Menstrual hygiene management among adolescent girls in West Africa: A systematic review.

A systematic literature review was conducted to examine all recent academic, peer-reviewed studies of menstrual hygiene management (MHM) across adolescent girls in Anglophone West Africa. The objective was to assess the status of the scholarship surrounding the knowledge, attitudes, and practices of MHM across English-speaking West African countries and identify gaps in the literature for further research. The authors searched the epidemiological literatures indexed in PubMed and cross-referenced bibliographies for studies published between 2010-2022.

Predictors of Seat-Belt Use among Bus Passengers in Ghana: An Application of the Theory of Planned Behaviour and Health Belief Model.

Background: Seat-belt use is effective in preventing traffic fatalities and injuries yet its use is not universal. This study sought to determine the predictors of self-reported seat-belt use among bus passengers in Ghana based on the theory of planned behaviour and health belief model.

Methods: A quantitative cross-sectional study design with 633 randomly selected intercity bus passengers was conducted using a structured questionnaire in Kumasi, Ghana.

Effect of a theory-based hand hygiene educational intervention for enhancing behavioural outcomes in Ghanaian schools: a cluster-randomised controlled trial.

Objectives: The study sought to determine whether a hand hygiene educational intervention underpinned by educational and psychosocial theories is effective in enhancing behavioural intention and proper handwashing practices among school children.

Methods: The study was a cluster-randomised controlled trial, with schools constituting the clusters. At baseline, 717 pupils organised in four clusters were recruited.

Insights into the Etiology of Mammalian Neural Tube Closure Defects from Developmental, Genetic and Evolutionary Studies.

The human neural tube defects (NTD), anencephaly, spina bifida and craniorachischisis, originate from a failure of the embryonic neural tube to close. Human NTD are relatively common and both complex and heterogeneous in genetic origin, but the genetic variants and developmental mechanisms are largely unknown. Here we review the numerous studies, mainly in mice, of normal neural tube closure, the mechanisms of failure caused by specific gene mutations, and the evolution of the vertebrate cranial neural tube and its genetic processes, seeking insights into the etiology of human NTD.

Examining school-based hygiene facilities: a quantitative assessment in a Ghanaian municipality.

Background: The crucial role of adequate water, sanitation and hygiene (WASH) facilities in influencing children's handwashing behaviour is widely reported. Report from UNICEF indicates a dearth of adequate data on WASH facilities in schools, especially in the developing world. This study sought to contribute to building the evidence-base on school hygiene facilities in Ghana.

A framework for designing hand hygiene educational interventions in schools.

Objectives: Hygiene education appears to be the commonest school-based intervention for preventing infectious diseases, especially in the developing world. Nevertheless, there remains a gap in literature regarding a school-specific theory-based framework for designing a hand hygiene educational intervention in schools. We sought to suggest a framework underpinned by psychosocial theories towards bridging this knowledge gap.

Epigenetic mechanism causes Wnt9b deficiency and nonsyndromic cleft lip and palate in the A/WySn mouse strain.

Background: The heritable multifactorial etiology of human nonsyndromic cleft lip with or without cleft palate (CL ± P) is not understood. CL ± P occurs in 15% of neonates in the homozygous A/WySn mouse strain, with a multifactorial genetic etiology, the clf1 and clf2 variant genes. Clf1 acts as a mutant allele of Wnt9b but its coding sequence is normal.

An update to the list of mouse mutants with neural tube closure defects and advances toward a complete genetic perspective of neural tube closure.

The number of mouse mutants and strains with neural tube defects (NTDs) now exceeds 240, including 205 representing specific genes, 30 for unidentified genes, and 9 multifactorial strains. These mutants identify genes needed for embryonic neural tube closure. Reports of 50 new NTD mutants since our 2007 review (Harris and Juriloff, 2007) were considered in relation to the previously reviewed mutants to obtain new insights into mechanisms of NTD etiology.

Insights into prevention of human neural tube defects by folic acid arising from consideration of mouse mutants.

Almost 30 years after the initial study by Richard W. Smithells and coworkers, it is still unknown how maternal periconceptional folic acid supplementation prevents human neural tube defects (NTDs). In this article, questions about human NTD prevention are considered in relation to three groups of mouse models: NTD mutants that respond to folate, NTD mutants and strains that do not respond to folate, and mutants involving folate-pathway genes.

Accelerated embryonic development associated with increased risk of neural tube defects induced by maternal diet in offspring of SELH/Bc mice.

