He L, Harold SF, Frydrysiak–Brzozowska A. From Sanger to Single Molecules: How High-throughput Deoxyribonucleic Acid Sequencing Became Possible. Newborn 2026; 5(3):iv-xi. DOI: 10.5005/newborn-5-3-iv.

----------------------------------------------------------------------------------------------------------------------------------------------------

Joseph JE, Muthukumaran N, Sangeetha T. Improving Early Mother’s Own Milk Availability in Separated Dyads in an Extramural Neonatal Intensive Care Unit Using a Structured Lactation Support Protocol: A Quality Improvement Study. Newborn 2026;5(3):123–128. DOI: 10.5005/jp-journals-11002-0166.

 

Abstract:

Objective: To increase the proportion of separated neonates receiving mother’s own milk (MOM) within 48 hours of admission from a baseline of 25% to at least 50% over a 6-month period in an extramural neonatal intensive care unit (NICU).

Design: Prospective quality improvement study using the point-of-care quality improvement (POCQI) methodology. Setting: Extramural NICU of a tertiary care teaching hospital in South India. Participants: One hundred and eighty-six separated mother–infant dyads admitted within the first 5 days of life. Intervention: Sequential implementation of four plan–do–study–act (PDSA) cycles consisting of structured counseling, telelactation support, transportation support for expressed breast milk, and lactation counselor-led monitoring. Main outcome measures: Primary outcome was the proportion of neonates receiving MOM within 48 hours of admission. Secondary outcome was the proportion of MOM in total enteral feeds by day 5. Process measures included counseling within 6 hours of admission and milk expression frequency greater than eight times daily.

Results: A total of 186 mother–infant dyads were enrolled. The proportion of neonates receiving MOM within 48 hours increased from 25% at baseline to 94% during the sustenance phase. Counseling within 6 hours improved from 10% to 98%, while mothers expressing milk more than eight times daily increased from 0 to 96%. The proportion of MOM in total feeds by day 5 showed sustained improvement across successive PDSA cycles.

Conclusion: A structured lactation-support protocol significantly improved early MOM availability among separated dyads in an extramural NICU. The interventions were low-cost, feasible, and sustainable.

​

​Key scientific associations: Breastfeeding, Expressed breast milk, Mother’s own milk, Neonatal intensive care unit, Point-of-care quality improvement, Quality improvement, Telelactation.

-----------------------------------------------------------------------------------------------------------------------------------------------------------------

Agroya AS, Patil NB, Kavthekar SO. C-reactive Protein and Albumin Ratio as a Biomarker of Gram-negative Bacteremia in Neonatal Sepsis. Newborn 2026;5(3):129–132. DOI: 10.5005/jp-journals-11002-0168.

 

​Abstract:

Introduction: Many previous studies often focused on C-reactive protein (CRP) or albumin individually, without considering their combined effect in neonatal sepsis.

Aim: To evaluate the utility of the CRP and albumin ratio (CRP/albumin) for differentiating between Gram-positive or Gram-negative bacteremia in blood culture-positive neonatal sepsis.

Materials and methods: In this cross-sectional study, a total of 94 blood culture-positive (done by the automated BACTEC) septic neonates were included. The serum CRP and albumin levels were measured on a biochemistry analyzer, and the serum CRP/albumin ratio was calculated manually and compared with (Gram-positive/Gram-negative) blood culture reports.

Results: Neonates with Gram-positive and Gram-negative infections had a mean CRP of 32.98 ± 8.52 mg/L and 96.79 ± 13.05 mg/L, respectively. The mean serum albumin was 2.80 ± 0.13 gm/dL and 2.69 ± 0.14 gm/dL among neonates with Gram-positive and Gram-negative infections, respectively. The mean CRP/albumin ratio was 11.80 ± 3.20 and 36.16 ± 5.33 in Gram-positive and Gram-negative neonates, respectively, and was statistically significant (p< 0.001). Multivariable logistic regression analysis revealed CRP/albumin as the sole significant predictor of Gram-negative sepsis (OR: 1.291; 95% CI: 1.148–1.451).

Conclusion: The CRP/albumin ratio was significantly higher in Gram-negative neonatal sepsis than Gram-positive sepsis. The higher ratio can be used to predict Gram-negative neonatal sepsis, especially organisms like Klebsiella, Pseudomonas, and Escherichia coli species. Clinical significance: The CRP/albumin biomarker emerged as a cost-effective, gestational-age-independent tool. A markedly higher CRP/ albumin ratio >35 suggested Gram-negative sepsis, and it can be used as an adjunctive tool that complements clinical assessment while awaiting culture report confirmation.

 

​​Key scientific associations: Albumin, Blood culture, C-reactive protein, Neonatal sepsis, Organisms.

​-------------------------------------------------------------------------------------------------------------------------------------------------------------

Maheshwari A, Huisman TAGM. Zellweger Spectrum Disorders: Beyond the Peroxisome. Newborn 2026;5(3): 133–157. DOI: 10.5005/jp-journals-11002-0164. 

