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\"This is the memoir of J. R. Ritter (1902-1994), a civil engineer from Texas who became a U.S. Navy Seabee officer during World War II. The formal name of the Seabees is \"U.S. Naval Construction Battalions\" and they were responsible for building airstrips, barracks, and other infrastructure for the troops. Ritter was first stationed in Alaska when Japan was thought to be planning an invasion through the Aleutians, then in the Central Pacific, mainly on Tinian Island. He was on Tinian when the war ended\"-- Provided by publisher.

Diffuse white matter injury is common in very preterm infants; here, enhanced epidermal growth factor receptor signalling in oligodendrocyte precursor cells in a mouse model of such injury is shown to increase cellular and functional recovery. EGFR treatment of neonatal brain injury As the survival rates of premature babies have increased, so too has the incidence of chronic neurodevelopmental disorders in neonates. Diffuse white matter injury is common in preterm infants with neonatal brain injury and is partially the result of a failure in oligodendrocyte precursor cell maturation. Here, Vittorio Gallo and colleagues specifically enhanced epidermal growth factor receptor (EGFR) signalling in oligodendrocyte precursor cells in a model of diffuse white matter injury and found increased cellular and functional recovery post-injury. Oligodendrocyte cell death was decreased and the generation of new oligos was increased by the treatment. This identifies EGFR signalling as a potential therapeutic target in the treatment of premature children after white matter injury. There are no clinically relevant treatments available that improve function in the growing population of very preterm infants (less than 32 weeks’ gestation) with neonatal brain injury. Diffuse white matter injury (DWMI) is a common finding in these children and results in chronic neurodevelopmental impairments 1 , 2 . As shown recently, failure in oligodendrocyte progenitor cell maturation contributes to DWMI 3 . We demonstrated previously that the epidermal growth factor receptor (EGFR) has an important role in oligodendrocyte development 4 . Here we examine whether enhanced EGFR signalling stimulates the endogenous response of EGFR-expressing progenitor cells during a critical period after brain injury, and promotes cellular and behavioural recovery in the developing brain. Using an established mouse model of very preterm brain injury, we demonstrate that selective overexpression of human EGFR in oligodendrocyte lineage cells or the administration of intranasal heparin-binding EGF immediately after injury decreases oligodendroglia death, enhances generation of new oligodendrocytes from progenitor cells and promotes functional recovery. Furthermore, these interventions diminish ultrastructural abnormalities and alleviate behavioural deficits on white-matter-specific paradigms. Inhibition of EGFR signalling with a molecularly targeted agent used for cancer therapy demonstrates that EGFR activation is an important contributor to oligodendrocyte regeneration and functional recovery after DWMI. Thus, our study provides direct evidence that targeting EGFR in oligodendrocyte progenitor cells at a specific time after injury is clinically feasible and potentially applicable to the treatment of premature children with white matter injury.

This is the story of J. R. Ritter (1902-1994), a civil engineer from Texas who became a U.S. Navy Seabee officer during World War II. For his memoir he preserved personal papers, letters, photos, and other items, many of which are reproduced in this book. His narrative is edited and annotated by his grandson, Jonathan Templin Ritter. The U.S. Naval Construction Battalions, known as the “Seabees,” were formed in March 1942. Their duties were to build military facilities and airfields overseas, in both the European and Pacific Theaters. In the Pacific Theater alone, including the Aleutians, the Seabees built 111 major airstrips, 441 piers, 2258 ammunition magazines, and much more. Ritter tells the story of two Seabee Battalions, one in the Aleutians and one in the Central Pacific. He describes the Aleutian Islands Campaign during 1942-1943, when there was a real concern that Japan might try to attack Alaska and the continental United States through the “back door.” Ritter also gives an eyewitness account of the building of the airfields on Tinian Island in the Northern Marianas that enabled the B-29 fire raids on Japan—the “Empire Run”—which culminated in the two missions that dropped the atomic bombs in August 1945, ending the Pacific War. This book provides a major contribution to the wartime literature about the Seabees, those brave, resourceful, and hard-working American patriots, whose mottos were “Can do!” and “The difficult we do now; the impossible takes a little longer.”

