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W Freitag

Publications and source records attributed to W Freitag.

12 recordsLinked to original sources
PubMed2006

Age-dependent loss of insulin-like growth factor-1 receptor immunoreactive cells in the supraoptic hypothalamus is reduced in calorically restricted mice.

Both life-long caloric restriction (CR) and the suppression of insulin-like growth factor-1 (IGF-1) signaling reliably extend the mammalian lifespan. The neuroendocrine system, regulated by the hypothalamus, remains the most convincing site of action for both these modes of life extension. Yet, determining whether CR actions are mediated by the modulation of neuroendocrine IGF-1 signaling remains unclear. Of the hypothalamic nuclei that express the IGF-1 receptor (IGF-1R), the cells of the supraoptic nucleus (SON) display some of the most robust IGF-1R expression. Taking IGF-1R immunoreactivity as an index of sensitivity to IGF-1, we counted IGF-1R immunoreactive and non-immunoreactive cells in the SON of young-ad-libitum fed (young-Al, 6 weeks), old-ad-libitum fed (Old-Al, 22 months), and old-calorie-restricted (Old-CR, 22 months) female B6D2F1 mice. An automated imaging microscopy system (AIMS) was used to generate cell counts for each section of supraoptic hypothalamus. Results show that while the total number of cells in the SON of ad-libitum fed mice does not change significantly with aging, a significant reduction in IGF-1R immunoreactive cells does occur in ad-libitum fed mice with aging. In contrast to this, calorie restricted mice show both a decline in the total number of cells and IGF-1R immunoreactive cells in the SON with age, but with the decrease in the latter being notably attenuated when compared to the degree of loss seen in ad-libitum fed mice. Thus, while CR induces greater loss in the total number of cells in the SON with age, it reduces the degree of age-dependent loss seen in IGF-1R expressing cells. As a result, when compared to Old-AL mice, the SON of Old-CR mice displays a greater proportion of IGF-1R cells and thus possibly enhanced IGF-1 sensitivity with aging.

Age Factors↗
PubMed1986

Inhibitory effects of interferon-gamma on the T suppressor cell circuit in contact sensitivity.

The effects of a partially purified, splenocyte-derived murine interferon (MuIFN-gamma N) and a recombinant IFN-gamma (MuIFN-gamma R) on the T suppressor pathway and on the T effector cells of delayed type hypersensitivity were investigated in a 2,4-dinitrofluorobenzene contact sensitivity model. Various T cell subpopulations, suppressor T cells of afferent and efferent types, and an auxiliary T suppressor cells as well as a T effector cell of delayed type hypersensitivity were induced and the functions assessed in transfer experiments. Confirming the results of earlier experiments obtained with IFN-alpha, beta, the MuIFN-gamma N preparation and the rec. MuIFN-gamma R: enhanced the decreased response in animals sensitized with an antigen overload to an optimal response; inhibited the afferent-acting T suppressor cell in vivo and in vitro; inhibited the Ts-eff response; blocked the auxiliary T suppressor cell response after intravenous injection to recipients of Ts-eff cells on day 0 and 1; and did not suppress the activity of the T effector cell of delayed type hypersensitivity in vivo and in vitro (the MuIFN-gamma R was not tested). We conclude that IFN-gamma preferentially inhibited the T suppressor cell circuit of contact allergy. These results are similar to our observations on the inhibitory effects of a pure interferon-alpha, beta on the regulatory T suppressor cell circuit in contact allergy. Selective suppression of different T subpopulations by IFN-gamma may be an important regulatory mechanism in delayed type hypersensitivity.

Animals↗
PubMed1985

Inhibition of the anti-receptor antibody response of contact sensitivity by interferon.