​

Abstract: Zellweger spectrum disorders (ZSDs) are rare autosomal recessive peroxisomal biogenesis disorders caused by pathogenic variants in PEX genes encoding peroxins, proteins essential for peroxisome assembly, maintenance, and matrix protein import. Defective peroxisome biogenesis disrupts multiple metabolic pathways, resulting in accumulation of very-long-chain fatty acids (VLCFAs), phytanic and pristanic acids, pipecolic acid, and bile acid (BA) intermediates, together with impaired plasmalogen and docosahexaenoic acid (DHA) synthesis. These biochemical abnormalities produce a severe multisystem disorder involving the central nervous system, liver, kidneys, eyes, ears, adrenal glands, and skeleton. Clinical manifestations range from the classic neonatal Zellweger syndrome with profound hypotonia, refractory seizures, feeding difficulties, hepatic dysfunction, characteristic craniofacial features, and early mortality, to milder phenotypes that survive into childhood or adulthood. This review summarizes current knowledge regarding the epidemiology, molecular genetics, pathophysiology, developmental biology, and evolutionary conservation of peroxisomes, emphasizing the pivotal roles of peroxins, particularly peroxin 5 (PEX5), in peroxisomal protein import. Recent advances in understanding neuronal migration defects, oligodendrocyte maturation, microglial dysfunction, oxidative stress, mitochondrial–peroxisomal interactions, epigenetic regulation, and non-coding RNA (ncRNA) responses are discussed to provide an integrated view of disease mechanisms. Characteristic laboratory abnormalities, neuroimaging findings, ultrastructural changes, and molecular diagnostic strategies are reviewed, together with emerging concepts including uniparental disomy (UPD), genotype–phenotype correlations, and phylogenetic conservation of PEX genes. Although treatment remains largely supportive and multidisciplinary, improvements in biochemical testing, next-generation sequencing, newborn diagnosis, and comprehensive clinical care have expanded recognition of milder disease and improved long-term outcomes for selected patients. Continued advances in molecular biology, systems genomics, and targeted therapeutic development are expected to refine diagnosis, enhance prognostic assessment, and provide opportunities for future disease-modifying interventions in this complex group of inherited peroxisomal disorders.

