Authentic Narratives of Successful Pathways to Undergraduate Completion for Black Men

This qualitative narrative study examined the authentic lived experiences of eight Black male participants who successfully completed their college undergraduate degree at a private college in the southeast United States. The participants were recruited via LinkedIn, a professional social media, networking site. It explored family, K-12, co-curricular, and community factors that contributed to the academic success of the participants throughout their educational journey. This study drew upon Harper’s (2012) antideficit theory framing the study from the lens of the positive aspects of their academic experiences rather than focusing on the negative aspects of Black men that graduate college at the lowest rate of any subpopulation. This positive lens structured the one main research question, how did they describe their educational experience as a Black man. This question was followed by a series of open ended, semistructured questions to allow the participants to share their authentic stories. The interviews were conducted via Zoom allowing participants to confidentially share their authentic lived experiences. The eight participants disclosed significant influences leading to three categories or themes: Influential, Systemic, and Personal Investment. These themes emerged from their stories through analysis of the data highlighting the intrinsic and extrinsic support. Recommended actions provided to assist K-12 and college-level administrators in designing strategies for preparing and supporting Black men on their pathway to successful college completion

The Impact of Nursing Staff Adherence with Chlorhexidine Gluconate Bathing on Intensive Care Unit Patient Outcomes

Purpose: The purpose of this study is to evaluate nursing staff adherence to a chlorhexidine gluconate (CHG) bathing protocol in the intensive care unit at Norton Brownsboro Hospital. Methods: This study utilized a single-site, quasi-experimental, retrospective electronic medical record review format. The sample consisted of 200 patient records post CHG bathing protocol initiation from the Norton Brownsboro Hospital Intensive Care Unit during the period of March, 2015 to May, 2017. Results: The sample was divided into adherent and non-adherent groups. No significant differences in age, sex, race, ICU length of stay (LOS), BMI, or mortality scores, presence of indwelling medical device, or surgical procedure performed existed between the adherent and non-adherent groups. Adherence was low with only 61 or 30.5% of patients receiving CHG bathing as prescribed. No statistically significant relationship was identified between CHG bathing adherence and patient variables.Only three HAIs were captured in the sample; all were catheter-associated urinary tract infections (CAUTIs) in the adherent group. Conclusion: Low adherence and lack of statistical significance may indicate a charting discrepancy by ICU nursing staff. It is also reasonable to consider that this study is an actual reflection of the adherence rate. Education, chart audits, and change moles such as Plan-Do-Study-Act (PDSA) should be considered to optimize nursing staff adherence with CHG bathing

Successful Pathways to Undergraduate Completion

This article explores the critical factors that led to successful college completion for Black men. By focusing on success factors from Black male college graduates\u27 lived experiences, a roadmap to college success for this group may be shared with others to encourage increased degree attainment for this population. The lens for this study drew from Harper’s (2012) antideficit theory, which highlights students’ successes rather than problematic issues. A non-random approach of purposeful sampling from eight Black men from LinkedIn who had completed an undergraduate degree from a private, predominately White college in the southeast United States defined the sample size. Using one-on-one interviews, participants\u27 internal and external experiences leading up to and through college were revealed. The study will address their academic success in achieving undergraduate degree attainment. The first two categories, pre-college socialization and readiness and college achievement are the focus of this study

Soluble tau species, not neurofibrillary aggregates, disrupt neural system integration in a tau transgenic model

