization activity by vascular endothelial cells in a mouse corneal stroma. TRPV4 could be a therapeutic target to prevent unfavorable postinjury neovascularization in the cornea.

Delayed regression of laser-induced choroidal neovascularization in TNFα-null mice.

We investigated the effects of lacking TNFα on the development and regression of Argon-laser-induced choroidal neovascularization (CNV) in mice. We lasered ocular fundus for induction of CNV in both wild-type (WT) and TNFα-null (KO) mice. Fluorescence angiography was performed to examine the size of CNV lesions. Gene expression pattern of wound healing-related components was examined. The effects of exogenous TNFα on apoptosis of human retinal microvascular endothelial cells (HRMECs) and on the tube-like structure of the cells were investigated in vitro. The results showed that Argon-laser irradiation-induced CNV was significantly larger in KO mice than WT mice on Day 21, but not at other timepoints. Lacking TNFα increased neutrophil population in the lesion. The distribution of cleaved caspase3-labelled apoptotic cells was more frequently observed in the laser-irradiated tissue in a WT mouse as compared with a KO mouse. Exogenous TNFα induced apoptosis of HRMECs and accelerated regression of tube-like structure of HRMECs in cell culture. Taken together, TNFα gene knockout delays the regression of laser-induced CNV in mice. The mechanism underlying the phenotype might include the augmentation of neutrophil population in the treated tissue and attenuation of vascular endothelial cell apoptosis.

Loss of sphingosine 1-phosphate receptor 3 gene function impairs injury-induced stromal angiogenesis in mouse cornea.

Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid generated through sphingosine kinase1 (SPK1)-mediated phosphorylation of sphingosine. We show here that injury-induced S1P upregulation increases corneal neovascularization through stimulating S1PR3, a cognate receptor. since this response was suppressed in S1PR3-knockout mice. Furthermore, Cayman10444, a selective S1PR3 inhibitor, reduced this response in WT mice. Such reductions in neovascularization were associated with reduced vascular endothelial growth factor A (VEGF-A) mRNA expression levels in WT TKE2 corneal epithelial cells and macrophages treated with CAY10444 as well as macrophages isolated from S1PR3 KO mice. S1P increased tube-like vessel formation in human vascular endothelial cells (HUVEC) and human retinal microvascular endothelial cells (HRMECs) cells expressing S1PR3. In S1PR3 KO mice, TGFß1-induced increases in αSMA gene expression levels were suppressed relative to those in the WT counterparts. In S1PR3 deficient macrophages, VEGF-A expression levels were lower than in WT macrophages. Transforming growth factor ß1(TGFß1) upregulated SPK1 expression levels in ocular fibroblasts and TKE2 corneal epithelial cells. CAY10444 blocked S1P-induced increases in VEGF-A mRNA expression levels in TKE2 corneal epithelial cells. Endogenous S1P signaling upregulated VEGF-A and VE-cadherin mRNA expression levels in HUVEC. Unlike in TKE2 cells, SIS3 failed to block TGFß1-induced VEGF-A upregulation in ocular fibroblasts. Taken together, these results indicate that injury-induced TGFß1 upregulation increases S1P generation through increases in SPK1 activity. The rise in S1P formation stimulates the S1PR3-linked signaling pathway, which in turn increases VEGF-A expression levels and angiogenesis in mouse corneas.

Candida guilliermondii-induced chorioretinitis in a patient with eating disorder.

Candidemia is a life-threatening fungal infection among patients undergoing long-term intravenous catheterization, hematopoietic stem cell transplantation, or immunosuppressive therapy, as well as patients with severe immunodeficiency or cancer. Endophthalmitis is a rare but severe form of ocular inflammation caused by infection of the intraocular cavity, which can lead to irreversible visual loss if not treated properly and promptly. The initial manifestation typically involves chorioretinitis, which requires early diagnosis and appropriate treatment. Candida guilliermondii is a non-Candida albicans yeast species; its frequency of detection in Japan has increased in recent years, and many drug-resistant and less-chorioretinitis-related strains are known. Here, we describe a 17-year-old girl with an eating disorder who exhibited chorioretinitis because of catheter-related bloodstream infection (CRBSI) caused by C. guilliermondii. The patient was hospitalized with severe weight loss, and she was presumed to develop candidemia because of immunosuppression during central parenteral nutrition therapy with a peripherally inserted central catheter. After onset of CRBSI, the catheter was immediately removed. Antifungal therapy was modified following fundus examination, fungal species confirmation, and drug sensitivity confirmation; thus, the patient recovered without long-term complications. To the best of our knowledge, this is the first report of C. guilliermondii-induced chorioretinitis in a patient with an eating disorder. Prolonged malnutrition and immunosuppression during nutritional therapy create a risk of candidemia in patients with eating disorders. After the onset of CRBSI, early administration and appropriate use of antifungal agents, with respect to specific ocular complications, are important for reduction of both mortality and ocular complications.

