Publications by authors named "Wei Wei Liu"

237 Publications

Early Spontaneous Abortion in Fresh- and Frozen-Embryo Transfers: An Analysis of Over 35,000 Transfer Cycles.

Front Endocrinol (Lausanne) 2022 27;13:875798. Epub 2022 Jun 27.

Chongqing Reproduction and Genetics Institute, Chongqing Health Center for Women and Children, Chongqing, China.

Background: The aim of this study was to explore the risk factors for early spontaneous abortion (ESA) in fresh- and frozen-embryo transfers.

Methods: This retrospective cohort study comprised a total of 35,076 patients, including 15,557 women in the fresh-embryo transfer group and 19,519 women in the frozen-embryo transfer group from January 2016 to December 2020. The primary outcome of this study was ESA, which we defined as the termination of embryonic development before 12 weeks of pregnancy (i.e., an early abortion after artificial multi-fetal pregnancy reduction was excluded).

Results: In the 35,076 ART transfer cycles, the incidence of ESA was 5.77% (2023/35,076), and the incidence rates for ESA in fresh and frozen cycles were 4.93% (767 of 15,557) and 6.43% (1,256 of 19,519), respectively. Using a multivariate logistic regression analysis model, maternal age, body mass index (BMI), and number of embryos transferred were independent predictors for ESA. In addition, frozen-thawed transfer was a risk factor for ESA as compared with fresh transfer (OR = 1.207; 95% CI, 1.094-1.331; P = 0.000), blastocyst transfer was risk factor for ESA as compared with cleavage transfer (OR =1.373; 95% CI, 1.186-1.591; P = 0.000 in the total group; OR = 1.291; 95% CI, 1.111-1.499; P = 0.001 in the frozen-transfer group), and unexplained infertility was a protective factor for ESA only in the frozen group (OR = 0.746; 95% CI, 0.565-0.984; P = 0.038).

Conclusions: Maternal age, BMI, number of embryos transferred, and frozen-thawed transfer were independent risk factors for ESA in assisted reproductive technology treatment cycles.
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http://dx.doi.org/10.3389/fendo.2022.875798DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9271787PMC
June 2022

Silibinin inhibits ethanol- or acetaldehyde-induced ferroptosis in liver cell lines.

Toxicol In Vitro 2022 Aug 18;82:105388. Epub 2022 May 18.

Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning, PR China; Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research & Development, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning, PR China. Electronic address:

Alcoholic liver disease has become one of the main causes of liver injury, and its prevention and cure are important medical tasks. Silibinin, a natural flavonoid glycoside, is a conventional hepatic protectant. This study elucidates the modulation of ferroptosis in silibinin's protective effects on ethanol- or acetaldehyde-induced liver cell damage by using human carcinomatous liver HepG2 cells and immortalized liver HL7702 cells. Our results show that ferroptosis is induced in the cells treated with ethanol or acetaldehyde, as evidenced by the increased ROS stress and iron level. Silibinin resolves the oxidative stress and reduces iron level. Ferroptosis induced by ethanol- or acetaldehyde involving nuclear receptor co-activator 4 (NCOA4)-dependent autophagic degradation of ferritin, a protein for storing iron is rescued by silibinin. PINK1 and Parkin-mediated mitophagy is arrested in ethanol- or acetaldehyde-treated cells but reversed by silibinin. Ferritin degradation and ROS level are further increased when PINK1 or Parkin is silenced in the cells treated with ethanol or acetaldehyde. Collectively, our study reveals that silibinin inhibits ethanol- or acetaldehyde-induced ferroptosis in two liver cell lines, HepG2 and HL7702 cells, providing new therapeutic strategies for alcoholic liver injury.
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http://dx.doi.org/10.1016/j.tiv.2022.105388DOI Listing
August 2022

Internal heating method of loop-mediated isothermal amplification for detection of HPV-6 DNA.

Mikrochim Acta 2022 05 4;189(5):212. Epub 2022 May 4.

Department of Central Laboratory, Clinical Medicine Scientific and Technical Innovation Park, Shanghai Tenth People's Hospital, Shanghai, 200435, China.

Loop-mediated isothermal amplification (LAMP) is a promising diagnostic tool for genetic amplification, which is known for its rapid process, simple operation, high amplification efficiency, and excellent sensitivity. However, most of the existing heating methods are external for completion of molecular amplification with possibility of contamination of specimens. The present research provided an internal heating method for LAMP using magnetic nanoparticles (MNPs), which is called nano-LAMP. Near-infrared light with an excitation wavelength of 808 nm was employed as the heating source; hydroxy naphthol blue (HNB) was used as an indicator to conduct methodological research. We demonstrate that the best temperature was controlled at a working power of 2 W and 4.8 µg/µL concentration of nanoparticles. The lowest limit for the detection of HPV by the nano-LAMP method is 10 copies/mL, which was confirmed by a gel electrophoresis assay. In the feasibility investigation of validated clinical samples, all 10 positive HPV-6 specimens amplified by nano-LAMP were consistent with conventional LAMP methods. Therefore, the nano-LAMP detection method using internal heating of MNPs may bring a new vision to the exploration of thermostatic detection in the future.
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http://dx.doi.org/10.1007/s00604-022-05283-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9065241PMC
May 2022

Mismatch-fueled catalytic hairpin assembly mediated ultrasensitive biosensor for rapid detection of MicroRNA.

Anal Chim Acta 2022 Apr 15;1204:339663. Epub 2022 Mar 15.

Key Laboratory of Luminescence Analysis and Molecular Sensing Southwest University, Ministry of Education, College of Chemistry and Chemical Engineering, Southwest University, Chongqing, 400715, PR China. Electronic address:

Herein, a mismatch-fueled catalytic hairpin assembly (MCHA) was rationally engineered, which possessed higher amplification efficiency and faster rate than catalytic hairpin assembly (CHA). Once input target microRNA-21(miRNA-21) triggers the MCHA, the hairpin DNA H1 will be opened to form the duplex H1-miRNA-21, then the mismatched hairpin DNA H2 could easily hybridize with H1-miRNA-21 to generate duplex H1-H2 and the miRNA-21 could be released to enter next cycle, thus generating amounts of output products. Impressively, the MCHA realizes a pretty shorter complete reaction time of 40 min and quite higher amplification efficiency of 9.56 × 10, which dramatically transcended the barrier: low amplification times and long reaction time in traditional CHA. As a proof of the concept, the elaborated MCHA as a hyper-efficiency and high-speed DNA signal-magnifier was successfully applied in ultrasensitive and rapid detection of miRNA-21 with the detection limit of 0.17 fM, which exploited an ingenious nucleic acid signal amplification technique for sensitive and fast detection of biomarkers in biosensing assay and clinic diagnose.
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http://dx.doi.org/10.1016/j.aca.2022.339663DOI Listing
April 2022

gene disruption causes severe limb deformities in pigs.

