Nouveaux livres

Ohne Zusammenfassung

---

Reviews

---

Nouveaux livres

---

Recensioni

     

Zur Stratigraphie der säugetierführenden Schichten von Java

Summary According to recent geological and paleontological investigations thePithecanthropus-beds of Java are pleistocene in age. The examinations of the fossil mammalian faunæ of the island are of utmost importance for this age-determination and the following faunæ can be recognized:Tji Djolang-fauna: Middle Pliocene.Kali Glagah-fauna: Upper Pliocene.Djetis-fauna withPithecanthropus: Lower Pleistocene.Trinil-fauna withPithecanthropus: Middle Pleistocene.Ngandong-fauna withHomo neanderthalensis soloensis: Upper Pleistocene.Sampoeng-fauna with a primitive type of the Wedda-Dravida-Australoid group: Subrecent. — Micropaleontological examinations of smallerForaminifera from marine equivalents of thePithecanthropus-beds confirm the age-determinations based on mammalia. — Recent field investigations prove that the lower and middle pleistocenePithecanthropus-beds are distinctlyfolded by a post-middle-pleistocene movement; the upper pleistocene Ngandong-terraces are not folded at all.     

Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death

Mutations in ion channels involved in the generation and termination of action potentials constitute a family of molecular defects that underlie fatal cardiac arrhythmias in inherited long-QT syndrome. We report here that a loss-of-function (E1425G) mutation in ankyrin-B (also known as ankyrin 2), a member of a family of versatile membrane adapters, causes dominantly inherited type 4 long-QT cardiac arrhythmia in humans. Mice heterozygous for a null mutation in ankyrin-B are haploinsufficient and display arrhythmia similar to humans. Mutation of ankyrin-B results in disruption in the cellular organization of the sodium pump, the sodium/calcium exchanger, and inositol-1,4,5-trisphosphate receptors (all ankyrin-B-binding proteins), which reduces the targeting of these proteins to the transverse tubules as well as reducing overall protein level. Ankyrin-B mutation also leads to altered Ca2+ signalling in adult cardiomyocytes that results in extrasystoles, and provides a rationale for the arrhythmia. Thus, we identify a new mechanism for cardiac arrhythmia due to abnormal coordination of multiple functionally related ion channels and transporters.