bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of soil properties in urban and non‐urban grasslands in Budapest area
Authors: Mónok Dávid , Kardos Levente , Pabar Sándor Attila , Kotroczó Zsolt , Tóth Eszter , Végvári György 
Published: August 2020

AbstractThis study focused on the physical, chemical and microbiological characteristics of soils from different grasslands in the Budapest area. Our aim was to assess the influence of anthropogenic activities on these soils by comparing three types of site: urban, green‐urban and non‐urban. From these sites, a total of 72 topsoil samples were collected and analysed. The results indicated that many properties of soils varied greatly between the different types of site. Urban soils had significantly higher pH, carbonate and salt content, but smaller organic carbon content than the other soils. These differences could be explained in part by the greater artefact content, as the latter was significantly correlated with most of the main soil properties. Concentrations of the heavy metals measured (Co, Cu, Cr, Fe, Mn, Ni, Pb, Zn) were generally smaller in non‐urban soils. In urban and green‐urban soils, Cu, Cr, Ni and Pb levels were above the natural background levels, due to anthropogenic inputs in the city. Results of microbiological analyses were controversial. According to most probable number (MPN), there was no significant difference between types of site for bacterial and fungal numbers in soil. However, dehydrogenase activity and the number of bacterial cells were larger in non‐urban than in urban soils. It was also found that microbial parameters were influenced by many soil properties, for example organic matter and macronutrient (N, P, K) content of soils, the presence and amount of artefacts and metal concentrations in soil.
Rapid temperature responses of photosystem II efficiency forecast genotypic variation in rice vegetative heat tolerance
Authors: Ferguson John N. , McAusland Lorna , Smith Kellie E. , Price Adam H. , Wilson Zoe A. , Murchie Erik H. 
Published: August 2020

SUMMARYA key target for the improvement ofOryza sativa(rice) is the development of heat‐tolerant varieties. This necessitates the development of high‐throughput methodologies for the screening of heat tolerance. Progress has been made to this end via visual scoring and chlorophyll fluorescence; however, these approaches demand large infrastructural investments to expose large populations of adult plants to heat stress. To address this bottleneck, we investigated the response of the maximum quantum efficiency of photosystem II (PSII) to rapidly increasing temperatures in excised leaf segments of juvenile rice plants. Segmented models explained the majority of the observed variation in response. Coefficients from these models, i.e. critical temperature (Tcrit) and the initial response (m1), were evaluated for their usability for forecasting adult heat tolerance, measured as the vegetative heat tolerance of adult rice plants through visual (stay‐green) and chlorophyll fluorescence (ɸPSII) approaches. We detected substantial variation in heat tolerance of a randomly selected set ofindicarice varieties. BothTcritandm1were associated with measured heat tolerance in adult plants, highlighting their usability as high‐throughput proxies. Variation in heat tolerance was associated with daytime respiration but not with photosynthetic capacity, highlighting a role for the non‐photorespiratory release of CO2in heat tolerance. To date, this represents the first published instance of genetic variation in these key gas‐exchange traits being quantified in response to heat stress in a diverse set of rice accessions. These results outline an efficient strategy for screening heat tolerance and accentuate the need to focus on reduced rates of respiration to improve heat tolerance in rice.
The biosynthesis of the anti‐microbial diterpenoid leubethanol in Leucophyllum frutescens proceeds via an all‐cis prenyl intermediate
Authors: Miller Garret P. , Bhat Wajid Waheed , Lanier Emily R. , Johnson Sean R. , Mathieu Davis T. , Hamberger Björn 
Published: August 2020