Zool Res 2022 May;43(3):391-403

State Key Laboratory of Pig Genetic Improvement and Production Technology, Jiangxi Agricultural University, Nanchang, Jiangxi 330045, China.

In an attempt to generate g.A746G substitution in the gene, we unexpectedly obtained homozygous knockout piglets ( ) and heterogeneous knockout piglets with one copy of the A746G mutation ( ) via CRISPR/Cas9 editing. Polymerase chain reaction (PCR) and sequencing revealed complex genomic rearrangements in the target region. All -disrupted piglets showed an inability to stand and walk normally. Both and piglets exhibited severe skeletal dysplasia characterized by distorted and truncated forearms (ulna, radius) and disordered carpal, metacarpal, and phalangeal bones in the forelimbs. The piglets displayed more severe deformities in the hindlimbs by visual inspection, including fibular hemimelia, enlarged tarsal bone, and disordered toe joint bones. Limb deformities were more profound in piglets than in the piglets. Proteomic analysis identified 139 differentially expressed proteins (DEPs) in the hindlimb fibula of piglets compared to the wild-type (WT) controls. Most DEPs are involved in skeletal or embryonic development and/or the TGF-β pathway and tumor progression. Gene Ontology (GO) and protein domain enrichment analysis suggested alterations in these processes. Of the top 50 DEPs, a large proportion, e.g., C1QA, MYO1H, SRSF1, P3H1, GJA1, TCOF1, RBM10, SPP2, MMP13, and PHAX, were significantly associated with skeletal development. Our study provides novel findings on the role of in mammalian limb development.
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http://dx.doi.org/10.24272/j.issn.2095-8137.2021.291DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9113981PMC
May 2022

Protective effects of silibinin against ethanol- or acetaldehyde-caused damage in liver cell lines involve the repression of mitochondrial fission.

Toxicol In Vitro 2022 Apr 11;80:105330. Epub 2022 Feb 11.

Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning, PR China; Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research & Development, Shenyang 110016, Liaoning, PR China. Electronic address:

Silibinin is a natural polyphenolic flavonoid, isolated from the seeds of the milk thistle of Silybum marianum (L.) Gaertn. Silibinin has been widely used clinically as a traditional medicine for liver diseases. This study investigated the protective role of silibinin in ethanol- or acetaldehyde-induced apoptosis in human carcinomatous liver HepG2 cells and immortalized liver HL7702 cells, focusing on elucidation of the underlying mechanism in vitro. The toxicity of ethanol or acetaldehyde was evaluated by MTT assay. Apoptosis-related proteins, mitochondrial fission-associated proteins and mitochondrial fusion-associated proteins were analyzed by western blotting and immunofluorescence microscopy. Present experimental results demonstrated that silibinin improved cell viability, reduced the enzyme activities of AST/ALT and ALDH/ADH, inhibited apoptosis and recovered mitochondrial function in ethanol- or acetaldehyde-treated HepG2 or HL7702 cells. Silibinin reduced the expression of mitochondrial fission-associated proteins, dynamin-related protein 1 (DRP1), but increased mitochondrial fusion-associated proteins, optic atrophy 1 (OPA1) and mitofusin 1 (MFN1). Accordingly, inhibition of DRP1 activity with its pharmacological inhibitor or siDRP1 efficiently attenuated ethanol- or acetaldehyde-induced apoptosis, whereas activation of DRP1 by using staurosporine (STS) further increased apoptosis in ethanol- or acetaldehyde-treated HepG2 or HL7702 cells. The results show that silibinin protects cells against ethanol- or acetaldehyde-induced mitochondrial fission that results in apoptosis.
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http://dx.doi.org/10.1016/j.tiv.2022.105330DOI Listing
April 2022

PTP-PEST Regulated Membranous/Cytoplasmic Translocation of p120ctn in the Lung Cancer Resistance to Tyrosine Kinase Inhibitor.

Appl Immunohistochem Mol Morphol 2022 03;30(3):215-224

Department of Pathology, The First Hospital of China Medical University and College of Basic Medical Sciences, China Medical University.

Our previous studies indicate that resistance induction using first-generation tyrosine kinase inhibitors (TKIs) in lung cancer is accompanied with p120-catenin (p120ctn) cytoplasmic translocation from the membrane. However, the molecular mechanism underlying p120ctn intracytoplasmic translocation has not yet been reported. We performed immunohistochemistry to detect the correlation of p120ctn distribution with protein tyrosine phosphatase non-receptor type 12 (PTP-PEST) and p120ctn Y335 phosphorylation levels in non-small cell lung cancer (NSCLC) patients. After resistance induction using first-generation TKIs in lung cancer cells, Western blotting and substrate trapping were used to assess PTP-PEST expression and its influence on p120ctn Y335 phosphorylation, as well as the role of p120ctn Y335 phosphorylation on the association of p120ctn with E-cadherin and p120ctn membrane/cytoplasm translocation. In 197 samples collected from NSCLC patients, cytoplasmic p120ctn and enhanced p120ctn Y335 phosphorylation were associated with decreased PTP-PEST. After resistance induction using gefitinib, decreased PTP-PEST expression was accompanied by enhanced phosphorylation of p120ctn Y335 and p120ctn translocated to the cytoplasm. In gefitinib-resistant cells, PTP-PEST overexpression restrained p120ctn Y335 phosphorylation and restored membrane p120ctn expression. PTP-PEST enhanced the interaction of p120ctn with E-cadherin and elevated p120ctn membrane expression. However, increased p120ctn-Y335F mutant had no effect on p120ctn interaction with E-cadherin and membrane/cytoplasm translocation compared with the control group. In conclusion, resistance to first-generation TKIs inhibited PTP-PEST expression, which promoted p120ctn-Y335 phosphorylation and reduced the interaction of p120ctn with E-cadherin, resulting in p120ctn cytoplasmic translocation.
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http://dx.doi.org/10.1097/PAI.0000000000001008DOI Listing
March 2022

Novel pathogenic ALG2 mutation causing congenital myasthenic syndrome: A case report.

