Chlorhexidine digluconate is the active ingredient in mouthrinses used to prevent dental plaque and gingivitis. The in vitro cytotoxicity of chlorhexidine was evaluated with the Smulow-Glickman (S-G) gingival epithelial cell line. The potency of chlorhexidine was dependent on the length of exposure and composition of the exposure medium. The midpoint cytotoxicity values for 1-, 24-, and 72-h exposures were 0.106, 0.011, and 0.0045 mmol/L, respectively. S-G cells exposed for 2 h to chlorhexidine and then maintained for 48 h in chlorhexidine-free medium were unable to recover from the initial insult. The adverse effects of chlorhexidine on the plasma membrane were suggested by the leakage of lactic acid dehydrogenase from chlorhexidine-treated S-G cells and by the increased permeability of chlorhexidine-treated liposomes to Ca2+. The toxicity of a 24-h exposure to chlorhexidine to the S-G cells was progressively lessened as the content of fetal bovine serum (FBS) in the exposure medium was increased from 2% to 8%. The potency of a 1-h exposure to chlorhexidine was reduced in medium amended with albumin, lecithin, and heat-killed Escherichia coli. These reductions in toxicity were presumably due to the binding of the cationic chlorhexidine to the negatively charged chemical moieties of the components of FBS and of albumin and lecithin and of sites on the surfaces of bacteria. Combinations of chlorhexidine and carbamide peroxide were additive in their cytotoxicities.

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We investigated acute metabolic changes following parasagittal fluid-percussion brain injury in the rat, using high-resolution 1H nuclear magnetic resonance (NMR) spectroscopy. Sixty minutes following brain injury or sham (surgery, no injury) treatment, brains were rapidly removed and the injured and control cortices were isolated (n = 5/group). Isolates of brain cortices were then placed in buffer and studied in a 400-MHz spectrometer with measurements taken every 15 min over a 145-min period. At the initial NMR evaluation (immediately following dissection), we observed significantly lower levels of N-acetyl aspartic acid (NAA) in the injured group compared to the sham group. Surprisingly, a reciprocal increase in the concentration of acetate, a major metabolic product of NAA, was not observed at this timepoint. At subsequent timepoints, a progressive loss of NAA was observed in both injured and sham cortices, presumably due to ischemic conditions of the ex vivo samples. However, this progressive loss of NAA was now accompanied by a commensurate accumulation of acetate. These results suggest that (1) a decrease in the concentration of NAA occurs by 1 h following experimental brain trauma, potentially marking traumatic neural injury; (2) the initial absence of an expected reciprocal increase in acetate concentration may signify rapid utilization of acetate following trauma, potentially for reparative processes; and (3) in contrast to trauma alone, post mortem ischemic conditions may induce an increase in acetate concentrations.

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Air‐moisture maps were generated based on commercial microwave links data over N. Israel and compared for the first time to European Centre for Medium‐Range Weather Forecasts (ECMWF) ERA‐Interim maps for April 2017. Several skill scores of the different maps were calculated against the observed humidity from 39 weather stations. High correlations range, 0.75–0.9, were found between the new links' humidity fields and the stations. The numbers of best correlated links are found to be higher compared to ECMWF, that is, 31 stations versus 8. Also, in the measure of standard deviation the links performed better, 38 versus 1. However, for the mean humidity, the ECMWF is doing better, that is 14/25 for links/ECMWF. The links' humidity thus provides a more accurate picture of the observed moisture as compared to current weather prediction product. Consequently, the high‐resolution humidity fields obtained from the commercial microwave link seem to have the potential to improve future forecasting of precipitation.

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