Publications by authors named "Bo Jiao"

95 Publications

A prediction model incorporating the BRAF protein status for determining the risk of cervical lateral lymph node metastasis in papillary thyroid cancer patients with central lymph node metastasis.

Eur J Surg Oncol 2021 Aug 27. Epub 2021 Aug 27.

Department of Thyroid and Breast Surgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, 1095 Jiefang Avenue, Qiaokou District, Wuhan, Hubei Province, 430030, China. Electronic address:

Background And Objectives: Cervical lateral lymph node metastasis (LLNM) is a predictor of poor prognosis for papillary thyroid carcinoma (PTC) patients. However, the risk factors for LLNM remain unclear. The purpose of the study was to examine the risk factors for LLNM and construct a prediction model.

Methods: With Ethics Committee approval, a total of 1198 PTC patients were retrospectively included in our study. Univariate and multivariate analyses were performed to explore the relationship between clinicopathological characteristics and LLNM. A nomogram for predicting LLNM in PTC patients with central lymph node metastasis (CLNM) was constructed and validated.

Results: The negative BRAF protein expression was significantly correlated with positive LLNM status in PTC patients. In PTC patients with CLNM, the number of metastatic central lymph nodes (LNN) ≥ 3 and the ratio of metastatic central lymph nodes (LNR) ≥ 0.565 were found to be significantly associated with positive LLNM status. The nomogram for predicting LLNM risk in PTC patients with CLNM incorporated four risk factors: tumor size, the BRAF protein expression, LNN and LNR. The prediction model showed excellent discrimination, with a C-index of 0.714.

Conclusions: The negative BRAF protein expression was more likely to lead to LLNM. LNN ≥3 and LNR ≥0.565 were associated with LLNM risk in PTC patients with CLNM. Our nomogram might assist clinicians in developing individual suitable follow-up strategies for PTC patients with CLNM.
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http://dx.doi.org/10.1016/j.ejso.2021.08.033DOI Listing
August 2021

Cohesively Enhancing the Conductance, Mechanical Robustness, and Environmental Stability of Random Metallic Mesh Electrodes via Hot-Pressing-Induced In-Plane Configuration.

ACS Appl Mater Interfaces 2021 Sep 30;13(35):41836-41845. Epub 2021 Aug 30.

Key Laboratory for Physical Electronics and Devices of the Ministry of Education and Shaanxi Key Lab of Information Photonic Technique, School of Electronic Science and Engineering, Xi'an Jiaotong University, No. 28, Xianning West Road, Xi'an 710049, China.

Flexible transparent conductive electrode (FTCE) is highly desirable due to the fast-growing flexible optoelectronic devices. Several promising FTCEs based on metal material have been developed to replace conventional indium tin oxide (ITO). The random metal mesh is considered to be one of the competitive candidates. However, obtaining feasible random metal mesh with low sheet resistance, high transparency, good mechanical durability, and strong environmental stability is still a great challenge. Here, a random metal mesh-based FTCE with an in-plane structure, achieved by a facile hot-pressing process, is demonstrated. The hot-pressing process enables the fabrication of highly conductive FTCE with improved mechanical robustness and environmental stability. The in-plane FTCE shows a low sheet resistance of 1.63 Ω·sq with an 80.6% transmittance, low relative resistance increase (RRI) of 7.9% after 240 h 85 °C/85% RH test, and low RRI of 8.0% after 10 cycles of bending test. Besides, various applications of the in-plane FTCE were demonstrated, including the flexible heater, flexible touch screen, and flexible electroluminescence. We anticipate that these results will spark interest in in-plane random metal mesh electrodes and enable the application of random metal mesh in flexible optoelectronic devices.
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http://dx.doi.org/10.1021/acsami.1c12204DOI Listing
September 2021

IRF8 Impacts Self-Renewal of Hematopoietic Stem Cells by Regulating TLR9 Signaling Pathway of Innate Immune Cells.

Adv Sci (Weinh) 2021 Aug 8:e2101031. Epub 2021 Aug 8.

Shanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine, International Center for Aging and Cancer, Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.

IRF8 is a key regulator of innate immunity receptor signaling and plays diverse functions in the development of hematopoietic cells. The effects of IRF8 on hematopoietic stem cells (HSCs) are still unknown. Here, it is demonstrated that IRF8 deficiency results in a decreased number of long-term HSCs (LT-HSCs) in mice. However, the repopulation capacity of individual HSCs is significantly increased. Transcriptomic analysis shows that IFN-γ and IFN-α signaling is downregulated in IRF8-deficient HSCs, while their response to proinflammatory cytokines is unchanged ex vivo. Further tests show that Irf8 HSCs can not respond to CpG, an agonist of Toll-like receptor 9 (TLR9) in mice, while long-term CpG stimulation increases wild-type HSC abundance and decreases their bone marrow colony-forming capacity. Mechanistically, as the primary producer of proinflammatory cytokines in response to CpG stimulation, dendritic cells has a blocked TLR9 signaling due to developmental defect in Irf8 mice. Macrophages remain functionally intact but severely reduce in Irf8 mice. In NK cells, IRF8 directly regulates the expression of Tlr9 and its deficiency leads to no increased IFNγ production upon CpG stimulation. These results indicate that IRF8 regulates HSCs, at least in part, through controlling TLR9 signaling in diverse innate immune cells.
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http://dx.doi.org/10.1002/advs.202101031DOI Listing
August 2021

IRF4 and IRF8 expression are associated with clinical phenotype and clinico-hematological response to hydroxyurea in essential thrombocythemia.

Front Med 2021 Jul 31. Epub 2021 Jul 31.

