OBJECTIVES: Idiopathic REM sleep behavior disorder (RBD) is by far the strongest clinical predictor of neurodegenerative disease available. Several potential early diagnostic markers of neurodegenerative disease including autonomic symptoms have been proposed, but they have generally not been tested in presymptomatic neurodegenerative disease. So the authors investigated autonomic symptoms and their associated factors in idiopathic RBD patients. METHODS: 52 idiopathic RBD patients and 52 controls participated in the study. Autonomic symptoms were evaluated by applying the unified multiple system atrophy rating scale (UMSARS) and measuring orthostatic systolic blood pressure drop. RESULTS: Idiopathic RBD patients showed significantly higher UMSARS subscale scores and sharper drop of orthostatic systolic blood pressure than controls. In multiple linear regression analysis, all autonomic symptoms and measured orthostatic systolic blood pressure drop were associated with RBD. In addition, orthostatic symptoms were associated with medication and age, urinary function was associated with benign prostatic hyperplasia, and measured orthostatic systolic blood pressure drop was associated with hypertension. CONCLUSION: In this study, idiopathic RBD patients showed more autonomic symptoms than controls. However, other autonomic symptoms-related factors also influenced some autonomic symptoms. Prospective studies should be performed to evaluate autonomic symptoms as a potential predictor of neurodegenerative diseases.
Aged* ; Blood Pressure ; Humans ; Hypertension ; Linear Models ; Multiple System Atrophy ; Neurodegenerative Diseases ; Prostatic Hyperplasia ; REM Sleep Behavior Disorder* ; Sleep, REM*

Lectins are glycoproteins that specifically bind carbohydrate structures and may participate in the biodefense mechanisms of fish. In this study, the binding of three lectins, Dolichos biflorus agglutinin (DBA), soybean agglutinin (SBA), Bandeiraea simplicifolia BS-1 (isolectin B4), Triticum vulgaris (WGA), Arachis hypogaea (PNA) and Ulex europaeus (UEA-I) were studied in the gill, liver, intestine, kidney, heart, and spleen of the flat fish Paralichthys olivaceus. DBA was detected in intestinal mucous cells, as well as in gill epithelial and mucous cells. It was weakly detected in renal tubule epithelial cells and in bile duct epithelial cells. The strong SBA staining was seen in the intestinal club cells, in bile duct epithelial cells and renal tubule epithelial cells. There were intense positive reactions for isolectin B4 in gill epithelial and mucous cells, and the strong isolectin B4 staining was seen in epithelial cells of the bile duct and intestine. The strong WGA staining was seen in the gill mucosal cells, sinusoid, renal tubule epithelial cells and mucosal cells of the intestine. UEA-I was detected in the gill epithelial and mucosal cells, bile duct epithelial cells and renal tubular epithelial cells. These results suggest that the six lectins examined were localized in the covering epithelia of the various organs of the flat fish and they may participate in the biodefense mechanism of the intra body surface in which is exposed to various antigens.
Animals ; Epithelial Cells/metabolism ; Flatfishes/*metabolism ; Histocytochemistry/veterinary ; Lectins/*metabolism ; Mucus/metabolism ; Peanut Agglutinin/metabolism ; Plant Lectins/metabolism ; Soybean Proteins/metabolism ; Wheat Germ Agglutinins/metabolism

PURPOSE: To analyze the MR findings of chondroblastoma and peritumoral bone marrow, focussing on the enhancement pattern. MATERIALS AND METHODS: Enhanced MR images obtained from 23 patients with pathologically proven chondroblastoma were retrospectively reviewed by three radiologists. The enhancement pattern was classified as one of three types: homogeneous, heterogeneous, or peripheral rim, while peritumoral bone marrow enhancement was assigned one of four grades. Correlation between the enhancement pattern and T2 signal intensity of a tumor was analyzed by Fisher's exact test. RESULTS: The enhancement pattern was homogeneous in ten cases, heterogeneous in six, and involved the peripheral rim in seven. In 11 cases, peritumoral bone marrow enhancement was observed. Among the ten instances of homogeneous enhancement the signal intensity seen at T2WI was homogeneously iso or low in six cases, homogeneously high in two, and heterogeneous in two. Among the seven cases in which there was peripheral rim enhancement, the signal intensity observed at T2WI was homogeneously high in three, fluid-fluid level in three, and homogeneously iso or low in one. CONCLUSION: At MR imaging, chondroblastoma shows variable signal intensities and enhancement patterns. The peripheral rim enhancement observed at T2WI correlated with homogeneously high signal intensity or fluid-fluid levels.
Bone Marrow ; Chondroblastoma* ; Humans ; Magnetic Resonance Imaging ; Retrospective Studies

