Biomedical subjects

M Arai

Publications and source records attributed to M Arai.

At least 199 records · Page 11Linked to original sources

PubMed1998

N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly reduced infarct size in rabbit hearts.

BACKGROUND: N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, reduces the glycogenolytic rate by inhibiting the alpha-1,6-glucosidase of glycogen-debranching enzyme in the liver, in addition to possessing an antihyperglycemic action by blocking alpha-1,4-glucosidase in the intestine. Because the reduction of the glycogenolytic rate may be one of the mechanisms of myocardial protection in ischemic preconditioning, the compounds inhibiting myocardial alpha-1,6-glucosidase may be protective against ischemic damage. Thus, we investigated whether MOR-14 could inhibit alpha-1,6-glucosidase and reduce the infarct size in rabbit hearts without collateral circulation. METHODS AND RESULTS: MOR-14 dose-dependently decreased the alpha-1,6-glucosidase activity in rabbit heart extract. A tracer study demonstrated the myocardial uptake of a considerable amount of MOR-14 sufficient to fully inhibit alpha-1,6-glucosidase. To assess the infarct size-reducing effect of MOR-14, 54 rabbits were subjected to 30-minute coronary occlusion followed by 48-hour reperfusion. Preischemic treatment with 25, 50, and 100 mg/kg of MOR-14 dose-dependently reduced the infarct size (to 26+/-4%, 19+/-3%, and 14+/-2% of the area at risk, respectively), compared with the saline control (45+/-5%) without altering the blood pressure or heart rate. Another 40 rabbits given 100 mg of MOR-14 or saline 10 minutes before ischemia were euthanized at 10 or 30 minutes of ischemia for biochemical analysis. MOR-14 decreased the alpha-1,6-glucosidase activity to approximately 20% in vivo, reduced the glycogen breakdown, and attenuated the lactate accumulation at both 10 and 30 minutes of ischemia. CONCLUSIONS: Preischemic treatment with MOR-14 preserved glycogen, attenuated the accumulation of lactate, and reduced the myocardial infarct size by 69%. This cardioprotective effect was independent of changes of blood pressure and heart rate or regional blood flow. It may be associated with alpha-1,6-glucosidase inhibition, because MOR-14 markedly decreased the alpha-1,6-glucosidase activity in the heart.

1-Deoxynojirimycin↗

PubMed1998

Human T-cell leukemia virus type 1 Tax protein induces the expression of lymphocyte chemoattractant SDF-1/PBSF.

We investigated the mechanism of lymphocyte infiltration into tissues infected with human T-cell leukemia virus type 1 (HTLV-1). The cytokine SDF-1/PBSF is a highly efficient chemoattractant for lymphocytes. Reverse transcription-PCR analysis showed that among various human T-cell lines, those infected with HTLV-1 selectively expressed the SDF-1 gene. Expression of the viral protein Tax in a human T-cell line induced the expression of the SDF-1 gene, indicating that the constitutive expression of SDF-1 in virus-infected cell lines is at least in part mediated by Tax. HTLV-1-infected T-cell lines also expressed CXCR-4, a receptor for SDF-1. Moreover, chemotaxis assay showed that a HTLV-1-infected cell line migrated toward synthetic SDF-1. Thus, HTLV-1-infected cells are themselves responders for SDF-1. Our results suggest that SDF-1 induced by Tax may alter the distribution of HTLV-1-infected cells in vivo; hence it may contribute to their infiltration into affected tissues in HTLV-1-associated inflammatory diseases.

Animals↗

PubMed1998

Expression of FAP-1 (Fas-associated phosphatase) and resistance to Fas-mediated apoptosis in T cell lines derived from human T cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis patients.

