A case of Trousseau syndrome caused by pulmonary adenocarcinoma that was controlled for one year and 10 months with thrombosis treatment using an EGFR tyrosine kinase inhibitor and chemotherapy.

A 47-year-old female with no history of previous illnesses developed cerebral infarction and was diagnosed with lung cancer, specifically EGFR mutation-positive adenocarcinoma, and Trousseau syndrome. The patient's response to anticoagulant therapy with non-fractionated heparin was very poor; however we were able to control the thrombosis with chemotherapy. She survived for one year and 10 months following treatment with gefitinib, CBDCA + PEM and erlotinib, without recurrence of thrombosis.

Prostaglandin F2alpha inhibits SERCA2 gene transcription through an induction of Egr-1 in cultured neonatal rat cardiac myocytes.

Prostaglandin F(2alpha) (PGF(2alpha)) stimulates hypertrophic growth of neonatal rat cardiac myocytes, a feature of which includes downregulation of the Ca(2+)-ATPase (SERCA2), a major Ca(2+) transport protein in SR. The molecular mechanisms by which PGF(2alpha) inhibits SERCA2 gene expression remain unknown. We determined the cis-regulatory elements responsible for the regulation of the SERCA2 gene expression in cultured neonatal rat cardiac myocytes exposed to PGF(2alpha).

Competitive binding of CREB and ATF2 to cAMP/ATF responsive element regulates eNOS gene expression in endothelial cells.

Objective: Expression of endothelial nitric oxide synthase (eNOS) is a critical determinant for vascular homeostasis. We examined the effects of Beraprost sodium (BPS), a stable analogue of prostacyclin, on the eNOS gene expression in the presence of inflammatory cytokine interleukin (IL)-1beta in cultured endothelial cells.

Method And Results: Exposure of human and bovine endothelial cells to IL-1beta decreased eNOS expression.