Joined Spectral Trees for Scalable SPIHT-Based Multispectral Image Compression

In this paper, the compression of multispectral images is addressed. Such 3-D data are characterized by a high correlation across the spectral components. The efficiency of the state-of-the-art wavelet-based coder 3-D SPIHT is considered. Although the 3-D SPIHT algorithm provides the obvious way to process a multispectral image as a volumetric block and, consequently, maintain the attractive properties exhibited in 2-D (excellent performance, low complexity, and embeddedness of the bit-stream), its 3-D trees structure is shown to be not adequately suited for 3-D wavelet transformed (DWT) multispectral images. The fact that each parent has eight children in the 3-D structure considerably increases the list of insignificant sets (LIS) and the list of insignificant pixels (LIP) since the partitioning of any set produces eight subsets which will be processed similarly during the sorting pass. Thus, a significant portion from the overall bit-budget is wastedly spent to sort insignificant information. Through an investigation based on results analysis, we demonstrate that a straightforward 2-D SPIHT technique, when suitably adjusted to maintain the rate scalability and carried out in the 3-D DWT domain, overcomes this weakness. In addition, a new SPIHT-based scalable multispectral image compression algorithm is used in the initial iterations to exploit the redundancies within each group of two consecutive spectral bands. Numerical experiments on a number of multispectral images have shown that the proposed scheme provides significant improvements over related works.

SPECK-Based Lossless Multispectral Image Coding

This letter proposes an efficient extension of the set partitioning embedded block (SPECK) algorithm to lossless multispectral image coding. Such a wavelet-based coder is widely referred to in the literature, especially for lossless image coding, and is considered to be one of the most efficient techniques exhibiting very low computational complexity when compared with other state-of-the-art coders. The modification proposed in this letter is simple and provides significant improvement over the conventional SPECK. The key idea is to join each group of two consecutive wavelet-transformed spectral bands during the SPECK coding since they show high similarities with respect to insignificant sets at the same locations. Simulation results, carried out on a number of test images, demonstrate that this grouping procedure considerably saves on the bit budget for encoding the multispectral images.

Advanced glycation end products cause increased CCN family and extracellular matrix gene expression in the diabetic rodent retina

Aims/hypothesis: Referred to as CCN, the family of growth factors consisting of cystein-rich protein 61 (CYR61, also known as CCN1), connective tissue growth factor (CTGF, also known as CCN2), nephroblastoma overexpressed gene (NOV, also known as CCN3) and WNT1-inducible signalling pathway proteins 1, 2 and 3 (WISP1, -2 and -3; also known as CCN4, -5 and -6) affects cellular growth, differentiation, adhesion and locomotion in wound repair, fibrotic disorders, inflammation and angiogenesis. AGEs formed in the diabetic milieu affect the same processes, leading to diabetic complications including diabetic retinopathy. We hypothesised that pathological effects of AGEs in the diabetic retina are a consequence of AGE-induced alterations in CCN family expression.

Materials and methods: CCN gene expression levels were studied at the mRNA and protein level in retinas of control and diabetic rats using real-time quantitative PCR, western blotting and immunohistochemistry at 6 and 12 weeks of streptozotocin-induced diabetes in the presence or absence of aminoguanidine, an AGE inhibitor. In addition, C57BL/6 mice were repeatedly injected with exogenously formed AGE to establish whether AGE modulate retinal CCN growth factors in vivo.

Results: After 6 weeks of diabetes, Cyr61 expression levels were increased more than threefold. At 12 weeks of diabetes, Ctgf expression levels were increased twofold. Treatment with aminoguanidine inhibited Cyr61 and Ctgf expression in diabetic rats, with reductions of 31 and 36%, respectively, compared with untreated animals. Western blotting showed a twofold increase in CTGF production, which was prevented by aminoguanidine treatment. In mice infused with exogenous AGE, Cyr61 expression increased fourfold and Ctgf expression increased twofold in the retina.

Conclusions/interpolation: CTGF and CYR61 are downstream effectors of AGE in the diabetic retina, implicating them as possible targets for future intervention strategies against the development of diabetic retinopathy.

Proteomic profiling of the retinal dysplasia and degeneration chick retina

Purpose: In our previous paper we undertook proteomic analysis of the normal developing chick retina to identify proteins that were differentially expressed during retinal development. In the present paper we use the same proteomic approach to analyze the development and onset of degeneration in the retinal dysplasia and degeneration (rdd) chick. The pathology displayed by the rdd chick resembles that observed in some of the more severe forms of human retinitis pigmentosa.