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PubMed2006

Early gene expression profile in mouse brain after exposure to ionizing radiation.

Acute changes in the gene expression profile in mouse brain after exposure to ionizing radiation were studied using microarray analysis. RNA was isolated at 0.25, 1, 5 and 24 h after exposure to 20 Gy and at 5 h after exposure of the whole brain of adult mice to 2 or 10 Gy. RNA was hybridized onto 15K cDNA microarrays, and data were analyzed using GeneSpring and Significant Analysis of Microarray. Radiation modulated the expression of 128, 334, 325 and 155 genes and ESTs at 0.25, 1, 5 and 24 h after 20 Gy and 60 and 168 at 5 h after 2 and 10 Gy, respectively. The expression profiles showed dose- and time-dependent changes in both expression levels and numbers of differentially modulated genes and ESTs. Seventy-eight genes were modulated at two or more times. Differentially modulated genes were associated with 12 different classes of molecular function and 24 different biological pathways and showed time- and dose-dependent changes. The change in expression of four genes (Jak3, Dffb, Nsep1 and Terf1) after irradiation was validated using quantitative real-time PCR. Up-regulation of Jak3 was observed in another mouse strain. In mouse brain, there was an increase of Jak3 immunoreactivity after irradiation. In conclusion, changes in the gene profile in the brain after irradiation are complex and are dependent on time and dose, and genes with diverse functions and pathways are modulated.

Animals↗

PubMed2003

Gene expression profile in the regenerating rat liver after partial hepatectomy.

BACKGROUND/AIMS: When a loss of hepatic mass occurs, the expression of a large number of genes is either induced or altered, accompanying hepatocyte proliferation. In the present study, we made an in-house cDNA microarray containing 4608 elements (Liver chip), and analyzed extensively gene expression profiles of the regenerating liver after 70% partial hepatectomy (PHx) in rats. METHODS: RNAs were prepared from three rat livers at each time point (taken at 0, 6, 12, 18, 24, 48, 72 h, and 1 week after PHx). Using the liver chip, we performed large-scale analysis of gene expression during liver regeneration. Elements either up- or down-regulated more than twofold at one or more time points were selected. RESULTS: Among the 4608, 382 were identified. Using cluster analysis, we found great similarity between gene-expression profiles at 12 and 18 h after PHx as well as between 48 and 72 h after PHx. We also found that there are at least six distinct temporal patterns of gene expression in the regenerating rat liver after PHx. CONCLUSIONS: These results indicated that microarray analysis is a powerful approach for monitoring molecular events in the regenerating liver.

Animals↗

PubMed2005

Gene expression profiling in acute myeloid leukemia.

Over the last decades, significant advances have been made in the knowledge and treatment of acute myeloid leukemia (AML). The WHO has recognized this new information by incorporating into its classification morphologic, immunophenotypic, genetic, and clinical features in an attempt to define biologically and clinically relevant entities. Nevertheless, well-defined cytogenetic subgroups exhibit considerable heterogeneity, and in many AML subtypes the pathogenic event is still not known. A classification system based on the underlying molecular pathogenetic abnormalities would be ideal, but such detailed knowledge is not yet available. Novel approaches in genomics, such as surveying the expression levels of thousands of genes in parallel using DNA microarray technology, open possibilities to further refine the studies on AML. Today, gene expression profiling in AML is becoming well established and has already been proven to be valuable in diagnosing different cytogenetic subtypes, discovering novel AML subclasses, and predicting clinical outcome. Recently, gene expression profiling studies in AML showed a remarkable level of concordance in findings, which may ultimately lead to an increasingly refined molecular taxonomy. While many challenges remain to be overcome, a combination of gene expression profiling with other microarray-based applications, high-throughput mutational analyses and proteomic approaches will not only significantly contribute to the classification and therapeutic decision making of AML, but also give important insights into the true pathobiologic nature of this type of leukemia.

Cytogenetic Analysis↗

PubMed2002

Thomas A. Neff lecture. Application of expression profiling to the developing lung: identification of putative regulatory networks controlling matrix production.

