Ocular hypotensive effects of monoamine oxidase-A inhibitors in rabbit

The effects of monoamine oxidase-A (MAO-A) inhibitors with epinephrine on intraocular pressure in the pigmented rabbit were studied. MAO-A inhibitors were used topically with or without various concentrations of epinephrine. For the measurement of intraocular pressure, applanation pneumatonography was used and tissue MAO activities were determined by radiometric assay. After topical administration with clorgyline, MAO-A activities in the bulbar conjunctiva and the iris-ciliary body were remarkably inhibited, whereas MAO-B inhibition was minimal. Maximal reduction of intraocular pressure with 0.05% epinephrine was 3.2 mmHg. Single administration of clorgyline, amiflamine, moclobemide or CGP 11305-A caused decreases in the intraocular pressure of 2.0, 2.5, 1.8 and 2.4 mmHg, respectively. In the coadministration experiments with epinephrine, the ocular hypotensive effects of epinephrine were potentiated with clorgyline, amiflamine, moclobemide and CGP 11305-A (6.6, 4.8, 5.6 and 5.8 mmHg). On the contrary, they were not influenced by the MAO-B inhibitor deprenyl. These results indicated that MAO-A inhibitors potentiated the ocular hypotensive effects of epinephrine, and that the coadministration of a reversible MAO-A inhibitor with epinephrine might be useful for patients with glaucoma.     

Idiopathic membranous nephropathy in two brothers

Idiopathic membranous nephropathy has been reported rarely to develop in genetic association with certain HLA antigens. This paper describes two male siblings presenting with nephrotic syndrome with histologically proven membranous nephropathy. The younger brother maintained a normal renal function with slight proteinuria during the 3 years of follow-up, but the older one experienced a rapid decline in renal function and had to be put on maintenance hemodialysis. No clinical evidence of contributory underlying disease such as malignancy or systemic lupus erythematosus could be found. HLA typing was carried out in the two patients and in members of their family. Several HLA antigens were found to be shared by the two patients. However, the HLA antigens which have been reported to be associated with idiopathic membranous nephropathy were not found in either of them.     

Induction and separation of mouse helper T cells by lectins.

The capability of Lens culinaris agglutinin (LcA) to induce selectively the helper T cell activity affecting primary antibody response was demonstrated. In the presence of mouse spleen cells, activated with LcA at a concentration of 12 . 5 microgram/ml, optimal augmentation of the humoral immune response to sheep erythrocytes (SRBC) was observed. It was also demonstrated that Limulus polyphemus agglutinin (LPA), which was shown to possess carbohydrate-binding specificity directed to sialic acid residues, preferentially agglutinated helper T cells. Conversely, peanut agglutinin (PNA), which binds preferentially to the sugar sequence beta-D-Gal-(1 leads to 3)-D-GalNAc, did not agglutinate the helper cells. Furthermore, the stimulatory effect of LPA-agglutinated cells on the antibody response was abolished by treatment of the cells with anti-Thy-1 . 2 and complement. These results suggested that the helper cells induced by LcA were T cells and that they have abundant sialic acid residues exposed on the cell surface.     

Purification and characterization of a cell-associated hemagglutinin of Vibrio parahaemolyticus.

We found a positive correlation between cell-associated mannose-sensitive hemagglutination and adherence of Vibrio parahaemolyticus to rabbit enterocytes by investigating 35 strains of V. parahaemolyticus for cell-associated hemagglutinin (cHA) and for the ability to adhere to the enterocytes. We purified a mannose-sensitive cHA from a Kanagawa phenomenon-positive clinical strain of V. parahaemolyticus that exhibited a high level of mannose-sensitive hemagglutination and strongly adhered to the enterocytes. The purified cHA is a heat-labile, tetrameric protein consisting of four identical subunits of approximately 26 kDa each. The adherence to rabbit enterocytes was inhibited in a dose-dependent manner by pretreatment of the bacterial cells with D-mannose and with the Fab fraction of immunoglobulin G against the purified cHA. Furthermore, pretreatment of the enterocytes with the purified cHA inhibited the adherence of V. parahaemolyticus. Immunogold electron microscopy revealed that the cHA is located on the bacterial cell surface and is not associated with pili. These results suggest that cHA is involved in the adherence mechanisms of V. parahaemolyticus to the enterocytes and that the receptors for cHA on the enterocyte appear to be a D-mannose-containing compound.     

