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"Butler, G"
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Irish writers in the Irish American press, 1882-1964
\"Literary anthologies feature many of Ireland's most well-known authors, Oscar Wilde, W. B. Yeats, J. M. Synge, George Bernard Shaw, Seán O'Casey, James Joyce, and Brendan Behan among them. While a number of notable scholars have contended that middle-class Irish Americans rejected or ignored this rebellious group of poets, playwrights, and novelists in favor of a conservative Catholic subculture brought over with the mass migration of the mid-nineteenth century, Stephen G. Butler demonstrates that the transatlantic relationship between these figures and a segment of Irish American journalists and citizens is more complicated--and sometimes more collaborative--than previously acknowledged. Irish Writers in the Irish American Press spans the period from Oscar Wilde's 1882 American lecture tour to the months following JFK's assassination and covers the century in which Irish American identity was shaped by immigration, religion, politics, and economic advancement. Through a close engagement with Irish American periodicals, Butler offers a more nuanced understanding of the connections between Irish literary studies and Irish American culture during this period\" -- Provided by publisher.
Book
Clinical Assessment, Genetics, and Treatment Approaches in Autism Spectrum Disorder (ASD)
Autism spectrum disorder (ASD) consists of a genetically heterogenous group of neurobehavioral disorders characterized by impairment in three behavioral domains including communication, social interaction, and stereotypic repetitive behaviors. ASD affects more than 1% of children in Western societies, with diagnoses on the rise due to improved recognition, screening, clinical assessment, and diagnostic testing. We reviewed the role of genetic and metabolic factors which contribute to the causation of ASD with the use of new genetic technology. Up to 40 percent of individuals with ASD are now diagnosed with genetic syndromes or have chromosomal abnormalities including small DNA deletions or duplications, single gene conditions, or gene variants and metabolic disturbances with mitochondrial dysfunction. Although the heritability estimate for ASD is between 70 and 90%, there is a lower molecular diagnostic yield than anticipated. A likely explanation may relate to multifactorial causation with etiological heterogeneity and hundreds of genes involved with a complex interplay between inheritance and environmental factors influenced by epigenetics and capabilities to identify causative genes and their variants for ASD. Behavioral and psychiatric correlates, diagnosis and genetic evaluation with testing are discussed along with psychiatric treatment approaches and pharmacogenetics for selection of medication to treat challenging behaviors or comorbidities commonly seen in ASD. We emphasize prioritizing treatment based on targeted symptoms for individuals with ASD, as treatment will vary from patient to patient based on diagnosis, comorbidities, causation, and symptom severity.
Journal Article
The sitcom
\"In this new Routledge Television Guidebook, Jeremy G. Butler studies our love-hate relationship with the durable sitcom, analyzing the genre's position as a major media artefact within American culture and providing a historical overview of its evolution in the USA. Everyone loves the sitcom genre; and yet, paradoxically, everyone hates the sitcom, too. This book examines themes of gender, race, ethnicity, and the family that are always at the core of humor in our culture, tracking how those discourses are embedded in the sitcom's relatively rigid storytelling structures. Butler pays particular attention to the sitcom's position in today's post-network media landscape and sample analyses of Sex and the City, Black-ish, The Simpsons, and The Andy Griffith Show illuminate how the sitcom is infused with foundational American values. At once contemporary and reflective, The Sitcom is a must-read for students and scholars of television, comedy, and broader media studies, and a great classroom text\"-- Provided by publisher.
Book
Clinical Trials in Prader–Willi Syndrome: A Review
Prader–Willi syndrome (PWS) is a complex, genetic, neurodevelopmental disorder. PWS has three molecular genetic classes. The most common defect is due to a paternal 15q11-q13 deletion observed in about 60% of individuals. This is followed by maternal disomy 15 (both 15 s from the mother), found in approximately 35% of cases. the remaining individuals have a defect of the imprinting center that controls the activity of imprinted genes on chromosome 15. Mild cognitive impairment and behavior problems in PWS include self-injury, anxiety, compulsions, and outbursts in childhood, impacted by genetic subtypes. Food seeking and hyperphagia can lead to morbid obesity and contribute to diabetes and cardiovascular or orthopedic problems. The control of hyperphagia and improving food-related behaviors are the most important unmet needs in PWS and could be addressed with the development of a new therapeutic agent, as currently no approved therapeutics exist for PWS treatment. The status of clinical trials with existing results for the management of obesity and hyperphagia in PWS will be discussed in this review, including treatments such as beloranib, setmelanotide, a diazoxide choline controlled-release tablet (DCCR), an unacylated ghrelin analogue, oxytocin and related compounds, glucagon-like peptide 1 receptor agonists, surgical intervention, and transcranial direct-current stimulation.
