Biomedical subjects

Hiroyuki Arai

Publications and source records attributed to Hiroyuki Arai.

At least 55 records · Page 3Linked to original sources

PubMed2005

Anabolic five subunit-type pyruvate:ferredoxin oxidoreductase from Hydrogenobacter thermophilus TK-6.

The thermophilic, obligately chemolithoautotrophic hydrogen-oxidizing bacterium, Hydrogenobacter thermophilus TK-6, assimilates carbon dioxide via the reductive tricarboxylic acid cycle. A gene cluster, porEDABG, encoding pyruvate:ferredoxin oxidoreductase (POR), which plays a key role in this cycle, was cloned and sequenced. The nucleotide sequence and the gene organization were similar to those of the five subunit-type 2-oxoglutarate:ferredoxin oxidoreductase from this strain, although the anabolic POR had been previously reported to consist of four subunits. A small protein (8 kDa) encoded by porE, which had not been detected in the previous work, was identified in the purified recombinant POR expressed in Escherichia coli, indicating that the enzyme is also a five-subunit type. Incorporation of PorE in the wild-type POR enzyme was confirmed by immunological analysis. PorA, PorB, PorG, and PorE were similar to the alpha, beta, gamma, and delta subunits of the four subunit-type 2-oxoacid oxidoreductases, respectively, and had conserved specific motifs. PorD had no specific motifs but was essential for the expression of the active enzyme.

Amino Acid Sequence↗

PubMed2005

Quinoline and benzimidazole derivatives: candidate probes for in vivo imaging of tau pathology in Alzheimer's disease.

Neurofibrillary tangles (NFTs), neuropil threads, and neuritic elements of senile plaques predominantly comprise hyperphosphorylated tau protein and represent pathological characteristics of Alzheimer's disease (AD). These lesions occur before the presentation of clinical symptoms and correlate with the severity of dementia. In vivo detection of these lesions would thus prove useful for preclinical diagnosis of AD and for tracking disease progression. The present study introduces three novel compounds, 4-[2-(2-benzoimidazolyl)ethenyl]-N,N-diethylbenzenamine (BF-126), 2-[(4-methylamino)phenyl]quinoline (BF-158), and 2-(4-aminophenyl)quinoline (BF-170), as candidate probes for in vivo imaging of tau pathology in the AD brain. When solutions of these compounds are injected intravenously into normal mice, these agents exhibit excellent brain uptake and rapid clearance from normal brain tissue. These compounds display relatively lower binding affinity to beta-amyloid fibrils and higher binding affinity to tau fibrils, compared with previously reported probe BF-168. In neuropathological examination using AD brain sections, BF-126, BF-158, and BF-170 clearly visualize NFTs, neuropil threads, and paired helical filament-type neuritis. Autoradiography using 11C-labeled BF-158 further demonstrated labeling of NFTs in AD brain sections. These findings suggest the potential usefulness of quinoline and benzimidazole derivatives for in vivo imaging of tau pathology in AD.

Aged↗

PubMed2005

ADRP/adipophilin is degraded through the proteasome-dependent pathway during regression of lipid-storing cells.

Adipose differentiation-related protein (ADRP) is a major protein associated with lipid droplets in various types of cells, including macrophage-derived foam cells and liver cells. However, the role of ADRP in the processes of formation and regression of these cells is not understood. When J774 murine macrophages were incubated with either VLDL or oleic acid, their content of both ADRP and triacylglycerol (TG) increased 3- to 4-fold. Induction of ADRP during TG accumulation was also observed in oleic acid-treated HuH-7 human liver cells. Addition of triacsin C, a potent inhibitor of acyl-CoA synthase, for 6 h decreased the amount of TG in VLDL-induced foam cells and oleic acid-treated liver cells; it decreased the amount of ADRP protein in parallel, indicating the amount of ADRP reduced during regression of the lipid-storing cells. Addition of a proteasome inhibitor during triacsin C treatment abolished the ADRP decrease and accumulated polyubiquitinated ADRP. In addition, the proteasome inhibitor reversed not only the degradation of ADRP but also TG reduction by triacsin C. These results suggest that cellular amounts of ADRP and TG regulate each other and that the ubiquitin-proteasome system is involved in degradation of ADRP during regression of lipid-storing cells.

