bluuebunny/crossref_metadata_2025_split huggingface dataset:
Representation theoretic embedding of twisted Dirac operators
Authors: Mehdi S. , Pandžić P. 
Published: September 2021

Let

G
G

be a non-compact connected semisimple real Lie group with finite center. Suppose

L
L

is a non-compact connected closed subgroup of

G
G

acting transitively on a symmetric space

G

/

H

G/H

such that

L
∩
H

L\cap H

is compact. We study the action on

L

/

L
∩
H

L/L\cap H

of a Dirac operator

D

G

/

H

(
E
)

D_{G/H}(E)

acting on sections of an

E
E

-twist of the spin bundle over

G

/

H

G/H

. As a byproduct, in the case of

(
G
,
H
,
L
)
=
(
S
L
(
2
,

R

)
×
S
L
(
2
,

R

)
,
Δ
(
S
L
(
2
,

R

)
×
S
L
(
2
,

R

)
)
,
S
L
(
2
,

R

)
×
S
O
(
2
)
)

(G,H,L)=(SL(2,{\mathbb R})\times SL(2,{\mathbb R}),\Delta (SL(2,{\mathbb R})\times SL(2,{\mathbb R})),SL(2,{\mathbb R})\times SO(2))

, we identify certain representations of

L
L

which lie in the kernel of

D

G

/

H

(
E
)

D_{G/H}(E)

.
Evaluation of the risk of metachronous multiple squamous cell carcinoma of the head and neck after transoral surgery based on the genetic polymorphisms of alcohol dehydrogenase 1B and aldehyde dehydrogenase 2
Authors: Inoue Masaki , Shimizu Yuichi , Taniguchi Masanobu , Kimura Yuki , Furuhashi Hiroto , Dobashi Akira , Ikeya Takashi , Goda Kenichi , Kato Masayuki , Kato Mototsugu , Sakamoto Naoya , Watanabe Akihito 
Published: September 2021

Abstract
Patients with superficial head and neck squamous cell carcinoma (HNSCC) can be completely treated by techniques of transoral surgery (TOS). The aim of this study was to evaluate the risk of metachronous multiple HNSCC arising after TOS based on alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2). We registered patients who underwent TOS for superficial HNSCC. Buccal cell samples were obtained by using a cotton swab to examine two single nucleotide polymorphisms in ADH1B and ALDH2 genotyping. We used Cox proportional hazards models to examine the risk of metachronous HNSCC. A total of 198 patients who underwent TOS for HNSCC were evaluated. In multivariate analysis, risks for second HNSCC were ADH1B*1/*1 [hazard ratio (HR), 1.88; 95% confidence interval (CI), 1.11–3.19; P = 0.02], ALDH2*1/*2 (HR, 2.11; 95% CI, 1.00–5.16; P = 0.048) and alcohol consumption before TOS (HR, 1.17; 95% CI, 1.06–1.27; P = 0.01). The 5-year incidence rates of second primary HNSCC in the temperance group and the non-temperance group were 20.8 and 46.5%, respectively (HR, 0.54; 95% CI, 0.31–0.92; P = 0.02). Cumulative development rates of third HNSCC in the temperance group and non-temperance group at 10 years were 11.3 and 36.1%, respectively (HR, 0.19; 95% CI, 0.03–0.65; P = 0.006). ADH1B*1/*1, ALDH2*1/*2 and moderate or heavy alcohol consumption before treatment are independent risk factors of metachronous HNSCC. Since it was shown that temperance decreased the incidences of second and third metachronous HNSCC, advice to discontinue alcohol drinking is necessary.
Understanding the Potential Impact of Different Drug Properties on Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Transmission and Disease Burden: A Modelling Analysis
Authors: Whittaker Charles , Watson Oliver J , Alvarez-Moreno Carlos , Angkasekwinai Nasikarn , Boonyasiri Adhiratha , Carlos Triana Luis , Chanda Duncan , Charoenpong Lantharita , Chayakulkeeree Methee , Cooke Graham S , Croda Julio , Cucunubá Zulma M , Djaafara Bimandra A , Estofolete Cassia F , Grillet Maria Eugenia , Faria Nuno R , Figueiredo Costa Silvia , Forero-Peña David A , Gibb Diana M , Gordon Anthony C , Hamers Raph L , Hamlet Arran , Irawany Vera , Jitmuang Anupop , Keurueangkul Nukool , Kimani Teresia Njoki , Lampo Margarita , Levin Anna S , Lopardo Gustavo , Mustafa Rima , Nayagam Shevanthi , Ngamprasertchai Thundon , Njeri Ng’ang’a Irene Hannah , Nogueira Mauricio L , Ortiz-Prado Esteban , Perroud Mauricio W , Phillips Andrew N , Promsin Panuwat , Qavi Ambar , Rodger Alison J , Sabino Ester C , Sangkaew Sorawat , Sari Djayanti , Sirijatuphat Rujipas , Sposito Andrei C , Srisangthong Pratthana , Thompson Hayley A , Udwadia Zarir , Valderrama-Beltrán Sandra , Winskill Peter , Ghani Azra C , Walker Patrick G T , Hallett Timothy B 
Published: September 2021