Human T cell leukemia virus type 1 (HTLV-I) is the etiologic agent of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) with an autoimmune condition. We examined the sensitivity of HTLV-I-infected T cell lines to Fas-mediated apoptosis, which plays a critical role in the elimination of self-reactive T cells. Among 13 human T-cell lines, all 4 HAM-derived T cell lines and 4 of 6 non-HAM/HTLV-I T cell lines were resistant to apoptosis induced by anti-Fas antibody, whereas only 1 of 3 uninfected cell lines was resistant to apoptosis. The cell lines resistant to apoptosis expressed the viral tax gene and/or the cellular FAP-1 (Fas-associated phosphatase) gene, both of which inhibit Fas-mediated apoptosis in T cell lines. Although Tax is a transcriptional activator of a number of cellular genes, the expression of Tax in a T cell line did not induce the expression of FAP-1, suggesting that these two antiapoptotic proteins independently function in HTLV-I-infected cells. Seven of 10 HTLV-I-infected cell lines, compared with only 1 of 3 virus-negative cell lines, expressed FAP-1. All four HAM cell lines expressed the FAP-1 gene, and its level in these cells was higher than in other T cell lines. Our results suggest that virus-infected T cells escape Fas-mediated immune surveillance by the function of Tax and FAP-1, and this escape may be involved in the autoimmune condition observed in HAM/TSP patients.

Apoptosis↗

PubMed1998

Suppression of leukotriene formation in RBL-2H3 cells that overexpressed phospholipid hydroperoxide glutathione peroxidase.

The overexpression of phospholipid hydroperoxide glutathione peroxidase (PHGPx) by RBL-2H3 cells was used as the basis for an investigation of the effects of PHGPx on the formation of leukotrienes. The rates of production of leukotriene C4 (LTC4) and leukotriene B4 (LTB4) in cells that overexpressed PHGPx were 8 times lower than those in a control line of cells. The reduction in rates of production of leukotrienes apparently resulted from the increase in the PHGPx activity since control rates of formation of leukotrienes could be achieved in PHGPx-overexpressing cells upon inhibition of PHGPx activity by diethyl malate. The conversion of radioactively labeled arachidonic acid to intermediates in the lipoxygenase pathway, such as 5-hydroxyeicosatetraenoic acid (5-HETE), LTC4, and LTB4, was strongly inhibited in PHGPx-overexpressing cells that had been prelabeled with [14C]arachidonic acid. PHGPx apparently inactivated the 5-lipoxygenase that catalyzed the conversion of arachidonic acid to 5-hydroperoxyeicosatetraenoic acid (5-HPETE) since 5-HPETE is a common precursor of 5-HETE, LTC4, and LTB4. The rates of formation of LTC4 and LTB4 in PHGPx-overexpressing cells returned to control rates upon the addition of a small amount of 12-HPETE. Flow cytometric analysis revealed that the rapid burst of formation of lipid hydroperoxides induced by A23187 was suppressed in PHGPx-overexpressing cells as compared with the control lines of cells. Subcellular fractionation analysis showed that the amount of PHGPx associated with nuclear fractions from PHGPx-overexpressing cells was 3.5 times higher than that from the control line of cells. These results indicate that PHGPx might be involved in inactivation of 5-lipoxygenase via reductions in levels of the fatty acid hydroperoxides that are required for the full activation of 5-lipoxygenase. Thus, in addition to its role as an antioxidant enzyme, PHGPx appears to have a novel function as a modulator of the production of leukotrienes.

Animals↗

PubMed1998

Kinetic refolding of beta-lactoglobulin. Studies by synchrotron X-ray scattering, and circular dichroism, absorption and fluorescence spectroscopy.

