Kun Cao

Affiliated Hospital of Guizhou Medical University

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Rui Wang

Bengbu Medical College

Lingyun Wu

Fudan University

Yanjie Lu

Hainan University

Shi Zuo

Affiliated Hospital of Guizhou Medical University

Xianfeng Sun

Wuxi No.2 People's Hospital

Haiyang Li

Third Affiliated Hospital of Sun Yat-sen University

Bo Jiang

The University of Texas MD Anderson Cancer Center

Bo Li

Air Force Medical University

Jing Bian

Ministry of Agriculture and Rural Affairs

Yufeng Sun

China University of Petroleum, East China

Cooperative Institutions

Chinese Academy of Sciences

Peking University

Chinese Academy of Medical Sciences & Peking Union Medical College

Guiyang Medical University

Sun Yat-sen University

National Institute of Biological Sciences, Beijing

University of Saskatchewan

Nanjing Medical University

Peking University Cancer Hospital

Heilongjiang Academy of Sciences

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Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia

EP Europace (2005)

Mingfei Chen Bingwei Yang Jian Zou Qijun Shan Chao Chen

The reentry circuit of idiopathic left ventricular tachycardia (ILVT) has been demonstrated to be confined to the left posterior Purkinje network. We hypothesized that mapping and linear ablation of the left posterior fascicle (LPF) during sinus rhythm guided by non-contact mapping can effectively modify the arrhythmogenic substrate in patients with ILVT and abolish the tachycardia.Six patients with ILVT, consisting of one case in which conventional mapping failed three times, one recurrent case, one non-inducible case and three common cases, were included in the study. After a three-dimensional endocardial geometry of the left ventricle (LV) was created, the conduction system in the LV was mapped during sinus rhythm using a filter setting of 8 Hz. The His bundle area, left bundle branch, fascicles and sinus breakout point (SBO) were mapped in detail and tagged as special landmarks in the geometry. A linear lesion was placed perpendicular to the wave front propagation direction of the LPF, 1cm above the SBO. There was a small Purkinje potential preceding the ventricular activation at its starting and ending point.The mean tachycardia cycle length of ILVT in this study was 340.3+/-51.4ms. After a mean of 5.5+/-1.6 radiofrequency deliveries, the clinical tachycardias could not be induced and the 12-lead surface ECG showed right QRS axis deviation (mean 39.7+/-26.0 degrees) in all patients. The total procedure time was 160.0+/-32.2 min with fluoroscopic time of 26.0+/-6.8 min. No ILVT was inducible during control stimulation, and none recurred during a mean follow-up of 13.0+/-4.8 months.Mapping and linear ablation of the Purkinje network in LPF area guided by non-contact mapping is an effective and safe treatment of ILVT with radiofrequency energy, especially for those ILVTs which were unsuccessfully treated by conventional means or were non-inducible or non-sustained during the procedure.

Fascicle

10.1016/j.eupc.2004.12.011

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Citations (49)

Additional file 1 of Combined use of specific length amplified fragment sequencing (SLAF-seq) and bulked segregant analysis (BSA) for rapid identification of genes influencing fiber content of hemp (Cannabis sativa L.)

Figshare (2022)

Yue Zhao Yufeng Sun Kun Cao Xiaoyan Zhang Jing Bian

Additional file 1: Supplemental Table 1. Detailed information about the fresh fiber content of F1 bulk and mixed pool

Bulked segregant analysis

Identification

Cannabis sativa

10.6084/m9.figshare.19808042

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Calcium and polyamine regulated calcium‐sensing receptors in cardiac tissues

European Journal of Biochemistry (2003)

Rui Wang Changqing Xu Weimin Zhao Jing Zhang Kun Cao

Activation of a calcium‐sensing receptor (Ca‐SR) leads to increased intracellular calcium concentration and altered cellular activities. The expression of Ca‐SR has been identified in both nonexcitable and excitable cells, including neurons and smooth muscle cells. Whether Ca‐SR was expressed and functioning in cardiac myocytes remained unclear. In the present study, the transcripts of Ca‐SR were identified in rat heart tissues using RT‐PCR that was further confirmed by sequence analysis. Ca‐SR proteins were detected in rat ventricular and atrial tissues as well as in isolated cardiac myocytes. Anti‐(Ca‐SR) Ig did not detect any specific bands after preadsorption with standard Ca‐SR antigens. An immunohistochemistry study revealed the presence of Ca‐SR in rat cardiac as well as other tissues. An increase in extracellular calcium or gadolinium induced a concentration‐dependent sustained increase in [Ca 2+ ] i in isolated ventricular myocytes from adult rats. Spermine (1–10 m m ) also increased [Ca 2+ ] i . Pre‐treatment of cardiac myocytes with thapsigargin or U73122 abolished the extracellular calcium, gadolinium or spermine‐induced increase in [Ca 2+ ] i . The blockade of Na + /Ca 2+ exchanger or voltage‐dependent calcium channels did not alter the extracellular calcium‐induced increase in [Ca 2+ ] i . Finally, extracellular calcium, gadolinium and spermine all increased intracellular inositol 1,4,5‐triphosphate (IP 3 ) levels. Our results demonstrated that Ca‐SR was expressed in cardiac tissue and cardiomyocytes and its function was regulated by extracellular calcium and spermine.

