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in, abstract, authors, of, and, the, airway, cell, to, disease, muscle, with, cells, signaling, mice, by, human, fibrosis, smooth, through, associated, cd4, epithelial, reveals, induced, dependent, organ, lung, il, pulmonary, more, specific, growth, not, research, promotes, tumor, er, cancer, rna, protein, deficiency, impaired, genetic, background, program, hyperresponsiveness, progressive, via, identifies, as, for, single, involvement, transcriptomic, among, spatial, multiomics, biomedical, advances, beyond, transcriptomics, pathway, influences, developmental, susceptibility, from, mechanisms, development, remodeling, latest, physician, scientist, issue, characterizing, enteric, pathology, mps, iiia, suggests, vulnerability, lysosomal, storage, disorders, pik3ca, driven, cerebral, cavernous, malformations, does, require, microbiome, stimulation, estrogen, phenotypes, breast, ugdh, gpr30, noncoding, ty1, reverses, systemic, sclerosis, attenuating, cgas, sting, familial, case, flad1, adrenal, steroidogenesis, discovery, recognized, pertussis, antigens, that, reduce, colonization, glutamine, biosynthetic, pathways, fuel, autoreactive, foxp3, mediated, ketoglutarate, accelerates, cutaneous, wound, healing, modulating, fibroblast, niche, chromosome, pan, mapping, mosaic, loss, normal, specificity, frequency, phenotype, citrullinated, vary, activity, rheumatoid, arthritis, activation, megakaryocyte, α7, nachr, exacerbates, allergic, inflammation, 33, p38, mapk, pericardial, macrophages, suppress, cardiac, cystatin, after, myocardial, infarction, hypercapnia, enhances, contractility, stim1, ca2, role, mannose, binding, lectin, schistosoma, hypertension, regulation, purinergic, axis, contributes, cd8, dysregulation, stat3, gain, function, multiomic, analysis, subsets, interaction, idiopathic, 27, neutralization, without, antibiotics, an, approach, prevent, treat, neonatal, sepsis, local, hormone, benign, prostatic, hyperplasia, urinary, ykl, 40, diagnostic, biomarker, cystinosis, cxcr4, coordinates, adhesion, migration, nk, cross, model, atlas, conserved, osteopontin, polycystic, kidney, hypothalamic, neuroinflammation, ovariectomized, parallels, aging, related, changes, female, hypothalamus, sequencing, clonally, expanded, tissue, resident, memory, histidyl, trna, synthetase, myositis, plasma, proteins, chronic, graft, versus, host, zinc, restrains, multicellular, fibrotic, stabilization, pp2a, b56α, complex, overcomes, venetoclax, azacitidine, resistance, impairing, oxphos, aml, profiling, immune, malignant, pleural, effusions, macrophage, reprogramming, survival, feeding, mtorc1, regulates, postprandial, synthesis, endurance, but, size, endothelial, cycle, inhibition, enables, blood, vessel, maturation, normalize, vasculature, sign, up, email, alerts, cover, pdgfra, published, september, 2026, previous, press, preview, reviews, video, on, show, summary, otoshi, et, al, report, hyperactive, tgf, tnc, unleashed, brief, utero, exposure, vitamin, retinoic, acid, deficient, environment, resulting, structural, adult, image, shows, aberrant, ectopic, expansion, red, where, emerges, embryonic, near, distal, buds, sox9, green, progenitors, sox2, cyan, go, section, view, articles, topic, predoctoral, grant, writing, trainees, national, survey, barriers, facilitators, success, navigating, careers, insights, american, board, internal, medicine, graduates, shared, 21, expression, is, modulated, during, latent, coinfection,

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marbán view text pdf noncoding rna ty1 reverses fibrosis in systemic sclerosis by attenuating the cgas sting pathway text pdf abstract dna damage and the cgas sting innate immunity pathway have been associated with fibrosis in systemic sclerosis ssc but a cause and effect role has not been established here we report the effects of ty1 a noncoding rna drug of the exomer class that suppresses dna damage and thereby inhibits cgas sting in human ssc cells and in 2 preclinical models of ssc macrophages from patients with ssc exhibited high levels of phosphorylated dna damage cgas 2 3 cgamp sting and ifns all of which decreased after exposure to ty1 in mice that had been injected s c with bleomycin to model ssc exercise tolerance cardiac function lung hydroxyproline and skin thickness reverted to normal levels after oral administration of ty1 similar therapeutic benefits were evident in the genetic tsk 1 mouse model of ssc ty1 attenuated fibrosis and or fibrotic gene expression in both mouse models of ssc and in human ssc skin fibroblasts our findings support