The Ishikawa Classification of Cavernous Sinus Lesions by Clinico-anatomical Findings

Purpose: The Jefferson classification has been used to localize cavernous sinus lesions. However, this classification occasionally showed dissociation between identified localization and clinical findings. We investigated the clinical applicability of the newly proposed Ishikawa classification based on serial topographic sections of human cavernous sinus and the clinical findings. Methods: In the Ishikawa classification, the cavernous sinus is divided into three portions, that is, anterior, middle, and posterior, demarcated by the location of the intracranial orifice of the optic canal and the entry of the maxillary nerve into the cavernous sinus. A total of 162 patients with cavernous sinus lesions were classified using both the Jefferson and the Ishikawa classifications and the clinical applicability of these two classifications was studied. Characteristics of the localization of lesions were also examined in each etiological type. Results: By the Jefferson classification, 11% of the 162 patients had the anterior type of lesion, 12% the middle, 8% the posterior type, and 69% the unclassifiable type. However, by the Ishikawa classification, 35% had the anterior type, 10% the middle type, 22% the posterior type, 5% the whole type, and 28% the unclassifiable type of lesion. Furthermore, the Ishikawa classification revealed that the etiology of the anterior type was mainly inflammation, and that the etiology of the posterior and whole types was tumors. Conclusion: The Ishikawa classification is clinically useful to identify and classify the localization of cavernous sinus lesions. Jpn J Ophthalmol 2001;45:420-42

The nuclear isoform of protein-tyrosine phosphatase TC-PTP regulates interleukin-6-mediated signaling pathway through STAT3 dephosphorylation.

In the previous study, we demonstrated that the nuclear isoform of T-cell protein-tyrosine phosphatase (TC-PTP) dephosphorylated and deactivated signal transducer and activator of transcription 5a (STAT5a) and STAT5b, thereby negatively regulating prolactin (PRL)-mediated signaling pathway. In this study, we examined the involvement of the nuclear isoform of TC-PTP in interleukin-6 (IL-6)-mediated signaling pathway. IL-6 is a multifunctional cytokine that plays important roles in the immune system, hematopoiesis, and acute phase reactions, and has also implicated in IL-6-related diseases. Here, we demonstrate that IL-6-induced tyrosine-phosphorylation and activation of STAT3 were suppressed by overexpression of the nuclear isoform of TC-PTP in 293T cells. Tyrosine-phosphorylated STAT3 directly interacted with a substrate-trapping mutant of TC-PTP. Furthermore, retrovirus-mediated overexpression of the nuclear isoform of TC-PTP suppressed the IL-6-induced growth arrest of myeloid leukemia M1 cells. Endogenous TC-PTP complexed with STAT3 in the nucleus of M1 cells. These results strongly suggest that the nuclear isoform of TC-PTP may serve as a negative regulator of IL-6-mediated signaling pathway

Role of ICAM-1 in the aggregation and adhesion of human alveolar macrophages in response to TNF-α and INF-γ

Intracellular adhesion molecule-1 (ICAM-1)-mediated cell-cell adhesion is thought to play an important role at sites of inflammation. Recent evidence suggests that ICAM-1 surface expression on alveolar macrophages is increased in pulmonary sarcoidosis and that inflammatory granuloma formation is characterized by the aggregation of macrophages. The present study shows that ICAM-1 expression is significantly elevated on alveolar macrophages from patients with sarcoidosis in response to tumor necrosis factor-α (TNF-α) and interferon- γ (INF-γ) compared with healthy controls. Aggregation and adhesion were significantly increased in alveolar macrophages treated with TNF-α and INF-γ, and significantly inhibited in those pretreated with a monoclonal antibody to ICAM-1. Similarly, aggregation and adhesion were inhibited in macrophages treated with heparin, which then exhibited a wide range of biological activities relevant to inflammation. These results suggested that the surface expression of ICAM-1 on alveolar macrophages in response to TNF-α and INF-γ is important in mediating aggregation and adhesion. Additionally, heparin may be useful for developing novel therapeutic agents for fibrotic lung disease