beta-Lactoglobulin (beta LG) is a predominantly beta-sheet protein with a markedly high helical propensity and forms non-native alpha-helical intermediate in the refolding process. We measured the refolding reaction of beta LG with various techniques and characterized the folding kinetics and the structure of the intermediate formed within the burst phase of measurements, i.e. the burst-phase intermediate. Time-resolved stopped-flow X-ray scattering measurements using the integral intensity of scattering show that beta LG forms a compact, globular structure within 30 ms of refolding. The averaged radius of gyration within 100 ms is only 1.1 times larger than that in the native state, ensuring that the burst-phase intermediate is compact. The presence of a maximum peak in a Kratky plot shows a globular shape attained within 100 ms of refolding. Stopped-flow circular dichroism, tryptophan absorption and fluorescence spectroscopy show that pronounced secondary structure regains rapidly in the burst phase with concurrent non-native alpha-helix formation, and that the subsequent compaction process is accompanied by annealing of non-native secondary structure and slow acquisition of tertiary structure. These findings strongly suggest that both compaction and secondary structure formation in protein folding are quite rapid processes, taking place within a millisecond time-scale. The structure of the burst-phase intermediate in beta LG refolding was characterized as having a compact size, a globular shape, a hydrophobic core, substantial beta-sheets and remarkable non-native alpha-helical structure, but little tertiary structure. These results suggest that both local interactions and non-local hydrophobic interactions are dominant forces early in protein folding. The interplay of local and non-local interactions throughout folding processes is important in understanding the mechanisms of protein folding.

Animals↗

PubMed1998

Selective bowel decontamination of recipients for prevention against liver injury following orthotopic liver transplantation: evaluation with rat models.

Gut-derived substances can activate Kupffer cells to provoke hepatic necrosis after partial hepatectomy in rats. A similar situation may occur during orthotopic liver transplantation (OLT), as congestion in the intestinal wall, caused by portal vein occlusion, is inevitable during the operation. The contribution of such substances to liver injury following OLT was investigated in rats. Oral administration of polymyxin B sulfate for 7 days significantly altered intestinal bacterial flora in rats; Enterobacteriaceae diminished and anaerobes such as Bifidobacterium , Lactobacillus, Bacteroides, and Eubacterium increased in number, compared with the control rats. Also, this treatment significantly reduced endotoxin concentration in the portal blood 30 minutes after blood reflow following portal vein occlusion. When OLT was performed in rats using the liver preserved in cold University of Wisconsin solution for 18 hours, tissue factor activity in Kupffer cells (KC) isolated from the transplanted liver 1 hour after the operation was significantly higher than in that of normal rats. This increase was significantly reduced by pretreatment of the recipients with polymyxin B sulfate. In these recipients, serum alanine aminotransferase activity, tumor necrosis factor alpha (TNF alpha) concentration, and histological extent of liver necrosis were significantly attenuated at 24 hours after the operation compared with those of control rats. We conclude that the substances derived from bacilli sensitive to polymyxin B sulfate in the gut may be a contributing factor to liver injury following OLT in rats; we feel that this probably occurs by entering of the substances into the portal blood during the ahepatic phase of the operation to activate KC. Selective bowel decontamination of recipients with polymyxin B sulfate would be a candidate for protection against early graft failure following OLT.

Animals↗

PubMed1998

Equilibrium and kinetics of the folding of equine lysozyme studied by circular dichroism spectroscopy.

The equilibrium unfolding and the kinetics of unfolding and refolding of equine lysozyme, a Ca2+-binding protein, were studied by means of circular dichroism spectra in the far and near-ultraviolet regions. The transition curves of the guanidine hydrochloride-induced unfolding measured at 230 nm and 292.5 nm, and for the apo and holo forms of the protein have shown that the unfolding is well represented by a three-state mechanism in which the molten globule state is populated as a stable intermediate. The molten globule state of this protein is more stable and more native-like than that of alpha-lactalbumin, a homologous protein of equine lysozyme. The kinetic unfolding and refolding of the protein were induced by concentration jumps of the denaturant and measured by stopped-flow circular dichroism. The observed unfolding and refolding curves both agreed well with a single-exponential function. However, in the kinetic refolding reactions below 3 M guanidine hydrochloride, a burst-phase change in the circular dichroism was present, and the burst-phase intermediate in the kinetic refolding is shown to be identical with the molten globule state observed in the equilibrium unfolding. Under a strongly native condition, virtually all the molecules of equine lysozyme transform the structure from the unfolded state into the molten globule, and the subsequent refolding takes place from the molten globule state. The transition state of folding, which may exist between the molten globule and the native states, was characterized by investigating the guanidine hydrochloride concentration-dependence of the rate constants of refolding and unfolding. More than 80% of the hydrophobic surface of the protein is buried in the transition state, so that it is much closer to the native state than to the molten globule in which only 36% of the surface is buried in the interior of the molecule. It is concluded that all the present results are best explained by a sequential model of protein folding, in which the molten globule state is an obligatory folding intermediate on the pathway of folding.

