Postnatal Loss Research Articles

Postnatal weight loss and neurodevelopmental outcomes at age 3 years in extremely preterm infants: a cohort study

BackgroundPrevious research has suggested a correlation between postnatal maximum weight loss (MWL) and both neonatal mortality and morbidities in extremely preterm infants. However, the relationship between MWL and neurodevelopmental outcomes remains underexplored.MethodsIn a single-center, retrospective cohort study at Okayama Medical Center, we evaluated data from extremely preterm infants admitted to the neonatal intensive care unit from 2010 to 2020. Infants who died within the first 10 days of life were excluded. MWL in the first 10 days was the main exposure, categorized into three groups: >15%, 5–15%, and < 5%. The primary outcome evaluated was the occurrence of death or neurodevelopmental impairment (NDI) at age 3 years, defined as developmental impairments (developmental quotient [DQ] < 85), cerebral palsy, hearing impairments, or visual impairments. Data analysis involved robust Poisson regression, adjusted for perinatal confounders, with a restricted cubic spline function to examine the dose-response relationship. We also conducted a sensitivity analysis using a DQ of < 70 to define developmental impairment.ResultsAmong 135 infants assessed for neurodevelopmental outcomes, 40 were in the > 15% MWL group, 71 in the 5–15% group, and 24 in the < 5% group. Median gestational ages and birth weights were 25.9 weeks and 821 g for > 15% MWL; 26.1 weeks and 818 g for 5–15% MWL; and 26.0 weeks and 734 g for < 5% MWL. Compared with the 5–15% MWL group, the < 5% group exhibited a higher risk of death or NDI at age 3 years (62.8% vs. 80.8%, risk ratio [RR] 1.36, 95% confidence interval [CI] 1.04–1.79) and NDI alone (59.2% vs. 79.2%, RR 1.43, 95% CI 1.06–1.94). Furthermore, higher risks of developmental impairment were also noted in the > 15% (RR 1.32, 95% CI 1.00–1.75) and < 5% (RR 1.46, 95% CI 1.08–1.98) groups. These associations were confirmed by spline analyses. In contrast, the associations between MWL and neurodevelopmental outcomes using a DQ of < 70 were not apparent.ConclusionsMWL within the first 10 days of life may be associated with increased risks of NDI and developmental impairments by age 3 years in extremely preterm infants.

Effects of early parenteral nutrition on the development of premature infants born at 22-23 weeks of gestation: a retrospective cohort study evaluated by brain magnetic resonance imaging.

The effect of early parenteral nutrition (EPN) therapy on brain development in extremely premature infants at a gestational age (GA) of 22-25 weeks remains unknown. This study investigated the effect of EPN therapy on GA 22 to 25 weeks of gestation using magnetic resonance imaging (MRI) global brain abnormality score (GBAS). Forty-six preterm infants born before 26 weeks of gestation were divided into the GA 22-23 weeks (GA 22-23; n = 18) and GA 24-25 weeks (GA 24-25; n = 28) group. Each infant received ≥3.0 g/kg/day of amino acids from day 1 of life and ≥1.0 g/kg/day of lipid emulsion the next day. Weight change during hospitalization, GBAS at discharge, and developmental quotient (DQ) until three years old were compared between the groups. GA 22-23 showed long-term postnatal weight loss, but weight at 41 weeks of postmenstrual age did not differ between the groups. The GBAS score was not significantly different, but the head circumference was smaller in GA 22-23 than in GA 24-25 until 2 years old. The DQ at 1-1.5 years old was lower in GA 22-23 than that of GA 24-25; however, there was no significant difference in DQ after 2 years old between the groups. The effect of nutritional support with EPN therapy in premature neonates born at <24 weeks of gestation may still be inadequate. GBAS is useful for assessing brain development in very preterm infants, and the importance of nutritional support during the first few weeks of life should continue to be explored.