the hypothesis that cgas sting activated by dna damage is a key driver of fibrosis in ssc authors xaviar m jones salwa soussi alessandra ciullo kara tsi weixin liu liang li mario fournier thassio mesquita alberto m marchevsky nunzio bottini francesco boin ahmed g e ibrahim eduardo marbán a familial case of flad1 protein deficiency associated with impaired adrenal steroidogenesis olga a averina natalia yu kalinchenko vitaly a ioutsi andrey v pirogov alexander v bogachev oleg a permyakov vitaly s buev ekaterina a guseva anastasia v priymak olga a bazhanova mariia a emelianova olga o grigoryeva galina v baydakova maxim a abakumov vasily n manskikh olga a dontsova petr v sergiev anatoly n tiulpakov olga a averina natalia yu kalinchenko vitaly a ioutsi andrey v pirogov alexander v bogachev oleg a permyakov vitaly s buev ekaterina a guseva anastasia v priymak olga a bazhanova mariia a emelianova olga o grigoryeva galina v baydakova maxim a abakumov vasily n manskikh olga a dontsova petr v sergiev anatoly n tiulpakov view text pdf a familial case of flad1 protein deficiency associated with impaired adrenal steroidogenesis text pdf abstract the flad1 gene codes for flavin adenine dinucleotide fad synthase fad is a cofactor for many redox enzymes involved in vital processes from respiration to signal transduction in this work we described a clinical case of 2 siblings carrying compound heterozygous mutations in the flad1 gene resulting in the substitutions a418v and r542 at the protein level the patients demonstrate adrenal insufficiency which has not previously been associated with flad1 protein defects to verify that adrenal insufficiency is caused by flad1 mutations we created a personalized mouse model carrying the mutations found in the patients the mutation in the flad1 gene leading to the a418v substitution appeared viable in the homozygous state with minimal difference from the wt the flad1 gene mutation leading to the r542 truncation is lethal when homozygous the mouse model of the compound heterozygous flad1a418v r542 mutations recapitulated the physiological biochemical and endocrine manifestations of flad1 mutations in patients the mouse model created demonstrates the causal effect of flad1 mutations on the described pathology and potentially paves the way for understanding the disease s molecular mechanism and developing better therapies authors olga a averina natalia yu kalinchenko vitaly a ioutsi andrey v pirogov alexander v bogachev oleg a permyakov vitaly s buev ekaterina a guseva anastasia v priymak olga a bazhanova mariia a emelianova olga o grigoryeva galina v baydakova maxim a abakumov vasily n manskikh olga a dontsova petr v sergiev anatoly n tiulpakov discovery of cd4 t cell recognized b pertussis antigens that reduce airway colonization mohamed m shamseldin jesse m hall griffin m lawrence gabrielle m hernandez yue liu alexa r aubrey eva k verzani rajendar deora amy lovett racke jennifer g abelin purnima dubey mohamed m shamseldin jesse m hall griffin m lawrence gabrielle m hernandez yue liu alexa r aubrey eva k verzani rajendar deora amy lovett racke jennifer g abelin purnima dubey view text pdf discovery of cd4 t cell recognized b pertussis antigens that reduce airway colonization text pdf abstract despite widespread vaccination bordetella pertussis bp cases are resurging globally although cd4 t cells are known to be essential for sustained protection the antigens they recognize are not fully characterized hindering vaccine refinement using immunopeptidomics bioinformatics and functional t cell assays we identified high affinity epitopes from reference and clinical bp strains presented on mhc ii i ab a subset of these epitopes stimulated systemic and mucosal cd4 t cells of mice immunized with heat killed bp and peripheral blood t cells from humans vaccinated with the whole cell pertussis vaccine mice immunized with a subunit vaccine comprising two recombinant proteins identified in our screen were subsequently challenged with bp bacterial burden was nearly eliminated from the lower respiratory tract and significantly reduced in the upper respiratory tract th1 th17 polarized cd4 tissue resident memory t cells trms were induced in nasal and pulmonary tissues depleting memory cd4 t cells before challenge abolished protection confirming that antigen specific cd4 t cells are critical for clearing bp from the respiratory tract our integrated antigen identification and t cell assay approach revealed previously untested bp antigens that elicit protective cd4 t cell mediated immunity suggesting that incorporating them into new vaccines may help curb