Effect of stress ratio on near-threshold propagation of delimination fatigue cracks in unidirectional CFRP

The effect of the stress ratio on near-threshold growth of delamination fatigue cracks was investigated with unidirectional laminates made from Ciba Geigy 914C prepegs (T300/914) and from Toray P305 prepegs (T300/#2500). Tests of delamination fatigue crack propagation were carried out under mode I opening loading by using double cantilever beam specimens. The normalized gradient of energy release range was controlled in load-shedding tests. In the region of crack growth rates above about 5 × 10⁻¹⁰ m/cycle, the growth rate was expressed as a power function of fracture mechanics parameters. Below this region, there existed a growth threshold. The influence of the stress ratio became smaller when the rate was correlated to the energy release rate range than when the rate was correlated to the stress intensity range or the maximum energy release rate. A controlling fracture mechanics parameter is discussed on the basis of fractographic observation and mechanism consideration. A new phenomenological law of fatigue crack propagation is derived.     

The equivalent hours loss factor revisited [power systems]

Specific portions of electric systems experience losses, which are a function of load. In these cases utility engineers have historically used one of two equations to determine the equivalent-hours loss factor which can be used to determine the energy losses when the load factor is known. One of these two equations determines the equivalent-hours loss factor as a function of load factor and load factor squared. This equation was developed by F.H. Buller and C.A. Woodrow in 1928 with a recommended value of 0.3 for the constant coefficient term (the coefficient of the load factor term). The second equation determines the equivalent hours loss factor as a function of the load factor raised to a power. The value for the exponent commonly used in industry practice is 1.6. The authors argue that the values of 0.3 for the constant coefficient and 1.6 for the exponent no longer appear to be appropriate. In fact, analysis of a wide range of utility annual EEI-formatted load data sets results in a value of 0.08 for the constant coefficient and 1.912 for the exponent. Equations with revised coefficients are calculated and verified     

An experimental study and a thermodynamic evaluation of the cr- fe- w system

An experimental study of the Cr-Fe-W system has been made using a diffusion couple technique. A number of tie-lines have been determined using a scanning electron microscope with energy dispersive X-ray analysis equipment. The structures of the observed intermetallic phases were determined by means of X-ray diffraction. The experimental results are presented in tables and isothermal sections at 1173, 1273, 1373, 1473, 1573, and 1673 K. A thermodynamic evaluation has been made using a magnetic subregular model for the bcc and fcc solution phases, a multi-sublattice model for the intermetallic phases, and an ordinary subregular solution model for the liquid phase. The parameter values describing the Gibbs energy of each individual phase have been determined by means of a computerized optimization technique. The calculated sections of the Cr-Fe-W phase diagram are in satisfactory agreement with the experimental information. Formerly with the Division of Physical Metallurgy, Royal Institute of Technology, Stockholm, Sweden     

Steady-state electromagnetic shock in Kerr liquid

Solutions are obtained for a steady-state electromagnetic shock in a nonlinear Kerr liquid. The equations for the liquid are those of De Martini et al. [1]. It is found that a shock solution can always be found regardless of the magnitude of the nonlinear parameter relating the change of propagation velocity to the energy density. Every shock is described completely, for a given material, in terms of two parameters; e.g., the energy density on one side of the shock and the speed of the shock.     

Alcohol and disinhibition

This review investigates research evaluating the disinhibition hypothesis. This hypothesis postulates that in a sober state behavior is inhibited. When people are influenced by alcohol the inhibitions are supposed to be weakened and the motivating drives are postulated to become disinhibited and potent to influence behavior. This report reviews the effect of alcohol on nerve functions, on human sexuality, aggression, eating behavior, psychological conflicts, fluency in talk, social anxiety, violent crimes and the interaction of alcohol and social norms. It has been shown that individual subjective experiences sometimes indicate disinhibition (reduction of the forces holding back impulses) and objective behavior in some respects was different when the subject was intoxicated, but the mechanism that mediates behavior is not clear. It seems to be difficult to measure independently the forces restraining (inhibiting) the driving forces (uncontrolled impulses) at the same time as measuring these driving forces. The review concludes that there is no unambiguous support of the disinhibition hypothesis. An alternative hypothesis that seems to explain many behaviors in an inebriated individual is the 'time out' hypothesis which states that drunken behavior is influenced more by norms about what it should be than by the pharmacological effect of alcohol.     

