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This study examines the impact of a cultural center on students' views and perceptions of their own cultural competency learning and ability to manage their college experience at a large metropolitan university. This exploratory analysis highlights the views of ten students who frequently engaged with a cultural center. Emerging themes include: (a) how students at a metropolitan university defined cultural competence; (b) challenges, difficulties, and problems participants experienced interacting with people from other cultures (e.g. nationality, ethnicity); and (c) successful interactions participants experienced with people from other cultures. Findings and discussion from this study suggest: (a) identity, exposure, and critical awareness; (b) navigating and negotiating conflict; and (c) engaging cultural resources are the skills students develop, through experiences with a cultural center, that impact their ability to manage their college experience. This project studied a culturally mixed group of students using personal experiences, interviews, and focus group discussions to describe meaningful and defining moments. This study and its findings are noteworthy because there is little research in this subject area. All participants were frank, cooperative, and candid throughout the process. They offered insights and shared information regarding cultural competency at Metropolitan University (MU).

In study abroad programs, overall student participation and the representation of minoritized students continue to rise, but barriers to participation for minoritized students persist, especially in engineering. As we strive to broaden participation in engineering study abroad programs, we must critically examine the experiences of minoritized students who engage in these programs so we can facilitate supportive educational environments. This study examines the experiences of minoritized students in a global engineering study abroad program, using the concept of habitus, a student's collection of identities and embodied cultural capital. We find that students draw on various forms of habitus while studying abroad, connecting their new experiences abroad to their prior experiences. Based on these findings, we make recommendations for designing more equitable and inclusive study abroad programming elements.

IntroductionIndole-3-carbinol (I3C) is found in cruciferous vegetables and used as a dietary supplement. It is known to act as a ligand for aryl hydrocarbon receptor (AhR). In the current study, we investigated the role of AhR and the ability of I3C to attenuate LPS-induced Acute Respiratory Distress Syndrome (ARDS).MethodsTo that end, we induced ARDS in wild-type C57BL/6 mice, Ccr2gfp/gfp KI/KO mice (mice deficient in the CCR2 receptor), and LyZcreAhRfl/fl mice (mice deficient in the AhR on myeloid linage cells). Additionally, mice were treated with I3C (65 mg/kg) or vehicle to investigate its efficacy to treat ARDS.ResultsI3C decreased the neutrophils expressing CXCR2, a receptor associated with neutrophil recruitment in the lungs. In addition, LPS-exposed mice treated with I3C revealed downregulation of CCR2+ monocytes in the lungs and lowered CCL2 (MCP-1) protein levels in serum and bronchoalveolar lavage fluid. Loss of CCR2 on monocytes blocked the recruitment of CXCR2+ neutrophils and decreased the total number of immune cells in the lungs during ARDS. In addition, loss of the AhR on myeloid linage cells ablated I3C-mediated attenuation of CXCR2+ neutrophils and CCR2+ monocytes in the lungs from ARDS animals. Interestingly, scRNASeq showed that in macrophage/monocyte cell clusters of LPS-exposed mice, I3C reduced the expression of CXCL2 and CXCL3, which bind to CXCR2 and are involved in neutrophil recruitment to the disease site.DiscussionThese findings suggest that CCR2+ monocytes are involved in the migration and recruitment of CXCR2+ neutrophils during ARDS, and the AhR ligand, I3C, can suppress ARDS through the regulation of immune cell trafficking.

IntroductionThere is a critical need to foster inclusive educational spaces for Queer identifying students and to resist oppressive structures that seek to marginalize and inflict trauma on students because of their gender or sexual identity.MethodsDrawing on thematic analysis and Queer theory, we interviewed 11 Queer identifying STEM students to understand the navigational strategies they leveraged within higher education environments related to their Queer identity.ResultsWe developed a cyclical model of navigational strategies employed by Queer STEM students that involved evaluating the environments, performing psychological identity calculations, and engaging in behavioral actions. Students evaluated the environment by attending to the diversity of gender representation, presence of other Queer individuals, and contextual factors conveyed based on disciplinary expectations. Students engaged in psychological identity calculations whereby they assessed beliefs about the relevance, importance, and fears related to their Queer identity, with few perceiving any benefits. Behavioral actions resulted in students building a chosen community, disclosing or shelving their queer identity, and advocating for representation.DiscussionIn order to support Queer students to thrive in educational contexts, researchers and practitioners should examine ways to increase representation, use inclusive pedagogical strategies, and understand the relevance of Queerness within disciplinary fields. Questioning the relevance or presence of Queerness in higher education environments only further serves to oppress, inflict trauma, and marginalize Queer students.

