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Serrano, M.

Publications and source records attributed to Serrano, M..

32 records · Page 2Linked to original sources

Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming

The expression of the pluripotency factors OCT4, SOX2, KLF4 and MYC (OSKM) can convert somatic differentiated cells into pluripotent stem cells in a process known as reprogramming. Notably, cycles of brief OSKM expression do not change cell identity but can reverse markers of aging in cells and extend longevity in progeroid mice. However, little is known about the mechanisms involved. Here, we have studied changes in the DNA methylome, transcriptome and metabolome in naturally aged mice subject to a single period of transient OSKM expression. We found that this is sufficient to reverse DNA methylation changes that occur upon aging in the pancreas, liver, spleen and blood. Similarly, we observed reversion of transcriptional changes, especially regarding biological processes known to change during aging. Finally, some serum metabolites altered with aging were also restored to young levels upon transient reprogramming. These observations indicate that a single period of OSKM expression can drive epigenetic, transcriptomic and metabolomic changes towards a younger configuration in multiple tissues and in the serum.

cell biology↗

NeuroSCORE: A Genome-wide Omics-Based Model to Identify Candidate Disease Genes of the Central Nervous System

To identify and prioritize candidate disease genes of the central nervous system (CNS) we created the Neurogenetic Systematic Correlation of Omics-Related Evidence (NeuroSCORE). We used five genome-wide metrics highly associated with neurological phenotypes to score 19,598 protein-coding genes. Genes scored one point per metric, resulting in a range of scores from 0-5. Approximately 13,000 genes were then paired with phenotype data from the Online Mendelian Inheritance in Man (OMIM) database. We used logistic regression to determine the odds ratio of each metric and compared genes scoring 1+ to cause a known CNS-related phenotype compared to genes that scored zero. We tested NeuroSCORE using microarray copy number variants (CNVs) in case-control cohorts, mouse model phenotype data, and gene ontology (GO) and pathway analyses. NeuroSCORE identified 8,296 genes scored [&ge;]1, of which 1,580 are "high scoring" genes (scores [&ge;]3). High scoring genes are significantly associated with CNS phenotypes (OR=5.5, p<2x10-16), enriched in case CNVs, and enriched in mouse ortholog genes associated with behavioral and nervous system abnormalities. GO and pathway analyses showed high scoring genes were enriched in chromatin remodeling, mRNA splicing, dendrite development, and neuron projection. OMIM has no phenotype for 1,062 high scoring genes (67%). Top scoring genes include ANKRD17, CCAR1, CLASP1, DOCK9, EIF4G2, G3BP2, GRIA1, MAP4K4, MARK2, PCBP2, RNF145, SF1, SYNCRIP, TNPO2, and ZSWIM8. NeuroSCORE identifies and prioritizes CNS-disease candidate genes, many not yet associated with any phenotype in OMIM. These findings can help direct future research and improve molecular diagnostics for individuals with neurological conditions.

genomics↗

The morphogenetic protein CotE drives exosporium formation by positioning CotY and ExsY during sporulation of Bacillus cereus

The exosporium is the outermost spore layer of some Bacillus and Clostridium species and related organisms. It mediates interactions of spores with their environment, modulates spore adhesion and germination and could be implicated in pathogenesis. The exosporium is composed of a crystalline basal layer, formed mainly by the two cysteine-rich proteins CotY and ExsY, and surrounded by a glycoprotein hairy nap. The morphogenetic protein CotE is necessary for Bacillus cereus exosporium integrity, but how CotE directs exosporium assembly remains unknown. Here, we followed the localization of SNAP-tagged CotE, -CotY and -ExsY during B. cereus sporulation, using super-resolution fluorescence microscopy and evidenced interactions among these proteins. CotE, CotY and ExsY are present as complexes at all sporulation stages and follow a similar localization pattern during endospore formation that is reminiscent of the localization of Bacillus subtilis CotE. We show that B. cereus CotE drives the formation of one cap at both forespore poles by positioning CotY and then guides forespore encasement by ExsY, thereby promoting exosporium elongation. By these two actions, CotE ensures the formation of a complete exosporium. Importantly, we demonstrate that the assembly of the exosporium is not a unidirectional process as previously proposed but it is performed through the formation of two caps, as observed during B. subtilis coat morphogenesis. It appears that a general principle governs the assembly of the spore surface layers of Bacillaceae. IMPORTANCESpores of Bacillaceae are enveloped in a glycoprotein outermost layer. In the B. cereus group, encompassing the B. anthracis and B. cereus pathogens, this layer is easily recognizable by a characteristic balloon-like appearance separated from the underlying coat by an interspace. In spite of its importance for the environmental interactions of spores, including those with host cells, the mechanism of assembly of the exosporium is poorly understood. We used super-resolution fluorescence microscopy to directly visualize formation of the exosporium during sporulation of B. cereus and we studied the localization and interactions of proteins essential for exosporium morphogenesis. We discovered that these proteins form a morphogenetic scaf-fold, before a complete exosporium or coat are detectable. We describe how the different proteins localize to the scaffold and how they subsequently assemble around the spore and we present a model for the assembly of the exosporium.

