The role of epidemiology in cancer prevention

1. ISA Brown and Shaver 288 pullets were changed from 8 h to 8, 10, 13 or 16 h photoperiods at 42, 63, 84, 105, 126 or 142 d of age. 2. Age at first egg (AFE) was curvilinearly affected by the size and timing of the change in photoperiod. AFE was advanced most by a photoperiod change from 8 to 13 h made at 63 or 84 d. ISA birds were generally more responsive than Shaver to the photoperiod changes. 3. Longer photoperiods significantly increased survivors' egg production, but decreased liveability to 504 d. so that eggs per hen housed were unaffected. Retarding AFE by 10 d reduced survivors' egg numbers by 7.0, but increased mean egg weight by 1.26 g. Egg output by Shaver birds was unaffected by AFE, but that of ISA was curvilinearly affected, with an apogee at an AFE of 135 d. In both breeds, egg weight and egg output were greater following an early or late, rather than a mid-term photostimulation. 4. Photoperiod significantly increased mean daily food intake during lay by 1.26 g/h. A 10 d retardation in AFE resulted in a reduction in food intake of 1 g/d. Efficiency of food conversion deteriorated according to the square of the photoperiod, and changed curvilinearly according to age at photostimulation. Food conversion efficiency improved by 0.05 g/g for each 10 d delay in AFE. 5. Shell quality was unaffected by AFE, but deteriorated with increasing photoperiod and was curvilinearly affected by age at photostimulation with the smallest shell weights associated with photostimulation at 63 d. The incidence of double-yolked (DY) egg production increased with photoperiod and decreased with delayed photostimulation. There was an exponential regression of DY eggs on AFE. 6. Body weight at first egg increased by 75 g/d delay in AFE, but body weight at 504 d of age was unaffected by AFE, photoperiod or age at photostimulation. Body weight gain during lay increased by 15 g/h increase in photoperiod, decreased by 6 g per 10 d delay in photostimulation and by 40 g per 10 d delay in AFE. Fat content at 504 d increased by about 10 g/kg and by 23 g/bird for each 10 d delay in AFE. 7. Mortality in lay increased by 0.8%/h increase in photoperiod, but was unaffected by either age at photostimulation or AFE.     

Thrombolytic therapy in stroke. What do clinical tests prove?

Despite the increased risk of intracranial haemorrhage associated with the use of thrombolytic treatment of stroke. American studies have shown patients treated with rt-PA (recombinant plasminogen activator) within three hours of the onset of symptoms to manifest 30 per cent less disability at three-month follow-up than those placebo. However, until satisfactory criteria for the use of rt-PA are available, caution is essential, and thrombolytic therapy should be restricted to specialised centres. It is also important to promote public awareness of the stroke patient's need of immediate treatment at a specialised stroke unit.     

Psychosocial barriers to health promotion in an American Indian population

Northern Plains Indians (N = 200) completed the Indian Specific Health Risk Appraisal and measures assessing beliefs about risk factors and personal risk. Participants rated personal risk optimistically, judged their risk factor standing as superior to that of their peers, and neglected to consider risk factor standing when appraising personal risk. Moreover, participants were often not improving their standing on risk factors they considered relevant to their health. Such biases in health beliefs may prevent health interventions from being successful.     

The KDEL receptor, ERD2, regulates intracellular traffic by recruiting a GTPase-activating protein for ARF1

The small GTPase ADP-ribosylation factor 1 (ARF1) is a key regulator of intracellular membrane traffic. Regulators of ARF1, its GTPase-activating protein (GAP) and its guanine nucleotide exchange factor have been identified recently. However, it remains uncertain whether these regulators drive the GTPase cycle of ARF1 autonomously or whether their activities can be regulated by other proteins. Here, we demonstrate that the intracellular KDEL receptor, ERD2, self-oligomerizes and interacts with ARF1 GAP, and thereby regulates the recruitment of cytosolic ARF1 GAP to membranes. Because ERD2 overexpression enhances the recruitment of GAP to membranes and results in a phenotype that reflects ARF1 inactivation, our findings suggest that ERD2 regulates ARF1 GAP, and thus regulates ARF1-mediated transport.