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The solid electrolyte interphase (SEI) is a thin heterogeneous layer formed at the anode/electrolyte interface in lithium‐ion batteries as a consequence of the reduction of the electrolyte. The initial formation of the SEI inhibits the direct contact between the electrode and the electrolyte and thus protects the battery. However, the composition, structure, and size of the SEI evolve over time and the growth of the SEI is considered the primary mechanism leading to the gradual deterioration of the battery performance. Despite the importance of the SEI and its growth, the atomistic understanding of the underlying elementary reaction steps remains partial. Molecular modeling of the electrolyte decomposition is key to gain detailed insights that are complementary to experiments for the reactions occurring in this heterogenous interphase. In this perspective, the electron transport mechanisms are first described from the anode to the electrolyte through the SEI and highlight the importance of the inorganic/organic interface within the heterogeneous SEI: it is where the electrolyte decomposition reactions are likely to occur. Finally, a view is provided on the current progress on molecular modeling techniques (e.g., Density Functional Theory, force fields, machine learning potentials) of the SEI and the challenges each method faces. [ABSTRACT FROM AUTHOR]

Dajung J Kim, Hassan Jassar, Manyoel Lim, Thiago D Nascimento, Alexandre F DaSilva Headache and Orofacial Pain Effort (H.O.P.E.), Biologic and Material Sciences & Prosthodontics, University of Michigan School of Dentistry, Ann Arbor, MI, 48109, USACorrespondence: Alexandre F DaSilvaHeadache and Orofacial Pain Effort Lab (H.O.P.E.), Biologic and Material Sciences & Prosthodontics, University of Michigan School of Dentistry, 1011 N University Avenue, Ann Arbor, MI, 48109, USATel +1 734 615 3807Fax +1 734 763 3453Email adasilva@umich.eduPurpose: It has been suggested that reward system dysfunction may account for emotion and pain suffering in migraine. However, there is a lack of evidence whether the altered reward system connectivity is directly associated with clinical manifestations, including negative affect and ictal pain severity and, at the molecular level, the dopamine (DA) D2/D3 receptors (D2/3Rs) signaling implicated in encoding motivational and emotional cues.Patients and Methods: We acquired resting-state functional MRI from interictal episodic migraine (EM) patients and age-matched healthy controls, as well as positron emission tomography (PET) with [11C]raclopride, a selective radiotracer for DA D2/3Rs, from a subset of these participants. The nucleus accumbens (NAc) was seeded to measure functional connectivity (FC) and DA D2/3Rs availability based on its essential involvement in pain-related aversive/reward functions. Associations of the brain measures with positive/negative affect and ictal pain severity were also assessed.Results: Compared with controls, the EM group showed weaker right NAc connectivity with areas implicated in pain and emotional regulation, such as the amygdala, rostral anterior cingulate cortex, hippocampus, and thalamus; but showed stronger left NAc connectivity with the dorsolateral prefrontal cortex and lingual gyrus. Moreover, among the altered NAc connectivities, only right NAc-amygdala connectivity was inversely correlated with DA D2/3Rs availability in migraine patients (diagnostic group-by-D2/3Rs interaction p < 0.007). At a clinical level, such weaker NAc-amygdala connectivity was associated with lower interictal positive affect and greater ictal pain severity over the head and facial extension area (pain area and intensity number summation, PAINS).Conclusion: Together, our findings suggest that altered reward system connectivity, specifically between the NAc and amygdala, might be affected by endogenous DA D2/3Rs signaling, and such process might be a neural mechanism that underlies emotional and pain suffering in episodic migraineurs.Keywords: dopamine, nucleus accumbens, functional connectivity, migraine, reward system, craniofacial pain

Abstract Background The moment-to-moment variability of resting-state brain activity has been suggested to play an active role in chronic pain. Here, we investigated the regional blood-oxygen-level-dependent signal variability (BOLDSV) and inter-regional dynamic functional connectivity (dFC) in the interictal phase of migraine and its relationship with the attack severity. Methods We acquired resting-state functional magnetic resonance imaging from 20 migraine patients and 26 healthy controls (HC). We calculated the standard deviation (SD) of the BOLD time-series at each voxel as a measure of the BOLD signal variability (BOLDSV) and performed a whole-brain voxel-wise group comparison. The brain regions showing significant group differences in BOLDSV were used to define the regions of interest (ROIs). The SD and mean of the dynamic conditional correlation between those ROIs were calculated to measure the variability and strength of the dFC. Furthermore, patients’ experimental pain thresholds and headache pain area/intensity levels during the migraine ictal-phase were assessed for clinical correlations. Results We found that migraineurs, compared to HCs, displayed greater BOLDSV in the ascending trigeminal spinal-thalamo-cortical pathways, including the spinal trigeminal nucleus, pulvinar/ventral posteromedial (VPM) nuclei of the thalamus, primary somatosensory cortex (S1), and posterior insula. Conversely, migraine patients exhibited lower BOLDSV in the top-down modulatory pathways, including the dorsolateral prefrontal (dlPFC) and inferior parietal (IPC) cortices compared to HCs. Importantly, abnormal interictal BOLDSV in the ascending trigeminal spinal-thalamo-cortical and frontoparietal pathways were associated with the patient’s headache severity and thermal pain sensitivity during the migraine attack. Migraineurs also had significantly lower variability and greater strength of dFC within the thalamo-cortical pathway (VPM-S1) than HCs. In contrast, migraine patients showed greater variability and lower strength of dFC within the frontoparietal pathway (dlPFC-IPC). Conclusions Migraine is associated with alterations in temporal signal variability in the ascending trigeminal somatosensory and top-down modulatory pathways, which may explain migraine-related pain and allodynia. Contrasting patterns of time-varying connectivity within the thalamo-cortical and frontoparietal pathways could be linked to abnormal network integrity and instability for pain transmission and modulation.