Thapsigargin

Calcium in biology

10.1046/j.1432-1033.2003.03645.x

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KDM1A Promotes Immunosuppression in Hepatocellular Carcinoma by Regulating PD-L1 through Demethylating MEF2D

Journal of Immunology Research (2021)

Yonglan Wang Kun Cao

Immune checkpoint inhibitor therapy targeting antiprogrammed cell death-1 (anti-PD-1) or its ligand (anti-PD-L1) is effective in the treatment of some hepatocellular carcinomas (HCC). Hence, further identification of biological targets related to PD-L1 regulation in HCC is beneficial to improve the clinical efficacy of immunotherapy. Some HCC cells express lysine-specific demethylase 1A (KDM1A), which is implicated in the reduced survival time of patients. Here, we studied whether the level of PD-L1 and the immunosuppression are regulated by KDM1A and its miRNA in HCC cells.In the present study, we studied clinical data from The Cancer Genome Atlas (TCGA) database. We performed qPCR and western blotting assays to measure the expression level of genes of interest. PD-L1 expression was also analyzed by FACS. Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 was used to generate gene knockout cells to investigate the relationships of genes of interest. We also developed a reporter gene assay (RGA) to explore the changes in T cell-induced antitumor immunity relative to PD-L1 expression in HCC cells. The binding between proteins and promoters or miRNAs and their target genes was explored by luciferase reporter assays.The results showed that PD-L1 and KDM1A were increased in HCC patients and cells, and KDM1A promoted the expression of PD-L1 in HCC cells. Our findings showed that the enhancement of PD-L1 expression was not attributed to mitochondrial dysfunction caused by increases in KDM1A in HCC cells. Furthermore, we observed a lower level of MEF2D methylation in HCC cells than in normal human liver cells. Demethylated MEF2D could bind to the promoter of PD-L1 and activate its expression, while KDM1A interacted with MEF2D and acted as a demethylase to reduce its methylation. Moreover, a new miRNA, miR-329-3p, targeting KDM1A was found to regulate the PD-L1 expression profile in HCC cells. In the xenograft model, the tumors treated with miR-329-3p showed growth inhibition.Mechanistically, miR-329-3p inhibits tumor cellular immunosuppression and reinforces the response of tumor cells to T cell-induced cytotoxic effect by targeting KDM1A mRNA and downregulating its expression, which contributed to MEF2D demethylation and activation of PD-L1 expression.

Immunosuppression

10.1155/2021/9965099

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Endogenous Kv channels in human embryonic kidney (HEK-293) cells.

Molecular and Cellular Biochemistry (2002)

Bo Jiang Xianfeng Sun Kun Cao Rui Wang

HEK 293 cells

Tetraethylammonium chloride

4-Aminopyridine

Niflumic acid

Potassium channel blocker

10.1023/a:1019907104763

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Citations (86)

Acetylcholine directly opens Kir61 channels

The FASEB Journal (2003)

Salma Toma Hanna Kun Cao R. Wang

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Pancreatic islet overproduction of H2S and suppressed insulin release in Zucker diabetic rats

Laboratory Investigation (2008)

