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At least 109 records · Page 6Linked to original sources
PubMed2004

Recommendations for accelerating global action to prevent folic acid-preventable birth defects and other folate-deficiency diseases: meeting of experts on preventing folic acid-preventable neural tube defects.

BACKGROUND: In April of 2003, The Micronutrient Initiative, in collaboration with several other organizations, convened a group of knowledgeable scientists and policy experts to discuss ways to accelerate the global pace at which countries implement effective and sustainable programs to prevent folic acid-preventable birth defects and other folate-deficiency diseases. Programs implemented to date by fewer than 40 countries have prevented only 10% of the estimated 240,000 annual cases of folic acid-preventable spina bifida and anencephaly. METHODS: Participants in this meeting summarized and presented scientific evidence showing that increased consumption of synthetic folic acid prevents a large proportion of spina bifida and anencephaly cases. They also reviewed related guidance and endorsement issued by national professional societies and advisory bodies as well as policies and programs implemented by some countries that have already demonstrated successful results in terms of reduced rates of neural tube defects and improved folate nutrition. CONCLUSIONS: The group formulated and discussed recommendations and strategies for increasing the pace of neural tube defect prevention globally. The recommendations and strategies are published here.

Dietary Supplements↗
PubMed1988

Evidence that specific cellular immunity cannot account for death of Mus caroli embryos transferred to Mus musculus with severe combined immune deficiency disease.

Mus caroli blastocysts transferred to pseudopregnant Mus musculus implant but die about midgestation. Death of the M caroli embryos is associated with infiltration of the fetoplacental units by M musculus lymphocytes, including functional cytotoxic T lymphocytes (CTL). To determine if specific maternal antifetal immune responses are responsible for the initiation of M caroli failure, survival of M caroli embryos transferred to M musculus with severe combined immune deficiency disease (SCID) was studied. C.B.-17 scid mice, homozygous for the scid gene, are reported to be unresponsive to T cell or B cell mitogens and to alloantigens. We have evaluated responses of C.B.-17 scid mice to M caroli xenoantigens in vivo and in vitro. C.B.-17 scid fail to reject M caroli skin grafts, and their spleen cells do not proliferate when mixed with M caroli splenocytes in a 1-way mixed leukocyte culture. Further, neither primary nor secondary challenge of C.B.-17 scid footpads with M caroli splenocytes elicits a delayed-type hypersensitivity (DTH) response. These results suggest that C.B.-17 scid mice are unable to recognize or respond specifically to M caroli xenoantigens. M caroli embryos transferred to C.B.-17 scid mice implant but fail to survive while cotransferred M musculus embryos are normal. Histologic examination of resorbing embryos revealed granulocytes, macrophages, large granular lymphocytes, but very few small lymphocytes at the implantation sites. Thus, it appears that specific maternal antifetal immune responses are not responsible for initiation of M caroli embryo failure in the M musculus uterus. These studies also indicate that efficient resorption of embryos does not require the function of T cells or B cells.

Animals↗
PubMed1984

Changes in heart size and volume in certain endocrinal and nutritional deficiency diseases. A correlative study in twenty adult patients.

Twenty adult patients selected at random were studied because of a reduction in heart size, seen on routine chest radiographs. I analyzed etiologic factors, clinical, biochemical, and pathological abnormalities and cardiovascular status in relation to the radiographic findings and response to treatment. Reduction in heart size can occur as part of a wide spectrum of changes in certain endocrinal and nutritional deficiency diseases. Clinically there may be weakness as well as changes in heart rate, blood pressure, electrolytes, electrocardiograms, and loss of weight. All of these parameters improve with appropriate treatment.

Addison Disease↗
PubMed1998

Primary defect in CD8+ lymphocytes in the antibody deficiency disease (common variable immunodeficiency): abnormalities in intracellular production of interferon-gamma (IFN-gamma) in CD28+ ('cytotoxic') and CD28- ('suppressor') CD8+ subsets.

We have measured by flow cytometry the ability of subsets of CD8+CD3+ lymphocytes within mononuclear cell preparations to make intracellular cytokines (IL-2, tumour necrosis factor-alpha (TNF-alpha) and IFN-gamma) on stimulation in vitro with phorbol myristate acetate (PMA) and ionomycin for 16 h. These CD8+ subsets were defined by the presence or absence of CD28 or HLA-DR. Subsets of normal CD8+ cells were compared with cells from the antibody deficiency disease common variable immunodeficiency (CVID). In CVID there was a significant increase in the production of IFN-gamma in the CD8+CD28+ subset ('cytotoxic'). This reflects a shift in this disease towards an excessive Th1 response away from B cell help. Paradoxically, some CVID patients also showed a reduction in IFN-gamma production in the CD8+CD28- subset ('suppressor') which was associated with a failure of these cells to maintain a state of activation after a stimulus in vitro. The B cell problem in this disease is known to be related to a failure of T cell help shown by an inability to produce the antigen-specific CD4+ memory T cells needed for successful B cell maturation. The two pathological CD28 subsets of CD8+ cells we have found in CVID may both be detrimental to a normal CD4-dependent immune response. The CD28- suppressor subset expands and is unable to maintain activation and cytokine secretion, and the CD28+ cytotoxic subset is over-producing the Th1 cytokine IFN-gamma.

Adult↗
PubMed1980

The colonic epithelium in ulcerative colitis: an energy-deficiency disease?

Suspensions of colonocytes (isolated colonic epithelial cells) were prepared from mucosa of the descending colon from 6 patients with quiescent ulcerative colitis (UC), 4 with acute UC, and 7 control subjects. In each group metabolic performance was investigated by assessing utilisation of n-butyrate, the main respiratory fuel of the colonic mucosa, as well as utilisation of glucose and glutamine. In both acute and quiescent UC oxidation of butyrate to CO2 and ketones was significantly lower than in the control tissues, and the decrease correlated with the state of the disease. Enhanced glucose and glutamine oxidation compensated for decreased butyrate oxidation in UC, indicating that colonocytes in colitis were not metabolically degenerate cells. Failure of butyrate oxidation reflects a variable yet definite metabolic defect in the mucosa in UC. Diminished oxidation of butyrate can explain the characteristic distribution of colitis along the colon, especially the frequency of UC in the distal colon. It is suggested that failure of fatty-acid (n-butyrate) oxidation in UC is an expression of an energy-deficiency disease of the colonic mucosa.

Acute Disease↗