Effective laser ablation of enamel and dentine without thermal side effects.

We present a feasibility study into laser treating dental materials by using femtosecond pulses generated by a titanium:sapphire laser system which consisted of an oscillator and a regenerative amplifier. The pulse duration was varied between 200 fs and 2 ps. The observed energy thresholds for the ablation process of dentine and enamel were clearly smaller than those observed when longer pulse durations were used. The consequence of this observation is a lower thermal load within the vicinity of the radiated area. Thus no thermal damage or mechanical damage, such as cracks, were produced during the laser treatment. Commercially available femtosecond laser systems can produce ablation rates in healthy and in-vitro demineralized dental material 2 mm3 per min and 6-16 mm3 per min, respectively. These values are an order of magnitude larger than those produced by picosecond laser systems at the same time pulse energy and pulse repetition rate. The brightness of the plasma spark generated by the laser treatment depended on the dimineralization of the teeth. This may allow online control of the laser treatment.

Derivatives of 1-beta-D-ribofuranosylbenzimidazole 3',5'-phosphate that mimic the actions of adenosine 3',5'-phosphate (cAMP) and guanosine 3',5'-phosphate (cGMP).

A series of new analogues of 1-beta-D-ribofuranosylbenzimidazole 3',5'-phosphate (cBIMP) has been designed according to the properties predicted by the MNDO method, and synthesised from substituted benzimidazoles. Dipole vectors and HOMO and LUMO energies for each benzimidazole base were calculated by the MNDO method and the lipophilicities of the cBIMP derivatives were determined. In general, the cBIMP derivatives activate cAMP-dependent protein kinases I and II and preferentially bind to site B, especially for the type II kinase, with 2-trifluoromethyl-cBIMP and 5,6-difluoro-cBIMP exhibiting the highest site selectivity. Each cBIMP derivative can stimulate cGMP-stimulated cyclic phosphodiesterase (cGS-PDE), with 5,6-dimethyl-cBIMP being as potent as cGMP, and also inhibit cGMP-inhibited phosphodiesterase (cGI-PDE). Only the 2-trifluoromethyl-cBIMP and the Rp-phosphorothioates (cBIMPS) (equatorial P = S) were resistant to hydrolysis by cPDE. The Sp-phosphorothioates were hydrolysed slowly, if at all. In addition to exhibiting a high lipophilicity, the most active compounds for the induction of apoptosis and inhibition of proliferation were also resistant to cPDE (Sp-5,6-dichloro-cBIMPS) and/or were potent activators of cAMP-dependent protein kinase (5,6-dichloro-cBIMP).