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PubMed2000

Projective techniques and the detection of child sexual abuse.

Projective techniques (e.g., the Rorschach, Human Figure Drawings) are sometimes used to detect child sexual abuse. West recently conducted a meta-analysis on this topic, but she systematically excluded nonsignificant results. In this article, a reanalysis of her data is presented. The authors conclude that projective techniques should not be used to detect child sexual abuse. Many of the studies purportedly demonstrating validity are flawed, and none of the projective test scores have been well replicated.

Bias↗

PubMed1991

Reexamination of Eisen, Zellman, and McAlister's Health Belief Model questionnaire.

Eisen, Zellman, and McAlister proposed a 22-item scale to measure four Health Belief Model (HBM) constructs as applied to adolescent contraceptive behavior. Their factor analysis led them to conclude that there were several discrepancies in their proposed scales. We suggest that they were unduly pessimistic. Although their proposed scales could stand improvement, they are adequate preliminary tools. The major reason they concluded that the scales were deficient was that they applied criteria that are generally appropriate for continuous data to their inherently discrete (categorical) item response data. A secondary consideration is that confirmatory methods of factor analysis can yield results that bear more directly on their proposed organization of items than the traditional exploratory methods that they used. A reanalysis of their data suggests that their proposed scales have fewer problems than they believed they had. Our results increase the likelihood of standardizing HBM measures.

Adolescent↗

PubMed2001

The economic impact of autism in Britain.

Little is known about the economic impact of autism. This study estimated the economic consequences of autism in the United Kingdom, based on published evidence and on the reanalysis of data holdings at the Centre for the Economics of Mental Health (CEMH). With an assumed prevalence of 5 per 10,000, the annual societal cost for the UK was estimated to exceed ł1 billion. The lifetime cost for a person with autism exceeded ł2.4 million. The main costs were for living support and day activities. Family costs account for only 2.3 percent of the total cost, but a lack of relevant information limited our ability to estimate these costs. Minor improvements in life outcome for people with autism could substantially reduce costs over the lifetime.

Autistic Disorder↗

PubMed2026

Extreme Temperature and Incident Diabetes Risk Among Middle-Aged and Older Adults in China: A National Longitudinal Cohort Study.

BACKGROUND AND AIMS: The metabolic consequences of extreme temperature exposure in nondiabetic populations remain poorly understood. This study aimed to examine associations between heatwave and coldwave exposure and incident diabetes mellitus (DM) and impaired glucose tolerance (IGT) in middle-aged and older Chinese adults. METHODS: A total of 1803 China Health and Retirement Longitudinal Study participants aged ≥45 years with normoglycemia at baseline were followed from Wave 1 (2011) to Wave 3 (2015). Eighteen extreme-temperature indicators were derived from city-level fifth-generation European Centre for Medium-Range Weather Forecasts atmospheric reanalysis data. Outcomes were classified according to American Diabetes Association criteria. Generalized linear mixed-effects models (GLMMs) were pooled across five imputed datasets, with Bonferroni correction for multiple comparisons (α = 0.0028) and sensitivity analysis adjusting for individual follow-up duration. RESULTS: All nine heatwave indicators showed odds ratios (ORs) < 1.0 for DM and IGT. HT9 (≥97.5th percentile, ≥4 consecutive days) was the sole Bonferroni-significant result: OR = 0.845 (95% confidence interval [CI]: 0.802-0.890). Coldwave indicators showed no consistent associations. Age significantly modified the HT9 effect (P-interaction = 0.004): adults aged 65-84 showed a stronger inverse association (OR = 0.616) than those aged < 65 (OR = 0.921). CONCLUSION: Prolonged heatwave exposure was consistently associated with reduced diabetes risk, with pronounced age heterogeneity. Replication in larger prospective studies is warranted.

Humans↗

PubMed2003

ADAMTS13 gene mutation in congenital thrombotic thrombocytopenic purpura with previously reported normal VWF cleaving protease activity.

Deficiency of von Willebrand factor (VWF) cleaving protease ADAMTS13 is associated with the development of thrombotic thrombocytopenic purpura (TTP). A case of congenital TTP that was previously reported to have normal ADAMTS13 activity was analyzed at the molecular level. Reanalysis of plasma VWF cleaving protease activity using a different assay revealed that the patient had less than 0.1 U/L ADAMTS13 protease activity, while the parents were both partially deficient. Sequence analysis of DNA amplified by polymerase chain reaction showed that the patient was homozygous for a novel TT deletion in exon 15 of the ADAMTS13 gene resulting in a frameshift, while both parents were heterozygous for the same mutation. Taken together with other recent reports, all the cases of hereditary TTP studied by DNA sequence analysis to date appear to be due to mutations within the ADAMTS13 gene.

