Information on Scholarships and Concessions for Dependents of Active, Retired and Deceased Naval and Marine Corps Personnel

Mode of access: Internet.

Summarized Reports of Principal Investigations Being Conducted at the Mining Experiment Stations of the Bureau of Mines

Mode of access: Internet.

Decision list / United States Department of the Interior, Board on Geographic Names.

Mode of access: Internet.

Manual of meat inspection procedures of the United States Department of Agriculture.

Mode of access: Internet.

1963 census of commercial fisheries: number of operators and fishing vessels, employment and gross receipts, fishing regions, primary catch, and fishing gear, size of vessel, cost, and year purchased or built.

Cover title.

Annual reports of the United States Office of Education for the fiscal years ...

Fiscal year ends June 30.

Marine casualty report : entanglement of the submersible Johnson Sea Link with submerged wreckage off Key West, Florida on or about 17 June 1973 with loss of life : U.S. Coast Guard Marine Board of Investigation report and commandant's action : action by National Transportation Safety Board /

Cover title.

Marine casualty report : SS C. V. Sea Witch - SS Esso Brussels (Belgium) : collision and fire in New York Harbor on June 1973 with loss of life : U.S. Coast Guard Marine Board of Investigation report and commandant's action : action by National Transportation Safety Board.

"Report no. USCG/NTSB-MAR-75-6."

Occupational compensation survey--pay only. Connecticut / U.S. Department of Labor, Bureau of Labor Statistics.

Title from caption.

A subject-specific model of human buttocks and thighs in a seated posture

Finite element analyses of the human body in seated postures requires digital models capable of providing accurate and precise prediction of the tissue-level response of the body in the seated posture. To achieve such models, the human anatomy must be represented with high fidelity. This information can readily be defined using medical imaging techniques such as Magnetic Resonance Imaging (MRI) or Computed Tomography (CT). Current practices for constructing digital human models, based on the magnetic resonance (MR) images, in a lying down (supine) posture have reduced the error in the geometric representation of human anatomy relative to reconstructions based on data from cadaveric studies. Nonetheless, the significant differences between seated and supine postures in segment orientation, soft-tissue deformation and soft tissue strain create a need for data obtained in postures more similar to the application posture. In this study, we present a novel method for creating digital human models based on seated MR data. An adult-male volunteer was scanned in a simulated driving posture using a FONAR 0.6T upright MRI scanner with a T1 scanning protocol. To compensate for unavoidable image distortion near the edges of the study, images of the same anatomical structures were obtained in transverse and sagittal planes. Combinations of transverse and sagittal images were used to reconstruct the major anatomical features from the buttocks through the knees, including bone, muscle and fat tissue perimeters, using Solidworks® software. For each MR image, B-splines were created as contours for the anatomical structures of interest, and LOFT commands were used to interpolate between the generated Bsplines. The reconstruction of the pelvis, from MR data, was enhanced by the use of a template model generated in previous work CT images. A non-rigid registration algorithm was used to fit the pelvis template into the MR data. Additionally, MR image processing was conducted to both the left and the right sides of the model due to the intended asymmetric posture of the volunteer during the MR measurements. The presented subject-specific, three-dimensional model of the buttocks and thighs will add value to optimisation cycles in automotive seat development when used in simulating human interaction with automotive seats.

DNA damage recognition in the normal epithelium of human prostate and seminal vesicles