microbiology↗

Primate naive pluripotent stem cells stall in the G1 phase of the cell cycle and differentiate prematurely during embryo colonization

After reprogramming to naive pluripotency, human pluripotent stem cells (PSCs) still exhibit very low ability to make interspecies chimeras. Whether this is because they are inherently devoid of the attributes of chimeric competency or because naive PSCs cannot colonize embryos from distant species remains to be elucidated. Here, we have used different types of mouse, human and rhesus monkey naive PSCs and analyzed their ability to colonize rabbit and cynomolgus monkey embryos. Mouse embryonic stem cells (ESCs) remained mitotically active and efficiently colonized host embryos. In contrast, primate naive PSCs colonized host embryos with much lower efficiency. Unlike mouse ESCs, they slowed DNA replication after dissociation and, after injection into host embryos, they stalled in the G1 phase and differentiated prematurely, regardless of host species. We conclude that human and non-human primate naive PSCs do not efficiently make chimeras because they are inherently unfit to remain mitotically active during colonization.

cell biology↗

Cellular senescence limits acute lung injury induced by mechanical ventilation

The p53/p21 pathway is activated in response to cell stress. However, its role in acute lung injury has not been elucidated. Acute lung injury is associated with disruption of the alveolo-capillary barrier leading to acute respiratory distress syndrome (ARDS). Mechanical ventilation may be necessary to support gas exchange in patients with ARDS, however, high positive airway pressures can cause regional overdistension of alveolar units and aggravate lung injury. Here, we report that acute lung injury and alveolar overstretching activate the p53/p21 pathway to maintain homeostasis and avoid massive cell apoptosis. A systematic pooling of transcriptomic data from animal models of lung injury demonstrates the enrichment of specific p53- and p21-dependent gene signatures and a validated senescence profile. In a clinically relevant, murine model of acid aspiration and mechanical ventilation, we observed changes in the nuclear envelope and the underlying chromatin, DNA damage and activation of the Tp53/p21 pathway. Absence of Cdkn1a decreased the senescent response, but worsened lung injury due to increased cell apoptosis. Conversely, treatment with lopinavir/ritonavir led to Cdkn1a overexpression and ameliorated cell apoptosis and lung injury. The activation of these mechanisms was associated with early markers of senescence, including expression of senescence-related genes and increases in senescence-associated heterochromatin foci in alveolar cells. Autopsy samples from lungs of patients with ARDS revealed increased senescence-associated heterochromatin foci. Collectively, these results suggest that acute lung injury activates p53/p21 as an anti-apoptotic mechanism to ameliorate damage, but with the side effect of induction of senescence.

cell biology↗

A regulatory protein that represses sporulation in Clostridioides difficile

Bacteria that reside in the gastrointestinal tract of healthy humans are essential for our health, sustenance and well-being. About 50 to 60% of those bacteria have the ability to produce resilient spores, important for the life cycle in the gut and for host-to-host transmission. A genomic signature for sporulation in the human intestine was recently described, which spans both commensals and pathogens such as Clostridioides difficile, and contains several genes of unknown function. We report on the characterization of a signature gene, csiA, which, as we show, is involved in the control of sporulation initiation in C. difficile. Spo0A is the main regulatory protein controlling entry into sporulation and we show that an in-frame deletion of csiA results in increased sporulation, and increased expression of spo0A per cell. Spo0A also drives transcription of the spoIIA and spoIIG operons, coding for the first forespore-({sigma}F) and mother cell-specific ({sigma}E) RNA polymerase sigma factors. Strikingly, deletion of csiA increases expression of the spoIIG operon, but not that of the spoIIA operon. Increased expression of spoIIG results in increased production and proteolytic activation of pro-{sigma}E, suggesting that normally, the levels of active {sigma}E are limiting for sporulation. While other regulatory proteins affect both sporulation and several processes during the transition phase of growth, including toxin production or motility, deletion of the csiA gene does not alter the expression of the genes coding for the TcdA and TcdB cytotoxins or the genes involved in motility. Thus, our results establish that CsiA acts to modulate sporulation by reducing expression of the spo0A gene.