ADAM Proteins↗

PubMedDate not supplied

A region on chicken chromosome 2 affects both egg white thinning and egg weight.

We describe the results from genetic dissection of a QTL region on chicken chromosome 2, shown to affect egg weight and quality in an earlier genome scan of an F2 intercross between two divergent egg layer lines. As the 90% confidence intervals for the detected QTL covered tens of centiMorgans, new analyses were needed. The datasets were re-analysed with denser marker intervals to characterise the QTL region. Analysis of a candidate gene from the original QTL region, vimentin, did not support its role in controlling egg white thinning. Even after reanalysis with additional seven markers in the QTL area, the 90% confidence intervals remained large or even increased, suggesting the presence of multiple linked QTL for the traits. A grid search fitting two QTL on chromosome 2 for each trait suggested that there are two distinct QTL areas affecting egg white thinning in both production periods and egg weight in the late production period. The results indicate possible pleiotropic effects of some of the QTL on egg quality and egg weight. However, it was not possible to make a distinction between close linkage versus pleiotropic effects.

Animals↗

PubMed2006

Genetic heterogeneity of residual variance in broiler chickens.

Aims were to estimate the extent of genetic heterogeneity in environmental variance. Data comprised 99 535 records of 35-day body weights from broiler chickens reared in a controlled environment. Residual variance within dam families was estimated using ASREML, after fitting fixed effects such as genetic groups and hatches, for each of 377 genetically contemporary sires with a large number of progeny (>100 males or females each). Residual variance was computed separately for male and female offspring, and after correction for sampling, strong evidence for heterogeneity was found, the standard deviation between sires in within variance amounting to 15-18% of its mean. Reanalysis using log-transformed data gave similar results, and elimination of 2-3% of outlier data reduced the heterogeneity but it was still over 10%. The correlation between estimates for males and females was low, however. The correlation between sire effects on progeny mean and residual variance for body weight was small and negative (-0.1). Using a data set bigger than any yet presented and on a trait measurable in both sexes, this study has shown evidence for heterogeneity in the residual variance, which could not be explained by segregation of major genes unless very few determined the trait.

Animals↗

PubMed2005

Differences in codon bias cannot explain differences in translational power among microbes.

BACKGROUND: Translational power is the cellular rate of protein synthesis normalized to the biomass invested in translational machinery. Published data suggest a previously unrecognized pattern: translational power is higher among rapidly growing microbes, and lower among slowly growing microbes. One factor known to affect translational power is biased use of synonymous codons. The correlation within an organism between expression level and degree of codon bias among genes of Escherichia coli and other bacteria capable of rapid growth is commonly attributed to selection for high translational power. Conversely, the absence of such a correlation in some slowly growing microbes has been interpreted as the absence of selection for translational power. Because codon bias caused by translational selection varies between rapidly growing and slowly growing microbes, we investigated whether observed differences in translational power among microbes could be explained entirely by differences in the degree of codon bias. Although the data are not available to estimate the effect of codon bias in other species, we developed an empirically-based mathematical model to compare the translation rate of E. coli to the translation rate of a hypothetical strain which differs from E. coli only by lacking codon bias. RESULTS: Our reanalysis of data from the scientific literature suggests that translational power can differ by a factor of 5 or more between E. coli and slowly growing microbial species. Using empirical codon-specific in vivo translation rates for 29 codons, and several scenarios for extrapolating from these data to estimates over all codons, we find that codon bias cannot account for more than a doubling of the translation rate in E. coli, even with unrealistic simplifying assumptions that exaggerate the effect of codon bias. With more realistic assumptions, our best estimate is that codon bias accelerates translation in E. coli by no more than 60% in comparison to microbes with very little codon bias. CONCLUSIONS: While codon bias confers a substantial benefit of faster translation and hence greater translational power, the magnitude of this effect is insufficient to explain observed differences in translational power among bacterial and archaeal species, particularly the differences between slowly growing and rapidly growing species. Hence, large differences in translational power suggest that the translational apparatus itself differs among microbes in ways that influence translational performance.

Bacterial Physiological Phenomena↗

PubMed2006

In situ origin of deep rooting lineages of mitochondrial Macrohaplogroup 'M' in India.