Background: Research experiences for undergraduate and graduate students have the potential to provide significant learning experiences, but most research of these experiences focuses primarily on their outcomes. To better design such experiences for a diverse range of students, it is important to understand student narratives of researcher development and identify significant experiences in their development as researchers. Purpose: In this study, we explored narratives of researcher development for seven US civil engineering students in an eight-week research experience in Australia. Through these narratives, we sought to identify categories of significant experiences to characterize the early stage of the researcher development process. Method: Each student participated in a series of interviews throughout the program, which were used to construct narratives about their research experiences. Results: We identified several common significant experiences across the students’ narratives but observed that students navigated their fit within the research environment in different ways. We interpret these differences in the narratives using Person-Environment Fit theory and argue that this theory can support a complex analysis of students’ experiences in educational environments. Conclusions: Our findings suggest that assessing Person-Environment Fit is an important part of the early stages of researcher development. We recommend that the design of research programs should intentionally consider different levels of the environment and ensure sufficient challenge and support so that students can assess their fit with research as a career.

Graduate education in engineering is an extremely challenging, complex entity that is difficult to change. The purpose of this exploratory research paper was to investigate the applicability of the Collective Impact framework, which has been used within community organizing contexts, to organize the change efforts of a center focused on advancing equitable graduate education within engineering. We sought to understand how the conditions of Collective Impact (i.e., common agenda, backbone organization, mutually reinforcing activities, shared measurement system, and continuous communication) could facilitate the organization of equity-focused change efforts across a college of engineering at a single institution. To achieve this, we took an action research approach. We found the Collective Impact framework to be a useful tool for organizing cross-sectional partnerships to facilitate equity-focused change in graduate education; we also found the five conditions of Collective Impact to be applicable to the higher education context, with some intentional considerations and modifications. Through coordinated efforts, the Collective Impact framework can support the goal of reorienting existing decentralized structures, resource flows, and decision processes to foster bottom-up and top-down change processes to advance equitable support for graduate students.

This paper describes the redesign process for a Principal Preparation Program (PPP) that is grounded in strong service-learning elements and evidence-based outcomes. The PPP design team developed the Service Leadership Framework for Leadership Preparation (SLF4LP) which blends research-based service learning and servant leadership principles (Felten & Clayton, 2011; Greenleaf, 1990; Henderson & Mapp, 2002). The PPP and its faculty have a rich tradition of excellence in teaching, scholarship, and service. To preserve this legacy, the redesign process maintained a positive culture of teamwork, partnership, and collaboration among candidates, colleagues, administrators, and external stakeholders. An overview of the value-added SLF4LP components will be provided and the impact of each component will be discussed.

ABSTRACT Acute respiratory distress syndrome (ARDS) is triggered by a variety of insults, including bacterial and viral infections, and this leads to high mortality. While the role of the aryl hydrocarbon receptor (AhR) in mucosal immunity is being increasingly recognized, its function during ARDS is unclear. In the current study, we investigated the role of AhR in LPS-induced ARDS. AhR ligand, indole-3-carbinol (I3C), attenuated ARDS which was associated with a decrease in CD4+ RORγt +IL-17a+IL-22+ pathogenic Th17 cells, but not CD4+RORγt +IL-17a+IL-22− homeostatic Th 17 cells, in the lungs. AhR activation also led to a significant increase in CD4+IL-17a−IL-22+ Th22 cells. I3C-mediated Th22 cell expansion was dependent on the AhR expression on RORγt+ cells. AhR activation downregulated miR-29b-2-5p in immune cells from the lungs, which in turn downregulated RORc expression and upregulated IL-22. Collectively, the current study suggests that AhR activation can attenuate ARDS and may serve as a therapeutic modality by which to treat this complex disorder. IMPORTANCE Acute respiratory distress syndrome (ARDS) is a type of respiratory failure that is triggered by a variety of bacterial and viral infections, including the coronavirus SARS-CoV2. ARDS is associated with a hyperimmune response in the lungs that which is challenging to treat. Because of this difficulty, approximately 40% of patients with ARDS die. Thus, it is critical to understand the nature of the immune response that is functional in the lungs during ARDS as well as approaches by which to attenuate it. AhR is a transcription factor that is activated by a variety of endogenous and exogenous environmental chemicals as well as bacterial metabolites. While AhR has been shown to regulate inflammation, its role in ARDS is unclear. In the current study, we provide evidence that AhR activation can attenuate LPS-mediated ARDS through the activation of Th22 cells in the lungs, which are regulated through miR-29b-2-5p. Thus, AhR can be targeted to attenuate ARDS.

