Publications by authors named "Jingjing Liang"

152 Publications

Exchange Rate Forecasting Based on Deep Learning and NSGA-II Models.

Comput Intell Neurosci 2021 22;2021:2993870. Epub 2021 Sep 22.

SILC Business School, Shanghai University, Shanghai 201800, China.

Today, the global exchange market has been the world's largest trading market, whose volume could reach nearly 5.345 trillion US dollars, attracting a large number of investors. Based on the perspective of investors and investment institutions, this paper combines theory with practice and creatively puts forward an innovative model of double objective optimization measurement of exchange forecast analysis portfolio. To be more specific, this paper proposes two algorithms to predict the volatility of exchange, which are deep learning and NSGA-II-based dual-objective measurement optimization algorithms for the exchange investment portfolio. Compared with typical traditional exchange rate prediction algorithms, the deep learning model has more accurate results and the NSGA-II-based model further optimizes the selection of investment portfolios and finally gives investors a more reasonable investment portfolio plan. In summary, the proposal of this article can effectively help investors make better investments and decision-making in the exchange market.
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http://dx.doi.org/10.1155/2021/2993870DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8481046PMC
October 2021

Mitochondrial Fusion Suppresses Tau Pathology-Induced Neurodegeneration and Cognitive Decline.

J Alzheimers Dis 2021 Sep 30. Epub 2021 Sep 30.

Department of Pharmacology and Experimental Neurosciences, University of Nebraska Medical Centre, Omaha, NE, USA.

Background: Abnormalities of mitochondrial fission and fusion, dynamic processes known to be essential for various aspects of mitochondrial function, have repeatedly been reported to be altered in Alzheimer's disease (AD). Neurofibrillary tangles are known as a hallmark feature of AD and are commonly considered a likely cause of neurodegeneration in this devastating disease.

Objective: To understand the pathological role of mitochondrial dynamics in the context of tauopathy.

Methods: The widely used P301S transgenic mice of tauopathy (P301S mice) were crossed with transgenic TMFN mice with the forced expression of Mfn2 specifically in neurons to obtain double transgenic P301S/TMFN mice. Brain tissues from 11-month-old non-transgenic (NTG), TMFN, P301S, and P301S/TMFN mice were analyzed by electron microscopy, confocal microscopy, immunoblot, histological staining, and immunostaining for mitochondria, tau pathology, and tau pathology-induced neurodegeneration and gliosis. The cognitive function was assessed by the Barnes maze.

Results: P301S mice exhibited mitochondrial fragmentation and a consistent decrease in Mfn2 compared to age-matched NTG mice. When P301S mice were crossed with TMFN mice (P301S/TMFN mice), neuronal loss, as well as mitochondria fragmentation were significantly attenuated. Greatly alleviated tau hyperphosphorylation, filamentous aggregates, and thioflavin-S positive tangles were also noted in P301S/TMFN mice. Furthermore, P301S/TMFN mice showed marked suppression of neuroinflammation and improved cognitive performance in contrast to P301S mice.

Conclusion: These in vivo findings suggest that promoted mitochondrial fusion suppresses toxic tau accumulation and associated neurodegeneration, which may protect against the progression of AD and related tauopathies.
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http://dx.doi.org/10.3233/JAD-215175DOI Listing
September 2021

The ineffective emotion regulation strategies of heroin use disorder patients: An event-related potential study.

Drug Alcohol Depend 2021 Sep 24;228:109076. Epub 2021 Sep 24.

Lanzhou Drug Rehabilitation Hospital, Lanzhou, China.

Background: People with substance use disorders (SUDs) usually experience emotion dysregulation, which may be a consequence of or a risk factor for the development and maintenance of substance misuse. Despite growing evidence on emotion dysregulation among people with SUDs, relatively few studies have explored emotion dysregulation in heroin use disorder (HUD) patients.

Methods: Using event-related potentials (ERP), we compared the emotion regulation ability of 33 HUD patients and 30 healthy controls according to their average electroencephalogram amplitudes of the late positive potential (LPP) component in 400-1000 ms and 1000-2000 ms time windows, while viewing neutral and unpleasant emotional pictures, and using emotion regulation strategies (expressive suppression, cognitive reappraisal, and a combination) while viewing unpleasant pictures. We recorded their mood states and how successfully they used emotion regulation strategies in each block using 7-point scales.

Results: Relative to healthy controls, the LPP amplitudes of HUD patients were significantly lower when viewing emotional stimuli (p < 0.05) and using emotion regulation strategies (all p < 0.05). The left hemisphere was more active in healthy controls (p < 0.05, p < 0.01); there were no differences in scalp position activation among HUD patients.

Discussion: Compared to healthy controls, HUD patients' emotional arousal and emotion regulation ability were impaired, as reflected by the LPP component. Their abnormal scalp activation pattern may imply abnormal brain activity. Future research could explore this with electroencephalogram source analysis techniques, functional magnetic resonance imaging, or other technologies. Intervention effects for emotion dysregulation in HUD treatment are also worth exploring.
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http://dx.doi.org/10.1016/j.drugalcdep.2021.109076DOI Listing
September 2021

AKR1C3 and Its Transcription Factor HOXB4 Are Promising Diagnostic Biomarkers for Acute Myocardial Infarction.

