OH184 Douglas H. Cates Oral History

Douglas H. Cates provides a firsthand account of the Duvin Mine explosion that occurred on July 14, 1939 in Providence, Kentucky. The disaster killed twenty eight miners and left ten wounded. He describes the conditions faced by coal miners in central Kentucky in the first half of the twentieth century. Cates details various aspects of coal mining life, including the company stores, “flickers”, accident compensation, wages and comradely among miners. He concludes by describing various events related to the unionization of the coal miners in the 1930s

OH188 Nadine Weldon Oral History

Nadine Weldon discusses the Duvin Mine Explosion which occurred in Providency, Kentucky on July 14, 1939. She was a wister of a survivor and provides a detailed account of the events at the mine and the rescue efforts that followed the explosion. She describes life in a mining community in western Kentucky during the 1930s. She also discusses the relationship her family had with F.V. Ruckman, the owner of the mine

OH186 Patricia Green Oral History

Patricia Trisha Green provides a second hand account of the Duvin Mine explosion on July 14, 1939 at Providence, Kentucky. She received information of the disaster through her mother whose brother-in-law Carl Big Boy Holloman Jr., had perished in the mine explosion. She describes the rescue efforts and the impact that the disaster had on her family along with the community of Providence. She also explores aspects of the unionization of the miners, mining scripts or flickers , safety concerns, and racial issues

OH187 Linda Earl McDowell Oral History

Linda Earl McDowell discusses the Duvin Mine explosion on July 14, 1939 at Providence, Kentucky. Her account of the disaster was told by her mother, family members, newspaper clippings, other miners and F.V. Ruckman, the owner of the mine. She discusses her father, Earl White Woodring, one of the miners killed by the blast. She details the lives of the miners, including safety issues, script ( flickers ), and the unionization of the mines. She discusses Ruckman\u27s impact on her family and interactions with him following the explosion

OH185 Nettie Davis and Virginia Calbert Oral History

Nettie Davis and Virginia Calbert discuss their recollections of the Duvin Mine explosions on July 14, 1939 at Providence, Kentucky. They discuss James R. Gaither, the brother of Ms. Davis, and George Louis Springfield, the husband of Mrs. Calbert, who perished in the explosion. They describe the scene outside the mine in the hours and days following the explosion and the impact of the disaster on the community. They also recount the racial and economic conditions of the area at that time

Comparative analysis of anti-polyglutamine Fab crystals grown on Earth and in microgravity

Huntington's disease is one of nine neurodegenerative diseases caused by a polyglutamine (polyQ)-repeat expansion. An anti-polyQ antigen-binding fragment, MW1 Fab, was crystallized both on Earth and on the International Space Station, a microgravity environment where convection is limited. Once the crystals returned to Earth, the number, size and morphology of all crystals were recorded, and X-ray data were collected from representative crystals. The results generally agreed with previous microgravity crystallization studies. On average, microgravity-grown crystals were 20% larger than control crystals grown on Earth, and microgravity-grown crystals had a slightly improved mosaicity (decreased by 0.03°) and diffraction resolution (decreased by 0.2 Å) compared with control crystals grown on Earth. However, the highest resolution and lowest mosaicity crystals were formed on Earth, and the highest-quality crystal overall was formed on Earth after return from microgravity

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Hmox1 (Heme Oxygenase-1) Protects Against Ischemia-Mediated Injury via Stabilization of HIF-1α (Hypoxia-Inducible Factor-1α)

Objective: Hmox1 (heme oxygenase-1) is a stress-induced enzyme that catalyzes the degradation of heme to carbon monoxide, iron, and biliverdin. Induction of Hmox1 and its products protect against cardiovascular disease, including ischemic injury. Hmox1 is also a downstream target of the transcription factor HIF-1α (hypoxia-inducible factor-1α), a key regulator of the body's response to hypoxia. However, the mechanisms by which Hmox1 confers protection against ischemia-mediated injury remain to be fully understood.Approach and Results: Hmox1 deficient (Hmox1-/-) mice had impaired blood flow recovery with severe tissue necrosis and autoamputation following unilateral hindlimb ischemia. Autoamputation preceded the return of blood flow, and bone marrow transfer from littermate wild-type mice failed to prevent tissue injury and autoamputation. In wild-type mice, ischemia-induced expression of Hmox1 in skeletal muscle occurred before stabilization of HIF-1α. Moreover, HIF-1α stabilization and glucose utilization were impaired in Hmox1-/- mice compared with wild-type mice. Experiments exposing dermal fibroblasts to hypoxia (1% O2) recapitulated these key findings. Metabolomics analyses indicated a failure of Hmox1-/- mice to adapt cellular energy reprogramming in response to ischemia. Prolyl-4-hydroxylase inhibition stabilized HIF-1α in Hmox1-/- fibroblasts and ischemic skeletal muscle, decreased tissue necrosis and autoamputation, and restored cellular metabolism to that of wild-type mice. Mechanistic studies showed that carbon monoxide stabilized HIF-1α in Hmox1-/- fibroblasts in response to hypoxia.Conclusions: Our findings suggest that Hmox1 acts both downstream and upstream of HIF-1α, and that stabilization of HIF-1α contributes to Hmox1's protection against ischemic injury independent of neovascularization.</p

Lipoprotein Profiles in Class III Obese Caucasian and African American Women with Nonalcoholic Fatty Liver Disease

Triglyceride content in the liver is regulated by the uptake, production and elimination of lipoproteins, and derangements in these processes contribute to nonalcoholic fatty liver disease (NAFLD). Previous studies show a direct relationship between intrahepatic fat and production of apolipoprotein B100 (apoB100) containing particles, VLDL and LDL, but little consensus exists regarding changes in lipoprotein production in the development of simple steatosis (SS) versus nonalcoholic steatohepatitis (NASH). Further, ethnic variations in lipoproteins among SS and NASH are unknown as is how such variations might contribute to the differential prevalence of disease among Caucasians versus African Americans. In this study, we assessed plasma lipoprotein profiles by nuclear magnetic resonance (NMR) spectroscopy in 70 non-diabetic class III obese females recruited from the surgical weight loss clinic. Of these, 51 females were stratified by biopsy-staged NAFLD severity (histologically normal, SS, or NASH). NASH females displayed increased circulating triglycerides and increased VLDL particle number and size relative to those with histologically normal livers, while total and large LDL concentration decreased in SS versus NASH and correlated with increased insulin resistance (via HOMA2-IR). When Caucasian women were examined alone (n = 41), VLDL and triglycerides increased between normal and SS, while total LDL and apoB100 decreased between SS and NASH along with increased insulin resistance. Compared to Caucasians with SS, African American women with SS displayed reduced triglycerides, VLDL, and small LDL and a more favorable small to large HDL ratio despite having increased BMI and HOMA2-IR. These findings suggest that ApoB100 and lipoprotein subclass particle number and size can delineate steatosis from NASH in obese Caucasian females, but should be interpreted with caution in other ethnicities as African Americans with SS display relatively improved lipoprotein profiles. This may reflect variation in the relationship between dyslipidemia and NAFLD progression across gender and ethnicity