[Warranty Deed to a piece of property sold by J. J. and Emma Freeze to G. M. D. Bowers and B. R. Colson as trustees]

Warranty deed to a piece of property sold by J. J. and Emma Freeze to G. M. D. Bowers and B. R. Colson as trustees of Dixieland College. The deed is dated 28 September 1912

Letter from J. J. Freeze to B. R. Colson

Letter from J. J. Freeze to B. R. Colson dated January 4. Year of creation is estimated to be 1913

Option contract between J. J. and Emma S. Freeze and W. W. Colson

Option contract dated 18 April 1912 between J. J. and Emma S. Freeze and W. W. Colson

Preliminary results of noble metal thermocouple research program, 1000 - 2000 C

Noble metal thermocouple research involving combustion gase

Satisfaction of Mortgage

Satisfaction of Mortgage between J. J. Freeze to G. M. D. Bowers and B. R. Colson. The document is dated 11 April 1914

Extra employment policies in Texas law enforcement

Examines various extra employment policies within Texa

Separation of transport lifetimes in SrTi

Deviations from Landau Fermi liquid behavior are ubiquitous features of the normal state of unconventional superconductors. Despite several decades of investigation, the underlying mechanisms of these properties are still not completely understood. In this work, we show that two-dimensional electron liquids at SrTiO3/RTiO3 (R = Gd or Sm) interfaces reveal strikingly similar physics. Analysis of Hall and resistivity data show a clear separation of transport and Hall scattering rates, also known as "two-lifetime" behavior. This framework gives a remarkably simple and general description of the temperature dependence of the Hall coefficient. Distinct transport lifetimes accurately describe the transport phenomena irrespective of the nature of incipient magnetic ordering, the degree of disorder, confinement, or the emergence of non-Fermi liquid behavior. The Hall scattering rate diverges at a critical quantum well thickness, coinciding with a quantum phase transition. Collectively, these results introduce new constraints on the existing microscopic theories of lifetime separation and point to the need for unified understanding.Comment: Version accepted for publication in Phys. Rev.

Bicuspid Aortic Valve: a Review with Recommendations for Genetic Counseling

Bicuspid aortic valve (BAV) is the most common congenital heart defect and falls in the spectrum of left-sided heart defects, also known as left ventricular outflow tract obstructive (LVOTO) defects. BAV is often identified in otherwise healthy, asymptomatic individuals, but it is associated with serious long term health risks including progressive aortic valve disease (stenosis or regurgitation) and thoracic aortic aneurysm and dissection. BAV and other LVOTO defects have high heritability. Although recommendations for cardiac screening of BAV in at-risk relatives exist, there are no standard guidelines for providing genetic counseling to patients and families with BAV. This review describes current knowledge of BAV and associated aortopathy and provides guidance to genetic counselors involved in the care of patients and families with these malformations. The heritability of BAV and recommendations for screening are highlighted. While this review focuses specifically on BAV, the principles are applicable to counseling needs for other LVOTO defects

Pathogenic Variants in Fucokinase Cause a Congenital Disorder of Glycosylation

FUK encodes fucokinase, the only enzyme capable of converting L-fucose to fucose-1-phosphate, which will ultimately be used for synthesizing GDP-fucose, the donor substrate for all fucosyltransferases. Although it is essential for fucose salvage, this pathway is thought to make only a minor contribution to the total amount of GDP-fucose. A second pathway, the major de novo pathway, involves conversion of GDP-mannose to GDP-fucose. Here we describe two unrelated individuals who have pathogenic variants in FUK and who presented with severe developmental delays, encephalopathy, intractable seizures, and hypotonia. The first individual was compound heterozygous for c.667T>C (p.Ser223Pro) and c.2047C>T (p.Arg683Cys), and the second individual was homozygous for c.2980A>C (p.Lys994Gln). Skin fibroblasts from the first individual confirmed the variants as loss of function and showed significant decreases in total GDP-[3H] fucose and [3H] fucose-1-phosphate. There was also a decrease in the incorporation of [5,6-3H]-fucose into fucosylated glycoproteins. Lys994 has previously been shown to be an important site for ubiquitin conjugation. Here, we show that loss-of-function variants in FUK cause a congenital glycosylation disorder characterized by a defective fucose-salvage pathway