Effect of multi-month antiretroviral dispensing on HIV clinic attendance at 68 Nigerian Army Reference Hospital, Yaba, Nigeria.

Background: Multi-month dispensing (MMD) of antiretroviral therapy has demonstrated benefits for HIV patients and health service delivery systems, including reduced frequency of hospital visits and improved retention. We evaluated the effect of 6-monthly dispensing (MMD6) on patient clinic attendance at a single military facility in the one-year pre- and post-policy change.Methods: This was a descriptive, retrospective, cross-sectional study, exploring the relationship between MMD6 and clinic attendance numbers. We reviewed aggregate clinic attendance records for clients on ART and documented monthly trends in clinic attendance numbers, number of clients current on ART, and amount of ART dispensed.Results: In the pre-MMD6 group, 4 150 patients were included, and 4 190 in the post-MMD6 group. Clinic attendance was 30 407 visits (16 111 pre-MMD6 and 14 296 post-MMD6). An overall mean increase of 326.58 ± 861.81 (95% CI = -874.15 ± 220.98) drugs were dispensed per month; t(11) = -1.31, p = 0.22; mean monthly clinic attendance declined from 1342.8 ± 220.10 visits pre-MMD6 to 1191.33 ± 309.10 post-MMD6 with t(11) = 1.601, p = 0.14, but was not statistically significant.Conclusion: Six-monthly dispensing can be an important tool to reduce HIV clinic volumes and improve antiretroviral access. It is particularly important for care continuity in military facilities where service members may be deployed or transferred to other bases along with their dependents.

The Nigerian Military Public Health Response to COVID-19: A 14-Month Appraisal.

The COVID-19 pandemic has caused significant morbidity and mortality since its emergence in December 2019. In Nigeria, the government inaugurated the Presidential Task Force on COVID-19 to coordinate resources while the Nigeria Centre for Disease Control led the public health response. The Nigeria Ministry of Defence Health Implementation Programme (MODHIP), in partnership with the US Army Medical Research Directorate - Africa/Nigeria, responded immediately to the pandemic by establishing a public health emergency operations center to coordinate the military response in support of national efforts. MODHIP has 5 functional units and 6 pillars that coordinate testing, surveillance, case management, risk communication, logistics, research, and infection prevention and control. It developed an incident action plan and each pillar had its own terms of reference to guide specific response activities while preventing duplication of efforts within the military and the Nigeria Centre for Disease Control. In addition, awareness and sensitization sessions were conducted on preventive practices for COVID-19 and infrastructure was provided for hand hygiene and screening at all military facilities. Military laboratories were configured for SARS-CoV-2 testing while selected military health facilities were equipped and designated as COVID-19 treatment centers. Research proposals aimed at better understanding the disease and controlling it were also developed. The traditional combat role of the military was redirected to complement this public health emergency response. In this article, we highlight gaps, opportunities, and lessons to improve military participation in public health emergency response in the future. More funding and multisectoral collaboration with civilian institutions are key to strengthening military public health emergency preparedness and response capabilities.

Loss of the Tg737 protein results in skeletal patterning defects.

Tg737 mutant mice exhibit pathologic conditions in numerous tissues along with skeletal patterning defects. Herein, we characterize the skeletal pathologic conditions and confirm a role for Tg737 in skeletal patterning through transgenic rescue. Analyses were conducted in both the hypomorphic Tg737(orpk) allele that results in duplication of digit one and in the null Tg737(delta2-3betaGal) allele that is an embryonic lethal mutation exhibiting eight digits per limb. In early limb buds, Tg737 expression is detected throughout the mesenchyme becoming concentrated in precartilage condensations at later stages. In situ analyses indicate that the Tg737(orpk) mutant limb defects are not associated with changes in expression of Shh, Ihh, HoxD11-13, Patched, BMPs, or Glis. Likewise, in Tg737(delta2-3betaGal) mutant embryos, there was no change in Shh expression. However, in both alleles, Fgf4 was ectopically expressed on the anterior apical ectodermal ridge. Collectively, the data argue for a dosage effect of Tg737 on the limb phenotypes and that the polydactyly is independent of Shh misexpression.

EMR4, a novel epidermal growth factor (EGF)-TM7 molecule up-regulated in activated mouse macrophages, binds to a putative cellular ligand on B lymphoma cell line A20.

A novel member of the EGF-TM7 family, mEMR4, was identified and characterized. The full-length mouse EMR4 cDNA encodes a predicted 689-amino acid protein containing two epidermal growth factor (EGF)-like modules, a mucin-like spacer domain, and a seven-transmembrane domain with a cytoplasmic tail. Genetic mapping established that mEMR4 is localized in the distal region of mouse chromosome 17 in close proximity to another EGF-TM7 gene, F4/80 (Emr1). Similar to F4/80, mEMR4 is predominantly expressed on resident macrophages. However, a much lower expression level was also detected in thioglycollate-elicited peritoneal neutrophils and bone marrow-derived dendritic cells. The expression of mEMR4 is up-regulated following macrophage activation in Biogel and thioglycollate-elicited peritoneal macrophages. Similarly, mEMR4 is over-expressed in TNF-alpha-treated resident peritoneal macrophages, whereas interleukin-4 and -10 dramatically reduce the expression. mEMR4 was found to undergo proteolytic processing within the extracellular stalk region resulting in two protein subunits associated noncovalently as a heterodimer. The proteolytic cleavage site was identified by N-terminal amino acid sequencing and located at the conserved GPCR (G protein-coupled receptor) proteolytic site in the extracellular region. Using multivalent biotinylated mEMR4-mFc fusion proteins as a probe, a putative cell surface ligand was identified on a B lymphoma cell line, A20, in a cell-binding assay. The mEMR4-ligand interaction is Ca2+-independent and is mediated predominantly by the second EGF-like module. mEMR4 is the first EGF-TM7 receptor known to mediate the cellular interaction between myeloid cells and B cells.

A new mouse model for autosomal recessive polycystic kidney disease.

In the course of large-scale mutagenesis studies, we discovered a mutant that provides a new mouse model for human autosomal recessive polycystic kidney disease. Animals homozygous for this mutation, T(2;10)67Gso, present evidence of grossly cystic renal and hepatic tissue at birth and a limited survival time of 3-4 days. The recessively expressed phenotype is associated with inheritance of a reciprocal translocation involving mouse chromosomes 2 and 10. Here we describe the pathology and phenotype of this new mutation. The mapping of the chromosomal breakpoint to the 1.0-cM critical region defined for another mouse autosomal recessive polycystic kidney disease model, juvenile congenital polycystic kidney disease (jcpk), led us to undertake the complementation testing that confirmed T(2;10)67Gso and jcpk are allelic. Because of the strong resemblance between the phenotype associated with these mouse mutations and early childhood polycystic kidney disease, and because of advantages offered by reciprocal translocations for gene mapping and cloning, T(2;10)67Gso should prove a valuable asset for studies concerning this fatal disease.