Front Cardiovasc Med 2021 9;8:694238. Epub 2021 Sep 9.

Department of Cardiology, Shunde Hospital, Southern Medical University, Foshan, China.

A recent study disclosed that ferroptosis was an important myocyte death style in myocardial infarction (MI). However, the diagnostic value of ferroptosis regulators and correlated underlying mechanisms in acute myocardial infarction (AMI) remain unknown. Bioinformatical analyses were conducted to identify the candidate biomarkers for AMI, and the collected local samples were used to validate the findings real-time quantitative PCR. Bioinformatical analysis and luciferase reporter assay were implemented to identify the transcriptional factor. Transient transfection and ferroptosis characteristic measurement, including glutathione peroxidase 4, malondialdehyde, iron, and glutathione, was performed to verify the ability of the candidate gene to regulate the ferroptosis of cardiomyocytes. A meta-analysis was conducted in multiple independent cohorts to clarify the diagnostic value. A total of 121 ferroptosis regulators were extracted from previous studies, and aldo-keto reductase family 1 member C3 (AKR1C3) was significantly downregulated in the peripheral blood samples of AMI cases from the analysis of GSE48060 and GSE97320. HOXB4 served as a transcriptional activator for AKR1C3 and could suppress the ferroptosis of the H9C2 cells treated with erastin. Besides this, peripheral blood samples from 16 AMI patients and 16 patients without coronary atherosclerotic disease were collected, where AKR1C3 and HOXB4 both showed a high diagnostic ability. Furthermore, a nomogram including HOXB4 and AKR1C3 was established and successfully validated in six independent datasets. A clinical correlation analysis displayed that AKR1C3 and HOXB4 were correlated with smoking, CK, CK-MB, and N-terminal-pro-B-type natriuretic peptide. Taken together, this study demonstrates that AKR1C3 and HOXB4 are promising diagnostic biomarkers, providing novel insights into the ferroptosis mechanisms of AMI.
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http://dx.doi.org/10.3389/fcvm.2021.694238DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8458746PMC
September 2021

Edible fungal polysaccharides, the gut microbiota, and host health.

Carbohydr Polym 2021 Dec 14;273:118558. Epub 2021 Aug 14.

College of Food Science and Engineering, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address:

The plasticity of the gut microbiota (GM) creates an opportunity to reshape the biological output of gut microbes by manipulating external factors. It is well known that edible fungal polysaccharides (EFPs) can reach the distal intestine and be assimilated to reshape the GM. The GM has unique devices that utilize various EFPs and produce oligosaccharides, which can selectively promote the growth of beneficial bacteria and are fermented into short-chain fatty acids that interact closely with intestinal cells. Here we review EFPs-based interventions for the GM, particularly the key microorganisms, functions, and metabolites. In addition, we discuss the bi-directional causality between GM imbalance and diseases, and the beneficial effects of EFPs on host health via GM. This review can offer a valuable reference for the design of edible fungal polysaccharide- or oligosaccharide-based nutrition interventions or drug development for maintaining human health by targeted regulation of the GM.
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http://dx.doi.org/10.1016/j.carbpol.2021.118558DOI Listing
December 2021

Coronary Artery Disease: Optimal Lipoprotein(a) for Survival-Lower Is Better? A Large Cohort With 43,647 Patients.

Front Cardiovasc Med 2021 31;8:670859. Epub 2021 Aug 31.

Department of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.

A high level of lipoprotein(a) can lead to a high risk of cardiovascular events or mortality. However, the association of moderately elevated lipoprotein(a) levels (≥15 mg/dL) with long-term prognosis among patients with coronary artery disease (CAD) is still uncertain. Hence, we aim to systematically analyzed the relevance of baseline plasma lipoprotein(a) levels to long-term mortality in a large cohort of CAD patients. We obtained data from 43,647 patients who were diagnosed with CAD and had follow-up information from January 2007 to December 2018. The patients were divided into two groups (<15 and ≥15 mg/dL). The primary endpoint was long-term all-cause death. Kaplan-Meier curve analysis and Cox proportional hazards models were used to investigate the association between moderately elevated baseline lipoprotein(a) levels (≥15 mg/dL) and long-term all-cause mortality. During a median follow-up of 5.04 years, 3,941 (18.1%) patients died. We observed a linear association between lipoprotein(a) levels and long-term all-cause mortality. Compared with lipoprotein(a) concentrations <15 mg/dL, lipoprotein(a) ≥15 mg/dL was associated with a significantly higher risk of all-cause mortality [adjusted hazard ratio (aHR) 1.10, 95%CI: 1.04-1.16, -values = 0.001). Similar results were found for the subgroup analysis of non-acute myocardial infarction, non-percutaneous coronary intervention, chronic heart failure, diabetes mellitus, or non-chronic kidney diseases. Moderately elevated baseline plasma lipoprotein(a) levels (≥15 mg/dL) are significantly associated with higher all-cause mortality in patients with CAD. Our finding provides a rationale for testing the lipoprotein(a)-reducing hypothesis with lower targets (even <15 mg/dL) in CAD outcome trials.
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http://dx.doi.org/10.3389/fcvm.2021.670859DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8438333PMC
August 2021

Protective Effect of Remdesivir Against Pulmonary Fibrosis in Mice.

