The prevalence of hepatitis B (Australia) antigen in Southern Africa

The prevalence of hepatitis B (Australia) antigen (HBAg) in 38 941 apparently healthy persons of various ethnic groups living in the Transvaal was determined by countercurrent immuno-electrophoresis or by complement fixation. The prevalence was 0,09 - 0,6% in  healthy Whites, 0,9% in Coloured donors, 2,0% in urban Negroes and 7"10 in rural male Blacks. The positivity rate in 444 healthy Black subjects and in 423 Sana (Bushmen) inhabiting areas in the northern and north-western regions of Southern Africa ranged from 2,7 to 15,8%. An assessment of the frequency of HBAg in various tribal groups of either Sana (Bushmen) or rural Blacks indicated that geographical environment might be one of the factors influencing antigenaemia in healthy persons. The prevalence was highest in persons originating from the west coast regions of Southern Africa, in adjoining territories proceeding from the central plateau, and those countries north of this area (9,1 - 13,6%) An intermediate prevalence of 6 - 7% was noted in some regions abutting on the east coast strip, and a lower prevalence was recorded for inland regions, including Lesotho, the eastern Orange Free State, Natal Midlands and Zululand (4 - 4,7%), while the lowest frequency was found in northern Natal and the central Transvaal areas (2 - 3%). A small group of Sana in the north-eastern corner of South West Africa who had an incidence of 2,7% was the only one which did not fit in with the general geographical distribution of HBAg observed.S. Afr. Med. J., 48, 941 (1974)

Smad2 and Smad4 gene mutations in hepatocellular carcinoma

TGF-β is a negative regulator of liver growth. Smad family of genes, as mediators of TGF-β pathway, are candidate tumor suppressor genes in hepatocellular carcinoma (HCC). We studied 35 HCC and non-tumour liver tissues for possible mutations in Smad2 and Smad4 genes. Three tumours displayed somatic mutations; two in Smad4 (Asp332Gly and Cys401Arg) and one in Smad2 (Gln407Arg) genes. All three mutations were A:T → G:C transitions suspected to result from oxidative stress as observed in mitochondrial DNA. These observation demonstrate that TGF-β pathway is altered in hepatocellular carcinoma

National strategy for the prevention and management of transfusion-associated hepatitis

The screening of potential blood donors for the hepatitis B (HBV) and C (HCV) viruses has decreased the risk of transfusion-associated hepatitis, There remains. however, a lack of consensus on a number of issues including methods for screening of blood donors and the management of donors found to have markers of hepatitis virus infection. This document outlines the recommendations of a large group of interested individuals including blood transfusion service managers, primary care health authorities, epidemiologists, Virologists, pathologists, gastroenterologists and hepatologists drawn from both the public and the private sector

Associations Between Aldosterone-Renin-Ratio and Bone Parameters Derived from Peripheral Quantitative Computed Tomography and Impact Microindentation in Men

OnlinePublComponents of the renin-angiotensin-aldosterone system (RAAS) are present on bone cells. One measure of RAAS activity, the aldosterone-renin-ratio (ARR), is used to screen for primary aldosteronism. Associations between ARR and bone mineral density are conflicting. This study investigated associations between ARR and peripheral quantitative computed tomography (pQCT) and impact microindentation (IMI). Male participants (n = 431) were from the Geelong Osteoporosis Study. "Likely" primary aldosteronism was defined as ARR ≥ 70 pmol/mIU. Another group, "possible" primary aldosteronism, was defined as either ARR ≥ 70 pmol/mIU or taking a medication that affects the RAAS, but not a beta blocker, and renin  0.05). There were no associations between ARR or aldosterone and pQCT-derived bone parameters. Men with likely primary aldosteronism had lower bone area, suggesting clinically high levels of ARR may have a negative impact on bone health.Kara L. Holloway-Kew, Kara B. Anderson, Pamela Rufus, Membere, Monica C. Tembo, Sophia X. Sui, Natalie K. Hyde, Mark A. Kotowicz, Stella M. Gwini, Jun Yang, Adolfo Diez, Perez, Maciej Henneberg, Wan, Hui Liao, Julie A. Pasc