bluuebunny/crossref_metadata_2025_split huggingface dataset:
Black Feminist Philosophy and the Politics of Refusal
Authors: Karera Axelle 
Published: June 2021

Abstract
This chapter discusses the meaning, possibility, and contributions of Black feminist philosophy. The chapter discusses a politics of refusal that characterizes Black women’s theorizing and develops it as a framework for understanding how Black feminist philosophy is more than mere corrective and subversion of mainstream philosophy. As a framework, Black feminist philosophical “politics of refusal” depicts how Black feminist philosophers doing philosophy for Black women and girls refuse to sell themselves short, refuse institutionally imposed intellectual trajectories, and refuse to respond to philosophy’s call to order in their attempts to lay down uncompromisingly Black feminist research agendas in philosophy. The chapter offers an overview of important contributions to the field and discusses how a politics of refusal operates as critique and knowledge production within the field.
Public health activism amid the Covid-19 pandemic: the case of the Alliance of Health Workers
Authors: Macaraan Willard Enrique R 
Published: June 2021

Abstract
In an editorial, the editors note how crucial the role is of public health activism in enforcing efficient and effective public health management. The government is the lead institution in any national response to the pandemic and to ensure transparency on its end, it is important for any network of health organizations and associations not to shy away from embracing an activist role. In this correspondence, the author explores the case of the Alliance of Health Workers, a union of government and private health workers, and its advocacy towards an empowered status of healthcare professionals in the Philippines.
Retracted: Economic viability in free-range chicken production
Authors: Lourençoni Dian , Faustino Amelia Carvalho , Turco Sílvia Helena Nogueira , Bonfim Otoniel Cajuí , Carolina Luana , Silva Rocha E , De Sá Silva Lins Ana Carolina 
Published: June 2021

Abstract
Despite the lack of large-scale farming of free-range chickens in Brazil, their production generates income in the countryside and prevents exodus of rural families in agricultural regions. The objective of this study is to evaluate the economic viability of free-range broiler production in different facilities. The experiment was conducted in two different sheds (masonry shed-SM and wooden shed-SW) located in the Plural Space of the Universidade Federal do Vale São Francisco, municipality of Juazeiro, BA. Here, 200 heavy red French free-range chickens were distributed in the two sheds and were raised from the 1st to the 88th day (slaughter). Assuming that the minimum age for slaughter is 85 days, the results indicated that at least 205 birds in SM and 217 birds in SW were necessary for the producer to earn the minimum per capita monthly wage in Brazil (2020); at least 411 birds in CG and 600 birds in GM were found to be necessary to achieve maximum productivity at the end of the production cycle. The maximum profitability in the slaughter of the chickens was achieved at an age of 60 days.
Determining the effect of the WNT/b‐catenin pathway on the ischemic blood‐brain barrier in vitro and in vivo
Authors: Page Shyanne , Villalba Heidi , Al‐Ahmad Abraham 
Published: June 2021

The blood‐brain barrier (BBB) is a selectively permeable barrier made up of tight junctions formed by endothelial cells that separates the circulating blood from the brain extracellular fluid. The primary function of the BBB is to limit the movement of xenobiotics from the blood to the brain. In the event of an ischemic stroke, the BBB opens allowing water and ions to enter the brain, leading to excitotoxicity and edema formation. Targeting such opening of the barrier following ischemic stroke has become a focus in current stroke studies. It has been shown that the Wnt/b‐catenin pathway is important for barrier formation during embryonic development, therefore, we hypothesized that activation of this pathway following ischemic stroke would attenuate barrier dysfunction. Brain microvascular endothelial cells (BMECs) derived from iPSCs were cultured and placed in ischemic stress for 6hrs, followed by an 18‐hour period of re‐oxygenation. Wnt small molecule activators (CHIR99021 and SB‐216763) and inhibitors (XAV939, IWP‐4, IWR‐1) were introduced at different time points of differentiation, during ischemia, and during re‐oxygenation. Transendothelial Electrical Resistance (TEER) and permeability were performed to assess barrier integrity following re‐oxygenation. For in vivo studies, C57BL mice were subjected to one‐hour ischemia by MCAO. At the time of re‐oxygenation, mice were dosed with CHIR99021 (IP; 30mg/kg). 24‐hours post‐MCAO, TTC staining on brains was performed to determine infarct size and edema ratio. The results of the in vitro studies have shown that activation of the Wnt pathway during re‐oxygenation results in increased barrier function, suggesting that the Wnt pathway is a potential target for post‐stroke therapy.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
A zebrafish FASD model for congenital heart defects
Authors: Marrs James , Sarmah Swapnalee 
Published: June 2021