Microglia are found pathologically at all stages of multiple sclerosis (MS) lesion development and are hypothesized to contribute to both inflammatory injury and neuroprotection in the MS brain. Transient receptor potential vanilloid 4 (TRPV4) channels are widely expressed, play an important role as environmental sensors, and are involved in calcium homeostasis for a variety of cells. TRPV4 modulates myeloid cell phagocytosis in the periphery and microglial motility in the central nervous system. We hypothesized that TRPV4 deletion would alter microglia phagocytosis in vitro and lessen disease activity and demyelination in experimental autoimmune encephalitis (EAE) and cuprizone-induced demyelination. We found that genetic deletion of TRPV4 led to increased microglial phagocytosis in vitro but did not alter the degree of demyelination or remyelination in the cuprizone mouse model of MS. We also found no difference in disease in EAE following global or microglia-specific deletion of Trpv4. Additionally, lesioned and normal appearing white matter from MS brains exhibited similar TRPV4 expression compared to healthy brain tissue. Taken together, these findings indicate that TRPV4 modulates microglial activity but does not impact disease activity in mouse models of MS, suggesting a muted and/or redundant role in MS pathogenesis.

A major therapeutic goal in demyelinating diseases, such as Multiple Sclerosis, is to improve remyelination, thereby restoring effective axon conduction and preventing neurodegeneration. In the adult central nervous system (CNS), parenchymal oligodendrocyte progenitor cells (pOPCs) and, to a lesser extent, pre-existing oligodendrocytes (OLs) and oligodendrocytes generated from neural stem cells (NSCs) in the sub-ventricular zone (SVZ) are capable of forming new myelin sheaths. Due to their self-renewal capabilities and the ability of their progeny to migrate widely within the CNS, NSCs represent an additional source of remyelinating cells that may be targeted to supplement repair by pOPCs. However, in demyelinating disorders and disease models, the NSC contribution to myelin repair is modest and most evident in regions close to the SVZ. We hypothesized that NSC-derived cells may compete with OPCs to remyelinate the same axons, with pOPCs serving as the primary remyelinating cells due to their widespread distribution within the adult CNS, thereby limiting the contribution of NSC-progeny. Here, we have used a dual reporter, genetic fate mapping strategy, to characterize the contribution of pOPCs and NSC-derived OLs to remyelination after cuprizone-induced demyelination. We confirmed that, while pOPCs are the main remyelinating cells in the corpus callosum, NSC-derived cells are also activated and recruited to demyelinating lesions. Blocking pOPC differentiation genetically, resulted in a significant increase in the recruitment NSC-derived cells into the demyelinated corpus callosum and their differentiation into OLs. These results strongly suggest that pOPCs and NSC-progeny compete to repair white matter lesions. They underscore the potential significance of targeting NSCs to improve repair when the contribution of pOPCs is insufficient to affect full remyelination.

The aryl hydrocarbon receptor (AhR) is a ubiquitously expressed ligand-activated transcription factor. While initially identified as an environmental sensor, this receptor has been shown more recently to regulate a variety of immune functions. AhR ligands vary in structure and source from environmental chemicals such as 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and indoles found in cruciferous vegetables to endogenous ligands derived from tryptophan metabolism. In the current study, we used TCDD, a high affinity AhR ligand to study the impact of AhR activation in the murine model of autoimmune hepatitis (AIH). Primarily, we used single-cell RNA-sequencing (scRNA-seq) technology to study the nature of changes occurring in the immune cells in the liver at the cellular and molecular level. We found that AhR activation attenuated concanavalin A (ConA)-induced AIH by limiting chemotaxis of pro-inflammatory immune cell subsets, promoting anti-inflammatory cytokine production, and suppressing pro-inflammatory cytokine production. scRNA-seq analysis showed some unusual events upon ConA injection such as increased presence of mature B cells, natural killer (NK) T cells, CD4+ or CD8+ T cells, Kupffer cells, memory CD8+ T cells, and activated T cells while TCDD treatment led to the reversal of most of these events. Additionally, the immune cells showed significant alterations in the gene expression profiles. Specifically, we observed downregulation of inflammation-associated genes including Ptma, Hspe1, and CD52 in TCDD-treated AIH mice as well as alterations in the expression of migratory markers such as CXCR2. Together, the current study characterizes the nature of inflammatory changes occurring in the liver during AIH, and sheds light on how AhR activation during AIH attenuates liver inflammation by inducing phenotypic and genotypic changes in immune cells found in the liver.