Amino Acid Sequence↗

PubMed2005

Male elderly subthreshold depression patients have smaller volume of medial part of prefrontal cortex and precentral gyrus compared with age-matched normal subjects: a voxel-based morphometry.

BACKGROUND: The brain morphological changes in subthreshold depression (sD) have not been clarified. We examined the structural difference in regional gray matter volume between community-dwelling elderly subjects with sD and age-matched nondepressed normal subjects by voxel-based morphometry (VBM) based on magnetic resonance imaging (MRI). METHODS: Thirty-four community-dwelling elderly subjects with sD and 109 age-matched nondepressed normal subjects were studied by MRI. We defined subjects with sD as those who showed a Geriatric Depression Scale score of 15 or higher and a Mini Mental State Examination score of 22 or higher, and do not fulfill the criteria of major depressive disorder (MDD) in the Diagnostic and Statistical Manual for Mental Disorders IV. We collected brain magnetic resonance images of 34 subjects with sD and 109 age-matched normal subjects, and analyzed the difference in regional gray matter volume between these two groups by VBM. RESULTS: Male subjects with sD had significantly smaller volumes of the medial part of the bilateral frontal lobes and the right precentral gyrus than normal male subjects. LIMITATIONS: We have not clarified the discrepancy in the results of gender difference. CONCLUSIONS: Our study revealed that even community-dwelling elderly male subjects with sD show bilateral prefrontal gray matter volume reduction, which was reported to be observed in elderly patients with MDD, although there is no significant volume reduction in the hippocampus, which was also reported to be observed in MDD. Our study may contribute to clarifying the mechanism underlying brain pathological changes in sD.

Age of Onset↗

PubMed2005

Regulation of SR-BI protein levels by phosphorylation of its associated protein, PDZK1.

Scavenger receptor class B type I (SR-BI) is a high-density lipoprotein (HDL) receptor that mediates the selective uptake of HDL cholesterol and cholesterol secretion into bile in the liver. Previously, we identified an SR-BI-associated protein, termed PDZK1, from rat liver membrane extracts. PDZK1 contains four PSD-95/Dlg/ZO-1 (PDZ) domains, the first of which in the N-terminal region is responsible for the association with SR-BI. PDZK1 controls hepatic SR-BI expression in a posttranscriptional fashion both in cell culture and in vivo. In this study, we demonstrated that the C-terminal region of PDZK1 is crucial for up-regulating SR-BI protein expression. Metabolic labeling experiments and phosphoamino acid analysis revealed that PDZK1 is phosphorylated at Ser residues within this region. Point-mutation analysis demonstrated that PDZK1 is phosphorylated at Ser-509. Interestingly, a mutant PDZK1, in which Ser-509 was replaced with Ala, lost the ability to up-regulate SR-BI protein. We identified Ser-509 of PDZK1 as the residue that is phosphorylated by the cAMP-dependent PKA in vitro as well as in cell culture. Ser-509 of PDZK1 in rat liver was also phosphorylated, as shown by an Ab that specifically detects phosphorylated Ser-509. Administration of glucagon to Wistar rats increased PDZK1 phosphorylation as well as hepatic SR-BI and PDZK1 expression while it decreased plasma HDL levels, indicating that PDZK1 phosphorylation is hormonally regulated. These findings suggest that phosphorylation of PDZK1 has an important role in the regulation of hepatic SR-BI expression and, thus, influences plasma HDL levels.

Amino Acid Substitution↗

PubMed2005

MBR-1, a novel helix-turn-helix transcription factor, is required for pruning excessive neurites in Caenorhabditis elegans.

