Publications by authors named "Huizhen Zhang"

139 Publications

Advances in the toxicology research of microcystins based on Omics approaches.

Environ Int 2021 May 30;154:106661. Epub 2021 May 30.

College of Public Health, Zhengzhou University, Zhengzhou, PR China. Electronic address:

Microcystins (MCs) are the most widely distributed cyanotoxins, which can be ingested by animals and human body in multiple ways, resulting in a threat to human health and the biodiversity of wildlife. Therefore, the study on toxic effects and mechanisms of MCs is one of the focuses of attention. Recently, the Omics techniques, i.e. genomics, transcriptomics, proteomics and metabolomics, have significantly contributed to the comprehensive understanding and revealing of the molecular mechanisms about the toxicity of MCs. This paper mainly reviews current literature using the Omics approaches to explore the toxicity mechanism of MCs in liver, gonad, spleen, brain, intestine and lung of multiple species. It was found that MCs can exert strong toxic effects on various metabolic activities and cell signal transduction in cell cycle, apoptosis, destruction of cell cytoskeleton and redox disorder, at protein, transcription and metabolism level. Meanwhile, it was also revealed that the alteration of non-coding RNAs (miRNA, circRNA and lncRNA, etc.) and gut microbiota plays an essential regulatory role in the toxic effects of MCs, especially in hepatotoxicity and reproductive toxicity. In addition, we summarized current research gaps and pointed out the future directions for research. The detailed information in this paper shows that the application and development of Omics techniques have significantly promoted the research on MCs toxicity, and it is also a valuable resource for exploring the toxic mechanism of MCs.
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http://dx.doi.org/10.1016/j.envint.2021.106661DOI Listing
May 2021

Resveratrol improved hippocampal neurogenesis following lead exposure in rats through activation of SIRT1 signaling.

Environ Toxicol 2021 May 12. Epub 2021 May 12.

Department of Environmental Health, College of Public Health, Zhengzhou University, Zhengzhou, China.

Lead (Pb) poses a potential environmental risk factor for cognitive dysfunction during early life and childhood. Resveratrol is considered a promising antioxidant with respect to the prevention of cognitive deficits and act as a potent SIRT1 agonist. Here in, this study aims to investigate the profile of neurogenesis markers following Pb exposure and to determine the regulatory role of resveratrol in this process. We confirmed firstly the protective effects of resveratrol against Pb-induced impairments of hippocampal neurogenesis in Male SD rats. Pb exposure early in life caused the altered expression of Ki-67, NeuN, caspase-3 and SIRT1signaling, thereby resulting in spatial cognitive impairment of adolescent rats. As expected, resveratrol reduced cognitive damage and promoted neurogenesis in Pb-induced injury by regulation of SIRT1 pathway. Collectively, our study establishes the efficacy of resveratrol as a neuroprotective agent and providesa strong rationale for further studies on SIRT1-mediated mechanisms of neuroprotective functions.
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http://dx.doi.org/10.1002/tox.23162DOI Listing
May 2021

Update on the adverse effects of microcystins on the liver.

Environ Res 2021 04 19;195:110890. Epub 2021 Feb 19.

College of Public Health, Zhengzhou University, Zhengzhou, Henan, China. Electronic address:

Microcystins (MCs) are the most common cyanobacteria toxins in eutrophic water, which have strong hepatotoxicity. In the past decade, epidemiological and toxicological studies on liver damage caused by MCs have proliferated, and new mechanisms of hepatotoxicity induced by MCs have also been discovered and confirmed. However, there has not been a comprehensive and systematic review of these new findings. Therefore, this paper summarizes the latest advances in studies on the hepatotoxicity of MCs to reveal the effects and mechanisms of hepatotoxicity induced by MCs. Current epidemiological studies have confirmed that symptoms or signs of liver damage appear after human exposure to MCs, and a long time of exposure can even lead to liver cancer. Toxicological studies have shown that MCs can affect the expression of oncogenes by activating cell proliferation pathways such as MAPK and Akt, thereby promoting the occurrence and development of cancer. The latest evidence shows that epigenetic modifications may play an important role in MCs-induced liver cancer. MCs can cause damage to the liver by inducing hepatocyte death, mainly manifested as apoptosis and necrosis. The imbalance of liver metabolic homeostasis may be involved in hepatotoxicity induced by MCs. In addition, the combined toxicity of MCs and other toxins are also discussed in this article. This detailed information will be a valuable reference for further exploring of MCs-induced hepatotoxicity.
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http://dx.doi.org/10.1016/j.envres.2021.110890DOI Listing
April 2021

Microcystin-LR induces ovarian injury and apoptosis in mice via activating apoptosis signal-regulating kinase 1-mediated P38/JNK pathway.

Ecotoxicol Environ Saf 2021 Apr 18;213:112066. Epub 2021 Feb 18.

College of Public Health, Zhengzhou University, Zhengzhou 450001, China. Electronic address:

As an emerging pollutant in the aquatic environment, microcystin-LR (MC-LR) can enter the body through multiple pathways, and then induce apoptosis and gonadal damage, affecting reproductive function. Previous studies focused on male reproductive toxicity induced by MC-LR neglecting its effects on females. The apoptotic signal-regulated kinase 1 (ASK1) is an upstream protein of P38/JNK pathway, closely associated with apoptosis and organ damage. However, the role of ASK1 in MC-LR-induced reproductive toxicity is unclear. Therefore, this study investigated the role of ASK1 in mouse ovarian injury and apoptosis induced by MC-LR. After MC-LR exposure, ASK1 expression in mouse ovarian granulosa cells was increased at the protein and mRNA levels, and decreased following pretreatment by antioxidant N-acetylcysteine, suggesting that MC-LR-induced oxidative stress has a regulatory role in ASK1 expression. Inhibition of ASK1 expression with siASK1 and NQDI-1 could effectively alleviate MC-LR-induced mitochondrial membrane potential damage and apoptosis in ovarian granulosa cells, as well as pathological damage, apoptosis and the decreased gonadal index in ovaries of C57BL/6 mice. Moreover, the P38/JNK pathway and downstream apoptosis-related proteins (P-P38, P-JNK, P-P53, Fas) and genes (MKK4, MKK3, Ddit3, Mef2c) were activated in vivo and vitro, but their activation was restrained after ASK1 inhibition. Data presented herein suggest that the ASK1-mediated P38/JNK pathway is involved in ovarian injury and apoptosis induced by MC-LR in mice. It is confirmed that ASK1 has an important role in MC-LR-induced ovarian injury, which provides new insights for preventing MCs-induced reproductive toxicity in females.
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http://dx.doi.org/10.1016/j.ecoenv.2021.112066DOI Listing
April 2021

LncRNA SLC16A1-AS1 Suppresses Cell Proliferation in Cervical Squamous Cell Carcinoma (CSCC) Through the miR-194/SOCS2 Axis.

