Voluntary disclosure of forward-looking earnings forecasts in Australia

This study examines the voluntary disclosure of future earnings information in annual reports for Australian listed companies. We find that most Australian companies in our sample do not provide quantitative earnings, forecasts in their annual reports, although more than half of the sample do disclose forward-looking information relating to earnings, without specifically disclosing point estimates for the future. These companies mostly supply qualitative information with a positive bias, while the remainder of the sample discloses no forward-looking information relating to earnings. Our findings also suggest that larger companies with less volatile earnings tend to provide more future earnings information than smaller companies with relatively volatile earnings.

Genetic disruption of the growth hormone receptor does not influence motoneuron survival in the developing mouse

In the rodent central nervous system (CNS) during the five days prior to birth, both growth hormone (GH) and its receptor (GHR) undergo transient increases in expression to levels considerably higher than those found postnatally. This increase in expression coincides with the period of neuronal programmed cell death (PCD) in the developing CNS. To evaluate the involvement of growth hormone in the process of PCD, we have quantified the number of motoneurons in the spinal cord and brain stem of wild type and littermate GHR-deficient mice at the beginning and end of the neuronal PCD period. We found no change in motoneuron survival in either the brachial or lumbar lateral motor columns of the spinal cord or in the trochlear, trigeminal, facial or hypoglossal nuclei in the brain stem. We also found no significant differences in spinal cord volume, muscle fiber diameter, or body weight of GHR-deficient fetal mice when compared to their littermate controls. Therefore, despite considerable in vitro evidence for GH action on neurons and glia, genetic disruption of GHR signalling has no effect on prenatal motoneuron number in the mouse, under normal physiological conditions. This may be a result of compensation by the signalling of other neurotrophic cytokines.