​

​Key scientific associations: Peroxisomal biogenesis disorders, peroxisomal biogenesis factor, peroxins, PEX mutations, pathogenic variants, autosomal recessive inheritance, metabolic detoxification, ether lipid synthesis, bile acid metabolism, toxic metabolite accumulation, lipid deficiency, neonatal adrenoleukodystrophy, infantile Refsum disease, disease continuum, phenotypic spectrum, Hans Zellweger, Swiss-American pediatrician, University of Iowa, neonatal hypotonia, feeding difficulties, craniofacial dysmorphism, hepatic dysfunction, neurodevelopmental impairment, structural brain abnormalities, skeletal abnormalities, multisystem disease, neonatal presentation, supportive management, molecular diagnosis, carrier detection, founder mutations, carrier frequency, reproductive risk, live birth incidence, geographic variation, ethnic distribution, prenatal testing, asymptomatic carriers, peroxisome assembly, peroxisome function, phospholipid bilayer, transporter proteins, electron-dense core, crystalline matrix, fibrillar matrix, urate oxidase, D-amino acid oxidase, oxidative balance, metabolic compartment, eukaryotic organelles, Zellweger spectrum disorder, Zellweger syndrome, peroxisome, peroxisomal biogenesis, PEX gene, PEX1, PEX2, PEX3, PEX5, PEX6, PEX10, PEX12, PEX13, PEX14, PEX16, PEX19, autosomal recessive, inherited metabolic disease, very-long-chain fatty acids, VLCFA, plasmalogens, pipecolic acid, phytanic acid, pristanic acid, bile acid intermediates, DHCA, THCA, docosahexaenoic acid, DHA, polyunsaturated fatty acids, β-oxidation, α-oxidation, catalase, hydrogen peroxide, reactive oxygen species, oxidative stress, lipid metabolism, ether phospholipids, neuronal migration, cortical dysplasia, leukodystrophy, hypomyelination, oligodendrocytes, astrocytes, microglia, mitochondria, mitochondrial dysfunction, endoplasmic reticulum, lipid droplets, matrix protein import, PTS1, PTS2, PEX5 receptor, TPR domain, WxxxF motif, RING finger complex, ubiquitination, AAA ATPase, protein trafficking, membrane biogenesis, organelle dynamics, peroxisome proliferation, pexophagy, catalase deficiency, craniofacial dysmorphism, hypotonia, neonatal seizures, developmental delay, sensorineural hearing loss, retinal dystrophy, cataracts, hepatic dysfunction, cholestasis, adrenal insufficiency, renal cysts, skeletal dysplasia, chondrodysplasia punctata, newborn screening, tandem mass spectrometry, next-generation sequencing, whole-exome sequencing, whole-genome sequencing, genotype–phenotype correlation, uniparental disomy, copy number variation, phylogenetics, molecular evolution, evolutionary conservation, WAG model, LG model, JTT model, maximum likelihood, neighbor joining, fast minimum evolution, electron microscopy, crystalloid, immunofluorescence, fibroblast culture, precision medicine, gene therapy, pharmacological chaperones, supportive care, multidisciplinary management, Acyl-CoA oxidase, D-bifunctional protein, acyl-CoA, acyltransferase, alkylglycerone phosphate synthase, acyl-CoA synthetase, ABCD1, ABCD2, ABCD3, PMP70, PEX11, PEX26, PEX7, PEX8, PEX22, PEX4, PEX15, PEX17, PEX18, PEX20, PEX21, PEX25, PEX27, PEX28, PEX29, peroxisomal membrane protein, matrix enzymes, membrane assembly, organelle biogenesis, lipid homeostasis, redox balance, antioxidant defense, hydrogen peroxide detoxification, lipid peroxidation, ferroptosis, apoptosis, autophagy, mitophagy, organelle crosstalk, ER–peroxisome contact sites, mitochondria–peroxisome interactions, membrane contact sites, fatty acid elongation, branched-chain fatty acids, dicarboxylic acids, cholesterol metabolism, steroidogenesis, cholesterol side-chain cleavage, bile acid synthesis, glyoxylate metabolism, purine metabolism, amino acid metabolism, lysine degradation, neurotransmission, neuroinflammation, neurodegeneration, axonal degeneration, synaptic dysfunction, white matter disease, cerebellar hypoplasia, polymicrogyria, pachygyria, heterotopia, ventriculomegaly, corpus callosum abnormalities, magnetic resonance imaging, magnetic resonance spectroscopy, electroencephalography, visual evoked potentials, brainstem auditory evoked responses, adrenal cortex, hepatomegaly, splenomegaly, nephrocalcinosis, renal dysfunction, failure to thrive, dysphagia, aspiration, gastrostomy, nutritional support, rehabilitation, physical therapy, occupational therapy, speech therapy, genetic counseling, prenatal diagnosis, carrier screening, prenatal ultrasound, chorionic villus sampling, amniocentesis, induced pluripotent stem cells, animal models, mouse models, zebrafish models, CRISPR, transcriptomics, proteomics, metabolomics, lipidomics, biomarkers, natural history, clinical trials, disease progression, quality of life, personalized medicine, translational research, adrenoleukodystrophy protein, acyl-dihydroxyacetone phosphate, alkyl-dihydroxyacetone phosphate, plasmalogen biosynthesis, ether lipid biosynthesis, peroxisomal targeting signal, receptor recycling, cargo recognition, matrix import machinery, membrane docking complex, receptor ubiquitination, receptor export, importomer, peroxisomal membrane permeability, peroxisomal fission, organelle inheritance, membrane curvature, membrane remodeling, dynamin-related protein 1, mitochondrial fission factor, FIS1, MFF, PEX11β, de novo peroxisome formation, endoplasmic reticulum budding, vesicular trafficking, membrane fusion, intracellular transport, organelle quality control, metabolic compartmentalization, cellular homeostasis, lipid signaling, phosphatidylcholine, phosphatidylethanolamine, sphingolipids, ceramides, cholesterol esters, eicosanoids, docosanoids, resolvins, protectins, maresins, arachidonic acid, eicosapentaenoic acid, membrane phospholipids, membrane fluidity, oxidative phosphorylation, ATP metabolism, nicotinamide adenine dinucleotide, flavin adenine dinucleotide, flavoproteins, acyl-CoA metabolism, acetyl-CoA, acetylcarnitine, carnitine metabolism, metabolic profiling, targeted metabolomics, untargeted metabolomics, flux analysis, stable isotope tracing, systems biology, network biology, computational biology, bioinformatics, variant interpretation, pathogenic variant, likely pathogenic variant, variant of uncertain significance, missense mutation, nonsense mutation, frameshift mutation, splice-site mutation, founder mutation, allelic heterogeneity, locus heterogeneity, compound heterozygosity, homozygosity, allelic expression, nonsense-mediated decay, genotype-driven diagnosis, phenotype expansion, precision diagnostics, rare disease, orphan disease, Mendelian disorder, inborn error of metabolism, neonatal hypotonia, infantile encephalopathy, seizure disorders, epilepsy, visual impairment, optic nerve hypoplasia, pigmentary retinopathy, enamel hypoplasia, osteopenia, osteoporosis, digital anomalies, developmental pediatrics, clinical genetics, multidisciplinary clinic, longitudinal follow-up, patient registry, biomarker discovery, therapeutic targets, disease mechanisms, Acylcarnitine profile, adrenocorticotropic hormone, adrenal hypoplasia, alanine aminotransferase, alkaline phosphatase, amino acid oxidation, angiogenesis, apoptosis signaling, arginine metabolism, ATP-binding cassette transporters, auditory neuropathy, basal ganglia, bile alcohols, biomarker validation, biogenesis disorders, blood–brain barrier, brain development, calcium homeostasis, carbohydrate metabolism, cell differentiation, cell signaling, cellular stress response, central nervous system development, cerebellar ataxia, cerebellar development, chaperone proteins, cholic acid intermediates, chromosomal microarray, ciliogenesis, clinical phenotype, cognitive impairment, congenital cataracts, congenital hypotonia, connective tissue abnormalities, corpus callosum agenesis, cortical organization, cytoplasmic receptor recycling, developmental neurobiology, developmental pathology, diagnostic biomarkers, differential diagnosis, DNA sequencing, dominant-negative effect, electron transport chain, embryogenesis, endocrine dysfunction, endoplasmic reticulum stress, enzyme deficiency, exome analysis, exome capture, fibroblast complementation, fibroblast morphology, fetal development, fetal hypotonia, fibroblast proliferation, gene expression profiling, genomic medicine, glycine conjugates, growth retardation, hearing impairment, hepatocellular injury, hepatocyte biology, infant metabolism, infant nutrition, inflammatory signaling, intracellular lipid transport, intracellular trafficking, kidney development, lipid catabolism, liver fibrosis, liver transplantation, long-chain fatty acids, lysosomal interactions, matrix enzyme deficiency, membrane lipid composition, membrane protein insertion, metabolic adaptation, metabolic pathways, metabolic rescue, molecular chaperones, molecular pathology, motor impairment, multi-omics, neural progenitor cells, neuronal differentiation, neurodevelopment, neurogenetics, newborn metabolism, nuclear receptors, organ development, organ dysfunction, orphan drug development, patient-derived fibroblasts, pediatric neurology, peroxisomal enzymes, phospholipid remodeling, postnatal development, prenatal genetics, proteostasis, receptor-mediated import, secondary mitochondrial dysfunction, small-molecule therapy, sterol metabolism, substrate accumulation, systems medicine, therapeutic development, transcriptional regulation.​

------------------------------------------------------------------------------------------------------------------------------------------------------

Das JK, Maheshwari A. High-throughput Sequencing to Identify Errors in Deoxyribonucleic Acid Sequences and Chromosomal Abnormalities. Newborn 2026;5(3):158–172. DOI: 10.5005/jp-journals-11002-0171.

