University of Kentucky

About: University of Kentucky is a education organization based out in Lexington, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 43933 authors who have published 92195 publications receiving 3256087 citations. The organization is also known as: UK.

Effect of the Growth Temperature on the Diameter Distribution and Chirality of Single-Wall Carbon Nanotubes

Abstract: Pulsed laser vaporization of a heated, Fe/Ni or Co/Ni catalyzed, carbon target in argon gas has been used to synthesize single-wall carbon nanotubes (SWNTs). Electron microscopy, x-ray diffraction, and Raman spectroscopy were all used to study the effect of the catalyst on the tube yield, and the evolution of the tube diameter distribution with increasing growth environment temperature $T$. By controlling the temperature in the range $780lTl1050\ifmmode^\circ\else\textdegree\fi{}\mathrm{C}$, we have been able to tune the diameter of the tubules from $\ensuremath{\sim}0.81$ to $\ensuremath{\sim}1.51\mathrm{nm}$. The threshold temperature for significant SWNT production was found to be $\ensuremath{\sim}850\ifmmode^\circ\else\textdegree\fi{}\mathrm{C}$.

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report.

Abstract: We describe a recently recognized disease entity, limbic-predominant age-related TDP-43 encephalopathy (LATE). LATE neuropathological change (LATE-NC) is defined by a stereotypical TDP-43 proteinopathy in older adults, with or without coexisting hippocampal sclerosis pathology. LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-type dementia in retrospective autopsy studies. LATE is distinguished from frontotemporal lobar degeneration with TDP-43 pathology based on its epidemiology (LATE generally affects older subjects), and relatively restricted neuroanatomical distribution of TDP-43 proteinopathy. In community-based autopsy cohorts, ∼25% of brains had sufficient burden of LATE-NC to be associated with discernible cognitive impairment. Many subjects with LATE-NC have comorbid brain pathologies, often including amyloid-β plaques and tauopathy. Given that the 'oldest-old' are at greatest risk for LATE-NC, and subjects of advanced age constitute a rapidly growing demographic group in many countries, LATE has an expanding but under-recognized impact on public health. For these reasons, a working group was convened to develop diagnostic criteria for LATE, aiming both to stimulate research and to promote awareness of this pathway to dementia. We report consensus-based recommendations including guidelines for diagnosis and staging of LATE-NC. For routine autopsy workup of LATE-NC, an anatomically-based preliminary staging scheme is proposed with TDP-43 immunohistochemistry on tissue from three brain areas, reflecting a hierarchical pattern of brain involvement: amygdala, hippocampus, and middle frontal gyrus. LATE-NC appears to affect the medial temporal lobe structures preferentially, but other areas also are impacted. Neuroimaging studies demonstrated that subjects with LATE-NC also had atrophy in the medial temporal lobes, frontal cortex, and other brain regions. Genetic studies have thus far indicated five genes with risk alleles for LATE-NC: GRN, TMEM106B, ABCC9, KCNMB2, and APOE. The discovery of these genetic risk variants indicate that LATE shares pathogenetic mechanisms with both frontotemporal lobar degeneration and Alzheimer's disease, but also suggests disease-specific underlying mechanisms. Large gaps remain in our understanding of LATE. For advances in prevention, diagnosis, and treatment, there is an urgent need for research focused on LATE, including in vitro and animal models. An obstacle to clinical progress is lack of diagnostic tools, such as biofluid or neuroimaging biomarkers, for ante-mortem detection of LATE. Development of a disease biomarker would augment observational studies seeking to further define the risk factors, natural history, and clinical features of LATE, as well as eventual subject recruitment for targeted therapies in clinical trials.

Lifestyle transitions in plant pathogenic Colletotrichum fungi deciphered by genome and transcriptome analyses

Abstract: Colletotrichum species are fungal pathogens that devastate crop plants worldwide. Host infection involves the differentiation of specialized cell types that are associated with penetration, growth inside living host cells (biotrophy) and tissue destruction (necrotrophy). We report here genome and transcriptome analyses of Colletotrichum higginsianum infecting Arabidopsis thaliana and Colletotrichum graminicola infecting maize. Comparative genomics showed that both fungi have large sets of pathogenicity-related genes, but families of genes encoding secreted effectors, pectin-degrading enzymes, secondary metabolism enzymes, transporters and peptidases are expanded in C. higginsianum. Genome-wide expression profiling revealed that these genes are transcribed in successive waves that are linked to pathogenic transitions: effectors and secondary metabolism enzymes are induced before penetration and during biotrophy, whereas most hydrolases and transporters are upregulated later, at the switch to necrotrophy. Our findings show that preinvasion perception of plant-derived signals substantially reprograms fungal gene expression and indicate previously unknown functions for particular fungal cell types.

Iron deficiency anemia

Abstract: Iron is an essential mineral for oxygen transport and energy production. Increased requirements, as with pregnancy, or inadequate dietary intake of iron may lead to varying degrees of depletion. If iron depletion is severe, iron deficiency anemia (IDA) occurs. By World Health Organization standards, anemia during pregnancy is a hemoglobin (Hb) concentration ≤13.0 g/dl, and by this definition anemia may complicate over 50% of all gestations in the United States.1 Of pregnant women with an abnormally low Hb concentration and packed cell volume (PCV), 75–85% have IDA.2 Indeed, some degree of iron depletion appears to be almost universal during pregnancy. The problem is compounded by multiple gestations, successive pregnancies (<2–3 years apart), adolescent pregnancy, chronic blood loss, intravascular hemolysis, and poor iron absorption associated with certain medical conditions.