Sudden unexpected infant deaths in Dundee, 1882-1891: overlying or SIDS?

Using a cohort study of all deaths in infants under 12 months in Dundee born between 1882-91 we set out to compare the aetiology of sudden unexpected infant deaths in Dundee at the end of the 19th Century with the aetiology of present day Sudden Infant Death Syndrome (SIDS). During 1882-1891, 361 infants died suddenly and unexpectedly and without obvious cause while in bed with their parents. The sex ratio of deaths was even (0.51 male) whereas the typical male fraction of SIDS today is 0.61. The mean age at death was almost two and one-half weeks younger in the Dundee cohort than for SIDS in modern Scotland. The infants in the Dundee cohort were discovered more frequently early in the morning than is typical. Their social class distribution was different in that no overlying cases were found in the higher classes whereas SIDS affects all classes. The overlying rate for illegitimate infants was lower than that reported for SIDS today. The epidemiological characteristics of the Dundee cohort and of those dying from present day SIDS differ considerably. The Dundee cohort apparently died from overlying rather than from SIDS as it is classified today. Present day advice that co-sleeping is safe should be given more cautiously until the safety of co-sleeping is resolved. It might be prudent to inform parents that co-sleeping is a risk factor for SIDS and that it should therefore be avoided.

Fc alpha receptor cross-linking causes translocation of phosphatidylinositol-dependent protein kinase 1 and protein kinase B alpha to MHC class II peptide-loading-like compartments.

A20 IIA1.6 B cells cotransfected with FcalphaR and wild-type gamma-chain (wt-ITAM (immunoreceptor tyrosine-based activation motif)) or FcalphaR and gamma-chain, in which the wt-ITAM was substituted with the FcgammaRIIA ITAM (IIA-ITAM), were used to investigate cell signaling events influencing presentation of FcalphaR-targeted exogenous Ag in the context of MHC class II. wt-ITAM cells presented FcalphaR-targeted OVA more efficiently than IIA-ITAM transfectants to OVA-specific T cell hybridomas. Phosphatidylinositol 3-kinase (PI 3-kinase) inhibition abrogated Ag presentation, suggesting that FcalphaR may trigger a PI 3-kinase-dependent signal transduction pathway, and thus phosphatidylinositol-dependent protein kinase (PDK1) and protein kinase B alpha (PKBalpha) activation. Cross-linking FcalphaR on wt-ITAM or IIA-ITAM cells triggered equivalent PI 3-kinase-dependent activation of PKBalpha. Furthermore, FcalphaR cross-linking triggered recruitment of PDK1 and serine-phosphorylated PKBalpha to capped cell surface FcalphaR irrespective of the gamma-chain ITAM. Although FcalphaR endocytosis was accompanied by translocation of PDK1 and phospho-PKBalpha to FcalphaR-containing vesicles in both transfectants, this was decreased in IIA-ITAM cells, and a significant proportion of PDK1 and PKBalpha remained at the plasma membrane. In wt-ITAM cells, PDK1 and serine-phosphorylated PKBalpha translocated to lysosomal-associated membrane glycoprotein 1- and cathepsin B-containing vesicles, consistent with MHC class II peptide-loading compartments (MIIC) described by other groups. Our data indicate that translocation of signal transduction mediators to MIIC-like compartments accompanies efficient presentation of receptor-targeted Ag, and suggest a mechanism connecting signaling to the Ag-processing pathway.

Autoantibodies in endometriosis sera recognize a Thomsen-Friedenreich-like carbohydrate antigen.

Autoantibody responses to endometrial antigens are a common feature of endometriosis. Antibody responses to a number of serum and tissue antigens such as alpha(2)-Heremans Schmidt glycoprotein (alpha(2)-HSG), transferrin, and carbonic anhydrase have been identified. The nature of the epitopes recognized on these proteins has not been determined. In this study we show that the serum antibody response to alpha(2)-HSG and carbonic anhydrase is against a common carbohydrate epitope which is also expressed on bovine fetuin. Removal of carbohydrate moieties from these antigens resulted in loss of antibody binding. Antibody reactivity with alpha(2)-HSG, fetuin and other antigens was removed by binding with the lectin jacalin. Jacalin specifically binds the Thomsen-Friedenreich antigen (Galbeta1-3GalNAc). Demonstrating that the autoantibodies also reacted with other Thomsen-Friedenreich antigen-bearing proteins, serum IgA1 and haemopexin confirmed an association with this epitope. These antigens have not been previously described as autoantigens in endometriosis and are of interest since they raise the possibility that this autoimmune response may either play a direct role in the disease process or reflect an abnormality of glycosylation in endometriosis. These results may also prove useful in the development of a serum diagnostic test for endometriosis.

Extragenic suppressors of the nimX2(cdc2) mutation of Aspergillus nidulans affect nuclear division, septation and conidiation.

The Aspergillus nidulans NIMX(CDC2) protein kinase has been shown to be required for both the G(2)/M and G(1)/S transitions, and recent evidence has implicated a role for NIMX(CDC2) in septation and conidiation. While much is understood of its G(2)/M function, little is known about the functions of NIMX(CDC2) during G(1)/S, septation, and conidiophore development. In an attempt to better understand how NIMX(CDC2) is involved in these processes, we have isolated four extragenic suppressors of the A. nidulans nimX2(cdc2) temperature-sensitive mutation. Mutation of these suppressor genes, designated snxA-snxD for suppressor of nimX, affects nuclear division, septation, and conidiation. The cold-sensitive snxA1 mutation leads to arrest of nuclear division during G(1) or early S. snxB1 causes hyperseptation in the hyphae and sensitivity to hydroxyurea, while snxC1 causes septation in the conidiophore stalk and aberrant conidiophore structure. snxD1 leads to slight septation defects and hydroxyurea sensitivity. The additional phenotypes that result from the suppressor mutations provide genetic evidence that NIMX(CDC2) affects septation and conidiation in addition to nuclear division, and cloning and biochemical analysis of these will allow a better understanding of the role of NIMX(CDC2) in these processes.

Rapid antibody-based field test to distinguish between Helicoverpa armigera (Lepidoptera: Noctuidae) and Helicoverpa punctigera (Lepidoptera: Noctuidae).

Helicoverpa armigera (Hübner) and Helicoverpa punctigera (Wallengren) are the two most important insect pests of cotton production in Australia and require application of insecticides to control them. H. armigera has developed resistance to several insecticides but H. punctigera has not. Cost-effective management of insecticide resistance requires that growers be able to determine the proportion of H. armigera eggs or young larvae present on their crop before applying insecticides. This is impossible visually. We generated two monoclonal antibodies that reacted with the insect protein "lipophorin" and were capable of discriminating individuals of the two species at all life-stages. The antibodies were incorporated into a rapid test kit that was tested under field conditions over two growing seasons. Results obtained with the kit agreed closely with those obtained by rearing larvae through to second instar.