SUMMARYA simple procedure of obtaining flexibility matrices in terms of contact pressures at possible contact points of two bodies allows the frictionless contact pressures to be solved as a quasi-linear problem. Iteration is limited in general to very few cycles and, as small matrices are handled, can be very economical.Excellent accuracy of this procedure is demonstrated.

No abstract

The problem of minimizing stress concentrations in machinery components is formulated as one of unconstrained minimization by incorporating all ‘side’ constraints on design variables by use of penalty functions. Design parameters describing the transition are determined for an optimal fillet in a tension bar, as well as for a piston-rod ‘eye’. The procedure is generally applicable.

Fine balanced sequential changes of the levels of circulating hepatotrophic factors are essential for normal liver regeneration. Our recent studies have indicated that liver-resident natural killer (NK) cells are important regulators of liver regeneration and have raised the possibility that hepatotrophic factors might mediate their activities through NK cells. In the present study, we assessed the effects of in vivo administration of three hepatotrophic factors (augmenter of liver regeneration [ALR], insulin-like growth factor-II [IGF-II], and hepatocyte growth factor [HGF]) on NK cells in normal rats. Each of the three, given over a 1-day period in doses known to produce hepatotrophic activity, induced inhibition of NK cell cytotoxic activities in the population of mononuclear leukocytes (MNL) in the liver, but not in MNL from the spleen or peripheral blood. In contrast to these results obtained by the whole animal treatment, the three molecules had no effect on NK cell functions when added to cultures of MNL from the livers, spleens, or blood of untreated rats. These data support and extend our previously advanced hypothesis that ALR and other hepatotrophic factors play an important role in liver regeneration by regional regulation of NK cells through some as-yet-unknown intermediary mechanism.Hepatotrophic factors (Table 1) have been so characterized [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] by virtue of their ability to augment the hyperproliferative response induced by partial hepatectomy (PH) in rats 3,6 or dogs, 5 and to prevent the atrophy as well as augment the heightened cell renewal caused by portacaval shunt (Eck's fistula) in dogs. 2,4 Only two of the eight known hepatotrophic factors (hepatocyte growth factor [HGF] and transforming growth factor [TGF]-α) are primary mitogens capable of stimulating de novo hepatocyte proliferation in vitro without the requisite precondition of preexisting commitment to heightened cell renewal. Molecules with opposite effects have been called "antihepatotrophic." [16][17][18] After PH, there is an acute temporary increase in the circulating levels of several of the endogenous hepatotrophic factors 1,2,4,5,19 and multiple gene expression in the liver. 20 have speculated that the hepatocyte stimulatory activity of augmenter of liver regeneration (ALR) and the other hepatotrophic factors may be mediated through or by nonparenchymal cells. 1,9,21 This possibility was reinforced by the observation during the acute phase of regeneration after PH in rats of temporary suppression of natural killer (NK) cell functions of liver mononuclear leukocytes (MNL), followed by their recovery at the termination of regeneration. 21 These changes occurred contemporaneously with mirror-image susceptibility of the regenerating hepatocytes to NK-induced lysis.To test this immunologic hypothesis, we have determined in the present study whether the changes of NK cell function occurring after PH could be reproduced in unoperated naive rats by their treatment with three pot...