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Article ; Online: Experimental Investigation on the Penetrability Mechanism of Gel Slug During Well Completion Processes.

Dou, Xiangji / Du, Yong / Zhang, Yisong / Qian, Kun

ACS omega

2023 Volume 8, Issue 25, Page(s) 23112–23119

Abstract: Reservoir formation damage is an essential problem which troubled oil and gas well production, a smart packer is a promising technology to maintain sustainable development for the oil and gas fields. Currently, the "gel valve" technology has been proved ... ...

Abstract	Reservoir formation damage is an essential problem which troubled oil and gas well production, a smart packer is a promising technology to maintain sustainable development for the oil and gas fields. Currently, the "gel valve" technology has been proved to be feasible with gel slug to seal casing and descend the completion pipe string, while the systemic performance of ideal gel is still not clear. In the underbalanced completion stage with the gel valve, the downward completion string needs to penetrate the gel slug to form an oil and gas passage in the wellbore. The penetration of rod string to gel is a dynamic process. The gel-casing structure often shows a time-dependent mechanical response, which is different from the static response. In the process of penetration, the interaction force between the rod and gel is not only related to the properties of the interface between gel and string but also affected by the moving speed, rod diameter, and thickness of the gel. The dynamic penetration experiment was carried out to determine the penetrating force varied with depth. The research showed that the force curve was mainly composed of three parts, the rising curve of elastic deformation, decline curve for the surface worn out, and another curve of the rod wear into. By changing the rod diameter, gel thickness, and penetration speed, the change rules of forces in each stage were further analyzed, which would provide a scientific basis for a well completion design with a gel valve.
Language	English
Publishing date	2023-06-15
Publishing country	United States
Document type	Journal Article
ISSN	2470-1343
ISSN (online)	2470-1343
DOI	10.1021/acsomega.3c02494
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Article ; Online: Vascular Endothelial Glycocalyx Damage and Potential Targeted Therapy in COVID-19

Duoduo Zha / Mingui Fu / Yisong Qian

Cells, Vol 11, Iss 1972, p

2022 Volume 1972

Abstract: COVID-19 is a highly infectious respiratory disease caused by a new coronavirus known as SARS-CoV-2. COVID-19 is characterized by progressive respiratory failure resulting from diffuse alveolar damage, inflammatory infiltrates, endotheliitis, and ... ...

Abstract	COVID-19 is a highly infectious respiratory disease caused by a new coronavirus known as SARS-CoV-2. COVID-19 is characterized by progressive respiratory failure resulting from diffuse alveolar damage, inflammatory infiltrates, endotheliitis, and pulmonary and systemic coagulopathy forming obstructive microthrombi with multi-organ dysfunction, indicating that endothelial cells (ECs) play a central role in the pathogenesis of COVID-19. The glycocalyx is defined as a complex gel-like layer of glycosylated lipid–protein mixtures, which surrounds all living cells and acts as a buffer between the cell and the extracellular matrix. The endothelial glycocalyx layer (EGL) plays an important role in vascular homeostasis via regulating vascular permeability, cell adhesion, mechanosensing for hemodynamic shear stresses, and antithrombotic and anti-inflammatory functions. Here, we review the new findings that described EGL damage in ARDS, coagulopathy, and the multisystem inflammatory disease associated with COVID-19. Mechanistically, the inflammatory mediators, reactive oxygen species (ROS), matrix metalloproteases (MMPs), the glycocalyx fragments, and the viral proteins may contribute to endothelial glycocalyx damage in COVID-19. In addition, the potential therapeutic strategies targeting the EGL for the treatment of severe COVID-19 are summarized and discussed.
Keywords	COVID-19 ; endothelial cells ; glycocalyx ; syndecan-1 ; heparanase ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Vascular Endothelial Glycocalyx Damage and Potential Targeted Therapy in COVID-19.