Front Pharmacol 2021 26;12:692346. Epub 2021 Aug 26.

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin, China.

Pulmonary fibrosis is a known sequela of severe or persistent lung damage. Existing clinical, imaging and autopsy studies have shown that the lungs exhibit a pathological pulmonary fibrosis phenotype after infection with coronaviruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Pulmonary fibrosis may be one of the most serious sequelae associated with coronavirus disease 2019 (COVID-19). In this study, we aimed to examine the preventative effects of the antiviral drug remdesivir on pulmonary fibrosis. We used a mouse model of bleomycin-induced pulmonary fibrosis to evaluate the effects of remdesivir on pulmonary fibrosis and further explored the potential pharmacological mechanisms of remdesivir in lung fibroblasts and alveolar epithelial cells . The preventive remdesivir treatment was started on the day of bleomycin installation, and the results showed that remdesivir significantly alleviated bleomycin-induced collagen deposition and improved pulmonary function. experiments showed that remdesivir dose-dependently suppressed TGF-β1-induced lung fibroblast activation and improved TGF-β1-induced alveolar epithelial to mesenchymal transition. Our results indicate that remdesivir can preventatively alleviate the severity of pulmonary fibrosis and provide some reference for the prevention of pulmonary fibrosis in patients with COVID-19.
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http://dx.doi.org/10.3389/fphar.2021.692346DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8427522PMC
August 2021

Whole-genome association analyses of sleep-disordered breathing phenotypes in the NHLBI TOPMed program.

Genome Med 2021 Aug 26;13(1):136. Epub 2021 Aug 26.

Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, 10461, USA.

Background: Sleep-disordered breathing is a common disorder associated with significant morbidity. The genetic architecture of sleep-disordered breathing remains poorly understood. Through the NHLBI Trans-Omics for Precision Medicine (TOPMed) program, we performed the first whole-genome sequence analysis of sleep-disordered breathing.

Methods: The study sample was comprised of 7988 individuals of diverse ancestry. Common-variant and pathway analyses included an additional 13,257 individuals. We examined five complementary traits describing different aspects of sleep-disordered breathing: the apnea-hypopnea index, average oxyhemoglobin desaturation per event, average and minimum oxyhemoglobin saturation across the sleep episode, and the percentage of sleep with oxyhemoglobin saturation < 90%. We adjusted for age, sex, BMI, study, and family structure using MMSKAT and EMMAX mixed linear model approaches. Additional bioinformatics analyses were performed with MetaXcan, GIGSEA, and ReMap.

Results: We identified a multi-ethnic set-based rare-variant association (p = 3.48 × 10) on chromosome X with ARMCX3. Additional rare-variant associations include ARMCX3-AS1, MRPS33, and C16orf90. Novel common-variant loci were identified in the NRG1 and SLC45A2 regions, and previously associated loci in the IL18RAP and ATP2B4 regions were associated with novel phenotypes. Transcription factor binding site enrichment identified associations with genes implicated with respiratory and craniofacial traits. Additional analyses identified significantly associated pathways.

Conclusions: We have identified the first gene-based rare-variant associations with objectively measured sleep-disordered breathing traits. Our results increase the understanding of the genetic architecture of sleep-disordered breathing and highlight associations in genes that modulate lung development, inflammation, respiratory rhythmogenesis, and HIF1A-mediated hypoxic response.
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http://dx.doi.org/10.1186/s13073-021-00917-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8394596PMC
August 2021

Translational regulation in the brain by TDP-43 phase separation.

J Cell Biol 2021 Oct 24;220(10). Epub 2021 Aug 24.

Department of Pharmacology and Experimental Neurosciences, University of Nebraska Medical Center, Omaha, NE.

The in vivo physiological function of liquid-liquid phase separation (LLPS) that governs non-membrane-bound structures remains elusive. Among LLPS-prone proteins, TAR DNA-binding protein of 43 kD (TDP-43) is under intense investigation because of its close association with neurological disorders. Here, we generated mice expressing endogenous LLPS-deficient murine TDP-43. LLPS-deficient TDP-43 mice demonstrate impaired neuronal function and behavioral abnormalities specifically related to brain function. Brain neurons of these mice, however, did not show TDP-43 proteinopathy or neurodegeneration. Instead, the global rate of protein synthesis was found to be greatly enhanced by TDP-43 LLPS loss. Mechanistically, TDP-43 LLPS ablation increased its association with PABPC4, RPS6, RPL7, and other translational factors. The physical interactions between TDP-43 and translational factors relies on a motif, the deletion of which abolished the impact of LLPS-deficient TDP-43 on translation. Our findings show a specific physiological role for TDP-43 LLPS in the regulation of brain function and uncover an intriguing novel molecular mechanism of translational control by LLPS.
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http://dx.doi.org/10.1083/jcb.202101019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404466PMC
October 2021

Bergenin attenuates bleomycin-induced pulmonary fibrosis in mice via inhibiting TGF-β1 signaling pathway.

Phytother Res 2021 Aug 10. Epub 2021 Aug 10.

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin, China.