Effect of neointimal tissue morphology on vascular response to balloon angioplasty in lesions with in-stent restenosis after drug-eluting stent deployment: an optical coherence tomography analysis.

This study aimed to evaluate the vascular response to balloon angioplasty for drug-eluting stent (DES) in-stent restenosis (ISR) lesions based on our novel optical coherence tomography (OCT) classification to establish the optimal treatment strategy for ISR lesions after DES implantation. A total of 104 ISR lesions after DES implantation were imaged by OCT and categorized into the following six patterns: type I-homogeneous high-intensity tissue, type II-heterogeneous tissue with signal attenuation, type III-speckled heterogeneous tissue, type IV-mixed tissue containing poorly delineated region with invisible strut, type V-mixed tissue containing sharply delineated low-intensity region, and type VI-bright protruding tissue with an irregular surface. Serial volumetric OCT analysis was performed before and after balloon dilation to evaluate the vascular response to balloon angioplasty. After balloon dilation, the minimal decrease in neointimal volume was noted in type I lesions and maximal in type III lesions. In contrast, the increase in stent volume was significantly more in type I lesions than others. Neointimal tissue characterization by OCT allows us to provide useful information about the vascular response to balloon dilation, which can influence the therapeutic strategy for DES ISR lesions.

Optical coherence tomography characteristics of in-stent restenosis after drug-eluting stent implantation: a novel classification and its clinical significance.

This study aimed to establish a novel classification of in-stent restenosis (ISR) morphological characteristics after drug-eluting stent (DES) implantation as visualized by optical coherence tomography (OCT) and determine its clinical significance. A total of 133 lesions with intrastent restenosis after DES implantation were imaged by OCT. Neointimal tissue characteristics were categorized according to the classical classification as either homogeneous, heterogeneous, or layered. Then all tissues were also classified into six types as follows: homogeneous high-intensity tissue (type I), heterogeneous tissue with signal attenuation (type II), speckled heterogeneous tissue (type III), heterogeneous tissue containing poorly delineated region with invisible strut (type IV), heterogeneous tissue containing sharply delineated low-intensity region (type V), or bright protruding tissue with an irregular surface (type VI). The kappa value for interobserver agreement between the two observers was higher in the modified classification than in the classical classification (0.97 and 0.72, respectively). Most lesions classified as type V and VI were likely to be identified in patients on hemodialysis and located at the ostial right coronary artery. The duration from stent implantation to ISR was significantly longer in types IV and VI than in others. The incidence of stent fracture was significantly higher in types I and IV. This new modified classification enabled us to classify most ISR lesions easily with higher reproducibility. The clinical significance of neointimal restenotic tissue classification by OCT became clear while using the modified classification.

Utility and Validity of Intracoronary Administration of Nicorandil Alone for the Measurement of Fractional Flow Reserve in Patients With Intermediate Coronary Stenosis.

BACKGROUND: Intracoronary (IC) administration of nicorandil has been proposed as an alternative choice of hyperemic agent for fractional flow reserve (FFR) measurements. This study evaluated the utility and validity of IC nicorandil administration alone to induce maximal hyperemia.Methods and Results:Two-hundred-seven patients with coronary artery disease listed for coronary angiography with FFR were prospectively enrolled. FFR was measured after (1) IC administration of nicorandil 2 mg (ICNIC2 mg); (2) continuous intravenous (IV) adenosine triphosphatase (ATP) infusion at 150 µg/kg/min (IVATP150); (3) IV ATP infusion at 210 µg/kg/min (IVATP210); (4) IC administration of 0.5 mg nicorandil during IVATP150 (ICNIC0.5 mg+IVATP150); (5) IC administration of 1 mg nicorandil during IVATP150 (ICNIC1 mg+IVATP150); and (6) IC administration of 2 mg nicorandil during IVATP150 (ICNIC2 mg+IVATP150). The average FFR values and the rate of achieving maximum hyperemia after ICNIC2 mg, IVATP150, IVATP210, ICNIC0.5 mg+IVATP150, ICNIC1 mg+IVATP150, and ICNIC2 mg+IVATP150 were 0.85±0.08, 0.89±0.08, 0.85±0.09, 0.84±0.08, 0.83±0.08, 0.83±0.08 (P<0.01), and 92%, 54%, 91%, 96%, 99%, 99% (P<0.01), respectively. The incidence of systolic aortic pressure drop, chest discomfort, and transient atrioventricular block increased in a dose-dependent manner after IV ATP infusion, but almost no adverse effects were observed after ICNIC2 mg. CONCLUSIONS: ICNIC2 mg produced a more pronounced hyperemia than continuous IV ATP, and might be the preferred method for assessment of FFR.

