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Documenting the magnitude of finite strain within ductile shear zones is critical for understanding lithospheric deformation. However, pervasive recrystallization within shear zones often destroys the deformed markers from which strain can be measured. Intensity parameters calculated from quartz crystallographic preferred orientation (CPO) distributions have been interpreted as proxies for the relative strain magnitude within shear zones, but thus far have not been calibrated to absolute strain magnitude. Here, we present equations that quantify the relationship between CPO intensity parameters (cylindricity and density norm) and finite strain magnitude, which we calculate by integrating quartz CPO analyses (n = 87) with strain ellipsoids from stretched detrital quartz clasts (n = 49) and macro‐scale ductile thinning measurements (n = 7) from the footwall of the Northern Snake Range décollement (NSRD) in Nevada. The NSRD footwall exhibits a strain gradient, with Rs(XZ) values increasing from 5.4 ± 1.4 to 282 ± 122 eastward across the range. Cylindricity increases from 0.52 to 0.83 as Rs increases from 5.4 to 23.5, and increases gradually to 0.92 at Rs values between 160 and 404. Density norm increases from 1.68 to 2.97 as Rs increases from 5.4 to 23.5, but stays approximately constant until Rs values between 160 and 404. We present equations that express average finite strain as a function of average cylindricity and density norm, which provide a broadly applicable tool for estimating the first‐order finite strain magnitude within any shear zone from which quartz CPO intensity can be measured. To demonstrate their utility, we apply our equations to published data from Himalayan shear zones and a Cordilleran core complex. Key Point: Quantifying the relationship between crystallographic preferred orientation distribution intensity parameters and finite strain magnitude [ABSTRACT FROM AUTHOR]

Introduction and aims: There is emerging evidence that heavy long‐term alcohol consumption may alter the neuroimmune profile. We conducted a meta‐analysis of the association between alcohol use disorder (AUD) and the extent of neuroinflammation using cerebrospinal (CSF), PET (Positron Emission Tomography), and postmortem studies. Design and methods: A comprehensive search of electronic databases was conducted using the Preferred Reporting Items for Systematic Review and Meta‐Analysis Protocols (PRISMA‐P) for AUD‐related terms in combination with neuroinflammatory markers and cytokine‐ and chemokine‐related terms for CSF, PET, and postmortem studies. Participants had to meet established criteria for AUD and/or heavy alcohol consumption with dependence features and be compared with healthy controls. Papers retrieved were assessed for inclusion criteria and a critical appraisal was completed using the Newcastle‐Ottawa Scale. A meta‐analysis was conducted on postmortem and PET studies. Results: Eleven papers met the inclusion criteria with CSF, PET, and postmortem studies included in the final analysis. Postmortem studies demonstrate significant heterogeneity (푄 (14) = 62.02, 푝 < 0.001), with the alcohol group showing higher levels of neuroimmune markers than controls (푑 = 1.50 [95% CI 0.56, 2.45]). PET studies demonstrated a lower [11C] PBR28 total volume of distribution (VT) for translocator protein in the hippocampus (g = −1.95 [95% CI −2.72, −1.18], p < 0.001) of the alcohol group compared to controls. Conclusion: There is emerging evidence across multiple diagnostic modalities that alcohol impacts neuroimmune signaling in the human brain. [ABSTRACT FROM AUTHOR]