Zha, Duoduo / Fu, Mingui / Qian, Yisong

Cells

2022 Volume 11, Issue 12

Abstract	COVID-19 is a highly infectious respiratory disease caused by a new coronavirus known as SARS-CoV-2. COVID-19 is characterized by progressive respiratory failure resulting from diffuse alveolar damage, inflammatory infiltrates, endotheliitis, and pulmonary and systemic coagulopathy forming obstructive microthrombi with multi-organ dysfunction, indicating that endothelial cells (ECs) play a central role in the pathogenesis of COVID-19. The glycocalyx is defined as a complex gel-like layer of glycosylated lipid-protein mixtures, which surrounds all living cells and acts as a buffer between the cell and the extracellular matrix. The endothelial glycocalyx layer (EGL) plays an important role in vascular homeostasis via regulating vascular permeability, cell adhesion, mechanosensing for hemodynamic shear stresses, and antithrombotic and anti-inflammatory functions. Here, we review the new findings that described EGL damage in ARDS, coagulopathy, and the multisystem inflammatory disease associated with COVID-19. Mechanistically, the inflammatory mediators, reactive oxygen species (ROS), matrix metalloproteases (MMPs), the glycocalyx fragments, and the viral proteins may contribute to endothelial glycocalyx damage in COVID-19. In addition, the potential therapeutic strategies targeting the EGL for the treatment of severe COVID-19 are summarized and discussed.
MeSH term(s)	COVID-19/drug therapy ; Capillary Permeability ; Endothelial Cells/metabolism ; Glycocalyx/metabolism ; Humans ; SARS-CoV-2
Language	English
Publishing date	2022-06-19
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11121972
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Article ; Online: NMMHC IIA triggered lipid metabolize reprogramming resulting in vascular endothelial cellular tight junction injury.

Lv, Yanni / Hong, Daojun / Fu, Longsheng / Qian, Yisong

Molecular biology reports

2022 Volume 49, Issue 4, Page(s) 2805–2819

Abstract: Background and purpose: Nonmuscle myosin heavy chain IIA, played an essential role in the promotion of tight junction injury in vascular endothelial cells under oxygen glucose deprivation condition. Rat microvascular endothelial cells had been confirmed ...

Abstract	Background and purpose: Nonmuscle myosin heavy chain IIA, played an essential role in the promotion of tight junction injury in vascular endothelial cells under oxygen glucose deprivation condition. Rat microvascular endothelial cells had been confirmed to have the susceptibility to ox-LDL stimulation under OGD condition. We proposed the hypothesis that lipid metabolic reprogramming might be the root cause for damage to RBMCs tight junction. Methods: Untargeted shotgun and targeted lipid metabolomics mass spectrometry approaches combined with principal component analysis was applied to better define the lipids contributing to the variance observed between control and different OGD time. The protein expression of tight junction of RBMCs: occludin, claudin-5, and ZO-1 were detected with immunofluorescence staining and western blot. The proof of the interaction between NMMHC IIA and SREBP1 was investigated via GST-pull down, while their specific binding fragments were also confirmed. The regulation mechanism of NMMHC IIA on SREBP1 was investigated to explore downstream regulatory signaling pathways. Results: Untargeted and targeted shotgun lipidomics data revealed that OGD might be the conditional factor in reshaping lipid components. Mechanistic studies showed that with the increase of OGD time, PCA analysis of lipidomics obtained from RBMCs indicated their specificity in reshaping lipid components, while ≥80% major lipid components phospholipids and sphingolipids transferred from phospholipids, sphingolipids, and neutral lipids, of which neutral lipids taken the largest proportion with OGD time course. Perturbing reprogramming of lipid composition was less susceptible to OGD condition via knockdown of NMMHC IIA of vascular endothelial cells. Knockdown of NMMHC IIA could promote tight junction defense to OGD condition. NMMHC IIA could directly bind with SREBP1, then could affect sterol regulatory element binding protein-1 to adjust lipid metabolize reprogramming of RBMCs. Conclusions: Mechanistic studies showed that perturbing reprogramming of lipid composition could enhance tight junction damage, which was mediated by the opposing effects of NMMHC IIA.
MeSH term(s)	Animals ; Endothelial Cells/metabolism ; Glucose/metabolism ; Lipids ; Rats ; Signal Transduction ; Tight Junctions/metabolism
Chemical Substances	Lipids ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-01-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-021-07092-4
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Article ; Online: Mechanisms of Endothelial Cell Membrane Repair: Progress and Perspectives.