Background: The SELH/Bc mouse strain has a high risk of the NTD, exencephaly, caused by multifactorial genetics. All SELH/Bc embryos have delayed elevation of neural folds; some never elevate (future exencephalics). Maternal diets affect SELH/Bc exencephaly rates: 25-35% on Purina Diet 5015 versus 5-10% on Purina Diet 5001.

Mouse genetic models of cleft lip with or without cleft palate.

Nonsyndromic cleft lip and palate (CLP) is among the most common human birth defects. Transmission patterns suggest that the causes are "multifactorial" combinations of genetic and nongenetic factors, mostly distinct from those causing cleft secondary palate (CP). The major etiological factors are largely unknown, and the embryological mechanisms are not well understood.

Mouse mutants with neural tube closure defects and their role in understanding human neural tube defects.

Background: The number of mouse mutants and strains with neural tube closure defects (NTDs) now exceeds 190, including 155 involving known genes, 33 with unidentified genes, and eight "multifactorial" strains.

Methods: The emerging patterns of mouse NTDs are considered in relation to the unknown genetics of the common human NTDs, anencephaly, and spina bifida aperta.

Results: Of the 150 mouse mutants that survive past midgestation, 20% have risk of either exencephaly and spina bifida aperta or both, parallel to the majority of human NTDs, whereas 70% have only exencephaly, 5% have only spina bifida, and 5% have craniorachischisis.

Wnt9b is the mutated gene involved in multifactorial nonsyndromic cleft lip with or without cleft palate in A/WySn mice, as confirmed by a genetic complementation test.

Background: Nonsyndromic cleft lip (CL) with or without cleft palate (CLP) is a common human birth defect with complex genetic etiology. One of the unidentified genes maps to chromosome 17q21. A mouse strain, A/WySn, has CLP with complex genetic etiology that models the human defect, and 1 of its causative genes, clf1, maps to a region homologous to human 17q21.

Maternal diet alters exencephaly frequency in SELH/Bc strain mouse embryos.

Background: The SELH/Bc mouse inbred strain, with a high frequency of nonsyndromic, genetically-multifactorial exencephaly, is a model for human cranial neural tube defects (NTDs). Maternal diet affects risk of human NTDs.

Methods: Exencephaly frequencies in SELH/Bc embryos were compared in 8 studies in which dams were fed alternative commercial Purina diets (5015 and 5001) or semisynthetic diets, and in several studies in which maternal diet was supplemented with a specific nutrient, either in drinking water or food before and during pregnancy, or by intraperitoneal injection on E7 and/or E8.

Investigations of the genomic region that contains the clf1 mutation, a causal gene in multifactorial cleft lip and palate in mice.

Background: Human nonsyndromic cleft lip and palate, CL(P), is genetically complex, with one contributing gene on chromosome 17q. A potentially homologous gene, clf1 on distal chromosome 11, is part of the digenic cause of the 10-30% CL(P) in the A/WySn mouse strain. Here we report our progress toward identifying the clf1 mutation.

The open-eyelid mutation, lidgap-Gates, is an eight-exon deletion in the mouse Map3k1 gene.

The BALB/cGa mouse strain and its descendants, now called the SELH/Bc strain, have produced two waves of high frequency of spontaneous heritable mutations. One of these, the recessive lidgap-Gates (lg(Ga)) mutation, causes the same open-eyelids-at-birth phenotype as the gene knockout mutations of Map3k1 and co-maps to distal Chr 13. The lg(Ga) mutation is demonstrated to be a 27.

A digenic cause of cleft lip in A-strain mice and definition of candidate genes for the two loci.

Background: Nonsyndromic cleft lip with or without cleft palate, CL(P), is a common human birth defect with a complex unknown genetic cause. The mouse model is the "A/-" strains. Our previous studies mapped two loci: clf1 on Chr11 and clf2 on Chr13--with a strong genetic maternal effect on the level of risk.

Structure and expression of mobile ETnII retroelements and their coding-competent MusD relatives in the mouse.

ETnII elements are mobile members of the repetitive early transposon family of mouse long terminal repeat (LTR) retroelements and have caused a number of mutations by inserting into genes. ETnII sequences lack retroviral genes, but the recent discovery of related MusD retroviral elements with regions similar to gag, pro, and pol suggests that MusD provides the proteins necessary for ETnII transposition in trans. For this study, we analyzed all ETnII elements in the draft sequence of the C57BL/6J genome and classified them into three subtypes (alpha, beta, and gamma) based on structural differences.