Mothers who drink during pregnancy expose their developing babies to ethanol, and excessive drinking often produces devastating birth defects collectively termed fetal alcohol spectrum disorder (FASD). These defects include craniofacial defects, cognitive impairment, sensorimotor disabilities and organ deformities, including various congenital heart defects (CHDs), particularly septal and conotruncal defects. Genesis mechanisms for FASD‐associated CHDs are not well understood. Using a zebrafish model, experiments tested whether alcohol interferes with different heart development events or the multiple cardiac precursors that may contribute to CHD genesis. These experiments showed that ethanol affects various cardiac regulatory networks in multiple steps of cardiogenesis (specification, myocardial migration, differentiation, looping, chamber morphogenesis, and endocardial cushion formation). Retinoic acid and folic acid co‐treatment with ethanol had differential rescue effects on FASD‐induced cardiac defects. Early (first heart field) and late‐added (second heart field and cardiac neural crest precursors) cardiac precursors were reduced by ethanol exposure. Experiments showed dysregulation of BMP, Notch and other signaling pathways during atrioventricular valve formation produced persistent valve defects. Together, these results show that embryonic ethanol exposure disrupts critical cardiac morphogenic events and reduce cardiac precursor contributions to the growing heart. Additional mechanistic studies are needed to identify key events that can be targeted therapeutically.Support or Funding InformationNIH/NIAAA AA0022396 and AA026711This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Gait and Mobility Session: Teaching the Neurology and Neuroanatomy of Spinal Cord Injuries
Authors: Vogel Kristine S. , Palm Michael 
Published: June 2021

Medical student knowledge of key ascending and descending pathways (dorsal column/medial lemniscal, spinothalamic, lateral corticospinal) is essential to their ability to identify and assess spinal cord injuries (SCI). In addition, evaluation of gait is an important component of the neurological examination. To incorporate these clinical and neuroanatomical concepts into an interactive session, which is part of an integrated nine‐week neuroscience/neurology/psychiatry module, we combined a gait observation and analysis activity, a review of spinal cord anatomy and lesions, and a question and answer interview with the patient. Before the session, students watched a short, high‐resolution video of the patient, who has a Brown‐Sequard syndrome lesion, navigating stairs and level ground, with and without his cane. They were required to submit at least three observations on the patient's gait and mobility, but were not provided with specific prompts, nor given any information about the location or nature of the lesion. Analysis of over 750 student responses from four years of the module is ongoing, and includes tabulation of lesion localization (e.g. right or left side, upper motor neuron vs. lower motor neuron, cerebral cortex vs. cerebellum vs. spinal cord), aspects of mobility (e.g. use of cane, placement of feet on stairs, turning, balance), and gait descriptors (e.g. circumduction, foot drop, wide‐based). For example, in 2015, 83/213 students correctly identified the side with lower extremity weakness/stiffness, 17/213 identified the incorrect side, and the remainder (113/213) did not indicate the side on which weakness was observed. 66/213 students compared the patient's gait with and without his cane, and 62/213 noted the patient's foot placement while ascending or descending stairs. These classifications of student observations, combined with in‐class analysis and discussion of the video guided by neurology faculty, provide insight into the development of medical student observation skills and familiarity with the neurological examination and terminology. Moreover, the question and answer session with the patient (who is a physician) adds depth to the narrative, and encourages empathy for the mobility challenges faced by individuals who have SCI.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Pathology consultation in the gross anatomy laboratory–rationale and process
Authors: Husain Mujtaba 
Published: June 2021

The gross anatomy laboratory is a rich environment for learners to be exposed to a variety of pathology. In the course of dissection, students and anatomy faculty frequently encounter challenges in determining whether a finding is a normal variant or pathologic process that may or may have not led to the demise of their cadaver donors. The presence of a practicing pathologist faculty is an excellent adjunct to the learning environment, as they provide much needed context to help determine if a finding is normal or abnormal. The pathologist faculty guide the students in forming a differential diagnosis for the cause of death (COD), develop the rationale and indication for tissue biopsy and correlate histopathological with dissection and medical imaging findings. The pathologist also assist the learners in prioritizing all of the pathologic abnormalities as they relate to the COD (terminal, intermediate, and primary diagnoses) simulating a death certificate. Finally, the pathologist faculty facilitates the preparation of a clinico‐pathologic conference style format for student presentations. This mode of education provides an excellent opportunity to link the fundamentals of normal anatomy, learned traditionally in the first year of medical school, to the pathophysiology introduced in the second year of a four‐year curriculum. The process of pathology consultation in the gross anatomy laboratory will be discussed with respect to common scenarios, resources required, and successful communication strategies between the students and the pathology consultantSupport or Funding InformationNone.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Integrating anatomy teaching into the clinical medicine clerkship
Authors: Pasarica Magdalena 
Published: June 2021