Immunohistochemical findings of lens capsules obtained from patients with dead bag syndrome.

PURPOSE: To investigate the extracellular matrix and cellular components in lens capsules extracted from patients with dead bag syndrome (DBS) through immunohistochemistry. SETTING: Department of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan, and Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, University of Utah, Salt Lake City, Utah. DESIGN: Immunohistochemical experimental study. METHODS: 9 capsular bag specimens from DBS cases, as well as 2 control specimens from late-postoperative in-the-bag intraocular lens dislocation cases related to previous vitrectomy, pseudoexfoliation, and blunt trauma were included. They were processed for histopathology; unstained sections were obtained from each one and analyzed by immunohistochemistry targeting collagen type IV, laminin, vimentin, collagen type I, and fibronectin. RESULTS: Immunohistochemistry in DBS showed lens capsule stained for basement membrane components. The outer part of the anterior capsule that was split from the inner part was more markedly stained for type IV collagen as compared with the posterior part. Faint staining for fibrous posterior capsular opacification (PCO) components, for example, collagen type I and fibronectin, was detected in limited areas, but the major portion of the capsule was free from these components. Small spotty vimentin-positive materials, suggesting the presence of cell debris, were also detected in limited samples. CONCLUSIONS: Small amounts of fibrotic PCO components were detected in capsules extracted from patients with DBS, but their major parts were free from PCO components. Current findings suggest small amounts of lens epithelial cells were present after surgery and secreted fibrous components before undergoing cell death process.

Effects of Ripasudil Hydrochloride on Epithelial Repair in a Mouse Cornea.

PURPOSE: Effect of topical administration of a Rho kinase inhibitor, ripasudil, on epithelial wound healing in a mouse cornea was investigated. Effects of treatment of cultured human corneal epithelial cell (HCEC) line and organ-cultured corneal epithelium with ripasudil on expression of p-ERK was also examined. METHODS: Epithelial defects with a diameter of 2.0 mm were prepared in the central corneas of C57BL/6 mice with or without 1-week travoprost pre-treatment, to which ripasudil or PBS as a control was instilled every 6 h immediately after preparation. The mice eyes were cultured with or without travoprost for 24-hrs. The expression levels of p-ERK in epithelium of mice eyes were compared by immunostaining after further 24-hrs culture with or without ripasudil for 24-hrs. HCEC were cultured with or without ripasudil and processed for examination for proliferation activity and protein expression of p-ERK by either immunostaining or Western blotting. The cells were also treated with or without travoprost for 24-hrs, and were further cultured with or without ripasudil. Expression levels of p-ERK were examined by Western blotting. RESULTS: Ripasudil treatment suppressed post-debridement epithelial healing in association with reduced proliferation activity in peripheral (limbal) epithelium in cornea with or without pre-treatment with travoprost. Ripasudil treatment accelerated p-ERK expression. Ripasudil supplementation upregulated proliferation with increased p-ERK in HCEC. CONCLUSION: Ripasudil treatment promotes wound healing of the mouse corneal epithelium by enhancing cell proliferation on peripheral (limbal) epithelium.

Impaired T lymphocyte trafficking in mice deficient in an actin-nucleating protein, mDia1.