If we hope to repair damaged lung tissue associated with a variety of acquired and developmental diseases, we must first gain a full appreciation of normal lung development. As an approach, we have utilized Affymetrix (Santa Clara, CA) high-density, oligonucleotide-based microarrays to generate an expression profile of the entire process of rodent lung development, which will be made publicly available. Our initial results were internally consistent and correlated closely with those generated with standard expression techniques such as Northern hybridization. We have verified known expression of genes, found other genes with previously unsuspected expression during lung development, as well as uncovered many expressed sequence tags whose role in lung development awaits further study. Data mining reveals close relationships of expression profiles between specific genes, suggesting novel regulatory relationships. In the future, application of these methods to the study of gene-targeted mice with abnormal lung development should uncover pathways of airway and alveolar development. Ultimately, expression profiling of diseased lungs might allow us to understand why the lung fails to repair, and strategies to influence repair might become apparent.

Animals↗

PubMed2005

Gene expression profiling for pharmaceutical safety assessment.

Toxicogenomics is the application of gene expression profiling technology to toxicology. This results in the generation of very large and complex gene expression data sets associated with the development of toxicities. It is widely assumed that this data can be deconvoluted to reveal novel insights into toxicological processes that are of value to the task of risk assessment. More specifically, it is hoped that toxicogenomics will aid in the prediction of the toxic potential and mechanisms of toxicity of novel chemical entities. On the basis of such promise, the pharmaceutical industry has invested heavily in this area, as the perceived rewards in terms of improved pipeline efficiency and safer drugs are immense. Consequently, a great deal of groundwork has been done over the past several years to establish working methods in toxicogenomics, both within industry and academia, demonstrating utility in proof-of-concept studies, generating the databases on which some approaches depend, and developing new data analysis tools. Despite such activity, there is little reported evidence to suggest that toxicogenomics is making a significant impact on the discovery and development of drugs. This may partly reflect the understandable reluctance of pharmaceutical industries to share information in a competitive environment. It may also partly reflect difficulties in bridging the gap between theory and practice, as is required to deliver real value to the industry. This review will assess the successes and shortcomings of toxicogenomics, and consider how it can be usefully applied to a drug discovery pipeline.

Animals↗

PubMedDate not supplied

Altered gene expression profile in mouse bladder cancers induced by hydroxybutyl(butyl)nitrosamine.

A variety of genetic alterations and gene expression changes are involved in the pathogenesis of bladder tumor. To explore these changes, oligonucleotide array analysis was performed on RNA obtained from carcinogen-induced mouse bladder tumors and normal mouse bladder epithelia using Affymetrix (Santa Clara, CA) MGU74Av2 GeneChips. Analysis yielded 1164 known genes that were changed in the tumors. Certain of the upregulated genes included EGFR-Ras signaling genes, transcription factors, cell cycle-related genes, and intracellular signaling cascade genes. However, downregulated genes include mitogen-activated protein kinases, cell cycle checkpoint genes, Rab subfamily genes, Rho subfamily genes, and SH2 and SH3 domains-related genes. These genes are involved in a broad range of different pathways including control of cell proliferation, differentiation, cell cycle, signal transduction, and apoptosis. Using the pathway visualization tool GenMAPP, we found that several genes, including TbR-I, STAT1, Smad1, Smad2, Jun, NFkappaB, and so on, in the TGF-beta signaling pathway and p115 RhoGEF, RhoGDI3, MEKK4A/MEKK4B, PI3KA, and JNK in the G13 signaling pathway were differentially expressed in the tumors. In summary, we have determined the expression profiles of genes differentially expressed during mouse bladder tumorigenesis. Our results suggest that activation of the EGFR-Ras pathway, uncontrolled cell cycle, aberrant transcription factors, and G13 and TGF-beta pathways are involved, and the cross-talk between these pathways seems to play important roles in mouse bladder tumorigenesis.

Animals↗

PubMed2002

Integrated classification of lung tumors and cell lines by expression profiling.