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by epithelial cell damage, fibroblast activation, and collagen deposition. IPF has high mortality and limited therapies, which urgently needs to develop safe and effective therapeutic drugs. Bergenin, a compound derived from a variety of medicinal plants, has demonstrated multiple pharmacological activities including anti-inflammatory and anti-tumor, also acts as a traditional Chinese medicine to treat chronic bronchitis, but its effect on the pulmonary fibrosis is unknown. In this study, we demonstrated that bergenin could attenuate bleomycin (BLM)-induced pulmonary fibrosis in mice. In vitro studies indicated that bergenin inhibited the transforming growth factor-β1 (TGF-β1)-induced fibroblast activation and the extracellular matrix accumulation by inhibiting the TGF-β1/Smad signaling pathway. Further studies showed that bergenin could induce the autophagy formation of myofibroblasts by suppressing the mammalian target of rapamycin signaling and that bergenin could promote the myofibroblast apoptosis. In vivo experiments revealed that bergenin substantially inhibited the myofibroblast activation and the collagen deposition and promoted the autophagy formation. Overall, our results showed that bergenin attenuated the BLM-induced pulmonary fibrosis in mice by suppressing the myofibroblast activation and promoting the autophagy and the apoptosis of myofibroblasts.
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http://dx.doi.org/10.1002/ptr.7239DOI Listing
August 2021

Study of the pathology and the underlying molecular mechanism of tissue injury around hematoma following intracerebral hemorrhage.

Mol Med Rep 2021 Oct 9;24(4). Epub 2021 Aug 9.

Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China.

Intracerebral hemorrhage (ICH) refers to hemorrhage caused by spontaneous rupture of blood vessels in the brain. Brain injury due to ICH leads to catastrophic effects resulting from the formation of hematoma and oxidative stress caused by components of lysed erythrocytes. However, not all neurons in the area surrounding the hematoma die immediately: A number of neurons remain in a critical, but reversible, state; however, the genes involved in this critical state remain poorly understood. Gene chip technology was used identify changes in the area surrounding the hematoma associated with the upregulation of 210 and downregulation of 173 genes. Gene Ontology functional annotation revealed changes in the gene expression profile in the peripheral region of hematoma following ICH, which were primarily associated with the external stimulation received by the organism, the transmission of harmful information to the cell through the transport of cell membrane proteins, and the regulation of a series of biological processes. Protein interaction network analysis revealed that 11 up‑[secreted phosphoprotein 1, dual specificity phosphatase 9, catechol‑O‑methyltransferase, BAR/IMD domain‑containing adaptor protein 2‑like 1, plakophilin 2, homer scaffold protein 3, ret proto‑oncogene (RET), KIT proto‑oncogene, receptor tyrosine kinase, hepsin, connector enhancer of kinase suppressor of Ras 2 and kalirin RhoGEF kinase] and four downregulated genes (transcription factor AP‑2β, peptidylprolyl isomerase A, SHOC2 leucine rich repeat scaffold protein and synuclein α) may serve a significant role in the area around hematoma following ICH. Reverse transcription‑quantitative PCR was used to verify that these genes were differentially expressed in the ICH compared with the control group. Causal network analysis suggested that the Achaete‑scute homolog 1‑RET signaling axis served a key role in the repair of nerve injury in the peripheral region of hematoma following ICH. Additionally, experiments revealed that RET expression was upregulated and co‑localized with neurons. Taken together, these results suggested that the changes in the gene expression profile in the area around hematoma following ICH were primarily associated with the repair of damage caused to the nervous system.
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http://dx.doi.org/10.3892/mmr.2021.12341DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8365418PMC
October 2021

Development and validation of an intra-tumor heterogeneity-related signature to predict prognosis of bladder cancer: a study based on single-cell RNA-seq.

Aging (Albany NY) 2021 08 2;13(15):19415-19441. Epub 2021 Aug 2.

Department of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.

Intra-tumor heterogeneity (ITH) was a potential mechanism of progression and drug resistance in bladder cancer (BCa). However, the understanding of ITH in BCa remains insufficient. Single-cell RNA sequencing (scRNA-seq) profiles of 2075 cells were analyzed, and 2940 cell markers were screened. The ITH of 396 cases was evaluated, and 96 ITH-related genes were identified. Based on the gene-pair strategy, 96 genes were cyclically paired, and an 8-gene-pair model was successfully established to evaluate the overall survival of BCa through Lasso and multivariate Cox regressions. The risk model showed high predictive value in the training dataset ( = 396, = 0) and external validation datasets ( = 165, = 2.497e-02; = 224, = 3.423e-02). The model was also valuable for the prediction of clinical treatment outcomes. Totally, a prognostic model based on scRNA-seq and ITH was successfully constructed and validated in large cohorts, providing novel clues for ITH study of BCa.
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http://dx.doi.org/10.18632/aging.203353DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8386527PMC
August 2021

Defining the Immune Responses for SARS-CoV-2-Human Macrophage Interactions.

bioRxiv 2021 Jul 15. Epub 2021 Jul 15.

