Depression of macrophage functions and T-cell-mediated immunity to listeria infection in tumor-bearing mice and its prevention by PSK

Summary The effect of PSK on the depressed bactericidal activity of macrophages and delayed-type hypersensitivity (DTH) to Listeria monocytogenes in BALB/c mice bearing transplantable Meth A fibrosarcoma was studied. In tumor-bearing mice pretreated with PSK, L. monocytogenes was cleared rapidly from the circulating blood and bacterial growth in the liver was inhibited effectively in the early phase of infection. This resistance to the infection could be transferred with adherent peritoneal exudate cells (PEC) but not with nonadherent or adherent spleen cells of PSK-treated mice. In the early phase of infection, tumor-bearing mice developed a lower level of DTH to L. monocytogenes than nongrafted control mice. However, the control levels of DTH could be obtained by pretreatment with PSK in tumor-bearing mice. These results suggest that the restoration of DTH to L. monocytogenes by pretreatment with PSK may be attributable to the restoration of the depressed immunological responsiveness to the normal levels in tumor-bearing mice.     

Effects of MK-733 (simvastatin), an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on intestinal acylcoenzyme A:cholesterol acyltransferase activity in rabbits

MK-733 (simvastatin), a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, was found to inhibit the absorption of cholesterol from the gastrointestinal tract in cholesterol-fed rabbits (Ishida et al. (1988) Biochim. Biophys. Acta 963, 35-41). To clarify the mechanism of action, the effects of MK-733 on acyl coenzyme A:cholesterol acyltransferase (ACAT) and cholesterol esterase activities, which are thought to participate in the absorption of cholesterol, were examined. Dietary administration (0.03% in a 1% cholesterol diet for 7 days, approx. 10 mg/kg) of MK-733 to cholesterol-fed rabbits was found to inhibit the increase in serum total cholesterol levels, and caused a 70% reduction in ACAT activity in microsomes of intestinal mucosa relative to those observed in concurrent control rabbits. MK-733 did not affect cholesterol esterase activity in the cytosol of the intestinal mucosa. The inhibitory effect of MK-733 on cholesterol absorption in cholesterol-fed rabbits is though to be related to a reduction in microsomal ACAT activity in the intestinal mucosa.     

GENETICS OF SORDARIA FIMICOLA. IV. LINKAGE GROUP I

El -Ani , Arif S., L. S. Olive , and Y. Kitani . (Columbia U., New York City.) Genetics of Sordaria fimicola. IV. Linkage group I. Amer. Jour. Bot. 48(8): 716–723. Illus. 1961.—A general technique for isolating and testing various morphological mutants induced by X ray is described. Eleven mutants differing in ascospore color, fertility, and rate and type of growth were studied in different crosses. This has led to the construction of the first linkage group in S. fimicola. The chromosome on which the 11 mutant loci occur is marked by a single locus on one arm and 10 on the opposite arm. The ascospore color mutant gray is autonomous, maintaining the mutant spore color in both homozygous and heterozygous asci, whereas milky, the other color mutant studied. expresses its mutant effect only in asci homozygous for the factor. Certain crosses involving 2 sterility mutants controlled by 2 non-allelic loci are fertile, and the progeny give rise to parentals as well as double-mutant and fertile recombinants.     

The velocity of the reaction between ornithine decarboxylase and antizyme highly depends on the presence of salt and temperature

Antizyme reversibly inhibits ornithine decarboxylase activity by direct binding to the enzyme. The velocity of the reaction between ornithine decarboxylase and antizyme was markedly accelerated as the concentration of sodium chloride in the medium was increased and as the temperature of incubation was lowered. The equilibrium constant (binding constant) of the reaction between ornithine decarboxylase and antizyme was a little increased by decreasing salt concentrations in the medium and by decreasing the temperature of incubation.     

Biliary transport maximum of tauroursodeoxycholate is twice as high as that of taurocholate in the rat

Biliary excretory transport maximum (Tm) and choleretic efficiency were compared for tauroursodeoxycholate and taurocholate in Wistar male rats. Under a continuous iv infusion of bile salts with a stepwise increase in infusion rate, the Tm of tauroursodeoxycholate was found to be two times higher (2.25±0.07 μmole/min/100 g body weight, n=8, mean±SD) than that of taurocholate (0.97±0.05 μmole/min/100 g body weight, n=14, p<0.001). On the other hand, the amount of bile water obligated by the excretion of 1μmole of tauroursodeoxycholate was significantly lower than that of taurocholate. (4.71±0.08 μl/μmole for tauroursodeoxycholate, vs. 9.27±0.76 μl/μmole for taurocholate, mean±SD, p<0.001). It was concluded that tauroursodeoxycholate can be excreted into the bile in male rats twice as efficiently as taurocholate. Furthermore, the higher efficiency in the choleretic property of ursodeoxycholate previously reported by Dumont et al. appears to be specific to free ursodeoxycholate and not to its taurine conjugate used in the present experiment.     

The Activin A-Dependent Proliferation of PCC3/A/1 Embryonal Carcinoma Cells in Serum-Free Medium

Examination of the growth requirements of murine embryonal carcinoma cells (EC cells) or embryonic stem cells (ES cells) in serum-free medium revealed that PCC3 EC cells required activin A to grow and/or survive in such medium. In the absence of activin A, PCC3 cells began to disintegrate within 3 days under any serum-free conditions examined. P19 and AT805 EC cells grew even in serum-free medium without activin A but their growth rates were slightly facilitated by its addition. F9 EC cells also grew in the medium without activin A and its addition somewhat inhibited their growth rate. Three independently isolated ES cell lines and feeder-dependent PSA-1 EC cells also grew in serum-free medium without activin A if leukemia inhibitory factor (LIF) was supplemented. The addition of activin A had little effect on their growth rates. These findings suggest that PCC3 EC cells are a sort of nutritional mutant requiring activin A, thus making them useful in stidies on the growth regulatory mechanisms of EC/ES cells and/or the action of activin on EC/ES cells.