The utility of cancer cell lines depends largely on their accurate classification, commonly based on histopathological diagnosis of the cancers from which they were derived. However, because cancer is often heterogeneous, the cell line, which also has the opportunity to alter in vitro, may not be representative. Yet without the overall architecture used in histopathological diagnosis of fresh samples, reclassification of cell lines has been difficult. Gene-expression profiling accurately reproduces histopathological classification and is readily applicable to cell lines. Here, we compare the gene-expression profiles of 41 cell lines with 44 tumors from lung cancer. These profiles were generated after hybridization of samples to four replicate 7,685-element cDNA microarrays. After removal of genes that were uniformly up- or down-regulated in fresh compared with cell-line samples, cluster analysis produced four major branch groups. Within these major branches, fresh tumor samples essentially clustered according to pathological type, and further subclusters were seen for both adenocarcinoma (AC) and small cell lung carcinoma (SCLC). Four of eight squamous cell carcinoma (SCC) cell lines clustered with fresh SCC, and 11 of 13 SCLC cell lines grouped with fresh SCLC. In contrast, although none of the 11 AC cell lines clustered with AC tumors, three clustered with SCC tumors and six with SCLC tumors. Although it is possible that preexisting SCC or SCLC cells are being selected from AC tumors after establishment of cell lines, we propose that, even in situ, AC will ultimately progress toward one of two poorly differentiated phenotypes with expression profiles resembling SCC or SCLC.

Adenocarcinoma↗

PubMed2003

Gene expression profile analysis of AIDS-related primary effusion lymphoma (PEL) suggests a plasmablastic derivation and identifies PEL-specific transcripts.

AIDS-related primary effusion lymphoma (PEL) is an HIV-associated malignancy characterized by the ability of the tumor cells to specifically home in the serous body cavities. Here we used gene expression profile analysis (about 12 000 genes) to further define the phenotype of PEL and to investigate the lymphoma relationship to normal B cells and to other tumor subtypes, including non-Hodgkin lymphomas (NHLs) of immunocompetent hosts and AIDS-associated NHL (AIDS-NHL). The results showed that PEL displayed a common gene expression profile that is clearly distinct from all NHLs of immunocompetent hosts and AIDS-NHL subtypes and, in contrast to those, is not related to germinal center (GC) or memory B cells. The gene expression profile of PEL was defined as plasmablastic because it showed features of both immunoblasts identified by Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and AIDS immunoblastic lymphoma, and plasma cells, as defined by multiple myeloma cell lines. Finally, our results identify a set of genes specifically expressed in PEL tumor cells. Their expression was validated at the protein level, suggesting their potential pathogenetic and clinical significance.

Acquired Immunodeficiency Syndrome↗

PubMed2003

Blood genomic expression profile for neuronal injury.

This study determined whether stroke and other types of insults produced a gene expression profile in blood that correlated with the presence of neuronal injury. Adult rats were subjected to ischemic stroke, intracerebral hemorrhage, status epilepticus, and insulin-induced hypoglycemia and compared with untouched, sham surgery, and hypoxia animals that had no brain injury. One day later, microarray analyses showed that 117 genes were upregulated and 80 genes were downregulated in mononuclear blood cells of the "injury" (n = 12) compared with the "no injury" (n = 9) animals. A second experiment examined the whole blood genomic response of adult rats after global ischemia and kainate seizures. Animals with no brain injury were compared with those with brain injury documented by TUNEL and PANT staining. One day later, microarray analyses showed that 37 genes were upregulated and 67 genes were downregulated in whole blood of the injury (n = 4) animals compared with the no-injury (n = 4) animals. Quantitative reverse transcription-polymerase chain reaction confirmed that the vesicular monoamine transporter-2 increased 2.3- and 1.6-fold in animals with severe and mild brain injury, respectively, compared with no-injury animals. Vascular tyrosine phosphatase-1 increased 2.0-fold after severe injury compared with no injury. The data support the hypothesis that there is a peripheral blood genomic response to neuronal injury, and that this blood response is associated with a specific blood mRNA gene expression profile that can be used as a marker of the neuronal damage.

Animals↗

PubMed2006

Gene expression profiles of peripheral blood leukocytes after endotoxin challenge in humans.

