Understanding bamboo flowering based on large-scale analysis of expressed sequence tags.

Unlike other plants, bamboo (Bambusoideae) flowering is an elusive physiological phenomena, because it is unpredictable, long-periodic, gregarious, and uncontrollable; also, bamboo plants usually die after flowering. The flowering mechanism in Arabidopsis thaliana, a eudicot model species, is well established, but it remains unknown in bamboo species. We found 4470 and 3878 expressed sequence tags in the flower bud and vegetative shoot cDNA libraries, respectively, of the bamboo species, Bambusa oldhamii. Different genes were found expressed in bamboo flower buds compared to vegetative shoots, based on the Munich Information Center for Protein Sequences functional categorization; flowering-related genes were also identified in this species. We also identified Arabidopsis flowering-specific homologs that are involved in its photoperiod in this bamboo species, along with autonomous, vernalization and gibberellin-dependent pathways, indicating that bamboos may have a similar mechanism to control floral transition. Some bamboo expressed sequence tags shared high similarity with those of rice, but others did not match any known sequences. Our data lead us to conclude that bamboo may have its own unique flowering genes. This information can help us understand bamboo flowering and provides useful experimental methods to study the mechanisms involved.

Infusion of pH 2.0 D-chiro-inositol glycan insulin putative mediator normalizes plasma glucose in streptozotocin diabetic rats at a dose equivalent to insulin without inducing hypoglycaemia.

We compared the effects of infusing a chemically defined chiro-inositol glycan putative insulin mediator with an equivalent dose of insulin in low-dose (45 mg/kg) streptozotocin diabetic rats. Insulin decreased plasma glucose levels from 17.32 +/- 0.17 to 3.96 +/- 0.064 mmol/l (p < 0.0002) in 120 min, a decrease of 77.13%, while the putative mediator promoted a decrease in plasma glucose from 14.85 +/- 0.084 to 7.22 +/- 0.13 mmol/l (p < 0.007) in 60 min. The putative mediator maintained euglycaemia over the ensuing 60 min with a plasma glucose level of 7.01 +/- 0.10 mmol/l at 120 min. Thus, insulin further reduced the plasma glucose from euglycaemia at 60 min to produce hypoglycaemia at 120 min. The lack of production of hypoglycaemia by the putative mediator can be explained by its inhibition of glucose-stimulated insulin secretion by the islet beta cells, thus providing a potential negative feedback regulatory mechanism; or by its selective action on muscle to increase glycogen synthesis. The significance of these results in terms of future directions in drug design is herein considered.