The effect of dimethyl sulfoxide on tissue distribution of gentamicin

Summary Dimethyl sulfoxide (DMSO) and gentamicin were administered to rats i.p. No significant differences in gentamicin tissue concentrations were found between rats receiving DMSO and gentamicin, and rats receiving gentamicin alone. DMSO does not increase the tissue concentrations of gentamicin.     

Cerebrovascular reactivity to CO2: Modulation by arterial pressure

Summary Cerebrovascular reactivity to CO₂ (CO₂R), measured in halothane-anesthetized rabbits, decreased as arterial pressure was increased either pharmacologically or mechanically. On the other hand, hypotension, induced by bleeding, led to an increase in CO₂R. These responses were unaffected by denervation of baroreceptors.This work was supported by grants from NIH (HL 17903) and American Heart Association — Greater Los Angeles Affiliate (437IG). To whom requests for reprints should be sent.     

Compartmentalization of S-RNase and HT-B degradation in self-incompatible Nicotiana

Pollen-pistil interactions are crucial for controlling plant mating. For example, S-RNase-based self-incompatibility prevents inbreeding in diverse angiosperm species. S-RNases are thought to function as specific cytotoxins that inhibit pollen that has an S-haplotype that matches one of those in the pistil. Thus, pollen and pistil factors interact to prevent mating between closely related individuals. Other pistil factors, such as HT-B, 4936-factor and the 120 kDa glycoprotein, are also required for pollen rejection but do not contribute to S-haplotype-specificity per se. Here we show that S-RNase is taken up and sorted to a vacuolar compartment in the pollen tubes. Antibodies to the 120 kDa glycoprotein label the compartment membrane. When the pistil does not express HT-B or 4936-factor, S-RNase remains sequestered, unable to cause rejection. Similarly, in wild-type pistils, compatible pollen tubes degrade HT-B and sequester S-RNase. We suggest that S-RNase trafficking and the stability of HT-B are central to S-specific pollen rejection.