Year of the Snake

Year of the Snake is a travel narrative and family memoir that details a year of the author’s life as a Fulbright scholar in Vietnam. Twenty-five years after the author’s parents have fled Vietnam as war refugees, the author returns to her parents’ homeland. The author spends 2001 exploring and examining this forsaken homeland. She has three distinct experiences, as a student living with my uncle as his adopted daughter, as a backpacker exhilarated by the culture and land, and as a privileged ex-pat working among locals. Through these varied experiences, I began to see how Vietnam was trying to put resolution on the past while opening borders to a future of tourism and capitalistic enterprises. I also began to understand the trials my family endured and the connection between the relatives I loved in the U.S. and those left behind. Through field and academic research, I attempt to reconcile my parents and relatives\u27 lives with my own experiences growing up poor in Mobile, Alabama. My personal journey as a young and fearful, first-generation 22-year-old living, abroad for the first time, draws parallels between the struggle to attain the American dream with the struggle of living in Vietnam\u27s impoverished, communist world. My intent is to illuminate all that is both beautiful and sad about claiming identity as any ethnic minority in America. However, I push past the idea of being Vietnamese-American to point to the underlying humanity that brings us together. My stories of two different cultures delve into the tenderness of family and the common human experiences of fear, joy, and sacrifice. In our uncertain society today, there is added weight and virtue to finding likenesses and understanding between cultures. My audience will go beyond first-generation Americans to include those trying to find meaning in cultural differences, those who have ever felt an otherness, and those who appreciate stories of hope and perseverance

Telehealth Family Navigation for Early Autism Services Access: The Autism ALERT Project

Background: Delays in access to educational services for autism are common and more likely among children from families of color and/or with low income. In-person family navigation accelerates autism diagnosis; however, the effectiveness of telehealth autism diagnostic navigation is unknown. Objectives: To test preliminary feasibility and efficacy of a telehealth autism navigation program. Method: This was a site-randomized pilot trial of autism family navigation for Oregon children in 2021-2022. The intervention used layperson family resource specialists based at Oregon’s Help Me Grow program as navigators for families of children with autism symptoms. Pediatric clinics with \u3e30% Medicaid, located in 5 Oregon counties, were invited to enroll children in the study. 7 clinics (49 primary care providers [PCPs]) participated; 4 were randomized to the family navigation intervention and 3 to usual care. PCPs in both arms received training on autism screening and referral to medical/educational services. PCPs then referred any child age 1-55 months with a positive screen and/or provider autism concern to the study. For children in intervention arm clinics, the navigator called parents, providing information about autism and the autism diagnostic process, assistance with paperwork, social support, and appointment reminders. Control arm clinics/children received no calls. Study enrollment continued until 50 children (30 intervention, 20 control) enrolled. Child Early Intervention/Early Childhood Special Education (EI/ECSE) data were collected from Oregon’s state database 6 months after enrollment. Primary study outcomes compared intervention and control arms on: % of children receiving EI/ECSE referrals within 6 months, % receiving an evaluation in EI/ECSE within 6 months, time from enrollment to EI/ECSE evaluation, and % of evaluated children receiving an autism educational label within 6 months. Results: All clinics enrolled children; children were 40.8% (n=20) white, 26.5% (n=13) Latino, and 32.7% (n=9) multiracial and/or other race/ethnicity. 16% were female (n=8); median age was 2. Intervention families received a median of 12 navigator telehealth contacts. Overall, 70% (n=21) of intervention arm and 42% (n =8) of control arm families were successfully referred to EI/ECSE (p = 0.05). Of those referred, 86% (n=18) of intervention arm and 100% (n=8) of control arm children were evaluated in EI/ECSE (n.s.). Median time to EI/ECSE evaluation was 103 days in the intervention and 162 days in the control arm (p = 0.68; Figure 1). Overall, 40% of intervention arm (n = 12) and 21% (n = 4) of control arm children had an autism placement, with a trend toward autism as the primary placement type in the intervention arm (p = 0.12). Conclusion: Telehealth family navigation shows promise for improving access to autism services in EI/ECSE, especially for securing an early EI/ECSE evaluation, and increasing autism educational labels. A full-scale trial can investigate more distal outcomes including receipt of medical diagnosis and therapeutic services use

Acute invariant NKT cell activation triggers an immune response that drives prominent changes in iron homeostasis