Qki5 safeguards spinal motor neuron function by defining the motor neuron-specific transcriptome via pre-mRNA processing

Many RNA-binding proteins (RBPs) are linked to the dysregulation of RNA metabolism in motor neuron diseases (MNDs). However, the molecular mechanisms underlying MN vulnerability have yet to be elucidated. Here, we found that such an RBP, Quaking5 (Qki5), contributes to formation of the MN-specific transcriptome profile, termed "MN-ness," through the posttranscriptional network and maintenance of the mature MNs. Immunohistochemical analysis and single-cell RNA sequencing (scRNA-seq) revealed that Qki5 is predominantly expressed in MNs, but not in other neuronal populations of the spinal cord. Furthermore, comprehensive RNA sequencing (RNA-seq) analyses revealed that Qki5-dependent RNA regulation plays a pivotal role in generating the MN-specific transcriptome through pre-messenger ribonucleic acid (mRNA) splicing for the synapse-related molecules and c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pathways. Indeed, MN-specific ablation of the Qki5 caused neurodegeneration in postnatal mice and loss of Qki5 function resulted in the aberrant activation of stress-responsive JNK/SAPK pathway both in vitro and in vivo. These data suggested that Qki5 plays a crucial biological role in RNA regulation and safeguarding of MNs and might be associated with pathogenesis of MNDs.

Developmental Disruption of Mef2c in Medial Ganglionic Eminence–Derived Cortical Inhibitory Interneurons Impairs Cellular and Circuit Function

BackgroundMEF2C is strongly linked to various neurodevelopmental disorders including autism, intellectual disability, schizophrenia, and attention-deficit/hyperactivity disorder. Mice that constitutively lack 1 copy of Mef2c or selectively lack both copies of Mef2c in cortical excitatory neurons display a variety of behavioral phenotypes associated with neurodevelopmental disorders. The MEF2C protein is a transcription factor necessary for cellular development and synaptic modulation of excitatory neurons. MEF2C is also expressed in a subset of cortical GABAergic (gamma-aminobutyric acidergic) inhibitory neurons, but its function in those cell types remains largely unknown. MethodsUsing conditional deletions of the Mef2c gene in mice, we investigated the role of MEF2C in parvalbumin-expressing interneurons (PV-INs), the largest subpopulation of cortical GABAergic cells, at 2 developmental time points. We performed slice electrophysiology, in vivo recordings, and behavior assays to test how embryonic and late postnatal loss of MEF2C from GABAergic INs impacts their survival and maturation and alters brain function and behavior. ResultsLoss of MEF2C from PV-INs during embryonic, but not late postnatal, development resulted in reduced PV-IN number and failure of PV-INs to molecularly and synaptically mature. In association with these deficits, early loss of MEF2C in GABAergic INs led to abnormal cortical network activity, hyperactive and stereotypic behavior, and impaired cognitive and social behavior. ConclusionsMEF2C expression is critical for the development of cortical GABAergic INs, particularly PV-INs. Embryonic loss of function of MEF2C mediates dysfunction of GABAergic INs, leading to altered in vivo patterns of cortical activity and behavioral phenotypes associated with neurodevelopmental disorders.

Spontaneous immunological activities in the target tissue of vitiligo-prone Smyth and vitiligo-susceptible Brown lines of chicken.

Vitiligo is an acquired de-pigmentation disorder characterized by the post-natal loss of epidermal melanocytes (pigment-producing cells) resulting in the appearance of white patches in the skin. The Smyth chicken is the only model for vitiligo that shares all the characteristics of the human condition including: spontaneous post-natal loss of epidermal melanocytes, interactions between genetic, environmental and immunological factors, and associations with other autoimmune diseases. In addition, an avian model for vitiligo has the added benefit of an easily accessible target tissue (a growing feather) that allows for the repeated sampling of an individual and thus the continuous monitoring of local immune responses over time. Using a combination of flow cytometry and gene expression analyses, we sought to gain a comprehensive understanding of the initiating events leading to expression of vitiligo in growing feathers by monitoring the infiltration of leukocytes and concurrent immunological activities in the target tissue beginning prior to visual onset and continuing throughout disease development. Here, we document a sequence of immunologically significant events, including characteristic rises in infiltrating B and αβ T cells as well as evidence of active leukocyte recruitment and cell-mediated immune activities (CCL19, IFNG, GZMA) leading up to visual vitiligo onset. Examination of growing feathers from vitiligo-susceptible Brown line chickens revealed anti-inflammatory immune activities which may be responsible for preventing vitiligo (IL10, CTLA4, FOXP3). Furthermore, we detected positive correlations between infiltrating T cells and changes in their T cell receptor diversity supporting a T cell-specific immune response. Collectively, these results further support the notion of cell-mediated immune destruction of epidermal melanocytes in the pulp of growing feathers and open new avenues of study in the vitiligo-prone Smyth and vitiligo-susceptible Brown line chickens.

