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  • JAMA August 22, 2017

    Figure 2: Cumulative Incidence of Any Cytomegalovirus (CMV) Reactivationa and High-Grade CMV Reactivation in Plasmab Through Day 28

    Baseline positive DNA detections were excluded from this analysis. The median duration of follow-up for CMV reactivation at any level was 28 days (range, 1 to 28) for the ganciclovir group and 28 days (range, 1 to 28) for the placebo group. The median duration of follow-up for high-grade CMV reactivation was 28 days (range, 1 to 28) for the ganciclovir group and 28 days (range, 1 to 28) for the placebo group.aCMV DNA was quantified in specimens using a previously published polymerase chain reaction assay method. The frequency of assessment was every 3 days until day 35 for plasma; day 1 and then every fourth day while intubated for endotracheal tube aspirate samples; days 1 and 7 only for the first 10 patients for bronchoalveolar lavage; and every 3 days until day 35 for throat.bExcluding baseline positive DNA detection.
  • JAMA June 28, 2016

    Figure: Proposed Algorithm for Determining Etiology of Persistent Diarrhea in Adults in the United States

    aGiardia, Entamoeba, and Cryptosporidium by enzyme immunoassay; others: Cyclospora, Microsporidia species, Strongyloides, Dientamoeba fragilis, Schistosoma species (only in endemic areas). IBD indicates inflammatory bowel disease; IBS, irritable bowel syndrome; PCR, polymerase chain reaction.
  • JAMA August 25, 2015

    Figure 1: Flowchart Outlining the Selection of Samples and Sequencing Approaches in the Study

    aAML-RMG is a capture reagent consisting of all of the exons of the genes that are currently known to be recurrently mutated in acute myeloid leukemia, based on The Cancer Genome Atlas AML study.bThe only samples with sufficient day 30 DNA for sequencing and assessment of disease clearance (refractory group, 6 patients; R6-12 group, 8 patients; LFR group, 11 patients).cEnhanced exome sequencing is exome capture-based sequencing supplemented with the AML-RMG panel of target genes, to improve coverage of critical regions of the exome. dTargeted Ampliseq is a polymerase chain reaction–based digital sequencing approach that allows for accurate determination of the frequency of specific mutations in acute myeloid leukemia samples.
  • JAMA April 21, 2015

    Figure 1: Longitudinal Evaluation of Gene Marking in Blood Cells After Gene Therapy

    A, Gene marking in peripheral blood cells over time after gene therapy in patients 1 to 7, as expressed by vector copy number per peripheral blood mononuclear cell (PBMC) and measured by quantitative polymerase chain reaction. B, Gene marking in various blood cell subsets in each patient, expressed as vector copy number per cell in CD3+ T cells, CD56+ natural killer cells, CD19+ B cells, CD15+ neutrophils, and CD14+ monocytes.
  • JAMA March 24, 2015

    Figure 1: Transient Fever and Low-Level Viremia Postvaccination With VSVΔG-ZEBOV

    The VSVΔG-ZEBOV vaccine was made up of a replicating, attenuated, recombinant vesicular stomatitis virus (serotype Indiana) whose surface glycoprotein gene was replaced by the Zaire Ebola virus glycoprotein gene. Prevaccination blood samples were not available. The needlestick occurred 43 hours before vaccination. A, The dashed horizontal line indicates 38°C. B, The number of polymerase chain reaction cycles required to amplify and detect the target RNA is known as the threshold cycle; thus, a lower threshold cycle value indicates that a higher concentration of target template is present. The dashed horizontal line indicates the limit of detection. Further details of real-time reverse transcription–polymerase chain reaction appear in the eMethods section in the Supplement.
  • Diagnosis and Treatment of Clostridium difficile in Adults: A Systematic Review

    Abstract Full Text
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    JAMA. 2015; 313(4):398-408. doi: 10.1001/jama.2014.17103

    This systematic review summarizes the diagnostic approaches for Clostridium difficile infection and evaluates which therapeutic approaches should be used.

  • JAMA January 27, 2015

    Figure 2: Sample Multistep Algorithm for Rapid Diagnosis of Clostridium difficile Infection

    Abbreviations: EIA, enzyme immunoassay; GDH, glutamate dehydrogenase; PCR, polymerase chain reaction.aToxin-positive (+) indicates presence of either Toxin A or Toxin B when a combined test is performed, as in this example. Toxin-negative (−) indicates that neither Toxin A nor B is present. Adapted under Creative Commons License.
  • JAMA June 19, 2013

    Figure 3: Images From Magnetic Resonance Imaging of 3 Patients Exposed to Spinal and Paraspinal Injections With Contaminated Methylprednisolone