We sequenced the entire mitochondrial genome of Abispa ephippium (Hymenoptera: Vespoidea: Vespidae: Eumeninae) and most of the mitochondrial genome of Polistes humilis synoecus (Hymenoptera: Vespoidea: Vespidae: Polistinae). The arrangement of genes differed between the two genomes and also differed slightly from that inferred to be ancestral for the Hymenoptera. The genome organization for both vespids is different from that of all other mitochondrial genomes previously reported. A number of tRNA gene rearrangements were identified that represent potential synapomorphies for a subset of the Vespidae. Analysis of all available hymenopteran mitochondrial genome sequences recovered an uncontroversial phylogeny, one consistent with analyses of other types of data. Key words: Hymenoptera, phylogeny, mitochondrial, genome, social. Les auteurs ont sequence completement le genome mitochondrial de l'Abispa ephippium (Hymenoptera : Vespoidea : Vespidae : Eumeninae) et la majorite du genome mitochondrial du Polistes humilis synoecus (Hymenoptera : Vespoidea : Vespidae : Polistinae). La disposition des genes an sein des deux genomes etait differente et differait legerement de la disposition presumee ancestrale chez les hymenopteres. L'organisation du genome chez ces deux vespides differe de 'organisation decrite chez tons les autres genomes mitochondriaux rapportes a ce jour. Plusieurs rearrangements de genes codant pour des ARNt ont ete identifies et representent de possibles synapomorphies chez un sons-ensemble des vespides. Une analyse de toutes les sequences de genomes mitochondriaux disponibles chez les hymenopteres a permis de produire une phylogenie conforme a celle obtenue a l' aide de d' autres types de donnees. Mots-cles : Hymenoptera, phylogenie, mitochondrial, genome, social. [Traduit par la Redaction], Introduction Entire or nearly entire mitogenomic sequences have been increasingly employed to address long-standing phylogenetic questions (e.g., Hwang et al. 2001; Amason et al. 2002; Miya et al. 2003; Lavrov [...]

Background: Amyotrophic lateral sclerosis (ALS) is associated with a range of clinical phenotypes and shows progressive degeneration of upper and/or lower motor neurons, and phosphorylated 43 kDa TAR DNA‐binding protein (pTDP‐43) inclusions in motor and non‐motor pathways. Parkinsonian features have been reported in up to 30% of ALS patients, and Lewy bodies, normally associated with Lewy body disease (LBD), have been reported in a small number of ALS cases, with unknown clinical relevance. This study investigates the prevalence of clinically relevant LBD in a prospectively studied ALS cohort to determine whether concomitant pathology contributes to the clinical heterogeneity. Methods: All ALS cases held by the New South Wales Brain Bank (n = 97) were screened for coexisting LBD consistent with clinical disease (Braak ≥ stage IV). Relevant clinical and genetic associations were determined. Results: Six cases had coexisting LBD Braak ≥ stage IV pathology. The age at symptom onset (69 ± 7 years) and disease duration (4 ± 3 years) in ALS cases with coexisting LBD did not differ from ALS cases. Three patients had lower limb onset and two patients had bulbar onset. Two patients developed the clinical features of Parkinson's disease, with one receiving a dual diagnosis. All cases had no known relevant family history or genetic abnormalities. Conclusion: The prevalence of clinically relevant LBD pathology in ALS is higher than in the general population, and has implications for clinical and neuropathological diagnoses and the identification of biomarkers. [ABSTRACT FROM AUTHOR]

Describes an experiment designed to test the hypothesis that because of society's reaction to them, the facially attractive develop greater social skill. Shows that this experiment, in which faces and conversation of subjects were independently evaluated, found no evidence to support such hypothesis. (Author/MES)

The Caenorhabditis elegans early embryo is highly polarized, requiring sequestration of cytoplasmic polarity factors at the plasma membrane. This compartmentalization aids asymmetric distribution of lipids and proteins, which is partially responsible for the fates of the daughter cells. Since most plasma membrane proteins are glycosylated, we determined the effect of attenuation of N-glycosylation on cell polarity. While polarity establishment was not perturbed, the size difference between the two cells formed in first cell division (AB and P1) was more variable in embryos with reduced N-glycosylation than in the mock-treated embryos. In addition, among other deficiencies, we observed spindle orientation defects in two-cell embryos. Moreover, cell–cell adhesion was specifically lost at the two-cell stage when N-glycosylation was reduced. This loss-of-adhesion phenotype was rescued by interfering with polarity establishment, indicating that polarity establishment enforces plasma membrane compartmentalization. Consistent with this idea, the decreased plasma membrane levels of the adhesion proteins E-cadherin and MAGI-1 in ribo-1(RNAi) embryos were restored in the absence of functional PAR-2. Our data suggest a general role for N-glycosylation in plasma membrane compartmentalization and cell polarity. [ABSTRACT FROM AUTHOR]