A comparative analysis of TonEBP conditional knockout mouse models reveals inter-dependency between compartments of the intervertebral disc.

Interactions between notochord and sclerotome are required for normal embryonic spine patterning, but whether the postnatal derivatives of these tissues also require interactions for postnatal intervertebral disc (IVD) growth and maintenance is less established. We report here the comparative analysis of four conditional knockout mice deficient for TonEBP, a transcription factor known to allow cells to adapt to changes in extracellular osmotic pressure, in specific compartments of the IVD. We show that TonEBP deletion in nucleus pulposus (NP) cells does not affect their survival or aggrecan expression, but promoted cell proliferation in the NP and in adjacent vertebral growth plates (GPs). In cartilage end plates/GPs, TonEBP deletion induced cell death, but also structural alterations in the adjacent NP cells and vertebral bodies. Embryonic or postnatal TonEBP loss generated similar IVD changes. In addition to demonstrating the requirement of TonEBP in the different compartments of the IVD, this comparative analysis uncovers the in vivo interdependency of the different IVD compartments during the growth of the postnatal IVD-vertebral units.

The effects of unsupervised home-based exercise training during pregnancy: A systematic review.

Pregnant women may experience physical and emotional distress. Exercise is recommended for healthy pregnant women and is beneficial for their mental and physical health. Unsupervised home-based exercise is cost-effective for pregnant women as an occasional solution for their discomfort. However, no synthesis of randomized trials on this topic has been conducted. The aim of this study was to evaluate the effectiveness of unsupervised home-based exercise during pregnancy. A systematic search for randomized controlled trials was performed in electronic databases. The review extracted eligibility criteria based on unsupervised home-based exercise intervention. The quality of the included studies was performed using the Cochrane Risk of Bias Tool 2.0. This review was registered a priori in PROSPERO (CRD42023452966). In total, seven studies were selected for systematic review. Participant adherence rates for the three reported studies varied considerably, ranging from 33% to 75%. Two studies revealed that unsupervised home-based exercise improved symptom severity in relation to long-term adherence to exercise. Two studies suggested that maternal aerobic fitness increased due to exercise. One study revealed improved sleep quality. However, none of the studies supported the positive effects of exercise on fatigue, maternal insulin sensitivity, prenatal weight gain, postnatal weight loss, birth pain, and cesarean section. Unsupervised home-based exercise improves discomfort symptoms during pregnancy but requires a long intervention period. This finding suggests that the evaluation period needs to be longer to identify the effects of exercise. In addition, a theoretical-based integrity exercise plan should be considered to promote the effectiveness of unsupervised home-based exercise.

TMTC4 is a hair cell-specific human deafness gene.

Transmembrane and tetratricopeptide repeat 4 (Tmtc4) is a deafness gene in mice. Tmtc4-KO mice have rapidly progressive postnatal hearing loss due to overactivation of the unfolded protein response (UPR); however, the cellular basis and human relevance of Tmtc4-associated hearing loss in the cochlea was not heretofore appreciated. We created a hair cell-specific conditional KO mouse that phenocopies the constitutive KO with postnatal onset deafness, demonstrating that Tmtc4 is a hair cell-specific deafness gene. Furthermore, we identified a human family in which Tmtc4 variants segregate with adult-onset progressive hearing loss. Lymphoblastoid cells derived from multiple affected and unaffected family members, as well as human embryonic kidney cells engineered to harbor each of the variants, demonstrated that the human Tmtc4 variants confer hypersensitivity of the UPR toward apoptosis. These findings provide evidence that TMTC4 is a deafness gene in humans and further implicate the UPR in progressive hearing loss.

