Living in the same household - ‘Incest’ in the family of sport

This article focuses on the coach/athlete relationship in the self admitted sporting ‘family’ and, using both the provisions of the Sexual Offences Act 2003 and the civil law remedies of non-molestation orders argues that where matters of abuse are concerned, the private world of the surrogate family of sport could be just as liable under family law principles as any other modern day informal family

Circadian clocks and breast cancer

Circadian clocks respond to environmental time cues to coordinate 24-hour oscillations in almost every tissue of the body. In the breast, circadian clocks regulate the rhythmic expression of numerous genes. Disrupted expression of circadian genes can alter breast biology and may promote cancer. Here we overview circadian mechanisms, and the connection between the molecular clock and breast biology. We describe how disruption of circadian genes contributes to cancer via multiple mechanisms, and link this to increased tumour risk in women who work irregular shift patterns. Understanding the influence of circadian rhythms on breast cancer could lead to more efficacious therapies, reformed public health policy and improved patient outcome

Analysis of trends in total and aidsrelated deaths certified at Mosvold Hospital, Ingwavuma, KwaZulu-Natal, from 2003 to 2008

Objectives. To analyse mortality trends from deaths registered at Mosvold Hospital, Ingwavuma, KwaZulu-Natal, and possible impact of programmes to treat and prevent HIV infection. Design. Longitudinal study of death certifications from 2003 to 2008. Setting. Mosvold Hospital mortuary, Ingwavuma. Subjects. Counterfoils of form 83/BI-1663, Notification/Register of Death/Stillbirths (Republic of South Africa, Department of Home Affairs), completed at Mosvold Hospital from January 2003 to December 2008. Outcome measures. Age at death, cause of death, patterns of deaths grouped by age, gender and cause of death. Results. AIDS-related deaths were the cause of 53% of deaths, particularly affecting the 20 - 59-year and under-5 age groups. Since 2005 there has been a decline in deaths in the 20 - 59 age group and an increase in average age at death. Conclusions. The decrease in mortality from 2005 may be associated with antiretroviral roll-out reducing mortality from AIDS-related illnesses

Impact of HIV/AIDS on deaths certified at Mosvold Hospital, Ingwavuma, Northern KwaZulu- Natal from January to August 2003

An analysis of the causes of death certified at Mosvold Hospital, Ingwavuma demonstrates the impact of HIV/AIDS in the region. HIV/AIDS appears to be responsible for about 45% of registered deaths in both males and females after the age of nine years. There is a significant difference in the mean age at death between males and females succumbing to the disease after the age of nine years: the average age at death of females from HIV/AIDS is 35 years, and the average age for males is 40 years. The younger average age of death from HIV/AIDS in females, together with a higher expected age of death from non-HIV causes, means that females lose considerably more years of life due to HIV/AIDS than males. The figures for this part of northern KwaZulu-Natal indicate a higher impact of HIV/AIDS on deaths than in previous assessments for South Africa as a whole.SA Fam Pract 2005;47(1): 51-5

BRCA2 Regulates Transcription Elongation by RNA Polymerase II to Prevent R-Loop Accumulation.

The controlled release of RNA polymerase II (RNAPII) from promoter-proximal pausing (PPP) sites is critical for transcription elongation in metazoans. We show that the human tumor suppressor BRCA2 interacts with RNAPII to regulate PPP release, thereby preventing unscheduled RNA-DNA hybrids (R-loops) implicated in genomic instability and carcinogenesis. BRCA2 inactivation by depletion or cancer-causing mutations instigates RNAPII accumulation and R-loop accrual at PPP sites in actively transcribed genes, accompanied by γH2AX formation marking DNA breakage, which is reduced by ERCC4 endonuclease depletion. BRCA2 inactivation decreases RNAPII-associated factor 1 (PAF1) recruitment (which normally promotes RNAPII release) and diminishes H2B Lys120 ubiquitination, impeding nascent RNA synthesis. PAF1 depletion phenocopies, while its overexpression ameliorates, R-loop accumulation after BRCA2 inactivation. Thus, an unrecognized role for BRCA2 in the transition from promoter-proximal pausing to productive elongation via augmented PAF1 recruitment to RNAPII is subverted by disease-causing mutations, provoking R-loop-mediated DNA breakage in BRCA2-deficient cells

Audit of efficacy of CoartemTM to clear plasmodium falciparum malaria parasitaemia at single forty-two day follow-up