Neurofibrillary tangles are a feature of Alzheimer disease and other tauopathies, and while they are generally believed to be markers of neuronal pathology, there is little evidence evaluating whether tangles directly impact neuronal function. To investigate the response of cells in hippocampal circuits to complex behavioral stimuli, we used an environmental enrichment paradigm to induce expression of an immediate-early gene, Arc, in the rTg4510 mouse model of tauopathy. These mice reversibly overexpress P301L tau and exhibit substantial neurofibrillary tangle deposition, neuronal loss, and memory deficits. Employing fluorescent in situ hybridization to detect Arc mRNA, we found that rTg4510 mice have impaired hippocampal Arc expression both without stimulation and in response to environmental enrichment; this likely reflects the combination of functional impairments of existing neurons and loss of neurons. However, tangle-bearing cells were at least as likely as non-tangle-bearing neurons to exhibit Arc expression in response to enrichment. Transgene suppression with doxycycline for 6 weeks resulted in increased percentages of Arc-positive cells in rTg4510 brains compared to untreated transgenics, restoring enrichment-induced Arc mRNA levels to that of wild-type controls despite the continued presence of neurofibrillary pathology. We interpret these data to indicate that soluble tau contributes to impairment of hippocampal function, while tangles do not preclude neurons from responding in a functional circuit

Alzheimer's disease: synapses gone cold

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by insidious cognitive decline and memory dysfunction. Synapse loss is the best pathological correlate of cognitive decline in AD and mounting evidence suggests that AD is primarily a disease of synaptic dysfunction. Soluble oligomeric forms of amyloid beta (Aβ), the peptide that aggregates to form senile plaques in the brain of AD patients, have been shown to be toxic to neuronal synapses both in vitro and in vivo. Aβ oligomers inhibit long-term potentiation (LTP) and facilitate long-term depression (LTD), electrophysiological correlates of memory formation. Furthermore, oligomeric Aβ has also been shown to induce synapse loss and cognitive impairment in animals. The molecular underpinnings of these observations are now being elucidated, and may provide clear therapeutic targets for effectively treating the disease. Here, we review recent findings concerning AD pathogenesis with a particular focus on how Aβ impacts synapses

The Endowment Effect in Orangutans

The endowment effect is the tendency to, seemingly irrationally, immediately value a possessed item more than the opportunity to acquire the identical item when one does not already possess it. Although endowment effects are reported in chimpanzees (Brosnan, Jones, Lambeth, Mareno, Richardson, & Shapiro, 2007) and capuchin monkeys (Lakshminarayanan, Chen, & Santos, 2008), both species share social traits with humans that make convergence as likely an evolutionary mechanism as homology. Orangutans (Pongo spp.) provide a unique insight into the evolution of the endowment effect, along with other apparently irrational behaviors, because their less frequent social interactions and relatively more solitary social organization distinguishes them from the more gregarious apes, allowing a test of evolutionary homology. In the present study, we used pairs of both food and non-food objects, as in an earlier test on chimpanzees (Brosnan et al., 2007). We established the apes’ preferences in forced-choice tasks, then tested whether they showed an endowment effect in an exchange task, in which subjects were given one of the objects, followed by the option to exchange it for the other. Here, we report the first evidence of the endowment effect in a relatively less social primate, the orangutan. This indicates that this behavior may have evolved as a homology within the primates, rather than being due to convergent social pressures. These findings provide stronger evidence for the hypothesis that at least one bias, the endowment effect, may be common in primates and, potentially, other species

Propagation of tau pathology in Alzheimer’s disease: identification of novel therapeutic targets

Accumulation and aggregation of the microtubule-associated protein tau are a pathological hallmark of neurodegenerative disorders such as Alzheimer’s disease (AD). In AD, tau becomes abnormally phosphorylated and forms inclusions throughout the brain, starting in the entorhinal cortex and progressively affecting additional brain regions as the disease progresses. Formation of these inclusions is thought to lead to synapse loss and cell death. Tau is also found in the cerebrospinal fluid (CSF), and elevated levels are a biomarker for AD. Until recently, it was thought that the presence of tau in the CSF was due to the passive release of aggregated tau from dead or dying tangle-bearing neurons. However, accumulating evidence from different AD model systems suggests that tau is actively secreted and transferred between synaptically connected neurons. Transgenic mouse lines with localized expression of aggregating human tau in the entorhinal cortex have demonstrated that, as these animals age, tau becomes mislocalized from axons to cell bodies and dendrites and that human tau-positive aggregates form first in the entorhinal cortex and later in downstream projection targets. Numerous in vitro and in vivo studies have provided insight into the mechanisms by which tau may be released and internalized by neurons and have started to provide insight into how tau pathology may spread in AD. In this review, we discuss the evidence for regulated tau release and its specific uptake by neurons. Furthermore, we identify possible therapeutic targets for preventing the propagation of tau pathology, as inhibition of tau transfer may restrict development of tau tangles in a small subset of neurons affected in early stages of AD and therefore prevent widespread neuron loss and cognitive dysfunction associated with later stages of the disease

