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Fornminne: Steinsetting. Oval mot rektangulær steinsetting av flate heller. NS orientert. Steinene er hodestore og større og er delvis overgrodde. Ved prøvestikk fantes tre under torv og rett over sand/grus. 1,8 x 2,80 m.

Enkeltliggende kokegrop i dyrket mark. Mål: 90 x 80 cm, ujevn rund form. Dybde: 0-4,5 cm Plan: Kokegropen fremstår som meget ujevn i form i plan og veldig grunn. Kokegropen består av kullblandet leire, og det er noen skjørbrente steiner sentralt i strukturen. Det er skavet av masser sør og vest for kokegropen. Da strukturen fremstår som meget grunn er det ikke umulig at det også er skavet av noe av selve kokegropen. Sørøstlige halvdel av strukturen ble fjernet ved snitting. Profil: Meget grunn struktur med en maks dybde på 4,5 cm. Den sørøstlige delen av profilet var dypest og hadde en kullrand i bunn. I denne delen av kokegropen var det et parti som bestod av brunrød leire, og inneholdt ikke kull. En håndfull skjørbrente steiner ble fjernet ved snittingen.

Alphabetical and referenced investigations on the structure and internal dynamics of the political elites in the early modern age; extent, development and structure of the elevations in status under aspects of constitutional and government history. Topics: Country of origin, occupation, area of activity, title, year of elevation, Kaiser elevating, nobility title. Prosopographische Untersuchungen zur Struktur und inneren Dynamik der politischen Eliten in der frühen Neuzeit; Umfang, Entwicklung und Struktur der Standeserhebungen unter verfassungs- und verwaltungsgeschichtlichen Aspekten. Themen: Herkunftsland, Beruf, Tätigkeitsbereich, Titel, Jahr der Erhebung, erhebender Kaiser, Adelstitel. Random selection Zufallsauswahl Sources: Reich registers, further archive materials. Quellen: Reichsregister, weiteres Archivgut.

662200608 is a Populus nigra accession from GnpIS.

Magnetic hysteresis measurements of sediments have resulted in widespread reporting of “pseudo‐single‐domain”‐like magnetic properties. In contrast, the ideal single domain (SD) properties that would be expected to be responsible for high quality paleomagnetic records are rare. Determining whether SD particles are rare or common in sediments requires application of techniques that enable discrimination among different magnetic components in a sediment. We apply a range of such techniques and find that SD particles are much more common than has been reported in the literature and that magnetite magnetofossils (the inorganic remains of magnetotactic bacteria) are widely preserved at depth in a range of sediment types, including biogenic pelagic carbonates, lacustrine and marine clays, and possibly even in glaci‐marine sediments. Thus, instead of being rarely preserved in the geological record, we find that magnetofossils are widespread. This observation has important implications for our understanding of how sediments become magnetized and highlights the need to develop a more robust basis for understanding how biogenic magnetite contributes to the magnetization of sediments. Magnetofossils also have grain sizes that are substantially smaller than the 1–15μm size range for which there is reasonable empirical support for relative paleointensity studies. The different magnetic response of coexisting fine biogenic and coarser lithogenic particles is likely to complicate relative paleointensity studies. This issue needs much closer attention. Despite the fact that sediments have been subjected to paleomagnetic investigation for over 60 years, much remains to be understood about how they become magnetized National Oceanography Centre, University of Southampton, Reino Unido Research School of Earth Sciences, Australian National University, Australia Paleomagnetic Laboratory Fort Hoofddijk, Department of Earth Sciences, University of Utrecht, Holanda Istituto Nazionale di Geofisica e Vulcanologia, Italia Unidad de Zaragoza, Área de Cambio Global, Instituto Geológico y Minero de España, España Natural Environment Research Council, Reino Unido Australian Research Council, Australia Ministerio de Educación y Cultura, España

Let (X-t)(t >= 0) be a continuous-time irreducible Markov chain on a finite state space E, let v: E -> R \ {0}, and let (phi(t))(t >= 0) be defined by phi(t) = integral(0)(t) v(X-s) ds. We consider the case in which the process (phi(t))(t >= 0) is oscillating and that in which (phi(t))(t >= 0) has a negative drift. In each of these cases, we condition the process (X-t, phi(t))(t >= 0) on the event that (phi(t))(t >= 0) hits level y before hitting 0 and prove weak convergence of the conditioned process as y -> infinity. In addition, we show the relationship between the conditioning of the process (phi(t))(t >= 0) with a negative drift to oscillate and the conditioning of it to stay nonnegative for a long time, and the relationship between the conditioning of (phi(t))(t >= 0) with a negative drift to drift to infinity and the conditioning of it to hit large levels before hitting 0.

The primary aim of the Obemat2.0 trial was to evaluate the efficacy of a multicomponent motivational program for the treatment of childhood obesity, coordinated between primary care and hospital specialized services, compared to the usual intervention performed in primary care. This was a cluster randomized clinical trial conducted in Spain, with two intervention arms: motivational intervention group vs. usual care group (as control), including 167 participants in each. The motivational intervention consisted of motivational interviewing, educational materials, use of an eHealth physical activity monitor and three group-based sessions. The primary outcome was body mass index (BMI) z score increments before and after the 12 (+3) months of intervention. Secondary outcomes (pre-post intervention) were: adherence to treatment, waist circumference (cm), fat mass index (z score), fat free mass index (z score), total body water (kg), bone mineral density (z score), blood lipids profile, glucose metabolism, and psychosocial problems. Other assessments (pre and post-intervention) were: sociodemographic information, physical activity, sedentary activity, neuropsychological testing, perception of body image, quality of the diet, food frequency consumption and foods available at home. The results of this clinical trial could open a window of opportunity to support professionals at the primary care to treat childhood obesity.