BACKGROUND: Macrohaplogroups 'M' and 'N' have evolved almost in parallel from a founder haplogroup L3. Macrohaplogroup N in India has already been defined in previous studies and recently the macrohaplogroup M among the Indian populations has been characterized. In this study, we attempted to reconstruct and re-evaluate the phylogeny of Macrohaplogroup M, which harbors more than 60% of the Indian mtDNA lineage, and to shed light on the origin of its deep rooting haplogroups. RESULTS: Using 11 whole mtDNA and 2231 partial coding sequence of Indian M lineage selected from 8670 HVS1 sequences across India, we have reconstructed the tree including Andamanese-specific lineage M31 and calculated the time depth of all the nodes. We defined one novel haplogroup M41, and revised the classification of haplogroups M3, M18, and M31. CONCLUSION: Our result indicates that the Indian mtDNA pool consists of several deep rooting lineages of macrohaplogroup 'M' suggesting in-situ origin of these haplogroups in South Asia, most likely in the India. These deep rooting lineages are not language specific and spread over all the language groups in India. Moreover, our reanalysis of the Andamanese-specific lineage M31 suggests population specific two clear-cut subclades (M31a1 and M31a2). Onge and Jarwa share M31a1 branch while M31a2 clade is present in only Great Andamanese individuals. Overall our study supported the one wave, rapid dispersal theory of modern humans along the Asian coast.

DNA, Mitochondrial↗

PubMed2005

Structural equation model testing and the quality of natural killer cell activity measurements.

BACKGROUND: Browne et al. [Browne, MacCallum, Kim, Andersen, Glaser: When fit indices and residuals are incompatible. Psychol Methods 2002] employed a structural equation model of measurements of target cell lysing by natural killer cells as an example purportedly demonstrating that small but statistically significant ill model fit can be dismissed as "negligible from a practical point of view". METHODS: Reanalysis of the natural killer cell data reveals that the supposedly negligible ill fit obscured important, systematic, and substantial causal misspecifications. RESULTS: A clean-fitting structural equation model indicates that measurements employing higher natural-killer-cell to target-cell ratios are more strongly influenced by a progressively intrusive factor, whether or not the natural killer cell activity is activated by recombinant interferon gamma (rIFN gamma). The progressive influence may reflect independent rate limiting steps in cell recognition and attachment, spatial competition for cell attachment points, or the simultaneous lysings of single target cells by multiple natural killer cells. CONCLUSIONS: If the progressively influential factor is ultimately identified as a mere procedural impediment, the substantive conclusion will be that measurements of natural killer cell activity made at lower effector to target ratios are more valid. Alternatively, if the individual variations in the progressively influential factor are modifiable, this may presage a new therapeutic route to enhancing natural killer cell activity. The methodological conclusion is that, when using structural equation models, researchers should attend to significant model ill fit even if the degree of covariance ill fit is small, because small covariance residuals do not imply that the underlying model misspecifications are correspondingly small or inconsequential.

Child↗

PubMed2005

Kinetics of cancer: a method to test hypotheses of genetic causation.

BACKGROUND: Mouse studies have recently compared the age-onset patterns of cancer between different genotypes. Genes associated with earlier onset are tentatively assigned a causal role in carcinogenesis. These standard analyses ignore the great amount of information about kinetics contained in age-onset curves. We present a method for analyzing kinetics that measures quantitatively the causal role of candidate genes in cancer progression. We use our method to demonstrate a clear association between somatic mutation rates of different DNA mismatch repair (MMR) genotypes and the kinetics of cancer progression. METHODS: Most experimental studies report age-onset curves as the fraction diagnosed with tumors at each age for each group. We use such data to estimate smoothed survival curves, then measure incidence rates at each age by the slope of the fitted curve divided by the fraction of mice that remain undiagnosed for tumors at that age. With the estimated incidence curves, we compare between different genotypes the median age of cancer onset and the acceleration of cancer, which is the rate of increase in incidence with age. RESULTS: The direction of change in somatic mutation rate between MMR genotypes predicts the direction of change in the acceleration of cancer onset in all 7 cases (p approximately 0.008), with the same result for the association between mutation rate and the median age of onset. CONCLUSION: Many animal experiments compare qualitatively the onset curves for different genotypes. If such experiments were designed to analyze kinetics, the research could move to the next stage in which the mechanistic consequences of particular genetic pathways are related to the dynamics of carcinogenesis. The data we analyzed here were not collected to test mechanistic and quantitative hypotheses about kinetics. Even so, a simple reanalysis revealed significant insights about how DNA repair genotypes affect separately the age of onset and the acceleration of cancer. Our method of comparing genotypes provides good statistical tests even with small samples for each genotype.

