Decolonising multimorbidity? research gaps in low and middle-income countries.

Multimorbidity is defined as the co-existence of multiple health conditions in one person. However, its use in research has been predominantly applied to non-communicable diseases, because research was conducted almost exclusively in developed countries. More recently, infectious diseases of long duration, such as human immunodeficiency virus (HIV), have also been included in the conceptualization of multimorbidity.

The non-fatal disease burden caused by type 2 diabetes in South Africa, 2009.

Background: Increasing urbanisation and rising unhealthy lifestyle risk factors are contributing to a growing diabetes epidemic in South Africa. In 2000, a study estimated diabetes prevalence to be 5.5% in those aged over 30.

Diagnostic accuracy of clinical signs used to identify electrolyte disturbances in children with diarrhoea.

Background: No studies have assessed the diagnostic accuracy of clinical signs of electrolyte disturbances in children with dehydrating diarrhoea.

Aims: To assess the diagnostic accuracy and reliability of clinical signs previously reported to be associated with plasma sodium and potassium disturbances in children.

Methods: A cross-sectional analytical study of 476 children aged 6 weeks to 2 years, admitted to a rehydration unit in Cape Town, South Africa.

In vitro effect of a thrombin inhibition peptide selected by phage display technology.

A repeated selection of phages from a cyclic heptapeptide phage display library resulted in the enrichment of phages that bind to human alpha-thrombin. One clone of the binding phages that competed with PPACK for binding to thrombin and that had the best binding characteristics was chosen. The amino acid sequence of the peptide displayed on this phage was determined and a peptide with the sequence, Cys-Asn-Arg-Pro-Phe-Ile-Pro-Thr-Cys was synthesised.

Incorporation of an Asp-Ser sequence to form an RGDS-like motif in hirutonin: the effect on in vitro platelet function.

We investigated the effect on in vitro platelet function of hirutonin, a modified hirutonin with an RGD-like motif, a pseudo-RGDS peptide and a linear RGDS peptide. Inhibition of expression of surface fibrinogen on ADP-activated platelets with 40 microM of the peptide was as follows: hirutonin 10+/-3%, modified chimeric peptide 26+/-5%, pseudo-RGDS 66+/-11% and linear RGDS 93+/-13%. Both hirutonin and the chimeric peptide significantly inhibited ADP-induced platelet activation as detected by CD62 expression.