​

Abstract: High-throughput sequencing (HTS), also known as next-generation sequencing (NGS), has transformed genomic research and clinical diagnostics by enabling the rapid, parallel sequencing of millions to billions of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) fragments. Compared with conventional Sanger sequencing, HTS offers substantially greater speed, throughput, and analytical depth, permitting comprehensive investigation of genomes, transcriptomes, and microbial communities. This review provides an integrated overview of HTS technologies, including principles of nucleic acid preparation, sequencing workflows, and major biomedical applications. We summarize the use of HTS for identifying single nucleotide variants (SNVs), insertions and deletions, copy number variations (CNVs), repeat expansions, splice-site and regulatory mutations, as well as structural chromosomal abnormalities such as inversions, translocations, deletions, duplications, and complex genomic rearrangements. The biological mechanisms underlying these abnormalities, including replication errors, recombination defects, transposable element activity, DNA repair failure, and chromosomal instability, are discussed together with their relevance to human disease and genome evolution. Emerging applications in single-cell genomics, metagenomics, pathogen surveillance, cancer genomics, and precision medicine are highlighted, along with the expanding role of artificial intelligence and advanced bioinformatics in sequence interpretation. Finally, we discuss current limitations, including technical artifacts, variant interpretation, and overdiagnosis, and outline future directions that will further enhance the diagnostic accuracy, clinical utility, and research potential of HTS.

​

Key scientific associations: High-throughput sequencing, HTS, next-generation sequencing, NGS, DNA sequencing, RNA sequencing, RNA-seq, whole-genome sequencing, whole-exome sequencing, transcriptomics, genomics, functional genomics, precision medicine, molecular diagnostics, bioinformatics, variant calling, genome assembly, genome annotation, gene expression, transcriptome, complementary DNA, cDNA, messenger RNA, mRNA, DNA extraction, RNA extraction, library preparation, sequencing platform, sequencing workflow, sequencing depth, sequencing coverage, read alignment, read mapping, read depth, quality control, nucleic acid purification, genetic variants, single nucleotide variants, SNVs, insertions, deletions, indels, copy number variation, CNV, structural variants, chromosomal rearrangements, inversions, translocations, chromosomal deletions, chromosomal duplications, chromothripsis, repeat expansion, trinucleotide repeat expansion, tandem repeats, microsatellites, minisatellites, low-copy repeats, segmental duplications, transposable elements, retrotransposons, DNA transposons, LINE, LINE-1, SINE, long interspersed nuclear elements, short interspersed nuclear elements, long terminal repeat elements, LTR retrotransposons, splice-site mutations, regulatory mutations, promoters, enhancers, gene regulation, epigenetics, DNA methylation, replication stress, double-strand breaks, homologous recombination, non-homologous end joining, unequal crossing-over, template switching, replication fork collapse, chromosomal instability, genome evolution, genetic diversity, comparative genomics, evolutionary genomics, cancer genomics, rare disease diagnosis, inherited disorders, developmental disorders, pathogen detection, metagenomics, microbial communities, single-cell genomics, artificial intelligence, clinical genomics, personalized medicine, genomic medicine, diagnostic genomics, variant interpretation, genomic biomarkers, computational genomics, clinical bioinformatics, precision diagnostics.

​--------------------------------------------------------------------------------------------------------------------------------------------------------

Dahiya R, Patel B. The Multimodal Imperative: Reengineering Patient and Family Communication for Safety, Equity, and Understanding. Newborn. 2026;5(3):173–182. DOI: 10.5005/jp-journals-11002-0172.

​

Abstract:

Background: Effective patient and family–clinician communication is fundamental to safe, high-quality healthcare. Communication failures contribute to preventable harm, non-adherence, avoidable healthcare utilization, and medical liability. Yet clinical communication continues to rely heavily on brief verbal exchanges and text-based materials that may be poorly matched to differences in health literacy, language, cognitive load, sensory abilities, and the capacity of patients and families to process information during illness. This limitation is particularly important when patients cannot independently receive, interpret, or act upon medical information and families or caregivers become essential communication partners. A multimodal approach that communicates information through complementary verbal, written, visual, audiovisual, interactive, and digitally enabled formats may provide a more adaptable model for patient- and family-centered clinical communication.

Objective: This review examines the mechanisms and consequences of communication failure in contemporary healthcare and evaluates multimodal strategies for improving comprehension, information retention, participation in care, adherence, clinical safety, health equity, and healthcare efficiency. Methods: We synthesized evidence from patient-safety research, malpractice analyses, health-economic studies, cognitive science, health-literacy research, and digital-health literature. Evidence included randomized controlled trials (RCTs), systematic reviews, meta-analyses, observational studies, and legal datasets examining communication and communication-related interventions across inpatient and outpatient settings.