Neuromuscul Disord 2022 01 27;32(1):80-83. Epub 2021 Nov 27.

Clinical Neurophysiology, Department of Neuroscience, Uppsala University and Uppsala University Hospital; Uppsala, Sweden. Electronic address:

ALG2 mutations are extremely rare causes of congenital myasthenic syndromes (CMS). The clinical phenotype and treatment response is therefore not well described. We present the case of a baby who immediately after birth presented with pronounced truncal hypotonia, proximal muscle weakness and feeding difficulties. Single fibre electromyography showed neuromuscular transmission failure and salbutamol and ephedrine treatment improved both muscle weakness and neuromuscular transmission. Genetic analysis revealed a likely pathogenic variant c.1040del, p.(Gly347Valfs*27) in exon 2 and a variant of uncertain significance, c.239G>A, p.(Gly80Asp) in exon 1 of the ALG2 gene. Western blot in whole cell lysates of HEK293 cells transfected with p.Gly80Asp, or p.Gly347Valfs*27 expression constructs indicated that p.Gly347Valfs*27 is likely a null allele and p.Gly80Asp is pathogenic through marked reduction of ALG2 expression. This case highlights the utility of functional studies in clarifying variants of unknown significance, in suspected cases of CMS.
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http://dx.doi.org/10.1016/j.nmd.2021.11.012DOI Listing
January 2022

Inclusion of interleukin-6 improved performance of postoperative delirium prediction for patients undergoing coronary artery bypass graft (POD-CABG): A derivation and validation study.

J Cardiol 2022 05 23;79(5):634-641. Epub 2021 Dec 23.

School of Nursing, Capital Medical University, Beijing, China.

Background: Patients undergoing coronary artery bypass graft (CABG) are at high risk for developing postoperative delirium (POD). A simple prediction rule may benefit patients from early identification of POD followed by adequate preventive strategies. The purpose of the current study was to develop and validate a POD prediction rule for patients undergoing CABG (POD-CABG), by considering all possible perioperative factors.

Methods: In this prospective cohort study, patients who underwent first elective isolated CABG were continuously enrolled from May 2014 to November 2015 in a tertiary hospital. Delirium was assessed using the Confusion Assessment Method for Intensive Care Unit. Patients' perioperative risk factors were collected through interviews and review of medical records. The area under receiver-operating characteristic curve (AUC) was used to assess the overall performance of the predictive rule.

Results: A total of 242 and 148 patients were enrolled in the derivation and validation cohorts, respectively. Multiple logistic regression analysis identified seven variables that were independently associated with POD: age (≥65 years), gender (female), history of myocardial infarction and diabetes mellitus, postoperative atrial fibrillation, the use of intra-aortic balloon pump, and serum interleukin-6 ≥478 pg/ml at 18 hours after surgery. The AUC of the POD-CABG was 0.84 (95% CI, 0.79-0.90) in the derivation cohort, and was 0.86 (95% CI, 0.80-0.91) after bootstrap resampling. The AUC was 0.81 (95% CI, 0.73-0.88) after the POD-CABG was applied to the validation cohort.

Conclusions: The POD-CABG with inclusion of interleukin-6 demonstrated good performance in predicting POD.
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http://dx.doi.org/10.1016/j.jjcc.2021.12.003DOI Listing
May 2022

Silibinin relieves UVB-induced apoptosis of human skin cells by inhibiting the YAP-p73 pathway.

Acta Pharmacol Sin 2022 Aug 15;43(8):2156-2167. Epub 2021 Dec 15.

Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, 110016, China.

Excessive exposure to UVB induces skin diseases. Silibinin, a flavonolignan used for treating liver diseases, is found to be effective against UVB-caused skin epidermal and dermal cell damage. In this study we investigated the molecular mechanisms underlying. Human nonmalignant immortalized keratinocyte HaCaT cells and neonatal human foreskin fibroblasts HFFs were exposed to UVB irradiation. We showed that pre-treatment with silibinin dose-dependently decreased UVB-induced apoptosis of HaCaT cells. Furthermore, we showed that silibinin treatment inhibited nuclear translocation of YAP after UVB irradiation. Molecular docking analysis and DARTS assay confirmed the direct interaction of silibinin with YAP. Silencing YAP by siRNA had no influence on the survival of HaCaT cells, whereas inhibiting classical YAP-TEAD signaling pathway by siRNA targeting TEAD1 or its pharmaceutical inhibitor verteporfin further augmented UVB-induced apoptosis, suggesting that YAP-TEAD pathway was prosurvival, which did not participate in the protective effect of silibinin. We then explored the pro-apoptotic YAP-p73 pathway. p73 was upregulated in UVB-irradiated cells, but reduced by silibinin cotreatment. The mRNA and protein levels of p73 target genes (PML, p21 and Bax) were all increased by UVB but decreased by silibinin co-treatment. Inhibiting p73 by using siRNA reduced UVB-induced apoptosis, suggesting that downregulation of p73 was responsible for the cytoprotective effect of silibinin. In HFFs, the upregulated YAP-p73 pathway by UVB irradiation was also suppressed by silibinin. Collectively, YAP-p73 pathway is a major cause of the death of UVB-exposed epidermal HaCaT cells and dermal HFFs. Silibinin directly inhibits YAP-p73 pathway, exerting the protective action on UVB-irradiated skin cells.
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http://dx.doi.org/10.1038/s41401-021-00826-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9343358PMC
August 2022

Genetic defects are common in myopathies with tubular aggregates.

Ann Clin Transl Neurol 2022 01 15;9(1):4-15. Epub 2021 Dec 15.

Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London, UK.

Objective: A group of genes have been reported to be associated with myopathies with tubular aggregates (TAs). Many cases with TAs still lack of genetic clarification. This study aims to explore the genetic background of cases with TAs in order to improve our knowledge of the pathogenesis of these rare pathological structures.

Methods: Thirty-three patients including two family members with biopsy confirmed TAs were collected. Whole-exome sequencing was performed on 31 unrelated index patients and a candidate gene search strategy was conducted. The identified variants were confirmed by Sanger sequencing. The wild-type and the mutant p.Ala11Thr of ALG14 were transfected into human embryonic kidney 293 cells (HEK293), and western blot analysis was performed to quantify protein expression levels.

