Existence of a Meromorphic Extension of Spectral Zeta Functions on Fractals

We investigate the existence of the meromorphic extension of the spectral zeta function of the Laplacian on self-similar fractals using the classical results of Kigami and Lapidus (based on the renewal theory) and new results of Hambly and Kajino based on the heat kernel estimates and other probabilistic techniques. We also formulate conjectures which hold true in the examples that have been analyzed in the existing literature

Impact of Software Modeling on the Accuracy of Perfusion MRI in Glioma

PURPOSE: To determine whether differences in modeling implementation will impact the correction of leakage effects (from blood brain barrier disruption) and relative cerebral blood volume (rCBV) calculations as measured on T2*-weighted dynamic susceptibility-weighted contrast-enhanced (DSC)-MRI at 3T field strength. MATERIALS AND METHODS: This HIPAA-compliant study included 52 glioma patients undergoing DSC-MRI. Thirty-six patients underwent both non Preload Dose (PLD) and PLD-corrected DSC acquisitions, with sixteen patients undergoing PLD-corrected acquisitions only. For each acquisition, we generated two sets of rCBV metrics using two separate, widely published, FDA-approved commercial software packages: IB Neuro (IBN) and NordicICE (NICE). We calculated 4 rCBV metrics within tumor volumes: mean rCBV, mode rCBV, percentage of voxels with rCBV > 1.75 (%>1.75), and percentage of voxels with rCBV > 1.0 (Fractional Tumor Burden or FTB). We determined Pearson (r) and Spearman (ρ) correlations between non-PLD- and PLD-corrected metrics. In a subset of recurrent glioblastoma patients (n=25), we determined Receiver Operator Characteristic (ROC) Areas-Under-Curve (AUC) for FTB accuracy to predict the tissue diagnosis of tumor recurrence versus post-treatment effect (PTRE). We also determined correlations between rCBV and microvessel area (MVA) from stereotactic biopsies (n=29) in twelve patients. RESULTS: Using IBN, rCBV metrics correlated highly between non-PLD- and PLD-corrected conditions for FTB (r=0.96, ρ=0.94), %>1.75 (r=0.93, ρ=0.91), mean (r=0.87, ρ=0.86) and mode (r=0.78, ρ=0.76). These correlations dropped substantially with NICE. Using FTB, IBN was more accurate than NICE in diagnosing tumor vs PTRE (AUC=0.85 vs 0.67) (p<0.01). The highest rCBV-MVA correlations required PLD and IBN (r=0.64, ρ=0.58, p=0.001). CONCLUSIONS: Different implementations of perfusion MRI software modeling can impact the accuracy of leakage correction, rCBV calculation, and correlations with histologic benchmarks

Beyond the Global Brain Differences:Intraindividual Variability Differences in 1q21.1 Distal and 15q11.2 BP1-BP2 Deletion Carriers

BACKGROUND: Carriers of the 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants exhibit regional and globalbrain differences compared with noncarriers. However, interpreting regional differences is challenging if a globaldifference drives the regional brain differences. Intraindividual variability measures can be used to test for regionaldifferences beyond global differences in brain structure.METHODS: Magnetic resonance imaging data were used to obtain regional brain values for 1q21.1 distal deletion (n =30) and duplication (n = 27) and 15q11.2 BP1-BP2 deletion (n = 170) and duplication (n = 243) carriers and matchednoncarriers (n = 2350). Regional intra-deviation scores, i.e., the standardized difference between an individual’sregional difference and global difference, were used to test for regional differences that diverge from the globaldifference.RESULTS: For the 1q21.1 distal deletion carriers, cortical surface area for regions in the medial visual cortex, posterior cingulate, and temporal pole differed less and regions in the prefrontal and superior temporal cortex differedmore than the global difference in cortical surface area. For the 15q11.2 BP1-BP2 deletion carriers, cortical thicknessin regions in the medial visual cortex, auditory cortex, and temporal pole differed less and the prefrontal andsomatosensory cortex differed more than the global difference in cortical thickness.CONCLUSIONS: We find evidence for regional effects beyond differences in global brain measures in 1q21.1 distaland 15q11.2 BP1-BP2 copy number variants. The results provide new insight into brain profiling of the 1q21.1 distaland 15q11.2 BP1-BP2 copy number variants, with the potential to increase understanding of the mechanismsinvolved in altered neurodevelopment