SUMMARYSerrulatane diterpenoids are natural products found in plants from a subset of genera within the figwort family (Scrophulariaceae). Many of these compounds have been characterized as having anti‐microbial properties and share a common diterpene backbone. One example, leubethanol from Texas sage (Leucophyllum frutescens) has demonstrated activity against multi‐drug‐resistant tuberculosis. Leubethanol is the only serrulatane diterpenoid identified from this genus; however, a range of such compounds have been found throughout the closely related Eremophila genus. Despite their potential therapeutic relevance, the biosynthesis of serrulatane diterpenoids has not been previously reported. Here we leverage the simple product profile and high accumulation of leubethanol in the roots of L. frutescens and compare tissue‐specific transcriptomes with existing data from Eremophila serrulata to decipher the biosynthesis of leubethanol. A short‐chain cis‐prenyl transferase (LfCPT1) first produces the rare diterpene precursor nerylneryl diphosphate, which is cyclized by an unusual plastidial terpene synthase (LfTPS1) into the characteristic serrulatane diterpene backbone. Final conversion to leubethanol is catalyzed by a cytochrome P450 (CYP71D616) of the CYP71 clan. This pathway documents the presence of a short‐chain cis‐prenyl diphosphate synthase, previously only found in Solanaceae, which is likely involved in the biosynthesis of other known diterpene backbones in Eremophila. LfTPS1 represents neofunctionalization of a compartment‐switching terpene synthase accepting a novel substrate in the plastid. Biosynthetic access to leubethanol will enable pathway discovery to more complex serrulatane diterpenoids which share this common starting structure and provide a platform for the production and diversification of this class of promising anti‐microbial therapeutics in heterologous systems.
Rates and causes of mortality among children and young people with and without intellectual disabilities in Scotland: a record linkage cohort study of 796 190 school children
Authors: Smith Gillian S , Fleming Michael , Kinnear Deborah , Henderson Angela , Pell J P , Melville Craig , Cooper Sally-Ann 
Published: August 2020

ObjectivesTo investigate mortality rates and causes in children and young people with intellectual disabilities.DesignRetrospective cohort; individual record linkage between Scotland’s annual pupil census and National Records of Scotland death register.SettingGeneral community.ParticipantsPupils receiving local authority-funded schooling in Scotland, 2008 to 2013, with an Additional Support Need due to intellectual disabilities, compared with other pupils.Main outcome measuresDeaths up to 2015: age of death, age-standardised mortality ratios (age-SMRs); causes of death including cause-specific age-SMRs; avoidable deaths as defined by the UK Office of National Statistics.Results18 278/947 922 (1.9%) pupils had intellectual disabilities. 106 died over 67 342 person-years (crude mortality rate=157/100 000 person-years), compared with 458 controls over 3 672 224 person-years (crude mortality rate=12/100 000 person-years). Age-SMR was 11.6 (95% CI 9.6 to 14.0); 16.6 (95% CI 12.2 to 22.6) for female pupils and 9.8 (95% CI 7.7 to 12.5) for male pupils. Most common main underlying causes were diseases of the nervous system, followed by congenital anomalies; most common all-contributing causes were diseases of the nervous system, followed by respiratory system; most common specific contributing causes were cerebral palsy, pneumonia, respiratory failure and epilepsy. For all contributing causes, SMR was 98.8 (95% CI 69.9 to 139.7) for congenital anomalies, 76.5 (95% CI 58.9 to 99.4) for nervous system, 63.7 (95% CI 37.0 to 109.7) for digestive system, 55.3 (95% CI 42.5 to 72.1) for respiratory system, 32.1 (95% CI 17.8 to 57.9) for endocrine and 14.8 (95% CI 8.9 to 24.5) for circulatory system. External causes accounted for 46% of control deaths, but the SMR for external-related deaths was still higher (3.6 (95% CI 2.2 to 5.8)) for pupils with intellectual disabilities. Deaths amenable to good care were common.ConclusionPupils with intellectual disabilities were much more likely to die than their peers, and had a different pattern of causes, including amenable deaths across a wide range of disease categories. Improvements are needed to reduce amenable deaths, for example, epilepsy-related and dysphagia, and to support families of children with life-limiting conditions.
Constraining the tidal charge of brane black holes using their shadows
Authors: Neves Juliano C. S. 
Published: August 2020

AbstractA constraint on the tidal charge generated within a brane world is shown. Using the shadow of a rotating black hole in a brane context in order to describe the M87* parameters recently announced by the Event Horizon Telescope Collaboration, the deviation from circularity of the reported shadow produces an upper bound on the bulk’s nonlocal effect, which is conceived of as a tidal charge in the four-dimensional brane induced by the five-dimensional bulk. Therefore, a deviation from circularity $$\lesssim 10\%$$≲10% leads to an upper bound on the tidal charge $$\lesssim 0.004M^2$$≲0.004M2.
Clinical Characteristics of COVID-19 Patients with and without Diabetes in Wuhan Red Cross Hospital
Authors: Li Guozhen , Deng Qin , Feng Jiali , Li Fang , Xiong Nian , He Qiong 
Published: August 2020