Cancer Manag Res 2021 11;13:1299-1306. Epub 2021 Feb 11.

Department of Gynecology, Heping Hospital Affiliated to Changzhi Medical College, Changzi, Shanxi Province, 046000, People's Republic of China.

Background: SLC16A1-AS1 has been characterized as an oncogenic long non-coding (lncRNA) in breast cancer and bladder cancer, while its role in cervical squamous cell carcinoma (CSCC) is unknown.

Methods: CSCC and non-tumor tissue samples were collected from 60 female patients, and qPCR was performed to detect the expression of SLC16A1-AS1, miR-194 and SOCS2. Luciferase reporter assay was performed to detect the interaction between SLC16A1-AS1 and miR-194. Colony formation assay was used to detect cell proliferation.

Results: SLC16A1-AS1 was down-regulated in CSCC and correlated with poor survival. Overexpression of SLC16A1-AS1 could inhibit the proliferation of cervical cancer cells. In addition, SLC16A1-AS1 could sponge miR-194 and increase the expression levels of SOCS2, ultimately inhibiting the proliferation of cervical cancer cells.

Conclusion: SLC16A1-AS1 was downregulated in CSCC and suppressed cell proliferation in cervical squamous cell carcinoma (CSCC) through the miR-194/SOCS2 axis.
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http://dx.doi.org/10.2147/CMAR.S276629DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7884948PMC
February 2021

Mutations in Profilin 1 Cause Early-Onset Paget's Disease of Bone With Giant Cell Tumors.

J Bone Miner Res 2021 Feb 17. Epub 2021 Feb 17.

Shanghai Clinical Research Center of Bone Disease, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Paget's disease of bone (PDB) is a late-onset chronic progressive bone disease characterized by abnormal activation of osteoclasts that results in bone pain, deformities, and fractures. PDB is very rare in Asia. A subset of PDB patients have early onset and can develop malignant giant cell tumors (GCTs) of the bone (PDB/GCTs), which arise within Paget bone lesions; the result is a significantly higher mortality rate. SQSTM1, TNFRSF11A, OPG, VCP, and HNRNPA2B1 have been identified as pathogenic genes of PDB, and ZNF687 is the only confirmed gene to date known to cause PDB/GCT. However, the molecular mechanism underlying PDB/GCT has not been fully elucidated. Here, we investigate an extended Chinese pedigree with eight individuals affected by early-onset and polyostotic PDB, two of whom developed GCTs. We identified a heterozygous 4-bp deletion in the Profilin 1 (PFN1) gene (c.318_321delTGAC) by genetic linkage analysis and exome sequencing for the family. Sanger sequencing revealed another heterozygous 1-bp deletion in PFN1 (c.324_324delG) in a sporadic early-onset PDB/GCT patient, further proving its causative role. Interestingly, a heterozygous missense mutation of PFN1 (c.335 T > C) was identified in another PDB/GCT family, revealing that not only deletion but also missense mutations in PFN1 can cause PDB/GCT. Furthermore, we established a Pfn1-mutated mouse model (C57BL/6J mice) and successfully obtained Pagetic phenotypes in heterozygous mice, verifying loss of function of PFN1 as the cause of PDB/GCT development. In conclusion, our findings reveal mutations in PFN1 as the pathological mechanism in PDB/GCT, and we successfully established Pfn1-mutated mice as a suitable animal model for studying PDB-associated pathological mechanisms. The identification of PFN1 mutations has great diagnostic value for identifying PDB individuals predisposed toward developing GCTs. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
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http://dx.doi.org/10.1002/jbmr.4275DOI Listing
February 2021

Role of PRPS2 as a prognostic and therapeutic target in osteosarcoma.

J Clin Pathol 2021 May 15;74(5):321-326. Epub 2021 Feb 15.

Department of Pathology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China

Aims: Osteosarcoma (OS) is the most common primary malignant tumour of the bone. However, further improvement in survival has not been achieved due to a lack of well-validated prognostic markers and more effective therapeutic agents. Recently, the c-Myc-phosphoribosyl pyrophosphate synthetase 2 (PRPS2) pathway has been shown to promote nucleic acid metabolism and cancer cell proliferation in malignant melanoma; phosphorylated mammalian target of rapamycin (p-mTOR) has been upregulated and an effective therapeutic target in OS. However, the p-mTOR-PRPS2 pathway has not been evaluated in OS.

Methods: In this study, the expression level of PRPS2, p-mTOR and marker of proliferation (MKI-67) was observed in a cohort of specimens (including 236 OS cases and 56 control samples) using immunohistochemistry, and the association between expression level and clinicopathological characteristics of patients with OS was analysed.

Results: PRPS2 protein level, which is related to tumour proliferation, was higher in OS cells (p=0.003) than in fibrous dysplasia, and the higher PRPS2 protein level was associated with a higher tumour recurrence (p=0.001). In addition, our statistical analysis confirmed that PRPS2 is a novel, independent prognostic indicator of OS. Finally, we found that the expression of p-mTOR was associated with the poor prognosis of patients with OS (p<0.05).

Conclusions: PRPS2 is an independent prognostic marker and a potential therapeutic target for OS.
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http://dx.doi.org/10.1136/jclinpath-2020-206505DOI Listing
May 2021

Predictors of Quality of Life in Patients with Breast Cancer-Related Lymphedema: Effect of Age, Lymphedema Severity, and Anxiety.

Lymphat Res Biol 2021 Feb 8. Epub 2021 Feb 8.

State Key Laboratory of Oncology in South China, Guangzhou, China.

Patients with breast cancer-related lymphedema (BCRL) have lower quality of life (QOL). However, some important predictors, such as the effect of age, lymphedema severity, depression, and anxiety, have not yet been discovered. The overall objective of this study is to explore the QOL predictors associated with BCRL in China. A cross-sectional design was conducted. Data were collected before treatment, including sociodemographic characteristics (height, heaviness, age, education level, work status, marital status, and economic status), clinical characteristics (surgical method, clinical cancer stage, lymphedema severity, and lymphedema duration), the hospital anxiety (HA) and depression scale, and the functional assessment of cancer therapy-breast quality of life instrument. Univariate analysis or bivariate correlation was first made to explore the correlation of QOL with sociodemographic/clinical characteristics, anxiety, and depression. The multiple linear regression model was used to identify the independent QOL predictors. Seventy-one patients with BCRL were recruited. Age, education level, work status, family income, lymphedema duration, lymphedema severity, and HA and hospital depression scale scores are significantly correlated with QOL ( < 0.05). Age, lymphedema severity, and HA accounted for 85.9% in QOL ( = 62.76,  < 0.001). Age, lymphedema, and anxiety are the most important QOL predictors. Therefore, it is very important to establish a BCRL prevention system and pay attention to psychological distress in the patients with BCRL.
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http://dx.doi.org/10.1089/lrb.2020.0073DOI Listing
February 2021

Lipidomic profiling reveals triacylglycerol accumulation in the liver during pregnane X receptor activation-induced hepatomegaly.

