METHODOLOGY: All synthesized compounds were characterized by IR, NMR, Mass and elemental analysis followed by in vitro antimicrobial studies against Gram-positive (Staphylococcus aureus), Gram-negative (Salmonella typhi and Klebsiella pneumoniae) bacterial and fungal (Candida albicans and Aspergillus niger) strains by the tube dilution method. The in vitro anticancer evaluation was carried out against the human colorectal carcinoma cell line (HCT116), using the Sulforhodamine B assay.
RESULTS, DISCUSSION AND CONCLUSION: Compound W6 (MICsa, st, kp = 5.19 µM) emerged as a significant antibacterial agent against all tested bacterial strains i.e. Gram-positive (S. aureus), Gram-negative (S. typhi, K. pneumoniae) while compound W1 (MICca, an = 5.08 µM) was most potent against fungal strains (A. niger and C. albicans) and comparable to fluconazole (MIC = 8.16 µM). The anticancer screening demonstrated that compound W17 (IC50 = 4.12 µM) was most potent amongst the synthesized compounds and also more potent than the standard drug 5-FU (IC50 = 7.69 µM).
RESULTS: A comparative study between two methods, (microwave-assisted and conventional heating approaches), was performed to synthesise a new quinazoline derivative from 2-(2-aminophenyl)-1H-benzimidazole and octanal to produce 6-heptyl-5,6-dihydrobenzo[4,5]imidazo[1,2-c]quinazoline (OCT). The compound was characterised using FTIR, 1H and 13C NMR, DIMS, as well as X-ray crystallography. The most significant peak in the 13C NMR spectrum is C-7 at 65.5 ppm which confirms the cyclisation process. Crystal structure analysis revealed that the molecule grows in the monoclinic crystal system P21/n space group and stabilised by an intermolecular hydrogen bond between the N1-H1A…N3 atoms. The crystal packing analysis showed that the molecule adopts zig-zag one dimensional chains. Fluorescence study of OCT revealed that it produces blue light when expose to UV-light and its' quantum yield equal to 26%. Antioxidant activity, which included DPPH· and ABTS·+ assays was also performed and statistical analysis was achieved via a paired T-test using Minitab 16 software with P
METHODS: A total 98 in-hospital first ever acute stroke patients were recruited, and their Barthel Index scores were measured at the time of discharge, at 1 month and 3 months post-discharge. The Barthel Index was scored through telephone interviews. We employed the random intercept model from linear mixed effect regression to model the change of Barthel Index scores during the three months intervals. The prognostic factors included in the model were acute stroke subtypes, age, sex and time of measurement (at discharge, at 1 month and at 3 month post-discharge).
RESULTS: The crude mean Barthel Index scores showed an increased trend. The crude mean Barthel Index at the time of discharge, at 1-month post-discharge and 3 months post-discharge were 35.1 (SD = 39.4), 64.4 (SD = 39.5) and 68.8 (SD = 38.9) respectively. Over the same period, the adjusted mean Barthel Index scores estimated from the linear mixed effect model increased from 39.6 to 66.9 to 73.2. The adjusted mean Barthel Index scores decreased as the age increased, and haemorrhagic stroke patients had lower adjusted mean Barthel Index scores compared to the ischaemic stroke patients.
CONCLUSION: Overall, the crude and adjusted mean Barthel Index scores increase from the time of discharge up to 3-month post-discharge among acute stroke patients. Time after discharge, age and stroke subtypes are the significant prognostic factors for Barthel Index score changes over the period of 3 months.