When Is Domestic Political Unrest Related to International Conflict? Diversionary Theory and Japanese Foreign Policy, 1890–19411

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146888/1/j.1468-2478.2010.00620.x.pd

The Impact of Burnout Identification and Interventions in Nursing Students and Newly Licensed Nurses: A Literature Review

Burnout is a problem that is plaguing the healthcare system globally, potentially resulting in individuals leaving their respective professions. Worldwide, there is a shortage of over 6 million nurses. Newly licensed registered nurses, both the associates degree and baccalaureate prepared, are poorly equipped to manage the stress and emotional exhaustion of providing patient care resulting in new nurses leaving the nursing field within one to two years of graduation. The purpose of this project was to identify: (1) if burnout experienced during nursing school continues into the new graduate nurse’s career; (2) how this influences the new graduate as a newly licensed registered nurse’s choice to exit the profession within the first few years of work; and (3) what interventions can be implemented to minimize burnout and improve retention rates of new nurses. A literature review was conducted, and the Health Belief Model was utilized to guide appropriate recommendations to minimize the negative effects of burnout. Approximately 175,000 registered nurses within the United States will leave the profession each year for a wide range of reasons. If nursing students experience burnout while in their respective programs, job stressors and job demands can increase the probability of newly licensed nurses burning out and subsequently leaving the profession. Implementation of various interventions have been shown to minimize burnout in nursing students and new nurses and subsequent retention in the nursing profession. It is recommended that education regarding burnout be implemented in nursing programs to provide students with the necessary skills to mitigate burnout prior to entering the profession. &nbsp

Hospital-Based Harm Reduction Interventions: A Systematic Review

Background: In the U.S., the number of hospitalized patients diagnosed with a substance use disorder (SUD; e.g., opioid use disorder, alcohol use disorder) is growing at an alarming rate. Often negatively impacted by stigma, homelessness and physical and mental comorbidities, this vulnerable patient population may benefit from the use of hospital-based harm reduction interventions (HHRIs) to improve overall hospital care experiences and negative health outcomes. Purpose: To examine how harm reduction principles have been successfully applied to HHRIs resulting in decreased negative health outcomes associated with SUD, improved healthcare provider-patient relationships, and reduced financial burden of healthcare systems. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and flow diagram were utilized for this systematic review. Nineteen studies met the eligibility criteria for inclusion in the review. Implications: Four consistent themes that either inhibit or facilitate the implementation of HHRIs (e.g., establishing specialized SUD hospital units, employing peer support specialists, utilizing the clinical opiate withdrawal scale) were identified: ethical responsibility, stigma, structural changes to hospital systems, and noted gaps associated with post-discharge care. Conclusion: HHRIs are a useful treatment option to manage the unique needs associated with the growing SUD patient population

Identification of growth insensitive to ABA3 (gia3), a Recessive Mutation Affecting ABA Signaling for the Control of Early Post-Germination Growth in Arabidopsis thaliana

The stress phytohormone ABA inhibits the developmental transition taking the mature embryo in the dry seed towards a young seedling. ABA also induces the accumulation of the basic leucine zipper (bZIP) transcription factor ABA-insensitive 5 (ABI5) which, apart from blocking endosperm rupture, also protects the embryo by stimulating the expression of late embryogenesis abundant (LEA) genes that conferred osmotolerance during seed maturation. It is unknown whether ABA recruits additional embryonic pathways to control early seedling growth and fitness. Here we identify gia3 (growth insensitive to ABA3), a recessive locus in Arabidopsis mediating cotyledon cellular maturation and ABA-dependent repression of cotyledon expansion and greening. Microarray studies showed that expression of the essential mid-embryogenesis gene Maternal Embryo Effect 26 (MEE26) is induced by ABA during early seedling growth in wild-type (WT) or abi5 plants but not in gia3 mutants. However, we also show that the GIA3 locus controls ABA-dependent gene expression responses that partially overlap with those controlled by ABI5. Thus, the gia3 locus identifies an additional arm of ABA signaling, distinct from that controlled by ABI5, which recruits MEE26 expression and maintains cotyledon embryonic identity. Fine mapping localized the gia3 locus within a 1 Mb interval of chromosome 3, containing a large DNA insertion of a duplicated region of chromosome 2. It remains unknown at present whether gia3 phenotypes are the result of single or multiple genetic alteration