Wnt16 Promotes Vascular Smooth Muscle Contractile Phenotype and Function via Taz (Wwtr1) Activation in Male LDLR-/- Mice.

Wnt16 is expressed in bone and arteries, and maintains bone mass in mice and humans, but its role in cardiovascular physiology is unknown. We show that Wnt16 protein accumulates in murine and human vascular smooth muscle (VSM). WNT16 genotypes that convey risk for bone frailty also convey risk for cardiovascular events in the Dallas Heart Study. Murine Wnt16 deficiency, which causes postnatal bone loss, also reduced systolic blood pressure. Electron microscopy demonstrated abnormal VSM mitochondrial morphology in Wnt16-null mice, with reductions in mitochondrial respiration. Following angiotensin-II (AngII) infusion, thoracic ascending aorta (TAA) dilatation was greater in Wnt16-/- vs Wnt16+/+ mice (LDLR-/- background). Acta2 (vascular smooth muscle alpha actin) deficiency has been shown to impair contractile phenotype and worsen TAA aneurysm with concomitant reductions in blood pressure. Wnt16 deficiency reduced expression of Acta2, SM22 (transgelin), and other contractile genes, and reduced VSM contraction induced by TGFβ. Acta2 and SM22 proteins were reduced in Wnt16-/- VSM as was Ankrd1, a prototypic contractile target of Yap1 and Taz activation via TEA domain (TEAD)-directed transcription. Wnt16-/- VSM exhibited reduced nuclear Taz and Yap1 protein accumulation. SiRNA targeting Wnt16 or Taz, but not Yap1, phenocopied Wnt16 deficiency, and Taz siRNA inhibited contractile gene upregulation by Wnt16. Wnt16 incubation stimulated mitochondrial respiration and contraction (reversed by verteporfin, a Yap/Taz inhibitor). SiRNA targeting Taz inhibitors Ccm2 and Lats1/2 mimicked Wnt16 treatment. Wnt16 stimulated Taz binding to Acta2 chromatin and H3K4me3 methylation. TEAD cognates in the Acta2 promoter conveyed transcriptional responses to Wnt16 and Taz. Wnt16 regulates cardiovascular physiology and VSM contractile phenotype, mediated via Taz signaling.

Genome-wide profiling of miRNA-gene regulatory networks in mouse postnatal heart development-implications for cardiac regeneration.

After birth, mammalian cardiomyocytes substantially lose proliferative capacity with a concomitant switch from glycolytic to oxidative mitochondrial energy metabolism. Micro-RNAs (miRNAs) regulate gene expression and thus control various cellular processes. Their roles in the postnatal loss of cardiac regeneration are however still largely unclear. Here, we aimed to identify miRNA-gene regulatory networks in the neonatal heart to uncover role of miRNAs in regulation of cell cycle and metabolism. We performed global miRNA expression profiling using total RNA extracted from mouse ventricular tissue samples collected on postnatal day 1 (P01), P04, P09, and P23. We used the miRWalk database to predict the potential target genes of differentially expressed miRNAs and our previously published mRNA transcriptomics data to identify verified target genes that showed a concomitant differential expression in the neonatal heart. We then analyzed the biological functions of the identified miRNA-gene regulatory networks using enriched Gene Ontology (GO) and KEGG pathway analyses. Altogether 46 miRNAs were differentially expressed in the distinct stages of neonatal heart development. For twenty miRNAs, up- or downregulation took place within the first 9 postnatal days thus correlating temporally with the loss of cardiac regeneration. Importantly, for several miRNAs, including miR-150-5p, miR-484, and miR-210-3p there are no previous reports about their role in cardiac development or disease. The miRNA-gene regulatory networks of upregulated miRNAs negatively regulated biological processes and KEGG pathways related to cell proliferation, while downregulated miRNAs positively regulated biological processes and KEGG pathways associated with activation of mitochondrial metabolism and developmental hypertrophic growth. This study reports miRNAs and miRNA-gene regulatory networks with no previously described role in cardiac development or disease. These findings may help in elucidating regulatory mechanism of cardiac regeneration and in the development of regenerative therapies.

