We introduce a novel speckle noise reduction algorithm for OCT images. Contrary to present approaches, the algorithm does not rely on simple averaging of multiple image frames or denoising on the final averaged image. Instead it uses wavelet decompositions of the single frames for a local noise and structure estimation. Based on this analysis, the wavelet detail coefficients are weighted, averaged and reconstructed. At a signal-to-noise gain at about 100% we observe only a minor sharpness decrease, as measured by a full-width-half-maximum reduction of 10.5%. While a similar signal-to-noise gain would require averaging of 29 frames, we achieve this result using only 8 frames as input to the algorithm. A possible application of the proposed algorithm is preprocessing in retinal structure segmentation algorithms, to allow a better differentiation between real tissue information and unwanted speckle noise.

Oxidized low density lipoprotein (oxLDL) induces apoptosis in human macrophages (Mphi), a significant feature in atherogenesis. We found that induction of apoptosis in Mphi by oxLDL, C2-ceramide, tumor necrosis factor alpha (TNF-alpha), and hydrogen peroxide (H2O2) was associated with enhanced expression of manganese superoxide dismutase (MnSOD) and p53. Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis. Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein. In apoptotic macrophages of human atherosclerotic plaques, colocalization of MnSOD and p53 immunoreactivity was found. These results indicate that in oxLDL-induced apoptosis, a concomitant induction of p53 and MnSOD is critical, and suggest that it is at least in part due to an enhancement of the sphingomyelin/ceramide pathway.

Marginal zones (MZs) are microdomains in the spleen that contain various types of immune cells, including MZ B cells, MOMA1 ϩ metallophilic macrophages, and mucosal addressin cell adhesion molecule 1 (MAdCAM-1) ϩ endothelial cells. MAdCAM-1 ϩ and MOMA1 ϩ cells line the sinus, that separates MZs from splenic follicles. Here we show that a receptor for the lysophospholipid sphingosine-1-phosphate (S1P), S1P 3 , is required for normal numbers of splenic immature and MZ B cells, and for S1P-induced chemotaxis of MZ B cells. S1P 3 is also essential for proper alignment of MOMA1 ϩ macrophages and MAdCAM-1 ϩ endothelial cells along the marginal sinus. The lack of cohesion of the marginal sinus in S1P 3 Ϫ / Ϫ mice affects MZ B cell functions, as wild-type (WT) MZ B cells migrate more into S1P 3 Ϫ / Ϫ follicles than into WT follicles after treatment with lipopolysaccharide. Additionally, short-term homing experiments demonstrate that WT MZ B cells home to the S1P 3 Ϫ / Ϫ spleen in increased numbers, suggesting a role for the marginal sinus in regulating MZ B cells numbers. Moreover, S1P 3 Ϫ / Ϫ mice are defective in mounting immune responses to thymus-independent antigen type 2 due to defects in radiation-resistant cells in the spleen. These data identify lysophospholipids and the S1P 3 receptor as essential regulators of the MZ sinus and its role as a barrier to the follicle.

We report a patient with mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes treated with riboflavin and nicotinamide for 18 months, during which time previously frequent encephalopathic spells ceased. To confirm clinical benefit, we withdrew treatment and monitored response with muscle 31P magnetic resonance spectroscopy (MRS) and sural nerve conduction studies. Of three prospectively chosen MRS variables, two changed coincidentally with clinical end points; phosphocreatine (PCr)/adenosine triphosphate recovery rates fell in parallel with sural nerve sensory amplitudes, and a drop in muscle bioenergetic efficiency (relationship of inorganic phosphate/PCr to the accelerating force of contracting muscle) coincided with development of encephalopathy. Investigations revealed a deficiency of respiratory complex I and mutation of the mitochondrial tRNA(Leu)(UUR). We suggest that a defective cellular energy state in mitochondrial disease may be partially treatable and that changes seen in appropriate muscle spectroscopy studies may parallel improvement in brain and peripheral nerve function.

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