Compliance with diphtheria,tetanus, and pertussis immunisation in Bangladesh: factors identifying high risk groups.

OBJECTIVE--To evaluate factors associated with non-compliance with having second vaccination against diphtheria, tetanus, and pertussis in a treatment centre in Dhaka to determine which children were most at risk of not completing immunisation. DESIGN--Cohort study of infants given first dose of the vaccine and followed up six weeks later to ascertain compliance with having second dose. Factors associated with non-compliance were evaluated. SETTING--Dhaka treatment centre of the International Centre for Diarrhoeal Disease Research, Bangladesh. SUBJECTS--136 unimmunised children aged 6 weeks to 23 months who lived within reach of the treatment centre. At time of the six week follow up 16 of the children could not be traced and seven had died. INTERVENTIONS--All children received their first dose of the vaccine. In each case health education workers had informed the mother about the value of immunisation, and she was given clear instructions to bring the child back after four weeks for the second dose. MAIN OUTCOME MEASURE--Rate of non-compliance with advice to return child for second vaccination. RESULTS--46 of 113 children (41%) received the second dose of the vaccine. Factors most closely associated with mothers'' failure to comply with the second dose were lack of education and low income. Children whose mothers knew most about immunisation at first interview were more likely to have their second dose. CONCLUSIONS--Preventive health care services such as immunisation are appropriately offered in treatment centres, but compliance among children varies with socioeconomic status and mother''s education. Further research should be aimed at ways to make health education more effective among uneducated parents.     

Complex regulation of simple sugar transport in insulin-responsive cells.

Facilitated sugar entry into mammalian cells is catalysed by multiple isoforms of the glucose transporter and regulated by hormonal stimuli, nutritional status and oncogenesis. A large reserve of latent glucose transport capacity must be maintained by muscle and adipose cells that are sensitive to insulin, the primary activator of sugar uptake after feeding. Intracellular sequestration of sugar transporters accounts for a large part of this latent capacity, but new findings suggest that there is also reversible suppression of intrinsic catalytic activity of those glucose transporters residing at the cell surface. The mechanism of this suppression appears to be occlusion or disruption of the exofacial sugar-binding sites on the glucose-transporter proteins.     

Trypanosoma brucei brucei: variability in the association of some variant surface glycoproteins

In our isolation procedure, the surface antigens of the variants AnTat 1.1 and 1.10 (Trypanosoma brucei brucei) are essentially obtained as a disulfide-linked dimer while the AnTat 1.8 surface antigen is found as a mixture of monomer and disulfide-linked dimer. This observation may be related to the localization of the cysteine residues in the protein sequences. In the purification procedure using concanavalin-A Sepharose chromatography, besides the VSG elution by methyl-alpha-D-mannopyranoside, a quantitative elution of still bound VSG may be obtained by the addition of beta-mercaptoethanol to methyl-alpha-D-mannopyrannoside in the elution buffer. The surface antigen of the variant AnTat 1.1 was examined for molecular form at several different times during the release procedure. The disulfide-linked dimer could be observed within 30 min of the surface coat release, indicating its presence within the parasite.     

Immunocytochemical localization of glucocorticoid receptors in cells, cytoplasts, and nucleoplasts

A monoclonal antibody has been used to assess the intracellular localization of the glucocorticoid receptor in rodent L-929 fibroblasts and GH3 pituitary tumor cells. Whole cells from both cell lines showed immunoreactivity in the cytoplasm and nucleus. However, when cytoplasts and nucleoplasts of these cells were examined, only L-cells showed strong antibody binding in both fractions; in contrast, GH3 cells exhibited nuclear staining and slight cytoplasmic staining. These results are discussed in terms of the current findings regarding the intracellular location of steroid hormone receptors.     

Esterification by rat liver microsomes of retinol bound to cellular retinol-binding protein

We have investigated the esterification by liver membranes of retinol bound to cellular retinol-binding protein (CRBP). When CRBP carrying [3H]retinol as its ligand was purified from rat liver cytosol and incubated with rat liver microsomes, a significant fraction of the [3H]retinol was converted to [3H]retinyl ester. Esterification of the CRBP-bound [3H]retinol, which was maximal at pH 6-7, did not require the addition of an exogenous fatty acyl group. Indeed, when additional palmitoyl-CoA or coenzyme A was provided, the rate of esterification increased either very slightly or not at all. The esterification reaction had a Km for [3H]retinol-CRBP of 4 +/- 0.6 microM and a maximum velocity of 145 +/- 52 pmol/min/mg of microsomal protein (n = 4). The major products were retinyl palmitate/oleate and retinyl stearate in a ratio of approximately 2 to 1 over a range of [3H]retinol-CRBP concentrations from 1 to 8 microM. The addition of progesterone, a known inhibitor of the acyl-CoA:retinol acyltransferase reaction, consistently increased the rate of retinyl ester formation when [3H]retinol was delivered bound to CRBP. These experiments indicate that retinol presented to liver microsomal membranes by CRBP can be converted to retinyl ester and that this process, in contrast to the esterification of dispersed retinol, is independent of the addition of an activated fatty acid and produces a pattern of retinyl ester species similar to that observed in intact liver. A possible role of phospholipids as endogenous acyl donors in the esterification of retinol bound to CRBP is supported by our observations that depletion of microsomal phospholipid with phospholipase A2 prior to addition of retinol-CRBP decreased the retinol-esterifying activity almost 50%. Conversely, incubating microsomes with a lipid-generating system containing choline, CDP-choline, glycerol 3-phosphate, and an acyl-CoA-generating system prior to addition of retinol-CRBP increased retinol esterification significantly as compared to buffer-treated controls.     

