Subject(s)
Arthritis, Infectious , Arthritis , Bacteremia , Staphylococcal Infections , Sternoclavicular Joint , Humans , Staphylococcal Infections/diagnosis , Staphylococcal Infections/drug therapy , Staphylococcus aureus , Bacteremia/diagnosis , Bacteremia/drug therapy , Anti-Bacterial Agents/therapeutic use , Arthritis, Infectious/diagnosis , Arthritis, Infectious/drug therapy , Sternoclavicular Joint/diagnostic imagingSubject(s)
Antibiotics, Antitubercular/therapeutic use , Ascites/metabolism , CA-125 Antigen/metabolism , Peritoneal Neoplasms/diagnosis , Peritonitis, Tuberculous/diagnosis , Abdominal Pain , Aged , Diagnosis, Differential , Fatal Outcome , Female , Fever , Gastrointestinal Hemorrhage , Humans , Peritoneal Neoplasms/pathology , Peritonitis, Tuberculous/drug therapy , Peritonitis, Tuberculous/pathology , VomitingABSTRACT
In winter 2001, an outbreak of pertussis involving an estimated 75 people occurred among soldiers serving in an infantry regiment of the Israeli Defense Forces (IDF). Nasopharyngeal swabs were obtained from patients and contacts for culture and PCR. Serum samples were obtained and assayed by ELISA for the presence of IgA, IgM and IgG antibodies to a lysate antigen of Bordetella pertussis. The calculated attack rate was 21% based on clinical signs alone (cough lasting 30 days or longer) and 9.5% based on clinical signs with laboratory confirmation (by PCR, IgA or IgM). A high carriage rate was observed; 20% of the asymptomatic and previously symptomatic subjects were PCR-positive for B. pertussis. These findings emphasize the importance of B. pertussis as a causative agent of epidemic respiratory infections in young adults and reveal the occurrence of a significant proportion of pertussis transient carriers during an outbreak of the disease.
Subject(s)
Disease Outbreaks , Military Personnel , Whooping Cough/epidemiology , Adult , Bordetella pertussis/genetics , Bordetella pertussis/immunology , Bordetella pertussis/pathogenicity , Carrier State , Enzyme-Linked Immunosorbent Assay , Female , Humans , Immunoglobulin A/analysis , Immunoglobulin G/analysis , Immunoglobulin M/analysis , Israel/epidemiology , Male , Nasopharynx/microbiology , Pertussis Vaccine , Polymerase Chain Reaction , Whooping Cough/immunologyABSTRACT
Hairpin and tetrahelical structures of a d(CGG)(n) sequence in the FMR1 gene have been implicated in its expansion in fragile X syndrome. The identification of tetraplex d(CGG)(n) destabilizing proteins (Fry, M., and Loeb, L. A.(1999) J. Biol. Chem. 274, 12797-12803; Weisman-Shomer, P., Naot, Y., and Fry, M. (2000) J. Biol. Chem. 275, 2231-2238) suggested that proteins might modulate d(CGG)(n) folding and aggregation. We assayed human TK-6 lymphoblastoid cell extracts for d(CGG)(8) oligomer binding proteins. The principal binding protein was identified as Ku antigen by its partial amino acid sequence and antigenicity. The purified 88/75-kDa heterodimeric Ku bound with similar affinities (K(d) approximately 1. 8-10.2 x 10(-9) mol/liter) to double-stranded d(CGG)(8).d(CCG)(8), hairpin d(CGG)(8), single-stranded d(CII)(8), or tetraplex structures of telomeric or IgG switch region sequences. However, Ku associated more tightly with bimolecular G'2 tetraplex d(CGG)(8) (K(d) approximately 0.35 x 10(-9) mol/liter). Binding to Ku protected G'2 d(CGG)(8) against nuclease digestion and impeded its unwinding by the tetraplex destabilizing protein qTBP42. Stabilization of d(CGG)(n) tetraplex domains in FMR1 by Ku or other proteins might promote d(CGG) expansion and FMR1 silencing.