Universal neonatal hearing screening and delayed hearing loss or late-developmental hearing loss

ObjectiveTo determine the percentage of children with permanent bilateral postnatal hearing loss in order to study its incidence, related risk factors, diagnosis and treatment. MethodsRetrospective study to collect data on children diagnosed with hearing loss outside the neonatal period in the Hearing Loss Unit of the Hospital Universitario Central de Asturias, from April 2014 to April 2021. Results52 cases met the inclusion criteria. The detection rate of congenital hearing loss in the neonatal screening programme in the same study period was 1.5 children per thousand newborns per year, adding postnatal hearing loss results in a rate of infant bilateral hearing loss of 2.7 children per thousand (55.5% and 44.4% respectively). Thirty-five children presented risk factors for hearing loss, of which 23 were at retrocochlear risk. The mean age at referral was 91.9 (18–185) months. Hearing aid fitting was indicated in 44 cases (84.6%). Cochlear implantation was indicated in eight cases (15.4%). DiscussionAlthough congenital hearing loss accounts for the majority of childhood deafness, postnatal hearing loss has a significant incidence. This may be mainly due to: (1) that hearing impairment may arise in the first years of life, (2) that mild hearing loss as well as hearing loss in severe frequencies are undetectable by neonatal screening in some cases, (3) that some children may have false negative results. Conclusionpostnatal hearing loss requires identification of risk factors and long-term follow-up of children with hearing loss, as it needs to be detected and treated early.

Prenatal diagnosis and outcome of fetal urinomas in relation to the underlying etiology.

Evaluation of course and outcome of pregnancies with prenatally diagnosed fetal urinoma in a single center over a 20-year period. Retrospective study including all prenatally suspected or diagnosed fetal urinomas. Cases were analyzed by ultrasound findings during pregnancy, comparing urinomas caused by lower urinary tract obstruction (LUTO) and ureteropelvic or ureterovesical junction obstruction (UPJO/UVJO). Course of pregnancy and outcomes were compared according to the underlying etiology. 87 cases of fetal urinomas were identified between 2002 and 2022. The underlying etiology was LUTO in 56.3% and UPJO/UVJO in 43.7%. Complications mainly included oligo- or anhydramnios, thoracic hypoplasia as well as associated renal abnormalities. Postnatally, loss of function (LOF) in kidneys affected by urinomas was seen in 78.6% of children overall, but significantly more often in cases of UPJO/UVJO than in LUTO (86.2% vs. 70.2%, p<0.05). Association of prenatal urinoma and postnatal LOF of the affected kidney is high, especially in cases caused by UPJO/UVJO. In survivors with urinoma caused by UPJO/UVJO, the general prognosis is excellent if the contralateral kidney was normal. In survivors with urinomas caused by LUTO, long-term prognosis depends on postnatal renal and pulmonary function.

Modification of serum fatty acids in preterm infants by parenteral lipids and enteral docosahexaenoic acid/arachidonic acid: A secondary analysis of the Mega Donna Mega trial

