bluuebunny/crossref_metadata_2025_split huggingface dataset:
Routine snuffbox approach do not reduce radial artery occlusion in comparison with conventional transradial access
Authors: Kozinski L , Dabrowska-Kugacka A , Orzalkiewicz Z 
Published: October 2021

Abstract

Background/Introduction
Postprocedural radial artery occlusion (RAO) is still the Achilles' heel of conventional transradial approach (cTRA) as it limits its reuse for future coronary procedures. A distal transradial access (dTRA) via the anatomical snuffbox has been proposed as an alternative. It is hypothesised that dTRA may reduce the incidence of RAO.

Purpose
To assess whether routine dTRA reduce the risk of RAO in consecutive patients undergoing coronary angiography or intervention, in comparison with cTRA.

Methods
Out of 465 subjects, 400 patients were included in a prospective, single-center, randomized (1:1) study. Hemodynamic instability, ST-elevation myocardial infarction, forearm artery occlusion or prior radial access failure were the exclusion criteria. Ultrasound-guided follow-up was obtained after 1 day and 60 days to evaluate the incidence of acute and late RAO.

Results
Baseline characteristics of patients were matched. Results are presented in table 1.

Conclusion(s)
The incidence of postprocedural acute and late RAO after routine dTRA and cTRA is low and occur with similar frequency when evaluated by ultrasound.

Funding Acknowledgement
Type of funding sources: None. Table 1
Age and gender disparities in the prevalence of lipitension
Authors: Grinshtein Y U , Ruf R , Shabalin V 
Published: October 2021

Abstract

Introduction
Lipitension is the presence of hypertension and dyslipidaemia in one person. It multiplies cardiovascular risk up to three-fold and therefore requires timely diagnosing and treatment.

Purpose
In the present study, we calculated the prevalence of lipitension and its disparities depending on gender and age.

Methods
We used the randomized sample of the ESSE-RF study that included 1603 urban and rural Krasnoyarsk Krai inhabitants aged 25–64. Each study participant signed informed consent and underwent the questionnaire, office blood pressure measurement, anthropometry, and biochemical blood analysis. Hypertension criteria were the measured systolic blood pressure at 140 mm Hg or higher, the measured diastolic blood pressure at 90 mm Hg or higher, or antihypertensive medications intake. Dyslipidaemia criteria were the total cholesterol level higher than 5.0 mmol/l, the low-density lipoprotein level higher than 3.0 mmol/l, the high-density lipoprotein level lower than 1.0 mmol/l in males and 1.2 mmol/l in females, or triglycerides level higher than 1.7 mmol/l.

Results
In 40.0% of people, we found a combination of at least one hypertension criterion and at least one dyslipidaemia criterion. The prevalence of lipitension significantly (chi-square for trend; p&lt;0.001) increased from 10.7% in the 25–34 age group to 66.6% in the 55–64 age group. At a younger age, males had dyslipidaemia more frequently than females, while at 55–64, the prevalence of lipitension was higher in females. The details of age and gender disparities are shown in Table 1.

Conclusion
At least 40% of the general population and two-thirds of people older than 55 have lipitension and need a combined antihypertensive and lipid-lowering therapy.

Funding Acknowledgement
Type of funding sources: None. Table 1
DPP4 inhibitors as a risk factor for QTC interval prolongation among type 2 diabetic patients
Authors: Enero R J , Amora J 
Published: October 2021

Abstract

Introduction
Prolonged QT interval is associated with cardiac arrhythmias and sudden death. This study determined the prevalence of QT intervals corrected for heart rate (QTc) among adults admitted for executive check up in a tertiary hospital with Type 2 diabetes and its associations with metabolic control.

Methods
This cross-sectional study included 111 adult patients with Type 2 diabetes and 152 control patients admitted for executive check up in a tertiary hospital. A standard 12-lead electrocardiogram was recorded. Corrected QT interval (QTc) of &gt;440 ms was considered abnormally prolonged and QTc &gt;500 ms was considered a high-risk QTc. Demographic, clinical and laboratory data were collected. Independent risk factors for prolonged QTc were assessed using logistic regression analysis.