microbiology↗

Long reads from Nanopore sequencing as a tool for animal microbiome studies

In the era of bioinformatics and metagenomics, the study of the ruminal microbiome has gained considerable relevance in the field of animal breeding, since the composition of the rumen microbiota significantly impacts production and the environment. Illumina sequencing is considered the gold standard for the analysis of microbiomes, but it is limited by obtaining only short DNA sequences to analyze. As an alternative, Oxford Nanopore Technologies (ONT) has developed a new sequencing technique based on nanopores that can be carried out in the MinION, a portable device with a low initial cost which long DNA readings can be obtained with. The aim of this study was to compare the performance of both types of sequencing applied to samples of ruminal content using a similar pipeline. The ONT sequencing provided similar results to the Illumina sequencing, although it was able to classify a greater number of readings at the species level, possibly due to the increase in the read size. The results also suggest that, due to the size of the reads, it would be possible to obtain the same amount of information in a smaller number of hours. However, detection of archaeal and eukaryotic species is still difficult to accomplish due to their low abundance in the rumen compared to bacteria, suggesting different pipelines and strategies are needed to obtain a whole representation of the less abundant species in the rumen microbiota.

microbiology↗

A novel microRNA-based strategy to expand the differentiation potency of stem cells

Full differentiation potential along with self-renewal capacity is a major property of pluripotent stem cells (PSCs). However, the differentiation capacity frequently decreases during expansion of PSCs in vitro. We show here that transient exposure to a single microRNA, expressed at early stages during normal development, improves the differentiation capacity of already-established murine and human PSCs. Short exposure to miR-203 in PSCs (miPSCs) results in expanded differentiation potency as well as improved efficiency in stringent assays such as tetraploid complementation and human-mouse interspecies chimerism. Mechanistically, these effects are mediated by direct repression of de novo DNA methyltransferases Dnmt3a and Dnmt3b, leading to transient and reversible erasing of DNA methylation. As a proof of concept, miR-203 improves differentiation and maturation of PSCs into cardiomyocytes in vitro as well as cardiac regeneration in vivo, after cardiac injury. These data support the use of transient exposure to miR-203 as a general and single method to reset the epigenetic memory in PSCs, and improve their use in regenerative medicine.

cell biology↗

From root to tips: sporulation evolution and specialization in Bacillus subtilis and the intestinal pathogen Clostridioides difficile

Bacteria of the Firmicutes phylum are able to enter a developmental pathway that culminates with the formation of a highly resistant, dormant spore. Spores allow environmental persistence, dissemination and for pathogens, are infection vehicles. In both the model Bacillus subtilis, an aerobic species, and in the intestinal pathogen Clostridioides difficile, an obligate anaerobe, sporulation mobilizes hundreds of genes. Their expression is coordinated between the forespore and the mother cell, the two cells that participate in the process, and is kept in close register with the course of morphogenesis. The evolutionary mechanisms by which sporulation emerged and evolved in these two species, and more broadly across Firmicutes, remain largely unknown. Here, we trace the origin and evolution of sporulation. Using the genes involved in the process in B. subtilis and C. difficile, and estimating their gain-loss dynamics in a comprehensive bacterial macro-evolutionary framework we show that sporulation evolution was driven by two major gene gain events, the first at the base of the Firmicutes and the second at the base of the B. subtilis group and within the Peptostreptococcaceae family, which includes C. difficile. We also show that early and late sporulation regulons have been co-evolving and that sporulation genes entail greater innovation in B. subtilis with many Bacilli-lineage restricted genes. In contrast, C. difficile more often recruits new sporulation genes by horizontal gene transfer, which reflects both its highly mobile genome, the complexity of the gut microbiota and an adjustment of sporulation to this particular ecosystem.

