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  • JAMA January 10, 2017

    Figure 2: Parathyroid Hormone, Calcium, and Phosphate Concentrations in Patients Receiving Cinacalcet or Etelcalcetide by Study Week

    Data markers indicate the mean and error bars, 95% confidence intervals.
  • Tedizolid Phosphate vs Linezolid for Treatment of Acute Bacterial Skin and Skin Structure Infections: The ESTABLISH-1 Randomized Trial

    Abstract Full Text
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    JAMA. 2013; 309(6):559-569. doi: 10.1001/jama.2013.241
    Prokocimer and coauthors report the results from the ESTABLISH-1 randomized trial of tedizolid phosphate vs linezolid for the treatment of acute bacterial skin and skin structure infections. In an accompanying Editorial, Doron and Boucher discuss new study design and a step toward shorter course therapy of antibiotics for skin infections.
  • JAMA June 15, 2011

    Figure 1: Multivariable-Adjusted Hazard Function for Death According to Measured (Untransformed) Levels of Fibroblast Growth Factor 23

    The median fibroblast growth factor 23 (FGF-23) level within the lowest FGF-23 quartile (74 RU/mL) served as the referent value (hazard = 1.0). The model was stratified by center and adjusted for age; sex; race; ethnicity; estimated glomerular filtration rate; natural log-transformed urine albumin-to-creatinine ratio; hemoglobin; serum albumin; systolic blood pressure; body mass index; diabetes; smoking status; low-density lipoprotein; history of coronary artery disease, congestive heart failure, stroke, and peripheral vascular disease; use of aspirin, β-blockers, statins, and angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers; and serum calcium, phosphate, and natural log-transformed parathyroid hormone. Tick marks on the x-axis indicate individual observations at corresponding levels of FGF-23. The solid black line represents the multivariable-adjusted hazard of mortality as a function of the measured (nontransformed) FGF-23 level. The dashed lines indicate the 95% confidence intervals.
  • JAMA November 24, 2010

    Figure: Mechanism of Fructose-Induced Production of Uric Acid

    Fructose induces uric acid production by increasing adenosine triphosphate (ATP) degradation to adenosine monophosphate (AMP), a uric acid precursor. The phosphorylation of fructose to fructose-1-phosphate by fructokinase leads to the degradation of ATP to adenosine diphosphate (ADP). As fructose-1-phosphate entraps inorganic phosphate (Pi), intracellular Pi levels decrease. As a net result, intracellular ATP levels decrease and AMP levels increase, which also leads to increased inosine monophosphate (IMP) levels. Elevated AMP and IMP levels activate catabolic pathways, which leads to increased uric acid production.
  • JAMA March 17, 2010

    Figure 3: Dose-Response Relationship Between Blood PLP Level and Relative Risk of Colorectal Cancer

    Adjusted relative risks and 95% confidence intervals (CIs; dashed lines) are reported. Blood pyridoxal 5′-phosphate (PLP) levels were modeled with a linear trend in a random-effects meta-regression model. The median value of the lowest reference range (12.7 pmol/mL) was used to estimate all relative risks. The vertical axis is on a log scale.
  • JAMA March 17, 2010

    Figure 2: Adjusted Relative Risks of Colorectal Cancer for the Highest vs Lowest Categories of Vitamin B6 Intake or Blood PLP Level

    CI indicates confidence interval; PLP, pyridoxal 5′-phosphate. The size of each square is proportional to the study's weight (inverse of variance). aThe range is the difference in the midpoint between the highest and lowest categories of exposure. bExclusion of the study by de Vogel et al, which appeared to explain the study heterogeneity, yielded a pooled relative risk of 0.80 (95% CI, 0.69-0.92) with no heterogeneity among studies (P = .23; I2 = 24%; 95% CI, 0%-64%).
  • JAMA August 12, 2009

    Figure 1: COX-2 Immunohistochemistry in Colorectal Cancer

    Primary anti−cyclooxygenase 2 (COX-2) antibody diluted 1:300 in phosphate-buffered saline was applied overnight at 4°C. We then applied secondary anti-mouse antibody for 20 minutes followed by avidin-biotin complex conjugate. Sections were visualized by diaminobenzidine and methyl-green counterstain. A, Representative section from a COX-2–negative tumor (original magnification ×400). The gray arrowheads indicate colorectal cancer cells without COX-2 overexpression. B, Representative section from a COX-2–positive tumor (original magnification ×400). Black arrowheads indicate colorectal cancer cells with strong COX-2 expression (dark brown color) compared with normal colonic epithelium indicated by white arrowheads.
  • JAMA January 7, 2009

    Figure 1: Components and Structure of DNA

    The building block of DNA is the nucleotide—a sugar (deoxyribose) with a phosphate group at the 5′ carbon and a base (adenine, thymine, guanine, or cytosine) at the 1′ carbon. Nucleotides link together by a bond between the phosphate group of one nucleotide and the 3′ carbon of the previous nucleotide, to form a single DNA strand with a resulting directionality of 5′ to 3′. Two strands with opposite directionality combine to form a double helix that is held together by hydrogen bonds across the bases. Adenine always binds to thymine and guanine always binds to cytosine. The sequence of base pairs encodes the genetic information.
  • Efficacy and Safety of Pyridoxal 5′-Phosphate (MC-1) in High-Risk Patients Undergoing Coronary Artery Bypass Graft Surgery: The MEND-CABG II Randomized Clinical Trial

