We report herein the case of a 69-year-old man with basaloid-squamous carcinoma (BSC) of the esophagus. To the best of our knowledge, this is the 60th case of BSC of the esophagus to be reported in Japan, and a review of the other 59 cases is presented after this case report. In our patient, endoscopic findings revealed a circumferential erosion in the middle intrathoracic esophagus (Im), and a protruding tumor with friable ulceration in the center of the erosion. A biopsy suggested that it was moderately differentiated squamous cell carcinoma (SCC), and a thoracoscopic total thoracic esophagectomy was performed. Histologically, the protruding-type lesion with ulceration was composed of BSC, and the circumferential 0 -I + IIc type lesion was composed of moderately differentiated SCC. The immunohistochemical findings of these resected specimens led us to suspect that the basal-layer-type SCC had transformed into BSC by undergoing differentiation and expansive proliferation.
A BSTRACTBackground: Recently, a second prostaglandin D 2 (PGD 2 ) receptor, chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), was identified. Because PGD 2 was reported to have chemotactic activity on eosinophils, CRTH2 expressed on eosinophils attracted interest as a receptor associated with eosinophil migration to, and accumulation at, inflammatory sites. To elucidate the mechanism regulating the expression of CRTH2 on eosinophils, the effects of PGD 2 , interleukin (IL)-4, IL-5 and interferon (IFN)-γ on CRTH2 expression were investigated. Methods: Blood eosinophils were purified using Percoll and anti-CD16 antibody coated magnetic beads. Eosinophils were incubated with PGD 2 and/or IL-4, IL-5 and IFN-γ . The expression of CRTH2 on eosinophils was measured using a FACScan cytometer (Becton Dickinson Immunocytometry Systems, San Jose, CA, USA). Results: Prostaglandin D 2 and IL-5, but not IL-4 and IFN-γ , downregulated the expression of CRTH2 on eosinophils. Furthermore, PGD 2 -and IL-5-induced downregulation of CRTH2 on human eosinophils was inhibited by phenylarsine oxide, a receptor internalization inhibitor. Conclusions: These results suggest that PGD 2 and IL-5 regulate CRTH2 expression on eosinophils through
Metastatic retinoblastoma of the jaws is very rare. We present a 4-year-old boy with metastatic retinoblastoma that involved both the maxilla and mandible simultaneously. Enhanced CT indicated bone-destructive masses with partially non-enhanced area and enhanced margin in the right maxilla and left mandible. MRI showed well-delineated masses that were isointense on T(1) weighted images and hyperintense on T(2) weighted images. Four weeks after chemotherapy and bone marrow transplantation, the size of lesions remarkably decreased. The patient died 19 months later with extensive tumour metastases despite additional chemotherapy. In this case, the dental crypt of a permanent tooth was considered the potential target through which retinoblastoma metastasized to the jaws.
Eosinophils are major effector cells in allergic diseases including asthma. Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear receptor that regulates immune reaction. We have previously demonstrated that human eosinophils express PPARγ and that stimulation with a synthetic agonist for PPARγ attenuated the factor-induced eosinophil survival and chemotaxis. However, the modulator of the eosinophil PPARγ expression has not yet been studied. In this study, we investigated the effect of theophylline and dexamethasone (widely used drugs in the treatment of asthma) on PPARγ expression in eosinophils. Purified human peripheral blood eosinophils were cultured, and therapeutic concentrations of theophylline and dexamethasone were added. Subsequently, PPARγ was measured using quantitative real-time RT-PCR and flow cytometry. Theophylline and dexamethasone markedly enhanced both mRNA and protein levels of PPARγ. These findings suggest that the increase in PPARγ expression on eosinophils may play a role in the anti-inflammatory effects of theophylline and dexamethasone.
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