Change in body water distribution index in infants who become stunted between 4 and 18 months of age

OBJECTIVE: To evaluate body composition changes using bioelectrical impedance analysis and skinfold thickness measurements in infants from tropical areas who become stunted between 4-18 months of age. DESIGN AND MEASUREMENTS: Follow-up study. Extracellular water to total body water ratio index (length(2)/resistance at low to high frequency), peripheral fat (tricipital and subscapular skinfold thickness), and length-for-age index were studied at 4 and 18 months of age. SETTINGS: Low-income areas in four tropical regions (Congo, Senegal, Bolivia and New Caledonia). SUBJECTS: Infants were included in the analysis provided they were neither stunted nor wasted at 4 months. Two groups of infants were compared, those that were stunted at 18 months (n=61) or not (n=170). RESULTS: The extracellular water to total body water ratio index and the sum of skinfold thickness measurements were similar in the two groups at 4 months, and only the extracellular water to total body water ratio index was significantly different at 18 months. When no stunting appeared between 4 and 18 months, the change in the extracellular water to total body water ratio index was not linked with variations in length-for-age, and presented the expected pattern of variation in body water compartments. When stunting occurred, variation in length-for-age was related to significant changes in the extracellular water to total body water ratio index, the biggest increase in the proportion of extracellular water being found in the most stunted infants. Variations in the sum of the two skinfold thickness measurements presented the expected pattern for the 4-18 months growth and did not differ between the two groups. CONCLUSIONS: Multifrequency resistances suggested that stunting was associated with a lack of the expansion of the intracellular compartment that is expected during normal growth of cell mass, together with preserved fat mass. SPONSORSHIPS: Supported by grant 92L0623 from the French Ministry of Research, and by Institut de Recherche pour le Développement (IRD).     

GVHD-associated enteropathy and endotoxemia in F1-hybrid recipients of NK1.1-depleted grafts

Our previous work using a C57BL/6-->(C57BL/6 x DBA/2)F1-hybrid model of acute GVHD showed that mortality can be completely prevented if grafts are depleted of NK1.1+ cells in vitro. To achieve this protection, it was necessary to inject the donors with polyinosinic:polycytidylic acid 18 h before the graft was harvested. In another study, we showed that interferon (IFN)-gamma production and lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF)-alpha release are markedly reduced in these recipients, suggesting that this treatment abrogates the Th1-mediated immune response that underlies the development of this disease. However, because it has also been hypothesized that cytotoxic NK1.1+ cells mediate injury to tissues targeted by the GVH reaction, we wished to determine whether NK1.1 depletion of the graft would also prevent the development of GVHD-associated enteropathy and endotoxemia. We therefore induced GVH reactions in (C57BL/6 x DBA/2)F1 hybrids using either untreated grafts from unstimulated C57BL/6 donors, or NK1.1-depleted grafts from poly I:C-stimulated donors. We identified intestinal lesions morphologically in sections of ileum collected from each group of recipients but not in control mice. We also compared endotoxin levels in the sera. Our results indicate that GVHD-associated enteropathy occurs in both groups of recipients, and that the levels of LPS in the sera do not differ significantly.     

Distinct domains of alphaIIbbeta3 support different aspects of outside-in signal transduction and platelet activation induced by LSARLAF, an alphaIIbbeta3 interacting peptide

The peptide LSARLAF causes alphaIIbeta3-dependent platelet activation exemplified by secretion, aggregation, spreading and adhesion on fibrinogen, and tyrosine phosphorylation. alphaIIIbeta3-dependent outside-in signal transduction induced by LSARLAF was investigated in variant thrombasthenic platelets which lack most of the cytoplasmic domain of the integrin beta3 subunit (alphaIIbbeta3 delta724). These studies revealed that only certain aspects of this alphaIIbbeta3-dependent outside-in signaling were affected by the beta3 truncation. Specifically, alphaIIbbeta3 delta724 supported LSARLAF-induced platelet aggregation, agglutination and secretion, but failed to trigger cytoskeletal reorganization and platelet spreading on fibrinogen, despite the fact that PMA-induced non alphaIIbbeta3 mediated signaling caused spreading of these platelets on fibrinogen. Thus, distinct domains of alphaIIbbeta3 are required to support different aspects of LSARLAF-induced platelet activation. Furthermore, these studies suggest that not all alphaIIbbeta3-dependent platelet responses require an intact beta3 cytoplasmic tail.     

The Puerto Rico–New York Airbridge for Drug Users: Description and Relationship to HIV Risk Behaviors

This study examined mobility on the airbridge between New York (NY) and Puerto Rico (PR) for Puerto Rican drug users and its relationship to HIV risk. Over 1,200 Puerto Rican injection drug users (IDUs) and crack smokers were recruited by outreach workers in NY and PR; interview data included questions on mobility (lifetime residences and recent trips). Two-thirds of the NY sample had lived in PR; one-quarter of the PR sample had lived in NY; the most commonly sited reasons for moving were family-related. Fewer than 10% had visited the other location in the prior 3 years. Variables related to risk were number of moves, recent travel, and having used drugs in PR (all with p < 0.05). Implications included the need to enhance risk reduction efforts for IDUs in PR and address sexual risk among mobile drug users.     

Influence of maternal schistosomiasis on the immunity of adult offspring mice

Schistosoma mansoni infection modulates the immunity to unrelated antigens in the host. In this study, we have investigated the effect of pregnancy and nursing from schistosomotic mother mice on the immune response to ovalbumin (OA), in adult offspring. Then, newborn mice were divided into four groups: animals born from infected mothers (BIM) suckled by non-infected mothers; animals from non-infected mothers suckled by infected mothers (SIM); and two other groups that were mice born and suckled in infected mothers (BSIM) or non-infected (control) mothers. The adult offspring were immunized with OA plus adjuvant. We compared the OA-specific hypersensitivity reactions (HR), antibodies levels (IgG, IgG2a) and the cytokine production in splenocyte cultures. Remarkable interleukin (IL)-10 synthesis was observed in mice BIM; while the anti-OA antibodies levels and immediate HR were impaired. IL-10 neutralization recovered this suppression. Differently, in mice SIM and BSIM there was an enhancement in the anti-OA humoral response and high IL-2 production, however low level of the IL-10 was detected in mice BSIM. In conclusion, schistosomotic pregnancy provides an immunosuppressive potential, IL-10 dependent, which was sustained throughout adult life. Regardless, suckling by infected mothers induces great responsiveness to an unrelated antigen and repairs the inhibitory potential acquired during prenatal stage.