The Karitane mothercraft hospital current and future activities.
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Biomedical subjects
Publications and source records attributed to M J Harris.
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The global pandemic of HIV/AIDS is at catastrophic levels in sub-Saharan Africa, while the need for research and treatment initiatives throughout the developing world remains critical. The West African country of Sierra Leone is representative of both of these facts. The purposes of this study were to assess the HIV-related knowledge, attitudes, and behaviors of adult Sierra Leoneans to determine what type of HIV prevention efforts are needed in this population and to determine how such efforts could be developed and implemented. Interviews with 487 adults residing in the capital city of Freetown, Sierra Leone, and in the Northern Province of that country revealed HIV/AIDS-related knowledge, attitudes, and behaviors that reflect the impact of culture and tradition on the spread of HIV/AIDS. The challenges for HIV prevention raised through this study indicate the need to examine in greater depth the culturally specific use of traditional healers and traditional theater as channels of information that could serve to make HIV prevention initiatives more effective in Sierra Leone.
The first arch malformation arising in a BALB/c strain of mice, has been shown to be inherited as a single autosomal recessive gene and is given the provisional gene symbol far. Affected newborns have extensive bony defects of the face and skull, including a cleft secondary palate, and die within 24 hours of birth. Most of the abnormalities occur in bones derived from the first branchial arch and most of the bony derivatives of the first arch are abnormal in the mutant.
A new mutation causing spherocytic, hemolytic anemia has been discovered in the house mouse. It is inherited as a single autosomal recessive gene, allelic with both sph and ha, which, in turn, were shown to be allelic with each other. A revised nomenclature for the three apparent alleles is proposed: sph (formerly sph), sphha (formerly ha), and sph2Bc (the new mutation). Like the other murine hemolytic anemias, sph2Bc involves a defect in the red blood cell membrane protein, spectrin.
A short limb dwarfing syndrome that arose in BALB/cGaBc inbred mice appeared to segregate as a Mendelian autosomal recessive lethal mutation. Anatomical and histological studies of newborns showed shortening and widening of most cartilaginous bones, shortening of the head, subcutaneous edema, and engorgement of liver with blood. Cartilage showed deficiency of acid mucopolysaccharide in the extracellular matrix and strain excessively for collagen. The primary cause of death at birth is probably the extremely compressed anterior thorax. The new mutation behaves as an allele of cartilage matrix deficiency (cmd) and is provisionally named cmdBc.
We tested the hypothesis that differences in wild-type (+) alleles (isoalleles) at the first arch (far) locus between mouse strains ICR/Bc and BALB/cGaBc are responsible for the partially dominant expression of far in the ICR/Bc genetic background, in contrast to its recessive expression in the BALB/cGaBc background. A similar hypothesis concerning isoalleles has been suggested to explain differences in heterozygote expression in some human genetic diseases but appears not to have been tested directly in mammals. First arch is lethal when homozygous. The dominant effects in ICR/Bc mice include defects in mystacial vibrissa pattern formation and cleft palate. To test the isoallele hypothesis, we made the four appropriate genetic crosses between +/far and +/+ mice between strains. The F1 progeny were scored on day 16 of gestation for defective mystacial vibrissa pattern formation and cleft palate. From all four crosses, approximately 30% of F1 fetuses (i.e., 60% of +/far fetuses) had disrupted mystacial vibrissa patterns, and only one fetus had cleft palate. The fact that all crosses produced approximately equal rates of defective progeny disproves the isoallele hypothesis for far. Therefore, differences between strains in alleles at other loci (modifier loci) must cause the differences in heterozygote (+/far) expression. This genetic design can be used for other mutations with strain differences in heterozygote expression to test the importance of isoalleles in mammals.