Seminal magnetic fields from Inflato-electromagnetic Inflation

We extend some previous attempts to explain the origin and evolution of primordial magnetic fields during inflation induced from a 5D vacuum. We show that the usual quantum fluctuations of a generalized 5D electromagnetic field cannot provide us with the desired magnetic seeds. We show that special fields without propagation on the extra non-compact dimension are needed to arrive to appreciable magnetic strengths. We also identify a new magnetic tensor field $B_{ij}$ in this kind of extra dimensional theories. Our results are in very good agreement with observational requirements, in particular from TeV Blazars and CMB radiation limits we obtain that primordial cosmological magnetic fields should be close scale invariance.Comment: Improved version. arXiv admin note: text overlap with arXiv:1007.3891 by other author

BCOHTA 94:1T

The primary research question centers on whether any evidence, and if so what kind of evidence, supports use of SR-NG compared to regular release ISDN for the prophylactic treatment of stable angina pectoris.Family Practice, Department ofMedicine, Faculty ofPopulation and Public Health (SPPH), School ofReviewedFacultyResearche

Value of hepatic iron measurements in early hemochromatosis and determination of the critical iron level associated with fibrosis

The role of the measurement of hepatic iron in the diagnosis of genetic hemochromatosis was studied, with particular reference to the differentiation of early hemochromatosis from alcoholic siderosis and the critical hepatic iron concentration associated with fibrosis in hemochromatosis. Hepatic iron was measured in 30 homozygous relatives of 17 hemochromatosis probands, 8 heterozygous relatives, 51 patients with alcoholic liver disease and 40 control subjects. Hepatic iron concentrations were greatly increased in the majority of homozygous hemochromatosis subjects, and there was little overlapwith the other groups. In the absence of alcoholism, fibrosis or cirrhosis in hemochromatosis was present only with hepatic iron concentrations above a threshold of approximately 400 μmoles per gm (22.3 mg per gm) dry weight. In some heterozygous hemochromatosis subjects and in some alcoholic patients, hepatic iron concentrations were in the range seen in young homozygous subjects. However, an age‐related rise in hepatic iron was seen only in hemochromatosis homozygotes, and calculation of an hepatic iron index (hepatic iron/age) resulted in a clear distinction between homozygotes and the other three groups. It is concluded: (a) that chemical measurement of hepatic iron concentration, when corrected for the age of the subject, reliably distinguishes early hemochromatosis from alcoholic siderosis, and (b), that there appears to be a threshold level of hepatic iron above which there is a high risk of fibrosis

HLA typing in idiopathic hemochromatosis: Distinction between homozygotes and heterozygotes with biochemical expression

In a study of 20 families with idiopathic hemochromatosis, relatives of probands were classified as either homozygous, heterozygous, or normal according to their HLA phenotype. An abnormality in the serum iron concentration, total iron‐binding capacity, or serum ferritin concentration was present in all homozygotes and in 25% of heterozygotes. In heterozygotes, the mean total iron‐binding capacity was significantly decreased, and the mean hepatic iron concentration was significantly increased compared to normals. However, in contrast to homozygotes, clinical evidence of iron overload was not observed in heterozygotes, and there was no biochemical or histological evidence of liver disease resulting from excessive iron stores. Progressive iron overload did not develop in 44 heterozygotes who were studied for up to 16 yr