The Iowa Homemaker vol.7, no.10

The Iowa Homemaker Has a Birthday by Ruth Morrison, page 1 Chow Mein versus Chop Suey by Frances Thomas, page 2 Veishea, 1928 by Ruth M. Davis, page 3 News Bits by Margaret Davidson and Rosemary Koeberle, page 4 Sandwiches for Your Spring Menu by Caroline E. Morrell, page 5 4-H Club by Mrs. Edith Barker, page 6 State Association Page by Marcia E. Turner, page 8 Home Economics Research at Iowa State by Melba Nisewanger, page 10 Editorial, page 11 Who’s There and Where by Vera Caulum, page 12 Window Boxes by Gladys Parker, page 1

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Rapid linkage disequilibrium decay in the Lr10 gene in wild emmer wheat (Triticum dicoccoides) populations

INTRODUCTION: Recombination is a key evolutionary factor enhancing diversity. However, the effect of recombination on diversity in inbreeding species is expected to be low. To estimate this effect, recombination and diversity patterns of Lr10 gene were studied in natural populations of the inbreeder species, wild emmer wheat (Triticum dicoccoides). Wild emmer wheat is the progenitor of most cultivated wheats and it harbors rich genetic resources for disease resistance. Lr10 is a leaf rust resistance gene encoding three domains: a coiled-coil, nucleotide-binding site, and leucine-rich repeat (CC-NBS-LRR). RESULTS: Lr10 was sequenced from 58 accessions representing 12 diverse habitats in Israel. Diversity analysis revealed a high rate of synonymous and non-synonymous substitutions (d (S) = 0.029, d (N) = 0.018, respectively) in the NBS-LRR domains. Moreover, in contrast to other resistance genes, in Lr10 the CC domain was more diverse than the NBS-LRR domains (d (S) = 0.069 vs. 0.029, d (N) = 0.094 vs. 0.018) and was subjected to positive selection in some of the populations. Seventeen recombination events were detected between haplotypes, especially in the CC domain. Linkage disequilibrium (LD) analysis has shown a rapid decay from r (2) = 0.5 to r (2) = 0.1 within a 2-kb span. CONCLUSION: These results suggest that recombination is a diversifying force for the R-gene, Lr10, in the selfing species T. dicoccoides. This is the first report of a short-range LD decay in wild emmer wheat

The association between experiencing discrimination and physical and mental health among PWID

Background: Discrimination can be a daily issue in the lives of people who inject drugs (PWID). However, the extent to which discrimination is related to the health of PWID remains unclear. Methods: Data focusing on discrimination against PWID and potential health correlates were collected as part of the 2013 Illicit Drug Reporting System, a national survey with 887 PWID recruited in all Australian states and territories. Experience of discrimination, its setting, perceived reason and outcome, were self-reported by participants. The Kessler-10 scale and the mental component score of the Short Form 12-Item Health Survey were used to measure mental health. Physical health was assessed using the physical component score of the Short Form 12-Item Health Survey, specifically questions assessing injecting related problems and risk behaviour. Poisson and multinomial regression analyses were performed. Models were adjusted for socio-demographic and drug-related covariates. Findings: PWID reported experiencing discrimination in pharmacies, hospitals, government services and doctors/prescribers. The most commonly reported instances of discrimination were being refused service and experiencing abuse and/or violence. Experience of discrimination was associated with mental and physical health indicators. PWID who experienced discrimination were more likely to report high or very high mental distress (ARRR = 2.4, CI95 = 1.5–3.6) and mental health problems (ARRR = 1.4, CI95 = 1.2–1.7). The mental functioning (ARRR = 1.3, CI95 = 1.1–1.4) and physical functioning (ARRR = 1.1, CI95 = 1.1–1.4) of PWID, who experienced discrimination, were also more likely to be below Australian population mean scores. Conclusion: Self-reported experience of discrimination was associated with poor mental and physical health amongst PWID

Accelerating Medicines Partnership® Schizophrenia (AMP® SCZ):Rationale and Study Design of the Largest Global Prospective Cohort Study of Clinical High Risk for Psychosis

This article describes the rationale, aims, and methodology of the Accelerating Medicines Partnership® Schizophrenia (AMP® SCZ). This is the largest international collaboration to date that will develop algorithms to predict trajectories and outcomes of individuals at clinical high risk (CHR) for psychosis and to advance the development and use of novel pharmacological interventions for CHR individuals. We present a description of the participating research networks and the data processing analysis and coordination center, their processes for data harmonization across 43 sites from 13 participating countries (recruitment across North America, Australia, Europe, Asia, and South America), data flow and quality assessment processes, data analyses, and the transfer of data to the National Institute of Mental Health (NIMH) Data Archive (NDA) for use by the research community. In an expected sample of approximately 2000 CHR individuals and 640 matched healthy controls, AMP SCZ will collect clinical, environmental, and cognitive data along with multimodal biomarkers, including neuroimaging, electrophysiology, fluid biospecimens, speech and facial expression samples, novel measures derived from digital health technologies including smartphone-based daily surveys, and passive sensing as well as actigraphy. The study will investigate a range of clinical outcomes over a 2-year period, including transition to psychosis, remission or persistence of CHR status, attenuated positive symptoms, persistent negative symptoms, mood and anxiety symptoms, and psychosocial functioning. The global reach of AMP SCZ and its harmonized innovative methods promise to catalyze the development of new treatments to address critical unmet clinical and public health needs in CHR individuals.</p