Shanghai Institute of Hematology, State Key Laboratory for Medical Genomics, Collaborative Innovation Center of Hematology, National Research Center for translational Medicine (Shanghai), Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

The morbidity and mortality of myeloproliferative neoplasms (MPNs) are primarily caused by arterial and venous complications, progression to myelofibrosis, and transformation to acute leukemia. However, identifying molecular-based biomarkers for risk stratification of patients with MPNs remains a challenge. We have previously shown that interferon regulatory factor-8 (IRF8) and IRF4 serve as tumor suppressors in myeloid cells. In this study, we evaluated the expression of IRF4 and IRF8 and the JAK2V617F mutant allele burden in patients with MPNs. Patients with decreased IRF4 expression were correlated with a more developed MPN phenotype in myelofibrosis (MF) and secondary AML (sAML) transformed from MPNs versus essential thrombocythemia (ET). Negative correlations between the JAK2V617F allele burden and the expression of IRF8 (P < 0.05) and IRF4 (P < 0.001) and between white blood cell (WBC) count and IRF4 expression (P < 0.05) were found in ET patients. IRF8 expression was negatively correlated with the JAK2V617F allele burden (P < 0.05) in polycythemia vera patients. Complete response (CR), partial response (PR), and no response (NR) were observed in 67.5%,10%, and 22.5% of ET patients treated with hydroxyurea (HU), respectively, in 12 months. At 3 months, patients in the CR group showed high IRF4 and IRF8 expression compared with patients in the PR and NR groups. In the 12-month therapy period, low IRF4 and IRF8 expression were independently associated with the unfavorable response to HU and high WBC count. Our data indicate that the expression of IRF4 and IRF8 was associated with the MPN phenotype, which may serve as biomarkers for the response to HU in ET.
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http://dx.doi.org/10.1007/s11684-021-0858-1DOI Listing
July 2021

Comment on: The association of bispectral index values and metrics of cerebral perfusion during cardiopulmonary bypass.

J Clin Anesth 2021 Jul 24;75:110441. Epub 2021 Jul 24.

Department of Anesthesiology, West China Hospital, Sichuan University, China. Electronic address:

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http://dx.doi.org/10.1016/j.jclinane.2021.110441DOI Listing
July 2021

Fasting improves tolerance to acute hypoxia in rats.

Biochem Biophys Res Commun 2021 Sep 9;569:161-166. Epub 2021 Jul 9.

Department of Aerospace Physiology, Fourth Military Medical University, 169(#) Changle West Road, Xi'an, 710032, China. Electronic address:

Acute high-altitude illness seriously threatens the health and lives of people who rapidly ascend to high altitudes, but there is currently no particularly effective method for the prevention or treatment of acute high-altitude illness. In the present study, we found that fasting preconditioning effectively improved the survival rate of rats exposed to a simulated altitude of 7620 m for 24 h, and a novel animal model of rapid adaptation to acute hypoxia was established. Compared with control treatment, fasting preconditioning activated AMPK, induced autophagy, decreased ROS levels, and inhibited NF-κB signaling in the cardiac tissues of rats. Our results suggested that fasting effectively improved the acute hypoxia tolerance of rats, which was gradually enhanced with prolongation of fasting. In addition, the acute hypoxia tolerance of young rats was significantly higher than that of adult rats. These experimental results lay the foundation for achieving rapid adaptation to acute hypoxia in humans.
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http://dx.doi.org/10.1016/j.bbrc.2021.06.099DOI Listing
September 2021

The role of HMGB1 on TDI-induced NLPR3 inflammasome activation via ROS/NF-κB pathway in HBE cells.

Int Immunopharmacol 2021 Sep 18;98:107859. Epub 2021 Jun 18.

National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention (CDC), Beijing 100050, China. Electronic address:

To explore the potential role of HMGB1 on TDI-induced NLRP3 inflammasome activation, HBE cells were treated with TDI-HSA conjugate to observe the changes of HMGB1, TLR4, NF-κB, Nrf2 and NLRP3 inflammasome related proteins expressions, ROS release and MMP. NAC, TPCA-1 and Resatorvid pre-treatments were applied to explore the effects of ROS, NF-κB and TLR4 on TDI-induced NLRP3 inflammasome activation. The CRISPR/Cas9 system was used to construct HMGB1 gene knockout HBE cell line and then to explore the role of HMGB1 on TDI-HSA induced NLRP3 inflammasome activation. GL pre-treatment was applied to further confirm the role of HMGB1. Results showed that TDI increased HMGB1, TLR4, P-p65, Nrf2 proteins expressions and ROS release, decreased MMP level and activated NLRP3 inflammasome in HBE cells in a dose dependent manner. NAC, TPCA-1 and Resatorvid pre-treatments decreased the expression of P-p65 and inhibited NLRP3 inflammasome activation. Inhibition of HMGB1 decreased Nrf2 expression and ROS release, improved MMP level and reduced NLRP3 inflammasome activation. GL ameliorated NLRP3 inflammasome activation via inhibiting HMGB1 regulated ROS/NF-κB pathway. These results indicated that HMGB1 was involved in TDI-induced NLRP3 inflammasome activation as a positive regulatory mechanism. The study provided a potential target for early prevention and treatment of TDI-OA.
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http://dx.doi.org/10.1016/j.intimp.2021.107859DOI Listing
September 2021

Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK-YAP Signaling.

Adv Sci (Weinh) 2021 08 20;8(16):e2100250. Epub 2021 Jun 20.

Shanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine, International Center for Aging and Cancer, Collaborative Innovation Center of Hematology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

KRAS mutation is one of the most prevalent genetic drivers of cancer development, yet KRAS mutations are until very recently considered undruggable. There are ongoing trials of drugs that target the KRAS G12C mutation, yet acquired drug resistance from the extended use has already become a major concern. Here, it is demonstrated that KRAS G12C inhibition induces sustained activation of focal adhesive kinase (FAK) and show that a combination therapy comprising KRAS G12C inhibition and a FAK inhibitor (IN10018) achieves synergistic anticancer effects. It can simultaneously reduce the extent of drug resistance. Diverse CDX and PDX models of KRAS G12C mutant cancer are examined and synergistic benefits from the combination therapy are consistently observed. Mechanistically, it is found that both aberrant FAK-YAP signaling and FAK-related fibrogenesis impact on the development of KRAS G12C inhibitor resistance. This study thus illustrates the mechanism of resistance of cancer to the treatment of KRAS G12C inhibitor, as well as an innovative combination therapy to improve treatment outcomes for KRAS G12C mutant cancers.
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http://dx.doi.org/10.1002/advs.202100250DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8373085PMC
August 2021

Exploiting a Multiphase Pure Formamidinium Lead Perovskite for Efficient Green-Light-Emitting Diodes.