New fossil anthropoids from the middle Miocene of East Africa and their bearing on the origin of the oreopithecidae

Recent paleontological collections at the middle Miocene locality of Maboko Island in Kenya, dated at 15-16 million years, have yielded numerous new specimens belonging to at least five species of fossil anthropoids. The most common species of ape at the site, a medium-sized primate with a very distinctive dental morphology, clearly represents a previously undescribed taxon. When compared with other Miocene anthropoids from East Africa, it has its closest affinities with the poorly known species Rangwapithecus vancouveringi from the early Miocene locality of Rusinga Island. The species from Maboko Island is described here as belonging to a new genus of fossil anthropoid, to which "Rangwapithecus" vancouveringi is also referred. The new genus has a highly distinctive suite of derived characters of its molars and premolars, which it shares with Oreopithecus bambolii from the late Miocene of Europe. These synapomorphies indicate a close phyletic relationship between the East African species and Oreopithecus and form the basis for the inclusion of these taxa in a single family, the Oreopithecidae Schwalbe, 1915. In many respects, however, the East African forms are more conservative than Oreopithecus, and in a general sense they can be regarded as an intermediate grade between Oreopithecus and the more generalized early Miocene catarrhines, the proconsuloids. There is, therefore, good fossil evidence to indicate that the origins of the Oreopithecidae can be traced back to the early Miocene of Africa.     

Structure of turnip crinkle virus. III. Identification of a unique coat protein dimer

The minor structural protein (p80), found in about one copy per virion in turnip crinkle virus (TCV), is shown by amino acid analysis and peptide mapping to be a covalent dimer of the major coat protein (p40). The covalent linkage occurs near the N termini of the crosslinked chains. These data suggest that TGV and related viruses contain 178 copies of p40 (89 non-covalent dimers) and one copy of p80 (covalent dimer of two additional p40 chains). The presence of p80 in the salt-stable RNA-protein complex formed when TCV dissociates, as described in an accompanying paper, indicates that the covalent modification affects binding to RNA. We suggest that p80 might be the final dimer to be incorporated into the shell and that it might also be the site for initiation of uncoating.     

G-11 staining in Turner's syndrome with mos 45,X/46,X,r(?)

Mos 45,X/46,X,r(?) in 4 patients with Turner's syndrome and no signs of virilization, and in one pair of monozygotic twins, one of them with clitoral hypertrophy, was studied using combined cytogenetic techniques and specially G-11 staining for the characterization of the X or Y origin of the rings. In all 6 patients the ring was G-11 positive, attesting its Y origin. Both twins were operated and bilateral streak gonads with a bilateral nodule of testicular tissue were found. Similar small rings were also studied in one patient with mos 46,XX/46,X,r(X) and in one nonvirilized Turner's syndrome patient with a larger ring; in these two cases the ring was G-11 negative. It seems that the small rings occasionally found in Turner's syndrome are more frequently from Y origin and therefore prophylactic gonadectomy should be considered.     

Adipocyte conversion of CHEF cells in serum-free medium

When grown in the presence of serum with added insulin, Chinese hamster embryonic fibroblasts (CHEF/18) cells can be induced to become preadipocytes that are committed to the adipocyte pathway of terminal differentiation (Sager, R., and P. Kovac, 1982, Proc. Natl. Acad. Sci. USA, 79:480-484). We found that commitment to the adipocyte pathway, as well as terminal differentiation to form mature adipocytes, can occur in a defined serum-free medium containing insulin. When CHEF/18 cells are plated in serum-containing medium, only 5-10% of cells in each colony undergo terminal differentiation, whereas in serum-free medium, greater than 90% of the cells became adipocytes. These and other results show that CHEF/18 cells require no adipogenic factors in addition to insulin and the other components of the serum-free medium (transferrin, epithelial growth factor, thrombin) to form adipocytes, and furthermore, that serum inhibits the rate of terminal adipocyte differentiation of these cells. As little as 10 ng/ml insulin added to serum-containing medium can induce adipogenesis, suggesting that insulin rather than an insulinlike growth factor is the active agent. The results further demonstrate that virtually every CHEF/18 cell can be induced into the adipocyte pathway.     

Surface localization of an endogenous lectin in rabbit bone marrow

Summary A lectin, which may be involved in cell to cell adhesion during erythropoiesis in rabbit bone marrow, has been isolated and characterized. Several electron microscopical techniques have been used to investigate the cell surface distribution of this lectin in bone marrow utilizing colloidal gold conjugates of anti-lectin IgG or protein A. The lectin is present at the surface of erythroid cells at all stages of development but no lectin was detected on the surface of myeloid cells. The limitations and complementary nature of the techniques used are discussed.