Altered surface glycoproteins in melanoma cell variants with reduced metastasizing capacity selected for resistance to wheat germ agglutinin

Variants of B 16-F 1 mouse melanoma cells selected for resistance to wheat germ agglutinin (WGA) toxicity $\text{in}\text{vitro}$ were found to have undergone a stable surface change correlated both to lectin resistance and reduced metastasizing potential. The surface alteration, as indicated by the increased electrophoretic mobilities of several lactoperoxidase-iodinated cell surface proteins in SDS-PAGE, was restricted to polypeptides able to interact with WGA. The availability of lectin-resistant melanoma cell variants having altered metastasizing behavior provides a promising approach to studies of the role of specific cell surface components in the metastasizing process.     

A newborn child with karyotype 47,XX,+der(12) (12pter→12q12::8q24→8qter),t(8;12) (q24;q12) pat

Summary A case of Meckel or Gruber syndrome is reported, together with a survey of the relevant literature of recent years (1971–1977), in reference to a probably autosomal recessive inheritance of this malformation.     

Nerve growth factor-mediated induction of tyrosine hydroxylase in rat superior cervical ganglia in vitro.

Exposure of rat sympathetic ganglia to 3 microgram/ml of 2.5 S nerve growth factor (NGF) resulted in a 100% increase in tyrosine hydroxylase activity within 48 h. Pulselabeling of proteins with [3H]leucine, followed by immunoprecipitation with antibodies to tyrosine hydorxylase and isolation of the precipitated enzyme by gel electrophoresis, demonstrated that the increase in tyrosine hydroxylase activity was due to enhanced de novo synthesis. The incorporation of [3H]leucine into tyrosine hydroxylase was increased by 150% compared to a 17% increase in total protein synthesis, which was not statistically significant. The fact that the half-life of pulse-labeled tyrosine hydroxylase was the same for NGF-treated and control organ cultures of superior cervical ganglia excludes the possibility that enhanced tyrosine hydroxylase labeling by NGF is due to decreased degradation. We conclude that, without modulatory factors which play a role in vivo, NGF can enhance the synthesis of tyrosine hydroxylase in sympathetic ganglia in vitro, provided organ culture conditions which permit optimal survival of adrenergic neurons are selected.     

Ia-like alloantigens in the chicken: Serologic characterization an ontogeny of cellular expression

Alloantisera raised in highly inbred lines of chickens, 7(2) and 15I(5) , by reciprocal immunization with lymphocytes were shown by immunofluorescence to react with B cells, cells of the monocyte-macrophage series, and an unidentified population of mononuclear cells prevalent in the spleen and bone marrow. Variable immunogenicity of the 'Ia'(2) and 'Ia'(15) alloantigens was observed. The alloantigens detected by these sara could be redistributed on the B-cell surface independently of immunoglobulin determinants or previously recognized antigens encoded by the major histocompatibility complex (B locus), and were more resistant to proteolysis than slgM. Analysis of several inbred lines of chickens revealed an association between expression of these antigens and the B haplotype. Strains of the B(2) haplotype expressed the antigen detected by anti-7 2 and vice versa. These data suggest that the B-cell alloantigens detected are encoded by genes linked to the MHC and may be analogous to la antigens of mice and DR antigens of man. 'Ia' alleles were co dominantly expressed on lymphocytes of F(1) hybrids. During ontogeny 'a'(+) cells were first detected in the bursa at 10 days of incubation , 3 days before 'Ia'(+). IgM(+) cells could be detected. Both 'Ia'(+).IgM(+) and 'Ia'(+).IgM(-) populations of bursal cells increased in parallel until day 18, when plateau levels were reached. Development of 'Ia'(+).IgM(-) cells throughout the body was unaffected by bursectomy at hatching. Cell surface expression of 'Ia' antigens was apparently increased with B-Iymphocyte maturation and was detectable on most, but not all, mature plasma cells.     

Thermodynamic functions of biopolymer hydration. II. Enthalpy–entropy compensation in hydrophilic hydration processes