ACS Appl Mater Interfaces 2021 May 10;13(19):23067-23073. Epub 2021 May 10.

Key Laboratory for Physical Electronics and Devices of the Ministry of Education & Shaanxi Key Lab of Information Photonic Technique, School of Electronic Science and Engineering, Xi'an Jiaotong University, Xi'an 710049, China.

Formamidinium (FA)-based perovskites have demonstrated excellent advances in optoelectronics recently, but in terms of perovskite compounds, the optimal condition of their composition optimization remains controversial. Herein, we boosted the performance of perovskite light-emitting diodes (PeLEDs) in both efficiency and stability through composition and phase engineering. The low-dimensional FAPbBr particles emerged and mixed with the FAPbBr composites when the FABr content is excessive. By regulating the phase composition in multiphase FAPbBr perovskites, the maximum external quantum efficiency (EQE) of optimal PeLEDs (5.14%) is 2.7-fold higher than that of pure FAPbBr-based PeLEDs (1.90%), and device stability is improved. Further optimizing the film quality and emission efficiency with Rb ions, the EQE of PeLEDs can be increased to 6.01%, with a half-lifetime of about 185 s under the high current density. This strategy of phase composition optimization in FA-based perovskites provides an effective way to process high-efficiency and stable PeLEDs.
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http://dx.doi.org/10.1021/acsami.1c00116DOI Listing
May 2021

Vagus nerve stimulation in brain diseases: Therapeutic applications and biological mechanisms.

Neurosci Biobehav Rev 2021 08 21;127:37-53. Epub 2021 Apr 21.

Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:

Brain diseases, including neurodegenerative, cerebrovascular and neuropsychiatric diseases, have posed a deleterious threat to human health and brought a great burden to society and the healthcare system. With the development of medical technology, vagus nerve stimulation (VNS) has been approved by the Food and Drug Administration (FDA) as an alternative treatment for refractory epilepsy, refractory depression, cluster headaches, and migraines. Furthermore, current evidence showed promising results towards the treatment of more brain diseases, such as Parkinson's disease (PD), autistic spectrum disorder (ASD), traumatic brain injury (TBI), and stroke. Nonetheless, the biological mechanisms underlying the beneficial effects of VNS in brain diseases remain only partially elucidated. This review aims to delve into the relevant preclinical and clinical studies and update the progress of VNS applications and its potential mechanisms underlying the biological effects in brain diseases.
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http://dx.doi.org/10.1016/j.neubiorev.2021.04.018DOI Listing
August 2021

Oestrogen receptor alpha in papillary thyroid carcinoma: association with clinical features and BRAFV600E mutation.

Jpn J Clin Oncol 2021 Jul;51(7):1051-1058

Department of Thyroid and Breast Surgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Background: Papillary thyroid cancer cells can express oestrogen receptor alpha, which is encoded by the ESR1 gene and may bind to oestrogen to induce the occurrence and development of papillary thyroid cancer. The BRAFV600E mutation is also an important biomarker for the occurrence and progression of papillary thyroid cancer. However, the association between the BRAFV600E mutation and oestrogen receptor alpha expression has not been identified. This study aims to investigate the association between ESR1 expression and the BRAFV600E mutation and its clinical significance.

Methods: Oestrogen receptor alpha and BRAFV600E proteins were detected by immunohistochemical staining of formalin-fixed paraffin-embedded thyroid tissues from 1105 patients with papillary thyroid cancer at our institution. Messenger RNA expression counts of ESR1 and clinicopathologic information were obtained from The Cancer Genome Atlas database.

Results: Oestrogen receptor alpha protein expression was significantly associated with BRAFV600E protein. The positive rate of oestrogen receptor alpha protein in papillary thyroid cancer patients was significantly higher in males, younger patients and patients with the multifocal type. In papillary thyroid cancer patients with positive BRAFV600E protein, oestrogen receptor alpha expression was significantly correlated with central lymph node metastasis. Data from the The Cancer Genome Atlas database also suggested that the ESR1 messenger RNA level was associated with the BRAFV600E mutation. Furthermore, classification analysis performed according to a tree-based classification method demonstrated that higher ESR1 messenger RNA expression indicated poorer overall survival in papillary thyroid cancer patients with the BRAFV600E mutation.

Conclusions: The percentage of BRAFV600E mutations is increased in patients with higher ESR1 messenger RNA levels, and the BRAFV600E protein might be co-expressed with oestrogen receptor alpha, which could be an indicator of cervical lymph node metastasis and poor overall survival in patients with papillary thyroid cancer.
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http://dx.doi.org/10.1093/jjco/hyab058DOI Listing
July 2021

Nitric Oxide in the Spinal Cord Is Involved in the Hyperalgesia Induced by Tetrahydrobiopterin in Chronic Restraint Stress Rats.

Front Neurosci 2021 26;15:593654. Epub 2021 Mar 26.

Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

It has been well recognized that exposure to chronic stress could increase pain responding and exacerbate pain symptoms, resulting in stress-induced hyperalgesia. However, the mechanisms underlying stress-induced hyperalgesia are not yet fully elucidated. To this end, we observed that restraint as a stressful event exacerbated mechanical and thermal hyperalgesia, accompanied with up-regulation of nitric oxide (NO) ( < 0.001), GTP cyclohydrolase 1 (GCH1) (GCH1 mRNA: = 0.001; GCH1 protein: = 0.001), and tetrahydrobiopterin (BH4) concentration (plasma BH4: < 0.001; spinal BH4: < 0.001) on Day 7 in restraint stress (RS) rats. Intrathecal injection of -nitro-L-arginine methyl ester (L-NAME), a non-specific NO synthase inhibitor, or -([3-(aminomethyl)phenyl]methyl) ethanimidamide, a special inhibitor of inducible NO synthase (iNOS), for seven consecutive days attenuated stress-induced hyperalgesia and decreased the production of NO ( < 0.001). Interestingly, 7-nitro indazole, a special inhibitor of neuronal NO synthase, alleviated stress-induced hyperalgesia but did not affect spinal NO synthesis. Furthermore, intrathecal injection of BH4 not only aggravated stress-induced hyperalgesia but also up-regulated the expression of spinal iNOS (iNOS mRNA: = 0.015; iNOS protein: < 0.001) and NO production ( < 0.001). These findings suggest that hyperalgesia induced by RS is associated with the modulation of the GCH1-BH4 system and constitutively expressed spinal iNOS. Thus, the GCH1-BH4-iNOS signaling pathway may be a new novel therapeutic target for pain relief in the spinal cord.
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http://dx.doi.org/10.3389/fnins.2021.593654DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8044835PMC
March 2021

Comment on: Postoperative opioid administration characteristics associated with opioid-induced respiratory depression: Results from the PRODIGY trial.

