Intraracialized, Anti-Queer Microaggressions Towards Queer Black Men Research Prospectus

Microaggressions are the everyday verbal, nonverbal, and environmental slights, snubs, or insults, whether intentional or unintentional, that communicate hostile, derogatory, or negative messages to target persons based solely upon their marginalized group membership (Sue et al., 2007). As intersectional microaggression research remains understudied (Sterzing et al., 2017), the purpose of this project is to extend the platform by documenting the experiences that Queer Black males experience from microaggressions intraracially in their communities. Through qualitative research and an intersectional framework, I plan to examine the impacts, experiences, and coping methods that Queer Black men encounter from intersectional microaggressions, and additionally code how anti-Queer language is presented within Black vernacular language. Intersectional microaggression research is of high importance because prior research fails to take notice of the microaggressions that intersecting identity individuals encounter (Sterzing et. al., 2017). Although they might be invisible and subtle, microaggressions are truly damaging

Anti-Queer Microaggressions Towards Queer Black Men

Microaggressions are reoccurring derogatory messages that degrade and/ or discredit one’s identity. While invisible and unknown to many, they remain visible and apparent to those impacted by them. The research questions for this project are: (1) What microaggressions do Queer Black men experience within larger society? (2) To contrast with larger society, what microaggressions do Queer Black men experience within Black communities? By conducting focus groups, I will examine the intersectional microaggressions that Queer Black males experience in their own community, as well as document microaggression that they experience in larger society. After conducting my focus groups, I will be adopting Derald Wing Sue’s taxonomy of microaggression themes to translate the underlying messages behind delivered microaggressions. The results in this study will aide in addressing an appeared gap within microaggression literature by, documenting how Queer Black males experience these muted, normalized insults and invalidations in societ

(Kid) Gloves On or Off? Academic Conflict in Research Articles Across the Disciplines

El estudio interdisciplinar que se presenta en este artículo continúa en la línea de recientes investigaciones del conflicto académico. Examinamos artículos de investigación de seis disciplinas distintas. De los datos obtenidos, desarrollamos una taxonomía de las estrategias retóricas que emplean los autores en estos campos para expresar el conflicto académico, incluyendo el concepto de mediación del “redactor” en la expresión de la crítica. La aplicación de esta taxonomía mostró que disciplinas con contactos fuera de la comunidad académica normalmente evitaban o mitigaban la crítica, pero por otro lado no se pudo establecer ninguna otra correlación. Sugerimos que sucesivas investigaciones deberían aplicar un enfoque más cualitativo y tener más en cuenta la recepción.The interdisciplinary study of academic conflict (AC) presented in this paper expands on a growing body of research. We examined research articles from six distinct disciplines. From the data obtained, we developed a taxonomy of the rhetorical strategies used by the writers in these fields, expanding on earlier work by introducing the concept of writer mediation. The application of this taxonomy to the disciplines showed that those with extra-mural ties were more likely to avoid or mitigate AC, but few other correlations were discernible. It is suggested that future research on AC should take a qualitative approach and that more attention should be paid to reception

Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke

BACKGROUND: While gelatinase (MMP-2 and -9) activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown. RESULTS: Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9) expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change. CONCLUSION: The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke

Delayed minocycline inhibits ischemia-activated matrix metalloproteinases 2 and 9 after experimental stroke

BACKGROUND: Matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9) are increased in the brain after experimental ischemic stroke in rats. These two proteases are involved with the degradation of the basal lamina and loss of stability of the blood brain barrier that occurs after ischemia and that is associated with thrombolytic therapy in ischemic stroke. Minocycline is a lipophilic tetracycline and is neuroprotective in several models of brain injury. Minocycline inhibits inflammation, apoptosis and extracellular matrix degradation. In this study we investigated whether delayed minocycline inhibits brain MMPs activated by ischemia in a model of temporary occlusion in Wistar rats. RESULTS: Both MMP-2 and MMP-9 were elevated in the ischemic tissue as compared to the contra-lateral hemisphere after 3 hours occlusion and 21 hours survival (p < 0.0001 for MMP-9). Intraperitoneal minocycline at 45 mg/kg concentration twice a day (first dose immediately after the onset of reperfusion) significantly reduced gelatinolytic activity of ischemia-elevated MMP-2 and MMP-9 (p < 0.0003). Treatment also reduced protein concentration of both enzymes (p < 0.038 for MMP-9 and p < 0.018 for MMP-2). In vitro incubation of minocycline in concentrations as low as 0.1 μg/ml with recombinant MMP-2 and MMP-9 impaired enzymatic activity and MMP-9 was more sensitive at lower minocycline concentrations (p < 0.05). CONCLUSION: Minocycline inhibits enzymatic activity of gelatin proteases activated by ischemia after experimental stroke and is likely to be selective for MMP-9 at low doses. Minocycline is a potential new therapeutic agent to acute treatment of ischemic stroke

Increased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model type 2 diabetes

<p>Abstract</p> <p>Background</p> <p>Interruption of flow through of cerebral blood vessels results in acute ischemic stroke. Subsequent breakdown of the blood brain barrier increases cerebral injury by the development of vasogenic edema and secondary hemorrhage known as hemorrhagic transformation (HT). Diabetes is a risk factor for stroke as well as poor outcome of stroke. The current study tested the hypothesis that diabetes-induced changes in the cerebral vasculature increase the risk of HT and augment ischemic injury.</p> <p>Methods</p> <p>Diabetic Goto-Kakizaki (GK) or control rats underwent 3 hours of middle cerebral artery occlusion and 21 h reperfusion followed by evaluation of infarct size, hemorrhage and neurological outcome.</p> <p>Results</p> <p>Infarct size was significantly smaller in GK rats (10 ± 2 vs 30 ± 4%, p < 0.001). There was significantly more frequent hematoma formation in the ischemic hemisphere in GK rats as opposed to controls. Cerebrovascular tortuosity index was increased in the GK model (1.13 ± 0.01 vs 1.34 ± 0.06, P < 0.001) indicative of changes in vessel architecture.</p> <p>Conclusion</p> <p>These findings provide evidence that there is cerebrovascular remodeling in diabetes. While diabetes-induced remodeling appears to prevent infarct expansion, these changes in blood vessels increase the risk for HT possibly exacerbating neurovascular damage due to cerebral ischemia/reperfusion in diabetes.</p