Channel Mismatching in Sidelobe Canceler: Limitations and Remedies

After a brief recall of the Sidelobe Canceler (SLC) working principle, including the derivation of a general formula for the Cancellation Ratio (CR), the effects of channel mismatching are investigated. In particular, curves providing CRvalues as a function of amplitude and phase channel mismatching, radar bandwidth, and jammer direction of arrival (JDOA) are provided for the cases of one and two auxiliary antennas. Subsequently, a time -space processor for performance restoration is analyzed in detail. In addition to the above mentioned quantities, the attainable CR value is expressed as a function of the space-time processor parameters. The contribution of the paper is related to the derivation of a number of mathematical equations of CR for several cases of practical interest for the radar engineer. In addition, several curves are presented to assist design of SLC systems.     

Mutation of the matrix metalloproteinase 2 gene (MMP2) causes a multicentric osteolysis and arthritis syndrome.

The inherited osteolyses or 'vanishing bone' syndromes are a group of rare disorders of unknown etiology characterized by destruction and resorption of affected bones. The multicentric osteolyses are notable for interphalangeal joint erosions that mimic severe juvenile rheumatoid arthritis (OMIMs 166300, 259600, 259610 and 277950). We recently described an autosomal recessive form of multicentric osteolysis with carpal and tarsal resorption, crippling arthritic changes, marked osteoporosis, palmar and plantar subcutaneous nodules and distinctive facies in a number of consanguineous Saudi Arabian families. We localized the disease gene to 16q12-21 by using members of these families for a genome-wide search for homozygous-by-descent microsatellite markers. Haplotype analysis narrowed the critical region to a 1.2-cM region that spans the gene encoding MMP-2 (gelatinase A, collagenase type IV; (ref. 3). We detected no MMP2 enzymatic activity in the serum or fibroblasts of affected family members. We identified two family-specific homoallelic MMP2 mutations: R101H and Y244X. The nonsense mutation effects a deletion of the substrate-binding and catalytic sites and the fibronectin type II-like and hemopexin/TIMP2 binding domains. Based on molecular modeling, the missense mutation disrupts hydrogen bond formation within the highly conserved prodomain adjacent to the catalytic zinc ion.