Spinal cord injury : hope through research / [prepared by the Office of Scientific and Health Reports, National Institute of Neurological and Communicative Disorders and Stroke].

Mode of access: Internet.

The giant hand; our mobilization and control of industry and natural resources, 1917-1918,

Mode of access: Internet.

Incidence of disability and characteristics of clients closed from plan with severe spinal cord injury, fiscal year 1972-73 /

"December 30, 1975."

Patterns of education and employment : rehabilitants from severe spinal cord injuries, fiscal year 1972-73 /

"June 1, 1974."

An experimental study of the effects of viscous and capillary forces on the trapping and mobilization of oil drops in capillary constrictions /

Thesis--University of Kansas, Chemical and Petroleum Engineering.

Professor Schroeder van der Kolk on the minute structure and functions of the spinal cord and medulla oblongata : and on the proximate cause and rational treatment of epilepsy /

Translation of two memoirs: Anatomisch physiologisch onderzoek over het fijnere zamenstel en de werking van het ruggemerg, published 1854, and Over het fijnere zamenstel en de werking van het verlangde ruggemerg en over de naaste oorzaak van epilepsie en hare rationele behandeling, published 1858.

Myelitis of the anterior horns, or spinal paralysis of the adult and child,

Mode of access: Internet.

U.S. Army mobilization and logistics in the Korean War : a research approach /

Mode of access: Internet.

Health mobilization series.

Mode of access: Internet.

Industrial mobilization for war, history of the War Production Board and predecessor agencies, 1940-1945.

Mode of access: Internet.

Storage protein mobilization and thiol protease up-regulation by solid matrix priming in loblolly pine (Pinus taeda) seed embryos

Experiments were conducted to investigate physiological mechanisms of solid matrix priming (SMP) on germination enhancement of loblolly pine (Pinus taeda) seeds. During SMP, osmotic potential in the embryo decreased by 0.65 MPa, concentration of crystalloid proteins decreased to 62% and concentrations of buffer soluble proteins and free amino acids increased by 22% and by 166%, respectively. Observations under an electron microscope demonstrated protein bodies in the embryo were mobilized. Inhibitor analysis indicated thiol protease was the dominant enzyme among endopiptidases to degrade the reserved proteins. A fragment of thiol protease was cloned from the primed seed embryos and it has high identities to those thiol proteases responsive to water stress. RNA get blot analysis showed a 1.5 kb thiol protease gene was up-regulated by SMP. Treatment with E64, a thiol protease inhibitor, negated SMP effects on germination performance, water potentials and protein profiles. Based on the experimental results, reserve protein mobilization induced by SMP in the embryo before radicle emergence might be one of the mechanisms to enhance germination in loblolly pine seeds.

Mapping of autosomal recessive chronic distal spinal muscular atrophy to chromosome 11q13

Distal spinal muscular atrophy is a heterogeneous group of neuromuscular disorders caused by progressive anterior born cell degeneration and characterized by progressive motor weakness and muscular atrophy, predominantly in the distal parts of the limbs. Here we report on chronic autosomal recessive distal spinal muscular atrophy in a large, inbred family with onset at various ages. Because this condition had some of the same clinical features as spinal muscular atrophy with respiratory distress, we tested the disease gene for linkage to chromosome 11q and mapped the disease locus to chromosome 11q13 in the genetic interval that included the spinal muscular atrophy with respiratory distress gene (D11S1889-D11S1321, Z(max) = 4.59 at theta = 0 at locus D11S4136). The sequencing of IGHMBP2, the human homologue of the mouse neuromuscular degeneration gene (nmd) that accounts for spinal muscular atrophy with respiratory distress, failed to detect any mutation in our chronic distal spinal muscular atrophy patients, suggesting that spinal muscular atrophy with respiratory distress and chronic distal spinal muscular atrophy are caused by distinct genes located in the so-me chromosomal region. In addition, the high intrafamilial variability in age at onset raises the question of whether nonallelic modifying genes could be involved in chronic distal spinal muscular atrophy.