To define gene expression profiles that occur during the initial activation of human innate immunity, we administered intravenous endotoxin (n = 8) or saline (n = 4) to healthy subjects and hybridized RNA from blood mononuclear cells (0, 0.5, 6, 24, 168 h) or whole blood (0, 3, 6, 24, 168 h) to oligonucleotide probe arrays. The greatest change in mononuclear cell gene expression occurred at 6 h (439 induced and 428 repressed genes, 1% false discovery rate, and 50% fold change) including increased expression of genes associated with pathogen recognition molecules and signaling cascades linked to receptors associated with cell mobility and activation. Induced defense response genes included cytokines, chemokines, and their respective receptors, acute-phase transcription factors, proteases, arachidonate metabolites, and oxidases. Repressed defense response genes included those associated with co-stimulatory molecules, T and cytotoxic lymphocytes, natural killer (NK) cells, and protein synthesis. Gene expression profiles of whole blood had similar biological themes. Over 100 genes not typically associated with acute inflammation were differentially regulated after endotoxin. By 24 h, gene expression had returned to baseline values. Thus the inflammatory response of circulating leukocytes to endotoxin in humans is characterized by a rapid amplification and subsidence of gene expression. These results indicate that a single intravascular exposure to endotoxin produces a large but temporally short perturbation of the blood transcriptome.

Adult↗

PubMed2005

Gene expression profiling in squamous cell carcinoma of the oral cavity shows abnormalities in several signaling pathways.

OBJECTIVES/HYPOTHESIS: To examine gene expression profiles in squamous cell carcinoma of the oral cavity (oral SCC) compared with histologically matched normal tissue. STUDY DESIGN: Fresh-frozen tissue was prospectively obtained from individuals undergoing surgical resections for oral SCC. METHODS: RNA was extracted from seven sets of oral SCC and matched normal tissue. Gene expression profiles were obtained by interrogation of Affymetrix Gene Chip Arrays with cRNA prepared from the tissue. Expression values were subjected to a paired t test. Genes that were judged to differ between oral SCC and normal tissue were annotated according to their name in the Affymetrix Netaffx database and according to their function as indicated by their Gene Ontology Consortium number. RESULTS: Of the 10,599 probe sets that were analyzed, 523 genes were abnormally expressed in SCC of the head and neck (P < or = .01), and 417 of these genes were abnormally expressed in all seven tumors in the same manner. Hierarchical clustering of the 121 genes that were abnormally expressed in cancerous relative to normal tissue (P < or = .001) showed that the tissue segregated into two groups consisting of normal and transformed tissue, as expected. The abnormal expression of two genes that were up regulated in oral SCC (ADAM 12 and PTHLH) and two genes that were down-regulated in SCCHN (EMP-1 and P11) were confirmed by real-time polymerase chain reaction and immunohistochemistry (ADAM 12) using additional sets of tissue. CONCLUSIONS: The data showed that oral SCC aberrantly express genes in cellular pathways related to proliferation, apoptosis, extracellular matrix degradation, adhesion, transforming growth factor-beta signaling, and transcription. Further work is needed to determine the role of these genes in the development and progression of oral SCC.

ADAM Proteins↗

PubMed2006

MAP-ping genomic organization and organ-specific expression profiles of poplar MAP kinases and MAP kinase kinases.

BACKGROUND: As in other eukaryotes, plant mitogen-activated protein kinase (MAPK) cascades are composed of three classes of hierarchically organized protein kinases, namely MAPKKKs, MAPKKs, and MAPKs. These modules rapidly amplify and transduce extracellular signals into various appropriate intracellular responses. While extensive work has been conducted on the post-translational regulation of specific MAPKKs and MAPKs in various plant species, there has been no systematic investigation of the genomic organization and transcriptional regulation of these genes. RESULTS: Ten putative poplar MAPKK genes (PtMKKs) and 21 putative poplar MAPK genes (PtMPKs) have been identified and located within the poplar (Populus trichocarpa) genome. Analysis of exon-intron junctions and of intron phase inside the predicted coding region of each candidate gene has revealed high levels of conservation within and between phylogenetic groups. Expression profiles of all members of these two gene families were also analyzed in 17 different poplar organs, using gene-specific primers directed at the 3'-untranslated region of each candidate gene and real-time quantitative PCR. Most PtMKKs and PtMPKs were differentially expressed across this developmental series. CONCLUSION: This analysis provides a complete survey of MAPKK and MAPK gene expression profiles in poplar, a large woody perennial plant, and thus complements the extensive expression profiling data available for the herbaceous annual Arabidopsis thaliana. The poplar genome is marked by extensive segmental and chromosomal duplications, and within both kinase families, some recently duplicated paralogous gene pairs often display markedly different patterns of expression, consistent with the rapid evolution of specialized protein functions in this highly adaptive species.

3' Untranslated Regions↗

PubMed2006

Expression profiling of the mouse early embryo: reflections and perspectives.