J Clin Anesth 2021 08 11;71:110199. Epub 2021 Mar 11.

Department of Anesthesiology, West China Hospital, Sichuan University, China. Electronic address:

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http://dx.doi.org/10.1016/j.jclinane.2021.110199DOI Listing
August 2021

Class-3 semaphorins: Potent multifunctional modulators for angiogenesis-associated diseases.

Biomed Pharmacother 2021 May 3;137:111329. Epub 2021 Feb 3.

Department of Anesthesiology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address:

Semaphorins, the neuronal guidance cues, were shown to have broad influences on pathophysiological processes such as bone remodeling, immune responses, and angiogenesis. In particular, Class-3 Semaphorins (SEMA3) is considered a vital regulator involved in angiogenesis. Scientific evidence has pointed to the role of angiogenesis in many diseases, and numerous efforts have been made to explore the possibilities of curing those diseases by targeting angiogenesis. Nevertheless, the efficacies are limited owing to the complex mechanisms of angiogenesis. Hence, investigating the mechanisms of SEMA3 in angiogenesis may contribute to novel therapeutics for diseases. Previous reviews mainly focused on the various functions of semaphorins in one particular disease, and the specific angiogenesis mechanism of SEMA3 in diverse diseases has not been well elucidated. Additionally, the role of SEMA3 in angiogenesis remains elusive, as contradicting results have been found in different disease types. Some evidence from recent studies implies that, while most SEMA3 molecules inhibit pathological angiogenesis in different diseases, occasionally SEMA3 may also promote angiogenesis. This review summarizes the specific role of SEMA3 in a variety of angiogenesis-associated diseases, and documents SEMA3 may be a promising therapeutic target for treating angiogenesis-associated diseases.
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http://dx.doi.org/10.1016/j.biopha.2021.111329DOI Listing
May 2021

GNA13 regulates BCL2 expression and the sensitivity of GCB-DLBCL cells to BCL2 inhibitors in a palmitoylation-dependent manner.

Cell Death Dis 2021 01 9;12(1):54. Epub 2021 Jan 9.

Shanghai Institute of Hematology, State Key Laboratory for Medical Genomics, Collaborative Innovation Center of Hematology, National Research Center for Translational Medicine, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

GNA13, encoding one of the G protein alpha subunits of heterotrimeric G proteins that transduce signals of G protein-coupled receptors (GPCR), is frequently mutated in germinal center B-cell-like diffuse large B-cell lymphoma (GCB-DLBCL) with poor prognostic outcomes. Due to the "undruggable" nature of GNA13, targeted therapy for these patients is not available. In this study, we found that palmitoylation of GNA13 not only regulates its plasma membrane localization, but also regulates GNA13's stability. It is essential for the tumor suppressor function of GNA13 in GCB-DLBCL cells. Interestingly, GNA13 negatively regulates BCL2 expression in GCB-DLBCL cells in a palmitoylation-dependent manner. Consistently, BCL2 inhibitors were found to be effective in killing GNA13-deficient GCB-DLBCL cells in a cell-based chemical screen. Furthermore, we demonstrate that inactivating GNA13 by targeting its palmitoylation enhanced the sensitivity of GCB-DLBCL to the BCL2 inhibitor. These studies indicate that the loss-of-function mutation of GNA13 is a biomarker for BCL2 inhibitor therapy of GCB-DLBCL and that GNA13 palmitoylation is a potential target for combination therapy with BCL2 inhibitors to treat GCB-DLBCL with wild-type GNA13.
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http://dx.doi.org/10.1038/s41419-020-03311-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7797003PMC
January 2021

Adenomatous hyperplastic intratracheal ectopic thyroid tissue: a case report.

J Int Med Res 2020 Nov;48(11):300060520971435

Department of Thyroid and Breast Surgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Intratracheal ectopic thyroid (ITET) is a rare disease, with limited cases reported in the literature. ITET is an unusual congenital abnormality and can be easily mistaken for a respiratory illness. We present a case of a 61-year-old man with a history of slight discontinuous hemoptysis for 2 years. A tracheal mass, which appeared to be connected to the left thyroid gland, was found by chest computed tomography scan. Ultrasound revealed one suspiciously malignant, solid and hypoechoic nodule in the left thyroid gland. After the thyroid origin of the mass was confirmed by bronchoscopic biopsy, the patient underwent segmental resection and anastomosis of the trachea, together with left thyroidectomy. Histopathology of the tracheal tumor showed adenomatous hyperplastic ITET, and the orthotopic left thyroid gland showed nodular goiter with atypical adenomatous hyperplasia. Clinical suspicion is warranted in patients presenting with a tracheal tumor seemingly connected to the thyroid gland, particularly in patients who have imaging features suggestive of a malignant tumor in the orthotopic thyroid but without confirmative histopathology of malignancy before surgery.
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http://dx.doi.org/10.1177/0300060520971435DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686616PMC
November 2020

Vacuum Dual-Source Thermal-Deposited Lead-Free CsCuI Films with High Photoluminescence Quantum Yield for Deep-Blue Light-Emitting Diodes.

ACS Appl Mater Interfaces 2020 Nov 11;12(47):52967-52975. Epub 2020 Nov 11.

Key Laboratory for Physical Electronics and Devices of the Ministry of Education & Shaanxi Key Lab of Information Photonic Technique, School of Electronic Science and Engineering, Xi'an Jiaotong University, No. 28, Xianning West Road, Xi'an 710049, China.

