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A two-step strategy for endmember extraction is presented. The goal of the first step is to create two pools of spectra, one containing potential endmember candidates and the other one representing spectra that are unquestionably convex combinations (mixed spectra). The second step consists in the application of a sub-optimal subset search method that is applied for best endmember combination. In the first step, vector order statistics are used to identify a medoid spectrum within non-overlapping spatial windows. Endmember extraction based on the iterative error analysis algorithm is then performed on the medoid subset to identify a set of medoid endmembers. The latter are subsequently used to spectrally unmix the original dataset. Spectra that are outside the hyper-surface (outliers) derived from the medoid endmembers represent the pool of potential endmembers. Medoid spectra residing inside the hyper-surface (inliers) constitute the mixed spectra pool. The inliers/outliers status of each spectrum of the original dataset is derived from conditions on their computed unmixing fraction values. Clustering analysis is next performed on the endmember pool of candidates to produce a set of exemplars. Spectral screening is applied on the inliers set to eliminate redundancy. In the second step, the oscillating feature subset search algorithm is applied to identify the endmember combination that best reconstruct, in the least squares sense, the spectra in the joint pools. Results of the proposed strategy are presented for synthetic and real hyperspectral data.

Transforming growth factor beta (TGF-beta) signals through three high affinity cell surface receptors, TGF-beta type I, type II, and type III receptors. The type III receptor, also known as betaglycan, binds to the type II receptor and is thought to act solely by "presenting" the TGF-beta ligand to the type II receptor. The short cytoplasmic domain of the type III receptor is thought to have no role in TGF-beta signaling because deletion of this domain has no effect on association with the type II receptor, or with the presentation role of the type III receptor. Here we demonstrate that the cytoplasmic domains of the type III and type II receptors interact specifically in a manner dependent on the kinase activity of the type II receptor and the ability of the type II receptor to autophosphorylate. This interaction results in the phosphorylation of the cytoplasmic domain of the type III receptor by the type II receptor. The type III receptor with the cytoplasmic domain deleted is able to bind TGF-beta, to bind the type II receptor, and to enhance TGF-beta binding to the type II receptor but is unable to enhance TGF-beta2 signaling, determining that the cytoplasmic domain is essential for some functions of the type III receptor. The type III receptor functions by selectively binding the autophosphorylated type II receptor via its cytoplasmic domain, thus promoting the preferential formation of a complex between the autophosphorylated type II receptor and the type I receptor and then dissociating from this active signaling complex. These studies, for the first time, elucidate important functional roles of the cytoplasmic domain of the type III receptor and demonstrate that these roles are essential for regulating TGF-beta signaling.

Borra (1982) has argued that it is scientifically useful and should be technically feasible to build very large optical telescopes (diameters over 15 meters) having as primary mirror a rotating container filled with mercury. The authors report here the results of optical tests on prototype liquid mirrors. Knife-edge and Hartmann tests, as well as direct imagery, show that optical quality surfaces are attained. The largest mirror produced has a diameter of 1.65-m but the authors tested thoroughly only a 1-m diameter mirror.

‘Immobile’ (im) is a recessive lethal mutation discovered in the F3 of a Xenopus (Xenopus laevis laevis) originating from a mesodermal nucleus of a neurula transplanted into an enucleated egg. The im embryos do not contract after mechanical stimulation nor do they present any spontaneous contraction from the neurula stage onwards. Development proceeds normally during the first days after which deformation of the lower jaw and tail are observed. The im tadpoles die when normal controls are at the feeding stage. Nervous and muscular tissues are histologically normal in the mutant tadpoles; at advanced stages, however, an irregularity in the path of the myofibrils is observed which is especially conspicuous in the electron microscope. Cholinesterases and ATPase are present in the mutant muscles. Parabiosis and chimerae experiments have shown that parabionts and grafts behave according to their own genotype. Cultures of presumptive axial systems with or without ectoderm lead to the conclusion that, first of all, the abnormality is situated in the mesodermal cells and secondly that the first muscular contractions in normal Xenopus laevis are of myogenic origin. The banding pattern of the myofibrils is normal as was shown by obtaining contractions of glycerol extracted im myoblasts with ATP. It seems therefore that in this mutation, the abnormality is situated in the membranous system of the muscular cell, sarcoplasmic reticulum and/or tubular system as is probably the case in the mdg mutation of the mouse.

The behaviour of the egg pigment was studied by histological analysis of wild-type and ‘rusty’ embryos and tadpoles of Xenopus laevis as well as by experimental procedures. The histological analysis of the wild-type animals showed that the various tissues, notably the skin, neural tube, alimentary system and cement gland go through progressive stages of egg pigment migration and concentration at the apical ends of the cells. In the ‘rusty’ mutants the migration and concentration of pigment occur to a slight extent only, the majority of the pigment granules remaining dispersed. The experiments (tail cultures, squashes of cement gland mucus and of meconium) showed that in wild-type animals the pigment, after migration and concentration, is eliminated from the cells by expulsion. In ‘rusty’ animals, this expulsion does not take place. Parabiotic tadpoles of a ‘rusty’ wild-type combination possess a coloration corresponding to their genotype. Ectodermal grafts performed at the neurula stage between ‘rusty’ and wild-type embryos develop according to their origin. The amount of egg pigment found in wild-type and ‘rusty’ tadpoles, and the exceptional case of the cement gland are discussed. It is concluded that the behaviour of the egg pigment is an active cell-specific process, and that the pigment is eliminated by expulsion. The non-elimination of the egg pigment in the ‘rusty’ mutant, accounting for its characteristic colour, appears to be due to a failure of the expulsion mechanism.