Background. Since the end of December 2019, novel coronavirus- (SARS-CoV-2-) infected pneumonia (COVID-19) has spread rapidly in China. The study was designed to describe the clinical characteristics of COVID-19 patients with and without diabetes in Wuhan. Methods. 199 COVID-19 patients were admitted to Wuhan Red Cross Hospital in China from January 24th to March 15th. The cases were divided into the diabetic and nondiabetic groups according to the history of taking antidiabetic drugs or by plasma fasting blood glucose level at admission, and the differences between the groups were compared. A multivariable analysis of independent risk factors for in-hospital death was performed. Results. Among 199 COVID-19 patients, 76 were diabetic and 123 were nondiabetic. Compared with nondiabetics, patients with diabetes were older and had high levels of fasting plasma glucose (FPG), D-dimer, white blood cells, blood urea nitrogen (BUN), and total bilirubin (TBIL) and lower levels of lymphocytes, albumin and oxygen saturation (SaO2), and higher mortality (

P
<
0.05

). The two groups showed no difference in clinical symptoms. Diabetes (odds ratio (OR): 10.816, 95% CI (confidence interval): 1.895-61.741,

P
=
0.007

), higher level of D-dimer at admission (OR: 1.094, 95% CI: 1.017-1.178,

P
=
0.016

), and a

lymphocyte

count
<
0.6
×

10

9

/
L

at admission (OR: 7.609, 95% CI: 1.087-32.049,

P
=
0.006

) were associated with increasing odds of death. Antidiabetic drugs were associated with decreasing odds of death. Treatment with low molecular weight heparin was not related to odds of death. Conclusion. The mortality rate of COVID-19 patients with diabetes was significantly higher than those without diabetes. Diabetes, higher level of D-dimer, and a

lymphocyte

count
<
0.6
×

10

9

/
L

at admission were the risk factors associated with in-hospital death.
Association Between Mental Stress-Induced Inferior Frontal Cortex Activation and Angina in Coronary Artery Disease
Authors: Moazzami Kasra , Wittbrodt Matthew T. , Alkhalaf Mhmtjamil , Lima Bruno B. , Nye Jonathon A. , Mehta Puja K. , Quyyumi Arshed A. , Vaccarino Viola , Bremner J. Douglas , Shah Amit J. 
Published: August 2020

Background:
The inferior frontal lobe is an important area of the brain involved in the stress response, and higher activation with acute mental stress may indicate a more severe stress reaction. However, it is unclear if activation of this region with stress correlates with angina in individuals with coronary artery disease.

Methods:
Individuals with stable coronary artery disease underwent acute mental stress testing using a series of standardized speech/arithmetic stressors in conjunction with high resolution positron emission tomography imaging of the brain. Blood flow to the inferior frontal lobe was evaluated as a ratio compared with whole brain flow for each scan. Angina was assessed with the Seattle Angina Questionnaire’s angina frequency subscale at baseline and 2 years follow-up.

Results:

We analyzed 148 individuals with coronary artery disease (mean age [SD] 62 [8] years; 69% male, and 35.8% Black). For every doubling in the inferior frontal lobe activation, angina frequency was increased by 13.7 units at baseline (

, 13.7 [95% CI, 6.3–21.7];
P
=0.008) and 11.6 units during follow-up (

, 11.6 [95% CI, 4.1–19.2];
P
=0.01) in a model adjusted for baseline demographics. Mental stress-induced ischemia and activation of other brain pain processing regions (thalamus, insula, and amygdala) accounted for 40.0% and 13.1% of the total effect of inferior frontal lobe activation on angina severity, respectively.