In the developing brain, excessive neurites are actively pruned in the construction and remodeling of neural circuits. We demonstrate for the first time that the pruning of neurites occurs in the simple neural circuit of Caenorhabditis elegans and that a novel transcription factor, MBR-1, is involved in this process. We identified MBR-1 as a C. elegans ortholog of Mblk-1, a transcription factor that is expressed preferentially in the mushroom bodies of the honeybee brain. Although Mblk-1 homologs are conserved among animal species, their roles in the nervous system have never been analyzed. We used C. elegans as an ideal model animal for analysis of neuronal development. mbr-1 is expressed in various neurons in the head and tail ganglia. A comparison of the morphology of mbr-1-expressing neurons revealed that excessive neurites connecting the left and right AIM interneurons are eliminated during larval stages in wild-type but are sustained through the adult stage in the mbr-1 mutant. In addition, mbr-1 expression is regulated by UNC-86, a POU domain transcription factor, and the pruning of the excessive AIM connection is impaired in the unc-86 mutant. These findings provide an important clue for further genetic dissection of neurite pruning.

Amino Acid Sequence↗

PubMed2005

Vitamin E is essential for mouse placentation but not for embryonic development itself.

Vitamin E (alpha-tocopherol) was discovered 80 years ago to be an indispensable nutrient for reproduction in the female. However, it has not been clarified when or where vitamin E is required during pregnancy. We examined the role of alpha-tocopherol in pregnancy using alpha-tocopherol transfer protein (Ttpa)-deficient mice fed specific alpha-tocopherol diets that led to daily, measurable change in plasma alpha-tocopherol levels from nearly normal to almost undetectable levels. A dietary supplement of alpha-tocopherol to pregnant Ttpa-/- (homozygous null) mice was shown to be essential for maintenance of pregnancy from 6.5 to 13.5 days postcoitum but found not to be crucial before or after this time span, which corresponds to initial development and maturation of the placenta. In addition, exposure to a low alpha-tocopherol environment after initiation of placental formation might result in necrosis of placental syncytiotrophoblast cells, followed by necrosis of fetal blood vessel endothelial cells. When Ttpa(-/-)-fertilized eggs were transferred into Ttpa+/+ (wild-type) recipients, plasma alpha-tocopherol concentrations in the Ttpa-/- fetuses were below the detection limit but the fetuses grew normally. These results indicate that alpha-tocopherol is indispensable for the proliferation and/or function of the placenta but not necessary for development of the embryo itself.

Animals↗

PubMed2005

Induction of autotaxin by the Epstein-Barr virus promotes the growth and survival of Hodgkin lymphoma cells.

A proportion of patients with Hodgkin lymphoma carry Epstein-Barr virus (EBV), an oncogenic herpesvirus, in their tumor cells. Although it is generally assumed that EBV contributes to the malignant phenotype of Hodgkin lymphoma cells, direct evidence in support of this is lacking. Here we show that EBV infection of Hodgkin lymphoma cells results in the induction of autotaxin, a secreted tumor-associated factor with lysophospholipase-D activity. Up-regulation of autotaxin increased the generation of lysophosphatidic acid (LPA) and led to the enhanced growth and survival of Hodgkin lymphoma cells, whereas specific down-regulation of autotaxin decreased LPA levels and reduced cell growth and viability. In lymphoma tissues, autotaxin expression was mainly restricted to CD30+ anaplastic large-cell lymphomas and Hodgkin lymphoma; in the latter, high levels of autotaxin were strongly associated with EBV positivity (P = .006). Our results identify the induction of autotaxin and the subsequent generation of LPA as key molecular events that mediate the EBV-induced growth and survival of Hodgkin lymphoma cells and suggest that this pathway may provide opportunities for novel therapeutic intervention.

Cell Line, Tumor↗

PubMed2005

Structure-activity relationships of fluorinated lysophosphatidic acid analogues.