The laboratory mouse model plays important roles in our understanding of early mammalian development and provides an invaluable model for human early embryos, which are difficult to study for ethical and technical reasons. A comprehensive collection of cDNA clones, their sequences, and complete genome sequence information, which have been accumulated over the past two decades, reveal even further the value of the mouse models. Here, the progress in global gene expression profiling in early mouse embryos and, to some extent, stem cells is reviewed and future directions and challenges are discussed. The discussions include the restatement of global gene expression profiles as a snapshot of cellular status, and subsequent distinction between the differentiation state and physiological state of the cells. The discussions then extend to the biological problems that can be addressed only through global expression profiling, including a bird's-eye view of global gene expression changes, molecular index for developmental potency, cell lineage trajectory, microarray-guided cell manipulation, and the possibility of delineating gene regulatory cascades and networks.

Animals↗

PubMed2006

Exercise affects the gene expression profiles of human white blood cells.

White blood cells (WBCs) express tens of thousands of genes, whose expression levels are modified by genetic and external factors. The purpose of the present study was to investigate the effects of acute exercise on gene expression profiles (GEPs) of WBCs and to identify suitable genes that may serve as surrogate markers for monitoring exercise and training load. Five male participants performed an exhaustive treadmill test (ET) at 80% of their maximal O(2) uptake (Vo(2 max)) and a moderate treadmill test (MT) at 60% Vo(2 max) for exactly the same time approximately 2 wk later. WBCs were isolated by the erythrocyte lysis method. GEPs were measured using the Affymetrix GeneChip technology. After scaling, normalization, and filtering, groupwise comparisons of gene expression intensities were performed, and several measurements were validated by real-time PCR. We found 450 genes upregulated and 150 downregulated (>1.5-fold change; ANOVA with Benjamini-Hochberg correction, P < 0.05) after ET that were closely associated with the gene ontology lists "response to stress" and "inflammatory response". Analysis of mean expression levels after MT showed that the extent of up- and downregulation was workload dependent. The genes for the stress (heat shock) proteins HSPA1A and HSPH1 and for the matrix metalloproteinase MMP-9 showed the most prominent increases, whereas the YES1 oncogene (YES1) and CD160 (BY55) were most strongly reduced. Despite different methodological approaches used, the consistency of our results with the expression data of another study (Connolly PH, Caiozzo VJ, Zaldivar F, Nemet D, Larson J, Hung SP, Heck JD, Hatfield GW, Cooper DM. J Appl Physiol 97: 1461-1469, 2004) suggests that expression fingerprints are useful tools for monitoring exercise and training loads and thereby help to avoid training-associated health risks.

Adult↗

PubMed2001

Cytokeratin expression profiles in thyroid carcinomas.

AIMS: The aim of this study was to establish the cytokeratin expression profile of different types of thyroid carcinoma. MATERIALS AND METHODS: The expression of cytokeratins (CKs) 1, 4, 6, 7, 10/13, 18, 19 and 20 in 153 thyroid carcinomas were examined by immunohistochemistry. RESULTS: All papillary carcinomas (n=86) and follicular carcinomas (n=19) showed expression of CK7 and CK18. The staining was often diffuse. CK19 staining was expressed in all papillary carcinomas and the staining was often diffuse. The staining was noted in 68% of follicular carcinomas and the staining was often focal. No difference in the expression was noted between the minimally invasive and widely invasive follicular carcinomas. Poorly differentiated carcinomas (n=10) showed CK7, CK18, CK19 expression in 60%, 60% and 40%, respectively. Anaplastic carcinomas (n=25) expressed CK7 in 84%, CK18 in 80%, CK19 in 76% and CK10/13 in 16%. Medullary carcinomas (n=13) showed CK7 expression in 100%, CK18 in 85% and CK19 in 77%. None of the medullary carcinomas showed diffuse positivity to CK19. All the thyroid carcinomas were negative for CKs 1, 4, 6 and 20. CONCLUSIONS: Cytokeratin expression profile for each type of thyroid carcinoma was established.

Aged↗

PubMed2004

Gene expression profiling of rat livers reveals indicators of potential adverse effects.

