Publications by authors named "Meuwissen H"

The number of secondary cases, i.e. the number of new infections generated by an infectious individual, is an important parameter for the control of infectious diseases.

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The number of secondary cases is an important parameter for the control of infectious diseases. When individual variation in disease transmission is present, like for COVID-19, the number of secondary cases is often modelled using a negative binomial distribution. However, this may not be the best distribution to describe the underlying transmission process.

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Autosomal dominant gain of function mutations in the gene encoding PI3K p110δ were recently associated with a novel combined immune deficiency characterized by recurrent sinopulmonary infections, CD4 lymphopenia, reduced class-switched memory B cells, lymphadenopathy, CMV and/or EBV viremia and EBV-related lymphoma. A subset of affected patients also had elevated serum IgM. Here we describe three patients in two families who were diagnosed with HIGM at a young age and were recently found to carry heterozygous mutations in PIK3CD.

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Sera from patients with chronic renal failure (CRF) contain a factor(s) which enhances the oxidative metabolism of polymorphonuclear leukocytes (PMN) as assessed by chemiluminescence (CL), superoxide anion generation, and hexose monophosphate shunt activity. PMN oxidative metabolic activity was higher in CRF sera than in sera from hospitalized patients with normal renal function or in sera from normal healthy subjects. The enhancement occurred regardless of whether PMN were unstimulated or were stimulated by a nonspecific soluble membrane stimulant (phorbol myristate acetate), or by opsonized Candida albicans.

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Patients with Wiskott-Aldrich Syndrome have an increased incidence of serious infections, often with microorganisms that usually produce mild disease in immunologically normal subjects. Three patients with Wiskott-Aldrich syndrome complicated by progressive varicella are reported. There have been no previous reports of similar cases.

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Article Synopsis
  • In 1968, a 2-year-old boy with Wiskott-Aldrich syndrome suffered from severe eczema, repeated infections, and bleeding into various organs.
  • He received high-dose cyclophosphamide for immunosuppression and underwent a bone marrow transplant from his healthy sister.
  • After 15 years post-transplant, he showed improved immune function with no serious infections, despite ongoing low platelet counts.
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In most instances, marked deficiency of the purine catabolic enzyme adenosine deaminase results in lymphopenia and severe combined immunodeficiency disease. Over a 2-yr period, we studied a white male child with markedly deficient erythrocyte and lymphocyte adenosine deaminase activity and normal immune function. We have documented that (a) adenosine deaminase activity and immunoreactive protein are undetectable in erythrocytes, 0.

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Fibronectin is an important non-immune opsonic protein influencing phagocytic clearance of blood-borne nonbacterial particulates which may arise in association with septic shock, tissue injury, and intravascular coagulation. In the present study, serum fibronectin was measured by both electroimmunoassay as well as rapid immunoturbidimetric assay in healthy children (n = 114) ranging in age from 1 month to 15 years in order to delineate the temporal alterations in fibronectin with age. Normal adult serum fibronectin concentrations are typically 220 micrograms/ml +/- 20 micrograms/ml.

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Serum or plasma from 3 patients with C2 deficiency (C2D) and systemic lupus erythematosus (SLE) significantly enhanced chemiluminescence and superoxide anion production by polymorphonuclear leukocytes (PMN) after stimulation with phorbol myristate acetate or latex beads. PMN from patients and normal individuals were supranormally activated when resuspended in plasma from these patients. No such effect was seen with plasma from a patient with C2D but with no evidence of SLE, from patients with SLE but not C2D, from patients with C1q or C8 deficiency, from C4-deficient guinea pigs, or NZB-NZW mice.

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The capacity of phagocytes from animals or humans with complement component deficiency to ingest and kill Candida albicans has been much disputed. We show that peripheral blood polymorphonuclear leukocytes and mononuclear phagocytes from subjects with hereditary C2 deficiency (C2D) ingested C. albicans or Saccharomyces cerevisiae at an abnormally slow rate.

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The IgA system in a patient with SCID and ADA deficiency showed heterogeneity. Serum IgA and stool secretory IgA (SIgA) levels were normal, but with altered kappa/lambda and A1/A2 subclass ratios; IgA in saliva and urine was deficient. Amounts of secretory component were normal.

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A number of infants with an autosomal recessive form of combined immunodeficiency disease also lack adenosine deaminase (adenosine aminohydrolase; EC 3.5.4.

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Histobompatible sibling bone marrow was transplanted to a patient withsevere aplastic anemia. The first transplant failed, but a second transplantfrom the same donor was successfully performed with a new and more potentimmunosuppressive regimen. Successful retransplantation after marrow graftrejection is now possible.

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Fifty-five children with CID and known ADA status were studies at a workshop held in Albany, New York. Erythrocyte ADA determinations were performed in 22 of the 55 patients, 13 of whom were ADA negative. The ADA defect appears to be transmitted as an autosomal recessive trait.

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The recently discovered association of adenosine deaminase (ADA) deficiency and combined immune deficiency (CID) has emphasized the critical role of purine salvage in the function of lymphoid tissue. Known enzymatic properties of ADA are presented. In addition, known phenotypic data and possible genetic mechanisms for the occurrence of ADA deficiency in CID are discussed.

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