Mitochondria are essential eukaryotic organelles often forming intricate networks. The overall network morphology is determined by mitochondrial fusion and fission. Among the multiple mechanisms that appear to regulate mitochondrial fission, the ER and actin have recently been shown to play an important role by mediating mitochondrial constriction and promoting the action of a key fission factor, the dynamin-like protein Drp1. Here, we report that the cytoskeletal component septin 2 is involved in Drp1-dependent mitochondrial fission in mammalian cells. Septin 2 localizes to a subset of mitochondrial constrictions and directly binds Drp1, as shown by immunoprecipitation of the endogenous proteins and by pulldown assays with recombinant proteins. Depletion of septin 2 reduces Drp1 recruitment to mitochondria and results in hyperfused mitochondria and delayed FCCP-induced fission. Strikingly, septin depletion also affects mitochondrial morphology in Caenorhabditis elegans, strongly suggesting that the role of septins in mitochondrial dynamics is evolutionarily conserved. [ABSTRACT FROM AUTHOR]

The mammalian serum- and glucocorticoid-inducible kinase SGK1 regulates the endocytosis of ion channels. Here we report that in C. elegans sgk-1 null mutants, GFP-tagged MIG-14/Wntless, the sorting receptor of Wnt, failed to localize to the basolateral membrane of intestinal cells; instead, it was mis-sorted to lysosomes. This effect can be explained in part by altered sphingolipid levels, because reducing glucosylceramide biosynthesis restored the localization of MIG-14::GFP. Membrane traffic was not perturbed in general, as no obvious morphological defects were detected for early endosomes, the Golgi apparatus, and the endoplasmic reticulum (ER) in sgk-1 null animals. The recycling of MIG-14/Wntless through the Golgi might be partially responsible for the observed phenotype because the subcellular distribution of two plasma membrane cargoes that do not recycle through the trans-Golgi network (TGN) was affected to a lesser degree. Consistently, knockdown of the ArfGEF gbf-1 altered the distribution of SGK-1 at the basolateral membrane of intestinal cells. In addition, we found that sgk-1(RNAi) induced unfolded protein response in the ER, suggesting at least an indirect role of SGK-1 early in the secretory pathway. We propose that SGK-1 function is required for lipid homeostasis and that it acts at different intracellular trafficking steps. [ABSTRACT FROM AUTHOR]

N-glycosylation of proteins is an essential process, and N-glucans serve as important beacons in protein folding and ER associated degradation. More importantly, N-glycosylation increases the structural repertoire of proteins because the addition of the N-glucan on proteins will serve as a base for further sugar additions in the Golgi apparatus, and hence complex three-dimensional structures can be build. N-glycosylation is mediated by the ER-resident OST complex, which is essential throughout eukaryotes. Partial knockdown of conserved OST complex members, such as C. elegans RIBO-1, led to an embryonic lethal phenotype. Although the ER morphology was not grossly altered in ribo-1(RNAi) oocytes and embryos, secretion of yolk and of the yolk receptor RME-2 was perturbed in those worms. Perhaps as a consequence of reduced arrival of N-glycosylated proteins at the plasma membrane, cytokinesis occurred less efficiently leading to multinuclear cells. Unexpectedly, we detected a chromosome segregation defect in ribo-1(RNAi) embryos suggesting an essential role of at least one N-glycosylated protein in metaphase-anaphase transition. [ABSTRACT FROM AUTHOR]

We determined the prevalence of two common leucine-rich repeat kinase 2 (LRRK2) gene mutations in Australian patients with Parkinson's disease (PD). Of 830 affected patients, eight were heterozygous for the G2019S mutation, and two were heterozygous for the R1441H (4,322 G > A) mutation. In addition, one familial patient had a novel A1442P (4,324 G > C) mutation. Haplotype analysis showed that all LRRK2 G2019S-positive individuals carried the common founder haplotype 1 and a putative founder haplotype for the R1441H mutation carriers. Clinically, patients with LRRK2 mutations had typical levodopa responsive Parkinsonism with tremor being the commonest presenting feature. Patients with the G2019S mutation in our series had a similar age of onset of symptoms when compared with patients with other LRRK2 mutations or sporadic PD, although they were more likely to have a family history of PD (2.4% of Australian patients with familial PD and 0.3% of Australian patients with sporadic PD). Our results demonstrate that the G2019S mutation carriers share the same ancestors who migrated to Australia originally from Europe and that other LRRK2 mutations (R1441H and A1442P) can be found in this population. [ABSTRACT FROM AUTHOR]