Abstract

Background
The public health impact of the coronavirus disease 2019 (COVID-19) pandemic has motivated a rapid search for potential therapeutics, with some key successes. However, the potential impact of different treatments, and consequently research and procurement priorities, have not been clear.

Methods
Using a mathematical model of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission, COVID-19 disease and clinical care, we explore the public-health impact of different potential therapeutics, under a range of scenarios varying healthcare capacity, epidemic trajectories; and drug efficacy in the absence of supportive care.

Results
The impact of drugs like dexamethasone (delivered to the most critically-ill in hospital and whose therapeutic benefit is expected to depend on the availability of supportive care such as oxygen and mechanical ventilation) is likely to be limited in settings where healthcare capacity is lowest or where uncontrolled epidemics result in hospitals being overwhelmed. As such, it may avert 22% of deaths in high-income countries but only 8% in low-income countries (assuming R = 1.35). Therapeutics for different patient populations (those not in hospital, early in the course of infection) and types of benefit (reducing disease severity or infectiousness, preventing hospitalization) could have much greater benefits, particularly in resource-poor settings facing large epidemics.

Conclusions
Advances in the treatment of COVID-19 to date have been focused on hospitalized-patients and predicated on an assumption of adequate access to supportive care. Therapeutics delivered earlier in the course of infection that reduce the need for healthcare or reduce infectiousness could have significant impact, and research into their efficacy and means of delivery should be a priority.
Association Between Airborne Infection Isolation Room Utilization Rates and Healthcare Worker Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infections in 2 Academic Hospitals
Authors: Klompas Michael , Ye Shangyuan , Vaidya Vineeta , Ochoa Aileen , Baker Meghan A , Hopcia Karen , Hashimoto Dean , Wang Rui , Rhee Chanu 
Published: September 2021

Abstract
We compared healthcare worker severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection rates between March and August 2020 in 2 similar hospitals with high vs low airborne infection isolation room utilization rates but otherwise identical infection control policies. We found no difference in healthcare worker infection rates between the 2 hospitals, nor between patient-facing vs non-patient-facing providers.
Inflammation during the life cycle of the atherosclerotic plaque
Authors: Libby Peter 
Published: September 2021

Abstract
Inflammation orchestrates each stage of the life cycle of atherosclerotic plaques. Indeed, inflammatory mediators likely link many traditional and emerging risk factors with atherogenesis. Atheroma initiation involves endothelial activation with recruitment of leucocytes to the arterial intima, where they interact with lipoproteins or their derivatives that have accumulated in this layer. The prolonged and usually clinically silent progression of atherosclerosis involves periods of smouldering inflammation, punctuated by episodes of acute activation that may arise from inflammatory mediators released from sites of extravascular injury or infection or from subclinical disruptions of the plaque. Smooth muscle cells and infiltrating leucocytes can proliferate but also undergo various forms of cell death that typically lead to formation of a lipid-rich ‘necrotic’ core within the evolving intimal lesion. Extracellular matrix synthesized by smooth muscle cells can form a fibrous cap that overlies the lesion’s core. Thus, during progression of atheroma, cells not only procreate but perish. Inflammatory mediators participate in both processes. The ultimate clinical complication of atherosclerotic plaques involves disruption that provokes thrombosis, either by fracture of the plaque’s fibrous cap or superficial erosion. The consequent clots can cause acute ischaemic syndromes if they embarrass perfusion. Incorporation of the thrombi can promote plaque healing and progressive intimal thickening that can aggravate stenosis and further limit downstream blood flow. Inflammatory mediators regulate many aspects of both plaque disruption and healing process. Thus, inflammatory processes contribute to all phases of the life cycle of atherosclerotic plaques, and represent ripe targets for mitigating the disease.
CArdiac MagnEtic resonance assessment of bi-Atrial fibrosis in secundum atrial septal defects patients: CAMERA-ASD study
Authors: O’Neill Louisa , Sim Iain , O’Hare Daniel , Whitaker John , Mukherjee Rahul K , Razeghi Orod , Niederer Steven , Wright Matthew , Chiribiri Amedeo , Frigiola Alessandra , O’Neill Mark D , Williams Steven E 
Published: September 2021

