PubMed · 6942291
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M C Croxson. 1981-05-13. Which rubella screening test?. https://pubmed.ncbi.nlm.nih.gov/6942291/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
A solid-phase immunosorbent hemagglutination inhibition test (SPISHAI) was developed for hepatitis A virus-specific immunoglobulin M (IgM) antibody. Three hundred thirty and six sera were comparatively detected with both SPISHAI and ELISA. Among them 97 sera were positive and 237 were negative with both method. The crude agreement rate was 99.4%. With SPISHAI the titers of anti-HAV IgM ranged from 1:20 to 1:327,680 among tested sera from infected individuals by HAV. The specificity of SPISHAI was confirmed by 2-ME treatment method and blocking test. The patients with non-A hepatitis all got negative results. The SPISHAI does not require conjugated antibody and sophisticated equipment, and is not interfered with rheumatoid factor in sera. Furthermore, the result of the test can be got within 3 hours. Therefore, the SPISHAI is a cheap and simple, and could be applied for early diagnosis and epidemiological surveillance of hepatitis A in the community and in primary health care.
The aim of this work was to accelerate passive hemagglutination inhibition test, simplify it, perform it without an incubator and antibody diagnostic agent, and confirm the results of this test the characteristics permitting not only specific, but quantitative assessment of the results of passive hemagglutination test. To achieve this, the authors suggest the following modifications: the working dose of purified tetanus antitoxin is titered in relation to the standard serum; antibody erythrocytic diagnostic agent is modified by adding the working dose of purified tetanus antitoxin; the test is performed at room temperature.
Immunosuppressive acidic protein (IAP), an immunosuppressive substance produced mainly by macrophages, has previously been shown to increase in the serum of patients with inflammatory neurological diseases. In this study we assayed the IAP levels in cerebrospinal fluid (CSF) by a passive hemagglutination-inhibition test. CSF-IAP levels increased significantly in patients with multiple sclerosis (MS) during both the active and inactive stages and in patients with Guillain-Barré syndrome (GBS) or Miller Fisher syndrome (MFS) as compared with those of control patients, but not in patients with amyotrophic lateral sclerosis or spinocerebellar degeneration. During the active stage of MS, increased CSF-IAP levels together with the elevated IAP% (CSF-IAP/total CSF protein) and IAP index [(CSF-IAP/serum IAP)/(CSF albumin/serum albumin)] suggested the intrathecal synthesis of IAP. In contrast, in patients with GBS or MFS, increased CSF-IAP levels without elevation of IAP% could be attributed largely to increased total CSF protein levels. In patients with neuro-Behçet's disease, CSF-IAP levels and IAP% were elevated during the active stage, but remained normal levels during the inactive stage. Assaying CSF-IAP could provide useful information about inflammatory or immunopathological events within the central nervous system.