Field dependence of impact ionization coefficients in In/sub 0.53/Ga/sub 0.47/As

Electron and hole ionization coefficients in In/sub 0.53/Ga/sub 0.47/As are deduced from mixed carrier avalanche photomultiplication measurements on a series of p-i-n diode layers, eliminating other effects that can lead to an increase in photocurrent with reverse bias. Low field ionization is observed for electrons but not for holes, resulting in a larger ratio of ionization coefficients, even at moderately high electric fields than previously reported. The measured ionization coefficients are marginally lower than those of GaAs for fields above 250 kVcm/sup -1/, supporting reports of slightly higher avalanche breakdown voltages in In/sub 0.53/Ga/sub 0.47/As than in GaAs p-i-n diodes.     

mRNA for cardiac calcium channel is expressed during development of skeletal muscle

During the early development of skeletal muscle, cardiac isotypes of several contractile proteins are known to be transiently expressed. We report here that skeletal muscle developing in vivo, as well as primary cultures derived from skeletal muscle, express mRNA encoding the cardiac dihydropyridine-sensitive calcium channel. The mRNA is detectable at high concentration at the earliest stage tested in vivo and diminishes rapidly in concentration as myofibers mature. The concentration of the cardiac calcium channel mRNA also diminishes during the in vivo development of skeletal muscle in a genetically paralyzed mouse (mdg), indicating that muscle contractile activity is not necessary for the down-regulation. In contrast, mRNA for the skeletal muscle-specific calcium channel accumulates gradually in developing skeletal muscle. A similar temporal pattern of expression is also seen in primary cultures of skeletal myotubes. These results raise the question of whether the cardiac calcium channel may be functionally important during the early development of skeletal myofibers.     

The accuracy of mothers'' reports of child vaccination: evidence from rural Egypt

Accumulating evidence suggests that angiotensin-(1-7)(Ang-(1-7)) is an important component of the renin-angiotensin system and that the actions of the peptide may either contribute to or oppose those of Ang II. Ang-(1-7) can be converted directly from Ang I bypassing prerequisite formation of Ang II. Formation of Ang-(1-7) is under the control of at least three endopeptidases depending on the tissue compartment and include neprilysin, thimet oligopeptidase and prolyl oligopeptidase. Both neprilysin and thimet oligopeptidase are also involved in the metabolism of bradykinin and the atrial natriuretic peptide. Moreover, recent studies suggest that in addition to Ang I and bradykinin, Ang-(1-7) is an endogenous substrate for angiotensin converting enzyme. These enzymatic pathways may contribute to a complex relationship between the hypertensive actions of Ang II and various vasodepressor peptides from either the renin-angiotensin system or other peptide systems. Ang-(1-7) is devoid of the vasoconstrictor, central pressor, or thirst-stimulating actions associated with Ang II. In fact, new findings reveal depressor, vasodilator, and antihypertensive actions that may be more apparent in hypertensive animals or humans. Thus, Ang-(1-7) may oppose the actions of Ang II directly or as a result of increasing prostaglandins or nitric oxide. In this review, we examine the mechanisms by which Ang-(1-7) may contribute to cardiovascular regulation.     

Dependence of mutation induction on fast-neutron energy in a human epithelial teratocarcinoma cell line (P3)

Cultivation of Candida albicans NIH B-792 (serotype B) at high temperature (37 degrees C) for 48 h in yeast extract-containing Sabouraud liquid medium (YSLM) provided the following findings in comparison with the findings obtained after incubation at 27 degrees C. Growth of the blastoconidia of this strain was decreased, with a dry weight of 9%, and the cells were deficient in cytokinesis. The cells did not undergo agglutination with serum factor 5 from a commercially available serum factor kit (Candida Check). Mannan (B-37-M) obtained from the cells cultured at 37 degrees C had partially lost its reactivity against serum factor 4 and lost most of its reactivity against serum factor 5 in an enzyme-linked immunosorbent assay (ELISA) in contrast to that (B-27-M) at 27 degrees C. Both cells and mannan prepared by cultivation first at 37 degrees C and then at 27 degrees C entirely recovered their reactivities with serum factors 4 and 5. 1H-nuclear magnetic resonance analysis also revealed that B-37-M had lost a beta-1,2-linked mannopyranose unit and retained a phosphate group. Similar changes were observed in the three other serotype B strains used in the study. The beta-1,2-linked mannooligosaccharides longer than mannotetraose were not included among the products released from B-37-M by mild acid treatment. The results of the inhibition ELISA with a series of beta-1,2-linked mannooligosaccharides from biose to octaose (M2 to M8, respectively) showed that the reactivity against serum factor 4 was inhibited most strongly by the oligosaccharides M4 to M8 and that the reactivity against serum factor 5 was inhibited completely by relatively longer oligosaccharides, M5 to M8, indicating their participation as the antigenic factor 5 epitopes.     

Pigmentation phenotypes of variant extension locus alleles result from point mutations that alter MSH receptor function

Coat colors in the chestnut horse, the yellow Labrador retriever, the red fox, and one type of yellow mouse are due to recessive alleles at the extension locus. Similarly, dominant alleles at this locus are often responsible for dark coat colors in mammals, such as the melanic form of the leopard, Panthera pardus. We show here that the murine extension locus encodes the melanocyte-stimulating hormone (MSH) receptor. In mice, the recessive yellow allele (e) results from a frameshift that produces a prematurely terminated, nonfunctioning receptor. The sombre (Eso and Eso-3J) and tobacco darkening (Etob) alleles, which both have dominant melanizing effects, results from point mutations that produce hyperactive MSH receptors. The Eso-3J receptor is constitutively activated, while the Etob receptor remains hormone responsive and produces a greater activation of its effector, adenylyl cyclase, than does the wild-type allele.