J Pharm Biomed Anal 2021 Feb 17;195:113851. Epub 2020 Dec 17.

Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China. Electronic address:

Pregnane X receptor (PXR) is highly expressed in the liver and plays an integral role in the control of xenobiotic and endobiotic metabolism to maintain homeostasis. We previously reported that activation of PXR significantly induced liver enlargement. But the lipid profiling during PXR-induced hepatomegaly remains unclear. This study aimed to characterize the effect of PXR activation on hepatic lipid homeostasis by lipidomics analysis. Mice were intraperitoneally administered with the typical mPXR agonist, pregnenolone 16α-carbonitrile (PCN, 100 mg/kg/d), for 5 days. Liver and serum were collected for further analysis. The results confirmed that PXR activation can significantly induce liver enlargement. An obvious hepatic lipid accumulation was observed in PCN-treated mice, as determined by H&E and Oil Red O staining. Ultra-high performance liquid chromatography-Q Exactive Orbitrap high-resolution mass spectrometer (UHPLC-Q Exactive Orbitrap HRMS)-based lipidomics was performed to characterize the change in lipid species. A total of 20 potential lipid biomarkers were significantly perturbed. The most significant change was found in the triacylglycerol (TG), which constituted with the lower number of carbon atoms and double bonds. Moreover, the mRNA expression levels showed that PCN-induced PXR activation significantly regulated the expression of genes involved in the uptake, synthesis and metabolism of TG, which was consistent with increased TG levels. Collectively, these findings demonstrated that lipids such as TG were significantly accumulated during PXR-induced hepatomegaly.
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http://dx.doi.org/10.1016/j.jpba.2020.113851DOI Listing
February 2021

IRE1 and CaMKKβ pathways to reveal the mechanism involved in microcystin-LR-induced autophagy in mouse ovarian cells.

Food Chem Toxicol 2021 Jan 5;147:111911. Epub 2020 Dec 5.

College of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR China. Electronic address:

Microcystin-LR (MC-LR) is an emerging water pollutant produced by blooming cyanobacteria. It could be absorbed into human body via contaminated food and drinking water causing severe reproductive toxicity. Previous studies showed that MC-LR could regulate autophagy by inducing endoplasmic reticulum (ER) stress thereby causing female reproductive toxicity. However, the molecular mechanisms of MC-LR-induced autophagy remain to be elucidated. It is known that IRE1 and CaMKKβ pathways are two important pathways involved in autophagy induced by ER stress. Hence, this study investigated the roles of both pathways in MC-LR-induced autophagy in mouse ovarian cells. The results showed that MC-LR significantly up-regulated the expression of autophagy marker proteins LC3Ⅱ and BECLIN1 and down-regulated the expression of P62 in vivo and in vitro. MC-LR-caused increase of autophagosomes could be observed in KK-1 cells by MDC staining. MC-LR induced the formation of autolysosomes as indicated by the overlap of LAMP1 and LC3. Meanwhile, MC-LR significantly activated the proteins in IRE1 pathway (IRE1, XBP1 and JNK) and in CaMKKβ pathway (CaMKKβ, AMPK, mTOR). Furthermore, MC-LR caused weight loss and ovarian histopathological damage in mice. In contrast, after the expression and function of IRE1 and CaMKKβ were inhibited with siRNA in vitro and by inhibitors (4μ8C and STO-609, respectively) in vivo, the up-regulation of LC3Ⅱ and BECLIN1 and the degradation of P62 induced by MC-LR were significantly suppressed. MC-LR-induced autophagosomes in KK-1 cells and autolysosomes in mouse ovarian cells were also decreased. Moreover, the knockdown of IRE1 and CaMKKβ relieved MC-LR-induced histopathological injury to mouse ovaries. These results indicated that MC-LR induced ovarian cell autophagy and ovarian injury via IRE1 and CaMKKβ pathways. This study is the first study revealing the molecular mechanisms of MC-LR-induced autophagy of ovarian cells and providing new insights into the female reproductive toxicity of MC-LR.
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http://dx.doi.org/10.1016/j.fct.2020.111911DOI Listing
January 2021

Microcystin-leucine arginine exposure contributes to apoptosis and follicular atresia in mice ovaries by endoplasmic reticulum stress-upregulated Ddit3.

Sci Total Environ 2021 Feb 26;756:144070. Epub 2020 Nov 26.

College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Electronic address:

Microcystin-leucine arginine (MC-LR), an intracellular toxin to cause reproduction toxicity, is produced by blooming cyanobacteria and widely distributed in eutrophic waters. It is revealed that MC-LR-induced female reproductive toxicity is more severe than male reproductive toxicity. Previous studies mainly focused on male reproductive toxicity, and the molecular mechanisms of MC-LR-induced apoptosis, follicular atresia and infertility in female remain largely unclear. Here, it was found that MC-LR treatment could induce apoptosis, inflammation, follicular atresia, and decrease of gonadal index in mice ovaries. RNA-Seq data showed that the up-regulation of DNA-damage inducible transcript 3 (Ddit3) under endoplasmic reticulum (ER) stress had predominantly regulatory role in MC-LR-induced apoptotic pathway. Furthermore, MC-LR exposure promoted cleavage of activating transcription factor 6 (ATF6, 50kd), inositol-requiring enzyme 1 (Ire1) expression, phosphorylation of IRE1, mitogen-activated protein kinase 5 (Map3k5) and Ddit3 expression, which was accompanied by the upregulation of death receptor 5 (Dr5) and active-caspase-3, and a decrease in Bcl-2 expression. ER stress inhibitor 4-Phenyl butyric acid (4-PBA) ameliorated these MC-LR-induced changes in protein or mRNA level. More importantly, knockdown of Ddit3 suppressed MC-LR-induced cell apoptosis and follicular atresia by directly regulating Dr5 and Bcl-2. Additionally, it was also found that MC-LR increased Map3k5 phosphorylation by inhibiting protein phosphatase 2A (PP2A) activity, and then promoted Ddit3 expression. In short, our data suggests that Ddit3 promotes MC-LR-induced mice ovarian cells apoptosis and follicular atresia via ER stress activation, which provides a new insight into the relation between infertility in females and the emerging water pollutant MC-LR.
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http://dx.doi.org/10.1016/j.scitotenv.2020.144070DOI Listing
February 2021

Evaluation of the Antidepressant Effect of the Functional Beverage Containing Active Peptides, Menthol and Eleutheroside and Investigation of Its Mechanism of Action in Mice.