Results: Eleven index cases (33%) were found to have pathogenic variant or likely pathogenic variants in STIM1, ORAI1, PGAM2, SCN4A, CASQ1 and ALG14. Among them, the c.764A>T (p.Glu255Val) in STIM1 and the c.1333G>C (p.Val445Leu) in SCN4A were novel. Western blot analysis showed that the expression of ALG14 protein was severely reduced in the mutant ALG14 HEK293 cells (p.Ala11Thr) compared with wild type. The ALG14 variants might be associated with TAs in patients with complex multisystem disorders.

Interpretation: This study expands the phenotypic and genotypic spectrums of myopathies with TAs. Our findings further confirm previous hypothesis that genes related with calcium signalling pathway and N-linked glycosylation pathway are the main genetic causes of myopathies with TAs.
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http://dx.doi.org/10.1002/acn3.51477DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8791796PMC
January 2022

Efficiency Improvement of Quantum Dot Light-Emitting Diodes via Thermal Damage Suppression with HATCN.

ACS Appl Mater Interfaces 2021 Oct 11;13(41):49058-49065. Epub 2021 Oct 11.

Joint Key Laboratory of the Ministry of Education, Institute of Applied Physics and Materials Engineering, University of Macau, Avenida da Universidade, Taipa, Macao SAR 999078, China.

With many advantages including superior color saturation and efficiency, quantum dot light-emitting diodes (QLEDs) are considered a promising candidate for the next-generation displays. Emission uniformity over the entire device area is a critical factor to the overall performance and reliability of QLEDs. In this work, we performed a thorough study on the origin of dark spots commonly observed in operating QLEDs and developed a strategy to eliminate these defects. Using advanced cross section fabrication and imaging techniques, we discovered the occurrence of voids in the organic hole transport layer and directly correlated them to the observed emission nonuniformity. Further investigations revealed that these voids are thermal damages induced during the subsequent thermal deposition of other functional layers and can act as leakage paths in the device. By inserting a thermo-tolerant 1,4,5,8,9,11-hexaazatriphenylene-hexacarbonitrile (HATCN) interlayer with an optimized thickness, the thermally induced dark spots can be completely suppressed, leading to a current efficiency increase by 18%. We further demonstrated that such a thermal passivation strategy can work universally for various types of organic layers with low thermal stability. Our findings here provide important guidance in enhancing the performances and reliability of QLEDs and also other sandwich-structured devices via the passivation of heat-sensitive layers.
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http://dx.doi.org/10.1021/acsami.1c16034DOI Listing
October 2021

Alveolar-arterial partial pressure difference as an early predictor for patients with acute paraquat poisoning.

J Int Med Res 2021 Sep;49(9):3000605211043243

Department of Occupational Diseases and Poisoning, Guangzhou Occupational Disease Prevention and Treatment Hospital (Guangzhou Twelfth People's Hospital), Guangzhou 510620, China.

Objective: Paraquat (PQ) is associated with high mortality rates in acute poisoning. This study aimed to determine the importance of the alveolar-arterial partial pressure difference (A-aDo) in the expected consequences of acute PQ poisoning.

Methods: Patients who were hospitalized for PQ poisoning in 2018 were enrolled in this retrospective study. A-aDo data were collected. Multivariate analysis was performed using binary logistic regression to determine whether A-aDo is an independent risk factor for mortality from PQ.

Results: A total of 352 cases were analyzed. The mean PQ dose was 36.84 ± 50.30 mL (0.3-500 mL). There were 185 survivors and 167 non-survivors. The mean A-aDo was not significantly correlated between survivors and non-survivors on day 1. However, there were significant differences in A-aDo between survivors and non-survivors on days 3, 7, 14, and 21. Increased A-aDo values were correlated with an increased mortality rate. The mean A-aDo on day 14 showed the most significant difference between survivors and non-survivors.

Conclusion: Our study suggests that A-aDo plays an important role as a reference index, which could be a useful predictor in assessing acute PQ poisoning, especially on the 14th day after onset of poisoning.
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http://dx.doi.org/10.1177/03000605211043243DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8450997PMC
September 2021

Cytoplasmic P120ctn Promotes Gefitinib Resistance in Lung Cancer Cells by Activating PAK1 and ERK Pathway.

Appl Immunohistochem Mol Morphol 2021 Nov-Dec 01;29(10):750-758

Medical Microbiology and Human Parasitology, College of Basic Medical Sciences, China Medical University, Shenyang.

Our previous studies indicated that cytoplasmic p120ctn mediated epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKI) resistance in lung cancer. In the present study, we aim to further explore the underlying molecular mechanisms. Immunohistochemistry detected PAK1, Cdc42, and Rac1 expression in lung cancer with cytoplasmic p120ctn. Immunoblotting, protein activity analysis, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide evaluated p120ctn location, PAK1, Cdc42/Rac1, and extracellular signal-regulated kinase (ERK) activity in response to TKI treatment in HCC827 and PC9 cell lines, as well as the cell sensitivity to Gefitinib. Most non-small cell lung cancer patients with cytoplasmic p120ctn showed enhanced PAK1 and Cdc42/Rac1. When Gefitinib resistance was induced, cytoplasmic p120ctn is accompanied with increasing PAK1 and Cdc42/Rac1. Cytoplasmic p120ctn activated ERK via PAK1, while PAK1 downregulation attenuated ERK activation by cytoplasmic p120ctn. After Cdc42/Rac1 inhibition, cytoplasmic p120ctn could not activate PAK1. Cytoplasmic p120ctn activates PAK1 via Cdc42/Rac1 activation, constitutively activates ERK in the EGFR downstream signaling, and promotes EGFR-TKI resistance in lung cancer cells. The current study will aid to screen the subpopulation patients who would benefit from therapy with first-generation EGFR-TKIs.
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http://dx.doi.org/10.1097/PAI.0000000000000965DOI Listing
March 2022

Parotid mammary analogue secretory carcinoma: A case report and review of literature.

World J Clin Cases 2021 Jun;9(16):4052-4062

Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Jilin University, Changchun 130021, Jilin Province, China.

Background: Mammary analogue secretory carcinoma (MASC) is a rare low-grade malignant salivary gland tumor. The morphological and immunohistochemical features of MASC closely resemble those of breast secretory carcinoma. The key characteristics of the lesion are a lack of pain and slow growth. There is no obvious specificity in the clinical manifestations and imaging features. The diagnosis of the disease mainly depends on the detection of the MASC-specific fusion gene.