EuReCa ONE—27 Nations, ONE Europe, ONE Registry A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe

AbstractIntroductionThe aim of the EuReCa ONE study was to determine the incidence, process, and outcome for out of hospital cardiac arrest (OHCA) throughout Europe.MethodsThis was an international, prospective, multi-centre one-month study. Patients who suffered an OHCA during October 2014 who were attended and/or treated by an Emergency Medical Service (EMS) were eligible for inclusion in the study. Data were extracted from national, regional or local registries.ResultsData on 10,682 confirmed OHCAs from 248 regions in 27 countries, covering an estimated population of 174 million. In 7146 (66%) cases, CPR was started by a bystander or by the EMS. The incidence of CPR attempts ranged from 19.0 to 104.0 per 100,000 population per year. 1735 had ROSC on arrival at hospital (25.2%), Overall, 662/6414 (10.3%) in all cases with CPR attempted survived for at least 30 days or to hospital discharge.ConclusionThe results of EuReCa ONE highlight that OHCA is still a major public health problem accounting for a substantial number of deaths in Europe.EuReCa ONE very clearly demonstrates marked differences in the processes for data collection and reported outcomes following OHCA all over Europe. Using these data and analyses, different countries, regions, systems, and concepts can benchmark themselves and may learn from each other to further improve survival following one of our major health care events

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Relative importance of ozone energy transfer processes in the middle and upper atmosphere

The relative importance of different processes and transitions in the appearance of non-LTE populations for the fundamental levels of ozone was studied by quantifying the kinetic law of every process and transition that affect each level population. The vibrational temperatures and the relative contribution of every transition are presented as a function of altitude. The results show that the appearance of non-LTE Populations for the fundamental levels is not produced by a direct imbalance between absorption and emission but as a consequence of imbalanced collisional transitions provoked by the overpopulation of O-3(0 nu(2) 0) levels. This fact confirms that the relaxation cascade drives through the bending mode nu(2). (C) 2009 Elsevier Ltd. All rights reserved

Discriminating long myelitis of neuromyelitis optica from sarcoidosis

Objective To compare longitudinally extensive myelitis in neuromyelitis optica spectrum disorders (NMOSD) and spinal cord sarcoidosis (SCS). Methods We identified adult patients evaluated between 1996 and 2015 with SCS or NMOSD whose first myelitis episode was accompanied by a spinal cord lesion spanning 653 vertebral segments. All NMOSD patients were positive for aquaporin-4-immunoglobulin G, and all sarcoidosis cases were pathologically confirmed. Clinical characteristics were evaluated. Spine magnetic resonance imaging was reviewed by 2 neuroradiologists. Results We studied 71 patients (NMOSD, 37; SCS, 34). Sixteen (47%) SCS cases were initially diagnosed as NMOSD or idiopathic transverse myelitis. Median delay to diagnosis was longer for SCS than NMOSD (5 vs 1.5 months, p &lt; 0.01). NMOSD myelitis patients were more commonly women, had concurrent or prior optic neuritis or intractable vomiting episodes more frequently, had shorter time to maximum deficit, and had systemic autoimmunity more often than SCS (p &lt; 0.05). SCS patients had constitutional symptoms, cerebrospinal fluid (CSF) pleocytosis, and hilar adenopathy more frequently than NMOSD (p &lt; 0.05); CSF hypoglycorrhachia (11%, p = 0.25) and elevated angiotensin-converting enzyme (18%, p = 0.30) were exclusive to SCS. Dorsal cord subpial gadolinium enhancement extending 652 vertebral segments and persistent enhancement &gt;2 months favored SCS, and ringlike enhancement favored NMOSD (p &lt; 0.05). Maximum disability was similar in both disorders. Interpretation SCS is an under-recognized cause of longitudinally extensive myelitis that commonly mimics NMOSD. We identified clinical, laboratory, systemic, and radiologic features that, taken together, help discriminate SCS from NMOSD