Initiated chemical vapor deposition of antimicrobial polymer coatings.

The vapor phase deposition of polymeric antimicrobial coatings is reported. Initiated chemical vapor deposition (iCVD), a solventless low-temperature process, is used to form thin films of polymers on fragile substrates. For this work, finished nylon fabric is coated by iCVD with no affect on the color or feel of the fabric. Infrared characterization confirms the polymer structure. Coatings of poly(dimethylaminomethyl styrene) of up to 540 microg/cm2 were deposited on the fabric. The antimicrobial properties were tested using standard method ASTM E2149-01. A coating of 40 microg/cm2 of fabric was found to be very effective against gram-negative Escherichia coli, with over a 99.99%, or 4 log, kill in just 2 min continuing to over a 99.9999%, or 6 log, reduction in viable bacteria in 60 min. A coating of 120 microg/cm2 was most effective against the gram-positive Bacillus subtilis. Further tests confirmed that the iCVD polymer did not leach off the fabric.

Norepinephrine release in the rat pineal gland: the input from the biological clock measured by in vivo microdialysis.

The sympathetic innervation of the rat pineal gland was investigated, measuring the norepinephrine (NE) release by on-line in vivo microdialysis. NE was assayed using an HPLC method with precolumn derivatization and fluorescence detection. Its high sensitivity and reliability made it very suitable to monitor the low levels of NE in the dialysates (12.5 fmol during nighttime, 3 fmol during daytime). To increase NE levels, the monoamine reuptake inhibitor cocaine was added to Ringer's solution at concentrations of 10(-6) and 10(-5) M. This resulted in increases of neurotransmitter output of 167 and 219%, respectively, but did not change the qualitative and/or quantitative outcome of other experiments. Perfusion with 10(-6) M tetrodotoxin for 1 h resulted in a decrease of the NE release by >80%, whereas perfusion with the alpha 2-receptor antagonist yohimbine caused a twofold increase. These results indicate that the NE release in the rat pineal was of neuronal origin and regulated by a negative feedback mechanism involving inhibitory presynaptic alpha 2-receptors. Long-term (i.e., 16 h) measurements are described, showing the circadian properties of NE release. A pronounced rhythm is reported, showing extremely sharp transitions between low daytime and high nighttime values. Increases and decreases are reported to occur within the duration of collecting one sample (20 min). For comparison, the rhythm of melatonin release was also recorded. The on and off switches of the sympathetic input correlated well with the circadian rhythm of melatonin release and can thus be considered as the primary clock signal, inducing the nightly production of melatonin.