Electron beam relaxation in nonuniform plasma of a steady-state beam-plasma discharge at moderately low gas pressures

Electron beam relaxation in plasma under conditions typical of laboratory plasma devices based on a steady-state beam-plasma discharge was investigated. It is shown that the measured dependences of the beam loss factor in a discharge operating at a moderately low gas pressure disagree with theoretical dependences calculated for a longitudinally uniform plasma. Analytic dependences obtained in the framework of quasilinear theory with allowance for longitudinal plasma inhomogeneity agree with experimental data. Some effects caused by the influence of the main discharge parameters on electron beam relaxation are analyzed.     

Spontaneous and mitogen-induced proliferative activity of mononucleocytes in pollinosis patients

The proliferative response of lymphocytes to mitogens was studied in 17 patients according to 3H-thymidine incorporation. The patients had high sensitivity to timothy pollen, confirmed by the allergological anamnesis, skin tests, and the presence of allergen-specific IgE-antibodies. Mononuclears of peripheral blood were cultivated with a lipopolysaccharide (LPS) to study the response to the polyclonal B cell activator, while with PHA to study the response of T cells over 7 days. The patients with pollinosis manifested increased spontaneous cell proliferation. The degree of the proliferative response of the cells to LPS and PHA was similar in patients and normal subjects. It is suggested that the magnitude of spontaneous proliferation influences the degree of the mitogenic response of B cells.     

Localization of the α2-macroglobulin gene and Lpm gene family on mink chromosome 9

Summary Using cloned cDNA for human ₂-macroglobulin (A2M) as a probe, mink-Chinese hamster hybrid cells were analysed. The results allowed us to assign a gene for A2M to mink chromosome 9. Breeding tests demonstrated that the Lpm-locus coding for other related -macroglobulin protein and the gene for peptidase B (PEPB) are linked 11±3 cm apart. The PEPB gene is located on mink chromosome 9, and hence, the Lpw-locus is on the same mink chromosome. The relationship of the genetic systems controlling the isotypically different -macroglobulins in mink serum are discussed.     

Characterization of a new hybrid mink-mouse clone panel: chromosomal and regional assignments of the GLO,ACY, NP,CKBB, ADH2, and ME1 loci in mink (Mustela vison)

To expand the mink map, we established a new panel consisting of 23 mink-mouse clones. On the basis of statistical criteria (Wijnen et al. 1977; Burgerhout 1978), we developed a computer program for choice of clones of the panel. Assignments of the following mink genes were achieved with the use of the hybrid panel: glyoxalase (GLO), Chromosome (Chr) 1; acetyl acylase (ACY), Chr 5; creatine phosphokinase B (CKBB), Chr 10; alcohol dehydrogenase-2 (subunit B) (ADH2), Chr 8. Using a series of clones carrying rearrangements involving mink Chr 1 and 8, we assigned the gene for ME1 to the short arm of Chr 1 and that for ADH2 to Chr 8, in the region 8p12-p24. Mapping results confirm the ones we previously obtained with a mink-Chinese hamster panel. However, by means of an improved electrophoretic technique, we revised the localization of the gene for purine nucleoside phosphorylase (NP), which has been thought to be on mink Chr 2. It is reassigned to mink Chr 10.     

Localization of the multigene Lpm locus in chromosome 9 of the American mink

The results of genetic study on linkage of Lpm locus with peptidase B gene are presented. Investigation of 111 offspring back-crosses shows that Lpm allotypes and allelic variants of peptidase B are inherited in concert. The frequency of recombination between the Lpm locus and peptidase B gene is 11 +/- 3% in male. Since it was earlier established that peptidase B gene is a marker of chromosome 9, our data indicate that the Lpm loci family is situated in the chromosome 9 of domestic mink.     

