Possible mechanism for radial ion acceleration in a beam-plasma discharge

A mechanism is proposed that can lead to radial ion acceleration in a plasma discharge excited by an electron beam in a relatively weak longitudinal magnetic field. The mechanism operates as follows. The beam generates an azimuthally asymmetric slow potential wave, which traps electrons. Trapped magnetized electrons drift radially with a fairly high velocity under the combined action of the azimuthal wave field (which is constant for them) and a relatively weak external longitudinal magnetic field. The radial electron flux generates a radial charge-separation electric field, which accelerates unmagnetized plasma ions in the radial direction. The ion flux densities and energies achievable in experiments with kiloelectronvolt electron beams in magnetic fields of up to 100 G are estimated.     

Studies on theH-X locus of mice

The results of challenging F₁ hybrid male mice derived from strains BALB/c, A/J, C57BL/6J, C57BL/10ScSn and DBA/2J with small male ear skin grafts of paternal strain origin indicate thatH-X is highly polymorphic. Thus, with the exception of the B6 and B10 strains which may share oneH-X allele, each of these strains appears to have a different H-X genotype.     

Effect of neonatal androgenization on positive feedback in female mice

Exposure of female mice to androgens within 5 days of birth impairs fertility. Such treatment in rats results in a post-pubertal acyclic state of persistent vaginal cornification and in an inability, when ovariectomized, to show normal positive feedback on luteinizing hormone (LH) release in response to steroid challenge. In the present study, we explored whether neonatally androgenized mice demonstrate positive feedback. Female mice were administered 100 micrograms of testosterone propionate (TP) on either Day 1 (TP1) or Day 5 (TP5) after birth, or vehicle on Day 1 (SO1). Androgen-treated mice had a statistically significant advance in onset of vaginal opening as compared with vehicle-treated mice. All mice that received TP entered constant vaginal estrus, whereas those given vehicle showed variable cytology. All mice were ovariectomized at 7 wk of age and received Silastic capsules containing a priming dose of 17 beta-estradiol. When all mice were challenged 1 wk later with sequential administration of estradiol benzoate and progesterone, a significant increase in plasma LH level was present only in the vehicle-treated mice. We conclude that neonatal androgenization defeminizes the neuroendocrine mechanisms controlling gonadotropin release.     

Studies on sound-induced epilepsy in mice

The cerebral concentrations of pyridoxal-5'-phosphate and divalent transition metal ions (Cu2+ and Zn2+) are appreciably higher in the seizure-susceptible strain of mouse (DBA/2J) than those in normal strains (CBA/Ca and Parkes ). By injecting metal ions intracranially and pyridoxal-5'-phosphate intraperitoneally, we could render the normal mouse prone to sound-induced epilepsy. The behaviour of the treated seizure-susceptible strain of mouse. The levels of glutamate and aspartate in its inferior colliculus were elevated and the concentration of gamma-aminobutyrate was lowered. Glutaminase inhibitors, 6-diazo-5-oxo-L-norleucine (DON) and 0-diazo-acetyl-L-serine (azaserine), and a transaminase inhibitor, 4-amino-3- isoxazolidone (L-cycloserine), when injected intraperitoneally, protected the seizure-susceptible mouse from undergoing convulsions, whereas pyridoxal-5'-phosphate and methionine sulphoximine, a glutamine synthetase inhibitor, exacerbated its epileptic condition. We propose a possible sequence of biochemical events associated with susceptibility to audiogenic seizures.     

Studies on IgE production in mice

IgE levels after Nippostrongylus brasiliensis infestation were high in all strains of mice examined except in the SJA/9 strain. However, surface IgE levels on B cells were not different from those observed in the SJL strain. Most surface IgE-bearing cells also had surface IgM molecules. We suggest that the surface IgE-bearing cells are precursors of IgE-producing cells. In adoptive transfer, hapten-specific IgE antibody was produced when hapten-primed cells from SJA/9 mice were transferred together with cells from SJL donors infested with N. brasiliensis but not when the cells were from SJA/9 donors. It is suggested that the lack of collaboration between hapten-primed B cells and cells from infested mice is a genetic trait of the SJA/9 strain.     

Construction of transgenic mice with tissue-specific acceleration of mitochondrial DNA mutagenesis

Transgenic mice having rapid accumulation of mitochondrial DNA (mtDNA) mutations specifically in the heart were created. These mice contained a transgene encoding a proofreading-deficient, mouse mitochondrial DNA polymerase (pol gamma) driven by the promoter for the cardiac-specific alpha-myosin heavy chain. Starting shortly after birth greater than 95% of all pol gamma mRNA in the heart was transgene derived; expression in other tissues was low or absent. Mutations in cardiac mtDNA began to accumulate by 7 days after birth. At 1 month of age the frequency of point mutations was 0.014% as determined by DNA sequencing of cloned mtDNA. By long-extension PCR multiple different deletion mutations that had removed several thousand basepairs of genomic sequence were also detected. Sequencing of two deletion molecules showed that one was flanked at the breakpoint by direct repeat sequences. The expression of proofreading-deficient pol gamma had no apparent deleterious effect on mitochondrial DNA and protein content, gene expression, or respiratory function. However, associated with the rise in mtDNA mutation levels was the development of cardiomyopathy as evidenced by enlarged hearts in the transgenic mice. These mice may prove to be useful models to study the pathogenic effects of elevated levels of mitochondrial DNA mutations in specific tissues.     

正加速度应激致心脑损伤的动物实验研究综述

正加速度（ positive acceleration ,＋Gz）作用下机体的心脑功能防护是航空航天医学领域重点关注的课题。＋Gz作用致机体心脑等重要生命脏器损伤的特点和机制有待深入研究。本文就国内外有关＋Gz作用致实验动物心脑损伤及其机制的研究文献进行综述。