Iron homeostasis is an essential biological process that ensures the tissue distribution of iron for various cellular processes. As the major producer of hepcidin, the liver is central to the regulation of iron metabolism. The liver is also home to many immune cells, which upon activation may greatly impact iron metabolism. Here, we focus on the role of invariant natural killer T (iNKT) cells, a subset of T lymphocytes that, in mice, is most abundant in the liver. Activation of iNKT cells with the prototypical glycosphingolipid antigen, α-galactosylceramide, resulted in immune cell proliferation and biphasic changes in iron metabolism. This involved an early phase characterized by hypoferremia, hepcidin induction and ferroportin suppression, and a second phase associated with strong suppression of hepcidin despite elevated levels of circulating and tissue iron. We further show that these changes in iron metabolism are fully dependent on iNKT cell activation. Finally, we demonstrate that the biphasic regulation of hepcidin is independent of NK and Kupfer cells, and is initially driven by the STAT3 infammatory pathway, whereas the second phase is regulated by repression of the BMP/SMAD signaling pathway. These fndings indicate that iNKT activation and the resulting cell proliferation infuence iron homeostasis

Acute invariant NKT cell activation triggers an immune response that drives prominent changes in iron homeostasis

© The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licen ses/by/4.0/.Iron homeostasis is an essential biological process that ensures the tissue distribution of iron for various cellular processes. As the major producer of hepcidin, the liver is central to the regulation of iron metabolism. The liver is also home to many immune cells, which upon activation may greatly impact iron metabolism. Here, we focus on the role of invariant natural killer T (iNKT) cells, a subset of T lymphocytes that, in mice, is most abundant in the liver. Activation of iNKT cells with the prototypical glycosphingolipid antigen, α-galactosylceramide, resulted in immune cell proliferation and biphasic changes in iron metabolism. This involved an early phase characterized by hypoferremia, hepcidin induction and ferroportin suppression, and a second phase associated with strong suppression of hepcidin despite elevated levels of circulating and tissue iron. We further show that these changes in iron metabolism are fully dependent on iNKT cell activation. Finally, we demonstrate that the biphasic regulation of hepcidin is independent of NK and Kupffer cells, and is initially driven by the STAT3 inflammatory pathway, whereas the second phase is regulated by repression of the BMP/SMAD signaling pathway. These findings indicate that iNKT activation and the resulting cell proliferation influence iron homeostasis.This work was supported by grants from the Canadian Institutes of Health Research (CIHR, Grant no. PJT-159775) and Natural Sciences and Engineering Research Council of Canada (NSERC, Grant RGPIN-2018-06442) to MMS. HH received a PhD scholarship from the NSERC. SL is a Research Scholars Emeritus awardee from the FRQS.info:eu-repo/semantics/publishedVersio

New iron tetrazolate frameworks : synthesis temperature effect, thermal behaviour, Mössbauer and magnetic studies

The exploration of the FeF3/FeF2-Hamtetraz-HF system in dimethylformamide by solvothermal synthesis evidences two isostructural 3D hybrid fluoroferrates. They are prepared from the same starting mixture at two different synthesis temperatures: 120 °C for [Hdma]·(Fe4IIFeIIIF8(H2O)2(amtetraz)4) (1) and 140 °C for [Hdma]1.5·(Fe4.5IIFe0.5IIIF7(H2O)(HCOO)(amtetraz)4) (2). Both compounds are characterized by single crystal X-ray diffraction, X-ray thermodiffraction, TGA analysis, Mössbauer spectrometry and SQUID magnetometry. They crystallize in the monoclinic system and are built from two distinct chains connected by aminotetrazolate anions. The first chain ∞(FeIIFN4) is common to 1 and 2 and can be found in numerous fluorides. In the second chain ∞(Fe3X12) (X = F, N, O), iron cations adopt both valence states Fe(II)/Fe(III). The hydrolysis of DMF implies the formation of a [Hdma]+ cation and a (HCOO)− anion. The presence of Fe3+ in both phases is evidenced by 57Fe Mössbauer spectrometry. The magnetic properties are studied and two transitions from a paramagnetic regime to a long range ordered state below 30 K and 5 K are identified.PostprintPeer reviewe

The Type 2 Diabetes Knowledge Portal: an Open access Genetic Resource Dedicated to Type 2 Diabetes and Related Traits

