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We identify a reduction reaction of boron oxide by Si during melt fluxing of the Fe-Co-Si-B-P system, which results in an unexpected and significant B enrichment and Si depletion in the alloy. Taking this reaction into account, an optimized Fe-Co-Si-B-P alloy free from oxide inclusions and demonstrating a global peak in glass forming ability is formed. Following a 22-h high temperature fluxing of the melt, alloy with composition Fe_(57.5)Co_(20.2)Si_(10.2)B_(2.1)P_(10) transforms to Fe_(57)Co_(19.2)Si_(6.8)B_(7.4)P_(9.6), and its critical rod diameter increases from 1 mm to 5 mm. The alloy also demonstrates excellent soft ferromagnetic performance characterized by a magnetic saturation of 1.53 T.

We present and interpret newly determined site motions derived from GPS observations made from 2008 through 2016 in the Republic of Georgia, which constrain the rate and locus of active shortening in the Lesser–Greater Caucasus continental collision zone. Observation sites are located along two ∼160 km-long profiles crossing the Lesser–Greater Caucasus boundary zone: one crossing the Rioni Basin in western Georgia and the other crossing further east near the longitude of Tbilisi. Convergence across the Rioni Basin Profile occurs along the southern margin of the Greater Caucasus, near the surface trace of the north-dipping Main Caucasus Thrust Fault (MCTF) system, and is consistent with strain accumulation on the fault that generated the 1991 MW6.9 Racha earthquake. In contrast, convergence along the Tbilisi Profile occurs near Tbilisi and the northern boundary of the Lesser Caucasus (near the south-dipping Lesser Caucasus Thrust Fault), approximately 50–70 km south of the MCTF, which is inactive within the resolution of geodetic observations ( ± 0.5 mm/yr ) at the location of the Tbilisi Profile. We suggest that the southward offset of convergence along strike of the range is related to the incipient collision of the Lesser–Greater Caucasus, and closing of the intervening Kura Basin, which is most advanced along this segment of the collision zone. The identification of active shortening near Tbilisi requires a reevaluation of seismic hazards in this area.

Bulk platinum-rich glasses exhibiting high bulk moduli and Poisson ratios are introduced. A bulk modulus of 217 GPa and a Poisson’s ratio of 0.43 are measured, the highest values reported to date for a metallic glass. The present glasses demonstrate an unusual capacity for “liquid-like” deformation characterized by low resistance to shear flow and high resistance to cavitation, enabling extensive bending ductility in the absence of fracture. An indirect estimate of the fracture toughness yields a value of ∼125 MPa m^(1/2).

Superoxide anions react with nitric oxide to form peroxynitrite and hence reduce the bioavailability of nitric oxide in the arteries. Extracellular superoxide dismutase (EC-SOD) is a major superoxide scavenger in human plasma and vascular tissues. The objective of this study is to assess whether essential hypertension is associated with an alteration in EC-SOD activity. In this report, blood samples were obtained from hypertensive (n=39) and normotensive (n=37) African-Americans. Plasma EC-SOD activity was measured using in-gel activity staining and spectrophotometric assays, EC-SOD protein level was measured using Western blotting, nitrotyrosine was measured using slot blotting, 8-isoprostane was measured with an enzyme immunoassay, and plasma copper and zinc concentrations were measured using an atomic absorption assay. Our data demonstrate that the copper, zinc, and plasma EC-SOD protein concentrations in the hypertensive and normotensive subjects are indistinguishable. Compared to normotensive controls, hypertensive patients have significantly reduced plasma EC-SOD activity. Plasma nitrotyrosine and 8-isoprostane levels are significantly higher in the hypertensive patients than in normotensive controls. Results from this study suggest that a reduction in EC-SOD activity in hypertensive patients is not due to a down-regulation of the SOD3 gene (encoding EC-SOD) or deficiency in mineral cofactors. Furthermore, the reduced EC-SOD activity might be at least partially responsible for the increased oxidative stress, as reflected by increased plasma nitrotyrosine and 8-isoprostane, in hypertensive subjects.

Infantile nystagmus has many causes, some life threatening. We determined the most common diagnoses in order to develop a testing algorithm.Retrospective chart review. Exclusion criteria were no nystagmus, acquired after 6 months, or lack of examination.pediatric eye examination findings, ancillary testing, order of testing, referral, and final diagnoses. Final diagnosis was defined as meeting published clinical criteria and/or confirmed by diagnostic testing. Patients with a diagnosis not meeting the definition were "unknown." Patients with incomplete testing were "incomplete." Patients with multiple plausible etiologies were "multifactorial." Patients with negative complete workup were "motor."A total of 284 charts were identified; 202 met inclusion criteria. The three most common causes were Albinism (19%), Leber Congenital Amaurosis (LCA; 14%), and Non-LCA retinal dystrophy (13%). Anatomic retinal disorders comprised 10%, motor another 10%. The most common first test was MRI (74/202) with a diagnostic yield of 16%. For 28 MRI-first patients, nystagmus alone was the indication; for 46 MRI-first patients other neurologic signs were present. 0/28 nystagmus-only patients had a diagnostic MRI while 14/46 (30%) with neurologic signs did. The yield of ERG as first test was 56%, OCT 55%, and molecular genetic testing 47%. Overall, 90% of patients had an etiology identified.The most common causes of infantile nystagmus were retinal disorders (56%), however the most common first test was brain MRI. For patients without other neurologic stigmata complete pediatric eye examination, ERG, OCT, and molecular genetic testing had a higher yield than MRI scan. If MRI is not diagnostic, a complete ophthalmologic workup should be pursued.

Chronic graft-vs.-host disease occurs in 30%-50% of long-term survivors of allogeneic bone marrow grafts, and may eventuate in cirrhosis. In this study, a young woman, originally diagnosed as having acute myelogenous leukemia, underwent successful bone marrow transplantation but later developed graft-vs.-host disease-induced cirrhosis and recurrent variceal hemorrhage. She underwent successful orthotopic liver transplant. Her postoperative course was uncomplicated, with no evidence of rejection or recurrence of graft-vs.-host disease. As bone marrow transplantation is more widely used and survival improves, the number of patients with graft-vs.-host disease or venoocclusive disease resulting in cirrhosis is likely to increase. Hepatic transplantation should be considered for bone marrow transplant patients who develop end-stage liver disease.