Anatomy concepts are highly relevant for clinical teaching in the medical curriculum with many opportunities for implementation and integration. We will discuss here the most clinical relevant anatomical concepts that are relevant to a 3rd year Family Medicine clerkship experience. First, procedures are very important and common in the practice of family medicine. A baseline understanding of anatomy is necessary for procedure training. For example, at our institution, we teach join injections by using models and ultrasound to identify anatomic landmarks and then utilize cadavers for teaching the particular skill of injecting the joint. We also teach Intrauterine device insertion and cervical cytology, and for this we use models to teach the anatomy and to practice the skill. Second, interpreting radiographic studies is essential for any physician. For example, interpreting a chest x‐ray or a CT scan or an ultrasound requires a preliminary discussion of the normal anatomy, followed by pathology with integration of the clinical finding. Third, identifying abnormal pathology during clinical examination requires the knowledge of normal anatomy and pathology. For example, an abnormal musculoskeletal exam requires the knowledge of normal anatomy. As we use these pedagogies in our institutions, we learn about their advantages and disadvantages. One advantage is that the students have the opportunity to apply anatomy concepts in a clinically‐relevant real‐world scenario as they practice their skills, not only to improve their competency, but also their confidence in practicing these skills in the clinical education year and residency training. The disadvantages are that groups have to be small for maximal benefit, and also there are expensive resources to be used in addition to the requirement of knowledgeable facilitators. Other institutions interested in integrating anatomy in teaching pathology and clinical medicine in an active way could benefit from this approach.Support or Funding InformationnoneThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Characterization of the Role of Shroom3 in Nephron Formation
Authors: Kitala Patricia , Cunanan Joanna , Bridgewater Darren 
Published: June 2021

During kidney development the proper formation of the nephron, the functional unit of the kidney, is essential for normal kidney function. Nephrogenesis is the process in which nephron progenitors undergo cell shape changes and mesenchymal‐to‐epithelial transition to form mature nephrons. These cell shape changes are essential for the proper development of the nephron and for proper nephron function. Shroom3 is an actin‐binding protein that regulates epithelial cell shape. It regulates this morphogenesis by binding to F actin and interacting with Rho‐kinase. This leads to the phosphorylation of non‐muscle myosin II activating a signal pathway that causes contraction of the actomysoin network. This contraction causes the cell to form “pie” shaped cells, a process that is essential for tubule formation. Kidneys from shroom3 null mice have numerous abnormal nephrons with collapsing glomeruli at embryonic day E18.5, supporting a role for shroom3 in nephron formation. We hypothesize that Shroom3 is required for mesenchyme cells to cluster and form cell aggregates, pretubular aggregates, and renal vesicles. To support a role for Shroom3 in nephrogenesis we first localized Shroom3 expression. Shroom3 was highly expressed in the aggregating mesenchyme, renal vesicle, and parietal and visceral epithelial cells of the developing glomeruli. In contrast to wild‐type Shroom3 mice, E13.5 kidney histology of Shroom3 mutants demonstrated an increased distance of mesenchymal cells from the neighbouring ureteric bud tip cells (WT 3.85μm ± 0.30, MUT 14.80 μm ±1.22, n=9). These abnormalities were further observed by immunofluorescence (IF) using Six2 and Pax2, specific markers of the mesenchyme aggregates. In E13.5, the IF demonstrated an increased length in the cap mesenchyme (WT 179.6μm ± 24.96, MUT 306.4μm ± 33.30, n=9), and a lack of cap mesenchyme cell aggregation in Shroom3 mutants (WT 8804μm2 ±1250, MUT 12353 μm2 ±1504, n=9). In addition, E18.5 mutants displayed significantly less Six2+ cells in comparison to wild‐types (WT 149 ± 13.3, MUT 79.5 ± 7.47). The analysis for renal vesicles in Shroom3 mutants at E13.5 and E18.5 demonstrated abnormally forming renal vesicles that were few in number when compared to wild‐type (WT 3 ±0.58, MUT 1 ± 0, n=9). Taken together, our findings establish, for the first time, that Shroom3 is essential for the early stages of nephron formation, and suggest these early changes lead to improper migration and clustering of cap mesenchyme cells resulting in abnormal nephrons observed in null mice.Support or Funding InformationCIHR, NSERC, KFOCThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Metabolic Coordination of Tumor Suppression
Authors: Finley Lydia 
Published: June 2021