Case Summary: This report describes a rare case of a 32-year-old male patient who presented with a gradually growing lesion that was initially diagnosed as breast-like secretory carcinoma of the right parotid gland. Imaging and histological investigations were used to overcome the diagnostic difficulties. The lesion was managed with right parotidectomy, facial nerve preservation, biological patch implantation to restore the resulting defect, and postoperative radiotherapy. On postoperative follow-up, the patient reported a mild facial deformity with no complications, signs of facial paralysis, or Frey's syndrome.

Conclusion: The imaging and histological diagnostic challenges for MASC are discussed.
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http://dx.doi.org/10.12998/wjcc.v9.i16.4052DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8180236PMC
June 2021

Stable and Efficient Blue-Emitting CsPbBr Nanoplatelets with Potassium Bromide Surface Passivation.

Small 2021 Oct 13;17(43):e2101359. Epub 2021 Jun 13.

Institute of Applied Physics and Materials Engineering, University of Macau, Taipa, Macao SAR, 999078, China.

Colloidal all-inorganic perovskites nanocrystals (NCs) have emerged as a promising material for display and lighting due to their excellent optical properties. However, blue emissive NCs usually suffer from low photoluminescence quantum yields (PLQYs) and poor stability, rendering them the bottleneck for full-color all-perovskite optoelectronic applications. Herein, a facile approach is reported to enhance the emission efficiency and stability of blue emissive perovskite nano-structures via surface passivation with potassium bromide. By adding potassium oleate and excess PbBr to the perovskite precursor solutions, potassium bromide-passivated (KBr-passivated) blue-emitting (≈450 nm) CsPbBr nanoplatelets (NPLs) is successfully synthesized with a respectably high PLQY of 87%. In sharp contrast to most reported perovskite NPLs, no shifting in emission wavelength is observed in these passivated NPLs even after prolonged exposures to intense irradiations and elevated temperature, clearly revealing their excellent photo- and thermal-stabilities. The enhancements are attributed to the formation of K-Br bonding on the surface which suppresses ion migration and formation of Br-vacancies, thus improving both the PL emission and stability of CsPbBr NPLs. Furthermore, all-perovskite white light-emitting diodes (WLEDs) are successfully constructed, suggesting that the proposed KBr-passivated strategy can promote the development of the perovskite family for a wider range of optoelectronic applications.
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http://dx.doi.org/10.1002/smll.202101359DOI Listing
October 2021

[Spatial-Temporal Variation of Water Environment Quality and Pollution Source Analysis in Hengshui Lake].

Huan Jing Ke Xue 2021 Mar;42(3):1361-1371

National Ecosystem Research Station of Hengshui Lake Wetland, Hengshui 053000, China.

To study the spatial-temporal variation of water environment quality in Hengshui Lake and determine the associated pollution sources, we used historical water monitoring data (from 2000 onwards) and data from 17 sites sampled in 2019 to determine the trophic level index (TLI), comprehensive water quality index (WQI), and water environment quality index (EQI). The results showed that the proportion of monitoring points reaching level Ⅲ increased from 2000 to 2019. The permanganate index, total nitrogen, and total phosphorus were the main water environmental indicators. Spatially, TLI, WQI, and EQI all generally decreased from the south to the middle and west of the lake, and then further decreased towards the northeast. After the establishment of the Hengshui Lake National Nature Reserve, a series of water body protection policies and measures were implemented. These interventions are reflected in reductions in the TLI, WQI, and EQI between 2000 and 2019 by 20.9%, 53.4%, and 49.2%, respectively. However, side seepage and sewage discharge, agricultural non-point source pollutants transported by water diversion, and the decay of plants in the lake present significant challenges for water quality in Hengshui Lake.
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http://dx.doi.org/10.13227/j.hjkx.202008048DOI Listing
March 2021

Mandibular Reconstruction Using Free Fibular Flap Graft Following Excision of Calcifying Epithelial Odontogenic Tumor.

J Craniofac Surg 2021 Mar-Apr 01;32(2):e167-e171

Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Jilin University.

Abstract: The calcifying epithelial odontogenic tumor (CEOT) is a rare benign odontogenic tumor, which usually presents with distension of affected tissues. Radiologically, the lesions are often associated with an unerupted tooth and may have spot calcification shadows. The authors report a case of a CEOT in a 48-year-old male involving the right mandibular jaw bone and mentum soft tissues. The authors performed hemimandibulectomy and enucleation followed by reconstruction of the mandible using a vascularized free fibular flap through a digital surgical technique in order to restore the patient's facial symmetry and prepare the area for functional restorations. The case illustrates who the free fibular flap graft can be used for satisfactory mandibular reconstruction and restoration of the morphology and functions.
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http://dx.doi.org/10.1097/SCS.0000000000006955DOI Listing
June 2021

Imbalance of Molecular Module of TINCR-miR-761 Promotes the Metastatic Potential of Early Triple Negative Breast Cancer and Partially Offsets the Anti-Tumor Activity of Luteolin.

Cancer Manag Res 2021 23;13:1877-1886. Epub 2021 Feb 23.

Department of Breast Surgery, Cangzhou People's Hospital, Cangzhou City, 061001, Hebei Province, People's Republic of China.

Background: Triple negative breast cancer (TNBC) poses a great threat to patient prognosis. LncRNA-miRNA is a molecular module formed by a long non-coding RNA (LncRNA) and a microRNA (miRNA) that mediates the metastatic potential of tumours such as TNBC, and luteolin (LU) is a natural compound with anti-TNBC activity.

Objective: We aim to explore the regulatory mechanism of terminal differentiation-induced non-coding RNA (TINCR)-miR-761 molecular module in early TNBC, as well as its influence on anti-tumor activity of LU.

Methods: The serum was collected from TNBC patients in early stage to detect the expression of TINCR and miR-761 using RT-PCR. Transwell method was applied for the determination of cell migration and invasion, Western blot for epithelial-mesenchymal transition (EMT), flow cytometry (FCM) for cell apoptosis, and dual luciferase reporter and RNA pull-down experiment for the verification of the targeted relationship between TINCR and miR-761.