Trafficking of immune cells is controlled by directed migration of relevant cells toward chemotactic signals. Actin cytoskeleton undergoes continuous remodeling and serves as machinery for cell migration. The mDia family of formins and the Wiskott-Aldrich syndrome protein (WASP)-Arp2/3 system are two major actin nucleating-polymerizing systems in mammalian cells, with the former producing long straight actin filaments and the latter producing branched actin meshwork. Although much is known about the latter, the physiological functions of mDia proteins are unclear. We generated mice deficient in one mDia isoform, mDia1. Although mDia1(-/-) mice were born and developed without apparent abnormality, mDia1(-/-) T lymphocytes exhibited impaired trafficking to secondary lymphoid organs in vivo and showed reduced chemotaxis, little actin filament formation, and impaired polarity in response to chemotactic stimuli in vitro. Similarly, mDia1(-/-) thymocytes showed reduced chemotaxis and impaired egression from the thymus. These results suggest that mDia1 plays a distinct role in chemotaxis in T lymphocyte trafficking.

Rho GTPases in animal cell mitosis.

The Rho GTPases have been thought to influence cell morphogenesis through remodeling of the actin cytoskeleton. Consistently, downstream targets such as the mDia family of formins and the WASP family proteins induce actin nucleation and polymerization, and another set of downstream effectors, the ROCK family protein kinases, are involved in regulation of actomyosin contractility. However, evidence has now accumulated that Rho GTPases also regulate local dynamics of microtubules. The mDia family proteins, for example, function downstream of Rho to stabilize and align microtubules in interphase cells. Concomitantly, the role of Rho GTPases in animal cell division, once thought to be limited to cytokinesis, has now been shown to extend to mitosis. Recent work indicates that they may function during both spindle orientation and chromosome congression. However, their involvement is cell-type-specific, raising arguments for and against a mitotic role for Rho GTPases.

Impaired healing in an incision wound in corneal stroma in a lumican-null mouse.

PURPOSE: We investigated healing pattern of an incisional wound in corneal stroma of lumican-null (KO) mice. METHODS: C57BL/6 mice (wild-type, WT) and lumican-null (knockout, KO) mice were used. A linear full-thickness incision was produced in one cornea of each mouse. After intervals of healing, the corneas were processed for the following analyses. Histology was employed to measure the distance between each edge of the disrupted Descemet's membrane at the center of the cornea. Immunohistochemistry and real-time RT-PCR were employed to evaluate the expression of wound healing-related components in the tissue. Cultured ocular fibroblasts were obtained from cornea and sclera of WT and KO postnatal day 1 pups. The cells were subjected to examination for cell proliferation and expression of wound healing-related gene products. In vitro gel contraction assay was used to asses cell contractile activity of WT and KO cells. RESULTS: At day 5 of incision, the distance between the disrupted Descemet's membrane was larger in a KO mouse as compared with a WT mouse. Myofibroblast appearance in the wound was suppressed by the loss of lumican. The loss of lumican downregulated TGFß1's effects on mRNA expression of α-smooth muscle actin and collagen Ia1 in cultured ocular fibroblasts. Cell proliferation rate increased in injured stroma, which was further supported by in vitro datum of cell proliferation augmentation by the loss of lumican. Loss of lumican suppressed cell-mediated gel contraction. CONCLUSION: Loss of lumican perturbs the healing of penetrating incision in mouse corneal stroma in association with suppression of myofibroblast generation.

Anomaly of cornea and ocular adnexa in spinster homolog 2 (Spns2) knockout mice.

Spinster 2 (Spns2) is a transporter that pumps sphingosine-1-phosphate (S1P), a bioactive lipid mediator synthesized in the cytoplasm, out of cells into the inter cellular space. S1P is a signal that modulates cellular behavior during embryonic development, inflammation and tissue repair, etc. A Spns2-null (KO) mouse is born with failure of eyelid closure (eyelid-open-at birth; EOB) and develop corneal fibrosis in adulthood. It remains elusive whether corneal lesion is caused by exposure to keratitis (lagophthalmos) of EOB phenotype or the loss of Spns2 directly perturbs the corneal tissue morphogenesis and intra-eyelid structures. Therefore, we investigated differences between the cornea and ocular adnexa morphogenesis in KO and wild-type (WT) embryos and adults as well. The loss of Spns2 perturbs cornea morphogenesis during embryonic development as early as E16.5 besides EOB phenotype. Histology showed that the corneal stroma was thinner with less extracellular matrix accumulation, e.g., collagen and keratocan in the KO mouse. Epithelial stratification, expression of keratin 12 and formation of desmosomes and hemidesmosomes were also perturbed in these KO corneas. Lacking Spns2 impaired morphogenesis of the Meibomian glands and of orbicularis oculi muscles. KO glands were labeled for ELOVL4 and PPARγ and were Oil-Red O-positive, suggesting KO acinar cells possessed functionality as the glands. This is the first report on the roles of Spns2 in corneal and Meibomian gland morphogenesis. Corneal tissue destruction in an adult KO mouse might be due to not only lagophthalmos but also to an impaired morphogenesis of cornea, Meibomian glands, and orbicularis oculi muscle.