Animals↗

PubMed1998

Sarcoplasmic reticulum genes are selectively down-regulated in cardiomyopathy produced by doxorubicin in rabbits.

The clinical utility of doxorubicin, an antineoplastic agent, is limited by its cardiotoxicity. Our objective was to determine whether expression of genes encoding proteins that affect Ca2+ homeostasis were altered in the hearts of rabbits chronically treated with doxorubicin. Twelve male New Zealand white rabbits received an injection of doxorubicin (2.5 mg/kg i.v.) once a week for 8 weeks. Eight rabbits were similarly injected with saline as controls. The cardiac function of both groups was evaluated 8 weeks after the final injection, as were the levels of expression of mRNA for Ca2+ transport proteins in the sarcoplasmic reticulum and plasma membrane. The amount of the sarcoplasmic reticulum Ca2+-ATPase and the Ca2+ uptake capacity of the protein were also quantitated. Cardiac output was significantly decreased in the doxorubicin-treated group (71+/-21 ml/min, P<0.05) compared with the control group (118+/-15 ml/min). The mRNA levels for the sarcoplasmic reticulum proteins were significantly diminished in the doxorubicin-treated hearts: ryanodine receptor-2 (relative expression level compared with controls, 0.35+/-0.13, P<0.01), sarcoplasmic reticulum Ca2+-ATPase (0.56+/-0.13, P<0.01), phospholamban (0.62+/-0.20, P<0.01) and cardiac calsequestrin (0. 57+/-0.26, P<0.01). In addition, both relative amount of sarcoplasmic reticulum Ca2+-ATPase protein (doxorubicin-treated group, 69+/-17% of control, P<0.01) and the Ca2+ uptake capacity (46. 9+/-9.8 nmol Ca2+/mg protein-5 min in doxorubicin group v 63.2+/-10. 4 in the control group, P<0.01) were concomitantly decreased with its mRNA expression level. Conversely, the mRNA levels for the plasma membrane proteins did not differ from those of control rabbits: the dihydropyridine receptor (relative expression level, 1. 03+/-0.30, N.S.), plasma membrane Ca2+-ATPase (0.93+/-0.33, N.S.) and the Na+/Ca2+ exchanger (0.87+/-0.34, N.S.). These findings suggest that a selective decrease in mRNA expression for sarcoplasmic reticulum Ca2+ transport proteins is responsible for the impaired Ca2+ handling, and thus, for the reduced cardiac function seen in the cardiomyopathy induced in rabbits by the long-term treatment with doxorubicin.

Animals↗

PubMed1998

Epidural administration of droperidol suppresses cisplatin-induced emesis: preliminary findings.

To evaluate the antiemetic effect of the epidural administration of droperidol on cisplatin-induced emesis, nine adult gastric cancer patients receiving intraoperative cisplatin chemotherapy were studied. After removal of the stomach, 0.05 mg/kg droperidol with 5 ml saline was injected into the epidural space through the epidural catheter. Thirty minutes later, 60 mg/m2 cisplatin was administered intravenously over 1h. Subsequently, the same dose of droperidol was also injected epidurally every 6 h for 18 h. Postoperatively, the antiemetic effect was evaluated until 30 h after the first epidural droperidol. As a result, all patients expressed almost complete antiemesis until 25 h. After 26 h, some patients complained of mild emesis. No potential side effects, such as hypotension, consciousness disturbance, and extrapyramidal signs, were noticed. Therefore, the present pilot study implies that a sole epidural administration of droperidol remarkably suppresses cisplatin-induced emesis.

Adult↗

PubMed1998

Multifocal electroretinogram indicates visual field loss in acute zonal occult outer retinopathy.