Journal Article
Causes of death in Prader-Willi syndrome: Prader-Willi Syndrome Association (USA) 40-year mortality survey
Background:
Prader-Willi syndrome (PWS) is a rare, complex, neurodevelopmental genetic disorder that is associated with hyperphagia and morbid obesity in humans and leads to a shortened life expectancy. This report summarizes the primary causes of death and evaluates mortality trends in a large cohort of individuals with PWS.
Methods:
The US Prader-Willi Syndrome Association (PWSA (USA)) syndrome-specific database of death reports was collected through a cursory bereavement program for PWSA (USA) families using a brief survey created in 1999. Causes of death were descriptively characterized and statistically examined using Cox proportional hazards.
Results:
A total of 486 deaths were reported (263 males, 217 females, 6 unknown) between 1973 and 2015, with mean age of 29.5 ± 16 years (2 months–67 years); 70% occurred in adulthood. Respiratory failure was the most common cause, accounting for 31% of all deaths. Males were at increased risk for presumed hyperphagia-related accidents/injuries and cardiopulmonary factors compared to females. PWS maternal disomy 15 genetic subtype showed an increased risk of death from cardiopulmonary factors compared to the deletion subtype.
Conclusions:
These findings highlight the heightened vulnerability to obesity and hyperphagia-related mortality in PWS. Future research is needed to address critical vulnerabilities such as gender and genetic subtype in the cause of death in PWS.
Genet Med
advance online publication 17 November 2016
Journal Article
Origami toys & games.
Learn about the Japanese art of paper folding called origami, including the meaning behind the symbols that are used and how to make the different folds. Then, through easy step-by-step instructions and simple diagrams, you can create a fun tower puzzle or fishing game, a lively jumping frog or bobbing fox, an amazing magic square, and many other cool toys and games to play with friends and family!
Book
Naturally Occurring Mutations of SARS-CoV-2 Main Protease Confer Drug Resistance to Nirmatrelvir
The SARS-CoV-2 main protease (M
) is the drug target of Pfizer's oral drug nirmatrelvir. The emergence of SARS-CoV-2 variants with mutations in M
raised the alarm of potential drug resistance. To identify potential clinically relevant drug-resistant mutants, we systematically characterized 102 naturally occurring M
mutants located at 12 residues at the nirmatrelvir-binding site, among which 22 mutations in 5 residues, including S144M/F/A/G/Y, M165T, E166 V/G/A, H172Q/F, and Q192T/S/L/A/I/P/H/V/W/C/F, showed comparable enzymatic activity to the wild-type (
/
< 10-fold change) while being resistant to nirmatrelvir (
> 10-fold increase). X-ray crystal structures were determined for six representative mutants with and/or without GC-376/nirmatrelvir. Using recombinant SARS-CoV-2 viruses generated from reverse genetics, we confirmed the drug resistance in the antiviral assay and showed that M
mutants with reduced enzymatic activity had attenuated viral replication. Overall, our study identified several drug-resistant hotspots in M
that warrant close monitoring for possible clinical evidence of nirmatrelvir resistance, some of which have already emerged in independent viral passage assays conducted by others.
Journal Article
Origami animals
Learn about the Japanese art of paper folding called origami, including the meaning behind the symbols that are used and how to make the different folds. Then, through easy step-by-step instructions and simple diagrams, you can create a cute cat or duck, an amazing Apatosaurus or sea horse, a scary shark or bat, and many other awesome animals!
Book
Genomic imprinting disorders in humans: a mini-review
Mammals inherit two complete sets of chromosomes, one from the father and one from the mother, and most autosomal genes are expressed from both maternal and paternal alleles. Imprinted genes show expression from only one member of the gene pair (allele) and their expression are determined by the parent during production of the gametes. Imprinted genes represent only a small subset of mammalian genes that are present but not imprinted in other vertebrates. Genomic imprints are erased in both germlines and reset accordingly; thus, reversible depending on the parent of origin and leads to differential expression in the course of development. Genomic imprinting has been studied in humans since the early 1980’s and accounts for several human disorders. The first report in humans occurred in Prader-Willi syndrome due to a paternal deletion of chromosome 15 or uniparental disomy 15 (both chromosome 15s from only one parent) and similar genetic disturbances were reported later in Angelman syndrome.
Journal Article