On a direct algorithm for the generation of log-normal pseudo-random numbers

The random variable \(\left( {\prod {_{i = 1}^n {{X_i } \mathord{\left/ {\vphantom {{X_i } {X_{i + n} }}} \right. \kern-0em} {X_{i + n} }}} } \right)^{{1 \mathord{\left/ {\vphantom {1 {\sqrt {2n} }}} \right. \kern-0em} {\sqrt {2n} }}}\) is used to generate standard log-normal variables Λ(0, 1), where theX _i are independent uniform variables on [0, 1].     

Polynomoperatoren in C k [a,b]

Some estimations for the relative projection constantP(∏ _n+k ^k ,Csik[a,b]) are given. By constructing an associated polynomial operatorL _n :C ⁰[a,b]→∏ _n ⁰ to a given polynomial operatorH _n+k :C ^k [a,b]→∏ _n+k ^k we get a lower bound for the projection constant. An upper bound forP(∏ _n+k ^k ,C ^k [a,b]) is obtained by the determination of the norms of appropriate polynomial operatorsP _n+k :C ^k [a,b]→∏ _n+k ^k . Further we give a convergence property for the sequence (P _n+k ) _n∈?.     

Einleitung und Abbruch der künstlichen Ernährung beim einwilligungsunfähigen Patienten

Definition of the problem: In Austria the legal discussion on initiating and withdrawing artificial nutrition in incompetent patients has just begun. Arguments and conclusion: Legal regulations are lacking, but there appears to be agreement on accepting advance directives under specific criteria. This would mean that a presumed will and documented refusal of treatment and nutrition has to be respected by physicians. However, there is no consensus with regard to the “supposed will” of an incompetent patient to refuse treatment and nutrition. At present, surrogate decision making with regard to refusing life-sustaining treatment or nutrition is only accepted according to a declared and documented directive of the patient himself. When the patient’s will has to be “surmised” the protection of life has priority. In Austria this concept is based on the national constitution and its duty to protect life.     

Corticosterone Influences on Mammalian Neonatal Sensitive-Period Learning.

Infant rats exhibit sensitive-period odor learning characterized by olfactory bulb neural changes and odor preference acquisitions critical for survival. This sensitive period is coincident with low endogenous corticosterone (CORT) levels and stress hyporesponsivity. The authors hypothesized that low corticosterone levels modulate sensitive-period learning. They assessed the effects of manipulating CORT levels by increasing and removing CORT during (Postnatal Day 8) and after (Postnatal Day 12) the sensitive period. Results show that (a) exogenous CORT prematurely ends sensitive-period odor-shock-induced preferences; (b) adrenalectomy developmentally extends the sensitive period as indicated by odor-shock-induced odor-preference learning in older pups, whereas CORT replacement can reinstate fear learning; and (c) CORT manipulation modulates olfactory bulb correlates of sensitive-period odor learning in a manner consistent with behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Software specification using graph grammars

The following paper demonstrates that programmed sequential graph grammars can be used in a systematic proceeding to specify the changes of high level intermediate data structures arising in a programming support environment, in which all tools work in an incremental and syntax-driven mode. In this paper we lay stress upon the way to get the specification rather than on the result of this process. Therefore, we give here some approach to “specification engineering” using graph grammars. This approach is influenced by the syntactical definition of the underlying language for Programming in the Small, the module concept etc. to be supported on one side but also by the idea of the user interface.     

Sphk1 and Sphk2 Differentially Regulate Erythropoietin Synthesis in Mouse Renal Interstitial Fibroblast-like Cells

Erythropoietin (Epo) is a crucial hormone regulating red blood cell number and consequently the hematocrit. Epo is mainly produced in the kidney by interstitial fibroblast-like cells. Previously, we have shown that in cultures of the immortalized mouse renal fibroblast-like cell line FAIK F3-5, sphingosine 1-phosphate (S1P), by activating S1P₁ and S1P₃ receptors, can stabilize hypoxia-inducible factor (HIF)-2α and upregulate Epo mRNA and protein synthesis. In this study, we have addressed the role of intracellular iS1P derived from sphingosine kinases (Sphk) 1 and 2 on Epo synthesis in F3-5 cells and in mouse primary cultures of renal fibroblasts. We show that stable knockdown of Sphk2 in F3-5 cells increases HIF-2α protein and Epo mRNA and protein levels, while Sphk1 knockdown leads to a reduction of hypoxia-stimulated HIF-2α and Epo protein. A similar effect was obtained using primary cultures of renal fibroblasts isolated from wildtype mice, Sphk1−/−, or Sphk2−/− mice. Furthermore, selective Sphk2 inhibitors mimicked the effect of genetic Sphk2 depletion and also upregulated HIF-2α and Epo protein levels. The combined blockade of Sphk1 and Sphk2, using Sphk2−/− renal fibroblasts treated with the Sphk1 inhibitor PF543, resulted in reduced HIF-2α and Epo compared to the untreated Sphk2−/− cells. Exogenous sphingosine (Sph) enhanced HIF-2α and Epo, and this was abolished by the combined treatment with the selective S1P₁ and S1P₃ antagonists NIBR-0213 and TY52156, suggesting that Sph was taken up by cells and converted to iS1P and exported to then act in an autocrine manner through S1P₁ and S1P₃. The upregulation of HIF-2α and Epo synthesis by Sphk2 knockdown was confirmed in the human hepatoma cell line Hep3B, which is well-established to upregulate Epo production under hypoxia. In summary, these data show that sphingolipids have diverse effects on Epo synthesis. While accumulation of intracellular Sph reduces Epo synthesis, iS1P will be exported to act through S1P₁₊₃ to enhance Epo synthesis. Furthermore, these data suggest that selective inhibition of Sphk2 is an attractive new option to enhance Epo synthesis and thereby to reduce anemia development in chronic kidney disease.