Results: Communication failures are associated with adverse events, medication and treatment errors, non-adherence, avoidable readmissions, prolonged healthcare utilization, and malpractice claims. Limited health literacy, cognitive overload, linguistic and cultural differences, sensory and accessibility barriers, and disparities in digital access can further compromise comprehension. Established approaches, including plain language, teach-back, professional interpretation, accessible written materials, and shared decision-making, provide a clinical foundation for effective communication. Visual aids, pictograms, infographics, and audiovisual education can complement these approaches and improve comprehension, recall, engagement, and selected behavioral and clinical outcomes. Emerging technologies, including generative artificial intelligence (AI), conversational systems, digital human avatars, and immersive technologies, may further enable personalization, scalability, linguistic adaptation, and interactive communication, although their clinical effectiveness, safety, accessibility, and economic value require continued evaluation.

Conclusion: Patient- and family-centered communication should be regarded as a clinical and patient-safety function rather than an ancillary component of care. We propose a Multimodal Communication Principle in which the communication strategy is matched to the patient or family, the principal communication barrier, the clinical context, and the informational task, with complementary modalities combined when a single approach is insufficient. Thoughtful integration of established and emerging modalities may improve comprehension, safety, equity, and healthcare efficiency, provided that technological innovation remains clinically validated, accessible, and centered on human communication.

​

Key scientific associations: Artificial intelligence, Avatar communication, Digital health, Health equity, Health literacy, Healthcare communication, Infographics, Multimodal communication, Patient communication, Visual communication.

​----------------------------------------------------------------------------------------------------------------------------------------------------------------

Kaushal M, Ahmed S. Newborn Feeding and Human Milk: The Evolving Role of Specialized Lactation Consultants— An Expert Review. Newborn 2026;5(3):183–192. DOI: 10.5005/jp-journals-11002-0170.

​

Abstract: 

Background: Breastfeeding and human-milk feeding are fundamental components of newborn nutrition and provide important benefits for infants and mothers. The World Health Organization (WHO) and the United Nations Children’s Fund (UNICEF) recommend exclusive breastfeeding for the first 6 months of life, followed by continued breastfeeding with appropriate complementary foods up to 2 years of age or beyond. Despite these recommendations, establishing and sustaining breastfeeding can be limited by maternal, infant, psychological, clinical, and health-system barriers.

Objective: This Expert Review examines newborn feeding and human-milk feeding with particular emphasis on the role of International Boardcertified Lactation Consultants and other specialized lactation professionals in establishing, protecting, and sustaining breastfeeding across the maternal–infant care continuum. Methods: A narrative review of international guidance and peer-reviewed literature was undertaken, including publications from the WHO, UNICEF, the Academy of Breastfeeding Medicine, and clinical and health-economic studies. Published evidence was integrated with clinical and institutional experience to examine practical approaches to specialized lactation care and its implementation within healthcare systems.

Results: Successful breastfeeding and human-milk feeding require assessment of the mother–infant dyad and timely recognition of maternal and infant feeding difficulties. Specialized lactation consultants provide evidence-based assessment and management of ineffective latch and milk transfer, nipple trauma, engorgement, the mastitis spectrum, perceived or actual low milk supply, and infant feeding dysfunction. Professional lactation support can improve breastfeeding initiation, exclusivity, and duration, and strengthen maternal breastfeeding self-efficacy. Integration of specialized lactation care across maternity, neonatal, pediatric, and primary care settings can facilitate continuity, multidisciplinary management, and family-centered feeding support.

Conclusion:Newborn feeding should be supported as a continuum of care rather than as an isolated maternal or infant intervention. Specialized lactation consultants provide important expertise within this continuum, particularly when breastfeeding difficulties are complex or persistent. Equitable access, effective referral pathways, continuity of support, telelactation, and integration of lactation expertise into healthcare systems may strengthen breastfeeding and human-milk feeding and improve maternal and infant outcomes.

​

Key scientific associations: Breastfeeding, exclusive breastfeeding, human milk, lactation, lactation consultant, International Board Certified Lactation Consultant (IBCLC), lactation medicine, breastfeeding support, breastfeeding counseling, breastfeeding management, breastfeeding education, maternal health, infant health, newborn, neonate, neonatal care, perinatal care, postpartum care, maternal-infant dyad, breastfeeding initiation, breastfeeding continuation, breastfeeding duration, breastfeeding exclusivity, breastfeeding self-efficacy, maternal confidence, maternal anxiety, psychological support, family-centered care, continuity of care, clinical assessment, comprehensive lactation assessment, infant feeding, infant nutrition, human lactation, lactogenesis, milk production, milk transfer, low milk supply, insufficient milk supply, nipple pain, breast engorgement, mastitis, breast abscess, hyperlactation, reverse pressure softening, skin-to-skin care, latch optimization, infant latch, oral function, ankyloglossia, tongue-tie, frenotomy, breast pump, milk expression, lactation physiology, oxytocin, prolactin, Baby-Friendly Hospital Initiative, BFHI, World Health Organization, WHO, UNICEF, multidisciplinary care, interprofessional collaboration, primary care, neonatal intensive care unit, NICU, telelactation, telehealth, digital health, health systems, health policy, preventive medicine, public health, health economics, cost-effectiveness, value-based care, infant growth, neonatal jaundice, hyperbilirubinemia, dehydration, formula supplementation, infant microbiome, immune development, child health, women's health, breast cancer prevention, ovarian cancer prevention, cardiovascular health, evidence-based practice, lactation science.​

---------------------------------------------------------------------------------------------------------------------------------------------------------------------

Michie CA. Maternal Immunization: Optimizing Passive Immunity in the Newborn. Newborn 2026;5(3):193–204. DOI: 10.5005/jp-journals-11002-0173.

