Leaders of Reform: Progressive Republicans in Kansas, 1900-1916

Robert Sherman La Forte was professor of history at the University of North Texas, where he taught for thirty years. In addition to this book, he coauthored three books on World War II history and the authorized history of the University of North Texas. With a New Foreword by Charles Delgadillo. Charles Delgadillo is lecturer in history at the California State Polytechnic University, Pomona, and Norco College, in California. He is the author of Crusader for Democracy: The Political Life of William Allen White.This Kansas Open Books title is funded by a grant from the National Endowment for the Humanities and the Andrew W. Mellon Foundation Humanities Open Book Program.In Leaders of Reform Robert Sherman La Forte examines the intricacies of shifting factions within the state majority party over a two decade period, from the Boss-Busters and political machines of the early 1900s through the formation of a new party behind Theodore Roosevelt in 1913. He discusses the motives, activities, accomplishments, and failures of the progressive Republicans. He provides excellent vignettes of major leaders such as William Allen White, Arthur Capper, Joseph L. Bristow, and Charles Curtis, as well as lesser-known characters such as Walter Roscoe Stubbs, Edward H. Hoch, and Cy Leland, Jr. In providing a detailed analysis of virtually all Kansas progressive Republican leaders during the era, La Forte has made a valuable contribution to both state and national political history

The role of microRNAs in thyroid carcinomas

Thyroid cancers (TCs) are the most common malignancies of endocrine organs. They originate from cells of different origin within the thyroid gland, which is located at the base of the neck. Several forms of TCs have been classified and great variability is observed in molecular, cellular and clinical features. The most common forms have favorable prognosis but a number of very aggressive TCs, which are characterized by a less differentiated cellular phenotype, have no effective treatment at the moment. While TC causes are not completely understood, many genetic factors involved in their onset have been discovered. In particular, activating mutations of BRAF, RET or RAS genes are known to be specifically associated with TC initiation, progression and outcome. The involvement of microRNAs in thyroid neoplasms has recently changed the paradigm for biomarker discovery in TC, suggesting that these small non-coding RNAs could be used to develop, refine or strengthen strategies for diagnosis and management of TCs. In this review, the importance of microRNA profiling in TC is explored suggesting that these molecules can be included in procedures that can perform better than any known clinical index in the identification of adverse outcomes

Leaders of Reform: Progressive Republicans in Kansas, 1900-1916

In Leaders of Reform Robert Sherman La Forte examines the intricacies of shifting factions within the state majority party over a two decade period, from the Boss-Busters and political machines of the early 1900s through the formation of a new party behind Theodore Roosevelt in 1913. He discusses the motives, activities, accomplishments, and failures of the progressive Republicans. He provides excellent vignettes of major leaders such as William Allen White, Arthur Capper, Joseph L. Bristow, and Charles Curtis, as well as lesser-known characters such as Walter Roscoe Stubbs, Edward H. Hoch, and Cy Leland, Jr. In providing a detailed analysis of virtually all Kansas progressive Republican leaders during the era, La Forte has made a valuable contribution to both state and national political history. Description Robert Sherman La Forte was professor of history at the University of North Texas, where he taught for thirty years. In addition to this book, he coauthored three books on World War II history and the authorized history of the University of North Texas. With a New Foreword by Charles Delgadillo. Charles Delgadillo is lecturer in history at the California State Polytechnic University, Pomona, and Norco College, in California. He is the author of Crusader for Democracy: The Political Life of William Allen White. This Kansas Open Books title is funded by a grant from the National Endowment for the Humanities and the Andrew W. Mellon Foundation Humanities Open Book Program.https://digitalcommons.pittstate.edu/kansas_open_books/1038/thumbnail.jp