Late peri-stent contrast staining appearance due to rupture of atherogenic neointima following drug-eluting stent.

The development of peri-stent contrast staining (PSS) after coronary intervention with implantation of a stent is observed in approximately 1-3% of patients treated with drug-eluting stent. Although the cumulative incidences of late in-stent restenosis and stent thrombosis are significantly higher in lesions with PSS than in those without the finding, the mechanisms for the development of PSS have not yet been fully elucidated. In this report, we describe a case of rapid development of PSS with ulcer formation caused by rupture of atherogenic neointima, which was observed by serial optical coherence tomography examinations over 6 months. Protrusion of the stent-jailed underlying necrotic core toward the lumen by the contracting force might have resulted in formation of atherogenic neointima within the stent. Subsequently, rupture of this necrotic core induced by iatrogenic neointimal injury due to balloon dilation and dissolution of the accumulated necrotic core may have resulted in PSS formation 6 months after the procedure. These findings may be helpful for consideration of etiology and therapeutic strategy for lesions with PSS. .

Acute myocardial infarction in a patient with uncorrected tetralogy of Fallot accompanied by coronary artery ectasia: A case report.

A 63-year-old male with a medical history of uncorrected tetralogy of Fallot (TOF) presented to our hospital due to acute myocardial infarction (AMI). Emergency coronary angiography (CAG) was performed and it showed a severe thrombotic stenosis in the middle right coronary artery (RCA) and total thrombotic occlusion of the posterior descending branch of the RCA. Subsequently, percutaneous coronary artery intervention (PCI) under the guidance of intravascular ultrasound (IVUS) was performed. He was discharged on the 14th day in stable condition. Nine months after the PCI procedure, coronary computed tomography angiography was performed for follow-up, which revealed tetralogy of Fallot and complete resolution of the thrombus and ectasic coronary artery without stenosis. When he was 70 years old, he was transferred to our hospital because of recurrent AMI. As emergency CAG showed total thrombotic occlusion of the middle RCA, IVUS-guided PCI was performed. We experienced a very rare case of AMI in an adult patient with uncorrected TOF accompanied by coronary artery ectasia (CAE). To the best of our knowledge, this is the first case of AMI in an adult patient with uncorrected TOF accompanied by CAE. .

Ect2 and MgcRacGAP regulate the activation and function of Cdc42 in mitosis.

Although Rho regulates cytokinesis, little was known about the functions in mitosis of Cdc42 and Rac. We recently suggested that Cdc42 works in metaphase by regulating bi-orient attachment of spindle microtubules to kinetochores. We now confirm the role of Cdc42 by RNA interference and identify the mechanisms for activation and down-regulation of Cdc42. Using a pull-down assay, we found that the level of GTP-Cdc42 elevates in metaphase, whereas the level of GTP-Rac does not change significantly in mitosis. Overexpression of dominant-negative mutants of Ect2 and MgcRacGAP, a Rho GTPase guanine nucleotide exchange factor and GTPase activating protein, respectively, or depletion of Ect2 by RNA interference suppresses this change of GTP-Cdc42 in mitosis. Depletion of Ect2 also impairs microtubule attachment to kinetochores and causes prometaphase delay and abnormal chromosomal segregation, as does depletion of Cdc42 or expression of the Ect2 and MgcRacGAP mutants. These results suggest that Ect2 and MgcRacGAP regulate the activation and function of Cdc42 in mitosis.

Cdc42 and mDia3 regulate microtubule attachment to kinetochores.

During mitosis, the mitotic spindle, a bipolar structure composed of microtubules (MTs) and associated motor proteins, segregates sister chromatids to daughter cells. Initially some MTs emanating from one centrosome attach to the kinetochore at the centromere of one of the duplicated chromosomes. This attachment allows rapid poleward movement of the bound chromosome. Subsequent attachment of the sister kinetochore to MTs growing from the other centrosome results in the bi-orientation of the chromosome, in which interactions between kinetochores and the plus ends of MTs are formed and stabilized. These processes ensure alignment of chromosomes during metaphase and their correct segregation during anaphase. Although many proteins constituting the kinetochore have been identified and extensively studied, the signalling responsible for MT capture and stabilization is unclear. Small GTPases of the Rho family regulate cell morphogenesis by organizing the actin cytoskeleton and regulating MT alignment and stabilization. We now show that one member of this family, Cdc42, and its effector, mDia3, regulate MT attachment to kinetochores.