PURPOSE: To report alterations of electrophysiologic tests, including the multifocal electroretinogram, in a case of acute zonal occult outer retinopathy. METHOD: We recorded photopic, scotopic, and single-flash electroretinograms and a multifocal electroretinogram in a 47-year-old woman with acute zonal occult outer retinopathy in the right eye. RESULTS: Her visual acuity was 20/20 in the right eye throughout the follow-up period. The electroretinograms indicated retinal impairment of the right eye, predominantly in the cones. The multifocal electroretinogram showed reduced responses corresponding to the visual field defect of the static perimetry. CONCLUSIONS: In acute zonal occult outer retinopathy, impairment of the retinal area results in a visual field defect. The multifocal electroretinogram can be useful in determining the location of the defect.

Acute Disease↗

PubMed1998

Oxidation of cysteamine induced by gas-phase radicals from combustion smoke of poly (methyl methacrylate).

In order to obtain fundamental knowledge on biological damage caused by the smoke from combustion of poly(methyl-methacrylate) (PMMA), we investigated the oxidation of cysteamine induced by PMMA smoke. We suggest that the long-lived and oxygen-centered radicals involved in PMMA smoke should play an important role in the oxidation of cysteamine. The mechanism for the oxidation of cysteamine by combustion smoke of PMMA was postulated as radical initiated chain reactions, taking into account the effect of pH, oxygen and radical concentrations.

Chromatography, High Pressure Liquid↗

PubMed1998

Neutrophils, lipid peroxidation, and nitric oxide in gastric reperfusion injury in rats.

Nitric oxide (NO) modulation of ischemia-reperfusion injury was investigated by measuring lipid peroxide and neutrophil accumulation in rat stomachs treated with NG-nitro-L-arginine (L-NNA), a specific NO synthase inhibitor. Ischemia-reperfusion injury was induced in the rat stomach. Treatment with L-NNA for 3 days at a dose of 3 mg/kg/day significantly enhanced this injury. This enhancement was reversed by the simultaneous administration of L-arginine at a dose of 30 mg/kg/day. Both thiobarbituric acid (TBA)-reactive substances, an index of lipid peroxidation, and myeloperoxidase (MPO) activity, an index of tissue-associated neutrophil accumulation, were increased in the gastric mucosa after ischemia-reperfusion. L-NNA treatment enhanced these increases in TBA-reactive substances and MPO activity. The increase in the area of gastric erosions correlated closely with accumulation of TBA-reactive substances as well as the increase in MPO activity. Enhancement of ischemia-reperfusion injury by L-NNA treatment was inhibited by injection with anti-neutrophil antibody, anti-platelet activating factor (PAF) antagonist, and anti-leukotriene B4 (LTB4) receptor antagonist. In addition, the increase in TBA-reactive substances and MPO activity was decreased by these antibodies or antagonists. Enhancement of reperfusion-induced gastric mucosal injury associated with inhibition of NO synthesis may involve neutrophil infiltration and lipid peroxide accumulation in the gastric mucosa, mediated by PAF and LTB4.

Animals↗

PubMed1998

Lipid transfer particle catalyzes transfer of carotenoids between lipophorins of Bombyx mori.