Adenoma↗

PubMed2006

Tamoxifen is not effective in good prognosis patients with hepatocellular carcinoma.

BACKGROUND: Large randomised clinical trials and systematic reviews substantiate that tamoxifen is ineffective in improving survival of patients with hepatocellular carcinoma (HCC). However, a recent report suggested that the drug might prolong survival among patients with well preserved liver function. The aim of this paper is to validate this hypothesis. METHODS: We used the updated database of the phase 3 randomised CLIP-1 trial that compared tamoxifen with supportive therapy. Primary endpoint was overall survival. Treatment arms were compared within strata defined according to the Okuda stage and the CLIP-score. Survival differences were tested by the Log-rank test. RESULTS: Tamoxifen was not effective in prolonging survival in Okuda I-II subgroup (p = 0.501). Median survival times were equal to 16.8 (95%CI 12.7-18.5) months for tamoxifen and 16.8 (95%CI 13.5-22.4) months for the control arms; 1-year survival probabilities were equal to 58.8% (95%CI 51.7-65.8) and 59.4 (95%CI 52.5-66.2), respectively. Similar results were observed in the better CLIP subgroup (score 0/1), without evidence of difference between the two treatment arms (p = 0.734). Median survival times were equal to 29.2 (95%CI 20.1-36.4) months with tamoxifen and 29.0 (95%CI 23.3-35.2) months without; 1-year survival probabilities were equal to 80.9% (95%CI 72.5-89.3) with tamoxifen and 77.1% (95%CI 68.6-85.7) for the control arm. CONCLUSION: The recent suggestion that tamoxifen might be effective in the subgroup of patients with better prognosis is not supported by a reanalysis of the CLIP-1 trial. Tamoxifen should no longer be considered for the treatment of HCC patients and future trials of medical treatment should concentrate on different drugs.

Adult↗

PubMed2001

Time course of muscle soreness following different types of exercise.

BACKGROUND: Post-exercise muscle soreness is a dull, aching sensation that follows unaccustomed muscular exertion. Primarily on the basis of previous laboratory-based research on eccentric exercise, soreness is usually said to follow an inverted U-shaped curve over time, peaking 24 - 48 hours after exercise. As such, it is often described as "delayed-onset" muscle soreness. In a study of long-distance runners, soreness seemed to peak immediately and then reduce gradually over time. The study is a secondary analysis of clinical trial data that aims to determine whether the time course of soreness following a natural exercise, long-distance running, is different from that following a laboratory-based exercise, bench-stepping. METHODS: This is a reanalysis of data from three previous clinical trials. The trials included 400 runners taking part in long-distance races and 82 untrained volunteers performing a bench-stepping test. Subjects completed a Likert scale of muscle soreness every morning and evening for the five days following their exercise. RESULTS: Interaction between trial and time is highly significant, suggesting a different time course of soreness following running and bench-stepping. 45% of subjects in the bench-stepping trial experienced peak soreness at the third or fourth follow-up (approximately 36 - 48 hours after exercise) compared to only 14% of those in the running trial. The difference between groups is robust to multivariate analysis incorporating possible confounding variables. CONCLUSION: Soreness in runners following long-distance running follows a different time course to that in untrained individuals undertaking bench-stepping. Research on exercise taking place in the laboratory context does not necessarily generalize to exercise undertaken by trained athletes when engaged in their chosen sport.

Journal Article↗

PubMed2006

Rural-urban differentials of premature mortality burden in south-west China.

BACKGROUND: Yunnan province is located in south western China and is one of the poorest provinces of the country. This study examines the premature mortality burden from common causes of deaths among an urban region, suburban region and rural region of Kunming, the capital of Yunnan. METHODS: Years of life lost (YLL) rate per 1,000 and mortality rate per 100,000 were calculated from medical death certificates in 2003 and broken down by cause of death, age and gender among urban, suburban and rural regions. YLL was calculated without age-weighting and discounting rate. Rates were age-adjusted to the combined population of three regions. However, 3% discounting rate and a standard age-weighting function were included in the sensitivity analysis. RESULTS: Non-communicable diseases contributed the most YLL in all three regions. The rural region had about 50% higher premature mortality burden compared to the other two regions. YLL from infectious diseases and perinatal problems was still a major problem in the rural region. Among non-communicable diseases, YLL from stroke was the highest in the urban/suburban regions; COPD followed as the second and was the highest in the rural region. Mortality burden from injuries was however higher in the rural region than the other two regions, especially for men. Self-inflicted injuries were between 2-8 times more serious among women. The use of either mortality rate or YLL gives a similar conclusion regarding the order of priority. Reanalysis with age-weighting and 3% discounting rate gave similar results. CONCLUSION: Urban south western China has already engaged in epidemiological pattern of developed countries. The rural region is additionally burdened by diseases of poverty and injury on top of the non-communicable diseases.