Food Technol Biotechnol 2020 Sep;58(3):295-302

College of Food Science and Engineering, Northwest A&F University, 22 Xinong Road, 712100 Yangling, PR China.

Research Background: Depression has become a global threat to human health. In order to solve it, researchers have conducted multi-faceted studies including diet. Many food-derived bioactive substances have shown antidepressant effects. However, there are few studies on the design of industrialized food with antidepressant effect. This study aims to evaluate the antidepressant effect of a functional beverage made from several ingredients with potential antidepressant function and investigate its antidepressant mechanisms.

Experimental Approach: The beverage consists of peppermint oil, active peptides derived from bovine milk casein and extract (ASE) whose active ingredient is eleutheroside. Different amounts of ASE were evaluated to determine the optimal concentration of eleutheroside in this functional beverage to deliver the best antidepressant effect through extensive behavioral testing, including preliminary acute stress experiments and further chronic unpredictable mild stress test.

Results And Conclusions: The results demonstrated that the beverage with 15 mg/kg of eleutheroside could significantly reduce the mice's immobility time of tail suspension test and forced swimming test, recover mice's sucrose preference and behavior changes in the open field test, improve the contents of dopamine, norepinephrine, 5-hydroxytryptamine and the activity of superoxide dismutase and reduce the content of malondialdehyde in mice's brains, which indicated that the improvement of monoamine neurotransmitter systems and antioxidation was one potential mechanism of antidepressant action.

Novelty And Scientific Contribution: This study provides a design of antidepressant functional beverage and an efficient way for the prevention and treatment of depression.
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http://dx.doi.org/10.17113/ftb.58.03.20.6568DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709459PMC
September 2020

Primary perivascular epithelioid cell tumor (PEComa) in bone: A review of the literature and a case arising in the humerus with multiple metastases.

J Bone Oncol 2021 Feb 5;26:100336. Epub 2020 Nov 5.

Department of Imaging, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 XianXia Road, Shanghai 200336, China.

Introduction: Perivascular epithelioid cell tumors (PEComas) are a family of mesenchymal tumors that rarely arise as a primary bone tumor.

Material And Methods: We report a case of primary malignant bone PEComa. A literature review via PubMed, Embase and Web of Science databases with the keyword "PEComa" and "bone" was performed.

Results: We reported a 33-year-old female with primary malignant bone PEComa in right distal humerus. The patient received an inhibitor of the mammalian target of rapamycin (mTOR) protein based on negative molecular investigation result of transcription factor E3 () rearrangement, and additional therapies including palliative radiotherapy, anti-angiogenics and immunotherapy when the disease progression was detected. The patient was alive with the disease twenty-three months postoperatively. A total of nineteen related literature cases were retrieved and reviewed. Taking current case into account, ten males and ten females with median age of 24 years (range, 3-93 years) were identified, who were most frequently affected in tibia. The median follow-up duration of 24 months (range, 3-96 months). One patient died due to this disease, and six patients showed metastases. Three patients experienced recurrence, and two of them experienced twice and three times, respectively.

Conclusion: To our knowledge, this is the first case of primary malignant bone PEComa arising in humerus. Clinicopathological and radiological correlation is mandatory to the correct diagnosis and to determine its malignancy. More studies are required to understand the role of molecular test and imaging in selecting suitable treatment and mechanisms of treatment resistance.
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http://dx.doi.org/10.1016/j.jbo.2020.100336DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7674509PMC
February 2021

Monitoring the Changes of Upper Limb Water in Breast Cancer Patients by Segmental Multi-Frequency Bioelectrical Impedance Analysis.

Med Sci Monit 2020 Oct 31;26:e927804. Epub 2020 Oct 31.

Department of Breast Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China (mainland).

BACKGROUND Our study aims to investigate the role of segmental multi-frequency bioelectrical impedance analysis (SMF-BIA) in the monitoring of upper limb water changes of patients with breast cancer before and after surgery to aid in establishing a new approach to preventing lymphedema. MATERIAL AND METHODS This study included 442 female patients with breast cancer. We used SMF-BIA to monitor changes in body composition. Data were collected 1 day before surgery and 7 days and 3 months after surgery. RESULTS The average body mass index (BMI) of patients was normal but, in 22.8% of patients, the percentage of body fat exceeded the average, which is known as invisible obesity. Moreover, the weight, BMI, basal metabolic rate, inorganic salt content, muscle content, total body water, and extracellular water of patients increased 7 days after surgery (P<0.05), but recovered to preoperative levels within 3 months. In addition, protein content, skeletal muscle content, and intracellular water increased 7 days after surgery, but decreased within 3 months to even lower levels than before surgery (P<0.05). The extracellular water and total body water ratios increased continuously within the 3 months after surgery. Finally, the segmental water ratio of the healthy and affected upper limbs increased, while the bioelectrical impedance value decreased; however, they were still within the normal range. CONCLUSIONS SMF-BIA monitoring may provide more detailed information for making individual nursing care plans in patients with breast cancer. Further studies with long-term follow-up are urgently needed to establishment a lymphedema risk predictive model.
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http://dx.doi.org/10.12659/MSM.927804DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7640375PMC
October 2020

The latest advances in the reproductive toxicity of microcystin-LR.

Environ Res 2021 01 28;192:110254. Epub 2020 Sep 28.

College of Public Health, Zhengzhou University, Zhengzhou, Henan, China. Electronic address:

Microcystin-LR (MC-LR) is an emerging environmental pollutant produced by cyanobacteria that poses a threat to wild life and human health. In recent years, the reproductive toxicity of MC-LR has gained widespread attention, a large number of toxicological studies have filled the gaps in past research and more molecular mechanisms have been elucidated. Hence, this paper reviews the latest research advances on MC-LR-induced reproductive toxicity. MC-LR can damage the structure and function of the testis, ovary, prostate, placenta and other organs of animals and then reduce their fertility. Meanwhile, MC-LR can also be transmitted through the placenta to the offspring causing trans-generational and developmental toxicity including death, malformation, growth retardation, and organ dysfunction in embryos and juveniles. The mechanisms of MC-LR-induced reproductive toxicity mainly include the inhibition of protein phosphatase 1/2 A (PP1/2 A) activity and the induction of oxidative stress. On the one hand, MC-LR triggers the hyperphosphorylation of certain proteins by inhibiting intracellular PP1/2 A activity, thereby activating multiple signaling pathways that cause inflammation and blood-testis barrier destruction, etc. On the other hand, MC-LR-induced oxidative stress can result in cell programmed death via the mitochondrial and endoplasmic reticulum pathways. It is worth noting that epigenetic modifications are also involved in reproductive cell apoptosis, which may be an important direction for future research. Furthermore, this paper proposes for the first time that MC-LR can produce estrogenic effects in animals as an environmental estrogen. New findings and suggestions in this review could be areas of interest for future research.
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http://dx.doi.org/10.1016/j.envres.2020.110254DOI Listing
January 2021

Joint replenishment of zinc and folic acid enhances the anti-depressive effect of paroxetine via increasing serum calcium and copper and decreasing serum arsenic.