الأهداف: هدفت الدّراسة إلى اقتراح رؤية لتطوير إدارة تعليم رياض الأطفال في الأردن استناداً إلى القيادة الإبداعيّة، وتكوّن مجتمع الدّراسة من جميع مديرات ومعلّمات رياض الأطفال الخاصّة في عمّان، اختيرت عيّنة طبقيّة عشوائيّة بواقع 404 مديرة، ومعلّمة في العام الدّراسي 2020/2021. المنهجية: لتحقيق هدف الدّراسة جرى استخدام المنهج الوصفي التّطويري، إذ جرى بناء استبانة مكوّنة من 55 فقرة، وذلك للكشف عن درجة الواقع والأهميّة والحاجة لتوفّر رؤية من وجهة نظر أفراد عيّنة الدّراسة. النتائج: أظهرت النّتائج أن درجة الحاجة لتوفّر رؤية جاءت بدرجة عالية، وقدمت الدّراسة رؤية مقترحة بعد تحكيمها، إذ أظهرت النّتائج أن وضوح الرّؤية وواقعيّتها ومرونتها، وقابليّتها للتّطبيق جاءت بدرجة عالية. التوصيات: توصي الدّراسة بتبني الرؤية المقترحة كأداة تطويريّة.

Background Many patients with severe aortic stenosis (AS) and an indication for aortic valve replacement (AVR) do not undergo treatment. The reasons for this have not been well studied in the transcatheter AVR era. We sought to determine how patient‐ and process‐specific factors affected AVR use in patients with severe AS. Methods and Results We identified ambulatory patients from 2016 to 2018 demonstrating severe AS, defined by aortic valve area ≤1.0 cm2. Propensity scoring analysis with inverse probability of treatment weighting was used to evaluate associations between predictors and the odds of undergoing AVR at 365 days and subsequent mortality at 730 days. Of 324 patients with an indication for AVR (79.3±9.7 years, 57.4% men), 140 patients (43.2%) did not undergo AVR. The odds of AVR were reduced in patients aged >90 years (odds ratio [OR], 0.24 [95% CI, 0.08–0.69]; P=0.01), greater comorbid conditions (OR, 0.88 per 1‐point increase in Combined Comorbidity Index [95% CI, 0.79–0.97]; P=0.01), low‐flow, low‐gradient AS with preserved left ventricular ejection fraction (OR, 0.11 [95% CI, 0.06–0.21]), and low‐gradient AS with reduced left ventricular ejection fraction (OR, 0.18 [95% CI, 0.08–0.40]) and were increased if the transthoracic echocardiogram ordering provider was a cardiologist (OR, 2.46 [95% CI, 1.38–4.38]). Patients who underwent AVR gained an average of 85.8 days of life (95% CI, 40.9–130.6) at 730 days. Conclusions The proportion of ambulatory patients with severe AS and an indication for AVR who do not receive AVR remains significant. Efforts are needed to maximize the recognition of severe AS, especially low‐gradient subtypes, and to encourage patient referral to multidisciplinary heart valve teams.

Health disparity in Canada is continuing to grow with marginalized communities being disproportionately affected. Policies and actions implemented by the federal government have been ineffective in addressing underlying causes of poor health. Framing access to justice as a social determinant of health is a necessary first step to establish a comprehensive and interdisciplinary approach to address poor health outcomes. Through an analysis of the limitations of access to justice as a legal term and the application of access to justice in health outcomes, this article hopes to foster further collaboration between the medical and legal communities in this area. art I of this paper argues the need to expand the scope of access to justice beyond the legal realm. Part II highlights the increasing health disparity within Canada and critiques the current approach. Part III outlines the ways in which health disparity can be improved if access to justice is recognized as a social determinant of health. The paper concludes with discussing progress that can be made in both the legal and medical community as a result of widening the scope of access to justice. Through an analysis of the limitations of access to justice as a legal term and the application of access to justice in health outcomes, this paper hopes to foster further collaboration between the medical and legal communities in this area.