Conclusions:
Inferior frontal lobe activation with mental stress is independently associated with angina at baseline and during follow-up. Mental stress-induced ischemia and other pain processing brain regions may play a contributory role.
Management of Aortic Stenosis in Patients With End-Stage Renal Disease on Hemodialysis
Authors: Mentias Amgad , Desai Milind Y. , Saad Marwan , Horwitz Phillip A. , Rossen James D. , Panaich Sidakpal , Jneid Hani , Kapadia Samir , Vaughan-Sarrazin Mary 
Published: August 2020

Background:
Patients with end-stage renal disease on hemodialysis (ESRD-HD) and aortic stenosis have poor prognosis. The role of transcatheter aortic valve replacement (TAVR) in this high-risk population is debated.

Methods:
We compared the outcomes among ESRD-HD Medicare beneficiaries who were managed with TAVR, surgical AVR (SAVR), or conservative management for aortic stenosis between 2015 and 2017, using overlap propensity score weighting analysis to control for differences in treatment assignment. The primary outcome was all-cause mortality and was compared between treatment groups as well as to age-sex matched mortality for ESRD-HD in the US population. Secondary outcomes included trend of heart failure hospitalizations.

Results:

A total of 8107 ESRD-HD patients with aortic stenosis were included, 4130 (50%) underwent TAVR, 2565 (31.6%) underwent SAVR, and 1412 (17.4%) were managed conservatively. TAVR patients had more comorbidities and higher frailty compared with the other 2 groups. Thirty-day mortality was lower with TAVR compared with SAVR (4.6% versus 12.8%,
P
<0.01). After a median follow-up of 465 days (interquartile range, 261–759), on overlap propensity score weighting analysis, there was no difference in mortality between TAVR and SAVR (adjusted hazard ratio, 1.02 [95% CI, 0.91–1.15],
P
=0.7), and mortality was lower with TAVR compared with conservative management (adjusted hazard ratio, 0.53 [95% CI, 0.47–0.60],
P
<0.001). Standardized mortality ratios with TAVR, SAVR, and conservative management compared with age-sex matched ESRD-HD US population were 1.24, 1.27, and 1.83, respectively. The rate of heart failure admissions declined after TAVR (incidence rate ratio, 0.55 [95% CI, 0.48–0.62],
P
<0.001) and SAVR (incidence rate ratio, 0.76 [95% CI, 0.65–0.88],
P
<0.001).

Conclusions:
In ESRD-HD patients with aortic stenosis, mortality was lower in the short-term with TAVR compared with SAVR but comparable in the mid-term. AVR is associated with an improvement in survival and reduction in heart failure hospitalizations compared with conservative management.
Epigenomic and Transcriptomic Dynamics During Human Heart Organogenesis
Authors: VanOudenhove Jennifer , Yankee Tara N. , Wilderman Andrea , Cotney Justin 
Published: August 2020

Rationale:
There is growing evidence that common variants and rare sequence alterations in regulatory sequences can result in birth defects or predisposition to disease. Congenital heart defects are the most common birth defect and have a clear genetic component, yet only a third of cases can be attributed to structural variation in the genome or a mutation in a gene. The remaining unknown cases could be caused by alterations in regulatory sequences.

Objective:
Identify regulatory sequences and gene expression networks that are active during organogenesis of the human heart. Determine whether these sites and networks are enriched for disease-relevant genes and associated genetic variation.

Methods and Results:

We characterized ChromHMM (chromatin state) and gene expression dynamics during human heart organogenesis. We profiled 7 histone modifications in embryonic hearts from each of 9 distinct Carnegie stages (13–14, 16–21, and 23), annotated chromatin states, and compared these maps to over 100 human tissues and cell types. We also generated RNA-sequencing data, performed differential expression, and constructed weighted gene coexpression networks. We identified 177 412 heart enhancers; 12 395 had not been previously annotated as strong enhancers. We identified 92% of all functionally validated heart-positive enhancers (n=281; 7.5× enrichment;
P
<2.2×10
−16
). Integration of these data demonstrated novel heart enhancers are enriched near genes expressed more strongly in cardiac tissue and are enriched for variants associated with ECG measures and atrial fibrillation. Our gene expression network analysis identified gene modules strongly enriched for heart-related functions, regulatory control by heart-specific enhancers, and putative disease genes.