Neurosci Lett 2020 10 7;737:135270. Epub 2020 Aug 7.

Department of Human Nutrition, College of Public Health, Qingdao University, Qingdao 266000, China. Electronic address:

Insufficient zinc and folic acid levels are associated with depression and poor response to antidepressants. This study aimed to investigate the influences of combined zinc and folic acid replenishment on the anti-depressive effect of paroxetine. Male rats were randomly divided into five groups: control (C), model (M), paroxetine (MP), zinc + folic acid (MZnF), and zinc + folic acid + paroxetine (MZnFP) groups. Rats were exposed to mild unpredictable stress for 3 weeks as a depression model. The combinations of drug and supplements were applied via daily gavage for 4 weeks. The open field test was conducted to observe behavioral changes. A chemiluminescence method was used to detect folacin, and inductively coupled plasma mass spectrometry was used to detect serum elements. Supplementation of zinc and folic acid significantly improved behavior responses to paroxetine, including movement speed, total distance, and central zone frequency. In addition, higher calcium and copper levels and a lower arsenic level were found in the serum of the MZnFP group. Thus, supplementation of zinc and folacin can enhance the anti-depressive effect of paroxetine, and the mechanism is potentially related to the improved levels of calcium and copper and a reduced level of arsenic.
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http://dx.doi.org/10.1016/j.neulet.2020.135270DOI Listing
October 2020

Clarifying prognostic factors of small cell osteosarcoma: A pooled analysis of 20 cases and the literature.

J Bone Oncol 2020 Oct 15;24:100305. Epub 2020 Jul 15.

Department of Imaging, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200050, China.

Introduction: Small cell osteosarcoma (SCOS) is a rare subtype of osteosarcoma, with limited studies mainly focusing on histological features. Our study aims to analyze our own patients and those reported in the literature to increase the recognition of this rare disease, to evaluate patient survival and to further determine potential prognostic factors.

Material And Methods: Twenty patients with SCOS were treated in our hospital between 2010 and 2019. Their follow-up data were collected retrospectively. A total of 336 literature cases from 58 manuscripts were retrieved by means of a PubMed search with the key word "small cell osteosarcoma". Data pertaining to treatment and follow-up were extracted. We performed a pooled analysis for the survival of patients and the risk factors for local recurrence (LR), as well as metastatic disease (MD), in a total of 160 patients using the Kaplan-Meier method and Cox regression method.

Results: We reported our experience in diagnosing and treating SCOS. In our cases, elevated alkaline phosphatase (P = 0.013) and lactate dehydrogenase (P = 0.001) significantly impaired overall survival. In the pooled analysis, SCOS was diagnosed at the median age of 17 years and affected both sexes almost equally. The median follow-up duration was 19.5 months. In the pooled analysis cases, the 5-year overall survival rate was 38.6%, and 36.4% of patients survived 10 years. However, an increasing trend was detected, indicating recent improvements in management. The surgical margin status (P = 0.024) and metastases (P = 0.008) significantly impaired overall survival, and the response to chemotherapy was related to disease-free survival (P = 0.012). LR and MD were significantly correlated (P = 0.002) and could be observed after 5 years of follow-up. LR was significantly dependent on response to chemotherapy (P = 0.020). The development of MD seemed to be affected by response to chemotherapy (P = 0.060). Correlations between imaging features and prognosis were not detected.

Conclusions: This study suggested that positive margins, poor response to chemotherapy and MD are negative prognostic factors for SCOS, implied the potential role of laboratory examinations in the survival prediction and supported the need for prolonged or more intensive surveillance in patients with MD or LR. More well-documented literatures are encouraged to allow further confirmations.
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http://dx.doi.org/10.1016/j.jbo.2020.100305DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394919PMC
October 2020

HIF-1α-Mediated Telomerase Reverse Transcriptase Activation Inducing Autophagy Through Mammalian Target of Rapamycin Promotes Papillary Thyroid Carcinoma Progression During Hypoxia Stress.

Thyroid 2021 02 9;31(2):233-246. Epub 2020 Sep 9.

Department of Nuclear Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

It is important to properly understand the molecular mechanisms of aggressive tumors among papillary thyroid carcinomas (PTCs) that are often the most indolent. Hypoxia inducible factor-1α (HIF-1α), induced by hypoxia, plays pivotal roles in the development and metastasis of the many tumors, including PTCs. Upregulation of telomerase reverse transcriptase (TERT) activity is found in highly invasive PTCs. Further, previous studies have reported that autophagy serves as a protective mechanism to facilitate PTC cell survival. We, therefore, hypothesized that there was a link between HIF-1α, TERT, and autophagy in promoting PTC progression. Immunohistochemistry staining was conducted to evaluate the expressions of HIF-1α, TERT, and autophagy marker, LC3-II, in matched PTC tumors and corresponding nontumor tissues. Two PTC cell lines (TPC-1 and BCPAP) were used in subsequent cytological function studies. Cell viability, proliferation, apoptosis, migration, and invasion were assessed during hypoxia, genetic enhancement and inhibition of TERT, and chemical and genetic inhibition of autophagy. The protein expression levels of the corresponding biomarkers were determined by Western blotting, and autophagy flow was detected. We characterized the molecular mechanism of PTC cell progression. The protein expression levels of HIF-1α, TERT, and LC3-II were upregulated in PTCs and were significantly correlated with high tumor-node-metastasis stage. Further, an study indicated that HIF-1α induced by hypoxia functioned as a transcriptional activator by binding with sequences potentially located in the TERT promoter and was positively correlated with the malignant behavior of PTC cell lines. Overexpression of TERT inhibited the kinase activity of mammalian target of rapamycin (mTOR), resulting in the activation of autophagy. Functionally, TERT-induced autophagy provided a survival advantage to PTC cells during hypoxia stress. We identified a novel molecular mechanism involving the HIF-1α/TERT axis, which promoted PTC progression by inducing autophagy through mTOR during hypoxia stress. These findings may provide a basis for the new treatment of aggressive PTCs.
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http://dx.doi.org/10.1089/thy.2020.0023DOI Listing
February 2021

Clonality analysis and and mutation detection in both components of dedifferentiated chondrosarcoma, implicated its monoclonal origin.

J Bone Oncol 2020 Jun 4;22:100293. Epub 2020 May 4.

Department of Pathology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yi-Shan Road, Shanghai 200233, PR China.