Mice sensitized with optimal doses of 2,4-dinitrofluorobenzene (DNFB) develop maximum delayed hypersensitivity in 4-5 days; the intensity of this reaction declines rapidly 14 days after sensitization. In the serum of mice 14 days after sensitization, an anti-receptor antibody has been described. It has been suggested that this antibody might be responsible for this rapid decline of contact sensitivity. We studied the effect of interferon alpha, beta (IFN alpha, beta) and cyclophosphamide (Cy) in this model. IFN alpha, beta (2 X 10(4) units/ mouse) or Cy (200 mg/kg) injected at Days 0 and 1 during sensitization, or at Day -2 before sensitization, respectively, partially prevented the decline of contact sensitivity as compared to the controls. In the serum of mice treated with IFN or Cy, no anti-receptor antibody could be detected 14 days after sensitization. These results suggest that anti-receptor antibody may be partially responsible for the waning of contact sensitivity. It is further suggested that IFN inhibited the anti-receptor antibody response by preventing the generation of the anti-receptor-antibody-inducing auxiliar T-suppressor cell. It is concluded that IFN alpha, beta enhances the delayed hypersensitivity response in contact allergy by inhibition of the T-suppressor circuit, as previously reported, and by suppression of the anti-receptor antibody response.

Animals↗
PubMed1984

Inhibition of the T suppressor circuit of delayed-type hypersensitivity by interferon.

The effects of electrophoretically pure murine interferon (Mu-IFN-alpha beta) on the T suppressor pathway and on the T effector cell of delayed hypersensitivity (TDH) were investigated in BALB/c mice, in a 2,4-dinitrofluorobenzene (DNFB) contact-sensitivity model. Various T cell subpopulations, suppressor T cells of the afferent (Ts-aff) and efferent (Ts-eff) types, an auxiliary Ts (Ts-aux), as well as TDH were induced, and their function was assessed in transfer experiments. The results were as follows. At a dose of 5 X 10(3) U, IFN was shown to inhibit the Ts-aff response, when given to the donor animal shortly after induction of the Ts-aff subpopulation or when injected into the recipient 2 hr after spleen cell transfer. Pretreatment in vitro with IFN of the splenic cells to be transferred also abolished the Ts-aff response. Similar amounts of IFN were able to inhibit the generation of Ts-eff in the donor animals, whereas 10-fold-higher amounts were needed in vivo or in vitro to block the functional expression of Ts-eff in the recipient animal. Intravenous injection of IFN into recipients of Ts-eff on day 0 and 1 after sensitization inhibited the expression of the Ts-eff transferred 1 day before ear challenge. This suggests that the Ts-aux response required for the TDH suppression by Ts-eff is blocked by IFN. Secretion of a suppressor factor by Ts in vitro was not blocked by IFN. Treatment of the donor of suppressor factor-secreting Ts with IFN, however, blocked the induction of this Ts. The TDH were not sensitive to IFN even at amounts approximately 100 times higher than those used for the Ts inhibition in vivo as well as in vitro. These results demonstrate that low amounts of IFN may selectively block the suppressor pathway, because induction of these regulatory T cell subsets appears to be particularly sensitive to IFN. The exact mechanism of the IFN-mediated inhibition of Ts is not yet clear. The data suggest an important regulatory function of IFN in delayed-type hypersensitivity (DTH) reactions.

Animals↗
PubMed1980

The changing role of the hospital chief financial officer.

Things are changing. That statement is obviously true of things political, economic and scientific. Not surprisingly, therefore, the statement applies to the activities, responsibilities, qualifications and, ultimately, status of the hospital chief financial officer (CFO).

Administrative Personnel↗
PubMedDate not supplied

[Swimming performance in the aged].

The deterioration of performance caused by aging was examined in 3,469 swimmers divided into 9 age groups and 4 styles of swimming. Comparisons using cross and longitudinal sections show that older swimmers become progressively slower, and the reduction of speed in all styles of swimming follows a quadratic trend. The losses of efficiency increase with age group, being by far the most in back-stroke and the least in crawl swimming. The combined longitudinal and cross sectional comparisons confirm this result, but not without any exception, for very often no statistically significant differences could be recognized between adjacent age groups. The interindividual comparison shows that it is also possible to maintain or even improve the efficiency over 10 to 12 years, even in the fifth or sixth decade of age, if the intensity and volume of training can be increased. The curve comprising reductions in the later stages of life may additionally be caused by the smaller number of persons per group and the deficient homogeneity within these groups. In addition to this, the tendency towards higher losses in older age groups is not significant, if only the best competitors of each age group are compared.

Adult↗