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1,022 result(s) for "McDonald, Mary"
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Robust performance of a live bacterial therapeutic chassis lacking the colibactin gene cluster
E . coli Nissle (EcN) is a non-pathogenic probiotic bacterium of the Enterobacteriaceae family that has been used for over a century to promote general gut health. Despite the history of safe usage of EcN, concerns have been raised regarding the presence of the pks gene cluster, encoding the genotoxin colibactin, due to its association with colorectal cancer. Here, we sought to determine the effect of pks island removal on the in vitro and in vivo robustness and activity of EcN and EcN-derived strains. A deletion of the pks island ( Δpks ) was constructed in wild type and engineered strains of EcN using lambda red recombineering. Mass spectrometric measurement of N-myristoyl-D-asparagine, released during colibactin maturation, confirmed that the pks deletion abrogated colibactin production. Growth curves were comparable between Δpks strains and their isogenic parents, and wild type EcN displayed no competitive advantage to the Δpks strain in mixed culture. Deletion of pks also had no effect on the activity of strains engineered to degrade phenylalanine (SYNB1618 and SYNB1934) or oxalate (SYNB8802). Furthermore, 1:1 mixed dosing of wild type and Δpks EcN in preclinical mouse and nonhuman primate models demonstrated no competitive disadvantage for the Δpks strain with regards to transit time or colonization. Importantly, there was no significant difference on in vivo strain performance between the clinical-stage strain SYNB1934 and its isogenic Δpks variant with regards to recovery of the quantitative strain-specific biomarkers d5- trans -cinnamic acid, and d5-hippuric acid. Taken together, these data support that the pks island is dispensable for Synthetic Biotic fitness and activity in vivo and that its removal from engineered strains of EcN will not have a deleterious effect on strain efficacy.
Disorderly conduct
With a devastating wildfire spreading to Silicon Valley, Maggie preps her family for a rapid evacuation. The heat rises when firefighters discover the body of her best friend Tess Olmos's athletic husband, whose untimely death was anything but accidental. And as Tess agonizes over the whereabouts of her spouse's drop-dead gorgeous running mate, she becomes the prime suspect in what's shaping up to become a double murder case. Determined to set the record straight, Maggie sorts through clues in an investigation more dangerous than the flames approaching her home. But when her own loved ones are threatened, can she catch the meticulous killer before everything falls apart.
Characterization of a virulence factor in Plasmodiophora brassicae, with molecular markers for identification
Symptom severity on differential host lines is currently used to characterize and identify pathotypes of Plasmodiophora brassicae , which is an obligate, soil-borne chromist pathogen that causes clubroot disease on canola ( Brassica napus ) and other brassica crops. This process is slow, variable and resource intensive; development of molecular markers could make identification of important pathotypes faster and more consistent for deployment of cultivars with pathotype-specific resistance. In the current study, a variant of gene 9171 was identified in the whole-genome sequences of only the highly virulent pathotypes of P . brassicae from around the world, including the new cohort of virulent pathotypes in Canada; its presence was confirmed using three KASP marker pairs. The gene was not present in the initial cohort of pathotypes identified in Canada. The putative structure, domains, and gene ontogeny of the protein product of gene 9171 were assessed using on-line software resources. Structural analysis of the putative protein produced by gene 9171 indicated that it was localized in the cytosol, and likely involved in cellular processes and catalytic activity. Identification of gene 9171 represents a potentially useful step toward molecular identification of the pathotypes of P . brassicae .
Scheduled to death
\"Maggie McDonald is hoping to raise the profile of her new Orchard View organizing business via her first high-profile client. Professor Lincoln Sinclair may be up for a Nobel Prize, but he's hopeless when it comes to organizing anything other than his thoughts. For an academic, he's also amassed more than his share of enemies. When Sinclair's fiancâee is found dead on the floor of his home laboratory -- electrocuted in a puddle of water -- Maggie takes on the added task of finding the woman's murderer. To do so, she'll have to outmaneuver the suspicious, obnoxious police investigator she's nicknamed 'Detective Awful' before a shadowy figure can check off the first item on their personal to-do list-- Kill Maggie McDonald.\" -- From back cover.