Deep-blue emitters are greatly desirable for preparing white light-emitting diodes and enhancing the color gamut of full-color display. The deep-blue lead halide perovskite light-emitting diodes (PeLEDs) exhibit far inferior performance compared to green and red counterparts and suffer from lead toxicity, hampering their applications. Nontoxic, stable, and wide band gap zero-dimensional (0D) CsCuI with relatively high exciton binding energy has great potential as deep-blue emitters. However, the development of PeLEDs remains a huge challenge due to the difficulties in preparing a high-quality CsCuI film and device design, arising from an inherent wide band gap together with deep ionization potential. Here, a continuous and pin-hole-free CsCuI thin film with deep-blue emission centered at 440 nm was prepared by the dual-source thermal evaporation approach, and a high photoluminescence quantum yield of 58% was achieved, corresponding to significant enhancement of 61% compared with that of the CsCuI thin film synthesized by solution processes. Furthermore, saturated deep-blue PeLEDs at the Commission Internationale de L'Eclairage (CIE) coordinates (0.15, 0.08) were obtained by employing an electron-transfer layer composed of a 1,4,5,8,9,11-hexa-azatriphenylene hexacarboni-trile (HAT-CN) and ,'-bis(naphthalen-1-yl)-,'-bis(phenyl)benzidine (NPB) organic heterojunction to realize the effective hole blocking, rendering an external quantum efficiency of approximately 0.1%. These results will be extensively beneficial to wide band gap material and device preparation.
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http://dx.doi.org/10.1021/acsami.0c17029DOI Listing
November 2020

Toluene diisocyanate-induced inflammation and airway remodeling involves autophagy in human bronchial epithelial cells.

Toxicol In Vitro 2021 Feb 27;70:105040. Epub 2020 Oct 27.

Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong 250062, China.

Toluene-diisocyanate (TDI) is one of the main causes of occupational asthma. To study the role of autophagy in TDI-induced airway inflammation and airway remodeling in bronchial airway epithelial (16HBE) cells. We treated 16HBE cells with TDI-human serum albumin (TDI-HSA) conjugate to observe reactive oxygen species (ROS) release, autophagy activation, airway inflammation and airway remodeling. 3-Methyladenine (3-MA) and Rapamycin (Rapa) intervention were used to explore the effects of autophagy on inflammatory response and protein expression related to airway remodeling in 16HBE cells treated with TDI-HSA. Experimental results suggested that various concentrations of TDI-HSA (0, 40, 80 and 120 μg/mL) increased the release of ROS and the expression of Nrf2, activated autophagy and increased the expression of AMPK, Beclin-1, LC3 and decreased the expression of p62, promoted the levels of IL-5, IL-6 and IL-8 in 16HBE cells. Results also showed that E-cadherin expression decreased but an increase was observed in α-SMA and MMP-9 in the TDI-HSA group. The treatment of TDI-HSA combined with Rapa aggravated the above reaction whereas the inverse was true for TDI-HSA combined with 3-MA. These results indicated that autophagy is involved in TDI-induced airway inflammation and airway remodeling as a positive regulatory mechanism, inhibiting autophagy can significantly alleviate the TDI-induced inflammatory response and attenuate airway remodeling protein expression in 16HBE cells.
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http://dx.doi.org/10.1016/j.tiv.2020.105040DOI Listing
February 2021

PTPN2 regulates the activation of KRAS and plays a critical role in proliferation and survival of KRAS-driven cancer cells.

J Biol Chem 2020 12 29;295(52):18343-18354. Epub 2020 Oct 29.

Shanghai Institute of Hematology, State Key Laboratory for Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:

genes are the most commonly mutated in human cancers and play critical roles in tumor initiation, progression, and drug resistance. Identification of targets that block RAS signaling is pivotal to develop therapies for -related cancer. As RAS translocation to the plasma membrane (PM) is essential for its effective signal transduction, we devised a high-content screening assay to search for genes regulating KRAS membrane association. We found that the tyrosine phosphatase PTPN2 regulates the plasma membrane localization of KRAS. Knockdown of PTPN2 reduced the proliferation and promoted apoptosis in KRAS-dependent cancer cells, but not in KRAS-independent cells. Mechanistically, PTPN2 negatively regulates tyrosine phosphorylation of KRAS, which, in turn, affects the activation KRAS and its downstream signaling. Consistently, analysis of the TCGA database demonstrates that high expression of PTPN2 is significantly associated with poor prognosis of patients with KRAS-mutant pancreatic adenocarcinoma. These results indicate that PTPN2 is a key regulator of KRAS and may serve as a new target for therapy of -driven cancer.
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http://dx.doi.org/10.1074/jbc.RA119.011060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7939389PMC
December 2020

COVID-19: a risk factor for fatal outcomes in patients with comorbid cardiovascular disease.

Aging (Albany NY) 2020 Oct 9;12(19):18866-18877. Epub 2020 Oct 9.

Department of Emergency, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Objectives: To evaluate the fatal impact of COVID-19 on patients with comorbid cardiovascular disease (CVD).

Results: Overall, the 28-day mortality of patients with comorbid CVD was 3.25 times of that of patients without comorbid CVD (40.63% vs 12.50%, P=0.011). Clinic symptoms on admission were similar for the two groups. However, patients with comorbid CVD had higher levels of Interleukin-10 (22.22% vs 0%, P=0.034), procalcitonin (22.6% vs 3.13%, P<0.001), high-sensitivity troponin I (20 pg/mL vs 16.05 pg/mL, P=0.019), and lactic dehydrogenase (437 U/L vs 310 U/L, P=0.015). In addition, patients with comorbid CVD experienced a high incidence of acute respiratory distress syndrome (59.38% vs 15.63%, P<0.001), and required more invasive mechanical ventilation (40.63% vs 12.50%, P=0.011). Methylprednisolone was found to improve the survival of patients without comorbid CVD (p = 0.05).

Conclusions: Comorbid CVD resulted in a higher mortality rate for COVID-19 patients. Acute respiratory distress syndrome was the primary reason of death for COVID-19 patients with comorbid CVD, followed by acute myocardial infarction.