Results: Both TINCR and miR-761 were up-regulated in the serum of patients with early TNBC and the area under the curve (AUC) of the two for distinguishing TNBC from BC was not less than 0.850. In the cell function tests, down-regulation of TINCR or miR-761 notably suppressed the metastatic potentials (cell migration, invasion and EMT) of TNBC cells were remarkably inhibited, while up-regulation of TINCR or miR-761 notably promoted the metastatic potentials. We also confirmed that TINCR acts as the molecular sponge of miR-761, and has positive regulation on it. Besides, LU can significantly down-regulate TINCR and miR-761, and partially offset the anti-TNBC activity of LU when they were abnormally up-regulated, which was mainly reflected in the decrease of anti-proliferation and pro-apoptotic ability of LU against TNBC.

Conclusion: There is an imbalance of TINCR-miR-761 molecular module in early TNBC, which may be a potential new therapeutic target of TNBC.
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http://dx.doi.org/10.2147/CMAR.S288271DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7914057PMC
February 2021

Regulatory Effect of miR497-5p- Axis in Triple-Negative Breast Cancer Cells and Its Predictive Value for Early Diagnosis.

Cancer Manag Res 2021 18;13:439-447. Epub 2021 Jan 18.

Breast Center, Cangzhou People's Hospital, Cangzhou 061000, Hebei Province, People's Republic of China.

Objective: To explore the regulatory role of miR497-5p- axis in triple-negative breast cancer (TNBC) cells and its predictive value for early diagnosis.

Methods: Cancer tissue and adjacent tissue samples were collected from 86 patients with TNBC.RT-PCR was used to detect the expression of miR497-5p and (target gene) mRNA, determined by biological prediction in tissue and TNBC cells. ROC was used to analyze the diagnostic value of miR497-5p in TNBC. MTT, invasion, and flow cytometry were used to detect the proliferation, invasion, cycle, apoptosis rate, and expression of related proteins of TNBC cells with overexpression of miR497-5p or knockdown of .

Results: RT-qPCR results showed that miR497-5p levels were significantly downregulated in TNBC tissue and cells, while CCNE1 expression was significantly upregulated, and miR497-5p expression was negatively correlated with that of CCNE1 (<0.001). ROC analysis showed that the AUC of miR497-5p for TNBC was >0.9, which had better diagnostic value. The cell tests revealed that miR497-5p played a role in tumor inhibition, including inhibiting proliferation and invasion of TNBC cells, blocking the cell cycle, and promoting apoptosis. Bioinformatic prediction and subsequent experiments revealed that was the direct target of miR497-5p. Furthermore, after knocking down the expression of in TNBC cells, the proliferation and invasion of TNBC cells were significantly inhibited, the cell cycle blocked, and the apoptosis rate significantly increased (<0.001), and expression of the proapoptosis-related proteins Bax and caspase 3 (cleaved) were upregulated, while expression of the antiapoptosis-related protein BCL2 was downregulated (<0.001).

Conclusion: miR497-5p inhibited the proliferation and invasion of TNBC cells by targeting CCNE1, blocked the cell cycle and promoted the apoptosis of TNBC cells, and had better diagnostic value for TNBC. miR497-5p can be used as a new potential target for the treatment of TNBC.
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http://dx.doi.org/10.2147/CMAR.S284277DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7823138PMC
January 2021

Discontinuous polyostotic fibrous dysplasia with multiple systemic disorders and unique genetic mutations: A case report.

World J Clin Cases 2020 Dec;8(23):6197-6205

Department of Musculoskeletal Oncology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China.

Background: Polyostotic fibrous dysplasia (PFD) is an uncommon developmental bone disease in which normal bone and marrow are replaced by pseudotumoral tissue. The etiology of PFD is unclear, but it is generally thought to be caused by sporadic, post-zygotic mutations in the gene. Herein, we report the case of a young female with bone pain and lesions consistent with PFD, unique physical findings, and gene mutations.

Case Summary: A 27-year-old female presented with unbearable bone pain in her left foot for 4 years. Multiple bone lesions were detected by radiographic examinations, and a diagnosis of PFD was made after a biopsy of her left calcaneus with symptoms including pre-axial polydactyly on her left hand and severe ophthalmological problems such as high myopia, vitreous opacity, and choroidal atrophy. Her serum cortisol level was high, consistent with Cushing syndrome. Due to consanguineous marriage of her grandparents, boosted whole exome screening was performed to identify gene mutations. The results revealed mutations in and , which may be contributing factors to her unique findings.

Conclusion: The unique findings in this patient with PFD may be related to mutations in the and genes.
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http://dx.doi.org/10.12998/wjcc.v8.i23.6197DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723713PMC
December 2020

Effect of silibinin on ethanol- or acetaldehyde-induced damge of mouse primary hepatocytes in vitro.

Toxicol In Vitro 2021 Feb 30;70:105047. Epub 2020 Oct 30.

Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning, PR China; Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research & Development, Liaoning Province, PR China. Electronic address:

Silibinin, one of the flavonoids isolated from milk thistle seeds of Silybum marianum, has hepatoprotective properties against toxins in clinical. However, the detailed mechanisms have remained unclear. This study investigates the underlying mechanism of silibinin in the protection against ethanol- or acetaldehyde-induced damage of neonatal mouse primary hepatocytes in vitro. The results show that ethanol inhibited proliferation of hepatocytes in a time (12, 24, 36 h) and dose-dependent (0-800 mM) manner. However, silibinin did not show protective effect on ethanol (500 mM)-induced suppression of hepatocyte proliferation. Acetaldehyde, the toxic metabolite of ethanol, appearing immediately in individuals after drink also inhibited the proliferation of hepatocytes in a dose-dependent (0-12 mM) manner. Surprisingly, silibinin significantly increased the cell viability and reduced the leakage of alanine amino transferase (ALT) and aspartate amino transferase (AST) in acetaldehyde-treated hepatocytes, suggesting that silibinin protected cell injury caused by acetaldehyde treatment. The apoptosis-inducing effect of acetaldehyde was demonstrated by the increased number of cells in sub-G1 phase as well as caspase-3 activation. Further study shows that acetaldehyde induced autophagy in the hepatocytes. The autophagy inhibitors, 3-Methyladenine (3-MA) and chloroquine (CQ), further decreased the viability of cells treated with acetaldehyde, suggesting that autophagy plays a protective role against apoptosis. Consistently, silibinin (20 μM) significantly reduced the activation of caspase 3 or apoptosis and increased the conversion of LC3-I to LC3-II or autophagy. Taken together, it is concluded that silibinin does not repress the ethanol- induced hepatocyte injury, whereas silibinin reduces acetaldehyde-caused hepatocyte injury through down-regulation of apoptosis and up-regulation of autophagy.
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http://dx.doi.org/10.1016/j.tiv.2020.105047DOI Listing
February 2021

Identifying VoIP traffic in VPN tunnel via Flow Spatio-Temporal Features.