Host innate immune response follows severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and it is the driver of the acute respiratory distress syndrome (ARDS) amongst other inflammatory end-organ morbidities. Such life-threatening coronavirus disease 2019 (COVID-19) is heralded by virus-induced activation of mononuclear phagocytes (MPs; monocytes, macrophages, and dendritic cells). MPs play substantial roles in aberrant immune secretory activities affecting profound systemic inflammation and end organ malfunctions. All follow an abortive viral infection. To elucidate SARS-CoV-2-MP interactions we investigated transcriptomic and proteomic profiles of human monocyte-derived macrophages. While expression of the SARS-CoV-2 receptor, the angiotensin-converting enzyme 2, paralleled monocyte-macrophage differentiation it failed to affect productive viral infection. In contrast, simple macrophage viral exposure led to robust pro-inflammatory cytokine and chemokine expression but attenuated type I interferon (IFN) activity. Both paralleled dysregulation of innate immune signaling pathways specifically those linked to IFN. We conclude that the SARS-CoV-2-infected host mounts a robust innate immune response characterized by a pro-inflammatory storm heralding consequent end-organ tissue damage.
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http://dx.doi.org/10.1101/2021.07.07.449660DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8282098PMC
July 2021

Development of a Ferroptosis-Related lncRNA Signature to Predict the Prognosis and Immune Landscape of Bladder Cancer.

Dis Markers 2021 20;2021:1031906. Epub 2021 Jun 20.

Department of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510000, China.

The tight relationship between ferroptotic cell death and immune response demonstrated by recent studies enlightened us to detect the underlying roles of ferroptosis-related long noncoding RNAs (frlncRNAs) in the tumor microenvironment of bladder cancer (BCa). We collected 121 ferroptosis regulators from previous studies. Based on their expression values, 408 cases with BCa were clustered. The patients in different clusters showed diverse immune infiltration, immunotherapy response, and chemotherapy effectiveness, revalidating the tight correlation with ferroptosis and tumor immunity. Through differential, coexpression, Kaplan-Meier, Lasso, and Cox analysis, we developed a 22-lncRNA-pair signature to predict the prognosis of BCa based on gene-pair strategy, where there is no need for definite expression values. The areas under the curves are all over 0.8. The risk model also helped to predict immune infiltration, immunotherapeutic outcomes, and chemotherapy sensitivity. Totally, the prognostic assessment model indicated a promising predictive value, also providing clues for the interaction between ferroptosis and BCa immunity.
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http://dx.doi.org/10.1155/2021/1031906DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8238626PMC
June 2021

Malnutrition and the risk for contrast-induced acute kidney injury in patients with coronary artery disease.

Int Urol Nephrol 2021 Jun 25. Epub 2021 Jun 25.

Department of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.

Purpose: Malnutrition is a common comorbidity of coronary artery disease (CAD) and is often associated with adverse events. The malnutrition often means lower cholesterol, albumin and high lymphocyte, as risk factors of Contrast-Induced Acute Kidney Injury (CI-AKI). We aim to evaluate the association between malnutrition and CI-AKI following coronary angiography (CAG) in CAD patients.

Methods: We analyzed 3170 CAD patients with variables of nutritional status (Controlling Nutritional Status score (CONUT)) from the prospective multicenter study, REICIN (NCT01402232) including 4,271 consecutive patients undergoing CAG from January 2013 to February 2016. Patients were divided into the normal group (CONUT score 0-1) and malnutrition group (CONUT score > 1). The association of malnutrition and the risk of CI-AKI was examined in all CAD patients using multivariable logistics regression analysis.

Results: Among the 3170 patients (mean age: 63.1 ± 10.7 years), 1865 (58.8%) suffered from malnutrition, 111 (3.5%) developed CI-AKI, including 23 (1.76%) in normal group and 88 (4.72%) in malnutrition group (p < 0.01). The malnourished patients were older, and likely had anemia and worse cardiorenal function. After adjustment for confounders, the risk of CI-AKI was 1.04 times higher in the malnutrition group than in the normal group (adjusted OR: 2.04, 95% CI 1.28-3.38, p < 0.01).

Conclusions: Among CAD patients undergoing CAG, malnutrition is extremely common and associated with a double risk of CI-AKI. Further studies are needed to investigate the potential renal protection of intervening malnutrition in CAD patients.
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http://dx.doi.org/10.1007/s11255-021-02915-6DOI Listing
June 2021

Correction to: The global incidence and mortality of contrast-associated acute kidney injury following coronary angiography: a meta-analysis of 1.2 million patients.

J Nephrol 2021 Oct;34(5):1785

Department of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.

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http://dx.doi.org/10.1007/s40620-021-01090-2DOI Listing
October 2021

Next generation sequencing in children with unexplained epilepsy: A retrospective cohort study.

Brain Dev 2021 Jun 10. Epub 2021 Jun 10.

Department of Paediatrics, Peking University People's Hospital, Beijing 100044, China.

Objective: To evaluate the clinical utility of next-generation sequencing (NGS) in unexplained pediatric epilepsy, and to identify the potential predictors associated with Mendelian genetic causes.

Methods: Two hundred and ten children with unexplained epilepsy, who underwent NGS test were included. We analyzed the demographic, clinical and genetic characteristics, and executed a Logistic regression analysis for identifying predictors for Mendelian genetic causes. Patients were classified as either with isolated epilepsy or syndromic epilepsy with concurrent neurodevelopmental phenotypes.