The telomere G-strand binding protein Pot1 plays multifaceted roles in telomere maintenance and protection. We examined the structure and activities of Pot1 in Ustilago maydis, a fungal model that recapitulates key features of mammalian telomere regulation. Compared to the well-characterized primate and fission yeast Pot1 orthologs, UmPot1 harbors an extra N-terminal OB-fold domain (OB-N), which was recently shown to be present in most metazoans. UmPot1 binds directly to Rad51 and regulates the latter's strand exchange activity. Deleting the OB-N domain, which is implicated in Rad51-binding, caused telomere shortening, suggesting that Pot1-Rad51 interaction facilitates telomere maintenance. Depleting Pot1 through transcriptional repression triggered growth arrest as well as rampant recombination, leading to multiple telomere aberrations. In addition, telomere repeat RNAs transcribed from both the G- and C-strand were dramatically up-regulated, and this was accompanied by elevated levels of telomere RNA-DNA hybrids. Telomere abnormalities of pot1-deficient cells were suppressed, and cell viability was restored by the deletion of genes encoding Rad51 or Brh2 (the BRCA2 ortholog), indicating that homology-directed repair (HDR) proteins are key mediators of telomere aberrations and cellular toxicity. Together, these observations underscore the complex physical and functional interactions between Pot1 and DNA repair factors, leading to context-dependent and dichotomous effects of HDR proteins on telomere maintenance and protection.

Yu et al. provide evidence that Ustilago maydis employs two structurally distinct telomere-binding proteins to perform complementary functions in telomere maintenance in this organism. While UmTay1 regulates primarily telomere replication and recombination, UmTrf2 is responsible for telomere protection.

Managing the vast amounts of eggshell and sea-shell waste that is produced globally each year is becoming very problematic as this material is simply disposed of in landfills. This waste results in odor production and microbial growth directly leading to environmental stresses. Transforming this waste into valuable biomaterials pose significant environmental and economic advantages as discarded waste have materials that can be utilized. The objective of this work was to develop inexpensive, bioactive hydroxyapatite-based scaffolds for tissue engineering applications by using an eco-friendly and sustainable approach. Engineering nano hydroxyapatite (EnHA) was derived from chicken eggshell and clam sea-shell waste by using an energy efficient microwave assisted wet chemical precipitation method. X-ray diffraction (XRD), Field emission scanning electron microscopy (FESEM), Transmission electron microscopy (TEM), and Energy dispersive spectroscopy (EDS) were used to analyze the biomaterials. Results show that the particles are highly crystalline hydroxyapatite (HA) with acicular shapes and within nanometer size ranges. The chemical compositions match exactly that of naturally occurring HA. The EnHA infused polymer scaffolds were fabricated using slurry-based solution 3D printing techniques. The slurry solutions composed of 70 wt% EnHA and 30 wt% Polycarpolactone (PCL). The XRD, SEM, EDS, and in vitro cell studies were conducted to determine the ability of the scaffolds to support cell adhesion and maintain viability. The scaffolds supported cellular attachment and maintenance when observed over a period of several days, suggesting their potential for future tissue regeneration research and applications.

Abstract Background Racial minority children, particularly from low-income households, are at risk for obesity. Family meals have a protective effect on child nutritional health. However, the current evidence is limited in racial and socioeconomic diversity. The objective of this study was to evaluate the impact of a family meals intervention, Simple Suppers, on improvements in diet and health outcomes from baseline (T0) to post-intervention (T1) in intervention compared to waitlist control participants, and determine retention of change in outcomes among intervention participants at 10-week follow-up (T2). Methods Simple Suppers was a 10-week family meals intervention implemented as a 2-group quasi-experimental trial. Ten 90-min lessons were delivered weekly. Data were collected at T0 and T1, and from intervention participants at T2. Participants were racially diverse 4–10 year-old children from low-income households. Setting was a faith-based community center. Main outcomes were daily servings of fruit, vegetables, and sugar-sweetened beverages and diet quality; z-scores for body mass index (BMI), waist circumference, systolic and diastolic blood pressure (BP); weight status categories; food preparation skills; and family meals (frequency of dinner, breakfast, TV viewing during meals, meals in dining area). Generalized linear mixed models (GLMMs) and mixed-effects ordinal regression models were used to assess intervention impact (T0:T1). Paired t-tests examined retention of change among intervention participants (T1:T2). Results One hundred forty children enrolled and 126 completed T1 (90% retention); 71 of 87 intervention participants completed T2(79% retention). Mean (SD) age was 6.9(1.9) yr, 62% female, 60% Black, and 42% low-income. Intervention vs waitlist controls had higher food preparation skills (p

