The hide-and-seek game: men's perspectives on abortion and contraceptive use within marriage in a rural community in Zimbabwe

This paper is based on a study aimed at understanding the perceptions of men to induced abortion and contraceptive use within marriage in rural Zimbabwe. Two qualitative methods were combined. Men were found to view abortion not as a reproductive health problem for women. Instead, they described abortion as a sign of illicit sexual activity and contraceptive use as a strategy married women use to conceal their involvement in extramarital sexual activity. Men felt anxious and vulnerable for lack of control over women. In the absence of verbal communication on sexual matters, women and men resort to what are called here 'hide-and-seek' strategies, where women acquire and use contraceptives secretly while men search for evidence of such use. It is concluded that promoting women's sexual and reproductive health requires both short- and long-term strategies. The short-term strategy would entail providing women with reproductive technology they can use without risking violence. The long-term strategy would entail understanding men's concerns and the way these are manifested. In turn this requires the use of methodologies that encourage dialogue with research participants, in order to capture their deep meanings and experiences.     

Bovine viral diarrhoea virus antigenic diversity: impact on disease and vaccination programmes.

Bovine viral diarrhoea virus (BVDV) infections in cattle are associated with a variety or "diverse" clinical forms. These include digestive tract, respiratory, foetal (varied, dependent on foetal age), haemorrhagic and systemic diseases such as mucosal disease, and immunosuppression and inapparent infections. The BVDV isolates themselves are "diverse" with genotype differences based on nucleotide sequences, antigenic variability and biotypes (presence or absence of cytopathology in cell culture). Two predominant genotypes are present in the US, BVDV1 and BVDV2. There are subtypes of BVDV1, namely BVDV1a and BVDV1b. Examination of BVDV isolates from cattle derived from diagnostic laboratory submissions indicates that BVDV1b subtype isolates were as prevalent if not more prevalent than BVDV1a isolates. There was an almost equal distribution of BVDV1b and BVDV1a isolates from cattle with history of respiratory disease, and more isolates, 6 versus 2, of BVDV1b than for BVDV1a in necropsy cases of pneumonia. There were significant antibody titre differences in sera from calves receiving modified live virus vaccines containing BVDV1a, with the BVDV1b antibody titres being significantly lower. A survey of the US licensed and marketed BVDV vaccines indicates that only one vaccine contains BVDV1b with the others containing BVDV1a or undesignated BVDV1.     

Identification of a novel membrane-associated gene product that suppresses toxicity of a TrfA peptide from plasmid RK2 and its relationship to the DnaA host initiation protein

The toxicity of a peptide derived from the amino-terminal portion of 33-kDa TrfA, one of the initiation proteins encoded by the broad-host-range plasmid RK2, was suppressed by a host protein related to DnaA, the initiation protein of Escherichia coli. The newly identified 28.4-kDa protein, termed a DnaA paralog (Dp) because it is similar to a region of DnaA but likely has a different function in initiation of plasmid RK2 replication, interacts physically with the 33-kDa TrfA initiation protein, including the initiation-active monomeric form. The Dp has a cellular distribution similar to that of the 33-kDa TrfA initiation protein, being found primarily in the inner membrane fraction, with lesser amounts detected in the outer membrane fraction and almost none in the soluble fraction of E. coli. Maintenance and inner membrane-associated replication of plasmid RK2 were enhanced in a Dp knockout strain and inhibited in strains containing extra copies of the Dp gene or in membrane extracts to which a tagged form of Dp was added. Recently, the Dp was independently shown to help prevent overinitiation in E. coli and was termed Hda (S. Kato and T. Katayama, EMBO J. 20:4253-4262, 2001).     

Sleep in mice with nonfunctional growth hormone-releasing hormone receptors

The role of the somatotropic axis in sleep regulation was studied by using the lit/lit mouse with nonfunctional growth hormone (GH)-releasing hormone (GHRH) receptors (GHRH-Rs) and control heterozygous C57BL/6J mice, which have a normal phenotype. During the light period, the lit/lit mice displayed significantly less spontaneous rapid eye movement sleep (REMS) and non-REMS (NREMS) than the controls. Intraperitoneal injection of GHRH (50 microg/kg) failed to promote sleep in the lit/lit mice, whereas it enhanced NREMS in the heterozygous mice. Subcutaneous infusion of GH replacement stimulated weight gain, increased the concentration of plasma insulin-like growth factor-1 (IGF-1), and normalized REMS, but failed to restore normal NREMS in the lit/lit mice. The NREMS response to a 4-h sleep deprivation was attenuated in the lit/lit mice. In control mice, intraperitoneal injection of ghrelin (400 microg/kg) elicited GH secretion and promoted NREMS, and intraperitoneal administration of the somatostatin analog octretotide (Oct, 200 microg/kg) inhibited sleep. In contrast, these responses were missing in the lit/lit mice. The results suggest that GH promotes REMS whereas GHRH stimulates NREMS via central GHRH-Rs and that GHRH is involved in the mediation of the sleep effects of ghrelin and somatostatin.     