Inactivation of Rho GTPases with Clostridium difficile toxin B impairs centrosomal activation of Aurora-A in G2/M transition of HeLa cells.

During G2 phase of cell cycle, centrosomes function as a scaffold for activation of mitotic kinases. Aurora-A is first activated at late G2 phase at the centrosome, facilitates centrosome maturation, and induces activation of cyclin B-Cdk1 at the centrosome for mitotic entry. Although several molecules including HEF1 and PAK are implicated in centrosomal activation of Aurora-A, signaling pathways leading to Aurora-A activation at the centrosome, and hence mitotic commitment in vertebrate cells remains largely unknown. Here, we have used Clostridium difficile toxin B and examined the role of Rho GTPases in G2/M transition of HeLa cells. Inactivation of Rho GTPases by the toxin B treatment delayed by 2 h histone H3 phosphorylation, Cdk1/cyclin B activation, and Aurora-A activation. Furthermore, PAK activation at the centrosome that was already present before the toxin addition was significantly attenuated for 2 h by the addition of toxin B, and HEF1 accumulation at the centrosome that occurred in late G2 phase was also delayed. These results suggest that Rho GTPases function in G2/M transition of mammalian cells by mediating multiple signaling pathways converging to centrosomal activation of Aurora-A.

A Case of Repeating Transient Increase in Intraocular Pressure by Instability of an Intraocular Lens Implanted in the Capsular Bag.

We observed repeated episodes of rapid increases in intraocular pressure (IOP) considered to be caused by an in-the-bag intraocular lens (IOL) instability in a patient with an implanted IOL. As acute glaucoma attack-like increase in IOP was noted in the left eye on November 8, she was admitted to Wakayama Medical University Hospital. The findings at the first examination included an IOP of 62 mm Hg, instability of a PMMA one-piece IOL, shallow anterior chamber, narrow angle, moderate mydriasis, and loss of pupillary light reaction in the left avitreous eye. On November 15, a 6-mm Hg increase in IOP was observed during 60-min dark room prone provocative testing. After the first examination, the patient perceived pain and reduced visual acuity of the left eye and emergently consulted our hospital twice. Despite miosis, normalization of the anterior chamber depth and IOP with widening of the angle were achieved by resting in the supine position. These episodes were thought to be caused by instability and anterior shift of the IOL. On January 17, 2018, suture fixation of the in-the-bag IOL was performed. The IOL was fixed by transscleral suturing of the bilateral supporting parts to the sclera. Recurrence of sudden ophthalmalgia, instability of the in-the-bag IOL, and an increase in IOP have not been observed for 1 year after surgical treatment. Instability of an in-the-bag IOL caused repeated acute angle-closure glaucoma-like attacks. The situation was well treated by suturing and fixing the haptics of IOL to the sclera.

Successful percutaneous removal of dislodged ring-marker of optical coherence tomography catheter using the twisted wire technique with a guide-extension catheter: A case report.

An 81-year-old male with diabetes and hypertension was admitted to our hospital due to chest pain on exertion. Coronary angiography revealed a severe stenosis at the middle of right coronary artery (RCA). We performed percutaneous coronary intervention under the guidance of optical coherence tomography (OCT) to the lesion in the middle RCA. After balloon dilations, a drug-eluting stent was deployed to the lesion. Then, OCT examination was performed. At that time, fluoroscopy revealed a foreign body over the 0.014-inch guidewire in the distal RCA, which was the ring-marker of OCT catheter. As RCA blood flow was well preserved, percutaneous removal of the dislodged ring-marker was immediately attempted. At first, we tried to remove the dislodged ring-marker with the guide-extension catheter trapping technique. However, it failed and advanced balloon catheter made the dislodged ring-marker migrate more distally. Therefore, we tried the twisted wire technique with the guide-extension catheter and finally the dislodged ring-marker was removed with it. To the best of our knowledge, this is the first case report of a successful percutaneous removal of a dislodged ring-marker of OCT catheter using the twisted wire technique with a guide-extension catheter. .