Methods: This retrospective study used propensity score matching to divide 64 COVID-19 patients into two groups with and without comorbid CVD. Clinic symptoms, laboratory features, treatments, and 28-day mortality were compared between the two groups.
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http://dx.doi.org/10.18632/aging.103944DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7732330PMC
October 2020

Elevated ROS depress mitochondrial oxygen utilization efficiency in cardiomyocytes during acute hypoxia.

Pflugers Arch 2020 11 17;472(11):1619-1630. Epub 2020 Sep 17.

Department of Aerospace Physiology, Fourth Military Medical University, 169# Changle West Road, Xi'an, 710032, China.

Mitochondria are important sites for the production of ATP and the generation of ROS in cells. However, whether acute hypoxia increases ROS generation in cells or affects ATP production remains unclear, and therefore, monitoring the changes in ATP and ROS in living cells in real time is important. In this study, cardiomyocytes were transfected with RoGFP for ROS detection and MitGO-Ateam2 for ATP detection, whereby ROS and ATP production in cardiomyocytes were respectively monitored in real time. Furthermore, the oxygen consumption rate (OCR) of cardiomyocytes was measured. Similar results were produced for adult and neonatal rat cardiomyocytes. Hypoxia (1% O) reduced the basal OCR, ATP-linked OCR, and maximal OCR in cardiomyocytes compared with these OCR levels in the cardiomyocytes in the normoxic group (21% O). However, ATP-linked OCR, normalized to maximal OCR, was increased during hypoxia, indicating that the electron leakage of complex III exacerbated the increase of ATP-linked oxygen consumption during hypoxia and vice versa. Combined with the result that cardiomyocytes expressing MitGO-Ateam2 showed a significant decrease in ATP production during hypoxia compared with that of normoxic group, acute hypoxia might depress the mitochondrial oxygen utilization efficiency of the cardiomyocytes. Moreover, cardiomyocytes expressing Cyto-RoGFP or IMS-RoGFP showed an increase in ROS generation in the cytosol and the mitochondrial intermembrane space (IMS) during hypoxia. All of these results indicate that acute hypoxia generated more ROS in complex III and increased mitochondrial oxygen consumption, leading to less ATP production. In conclusion, acute hypoxia depresses the mitochondrial oxygen utilization efficiency by decreasing ATP production and increasing oxygen consumption as a result of the enhanced ROS generation at mitochondrial complex III.
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http://dx.doi.org/10.1007/s00424-020-02463-5DOI Listing
November 2020

Monitoring and Management of Home-Quarantined Patients With COVID-19 Using a WeChat-Based Telemedicine System: Retrospective Cohort Study.

J Med Internet Res 2020 07 2;22(7):e19514. Epub 2020 Jul 2.

Department of Emergency Medicine, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Background: Most patients with coronavirus disease (COVID-19) who show mild symptoms are sent home by physicians to recover. However, the condition of some of these patients becomes severe or critical as the disease progresses.

Objective: The aim of this study was to evaluate a telemedicine model that was developed to address the challenges of treating patients with progressive COVID-19 who are home-quarantined and shortages in the medical workforce.

Methods: A telemedicine system was developed to continuously monitor the progression of home-quarantined patients with COVID-19. The system was built based on a popular social media smartphone app called WeChat; the app was used to establish two-way communication between a multidisciplinary team consisting of 7 medical workers and 188 home-quarantined individuals (including 74 confirmed patients with COVID-19). The system helped patients self-assess their conditions and update the multidisciplinary team through a telemedicine form stored on a cloud service, based on which the multidisciplinary team made treatment decisions. We evaluated this telemedicine system via a single-center retrospective study conducted at Tongji Hospital in Wuhan, China, in January 2020.

Results: Among 188 individuals using the telemedicine system, 114 (60.6%) were not infected with COVID-19 and were dismissed. Of the 74 confirmed patients with COVID-19, 26 (35%) recovered during the study period and voluntarily stopped using the system. The remaining 48/76 confirmed patients with COVID-19 (63%) used the system until the end of the study, including 6 patients whose conditions progressed to severe or critical. These 6 patients were admitted to hospital and were stabilized (one received extracorporeal membrane oxygenation support for 17 days). All 74 patients with COVID-19 eventually recovered. Through a comparison of the monitored symptoms between hospitalized and nonhospitalized patients, we found prolonged persistence and deterioration of fever, dyspnea, lack of strength, and muscle soreness to be diagnostic of need for hospitalization.

Conclusions: By continuously monitoring the changes in several key symptoms, the telemedicine system reduces the risks of delayed hospitalization due to disease progression for patients with COVID-19 quarantined at home. The system uses a set of scales for quarantine management assessment that enables patients to self-assess their conditions. The results are useful for medical staff to identify disease progression and, hence, make appropriate and timely treatment decisions. The system requires few staff to manage a large cohort of patients. In addition, the system can solicit help from recovered but self-quarantined medical workers to alleviate shortages in the medical workforce and free healthy medical workers to fight COVID-19 on the front line. Thus, it optimizes the usage of local medical resources and prevents cross-infections among medical workers and patients.
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http://dx.doi.org/10.2196/19514DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7333794PMC
July 2020

Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition.

J Hematol Oncol 2020 06 18;13(1):80. Epub 2020 Jun 18.

Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Background: The Philadelphia chromosome (Ph), which leads to the creation and expression of the fusion gene product BCR-ABL, underlines the pathogenesis of chronic myelogenous leukemia (CML) and a fraction of adult and pediatric acute B-lymphoblastic leukemia (B-ALL). The BCR-ABL tyrosine kinase inhibitors (TKIs) have shown a remarkable clinical activity in patients with CML, but their efficacy in treating Ph B-ALL is limited. Identifying additional therapeutic targets is important for the effective treatment of Ph B-ALL.

