No abstract available.
Intercellular Adhesion Molecule-1* ; Prurigo*

No abstract available.
Intercellular Adhesion Molecule-1* ; Interleukin-6* ; Keratinocytes*

No abstract available.
Animals ; Intercellular Adhesion Molecule-1* ; Macrophages* ; Neutrophils* ; Rats* ; Urinary Bladder*

No abstract available.
Animals ; Intercellular Adhesion Molecule-1* ; Macrophages* ; Neutrophils* ; Rats* ; Urinary Bladder*

No abstract available.
Colonic Neoplasms* ; Humans ; Hydromorphone* ; Intercellular Adhesion Molecule-1*

No abstract available.
Humans* ; Intercellular Adhesion Molecule-1* ; Lung Neoplasms* ; Lung*

OBJECTIVETo observe effects of acupuncture on serum interleukin-1 (IL-1) and soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in the patient of cerebral infarction.

METHODSEighty-two cases of cerebral infarction were randomly divided into a treatment group treated by balanced muscular tension needling method, and a control group by traditional needling method. The levels of serum IL-1, sICAM-1 and sVCAM-1 were determined with enzyme-linked immunosorbent assay (ELISA).

RESULTSThe levels of serum IL-1, sICAM-1 and sVCAM-1 in the patient of cerebral infarction were significantly higher than those in the healthy persons (P < 0.01); there were positive correlation between sICAM-1 or sVCAM-1 level and IL-1 level (r = 0.743, P < 0.001; r = 0.862, P < 0.001). The three indexes improved to a certain extent in the two groups, with the treatment group superior to the control group (P < 0.01).

CONCLUSIONThe improvement of nervous function by the balanced muscular tension needling method in the patient of cerebral infarction is possibly related with decrease of IL-1, sICAM-1 and sVCAM-1 levels.

BACKGROUND: Angiotensin II (AngII) and abnormal oscillatory shear stress are highly associated with vascular inflammation including atherosclerosis. However, it is poorly understood how interactions between AngII and shear stress in human aortic endothelial cells (HAEC) are involved in mechanisms by which cellular adhesion molecules are expressed. The purpose of this study was to improve that understanding. METHODS: AngII (10(-7)M for 6 hr) and two-types of shear stress treatments were used: laminar shear stress (LS: unidirectional, 12 dynes/cm2) and oscillatory shear stress (OS: bi-directional, 5 dynes/cm2, 1 Hz) in HAEC. Immunoblotting was used to detect expression of cellular adhesion molecules markers such as vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM1). RESULTS: AngII significantly increased VCAM1 and ICAM1 expression in HAEC that had been reduced due to pretreatment with telmisartan. AngII-LS co-stimulation and AngII-OS co-stimulation significantly increased VCAM1 and ICAM1 expression in HAEC. The expression levels of VCAM1 and ICAM1 were also, significantly reduced when pretreated with telmisartan. However, VCAM1 and ICAM1 expression were significantly reduced under LS and OS stimulation. CONCLUSIONS: Telmisartan may modulate the expressions of VCAM1 and ICAM1 via different types of shear stress in HAEC that are activated by AngII.
Angiotensin II ; Angiotensins ; Atherosclerosis ; Benzimidazoles ; Benzoates ; Endothelial Cells ; Humans ; Immunoblotting ; Inflammation ; Intercellular Adhesion Molecule-1 ; Vascular Cell Adhesion Molecule-1

PURPOSE: To clarify the relationship between aseptic loosening of hip arthroplasty and adhesion molecules on interfacial membrane from revisional hip arthroplasty. MATERIALS AND METHODS: We studied 26 revisional total hip arthroplasties between May 2004 and July 2006, and 15 synovial tissues from hip fractures were selected as the control group. We analyzed the degree of femoral osteolysis by Paprosky's classification. We examined the expression of soluble endothelial leukocyte adhesion molecule-1 (E-selectin), vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) by immunohistochemical staining technique. We compared and analyzed radiologic evaluation and expression of adhesion molecules. RESULTS: Expression of E-selectin was observed in 100%, VCAM-1 in 42.3% and ICAM-1 in 34.6%. Expression of adhesion molecules were increased compared to the control group (p<0.05). The higher the expression of E-selectin, the higher the degree of osteolysis (p=0.023). CONCLUSION: These results showed that adhesion molecules are involved in aseptic loosening of hip arthroplasties, and we proposed that E-selectin may strongly engage in the cascade of aseptic loosening in hip arthroplasty.
Arthroplasty* ; Classification ; E-Selectin ; Hip Fractures ; Hip* ; Intercellular Adhesion Molecule-1 ; Membranes* ; Osteolysis ; Vascular Cell Adhesion Molecule-1

Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD (P) H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 (3.5+/-0.4) and VCAM-1 (3.8+/-0.3) in diabetic aorta was significantly higher than those in control aorta (0.9+/-0.5 and 1.6+/-0.3, respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD (P) H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P< 0.01 in ICAM-1 and r=0.88, P< 0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD (P) H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.
Animals ; Aorta* ; Atherosclerosis ; Cell Adhesion Molecules* ; Cell Adhesion* ; E-Selectin ; Intercellular Adhesion Molecule-1 ; Membranes ; Mice* ; NAD ; Oxidoreductases ; P-Selectin ; Superoxides* ; Vascular Cell Adhesion Molecule-1