Dedifferentiated chondrosarcoma (DDCS) is a highly malignant tumor that belongs to an uncommon subtype of chondrosarcoma with a poor prognosis. Microscopically, it is composed of highly differentiated chondrosarcoma and highly malignant noncartilaginous sarcomas with an abrupt interface. The question of whether the two components originated from the same archaeocyte has not yet been clarified. To further investigate this issue, DNA was separately extracted from the two components of the same patient. In total, 18 DDCS patients were analyzed. A portion of DNA samples from 9 female patients was used for clonality analysis. Another portion of DNA from 9 female and DNA from 9 male patients was used for isocitrate dehydrogenase 1() and gene mutation detection. The results of clonality analysis showed that the same X chromosome inactivation and consistent mutation states of the and genes in the two DDCS components. We conclude that the two DDCS components originate from the same primitive cell and that DDCS is monoclonal in origin.
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http://dx.doi.org/10.1016/j.jbo.2020.100293DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7385535PMC
June 2020

Carnitine palmitoyltransferase 1C reverses cellular senescence of MRC-5 fibroblasts via regulating lipid accumulation and mitochondrial function.

J Cell Physiol 2021 Feb 6;236(2):958-970. Epub 2020 Jul 6.

Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.

Cellular senescence, a state of growth arrest, is involved in various age-related diseases. We previously found that carnitine palmitoyltransferase 1C (CPT1C) is a key regulator of cancer cell proliferation and senescence, but it is unclear whether CPT1C plays a similar role in normal cells. Therefore, this study aimed to investigate the role of CPT1C in cellular proliferation and senescence of human embryonic lung MRC-5 fibroblasts and the involved mechanisms. The results showed that CPT1C could reverse the cellular senescence of MRC-5 fibroblasts, as evidenced by reduced senescence-associated β-galactosidase activity, downregulated messenger RNA (mRNA) expression of senescence-associated secretory phenotype factors, and enhanced bromodeoxyuridine incorporation. Lipidomics analysis further revealed that CPT1C gain-of-function reduced lipid accumulation and reversed abnormal metabolic reprogramming of lipids in late MRC-5 cells. Oil Red O staining and Nile red fluorescence also indicated significant reduction of lipid accumulation after CPT1C gain-of-function. Consequently, CPT1C gain-of-function significantly reversed mitochondrial dysfunction, as evaluated by increased adenosine triphosphate synthesis and mitochondrial transmembrane potential, decreased radical oxygen species, upregulated respiratory capacity and mRNA expression of genes related to mitochondrial function. In summary, CPT1C plays a vital role in MRC-5 cellular proliferation and can reverse MRC-5 cellular senescence through the regulation of lipid metabolism and mitochondrial function, which supports the role of CPT1C as a novel target for intervention into cellular proliferation and senescence and suggests CPT1C as a new strategy for antiaging.
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http://dx.doi.org/10.1002/jcp.29906DOI Listing
February 2021

A Salt Tolerance Evaluation Method for Sunflower (Helianthus annuus L.) at the Seed Germination Stage.

Sci Rep 2020 06 30;10(1):10626. Epub 2020 Jun 30.

Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, 830046, China.

Salinity is a major abiotic stress that affects plant growth and development and leads to crop yield loss. Many crop species are more sensitive to salinity stress at the seed germination stage than at other developmental stages. Some studies have shown that sunflower is tolerant to salinity to a certain degree. However, no systematic screening data for sunflower germplasms are available for salinity stress. In this study, 552 sunflower germplasms with different genetic backgrounds were evaluated for salt tolerance. Among them, 30 and 53 sunflower germplasms were identified as highly salt-tolerant and salt-tolerant germplasms, respectively, while 80 and 23 were grouped as salt-sensitive and highly salt-sensitive materials, respectively. Of all the traits tested, the germination index and the germination vigor index were the two most reliable traits, showing the highest correlation with salt tolerance during the seed germination stage of sunflower. Thus, a highly efficient and reliable method for evaluating salinity tolerance of sunflower seed germination was established. These results provided a good foundation for studying salt-tolerance mechanisms and breeding highly salt-tolerant sunflower cultivars.
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http://dx.doi.org/10.1038/s41598-020-67210-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326917PMC
June 2020

The Anti-Proliferative Effect of Flavonoid Nanoparticles on the Human Ovarian Cancer Cell Line SK0V3.

J Nanosci Nanotechnol 2020 10;20(10):6040-6046

Department of Biochemistry, Changzhi Medical College, Changzhi 046000, Shanxi, PR China.

To investigate the anti-proliferative effect of flavonoid nanoparticles on the human ovarian cancer cell line SKOV3. Ten nude mice were intraperitoneally inoculated with the human ovarian cancer SKOV3 cell mixture. The treatment group received tail vein injections with 1.25 mg/kg of flavonol, once every 3 days, 0.2 mL each time, for a total of 12 times. The control group was a tumor model that was injected with 50 mL/L glucose solution; it was observed in Lacquerin Group as the Laccase Nanoparticle Group. Tumor quality was recorded after treatment. The morphology of tumor cells in the two groups was observed by fluorescence microscopy. MTS was used to measure the value of tumor cells in the two groups after administration. Apoptosis of SKOV3 cells was detected by flow cytometry using a tumor cell suspension. The MTT results showed a decreased growth rate of SKOV3 cells with an increase in the mass concentration of flavonoid nanoparticles. The nude mice in the control group had scattered cauliflower-like tumor nodules. The treatment group only showed very small granular tumor nodules. The tumor mass within the treatment group was comparable ( > 0.05), but was lower than that in the control group ( < 0.05). The morphology of the tumor cells in the treatment group became longer and thinner and showed a slender spindle shape. Some high-temperature treated cells even appeared star-shaped, and the cell bodies were significantly broadened. Flow cytometry results showed significantly increased apoptosis of the SKOV3 cells after treatment with flavonoid nanoparticles. The MTS results showed a significantly slowed proliferation rate of SKOV3 cells after two days of administering flavonoid nanoparticles ( < 0.05). Flavonoid nanoparticles were nontoxic, and decreased cell proliferation of and promoted apoptosis in an ovarian cancer cell line.
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http://dx.doi.org/10.1166/jnn.2020.18119DOI Listing
October 2020

Carnitine palmitoyltransferase 1C contributes to progressive cellular senescence.

Aging (Albany NY) 2020 04 14;12(8):6733-6755. Epub 2020 Apr 14.

School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, P.R. China.