    A, Axial T1 postcontrast image shows avid enhancement of nerve roots (yellow arrowheads) as well as clumped intradural enhancement (blue arrowhead) consistent with arachnoiditis. Tissue obtained during operation showed fungal hyphae, and polymerase chain reaction was positive for Exserohilum species. B, Sagittal T1 fat-saturated, postcontrast images of the lumbar spine shows a rim-enhancing fluid collection in the dorsal epidural space (pink arrowhead) in a patient who was asymptomatic. Tissue obtained at surgery showed fungal hyphae. C, Linear end-plate enhancement (black arrowheads) consistent with diskitis or osteomyelitis in another patient in whom tissue obtained at surgery showed fungal hyphae; cultures yielded Exserohilum species.
  • JAMA March 14, 2012

    Figure 2: Telomere Analysis in Neuroblastoma

    A, Difference in telomeric reads for each of the 40 tumors in the discovery cohort based on the whole genome sequencing data. The reference value for each tumor was the telomere length from matched normal DNA from the same patient. The actual value for SJNBL008 was −57; SJNBL016, −39; and SJNBL023, 27. B, Box plot of normalized telomeric reads for the germline DNA and the diagnostic tumor from whole genome sequencing data for the 40 tumors and matched germline samples in the discovery cohort. The number of telomeric reads was normalized to the average genomic coverage for that particular sample. The upper and lower edges of the box represent the 75th and 25th percentile, respectively. The median is indicated as a horizontal line within the box and the error bars represent the lowest and highest values still within 1.5 of the interquartile range. C, Quantitative polymerase chain reaction for telomeres in the 10 samples in the discovery cohort with ATRX mutations as well as 4 controls with wild-type ATRX. Data are plotted as difference between tumor and germline for each patient. The actual value for SJNBL003 was 10 939; SJNBL032, 8171; and SJNBL039, 106 121.
  • JAMA March 14, 2012

    Figure 1:  ATRX Mutations in Neuroblastoma

    A, Diagram of the ATRX protein and changes that result from the 5 single nucleotide variations and 5 in-frame deletions found in the ATRX gene. B, Ethidium bromide–stained agarose gel with the PCR products for each of the 5 deletions shown in panel A. C, Sanger sequence traces of the PCR amplicons from panel B with junction break points (arrows). D, Sanger sequence traces of the PCR amplicon spanning the frameshift mutation K425_E426fs. NLS indicates nuclear localization signal.
  • Noninvasive Fetal Sex Determination Using Cell-Free Fetal DNA: A Systematic Review and Meta-analysis

    Abstract Full Text
    JAMA. 2011; 306(6):627-636. doi: 10.1001/jama.2011.1114
  • JAMA April 20, 2011

    Figure 1: TP53 Germline Deletion in Patient With t-AML

    A, Changes in sequence read depth indicate a heterozygous and homozygous deletion of TP53 in the skin and bone marrow samples, respectively. B, The deletion (indicated by dotted lines) includes exons 7-9 of TP53 (based on transcript ID ENST00000269305). Genomic coordinates of the deletion boundaries are shown. C, Genomic DNA isolated from the patient's skin or bone marrow or maternal blood was amplified by polymerase chain reaction (PCR) using the 2 primer sets depicted in B. The first primer set (1) produces a 2924–base pair (bp) product from the wild-type but not mutant TP53 allele. The second primer set (2) is predicted to amplify 4169-bp and 1179-bp products from the wild-type and mutant TP53 alleles, respectively. However, because of its smaller size, only the mutant band was consistently seen. Ref indicates DNA ladder reference; t-AML, therapy-related acute myeloid leukemia.
  • JAMA April 20, 2011

    Figure 2:TP53 Messenger RNA Expression in Patient With t-AML and Controls

    A, TP53 messenger RNA (mRNA) expression profiling used Affymetrix Exon 1.0 arrays (Affymetrix, Santa Clara, California). The probe signal value for each exon is plotted from the patient with therapy-related acute myeloid leukemia (t-AML) along with the signal for 6 AML samples without TP53 mutations. There are 2 probe sets for exon 7. B, Reverse-transcription polymerase chain reaction (RT-PCR) of the patient's bone marrow RNA was performed using primers in exons 6 and 11 of TP53. The wild-type (normal control) and mutant TP53 transcripts produced the predicted bands of 614 base pairs (bp) and 204 bp, respectively. C, Sequencing of the mutant band demonstrated the in-frame splicing of exon 6 to exon 10 (beginning with “ATC”). cDNA indicates complementary DNA.
  • JAMA April 20, 2011

    Figure 7: Reciprocal Translocation Between Chromosomes 3 and 4 Involving DGKG and BST1