Results
QTc duration was statistically significant between subjects with Type 2 diabetes and control subjects (mean duration 434 vs 419 ms; P=0.003). Prevalence of prolonged QTc among type 2 diabetics is 41.4% and 28% in the control group. In the diabetic group 2.7% has a QTc of &gt;500. Independent risk factors for prolonged QTc using univariate logistic regression analysis is presence of diabetes type 2 (OR = 2.00, p=0.008), HBA1c (OR = 1.23, p=0.050) and intake of DPP4 (OR=6.46, (p≤0.001). Independent risk factors for prolonged QTc using multivariate logistic regression analysis is intake of DPP4 inhibitors (OR=6.26, p=0.023).

Conclusion
There is no significant correlation between HBA1C and QTc interval. The prevalence of prolonged QTc is relatively high among diabetics but the prevalence of high risk QTc interval is relatively low. Intake of DPP4 inhibitors is an independent risk factor in QT prolongation.

Funding Acknowledgement
Type of funding sources: None.
Feasibility of remote support for electrophysiological ablation procedures during CoVid-19 pandemics
Authors: Muessigbrodt A , Demoniere F , Finoly S , Mommarche M , Inamo J 
Published: October 2021

Abstract

The COVID-19 pandemics is a global challenge with a huge impact on medicine, politics, economy, education, travel and many other aspects of human life.
The treatment of heart rhythm disorders has also been affected by the disease itself and by restrictions in order to constrain the spread of the virus.
Catheter ablations of cardiac arrhythmias are nowadays frequently guided by electro-anatomic mapping systems. Technical staff with medical training, or medical staff with technical training, is needed to assist the operator. Travel restrictions due to current COVID-19 pandemics have limited the in person availability for technical support staff. To overcome these limitations we explored the feasibility of remote support with an internet based communication platform.
A total of 9 patients (87,5% male, mean age 66,6 years) with different arrhythmias (atrial fibrillation, left atrial flutter, typical right atrial flutter, left ventricular tachycardia), having undergone ablation procedures between October 2020 and February 2021, were included. Acute procedural success was obtained in 9 out of 9 procedures. No complications occurred.
Our experience with remote support for electro-anatomic mapping for complex electrophysiological ablation procedures, show the feasibility and safety of this approach. It increases the availability of technical support at reduced costs and a reduced CO2 footprint. Remote support for electro-anatomic mapping may therefore facilitate continuous care for patients with arrhythmias during the COVID-19 pandemics. Due to its advantages beyond COVID-19 pandemics related problems, it will likely play a greater role in the future.

Funding Acknowledgement
Type of funding sources: None.
The biomarker macrophage migration inhibitory factor as a predictor of no-reflow phenomenon and other adverse events in patients with ST-segment elevation myocardial infarction
Authors: Vishnevskaya I , Kopytsya M P , Storozhenko T Y E 
Published: October 2021

Abstract

Major adverse cardiovascular events (MACE) in patients with ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI) may be caused by the “no-reflow” phenomenon. Biomarkers for the “no-reflow” phenomenon prediction is being actively studied. Proinflammatory cytokine macrophage migration inhibitory factor (MIF) is one of the promising biomarkers.

Purpose
To estimate the role of MIF in the prediction of early reperfusion myocardial injury and MACE in patients with STEMI.

Methods
The study involved 341 STEMI patients (78.6% male and 21.4% female) with an average age of 59.08±9.65 years. Control group of 12 healthy volunteers included. All patients were made to undergo a baseline investigation. In addition, the level of MIF and soluble suppression of tumorigenicity-2 (sST2) determined twice during the first 12 hours of STEMI, before the PCI and 24 hours after the procedure. Coronary blood flow evaluated using TIMI flow grade and myocardial blush grade (MBG). All patients had epicardial blood flow TIMI 3. The criteria for “no-reflow” diagnosis were myocardial perfusion at MBG 0 or MBG 1 level with complete recovery of epicardial blood flow or ST-segment resolution (rST) of less than 70% from baseline within 2 hours after PCI. All patients were divided into two groups according to MBG and rST after PCI more and less than 70%: 147 patients in the first group with MBG stage 0–1, 182 patients with MBG stage 2–3.