Protein arginine methylation is important for a variety of cellular processes including transcriptional regulation, mRNA splicing, DNA repair, nuclear/cytoplasmic shuttling and various signal transduction pathways. However, the role of arginine methylation in protein biosynthesis and the extracellular signals that control arginine methylation are not fully understood. Basic fibroblast growth factor (bFGF) has been identified as a potent stimulator of myofibroblast dedifferentiation into fibroblasts. We demonstrated that symmetric arginine dimethylation of eukaryotic elongation factor 2 (eEF2) is induced by bFGF without the change in the expression level of eEF2 in mouse embryo fibroblast NIH3T3 cells. The eEF2 methylation is preceded by ras-raf-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-p21(Cip/WAF1) activation, and suppressed by the mitogen-activated protein kinase (MAPK) inhibitor PD98059 and p21(Cip/WAF1) short interfering RNA (siRNA). We determined that protein arginine methyltransferase 7 (PRMT7) is responsible for the methylation, and that PRMT5 acts as a coordinator. Collectively, we demonstrated that eEF2, a key factor involved in protein translational elongation is symmetrically arginine-methylated in a reversible manner, being regulated by bFGF through MAPK signaling pathway.
Animals ; Arginine ; Cell Dedifferentiation ; Cyclin-Dependent Kinase Inhibitor p21/genetics/metabolism ; Elongation Factor 2 Kinase/*metabolism ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*metabolism/pathology ; Flavonoids/pharmacology ; MAP Kinase Signaling System/drug effects/genetics ; Methylation ; Mice ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Myofibroblasts/pathology ; NIH 3T3 Cells ; Protein Methyltransferases/*metabolism ; Protein-Arginine N-Methyltransferases/*metabolism ; RNA, Small Interfering/genetics

Protein arginine methylation is important for a variety of cellular processes including transcriptional regulation, mRNA splicing, DNA repair, nuclear/cytoplasmic shuttling and various signal transduction pathways. However, the role of arginine methylation in protein biosynthesis and the extracellular signals that control arginine methylation are not fully understood. Basic fibroblast growth factor (bFGF) has been identified as a potent stimulator of myofibroblast dedifferentiation into fibroblasts. We demonstrated that symmetric arginine dimethylation of eukaryotic elongation factor 2 (eEF2) is induced by bFGF without the change in the expression level of eEF2 in mouse embryo fibroblast NIH3T3 cells. The eEF2 methylation is preceded by ras-raf-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-p21(Cip/WAF1) activation, and suppressed by the mitogen-activated protein kinase (MAPK) inhibitor PD98059 and p21(Cip/WAF1) short interfering RNA (siRNA). We determined that protein arginine methyltransferase 7 (PRMT7) is responsible for the methylation, and that PRMT5 acts as a coordinator. Collectively, we demonstrated that eEF2, a key factor involved in protein translational elongation is symmetrically arginine-methylated in a reversible manner, being regulated by bFGF through MAPK signaling pathway.
Animals ; Arginine ; Cell Dedifferentiation ; Cyclin-Dependent Kinase Inhibitor p21/genetics/metabolism ; Elongation Factor 2 Kinase/*metabolism ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*metabolism/pathology ; Flavonoids/pharmacology ; MAP Kinase Signaling System/drug effects/genetics ; Methylation ; Mice ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Myofibroblasts/pathology ; NIH 3T3 Cells ; Protein Methyltransferases/*metabolism ; Protein-Arginine N-Methyltransferases/*metabolism ; RNA, Small Interfering/genetics