    A t(3;4) reciprocal translocation resulted in the fusion of DGKG (chromosome 3) and BST1 (chromosome 4). There is also a duplication of exons 10-14 of DGKG. Shown is a schematic of the translocation break point and the primers used to confirm expression of the fusion transcripts by reverse-transcription polymerase chain reaction (RT-PCR). The DGKG-BST1 fusion results in the splicing of exon 14 of DGKG with exon 6 of BST1 (starting with “TAT”). The BST1-DGKG fusion results in the splicing of exon 5 of BST1 with exon 10 of DGKG (starting with “GGC”). Exons and introns are not drawn to scale. Sequencing of the PCR products showed that both fusion genes were expressed in frame. cDNA indicates complementary DNA.
  • JAMA April 20, 2011

    Figure 5: PCR and Reverse Transcription (RT) PCR Validation of PML-RARA Expression From Case Patient

    A, Polymerase chain reaction (PCR) of genomic DNA from the case patient's skin (normal) and leukemia (tumor) using primers that span the junction of RARA-LOXL1 (P1/P2), PML-RARA (P3/P4), del(12), del(14), LOXL1-PML (P5/P6), and del(19). Note amplification across fusion breakpoints in the leukemia sample but not in the skin sample for all but del(19). DNA ladder: 2176, 1766, 1230, 1033, 653, 517, 453, 394, 298, 234, and 154 base-pairs (bp). B, RNA prepared from cryopreserved leukemia cells from case patient was amplified with a forward primer in PML exon 3 and a reverse primer in RARA exon 3. DNA ladder: 1500, 800, 500, 300, 200, 150, 100, and 50 bp.
  • JAMA March 2, 2011

    Figure 6: Expression of High-Mobility Group A1 (HMGA1) and Insulin Receptor (INSR) Messenger RNA (mRNA) and Protein in Monocytes

    There were 120 controls, 120 patients with nonvariant wild-type type 2 diabetes mellitus (DM), and 81 patients with 3 other variant type 2 DM. RT-PCR indicates reverse-transcriptase polymerase chain reaction.
  • JAMA March 2, 2011

    Figure 3: Expression of High-Mobility Group A1 (HMGA1) and Insulin Receptor (INSR)

    The HMGA1 and INSR messenger RNA and protein were obtained from blood monocytes of healthy wild-type controls (n = 120), patients with nonvariant wild-type type 2 diabetes mellitus (DM) (n = 120), and patients with IVS5-13insC variant type 2 DM (n = 120). Right panels, the bars indicate the mean and 95% confidence intervals. P < .001 for comparison between patients with carrier type 2 DM and both nondiabetic controls and patients with nonvariant wild-type type 2 DM. RT-PCR indicates reverse-transcriptase polymerase chain reaction.
  • JAMA January 5, 2011

    Figure 7: Quantification of Expression Levels of MicroRNAs let-7a and miR-345 by Real-Time Polymerase Chain Reaction in Frozen Tissues

    miR-345 and let-7a are down-regulated in goiter tissue from individual III-3 from family E compared with normal thyroid and follicular thyroid cancer (FTC) tissues from noncarriers of DICER1 mutations. Error bars indicate 95% confidence intervals; U6 snRNA indicates the noncoding small nuclear RNA part of U6 small nuclear ribosomal ribonucleoprotein.
  • JAMA January 5, 2011

    Figure 3:DICER1 Messenger RNA Levels in Mutation Carriers and Noncarriers Relative to GAPDH

    DICER1 expression was measured in lymphoblastoid cell lines derived from carriers and noncarriers from families A through E and from 2 unrelated noncarriers by real-time polymerase chain reaction. There are no significant differences in the level of DICER1 expression when comparing mutation carriers and noncarriers (P = .55) and when comparing carriers of truncating mutations (families A and C) and carriers of nontruncating mutations (families B, D, and E) (P = .49). The identity of each individual carrier is indicated on the x-axis; Con1 through Con5 are noncarrier controls. Error bars indicate 95% confidence intervals.
  • JAMA January 5, 2011

    Figure 3: Transactivation of miR-15a/miR-16-1 and miR-34b/miR-34c Clusters by TP53

    A, Promoter luciferase assay in tumor protein p53 (TP53)-null H1299 cells reported as means (error bars indicate 95% confidence intervals) of experiments performed in sextuplicate. The indicated TP53 binding site (BS) numbers correspond to those shown in red in eFigures 9 and 12. Control indicates the results obtained using the promoter vector with no binding site cloned in it. BAX indicates BCL2-associated X protein; Chr, chromosome. P values were calculated for TP53 vs empty for each group; all values were statistically significant (P < .05). B, Quantified real-time polymerase chain reaction (error bars indicate 95% confidence intervals) for microRNA 15b (miR-15b), microRNA 16 (miR-16), and microRNA 34b (miR-34b) performed on MEG-01 cells 24 hours after transfection with empty or TP53-expressing vectors. P values were calculated for TP53 vs empty for each group; all values were statistically significant (P < .05).