The thermodynamic functions of biopolymer hydration were investigated by multitemperature vapor pressure studies. Desorption measurements were performed that allowed determination of reversible isotherms in the hydration range of 0.1 to 0.3–0.5 g H₂O/g dry polymer. These isotherms are accessible to thermodynamic interpretation and are relevant to the interaction of water with biopolymers in their solution conformation. The results obtained on a series of different biopolymers (lysozyme, α-chymotrypsin, apo-lactoferrin, and desoxyribonucleic acid), show the following common features of interest: (1) The differential excess enthalpies (ΔH^e ) and entropies (ΔS^e ) are negative, and exhibit pronounced anomalies in a well-defined low-humidity range (approx. 0.1 g H₂O/g dry polymer). These initial extrema are interpretable by structural changes, induced in the native biopolymer structures by water removal below a critical degree of hydration. (2) The ΔH^e and ΔS^e terms exhibit statistically significant linear enthalpy–entropy compensation effects in all biopolymer–water systems investigated. The compensation temperatures \documentclass{article}\pagestyle{empty}\begin{document}$ \hat \beta = \overline {\Delta H} ^e /\overline {\Delta S} ^e $\end{document} are approximately identical for all biopolymers, ranging from 360 to 500 K. The compensation effects are attributable to phase transitions of water molecules between the bulk liquid and the inner-sphere hydration shell of native biopolymers. (3) The negative excess free energies (ΔG^e ) decrease monotonically with increasing water content and are close to zero at 0.3 to 0.5 g H₂O/g polymer. This result indicates that only transitions between the bulk liquid and the inner-sphere hydration shell are associated with significant net free energy effects. The outer-sphere hydration water is thermodynamically comparable to bulk water. The importance of the proportionality factor \documentclass{article}\pagestyle{empty}\begin{document}$ \hat \beta $\end{document} in the control of the free energy term is discussed.     

Neural control of muscle

Cholinergic innervation regulates the physiological and biochemical properties of skeletal muscle. The mechanisms that appear to be involved in this regulation include soluble, neurally-derived polypeptides, transmitter-evoked muscle activity and the neurotransmitter, acetylcholine, itself. Despite extensive research, the interacting neural mechanisms that control such macromolecules as acetylcholinesterase, the acetylcholine receptor and glucose 6-phosphate dehydrogenase remain unclear. It may be that more simplified in vitro model systems coupled with recent dramatic advances in the molecular biology of neurally-regulated proteins will begin to allow researchers to unravel the mechanisms controlling the expression and maintenance of these macromolecules.     

A Specific Transduction Mechanism for the Glutamate Action on Phosphoinositide Metabolism via the Quisqualate Metabotropic Receptor in Rat Brain Synaptoneurosomes: II. Calcium Dependency, Cadmium Inhibition

In this article, we demonstrate that an increase in intracellular Ca2+ concentration may represent a specific common step(s) in the mechanism(s) of action of glutamate (Glu) and depolarizing agents on formation of inositol phosphates (IPs) in 8-day-old rat forebrain synaptoneurosomes. In fact, A23187, a Ca2+ ionophore, induces a dose-dependent accumulation of IPs, which is not additive with that evoked by Glu and K+ but is slightly synergistic with that induced by carbachol. In addition, Glu and K+ augment the intracellular Ca2+ concentration in synaptoneurosome preparations as measured by the fura-2 assay. The absence of external Ca2+ decreases basal and Glu-, and K(+)-stimulated formation of IPs. Cd2+ (100 microM) fully inhibits both Glu- and K(+)-evoked formation of IPs without affecting the carbachol-elicited response of IPs. Zn2+ inhibits Glu- and K(+)-stimulated accumulation of IPs (IC50 approximately 0.4 mM) but with a lower affinity than Cd2+ (IC50 approximately 0.035 mM). The organic Ca2+ channel blockers verapamil (10 microM), nifedipine (10 microM), omega-conotoxin (2 microM), and amiloride (10 microM) as well as the inorganic blockers Co2+ (100 microM) and La3+ (100 microM) block neither Glu- nor K(+)-evoked formation of IPs, a result suggesting that the opening of the L-, T-, N-, or P-type Ca2+ channels does not participate in these responses. All these data suggest that an increase in intracellular Ca2+ concentration resulting from an influx of Ca2+, sensitive to Cd2+ but not to other classical Ca2+ antagonists, may play a key role in the transduction mechanism activated by Glu or depolarizing agents.     

Stage-specific cuticular proteins of Ostertagia circumcincta and Ostertagia ostertagi

In this study we have shown that NHS-biotin and I¹²⁵-streptavidin can detect cuticular polypeptides of Ostertagia spp. The labelled polypeptide profile of intact nematodes is simple compared to the profile obtained by labelling homogenates. None of the major internal polypeptides are labelled and the subset of proteins labelled in intact nematodes appears to be mainly surface associated. The results presented here demonstrate that NHS-biotin may be used as a reagent for the analysis of surface polypeptides. The surface polypeptide profiles of the five major developmental stages (L1, L2, L3, L4 and adult) of Ostertagia circumcincta show a series of stage-specific molecules with no polypeptides common to all stages, indicating that the cuticle is a dynamic structure which changes throughout the life cycle. Similarity comparison of Ostertagia ostertagi L3 and L4 stage surface profiles showed that each stage is clearly distinct; comparison of these stages between the two species shows an overall similarity.