HPCSA serious injury narrative test guideline.

Current South African Road Accident Fund (RAF) legislation requires a medical determination of the seriousness of injuries sustained in motor vehicle accidents to determine whether the claimant is entitled to a claim for general damages. Such medical assessments are submitted in the form of RAF 4 Serious Injury Assessment Reports. Contested claims for serious injury are referred to the Health Professions Council of South Africa (HPCSA) Appeal Tribunals for final determination. The legislation prescribes 2 instruments, namely the American Medical Association (AMA) Guides (6th edition) and the Narrative Test for this purpose. Whereas the AMA Guides are published in a comprehensive book, and training courses are provided in their use, existing legislation does not provide any indication of the required structure, content or criteria of a Narrative Test report. This document is published by the HPCSA Appeal Tribunals as a guideline to the performance of the Narrative Test; what it is, reasons for applying it and who should compile it, as well as the required structure, content and criteria thereof. A Narrative Test Report should include relevant and meaningful comment in relation to each of the 6 sections described in the article. 

Long-chain polyunsaturated fatty acids protect the heart against ischemia/reperfusion-induced injury via a MAPK dependent pathway.

The mechanisms by which long-chain dietary polyunsaturated fatty acids (PUFAs) protect against cardiovascular disease are largely unknown. The present study determines the effects of eicosapentaenoic acid (EPA) and arachidonic acid (ARA) on the response of neonatal rat cardiomyocytes to simulated ischaemia (SI) and reperfusion (R). Myocytes isolated from 1-2 day old Wistar rat hearts were cultured with or without EPA or ARA and exposed to 1 h SI followed by 30 minutes reperfusion. Apoptosis was evaluated by caspase-3 activation, poly-(ADP-ribose) polymerase (PARP) cleavage and nuclear condensation. EPA (20microM) and ARA (20microM) significantly inhibited caspase-3 activation and PARP-cleavage and reduced the apoptotic index during reperfusion. Both fatty acids significantly increased ERK phosphorylation and decreased p38 phosphorylation during reperfusion. The mechanism of action of ARA on the MAPKs was further investigated with okadaic acid (to inhibit serine-threonine phosphatases) and orthovanadate (to inhibit tyrosine phosphatases). Vanadate, but not okadaic acid, significantly reduced ARA-induced inhibition of p38 phosphorylation, suggesting the involvement a tyrosine phosphatase during SI/R. Mitogen-activated protein kinase phosphatase-1 (MKP-1), a dual-specificity phosphatase, was targeted and a significant induction of MKP-1 by ARA and EPA was observed. It was demonstrated for the first time that EPA and ARA protect neonatal cardiac myocytes from ischaemia/reperfusion-induced apoptosis through activation of ERK as well as induction of a dual-specific phosphatase, causing dephosphorylation of the pro-apoptotic kinase, p38. The cardioprotective effects of EPA and ARA could also be demonstrated on the functional recovery of isolated perfused hearts subjected to global ischemia.

Traumatic dislocation of the hip in children. A report of 4 cases.

During a 1-year period 4 children, aged 4-14 years, suffering from traumatic dislocation of the hip were treated at H. F. Verwoerd Hospital. This is a rare injury and constitutes 0.335% of injuries seen in this unit. Two cases of anterior dislocations, which are even more rare, are included in this study. This article emphasises the importance of this injury in all cases of children subjected to severe trauma. However, as illustrated by 1 case, mild trauma may be sufficient to cause a dislocated hip in the young child.

Some effects of the essential fatty acids linoleic acid and alpha-linolenic acid and of their metabolites gamma-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and of prostaglandins A1 and E1 on the proliferation of human osteogenic sarcoma cells in culture.

Gamma-linolenic acid has been shown to suppress the rate of proliferation of a number of malignant cell lines in culture. To test the proposal that this was a specific prostaglandin 1- or 2-series effect, 379 batches of MG63 human osteogenic sarcoma cells were seeded in Greiner flasks and cultured in media supplemented with a range of unsaturated fatty acids and prostaglandins. The monounsaturated fatty acid oleic acid enhanced the rate of cancer cell proliferation. The polyunsaturated fatty acids linoleic acid, gamma-linolenic acid, arachidonic acid, alpha-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid, as well as prostaglandins E1 and A1 suppressed the rate of cell proliferation. Total suppression of colony forming and cell proliferation occurred at high levels of polyunsaturated fatty acid supplementation. In addition gamma-linolenic in the form of evening primrose seed oil and vitamin C has been given to 6 patients with histologically diagnosed primary liver cell cancer. Some clinical improvement and reduction in tumor size occurred in 3 cases. One patient has shown remarkable improvement in reduction of liver and tumor size on the CAT scan and reduction of the serum alkaline phosphatase from 2830 to 295 units and gamma-glutamyl transaminase from 274 to 82 units. Thus preliminary clinical results suggest that gamma-linolenic acid may be effective in the management of human cancer patients and further trials should be conducted. However, the cell culture results suggest that although the essential fatty acids suppress proliferation, eicosanoids of all 3 series may be involved. The proliferation suppressive effect of docosahexaenoic acid suggests that other aspects than only eicosanoid activity may also be important in the suppression of cancer cell proliferation.

Some effects of linoleic acid and gamma-linolenic acid on the proliferation of human hepatoma cells in culture.

In previous communications the growth-suppressive effect of gamma-linolenic acid (GLA) dissolved in sodium carbonate in the culture media of malignant cells has been reported. In this study we show that linoleic acid (LA), the fatty acid precursor of GLA, had no growth-suppressive effect on human hepatoma cells in culture while a similar concentration of GLA suppressed malignant cell growth in culture by 69% after 10 days. This growth-suppressive effect must therefore be seen as an effect of GLA and not as a 'soap' effect. It has also been shown that the growth rate of human hepatoma cells in culture to which GLA was added daily for 5 consecutive days remained suppressed after the withdrawal of GLA from the growth medium for a further 5-day period. The striking difference between GLA and LA as regards growth suppression of human hepatoma cells in culture appears to imply a metabolic block in the hepatoma cells, involving the enzyme delta-6-desaturase, in the conversion of LA to GLA and thence via dihomo-gamma-linolenic acid to the prostaglandins of the 1 series.

The effect of gamma-linolenic acid on the growth of human osteogenic sarcoma and oesophageal carcinoma cells in culture.

A statistically highly significant growth-suppressive effect of the prostaglandin precursor gamma-linolenic acid (GLA) on MG63 human osteogenic sarcoma and oesophageal carcinoma cells in culture was found. In view of the results reported on the growth-suppressive effect of GLA on cancer cells in culture, on transplanted mammary tumours in rats and in primary liver cancer patients, it would appear that further investigation of the effects of this fatty acid on cancer cell growth both in vitro and in vivo is warranted.

The reversibility of cancer: evidence that malignancy in human hepatoma cells is gamma-linolenic acid deficiency-dependent.

A further critical test of Horrobin's hypothesis that malignancy in cells may be dependent on gamma-linolenic acid (GLA) deficiency, has revealed that GLA supplementation produces a highly significant reduction in the growth rate (up to 87%) of a cultured human hepatoma cell line, compared with the growth rate of untreated hepatoma cells. This supports our previous suggestion that this hypothesis requires urgent further investigation at all levels including trials in human cancer patients.