Chloroquine (CQ) is highly effective against P. vivax, due to the rapid spread of CQ resistance in P. falciparum parasites; it is no longer the drug of choice against P. falciparum. This study elucidates the scenario of chloroquine efficacy at times that coincided with a new drug policy and especially assessed the chloroquine resistant molecular markers after withdrawal of chloroquine in Kolkata and Purulia, two malaria endemic zones of West Bengal, India. In vitro CQ susceptibility was tested in 781 patients with P. falciparum mono infections between 2008 and 2013, of which 338 patients had received CQ in 2008–2009. Genotyping of the pfcrt and the pfmdr1 gene was carried out in all isolates. Early treatment failure was detected in 114 patients {43 (31·39%) from Kolkata and 71 (35·32%) from Purulia} while recrudescence was identified in 13 (9.49%) and 17 (8.46%) patients from Kolkata and Purulia respectively. In vivo chloroquine resistance was strongly associated with CVMNT-YYSNY (p < 0.01) and SVMNT-YYSNY (p < 0.05) allele in Kolkata. In Purulia chloroquine resistance was associated with CVMNK-YYSNY (P < 0.005), SVMNT-YYSNY (P < 0.01) allele. The proportion of in vitro chloroquine resistance increased in subsequent years to 87.23% and 93·10% in 2013, in Kolkata and Purulia, respectively. Isolates with SVMNT-YFSND, SVMNT-YFSNY, CVIET-YFSND and CVIET-YYSNY haplotypes increased gradually (p < 0.05) from 2010 to 2013, leading to a rise in IC50 (p < 0.05) of chloroquine. An increase in in vitro chloroquine resistance and candidate gene mutations even after five years of chloroquine withdrawal against P. falciparum calls for synchronized research surveillance and proper containment strategies.
Objective: Objective: To investigate the effect of the bioactive F-3 fraction from the rhizomes of Acorus calamus in experimentally induced hyperlipidemic rats. Materials and Methods: Materials and Methods: Doses of 10, 20 and 40 mg/kg of the bioactive fraction were evaluated for its effect on the lipid profile and fibrinogen levels in diet-induced hyperlipidemia. Additionally, apoprotein A1 and apoprotein B levels were estimated using immunoturbidimetric assays. Furthermore, the bioactive F-3 fraction was investigated for its mechanism of action by estimating HMG-CoA reductase activity and fecal cholesterol levels. Besides evaluating the free radical-scavenging activity using the Diphenyl picryl hydrazyl (DPPH) method, the high performance thin layer chromatography (HPTLC) fingerprint of the bioactive fraction was also developed. Results: Results: At doses of 20 and 40 mg/kg, the bioactive fraction significantly (P < 0.05) decreased the total cholesterol (TC) and low-density lipoprotein (LDL) levels. The bioactive F-3 fraction also attenuated the raised plasma fibrinogen levels. Fecal cholesterol excretion was significantly (P < 0.05) enhanced by the F-3 fraction while 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase) activity was depressed. Furthermore, the F-3 fraction also possessed an appreciable free radical scavenging activity. Conclusion: Conclusion: The results of the present study revealed that the bioactive F-3 fraction demonstrated its cholesterol-reducing effect by increasing fecal cholesterol excretion and decreasing cholesterol biosynthesis in the liver. Additionally, the effects on fibrinogen levels and free radicals indicate that the bioactive F-3 fraction could have a potentially beneficial effect in atherosclerosis associated with hyperlipidemia.
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