​

Abstract: Maternal immunization has emerged as an important strategy for preventing infectious disease in pregnant mothers and newborn infants by extending immune protection across pregnancy, birth, and early infancy. Vaccination during pregnancy augments naturally occurring maternal passive immunity, increasing pathogen-specific immunoglobulin G (IgG) available for neonatal Fc receptor-mediated placental transfer and complementing postnatal mucosal protection provided by secretory immunoglobulin A and other immune factors in human milk. Maternal vaccination against tetanus, influenza, pertussis, coronavirus disease 2019 (COVID-19), and respiratory syncytial virus has demonstrated that an intervention administered to the mother can support healthy pregnancies and reduce serious disease, morbidity, and mortality in young infants before direct infant vaccination provides effective protection. Maternal immunization should, therefore, be considered a safe preventive medicine, in which pregnancy becomes an opportunity to modify newborn immune protection early. This approach may be particularly important for premature infants because shortened gestation interrupts the rapid acquisition of maternal IgG during the third trimester, leaving these infants with lower passive antibody concentrations at birth during a period of developmental immune vulnerability. Neonatologists can contribute to maternal immunization through counseling families, supporting clinical investigation, interpreting maternal vaccination history in neonatal care, and collaborating with obstetric and public health teams. The success of existing programs provides a foundation for expanding maternal vaccines against pathogens, including group B Streptococcus and cytomegalovirus. Advances in structural biology, computational protein design, systems immunology, vaccine platforms, and artificial intelligence may enable precision maternal vaccinology, with vaccine selection and gestational timing increasingly optimized according to maternal immunity, placental functions, gestational age, pathogen exposure, geography, and epidemiological risk. Maternal immunization represents protection for the maternal–newborn dyad. It bridges fetal and infant immunity, expanding prenatal prevention against neonatal diseases and strengthening preparedness against emerging infections and future pandemics.

​

Key scientific associations: Maternal immunization, maternal vaccination, pregnancy vaccination, pregnancy vaccines, maternal passive immunity, passive immunity, neonatal immunity, newborn immunity, fetal immunity, placental antibody transfer, transplacental antibody transfer, neonatal Fc receptor, FcRn, immunoglobulin G, IgG, secretory immunoglobulin A, sIgA, microchimaerism, milk immunity, breastfeeding immunity, human milk immunology, colostrum, maternal antibodies, antibody transfer, maternal-fetal immunology, placental immunology, neonatal immune protection, infant immunity, early-life immunity, congenital infections, neonatal infections, newborn infectious diseases, neonatal infectious morbidity, infection prevention, vaccine-preventable diseases, respiratory syncytial virus, RSV, RSV vaccine, influenza vaccine, influenza immunization, pertussis vaccine, tetanus vaccine, COVID-19 vaccine, coronavirus vaccination, Group B Streptococcus, GBS vaccine, cytomegalovirus, CMV vaccine, enteric pathogens, respiratory pathogens, neonatal sepsis, pneumonia prevention, meningitis prevention, vaccine safety, maternal vaccine safety, pregnancy safety, fetal safety, vaccine efficacy, vaccine effectiveness, vaccine immunogenicity, vaccine durability, neutralizing antibodies, opsonizing antibodies, functional antibodies, antibody quality, antibody function, immune memory, memory B cells, booster vaccination, booster immunization, anamnestic response, adaptive immunity, innate immunity, mucosal immunity, systemic immunity, immune protection, immunological memory, structural biology, structure-guided vaccine design, antigen design, protective epitopes, computational protein design, protein engineering, systems biology, systems immunology, artificial intelligence, AI in vaccinology, computational vaccinology, precision vaccinology, personalized vaccinology, personalized medicine, biomarker-guided vaccination, maternal biomarkers, placental function, placental health, gestational age, preterm birth, prematurity, premature infants, high-risk pregnancy, adjuvants, vaccine adjuvants, mucosal vaccinology, entero-mammary immune axis, immune modulation, maternal immune response, pregnancy immunology, immune adaptation, maternal health, newborn health, infant health, neonatal outcomes, maternal outcomes, maternal-fetal medicine, obstetrics, neonatology, perinatology, pediatric infectious diseases, preventive medicine, preventive pediatrics, global health, global newborn health, vaccine development, next-generation vaccines, vaccine innovation, translational medicine, translational immunology, clinical immunology, reproductive immunology, immune ontogeny, developmental immunology, early immune development, immune maturation, neonatal host defense, infectious disease prevention, maternal antibody kinetics, antibody persistence, antibody half-life, placental transport, Fc receptor biology, immunoglobulin subclasses, IgG1, maternal vaccination timing, vaccine timing, trimester-specific vaccination, prenatal care, antenatal care, maternal screening, individualized vaccination, risk-based immunization, epidemiology, global disease surveillance, emerging infectious diseases, pandemic preparedness, outbreak response, humanitarian health, maternal nutrition, obesity, autoimmune disease, immunosuppression, vaccine confidence, evidence-based medicine, clinical guidelines, WHO recommendations, CDC recommendations, public health, maternal-child health, newborn protection, infant protection, neonatal passive protection, fetal protection, continuum of protection, lifelong immunity, vaccine platforms, protein vaccines, mRNA vaccines, recombinant vaccines, immunoprophylaxis, maternal immune transfer, placental IgG transfer, breast milk antibodies, maternal antibody optimization, neonatal passive immunity, maternal vaccine research, future directions, maternal vaccine portfolio, precision maternal immunization, personalized maternal immunization, risk-based maternal immunization, vaccine engineering, rational vaccine design, neonatal disease prevention, maternal infectious diseases, infant infectious diseases, pregnancy outcomes, healthy newborns, newborn survival, maternal immunology, neonatal vaccinology.