Regional assignment of the genes for TK1, GALK, ALDC, and ESD on chromosome 8 in the American mink by chromosome-mediated gene transfer

Summary A panel of clones of mink-Chinese hamster somatic cell hybrids was analysed to obtain data for assigning the genes for thymidine kinase-1 (TK1), galactokinase (GALK), subunit C of aldolase (ALDC), and esterase D (ESD) to specific mink chromosomes. The results demonstrate that the genes for TK1, GALK, ALDC and ESD are syntenic and located on mink chromosome 8. Prometaphase analysis of transformed mouse cells obtained by transfer of mink genes by means of metaphase chromosomes demonstrated the presence of mink chromosome 8 fragments of different sizes in some of the independent transformants. Segregation analysis of these fragments and mink TK1, GALK, ALDC and ESD allowed us to assign the genes for TK1 and GALK to 8p24, ALDC to pter-8p25, and ESD to 8q24-8qter.     

Embryonic stem cells derived from morulae,inner cell mass,and blastocysts of mink: Comparisons of their pluripotencies

A characterization of cell lines that we derived from morulae (three lines), blastocysts (two lines), and the inner cell mass (ICM) is given. The karyotype of all the lines was normal; the genotype of four lines was XX, and four lines were genotypically XY. The pluripotencies and commitment status of the derived lines were estimated. First, there were not less than two-thirds of cells in the populations of the lines derived from morulae and the lCM with both Xs active; 70–100% of cells of the blastocyst-derived lines had one of the Xs in an inactive state. The activity of glucose-6-phosphate dehydrogenase (G6PD) in the lines (genotype XX) derived from morulae and ICM was found to be twofold higher than in lines with genotype XY, and G6PD activity was the same in the blastocyst-derived XX lines and XY lines. Second, when injected intraperitoneally into athymic mice, morulae- and ICM-derived cells gave rise to simple and complex embryoid bodies (EB) resembling to typical “cystic” mouse EBs. Third, when injected subcutaneously to athymic mice, the ICM- or morula-derived cells gave rise to typical teratomas containing derivatives of the three germ layers and components of organogenesis. Comparisons of cell lines of different derivations demonstrated that the pluripotencies of the ES cells derived from morulae or the ICM are higher than those of blastocyst derivation. © 1993 Wiley-Liss, Inc.     

Soluble Sema4D cleaved from osteoclast precursors by TACE suppresses osteoblastogenesis

Bone remodelling is mediated by orchestrated communication between osteoclasts and osteoblasts which, in part, is regulated by coupling and anti-coupling factors. Amongst formally known anti-coupling factors, Semaphorin 4D (Sema4D), produced by osteoclasts, plays a key role in downmodulating osteoblastogenesis. Sema4D is produced in both membrane-bound and soluble forms; however, the mechanism responsible for producing sSema4D from osteoclasts is unknown. Sema4D, TACE and MT1-MMP are all expressed on the surface of RANKL-primed osteoclast precursors. However, only Sema4D and TACE were colocalized, not Sema4D and MT1-MMP. When TACE and MT1-MMP were either chemically inhibited or suppressed by siRNA, TACE was found to be more engaged in shedding Sema4D. Anti-TACE-mAb inhibited sSema4D release from osteoclast precursors by ~90%. Supernatant collected from osteoclast precursors (OC-sup) suppressed osteoblastogenesis from MC3T3-E1 cells, as measured by alkaline phosphatase activity, but OC-sup harvested from the osteoclast precursors treated with anti-TACE-mAb restored osteoblastogenesis activity in a manner that compensates for diminished sSema4D. Finally, systemic administration of anti-TACE-mAb downregulated the generation of sSema4D in the mouse model of critical-sized bone defect, whereas local injection of recombinant sSema4D to anti-TACE-mAb-treated defect upregulated local osteoblastogenesis. Therefore, a novel pathway is proposed whereby TACE-mediated shedding of Sema4D expressed on the osteoclast precursors generates functionally active sSema4D to suppress osteoblastogenesis.     

Genetic control of PI and GC variants in the American Mink

Genetic polymorphism of the serum α-protease inhibitor (PI) and group-specific component (GC) in minks was revealed using one-dimensional polyacrylamide gel electrophoresis and immunoblotting. Two codominant alleles were identified at each of the two loci. The data ruled out the possibility of any linkage between the PI, GC and the coat colour gene Crystal ( Cr ).