Results
The level of MIF biomarker determined before PCI was significantly higher in the group of patients with MBG 0–1 in comparison to MBG 2–3. (4386,750±676 pg/ml vs 2935±350 pg/ml; p=0,05). Also, the level of sST2, left ventricular mass index and blood glucose were significantly higher in the group of MBG 0–1 (p=0.03, p=0.006 and p=0.0085, respectively). The difference in left ventricle posterior wall thickness and early to late diastolic transmitral flow velocity (p=0.045) was found between two groups. In the group of MBG 0–1 and rST&lt;70% these parameters were significantly lower (p=0,04 and p=0,05, respectively).
Using the multivariate regression analysis, the dependency of the biomarker MIF on the parameters of the reperfusion myocardial injuries were obtained. MIF measured before revascularization was an independent predictor of MBG 0–1 and rST less than 70% (coefficients Beta 0,00057; odd ratio 1,0; 95%confidential interval (CI) 1,0–1,001; p=0,038). The Kaplan-Meier survival analysis showed that long-term adverse outcomes rate after STEMI was significantly higher in patient with the level of MIF determined during the first 12 hours after the event more than 2988 pg/ml (Log-rank = −4,891, p=0.014).

Conclusions
Biomarkers MIF has a capacity as predictive tool for MACE and “no-reflow” phenomenon in STEMI patients.

Funding Acknowledgement
Type of funding sources: None.
Lifelong dietary omega-3 fatty acid reverses cardiac and vascular dysfunction via MMP-2 modulation in aged mice
Authors: Saeedi Saravi S S , Bonetti N R , Vukolic A , Liberale L , Vdovenko D , Luscher T F , Camici G G , Beer J H 
Published: October 2021

Abstract

Background
Aging has a remarkable effect on the cardiovascular system, and negatively causes structural and functional changes in the heart including diastolic/systolic dysfunction and left ventricular (LV) dyssynchrony, as well as, arterial stiffness which may develop to heart failure with preserved ejection fraction (HFpEF) in aged adults. We recently showed that the plant-derived omega-3-fatty-acid α-linolenic-acid (ALA) has emerged to confer potential protective effects against cardiovascular disease. Since cardiovascular aging is a chronic process, we hypothesized that a lifelong effective dietary supplementation with ALA will reverse or prevent age-related diastolic and arterial dysfunction during aging.

Purpose
Here, we test the hypotheses that (1) lifelong dietary ALA will prevent LV diastolic and arterial dysfunction in aged mice and that (2) lifelong dietary ALA will prevent the age-related cardiovascular dysfunction through modiulation of matrix-metalloproteinase-2 (MMP-2) in the heart and arteries.

Methods and results
6-month-old (young) wild-type C57BL/6J mice were fed a low (0.03%), as control, or high ALA (7.3%) diet for more than 12 months. Our results show that aged (&gt;18 months) mice on low ALA diet recapitulate major hallmarks of HFpEF, including diastolic dysfunction with preserved left ventricular ejection fraction, cardiac interstitial fibrosis, impaired acetylcholine-induced relaxation of aortic segments, and arterial stiffness. Intriguingly, we revealed that lifelong ALA-rich diet prevents diastolic dysfunction, vascular relaxation capacity, reduced pulse wave velocity, interstitial fibrosis, and coincident hemodynamic abnormalities in aged mice. Lifelong dietary ALA-in the prevention strategy-was associated with remarkably reduced cardiac and aortic MMP-2 and COX-2 expression, lower levels of pro-inflammatory cytokine TNF-α, and increased isocitrate dehydrogenase 2 (Idh2) expression, decreased function of which has previously been associated with cardiac dysfunction.

