Family planning among people living with HIV in post-conflict Northern Uganda: A mixed methods study

<p>Abstract</p> <p>Background</p> <p>Northern Uganda experienced severe civil conflict for over 20 years and is also a region of high HIV prevalence. This study examined knowledge of, access to, and factors associated with use of family planning services among people living with HIV (PLHIV) in this region.</p> <p>Methods</p> <p>Between February and May 2009, a total of 476 HIV clinic attendees from three health facilities in Gulu, Northern Uganda, were interviewed using a structured questionnaire. Semi-structured interviews were conducted with another 26 participants. Factors associated with use of family planning methods were examined using logistic regression methods, while qualitative data was analyzed within a social-ecological framework using thematic analysis.</p> <p>Results</p> <p>There was a high level of knowledge about family planning methods among the PLHIV surveyed (96%). However, there were a significantly higher proportion of males (52%) than females (25%) who reported using contraception. Factors significantly associated with the use of contraception were having ever gone to school [adjusted odds ratio (AOR) = 4.32, 95% confidence interval (CI): 1.33-14.07; p = .015], discussion of family planning with a health worker (AOR = 2.08, 95% CI: 1.01-4.27; p = .046), or with one's spouse (AOR = 5.13, 95% CI: 2.35-11.16; p = .000), not attending the Catholic-run clinic (AOR = 3.67, 95% CI: 1.79-7.54; p = .000), and spouses' non-desire for children (AOR = 2.19, 95% CI: 1.10-4.36; p = .025). Qualitative data revealed six major factors influencing contraception use among PLHIV in Gulu including personal and structural barriers to contraceptive use, perceptions of family planning, decision making, covert use of family planning methods and targeting of women for family planning services.</p> <p>Conclusions</p> <p>Multilevel, context-specific health interventions including an integration of family planning services into HIV clinics could help overcome some of the individual and structural barriers to accessing family planning services among PLHIV in Gulu. The integration also has the potential to reduce HIV incidence in this post-conflict region.</p

Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk

An enhanced thrombotic environment and premature atherosclerosis are key factors for the increased cardiovascular risk in diabetes. The occlusive vascular thrombus, formed secondary to interactions between platelets and coagulation proteins, is composed of a skeleton of fibrin fibres with cellular elements embedded in this network. Diabetes is characterised by quantitative and qualitative changes in coagulation proteins, which collectively increase resistance to fibrinolysis, consequently augmenting thrombosis risk. Current long-term therapies to prevent arterial occlusion in diabetes are focussed on anti-platelet agents, a strategy that fails to address the contribution of coagulation proteins to the enhanced thrombotic milieu. Moreover, antiplatelet treatment is associated with bleeding complications, particularly with newer agents and more aggressive combination therapies, questioning the safety of this approach. Therefore, to safely control thrombosis risk in diabetes, an alternative approach is required with the fibrin network representing a credible therapeutic target. In the current review, we address diabetes-specific mechanistic pathways responsible for hypofibrinolysis including the role of clot structure, defects in the fibrinolytic system and increased incorporation of anti-fibrinolytic proteins into the clot. Future anti-thrombotic therapeutic options are discussed with special emphasis on the potential advantages of modulating incorporation of the anti-fibrinolytic proteins into fibrin networks. This latter approach carries theoretical advantages, including specificity for diabetes, ability to target a particular protein with a possible favourable risk of bleeding. The development of alternative treatment strategies to better control residual thrombosis risk in diabetes will help to reduce vascular events, which remain the main cause of mortality in this condition

The FSHD2 Gene SMCHD1 Is a Modifier of Disease Severity in Families Affected by FSHD1.

Facioscapulohumeral muscular dystrophy type 1 (FSHD1) is caused by contraction of the D4Z4 repeat array on chromosome 4 to a size of 1-10 units. The residual number of D4Z4 units inversely correlates with clinical severity, but significant clinical variability exists. Each unit contains a copy of the DUX4 retrogene. Repeat contractions are associated with changes in D4Z4 chromatin structure that increase the likelihood of DUX4 expression in skeletal muscle, but only when the repeat resides in a genetic background that contains a DUX4 polyadenylation signal. Mutations in the structural maintenance of chromosomes flexible hinge domain containing 1 (SMCHD1) gene, encoding a chromatin modifier of D4Z4, also result in the increased likelihood of DUX4 expression in individuals with a rare form of FSHD (FSHD2). Because SMCHD1 directly binds to D4Z4 and suppresses somatic expression of DUX4, we hypothesized that SMCHD1 may act as a genetic modifier in FSHD1. We describe three unrelated individuals with FSHD1 presenting an unusual high clinical severity based on their upper-sized FSHD1 repeat array of nine units. Each of these individuals also carries a mutation in the SMCHD1 gene. Familial carriers of the FSHD1 allele without the SMCHD1 mutation were only mildly affected, suggesting a modifier effect of the SMCHD1 mutation. Knocking down SMCHD1 in FSHD1 myotubes increased DUX4 expression, lending molecular support to a modifier role for SMCHD1 in FSHD1. We conclude that FSHD1 and FSHD2 share a common pathophysiological pathway in which the FSHD2 gene can act as modifier for disease severity in families affected by FSHD1

The FSHD2 Gene SMCHD1 Is a Modifier of Disease Severity in Families Affected by FSHD1.

Facioscapulohumeral muscular dystrophy type 1 (FSHD1) is caused by contraction of the D4Z4 repeat array on chromosome 4 to a size of 1-10 units. The residual number of D4Z4 units inversely correlates with clinical severity, but significant clinical variability exists. Each unit contains a copy of the DUX4 retrogene. Repeat contractions are associated with changes in D4Z4 chromatin structure that increase the likelihood of DUX4 expression in skeletal muscle, but only when the repeat resides in a genetic background that contains a DUX4 polyadenylation signal. Mutations in the structural maintenance of chromosomes flexible hinge domain containing 1 (SMCHD1) gene, encoding a chromatin modifier of D4Z4, also result in the increased likelihood of DUX4 expression in individuals with a rare form of FSHD (FSHD2). Because SMCHD1 directly binds to D4Z4 and suppresses somatic expression of DUX4, we hypothesized that SMCHD1 may act as a genetic modifier in FSHD1. We describe three unrelated individuals with FSHD1 presenting an unusual high clinical severity based on their upper-sized FSHD1 repeat array of nine units. Each of these individuals also carries a mutation in the SMCHD1 gene. Familial carriers of the FSHD1 allele without the SMCHD1 mutation were only mildly affected, suggesting a modifier effect of the SMCHD1 mutation. Knocking down SMCHD1 in FSHD1 myotubes increased DUX4 expression, lending molecular support to a modifier role for SMCHD1 in FSHD1. We conclude that FSHD1 and FSHD2 share a common pathophysiological pathway in which the FSHD2 gene can act as modifier for disease severity in families affected by FSHD1