Results: The overall diagnostic yield was 29.0% (61/210). A total of 68 variants spanning 39 genes were identified in 58 patients (27.6%, 58/210) from exome sequencing based testing. Of the 68 variants, 33 were novel ones. Besides, STAR and CNTN2 were identified to be a candidate gene for epilepsy. Patients with syndromic epilepsy had a much higher diagnostic yield than that of isolated epilepsy (53/135, 39.3% vs. 8/75, 10.7%, p = 0.000). The odds ratio of detecting genetic cause was 3.939 (95% CI 1.369-11.332) for syndromic epilepsy without epileptic encephalopathy (EE), 5.814 (95% CI 2.208-15.306) for EE, 2.958 (95% CI 1.093-8.000) for patients with seizure onset <12 months, and 2.932 (95%CI 1.414-6.080) for female. Of the 210 patients, 78.4% of patients (145/185) had at least a 50% reduction in seizure frequency and 58.9% (109/185) reached seizure freedom. There was no difference between seizure prognosis and diagnostic outcomes.

Significance: NGS is effective for Mendelian genetic etiological diagnosis for unexplained pediatric epilepsy. Female patients with syndromic epilepsy with onset within the first year of life are most likely to yield a positive test result.
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http://dx.doi.org/10.1016/j.braindev.2021.05.014DOI Listing
June 2021

SARS-CoV-2 Envelope (E) protein interacts with PDZ-domain-2 of host tight junction protein ZO1.

PLoS One 2021 9;16(6):e0251955. Epub 2021 Jun 9.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.

Newly emerged SARS-CoV-2 is the cause of an ongoing global pandemic leading to severe respiratory disease in humans. SARS-CoV-2 targets epithelial cells in the respiratory tract and lungs, which can lead to amplified chloride secretion and increased leak across epithelial barriers, contributing to severe pneumonia and consolidation of the lungs as seen in many COVID-19 patients. There is an urgent need for a better understanding of the molecular aspects that contribute to SARS-CoV-2-induced pathogenesis and for the development of approaches to mitigate these damaging pathologies. The multifunctional SARS-CoV-2 Envelope (E) protein contributes to virus assembly/egress, and as a membrane protein, also possesses viroporin channel properties that may contribute to epithelial barrier damage, pathogenesis, and disease severity. The extreme C-terminal (ECT) sequence of E also contains a putative PDZ-domain binding motif (PBM), similar to that identified in the E protein of SARS-CoV-1. Here, we screened an array of GST-PDZ domain fusion proteins using either a biotin-labeled WT or mutant ECT peptide from the SARS-CoV-2 E protein. Notably, we identified a singular specific interaction between the WT E peptide and the second PDZ domain of human Zona Occludens-1 (ZO1), one of the key regulators of TJ formation/integrity in all epithelial tissues. We used homogenous time resolve fluorescence (HTRF) as a second complementary approach to further validate this novel modular E-ZO1 interaction. We postulate that SARS-CoV-2 E interacts with ZO1 in infected epithelial cells, and this interaction may contribute, in part, to tight junction damage and epithelial barrier compromise in these cell layers leading to enhanced virus spread and severe dysfunction that leads to morbidity. Prophylactic/therapeutic intervention targeting this virus-host interaction may effectively reduce airway and/or gastrointestinal barrier damage and mitigate virus spread.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0251955PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8189464PMC
July 2021

The global incidence and mortality of contrast-associated acute kidney injury following coronary angiography: a meta-analysis of 1.2 million patients.

J Nephrol 2021 10 2;34(5):1479-1489. Epub 2021 Jun 2.

Department of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.

Background: Contrast-associated acute kidney injury (CA-AKI) is a common complication after coronary angiography (CAG), which brings a poor prognosis. But up to now, there were fewer studies to discuss the incidence of CA-AKI comprehensively. We comprehensively explore the incidence of CA-AKI after coronary angiography.

Methods: We searched Medline, Embase, and Cochrane Database of Systematic Reviews (to 30th June 2019). We evaluated the world's incidence of the CA-AKI, and associated mortality, and to described geographic variations according to countries, regions, and economies. CA-AKI was defined as an increase in serum creatinine ≥ 0.5 mg/dl or ≥ 25% within 72 h. Random effects model meta-analyses and meta-regressions was performed to derive the sources of heterogeneity.

Results: A total of 134 articles (1,211,106 participants) were included in our meta-analysis. Most studies originated from China, Japan, Turkey and United States, from upper middle income and high income countries. The pooled incidence of CA-AKI after coronary angiography was 12.8% (95% CI 11.7-13.9%), and the CA-AKI associated mortality was 20.2% (95% CI 10.7-29.7%). The incidence of CA-AKI and the CA-AKI associated mortality were not declined over time (Incidence rate change: 0.23% 95% CI - 0.050 to 0.510 p = 0.617; Mortality rate change: - 1.05% 95% CI - 3.070 to 0.970 p = 0.308, respectively).

Conclusion: CA-AKI was a universal complication in many regions, and the burden of CA-AKI remains severe. In clinical practice, physicians should pay more attention to the occurrence and active prevention and treatment of CA-AKI.
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http://dx.doi.org/10.1007/s40620-021-01021-1DOI Listing
October 2021

A Ketogenic Diet and the Treatment of Autism Spectrum Disorder.