Lysophosphatidic acid (LPA, 1- or 2-acyl-sn-glycerol 3-phosphate) displays an intriguing cell biology that is mediated via interactions with seven-transmembrane G-protein-coupled receptors (GPCRs) and the nuclear hormone receptor PPARgamma. To identify receptor-selective LPA analogues, we describe a series of fluorinated LPA analogues in which either the sn-1 or sn-2 hydroxyl group was replaced by a fluoro or fluoromethyl substituent. We also describe stabilized phosphonate analogues in which the bridging oxygen of the monophosphate was replaced by an alpha-monofluoromethylene (-CHF-) or alpha-difluoromethylene (-CF(2)-) moiety. The sn-2- and sn-1-fluoro-LPA analogues were unable to undergo acyl migration, effectively "freezing" them in the sn-1-O-acyl or sn-2-O-acyl forms, respectively. We first tested these LPA analogues on insect Sf9 cells induced to express human LPA(1), LPA(2), and LPA(3) receptors. While none of the analogues were found to be more potent than 1-oleoyl-LPA at LPA(1) and LPA(2), several LPA analogues were potent LPA(3)-selective agonists. In contrast, 1-oleoyl-LPA had similar activity at all three receptors. The alpha-fluoromethylene phosphonate analogue 15 activated calcium release in LPA(3)-transfected insect Sf9 cells at a concentration 100-fold lower than that of 1-oleoyl-LPA. This activation was enantioselective, with the (2S)-enantiomer showing 1000-fold more activity than the (2R)-enantiomer. Similar results were found for calcium release in HT-29 and OVCAR8 cells. Analogue 15 was also more effective than 1-oleoyl-LPA in activating MAPK and AKT in cells expressing high levels of LPA(3). The alpha-fluoromethylene phosphonate moiety greatly increased the half-life of 15 in cell culture. Thus, alpha-fluoromethylene LPA analogues are unique new phosphatase-resistant ligands that provide enantiospecific and receptor-specific biological readouts.

Animals↗

PubMed2005

LPA3-mediated lysophosphatidic acid signalling in embryo implantation and spacing.

Every successful pregnancy requires proper embryo implantation. Low implantation rate is a major problem during infertility treatments using assisted reproductive technologies. Here we report a newly discovered molecular influence on implantation through the lysophosphatidic acid (LPA) receptor LPA3 (refs 2-4). Targeted deletion of LPA3 in mice resulted in significantly reduced litter size, which could be attributed to delayed implantation and altered embryo spacing. These two events led to delayed embryonic development, hypertrophic placentas shared by multiple embryos and embryonic death. An enzyme demonstrated to influence implantation, cyclooxygenase 2 (COX2) (ref. 5), was downregulated in LPA3-deficient uteri during pre-implantation. Downregulation of COX2 led to reduced levels of prostaglandins E2 and I2 (PGE2 and PGI2), which are critical for implantation. Exogenous administration of PGE2 or carbaprostacyclin (a stable analogue of PGI2) into LPA3-deficient female mice rescued delayed implantation but did not rescue defects in embryo spacing. These data identify LPA3 receptor-mediated signalling as having an influence on implantation, and further indicate linkage between LPA signalling and prostaglandin biosynthesis.

Animals↗

PubMed2005

Biochemical and molecular characterization of a novel choline-specific glycerophosphodiester phosphodiesterase belonging to the nucleotide pyrophosphatase/phosphodiesterase family.

