Semidistributive Inverse Semigroups, II

The description by Johnston-Thom and the second author of the inverse semigroups S for which the lattice LJ(S) of full inverse subsemigroups of S is join semidistributive is used to describe those for which (a) the lattice L(S) of all inverse subsemigroups or (b) the lattice lo(S) of convex inverse subsemigroups have that property. In contrast with the methods used by the authors to investigate lower semimodularity, the methods are based on decompositions via GS, the union of the subgroups of the semigroup (which is necessarily cryptic)

Lower Semimodular Inverse Semigroups, II

The authors’ description of the inverse semigroups S for which the lattice ℒℱ(S) of full inverse subsemigroups is lower semimodular is used to describe those for which (a) the lattice ℒ(S) of all inverse subsemigroups or (b) the lattice �o(S) of convex inverse subsemigroups has that property. In each case, we show that this occurs if and only if the entire lattice is a subdirect product of ℒℱ(S) with ℒ(E S ), or �o(E S ), respectively, where E S is the semilattice of idempotents of S; a simple necessary and sufficient condition is found for each decomposition. For a semilattice E, ℒ(E) is in fact always lower semimodular, and �o(E) is lower semimodular if and only if E is a tree. The conjunction of these results leads to quite a divergence between the ultimate descriptions in the two cases, ℒ(S) and �o(S), with the latter being substantially richer

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Acute pulmonary toxicity and body distribution of inhaled metallic silver nanoparticles

The purpose of this study was to determine the acute pulmonary toxicity of metallic silver nanoparticles (MSNPs, 20.30 nm in diameter). Acute pulmonary toxicity and body distribution of inhaled MSNPs in mice were evaluated using a nose-only exposure chamber (NOEC) system. Bronchoalveolar lavage (BAL) fluid analysis, Western blotting, histopathological changes, and silver burdens in various organs were determined in mice. Mice were exposed to MSNPs for 6 hrs. The mean concentration, total surface area, volume and mass concentrations in the NOEC were maintained at 1.93 × 107 particles/cm3, 1.09 × 1010 nm2/cm3, 2.72 × 1011 nm3/cm3, and 2854.62 μg/m3, respectively. Inhalation of MSPNs caused mild pulmonary toxicity with distribution of silver in various organs but the silver burdens decreased rapidly at 24-hrs post-exposure in the lung. Furthermore, inhaled MSNPs induced activation of mitogen-activated protein kinase (MAPK) signaling in the lung. In summary, single inhaled MSNPs caused mild pulmonary toxicity, which was associated with activated MAPK signaling. Taken together, our results suggest that the inhalation toxicity of MSNPs should be carefully considered at the molecular level