Methods: Activation of the JNK signaling pathway in human and mouse BCR-ABL B-ALL cells with or without dasatinib treatment was analyzed by Western blotting. JNK was inhibited either by RNA interference or chemical inhibitors, such as JNK-IN-8. The effect of JNK inhibition with or without BCR-ABL TKI dasatinib on BCR-ABL B-ALL cells was analyzed by the CellTiter-Glo® Luminescent Cell Viability Assay. The in vivo effects of JNK-IN-8 and dasatinib alone or in combination were tested using a BCR-ABL induced B-ALL mouse model.

Results: We found that the c-JUN N-terminal kinase (JNK) signaling pathway is abnormally activated in both human and mouse BCR-ABL B-ALL cells, but the BCR-ABL TKI does not inhibit JNK activation in these cells. Inhibition of JNK, either by RNAi-mediated downregulation or by JNK inhibitors, could significantly reduce viability of Ph B-ALL cells. JNK inhibition by RNAi-mediated downregulation or JNK inhibitors also showed a synergistic effect with the BCR-ABL TKI, dasatinib, in killing Ph B-ALL cells in vitro. Furthermore, a potent JNK inhibitor, JNK-IN-8, in combination with dasatinib markedly improved the survival of mice with BCR-ABL induced B-ALL, as compared to the treatment with dasatinib alone.

Conclusions: Our findings indicate that simultaneously targeting both BCR-ABL and JNK kinase might serve as a promising therapeutic strategy for Ph B-ALL.
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http://dx.doi.org/10.1186/s13045-020-00912-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7302132PMC
June 2020

High-Brightness and Color-Tunable FAPbBr Perovskite Nanocrystals 2.0 Enable Ultrapure Green Luminescence for Achieving Recommendation 2020 Displays.

ACS Appl Mater Interfaces 2020 Jan 6;12(2):2835-2841. Epub 2020 Jan 6.

Department of Electronic Science and Technology, School of Electronic and Information Engineering , Xi'an Jiaotong University , Xi'an 710049 , Shaanxi , People's Republic of China.

To best catch human eyes in next-generation displays, the updated recommendation 2020 (Rec. 2020) standard has called for ultrapure green emitters to be qualified with a narrow emission of 525-535 nm with a full width at half-maximum (fwhm) below 25 nm. However, it is still challenging to find an emitter which can simultaneously cover these two criteria. Instead of traditional II-VI group semiconductor quantum dots, perovskite nanocrystals (NCs) can render versatile emitting tunability to allow them access to the Rec. 2020 standard. Herein, to realize the critical window of Rec. 2020, we have proposed a scalable, room temperature synthesis route of formamidinium lead bromide (FAPbBr) NCs using a sole ligand of sulfobetaine-18 (SBE-18). The as-synthesized FAPbBr NCs exhibit an ideal emission at 534 nm with an ultranarrow fwhm of 20.5 nm and a high photoluminescence quantum yield of 90.6%, overwhelming the FAPbBr nanoplates capped with oleic acid/oleylamine (OA/OAM). Introducing these high quality NCs into backlight displays, an ultrapure green backlight which covers ≈85.7% of the Rec. 2020 standard in the CIE 1931 color space is achieved, signifying the "greenest" backlight till now. Thus, we can foresee perovskite NCs as the most potential candidates for next-generation displays.
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http://dx.doi.org/10.1021/acsami.9b18140DOI Listing
January 2020

Flexible and Transparent Ferroferric Oxide-Modified Silver Nanowire Film for Efficient Electromagnetic Interference Shielding.

ACS Appl Mater Interfaces 2020 Jan 31;12(2):2826-2834. Epub 2019 Dec 31.

Key Laboratory for Physical Electronics and Devices of the Ministry of Education and Shaanxi Key Lab of Information Photonic Technique, School of Electronic Science and Engineering , Xi'an Jiaotong University , No.28, Xianning West Road , Xi'an 710049 , China.

Transparent and flexible electromagnetic interference (EMI) shielding film is highly desirable due to the fast-growing flexible electronics. A silver nanowire (Ag NW) film is considered to be an ideal candidate for a transparent and flexible EMI shielding film but suffers low EMI shielding effectiveness (SE) at high transparency and poor bending durability. Herein, we introduce ferroferric oxide (FeO) into a Ag NW film and demonstrate a robust EMI shielding film, which exhibits SE of 24.9 dB at 8.2 GHz and optical transparency of 90%. FeO exhibits roles of the improved absorption loss for electromagnetic radiation due to its high permeability, the enhanced reflection loss for electromagnetic radiation by increasing the conductivity of Ag NWs film, and the improved stability for the enhanced adhesion of the Ag NW EMI shielding film. Our work provides a facile method for high-performance transparent EMI shielding film, which exhibits great potential for protection for electronic devices.
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http://dx.doi.org/10.1021/acsami.9b17513DOI Listing
January 2020

Synthesis, Purification, and Selective β-AR Agonist and Bronchodilatory Effects of Catecholic Tetrahydroisoquinolines from .

J Nat Prod 2019 11 18;82(11):2986-2993. Epub 2019 Oct 18.

Key Laboratory of Chemical Biology (Ministry of Education), Institute of Pharmacognosy, School of Pharmaceutical Sciences , Shandong University , Jinan , Shandong 250012 , People's Republic of China.

A green, biomimetic, phosphate-mediated Pictet-Spengler reaction was used in the synthesis of three catecholic tetrahydroisoquinolines, , , and , present in the medicinal plant , as well as their analogues -, , and , with dopamine hydrochloride and aldehydes as the substrates. AB-8 macroporous resin column chromatography was applied for purification of the products from the one-step high-efficacy synthesis. It eliminated the difficulties in the isolation of catecholic tetrahydroisoquinolines from the aqueous reaction system and unreacted dopamine hydrochloride. Activity screening in CHO-K1/Gα15 cell models consistently expressing α-, β-, or β-adrenergic receptors indicated that and , compounds that are present in , possessed the most potent β-adrenergic receptor agonist activity and was a selective β-adrenergic receptor agonist at the concentration of 100 μM. Both and exhibited dose-dependent bronchodilator effects on the histamine-induced contraction of isolated guinea-pig tracheal smooth muscle, with EC values of 0.8 and 2.8 μM, respectively. These findings explain the scientific rationale of use as an antiasthmatic herb in folk medicine and provide the basis for the discovery of novel antiasthma drugs.
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http://dx.doi.org/10.1021/acs.jnatprod.9b00418DOI Listing
November 2019

Modulated light-activated electrochemistry at silicon functionalized with metal-organic frameworks towards addressable DNA chips.