Conclusions
Our data support that lifelong ALA-rich diet restores normal cardiac and vascular function in aged mice with LV diastolic and arterial dysfunction and prevents development of age-related cardiovascular dysfunction through the modulation of MMP-2 signaling.

Funding Acknowledgement
Type of funding sources: Public Institution(s). Main funding source(s): 1. Swiss National Science Foundation (number 324730_182328)2. the Kardio Stiftung, Baden, Switzerland
A pro-resolving phenotype underpins the anti-inflammatory effects of inorganic nitrate
Authors: Primus C , Masucci M , Whitear C , Montalvo Moreira S A , Ajit Kumar N , Chhetri I , Rathod K S , Khambata R , Kapil V , Ahluwalia A 
Published: October 2021

Abstract

Introduction
Increasing evidence highlights the critical role of chronic inflammation in cardiovascular disease (CVD). Targeting inflammatory pathways in patients with CVD has been associated with improved CV function in pre-clinical (Gee, 2017), early clinical (Yndestad, 2006; Velmurugan 2013; Jones, 2016) and large phase III studies (Ridker, 2017).
The resolution of inflammation is an active process and its failure has also been proposed to contribute to CVD progression. At least one mechanism thought to underlie this failure is dysfunction of the canonical pathway for anti-inflammatory nitric oxide (NO) production. Restoring NO through provision of inorganic nitrate (NO3-) and subsequent bioactivation via the non-canonical pathway may offer therapeutic benefit.

Aim
To test whether dietary NO3–derived NO accelerates resolution of inflammation.

Methods
Randomised, double-blind, placebo-controlled, parallel limb study of 8–10mmol dietary NO3- supplementation versus NO3–deplete placebo beetroot juice in 36 healthy male volunteers (NCT03183830). Using a cantharadin-induced skin blister model (Day, 2001), acute (24h) and chronic (72h)-phase blisters were harvested pre- and post-treatment. Blister exudate was analysed for leucocyte activation state (CD11b, CD62L, CD162) by flow cytometry and cytokine/chemokine composition by ELISA. Ozone chemiluminescence established NO3-/NO2- levels in key biological matrices: plasma, urine and saliva.

Results
9.3mmol inorganic NO3- led to a significant rise (versus placebo, p&lt;0.001) of NO3-/NO2- in plasma, saliva and urine NO2- (p&lt;0.02). No differences were seen in blister volumes, cell counts or markers of systemic inflammation. Whilst no differences were seen in the proportions of cellular infiltrate in 24h blisters, there were significant reductions of neutrophil (p=0.017) and intermediate monocyte proportions (p=0.001) and cellular adhesion molecules across inflammatory, intermediate and resolving monocytes at 72h (Figure 1). Generally, no differences in blister cytokine/chemokine profile was evident except for borderline significant suppression of TNFα at 24hrs with dietary NO3- treatment (P=0.057).

Conclusion
Whilst dietary inorganic NO3- does not impair the essential host defence response it does accelerate resolution: enhanced pro- to anti-inflammatory monocyte subtype switching and curtailed neutrophil recruitment, likely via attenuated TNFα production. These actions offer a novel, easy to administer, approach to influence inflammatory responses without impairing host defence.

Funding Acknowledgement
Type of funding sources: Public Institution(s). Main funding source(s): Derek Willoughby Trust and British Heart Foundation
The endothelial-enriched lncRNA LINC01235 regulates hypoxia response via HIF-3a
Authors: Gimbel A , Koziarek S , Pham T P , Dimmeler S , Maegdefessel L , Boon R A 
Published: October 2021

Abstract

Background
Cardiovascular diseases (CVDs) remain the leading cause of death worldwide. Hypoxia induces significant changes in cardiovascular control mechanisms potentially resulting in pathophysiology. Recently, an increasing number of long non-coding RNAs (lncRNAs) was reported to participate in the regulation of Hypoxia-inducible factors (HIF). Analysis of single-cell RNA-sequencing of human Abdominal Aortic Aneurysms pinpointed the endothelial-enriched lncRNA LINC01235. LINC01235 was previously correlated with tumour progression in gastric cancer and worse patient prognosis in breast cancer. Globally, the role of LINC01235 in the cardiovascular system remains unknown.