Zha, Duoduo / Wang, Shizhen / Monaghan-Nichols, Paula / Qian, Yisong / Sampath, Venkatesh / Fu, Mingui

Cells

2023 Volume 12, Issue 22

Abstract: Endothelial cells are the crucial inner lining of blood vessels, which are pivotal in vascular homeostasis and integrity. However, these cells are perpetually subjected to a myriad of mechanical, chemical, and biological stresses that can compromise ... ...

Abstract	Endothelial cells are the crucial inner lining of blood vessels, which are pivotal in vascular homeostasis and integrity. However, these cells are perpetually subjected to a myriad of mechanical, chemical, and biological stresses that can compromise their plasma membranes. A sophisticated repair system involving key molecules, such as calcium, annexins, dysferlin, and MG53, is essential for maintaining endothelial viability. These components orchestrate complex mechanisms, including exocytosis and endocytosis, to repair membrane disruptions. Dysfunctions in this repair machinery, often exacerbated by aging, are linked to endothelial cell death, subsequently contributing to the onset of atherosclerosis and the progression of cardiovascular diseases (CVD) and stroke, major causes of mortality in the United States. Thus, identifying the core machinery for endothelial cell membrane repair is critically important for understanding the pathogenesis of CVD and stroke and developing novel therapeutic strategies for combating CVD and stroke. This review summarizes the recent advances in understanding the mechanisms of endothelial cell membrane repair. The future directions of this research area are also highlighted.
MeSH term(s)	Humans ; Endothelial Cells ; Cell Membrane/metabolism ; Membranes ; Cardiovascular Diseases/metabolism ; Stroke/metabolism
Language	English
Publishing date	2023-11-17
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12222648
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Article: NMMHC IIA triggered lipid metabolize reprogramming resulting in vascular endothelial cellular tight junction injury

Lv, Yanni / Hong, Daojun / Fu, Longsheng / Qian, Yisong

Molecular biology reports. 2022 Apr., v. 49, no. 4

2022

Abstract: BACKGROUND AND PURPOSE: Nonmuscle myosin heavy chain IIA, played an essential role in the promotion of tight junction injury in vascular endothelial cells under oxygen glucose deprivation condition. Rat microvascular endothelial cells had been confirmed ... ...

Abstract	BACKGROUND AND PURPOSE: Nonmuscle myosin heavy chain IIA, played an essential role in the promotion of tight junction injury in vascular endothelial cells under oxygen glucose deprivation condition. Rat microvascular endothelial cells had been confirmed to have the susceptibility to ox-LDL stimulation under OGD condition. We proposed the hypothesis that lipid metabolic reprogramming might be the root cause for damage to RBMCs tight junction. METHODS: Untargeted shotgun and targeted lipid metabolomics mass spectrometry approaches combined with principal component analysis was applied to better define the lipids contributing to the variance observed between control and different OGD time. The protein expression of tight junction of RBMCs: occludin, claudin-5, and ZO-1 were detected with immunofluorescence staining and western blot. The proof of the interaction between NMMHC IIA and SREBP1 was investigated via GST-pull down, while their specific binding fragments were also confirmed. The regulation mechanism of NMMHC IIA on SREBP1 was investigated to explore downstream regulatory signaling pathways. RESULTS: Untargeted and targeted shotgun lipidomics data revealed that OGD might be the conditional factor in reshaping lipid components. Mechanistic studies showed that with the increase of OGD time, PCA analysis of lipidomics obtained from RBMCs indicated their specificity in reshaping lipid components, while ≥80% major lipid components phospholipids and sphingolipids transferred from phospholipids, sphingolipids, and neutral lipids, of which neutral lipids taken the largest proportion with OGD time course. Perturbing reprogramming of lipid composition was less susceptible to OGD condition via knockdown of NMMHC IIA of vascular endothelial cells. Knockdown of NMMHC IIA could promote tight junction defense to OGD condition. NMMHC IIA could directly bind with SREBP1, then could affect sterol regulatory element binding protein-1 to adjust lipid metabolize reprogramming of RBMCs. CONCLUSIONS: Mechanistic studies showed that perturbing reprogramming of lipid composition could enhance tight junction damage, which was mediated by the opposing effects of NMMHC IIA.
Keywords	Western blotting ; fluorescent antibody technique ; glucose ; lipid composition ; lipidomics ; mass spectrometry ; molecular biology ; myosin heavy chains ; occludins ; oxygen ; phospholipids ; principal component analysis ; protein synthesis ; rats ; sphingolipids ; sterols ; tight junctions ; variance
Language	English
Dates of publication	2022-04
Size	p. 2805-2819.
Publishing place	Springer Netherlands
Document type	Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-021-07092-4
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Article ; Online: E3 Ubiquitin Ligases in Endothelial Dysfunction and Vascular Diseases: Roles and Potential Therapies.

