Background:Pharmacovigilance is a useful to assure the safety of medicines and protect consumers from their harmful effects. Healthcare professionals should consider Adverse Drug Reaction (ADR) reporting as part of their professional obligation and participate in the existent pharmacovigilance programs in their countries. In India, the National PV Program was re-launched in July 2010.Objectives:This survey was conducted in order to assess the knowledge, attitude and practice of Indian pharmacists with the aim of exploring the pharmacists’ participation in ADR reporting system, identifying the reasons of under reporting and determining the steps that could be adopted to increase reporting rates.Materials and Methods:A cross-sectional survey was carried out among the pharmacists in India using a pretested questionnaire with 33 questions (10 questions on knowledge, 6 on attitude, 7 on practice, 7 on future of ADR reporting in India and 3 on benefits of reporting ADRs.). The study was conducted, over a period of 3 months from May 2012 to July 2012.Results:Out of the 600 participants to whom the survey was administered, a total of 400 were filled. The response rate of the survey was 67%. 95% responders were knowledgeable about ADRs. 90% participants had a positive attitude towards making ADRs reporting mandatory for practicing pharmacists. 87.5% participants were interested in participating in the National Pharmacovigilance program, in India. 47.5% respondents had observed ADRs in their practice, and 37% had reported it to the national pharmacovigilance center. 92% pharmacists believed reporting ADRs immensely helped in providing quality care to patients.Conclusion:The Indian pharmacists have poor knowledge, attitude, and practice (KAP) towards ADR reporting and pharmacovigilance. Pharmacists with higher qualifications such as the pharmacists with a PharmD have better KAP. With additional training on Pharmacovigilance, the Indian Pharmacists working in different sectors can become part of ADR reporting system.

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The main purpose of this research was to study the mechanism of drug release from solid dispersions of albendazole, giving special emphasis to particle size of the drug in solid dispersions. Solid dispersions were prepared using three different carriers, mixing ratios and methods in an attempt to improve the solubility and dissolution rate of albendazole. The mechanism of enhanced dissolution was investigated by a novel dissolution technique as an adjunct to phase solubility study, wettability test, differential scanning calorimetry, X-ray diffractometry, infrared spectroscopy and scanning electron microscopy. The solubility of albendazole was greater with albendazole-poloxamer 407 system, while polyethylene glycol dispersions showed predominant wettability. Physical mixtures showed enhanced dissolution compared with the pure drug, due to improved wetting and solubilization of drug in the diffusion layer offering carrier-rich microenvironment. Preparation of solid dispersion further improved the dissolution compared to the physical mixture, owing to increased surface area for mass transfer, thermodynamically enhanced dissolution of a higher energy amorphous form from the carrier, in addition to improved wetting and solubilization. All carriers showed comparable degree of drug particle size reduction, whereas mixing ratio and method of preparation substantially affected the particle size. Intermolecular association of drug with the carrier led to inhibition of drug recrystallization.

The compound 5-(4-methoxyarylimino)-2-N-(3,4-dichlorophenyl)-3-oxo-1,2,4-thiadiazolidine (P 3 -25) is known to possess antibacterial, anti-fungal, anti-tubercular, and local anesthetic activities. We studied the anti-tumorigenic activity of P 3 -25 and the role of nuclear transcription factor kappaB (NF-jB) in this process. In constitutive NF-jB-expressing cells, treatment with P 3 -25 inhibited the expression of NF-jB-dependent reporter gene, adhesion molecules, and cyclooxygenase. It downregulated phosphorylation of p65 by inhibiting upstream kinases, such as protein kinase A and casein kinase II, but did not alter NF-jB DNA-binding activity. Alone, P 3 -25 induced apoptosis in NF-jB-expressing and doxorubicin-resistant breast cancer cells, and in the presence of other chemotherapeutic agents, it potentiated apoptosis. Overall, our results suggest that P 3 -25 exerts antitumorigenic activity by inhibiting phosphorylation of p65, the transcriptionally active subunit of NF-jB by inhibiting its upstream kinases, and potentiates apoptosis mediated by chemotherapeutic agents. These results suggest novel approaches for designing of anticancer drugs for combination chemotherapy.

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