This study tested the hypothesis that gene expression profiling can reveal indicators of subtle injury to the liver induced by a low dose of a substance that does not cause overt toxicity as defined by conventional criteria of toxicology (e.g., abnormal clinical chemistry and histopathology). For the purpose of this study we defined this low dose as subtoxic, i.e., a dose that elicits effects which are below the detection of conventional toxicological parameters. Acetaminophen (APAP) was selected as a model hepatotoxicant because (1) considerable information exists concerning the mechanism of APAP hepatotoxicity that can occur following high doses, (2) intoxication with APAP is the leading cause of emergency room visits involving acute liver failure within the United States, and (3) conventional clinical markers have poor predictive value. Rats treated with a single dose of 0, 50, 150, or 1500 mg/kg APAP were examined at 6, 24, or 48 h after exposure for conventional toxicological parameters and for gene expression alterations. Patterns of gene expression were found which indicated cellular energy loss as a consequence of APAP toxicity. Elements of these patterns were apparent even after exposure to subtoxic doses. With increasing dose, the magnitude of changes increased and additional members of the same biological pathways were differentially expressed. The energy loss suggested by gene expression changes was confirmed at the 1500 mg/kg dose exposure by measuring ATP levels. Only by ultrastructural examination could any indication of toxicity be identified after exposure to a subtoxic dose of APAP and that was occasional mitochondrial damage. In conclusion, this study provides evidence that supports the hypothesis that gene expression profiling may be a sensitive means of identifying indicators of potential adverse effects in the absence of the occurrence of overt toxicity.

Acetaminophen↗

PubMed2004

Cytokine gene expression profiles in kidney medulla and cortex of obese hypertensive dogs.

BACKGROUND: The molecular mechanisms linking abnormal kidney function and obesity hypertension are poorly understood. This study compared gene expression profiles in the kidney medulla and cortex of obese and lean dogs. METHODS: Lean dogs (N= 4) were fed a standard kennel ration and obese dogs (N= 4) were fed the standard diet plus 0.5 to 0.9 kg of cooked beef fat per day for 10 weeks. The dogs were instrumented for continuous monitoring of mean arterial pressure (MAP), heart rate, glomerular filtration rate (GFR), and effective renal plasma flow (RPF). The relative mRNA levels of 375 genes in renal cortex and medulla were determined simultaneously using cDNA membrane arrays (R&D Systems). RESULTS: The high fat diet increased body weight by 57% and MAP increased by 24 mm Hg (112 +/- 1 mm Hg vs. 88 +/- 3 mm Hg) in obese compared to lean dogs. In obese dogs, expression of 11 and 13 genes changed significantly (N= 4; P < 0.05) in the renal medulla and the cortex, respectively, relative to the lean dogs. Differences in renal gene expression profiles between lean and obese dogs were closely related to functional pathways, including those associated with sympathetic activation, inflammatory response, matrix formation, angiogenesis, endothelial dysfunction, attenuated actions of leptin, and attenuated cell survival. CONCLUSION: A high fat diet in dogs is associated with marked changes in renal gene expression profiles that provide potential molecular links to pathways associated with altered renal function and structure in obesity hypertension.

Animals↗

PubMed2006

Examination of gene expression profile of functional human pancreatic islets after 2-week culture.

Islet transplant faces significant challenges, mainly because of the high incidence of primary nonfunction of transplanted islets. Protocol modifications to improve the rate of islet function have included changes in pancreatic preservation and the introduction of short-term culture. Islet culture for 48 to 72 hours has become a standard part of most successful protocols for clinical islet transplantation. We have previously reported gene expression profiles associated with human pancreatic islet function. The aim of this study was to determine the change in gene expression profiles of functional islets after 2 weeks of culture in Memphis-serum free media. Human islets from four isolations were maintained in culture for 14 days in Memphis-serum free media. RNA was extracted from 10000 IEQ for analysis of the gene expression profiles using high-density Affymetrix U133A GeneChips and Genespring software. Islet function was assessed by measurements of human C-peptide at days 7 and 14 posttransplant into NOD-SCID mice. Human C-peptide levels were determined by radioimmunoassay. Our preliminary data showed that genes related to functionality, such as those directed toward insulin processing and secretion, did not vary over 14 days of culture, while genes related to exocrine pancreas and organ architecture and immune-associated genes decreased over time. The ability to maintain islets in culture is an important step toward the development of islet tissue repositories, as well as toward screening human islet preparations for additional pathogens.

Animals↗