Wang, Yihan / Zhan, Yixiong / Wang, Linsiqi / Huang, Xuan / Xin, Hong-Bo / Fu, Mingui / Qian, Yisong

Journal of cardiovascular pharmacology

2023 Volume 82, Issue 2, Page(s) 93–103

Abstract: Abstract: Ubiquitin E3 ligases are a structurally conserved family of enzymes that exert a variety of regulatory functions in immunity, cell death, and tumorigenesis through the ubiquitination of target proteins. Emerging evidence has shown that E3 ... ...

Abstract	Abstract: Ubiquitin E3 ligases are a structurally conserved family of enzymes that exert a variety of regulatory functions in immunity, cell death, and tumorigenesis through the ubiquitination of target proteins. Emerging evidence has shown that E3 ubiquitin ligases play crucial roles in the pathogenesis of endothelial dysfunction and related vascular diseases. Here, we reviewed the new findings of E3 ubiquitin ligases in regulating endothelial dysfunction, including endothelial junctions and vascular integrity, endothelial activation, and endothelial apoptosis. The critical role and potential mechanism of E3 ubiquitin ligases in vascular diseases, such as atherosclerosis, diabetes, hypertension, pulmonary hypertension, and acute lung injury, were summarized. Finally, the clinical significance and potential therapeutic strategies associated with the regulation of E3 ubiquitin ligases were also proposed.
MeSH term(s)	Humans ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Ubiquitin/metabolism ; Proteins ; Vascular Diseases/drug therapy
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Ubiquitin ; Proteins
Language	English
Publishing date	2023-08-01
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000001441
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Article ; Online: Single-cell RNA sequencing unveils Lrg1's role in cerebral ischemia‒reperfusion injury by modulating various cells.

Ruan, Zhaohui / Cao, Guosheng / Qian, Yisong / Fu, Longsheng / Hu, Jinfang / Xu, Tiantian / Wu, Yaoqi / Lv, Yanni

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 285

Abstract: Background and purpose: Cerebral ischemia‒reperfusion injury causes significant harm to human health and is a major contributor to stroke-related deaths worldwide. Current treatments are limited, and new, more effective prevention and treatment ... ...

Abstract	Background and purpose: Cerebral ischemia‒reperfusion injury causes significant harm to human health and is a major contributor to stroke-related deaths worldwide. Current treatments are limited, and new, more effective prevention and treatment strategies that target multiple cell components are urgently needed. Leucine-rich alpha-2 glycoprotein 1 (Lrg1) appears to be associated with the progression of cerebral ischemia‒reperfusion injury, but the exact mechanism of it is unknown. Methods: Wild-type (WT) and Lrg1 knockout (Lrg1 Results: Lrg1 expression was increased in various cell types of brain tissue after cerebral ischemia‒reperfusion injury. Lrg1 knockout reduced cerebral edema and infarct size and improved neurological function after cerebral ischemia‒reperfusion injury. Single-cell RNA sequencing analysis of WT and Lrg1 Conclusions: Our results has shown that Lrg1 mediates numerous pathological processes involved in cerebral ischemia‒reperfusion injury by altering the functional states of various cell types, thereby rendering it a promising therapeutic target for cerebral ischemia‒reperfusion injury.
MeSH term(s)	Animals ; Humans ; Mice ; Blood-Brain Barrier/metabolism ; Brain/metabolism ; Brain Ischemia/metabolism ; Reperfusion Injury/metabolism ; Sequence Analysis, RNA
Chemical Substances	LRG1 protein, mouse
Language	English
Publishing date	2023-11-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02941-4
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Article: Twin PdPtIr porous nanotubes as a dual-functional catalyst for oxygen reduction and evolution reactions