Math Biosci Eng 2020 07;17(5):4747-4772

School of Automation, Nanjing University of Science and Technology, Nanjing 210094, China.

The persistent emergence of new network applications, along with encrypted network communication, has make traffic analysis become a challenging issue in network management and cyberspace security. Currently, virtual private network (VPNs) has become one of the most popular encrypted communication services for bypassing censorship and guarantee remote access to geographically locked services. In this paper, a novel identification scheme of VoIP traffic tunneled through VPN is proposed. We employed a set of Flow Spatio-Temporal Features (FSTF) to six well-known classifiers, including decision trees, K-Nearest Neighbor (KNN), Bagging and Boosting via C4.5, and Multi-Layer perceptron (MLP). The overall accuracy, precision, sensitivity, and F-measure verify that the proposed scheme can effectively distinguish between the VoIP flows and Non-VoIP ones in VPN traffic.
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http://dx.doi.org/10.3934/mbe.2020260DOI Listing
July 2020

Light-Responsive Core-Shell Nanoplatform for Bimodal Imaging-Guided Photothermal Therapy-Primed Cancer Immunotherapy.

ACS Appl Mater Interfaces 2020 Oct 19;12(43):48420-48431. Epub 2020 Oct 19.

Chongqing Key Laboratory of Ultrasound Molecular Imaging, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.

Photothermal therapy (PTT) as a noninvasive and effective thermal therapeutic approach has attracted tremendously increasing interest because it can effectively eliminate the primary tumor and generate tumor-associated antigens, which could elicit antitumor immune responses. Herein, we report on the rational design and fabrication of copper sulfide (CuS)-based nanoplatform for cancer photothermal immunotherapy. The as-prepared core-shell [email protected] (CPPs) nanocomposites possess high biocompatibility, photoacoustic (PA)/ultrasound (US) imaging, and strong PTT effect upon 808 nm laser irradiation, indicating that the nanocomposites have a promising application in diagnosis and treatment of breast cancer with molecular classification. Importantly, we also elucidated that the CPP-triggered PTT in combination with -PD-1 checkpoint blockade therapy can not only obliterate primary tumor but also inhibit metastatic tumor in tumor-bearing mice. We believe that the CPPs have a good probability to serve as a useful nanoplatform for PTT, and this approach may provide a promising strategy for tumor-therapeutic modality with immunotherapy.
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http://dx.doi.org/10.1021/acsami.0c16526DOI Listing
October 2020

Regulation of γδT17 cells by Mycobacterium vaccae through interference with Notch/Jagged1 signaling pathway.

Braz J Med Biol Res 2020 7;53(11):e9551. Epub 2020 Oct 7.

Department of Respiratory Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.

The objective of this study was to investigate the effect of Mycobacterium vaccae on Jagged 1 and gamma delta T17 (γδT17) cells in asthmatic mice. An asthma mouse model was established through immunization with ovalbumin (OVA). Gamma-secretase inhibitor (DAPT) was used to block the Notch signaling pathway. M. vaccae was used to treat asthma, and related indicators were measured. Blocking Notch signaling inhibited the production of γδT17 cells and secretion of cytokine interleukin (IL)-17, which was accompanied by a decrease in Jagged1 mRNA and protein expression in the treated asthma group compared with the untreated asthma group. Similarly, treatment with M. vaccae inhibited Jagged1 expression and γδT17 cell production, which was associated with decreased airway inflammation and reactivity. The Notch signaling pathway may play a role in the pathogenesis of asthma through the induction of Jagged1 receptor. On the other hand, the inhibitory effect of M. vaccae on Jagged1 receptor in γδT17 cells could be used for the prevention and treatment of asthma.
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http://dx.doi.org/10.1590/1414-431X20209551DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7552905PMC
December 2020

Changes in preventive care utilisation and its influencing factors among Chinese adults before and after the healthcare reform: cross-sectional evidence from the China Health and Nutrition Survey in 2004-2015.

BMJ Open 2020 10 1;10(10):e038763. Epub 2020 Oct 1.

Human Nutrition Department, QU Health, Qatar University, Doha, Ad Dawhah, Qatar.

Objective: China launched its health reform in 2009. This study aimed to assess changes in preventive care utilisation (PCU) and its relationship with the healthcare reform.

Design: A cross-sectional study using demographic characteristics, socioeconomic status, environmental factors, and lifestyle and health status data of adults from five waves (2004-2015) of the China Health and Nutrition Survey (CHNS) was conducted. Multilevel mixed-effects logistic regression models were used.

Setting: Data were derived from urban and rural communities of nine provinces in China.

Participants: Data were obtained from five waves of the CHNS, with 9960 participants in 2004, 9888 in 2006, 10 286 in 2009, 9709 in 2011, and 10 628 in 2015.

Outcome: The primary outcome was PCU.

Results: PCU in 2004-2015 among adults was 3.29%, 3.13%, 3.77%, 4.95% and 2.73%, respectively. Whether before or after the health reform, having a history of disease and female gender were positive influencing factors of PCU. Before 2009, PCU was significantly associated with gender, income, medical insurance status and region. Age, medical insurance status, history of drinking and education level significantly affected PCU in 2009-2011. Having medical insurance was no longer a positive influencing factor of PCU, while high income had a negative effect on PCU, in 2011-2015.

Conclusions: PCU from 2004 to 2015 was low and the health reform in China may lack sustainable effect on PCU. Further studies on how to ensure sustainability of PCU are necessary, and further reforms on preventive care services should be aimed at different ages, rural areas and participants without history of disease.
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http://dx.doi.org/10.1136/bmjopen-2020-038763DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7534708PMC
October 2020

Genome-wide association study of bone quality and feed efficiency-related traits in Pekin ducks.

Genomics 2020 11 11;112(6):5021-5028. Epub 2020 Sep 11.