In this article, the authors convincingly demonstrate that the ubiquitin E3 ligase HOIL-1 can ubiquitylate in vitro oligosaccharides, only the second example ever reported of a non-proteinaceous ubiquitylation substrate. They also observe that mice harbouring a catalytic dead version of HOIL-1 cannot efficiently clear polyglucosan from relevant tissues, thereby hypothesising that this aberrant phenotype may arise due to such inclusions not being removed in a HOIL-1 dependent manner. The presented in vitro data are robust, stemming from meticulously-thought, well-controlled experiments. The in vivo observations are interesting, with fascinating appeal should the hypothetical model the authors put forward be true. Having said so, it is surprising to me that the authors have not validated some of their in vitro findings or investigated potential functional implications in in vivo settings. This is my main point of concern, on which I elaborate subsequently, providing a few experimental suggestions that may help address such potential criticism that may come up in the input of other reviewers. I also provide feedback with respect to some additional controls and minor technical issues that may help cover all bases. Though the in vitro data of HOIL-1 dependent ubiquitylation of glycogen and maltoheptaose are abundantly clear, there is no evidence that this occurs in cells. Furthermore, even if HOIL-1 indeed ubiquitylates those biomolecules in vivo, the mechanism (monoubiquitylation? multi-monoubiquitylation? en bloc polyubiquitylation? chains of what linkage? what proportion of the a1:4 gets ubiquitylated?) and the functional implications (different glycophagy rates? different lysosomal activity? how is the lack of a1:6 signalled?) are still completely unclear. I think that any in vivo/cell data that (in)directly corroborate their in vitro findings would substantially increase the impact of and interest in their study. Here are some experiments that may help the authors further validate their conclusions: The authors could repeat the experiments carried out in Figure 2 and/or 4, using HOIL-1 containing complexes isolated (immnoprecipitated) from wt or C458S cells instead of recombinant proteins, to demonstrate that endogenous HOIL-1 complexes recapitulate the in vitro results, namely that they ubiquitylate recombinant glycogen and directly interact with oligosaccharides. Using a non-basic purification method, the authors could try to isolate glycogen from wt or C458S cells and investigate its ubiquitylation status either by blotting or mass spectrometry. To functionally connect the phenotype of aberrant glycogen to the lack of HOIL-1 ubiquitylation activity with actual in vivo implications, the authors could test what happens to glycophagy in wt versus C458S cells. Do C458S cells exhibit increased authophagy markers? Do those markers colocalise with PAS staining at those cells? Does the expression of lysosomal a1:4 glycosylase or Stbd1 increase in C458S cells? Do those proteins increasingly colocalise with PAS staining at those cells? Can you rescue the C458S phenotypes of aberrant glycogen deposits by overexpressing Stdb1 or another way of artificially stimulating glycophagy? The authors could exogenously produce glycogen lacking a1:6 junctions and put it in cells. Would it recapitulate the HOIL-1 (C458S) phenotypes? Would the HOIL-1 (C458S) be less susceptible to such a substance? The authors claim in their discussion that HOIP-produced M1 oligomers may be powerful allosteric activators of HOIL-1 ubiquitylation of glycogen. That is just one of many possibilities. Trying to exclude other possibilities, the authors could test the effect of other ubiquitin polymers (e.g. K48- or K11-polyubiquitin tetramers) on recombinant HOIL-1 reactions. They could also investigate if cells exclusively expressing catalytically inactive HOIP exhibit similar aberrant glycogen structures as HOIL-1 (C448S) cells do. If so, are the HOIP-CS/HOIL-1 CS phenotypes epistatic? Furthemore, the authors could investigate if other IBR E3 ligases (e.g. HHAR1/ARIH1 or Parkin) can in vitro ubiquitylate maltoheptaose or if this is a property unique to HOIL-1. Such data would complement well their current data exhibiting that other IBRs do not bind oligosaccharides in vitro. In my opinion, the authors would benefit by staining for specific molecules (e.g. by western blotting or PAS staining), in parallel to their coomassie stainings, particularly in Figures 5-7 where differences based solely on molecular weight are sometimes quite hard to discern. Some minor points: In figure 1, the authors could show PES stainings of tissues that do not show any increase, as a negative control. In figure 2, the authors could treat ubiquitylated glycogen with recombinant USP2 to further validate the fact that this is a ubiquitylation event. Though panels 4F, 6G and 6H are informative, they are not representing actual data but theoretical projections, as such I think that they would be more suited for supplementary information. Panels 5B and 5C/5D are somewhat at odds with one another with respect to the remaining, unmodified maltoheptaose. Though the levels of modified maltoheptaose increase similarly, the levels of unmodified maltoheptaose are visibly higher in the NZF mutants/deletion when ubiquitin tetramers are used.