Canonical pathway of nuclear factor kappa B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis

Nuclear factor kappa B (NF-kappa B) activation has been observed in human atherosclerotic plaques and is enhanced in unstable coronary plaques, but whether such activation has a protective or pathophysiological role remains to be determined. We addressed this question by developing a short-term culture system of cells isolated from human atherosclerotic tissue, allowing efficient gene transfer to directly investigate signaling pathways in human atherosclerosis. We found that NF-kappa B is activated in these cells and that this activity involves p65, p50, and c-Rel but not p52 or RelB. This NF-kappa B activation can be blocked by overexpression of I kappa B alpha or dominant-negative I kappa B kinase (IKK)-2 but not dominant-negative IKK-1 or NF-kappa B-inducing kinase, resulting in selective inhibition of inflammatory cytokines (tumor necrosis factor alpha, IL-6, and IL-8), tissue factor, and matrix metalloproteinases without affecting the antiinflammatory cytokine IL-10 or tissue inhibitor of matrix metalloproteinases. Our results demonstrate that the canonical pathway of NF-kappa B activation that involves p65, p50, c-Rel, and IKK-2 is activated in human atherosclerosis and results in selective up-regulation of major proinflammatory and prothrombotic mediators of the disease.     

A giant inguinoscrotal bladder hernia as a cause of chronic renal failure: A rare case

INTRODUCTIONGiant inguinoscrotal bladder hernias are very rare and require surgical intervention. They usually do not cause any specific symptoms and thus, they are often misdiagnosed. If left untreated though, they might lead to severe medical conditions, such as renal failure.PRESENTATION OF CASEWe present the case of a 71-year-old male patient suffering from a giant inguinoscrotal mass, accompanied by symptoms of the lower urinary track (LUTS) and chronic renal failure.DISCUSSIONIn our case, the patient presented with bladder hernia causing non specific symptoms of renal failure. In contrast to acute renal failure, a chronic renal impairment most often comes with no specific symptoms and thus, it can be present for many years before the diagnosis is made. It is evident that such serious conditions should be suspected and treated.CONCLUSIONInguinoscrotal bladder hernias may be associated with severe medical conditions, such as renal deterioration, and should be considered in the differential diagnosis of renal failure, when accompanied by any inguinal, scrotal, or low abdominal wall hernia.     

Guided growth of neurons and glia using microfabricated patterns of parylene-C on a SiO2 background

This paper describes a simple technique for the patterning of glia and neurons. The integration of neuronal patterning to Multi-Electrode Arrays (MEAs), planar patch clamp and silicon based ‘lab on a chip’ technologies necessitates the development of a microfabrication-compatible method, which will be reliable and easy to implement. In this study a highly consistent, straightforward and cost effective cell patterning scheme has been developed. It is based on two common ingredients: the polymer parylene-C and horse serum. Parylene-C is deposited and photo-lithographically patterned on silicon oxide (SiO₂) surfaces. Subsequently, the patterns are activated via immersion in horse serum. Compared to non-activated controls, cells on the treated samples exhibited a significantly higher conformity to underlying parylene stripes. The immersion time of the patterns was reduced from 24 to 3 h without compromising the technique. X-ray photoelectron spectroscopy (XPS) analysis of parylene and SiO₂ surfaces before and after immersion in horse serum and gel based eluant analysis suggests that the quantity and conformation of proteins on the parylene and SiO₂ substrates might be responsible for inducing glial and neuronal patterning.     

Delayed suture intravesical migration as a complication of a stamey endoscopic bladder neck suspension

We report our experience with two cases of latemigration of the suture and bolster occurring 2years after a modified Stamey endoscopicbladder neck suspension. Delayed migration ofthe suture and bolster after an endoscopicbladder neck suspension across tissue planes,with subsequent erosion into the bladder, isuncommon. Recurrent urinary tract infection andmild suprapubic discomfort were the onlysymptoms. Cystoscopy was the only helpfuldiagnostic tool and should be considered earlyin the evaluation of this kind of patients. Themechanism of migration of the cuff and theoperative technique are discussed.     

Expression of pigment epithelium-derived factor in experimental choroidal neovascularization

PURPOSE: To investigate the expression of pigment epithelium-derived factor (PEDF) in the rat laser-injury model of choroidal neovascularization (CNV). METHODS: Retinas were immunostained for PEDF at different times (1, 2, and 3 weeks) after laser injury. Levels of PEDF protein in the vitreous at 1, 3, 7, 14, and 28 days after laser injury were also assayed by Western blot. RESULTS: Protein levels of PEDF in the vitreous were increased during the first 7 days after CNV induction. Immunostaining for PEDF was observed throughout normal nonlasered control retinas, sham-lasered retinas, and areas remote to laser lesions, which were generally more intense in the outer nuclear layer (ONL) and less intense in the internal nuclear layer (INL). Decreased expression of PEDF was observed in flanking areas adjacent to the injury site and was confined mainly to the ONL. In the injury sites, immunostaining within the ONL was either absent or decreased for up to 3 weeks after laser injury (the duration of the study). Preadsorption of the anti-PEDF antibody with the immunizing peptide blocked specific labeling in the retina. CONCLUSIONS: These results demonstrate an inverse correlation of expression of PEDF and formation of CNV in the experimental model and suggest that decreased expression of PEDF plays a permissive role in the formation of CNV. PEDF analogues may be a reasonable treatment strategy for CNV.