Ceric-induced grafting of ethyl-acrylate onto sodium alginate

Sodium alginate was graft-copolymerized with ethyl acrylate using ceric ammonium nitrate as an initiator. In order to optimize the conditions for grafting, the concentrations of nitric acid, initiator and monomer together with temperature, time and amount of substrate were varied. The kinetic scheme of free radical graft copolymerization has been proposed and the equations relating the values of rate of polymerization, rate of graft copolymerization and rate of homopolymerization are also suggested. The experimental results agree very well with the proposed kinetic scheme.     

Plastic deformation of forearm

The unusual occurrence of plastic deformation in an adult is described.     

Alternative Granulation Technique: Melt Granulation

A melt granulation process has been investigated (1, 2) which efficiently agglomerates pharmaceutical powders for use in both immediate- and sustained-release solid dosage forms. The process utilizes materials that are effective as granulating fluids when they are in the molten state. Cooling of the agglomerated powders and the resultant solidification of the molten materials completes the granulation process. Both the molten agglomeration and cooling solidification were accomplished in a high shear Collette Gral mixer equipped with a jacketed bowl. Hence, the melt granulation process replaces the conventional granulation and drying operations which use water or alcohol solutions. The melt granulation process has been investigated using immediate- and sustained-release TAVIST® (clemastine fumarate USP) tablet formulations. The TAVIST granulations have been characterized by power consumption monitoring, measurement of the granulation particle size distribution, bulk and tapped density determinations, and loss-on-drying measurements. Scale-up of the melt granulation process for the sustained release TAVIST tablet formulation was judged successful based on a comparison of the hardness, friability, weight uniformity during compression, disintegration time, and dissolution rate data obtained at different manufacturing scales.     

Throughput and Delay in Random Wireless Networks With Restricted Mobility

Grossglauser and Tse (2001) introduced a mobile random network model where each node moves independently on a unit disk according to a stationary uniform distribution and showed that a throughput of Theta(1) is achievable. El Gamal, Mammen, Prabhakar, and Shah (2004) showed that the delay associated with this throughput scales as Theta(nlogn), when each node moves according to an independent random walk. In a later work, Diggavi, Grossglauser, and Tse (2002) considered a random network on a sphere with a restricted mobility model, where each node moves along a randomly chosen great circle on the unit sphere. They showed that even with this one-dimensional restriction on mobility, constant throughput scaling is achievable. Thus, this particular mobility restriction does not affect the throughput scaling. This raises the question whether this mobility restriction affects the delay scaling. This correspondence studies the delay scaling at Theta(1) throughput for a random network with restricted mobility. First, a variant of the scheme presented by Diggavi, Grossglauser, and Tse (2002) is presented and it is shown to achieve Theta(1) throughput using different (and perhaps simpler) techniques. The exact order of delay scaling for this scheme is determined, somewhat surprisingly, to be of Theta(nlogn), which is the same as that without the mobility restriction. Thus, this particular mobility restriction does not affect either the maximal throughput scaling or the corresponding delay scaling of the network. This happens because under this 1-D restriction, each node is in the proximity of every other node in essentially the same manner as without this restriction     

Deformable template recognition of multiple occluded objects

Based on deformable templates, the paper formulates an integrated and flexible Bayesian recognition system of multiple occluded objects. Various local dependence properties of the model are obtained to reduce the computational cost with the increase in the number of objects. Numerical results for a synthetic image and for a real image of mushrooms are discussed     

Interferometric noise limitations in fibre-amplifier cascades

Phase-induced intensity noise from weak multiple reflectors is evaluated theoretically and experimentally in amplifier cascades without isolators. Rayleigh backscattering alone significantly limits the number of amplifiers in the span. Theory and experiment agree closely for a six-amplifier cascade.<>     

SPARC deficiency leads to early-onset cataractogenesis

PURPOSE: To determine the role of SPARC (secreted protein, acidic, and rich in cysteine) in cataractogenesis by examining mice deficient in a matricellular protein SPARC. METHODS: Mice were rendered SPARC-deficient by a targeted disruption of the gene. Slit-lamp microscopy and histology were used to examine the eyes of SPARC-null and wild-type mice from birth to 14 months of age. RESULTS: SPARC-null mice developed opacities in the posterior cortex of the eye as early as 1.5 months after birth. The diffuse cataracts appeared to progress toward the anterior cortex and reached maturity in many animals by 3.5 months of age. Early stages of cataractogenesis in SPARC-null mice included inhibition of normal lens fiber cell differentiation, degeneration of fiber cells, vacuole formation at the equator, and liquefaction of the cortex. No cataracts were detected in wild-type mice up to the age of 8 months. CONCLUSIONS: The early onset of cataracts in SPARC-null mice establishes that the gene is essential to the maintenance of lens transparency.     

Meprin A, the major matrix degrading enzyme in renal tubules, produces a novel nidogen fragment in vitro and in vivo

We examined the effect of meprin A, the major matrix degrading metalloproteinase in rat kidney, on the laminin-nidogen complex. N-terminal sequence information from the most abundant 55 kDa fragment revealed that it was a breakdown product of nidogen rather than laminin. In comparison with over 50 nidogen cleavage sites produced by other proteases, the meprin A-induced nidogen cleavage site at amino acid position 899-900, a glutamine-glycine site in the G3 domain, is unique. In addition, these data demonstrate that meprin A degrades the G3 domain of nidogen even in the presence of laminin binding, which usually accords protection from proteolytic degradation. Meprin A also degraded purified nidogen into similar breakdown products. Given that the tubular basement membrane is located on the basilar side of the cell, the location of meprin A on the apical brush border makes it difficult to envision a role for meprin A in injury-induced basement membrane component breakdown. Thus, we examined the possibility that following renal tubular epithelial cell injury, meprin A undergoes a translocation to reach the underlying basement membrane. After renal ischemia-reperfusion there was a marked alteration in meprin A staining with meprin A now distributed throughout the renal tubular cell cytoplasm and directly adherent to the tubular basement membrane. This was in contrast to the usual linear staining of the brush border of tubules in the corticomedullary junction. These data provide unequivocal evidence that following injury, meprin A undergoes redistribution and/or adherence to the tubular basement membrane. Since in our in vitro studies, we identified a distinct meprin-induced 55 kDa nidogen breakdown product, the urine was also examined for the presence of nidogen degradation products after rat renal ischemia-reperfusion injury. Western blots showed a marked increase in the urinary 55 kDa nidogen fragment as early as the first day following ischemia-reperfusion injury and continuing for six days. Taken together, these in vivo data strongly support the notion that the nidogen breakdown products are the result of partial degradation of tubular basement membrane by meprin A following renal tubular ischemia-reperfusion injury.