Abstract

Aims
Atrial septal defects (ASD) are associated with atrial arrhythmias, but the arrhythmia substrate in these patients is poorly defined. We hypothesized that bi-atrial fibrosis is present and that right atrial fibrosis is associated with atrial arrhythmias in ASD patients. We aimed to evaluate the extent of bi-atrial fibrosis in ASD patients and to investigate the relationships between bi-atrial fibrosis, atrial arrhythmias, shunt fraction, and age.

Methods and results
Patients with uncorrected secundum ASDs (n = 36; 50.4 ± 13.6 years) underwent cardiac magnetic resonance imaging with atrial late gadolinium enhancement. Comparison was made to non-congenital heart disease patients (n = 36; 60.3 ± 10.5 years) with paroxysmal atrial fibrillation (AF). Cardiac magnetic resonance parameters associated with atrial arrhythmias were identified and the relationship between bi-atrial structure, age, and shunt fraction studied. Bi-atrial fibrosis burden was greater in ASD patients than paroxysmal AF patients (20.7 ± 14% vs. 10.1 ± 8.6% and 14.8 ± 8.5% vs. 8.6 ± 6.1% for right and left atria respectively, P = 0.001 for both). In ASD patients, right atrial fibrosis burden was greater in those with than without atrial arrhythmias (33.4 ± 18.7% vs. 16.8 ± 10.3%, P = 0.034). On receiver operating characteristic analysis, a right atrial fibrosis burden of 32% had a 92% specificity and 71% sensitivity for predicting the presence of atrial arrhythmias. Neither age nor shunt fraction was associated with bi-atrial fibrosis burden.

Conclusion
Bi-atrial fibrosis burden is greater in ASD patients than non-congenital heart disease patients with paroxysmal AF. Right atrial fibrosis is associated with the presence of atrial arrhythmias in ASD patients. These findings highlight the importance of right atrial fibrosis to atrial arrhythmogenesis in ASD patients.
Primary care consultations for respiratory tract symptoms during the COVID-19 pandemic: a cohort study including 70,000 people in South West England
Authors: Dambha-Miller Hajira , Hounkpatin Hilda O , Morgan-Harrisskitt Jeffrey , Stuart Beth , Fraser Simon D S , Roderick Paul 
Published: September 2021

Abstract

Background
Primary care consultations for respiratory tract symptoms including identifying and managing COVID-19 during the pandemic have not been characterized.

Methods
A retrospective cohort analysis using routinely collected records from 70,431 adults aged 18+ in South England within the Electronic Care and Health Information Analytics (CHIA) database. Total volume and type of consultations (face-to-face, home visits, telephone, email/video, or out of hours) for respiratory tract symptoms between 1 January and 31 July 2020 (during the first wave of the pandemic) were compared with the equivalent period in 2019 for the same cohort. Descriptive statistics were used to summarize consultations by sociodemographic and clinical characteristics, and by COVID-19 diagnosis and outcomes (death, hospitalization, and pneumonia).

Results
Overall consultations for respiratory tract symptoms increased by 229% during the pandemic compared with the preceding year. This included significant increases in telephone consultations by 250%, a 1,574% increase in video/email consultations, 105% increase in home visits, and 92% increase in face-to-face consultations. Nearly 60% of people who presented with respiratory symptoms were tested for COVID-19 and 16% confirmed or clinically suspected to have the virus. Those with complications including pneumonia, requiring hospitalization, and who died were more likely to be seen in-person.

