Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma

The prevalence and cost of chronic pain is a major physical and mental health care problem in the United States today. As a result, there has been a recent explosion of research on chronic pain, with significant advances in better understanding its etiology, assessment, and treatment. The purpose of the present article is to provide a review of the most noteworthy developments in the field. The biopsychosocial model is now widely accepted as the most heuristic approach to chronic pain. With this model in mind, a review of the basic neuroscience processes of pain (the bio part of biopsychosocial), as well as the psychosocial factors, is presented. This spans research on how psychological and social factors can interact with brain processes to influence health and illness as well as on the development of new technologies, such as brain imaging, that provide new insights into brain-pain mechanisms.

/pdf/the-biopsychosocial-approach-to-chronic-pain-scientific-1047fjbjjh.pdf

The Biopsychosocial Approach to Chronic Pain: Scientific Advances and Future Directions

National Asthma Education and Prevention Program.

SWISS-MODEL pioneered the field of automated modeling as the first protein modeling service on the Internet. In combination with the visualization tool Swiss-PdbViewer, the Internet-based Workspace and the SWISS-MODEL Repository, it provides a fully integrated sequence to structure analysis and modeling platform. This computational environment is made freely available to the scientific community with the aim to hide the computational complexity of structural bioinformatics and encourage bench scientists to make use of the ever-increasing structural information available. Indeed, over the last decade, the availability of structural information has significantly increased for many organisms as a direct consequence of the complementary nature of comparative protein modeling and experimental structure determination. This has a very positive and enabling impact on many different applications in biomedical research as described in this paper.

Automated comparative protein structure modeling with SWISS-MODEL and Swiss-PdbViewer: a historical perspective.

Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).

Mechanisms of action of the antioxidant lycopene in cancer.

Characterization ofNineNovelMutations intheCD40Ligand GeneinPatients withX-Linked HyperIgMSyndrome ofVarious Ancestry

Objective:To evaluate the efficacy of oral d-penicillamine therapy in children with high blood lead concentrations.Design:A prospective, uncontrolled study.Methods and Patients:Seven children (2–16 y old; mean 8.7) with elevated blood lead concentrations but no symptoms of lead poisoning were treated with oral d-penicillamine. Lead-contaminated homemade flour as found to be the source of poisoning. Mean ± SD blood lead concentrations prior to therapy were 60.3 ± 12.9 μg/dL (range 47.8–83). Mean blood zinc protoporphyrin (ZPP) was 337.86 ± 58.55 μmol/mol hemoglobin (Hb) (range 247–394).Results:Ninety days of treatment with d-penicillamine lowered the mean blood lead concentration by 31.7% to a mean of 40.7 ± 8.6 μg/dL (range 30–53) and lowered mean ZPP blood concentrations by 40% to a mean of 201.14 ± 14 μmol/mol Hb (range 150–278). Three patients with blood lead concentrations >45 μg/mL at the end of this therapy were subsequently treated with succimer, an alternative oral chelator; the blood lead concent...

Efficacy of d-Penicillamine in Reducing Lead Concentrations in Children: A Prospective, Uncontrolled Study

Chronic granulomatous disease is a primary immunodeficiency disease caused by a genetic mutation in any of the 5 genes encoding the different components of the Nicotinamide Adenine Dinucleotide Phosphate reduced (NADPH)-Oxidase enzyme complex. Since primary immunodeficiency diseases are considered to be rare diseases, the genetic diagnosis of a certain primary immunodeficiency leads to the reasonable assumption that all patients with the same disease within the same family will have the same genetic mutation. We report 2 patients with chronic granulomatous disease from the same extended consanguineous family who had different genetic causes of their disease. Therefore, it is crucial to obtain a definitive genetic diagnosis of primary immunodeficiency disease even in patients from the same family, where the same genetic diagnosis is presumed to be the cause of the disease.Statement of novelty: Genetic causes of chronic granulomatous disease may be different in patients from the same family.

https://lymphosign.com/doi/pdf/10.14785/lymphosign-2018-0004

Chronic granulomatous disease due to different mutations in patients from the same consanguineous extended family

HLA-identical bone marrow or peripheral blood stem cell (PBSC) transplantation is the treatment of choice for severe combined immunodeficiency (SCID) (1). However, HLA-matched sibling donors for patients with SCID may be unavailable; therefore HLA-haploidentical donors are chosen (2, 3). In general, immune functions are restored following haploidentical stem cell engraftment within 4–7 mo for T cells (2, 4), whereas for B cell functions, complete recovery is achieved much later, and only in a few patients (5, 6). Here we report on a patient with SCID who received peripheral stem cells from his haploidentically mismatched father, which led to a transient induction of his own cellular immune system despite lack of any evidence of engraftment.

Transient recovery of endogenous immune function following haploidentical peripheral stem cell transplantation in a patient with severe combined immunodeficiency without evidence of engraftment.

Jacov Levy

Papers

Mechanisms of action of the antioxidant lycopene in cancer.

Characterization ofNineNovelMutations intheCD40Ligand GeneinPatients withX-Linked HyperIgMSyndrome ofVarious Ancestry

Efficacy of d-Penicillamine in Reducing Lead Concentrations in Children: A Prospective, Uncontrolled Study

Chronic granulomatous disease due to different mutations in patients from the same consanguineous extended family

Transient recovery of endogenous immune function following haploidentical peripheral stem cell transplantation in a patient with severe combined immunodeficiency without evidence of engraftment.