The success of ocrelizumab in reducing confirmed disability accumulation in primary progressive multiple sclerosis (PPMS) via CD20-targeted depletion implicates B cells as causal agents in the pathogenesis of PPMS. This review explores the possible mechanisms by which B cells contribute to disease progression in PPMS, specifically exploring cytokine production, antigen presentation, and antibody synthesis. B cells may contribute to disease progression in PPMS through cytokine production, specifically GM-CSF and IL-6, which can drive naïve T-cell differentiation into pro-inflammatory Th1/Th17 cells. B cell production of the cytokine LT-α may induce follicular dendritic cell production of CXCL13 and lead indirectly to T and B cell infiltration into the CNS. In contrast, production of IL-10 by B cells likely induces an anti-inflammatory effect that may play a role in reducing neuroinflammation in PPMS. Therefore, reduced production of IL-10 may contribute to disease worsening. B cells are also capable of potent antigen presentation and may induce pro-inflammatory T-cell differentiation via cognate interactions. B cells may also contribute to disease activity via antibody synthesis, although it's unlikely the benefit of ocrelizumab in PPMS occurs via antibody decrement. Finally, various B cell subsets likely promulgate pro- or anti-inflammatory effects in MS.

ObjectiveEarly-onset epileptic encephalopathies have been associated with de novo mutations of numerous ion channel genes. We employed techniques of modern translational medicine to identify a disease-causing mutation, analyze its altered behavior, and screen for therapeutic compounds to treat the proband.MethodsThree modern translational medicine tools were utilized: 1) high-throughput sequencing technology to identify a novel de novo mutation; 2) in vitro expression and electrophysiology assays to confirm the variant protein's dysfunction; and 3) screening of existing drug libraries to identify potential therapeutic compounds.ResultsA de novo GRIN2A missense mutation (c.2434C>A; p.L812M) increased the charge transfer mediated by NMDA receptors containing the mutant GluN2A-L812M subunit. In vitro analysis with NMDA receptor blockers indicated that GLuN2A-L812M-containing NMDARs retained their sensitivity to the use-dependent channel blocker memantine; while screening of a previously reported GRIN2A mutation (N615K) with these compounds produced contrasting results. Consistent with these data, adjunct memantine therapy reduced our proband's seizure burden.InterpretationThis case exemplifies the potential for personalized genomics and therapeutics to be utilized for the early diagnosis and treatment of infantile-onset neurological disease.

NMDA receptors (NMDARs), ligand-gated ion channels, play important roles in various neurological disorders, including epilepsy. Here we show the functional analysis of a de novo missense mutation (L812M) in a gene encoding NMDAR subunit GluN2A (GRIN2A). The mutation, identified in a patient with early-onset epileptic encephalopathy and profound developmental delay, is located in the linker region between the ligand-binding and transmembrane domains. Electrophysiological recordings revealed that the mutation enhances agonist potency, decreases sensitivity to negative modulators including magnesium, protons and zinc, prolongs the synaptic response time course and increases single-channel open probability. The functional changes of this amino acid apply to all other NMDAR subunits, suggesting an important role of this residue on the function of NMDARs. Taken together, these data suggest that the L812M mutation causes overactivation of NMDARs and drives neuronal hyperexcitability. We hypothesize that this mechanism underlies the patient's epileptic phenotype as well as cerebral atrophy.

Graduate education in engineering is an extremely challenging, complex entity that is difficult to change. The purpose of this exploratory research paper was to investigate the applicability of the Collective Impact framework, which has been used within community organizing contexts, to organize the change efforts of a center focused on advancing equitable graduate education within engineering. We sought to understand how the conditions of Collective Impact (i.e., common agenda, backbone organization, mutually reinforcing activities, shared measurement system, and continuous communication) could facilitate the organization of equity-focused change efforts across a college of engineering at a single institution. To achieve this, we took an action research approach. We found the Collective Impact framework to be a useful tool for organizing cross-sectional partnerships to facilitate equity-focused change in graduate education; we also found the five conditions of Collective Impact to be applicable to the higher education context, with some intentional considerations and modifications. Through coordinated efforts, the Collective Impact framework can support the goal of reorienting existing decentralized structures, resource flows, and decision processes to foster bottom-up and top-down change processes to advance equitable support for graduate students. [ABSTRACT FROM AUTHOR]

