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Tephra fall (volcanic ash) studies are a key component to understanding the frequency and magnitude of volcanic eruptions and conducting volcano-hazard assessments. In addition, many interdisciplinary studies rely on tephra fall deposits as time-stratigraphic markers. Information on tephra deposits in Alaska has previously been dispersed amongst hundreds of publications that span numerous research disciplines. In order to streamline tephra occurrence data, information from these disparate publications have been compiled into one comprehensive geospatial dataset. Pleistocene, Holocene, and historical tephra deposit distribution information has been digitized for more than 120 published resources, including peer-reviewed articles, reports, and theses/dissertations. The dataset includes tephra fall distribution information pertaining to 39 eruptions from at least 19 volcanoes in Alaska. All files can be downloaded free of charge from the DGGS website (http://doi.org/10.14509/29847).

Mount Chiginagak is a hydrothermally active volcano on the Alaska Peninsula, approximately 170 km south-southwest of King Salmon, Alaska. This small stratovolcano, approximately 8 km in diameter, has erupted through Tertiary to Permian sedimentary and igneous rocks. The eruptive products of Chiginagak volcano record a history of chiefly andesite lava flows and associated block-and-ash flows. The oldest lavas exposed are Pleistocene in age and are found everywhere around the edifice except in the northeast sector, where Holocene lava flows dominate the landscape. Holocene activity has covered the northeast flank with rubbly-topped andesite lava flows that extend as far as 4.6 km from their source vent at the summit crater. The farthest-reaching volcanic deposits are on the southeast flank, where block-and-ash-flow, pyroclastic-flow, and lahar deposits extend down valley as far as 9 km from the summit. Limited exposure of deposits of a presumed plinian eruption of middle Pleistocene age indicate at least one episode of explosive activity in Chiginagak's past. This 1:25,000 scale geologic map and accompanying report document the age, geochemical, and spatial distribution of eruptive products of the Mount Chiginagak volcano. Map units are interpreted from field observations, satellite imagery interpretation, geochemical and geochronological analysis.

ZusammenfassungKürzlich wurde im Namen der American Heart Association und des American College of Cardiology eine Leitlinie zur Cholesterinsenkung und Reduktion des Risikos für arteriosklerotische Herz-Kreislauf-Erkrankungen veröffentlicht. Sie nimmt für sich in Anspruch, auf Evidenz randomisierter, kontrollierter Studien zu beruhen, und beschränkt sich deshalb auf die Behandlungsoptionen mit Statinen. Vor diesem Hintergrund gibt die Leitlinie keine Zielwerte mehr vor, sondern bezieht sich auf prozentuale Cholesterinsenkungen durch Statinmedikationen mit niedriger, moderater oder hoher Intensität, die allerdings genauso wenig als Vorgaben in randomisierten Studien geprüft worden sind wie die an der Praxis orientierten Zielwerte. Ähnliches gilt für die vier Patientengruppen, die die Leitlinie aufgrund ihres Risikos als therapiebedürftig definiert. Keine größere Statinstudie hat Probanden aufgrund eines errechneten globalen Risikos eingeschlossen, sodass auch die Zuordnungskriterien willkürlich gewählt sind. Sie würden zu einer erheblichen Ausweitung der Primärprävention mit hohen und maximalen Statindosen führen. Die Festlegung auf Statindosierungen statt Cholesterinzielwerte steht dem Prinzip einer individualisierten Behandlung entgegen. Zu begrüßen ist die Möglichkeit des neuen Risikoscores, zusätzlich zum 10-Jahres-Risiko das Lebenszeitrisiko bis zum 80. Lebensjahr zu ermitteln. Allerdings fließt dies nicht in die Behandlungsempfehlungen ein, obgleich Evidenz von Populations- und genetischen Studien darauf hinweist, dass die früh- und langzeitige moderate Senkung des Low-density-lipoprotein(LDL)- oder Non-high-density-lipoprotein(HDL)-Cholesterins eine weitaus stärkere Wirkung hat als eine intensive Behandlung im fortgeschrittenen Alter. Hinsichtlich der Sekundärprävention stimmt die neue Leitlinie mit der europäischen weitgehend überein. Die beteiligten Fachgesellschaften des D•A•CH-Bereichs empfehlen, weiterhin entsprechend den bewährten Richtlinien wie den Leitlinien der European Society of Cardiology und der European Atherosclerosis Society zu verfahren.