Nucleotide pyrophosphatases/phosphodiesterases (NPPs) are ubiquitous membrane-associated or secreted ectoenzymes that release nucleoside 5'-monophosphate from a variety of nucleotides and nucleotide derivatives. The mammalian NPP family comprises seven members, but only three of these (NPP1-3) have been studied in some detail. Previously we showed that lysophospholipase D, which hydrolyzes lysophosphatidylcholine (LPC) to produce lysophosphatidic acid, is identical to NPP2. More recently an uncharacterized novel NPP member (NPP7) was shown to have alkaline sphingomyelinase activity. These findings raised the possibility that other members of the NPP family act on phospholipids. Here we show that the sixth member of the NPP family, NPP6, is a choline-specific glycerophosphodiester phosphodiesterase. The sequence of NPP6 encodes a transmembrane protein containing an NPP domain with significant homology to NPP4, NPP5, and NPP7/alkaline sphingomyelinase. When expressed in HeLa cells, NPP6 was detected in both the cells and the cell culture medium as judged by Western blotting and by enzymatic activity. Recombinant NPP6 efficiently hydrolyzed the classical substrate for phospholipase C, p-nitrophenyl phosphorylcholine, but not the classical nucleotide phosphodiesterase substrate, p-nitrophenyl thymidine 5'-monophosphate. In addition, NPP6 hydrolyzed LPC to form monoacylglycerol and phosphorylcholine but not lysophosphatidic acid, showing it has a lysophospholipase C activity. NPP6 showed a preference for LPC with short (12:0 and 14:0) or polyunsaturated (18:2 and 20:4) fatty acids. It also hydrolyzed glycerophosphorylcholine and sphingosylphosphorylcholine efficiently. In mice, NPP6 mRNA was predominantly detected in kidney with a lesser expression in brain and heart, and in human it was detected in kidney and brain. The present results suggest that NPP6 has a specific role through the hydrolysis of polyunsaturated LPC, glycerophosphorylcholine, or sphingosylphosphorylcholine in these organs.

Amino Acid Sequence↗

PubMed2005

Neuronal expression and neuritogenic action of group X secreted phospholipase A2.

Although individual mammalian secreted phospholipase A(2) (sPLA(2)) enzymes exhibit unique tissue and cellular distributions, the cell type-specific functions of each enzyme remain largely unknown. In this study, we found by immunohistochemistry that group X sPLA(2) (sPLA(2)-X) is uniquely located in the peripheral neuronal fibers, an observation that was supported by detection of its transcript and protein in the neuronal cell line PC12 and in primary dorsal root ganglia neurons. Adenoviral expression of sPLA(2)-X in PC12 cells facilitated neurite outgrowth, particularly when combined with a suboptimal concentration of nerve growth factor. In neuronally differentiated PC12 cells, sPLA(2)-X was preferentially localized in the Golgi apparatus and growth cones, and proteolytic conversion of the proenzyme to mature enzyme mainly occurred after the secretion process. The neurite-extending ability of sPLA(2)-X depended on the production of its catalytic product, lysophosphatidylcholine. Moreover, nerve growth factor-induced neurite extension of PC12 cells was modestly but significantly attenuated by an anti-sPLA(2)-X antibody or by a small interfering RNA for sPLA(2)-X. These observations suggest the potential contribution of sPLA(2)-X to neuronal differentiation, and possibly repair, under certain conditions.

Adenoviridae↗

PubMed2005

Group VIB Ca2+-independent phospholipase A2gamma promotes cellular membrane hydrolysis and prostaglandin production in a manner distinct from other intracellular phospholipases A2.

Although group VIA Ca2+-independent phospholipase A2beta (iPLA2beta) has been implicated in various cellular events, the functions of other iPLA2 isozymes remain largely elusive. In this study, we examined the cellular functions of group VIB iPLA2gamma. Lentiviral transfection of iPLA2gamma into HEK293 cells resulted in marked increases in spontaneous, stimulus-coupled, and cell death-associated release of arachidonic acid (AA), which was converted to prostaglandin E2 with preferred cyclooxygenase (COX)-1 coupling. Conversely, treatment of HEK293 cells with iPLA2gamma small interfering RNA significantly reduced AA release, indicating the participation of endogenous iPLA2gamma. iPLA2gamma protein appeared in multiple sizes according to cell types, and a 63-kDa form was localized mainly in peroxisomes. Electrospray ionization mass spectrometry of cellular phospholipids revealed that iPLA2gamma and other intracellular PLA2 enzymes acted on different phospholipid subclasses. Transfection of iPLA2gamma into HCA-7 cells also led to increased AA release and prostaglandin E2 synthesis via both COX-1 and COX-2, with a concomitant increase in cell growth. Immunohistochemistry of human colorectal cancer tissues showed elevated expression of iPLA2gamma in adenocarcinoma cells. These results collectively suggest distinct roles for iPLA2beta and iPLA2gamma in cellular homeostasis and signaling, a functional link between peroxisomal AA release and eicosanoid generation, and a potential contribution of iPLA2gamma to tumorigenesis.