Stable transfection manipulation with antibiotic selection and passaging induces progressive cellular senescence phenotypes. However, the underlying mechanisms remain poorly understood. This study demonstrated that stable transfection of the empty vector induced PANC-1 cells into cellular senescence. Metabolomics revealed several acylcarnitines and their upstream regulatory gene, carnitine palmitoyltransferase 1C (CPT1C) involved in fatty acid β-oxidation in mitochondria, were strikingly decreased in senescent PANC-1 cells. Low CPT1C expression triggered mitochondrial dysfunction, inhibited telomere elongation, impaired cell survival under metabolic stress, and hindered the malignance and tumorigenesis of senescent cells. On the contrary, mitochondrial activity was restored by CPT1C gain-of-function in senescent vector PANC-1 cells. PPARα and TP53/CDKN1A, crucial signaling components in cellular senescence, were downregulated in senescent PANC-1 cells. This study identifies CPT1C as a key regulator of stable transfection-induced progressive PANC-1 cell senescence that inhibits mitochondrial function-associated metabolic reprogramming. These findings confirm the need to identify cell culture alterations after stable transfection, particularly when cells are used for metabolomics and mitochondria-associated studies, and suggest inhibition of CPT1C could be a promising target to intervene pancreatic tumorigenesis.
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http://dx.doi.org/10.18632/aging.103033DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202531PMC
April 2020

Binder-Free Charantia-Like Metal-Oxide Core/Shell Nanotube Arrays for High-Performance Lithium-Ion Anodes.

Front Chem 2020 6;8:159. Epub 2020 Mar 6.

School of Materials Engineering, Shanghai University of Engineering Science, Shanghai, China.

The performance of anodes of lithium-ion batteries relies largely on the architecture and composition of the hybrid active materials. We present a two-step, seed-free, solution-based method for the direct growth of hierarchical charantia-like TiO/FeO core/shell nanotube arrays on carbon cloth substrates. An ultrahigh loading of the nanomaterial on carbon fibers was achieved with this method without the use of a binder. This three-dimensional porous hollow architecture and its direct contact with the CC current collector ensure an efficient electronic pathway. The hollow TiO framework effectively protects the hierarchical charantia-like TiO/FeO hollow core/shell arrays from collapsing because of its negligible volume change during cycling. Meanwhile, the self-assembled α-FeO hollow nanospheres guarantee a large capacity and contact area with the electrolyte. This flexible anode with a 3D porous charantia-like hollow architecture exhibits high cycle performance, reversible capacity, and rate capability. These nanotube arrays maintain a high reversible capacity of 875 mAh g after 200 cycles at a current density of 200 mA g. This simple, cost-effective, and scalable electrode fabrication strategy can be implemented in the fabrication of high-performance wearable energy storage devices.
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http://dx.doi.org/10.3389/fchem.2020.00159DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7067744PMC
March 2020

Three-Dimensional PrGO-Based Sandwich Composites With MoS Flowers as Stuffings for Superior Lithium Storage.

Front Chem 2020 28;8:94. Epub 2020 Feb 28.

School of Information Science and Engineering, Fudan University, Shanghai, China.

Graphene-based MoS nanocomposites are expected to be promising anode materials for lithium ion batteries because of their large specific capacity and high conductivity. However, the aggregation of graphene and the weak interaction between the two components hinder their practical application. Inspired by the sandwich structure, novel three-dimensional flower-like MoS-PrGO sandwich composites were proposed as an advanced anode material for lithium-ion batteries. The separated 2D ultrathin rGO nano-sheets were connected by PEO chains and assembled into a well-organized 3D layered spatial structure, which not only avoids the aggregation of graphene but also accommodates a high mass loading of the micro-scale MoS nano-flowers. MoS nano-flowers with open architecture deliver large specific area. The rGO interlayers act as a conductive framework, making all flower-like MoS nano-stuffing electrochemically active. The ultra-thin 2D nano-sheets provide excellent cycle stability due to their neglectable volume changes during cycling. The 3D flower-like MoS-PrGO sandwich composites deliver high energy density, excellent conductivity and stable cyclic performance during charge-discharge process. With a nearly 100% coulombic efficiency, their reversible capacity is retained at 1,036 mA h g even after 500 cycles at current densities of 100 mA g. This novel design strategy provides a broad prospect for the development of advanced anode materials for superior lithium storage.
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http://dx.doi.org/10.3389/fchem.2020.00094DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058583PMC
February 2020

Role of microRNA-122 in microcystin-leucine arginine-induced dysregulation of hepatic iron homeostasis in mice.

Environ Toxicol 2020 Aug 14;35(8):822-830. Epub 2020 Mar 14.

College of Public Health, Zhengzhou University, Zhengzhou, People's Republic of China.

Microcystin-leucine arginine (MC-LR) is a cyclic heptapeptide hepatotoxin produced by cyanobacteria. MicroRNA-122 (miR-122) is specifically expressed in the liver. This study focuses on the role of miR-122 in MC-LR-induced dysregulation of hepatic iron homeostasis in C57BL/6 mice. The thirty mice were randomly divided into five groups (Control, 12.5 μg/kg·BW MC-LR, 25 μg/kg·BW MC-LR, Negative control agomir and 25 μg/kg·BW MC-LR + miR-122 agomir). The results show that MC-LR decreases the expressions of miR-122, Hamp, and its related regulators, while increasing the content of hepatic iron and the expressions of FPN1 and Tmprss6. Furthermore, miR-122 agomir pretreatment improves MC-LR induced dysregulation of hepatic iron homeostasis by arousing the related regulators and reducing the expression of Tmprss6. These results suggest that miR-122 agomir can prevent the accumulation of hepatic iron induced by MC-LR, which may be related to the regulation of hepcidin by BMP/SMAD and IL-6/STAT signaling pathways.
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http://dx.doi.org/10.1002/tox.22918DOI Listing
August 2020

Vector Exceptional Points with Strong Superchiral Fields.

Phys Rev Lett 2020 Feb;124(8):083901

Key Laboratory of Advanced Optoelectronic Quantum Architecture and Measurements of Ministry of Education, Beijing Key Laboratory of Nanophotonics and Ultrafine Optoelectronic Systems, School of Physics, Beijing Institute of Technology, Beijing 100081, China.

Exceptional points (EPs), branch points of complex energy surfaces at which eigenvalues and eigenvectors coalesce, are ubiquitous in non-Hermitian systems. Many novel properties and applications have been proposed around the EPs. One of the important applications is to enhance the detection sensitivity. However, due to the lack of single-handed superchiral fields, all of the proposed EP-based sensing mechanisms are only useful for the nonchiral discrimination. Here, we propose theoretically and demonstrate experimentally a new type of EP, which is called a radiation vector EP, to fulfill the homogeneous superchiral fields for chiral sensing. This type of EP is realized by suitably tuning the coupling strength and radiation losses for a pair of orthogonal polarization modes in the photonic crystal slab. Based on the unique modal-coupling property at the vector EP, we demonstrate that the uniform superchiral fields can be generated with two beams of lights illuminating the photonic crystal slab from opposite directions. Thus, the designed photonic crystal slab, which supports the vector EP, can be used to perform surface-enhanced chiral detection. Our findings provide a new strategy for ultrasensitive characterization and quantification of molecular chirality, a key aspect for various bioscience and biomedicine applications.
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http://dx.doi.org/10.1103/PhysRevLett.124.083901DOI Listing
February 2020

Disruption of synaptic expression pattern and age-related DNA oxidation in a neuronal model of lead-induced toxicity.