The evolution of self-compatibility in geographically peripheral populations of Leavenworthia alabamica (Brassicaceae)

Self-compatibility and adaptations to self-fertilization are often found in plant populations at the periphery of species' ranges or on islands. Self-compatibility may predominate in these environments because it provides reproductive assurance when pollinators or availability of mates limits seed production. This possibility was studied in Leavenworthia alabamica, a flowering plant endemic to the southeastern United States. Populations at the center of the species' range retain sporophytic self-incompatibility, but peripheral populations are smaller, self-compatible, and have adaptations for self-fertilization. A reciprocal-transplant experiment was designed to test whether there is pollen limitation of seed set and to examine its strength in central and peripheral populations. Self-compatible genotypes produced more fruit and 17-22% more seed than self-incompatible genotypes in all environments, suggesting that the transition to self-compatibility may be favored by natural selection in all populations inhabited by L. alabamica. Sequence analyses demonstrated that two peripheral populations have 90-100% reductions in genetic variation, consistent with the effects of small population size or historical bottlenecks. Although pollen limitation of seed set occurs in all environments, self-compatibility may evolve at the periphery in L. alabamica because the benefits of reproductive assurance are influenced by population size or bottlenecks following extinction and colonization.     

Clusters of transmembrane residues are critical for human prostacyclin receptor activation

Relaxation of vascular smooth muscle and prevention of blood coagulation are mediated by ligand-induced activation of the human prostacyclin (hIP) receptor, a seven-transmembrane-domain G-protein-coupled receptor (GPCR). In this study, we elucidate the molecular requirements for receptor activation within the region of the ligand-binding pocket, identifying transmembrane residues affecting potency. Eleven of 30 mutated residues in the region of the ligand-binding domain exhibited defective activation (decreased potency). These critical residues localized to four distinct clusters (analysis via a rhodopsin-based human prostacyclin receptor homology model). Residues Y75(2.65) (TMII), F95(3.28) (TMIII), and R279(7.40) (TMVII) comprised the immediate binding-pocket cluster and were shown to be essential for proper receptor activation, compared to equivalent expression levels of the wild-type hIP (WT EC(50) = 1.2 +/- 0.1 nM; Y75(2.65)A EC(50) = 347.3 +/- 62.8 nM, p < 0.001; F95(3.28)A EC(50) = 8.0 +/- 0.6 nM, p < 0.001; R279(7.40)A EC(50) = 130 +/- 63.0 nM, p < 0.001). Residues S20(1.39) (TMI), F24(1.43) (TMI), and F72(2.62) (TMII) were localized to a cluster involving P17(1.36), a critical residue thought to facilitate transmembrane movement during changes in activation conformation. A third cluster formed around amino acid D60(2.50) (TMII), containing the highly conserved (100% of prostanoid receptors) D288(7.49)/P289(7.50) motif located in TMVII. Last, a large hydrophobic cluster composed of aromatic residues F146(4.52) (TMIV), F150(4.56) (TMIV), F184(5.40) (TMV), and Y188(5.44) (TMV) was observed away from the ligand-binding pocket, but still necessary for hIP activation. These results assist in delineating the potential molecular requirements for agonist-induced signaling through the transmembrane domain. Such observations may be generally applicable, as many of these clusters are highly conserved among the prostanoid receptors as well as other class A GPCRs.     

The SPCH1 region on human 7q31: genomic characterization of the critical interval and localization of translocations associated with speech and language disorder

The KE family is a large three-generation pedigree in which half the members are affected with a severe speech and language disorder that is transmitted as an autosomal dominant monogenic trait. In previously published work, we localized the gene responsible (SPCH1) to a 5.6-cM region of 7q31 between D7S2459 and D7S643. In the present study, we have employed bioinformatic analyses to assemble a detailed BAC-/PAC-based sequence map of this interval, containing 152 sequence tagged sites (STSs), 20 known genes, and >7.75 Mb of completed genomic sequence. We screened the affected chromosome 7 from the KE family with 120 of these STSs (average spacing <100 kb), but we did not detect any evidence of a microdeletion. Novel polymorphic markers were generated from the sequence and were used to further localize critical recombination breakpoints in the KE family. This allowed refinement of the SPCH1 interval to a region between new markers 013A and 330B, containing approximately 6.1 Mb of completed sequence. In addition, we have studied two unrelated patients with a similar speech and language disorder, who have de novo translocations involving 7q31. Fluorescence in situ hybridization analyses with BACs/PACs from the sequence map localized the t(5;7)(q22;q31.2) breakpoint in the first patient (CS) to a single clone within the newly refined SPCH1 interval. This clone contains the CAGH44 gene, which encodes a brain-expressed protein containing a large polyglutamine stretch. However, we found that the t(2;7)(p23;q31.3) breakpoint in the second patient (BRD) resides within a BAC clone mapping >3.7 Mb distal to this, outside the current SPCH1 critical interval. Finally, we investigated the CAGH44 gene in affected individuals of the KE family, but we found no mutations in the currently known coding sequence. These studies represent further steps toward the isolation of the first gene to be implicated in the development of speech and language.