Journal Article↗

PubMed2004

Passive immunotherapy against Abeta in aged APP-transgenic mice reverses cognitive deficits and depletes parenchymal amyloid deposits in spite of increased vascular amyloid and microhemorrhage.

BACKGROUND: Anti-Abeta immunotherapy in transgenic mice reduces both diffuse and compact amyloid deposits, improves memory function and clears early-stage phospho-tau aggregates. As most Alzheimer disease cases occur well past midlife, the current study examined adoptive transfer of anti-Abeta antibodies to 19- and 23-month old APP-transgenic mice. METHODS: We investigated the effects of weekly anti-Abeta antibody treatment on radial-arm water-maze performance, parenchymal and vascular amyloid loads, and the presence of microhemorrhage in the brain. 19-month-old mice were treated for 1, 2 or 3 months while 23-month-old mice were treated for 5 months. Only the 23-month-old mice were subject to radial-arm water-maze testing. RESULTS: After 3 months of weekly injections, this passive immunization protocol completely reversed learning and memory deficits in these mice, a benefit that was undiminished after 5 months of treatment. Dramatic reductions of diffuse Abeta immunostaining and parenchymal Congophilic amyloid deposits were observed after five months, indicating that even well-established amyloid deposits are susceptible to immunotherapy. However, cerebral amyloid angiopathy increased substantially with immunotherapy, and some deposits were associated with microhemorrhage. Reanalysis of results collected from an earlier time-course study demonstrated that these increases in vascular deposits were dependent on the duration of immunotherapy. CONCLUSIONS: The cognitive benefits of passive immunotherapy persist in spite of the presence of vascular amyloid and small hemorrhages. These data suggest that clinical trials evaluating such treatments will require precautions to minimize potential adverse events associated with microhemorrhage.

Journal Article↗

PubMed2026

Clinical and genomic features of mitis group streptococcal bacteremia in patients with febrile neutropenia.

BACKGROUND: Viridans group streptococci (VGS) can cause the life-threatening viridans streptococcal shock syndrome (VSSS) in patients with febrile neutropenia (FN). The Mitis group, a major subgroup of VGS, is frequently implicated in these severe infections, but its specific clinical and genomic characteristics remain incompletely characterized, particularly in patients with FN. This study aimed to systematically describe these features in this population. METHODS: In this single-center retrospective study, we compared the clinical data and whole-genome sequencing (WGS) results of Mitis group streptococcal isolates from patients with and without FN. Virulence-associated and antimicrobial resistance genes were initially screened using a reference-based approach, followed by assembly-based reanalysis and manual sequence validation. RESULTS: Compared with the non-FN cohort (n = 34), the FN cohort (n = 61) was significantly younger, had a higher prevalence of hematologic malignancy, and more frequently presented with primary bacteremia. VSSS occurred exclusively in the FN group (11.5%) and was associated with high mortality (14-day mortality, 42.9%), which did not correlate with in vitro antimicrobial susceptibility. Genomic analyses revealed marked diversity among isolates. Initial screening suggested variable detection of several virulence-associated loci, including pavA, slrA, and rfb-related loci; however, subsequent assembly-based analyses indicated that many apparent absences were attributable to extreme allelic divergence rather than true gene loss. No single virulence determinant clearly segregated with clinical severity. CONCLUSIONS: Mitis group bacteremia in patients with FN appears to be characterized by distinct clinical features and marked genomic diversity. Our findings suggest that the development of severe disease, including VSSS, may not be explained by microbial factors alone and potentially reflects complex host-pathogen interactions. CLINICAL TRIAL: Not applicable.

Humans↗

PubMed2026

Evaluation of the efficacy of optical genome mapping in prenatal diagnosis: a retrospective cohort study.

