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  • To Prevent Rheumatoid Arthritis, Look Past the Joints to the Gums

    Abstract Full Text
    JAMA. 2017; 317(12):1201-1202. doi: 10.1001/jama.2017.0764

    This Medical News article discusses the discovery of a microbe that may trigger rheumatoid arthritis.

  • Researchers Trigger Prion Formation in Mouse Models of Disease

    Abstract Full Text
    JAMA. 2013; 310(13):1331-1331. doi: 10.1001/jama.2013.279213
  • FDA: Acetaminophen May Trigger Serious Skin Problems

    Abstract Full Text
    JAMA. 2013; 310(8):785-785. doi: 10.1001/jama.2013.276938
  • Asthma Forecast: Why Heat, Humidity Trigger Symptoms

    Abstract Full Text
    JAMA. 2012; 308(1):20-20. doi: 10.1001/jama.2012.7533
  • Deciphering Harm Measurement

    Abstract Full Text
    JAMA. 2012; 307(20):2155-2156. doi: 10.1001/jama.2012.3649
  • JAMA October 21, 2009

    Figure: Strep and OCD, Tourette

    Group A streptococcal infections such as strep throat do not appear to trigger Tourette syndrome or obsessive-compulsive disorder, according to findings of a new study.
  • JAMA April 15, 2009

    Figure: Diabetes Viral Trigger?

    Scientists have discovered that infection with an enterovirus, such as cocksackie B virus, might trigger type 1 diabetes.
  • Diabetes Viral Trigger?

    Abstract Full Text
    JAMA. 2009; 301(15):1529-1529. doi: 10.1001/jama.2009.504
  • Alzheimer Disease Trigger

    Abstract Full Text
    JAMA. 2008; 299(5):513-513. doi: 10.1001/jama.299.5.513-a
  • JAMA March 22, 2006

    Figure: Sleeping Poorly While Pregnant May Not Be “Normal”

    Disturbed sleep during and after pregnancy is common but can trigger or worsen depression and anxiety, disrupt relationships, and hamper a mother’s bonding with her newborn.
  • JAMA August 24, 2005

    Figure: Spinal Reflex and Pain Perception Pathways

    A, Reflex responses to noxious stimuli occur early in development, before thalamocortical circuits are functional; noxious stimuli trigger reflex movement without cortical involvement. Activated by a noxious stimulus (1), a peripheral sensory neuron (2) synapses on a dorsal horn interneuron (3) that in turn synapses on a ventral horn motor neuron (4), leading to reflex muscle contraction and limb withdrawal (5). B, Later in development, noxious stimuli (1) activate peripheral sensory neurons (2) that synapse on spinothalamic tract neurons (3), the axons of which extend up the spinal cord as the spinothalamic tract (4) to synapse on neurons of the thalamus (5). From here, thalamocortical axons synapse on cortical neurons, resulting in the conscious perception of pain.
  • Early Obesity Trigger?

    Abstract Full Text
    JAMA. 2005; 294(3):297-297. doi: 10.1001/jama.294.3.297-c
  • JAMA March 9, 2005

    Figure: Molecular Switch Triggers Fats’ Harm

    Scientists are gaining insights into how foods rich in saturated and trans-fats trigger a rise in blood cholesterol and triglycerides.
  • Molecular Switch Triggers Fats’ Harm

    Abstract Full Text
    JAMA. 2005; 293(10):1180-1180. doi: 10.1001/jama.293.10.1180
  • JAMA November 10, 2004

    Figure 1: Peripheral Blood Smear and Replication of Ehrlichia chaffeensis and Cellular Response