Background; A study, which included a follow-up study, was undertaken to assess the efficacy of CoartemTM tablets (20 mg artemether and 120 mg lumefantrine – Novartis South Africa (Pty) Ltd) to clear plasmodium falciparum malaria parasitaemia at a single 42-day follow-up, with 42 days being chosen in order to detect early emergence of resistance. The study was done at Ndumo Clinic and Mosvold Hospital in the Ingwavuma District of KwaZulu-Natal, South Africa in January/February 2002. Method: The study included 37 patients presenting to Ndumo Clinic and two presenting to Mosvold Hospital with uncomplicated malaria diagnosed by symptoms and a positive immunochromographic test (ICT) for plasmodium falciparum. The main outcome measures were done using a Trophozoite count on thick film and polymerase chain reaction parasite analysis of blood spot at day 42. Results: Only 31 of the 37 recruited patients were confirmed to be suffering from malaria by polymerase chain reaction (PCR). Of the 31, 24 returned for follow-up. One patient had parasitaemia at day 33, but tested negative at day 42 after re-treatment with Coartem™. It was not determined whether this patient was suffering from a recrudescence or re-infection of falciparum malaria. All the other returning patients tested negative for falciparum malaria on blood film and PCR examination. Conclusions : CoartemTM still appears to be an effective treatment for falciparum malaria. Regular assessment of its efficacy is desirable. For full text, click here:SA Family Pract 2004;46(6): 21-2

Audit of failure rate of sulfadoxine/pyrimethamine combined with chloroquine to treat falciparum malaria at single fourteen-day follow-up

Objective. To assess the failure rate of the present first line treatment regime for uncomplicated falciparum malaria of sulfadoxine/pyrimethamine combined with chloroquine. Design. A before-after study1 Setting. Ndumo Clinic, Ingwavuma District, South Africa, October 2000 Study Group. 55 patients presenting to Ndumo clinic with uncomplicated malaria and malaria trophozoites visible on thin film. Main outcome measures:Trophozoite count on thick film at day 14. Results. 15 out of 37 patients who returned for follow-up still had trophozoites on thick film. Symptoms of most patients at day 0 and day 14 were mild, parasite counts before and after treatment were low, and trophozoites were atypical. Conclusions. There appears to be an unacceptably high day 14 failure rate with the combination of sulfadoxine/pyrimethamine and chloroquine.The mildness of symptoms, low parasite counts and atypical trophozoites suggest immunity to falciparum malaria amongst the local population. With few antimalarials to chose from, the difficult question as to future treatment of uncomplicated malaria arises. Keywords: Falciparum malaria, chloroquine, sulfadoxine, pyrimethamine SA Fam Prac Vol.25(3) 2002: 4-

Hooge's Constant of Carbon Nanotube Field Effect Transistors

The 1/f noise in individual semiconducting carbon nanotubes (s-CNT) in a field effect transistor configuration has been measured in ultra-high vacuum and following exposure to air. The amplitude of the normalized current spectral noise density is independent of source-drain current, indicating the noise is due to mobility rather than number fluctuations. Hooge's constant for s-CNT is found to be 9.3 plus minus 0.4x10^-3. The magnitude of the 1/f noise is substantially degreased by exposing the devices to air

Molecular analysis of an echovirus 3 strain isolated from an individual concurrently with appearance of islet cell and IA-2 autoantibodies

Growing evidence has implicated members of the genus Enterovirus of the family Picornaviridae in the etiology of some cases of type I diabetes (T1D). To contribute to an understanding of the molecular determinants underlying this association, we determined the complete nucleotide sequence of a strain of echovirus 3 (E3), Human enterovirus B (HEV-B) species, isolated from an individual who soon after virus isolation developed autoantibodies characteristic of T1D. The individual has remained positive for over 6 years for tyrosine phosphatase-related IA-2 protein autoantibodies and islet cell autoantibodies, indicating an ongoing autoimmune process, although he has not yet developed clinical T1D. The sequence obtained adds weight to the observation that recent enterovirus isolates differ significantly from prototype strains and provides further evidence of a role for recombination in enterovirus evolution. In common with most HEV-B species members, the isolate exhibits 2C and VP1 sequences suggested as triggers of autoimmunity through molecular mimicry. However, comparisons with the E3 prototype strain and previously reported diabetogenic and nondiabetogenic HEV-B strains do not reveal clear candidates for sequence features of PicoBank/DM1/E3 that could be associated with autoantibody appearance. This is the first time a virus strain isolated at the time of commencement of beta-cell damage has been analyzed and is an invaluable addition to enterovirus strains isolated previously at the onset of T1D in the search for specific molecular features which could be associated with diabetes induction