Changing patterns of iron deficiency anaemia in the second year of life.
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Anemia, Iron-Deficiency↗
Biomedical subjects
S Logan
Publications and source records attributed to S Logan.
Need to avoid bias in controlled trials.
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Bias↗
Congenital cytomegalovirus infection and maternal antibody status.
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Cytomegalovirus Infections↗
Outcome measures in child health.
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Asthma↗
Production and characterization of monoclonal antibodies to N-acetyl-aspartyl-glutamate.
N-acetyl-aspartyl-glutamate (NAAG) is a putative neuromodulator/neurotransmitter in the mammalian nervous system. Immunohistochemical studies with polyclonal NAAG antisera have revealed immunoreactive neurons and processes in several brain regions. However, these antisera crossreact to some degree with N-acetyl-aspartate (NAA), which is present in mM concentrations in brain, prompting the development of monoclonal antibodies (MAb) more specific for NAAG. By fusing spleen lymphocytes obtained from BALB/c mice pre-immunized with NAAG covalently linked to bovine serum albumin by carbodiimide with SP2/0-Ag 14 mouse myeloma cells, we produced three IgG2a (kappa) MAb which specifically reacted with NAAG. These MAb exhibited negligible crossreactivity with NAA or with structurally similar peptides, as shown by solid-phase radioimmunoassay. Antibody activity was absorbed out selectively by both NAAG-thyroglobulin conjugate and free NAAG. These MAb stained many nuclei of the medulla-pons and midbrain, mitral cells in the olfactory bulb, pyramidal neurons in sensorimotor cortex, locus ceruleus, and several cholinergic cranial nuclei. The staining pattern strongly correlated with NAAG levels determined by HPLC. Monoclonal antibodies significantly enhanced sensitivity of staining, allowing visualization of dorsal horn neurons in spinal cord, which were not readily detectable with polyclonal antiserum. Availability of these MAb now facilitates further clarification of the role of NAAG in the brain.
Animals↗
The Replogle tube.
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Bulbar Palsy, Progressive↗
60% of women born in England to immigrant parents are seropositive to CMV.
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Adult↗
Cytomegalovirus screened blood for neonatal intensive care units.
Two infants were considered to have acquired cytomegalovirus (CMV) infection from blood transfusions screened for the presence of CMV antibody by a haemagglutination assay. Further samples from the same donors were tested by a latex agglutination test; six of 18 (33%) previously believed seronegative were found to be seropositive.
Agglutination Tests↗
Six independent neoplasms in one woman. A case report.
A woman had six independent neoplasms. In reviewing the world literature, no case report was found of a patient with carcinomas of the skin, cecum, kidney, ovaries (bilateral, independent and synchronous) and endometrium.
Adenocarcinoma↗
Young children as a probable source of maternal and congenital cytomegalovirus infection.
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Child Day Care Centers↗
The immunocytochemical demonstration of Toxoplasma antigen in the brains of congenitally infected mice.
The peroxidase anti-peroxidase immunocytochemical staining method was used to identify Toxoplasma antigen in paraffin embedded sections of the brains of 22 mice congenitally infected with the parasite. Intact Toxoplasma tissue cysts were readily demonstrated in the brain in all cases. In 4 of the 22 infected mice there was evidence of rupture of the cyst wall and/or presence of extra-cystic Toxoplasma antigen. Further support for the extra-cystic location of Toxoplasma antigen was obtained by electron microscopy of reprocessed tissue which revealed endozoites in the area immediately surrounding a ruptured cyst. The possible implications of these findings in relation to the pathogenesis of congenital toxoplasmic meningo-encephalitis are discussed.
Animals↗
Intraventricular xenografts: chronic injection of antibodies into the CSF provokes granulomatosis reactions but Ia antibodies do not enhance graft survival.
We have studied the influence of chronic infusions of antibodies against Ia antigen into the CSF on immunological reactions to intraventricular xenografts in rats. The antibodies were infused with osmotic pumps implanted one day before grafting. One set of control groups consisted of animals with xenografts which simultaneously received antibody against penicillin or vehicle with no antibody. In a second set of control groups, antibodies against Ia antigen, penicillin, rat anti-mouse IgG or vehicle (no antibody) were administered alone, without grafts. In the animals that received infusions of antibodies against either Ia antigen or penicillin plus xenografts, intense granulomatosis reactions were observed in the host brains. These reactions were not observed in the animals that received antibody infusions without xenografts. It appears that this reaction was produced by the massive and persistent injection of immunoglobulins, together with the presence of xenograft tissue. The chronic infusion of Ia antibodies did not prolong xenograft survival.
Animals↗