Inhibition of Sirtuin 2 with Sulfobenzoic Acid Derivative AK1 is Non-Toxic and Potentially Neuroprotective in a Mouse Model of Frontotemporal Dementia

Tauopathies including tau-associated Frontotemporal dementia (FTD) and Alzheimer’s disease are characterized pathologically by the formation of tau-containing neurofibrillary aggregates and neuronal loss, which contribute to cognitive decline. There are currently no effective treatments to prevent or slow this neural systems failure. The rTg4510 mouse model, which expresses a mutant form of the tau protein associated with FTD with Parkinsonism-17, undergoes dramatic hippocampal and cortical neuronal loss making it an ideal model to study treatments for FTD-related neuronal loss. Sirtuins are a family of proteins involved in cell survival that have the potential to modulate neuronal loss in neurodegenerative disorders. Here we tested the hypothesis that sirtuin 2 (SIRT2) inhibition would be non-toxic and prevent neurodegeneration in rTg4510 brain. In this study we delivered SIRT2 inhibitor AK1 directly to the hippocampus with an osmotic minipump and confirmed that it reached the target region both with histological assessment of delivery of a dye and with a pharmacodynamic marker, ABCA1 transcription, which was upregulated with AK1 treatment. AK1 treatment was found to be safe in wild-type mice and in the rTg4510 mouse model, and further, it provided some neuroprotection in the rTg4510 hippocampal circuitry. This study provides proof-of-concept for therapeutic benefits of SIRT2 inhibitors in both tau-associated FTD and Alzheimer’s disease, and suggests that development of potent, brain permeable SIRT2 inhibitors is warranted

Modulation of the Intestinal Microbiota Alters Colitis-Associated Colorectal Cancer Susceptibility

It is well established that the intestinal microbiota plays a key role in the pathogenesis of Crohn's disease (CD) and ulcerative colitis (UC) collectively referred to as inflammatory bowel disease (IBD). Epidemiological studies have provided strong evidence that IBD patients bear increased risk for the development of colorectal cancer (CRC). However, the impact of the microbiota on the development of colitis-associated cancer (CAC) remains largely unknown. In this study, we established a new model of CAC using azoxymethane (AOM)-exposed, conventionalized-Il10−/− mice and have explored the contribution of the host intestinal microbiota and MyD88 signaling to the development of CAC. We show that 8/13 (62%) of AOM-Il10−/− mice developed colon tumors compared to only 3/15 (20%) of AOM- wild-type (WT) mice. Conventionalized AOM-Il10−/− mice developed spontaneous colitis and colorectal carcinomas while AOM-WT mice were colitis-free and developed only rare adenomas. Importantly, tumor multiplicity directly correlated with the presence of colitis. Il10−/− mice mono-associated with the mildly colitogenic bacterium Bacteroides vulgatus displayed significantly reduced colitis and colorectal tumor multiplicity compared to Il10−/− mice. Germ-free AOM-treated Il10−/− mice showed normal colon histology and were devoid of tumors. Il10−/−; Myd88−/− mice treated with AOM displayed reduced expression of Il12p40 and Tnfα mRNA and showed no signs of tumor development. We present the first direct demonstration that manipulation of the intestinal microbiota alters the development of CAC. The TLR/MyD88 pathway is essential for microbiota-induced development of CAC. Unlike findings obtained using the AOM/DSS model, we demonstrate that the severity of chronic colitis directly correlates to colorectal tumor development and that bacterial-induced inflammation drives progression from adenoma to invasive carcinoma