DAT (deacylating autotransporter toxin) from Bordetella parapertussis demyristoylates Gαi GTPases and contributes to cough

The pathogenic bacteria Bordetella pertussis and Bordetella parapertussis cause pertussis (whooping cough) and pertussis-like disease, respectively, both of which are characterized by paroxysmal coughing. We previously reported that pertussis toxin (PTx), which inactivates heterotrimeric GTPases of the Gi family through ADP-ribosylation of their α subunits, causes coughing in combination with Vag8 and lipid A in B. pertussis infection. In contrast, the mechanism of cough induced by B. parapertussis, which produces Vag8 and lipopolysaccharide (LPS) containing lipid A, but not PTx, remained to be elucidated. Here, we show that a toxin we named deacylating autotransporter toxin (DAT) of B. parapertussis inactivates heterotrimeric Gi GTPases through demyristoylation of their α subunits and contributes to cough production along with Vag8 and LPS. These results indicate that DAT plays a role in B. parapertussis infection in place of PTx.Hiramatsu Y., Nishida T., Ota N., et al. DAT (deacylating autotransporter toxin) from Bordetella parapertussis demyristoylates Gαi GTPases and contributes to cough. Proceedings of the National Academy of Sciences of the United States of America 120, e2308260120 (2023); https://doi.org/10.1073/pnas.2308260120

Identification of novel clostridium perfringens type E strains that carry an iota toxin plasmid with a functional enterotoxin gene

Clostridium perfringens enterotoxin (CPE) is a major virulence factor for human gastrointestinal diseases, such as food poisoning and antibiotic associated diarrhea. The CPE-encoding gene (cpe) can be chromosomal or plasmid-borne. Recent development of conventional PCR cpe-genotyping assays makes it possible to identify cpe location (chromosomal or plasmid) in type A isolates. Initial studies for developing cpe genotyping assays indicated that all cpe-positive strains isolated from sickened patients were typable by cpe-genotypes, but surveys of C. perfringens environmental strains or strains from feces of healthy people suggested that this assay might not be useful for some cpe-carrying type A isolates. In the current study, a pulsed-field gel electrophoresis Southern blot assay showed that four cpe-genotype untypable isolates carried their cpe gene on a plasmid of ~65 kb. Complete sequence analysis of the ~65 kb variant cpe-carrying plasmid revealed no intact IS elements and a disrupted cytosine methyltransferase (dcm) gene. More importantly, this plasmid contains a conjugative transfer region, a variant cpe gene and variant iota toxin genes. The toxin genes encoded by this plasmid are expressed based upon the results of RT-PCR assays. The ~65 kb plasmid is closely related to the pCPF4969 cpe plasmid of type A isolates. MLST analyses indicated these isolates belong to a unique cluster of C. perfringens. Overall, these isolates carrying a variant functional cpe gene and iota toxin genes represent unique type E strains. © 2011 Miyamoto et al

Genotoxic Stress Abrogates Renewal of Melanocyte Stem Cells by Triggering Their Differentiation

SummarySomatic stem cell depletion due to the accumulation of DNA damage has been implicated in the appearance of aging-related phenotypes. Hair graying, a typical sign of aging in mammals, is caused by the incomplete maintenance of melanocyte stem cells (MSCs) with age. Here, we report that irreparable DNA damage, as caused by ionizing radiation, abrogates renewal of MSCs in mice. Surprisingly, the DNA-damage response triggers MSC differentiation into mature melanocytes in the niche, rather than inducing their apoptosis or senescence. The resulting MSC depletion leads to irreversible hair graying. Furthermore, deficiency of Ataxia-telangiectasia mutated (ATM), a central transducer kinase of the DNA-damage response, sensitizes MSCs to ectopic differentiation, demonstrating that the kinase protects MSCs from their premature differentiation by functioning as a “stemness checkpoint” to maintain the stem cell quality and quantity