Fine Mapping of a Clubroot Resistance Gene in Chinese Cabbage Using SNP Markers Identified from Bulked Segregant RNA Sequencing
Clubroot, caused by , is an important disease of canola ( ) in western Canada and worldwide. In this study, a clubroot resistance gene ( ) was identified and fine mapped in Chinese cabbage cv. \"Jazz\" using single-nucleotide polymorphisms (SNP) markers identified from bulked segregant RNA sequencing (BSR-Seq) and molecular markers were developed for use in marker assisted selection. In total, 203.9 million raw reads were generated from one pooled resistant (R) and one pooled susceptible (S) sample, and >173,000 polymorphic SNP sites were identified between the R and S samples. One significant peak was observed between 22 and 26 Mb of chromosome A03, which had been predicted by BSR-Seq to contain the causal gene . There were 490 polymorphic SNP sites identified in the region. A segregating population consisting of 675 plants was analyzed with 15 SNP sites in the region using the Kompetitive Allele Specific PCR method, and was fine mapped between two SNP markers, SNP_A03_32 and SNP_A03_67 with 0.1 and 0.3 cM from , respectively. Five SNP markers co-segregated with in this region. Variants were identified in 14 of 36 genes annotated in the target region. The numbers of poly variants differed among the genes. Four genes encode TIR-NBS-LRR proteins and two of them and , had high numbers of polymorphic variants and so are the most likely candidates of .
Dead storage
\"Despite a looming deadline, Maggie thinks she has what it takes to help friends Jason and Stephen unclutter their large Victorian in time for its scheduled renovation. But before she can fill a single bin with unused junk, Jason leaves for Texas on an emergency business trip, Stephen's injured mastiff limps home--and Stephen himself lands in jail for murder. Someone killed the owner of a local Chinese restaurant and stuffed him in the freezer. Stephen, caught at the crime scene covered in blood, is the number one suspect. Now Maggie must devise a strategy to sort through secrets and set him free--before she's tossed into permanent storage next.\"-- From back cover.
Identification of Genome-Wide Variants and Discovery of Variants Associated with Brassica rapa Clubroot Resistance Gene Rcr1 through Bulked Segregant RNA Sequencing
Clubroot, caused by Plasmodiophora brassicae, is an important disease on Brassica species worldwide. A clubroot resistance gene, Rcr1, with efficacy against pathotype 3 of P. brassicae, was previously mapped to chromosome A03 of B. rapa in pak choy cultivar \"Flower Nabana\". In the current study, resistance to pathotypes 2, 5 and 6 was shown to be associated with Rcr1 region on chromosome A03. Bulked segregant RNA sequencing was performed and short read sequences were assembled into 10 chromosomes of the B. rapa reference genome v1.5. For the resistant (R) bulks, a total of 351.8 million (M) sequences, 30,836.5 million bases (Mb) in length, produced 120-fold coverage of the reference genome. For the susceptible (S) bulks, 322.9 M sequences, 28,216.6 Mb in length, produced 109-fold coverage. In total, 776.2 K single nucleotide polymorphisms (SNPs) and 122.2 K insertion / deletion (InDels) in R bulks and 762.8 K SNPs and 118.7 K InDels in S bulks were identified; each chromosome had about 87% SNPs and 13% InDels, with 78% monomorphic and 22% polymorphic variants between the R and S bulks. Polymorphic variants on each chromosome were usually below 23%, but made up 34% of the variants on chromosome A03. There were 35 genes annotated in the Rcr1 target region and variants were identified in 21 genes. The numbers of poly variants differed significantly among the genes. Four out of them encode Toll-Interleukin-1 receptor / nucleotide-binding site / leucine-rich-repeat proteins; Bra019409 and Bra019410 harbored the higher numbers of polymorphic variants, which indicates that they are more likely candidates of Rcr1. Fourteen SNP markers in the target region were genotyped using the Kompetitive Allele Specific PCR method and were confirmed to associate with Rcr1. Selected SNP markers were analyzed with 26 recombinants obtained from a segregating population consisting of 1587 plants, indicating that they were completely linked to Rcr1. Nine SNP markers were used for marker-assisted introgression of Rcr1 into B. napus canola from B. rapa, with 100% accuracy in this study.
Dialogues on Whiteness, Leisure and (Anti)Racism
This essay offers one response to recent calls for leisure studies scholars to more effectively integrate race into their analyses. Drawing from interdisciplinary scholarship within ethnic studies, cultural studies, and gender/women's studies the article initiates a broader dialogue about the possibilities and dangers of analyzing whiteness within leisure contexts. The article outlines several studies that demonstrate ways in which whiteness operates to advantage white hegemony. It suggests how the concepts of power evasiveness, normalization and intersectionality might be applied to leisure settings and concludes with a discussion of some problems associated with the study of whiteness. The ultimate aim of the essay is to provoke further dialogue as a step toward documenting and overturning inequitable social arrangements in the movement toward justice.