Environ Toxicol Pharmacol 2020 May 3;76:103350. Epub 2020 Feb 3.

College of Public Health, Zhengzhou University, Zhengzhou, PR China. Electronic address:

Lead (Pb) is recognized as a potent inducer of synaptic toxicity generally associated with reduced synaptic transmission and increased neuronal fiber excitability, becoming an environmental risk for neurodegenerative processes. Despite numerous toxicological studies on Pb have been directed to the developing brain, attention concerning long-term consequences of pubertal chronic Pb exposure on neuronal activity is still lacking. Thus, we exposed 4-week-old male mice to 0.2 % lead acetate solution for one month, then, conducted behavioral tests or extracted brain homogenate from mice prefrontal cortex (PFC) and hippocampus at the age of 4, 13 and 16-month-old respectively. Our results showed that treated mice exhibited an evident increase in latency to reach platform following pubertal Pb exposure and aging. The increase of 8-OHdG revealed evident neural DNA oxidative damage across time upon pubertal Pb exposure. In the hippocampus of lead exposed mice at three age nodes, the expression of brain-derived neurotrophic factor precursor (proBDNF) increased, while that of mature BDNF (mBDNF), cAMP-response element binding protein (CREB) and phosphorylated CREB (pCREB) decreased compared with the control group. Furthermore, the expression of BACE1 protein and tau phosphorylation level in PFC and hippocampus increased, APP mRNAs in PFC and prolonged induction of BACE1 in hippocampus. Our results show that chronic Pb exposure from pubertal stage onward can either initiate divergent synaptic-related gene expression patterns in adulthood or trigger time-course of neurodegenerative profile within the PFC or hippocampus, which can contribute consistent deficits of cognition across subsequent age-nodes.
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http://dx.doi.org/10.1016/j.etap.2020.103350DOI Listing
May 2020

Lipidomics-based study on the neuroprotective effect of geissoschizine methyl ether against oxidative stress-induced cytotoxicity.

J Ethnopharmacol 2020 May 28;253:112636. Epub 2020 Jan 28.

Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, 510006, China. Electronic address:

Ethnopharmacological Relevance: Lipid homoeostasis is important for neurodevelopment, cell signaling and neurotransmission. Alteration of lipid metabolism has been demonstrated in many neurological disorders and neurodegenerative diseases. Geissoschizine methyl ether (GM) is an active alkaloid ingredient in the traditional Chinese medicine Uncaria hook. It has been shown that GM has strong potency in neuroprotective activity and GM reduces the production of reactive oxygen species by regulating glucose metabolism, which protects neurons against oxidative stress-induced cell death. However, it is unknown whether GM could regulate neuronal lipid metabolism during oxidative challenge.

Aim Of The Study: The current study aimed to explore whether GM regulates lipid metabolism in oxidative damaged neurons and to determine the underlying mechanism involved in this neuro-protection.

Materials And Methods: Using a glutamate-induced oxidative toxicity model in mouse hippocampal neuronal cell line (HT-22 cells), we investigated the effect of GM on glutamate-induced lipid peroxidation, lipotoxicity and mitochondrial dysfunction. In order to clarify the mechanism underlying the neuroprotection by GM, lipid metabolomics was performed to investigate whether GM prevent oxidative stress-induced lipid metabolism disruption. Furthermore, the expression of lipid metabolism-related genes was measured.

Results: The results show the protective effect of GM against oxidative stress through blocking glutamate-induced lipid peroxidation and lipotoxicity. Overall, lipidomics analysis revealed that glutamate treatment resulted in different extents of changes in a wide range of lipid classes such as fatty acids (FA), triacylglycerol (TG), sphingomyelin (SM), cardiolipin (CL), lysophosphatidylcholines (LPC). However, GM treatment can significantly reverse glutamate-induced lipids disorder to the homeostasis level. GM prevented the disruption of lipid metabolism by regulating the expression of lipid homeostasis related genes, which contributes to preserve mitochondrial function under oxidative damage.

Conclusion: These findings clearly demonstrated a novel protective mechanism of GM against glutamate-induced oxidative toxicity in neurons via regulating lipid metabolism. GM may provide an effective approach for the prevention and treatment of oxidative damaged neurons.
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http://dx.doi.org/10.1016/j.jep.2020.112636DOI Listing
May 2020

Chondromyxoid fibroma-like osteosarcoma: a case series and literature review.

BMC Musculoskelet Disord 2020 Jan 29;21(1):53. Epub 2020 Jan 29.

Department of Imaging, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 Xian Xia Road, Shanghai, 200050, China.

Background: Chondromyxoid fibroma-like osteosarcoma (CMF-OS) is an exceedingly rare subtype of low-grade central osteosarcoma (LGCO), accounting for up to 10% of cases and making it difficult to diagnose. CMF-OS is frequently misdiagnosed on a radiological examination and biopsy, even after the initial operation. Its treatment is a controversial issue due to its low-grade classification and actual high-grade behavior.

Case Presentation: We retrospectively reviewed the medical charts of more than 2000 osteosarcoma patients between 2008 and 2019; 11 patients with CMF-OS were identified, of which six patients were treated by our institution with complete clinical characteristics, including treatment and prognosis, radiological and pathological features were reviewed. Three males and three females with a median age of 46 (range 22-56) years were pathologically proven to have CMF-OS. The radiological presentation of CMF-OS is variable, thus radiological misdiagnoses are common. However, one must not ignore a malignant radiologic appearance. The most distinctive pathological feature conferring the diagnosis of CMF-OS is the presence of osteoid production directly by the tumor cells under a chondromyxoid fibroma (CMF)-like background. Differential diagnoses based on comprehensive data from CMF, LGCO, chondrosarcoma (CHS), conventional osteosarcoma (COS), etc., are needed. All patients were treated with an operation and chemotherapy, and one patient received additional radiotherapy. Nevertheless, recurrence and metastasis are common in CMF-OS patients. Relatively invasive biological behavior of CMF-OS is against the low-grade classification of this disease.

Conclusions: It is important to recognize CMF-OS and distinguish it from CMF, CHS, COS and other LGCOs. CMF-OS has a relatively poor prognosis despite its low-grade classification.
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http://dx.doi.org/10.1186/s12891-020-3063-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990471PMC
January 2020