    Abstract Full Text
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    JAMA. 2008; 299(15):1777-1787. doi: 10.1001/jama.299.15.joc80027
  • JAMA November 7, 2007

    Figure: Study Probes Best Choice of Drug to Reduce Phosphate in Patients on Dialysis

    Maintaining appropriate levels of phosphate is important for patients on hemodialysis, but the best way to do so remains open to debate.
  • Study Probes Best Choice of Drug to Reduce Phosphate in Patients on Dialysis

    Abstract Full Text
    JAMA. 2007; 298(17):1995-1996. doi: 10.1001/jama.298.17.1995
  • JAMA July 4, 2007

    Figure: Epidermal Growth Factor Receptor Activation, Processing, and Signaling

    ATP indicates adenosine triphosphate; Cbl, a ubiquitin E3 ligase; IGF, insulinlike growth factor; JAK, Janus kinase; MAPK, mitogen-activated protein kinase; P, phosphate; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol-3-kinase; PKC, protein kinase C; PLC-γ, phospholipase Cγ; STAT, signal transducers and activators of transcription; TK, tyrosine kinase; and Ub, ubiquitin.
  • JAMA September 14, 2005

    Figure 1: Phosphate Homeostasis

  • JAMA September 14, 2005

    Figure 3: Mechanisms of FGF-23 Excess in Renal Phosphate-Wasting Syndromes

    In tumor-induced osteomalacia, fibroblast growth factor 23 (FGF-23) and other phosphatonins ectopically produced by a mesenchymal tumor lead to excess circulating FGF-23 levels. In autosomal dominant hypophosphatemic rickets, FGF-23 excess results from mutations in the FGF-23 gene that render the protein resistant to cleavage and inactivation. In X-linked hypophosphatemia, the mechanism of FGF-23 excess is more speculative; mutations in the PHEX endopeptidase (presumably located on osteoblasts or osteocytes), are thought to either directly or indirectly result in FGF-23 excess by interfering with processing and inactivation of FGF-23.
  • Tumor-Induced Osteomalacia

    Abstract Full Text
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    JAMA. 2005; 294(10):1260-1267. doi: 10.1001/jama.294.10.1260
  • JAMA November 8, 2000

    Figure: Age-Specific Protection Against Haemophilus influenzae Type b (Hib) Disease After 3 Doses of Hib Vaccine in Infancy: Estimations From Surveillance Data and Predictions From Immunogenicity Data

    Effectiveness data, based on clinical vaccine failure rates, are shown on the left y-axis (closed data markers). The closed triangles indicate the potential effect of underascertainment. The percentage of patients with anti-PRP (polyribosylribitol phosphate) antibody levels greater than 0.15 µg/mL and greater than 1.0 µg/mL are shown on the right y-axis (open data markers). Clinical protection (based on surveillance data) appears to persist despite antibody levels considered not to be protective. Error bars indicate 95% confidence intervals.
  • JAMA November 3, 1999

    Figure 1: Phosphorus P 31 Nuclear Magnetic Resonance Spectra From the Liver of a Representative Healthy Control

    Hepatic 31P spectra were monitored for a 10-minute period before subjects were given an intravenous bolus injection of fructose. The average amplitude of the β–adenosine triphosphate (ATP) peak obtained for the 10-minute period before fructose injection was considered to be representative of baseline hepatic ATP stores (left). The gray line indicates the height of the baseline β-ATP response. Hepatic 31P spectra were monitored continuously for 60 minutes following fructose administration. The smallest amplitude β-ATP peak that was measured after fructose injection was taken as representative of minimum hepatic ATP content (middle). Minimum ATP levels typically occurred within 15 minutes after fructose injection. The amplitude of the β-ATP spectra obtained during the final 10 minutes of the 60-minute monitoring period was used as a measure of hepatic ATP recovery (right). Inspection of the β-ATP peaks in these 3 phosphorus spectra from a representative control subject illustrate that a decrease in amplitude occurred after fructose administration and that the β-ATP peak had returned toward its baseline level by the end of the study period. PME indicates phosphomonoesters (primarily phosphorylated carbohydrates); PDE, phosphodiesters (primarily glycerophosphorocholine and ethanolamine); and Pi, inorganic phosphate.
  • JAMA November 3, 1999

    Figure 2: Hepatic ATP Response to an ATP-Depleting Interference in Control and Patient Groups

    Phosphorus P 31 nuclear magnetic resonance spectroscopy was performed as described in the "Methods" section of the text. For each subject, hepatic phosphorus spectra were normalized to the phosphorus spectra obtained from a phosphate standard attached to the receiver that was positioned on the skin of the back, beneath the center of the liver. The phosphorus spectra were recorded from an area of the liver that was equidistant from the standard in all subjects. Baseline adenosine triphosphate (ATP) content was derived from β-ATP spectra obtained during the 10-minute period before fructose administration. The minimum ATP content was calculated from the lowest amplitude β-ATP spectra in each patient. The ATP content after recovery was determined by evaluating the amplitude of β-ATP spectra during the final 10-minute interval of the 60-minute observation period that followed fructose injection. Hepatic ATP content recovered back to baseline values in controls. The difference between the minimum ATP content and the recovery ATP content was significantly different in controls (P<.02). In contrast, after recovery, liver ATP content in patients was not significantly different than their minimum ATP content. Hence, after recovery, the liver ATP content of the patients was significantly lower than that of the controls at the same point (P<.04).