Front Pediatr 2021 11;9:650624. Epub 2021 May 11.

Department of Pediatrics, Peking University People's Hospital, Beijing, China.

Autism spectrum disorder (ASD) is characterized by stereotyped behavior and deficits in communication and social interaction. There are no curative treatments for children with ASD. The ketogenic diet (KD) is a high-fat, appropriate-protein, and low-carbohydrate diet that mimics the fasting state of the body and is proven beneficial in drug-resistant epilepsy and some other brain diseases. An increasing number of studies demonstrated that a KD improved autistic behavior, but the underlying mechanisms are not known. We reviewed the neuroprotective role of a KD in ASD, which is likely mediated improvements in energy metabolism, reductions in antioxidative stress levels, control of neurotransmitters, inhibition of the mammalian target of rapamycin (mTOR) signaling pathway, and modulation of the gut microbiota. A KD is likely a safe and effective treatment for ASD.
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http://dx.doi.org/10.3389/fped.2021.650624DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8146910PMC
May 2021

The intervention of intestinal Wnt/β-catenin pathway alters inflammation and disease severity of CIA.

Immunol Res 2021 08 26;69(4):323-333. Epub 2021 May 26.

Department of Rheumatology and Immunology, Changhai Hospital, The Second Military Medical University, Shanghai, China.

Autoreactive T cell is one of the leading causes of immunological tolerance defects in the chronic inflammatory lesions of rheumatoid arthritis (RA). There have been several extracellular signals and intracellular pathways reported in regulating this process but largely remain unknown yet. In this study, we explored the roles of intestinal Wnt/β-catenin on disease severity during collagen-induced arthritis model (CIA), an animal model of RA. We first testified the activity pattern Wnt/β-catenin shifted by intragastric administration of LiCl and DKK-1 in the intestine by real-time PCR and WB analysis. The arthritis scores showing the disease severity in the DKK-1 group was significantly ameliorated compared with the control group at the late stage of the disease, while in the LiCl group, the scores were significantly elevated which was consistent with pathology score analysis of H&E staining. Next, ELISA was performed and showed that TNF-α and IL-17 in the LiCl group were significantly higher than that of the control group. IL-10 in the DKK-1 group was significantly higher than that in the LiCl-1 group and control group, P < 0.05. Flow cytometry of spleen T cells differentiation ratio showed that: Th1 from the DKK-1 and LiCl groups and Th17 from the LiCl group was significantly different from that of the blank model group, P < 0.05. Finally, we explored the effects of intestinal Wnt/β-catenin on T cell differentiation regulator ROR-γt and TCF1 and found that both transcription factors were up-regulated in the LiCl group. Together, these data suggested the pro-information role of Wnt/β-catenin pathway from the intestine in the CIA mouse, implying its use as a potential therapeutic target for the treatment of inflammatory diseases such as RA.
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http://dx.doi.org/10.1007/s12026-021-09190-8DOI Listing
August 2021

Detection of Hepatitis B Virus M204V Mutation Quantitatively via Real-time PCR.

J Clin Transl Hepatol 2021 Apr 16;9(2):143-148. Epub 2021 Mar 16.

Liver Research Center, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center of Digestive Diseases, Beijing, China.

Background And Aims: Drug-resistant DNA mutations of the hepatitis B virus (HBV) affect treatment response in chronic hepatitis B patients. We have established a new, sensitive, specific, accurate and convenient real-time PCR method to detect HBV mutations quantitatively.

Methods: Blood samples were collected from patients showing viral breakthrough, primary nonresponse, or poor response during treatment, and mutations were detected via direct sequencing to assess our method. A plasmid containing the M204V mutation was synthesized and standard curves plotted.

Results: The determination coefficient for linear correlation between Ct and log plasmid copy numbers was 0.996, where Ct value was -3.723log (DNA concentration) +48.647. Coefficients of variation indicated good reproducibility. Correctness was within tolerable bias. Limit of detection was 10 copies/mL. Specificity, accuracy, positive predictive value and negative predictive value were 92.86%, 100%, 96.88%, 100% and 94.74%, respectively.

Conclusions: These results show that our method can be used to detect HBV M204V mutations with the advantages of sensitivity, specificity and efficiency, providing a new choice for monitoring drug resistance.
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http://dx.doi.org/10.14218/JCTH.2020.00118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8111100PMC
April 2021

PGE1 triggers Nrf2/HO-1 signal pathway to resist hemin-induced toxicity in mouse cortical neurons.

Ann Transl Med 2021 Apr;9(8):634

Department of Neurology, Affiliated Hospital of Nantong University, Nantong, China.

Background: Prostaglandin E1 (PGE1) exerts various pharmacological effects such as membrane stabilization, anti-inflammatory functions, vasodilation, and platelet aggregation inhibition. We have previously demonstrated that PGE1 has a beneficial impact on patients suffering from intracerebral hemorrhage (ICH). The related mechanism underlying PGE1's beneficial effect on ICH treatment needs further exploration.