Biosens Bioelectron 2019 Dec 3;146:111750. Epub 2019 Oct 3.

Institute of Medical Engineering, School of Basic Medical Sciences, Health Science Center, Xi'an Jiaotong University, Xi'an, 710061, China. Electronic address:

Modulated light-activated electrochemistry (MLAE) at semiconductor/liquid interfaces derived from light-addressable potentiometric sensor (LAPS) and light-activated electrochemistry (LAE) for addressable photoelectrochemical sensing has been proposed as a new sensor platform. In this system, a bias voltage is applied to create a depletion layer at the silicon/electrolyte interface. Meanwhile, intensity-modulated light illuminates the movable electrode to generate electron/hole pairs and causes a detectable local AC photocurrent. The AC measurement showed a higher signal-to-noise ratio (SNR) of photocurrents compared to the traditional DC response, while a steeper photocurrent-voltage (I-V) curve than that of LAPS with an insulating layer was obtained. Furthermore, to stabilize and functionalize the silicon substrate, metal-organic framework (MOF) nanoparticles were grown in-situ on the silicon electrode. The successful modification was validated by X-ray diffraction (XRD) and scanning electron microscopy (SEM). The AC photocurrent increased as a result of the adsorption of negatively charged DNA, which contributed to the enhancement of the cathodic reduction process at the semiconductor electrodes, indicating a different response mechanism of MLAE from LAPS. The results obtained demonstrate the potential of MOF functionalized MLAE as a robust platform for light-addressable DNA chips with high sensitivity and specificity.
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http://dx.doi.org/10.1016/j.bios.2019.111750DOI Listing
December 2019

Comparison of hypoxic effects induced by chemical and physical hypoxia on cardiomyocytes.

Can J Physiol Pharmacol 2019 Oct 28;97(10):980-988. Epub 2019 May 28.

Department of Aerospace Physiology, Fourth Military Medical University, Key Laboratory of Aerospace Medicine, Ministry of China, Xi'an 710032, China.

The degree and duration of chemical hypoxia induced by sodium dithionite (NaSO) have not been reported. It is not yet clear how much reduction in the O concentration (physical hypoxia) can lead to hypoxia in cultured cardiomyocytes. In this study, oxygen microelectrodes were used to measure changes in the O concentration in media containing different concentrations of NaSO. Then, hypoxic effects of 0.8, 1.0, and 2.0 mM NaSO or 1%, 3%, and 5% O in cultured cardiomyocytes from neonatal rats were observed and compared. The results showed that the O concentration failed to remain constant by NaSO treatment during the 180-minute observation period. Only the 2.0 mM NaSO group significantly increased the expression of hypoxia-inducible factor 1α (HIF-1α) and hypoxic responses. Notably, 3% O only significantly increased the expression of HIF-1α in cardiomyocytes, while 1% O not only increased the expression of HIF-1α but also increased the apoptotic rate in cardiomyocytes. These results suggest that NaSO is not suitable for establishing a hypoxic model in cultured neonatal rat cardiomyocytes, and neonatal rat cardiomyocytes cultured at or below 1% O induced significant hypoxic effects, which can be used as a starting O concentration for establishing a hypoxic cell model.
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http://dx.doi.org/10.1139/cjpp-2019-0092DOI Listing
October 2019

The R2R3 MYB transcription factor MYB189 negatively regulates secondary cell wall biosynthesis in Populus.

Tree Physiol 2019 07;39(7):1187-1200

Chongqing Key Laboratory of Plant Resource Conservation and Germplasm Innovation, School of Life Sciences, Southwest University, Chongqing, China.

Secondary cell wall (SCW) biosynthesis during wood formation in trees is controlled by a multilevel regulatory network that coordinates the expression of substantial genes. However, few transcription factors involved in the negative regulation of secondary wall biosynthesis have been characterized in tree species. In this study, we isolated an R2R3 MYB transcription factor MYB189 from Populus trichocarpa, which is expressed predominantly in secondary vascular tissues, especially in the xylem. A novel repression motif was identified in the C-terminal region of MYB189, which indicates this factor was a transcriptional repressor. Overexpression (OE) of MYB189 in Arabidopsis and poplar resulted in a significant reduction in the contents of lignin, cellulose and hemicelluloses. Vascular development in stems of MYB189 OE lines was markedly inhibited, leading to a dramatic decrease in SCW thickness of xylem fibers. Gene expression analyses showed that most of the structural genes involved in the biosynthesis of lignin, cellulose and xylans were significantly downregulated in MYB189-overexpressing poplars compared with the wild-type control. Chromatin immunoprecipitation-quantitative real-time polymerase chain reaction and transient expression assays revealed that MYB189 could directly bind to the promoters of secondary wall biosynthetic genes to repress their expression. Together, these data suggest that MYB189 acts as a repressor to regulate SCW biosynthesis in poplar.
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http://dx.doi.org/10.1093/treephys/tpz040DOI Listing
July 2019

Relationship between Volatile Anesthetics and Tumor Progression: Unveiling the Mystery.

Curr Med Sci 2018 Dec 7;38(6):962-967. Epub 2018 Dec 7.

Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

A series of factors can be involved in the perioperative period to cause an increase in cancer-related mortality. Unfortunately, volatile anesthesia might aggravate the deleterious effects. In this article, we review the association of diverse volatile anesthetic agents with immune system and cancer cell biology, and examine the effects on angeogenesis and postoperative metastasis or recurrence. Isoflurane, haloflurane and enflurane enhance immunosuppression and upregulate hypoxia-inducible-factor 1 and matrix metalloproteinases, leading to the cancer malignant progression, whereas roles of desflurane and sevoflurane are still unclear. As the effects of volatile anesthetics on tumor immunity have been known, it will be beneficial for using selective drugs into anesthesia and operation in cancer patients.
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http://dx.doi.org/10.1007/s11596-018-1970-6DOI Listing
December 2018
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