National Engineering Laboratory for Animal Breeding and Key Laboratory of Animal Genetics, Breeding and Reproduction, MARA; College of Animal Science and Technology, China Agricultural University, Beijing 100193, China. Electronic address:

Feeding and bone traits are vital for breeding and reproduction in the commercial duck industry. In this study, we performed a genome-wide association study for feeding and bone traits in a population of 540 lean-type Pekin ducks, followed by genotyping-by-sequencing procedures. The genetic parameters of feeding and bone traits were also estimated using genomic information. In total, seventy-eight significant SNPs were determined, and eleven of them reached the genome-wide significant level for 7 traits except for body weight at 42-day old. A peak of genome-wide significant SNPs was detected on chromosome 2 for feed conversion ratio (P-value = 7.46E-11), and the top SNP (P-value = 2.23E-08) for bone-breaking strength was also obtained in the upstream of gene RAPGEF5. This study provided a list of novel markers and candidate genes associated with feeding and bone traits in Pekin ducks, which could contribute to the genetic selection in duck breeding.
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http://dx.doi.org/10.1016/j.ygeno.2020.09.023DOI Listing
November 2020

Nucleolin Mediates LPS-induced Expression of Inflammatory Mediators and Activation of Signaling Pathways.

Curr Med Sci 2020 Aug 29;40(4):646-653. Epub 2020 Aug 29.

Department of Cardiology, the First Hospital of Changsha, Changsha, 410008, China.

In this study, we investigated the effects of nucleolin on lipopolysaccharide (LPS)-induced activation of MAPK and NF-KappaB (NF-κB) signaling pathways and secretion of TNF-α, IL-1β and HMGB1 in THP-1 monocytes. Immunofluorescence assay and Western blotting were used to identify the nucleolin expression in cell membrane, cytoplasm and nucleus of THP-1 monocytes. Inactivation of nucleolin was induced by neutralizing antibody against nucleolin. THP-1 monocytes were pretreated with anti-nucleolin antibody for 1 h prior to LPS challenge. The irrelevant IgG group was used as control. Secretion of inflammatory mediators (TNF-α, IL-1β and HMGB1) and activation of MAPK and NF-κB/I-κB signaling pathways were examined to assess the effects of nucleolin on LPS-mediated inflammatory response. Nucleolin existed in cell membrane, cytoplasm and nucleus of THP-1 monocytes. Pretreatment of anti-nucleolin antibody significantly inhibited the LPS-induced secretion of TNF-α, IL-1β and HMGB1. P38, JNK, ERK and NF-κB subunit p65 inhibitors could significantly inhibit the secretion of IL-1β, TNF-α and HMGB1 induced by LPS. Moreover, the phosphorylation of p38, JNK, ERK and p65 (or nuclear translocation of p65) was significantly increased after LPS challenge. In contrast, pretreatment of anti-nucleolin antibody could significantly inhibit the LPS-induced phosphorylation of p38, JNK, ERK and p65 (or nuclear translocation of p65). However, the irrelevant IgG, as a negative control, had no effect on LPS-induced secretion of TNF-α and IL-1β and phosphorylation of p38, JNK, ERK and p65 (or nuclear translocation of p65). We demonstrated that nucleolin mediated the LPS-induced activation of MAPK and NF-κB signaling pathways, and regulated the secretion of inflammatory mediators (TNF-α, IL-1β and HMGB1).
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http://dx.doi.org/10.1007/s11596-020-2229-6DOI Listing
August 2020

Clinical and molecular characteristics of secondary breast metastases from primary lung cancer: a study of 22 Chinese cases.

Int J Clin Exp Pathol 2020 1;13(7):1880-1885. Epub 2020 Jul 1.

Department of Medical Oncology, The First Affiliated Hospital of Bengbu Medical College Bengbu 233004, Anhui, People's Republic of China.

Background: To analyze the clinical and molecular characteristics, as well as pathologic diagnosis and treatment of lung tumors that spread to the breast in 22 Chinese patients.

Materials And Methods: A systematic literature search of PubMed, Embase, ScienceDirect, Chinese National Knowledge Infrastructure (CNKI), Chinese Science and Technology Journal Database and Wanfang Databases was conducted to identify the related studies published before March 31, 2020. A case of a 64-year-old man who underwent pneumonectomy and who was eventually diagnosed with a breast lump 5 years after surgery at our hospital, was also included in the present study. We analyzed the clinical and immunohistochemical characteristics from these case reports.

Results: The analysis totally incorporates 21 case reports and our own case, covering 22 subjects. Among all cases we found 11 adenocarcinomas, 7 small-cell carcinomas, and 4 squamous carcinomas. In addition, most of metastatic breast masses were located below or near the nipple, rather than in the outer quadrant. The results of immunohistochemistry mostly showed triple negative breast cancers.

Conclusion: A lung cancer patient with a breast tumor should suggest the possibility of metastasis. It is extremely difficult to distinguish secondary breast cancer from primary simply through medical observation and pathologic testing. Additional immunohistochemical examinations are necessary to avoid delays in diagnosis and treatment.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7414484PMC
July 2020

Severe congenital myasthenic syndrome associated with novel biallelic mutation of the CHRND gene.

Neuromuscul Disord 2020 04 24;30(4):336-339. Epub 2020 Feb 24.

Department of Neuropediatrics and Muscle Disorders, Faculty of Medicine, Medical Center - University of Freiburg, Freiburg, Germany; Centro Nacional de Análisis Genómico (CNAG-CRG), Center for Genomic Regulation, Barcelona Institute of Science and Technology (BIST), Barcelona, Catalonia, Spain; Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Canada; Department of Medicine, Division of Neurology, The Ottawa Hospital, Ottawa, Canada.

Congenital myasthenic syndromes (CMS) are a group of inherited disorders caused by mutations in genes encoding proteins essential for neuromuscular transmission. CMS is characterized by fatigable muscle weakness with onset at birth or in early childhood; rarely, symptoms may present later. The most frequently involved proteins are choline acetyltransferase, the endplate species of acetylcholinesterase and the acetylcholine receptor subunits. Defects in the cholinergic receptor nicotinic delta subunit (CHRND) are a rare cause for CMS but they should be considered in patients with a severe, early onset disease, with respiratory distress. We describe two sisters, clinically and genetically diagnosed with CMS, carrying two heteroallelic variants in the CHRND gene: c.730C>T; p.(Arg244Cys) and c.1304T>C; p.(Leu435Pro). The first variant has already been described yet no clinical relevance has been proved; the second one, is a novel variant documented here for the first time. These two cases expand the clinical spectrum of CMS linked to CHRND mutations.
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http://dx.doi.org/10.1016/j.nmd.2020.02.012DOI Listing
April 2020
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