A receptor subtype involved in neuropeptide-Y-induced food intake

Neuropeptide Y (NPY) is a powerful stimulant of food intake and is proposed to activate a hypothalamic 'feeding' receptor distinct from previously cloned Y-type receptors. This receptor was first suggested to explain a feeding response to NPY and related peptides, including NPY2-36, that differed from their activities at the Y1 receptor. Here we report the expression cloning of a novel Y-type receptor from rat hypothalamus, which we name Y5. The complementary DNA encodes a 456-amino-acid protein with less than 35% overall identity to known Y-type receptors. The messenger RNA is found primarily in the central nervous system, including the paraventricular nucleus of the hypothalamus. The extent to which selected peptides can inhibit adenylate cyclase through the Y5 receptor and stimulate food intake in rats correspond well. Our data support the idea that the Y5 receptor is the postulated 'feeding' receptor, and may provide a new method for the study and treatment of obesity and eating disorders.     

Identification of SH2-Bbeta as a substrate of the tyrosine kinase JAK2 involved in growth hormone signaling

Activation of the tyrosine kinase JAK2 is an essential step in cellular signaling by growth hormone (GH) and multiple other hormones and cytokines. Murine JAK2 has a total of 49 tyrosines which, if phosphorylated, could serve as docking sites for Src homology 2 (SH2) or phosphotyrosine binding domain-containing signaling molecules. Using a yeast two-hybrid screen of a rat adipocyte cDNA library, we identified a splicing variant of the SH2 domain-containing protein SH2-B, designated SH2-Bbeta, as a JAK2-interacting protein. The carboxyl terminus of SH2-Bbeta (SH2-Bbetac), which contains the SH2 domain, specifically interacts with kinase-active, tyrosyl-phosphorylated JAK2 but not kinase-inactive, unphosphorylated JAK2 in the yeast two-hybrid system. In COS cells coexpressing SH2-Bbeta or SH2-Bbetac and murine JAK2, both SH2-Bbetac and SH2-Bbeta coimmunoprecipitate to a significantly greater extent with wild-type, tyrosyl-phosphorylated JAK2 than with kinase-inactive, unphosphorylated JAK2. SH2-Bbetac also binds to immunoprecipitated wild-type but not kinase-inactive JAK2 in a far Western blot. In 3T3-F442A cells, GH stimulates the interaction of SH2-Bbeta with tyrosyl-phosphorylated JAK2 both in vitro, as assessed by binding of JAK2 in cell lysates to glutathione S-transferase (GST)-SH2-Bbetac or GST-SH2-Bbeta fusion proteins, and in vivo, as assessed by coimmunoprecipitation of JAK2 with SH2-Bbeta. GH promoted a transient and dose-dependent tyrosyl phosphorylation of SH2-Bbeta in 3T3-F442A cells, further suggesting the involvement of SH2-Bbeta in GH signaling. Consistent with SH2-Bbeta being a substrate of JAK2, SH2-Bbetac is tyrosyl phosphorylated when coexpressed with wild-type but not kinase-inactive JAK2 in both yeast and COS cells. SH2-Bbeta was also tyrosyl phosphorylated in response to gamma interferon, a cytokine that activates JAK2 and JAK1. These data suggest that GH-induced activation and phosphorylation of JAK2 recruits SH2-Bbeta and its associated signaling molecules into a GHR-JAK2 complex, thereby initiating some as yet unidentified signal transduction pathways. These pathways are likely to be shared by other cytokines that activate JAK2.