The present study concentrates on the catalytic pyrolysis of a waste bio-packaging material, namely, jute, under iso-thermal and non-isothermal conditions using a 50 mm diameter and 164 mm long semi-batch pyrolyzer and a TGA set-up, respectively.
Aim and objectives: Among the various SSRI and 5-HT-1A, partial agonist vilazodone is one of them. It has antidepressant and anti-anxiety activities. This method's main aim and the objective was to develop and validate a bio-analytical method of Vilazodone in human plasma by LC-MS/MS (API-4000) and its application to estimate pharmacokinetics. Method: For reporting this investigation, Analyst software, 1.6.3 used. The mobile phase was acetonitrile with 0.1% formic acid as an organic solvent and Milli Q water with 10Mm ammonium acetate and 0.1% formic acid using the gradation method 7.0min run time. The calibration standard concentrations were 1.0 to 64 ng/ml. Plasma precipitation was by protein precipitation technique. Result: The accuracy of calibration concentrations of Vilazodone was 93.5-104.39% and stability study showed 96.41-106.71%, 94.77-96.36%, 92.22-101.38%, 94.15-98.47%, 93.95-95.75% remaining for freeze-thaw, short term, long term, benchtop and autosampler stability respectively. Recovery was to be 98.10-98.99%; the matrix factor was 0.94-0.96. The maximum plasma concentration of reference preparation was 13.445±2.842ng/ml (Cmax) at a time 6.792±0.846hr. (Tmax). The maximum plasma concentration of test preparation was 13.218±3.231ng/ml (Cmax) at a time 6.958±0.793hr (Tmax) The relative bioavailability of the test preparation was to be 94.66 % of that of the reference preparation. Conclusion: The present investigation was highly selective, sensitive, reproducible, low matrix effect, high recovery and low time-consuming method. It was validated as per USFDA and EMA guideline and successfully used in comparative pharmacokinetics.
The role of macrophage activation in the candidacidal activity of liposome-incorporated (L) amphotericin B was investigated. Macrophages treated with L-amphotericin B killed Candida albicans more effectively than did macrophages treated with free (F) amphotericin B. However, macrophages treated with neither F- nor L-amphotericin B killed amphotericin B-resistant Candida tropicalis. In vivo stimulation of macrophages by intraperitoneal administration of thioglycollate, Freund's complete adjuvant, or heat-killed C. albicans followed by in vitro treatment with F- or L-amphotericin B, did not enhance their candidacidal activity. Intravenous administration of F- or L-amphotericin B did not augment the candidacidal activity of macrophages sensitized in vivo; however, sensitized macrophages showed enhanced killing compared with resident unstimulated cells. These studies suggest that macrophage-mediated enhancement of C. albicans killing may be due to uptake, transport, and delivery of L-amphotericin B to infected sites rather than to macrophage activation.
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