Iron reserves in the female body and susceptibility to colds

Levels of temporary invalidity because of catching cold were analyzed in 101 working women over two years and these women's levels of serum iron, total iron-binding capacity of the serum, transferrin saturation with iron, serum ferritin, and red cell ferritin measured. Women with stable iron reserves in the body virtually have no sick leaves because of catching cold, whereas in those with iron deficiency susceptibility to catching cold is increased, and if iron metabolism intensity in the body grows, invalidity periods are much longer. Normalization of not only iron reserves in the body, but correction of iron metabolism as well should be regarded as a factor exerting a favorable effect on body resistance to catching cold.     

SQUID NMR Studies of the Second Layer of 3He at High Density

Nuclear magnetism in the second layer of ³He films on graphite has been studied as a function of density in the zero-field limit at temperatures down to 300 µK. Total surface coverages in this study ranged from 20 atoms/nm² (the lowest coverage at which the effective exchange parameter turns ferromagnetic) through the two-phase region (ending at about 24 atoms/nm²) and into the single-phase imcommensurate solid region up to 31.2 atoms/nm². The surface layers were studied using both pulsed and cw NMR measured with our SQUID NMR system in magnetic fields of 500 µT and lower. As the surface density continues to increase in the single-phase region, the exchange constant decreases consistently with a picture of steric hindrance impeding ferromagnetic exchange. Several different observational features scale with this inferred exchange: low-field magnetization, NMR frequency shift, and the temperature of onset of significant magnetization.     

Inclusion body fibromatosis of the breast. Two cases with immunohistochemical and ultrastructural findings

Two cases of fibromatosis of the breast, characterized by a proliferation of spindle cells containing intracytoplasmic, spherical, eosinophilic inclusion bodies, are reported. The light and electron microscopic features, as well as the immunohistochemical features, are indistinguishable from those found in infantile digital fibromatosis. The proliferating spindle cells are characterized as myofibroblasts, whereas the inclusion bodies show an immunohistochemically nonreactive, hollow-like pattern with peripheral reactivity for actin filaments. This lesion, observed for the first time in the breast, expands the number of extradigital inclusion body fibromatoses.     

Congenic rats reveal three independent Copenhagen alleles within the Mcs1 quantitative trait locus that confer resistance to mammary cancer

It has previously been shown that the Copenhagen (COP) rat contains several genetic loci that contribute to its mammary tumor-resistant phenotype after 7,12-dimethylbenz(a)anthracene (DMBA) administration. One of these loci, mammary carcinoma susceptibility 1 (Mcs1), is located on the centromeric end of chromosome 2 and appears to act in a semidominant fashion. To confirm the existence and independent action of this locus and also aid in the identification of the physical location of the Mcs1 gene, congenic lines were generated by transferring the Mcs1 COP allele onto a Wistar Furth (WF) genetic background. Male carriers were genotyped using microsatellite markers spanning 20-30 cM of the Mcs1 locus. One of the congenic lines minimally retained the COP allele at D2Mit29 on the centromeric end of chromosome 2 and extended distally to D2Rat201. Heterozygous Mcs1 carrier rats were interbred, and the female offspring were treated with DMBA. The female rats from the Mcs1 congenic line that carried one or two COP alleles of the Mcs1 region had a significantly reduced (65 and 85%, respectively) tumor development (P < 0.001) compared with rats carrying zero COP alleles at this locus. A WF.COP-D2Mit29/D2Rat201 homozygous congenic strain derived at the N10 generation was treated with DMBA, and the COP homozygous rats developed 1.5 +/- 0.3 carcinomas/rat versus 6.3 +/- 0.5 in WF control rats (P < 0.0001). Fine mapping of this congenic interval using several recombinant lines identified three genetic loci within the Mcs1 congenic region that independently supported a tumor resistance phenotype. These genetic loci have been termed Mcs1a, Mcs1b, and Mcs1c. In rats for which each locus was homozygous for the COP allele, tumor development was reduced by approximately 60% compared with littermate controls. The identification of these independent loci within the Mcs1 COP allele provide a model of the genetic complexity of cancer.     

Single-chip design of bit-error-correcting stack decoders

The design of a single-chip VLSI system to implement the Zigangirov-Jelinek sequential decoding algorithm for bit-error-correction is described and the dependence of performance on design parameters is discussed. By virtue of being self-contained, having few input and output pins, and processing stack elements once each clock cycle, the system should be capable of high-speed decoding. For constraint length 21, rate 1/2 codes, and 3-b soft decision detection, it is found that a system containing approximately 25000 stack cells reduces errors in a 3-dB signal-to-noise level environment, corresponding to 7.8% hard decision error rate, by two orders of magnitude. Higher decoding gain is obtained at lower noise levels through the use of a relatively long constraint length. The constraint length is not limited by the architecture. Chip area estimates needed to obtain prescribed decoded error rates and average decoding rates are also described and indicate that an effective system is potentially achievable with current technology