The yellow color of Bombyx mori hemolymph is due to the presence of carotenoids, which are primarily associated with lipophorin particles. Carotenoids were extracted from high density lipophorin (HDLp) of B. mori and analyzed by HPLC. HDLp contained 33 micrograms of carotenoids per mg protein. Over 90% of carotenoids were lutein while alpha-carotene and beta-carotene were minor components. When larval hemolymph was subjected to density gradient ultracentrifugation, a second minor yellow band was present, which was identified as B. mori lipid transfer particle (LTP). During other life stages examined however, this second band was not visible. To determine if coloration of LTP may fluctuate during development, we determined its concentration in hemolymph and compared it to that of lipophorin. Both proteins were present during all life stages and their concentrations gradually increased. The ratio of lipophorin: LTP was 10-15:1 during the fourth and fifth instar larval stages, and 20-30:1 during the pupal and adult stages. Thus, there was no correlation between the yellow color attributed to LTP and its hemolymph concentration. It is possible that yellow coloration of the LTP fraction corresponds to developmental stages when the particle is active in carotene transport. To determine if LTP is capable of facilitating carotene transfer, we took advantage of a white hemolymph B. mori strain which, when fed artificial diet containing a low carotene content, gives rise to a lipophorin that is nearly colorless. A spectrophotometric, carotene specific, transfer assay was developed which employed wild type, carotene-rich HDLp as donor particle and colorless low density lipophorin, derived from the white hemolymph strain animals, as acceptor particle. In incubations lacking LTP carotenes remained associated with HDLp while inclusion of LTP induced a redistribution of carotenes between the donor and acceptor in a time and concentration dependent manner. Time course studies suggested the rate of LTP-mediated carotene transfer was relatively slow, requiring up to 4 h to reach equilibrium. By contrast, studies employing 3H-diacylglycerol labeled HDLp as donor particle in lipid transfer assays revealed a rapid equilibration of label between the particles. Thus, it is plausible that the slower rate of LTP-mediated carotene transfer is due to its probable sequestration in the core of HDLp.

Animals↗

PubMed1998

Impaired expression of brain natriuretic peptide gene in diabetic rats with myocardial infarction.

Accordingly, we induced streptozotocin diabetes in rats and evaluated the effects of ligating the coronary artery to produce myocardial infarct by analyzing hemodynamics and the expression of brain natriuretic peptide (BNP) messenger (m) RNA. Eight-week diabetic rats and age-matched nondiabetic rats underwent ligation of the coronary artery for 1 week. Left ventricular end-diastolic pressure (LVEDP) was not statistically different between diabetic rats (15+/-6 mmHg) and nondiabetic rats (13+/-9 mmHg) 1 week after coronary ligation, size of infarct, systolic blood pressure were also similar in both groups after coronary ligation. The BNP mRNA/beta-actin mRNA ratio in right ventricle of nondiabetic rats with MI was increased to 350+/-60%, however, in diabetic rats with MI, that was slightly increased to 200+/-50% (P < 0.01). The level of BNP mRNA in the left ventricle of diabetic rats with MI was not increased significantly (120+/-30% versus that in diabetic rats without MI), although that in left ventricle of nondiabetic rats with MI was increased to 280+/-40% versus nondiabetic rats without MI (P < 0.01). Cardiac BNP synthesis in diabetic rats completely reverted to control levels after insulin therapy.

Animals↗

PubMed1998

Assimilation of cellooligosaccharides by a cell surface-engineered yeast expressing beta-glucosidase and carboxymethylcellulase from aspergillus aculeatus

Since Saccharomyces cerevisiae lacks the cellulase complexes that hydrolyze cellulosic materials, which are abundant in the world, two types of hydrolytic enzymes involved in the degradation of cellulosic materials to glucose were genetically co-immobilized on its cell surface for direct utilization of cellulosic materials, one of the final goals of our studies. The genes encoding FI-carboxymethylcellulase (CMCase) and beta-glucosidase from the fungus Aspergillus aculeatus were individually fused with the gene encoding the C-terminal half (320 amino acid residues from the C terminus) of yeast alpha-agglutinin and introduced into S. cerevisiae. The delivery of CMCase and beta-glucosidase to the cell surface was carried out by the secretion signal sequence of the native signal sequence of CMCase and by the secretion signal sequence of glucoamylase from Rhizopus oryzae for beta-glucosidase, respectively. The genes were expressed by the glyceraldehyde-3-phosphate dehydrogenase promoter from S. cerevisiae. The CMCase and beta-glucosidase activities were detected in the cell pellet fraction, not in the culture supernatant. The display of CMCase and beta-glucosidase proteins on the cell surface was confirmed by immunofluorescence microscopy. The cells displaying these cellulases could grow on cellobiose or water-soluble cellooligosaccharides as the sole carbon source. The degradation and assimilation of cellooligosaccharides were confirmed by thin-layer chromatography. This result showed that the cell surface-engineered yeast with these enzymes can be endowed with the ability to assimilate cellooligosaccharides. This is the first step in the assimilation of cellulosic materials by S. cerevisiae expressing heterologous cellulase genes.

