Montera: A Framework for Efficient Execution of Monte Carlo Codes on Grid Infrastructures

he objective of this work is to improve the performance of Monte Carlo codes on Grid production infrastructures. To do so, the codes and the grid sites are characterized with simple parameters to model their behaviors. Then, a new performance model for grid infrastructures is proposed, and an algorithm that employs this information is described. This algorithm dynamically calculates the number and size of tasks to execute on each site to maximize the performance and reduce makespan. Finally, a newly developed framework called Montera is presented. Montera deals with the execution of Monte Carlo codes in an unattended way, isolating the complexity of the problem from the final user. By employing two fusion Monte Carlo codes as example cases, along with the described characterizations and scheduling algorithm, a performance improvement up to 650 % over current best results is obtained on a real production infrastructure, together with enhanced stability and robustness

Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson’s disease (PD) and Alzheimer’s disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues