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Armstrong Boel posted an update 6 months, 2 weeks ago
Interference from related memories is generally considered one of the major causes of forgetting in human memory. The most prevalent form of interference may be proactive interference (PI), which refers to the finding that memory of more recently studied information can be impaired by the previous study of other information. PI is a fairly persistent effect, but numerous studies have shown that there can also be release from PI. PI buildup and release have primarily been studied using paired-associate learning, the Brown-Peterson task, or multiple-list learning. The review first introduces the three experimental tasks and, for each task, summarizes critical findings on PI buildup and release, from both behavioral and imaging work. Then, an overview is provided of suggested cognitive mechanisms operating on the encoding and retrieval stages as well as of neural correlates of these mechanisms. The results indicate that, in general, both encoding and retrieval processes contribute to PI buildup and release. Finally, empirical gaps in the current work are emphasized and suggestions for future studies are provided.The drug resistance of Plasmodium vivax in clinical cases remains largely unknown till date because of the difficulty in diagnosing the resistant P. vivax strains. The present study was undertaken to determine the prevalence of mutant alleles in drug resistance genes viz P. vivax multi-drug resistance (pvmdr-1), chloroquine resistance transporter (pvcrt-o), dihydrofolate reductase (pvdhfr) and dihydropteroate synthase (pvdhps) along with in vitro chloroquine (CQ) sensitivity in P. vivax clinical isolates. During August-October 2017 a total of 86 samples of the febrile patients were screened and 31 samples were found to be positive for P. vivax in Safdarjung hospital, New Delhi. Sequence genotyping of the drug resistance genes was carried out in these P. Selleckchem Varoglutamstat vivax samples and in vitro CQ susceptibility for 23 isolates was determined by the schizont maturation assay (SMA). The CQ inhibitory concentrations (IC50) for the clinical isolates was found to be in the range of 25.6-176.7 nM. All the 31 clinical isolates analyzed for pvmdr-1 gene, showed mutant alleles and in only two isolates novel mutations at 861 and 898 codons were observed. Sequence analysis of pvcrt-o, pvdhfr and pvdhps genes revealed wild type genotypes in all the 31 studied isolates. The presence of mutations in pvmdr-1 gene and the increase in the CQ IC50 value indicates the possibility of shift in drug tolerance where CQ with primaquine (PQ) is still the first line of treatment for P. vivax malaria in the country. The regular molecular surveillance in P. vivax would provide useful information for the policy makers of the malaria control programme.
The orbitofrontal cortex (OFC) is implicated in depression. The hypothesis investigated was whether the OFC sensitivity to reward and nonreward is related to the severity of depressive symptoms.
Activations in the monetary incentive delay task were measured in the IMAGEN cohort at ages 14 years (n= 1877) and 19 years (n= 1140) with a longitudinal design. Clinically relevant subgroups were compared at ages 19 (high-severity group n= 116; low-severity group n= 206) and 14.
The medial OFC exhibited graded activation increases to reward, and the lateral OFC had graded activation increases to nonreward. In this general population, the medial and lateral OFC activations were associated with concurrent depressive symptoms at both ages 14 and 19 years. In a stratified high-severity depressive symptom group versus control group comparison, the lateral OFC showed greater sensitivity for the magnitudes of activations related to nonreward in the high-severity group at age 19 (p= .027), and the medial OFC showed decreased sensitivity to the reward magnitudes in the high-severity group at both ages 14 (p= .002) and 19 (p= .002). In a longitudinal design, there was greater sensitivity to nonreward of the lateral OFC at age 14 for those who exhibited high depressive symptom severity later at age 19 (p= .003).
Activations in the lateral OFC relate to sensitivity to not winning, were associated with high depressive symptom scores, and at age 14 predicted the depressive symptoms at ages 16 and 19. Activations in the medial OFC were related to sensitivity to winning, and reduced reward sensitivity was associated with concurrent high depressive symptom scores.
Activations in the lateral OFC relate to sensitivity to not winning, were associated with high depressive symptom scores, and at age 14 predicted the depressive symptoms at ages 16 and 19. Activations in the medial OFC were related to sensitivity to winning, and reduced reward sensitivity was associated with concurrent high depressive symptom scores.
To report the 2-year efficacy and safety of abicipar every 8 weeks and quarterly (after initial doses) compared with monthly ranibizumab in patients with treatment-naïve neovascular age-related macular degeneration (nAMD).
Two multicenter, randomized, phase 3 clinical trials with identical protocols (CEDAR and SEQUOIA). Analyses used pooled trial data.
The trials enrolled 1888 patients (1 eye/patient) with active choroidal neovascularization secondary to age-related macular degeneration and best-corrected visual acuity (BCVA) of 24 to 73 Early Treatment Diabetic Retinopathy Study letters.
At enrollment, patients were assigned to study eye treatment with abicipar 2 mg every 8 weeks after initial doses at baseline and weeks 4 and 8 (abicipar Q8, n= 630), abicipar 2 mg every 12 weeks after initial doses at baseline and weeks 4 and 12 (abicipar Q12, n= 628), or ranibizumab 0.5 mg every 4 weeks (ranibizumab Q4, n= 630).
Efficacy measures included stable vision (<15-letter loss in BCVA from baseline) a with ranibizumab (0.8% and 2.3% vs. 1.0%). The extended duration of effect of abicipar allows for quarterly dosing and reduced treatment burden.
Two-year results show efficacy of abicipar Q8 and Q12 in nAMD. First onset of IOI events with abicipar was much reduced in the second year and comparable with ranibizumab (0.8% and 2.3% vs. 1.0%). The extended duration of effect of abicipar allows for quarterly dosing and reduced treatment burden.
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