Preterm infants risk deficits of long-chain polyunsaturated fatty acids (LCPUFAs) that may contribute to morbidities and hamper neurodevelopment. We aimed to determine longitudinal serum fatty acid profiles in preterm infants and how the profiles are affected by enteral and parenteral lipid sources. Cohort study analyzing fatty acid data from the Mega Donna Mega study, a randomized control trial with infants born <28 weeks of gestation (n=204) receiving standard nutrition or daily enteral lipid supplementation with arachidonic acid (AA):docosahexaenoic acid (DHA) (100:50mg/kg/day). Infants received an intravenous lipid emulsion containing olive oil:soybean oil (4:1). Infants were followed from birth to postmenstrual age 40 weeks. Levels of 31 different fatty acids from serum phospholipids were determined by GC-MS and reported in relative (mol%) and absolute concentration (μmol l-1) units. Higher parenteral lipid administration resulted in lower serum proportion of AA and DHA relative to other fatty acids during the first 13 weeks of life (p<0.001 for the 25th vs the 75th percentile). The enteral AA:DHA supplement increased the target fatty acids with little impact on other fatty acids. The absolute concentration of total phospholipid fatty acids changed rapidly in the first weeks of life, peaking at day 3, median (Q1-Q3) 4452 (3645-5466) μmol l-1, and was positively correlated to the intake of parenteral lipids. Overall, infants displayed common fatty acid trajectories over the study period. However, remarkable differences in fatty acid patterns were observed depending on whether levels were expressed in relative or absolute units. For example, the relative levels of many LCPUFAs, including DHA and AA, declined rapidly after birth while their absolute concentrations increased in the first week of life. For DHA, absolute levels were significantly higher compared to cord blood from day 1 until postnatal week 16 (p<0.001). For AA, absolute postnatal levels were lower compared to cord blood from week 4 throughout the study period (p<0.05). Our data show that parenteral lipids aggravate the postnatal loss of LCPUFAs seen in preterm infants and that serum AA available for accretion is below that in utero. Further research is needed to establish optimal postnatal fatty acid supplementation and profiles in extremely preterm infants to promote development and long-term health. ClinicalTrials.gov, identifier: NCT03201588.

Cribado auditivo neonatal universal e hipoacusia diferida o de desarrollo tardío

ObjectiveTo determine the percentage of children with permanent bilateral postnatal hearing loss in order to study its incidence, related risk factors, diagnosis and treatment. MethodsRetrospective study to collect data on children diagnosed with hearing loss outside the neonatal period in the Hearing Loss Unit of the Hospital Universitario Central de Asturias, from April 2014 to April 2021. Results52 cases met the inclusion criteria. The detection rate of congenital hearing loss in the neonatal screening programme in the same study period was 1.5 children per thousand newborns per year, adding postnatal hearing loss results in a rate of infant bilateral hearing loss of 2.7 children per thousand (55.5% and 44.4% respectively). Thirty-five children presented risk factors for hearing loss, of which 23 were at retrocochlear risk. The mean age at referral was 91.9 (18-185) months. Hearing aid fitting was indicated in 44 cases (84.6%). Cochlear implantation was indicated in eight cases (15.4%). DiscussionAlthough congenital hearing loss accounts for the majority of childhood deafness, postnatal hearing loss has a significant incidence. This may be mainly due to: 1) that hearing impairment may arise in the first years of life, 2) that mild hearing loss as well as hearing loss in severe frequencies are undetectable by neonatal screening in some cases, 3) that some children may have false negative results. ConclusionPostnatal hearing loss requires identification of risk factors and long-term follow-up of children with hearing loss, as it needs to be detected and treated early.

A defect in mitochondrial protein translation influences mitonuclear communication in the heart

The regulation of the informational flow from the mitochondria to the nucleus (mitonuclear communication) is not fully characterized in the heart. We have determined that mitochondrial ribosomal protein S5 (MRPS5/uS5m) can regulate cardiac function and key pathways to coordinate this process during cardiac stress. We demonstrate that loss of Mrps5 in the developing heart leads to cardiac defects and embryonic lethality while postnatal loss induces cardiac hypertrophy and heart failure. The structure and function of mitochondria is disrupted in Mrps5 mutant cardiomyocytes, impairing mitochondrial protein translation and OXPHOS. We identify Klf15 as a Mrps5 downstream target and demonstrate that exogenous Klf15 is able to rescue the overt defects and re-balance the cardiac metabolome. We further show that Mrps5 represses Klf15 expression through c-myc, together with the metabolite L-phenylalanine. This critical role for Mrps5 in cardiac metabolism and mitonuclear communication highlights its potential as a target for heart failure therapies.