Increasing evidence demonstrates that intracellular metabolic pathways can be critical drivers of tumor progression. Metabolites provide the biomass required for cancer cell proliferation and contribute to antioxidant defenses that promote survival and metastatic dissemination. Moreover, oncogenic mutations in several metabolic enzymes lead to accumulation of pathological levels of metabolites that interfere with histone and DNA demethylation and impose a block to differentiation. Thus, while the ability of metabolites to contribute directly to malignant progression is well established, whether metabolites can contribute to the cell fate changes that occur during tumor suppression remains an open question. To study the role of metabolism during tumor suppression, we took advantage of a mouse model of pancreatic ductal adenocarcinoma driven by mutant Kras and inducible suppression of p53 to enable temporal control of tumor suppression. Using cell lines derived from these tumors, we found that p53 restoration is accompanied by metabolic alterations that can be uncoupled from changes in cell cycle progression. Recapitulating these metabolic alterations with pharmacologic or genetic interventions in malignant cells is sufficient to phenocopy the effects of p53 restoration on differentiation and tumor progression. These results suggest that p53‐driven metabolic rewiring directly contributes to the cell fate changes that occur during tumor suppression.Support or Funding InformationThis work was supported by the Searle Scholars Program, the Damon Runyon Cancer Research Foundation (DFS‐23‐17) and The Starr Foundation (I11‐0039).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Proteomic Approaches to Better Understand Transcriptional Regulation
Authors: Myers Sam 
Published: June 2021

Cellular differentiation is often driven by gradients of multiple, simultaneous extracellular cues that must be transduced across the membrane, interpreted, and integrated to enact appropriate transcriptional responses. These processes are typically studied by measuring either a small number of proteins or post‐translationally modified sites, or the resultant changes in mRNA levels. While powerful, these approaches overlook hundreds of dynamic signaling events, changes to protein complex composition, and the subcellular localization of regulatory proteins. Here, we will show the interdisciplinary tools and approaches being developed to better understand the principles and mechanisms underlying how signal transduction orchestrates changes in gene expression.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Chlorolipids: Mediators and Outcome Predictors of Sepsis
Authors: Pike Daniel , Hartman Celine , Palladino Elisa , Albert Carolyn , Ford David 
Published: June 2021

Sepsis is a serious cause of morbidity and mortality worldwide. Sepsis is the life‐threatening organ dysfunction caused by the dysregulation of the inflammatory response to an infection. One aspect of this immune response is the systemic activation of neutrophils. Intended to combat microbes through phagocytosis, production of reactive oxygen species, and the release of antimicrobial enzymes through degranulation, neutrophil defense mechanisms can also damage host tissue. Neutrophil myeloperoxidase (MPO) catalyzes the production of hypochlorous acid (HOCl). In addition to microbial targets, HOCl can attack the vinyl ether bond of host membrane plasmalogens, releasing 2‐chlorofatty aldehyde (2‐ClFALD), which is oxidized to 2‐chlorofatty acid (2‐ClFA). Collectively, these plasmalogen oxidation products are members of the chlorolipid family. Human plasma levels of the chlorolipid, 2‐ClFA, predict 30‐day mortality and acute respiratory distress syndrome (ARDS) in sepsis patients. Similarly, septic rats have time‐dependent increases in the plasma, lung, kidney, and intestine levels of 2‐ClFA. For these studies rat sepsis was caused by intraperitoneal injections of 15mL of cecal slurry (isolated from donor rats)/kg body weight. In vitro studies using a click chemistry analog of 2‐ClFA have shown 2‐ClFA localizes to the Weibel‐Palade bodies of human coronary artery endothelial cells and induce the release of their contents. Release of von Willebrand factor, angiopoietin‐2, and P‐ and E‐selectin surface expression were caused by 2‐ClFA exposure to endothelial cells from several vascular beds including human coronary artery endothelial cells and human lung microvascular endothelial cells. The release of these molecules elicits endothelial activation/dysfunction including neutrophil and platelet adherence as well as loss of the endothelial permeability barrier. Additionally, 2‐ClFA induces human neutrophils to release their DNA as neutrophil extracellular traps (NETs) in the process known as NETosis, also implicated in organ failure in sepsis. These in vitro studies with human endothelial cells and human neutrophils suggest 2‐ClFA may mediate the microvascular failure associated with sepsis including endothelial dysfunction and microvascular plugging by NETs. Overall, these studies indicate the importance of chlorolipids in sepsis as prognostic biomarkers of human sepsis outcomes and potential mediators of multi‐organ failure associated with sepsis mortality.Support or Funding InformationFord, PI, Multi‐PI R01 grant (GM115553), Chlorinated lipids in sepsis, NIH Ford, PI, Multi‐PI R01 grant (GM129508), Neutrophil‐dependent mediators of sepsis, NIH Pike, PI, F30 Fellowship grant (F30HL142193), Plasmalogen‐Derived Chlorinated Lipids: Mediators of Acute Lung Injury in Sepsis, NIHThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.