Associations between human genetic variation and clinical phenotypes have become a foundation of biomedical research. Most repositories of these data seek to be disease-agnostic and therefore lack disease-focused views. The Type 2 Diabetes Knowledge Portal (T2DKP) is a public resource of genetic datasets and genomic annotations dedicated to type 2 diabetes (T2D) and related traits. Here, we seek to make the T2DKP more accessible to prospective users and more useful to existing users. First, we evaluate the T2DKP\u27s comprehensiveness by comparing its datasets with those of other repositories. Second, we describe how researchers unfamiliar with human genetic data can begin using and correctly interpreting them via the T2DKP. Third, we describe how existing users can extend their current workflows to use the full suite of tools offered by the T2DKP. We finally discuss the lessons offered by the T2DKP toward the goal of democratizing access to complex disease genetic results

Mapping 123 million neonatal, infant and child deaths between 2000 and 2017

Since 2000, many countries have achieved considerable success in improving child survival, but localized progress remains unclear. To inform efforts towards United Nations Sustainable Development Goal 3.2—to end preventable child deaths by 2030—we need consistently estimated data at the subnational level regarding child mortality rates and trends. Here we quantified, for the period 2000–2017, the subnational variation in mortality rates and number of deaths of neonates, infants and children under 5 years of age within 99 low- and middle-income countries using a geostatistical survival model. We estimated that 32% of children under 5 in these countries lived in districts that had attained rates of 25 or fewer child deaths per 1,000 live births by 2017, and that 58% of child deaths between 2000 and 2017 in these countries could have been averted in the absence of geographical inequality. This study enables the identification of high-mortality clusters, patterns of progress and geographical inequalities to inform appropriate investments and implementations that will help to improve the health of all populations

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Safety and efficacy of fluoxetine on functional outcome after acute stroke (AFFINITY): a randomised, double-blind, placebo-controlled trial

Background Trials of fluoxetine for recovery after stroke report conflicting results. The Assessment oF FluoxetINe In sTroke recoverY (AFFINITY) trial aimed to show if daily oral fluoxetine for 6 months after stroke improves functional outcome in an ethnically diverse population. Methods AFFINITY was a randomised, parallel-group, double-blind, placebo-controlled trial done in 43 hospital stroke units in Australia (n=29), New Zealand (four), and Vietnam (ten). Eligible patients were adults (aged ≥18 years) with a clinical diagnosis of acute stroke in the previous 2–15 days, brain imaging consistent with ischaemic or haemorrhagic stroke, and a persisting neurological deficit that produced a modified Rankin Scale (mRS) score of 1 or more. Patients were randomly assigned 1:1 via a web-based system using a minimisation algorithm to once daily, oral fluoxetine 20 mg capsules or matching placebo for 6 months. Patients, carers, investigators, and outcome assessors were masked to the treatment allocation. The primary outcome was functional status, measured by the mRS, at 6 months. The primary analysis was an ordinal logistic regression of the mRS at 6 months, adjusted for minimisation variables. Primary and safety analyses were done according to the patient's treatment allocation. The trial is registered with the Australian New Zealand Clinical Trials Registry, ACTRN12611000774921. Findings Between Jan 11, 2013, and June 30, 2019, 1280 patients were recruited in Australia (n=532), New Zealand (n=42), and Vietnam (n=706), of whom 642 were randomly assigned to fluoxetine and 638 were randomly assigned to placebo. Mean duration of trial treatment was 167 days (SD 48·1). At 6 months, mRS data were available in 624 (97%) patients in the fluoxetine group and 632 (99%) in the placebo group. The distribution of mRS categories was similar in the fluoxetine and placebo groups (adjusted common odds ratio 0·94, 95% CI 0·76–1·15; p=0·53). Compared with patients in the placebo group, patients in the fluoxetine group had more falls (20 [3%] vs seven [1%]; p=0·018), bone fractures (19 [3%] vs six [1%]; p=0·014), and epileptic seizures (ten [2%] vs two [<1%]; p=0·038) at 6 months. Interpretation Oral fluoxetine 20 mg daily for 6 months after acute stroke did not improve functional outcome and increased the risk of falls, bone fractures, and epileptic seizures. These results do not support the use of fluoxetine to improve functional outcome after stroke