Interleukin-10 suppresses tissue factor expression in lipopolysaccharide-stimulated macrophages via inhibition of Egr-1 and a serum response element/MEK-ERK1/2 pathway.

Atherosclerosis is considered to be an inflammatory disease. Tissue factor (TF), a prothrombotic molecule expressed by various cell types within atherosclerotic plaques, is thought to play an essential role in thrombus formation after atherosclerotic plaque rupture. Recent studies suggest that the antiinflammatory cytokine interleukin-10 (IL-10) has many antiatherosclerotic properties.

Symptomatic bradycardia probably due to tizanidine hydrochloride in a chronic hemodialysis patient.

A 71-year-old woman was admitted to the Wakayama Medical University Hospital with dizziness and loss of body balance. She had started hemodialysis at the age of 70. During the 33 days before admission, she received oral tizanidine hydrochloride at 3 mg/day for leg cramps.

Platelet-derived growth factor induces tissue factor expression in vascular smooth muscle cells via activation of Egr-1.

Activation of vascular smooth muscle cells (SMCs) by platelet-derived growth factor (PDGF) is a seminal event in the initiation and progression of the atherosclerotic lesion and may contribute to atherosclerotic plaque instability with plaque rupture and thrombus formation. Tissue factor (TF), a prothrombotic molecule expressed by various cell types within atherosclerotic plaques, is thought to play a major role in thrombus formation after plaque rupture. This study examined intracellular signaling pathways leading to TF expression and Egr-1 activation, a key element in tissue factor transcription, by PDGF-BB in rat SMCs.

Management of secondary hyperparathyroidism of dialysis patients.

Hyperphosphatemia, vitamin D deficiency, and resulted hypocalcemia have been regarded as classical pathogeneses of secondary hyperparathyroidism. These factors have been treated by the administration of phosphorus binder and vitamin D derivatives. However, these therapies have not brought about a successful result for the prevention and treatment of secondary hyperparathyroidism.

Role of p22phox in angiotensin II and platelet-derived growth factor AA induced activator protein 1 activation in vascular smooth muscle cells.

Reactive oxygen species (ROS) are involved in the transcriptional response to angiotensin (ANG) II. In this setting the role of NAD(P)H oxidase, an important source of ROS as second messengers, is not completely understood. In particular in human cells detailed insights into this mechanism are lacking.

HMG-CoA reductase inhibition reduces the proinflammatory activation of human vascular smooth muscle cells by the terminal complement factor C5b-9.

The terminal complement complex C5b-9 is known to participate in inflammatory processes including atherosclerosis. Inflammation appears to be a direct consequence of C5b-9-mediated cell stimulation. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors may exert anti-inflammatory effects on vascular cells independent of lowering plasma cholesterol.

Effect of beta(2)-microglobulin adsorption column on dialysis-related amyloidosis.

Background: beta2-microglobulin (beta2-m) is considered a major pathogenic factor in dialysis-related amyloidosis (DRA), often seen in long-term dialysis patients. No effective therapy for this severely debilitating disease is currently available. Lixelle, an adsorption column, has been developed for the elimination of beta2-m; the efficacy of this column has been evaluated in this study.

New strategies for the treatment of secondary hyperparathyroidism.

Classic pathogeneses of secondary hyperparathyroidism (2HPT), hyperphosphatemia, vitamin D deficiency, and hypocalcemia, have been treated by the administration of phosphorus binders and vitamin D derivatives. However, these therapies have not brought about a successful result. The main reason could be attributed to hypercalcemia resulting from the administration of calcium salts as a phosphorus binder and the calcemic action of vitamin D.

Improvements in artery occlusion by low-density lipoprotein apheresis in a patient with peripheral arterial disease.

Peripheral arterial disease (PAD; arteriosclerosis obliterans) shows ischemic symptoms along the peripheral arteries due to reduced blood flow, and the number of patients with PAD is increasing. Several papers have reported on the clinical effect of low-density lipoprotein apheresis (LDL-A) on PAD, but there has been no report so far on the improvement of total peripheral artery stenosis by LDL-A. We report on the clinical course of a female PAD patient with intractable decubitus in her heel due to the complete occlusion of anterior tibial artery who was treated by a series of LDL-A sessions.