Neonatal loss of FGFR2 in astroglial cells affects locomotion, sociability, working memory, and glia-neuron interactions in mice

Fibroblast growth factor receptor 2 (FGFR2) is almost exclusively expressed in glial cells in postnatal mouse brain, but its impact in glia for brain behavioral functioning is poorly understood. We compared behavioral effects from FGFR2 loss in both neurons and astroglial cells and from FGFR2 loss in astroglial cells by using either the pluripotent progenitor-driven hGFAP-cre or the tamoxifen-inducible astrocyte-driven GFAP-creERT2 in Fgfr2 floxed mice. When FGFR2 was eliminated in embryonic pluripotent precursors or in early postnatal astroglia, mice were hyperactive, and had small changes in working memory, sociability, and anxiety-like behavior. In contrast, FGFR2 loss in astrocytes starting at 8 weeks of age resulted only in reduced anxiety-like behavior. Therefore, early postnatal loss of FGFR2 in astroglia is critical for broad behavioral dysregulation. Neurobiological assessments demonstrated that astrocyte-neuron membrane contact was reduced and glial glutamine synthetase expression increased only by early postnatal FGFR2 loss. We conclude that altered astroglial cell function dependent on FGFR2 in the early postnatal period may result in impaired synaptic development and behavioral regulation, modeling childhood behavioral deficits like attention deficit hyperactivity disorder (ADHD).

Early postnatal weight loss does not affect the 2-year neurodevelopment in preterm infants of less than 32 weeks.

It is still unclear if the magnitude of early postnatal weight loss (PWL) could be associated with neurodevelopmental outcomes in preterm infants. We studied the association between PWL and neurodevelopment at 2-year corrected age in preterm infants. We retrospectively reviewed data of preterm infants with a gestational age between 24 +0 and 31 +6 weeks/days, admitted at the G.Salesi Children's Hospital, Ancona, Italy, between 1 January 2006 and 31 December 2019. Infants with PWL greater than or equal to 10% (PWL ≥ 10%) were compared with those with PWL of less than 10% (PWL < 10%). A matched cohort analysis was also performed using gestational age and birth weight as matching variables. We analysed 812 infants: 471 (58%) PWL ≥ 10% and 341 (42%) PWL < 10%. A subgroup of 247 PWL ≥ 10% was closely match-paired with 247 PWL < 10% infants. There were no differences in amino acid and energy intakes from birth to day 14 of life and from birth to 36 weeks. Although at 36 weeks, body weight and total length were lower in PWL ≥ 10% than PWL < 10%, anthropometry and neurodevelopment at 2 years were similar between groups. Given similar amino acid and energy intakes on PWL ≥ 10% and PWL < 10% preterm infants of less than 32 +0 weeks/days, PWL does not affect 2-year neurodevelopment.

Postnatal growth and body composition in extremely low birth weight infants fed with individually adjusted fortified human milk: a cohort study

This cohort study aimed to evaluate the impact of an individualised nutritional care approach combining standardised fortification with adjustable fortification on postnatal growth and body composition in extremely low birth weight (ELBW) infants. We included ELBW infants admitted to a neonatal intensive care unit and still hospitalised at 35 weeks postmenstrual age (PMA). The fortification of human milk was standardised (multicomponent fortifier) between 70 mL/kg/day and full enteral feeding, and then individualised using adjustable fortification. When weight gain was below 20 g/kg/day, protein or energy was added when serum urea was below or above 3.5 mmol/L, respectively. Postnatal growth failure (PNGF) was defined as being small for gestational age at discharge and/or when the Z-score loss between birth and discharge was higher than 1. Body composition was assessed between 35 and 41 weeks of PMA. Among the 310 ELBW infants included, the gestational age of birth was 26.7 ± 1.8 weeks, and the birth weight was 800 ± 128 g. The mean Z-score difference between birth and discharge was moderately negative for the weight (−0.32), more strongly negative for length (−1.21), and almost nil for head circumference (+ 0.03). Only 27% of infants presented PNGF. At discharge, fat mass was 19.8 ± 3.6%. Multivariable analysis showed that the proportion of preterm formula received and gestational age at birth were independently associated with the percentage of fat mass. Conclusion: The individualised nutritional care approach applied herein prevented postnatal weight loss in most infants, limited length growth deficit, and supported excellent head circumference growth.What is Known:• At least half of extremely low birth weight infants are small for gestational age at discharge and postnatal growth deficit has been associated with impaired neurocognitive and renal development.• Human milk is the main milk used in neonatology and, although fortification of human milk is a standard of care, there is no consensus regarding the optimal fortification strategy to be adopted.What is New:• Using an approach combining standardised fortification followed by individualised adjustable fortification limited postnatal growth deficit for body weight and head circumference. Postnatal growth failure is not a fatality in extremely low birth weight infants.• Each additional gestational age week at birth resulted in a decrease in fat mass percentage at discharge, which was higher than in foetuses of the same gestational age, likely representing a necessary adaptation to extra-uterine life.