Prostate cancer is one of the most prevalent cancer types in men. The development of prostate tumors is known to require androgen exposure, and several pathways governing cell growth are deregulated in prostate tumorigenesis. Recent genetic studies have revealed that complex gene fusions and copy - number alterations are frequent in prostate cancer, a unique feature among solid tumors. These chromosomal aberrations are though to arise as a consequence of faulty repair of DNA double strand breaks (DSB). Most repair mechanisms have been studied in detail in cancer cell lines, but how DNA damage is detected and repaired in normal differentiated human cells has not been widely addressed. The events leading to the gene fusions in prostate cancer are under rigorous studies, as they not only shed light on the basic pathobiologic mechanisms but may also produce molecular targets for prostate cancer treatment and prevention. Prostate and seminal vesicles are part of the male reproductive system. They share similar structure and function but differ dramatically in their cancer incidence. Approximately fifty primary seminal vesicle carcinomas have been reported worldwide. Surprisingly, only little is known on why seminal vesicles are resistant to neoplastic changes. As both tissues are androgen dependent, it is a mystery that androgen signaling would only lead to tumors in prostate tissue. In this work, we set up novel ex vivo human tissue culture models of prostate and seminal vesicles, and used them to study how DNA damage is recognized in normal epithelium. One of the major DNA - damage inducible pathways, mediated by the ATM kinase, was robustly activated in all main cell types of both tissues. Interestingly, we discovered that secretory epithelial cells had less histone variant H2A.X and after DNA damage lower levels of H2AX were phosphorylated on serine 139 (γH2AX) than in basal or stromal cells. γH2AX has been considered essential for efficient DSB repair, but as there were no significant differences in the γH2AX levels between the two tissues, it seems more likely that the role of γH2AX is less important in postmitotic cells. We also gained insight into the regulation of p53, an important transcription factor that protects genomic integrity via multiple mechanisms, in human tissues. DSBs did not lead to a pronounced activation of p53, but treatments causing transcriptional stress, on the other hand, were able to launch a notable p53 response in both tissue types. In general, ex vivo culturing of human tissues provided unique means to study differentiated cells in their relevant tissue context, and is suited for testing novel therapeutic drugs before clinical trials. In order to study how prostate and seminal vesicle epithelial cells are able to activate DNA damage induced cell cycle checkpoints, we used primary cultures of prostate and seminal vesicle epithelial cells. To our knowledge, we are the first to report isolation of human primary seminal vesicle cells. Surprisingly, human prostate epithelial cells did not activate cell cycle checkpoints after DSBs in part due to low levels of Wee1A, a kinase regulating CDK activity, while primary seminal vesicle epithelial cells possessed proficient cell cycle checkpoints and expressed high levels of Wee1A. Similarly, seminal vesicle cells showed a distinct activation of the p53 - pathway after DSBs that did not occur in prostate epithelial cells. This indicates that p53 protein function is under different control mechanisms in the two cell types, which together with proficient cell cycle checkpoints may be crucial in protecting seminal vesicles from endogenous and exogenous DNA damaging factors and, as a consequence, from carcinogenesis. These data indicate that two very similar organs of male reproductive system do not respond to DNA damage similarly. The differentiated, non - replicating cells of both tissues were able to recognize DSBs, but under proliferation human prostate epithelial cells had deficient activation of the DNA damage response. This suggests that prostate epithelium is most vulnerable to accumulating genomic aberrations under conditions where it needs to proliferate, for example after inflammatory cellular damage.

Design and Characterization of Stabilized Derivatives of Human CD4D12 and CD4D1

CD4 is present on the surface of T-lymphocytes and is the primary cellular receptor for HIV-1. CD4 consists of a cytoplasmic tail, one transmembrane region, and four extracellular domains, D1-D4. A construct consisting of the first two domains of CD4 (CD4D12) is folded and binds gp120 with similar affinity as soluble 4-domain CD4 (sCD4). However, the first domain alone (CD4D1) was previously shown to be largely unfolded and had 3-fold weaker affinity for gp120 when compared to sCD4 [Sharma, D.; et al. (2005) Biochemistry 44, 16192-16202]. We now report the design and characterization of three single-site mutants of CD4D12 (G6A, L51I, and V86L) and one multisite mutant of CD4D1 (G6A/L511/L5K/F98T). G6A, L51I, and V86L are cavity-filling mutations while L5K and F98T are surface mutations which were introduced to minimize the aggregation of CD4D1 upon removal of the second domain. Two mutations, G6A and V86L in CD4D12 increased the stability and yield of the protein relative to the wild-type protein. The mutant CD4D1 (CD4D1a) with the 4 mutations was folded and more stable compared to the original CD4D1, but both bound gp120 with comparable affinity. In in vitro neutralization assays, both CD4D1a and G6A-CD4D12 were able to neutralize diverse HIV-1 viruses with similar IC(50)s as 4-domain CD4. These stabilized derivatives of human CD4 can be useful starting points for the design of other more complex viral entry inhibitors.

Infection of human amniotic and endothelial cells by Japanese encephalitis virus: Increased expression of HLA-F

Productive infection of human amniotic and endothelial cell lines with Japanese encephalitis virus (JEV) was established leading to the induction of NF kappa B and HLA-F, a non-classical MHC molecule. Induction of the HLA-F gene and protein in JEV-infected cells was shown to be NF kappa B dependent since it was blocked by inhibitors of NF kappa B activation. ShRNA targeting lentivirus-mediated stable knockdown of the p65 subunit of NF kappa B inhibited JEV-mediated induction of HLA-F both in the amniotic cell line, AV-3 as well as the human brain microendothelial cell line, HBMEC. The induction of HLA-F by treatment of AV-3 with TNF-alpha was also inhibited by ShRNA mediated knockdown of NF kappa B. TNF-alpha treatment of HEK293T cells that were transfected with reporter plasmids under the control of HLA-F enhancer A elements resulted in significant transactivation of the luciferase reporter gene. NF kappa B-mediated induction of HLA-F following JEV infection and TNF-alpha exposure is being suggested for the first time. (C) 2014 Elsevier Inc. All rights reserved.