Individuals from racial minority backgrounds, especially those in low income situations, are at increased risk for obesity. Family meals positively impact child nutritional health; however, there is limited evidence examining the impact on caregivers, particularly racial minority and income-restricted individuals. The objective of this intervention study was to determine the effect of Simple Suppers, a 10 week family meals program, on caregiver diet and nutrition outcomes. Intervention versus waitlist control participants were compared from baseline (T0) to post-intervention (T1). In addition, intervention participants were assessed at a 10 week follow-up time point (T2). This study was a two-group quasi-experimental intervention trial. Lessons (10 total) were delivered on a weekly basis for 90 min. Data were collected from intervention and waitlist control participants at T0 and T1, and intervention participants at T2. After baseline (T0) data collection, families enrolled in the immediate upcoming session of Simple Suppers (intervention group) or waited for 10 weeks (waitlist control group) to begin the program. Participants were caregivers of children ages 4–10 years. This study was conducted in a faith-based community center for underserved families in Columbus, Ohio. Primary outcomes were: diet quality assessed by Healthy Eating Index (HEI) total and component scores, and total energy intake (kcal/day); body mass index (BMI) (kg/m2), waist circumference (cm), systolic and diastolic blood pressure (BP) (mmHG); and self-efficacy for having healthy meals and menu planning (both scalar). The impact of the intervention (T0:T1) was assessed using generalized mixed-effects linear regression models. Maintenance of change in study outcomes among intervention participants (T1:T2) was examined with paired t-tests. 109 caregivers enrolled in this study. The retention rate at T1 was 90% (i.e., 98 participants). 56 of 68 intervention participants completed T2, resulting in a retention rate of 82%. Almost all (99%) were female, 61% were Black, and 50% were between 31 and 40 years old. In total, 40% had low income and 37% had low or very low food security. At T1, intervention vs. waitlist controls had a lower daily energy intake (p = 0.04), but an HEI-2010 component score for fatty acids (adequacy) that was lower indicating a lower dietary intake of fatty acids (p = 0.02), and a component score for empty calories (moderation) that was significantly lower indicating a higher intake of empty calorie foods (p = 0.03). At T1, intervention vs. waitlist controls also had a lower BMI (p < 0.001) and systolic BP (p = 0.04), and higher self-efficacy (p = 0.03). There were no group differences in other outcomes. At T2, intervention participants maintained the changes in daily energy intake, BMI, systolic BP, and self-efficacy that improved during the intervention period. There was no change (improvement) in the component score for fatty acids; however, the component score for empty calories significantly improved (p = 0.02). Engagement in the Simple Suppers program led to improvements in caregivers’ daily caloric intake, weight status, systolic blood pressure, and self-efficacy for family meals. Future research should further explore the dietary and nutritional health benefits of family meals among caregivers at the highest risk for obesity.

ภาวะกายใจไม่สงบ(agitation)พบบ่อยทั้งในภาวะฉุกเฉินทางอายุรกรรมและจิตเวช การรักษาพยาบาลได้อย่าง เหมาะสมในกรณีดังกล่าวถือเป็นสมรรถนะหลักอย่างหนึ่งของแพทย์เวชศาสตร์ฉุกเฉิน ในบทความนี้ผู้นิพนธ์ ได้รวบรวมการใช้ยารักษาโรคจิตในกลุ่ม first-generation second-generation และยา benzodiazepines เพื่อใช้ ในการรักษาภาวะกายใจไม่สงบ(agitation)ชนิดเฉียบพลัน รวมทั้งนำ�เสนอแนวทางจำ�เพาะในการรักษาภาวะกาย ใจไม่สงบ(agitation)ที่สัมพันธ์กับภาวะต่างๆได้แก่ การได้รับสารพิษ ภาวะจิตเภท อาการเพ้อ(delirium) รวมทั้ง เกิดขึ้นโดยไม่ทราบสาเหตุ การใช้ยาเพื่อรักษาภาวะกายใจไม่สงบควรพิจารณาตามสาเหตุก่อโรคที่เป็นไปได้มาก ที่สุด ถ้าภาวะกายใจไม่สงบเกิดจากอาการเพ้อ(delirium)หรือโรคทางกายอื่นๆ แพทย์ควรทำ�การรักษาสาเหตุก่อ โรคเป็นลำ�ดับแรกแทนที่จะให้เพียงแค่ยารักษาโรคจิตหรือยา benzodiazepines เท่านั้น [West J Emerg Med. 2012;13(1):26–34.]