evolutionary biology↗

Structure and assembly of a Clostridioides difficile spore polar appendage

Clostridioides difficile, a strict anaerobic spore-former, is the main cause of nosocomial disease associated to antibiotic therapy in adults and a growing concern in the community. Spores are the main infectious, persistence and transmission vehicle. Spore germination occurs in the intestine and the resulting vegetative cells will produce the toxins responsible for the disease symptoms, and spores. During sporulation, a wild type population bifurcates into two main spore morphotypes, with or without a thick exosporium. We show that this bifurcation extends to the formation of spores with a robust polar appendage or spores with a short appendage or that lack this structure. The cysteine-rich CdeM protein localizes to the appendage and around the entire surface of the spore, and is a major structural component of the exosporium, which we show is continuous with the appendage. In a CdeM mutant, when present, the polar appendage is short and disorganized. We show that wild type and cdeM spores with a short or no appendage germinate poorly in response to taurocholate, compared to those with an appendage. cdeM spores of the two types, however, germinate faster than their wild type counterparts. Thus, while the absence of CdeM may increase the permeability of spores to taurocholate, proper assembly of the appendage is also important for germination. Consistent with an overall enhancement of germination, a cdeM mutant shows increased virulence in a hamster model of disease. For a wild type population, spores with a short or no appendage germinate slower than the appendage-bearing spores. Differences in transmission, persistence and disease severity may result, in part, from their proportion in a spore population.

microbiology↗

A protein phosphorylation module patterns the Bacillus subtilis spore outer coat

Assembly of the Bacillus subtilis spore coat involves over 80 protein components, which self-organize into a basal layer, a lamellar inner coat, a striated electrondense outer coat and a more external crust. CotB is an abundant component of the outer coat. Its C-terminal moiety contains a region, termed SKRB, formed by a series of serine-rich repeats, which we show is phosphorylated by the coat-associated Ser/Thr kinase CotH at multiple Ser residues. Another coat protein, CotG, which contains a central repeat region, SKRG, interacts with the C-terminal moiety of CotB and promotes its phosphorylation by CotH in vivo and in a heterologous system. CotG itself is phosphorylated by CotH but phosphorylation is enhanced in the absence of CotB. Spores of a cotHD288A strain, producing an inactive form of the kinase, like those formed by a cotG deletion mutant, lack the characteristic pattern of electrondense outer coat striations, while retaining the crust. Specifically, in the absence of CotG or CotH activity, most of the outer coat proteins are assembled but form a layer of amorphous material that peels-off the spore if crust formation is genetically ablated. In contrast, deletion of the SKRB region, has no major impact on the structure of the outer coat. Thus, phosphorylation of CotG by CotH is the principal factor establishing the structural pattern of the spore outer coat. The presence of the cotB/cotH/cotG cluster in several species closely related to B. subtilis and of cotG-like proteins in nearly all spore-formers that also code for a CotH homologue hints at the importance of this protein phosphorylation module in the morphogenesis of the spore outer layers.

microbiology↗

Determining the Quantitative Principles of T Cell Response to Antigenic Disparity: The Case of Stem Cell Transplant Donor-Recipient Exome Wide Mismatching and HLA Bound Alloreactive Peptides

Alloreactivity compromising clinical outcomes in stem cell transplantation is observed despite HLA matching of donors and recipients. This has its origin in the variation between the exomes of the two, which provides the basis for minor histocompatibility antigens (mHA). The mHA presented on the HLA class I and II molecules and the ensuing T cell response to these antigens results in graft versus host disease. In this paper, results of a whole exome sequencing study are presented, with resulting alloreactive polymorphic peptides and their HLA class I and HLA class II (DRB1) binding affinity quantified. Large libraries of potentially alloreactive recipient peptides binding both sets of molecules were identified, with HLA-DRB1 presenting an order of magnitude greater number of peptides. These results are used to develop a quantitative framework to understand the immunobiology of transplantation. A tensor-based approach is used to derive the equations needed to determine the alloreactive donor T cell response from the mHA-HLA binding affinity and protein expression data. This approach may be used in future studies to simulate the magnitude of expected donor T cell response and risk for alloreactive complications in HLA matched or mismatched hematopoietic cell and solid organ transplantation.

