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Numerical tesseroid and radial-type approaches are presented and compared in terms of their efficiency for deriving the regional geoid height, vertical gravity, and gradiometric anomalies from sea floor topography grids. The vertical gradient function is particularly suitable for representing shorter wavelengths of gravity, typically less than 10 km. These two modeling methods were applied to the Great Meteor guyot in the Atlantic Ocean using its bathymetry. To optimize the computation of high-resolution gravity anomalies, the Armadillo, GSL, and OpenMP libraries were used to provide an environment for fast vector implementation, numerical integration for tesseroid calculation, and parallelization for loop iterations, resulting in a computation speed increase. The tesseroid and radial methods remain equivalent up to a resolution of about 1 min, with the radial method being faster when dealing with a large number of model points for the geoid. Aside from optimization enabling high-resolution gravity simulations, these fast modeling data can be used as the main operators in gravimetric inversion or to reduce the terrain effects in gravity observations, revealing gravity and sedimentary layers.

Abstract Background In the last decade, Ibrutinib has become the standard of care in the treatment of several lymphoproliferative diseases such as chronic lymphocytic leukemia (CLL) and several non-Hodgkin lymphoma. Beyond Bruton tyrosine kinase inhibition, Ibrutinib shows broad immunomodulatory effects that may promote the occurrence of infectious complications, including opportunistic infections. The infectious burden has been shown to vary by disease status, neutropenia, and prior therapy but data focusing on severe infections requiring intensive care unit (ICU) admission remain scarce. We sought to investigate features and outcomes of severe infections in a multicenter cohort of 69 patients receiving ibrutinib admitted to 10 French intensive care units (ICU) from 1 January 2015 to 31 December 2020. Results Median time from ibrutinib initiation was 6.6 [3–18] months. Invasive fungal infections (IFI) accounted for 19% (n = 13/69) of severe infections, including 9 (69%; n = 9/13) invasive aspergillosis, 3 (23%; n = 3/13) Pneumocystis pneumonia, and 1 (8%; n = 1/13) cryptococcosis. Most common organ injury was acute respiratory failure (ARF) (71%; n = 49/69) and 41% (n = 28/69) of patients required mechanical ventilation. Twenty (29%; n = 20/69) patients died in the ICU while day-90 mortality reached 55% (n = 35/64). In comparison with survivors, decedents displayed more severe organ dysfunctions (SOFA 7 [5–11] vs. 4 [3–7], p = 0.004) and were more likely to undergo mechanical ventilation (68% vs. 31%, p = 0.010). Sixty-three ibrutinib-treated patients were matched based on age and underlying malignancy with 63 controls receiving conventional chemotherapy from an historic cohort. Despite a higher median number of prior chemotherapy lines (2 [1–2] vs. 0 [0–2]; p

Abstract Background Von Willebrand disease was diagnosed in two Afro‐Caribbean patients and sequencing of the VWF gene (VWF) revealed the presence of multiple variants located throughout the gene, including variants located in the D4 domain of VWF: p.(Pro2145Thrfs*5) in one patient and p.(Cys2216Phefs*9) in the other patient. Interestingly, D4 variants have not been studied often. Objectives Our goal was to characterize how the D4 variants p.(Pro2145Thrfs*5) and p.(Cys2216Phefs*9) influenced VWF biosynthesis/secretion and functions using in vitro assays. Methods Recombinant VWF (rVWF), mutant or wild‐type, was produced via transient transfection of the human embryonic kidney cell line 293T. The use of different tags for the wild‐type and the mutant allele allowed us to distinguish between the two forms when measuring VWF antigen in medium and cell lysates. Binding of rVWF to its ligands, collagen, factor VIII, ADAMTS13, and platelet receptors was also investigated. Results Homozygous expression of the p.(Cys2216Phefs*9)‐rVWF mutation resulted in an almost complete intracellular retention of the protein. Heterozygous expression led to secretion of almost exclusively wild‐type‐rVWF, logically capable of normal interaction with the different ligands. In contrast, the p.(Pro2145Thrfs*5)‐rVWF exhibited reduced binding to type III collagen and αIIbβ3 integrin compared to wild‐type‐rVWF. Conclusions We report two mutations of the D4 domains that induced combined qualitative and quantitative defects.

Background: Urinary tract infections (UTI) are among the most common infections in pediatric patients. The main etiopathogenic agent is Escherichia coli. The purpose of this study was to determine the antimicrobial resistance pattern of E. coli in pediatric patients and to understand their main clinical and laboratory manifestations. Methods: Fifty-nine patients were included in the study and classified into two groups: hospitalization (H) and external consultation (EC). Every patient presented urine cultures with the isolation of E. coli that included an antibiogram. Clinical signs and symptoms, urinalysis, complete blood count (CBC) and serum inflammatory markers were analyzed. Results: The most common clinical manifestations were fever (H: 76.5%; EC: 88%), vomiting (H: 32.4%; EC: 32%), hyporexia (H: 20.6%; EC: 16%), abdominal pain (H: 20.6%: EC: 28%), and dysuria (H: 14.7%; EC: 32%). Ten patients (16.95%) presented UTI for extended spectrum beta-lactamase (ESBL) E. coli. Ampicillin, nalidixic acid, and trimethoprim-sulfamethoxazole showed a higher resistance rate, being ampicillin the most significant (H: 88.2%; EC: 92%). Leukocyturia, bacteriuria and urine nitrites were frequent alterations in urinalysis (H: 52.9%; EC: 92%). In ESBL E. coli patients, a positive correlation was found between leukocytes in CBC and C-reactive protein (r = 0.9, p < 0.01). Diarrhea and foul-smelling urine were associated with E. coli resistance. Conclusions: The presence of leukocytes, bacteria, nitrites and the Gram stain are the most common indicators. Nitrofurantoin and phosphomycin are good therapeutic options. However, an antibiogram must be conducted to determine the best therapeutic agent.