---------------------------------------------------------------------------------------------------------------------------------------------------------------------

Lodha A, Zein H, Al Awad EH, et al. Bilaterally Enlarged Echogenic and Cystic Fetal Kidneys: HNF1B-Related Disease in the Differential Diagnosis. Newborn 2026;5(3):205–211. DOI: 10.5005/jp-journals-11002-0169.

​

Abstract: Bilaterally enlarged hyperechogenic fetal kidneys with visible cysts represent a diagnostically challenging phenotype that may occur in hepatocyte nuclear factor 1 homeobox B (HNF1B)-related disease, autosomal dominant polycystic kidney disease (ADPKD), autosomal recessive polycystic kidney disease (ARPKD), renal dysplasia, and other developmental or cystic kidney disorders. We describe a fetus identified at 22 weeks’ gestation with progressive bilateral nephromegaly, markedly increased renal echogenicity, reduced corticomedullary differentiation, and multiple small cortical/subcapsular cysts, with preserved bladder filling, amniotic fluid volume, fetal growth, and no major extrarenal abnormalities. Chromosomal microarray analysis (CMA) demonstrated no pathogenic copy-number abnormality, including deletion of the HNF1B-containing 17q12 region. Subsequent trio genomic sequencing identified a heterozygous pathogenic HNF1B nonsense variant, NM_000458.4:c.826C>T (p.Arg276Ter). The same variant was unexpectedly identified in the clinically asymptomatic mother, whose subsequent evaluation revealed subtle renal abnormalities and hypomagnesemia, illustrating marked intrafamilial variable expressivity. The infant was delivered at term with preserved urine output; postnatal imaging reproduced the prenatal renal phenotype, and follow-up demonstrated mild renal dysfunction and hypomagnesemia. Importantly, visible fetal renal cysts are a morphologic finding rather than a molecular diagnosis: Cysts may occur in HNF1B-related disease, ADPKD, ARPKD, and renal dysplasia, although conspicuous macrocysts are not typically the dominant early prenatal feature of classic ARPKD. The subsequent behavior of cysts in HNF1B-related disease also should not be assumed to follow the progressive cyst-expansion paradigm of ADPKD, because cyst burden may remain stable in many affected children and renal morphology may evolve variably over time. This case demonstrates the complementary roles of detailed fetal phenotyping, CMA, sequence analysis, parental testing, and longitudinal surveillance and emphasizes that molecular diagnosis establishes etiology but does not reliably predict renal progression or overall phenotypic severity.

