[Effects and safety of infliximab administration in refractory uveoretinitis with Behçet's disease].

Purpose: To evaluate the efficacy and safety of infliximab administration in refractory uveoretinitis in Behçet's disease (BD).

Methods: The subjects were 22 consecutive BD patients with refractory uveoretinitis treated with infliximab. Three patients dropped out from the therapy.

[Primary intraocular lymphoma invaded to the central nervous system after successful treatment with intraocular methotrexate injection].

A 57-year-old man was admitted to our hospital because of persistent blurred vision for 5 months. He had opacity in the vitreous body and white lesions in the retina of the right eye. Although cytological examinations of the vitreous samples revealed Class II, the diagnosis of primary intraocular lymphoma (PIOL) was made by detecting both IgH rearrangement by PCR and an elevated ratio of IL-10/IL-6 concentration in the vitreous sample.

Macular retinal detachment associated with peripapillary detachment in pathologic myopia.

Purpose: A peripapillary detachment in pathologic myopia (PDPM) appears as a yellowish-orange lesion around the optic disc in highly myopic eyes. We report a case in which a macular retinal detachment (RD) accompanied a PDPM.

Method: A case report was used in this study.

Heterozygous deletion of mitotic arrest-deficient protein 1 (MAD1) increases the incidence of tumors in mice.

Mitotic arrest-deficient protein 1 (MAD1) is a component of the mitotic spindle assembly checkpoint. We have created a knockout mouse model to examine the physiologic consequence of reduced MAD1 function. Mad1(+/-) mice were successfully generated, but repeated paired mating of Mad1(+/-) with Mad1(+/-) mice failed to produce a single Mad1(-/-) animal, suggesting that the latter genotype is embryonic lethal.

Altered host:pathogen interactions conferred by the Blau syndrome mutation of NOD2.

Blau syndrome (BS) is a rare familial granulomatous disease manifested by uveitis, arthritis and skin rash. BS has recently been found to be associated with a distinctive mutation in NOD2, which encodes an intracellular toll-like receptor. We have compared host cell interaction with bacterial challenge in U937 cells expressing wild type human NOD2 (NOD2(wt)), mutant NOD2 (NOD2(Blau)), or a vector control (VC).

Spondylodiscitis: diagnosis and treatment.

Background: We present our experience in the diagnosis and treatment of spondylodiscitis.

Methods: 27 patients with spondylodiscitis were studied. There were 15 men and 12 women, with ages ranging from 26 to 85 years.

Ku protein as a potential human T-cell leukemia virus type 1 (HTLV-1) Tax target in clastogenic chromosomal instability of mammalian cells.

The HTLV-1 Tax oncoprotein rapidly induces cytogenetic damage which can be measured by a significant increase in the number of micronuclei (MN) in cells. Tax is thought to have both aneuploidogenic and clastogenic effects. To examine the cellular target for Tax which might mechanistically explain the clastogenic phenomenon, we tested the ability of Tax to induce MN in rodents cells genetically defective for either the Ku80 protein or the catalytic subunit of DNA protein kinase (DNAPKcs).

With a mere nod, uveitis enters a new era.

Purpose: To advance the knowledge of the ophthalmologist with regard to new developments in the genetics and pathologic mechanisms of uveitis.

Design: A review of recently published literature exploring the relationship between the nucleotide oligomerization domain (NOD2) gene and uveitis.

Results: Mutations in the nucleotide-binding region of NOD2 were found to be responsible for familial juvenile systemic granulomatosis (Blau syndrome or Jabs disease), a rare form of uveitis, arthritis, and dermatitis.

Characterization of regions in hsMAD1 needed for binding hsMAD2. A polymorphic change in an hsMAD1 leucine zipper affects MAD1-MAD2 interaction and spindle checkpoint function.

In eukaryotes, the mitotic spindle assembly checkpoint provides a monitor for the fidelity of chromosomal segregation. In this context, the mitotic arrest deficiency protein 2 (MAD2) censors chromosomal mis-segregation by monitoring microtubule attachment/tension, a role that requires its attachment to kinetochores. Studies in yeast have shown that binding of MAD1 to MAD2 is important for the checkpoint function of the latter.

Expression of mitotic spindle checkpoint protein hsMAD1 correlates with cellular proliferation and is activated by a gain-of-function p53 mutant.

Human mitotic arrest deficiency protein 1, hsMAD1, is a component of the mitotic spindle assembly checkpoint (MSC) that monitors fidelity of chromosomal segregation and guards against emergence of cellular aneuploidy. Because aneuploidy is a pervasive characteristic of human cancers, understanding how MSC genes are regulated is important. Here, we have analyzed human genomic sequences upstream of the 5' most hsMAD1 coding exon and have identified a 1.

Prevalent loss of mitotic spindle checkpoint in adult T-cell leukemia confers resistance to microtubule inhibitors.

Human T-cell leukemia virus type I (HTLV-I) is the causative agent for adult T-cell leukemia (ATL). Molecularly, ATL cells have extensive aneugenic abnormalities that occur, at least in part, from cell cycle dysregulation by the HTLV-I-encoded Tax oncoprotein. Here, we compared six HTLV-I-transformed cells to Jurkat and primary peripheral blood mononuclear cells (PBMC) in their responses to treatment with microtubule inhibitors.