the resurgence of pertussis authors mohamed m shamseldin jesse m hall griffin m lawrence gabrielle m hernandez yue liu alexa r aubrey eva k verzani rajendar deora amy lovett racke jennifer g abelin purnima dubey glutamine dependent biosynthetic pathways fuel autoreactive t and b cells in foxp3 deficiency mediated disease mohammad adeel zafar charlotte n hill machado jyotirmaya behera yuelin zhong xiao li shakchhi joshi yassine el fazaa virginia camacho peter georgiev kiran kurmi marcia haigis louis marie charbonnier mohammad adeel zafar charlotte n hill machado jyotirmaya behera yuelin zhong xiao li shakchhi joshi yassine el fazaa virginia camacho peter georgiev kiran kurmi marcia haigis louis marie charbonnier view text pdf glutamine dependent biosynthetic pathways fuel autoreactive t and b cells in foxp3 deficiency mediated disease text pdf abstract foxp3 deficiency causes a profound loss of immune tolerance unleashing autoreactive t and b cells lymphoproliferation cytokine driven inflammation and autoantibody production this autoimmune pathology is fueled by increased glutamine usage but it remains unresolved whether glutamine is necessary to produce energy or for intermediate metabolite biosynthesis responsible for immunomodulation here we demonstrate that glutamine utilization for biosynthetic pathways supported autoimmune inflammation in the settings of foxp3 deficiency and dextran sodium sulfate induced colitis by employing a model of autoimmunity driven by treg specific loss of foxp3 we showed that this effect is independent of pathogenic foxp3 deficient treg reprogramming mechanistically glutamine biosynthetic pathways sustained conventional t cell activation and proinflammatory cytokine production by preventing inosine accumulation and signaling thus implicating adenosine pathway modulation in autoreactive t cell dysregulation conversely autoreactive b cell activation and autoantibody production relied on glutamine dependent asparagine availability which we identified as a targetable vulnerability for autoantibody formation these findings highlighted glutamine driven biosynthetic processes as critical drivers of autoimmunity and revealed distinct metabolic vulnerabilities in autoreactive t and b cells that could be targeted for therapeutic intervention authors mohammad adeel zafar charlotte n hill machado jyotirmaya behera yuelin zhong xiao li shakchhi joshi yassine el fazaa virginia camacho peter georgiev kiran kurmi marcia haigis louis marie charbonnier genetic background influences developmental airway smooth muscle program and susceptibility to airway hyperresponsiveness in mice takehiro otoshi benjamin d kotton ayyappa k s kameshwar yoshinori seki zachary cardell xiangyi ke yuta matsuno pooja rajaram youn kyung kim sarah m sharpton loredana quadro wellington v cardoso masako suzuki takehiro otoshi benjamin d kotton ayyappa k s kameshwar yoshinori seki zachary cardell xiangyi ke yuta matsuno pooja rajaram youn kyung kim sarah m sharpton loredana quadro wellington v cardoso masako suzuki view text pdf genetic background influences developmental airway smooth muscle program and susceptibility to airway hyperresponsiveness in mice text pdf abstract airway structural remodeling and hyperresponsiveness ahr hallmarks of asthma are influenced by genetic variations and adverse exposures while intrauterine perturbations in lung development have been linked to adult pulmonary disease the developmental origins of these abnormalities remain poorly understood here we provide evidence of genetic background playing a key role in this process using a j and c57bl 6j mice known for their distinct susceptibility to ahr we show that a j embryos selectively develop an aberrant airway smooth muscle sm program and ahr in adulthood when exposed transiently to a vitamin a retinoic acid ra disrupted intrauterine environment in vivo by maternal bms493 administration single nucleus multiomics identified a mesenchymal cell population overactivating tgf β targets in response to bms493 selectively in a j lungs these cells localized to sites of airway sm initiation and p smad2 and 3 exhibited robust bms493 mediated upregulation of smad2 3 targets including regulators of sm program pdgfra and tnc functional analyses in vivo and cultured lungs showed aberrant sm formation in areas of overactive tgf β of bms493 exposed lungs these abnormalities were prevented by inhibiting tgf β signaling in utero in ra deficient embryos these findings underscore how distinct genetic backgrounds respond to intrauterine perturbations that program airway structure and function with potential lasting