30 years of Deadly Hate and Bias Crimes

The Bias Homicide Database (BHDB) is an open-source, relational database housed in the Terrorism Research Center (TRC), which is located in the J.W. Fulbright college of Arts and Sciences at the University of Arkansas. Created in 2003, the TRC harnesses science and data analytics to promote safer communities, inform evidence-based policies, and train the next generation of law enforcement and intelligence professionals. The TRC also hosts the Crime and Security Data Analytics Lab. This brief was prepared by Terrorism Research Center (TRC) staff. The TRC is a non-profit, nonpartisan research organization

Delirium Reduction Strategies For The Critically Ill

Delirium, an acute and fluctuating disturbance of consciousness and cognition, is a common manifestation of acute brain dysfunction in critically ill patients. Patients with delirium have longer hospital stays and a lower 6-month survival rate than do patients without delirium. Preliminary research suggests that delirium may be associated with cognitive impairment that persists months to years after discharge. In a large acute care hospital, the cardiac intensive care staff became interested in mitigating their unit’s high delirium rate of ventilated patients. At baseline, many members of the healthcare team did not believe that delirium could be prevented and the predominant view was that critically ill patients were too ill to mobilize. An extensive literature review suggested that early mobilization was extremely beneficial in delirium reduction. As a result, the goal of this performance improvement project was to reduce the prevalence and severity of delirium through progressive mobilization. Several barriers to preventing delirium were identified through a root cause analysis. Using improvement measures of operational excellence, a number of countermeasures were established. Several positive outcomes of this project were realized to include the development of an early mobility pathway and a bedside mobility assessment tool. Next steps include a prospective study of the effect this KPI might have on decreasing duration of ventilation days as well as overall length of hospital stay

Pregnant during the COVID-19 pandemic: an exploration of patients’ lived experiences

Abstract Background Infectious outbreaks are known to cause fear and panic. Exploration of pregnant individuals’ psychosocial condition using a qualitative lens during an infectious outbreak is limited. In this study we explore pregnant individuals’ lived experiences as well as their psychological and behavioural responses during COVID-19 with the goal of providing useful strategies from the patient’s perspective to enable health care providers to help pregnant patients navigate this and future pandemics. Methods Pregnant individuals between 20-weeks gestation and 3 months postpartum who received maternity care from an urban academic interprofessional teaching unit in Toronto, Canada were invited to participate. Semi-structured 60 min interviews were audio-recorded, transcribed and analyzed using descriptive thematic analysis. Interview questions probed psychological responses to the pandemic, behavioural and lifestyle changes, strategies to mitigate distress while pregnant during COVID-19 and advice for other patients and the healthcare team. Results There were 12 participants, mean age 35 years (range 30–43 years), all 1 to 6 months postpartum. Six main themes emerged: 1) Childbearing-related challenges to everyday life; 2) Increased worry, uncertainty and fear; 3) Pervasive sense of loss; 4) Challenges accessing care; 5) Strategies for coping with pandemic stress; 6) Reflections and advice to other pregnant people and health care professionals. Pregnant individuals described lack of social support due to COVID-19 pandemic restrictions and a profound sense of loss of what they thought their pregnancy and postpartum period should have been. Advice to healthcare providers included providing mental health support, clear and up to date communication as well as more postpartum and breastfeeding support. Conclusions These participants described experiencing psychosocial distress during their pregnancies and postpartum. In a stressful situation such as a global pandemic, health care providers need to play a pivotal role to ensure pregnant individuals feel supported and receive consistent care throughout the pregnancy and postpartum period. The health care provider should ensure that mental health concerns are addressed and provide postpartum and breastfeeding support. Without addressing this need for support, parental mental health, relationships, parent-infant bonding, and infant development may be negatively impacted

Effect of Online 1-Day Cognitive Behavioral Therapy-Based Workshops plus Usual Care vs Usual Care Alone for Postpartum Depression:A Randomized Clinical Trial

