Iron reserves in the female body and susceptibility to colds

Levels of temporary invalidity because of catching cold were analyzed in 101 working women over two years and these women's levels of serum iron, total iron-binding capacity of the serum, transferrin saturation with iron, serum ferritin, and red cell ferritin measured. Women with stable iron reserves in the body virtually have no sick leaves because of catching cold, whereas in those with iron deficiency susceptibility to catching cold is increased, and if iron metabolism intensity in the body grows, invalidity periods are much longer. Normalization of not only iron reserves in the body, but correction of iron metabolism as well should be regarded as a factor exerting a favorable effect on body resistance to catching cold.     

Memory complaints in epilepsy: correlations with cognitive performance and neuroticism

Experimental results are presented to show that the adhesion force is the single most important limiting factor in high-resolution atomic force microscopy of DNA in air, prepared by the cytochrome-C-assisted spreading method. It is also shown that humidity plays a minor role in the control of probe force. Using a pure carbon film as the substrate to clean the AFM tip prior to imaging, it is demonstrated that 4-6 nm resolution on DNA can be routinely obtained by the atomic force microscope with commercial Si3N4 pyramid cantilevers. We also show that in organic solvents a resolution of up to 3 nm can be obtained under optimal conditions.     

Phase equilibrium in a polarized saturated3He—4He mixture

We present experimental results on the phase equilibrium of a saturated³He−⁴He mixture, which has been cooled to a temperature of 10–15 mK and polarized in a⁴He circulating dilution refrigerator to a stationary polarization of 15%, 7 times higher than the equilibrium polarization in the external field of 7 T. The pressure dependence of the polarization enhancement in the refrigerator shows that the molar susceptibilities of the concentrated and dilute phase of a saturared³He-⁴He mixture are equal atp=2.60±0.04 bar. This result affects the Fermi liquid parameters of the dilute phase. The osmotic pressure in the dilute phase has been measured as a function of the polarization of the coexisting concentrated phase up to 15%. We find that the osmotic pressure at low polarization (<7%) agrees well with thermodynamics using the new Fermi liquid parameters of the dilute phase.     

Insulin-like growth factor I activates the invasion suppressor function of E-cadherin in MCF-7 human mammary carcinoma cells in vitro

The calcium-dependent cell-cell adhesion molecule E-cadherin has been shown to counteract invasion of epithelial neoplastic cells. Using three monoclonal antibodies, we have demonstrated the presence of E-cadherin at the surface of human MCF-7/6 mammary carcinoma cells by indirect immunofluorescence coupled to flow cytometry and by immunocytochemistry. Nevertheless, MCF-7/6 cells failed to aggregate in a medium containing 1.25 mM CaCl2, and they were invasive after confrontation with embryonic chick heart fragments in organ culture. Treatment of MCF-7/6 cells with 0.5 microgram ml-1 insulin-like growth factor I (IGF-I) led to homotypic aggregation within 5 to 10 min and inhibited invasion in vitro during at least 8 days. The effect of IGF-I on cellular aggregation was insensitive to cycloheximide. However, monoclonal antibodies that interfered with the function of either the IGF-I receptor (alpha IR3) or E-cadherin (HECD-1, MB2) blocked the effect of IGF-I on aggregation. The effects of IGF-I on aggregation and on invasion could be mimicked by 1 microgram ml-1 insulin, but not by 0.5 microgram ml-1 IGF-II. The insulin effects were presumably not mediated by the IGF-I receptor, since they could not be blocked by an antibody against this receptor (alpha IR3). Our results indicate that IGF-I activates the invasion suppressor role of E-cadherin in MCF-7/6 cells.     

Glucuronidation of N-hydroxy heterocyclic amines by human and rat liver microsomes

The food-borne carcinogenic and mutagenic heterocyclic aromatic amines undergo bioactivation to the corresponding N-hydroxy (OH)-arylamines and the subsequent N-glucuronidation of these metabolites is regarded as an important detoxification reaction. In this study, the rates of glucuronidation for the N-OH derivatives of 2-amino-3-methylimidazo[4,5-f]-quinoline (IQ), 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP), 2-amino-6-methyl-dipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) by liver microsomal glucuronosyltransferase were compared to that of the proximate human urinary bladder carcinogen, N-OH-aminobiphenyl (N-OH-ABP) and the proximate rat colon carcinogen N-OH-3,2'-dimethyl-4-amino-biphenyl (N-OH-DMABP). Human liver microsomes catalyzed the uridine 5'-diphosphoglucuronic acid (UDPGA)-dependent glucuroidation of N-OH-IQ, N-OH-PhIP, N-OH-Glu-P-1 and N-OH-MeIQx at rates of 59%, 42%, 35% and 27%, respectively, of that measured for N-OH-ABP (11.5 nmol/min/mg). Rat liver microsomes also catalyzed the UDPGA-dependent glucuronidation of N-OH-PhIP, N-OH-Glu-P-1 and N-OH-IQ at rates of 30%, 20% and 10%, respectively of that measured for N-OH-DMABP (11.2 nmol/min/mg); activity towards N-OH-MeIQx was not detected. Two glucuronide(s) of N-OH-PhIP, designated I and II, were separated by HPLC. Conjugate II was found to be chromatographically and spectrally identical with a previously reported major biliary metabolite of PhIP in the rat, while conjugate I was identical with a major urinary metabolite of PhIP in the dog. Hepatic microsomes from rat, dog and human were found to catalyze the formation of both conjugates. The rat preferentially formed conjugate II (I to II ratio of 1:15), while the dog and human formed higher relative amounts of conjugate I (I to II ratio of 2.5:1.0 and 1.3:1.0 respectively). Fast atom bombardment mass spectrometry of conjugates I and II gave the corresponding molecular ions and showed nearly identical primary spectra. However, collision-induced spectra were distinct and were consistent with the identity of conjugates I and II as structural isomers. Moreover, the UV spectrum of conjugate I exhibited a lambda max at 317 nm and was essentially identical to that of N-OH-PhIP, while conjugate II was markedly different with a lambda max of 331 nm. Both conjugates were stable in 0.1 N HCl and were resistant to hydrolysis by rat, dog and human liver microsomal beta-glucuronidases.(ABSTRACT TRUNCATED AT 400 WORDS)