Background: Adrenoleukodystrophy (ALD), including its adult variant adrenomyeloneuropathy (AMN), is an X-linked recessive trait characterized by progressive demyelinization of the nervous system. The gene defect involves a peroxisomal transporter protein, resulting in accumulation of very-long-chain fatty acids in the brain and other organs such as the adrenal glands. Affected men show various endocrine disorders. Moreover, disturbances of hair growth are frequently mentioned in reports on ALD/AMN. Objective: This study was performed to delineate further the hair status and type of hair loss in men with AMN. Methods: We examined and documented the status of hair growth in 16 men suffering from AMN. A meticulous history with particular regard to hair changes was taken from all patients and their family members. Results: The age of the patients varied between 27 and 62 years, their mean age was 39.8 years. Twelve men showed male-pattern androgenetic alopecia (AGA), Hamilton grades IV–VIII, 3 men had a female-pattern AGA (Ludwig grade I or II). Ten of the patients with male-pattern AGA had reached Hamilton stage VII or VIII. The remaining scalp hair was unusually scarce and thin in 11 cases, regardless of the grade of AGA. Moreover, in 10 of 16 patients the eyelids showed pronounced madarosis. The remaining body hair was found to be normal. If present, endocrine manifestations had started prior to the onset of alopecia, and in 11 of 12 patients hair loss was apparent before neurological symptoms were noted. Conclusion: ALD/AMN gives rise to two different types of hair loss. Firstly, affected men show diffuse hair loss involving the entire scalp and the eyelashes. Secondly, they tend to develop AGA more frequently and earlier and in a severer form. Paradoxically, pronounced AGA is present although the patients may simultaneously show some degree of hypogonadism. Hence, the X-linked ALD mutation can be taken as a well-defined gene within the polygenic spectrum of genes responsible for AGA. This may be of theoretical importance for the elucidation of the pathogenetic pathways of AGA.

Alterations of lipid metabolism play a pivotal role in the development of atherosclerosis and its complications, today's major mortality risks. The predominant regulators controlling cholesterol- and fatty acids synthesis in liver are the sterol regulatory element-binding proteins (SREBPs), a family of transcription factors that were formerly identified as cholesterol sensor for LDLR gene expression. Variation of gene structure in these genes might therefore indicate a predisposition to develop complications like myocardial infarction and stroke.We investigated 190 unrelated German subjects, including 69 subjects with LDL-cholesterol55mg/dl, for mutations in SREBP genes SREBF-1 and SREBF-2 by direct sequencing. The impact on SREBP functionality was analyzed by protein biochemical analyses, promoter reporter gene assays and gene expression studies.A missense mutation in SREBF-1 (c.332 CT; P111L) was identified in a subject with LDL-cholesterol5mg/dl. Examination of the subject's family confirmed the mutation in two of three siblings. Detailed clinical evaluation of these subjects disclose a novel form of primary combined hypolipidemia only in SREBP-1a P111L carriers, characterized by low levels of apoB and apoA1, low triglyceride, LDL-cholesterol and HDL-cholesterol levels. Functional analyses indicated that the mutation abolishes phosphorylation of SREBP-1. As a consequence transcriptional activation of classical target genes, i.e. LDLR, HMG-CoAR, FAS, ABCA1, but also MTTP, was dramatically reduced.Phosphorylation of SREBP-1, the master regulator of genes for central rate limiting enzymes of cholesterol and lipid metabolism, appears to be a biological principle with clinical implications.