IMPORTANCE: Postpartum depression (PPD) affects as many as 20% of mothers, yet just 1 in 10 of these women receives evidence-based treatment. The COVID-19 pandemic has increased PPD risk, reduced treatment access, and shifted preferences toward virtual care. OBJECTIVE: To determine whether an online 1-day cognitive behavioral therapy (CBT)–based workshop added to treatment as usual improves PPD, anxiety, social support, mother-infant relationship quality, and infant temperament more than treatment as usual alone. DESIGN, SETTING, AND PARTICIPANTS: This randomized clinical trial included 403 women with PPD who were recruited across Ontario, Canada, during the COVID-19 pandemic (April 20 to October 4, 2020). Women with Edinburgh Postnatal Depression Scale (EPDS) scores of at least 10 who were 18 years or older and had an infant younger than 12 months were eligible. INTERVENTIONS: Women were randomly assigned to receive a live, interactive online 1-day CBT-based workshop delivered by a registered psychotherapist, psychiatrist, or clinical psychology graduate student in addition to treatment as usual (n = 202) or to receive treatment as usual and wait-listed to receive the workshop 12 weeks later (n = 201). MAIN OUTCOMES AND MEASURES: The primary outcome was change in PPD (EPDS scores) in experimental and wait list control groups 12 weeks after baseline. Secondary outcomes included maternal anxiety (7-item Generalized Anxiety Disorder Questionnaire [GAD-7]), social support (Social Provisions Scale), quality of the mother-infant relationship (Postpartum Bonding Questionnaire), and infant temperament (Infant Behavior Questionnaire–Revised Very Short Form). RESULTS: Participants all identified as women with a mean (SD) age of 31.8 (4.4) years. The workshop led to significant mean (SD) reductions in EPDS scores (from 16.47 [4.41] to 11.65 [4.83]; B = −4.82; P < .001) and was associated with a higher odds of exhibiting a clinically significant decrease in EPDS scores (odds ratio, 4.15; 95% CI, 2.66-6.46). The mean (SD) GAD-7 scores decreased from 12.41 (5.12) to 7.97 (5.54) after the workshop (B = −4.44; 95% CI, −5.47 to −3.38; P < .001) and participants were more likely to experience a clinically significant change (odds ratio, 3.09; 95% CI, 1.99-4.81). Mothers also reported improvements in bonding (B = −3.22; 95% CI, −4.72 to −1.71; P < .001), infant-focused anxiety (B = −1.64; 95% CI, −2.25 to 1.00; P < .001), social support (B = 3.31; 95% CI, 1.04 to 5.57; P < .001), and positive affectivity/surgency in infants (B = 0.31; 95% CI, 0.05 to 0.56; P < .001). CONCLUSIONS AND RELEVANCE: In this randomized clinical trial, an online 1-day CBT-based workshop for PPD provides an effective, brief option for mothers, reducing PPD and anxiety as well as improving social support, the mother-infant relationship, and positive affectivity/surgency in offspring. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT0448500

Smyd1 facilitates heart development by antagonizing oxidative and ER stress responses.

Smyd1/Bop is an evolutionary conserved histone methyltransferase previously shown by conventional knockout to be critical for embryonic heart development. To further explore the mechanism(s) in a cell autonomous context, we conditionally ablated Smyd1 in the first and second heart fields of mice using a knock-in (KI) Nkx2.5-cre driver. Robust deletion of floxed-Smyd1 in cardiomyocytes and the outflow tract (OFT) resulted in embryonic lethality at E9.5, truncation of the OFT and right ventricle, and additional defects consistent with impaired expansion and proliferation of the second heart field (SHF). Using a transgenic (Tg) Nkx2.5-cre driver previously shown to not delete in the SHF and OFT, early embryonic lethality was bypassed and both ventricular chambers were formed; however, reduced cardiomyocyte proliferation and other heart defects resulted in later embryonic death at E11.5-12.5. Proliferative impairment prior to both early and mid-gestational lethality was accompanied by dysregulation of transcripts critical for endoplasmic reticulum (ER) stress. Mid-gestational death was also associated with impairment of oxidative stress defense-a phenotype highly similar to the previously characterized knockout of the Smyd1-interacting transcription factor, skNAC. We describe a potential feedback mechanism in which the stress response factor Tribbles3/TRB3, when directly methylated by Smyd1, acts as a co-repressor of Smyd1-mediated transcription. Our findings suggest that Smyd1 is required for maintaining cardiomyocyte proliferation at minimally two different embryonic heart developmental stages, and its loss leads to linked stress responses that signal ensuing lethality

Smyd1 Facilitates Heart Development by Antagonizing Oxidative and ER Stress Responses

<div><p>Smyd1/Bop is an evolutionary conserved histone methyltransferase previously shown by conventional knockout to be critical for embryonic heart development. To further explore the mechanism(s) in a cell autonomous context, we conditionally ablated <i>Smyd1</i> in the first and second heart fields of mice using a knock-in (KI) <i>Nkx2</i>.<i>5-cre</i> driver. Robust deletion of <i>floxed-Smyd1</i> in cardiomyocytes and the outflow tract (OFT) resulted in embryonic lethality at E9.5, truncation of the OFT and right ventricle, and additional defects consistent with impaired expansion and proliferation of the second heart field (SHF). Using a transgenic (Tg) <i>Nkx2</i>.<i>5-cre</i> driver previously shown to not delete in the SHF and OFT, early embryonic lethality was bypassed and both ventricular chambers were formed; however, reduced cardiomyocyte proliferation and other heart defects resulted in later embryonic death at E11.5-12.5. Proliferative impairment prior to both early and mid-gestational lethality was accompanied by dysregulation of transcripts critical for endoplasmic reticulum (ER) stress. Mid-gestational death was also associated with impairment of oxidative stress defense—a phenotype highly similar to the previously characterized knockout of the Smyd1-interacting transcription factor, skNAC. We describe a potential feedback mechanism in which the stress response factor Tribbles3/TRB3, when directly methylated by Smyd1, acts as a co-repressor of Smyd1-mediated transcription. Our findings suggest that Smyd1 is required for maintaining cardiomyocyte proliferation at minimally two different embryonic heart developmental stages, and its loss leads to linked stress responses that signal ensuing lethality.</p></div