Pericardial–esophageal fistula and/or atrial–esophageal fistula after cardiac ablation is nearly universally fatal if not detected and treated expeditiously. This condition should be assumed and ruled out in anyone with a recent history of cardiac ablation presenting with signs of sepsis, pneumomediastinum, pneumopericardium, or chest pain. Computed tomography scan of the chest is a rapid and a sensitive diagnostic modality. Tenets of treatment and repair consist of preventing an air embolism, repairing the esophageal perforation and atrial defect, and interposing autologous tissue between the esophagus and heart.

Abstract Background Guidelines suggest that patients discontinue Clopidogrel at least 5 days prior to coronary artery bypass grafting (CABG). Those with acute coronary syndrome (ACS) are at high risk for myocardial infarction (MI) if not treated with dual antiplatelet therapy (DAPT). We sought to assess pre and post-operative outcomes of patients maintained on Clopidogrel and aspirin up to the time of surgery and compare them with those on aspirin alone. Methods From the cardiac surgery database, 240 patients were retrospectively registered between January and May 2017. There were 126 patients with ACS who underwent CABG on DAPT (Clopidogrel group [CG]) and 114 patients who underwent elective CABG on aspirin alone (control). The CG received intraoperative prophylactic platelet transfusion (PPT). Demographics, comorbidities, and laboratory data were prospectively entered at the time of surgery and were subsequently retrieved for analysis. Per and postoperative findings were identified and compared between both groups. Results The cohort consisted of 240 patients (mean age 61 years, 81.3% were male, SD ± 9.58). Patients in the CG were younger (Median 57 vs. 63, P-value 0.001), and with male predominance (86% versus 75%, P-value 0.028). In addition, they had less prevalence for diabetes and renal failure as compared to control (P-values 0.003, and 0.005, respectively). There were no significant differences between both groups in number of vessels grafts, duration of on-pump and aortic clamp. Hematologic laboratory data had also similar baseline values. The CG had similar bleeding rate, redo surgery and in-hospital death (P-values non-significant), however more infection and total hospital stay as compared to control (p-values 0.048 and 0.001). Conclusion Patients who are at increased risk for MI can be maintained on DAPT up to the time of CABG because surgery is safe when patients are offered PPT.

Ciliopathies are a group of genetic disorders caused by a failure to form functional cilia. Due to a lack of structural information, it is currently poorly understood how ciliopathic mutations affect protein functionality to give rise to the underlying disease. Using X-ray crystallography, we show that the ciliopathy-associated centriolar protein CEP120 contains three C2 domains. The point mutations V194A and A199P, which cause Joubert syndrome (JS) and Jeune asphyxiating thoracic dystrophy (JATD), respectively, both reduce the thermostability of the second C2 domain by targeting residues that point toward its hydrophobic core. Genome-engineered cells homozygous for these mutations have largely normal centriole numbers but show reduced CEP120 levels, compromised recruitment of distal centriole markers, and deficient cilia formation. Our results provide insight into the disease mechanism of two ciliopathic mutations in CEP120, identify putative binding partners of CEP120 C2B, and suggest a complex genotype-phenotype relation of the CEP120 ciliopathy alleles.

Tuberculosis (TB) and Non-Hodgkins lymphoma (NHL) share similar clinical and radiological features, which make diagnosis a challenge. It is often difficult to rule out a diagnosis of extrapulmonary and/or disseminated TB because of its paucibacillary nature and difficulty in accessing the involved organs. In countries with high prevalence of TB like ours, empirical antitubercular treatment (ATT) is started, and the patient is followed up closely for response. We present a rare case of a 54-year old diabetic male who was suspected to be a case of disseminated TB but had a rapid downhill course despite ATT. A postmortem revealed features of a rare, aggressive T-cell NHL masquerading as disseminated TB.

A 43-year-old apparently healthy male presented with fever and presyncope. He was suspected to have massive pulmonary thromboembolism based on the clinico-biochemical profile. Despite aggressive thrombolytic therapy, he succumbed to his illness within 12 h of admission. Postmortem examination showed massive pulmonary thromboembolism and hyperhomocysteinemia with low high-density lipoproteins (HDL) cholesterol with antemortem blood sample. Herein, we report autopsy findings in a rare case of a young male with occult massive pulmonary thromboembolism without deep vein thrombosis, who had an atypical clinical presentation and was found to have underlying hyperhomocysteinemia and decreased HDLc. An acute, massive PE can present a diagnostic challenge due to the rate and severity of decompensation seen in afflicted patients. A high index of suspicion is required for early detection of pulmonary embolism in a young patient with atypical presentation and without obvious risk factors.