Lingyun Wu Wei Yang Xuming Jia Guangdong Yang Dessislava Duridanova

Hydrogen sulfide (H(2)S) has been traditionally known for its toxic effects on living organisms. The role of H(2)S in the homeostatic regulation of pancreatic insulin metabolism has been unclear. The present study is aimed at elucidating the effect of endogenously produced H(2)S on pancreatic insulin release and its role in diabetes development. Diabetes development in Zucker diabetic fatty (ZDF) rats was evaluated in comparison with Zucker fatty (ZF) and Zucker lean (ZL) rats. Pancreatic H(2)S production and insulin release were also assayed. It was found that H(2)S was generated in rat pancreas islets, catalyzed predominantly by cystathionine gamma-lyase (CSE). Pancreatic CSE expression and H(2)S production were greater in ZDF rats than in ZF or ZL rats. ZDF rats exhibited reduced serum insulin level, hyperglycemia, and insulin resistance. Inhibition of pancreatic H(2)S production in ZDF rats by intraperitoneal injection of DL-propargylglycine (PPG) for 4 weeks increased serum insulin level, lowered hyperglycemia, and reduced hemoglobin A1c level (P<0.05). Although in ZF rats it also reduced pancreatic H(2)S production and serum H(2)S level, PPG treatment did not alter serum insulin and glucose level. Finally, H(2)S significantly increased K(ATP) channel activity in freshly isolated rat pancreatic beta-cells. It appears that insulin release is impaired in ZDF because of abnormally high pancreatic production of H(2)S. New therapeutic approach for diabetes management can be devised based on our observation by inhibiting endogenous H(2)S production from pancreas.

Pancreatic Islets

10.1038/labinvest.2008.109

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Citations (212)

A pan-cancer analysis of HAVCR1 with a focus on diagnostic, prognostic and immunological roles in human cancers.

PubMed (2023)

Guangyao Li Muhammad Rizwan Javed Rubab Rasool Mostafa A. Abdel-Maksoud Ayman Mubarak

Cancer is one of the most prominent causes of death world wide. Identification of novel cancer biomarkers woud help with cancer diagnosis and possible treatment.In this study, we comprehensively studied the diagnostic, prognostic, and therapeutic values of the hepatitis A virus cellular receptor 1 (HAVCR1) gene across multiple cancers from a pan-cancer point of view via a detailed in silico approach.HAVCR1 expression was up-regulated in a variety of malignancies. The up-regulated HAVCR1 was closely related to the poor prognosis in patients with esophageal carcinoma (ESCA), lung adenocarcinoma (LUAD), and stomach adenocarcinoma (STAD). Moreover, DAVID analysis showed that HAVCR1, along with different other associated genes, was involved in numerous cancer-associated signaling pathways across ESCA, STAD, and LUAD. Furthermore, in these cancers, HAVCR1 was also found closely associated with some other parameters such as promoter methylation, tumor purity, level of CD8+ T immune cells, genomic alterations, and chemotherapeutic drugs.HAVCR1 was overexpressed in multiple tumors. However, the up-regulated HAVCR1 is a valuable diagnostic and prognostic biomarker as well as a therapeutic target in only ESCA, STAD, and LUAD patients.

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Inhibitory effect of protopine on KATP channel subunits expressed in HEK-293 cells

European Journal of Pharmacology (2004)

Bo Jiang Kun Cao Rui Wang

Protopine

HEK 293 cells

Heterotetramer

Sulfonylurea receptor

10.1016/j.ejphar.2004.11.004

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Citations (21)

miR-29a promotes osteoblast proliferation by downregulating DKK-1 expression and activating Wnt/β-catenin signaling pathway

Advances in Clinical and Experimental Medicine (2019)

Fuwen Zhang Kun Cao Gongwen Du Qi Zhang Zongsheng Yin

MicroRNA (miRNA) is a kind of non-coding small RNA with a negative regulating function. Some miRNAs play a role in regulating the differentiation and function of osteoblasts, chondrocytes and osteoclasts.In this study, we analyzed the role of miR-29a and dickkopf-1 (DKK-1) in osteoblast differentiation.Specimens were collected from the surgical resection of pathological ankylosing spondylitis (AS) tissue and some normal tissues. The expression of miR-29a, DKK-1 and β-catenin in normal and AS tissues were detected with real-time polymerase chain reaction (RT-PCR) and western blotting. Cell proliferation was detected with a Cell Counting Kit-8, cell migration and invasion were determined using a Transwell system and cell apoptosis was analyzed with flow cytometry. The luciferase reporter gene plasmid pGL3-DKK-1 and a point-mutation of the luciferase reporter gene plasmid mut-pGL3-DKK-1 were constructed.It was found that miR-29a could promote the proliferation of hFOB1.19 cells, while DKK-1 inhibited their proliferation. Also, miR-29a was able to inhibit the apoptosis of hFOB1.19 cells, while DKK-1 was able to promote the apoptosis of hFOB1.19 cells. When it comes to the invasion and migration of hFOB1.19 cells, miR-29a was found to promote it, while DKK-1 did not.These findings will lead to a better understanding of the proliferation and differentiation of osteoblasts and will provide new insights for the treatment of this disease.

Beta-catenin

LRP5

10.17219/acem/104533

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Citations (23)