    A, Peripheral blood smear obtained on hospital day 1 showing a monocyte with 2 vacuoles (morulae) that contain E chaffeensis clusters (arrowheads) (Wright stain; original magnification ×240). B, E chaffeensis infects mononuclear phagocytes in blood and in tissues. In the absence of an immune response, the bacterium is internalized via endocytosis. After entry, dense core cells differentiate into reticulate cells that are suspected to be the metabolically active and replicative stage. By poorly understood mechanisms, E chaffeensis directs early endosomes containing the bacteria into a receptor-salvage pathway that precludes lysosomal fusion. Likewise, infection alters signal transduction pathways and is associated with significant changes in host cell gene transcription. These events lead to global down-regulation of innate immune response pathways and receptor expression, intracellular vesicular trafficking, and activation of antiapoptotic survival mechanisms. The net effect is a more hospitable environment for intracellular replication. Replicated bacteria are released by cell lysis or exocytosis to infect other mononuclear phagocytes nearby or at disseminated sites. C, With emerging immune response, the bacteria are opsonized by anti–E chaffeensis antibodies, bound to Fc receptors, and phagocytosed. Ligation of antibody-bound E chaffeensis to Fc receptors triggers G-protein–coupled intracellular signaling that results in destruction of the bacterium, degradation and presentation of antigens for maturing adaptive immune response, and activation of innate immune pathways. This process leads to the production of proinflammatory cytokines and chemokines. Such responses are ultimately beneficial to the host by activation of crucial CD4- and CD8-mediated immunity dominated by IFN-γ. However, induction of proinflammatory mediators, including TNF-α, has the potential to cause transient local tissue and organ injury or systemic manifestations.
  • Study Finds Carbon Monoxide Can Trigger Brain-Damaging Attack by Immune System

    Abstract Full Text
    JAMA. 2004; 292(13):1542-1542. doi: 10.1001/jama.292.13.1542
  • JAMA May 19, 2004

    Figure 1: Immunomodulatory Actions of IVIG in Autoimmune Neuromuscular Diseases

    Intravenous immunoglobulin (IVIG) modulates multiple immunologic events (blue boxes) involved in the pathogenesis of autoimmune neuromuscular diseases. Diseases for which specific therapeutic actions of IVIG are supported by experimental evidence are listed in each box. In autoimmune neuromuscular diseases, an antigen, through molecular mimicry, defective clonal deletion, or other mechanisms, triggers an immune response that results in loss of immune tolerance to self-antigens. Infused IVIG interferes with costimulatory molecules involved in antigen presentation and modulates subsequent immunologic events. These events, mediated by activation of B cells with production of autoantibodies and by T cells, lead to tissue damage via complement activation, macrophage–Fc receptor interaction, and cytotoxic T cells. Other possible therapeutic actions of IVIG not shown in this illustration include increased catabolism of IgG, alteration of effector functions of T cells, and modulation of apoptosis. CIDP indicates chronic inflammatory demyelinating polyneuropathy; DM, dermatomyositis; GBS, Guillain-Barré syndrome; ICAM-1, intercellular adhesion molecule 1; IFN-γ, interferon γ; IL, interleukin; LEMS, Lambert-Eaton myasthenic syndrome; MAC, membrane attack complex; MG, myasthenia gravis; MMP, matrix metalloproteinase; NO, nitric oxide; PM, polymyositis; SPS, stiff-person syndrome; TGF-β, transforming growth factor β; TNF-α, tumor necrosis factor α; VCAM-1, vascular cell adhesion molecule 1.
  • JAMA February 4, 2004

    Figure: Cancer Vaccine Research Inches Forward

    One cancer vaccine under study makes use of recombinant vaccinia virus containing genes for both tumor-associated antigen and costimulatory molecules (which increase immunogenicity). Cells infected with the attenuated vaccinia virus present tumor antigen on their surface. Antigen presentation (in the context of MHC 1) to resting T-lymphocytes and costimulation trigger a T-lymphocyte-mediated immune response, as opposed to a traditional antibody-mediated response.
  • JAMA November 12, 2003

    Figure: Scientists Find Connections in the Brain Between Physical and Emotional Pain

    Imaging studies have revealed that the emotional pain of social rejection activates two brain regions that are also important in the response to physical pain. Pain activates the anterior cingulate cortex, which signals higher brain regions that impel an individual to act to stop the pain; social rejection similarly triggers activity in this region. Activation of the right ventral prefrontal cortex appears to help dampen the distress of both physical pain and social exclusion.
  • All Night Diners

    Abstract Full Text
    JAMA. 2003; 290(11):1442-1442. doi: 10.1001/jama.290.11.1442