The melting behaviour of gel-spun, ultra-high molecular weight polyethylene fibres was investigated in an attempt to characterize their morphology after various stages of hot-drawing at 148 ~ In this drawing process a shish-kebab morphology is transformed into a smooth fibrillar structure. It was concluded that this transition initially proceeds by pulling elastically inactive loops, originally present in the folded chain lamellae of the shish-kebabs, taut between entanglements. Thereafter a considerable amount of entanglements is removed by pulling molecular chain ends through them, until ca. 2.5 entangelements per molecule remain in the ultimately drawn fibres. The fibrils in the fully drawn fibres were found to be composed of chain-extended orthorhombic crystallites with an average length of 70 nm, which are interrupted by defect regions (containing trapped entanglements and chain ends) of about 4 nm in length. If free shrinkage of the fibre was allowed, this structure had an equilibrium melting temperature of 140.5 ~ Upon constrained melting of the filaments, a solid-solid phase transition could be observed in the DSC thermograms (at a temperature of ca. 150 ~ associated with a transition of the chain-extended orthorhombic blocks in the fibrils into a hexagonal phase. The heat effect associated with this solid-solid transition in perfectly crystalline polyethylene (AHo_ h) was estimated to be 205 kJ/kg, whereas for the heat of fusion of the hexagonal phase (AHh _ m) a value of 81 kJ/kg was assessed.

Increasing numbers of individuals are being referred to cardiogenetics outpatient clinics with potentially inherited arrhythmia (ARR) or cardiomyopathy (CM). To inform relatives at-risk, we ask index patients to distribute "family letters" containing information on the risks, possible genetic and other screenings, and preventive options. We assessed the responses to these letters in terms of referrals to a cardiologist and/or clinical geneticist. Fifty-six index patients were asked to distribute 249 family letters: 85 in the ARR group and 164 in the CM group. Within a mean follow-up period of 2 years (range 1-5 years) the number of relatives actually referred to the clinical geneticist and/or cardiologist was 57% (142 of 249). There was a significant difference (P < 0.01) between the ARR (80%) and CM groups (45.1%). To verify the results obtained from our files at the cardiogenetics department we sent a questionnaire to 52 index patients (response 50%). This showed that 23/26 (88%) index patients had distributed the letters to their relatives and that for 19/23 index patients one or more relatives had been screened. This is comparable with our files, which showed that 57% of relatives of index patients with a potentially inherited cardiac disease underwent screening, particularly in the ARR group. The actual response was underestimated because some relatives were investigated elsewhere or may still decide to be screened in the future. We conclude that distributing family letters is an effective way to inform and encourage relatives to undergo screening for high-risk inherited cardiac disease.