[West J Emerg Med. 2012;13(1):1–2.]

Agitation is an acute behavioral emergency requiring immediate intervention. Traditional methods of treating agitated patients, ie, routine restraints and involuntary medication, have been replaced with a much greater emphasis on a noncoercive approach. Experienced practitioners have found that if such interventions are undertaken with genuine commitment, successful outcomes can occur far more often than previously thought possible. In the new paradigm, a 3-step approach is used. First, the patient is verbally engaged; then a collaborative relationship is established; and, finally, the patient is verbally deescalated out of the agitated state. Verbal de-escalation is usually the key to engaging the patient and helping him become an active partner in his evaluation and treatment; although, we also recognize that in some cases nonverbal approaches, such as voluntary medication and environment planning, are also important. When working with an agitated patient, there are 4 main objectives: (1) ensure the safety of the patient, staff, and others in the area; (2) help the patient manage his emotions and distress and maintain or regain control of his behavior; (3) avoid the use of restraint when at all possible; and (4) avoid coercive interventions that escalate agitation. The authors detail the proper foundations for appropriate training for de-escalation and provide intervention guidelines, using the ‘‘10 domains of deescalation.’’ [West J Emerg Med. 2012;13(1):17–25.]

Issues surrounding reduction and/or elimination of episodes of seclusion and restraint for patients with behavioral problems in crisis clinics, emergency departments, inpatient psychiatric units and specialized psychiatric emergency services continue to be an area of concern and debate among mental health clinicians. An important underlying principle of Project BETA is non-coercive de-escalation as the intervention of choice in the management of acute agitation and threatening behavior.In this paper, the authors discuss several aspects of seclusion and restraint, including review of CMS guidelines regulating their use in medical behavioral settings, negative consequences of this intervention to patients and staff and a review of quality improvement and risk management strategies that have been effective in decreasing its use in various treatment settings. An algorithm designed to help the clinician determine when seclusion or restraint is most appropriate is introduced. The authors conclude that the specialized psychiatric emergency services and emergency departments, because of their treatment of primarily acute patients, may not be able to entirely eliminate the use of seclusion and restraint events, but these programs can adopt strategies to reduce the utilization rate of these interventions. [West J Emerg Med. 2012;13(1):35–40.]

Agitation is common in the medical and psychiatric emergency department, and appropriate management of agitation is a core competency for emergency clinicians. In this article, the authors review the use of a variety of first-generation antipsychotic drugs, second-generation antipsychotic agents, and benzodiazepines for treatment of acute agitation, and propose specific guidelines for treatment of agitation associated with a variety of conditions, including acute intoxication, psychiatric illness, delirium, and multifocal or idiopathic causes. Pharmacologic treatment of agitation should be based on an assessment of the most likely cause for the agitation. If agitation results from a medical condition or delirium, clinicians should first attempt to treat this underlying cause instead of simply medicating with antipsychotics or benzodiazepines. [West J Emerg Med. 2012;13(1):26–34.]

Abstract Background The most efficacious childhood obesity prevention interventions have involved caregivers directly or indirectly. Due to the high reliance on technology, research examining technological intervention approaches is warranted, particularly during the summer when parents may be more difficult to engage and the risk for excess weight gain among children is high. Methods The feasibility and acceptability of a multi-component childhood obesity prevention intervention incorporating a caregiver component utilizing technology-based approaches—texting and social media—was explored. This was an internal pilot of the Camp Nutrition Education Recreation and Fitness (NERF) study, a group RCT for school-age children coupled to the USDA Summer Food Service Program. Feasibility and acceptability of the technology caregiver engagement component were assessed via process outcomes (participation rates) and in-depth interviews. Results Participants (n = 37) were 91.9% female, 91.8% Black, 58.7% low-income, and 75.0% overweight/obese. Participation rates in texting and social media were 62.2% and