Transport of apolipoproteins A-I and A-II by human thoracic duct lymph

The daily transport of human plasma apolipoproteins A-I and A-II, triglyceride, and total cholesterol from the thoracic duct lymph into plasma was measured in 2 subjects before and 3 subjects after renal transplantation. Lymph triglyceride transport was ~83% of the daily ingested fat loads, whereas lymph cholesterol transport was consistently greater than the amount of daily ingested cholesterol. Lymph apolipoprotein transport significantly (P < 0.05) exceeded the predicted apolipoprotein synthesis rate by an average of 659±578 mg/d for apolipoprotein A-I and 109±59 mg/d for apolipoprotein A-II among the 5 subjects. It is estimated that 22-77% (apolipoprotein A-I) and 28-82% (apolipoprotein A-II) of daily total body apolipoprotein synthesis takes place in the intestine. Lymph high density lipoprotein particles are mostly high density lipoprotein(2b) and high density lipoprotein(2a) and have a greater overall relative triglyceride content and a smaller relative cholesteryl ester content when compared with homologous plasma high density lipoproteins. The major quantity of both lymph apolipoprotein A-I (81±8%) and apolipoprotein A-II (90±11%) was found within high density lipoproteins with almost all of the remainder found in chylomicrons and very low density lipoproteins. The combined results are consistent with a major contribution of the intestine to total body synthesis of apolipoprotein A-I and apolipoprotein A-II. An important role of lymph in returning filtered apolipoprotein to plasma in association with high density lipoproteins is proposed. Accompanying the return of filtered apolipoprotein to the plasma is a probable transformation, both in size and composition, of at least some of the lymph high density lipoprotein(2b) and high density lipoprotein(2a) particles into high density lipoprotein3

The globular clusters-stellar haloes connection in early type galaxies

This paper explores if, and to what an extent, the stellar populations of early type galaxies can be traced through the colour distribution of their globular cluster systems. The analysis, based on a galaxy sample from the Virgo ACS data, is an extension of a previous approach that has been successful in the cases of the giant ellipticals NGC 1399 and NGC 4486, and assumes that the two dominant GC populations form along diffuse stellar populations sharing the cluster chemical abundances and spatial distributions. The results show that a) Integrated galaxy colours can be matched to within the photometric uncertainties and are consistent with a narrow range of ages; b) The inferred mass to luminosity ratios and stellar masses are within the range of values available in the literature; c) Most globular cluster systems occupy a thick plane in the volume space defined by the cluster formation efficiency, total stellar mass and projected surface mass density. The formation efficiency parameter of the red clusters shows a dependency with projected stellar mass density that is absent for the blue globulars. In turn, the brightest galaxies appear clearly detached from that plane as a possible consequence of major past mergers; d) The stellar mass-metallicity relation is relatively shallow but shows a slope change at $M_*\approx 10^{10} M_\odot$. Galaxies with smaller stellar masses show predominantly unimodal globular cluster colour distributions. This result may indicate that less massive galaxies are not able to retain chemically enriched intestellar matter.Comment: 19 pages, 10 figure

Adsorption of NGF and BDNF derived peptides on gold surfaces

This study tackles the interaction between gold surfaces and two peptide fragments named NGF(1-14) and BDNF(1-12), able to mimic the proliferative activity of nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF), respectively. The physical adsorption processes at the solid surface from both single and binary peptide solutions, at physiological and acid pH, were investigated by QCM-D and CD experiments, as well as by molecular dynamics calculations. The relevant physicochemical properties at the hybrid bio-interface, including peptide-surface interaction, conformational changes, hydrodynamic thickness, viscoelastic parameters, competitive vs. synergic behaviour of the two peptide fragments towards the surface were scrutinized. Biological assays with neuronal cells pointed to the maintenance in the biological activity of NGF(1-14) and BDNF(1-12) peptide molecules within the adlayers on the gold surface

Combined kinase inhibition modulates parkin inactivation

Mutations in the parkin gene cause autosomal-recessive, juvenile-onset parkinsonism, and parkin dysfunction may also play a role in the pathogenesis of sporadic Parkinson disease (PD). Although its precise function remains largely unknown, parkin seems to play a neuroprotective role. Several studies indicate that changes in parkin solubility induced by post-translational modifications, such as S-nitrosylation or dopamine modification, comprise one mechanism of parkin inactivation associated with disease. Protein phosphorylation events have recently been linked to the molecular mechanism(s) underlying PD, but the role of this post-translational modification for parkin function has remained unclear. Here we report that compound phosphorylation of parkin by both casein kinase I and cyclin-dependent kinase 5 (cdk5) decreases parkin solubility, leading to its aggregation and inactivation. Combined kinase inhibition partially reverses the aggregative properties of several pathogenic point mutants in cultured cells. Enhanced parkin phosphorylation is detected in distinct brain areas of individuals with sporadic PD and correlates with increases in the levels of p25, the activator of cdk5. These findings indicate that casein kinase I and cdk5 may represent novel combinatorial therapeutic targets for treating PD