immunology↗

Dynamical System Modeling to Simulate Donor T Cell Response to Whole Exome Sequencing-Derived Recipient Peptides: Understanding Randomness in Clinical Outcomes Following Stem Cell Transplantation

The quantitative relationship between the magnitude of variation in minor histocompatibility antigens (mHA) and graft versus host disease (GVHD) pathophysiology in stem cell transplant (SCT) donor-recipient pairs (DRP) is not established. In order to elucidate this relationship, whole exome sequencing (WES) was performed on 27 HLA matched related (MRD), & 50 unrelated donors (URD), to identify nonsynonymous single nucleotide polymorphisms (SNPs). An average 2,463 SNPs were identified in MRD, and 4,287 in URD DRP (p<0.01); resulting peptide antigens that may be presented on HLA class I molecules in each DRP were derived in silico (NetMHCpan ver2.0) and the tissue expression of proteins these were derived from determined (GTex). MRD DRP had an average 3,670 HLA-binding-alloreactive peptides, putative mHA (pmHA) with an IC50 of <500 nM, and URD, had 5,386 (p<0.01). To simulate an alloreactive donor cytotoxic T cell response, the array of pmHA in each patient was considered as an operator matrix modifying a hypothetical cytotoxic T cell clonal vector matrix; each responding T cell clones proliferation was determined by the logistic equation of growth, accounting for HLA binding affinity and tissue expression of each alloreactive peptide. The resulting simulated organ-specific alloreactive T cell clonal growth revealed marked variability, with the T cell count differences spanning orders of magnitude between different DRP. Despite an estimated, uniform set of constants used in the model for all DRP, and a heterogeneously treated group of patients higher total and organ-specific T cell counts were associated with cumulative incidence of GVHD in recipients in Cox proportional hazard models. In conclusion, exome wide sequence differences and the variable alloreactive peptide binding to HLA in each DRP yields a large range of possible alloreactive donor T cell responses. Our findings also help understand the apparent randomness observed in the development of alloimmune responses.

immunology↗

Analytical and Clinical Validity Study of FirstStepDx PLUS: A Chromosomal Microarray Optimized for Patients with Neurodevelopmental Conditions

