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non-nucleoside reverse transcriptase inhibitor resistance due to the low genetic barrier to resistance and relatively preserved fitness of non-nucleoside reverse transcriptase inhibitor-resistant virus. 9 While the relationship between adherence and resistance may be complex, we want to be completely clear that we are not suggesting that good adherence is bad. Even with early HAART, every 10% improvement in adherence was associated with a 20% decrease in the risk of progression to AIDS and death. 10,11 Disease progression was slowed or halted in many highly adherent individuals who developed resistance on early HAART. Individuals who took too little of their medication to create drug resistance, in contrast, suffered the natural history of untreated HIV infection. Because of the unfortunate manner in which partially suppressive HAART became available in many western countries, we now have large populations of maximally adherent patients with highly resistant HIV. The goal now is to define optimal strategies for such patients while working to prevent this from happening in the future. High levels of adherence do not prevent the accumulation of drug resistance mutations to HIV antiretroviral therapy. Modeling the HIV protease inhibitor adherence-resistance curve by use of empirically derived estimates. the effects of adherence on resistance: use of local linear regression to reveal relationships between adherence and resistance in antire-troviral-naive patients treated with lopinavir/ritonavir or nelfinavir. Virologic rebound on HAART in the context of low treatment adherence is associated with a low prevalence of antiretroviral drug resistance. Drug resistance in patients experiencing early virological failure under a triple combination including indinavir. Low levels of adherence confer greater risk for non-nucleoside reverse transcrip-tase inhibitor resistance than protease-inhibitor resistance. (2002). Intermittent use of triple-combination therapy is predictive of mortality at baseline and after one year of follow-up. Novel gyrA and parC point mutations in two strains of Acinetobacter baumannii resistant to ciprofloxacin Sir, Acinetobacter baumannii are now resistant to most antibacterial drugs, with some centres reporting up to 80% of strains resistant to all aminoglycosides, and there is resistance to imipenem and sulbactam. In addition, resistance to ciprofloxacin has rapidly emerged in clinical isolates. 1 Fluoroquinolone resistance in A. baumannii has been associated with mutations in the gyrA and parC genes. 2,3 It has been found that the amino acid residues most frequently mutated in GyrA from A. baumannii occur at Ser-83 and Gly-81. 2 Ser-80 and Glu-84 were hotspots for mutation within ParC. 3 The purpose of …