Chronic inflammation is considered to be a silent killer because it is the underlying cause of a wide range of clinical disorders, from cardiovascular to neurological diseases, and from cancer to obesity. In addition, there are over 80 different types of debilitating autoimmune diseases for which there are no cure. Currently, the drugs that are available to suppress chronic inflammation are either ineffective or overtly suppress the inflammation, thereby causing increased susceptibility to infections and cancer. Thus, the development of a new class of drugs that can suppress chronic inflammation is imperative. Cannabinoids are a group of compounds produced in the body (endocannabinoids) or found in cannabis (phytocannabinoids) that act through cannabinoid receptors and various other receptors expressed widely in the brain and immune system. In the last decade, cannabinoids have been well established experimentally to mediate anti-inflammatory properties. Research has shown that they suppress inflammation through multiple pathways, including apoptosis and inducing immunosuppressive T regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs). Interestingly, cannabinoids also mediate epigenetic alterations in genes that regulate inflammation. In the current review, we highlight how the epigenetic modulations caused by cannabinoids lead to the suppression of inflammation and help identify novel pathways that can be used to target autoimmune diseases.

Introduction: There is a critical need to foster inclusive educational spaces for Queer identifying students and to resist oppressive structures that seek to marginalize and inflict trauma on students because of their gender or sexual identity. Methods: Drawing on thematic analysis and Queer theory, we interviewed 11 Queer identifying STEM students to understand the navigational strategies they leveraged within higher education environments related to their Queer identity. Results: We developed a cyclical model of navigational strategies employed by Queer STEM students that involved evaluating the environments, performing psychological identity calculations, and engaging in behavioral actions. Students evaluated the environment by attending to the diversity of gender representation, presence of other Queer individuals, and contextual factors conveyed based on disciplinary expectations. Students engaged in psychological identity calculations whereby they assessed beliefs about the relevance, importance, and fears related to their Queer identity, with few perceiving any benefits. Behavioral actions resulted in students building a chosen community, disclosing or shelving their queer identity, and advocating for representation. Discussion: In order to support Queer students to thrive in educational contexts, researchers and practitioners should examine ways to increase representation, use inclusive pedagogical strategies, and understand the relevance of Queerness within disciplinary fields. Questioning the relevance or presence of Queerness in higher education environments only further serves to oppress, inflict trauma, and marginalize Queer students. [ABSTRACT FROM AUTHOR]

Microglia are found pathologically at all stages of multiple sclerosis (MS) lesion development and are hypothesized to contribute to both inflammatory injury and neuroprotection in the MS brain. Transient receptor potential vanilloid 4 (TRPV4) channels are widely expressed, play an important role as environmental sensors, and are involved in calcium homeostasis for a variety of cells. TRPV4 modulates myeloid cell phagocytosis in the periphery and microglial motility in the central nervous system. We hypothesized that TRPV4 deletion would alter microglia phagocytosis in vitro and lessen disease activity and demyelination in experimental autoimmune encephalitis (EAE) and cuprizone-induced demyelination. We found that genetic deletion of TRPV4 led to increased microglial phagocytosis in vitro but did not alter the degree of demyelination or remyelination in the cuprizone mouse model of MS. We also found no difference in disease in EAE following global or microglia-specific deletion of Trpv4. Additionally, lesioned and normal appearing white matter from MS brains exhibited similar TRPV4 expression compared to healthy brain tissue. Taken together, these findings indicate that TRPV4 modulates microglial activity but does not impact disease activity in mouse models of MS, suggesting a muted and/or redundant role in MS pathogenesis. [ABSTRACT FROM AUTHOR]

Abstract Background The incidence of invasive cancer within a mucinous cystic neoplasm of the pancreas varies between 6 and 36%. Polycystic ovarian syndrome is a disorder characterized by hyperandrogenism and anovulatory infertility. One surgical treatment that can restore endocrine balance and ovulation in polycystic ovarian syndrome is partial ovarian destruction. Successful pregnancies following preconception pancreaticoduodenectomies (Whipple procedures) and chemoradiation to treat pancreatic neoplasms have been reported rarely but none were diagnosed with pre-cancer polycystic ovarian syndrome-associated infertility. Gemcitabine is an antimetabolite drug used for the treatment of pancreatic cancer that can have profound detrimental effects on oogenesis and ovarian function. Whether the ovarian destructive property of gemcitabine could act as a method to restore ovulation potential in polycystic ovarian syndrome is unknown. Case presentation A 40-year-old white American woman with a history of pancreatic cancer treatment with a Whipple procedure and chemoradiation with gemcitabine had a successful pregnancy after years of pre-cancerous anovulatory infertility and polycystic ovarian syndrome. She received no fertility agents and delivered full term via a spontaneous vaginal delivery with no pregnancy complications. Conclusion Gemcitabine treatment for pancreatic cancer may result in resumption of ovulation in women with polycystic ovarian syndrome and these women should be counseled accordingly.