Adenocarcinoma↗

PubMed2005

Cerebrospinal fluid neprilysin is reduced in prodromal Alzheimer's disease.

Amyloid beta peptide (A beta) has been implicated in Alzheimer's disease (AD) as an initiator of the pathological cascades. Several lines of compelling evidence have supported major roles of A beta-degrading enzyme neprilysin in the pathogenesis of sporadic AD. Here, we have shown a substantial reduction of cerebrospinal fluid (CSF) neprilysin activity (CSF-NEP) in patients with AD-converted mild cognitive impairment and early AD as compared with age-matched control subjects. The altered CSF-NEP likely reflects changes in neuronal neprilysin, since transfer of neprilysin from brain tissue into CSF was demonstrated by injecting neprilysin-carrying viral vector into the brains of neprilysin-deficient mice. Interestingly, CSF-NEP showed an elevation with the progression of AD. Along with a close association of CSF-NEP with CSF tau proteins, this finding suggests that presynaptically located neprilysin can be released into CSF as a consequence of synaptic disruption. The impact of neuronal damages on CSF-NEP was further demonstrated by a prominent increase of CSF-NEP in rats exhibiting kainate-induced neurodegeneration. Our results unequivocally indicate significance of CSF-NEP as a biochemical indicator to pursue a pathological process that involves decreased neprilysin activity and A beta-induced synaptic toxicity, and the support the potential benefits of neprilysin up-regulation in ameliorating neuropathology in prodromal and early AD.

Aged↗

PubMed2005

The relationship between body mass index and a plasma lipid peroxidation biomarker in an older, healthy Asian community.

PURPOSE: To examine the association between body mass index (BMI) and the plasma level of a lipid peroxidation biomarker in a large sample of elderly healthy Asian population. This cross-sectional study included 1150 community-dwelling Japanese aged 70 years or older in 2002. METHODS: We measured the lipid peroxidation biomarker 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) using the ELISA method. We also measured the weight and height and calculated the BMI as weight (kg)/height (m)2. RESULTS: After adjustment for potential confounders, the mean +/- SE plasma 8-iso-PGF(2alpha) level was significantly higher in subjects with higher BMI: 21.1 +/- 0.8 pg/ml in those with BMI of 30.0 or more; 20.5 +/- 0.3 pg/ml in those with BMI between 25.0 and 29.9; 20.0 +/- 0.2 pg/ml in those with BMI between 18.5 and 24.9; and 19.0 +/- 0.7 pg/ml in those with BMI of less than 18.5 (p for trend = 0.011). CONCLUSIONS: Our results demonstrated that in the healthy Asian population, there was a modest but significant relationship between BMI and the plasma lipid peroxidation level.

Aged↗

PubMed2005

Acupuncture for patients with glaucoma.

CONTEXT: Research of the effects of one acupuncture method for patients with glaucoma, focusing on intraocular pressure (IOP) and visual acuity. OBJECTIVE: To explore the possibility of using acupuncture for patients with glaucoma. DESIGN: Pilot study utilizing a one-group preintervention, postintervention design. SETTING: Eleven patients with glaucoma were recruited through advertisement at the clinic for glaucoma. INTERVENTION: Acupuncture was carried out twice a week over 5 weeks. OUTCOME MEASURES: IOP, visual acuity, and subjective symptoms were observed at 15 minutes before and after acupuncture once a week and in a four-week follow-up. RESULTS: IOP was significantly improved at 15 minutes after acupuncture, at one week, two weeks, and five weeks and tended to be lower weekly. Uncorrected visual acuity was significantly improved at three weeks, four weeks, and five weeks, and best corrected visual acuity was significantly improved at five weeks. However at the four-week follow-up, significance remained only in uncorrected visual acuity. CONCLUSIONS: Although these results should be interpreted cautiously, acupuncture can be used to supplement the conventional therapy for glaucoma.