Deletion of <i>Smyd1</i> by <i>Tg-Nkx2</i>.<i>5-cre</i> leads to a delayed embryonic lethal cardiac phenotype.

<p><b>A.</b><i>Smyd1</i>^{<i>flox/flox</i>}; <i>Tg-Nkx2</i>.<i>5-cre</i> (Tg-CKO) embryos die at midgestation. Table numbers are total recovered embryos of each genotype. The number of dead or abnormal embryos is given in parentheses. <b>B, C.</b><i>Smyd1</i> mRNA expression at E10.5 assayed by RT-PCR (B) and real-time PCR (C). <b>D.</b> H&E-stained transverse sections of E11.5 control (Cx) and Tg-CKO embryos showing pericardial edema, thinned pericardium and decreased trabeculation. <b>E.</b> Decreased proliferation was observed in the hearts of E10.5 <i>Smyd1</i> Tg-CKO embryos. Representative images of Cx and Tg-CKO hearts stained with H&E (upper panels) and the mitosis marker phospho-histone H3 serine 10 (p-H3) (lower panels). <b>F.</b> Quantification of p-H3 positive cells within the heart from three sections for three independent embryos (n = 3). <b>G.</b> Comparison of <i>skNAC</i> knockout and <i>Smyd1 Tg-CKO</i> heart gene expression by real-time PCR at E11.5. Data, focused primarily on oxidative response deregulation, are presented as mean for each genotype (<i>skNAC</i>^-/-, n = 5; <i>Smyd1</i> Tg-CKO, n = 4). Error bars indicate SEM. <b>H.</b> Genes encoding mediators of ER stress are deregulated by loss of Smyd1. Real-time PCR data represents average of 3 biological replicates each with 3 technical replicates; error bars indicate SEM. Data were analyzed by Student’s t-test (*P < 0.05, **P <0.01, ***P < 0.001, ****P < 0.0001).</p

Loss of <i>Smyd1</i> using <i>Ki-Nkx2</i>.<i>5</i>^<i>cre/+</i> disrupts looping morphogenesis and chamber formation through perturbation of the SHF and activation of ER stress.

<p><b>A.</b> Gross morphological comparison of control (Cx: <i>Nkx2</i>.<i>5</i>^<i>+/+</i>; <i>Smyd1</i>^{<i>Flox/Flox</i>}) and <i>Smyd1</i> Ki-CKO (CKO: <i>Nkx2</i>.<i>5</i>^<i>cre/+</i>; <i>Smyd1</i>^{<i>Flox/Flox</i>}) hearts at E9.5. Scale bar = 200 μm. <b>B, C</b>. The lengths of the outflow tract (OFT) (B) and right ventricle (RV) (C) were significantly reduced in Ki-CKO embryos at E9.5 (n = 6/group). <b>D.</b> Representative results of microarray gene expression comparison of transcripts critical to SHF and chamber formation at E9.5. Data are presented as expression values of 2 independent biological replicas of each genotype averaged from 2 technical replicas. <b>E.</b> Confirmation of microarray for deregulated transcripts critical to SHF and chamber formation by real-time PCR using RNA from E9.5 heart/pharyngeal mesoderm (n = 9/group). <b>F</b>. Whole mount <i>in situ</i> hybridization comparison of selected SHF and chamber formation transcripts deregulated and/or mislocalized in CKO hearts at E9.5 (n = 3/group). Arrows denote areas of differential expression. <b>G.</b> Comparison of cell proliferation in the outflow tract of Control (Cx) and Ki-CKO by BrdU immunohistochemistry. PE, Pharyngeal Endoderm. OFT, outflow tract. V, ventricle. Scale bar = 100 μm. <b>H.</b> Quantification of anti-BrdU staining in the outflow tract (n = 6/group). <b>I.</b> Loss of Smyd1 leads to deregulation of genes critical to anti-proliferative responses to ER stress. Data are presented as a heat map with expression values of 2 independent biological replicas of each genotype averaged from 2 technical replicas plotted as log² expression values. For B, C, E and H, data were analyzed by Student’s t-test (*P < 0.05).</p