Conclusions:
Well-connected hub genes with heart-specific expression targeted by embryonic heart-specific enhancers are likely disease candidates. Our functional annotations will allow for better interpretation of whole genome sequencing data in the large number of patients affected by congenital heart defects.
Vascular Endothelial Growth Factor 165-Binding Heparan Sulfate Promotes Functional Recovery From Cerebral Ischemia
Authors: Chan Su Jing , Esposito Elga , Hayakawa Kazuhide , Mandaville Emiri , Smith Raymond A.A. , Guo Shuzhen , Niu Wanting , Wong Peter Tsun-Hong , Cool Simon M. , Lo Eng H. , Nurcombe Victor 
Published: August 2020

Background and Purpose:

Although VEGF
165
(vascular endothelial growth factor-165) is able to enhance both angiogenesis and neurogenesis, it also increases vascular permeability through the blood-brain barrier. Heparan sulfate (HS) sugars play important roles in regulating VEGF bioactivity in the pericellular compartment. Here we asked whether an affinity-purified VEGF
165
-binding HS (HS7) could augment endogenous VEGF activity during stroke recovery without affecting blood-brain barrier function.

Methods:
Both rat brain endothelial cell line 4 and primary rat neural progenitor cells were used to evaluate the potential angiogenic and neurogenic effects of HS7 in vitro. For in vivo experiments, male Sprague-Dawley rats were subjected to 100 minutes of transient focal cerebral ischemia, then treated after 4 days with either PBS or HS7. One week later, infarct volume, behavioral sequelae, immunohistochemical markers of angiogenesis and neural stem cell proliferation were assessed.

Results:

HS7 significantly enhanced VEGF
165
-mediated angiogenesis in rat brain endothelial cell line 4 brain endothelial cells, and increased the proliferation and differentiation of primary neural progenitor cells, both via the VEGFR2 (vascular endothelial growth factor receptor 2) pathway. Intracerebroventricular injection of HS7 improved neurological outcome in ischemic rats without changing infarct volumes. Immunostaining of the compromised cerebrum demonstrated increases in collagen IV/Ki67 and nestin/Ki67 after HS7 exposure, consistent with its ability to promote angiogenesis and neurogenesis, without compromising blood-brain barrier integrity.

Conclusions:

A VEGF-activating glycosaminoglycan sugar, by itself, is able to enhance endogenous VEGF
165
activity during the post-ischemic recovery phase of stroke.
Dynamic Regional Brain Atrophy Rates in the First Year After Ischemic Stroke
Authors: Brodtmann Amy , Khlif Mohamed Salah , Egorova Natalia , Veldsman Michele , Bird Laura J. , Werden Emilio 
Published: August 2020

Background and Purpose:
Brain atrophy can be regarded as an end-organ effect of cumulative cardiovascular risk factors. Accelerated brain atrophy is described following ischemic stroke, but it is not known whether atrophy rates vary over the poststroke period. Examining rates of brain atrophy allows the identification of potential therapeutic windows for interventions to prevent poststroke brain atrophy.

Methods:
We charted total and regional brain volume and cortical thickness trajectories, comparing atrophy rates over 2 time periods in the first year after ischemic stroke: within 3 months (early period) and between 3 and 12 months (later period). Patients with first-ever or recurrent ischemic stroke were recruited from 3 Melbourne hospitals at 1 of 2 poststroke time points: within 6 weeks (baseline) or 3 months. Whole-brain 3T magnetic resonance imaging was performed at 3 time points: baseline, 3 months, and 12 months. Eighty-six stroke participants completed testing at baseline; 125 at 3 months (76 baseline follow-up plus 49 delayed recruitment); and 113 participants at 12 months. Their data were compared with 40 healthy control participants with identical testing. We examined 5 brain measures: hippocampal volume, thalamic volume, total brain and hemispheric brain volume, and cortical thickness. We tested whether brain atrophy rates differed between time points and groups. A linear mixed-effect model was used to compare brain structural changes, including age, sex, years of education, a composite cerebrovascular risk factor score, and total intracranial volume as covariates.

Results:
Atrophy rates were greater in stroke than control participants. Ipsilesional hemispheric, hippocampal, and thalamic atrophy rates were 2 to 4 times greater in the early versus later period.

Conclusions:
Regional atrophy rates vary over the first year after stroke. Rapid brain volume loss in the first 3 months after stroke may represent a potential window for intervention.

Registration:

URL:
https://www.clinicaltrials.gov
. Unique identifier: NCT02205424.