High incidence of pre-excitation syndrome in Japanese families with Leber's hereditary optic neuropathy

Cardiac conduction abnormalities have been reported in families with Leber's hereditary optic neuropathy (LHON). The pre-excitation syndrome, Wolff-Parkinson-White syndrome or Lown-Ganong-Levine syndrome, is reportedly common in Finns with LHON, being seen in 14 (9%) of the 163 individuals with mitochondrial DNA (mtDNA) mutations. While this syndrome is thought to be rare in other ethnic groups with LHON, the present study of 35 Japanese LHON families confirmed that it is also relatively common among Japanese families, being seen in 5 (8%) of the 63 individuals with mtDNA mutations. It remains to be determined whether the high incidence of the pre-excitation syndrome in Finnish and Japanese LHON families is due to a particular genetic composition of ethnic groups such as in Finland and in Japan, or only to a reporting bias.     

Identification of four novel mutations of the XLRS1 gene in Japanese patients with X-linked juvenile retinoschisis. Mutation in brief no. 234. Online

The XLRS1 gene (HUGO-approved symbol, RS1) has been found to cause X-linked recessive retinoschisis (RS) which is characterized by splitting of the superficial layer of the retina. Recent mutation analysis of this gene revealed 82 different mutations in 214 patients with RS. We have now identified 10 mutations of the XLRS1 gene in 11 unrelated Japanese males with RS. Mutations found in these patients were; 1) a 20-kb deletion in exon 1 region; 2) mutations in the initiation sequence (M1V); 3) mutations in the splice donor site (IVS1 + 1 g-->a); 4) two nonsense mutations (Q88X, W163X); and 5) five missense mutations (E72K, Y89C, R182C, G109E, P203L). Four (M1V, Q88X, G109E, and W163X) of the 10 mutations were novel. The R182C mutation was identified in 2 unrelated patients. The 3 mutations found between exons 1 and 3 cause premature translation termination in the XLRS1 protein. The rest of the 7 mutations were clustered between exons 4 and 6. This region of the protein is homologous to the proteins implicated in cell-cell adhesion.     

Deproteinizing effects on resin-tooth bond structures

This study investigated the effects of NaOCl on resin-tooth bonds to simulate the situations of long-term durability and caries invasion. Resin-tooth bonded specimens were produced with the use of two resin adhesives (Excite and One-Bond). Resin-tooth bonded beams (adhesive area; 0.9 mm2) were serially sectioned and the specimens were immersed in 10% NaOCl medium for 0 (control), 2, 4, and 6 h after being stored in water for 24 h. After immersion, microtensile bond tests were performed. SEM fractography was conducted to calculate each failure mode by image analysis. In addition, the adhesive interface was examined with the use of TEM. In the control specimens, enamel bond strengths had no difference between Excite (45.6 +/- 15.0) and One-Bond (56.9 +/- 12.9). On the other hand, dentin bond strengths had significant difference between Excite (80.6 +/- 21.2) and One-Bond (50.7 +/- 11.2). The bond strengths decreased with increased storage time for both systems with enamel and dentin bonds. The deteriorated mineralized dentin of beams resulted in bond-strength reduction for resin-enamel bonds. For dentin bonding, the adhesive interface was gradually dissolved from the outer to the center portion of the beam. The depletion of collagen fibrils within the demineralized dentin or hybrid layer deformation was found under SEM and TEM examinations. These morphological changes are responsible for bond strength reduction of resin-dentin bonds.     

A digest of the Evidence-Based Clinical Practice Guideline for Nephrotic Syndrome 2020

Clinical and Experimental Nephrology -     

Protective effect of nitric oxide against iron-induced neuronal damage

We investigated the effect of nitric oxide (NO) on iron-induced neuronal damage. Incubation of PC12 cells after the addition of FeCl2 induced rapid increases (within 1 hr) in lipid peroxidation and a concentration (0.1-2 mM)-dependent decrease in cell viability at 48 hr, both of which were blocked by deferoxamine and 2-methyl-6-(p-methoxyphenyl)-3,7-dihydroimidazo[1,2-a]pyrazine-3-o ne hydrochloride (MCLA) (a superoxide scavenger) but not by mannitol (a hydroxyl radical scavenger). Iron-induced cytotoxicity was also antagonized by superoxide dismutase with catalase. On the other hand, the NO donors S-nitroso-N-acetylpenicillamine (SNAP), 3-?(+/-)-(E)-ethyl-2'-[(E)-hydroxylamino]-5-nitro-3-hexenecarbo moyl?-pyridine (NOR-4), and 2,2'-(hydroxynitrosohydrazono)bis-ethanamine (NOC-18) decreased cell viability 48 hr after addition without increasing lipid peroxidation. However, when added with 1 mM FeCl2, NO donors including NOC-18, SNAP and NOR-4 (0.1-1 mM) inhibited lipid peroxidation in a concentration-dependent manner and suppressed cell death at lower concentrations. Addition of MCLA and NOC-18 also suppressed decreases in iron-induced [3H]thymidine incorporation. In rat brain homogenate, NOC-18 and SNAP both suppressed iron-induced lipid peroxidation. These findings suggest that NO has a dual effect on neuronal viability and can act as an antioxidant which protects neurons from iron-induced damage.