Journal Article↗

PubMed1998

Modified Bagolini striated glass test: clinical applications of starlight test in binocular visual field screening.

AIM: To introduce the "starlight" test which was devised to check binocular vision in normal conditions of seeing in a rapid, easy, and cost effective manner and to estimate the possibility of its clinical use in screening the binocular visual field of patients. METHOD: The Bagolini striated glass test consists of optically plano lenses with imperceptible parallel scratches that barely blur the environment but produce two perpendicular luminous stripes (right eye stripe of 45 degrees and left eye stripe of 135 degrees) when subjects with normal binocular vision view one light source. Unlike the original Bagolini test, the starlight test uses three light sources in horizontal or vertical lines according to the testing purposes and the subject is asked to fixate upon the centre light. Through Bagolini glasses, the subject observes the resulting grid-like pattern and the state of binocular visual field of the subject can be roughly estimated. RESULTS: Normal subjects and patients with strabismus, visual field loss from intracranial diseases, glaucoma, retinitis pigmentosa, and functional visual loss were examined using the starlight test and findings from each case were discussed. CONCLUSIONS: The starlight test, which was made by hand at a low cost, is a simple test that can be used clinically. It provides information about the state of binocular vision of patients in normal conditions of seeing. It is also useful because it enables the examiner to share similar experiences with the examinee. The results suggest it can be effective in visual field screening.

Adult↗

PubMed1998

Objective measurement of contrast sensitivity function using contrast sweep visual evoked responses.

AIM/BACKGROUND: The contrast sensitivity function (CSF) measurement provides information that is not accessible by standard visual acuity determinations. The contrast sweep pattern reversal visual evoked responses (CSVER) technique was used to objectively measure the CSF in clinical practice. METHODS: The contrast thresholds were measured at five spatial frequencies in 10 normal subjects. The CSVER were recorded with sinusoidally modulated vertical gratings at 10 contrast levels (96, 64, 48, 32, 16, 8, 4, 2, 1, and 0.5%) presented in five spatial frequencies (0.5, 1.0, 2.0, 4.0, and 8.0 cycles per degree). Each of 10 contrast levels was displayed for 2 seconds at the desired spatial frequency. The CSVER amplitudes at the second harmonic were calculated by discrete Fourier transform. The results were compared with those obtained using a psychophysical method. RESULTS: An inverted U-shaped CSF which peaked at 2.0 cycles per degree with a contrast sensitivity of 34.5 (contrast, 2.9%) was observed. The CSF assessed electrophysiologically was 0.62 to 0.79 log units lower than the sensitivity measured using the psychophysical method. However, the overall shapes were highly correlated. CONCLUSION: One can objectively measure CSF with CSVER and this may be useful in patients in whom the psychophysical method is limited.

Adult↗

PubMed1998

Advillin (p92): a new member of the gelsolin/villin family of actin regulatory proteins.

A new member of the gelsolin/villin family of actin regulatory proteins was initially identified by screening an adult murine brain cDNA library with a probe for bovine adseverin. The predicted amino acid sequence of the 92 kDa murine protein p92 (advillin) is 75% homologous to villin and 65% homologous to gelsolin and adseverin. It shares a six domain structure with other gelsolin family members and has a carboxy-terminal headpiece, similar to, yet distinct from, villin. Northern blot analysis shows a high level of mRNA expression in murine uterus and human intestine. In situ mRNA analysis of adult murine tissues demonstrates that the message is most highly expressed in the endometrium of the uterus, the intestinal lining, and at the surface of the tongue. In murine embryonic development, strong expression of the message is observed by day 14.5 in dorsal root ganglia and trigeminal ganglia. Expression is also noted at day 16.5 in cerebral cortex. We propose that p92 (advillin) has unique functions in the morphogenesis of neuronal cells which form ganglia, and that it may compensate to explain the near normal phenotype observed in villin-deficient mice.

Amino Acid Sequence↗