IntroductionChromosomal microarray analysis (CMA) is recognized as the first-tier test in the genetic evaluation of children with developmental delays, intellectual disabilities, congenital anomalies and autism spectrum disorders of unknown etiology.\n\nArray DesignTo optimize detection of clinically relevant copy number variants associated with these conditions, we designed a whole-genome microarray, FirstStepDx PLUS (FSDX). A set of 88,435 custom probes was added to the Affymetrix CytoScanHD platform targeting genomic regions strongly associated with these conditions. This combination of 2,784,985 total probes results in the highest probe coverage and clinical yield for these disorders.\n\nResults and DiscussionClinical testing of this patient population is validated on DNA from either non-invasive buccal swabs or traditional blood samples. In this report we provide data demonstrating the analytic and clinical validity of FSDX and provide an overview of results from the first 7,570 consecutive patients tested clinically. We further demonstrate that buccal sampling is an effective method of obtaining DNA samples, which may provide improved results compared to traditional blood sampling for patients with neurodevelopmental disorders who exhibit somatic mosaicism.\n\nClinical scenarioNeurodevelopmental disabilities, including developmental delays (DD), intellectual disabilities (ID), and autism spectrum disorders (ASD), affect up to 15% of children (1). In the majority of cases, a childs clinical presentation does not allow for a definitive etiological diagnosis. In such cases, CMA is recommended as the first-tier test that should be used to evaluate for a potential genetic etiology (2-7). A definitive genetic diagnosis allows patients to more often receive appropriate medical care tailored to their condition, as reflected by medical management changes and improved access to necessary support and educational services (8-13).\n\nTest descriptionFirstStepDx PLUS (FSDX) is an optimized clinical microarray test provided in the context of a comprehensive clinical service. Testing starts with either a non-invasive buccal swab sample or traditional blood sample from which DNA extraction using a Gentra Puregene(R) kit specific to the sample type (Qiagen, Inc., Valencia, CA) is performed in one of several contracted CLIA/CAP credentialed laboratories according to manufacturers protocols. High quality genomic DNA is fragmented, labeled and hybridized to FSDX arrays using reagents, equipment and methodology as specified by by the manufacturer (Affymetrix, Inc., Santa Clara, CA)(14). Washed arrays are scanned and raw data files are processed to CYCHP files using a reference file comprising at least 100 samples with normal array findings. Data analysis is performed using Chromosome Analysis Suite software version 2.0.1 (Affymetrix). Hybridization of patient DNA to oligonucleotide and SNP probes is independently compared against a previously analyzed cohort of normal samples to call CNVs and allele genotypes. The percentage mosaicism of whole-chromosome aneuploidies is determined using the average log2 ratio of the entire chromosome (14).\n\nMicroarray designFSDX was optimized by the addition of 88,435 custom probes targeting genomic regions strongly associated with ID/DD/ASD (15-24). This was effected, under GMP by Affymetrix, to the CytoScanHD platform using their microarray design process specifications which have been previously described (14). This is consistent with the ACMG recommendation of \"enrichment of probes targeting dosage-sensitive genes known to result in phenotypes consistent with common indications for a genomic screen\" (25). Critical regions that did not meet a desired probe density [&ge;]1 probe/1000 bp on the CytoScanHD were supplemented with additional probe content to allow for improved detection of smaller deletions and duplications in these critical regions. Finally, additional probes were added to improve detection of CNVs encompassing genes involved in other well-characterized neurodevelopmental disorders, for example GAMT (26) and GATM (27). All incremental probes were added in substitution for probes deemed sub-optimal by Affymetrix and previously masked, bringing FSDX to a grand total of 2,784,985 probes. Custom SNP probes (n =416) on FSDX are targeted by 12 oligonucleotides, three for each strand of each allele, which is approximately double the typical probe coverage for SNPs.\n\nTest interpretationCYCHP files are evaluated by ABMG certified cytogeneticists. Determination of CNVs is consistent with established cytogenetic standards. A minimum of 25-consecutive impacted probes is the baseline determinant for deletions and 50 probes for duplications independent of variant size. Rare CNVs are determined to be \"pathogenic\" if there is sufficient evidence published (at least two independent publications) to indicate that haploinsufficiency or triplosensitivity of the region or gene(s) involved is causative of clinical features or of sufficient overall size (28). If however, there is insufficient but at least preliminary evidence for a causative role for the region or gene(s) therein they are classified as variants of unknown significance (VOUS) independent of CNV size. Areas of absence of heterozygosity (AOH) are also classed as VOUS if of sufficient size and location to increase the risk for conditions with autosomal recessive inheritance or conditions with parent-of-origin/imprinting effects. Other CNVs are typically not reported after determination that they most likely represent normal common population variants and are contained in databases documenting presumptively benign CNVs, e.g., the Database of Genomic Variants (DGV) (29). These parameters were standard independent of the microarray used for analysis in comparative studies.\n\nPublic health importanceA definitive genetic diagnosis facilitates patient access to appropriate and necessary medical and support services. Defining the underlying genetic cause of DD/ID/ASD and/or multiple congenital anomalies (MCA) in each unique patient is vital to understanding etiology, prognosis, and course. It informs physicians of potential comorbid conditions for which a patient should be evaluated and treated proactively and optimally. Improved understandings of the appropriate therapeutic and behavioral approaches to that patient are also enabled. Genetic testing is best provided in the context of an integrated service (30), so FSDX provides comprehensive, clear, readable, and personalized reports for the healthcare provider and a family-friendly section to facilitate understanding of the often-complex results. The report is complemented by availability of pre- and post-test genetic counseling and technical support to providers. Moreover, FSDX includes personalized insurance pre-authorization and appeals assistance to overcome barriers encountered by both providers and families that, in many circumstances, prevent access to crucial genetic testing services (10-11).\n\nPublished reviews, recommendations and guidelinesThe American College of Medical Genetics (ACMG) (2,3), the American Academy of Child and Adolescent Psychiatry (4,7), the American Academy of Pediatrics (5), and the American Academy of Neurology/Child Neurology Society (6) recommend CMA as the first-tier test in the genetic evaluation of children with unexplained DD, ID, or ASD. Considerable data supporting these guidelines are documented in numerous reviews and publications (31-36). The ACMG has also published guidelines on both array design (25) and the validation of arrays, including validation of a new version of a platform in use by the laboratory from the same manufacturer, and of additional sample types (28).

genomics↗