What is the Minnesota Cooperative Soil Survey?

This archival publication may not reflect current scientific knowledge or recommendations. Current information available from the University of Minnesota Extension: https://www.extension.umn.edu

Differences in neural crest sensitivity to ethanol account for the infrequency of anterior segment defects in the eye compared with craniofacial anomalies in a zebrafish model of fetal alcohol syndrome

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138404/1/bdr21069.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138404/2/bdr21069_am.pd

Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response

Ribosome is responsible for protein synthesis in all organisms and ribosomal proteins (RPs) play important roles in the formation of a functional ribosome. L11 was recently shown to regulate p53 activity through a direct binding with MDM2 and abrogating the MDM2-induced p53 degradation in response to ribosomal stress. However, the studies were performed in cell lines and the significance of this tumor suppressor function of L11 has yet to be explored in animal models. To investigate the effects of the deletion of L11 and its physiological relevance to p53 activity, we knocked down the rpl11 gene in zebrafish and analyzed the p53 response. Contrary to the cell line-based results, our data indicate that an L11 deficiency in a model organism activates the p53 pathway. The L11-deficient embryos (morphants) displayed developmental abnormalities primarily in the brain, leading to embryonic lethality within 6–7 days post fertilization. Extensive apoptosis was observed in the head region of the morphants, thus correlating the morphological defects with apparent cell death. A decrease in total abundance of genes involved in neural patterning of the brain was observed in the morphants, suggesting a reduction in neural progenitor cells. Upregulation of the genes involved in the p53 pathway were observed in the morphants. Simultaneous knockdown of the p53 gene rescued the developmental defects and apoptosis in the morphants. These results suggest that ribosomal dysfunction due to the loss of L11 activates a p53-dependent checkpoint response to prevent improper embryonic development

Foxf2: A Novel Locus for Anterior Segment Dysgenesis Adjacent to the Foxc1 Gene

Anterior segment dysgenesis (ASD) is characterised by an abnormal migration of neural crest cells or an aberrant differentiation of the mesenchymal cells during the formation of the eye's anterior segment. These abnormalities result in multiple tissue defects affecting the iris, cornea and drainage structures of the iridocorneal angle including the ciliary body, trabecular meshwork and Schlemm's canal. In some cases, abnormal ASD development leads to glaucoma, which is usually associated with increased intraocular pressure. Haploinsufficiency through mutation or chromosomal deletion of the human FOXC1 transcription factor gene or duplications of the 6p25 region is associated with a spectrum of ocular abnormalities including ASD. However, mapping data and phenotype analysis of human deletions suggests that an additional locus for this condition may be present in the same chromosomal region as FOXC1. DHPLC screening of ENU mutagenised mouse archival tissue revealed five novel mouse Foxf2 mutations. Re-derivation of one of these (the Foxf2W174R mouse lineage) resulted in heterozygote mice that exhibited thinning of the iris stroma, hyperplasia of the trabecular meshwork, small or absent Schlemm's canal and a reduction in the iridocorneal angle. Homozygous E18.5 mice showed absence of ciliary body projections, demonstrating a critical role for Foxf2 in the developing eye. These data provide evidence that the Foxf2 gene, separated from Foxc1 by less than 70 kb of genomic sequence (250 kb in human DNA), may explain human abnormalities in some cases of ASD where FOXC1 has been excluded genetically

Cooperative Soil Survey Shows Soil Types

This archival publication may not reflect current scientific knowledge or recommendations. Current information available from the University of Minnesota Extension: https://www.extension.umn.edu

SCRAP: A Statistical Approach for Creating a Database Query Workload Based on Performance Bottlenecks

Abstract—With the tremendous growth in stored data, the role of database systems has become more significant than ever before. Standard query workloads, such as the TPC-C and TPC-H benchmark suites, are used to evaluate and tune the functionality and performance of database systems. Running and configuring benchmarks is a time consuming task. It requires substantial statistical expertise due to the enormous data size and large number of queries in the workload. Subsetting can be used to reduce the number of queries in a workload. An existing workload subsetting technique selected queries based on similarities of the ranks of the queries for low-level characteristics, such as cache miss rates, or based on the execution time required in different computer systems. However, many low-level characteristics are correlated, produce similar behaviors. Also, raw execution time as a metric is too diffuse to capture important performance bottlenecks. Our goal is to select a subset of queries that can reproduce the same bottlenecks in the system as the original workload. In this paper, we propose a statistical approach for creating a database query workload based on performance bottlenecks (SCRAP). Our methodology takes a query workload and a set of system configuration parameters as inputs, and selects a subset of the queries from the workload based on the similarity of performance bottlenecks. Experimental results using the TPC-H benchmark and the PostgreSQL database system, show that the reduced workload and the original workload produce similar performance bottlenecks, and the subset accurately estimates the total execution time. I