Atrial septal defect (ASD) coexisting with mitral valve regurgitation has been described in literature with various aetiologies and pathophysiologic mechanisms. Mitral valve lesions coexisting with an ASD could either be congenital or acquired. The most prominent congenital mitral valve pathology is a cleft in the anterior leaflet of the mitral valve, as seen in patients with partial atrio-ventricular septal defects. Acquired mitral valve lesions include, hemodynamic induced annular dilatation resulting in significant mitral regurgitation, iatrogenic leaflet perforation and coexisting diseases such as infective endocarditis or rheumatic valve disease. However, the aetiology of the mitral valve regurgitation being due to rheumatic heart disease is uncommon. We report the case of a 12-year-old female who presented with easy fatigability, palpitation and a precordial bulge dating about 2 years. Examination revealed cardiac murmurs in the apex and pulmonary areas and transthoracic echocardiography confirmed the presence of an Ostium Secundum ASD and features of severe rheumatic mitral valve regurgitation. Child was initially placed on medications which included diuretics and an Angiotensin converting enzyme inhibitor ACEi, before she eventually had surgical closure of ASD and mitral valve replacement. The purpose of this case report is to highlight the symptomatology, diagnosis and treatment of this rare association, particularly in our environment.

The objective of this study was to assess the adoption level of Total Quality Management (TQM) in pharmaceutical manufacturing industry in Southwestern Nigeria by a cross-sectional survey of staff in Lagos, Ogun and Oyo States of Nigeria involving 348 of the 2,649 members, selected by multi-stage sampling. Primary data were collected using a set of pre-tested semi-structured questionnaire which sought to elicit information on the level of TQM adoption and designed with items on a Likert–type scale of seven alternative responses with weighting scores of 0 through 6, representing seven stages (levels) in the adoption process. Adoption was taken as becoming effective from the sixth stage (level 5). Factors influencing TQM adoption were identified by employing a Likert-type influence scale with five alternative responses and weighting scores of 0 - 4. Weighted averages (WA) and means of weighted averages (MWA) were employed in summarising the data while t-test and regression analyses were used in identifying significant relationships between variables at 5% significance level. The results showed that TQM adoption was at implementation (trial) level (MWA ≈ 4) and had not become actualised in the industry (t = 11.906, df = 3, p = .000). The study concluded that the adoption level of TQM in this industry was at trial level and TQM adoption was ineffective. Thus, there is need for improved adoption of the various components of TQM, particularly ‘leadership commitment’ and this can be achieved through sustained TQM training and advocacy by professional associations within the industry such as Nigerian Association of Industrial Pharmacists (NAIP) and Pharmaceutical Society of Nigeria (PSN).

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a decrease in agonist-evoked current mediated by mutant subunits compared to wild-type channels. When GluA2 subunits are co-expressed with GluA1, most GRIA2 mutations cause a decreased current amplitude and some also affect voltage rectification. Our results show that de-novo variants in GRIA2 can cause neurodevelopmental disorders, complementing evidence that other genetic causes of ID, ASD and DEE also disrupt glutamatergic synaptic transmission.