Modeling of the determinants of Low-birth weight among children in Uganda

Birthweight is the first weight of the baby obtained after birth. For live childbirths, birthweight should preferably be measured within the first hour of life, before substantial post-natal weight loss has occurred. Low birth weight renders children exposed to infectious disease morbidity and mortality during both infancy and childhood. The objective of the study was to apply the modified binary logistic model to determine the factors associated with low birth weight among children in Uganda. The data used for this study was the Uganda Demographic and Health Survey (UDHS- 2016), the UDH survey selected 20615 households where 15522 women were successfully interviewed with known child birth weight out of which 5498 observations were considered after data cleaning. The results of the study revealed that the association between the age of the mother and low birth was statistically significant with a p-value of 0.044. The study also found that the risk of low birth weight babies was low for married women as compared to non-married women with a p-value of 0.003. Antenatal visit during pregnancy decreases the chances of having an infant with low birth weight. The association between low birth weight and the employed was statistically significant with a p-value of 0.007 and the likelihood of low birth weight infants for the rich was low as compared to the poor. The study concluded that the association between age, antenatal visits during pregnancy, occupation, wealth status of the mother and low birth weight were statistically significant.

Analysis of Patient Cues in Asynchronous Health Interactions: Pilot Study Combining Empathy Appraisal and Systemic Functional Linguistics.

Lifestyle-related diseases are among the leading causes of death and disability. Their rapid increase worldwide has called for low-cost, scalable solutions to promote health behavior changes. Digital health coaching has proved to be effective in delivering affordable, scalable programs to support lifestyle change. This approach increasingly relies on asynchronous text-based interventions to motivate and support behavior change. Although we know that empathy is a core element for a successful coach-user relationship and positive patient outcomes, we lack research on how this is realized in text-based interactions. Systemic functional linguistics (SFL) is a linguistic theory that may support the identification of empathy opportunities (EOs) in text-based interactions, as well as the reasoning behind patients' linguistic choices in their formulation. This study aims to determine whether empathy and SFL approaches correspond and complement each other satisfactorily to study text-based communication in a health coaching context. We sought to explore whether combining empathic assessment with SFL categories can provide a means to understand client-coach interactions in asynchronous text-based coaching interactions. We retrieved 148 text messages sent by 29 women who participated in a randomized trial of telecoaching for the prevention of gestational diabetes mellitus (GDM) and postnatal weight loss. We conducted a pilot study to identify users' explicit and implicit EOs and further investigated these statements using the SFL approach, focusing on the analysis of transitivity and thematic analysis. We identified 164 EOs present in 42.37% (3478/8209) of the word count in the corpus. These were mainly negative (n=90, 54.88%) and implicit (n=55, 60.00%). We distinguished opening, content and closing messages structures. Most of the wording was found in the content (n=7077, 86.21%) with a declarative structure (n=7084, 86.30%). Processes represented 22.4% (n=1839) of the corpus, with half being material (n=876, 10.67%) and mostly related to food and diet (n=196, 54.92%), physical activity (n=96, 26.89%), and lifestyle goals (n=40, 11.20%). Our findings show that empathy and SFL approaches are compatible. The results from our transitivity analysis reveal novel insights into the meanings of the users' EOs, such as their seek for help or praise, often missed by health care professionals (HCPs), and on the coach-user relationship. The absence of explicit EOs and direct questions could be attributed to low trust on or information about the coach's abilities. In the future, we will conduct further research to explore additional linguistic features and code coach messages. Australian New Zealand Clinical Trials Registry (ANZCTR) ACTRN12620001240932; https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=380020.