•Pre-morbid, patient demographic and injury features can predict TBI outcome.•Previous psychiatric history had the largest predictive value of TBI outcome.•Employment before and after TBI also had a significant effect on outcome.•Aetiology of assault, GCS, severe CT scan were additional predictors. Traumatic Brain Injury (TBI) is the leading cause of death and disability in people aged under 40 in the UK. Many patients suffer residual deficits, which limits their functional recovery. The aim of this study was to determine independent predictors of functional outcome at 1-year post-TBI. Utilising a prospective observational cohort design, 1131 consecutive adult admissions with non-recurrent TBI were recruited from the ED (Emergency Department). Using routine consultant-led follow up clinics, data was collected between August 2011 and July 2015. The Rivermead Head Injury Follow Up Questionnaire (RHFUQ) was used to measure psychosocial function at 1 year. A multiple linear regression model showed that previous psychiatric history (p < 0.001), lower Glasgow Coma Scale (p < 0.001), a severe CT scan (p = 0.002), aetiology of assault compared to sport (p = 0.011) and falls (p = 0.005), initial unemployment (p < 0.001) and no job at 8–10 weeks (p < 0.001) after TBI had a significant association with a worse RHFUQ score at 1 year. Follow up rate was >90 %. This study adds valuable information on the prognostic indicators of TBI recovery and possible targets for intervention. Future development of a validated prognostic model to predict long term functional outcomes after TBI will help improve long-term treatment of the condition.

An important contribution to understanding the development of modern New York, focusing on elite domestic architecture--in particular the James B. Duke House--within the contexts of social history, urban planning, architecture and interiors, and adaptive reuse for new functions.

This article examines the radicalization of carnival practices and music in the Fajardo province of Ayacucho, Peru, at the outset of the Shining Path guerrilla war in 1980. The simultaneous rise of formal song contests and Shining Path organizing in Fajardo cannot be separated in this history as both were key elements in a popular regional discourse of modernization and development. Often interpreted as transparent statements of Maoist propaganda, or, conversely, as organic expressions of Andean peasant rebelliousness, revolutionary song performances are instead positioned here as complex sites where local attitudes to politics and ideology were created, debated and transformed.

Diffuse white matter injury is common in very preterm infants; here, enhanced epidermal growth factor receptor signalling in oligodendrocyte precursor cells in a mouse model of such injury is shown to increase cellular and functional recovery.

Diffuse white matter injury (DWMI) is frequently associated with impaired neurological development in pre-mature infants. To characterize the cellular, structural and functional basis of hyperoxia-induced DWMI, the cellular changes in the white matter (WM) were first characterized using mice exposed to 48 hours of 80% oxygen from postnatal day 6 (P6) to postnatal day 8 (P8). Myelin basic protein (MBP) expression and CC1+ oligodendroglia decreased following hyperoxia at P8, but returned to control levels by P15. Hyperoxia caused increased apoptosis and decreased proliferation of oligodendrocyte progenitor cells (OPCs), which was followed by the restoration of the NG2 + cell population and increased oligodendrogenesis in the WM. Hyperoxia, did not affect survival or proliferation of astrocytes in vivo, but modified glial fibrillary acidic protein (GFAP) and glutamate-aspartate transporter (GLAST) expression. The rate of 3H-D-aspartic acid uptake in WM tissue was also diminished at P8 and P12. In addition, cultured astrocytes exposed to hyperoxia showed a reduced capacity to protect OPCs against exogenous glutamate. Upon further analysis, the hyperoxia group was discovered to have decreased myelin associated glycoprotein (MAG) and proteolipid protein (PLP) expression and a decrease in the number of MAG+CC1+ oligodendrocytes until P30. Electron microscopy found this group to also have reduced myelin thickness and axon caliber at P30. The change in axon caliber was associated with diminished neurofilament phosphorylation in axons of the developing WM until P15. Altered paranodal organization was also observed in the hyperoxia group throughout WM maturation. Electrophysiological analysis of the corpus callosum (CC) revealed that mice exposed to neonatal hyperoxia exhibited significant decreases in both myelinated (M) and unmyelinated (UM) compound action potential (CAP) maximum amplitude as well as a reduction in the conduction velocity of myelinated axons. Fractional anisotropy (FA) determined with diffusion tensor imaging (DTI) found that hyperoxia caused a decrease in WM diffusivity at P30 and P60. These studies indicate that a hyperoxia-induced disruption of WM development, through a mechanism involving astrocyte dysfunction/altered glutamate homeostasis, leads to significant lasting changes in WM structure and function. Understanding the underlying pathogenesis of WM injury is important in developing interventional strategies to prevent such pathology.