BACKGROUND: Optical genome mapping (OGM) is an emerging cytogenetic method for concurrently detecting structural variants (SVs) and copy number variants (CNVs). However, its clinical application in prenatal diagnosis remains underexplored. METHODS: This study retrospectively evaluated the clinical validity of OGM in prenatal diagnosis by comparing with two routine genetic testing methods: karyotyping and chromosomal microarray analysis (CMA). Both positive and negative cases detected by routine genetic methods were enrolled to evaluate the technical concordance of OGM and its capability to improve diagnostic rate in negative cases. The exclusion criteria were balanced centromeric translocations, mosaic cases with cellular fractions < 20%, and loss of heterozygosity (LOH) < 25 Mb. All samples subjected to OGM testing were anonymized and analyzed blindly. The results from OGM were compared with those from routine genetic testing, and statistical analyses were performed to assess technical concordance and diagnostic rate. RESULTS: Of 217 samples (166 positive samples and 51 negative samples for routine genetic testing), all were successfully tested with OGM, including 2 umbilical cord blood samples, 4 chorionic villi samples, and 211 cultured amniotic fluid samples. Of the 207 reportable chromosomal aberrations from 166 positive samples, the blinded concordance between OGM and CMA, karyotyping, and combination of karyotyping plus CMA was 97.81%, 96.36%, and 97.10%, respectively. OGM missed six aberrations initially, including one LOH, two marker chromosomes, and three microdeletions. However, after reanalysis, its concordance improved to 100% with CMA and 99.03% with karyotyping plus CMA. OGM also diagnosed one additional case of a 3-kb deletion in 51 negative samples, improving the diagnostic rate by 1.96%. Moreover, OGM reclassified the pathogenicity of two microdeletions from pathogenic to uncertain significance in 2 positive cases. Furthermore, OGM clarified the diagnosis suspected by routine genetic testing and improved diagnostic accuracy in some cases. CONCLUSION: As far as we know, this is the largest retrospective study on OGM in prenatal diagnosis, and it includes a broad range of sample types. The results showed that OGM exhibits high concordance among the tested methods and increases the diagnostic rate. Thus, OGM has the potential to become a first-line technique for prenatal diagnosis in the future.

Humans↗

PubMed2025

Multi-omics analysis reveals distinct spatial compartmentalization of lung repair niches in pediatric ARDS.

BACKGROUND: Pediatric acute respiratory distress syndrome (PARDS), often triggered by viral infections, is a life-threatening condition. Despite its severity, children demonstrate significantly better survival rates and superior lung repair compared to adults. However, the mechanisms underlying this age-specific advantage remain incompletely understood. PATIENTS AND METHODS: We conducted a pilot multi-omics study of influenza-associated PARDS integrating single-cell RNA sequencing (scRNA-seq) of pediatric lung tissue and bronchoalveolar lavage fluid (BALF), spatial transcriptomics, and plasma proteomics. Analyses were harmonized with the Human Lung Cell Atlas (HLCA) reference, reanalysis of public pediatric PARDS airway scRNA-seq, and contextual comparisons to adult lethal COVID-19 lung. RESULTS: Tissue scRNA-seq and spatial data indicated outcome-linked divergence in PARDS. Survivor showed spatially restricted repair with preserved alveolar type II (AT2) cells, AT2-to-alveolar type I (AT1) differentiation signatures, and higher KRT17, whereas fatal case and adults exhibited diffuse immune activation with pro-fibrotic and pro-apoptotic signaling. In BALF, KRT17-positive airway stress–repair epithelial cells (hillock-like) increased from the acute to recovery phase, and plasma proteomics showed higher circulating KRT17 in survivors. HLCA-based label transfer strengthened cell-type definitions and enabled pediatric–adult comparisons suggesting biological and developmental differences; the adult lethal COVID-19 atlas provided a benchmark with attenuated epithelial repair and prominent collagen CTHRC1-pathologic fibroblasts. Fibroblast programs were regionally compartmentalized, with injury-enriched CTHRC1+ states versus alveolar fibroblasts in preserved areas, and showed stronger injury–homeostasis anti-correlation in fatalities. Myeloid remodeling included BALF transitions from FCN1-high inflammatory states toward FABP4-positive resident-like states, consistent with public pediatric datasets showing reduced inflammatory and interferon-stimulated gene (ISG) modules and severity-linked increases in aged neutrophils. CONCLUSIONS: This pilot multi-omics case series outlines putative pediatric lung repair niches in influenza-associated PARDS. KRT17-positive transitional epithelium, preserved AT2 differentiation, and restoration of resident-like macrophages may align with recovery, whereas diffuse immune activation and CTHRC1-enriched fibroblast programs may accompany worse outcomes. HLCA-guided annotations and adult benchmarks indicate possible age-related differences, warranting validation in larger multi-center cohorts.

Humans↗