Incidence rate of nontuberculous mycobacterial disease in immunocompetent children: a prospective nationwide surveillance study in Germany.

An increasing incidence in disease caused by nontuberculous mycobacteria is being reported. We investigated the burden of disease in immunocompetent German children in a prospective nationwide study from April 2003 to September 2005. Ninety-seven percent of children presented with lymphadenitis; median age was 2.

Molecular epidemiology of penicillin-non-susceptible Streptococcus pneumoniae isolates from children with invasive pneumococcal disease in Germany.

A population-based nationwide surveillance of antibiotic resistance associated with invasive pneumococcal disease (IPD) in children and adolescents (aged<16 years) was performed in Germany between 1997 and 2004. In total, 1517 isolates were collected, of which 5.1% and 1.

Induction of 2'-5' oligoadenylate synthetase during interferon treatment of chronic myelogenous leukemia.

Activity of the interferon-induced enzyme 2'-5' oligoadenylate synthetase (2-5 OAS) was measured in peripheral blood mononuclear cells (PBMCs) and serum of patients with chronic phase Ph'-positive chronic myelogenous leukemia (CML) treated with interferon-alpha (IFN-alpha) (4 x 10(6) IU/m2) alone or in combination with 50 micrograms IFN-gamma. At the beginning of IFN therapy, marked elevation of 2-5 OAS titers was detected in PBMCs (pretreatment 0.03-1.

Heparin trisaccharides with nonreducing 2-amino-2-deoxy-alpha-D-glucopyranosyl end-groups suitable as substrates for catabolic enzymes.

Heparin trisaccharides having the sequence O-(2-amino-2-deoxy-alpha-D-glucopyranosyl)-(1----4)-O-alpha-L- idopyranosyluronic acid-(1----4)-2,5-anhydro-D-[1-3H]mannitol have been prepared, as substrate models for studying sulfatases of heparan sulfate catabolism, by alpha-L-iduronidase cleavage of previously reported heparin tetrasaccharides, with additional chemical and enzymic modification as required. Three series are described, including isomeric sulfate esters of that trisaccharide with no N-substituent, with N-acetyl substitution, and with N-sulfate substitution. New features of the substrate specificity of the hydrolases used, including iduronate sulfatase, alpha-L-iduronidase, glucosamine 6-sulfate sulfatase, and heparin sulfamidase, were observed, and simple procedures for partial purification of these hydrolases are reported.

Flurbiprofen in the treatment of corneal neovascularization induced by contact lenses.

Cellulose acetate butyrate extended-wear contact lenses were fitted bilaterally on ten New Zealand albino rabbits. We administered flurbiprofen 0.03% solution topically to the experimental eyes and vehicle solution to the contralateral control eyes four times a day in a random, masked fashion beginning 24 hours before the contact lens was fitted.

4-Methylumbelliferyl 2-acetamido-2-deoxy-alpha-D-glucopyranoside, a fluorogenic substrate for N-acetyl-alpha-D-glucosaminidase.

Condensation of dimeric 3,4,6-tri-O-acetyl-2-deoxy-2-nitroso-alpha-D-glucopyranosyl chloride with 4-methylumbelliferone gave crystalline 4-methylumbelliferyl 3,4,6-tri-O-acetyl-2-deoxy-2-oximino-alpha-D-arabino-hexopyranoside. Acetylation of this adduct, reduction of the resulting crude O-acetyloxime with borane in oxolane, and acetylation gave the 3,4,6-tri-O-acetyl derivative of 4-methylumbelliferyl 2-acetamido-2-deoxy-alpha-D-glucopyranoside (1). A new sensitive assay of N-acetyl-alpha-D-glucosaminidase (EC 3.

Direct demonstration of binding of a lysosomal enzyme, alpha-L-iduronidase, to receptors on cultured fibroblasts.

Receptor-binding of "high-uptake" forms of lysosomal enzymes to human diploid skin fibroblasts had been predicted from the Michaelis--Menten kinetics of uptake of these enzymes [e.g., Sando, G.

The defect in the Hurler and Scheie syndromes: deficiency of -L-iduronidase.

Skin fibroblasts cultured from patients affected with the Hurler or Scheie syndromes (mucopoly-saccharidoses I or V, respectively) have a functional deficiency of a protein required for catabolism of sulfated mucopolysaccharide that has been designated the "Hurler corrective factor." We now show Hurler factor purified from normal human urine to be associated with alpha-L-iduronidase activity. Cell lines deficient in Hurler corrective factor have no detectable activity of alpha-L-iduronidase (less than 3% of that found in cells from individuals of other genotypes).