Yu, Dan / Liu, Qian / Chen, Bing / Zhao, Yisong / Jia, Peng / Sun, Keju / Gao, Faming

Journal of materials chemistry A. 2022 May 31, v. 10, no. 21

2022

Abstract: Twin defects, high index facets (HIFs), and high surface/volume ratios play an important role in improving the electrocatalytic performance of 1D nanocatalysts in oxygen reduction (ORR) and oxygen evolution reactions (OER). The design and synthesis of ... ...

Abstract	Twin defects, high index facets (HIFs), and high surface/volume ratios play an important role in improving the electrocatalytic performance of 1D nanocatalysts in oxygen reduction (ORR) and oxygen evolution reactions (OER). The design and synthesis of materials with such features is highly desirable, but challenging. Here, we successfully synthesized PdPtIr porous nanotubes (PdPtIr PNTs-400, PdPtIr PNTs annealed at 400 °C) combining the advantages of abundant twin defects, HIFs, and an ultrahigh surface/volume ratio. The mass activity of PdPtIr PNTs-400 is 1.26 A mgPd₊Pₜ₊Iᵣ⁻¹ and the specific activity is 1.3 A cm⁻² in acidic media. PdPtIr PNTs-400 are also stable in acidic electrolyte, and show little change after 30 000 cycles. Specifically, the overpotential gap between the ORR overpotential at −3 mA cm⁻² and OER overpotential at 10 mA cm⁻² (ORR-OER) is 642 mV, which is the lowest when compared with catalysts reported in the literature. Such an ultra-low overpotential gap reveals their superior oxygen reduction and evolution reaction activity. The DFT calculation results show that the adsorption energy E₀ of oxygen upon introducing Ir atoms into a Pt and Pd composite is optimal on the (211) facet. This study provides a new strategy for the effective design of multiple “active sites” in 1D nanomaterials, which is helpful when preparing oxygen electrocatalysts with superior performance.
Keywords	adsorption ; electrolytes ; energy ; nanocatalysts ; nanotubes ; oxygen ; oxygen production
Language	English
Dates of publication	2022-0531
Size	p. 11354-11362.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2702232-8
ISSN	2050-7496 ; 2050-7488
ISSN (online)	2050-7496
ISSN	2050-7488
DOI	10.1039/d2ta00459c
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Article ; Online: Electrochemical biosensor based on CuPt alloy NTs-AOE for the ultrasensitive detection of organophosphate pesticides.

Yang, Yunxia / Liu, Qian / Zhao, Yisong / Chen, Jianmin / Chen, Bing / Yan, Yanling / Gao, Faming

Nanotechnology

2021 Volume 33, Issue 10

Abstract: The electrode material is vital for the performance of the electrochemical biosensor. Lately, many nanomaterials have been developed to improve the sensitivity and detection efficiency of the biosensors. In this work, a kind of one-dimensional ... ...

Abstract	The electrode material is vital for the performance of the electrochemical biosensor. Lately, many nanomaterials have been developed to improve the sensitivity and detection efficiency of the biosensors. In this work, a kind of one-dimensional nanomaterials, the CuPt alloy nanotubes with an open end (CuPt alloy NTs-AOE), was explored. The nanotubes with an open end can provide a larger electrochemical active surface area and more active sites for the immobilization of enzyme. The CuPt alloy displays excellent conductivity and catalytic activity. In addition, the Cu shows the great affinity to thio-compounds, which can greatly enhance the detection efficiency and sensitivity. As a result, the prepared biosensor demonstrates the wider linear range of 9.98 × 10
Language	English
Publishing date	2021-12-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1362365-5
ISSN	1361-6528 ; 0957-4484
ISSN (online)	1361-6528
ISSN	0957-4484
DOI	10.1088/1361-6528/ac38e5
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