Serum samples from 31 children ≤4 years old who were convalescing after meningococcal disease were used in a quantitative hybridization assay to establish antibody reactivity to 94 candidate meningococcal vaccine antigens. Genes encoding 22 of 23 strongly recognized proteins were found in ≥94% of the patients' meningococcal strains, and most were also widely prevalent in Neisseria lactamica and other commensal Neisseria species. Similar antibody reactivity was found in serum samples from healthy control children, suggesting that these antibodies arose from asymptomatic colonization. The 23rd protein, NadA, elicited strong reactivity solely in convalescent patients previously infected with a nadA+ strain. nadA was not present in any of 29 diverse N. lactamica strains, suggesting that reactivity in these children arose from meningococcal infection. In contrast, serum samples from healthy adults contained anti-NadA immunoglobulin G at high levels. The correlation of NadA antibody level with natural acquisition of protective immunity suggests that NadA may be a valuable component of a childhood antimeningococcal vaccine. [ABSTRACT FROM AUTHOR]

Focuses on the relationship between ratings of persons' facial appearance and ratings of their conversations. Rejection of the view that the facially attractive develop greater social skill; Development of greater socialization; Conversational expertise.

The current economic policies in the federal government present an opportunity for the nursing profession to improve access to health care, providing high quality care to a greater segment of the population at lower cost. [ABSTRACT FROM AUTHOR]

This study examines the effects of penmanship and the physical attractiveness of the writer upon essay assessment. An essay which was always exactly the same in content was assessed by a large number of school teachers and by some students. Some of the assessors received the essay in typed form, for some it was written in good handwriting and for some the handwriting was poor. A photograph of the supposed author of the essay was attached to it via a report card. This portrait photograph was of a male or a female who was either highly physically attractive or rather unattractive. It was found that when the authors were female the ratings given to the essays were influenced by the factors of penmanship and attractiveness. No such effects were found if the authors were male. The implications of such findings for educational and employment application settings are discussed. [ABSTRACT FROM AUTHOR]

We present an unusual aneurysm in a pediatric patient. Due to the fusiform nature of the aneurysm and the small size of the patient, a unique surgical solution was applied. One year of clinical follow-up is also provided. [ABSTRACT FROM AUTHOR]

Abstract: Chimeric sequences falsely increase the apparent diversity within samples. To examine chimera formation in PCR products from environmental DNA, clone libraries were prepared using different ramp speeds to reach the designated temperatures for each step of the PCR program. Slowing the thermocycler ramp speed to 1°Cs−1 reduced chimera formation. [Copyright &y& Elsevier]

We have identified two redundant GTPase activating proteins (GAPs) - RGA-3 and RGA-4 - that regulate Rho GTPase function at the plasma membrane in early Caenorhabditis elegans embryos. Knockdown of both RhoGAPs resulted in extensive membrane ruffling, furrowing and pronounced pseudo-cleavages. In addition, the non-muscle myosin NMY-2 and RHO-1 accumulated on the cortex at sites of ruffling. RGA-3 and RGA-4 are GAPs for RHO-1, but most probably not for CDC-42, because only RHO-1 was epistatic to the two GAPs, and the GAPs had no obvious influence on CDC-42 function. Furthermore, knockdown of either the RHO-1 effector, LET-502, or the exchange factor for RHO-1, ECT-2, alleviated the membrane-ruffling phenotype caused by simultaneous knockdown of both RGA-3 and RGA-4 [rga-3/4 (RNAi)]. GFP::PAR-6 and GFP::PAR-2 were localized at the anterior and posterior part of the early C. elegans embryo, respectively showing that rga-3/4 (RNAi) did not interfere with polarity establishment. Most importantly, upon simultaneous knockdown of RGA-3, RGA-4 and the third RhoGAP present in the early embryo, CYK-4, NMY-2 spread over the entire cortex and GFP::PAR-2 localization at the posterior cortex was greatly diminished. These results indicate that the functions of CYK-4 are temporally and spatially distinct from RGA-3 and RGA-4 (RGA-3/4). RGA-3/4 and CYK-4 also play different roles in controlling LET-502 activation in the germ line, because rga-3/4 (RNAi), but not cyk-4 (RNAi), aggravated the let-502(sb106) phenotype. We propose that RGA-3/4 and CYK-4 control with which effector molecules RHO-1 interacts at particular sites at the cortex in the zygote and in the germ line. [ABSTRACT FROM AUTHOR]