Conversations With Health Care Providers and Parents Before Autism Diagnosis: A Qualitative Study

Introduction The purpose of this study was to explore communication with health care providers from the perceptions of parents before their child\u27s diagnosis of autism spectrum disorder and provide some examples of how communication may contribute to the autism diagnosis. Method This study used a qualitative descriptive design with multiple individual structured in-person interviews. Results Three themes captured parents’ (n = 8) descriptions of the phases of communication during their children\u27s diagnoses including, (1) anguished questioning, (2) urgently seeking help, and (3) expecting a diagnosis. In addition, three themes characterized the communication style that parents needed, although not always received, in each of the periods of diagnosis including (1) compassionate curiosity, (2) acknowledgment and affirmation, and (3) engagement with parents. Discussion Results point to opportunities for pediatric providers to use a more empathic and engaging communication style during the diagnostic process with better identification of education and support needed by parents and families

Oxo Ligand Substitution in a Cationic Uranyl Complex: Synergistic Interaction of an Electrophile and a Reductant

Reaction of [U^VIO₂(dppmo)₂(OTf)]­[OTf] (dppmo = Ph₂P­(O)­CH₂P­(O)­Ph₂) with 4 equiv of Ph₃SiOTf and 2 equiv of Cp₂Co generates the U­(IV) complex U^IV(OTf)₄­(dppmo)₂ (<b>1</b>), as a yellow-green crystalline solid in 83% yield, along with Ph₃SiOSiPh₃ and [Cp₂Co]­[OTf]. This reaction proceeds via a U­(IV) silyloxide intermediate, [U^IV(OSiPh₃)­(dppmo)₂­(OTf)₂]­[OTf] (<b>2</b>), which we have isolated and structurally characterized. Similarly, reaction of [U^VIO₂­(TPPO)₄]­[OTf]₂ (TPPO = Ph₃PO) with 6 equiv of Me₃SiOTf and 2 equiv of Cp₂Co generates the U­(IV) complex, [Cp₂Co]­[U^IV(OTf)₅­(TPPO)₂] (<b>3</b>), as a yellow-green crystalline solid in 76% yield, concomitant with formation of Me₃SiOSiMe₃, [Ph₃POSiMe₃]­[OTf], and [Cp₂Co]­[OTf]. Complexes <b>1</b> and <b>3</b> have been fully characterized, including analysis by X-ray crystallography. The conversion of [U^VIO₂(dppmo)₂­(OTf)]­[OTf] and [U^VIO₂(TPPO)₄]­[OTf]₂ to complexes <b>1</b> and <b>3</b>, respectively, represents rare examples of well-defined uranyl oxo ligand substitution

Early-childhood linear growth faltering in low- and middle-income countries

Globally, 149 million children under 5 years of age are estimated to be stunted (length more than 2 standard deviations below international growth standards)1,2. Stunting, a form of linear growth faltering, increases the risk of illness, impaired cognitive development and mortality. Global stunting estimates rely on cross-sectional surveys, which cannot provide direct information about the timing of onset or persistence of growth faltering—a key consideration for defining critical windows to deliver preventive interventions. Here we completed a pooled analysis of longitudinal studies in low- and middle-income countries (n = 32 cohorts, 52,640 children, ages 0–24 months), allowing us to identify the typical age of onset of linear growth faltering and to investigate recurrent faltering in early life. The highest incidence of stunting onset occurred from birth to the age of 3 months, with substantially higher stunting at birth in South Asia. From 0 to 15 months, stunting reversal was rare; children who reversed their stunting status frequently relapsed, and relapse rates were substantially higher among children born stunted. Early onset and low reversal rates suggest that improving children’s linear growth will require life course interventions for women of childbearing age and a greater emphasis on interventions for children under 6 months of age

Causes and consequences of child growth faltering in low-resource settings

Growth faltering in children (low length for age or low weight for length) during the first 1,000 days of life (from conception to 2 years of age) influences short-term and long-term health and survival1,2. Interventions such as nutritional supplementation during pregnancy and the postnatal period could help prevent growth faltering, but programmatic action has been insufficient to eliminate the high burden of stunting and wasting in low- and middle-income countries. Identification of age windows and population subgroups on which to focus will benefit future preventive efforts. Here we use a population intervention effects analysis of 33 longitudinal cohorts (83,671 children, 662,763 measurements) and 30 separate exposures to show that improving maternal anthropometry and child condition at birth accounted for population increases in length-for-age z-scores of up to 0.40 and weight-for-length z-scores of up to 0.15 by 24 months of age. Boys had consistently higher risk of all forms of growth faltering than girls. Early postnatal growth faltering predisposed children to subsequent and persistent growth faltering. Children with multiple growth deficits exhibited higher mortality rates from birth to 2 years of age than children without growth deficits (hazard ratios 1.9 to 8.7). The importance of prenatal causes and severe consequences for children who experienced early growth faltering support a focus on pre-conception and pregnancy as a key opportunity for new preventive interventions