New data on the scale insects (Hemiptera, Coccoidea) of Tenerife, Canary Islands

This short communication presents new data on 16 species of scale insects, belonging to 5 families of the Coccoidea (Hemiptera) which were collected by the author on April 1995 in the course of a short visit to Tenerife Island. Three species, indicated below with an asterisk *, are recorded here for the first time from the Canary Islands. Slide-mounted specimens of all the species recorded here are deposited in the Coccoidea Collection, Department of Entomology, Agricultural Research Organization, Bet Dagan, Israel. The collection number of each record is indicated in the Material Examined section

Environmental Drivers of Benthic-Interior Exchange Events Over the Continental Shelf of Monterey Bay, California

This study presents a comprehensive analysis of oceanographic data collected by an automated profiling mooring and fixed instrumentation platforms deployed over the mud belt on the southern continental shelf of Monterey Bay, California at 70 m depth during the fall of 2012. Physical and optical measurements taken at the study site documented the frequent occurrence of suspended particulate matter (SPM) layers in the mid-water column, the majority of which were detached from the seafloor and overlaid clearer water. This study examines the temporal and spatial variations of these detached SPM layers using time series analysis and modeling methods, and investigates how hydrographic and climatic phenomena relate to their appearance. The results indicate that the forcing of detached SPM layers appears to include not only large enough surface waves for recent seafloor resuspension in the bottom boundary layer but also, and of equal importance, energetic internal tides. A probabilistic model based on co-occurrence of the two environmental processes predicted the appearance of detached SPM layers with 77% accuracy. The ability of energetic internal tides to propagate into Monterey Bay appears to be, to some extent, connected to wind-driven shifts in stratification over the shelf

ISSIS-XII (Crete, Greece, April-2010) recognises Zvi Mendel for his excellence and outstanding contributions to scale insect studies

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Gene-environment interactions between HPA axis regulatory genes and stressful life events in suicide attempts

Suicide is a leading cause of death. In the future, treatment for suicidal behavior, as well as public health prevention and/or intervention efforts, may be guided by genetic epidemiology. This research is informed by biological alterations which have been previously observed in suicidal behavior. Such alterations include dysregulation of the cortisol response to psychosocial stress, which is in large part mediated by the hypothalamic-pituitary-adrenal (HPA) axis. HPA axis functioning is influenced e.g. by heritable variation in regulatory genes, by exposure to stressful life events (SLEs), and/or by gene-environment interactions (G x Es) of regulatory genetic variants with SLEs. Using a family-based design of proband offspring who have made a suicide attempt (SA) and their parents, we tested and characterized associations of transmitted variants in candidate genes that regulate HPA axis activation, as well as G x Es of these variants with SLEs, with SA and secondary outcomes. In Study 1, we showed a G x E between a variant in corticotropin releasing hormone receptor type-1 (CRHR1), a gene which has a major role in mediating HPA axis activation, and physical assault in childhood/adolescence. We further observed a novel and independent G x E between another unlinked variant and physical assault in adulthood. These findings confirmed and extended previous findings on adulthood depressive symptoms, cortisol response, and alcohol misuse by other groups. In Study 2, we investigated 98% of currently known common single nucleotide polymorphisms (SNPs) and certain low-frequency SNPs in serotonin receptor type-2a (HTR2A), a gene involved in serotonergic system modulation of HPA axis activation, and showed novel genetic linkage/association of a promoter SNP and a low frequency exon 2 SNP, as well as a novel G x E between a well-studied exon 1 SNP and exposure to cumulative lifetime SLEs. We further characterized this G x E, revealing a complex parent-of-origin effect in females, which may partly explain inconsistent findings in the literature. In study 3, we investigated twenty-four genes in the glutamatergic, γ-aminobutyric acid (GABA)-ergic, and polyaminergic systems that are known to link several brain areas involved in emotional processing with HPA axis activation. We showed linkage/association of 3 SNPs in an N-methyl-D-aspartate (NMDA) receptor subunit type-2B gene (GRIN2B), and 2 SNPs and 1 haplotype in a gene which codes for a rate limiting enzyme in polyamine biosynthesis (ODC1). A G x E was also observed between another ODC1 SNP and physical assault in childhood/adolescence. In study 4, we investigated 100% of currently known common SNPs and a low frequency SNP in arginine vasopressin receptor type-1B (AVPR1B), a gene involved with CRHR1 in partially overlapping roles in HPA axis activation. We showed linkage/association of two SNPs and a corresponding major allele haplotype across the gene predominantly on current depressive symptoms in SA. Interestingly, we found no evidence of a G x E between AVPR1B variants and SLEs, or any gene-gene interaction effects with CRHR1 variants. In all studies, the findings were complemented with casecontrol re-analysis of SA offspring with healthy volunteers; characterized with SA-concomitant outcomes, as well as lifetime psychiatric diagnoses, and/or other descriptive variables; and discussed with regard to previous findings by our group or others, and to potential mechanistic roles. These findings support a stress-diathesis model of suicidal behavior, and a potential etiological role in the suicidal process for novel genetic variants and variants that have previously associated with stress-related HPA axis dysregulation, maladaptive behaviors and neuropsychiatric outcomes. The strength of these results is supported by the family-based design, which is robust to population substructure, and relatively comprehensive investigations of genetic variation, signaling pathway, and/or G x E. Further investigation and consistent replication across samples are warranted before utility in clinical diagnosis, treatment and/or public health efforts