Purpose
The objective of this study is to unravel the function of LINC01235 in endothelial cells (ECs).

Methods and results
LINC01235 levels were elevated in human umbilical vein ECs (7.66 fold, p&lt;0.05), human aortic ECs (16.84 fold, p&lt;0.05) and human dermal microvascular ECs (639.73 fold, p&lt;0.05) over other human cardiovascular cells like vascular smooth muscle cells, aortic fibroblasts and cardiomyocytes. Severe hypoxia (0.2% O2 for 24h) reduced LINC01235 expression significantly (0.33 fold, p&lt;0.05). SiRNA-mediated LINC01235 silencing in HUVECs (0.12, p&lt;0.05) resulted in decreased proliferation (0.76 fold, p&lt;0.05) and vascular endothelial growth factor A (VEGFA)-stimulated angiogenic sprouting (0.39 fold, p&lt;0.05). Loss of LINC01235 did not affect apoptosis, metabolism or barrier function. Analysis of RNA-sequencing data revealed that many hypoxia-responsive genes were downregulated after knockdown of LINC01235 (siCtrl vs. siLINC01235). These included HIF-3α (0.24 fold, p&lt;5.86e-28) as a potential key regulator of the cellular feedback to hypoxia. Phenotypically, knockdown of HIF3A using siRNAs (0.07 fold, p&lt;0.05) resulted in decreased proliferation (0.82 fold, p&lt;0.05) and VEGFA-stimulated angiogenic sprouting (0.50 fold, p&lt;0.05). Accordingly, hypoxia response and LINC01235 knockdown exhibit a negative correlation based on transcriptomics data (R=−0.157, p&lt;2.2e-16), further emphasizing a role of LINC01235 in hypoxia response.

Conclusion
In summary, the EC-enriched lncRNA LINC01235 is likely required for the suppression of hypoxia-induced gene expression under normoxic conditions potentially mediated by HIF-3α. Functionally, loss of LINC01235 decreased proliferation and VEGFA-stimulated angiogenic sprouting without an effect on cell death, metabolism or barrier integrity.

Funding Acknowledgement
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): DFG - TRR267
Platelet-specific deletion of acetyl-CoA carboxylase 1 decreases phospholipid content and impairs platelet functions
Authors: Octave M , Pirotton L , Ginion A , Robaux V , Lepropre S , Kautbally S , Senis Y , Nagy Z , Ambroise J , Guigas B , Giera M , Bertrand L , Beauloye C , Horman S 
Published: October 2021

Abstract

Background
Acetyl-CoA carboxylase (ACC), the first enzyme regulating lipid synthesis, promotes thrombus formation by increasing platelet phospholipid content and thromboxane A2 generation.

Purpose
Our study sought to evaluate whether ACC1 platelet-specific deletion may affect platelet functions by decreasing phospholipid content.

Methods
We generated a new Cre transgenic mouse strain that allows megakaryocyte/platelet specific ACC1 deletion (GpIbCre+/− x ACC1 flx/flx mouse). In vitro, platelet functions were assessed by aggregometry and flow cytometry. In vivo, hemostasis was assessed via the measurement of bleeding time. Lipidomics analysis was carried out on the commercial Lipidyzer platform. Thromboxane A2 secretion was evaluated by ELISA.

