Cardiovascular Journal of Africa: Vol 25 No 5 (September/October 2014)

17 / 74

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 5, September/October 2014 AFRICA 211
aetiology and challenges in the management of congestive heart failure
in sub-Saharan Africa: experience of the Cardiac Centre in Shisong,
Cameroon. Pan Afr Med J 2011; 8: 11.
16. Ojji DB, Alfa J, Ajayi SO, et al. Pattern of heart failure in Abuja, Nigeria:
an echocardiographic study. Cardiovasc J Afr 2009; 20: 349–352.
17. Soliman EZ, Juma H. Cardiac disease patterns in northern Malawi:
epidemiologic transition perspective. J Epidemiol 2008; 18: 204–208.
18. Sliwa K, Carrington M, Mayosi BM, et al. Incidence and characteristics
of newly diagnosed rheumatic heart disease in urban African adults:
insights from the heart of Soweto study. Eur Heart J 2010; 31: 719–727.
19. Carapetis JR, Steer AC, Mulholland EK, et al. The global burden of
group A streptococcal diseases. Lancet Infect Dis 2005; 5: 685–694.
20. Marijon E, Mirabel M, Celermajer DS, et al. Rheumatic heart disease.
Lancet 2012; 379: 953–964.
21. Marijon E, Ou P, Celermajer DS, et al. Prevalence of rheumatic heart
disease detected by echocardiographic screening. N Engl J Med 2007;
357: 470–476.
22. Saxena A, Ramakrishnan S, Roy A, et al. Prevalence and outcome
of subclinical rheumatic heart disease in India: the RHEUMATIC
(Rheumatic Heart Echo Utilisation and Monitoring Actuarial Trends
in Indian Children) study. Heart 2011; 97: 2018–2022.
23. Roberts K, Colquhoun S, Steer A, et al. Screening for rheumatic heart
disease: current approaches and controversies. Nat Rev Cardiol 2013;
10: 49–58.
24. Mirabel M, Celermajer DS, Ferreira B, et al. Screening for rheu-
matic heart disease: evaluation of a simplified echocardiography-based
approach. Eur Heart J Cardiovasc Imaging 2012; 13: 1024–1029.
25. Mocumbi AO, Lameira E, Yaksh A, et al. Challenges on the manage-
ment of congenital heart disease in developing countries. Int J Cardiol
2011; 148: 285–288.
26. Freers J, Masembe V, Schmauz R, et al. Endomyocardial fibrosis
syndrome in Uganda. Lancet 2000; 355: 1994–1995.
27. Mocumbi AO, Ferreira MB, Sidi D, et al. A population study of endo-
myocardial fibrosis in a rural area of Mozambique. N Engl J Med 2008;
359: 43–49.
28. Ibrahim MM, Damasceno A. Hypertension in developing countries.
Lancet 2012; 380: 611–619.
29. World Health Organization (2005) Report of the Regional Committe
of Africa. 2005.
30. Von Elm E, Altman DG, Egger M, et al; STROBE initiative. The
Strengthening The Reporting of OBservational studies in Epidemiology
(STROBE) statement: guidelines for reporting observational studies.
Ann Intern Med 2007; 147: 573–577.
Diabetes researchers track cells’ ability to regenerate
Vanderbilt University scientists have found evidence that
the insulin-secreting beta-cells of the pancreas, which are
either killed or become dysfunctional in the two main forms
of diabetes, have the capacity to regenerate. The surprising
finding, posted online by Cell Metabolism earlier this year,
suggests that by understanding how regeneration occurs,
scientists may one day be able to stop or reverse the rising
tide of diabetes. ‘The study provides clues to how we might
learn what signals promote beta-cell regeneration in type 1
and type 2 diabetes’, said Dr Alvin Powers, the senior author
and director of the Vanderbilt Diabetes Center.
In the past three months, the Powers group at Vanderbilt,
in four separate articles, has reported important findings
about the ‘microenvironment’ of the insulin-secreting beta-
cells and glucagon-secreting alpha-cells, which are among
four types of cells clustered in islets in the pancreas. Both
hormones are important in regulating blood glucose levels
and ensuring that glucose is delivered to the muscles and
brain to be used as fuel, and stored in the liver. Powers called
the islets a ‘mini-organ’ because they are highly vascularised
and innervated, and exist within a specialised environment.
In type 1 diabetes, the beta-cells are destroyed and glucose
levels rise in the blood because not enough insulin is being
produced. In type 2 diabetes, a frequent consequence of
obesity, tissues become resistant to insulin, again causing
blood glucose to rise. Beta-cell function also becomes
abnormal.
In two articles in the journal Diabetes and one each in
Development and Cell Metabolism, the researchers described
four main findings about islet vascularisation and innervation.
First, vascular endothelial growth factor A (VEGF-A) is
important for development of the islets’ blood supply and
for beta-cell proliferation. Blocking the growth factor early in
development in a mouse model ultimately reduced beta-cell
mass and insulin release and impaired glucose clearance from
the bloodstream.
Second, VEGF and other ‘signals’ released by the
endothelial cells lining the islet blood vessels consequently
stimulated growth of islet nerves in mice that connected to the
brain. ‘If the islets don’t become vascularised properly, they
don’t become innervated properly’, Dr Marcela Brissova,
who was co-author on three of the four articles, said. ‘These
signals also promote beta-cell growth.’
Third, VEGF-A was not involved when the beta-cell
mass increased in an obese mouse model of type 2 diabetes
in response to rising glucose levels. Unlike tumours, which
sprout new blood vessels as they grow, the beta-cell tissue
increased its blood supply by dilating existing vessels.
Finally, too much VEGF-A can lead to beta-cell death.
But that sets up a regenerative micro-environment involving
an interaction of vascular endothelial cells and macrophages,
which, in turn, leads to beta-cell proliferation both in mice
and human islets. ‘That’s very unusual because islet cells are
like neurons; once they’re dead, they don’t usually regrow’,
Brissova said. ‘We think that the endothelial cells and
macrophages that are recruited from bone marrow create an
environment that promotes the proliferation and regeneration
of those beta-cells.’
Source
erate.html