Notch and bone morphogenetic protein differentially act on dermomyotome cells to generate endothelium, smooth, and striated muscle

We address the mechanisms underlying generation of skeletal muscle, smooth muscle, and endothelium from epithelial progenitors in the dermomyotome. Lineage analysis shows that of all epithelial domains, the lateral region is the most prolific producer of smooth muscle and endothelium. Importantly, individual labeled lateral somitic cells give rise to only endothelial or mural cells (not both), and endothelial and mural cell differentiation is driven by distinct signaling systems. Notch activity is necessary for smooth muscle production while inhibiting striated muscle differentiation, yet it does not affect initial development of endothelial cells. On the other hand, bone morphogenetic protein signaling is required for endothelial cell differentiation and/or migration but inhibits striated muscle differentiation and fails to impact smooth muscle cell production. Hence, although different mechanisms are responsible for smooth muscle and endothelium generation, the choice to become smooth versus striated muscle depends on a single signaling system. Altogether, these findings underscore the spatial and temporal complexity of lineage diversification in an apparently homogeneous epithelium

On ω\omega-Strongly Measurable Cardinals

We prove several consistency results concerning the notion of $\omega$-strongly measurable cardinal in HOD. In particular, we show that is it consistent, relative to a large cardinal hypothesis weaker than $o(\kappa) = \kappa$, that every successor of a regular cardinal is $\omega$-strongly measurable in HOD

Segregation of striated and smooth muscle lineages by a Notch-dependent regulatory network

Background: Lineage segregation from multipotent epithelia is a central theme in development and in adult stem cell plasticity. Previously, we demonstrated that striated and smooth muscle cells share a common progenitor within their epithelium of origin, the lateral domain of the somite-derived dermomyotome. However, what controls the segregation of these muscle subtypes remains unknown. We use this in vivo bifurcation of fates as an experimental model to uncover the underlying mechanisms of lineage diversification from bipotent progenitors. Results: Using the strength of spatio-temporally controlled gene missexpression in avian embryos, we report that Notch harbors distinct pro-smooth muscle activities depending on the duration of the signal; short periods prevent striated muscle development and extended periods, through Snail1, promote cell emigration from the dermomyotome towards a smooth muscle fate. Furthermore, we define a Muscle Regulatory Network, consisting of Id2, Id3, FoxC2 and Snail1, which acts in concert to promote smooth muscle by antagonizing the pro-myogenic activities of Myf5 and Pax7, which induce striated muscle fate. Notch and BMP closely regulate the network and reciprocally reinforce each other’s signal. In turn, components of the network strengthen Notch signaling, while Pax7 silences this signaling. These feedbacks augment the robustness and flexibility of the network regulating muscle subtype segregation. Conclusions: Our results demarcate the details of the Muscle Regulatory Network, underlying the segregation of muscle sublineages from the lateral dermomyotome, and exhibit how factors within the network promote the smooth muscle at the expense of the striated muscle fate. This network acts as an exemplar demonstrating how lineage segregation occurs within epithelial primordia by integrating inputs from competing factors

Quantized Convolutional Neural Networks Through the Lens of Partial Differential Equations

Quantization of Convolutional Neural Networks (CNNs) is a common approach to ease the computational burden involved in the deployment of CNNs, especially on low-resource edge devices. However, fixed-point arithmetic is not natural to the type of computations involved in neural networks. In this work, we explore ways to improve quantized CNNs using PDE-based perspective and analysis. First, we harness the total variation (TV) approach to apply edge-aware smoothing to the feature maps throughout the network. This aims to reduce outliers in the distribution of values and promote piece-wise constant maps, which are more suitable for quantization. Secondly, we consider symmetric and stable variants of common CNNs for image classification, and Graph Convolutional Networks (GCNs) for graph node-classification. We demonstrate through several experiments that the property of forward stability preserves the action of a network under different quantization rates. As a result, stable quantized networks behave similarly to their non-quantized counterparts even though they rely on fewer parameters. We also find that at times, stability even aids in improving accuracy. These properties are of particular interest for sensitive, resource-constrained, low-power or real-time applications like autonomous driving

Stationary Reflection and the failure of SCH

In this paper we prove that from large cardinals it is consistent that there is a singular strong limit cardinal $\nu$ such that the singular cardinal hypothesis fails at $\nu$ and every collection of fewer than $\mathrm{cf}(\nu)$ stationary subsets of $\nu^+$ reflects simultaneously. For uncountable cofinality, this situation was not previously known to be consistent. Using different methods, we reduce the upper bound on the consistency strength of this situation for $\mathrm{cf}(\nu) = \omega$ to below a single partially supercompact cardinal. The previous upper bound of infinitely many supercompact cardinals was due to Sharon.Comment: 23 page