Acupuncture Therapy↗

PubMed2005

Experience with the Artisan phakic intraocular lens in Asian eyes.

PURPOSE: To investigate the efficacy and safety of implantation of an iris-claw phakic intraocular lens (PIOL), Artisan Myopia, in Asian eyes. SETTING: Minamiaoyama Eye Clinic, Tokyo, Japan. METHODS: Forty-four eyes of 32 Japanese patients and 1 Korean patient with high myopia had Artisan Myopia lens implantation to correct their refractive errors. Lens models, 5/8.5 or 6/8.5 (optic diameter/overall diameter), were chosen as standard lens model. A smaller lens model (5/7.5-Artisan Myopia Small) was implanted in eyes with corneal diameter less than 11.0 mm. Postoperative examinations were performed on 1 day, 1 week, 1 month, 3 months, 6 months, 1 year, and 2 years after surgery. Uncorrected visual acuity (UCVA), best corrected visual acuity (BCVA), manifest refraction, corneal endothelial cell counts, intraocular pressure, and complications were evaluated. RESULTS: Artisan Myopia Small lenses were implanted in 4 eyes (9.1%) and 8.5 mm diameter lenses were implanted in 40 eyes. Preoperative UCVA (logMAR) improved from 1.57 to 0.09 at 1 month after surgery and no regression was observed thereafter. Postoperative manifest refraction was -1.02 +/- 0.87 D (-3.25 to -0.00 D), and within 1.0 D in 20 eyes (55.6%), within 2.0 D in 32 eyes (88.9%) at 1 month after surgery, and stable during the follow-up period. The final BCVA decreased 2 lines in 2 eyes (4.5%) due to progression of age-related cataract. No serious complications such as angle closure or progressive endothelial cell loss were observed. CONCLUSION: Implantation of an Artisan iris-claw PIOL implantation may be a safe and effective procedure for Asian eyes.

Adult↗

PubMed2005

Early visual results with the 1CU accommodating intraocular lens.

PURPOSE: To prospectively assess the clinical outcome after implantation of the 1CU accommodating intraocular lens (IOL) and a foldable acrylic IOL (AcrySof, Alcon). SETTING: Department of Ophthalmology, Tokyo Dental College, Ichikawa Hospital, Ichikawa, and Minami Aoyama Eye Clinics, Tokyo, Yokohama, Japan. METHODS: Twenty-two eyes of 16 patients with cataract had phacoemulsification implantation of 1CU accommodating IOL. Twenty eyes of 10 age-matched and sex-matched patients with cataract had the same surgery but with a foldable acrylic IOL. All patients had assessments of the amplitude of accommodation, refraction, uncorrected and best corrected distance and near visual acuity, and distance corrected near visual acuity before surgery up to 12 months after surgery. Contrast visual acuities were measured 1 year after surgery. Anterior segment photography, intraocular pressure measurements, specular microscopy, and computerized topography were also performed. RESULTS: The final best corrected distance visual acuity was above 20/25 in all eyes with the 1CU and the AcrySof IOLs. The mean distance corrected near visual acuity was significantly higher in the 1CU IOL group than in the acrylic IOL group after 3 months. None of the eyes with the AcrySof IOL implants displayed an accommodative response at any examination. The peak mean amplitude of accommodation with the 1CU IOLs was observed at 3 months and was 0.5 diopters +/- 0.44 (SD). Accommodation amplitude declined after 6 months. CONCLUSION: The 1CU IOL provided additional near acuity postoperatively, but the benefit disappeared at 12 months with a concomitant decrease in accommodation amplitude owing to an increase in anterior and posterior capsular opacities.

Accommodation, Ocular↗