Results
As expected, ACC1 deletion was restricted to the megakaryocytic lineage. Hematological parameters in platelet-specific ACC1 knockout mice showed a decrease in platelet count by 30% and an increase in platelet volume by 31%, compared to ACC1 flx/flx platelets. In vitro, platelets from platelet-specific ACC1 knockout mice displayed a decrease in thrombin and CRP-induced platelet aggregation, associated with impaired dense granules secretion. In contrast, ADP-induced platelet aggregation was higher in the absence of ACC1. In vivo, platelet-specific ACC1 knockout mice showed a normal bleeding time. In agreement with our hypothesis, lipidomics analyses showed that ACC1 deletion in platelets was associated with a significant decrease in arachidonic acid-contaning phosphatidylethanolamine plasmalogen, and subsequently with a reduced production of thromboxane A2 upon thrombin or CRP stimulation.

Conclusion
Platelet-specific ACC1 deletion led to a decrease in phospholipid content which, in turn, decreased platelet thromboxane A2 generation, dense granules secretion and aggregation upon thrombin and CRP, but not ADP stimulation. Further studies are needed to elucidate the impact of ADP on platelet functions

Funding Acknowledgement
Type of funding sources: Other. Main funding source(s): Fonds pour la formation à la Recherche dans l'Industrie et l'Agriculture (FRIA)
Chromosome-Level Genome Assembly of Nephotettix cincticeps (Uhler, 1896) (Hemiptera: Cicadellidae: Deltocephalinae)
Authors: Yan Bin , Yu Xiaofei , Dai Renhuai , Li Zizhong , Yang Maofa 
Published: October 2021

Abstract
The green rice leafhopper, Nephotettix cincticeps (Uhler), is an important rice pest and a vector of the rice dwarf virus in Asia. Here, we produced a high-quality chromosome-level genome assembly of 753.23 Mb using PacBio (∼110×) and Hi-C data (∼94×). It contained 163 scaffolds and 950 contigs, whose scaffold/contig N50 lengths reached 85.36/2.57 Mb. And 731.19 Mb (97.07%) of the assembly was anchored into eight pseudochromosomes. Genome completeness was attained to 97.0% according to the insect reference Benchmarking Universal Single-Copy Orthologs (BUSCO) gene set (n = 1,367). We masked 347.10 Mb (46.08%) of the genome as repetitive elements. Nine hundred sixty-two noncoding RNAs were identified and 14,337 protein-coding genes were predicted. We also assigned GO term and KEGG pathway annotations for 10,049 and 9,251 genes, respectively. Significantly expanded gene families were primarily involved in immunity, cuticle, digestion, detoxification, and embryonic development. This study provided a crucial genomic resource for better understanding on the biology and evolution in family Cicadellidae.
IPIP27A cooperates with OCRL to support endocytic traffic in the zebrafish pronephric tubule
Authors: Oltrabella Francesca , Jackson-Crawford Anthony , Yan Guanhua , Rixham Sarah , Starborg Tobias , Lowe Martin 
Published: October 2021

Abstract
Endocytosis is a fundamentally important process through which material is internalized into cells from the extracellular environment. In the renal proximal tubule, endocytosis of the abundant scavenger receptor megalin and its co-receptor cubilin play a vital role in retrieving low molecular weight proteins from the renal filtrate. Although we know much about megalin and its ligands, the machinery and mechanisms by which the receptor is trafficked through the endosomal system remain poorly defined. In this study, we show that inositol phosphatase interacting protein of 27 kDa (Ipip27A), an interacting partner of the Lowe syndrome protein oculocerebrorenal syndrome of Lowe (OCRL), is required for endocytic traffic of megalin within the proximal renal tubule of zebrafish larvae. Knockout of Ipip27A phenocopies the endocytic phenotype seen upon loss of OCRL, with a deficit in uptake of both fluid-phase and protein cargo, which is accompanied by a reduction in megalin abundance and altered endosome morphology. Rescue and co-depletion experiments indicate that Ipip27A functions together with OCRL to support proximal tubule endocytosis. The results therefore identify Ipip27A as a new player in endocytic traffic in the proximal tubule in vivo and support the view that defective endocytosis underlies the renal tubulopathy in Lowe syndrome and Dent-2 disease.