​

Key scientific associations: HNF1B, HNF1B-related disease, HNF1B mutation, HNF1B variant, HNF1B nephropathy, HNF1B syndrome, hepatocyte nuclear factor 1-beta, HNF1 homeobox B, renal cysts and diabetes syndrome, RCAD syndrome, MODY5, maturity-onset diabetes of the young type 5, 17q12, 17q12 deletion syndrome, 17q12 microdeletion, intragenic HNF1B variant, pathogenic HNF1B variant, nonsense mutation, nonsense variant, p.Arg276Ter, p.Arg276*, c.826C>T, NM_000458.4, chromosome 17, chromosome 17q12, fetal kidney, fetal renal disease, fetal renal anomaly, fetal renal abnormality, fetal nephromegaly, bilateral nephromegaly, enlarged fetal kidneys, echogenic fetal kidneys, hyperechogenic fetal kidneys, bilateral echogenic kidneys, bilateral hyperechogenic kidneys, cystic fetal kidneys, fetal renal cysts, cortical renal cysts, subcapsular renal cysts, fetal cystic kidney disease, cystic renal disease, fetal renal dysplasia, renal dysplasia, cystic dysplasia, bilateral renal dysplasia, congenital anomalies of the kidney and urinary tract, CAKUT, corticomedullary differentiation, reduced corticomedullary differentiation, loss of corticomedullary differentiation, renal parenchymal echogenicity, fetal renal parenchyma, fetal urinary bladder, fetal urine production, preserved bladder filling, amniotic fluid volume, normal amniotic fluid, oligohydramnios, polyhydramnios, fetal renal function, prenatal renal diagnosis, prenatal diagnosis, fetal diagnosis, prenatal nephrology, fetal nephrology, maternal-fetal medicine, fetal ultrasonography, prenatal ultrasonography, fetal ultrasound, renal ultrasound, fetal renal ultrasound, prenatal sonography, fetal sonography, high-resolution fetal ultrasound, serial fetal ultrasound, prenatal imaging, fetal MRI, fetal magnetic resonance imaging, renal MRI, quantitative fetal MRI, functional fetal MRI, genomic diagnosis, molecular diagnosis, genomic sequencing, trio genomic sequencing, trio sequencing, exome sequencing, prenatal exome sequencing, genome sequencing, prenatal genome sequencing, chromosomal microarray, chromosomal microarray analysis, CMA, copy-number variant, copy-number abnormality, 17q12 deletion testing, molecular genetic testing, fetal genetic testing, prenatal genetic testing, amniocentesis, chorionic villus sampling, CVS, fetal DNA, amniotic fluid DNA, cell-free fetal DNA, cfDNA, cell-free placental DNA, noninvasive prenatal diagnosis, NIPD, monogenic prenatal diagnosis, targeted prenatal diagnosis, fetal genotype, genotype-phenotype correlation, genotype-phenotype relationship, phenotype-genotype correlation, phenotype-positive genotype-negative, variable expressivity, intrafamilial variability, phenotypic heterogeneity, genotype severity, autosomal dominant inheritance, autosomal dominant disease, dominant inheritance, familial HNF1B disease, inherited HNF1B variant, maternal inheritance, paternal inheritance, parent-of-origin effect, uniparental disomy, UPD, gonadal mosaicism, germline mosaicism, somatic mosaicism, tissue-specific mosaicism, modifier genes, regulatory variants, epigenetic modification, epigenetics, DNA methylation, histone modification, chromatin remodeling, non-coding RNA, transcriptomics, epigenomics, metabolomics, mitochondrial biology, mitochondrial dysfunction, mitochondrial respiration, PPARGC1A, PGC-1alpha, renal bioenergetics, tubular metabolism, nephrogenesis, kidney development, renal development, nephron differentiation, tubular epithelial differentiation, epithelial polarity, renal tubular function, collecting duct development, cystogenesis, renal cystogenesis, primary cilium, primary cilia, ciliary signaling, ciliopathy, renal ciliopathy, syndromic ciliopathy, cilia-associated pathways, PKHD1, PKD1, PKD2, autosomal recessive polycystic kidney disease, ARPKD, autosomal dominant polycystic kidney disease, ADPKD, fetal ADPKD, fetal ARPKD, polycystic kidney disease, polycystic fetal kidneys, cystic kidney differential diagnosis, renal cystic differential diagnosis, congenital cystic kidney disease, developmental kidney disease, developmental renal disorder, hereditary renal disease, monogenic renal disease, monogenic cystic kidney disease, fetal renal genetics, pediatric nephrology, neonatal nephrology, neonatology, neonatal renal disease, newborn renal disease, postnatal renal ultrasound, neonatal renal ultrasound, neonatal kidney disease, neonatal follow-up, pediatric follow-up, longitudinal surveillance, renal surveillance, renal function monitoring, chronic kidney disease, CKD, pediatric chronic kidney disease, kidney failure, end-stage kidney disease, ESKD, kidney replacement therapy, renal replacement therapy, kidney transplantation, pediatric kidney transplantation, transplant planning, renal prognosis, fetal renal prognosis, neonatal renal prognosis, long-term renal prognosis, preserved urine output, serum creatinine, estimated glomerular filtration rate, eGFR, proteinuria, albuminuria, hypertension, pediatric hypertension, growth monitoring, electrolyte abnormalities, electrolyte homeostasis, hypomagnesemia, renal magnesium wasting, magnesium wasting, FXYD2, hyperuricemia, gout, acid-base balance, metabolic surveillance, glucose metabolism, diabetes mellitus, pediatric diabetes risk, pancreatic abnormalities, pancreatic function, hepatobiliary abnormalities, liver function abnormalities, genital tract abnormalities, reproductive tract abnormalities, genitourinary abnormalities, multisystem disease, multisystem disorder, neurodevelopment, neurodevelopmental follow-up, developmental delay, learning difficulties, learning disability, language development, motor development, cognition, school performance, behavior, seizures, neurodevelopmental surveillance, pulmonary follow-up, respiratory follow-up, reproductive counseling, genetic counseling, recurrence risk, 50 percent recurrence risk, preconception counseling, IVF, in vitro fertilization, preimplantation genetic testing, PGT-M, preimplantation genetic testing for monogenic disease, embryo testing, prenatal counseling, future pregnancy, familial mutation testing, carrier parent, affected parent, maternal diagnosis, asymptomatic parent, previously unrecognized familial disease, prenatal phenotype, sonographic phenotype, imaging phenotype, molecular phenotype, phenotype-guided diagnosis, imaging-guided genomic diagnosis, fetal phenotype-guided sequencing, bright fetal kidneys, bilateral bright kidneys, renal echogenicity, visible fetal renal cysts, macroscopic renal cysts, microscopic cysts, collecting duct ectasia, dysplastic kidney differential, polycystic versus dysplastic kidney disease, HNF1B versus ADPKD, HNF1B versus ARPKD, HNF1B versus renal ciliopathy, HNF1B versus renal dysplasia, prenatal cystic kidney differential, fetal cystic kidney phenotype, molecular differential diagnosis, prenatal precision medicine, fetal precision medicine, genomic medicine, developmental nephrology, congenital kidney disease, inherited kidney disease, fetal anomaly genetics, prenatal genetics, fetal medicine, neonatal genetics, pediatric genetics, clinical genetics, renal genetics, genetic nephrology, precision nephrology, translational nephrology, fetal renal counseling, perinatal counseling, perinatal planning, multidisciplinary fetal care, multidisciplinary neonatal care, maternal-fetal medicine genetics, fetal renal surveillance, neonatal renal surveillance, lifelong surveillance, multisystem surveillance, family screening, cascade testing, parental testing, maternal phenotype, renal cystic phenotype, fetal cystic dysplasia, bilateral renal cysts, small renal cysts, subcapsular cysts, cortical cysts, fetal kidney echogenicity, fetal kidney enlargement, fetal renal architecture, renal structural abnormality, renal developmental disorder, prenatal molecular diagnosis, family genetic diagnosis, hereditary cystic kidney disorder, and HNF1B prenatal presentation..