Pathological Findings in Myasthenia Gravis Patients with Thymic Hyperplasia and Thymoma.

Thymectomy is routinely carried out in patients with myasthenia gravis (MG) and thymomas. However, there is still a dispute as to whether MG patients with thymic hyperplasia should undergo thymectomy. We aimed to investigate the pathological findings in the thymus in patients with co-existing MG and thymic hyperplasia or thymomas treated with thymectomy, as well as effects of immunosuppression.

[Association of glucocorticoid receptor gene polymorphism with myasthenia gravis].

Objective: To investigate the association of two glucocorticoid receptor (GR) polymorphisms (BclI, ER22/23EK) with Myasthenia Gravis (MG).

Methods: The genotypes of GR in 61 MG patients (MGG) and 57 age and gender-matched healthy controls (HCG) were determined by polymerase chain reaction and nucleotide sequence determination.

Results: The frequencies of three genotypes (GG, CG, CC) in BclIwere 3.

[Identification of a functional ITAM-like sequence within G1 cytoplasmic tail of Hantaan virus].

The G1 cytoplasmic tail of Hantaan virus (HTNV) harbors a highly conserved region, which is homologous to immunoreceptor tyrosine-based activation motifs (ITAM) and is termed the ITAM-like sequence. To demonstrate the potential signal-transducing activity of G1 ITAM-like sequence resembling the canonical ITAM within immune and endothelial cells, a series of experiments were performed to define its interaction with cellular kinases. The synthesized G1 ITAM-like peptide was shown to coprecipitate with cellular phosphoprotein complexes by an immune-complex kinase assay.

Aberrant activation of CDK5 is involved in the pathogenesis of OPIDN.

Exposure to triorthocresyl phosphate (TOCP) may result in a late neurological complication, i.e. organophosphate-induced delayed neuropathy (OPIDN).

Cellular entry of Hantaan virus A9 strain: specific interactions with beta3 integrins and a novel 70kDa protein.

Cellular entry of pathogenic hantaviruses had been shown to be mediated by beta3 integrins. However, no direct evidence exists that hantavirus binds to beta3 integrins, and integrin beta3 subunit is not expressed on some cells permissive to hantavirus infection. In this report, utilizing beta3-integrin-transfected CHO cells, we demonstrated that integrin beta3 subunit renders CHO cells susceptible to Chinese Hantaan virus (HTN) strain A9 (isolated in China), and the viral infection was correspondingly inhibited by antibodies to alphavbeta3, alphaIIbbeta3, beta3, and alphav integrins.

[The relationship between cellular infection by Hantaan virus and expression of beta3 integrin].

Objective: To investigate the relationship between cellular entry of Hantaan virus (HTNV) and expression of beta3 integrin in beta3-integrin-deficient and HTNV-insusceptible China hamster ovary (CHO) cells.

Methods: Eukaryotic expression vector encoding human integrin beta3 and eukaryotic expression vector harboring human integrin alphav or alphaIIb subunit cDNA were transfected into HTNV non-permissive CHO cells individually or collectively. Screening for stable transfectant clones was performed using G418 selective (culture medium.

[Construction of human integrin beta3 subunit eukaryotic expression vector and efficient surface expression of integrin alphaIIbbeta3].

Aim: To establish efficient surface expression of Homo sapiens integrin alphaIIbbeta3 in beta3-integrin-deficient and HV-insusceptible CHO cells, so as to lay the foundation for the further study of cellular entry of hantavirus mediated by beta3 integrins.

Methods: Eukaryotic expression vector pcDNA3.1-beta3 harboring ORF region of human integrin beta3 subunit cDNA was constructed, then pcDNA3.

[Spinal cord neuronal apoptosis induced by triorthocresyl phosphate poisoning in hens].

Objective: To investigate the role of neuronal apoptosis in organophosphorus poisoning-induced delayed neuropathy (OPIDN) and its dynamic pathological changes.

Methods: To establish OPIDN animal model, triorthocresyl phosphate (TOCP)was given to hens with a single dose (1 000 mg/kg, im). Changes of neuropathology, number of neurons and apoptotic cells in the third lumbar spinal cord were observed by HE, Nissl and TUNEL methods 3, 5, 7, 10, 14, 18 days after injection.