Conclusion
During the pandemic, primary care substantially increased consultations for respiratory tract symptoms to identify and manage people with COVID-19. These findings should be balanced against national reports of reduced GP workload for non-COVID care.
Frequent lineage-specific substitution rate changes support an episodic model for protein evolution
Authors: Prabh Neel , Tautz Diethard 
Published: September 2021

Abstract
Since the inception of the molecular clock model for sequence evolution, the investigation of protein divergence has revolved around the question of a more or less constant change of amino acid sequences, with specific overall rates for each family. Although anomalies in clock-like divergence are well known, the assumption of a constant decay rate for a given protein family is usually taken as the null model for protein evolution. However, systematic tests of this null model at a genome-wide scale have lagged behind, despite the databases’ enormous growth. We focus here on divergence rate comparisons between very closely related lineages since this allows clear orthology assignments by synteny and reliable alignments, which are crucial for determining substitution rate changes. We generated a high-confidence dataset of syntenic orthologs from four ape species, including humans. We find that despite the appearance of an overall clock-like substitution pattern, several hundred protein families show lineage-specific acceleration and deceleration in divergence rates, or combinations of both in different lineages. Hence, our analysis uncovers a rather dynamic history of substitution rate changes, even between these closely related lineages, implying that one should expect that a large fraction of proteins will have had a history of episodic rate changes in deeper phylogenies. Furthermore, each of the lineages has a separate set of particularly fast diverging proteins. The genes with the highest percentage of branch-specific substitutions are ADCYAP1 in the human lineage (9.7%), CALU in chimpanzees (7.1%), SLC39A14 in the internal branch leading to humans and chimpanzees (4.1%), RNF128 in gorillas (9%), and S100Z in gibbons (15.2%). The mutational pattern in ADCYAP1 suggests a biased mutation process, possibly through asymmetric gene conversion effects. We conclude that a null model of constant change can be problematic for predicting the evolutionary trajectories of individual proteins.
Deep learning for velocity model building with common-image gather volumes
Authors: Geng Zhicheng , Zhao Zeyu , Shi Yunzhi , Wu Xinming , Fomel Sergey , Sen Mrinal 
Published: September 2021

SUMMARY
Subsurface velocity model building is a crucial step for seismic imaging. It is a challenging problem for conventional methods such as full-waveform inversion (FWI) and wave equation migration velocity analysis (WEMVA), due to the highly nonlinear relationship between subsurface velocity values and seismic responses. In addition, traditional FWI and WEMVA methods are often computationally expensive. In this paper, we propose to apply a deep learning technique to construct subsurface velocity models automatically from common-image gather (CIG) volumes. In our method, pairs of synthetic velocity models and CIG volumes are generated to train a convolutional neural network. Our proposed network achieves promising results on different synthetic data sets. The training performance of several commonly used loss functions is also studied.
Priority setting and equity in COVID-19 pandemic plans: a comparative analysis of 18 African countries
Authors: Kapiriri Lydia , Kiwanuka Suzanne , Biemba Godfrey , Velez Claudia , Razavi S Donya , Abelson Julia , Essue Beverley M , Danis Marion , Goold Susan , Noorulhuda Mariam , Nouvet Elysee , Sandman Lars , Williams Iestyn 
Published: September 2021

Abstract
Priority setting represents an even bigger challenge during public health emergencies than routine times. This is because such emergencies compete with routine programmes for the available health resources, strain health systems and shift health-care attention and resources towards containing the spread of the epidemic and treating those that fall seriously ill. This paper is part of a larger global study, the aim of which is to evaluate the degree to which national COVID-19 preparedness and response plans incorporated priority setting concepts. It provides important insights into what and how priority decisions were made in the context of a pandemic. Specifically, with a focus on a sample of 18 African countries’ pandemic plans, the paper aims to: (1) explore the degree to which the documented priority setting processes adhere to established quality indicators of effective priority setting and (2) examine if there is a relationship between the number of quality indicators present in the pandemic plans and the country’s economic context, health system and prior experiences with disease outbreaks. All the reviewed plans contained some aspects of expected priority setting processes but none of the national plans addressed all quality parameters. Most of the parameters were mentioned by less than 10 of the 18 country plans reviewed, and several plans identified one or two aspects of fair priority setting processes. Very few plans identified equity as a criterion for priority setting. Since the parameters are relevant to the quality of priority setting that is implemented during public health emergencies and most of the countries have pre-existing pandemic plans; it would be advisable that, for the future (if not already happening), countries consider priority setting as a critical part of their routine health emergency and disease outbreak plans. Such an approach would ensure that priority setting is integral to pandemic planning, response and recovery.
Adaptation of the heart to frataxin depletion: evidence that integrated stress response can predominate over mTORC1 activation
Authors: Vásquez-Trincado César , Patel Monika , Sivaramakrishnan Aishwarya , Bekeová Carmen , Anderson-Pullinger Lauren , Wang Nadan , Tang Hsin-Yao , Seifert Erin L 
Published: September 2021