consequences in postnatal pulmonary function authors takehiro otoshi benjamin d kotton ayyappa k s kameshwar yoshinori seki zachary cardell xiangyi ke yuta matsuno pooja rajaram youn kyung kim sarah m sharpton loredana quadro wellington v cardoso masako suzuki α ketoglutarate accelerates cutaneous wound healing through modulating the epithelial fibroblast niche yuhan li weimin lin denghao huang yueying wang yimeng cai jie xiang linfeng liu xinxing shuai qi yin shuang jiang malcolm xing yuan wang leixiao yu quan yuan yuhan li weimin lin denghao huang yueying wang yimeng cai jie xiang linfeng liu xinxing shuai qi yin shuang jiang malcolm xing yuan wang leixiao yu quan yuan view text pdf α ketoglutarate accelerates cutaneous wound healing through modulating the epithelial fibroblast niche text pdf abstract wound healing is a highly dynamic and metabolically demanding process however the primary drivers of metabolic alterations involved in this process remain incompletely understood here we employed multiomics profiling of clinical samples to investigate metabolic alterations during wound healing our analyses revealed significant activation of the tca cycle and identified α ketoglutarate αkg as a central regulator orchestrating the reparative phase systemic administration of αkg promoted wound closure and re epithelialization characterized by enhanced neo tissue formation with an extended epithelial tongue mechanistically αkg promoted cell proliferation via the cell cycle pathway and enhanced fibroblast derived tgf β signaling to induce epithelial mesenchymal transition like programs in epithelial cells to address the spatial metabolic heterogeneity we developed a transdermal mn platform based on gelatin methacryloyl for localized αkg delivery further accelerating tissue repair collectively these findings identify αkg as a metabolic driver of wound repair reveal its dual role in modulating the epithelial fibroblast microenvironment and introduce a targeted bioengineering strategy with translational potential for both acute and chronic wound management authors yuhan li weimin lin denghao huang yueying wang yimeng cai jie xiang linfeng liu xinxing shuai qi yin shuang jiang malcolm xing yuan wang leixiao yu quan yuan human y chromosome pan organ mapping reveals progressive mosaic loss from normal to cancer arkadiusz gertych huihui ye xingyu chen eric vail v krishnan ramanujan lauren brady lawrence d true peter s nelson peter r carroll dan theodorescu arkadiusz gertych huihui ye xingyu chen eric vail v krishnan ramanujan lauren brady lawrence d true peter s nelson peter r carroll dan theodorescu view text pdf human y chromosome pan organ mapping reveals progressive mosaic loss from normal to cancer text pdf abstract background loss of the y chromosome loy is a frequent event in male tumors and has been linked to cancer progression however the degree of mosaic loy mloy within normal tissues from men with or without cancer remains uncharacterized methods here we used a fish based assay targeting x and y chromosome centromeres to perform a pan organ analysis of mloy in 1 000 male tissue samples from 405 individuals representing 11 organs automated image processing generated a quantitative fish based mloy score ychrfish that we validated against a transcriptomic surrogate of y chromosome dosage from rna seq data results mloy burden varied by tumor type with highest degree in colorectal carcinoma across tissue groups ychrfish scores declined progressively from normal tissues of cancer free men to histologically normal tissues adjacent to cancer and carcinoma p 0 0001 paired analyses confirmed consistently greater mloy in malignant compared with tumor adjacent histologically normal tissue in different organs spatially resolved rna seq maps of bladders removed for cancer demonstrated a transcriptional gradient of y chromosome loss from normal urothelium through intraepithelial neoplasia to invasive carcinoma conclusion mloy gradients exist across histologically normal and malignant tissues consistent with the concept of field cancerization our findings support epithelial mloy as a biomarker of early malignant transformation and to our knowledge a previously unrecognized hallmark of male oncogenesis funding nih grants r35ca294022 p01ca163227 and p50ca97186 the pacific northwest prostate cancer spore and the institute for prostate cancer research authors arkadiusz gertych huihui ye xingyu chen eric vail v krishnan ramanujan lauren brady lawrence d true peter s nelson peter r carroll dan theodorescu specificity frequency and phenotype of citrullinated specific t cells var...