Abstract
Friedreich’s ataxia is an inherited disorder caused by depletion of frataxin (FXN), a mitochondrial protein required for iron–sulfur cluster (ISC) biogenesis. Cardiac dysfunction is the main cause of death. Yet pathogenesis, and, more generally, how the heart adapts to FXN loss, remains poorly understood, though it is expected to be linked to an energy deficit. We modified a transgenic (TG) mouse model of inducible FXN depletion that permits phenotypic evaluation of the heart at different FXN levels and focused on substrate-specific bioenergetics and stress signaling. When FXN protein in the TG heart was 17% of normal, bioenergetics and signaling were not different from control. When, 8 weeks later, FXN was ~ 97% depleted in the heart, TG heart mass and cardiomyocyte cross-sectional area were less, without evidence of fibrosis or apoptosis. mTORC1 signaling was activated, as was the integrated stress response, evidenced by greater phosphorylation of eIF2α relative to total eIF2α, and decreased protein translation. We interpret these results to suggest that, in TG hearts, an anabolic stimulus was constrained by eIF2α phosphorylation. Cardiac contractility was maintained in the 97% FXN-depleted hearts, possibly contributed by an unexpected preservation of β-oxidation, though pyruvate oxidation was lower. Bioenergetics alterations were matched by changes in the mitochondrial proteome, including a non-uniform decrease in abundance of ISC-containing proteins. Altogether, these findings suggest that the FXN-depleted heart can suppress a major ATP-demanding process such as protein translation, which, together with some preservation of β-oxidation, could be adaptive, at least in the short term.
Sarcospan increases laminin-binding capacity of α-dystroglycan to ameliorate DMD independent of Galgt2
Authors: Mamsa Hafsa , Stark Rachelle L , Shin Kara M , Beedle Aaron M , Crosbie Rachelle H 
Published: September 2021

Abstract
In Duchenne muscular dystrophy (DMD), mutations in dystrophin result in a loss of the dystrophin-glycoprotein complex (DGC) at the myofiber membrane, which functions to connect the extracellular matrix with the intracellular actin cytoskeleton. The dystroglycan subcomplex interacts with dystrophin and spans the sarcolemma where its extensive carbohydrates (matriglycan and CT2 glycan) directly interact with the extracellular matrix. In the current manuscript, we show that sarcospan overexpression enhances the laminin-binding capacity of dystroglycan in DMD muscle by increasing matriglycan glycosylation of α-dystroglycan. Furthermore, we find that this modification is not affected by loss of Galgt2, a glycotransferase, which catalyzes the CT2 glycan. Our findings reveal that the matriglycan carbohydrates, and not the CT2 glycan, are necessary for sarcospan-mediated amelioration of DMD. Overexpression of Galgt2 in the DMD mdx murine model prevents muscle pathology by increasing CT2 modified α-dystroglycan. Galgt2 also increases expression of utrophin, which compensates for the loss of dystrophin in DMD muscle. We found that combined loss of Galgt2 and dystrophin reduced utrophin expression; however, it did not interfere with sarcospan rescue of disease. These data reveal a partial dependence of sarcospan on Galgt2 for utrophin upregulation. In addition, sarcospan alters the cross-talk between the adhesion complexes by decreasing the association of integrin β1D with dystroglycan complexes. In conclusion, sarcospan functions to re-wire the cell to matrix connections by strengthening the cellular adhesion and signaling, which, in turn, increases the resilience of the myofiber membrane.