Methods: The present study elucidates the mechanism of PGE1 on ICH treatment using a neuronal apoptosis model . The mouse primary cortical neurons were pretreated with different concentrations of PGE1, followed by the treatment with hemin, the main catabolite in whole blood, to mimic the clinical ICH.

Results: Comparing with the vehicle-treated group, PGE1 prevented cultured cortical neurons from the accumulation of inhibited intracellular levels of reactive oxygen species (ROS), amelioration of mitochondrial membrane potential, and hemin-induced apoptosis. The reduction of ROS and apoptosis were associated with the up-regulation of Heme oxygenase-1 (HO-1) expression. Knockdown of nuclear transcription factor erythroid 2-related factor (Nrf2) by siRNA attenuated the upregulation of HO-1 as well as the protective effect of PGE1.

Conclusions: Our work suggests that the Nrf2/HO-1 molecular pathway may play a crucial role in treating ICH patients with PGE1 and may represent novel molecular targets, resulting in discovering new drugs for ICH treatment.
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http://dx.doi.org/10.21037/atm-20-5839DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8106031PMC
April 2021

Association of Early and Late Contrast-Associated Acute Kidney Injury and Long-Term Mortality in Patients Undergoing Coronary Angiography.

J Interv Cardiol 2021 8;2021:6641887. Epub 2021 Mar 8.

Department of Cardiology, Dongguan TCM Hospital, Dongguan 523000, China.

Background: Contrast-associated acute kidney injury (CA-AKI) is a common complication in patients undergoing coronary angiography (CAG). However, few studies demonstrate the association between the prognosis and developed CA-AKI in the different periods after the operation.

Methods: We retrospectively enrolled 3206 patients with preoperative serum creatinine (Scr) and at least twice SCr measurement after CAG. CA-AKI was defined as an increase ≥50% or ≥0.3 mg/dL from baseline in the 72 hours after the procedure. Early CA-AKI was defined as having the first increase in SCr within the early phase (<24 hours), and late CA-AKI was defined as an increase in SCr that occurred for the first time in the late phase (24-72 hours). The first endpoint of this study was long-term all-cause mortality. Kaplan-Meier analysis was used to count the cumulative mortality, and the log-rank test was used to assess differences between curves. Univariate and multivariate cox regression analyses were performed to assess whether patients who developed different type CA-AKI were at increased risk of long-term mortality.

Results: The number of deaths in the 3 groups was 407 for normal (12.7%), 106 for early CA-AKI (32.7%) and 57 for late CA-AKI (17.7%), during a median follow-up period of 3.95 years. After adjusting for important clinical variables, early CA-AKI (HR = 1.33, 95% CI: 1.02-1.74, =0.038) was significantly associated with mortality, while late CA-AKI (HR = 0.92, 95% CI: 0.65-1.31, =0.633) was not. The same results were found in patients with coronary artery disease, chronic kidney disease, diabetes mellitus, and percutaneous coronary intervention.

Conclusions: Early increases in Scr, i.e., early CA-AKI, have better predictive value for long-term mortality. Therefore, in clinical practice, physicians should pay more attention to patients with early renal injury related to long-term prognosis and give active treatment.
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http://dx.doi.org/10.1155/2021/6641887DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8074549PMC
July 2021

Association between baseline LDL-C and prognosis among patients with coronary artery disease and advanced kidney disease.

BMC Nephrol 2021 May 6;22(1):168. Epub 2021 May 6.

Department of Cardiology, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.

Background: Lower low-density lipoprotein cholesterol (LDL-C) is significantly associated with improved prognosis in patients with coronary artery disease (CAD). However, LDL-C reduction does not decrease all-cause mortality among CAD patients when renal function impairs. The association between low baseline LDL-C (< 1.8 mmol/L) and mortality is unknown among patients with CAD and advanced kidney disease (AKD). The current study aimed to evaluate prognostic value of low baseline LDL-C level for all-cause death in these patients.

Methods: In this observational study, 803 CAD patients complicated with AKD (eGFR < 30 mL/min/1.73 m) were enrolled between January 2008 to December 2018. Patients were divided into two groups (LDL-C < 1.8 mmol/L, n = 138; LDL-C ≥ 1.8 mmol/L, n = 665). We used Kaplan-Meier methods and Cox regression analyses to assess the association between baseline low LDL-C levels and long-term all-cause mortality.

Results: Among 803 participants (mean age 67.4 years; 68.5% male), there were 315 incidents of all-cause death during a median follow-up of 2.7 years. Kaplan-Meier analysis showed that low LDL-C levels were associated with worse prognosis. After adjusting for full 24 confounders (e.g., age, diabetes, heart failure, and dialysis, etc.), multivariate Cox regression analysis revealed that lower LDL-C level (< 1.8 mmol/L) was significantly associated with higher risk of all-cause death (adjusted HR, 1.38; 95% CI, 1.01-1.89).

Conclusions: Our data demonstrated that among patients with CAD and AKD, a lower baseline LDL-C level (< 1.8 mmol/L) did not present a higher survival rate but was related to a worse prognosis, suggesting a cautiousness of too low LDL-C levels among patients with CAD and AKD.
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http://dx.doi.org/10.1186/s12882-021-02375-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8101096PMC
May 2021

Ellagic Acid Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting Wnt Signaling Pathway.

Front Pharmacol 2021 12;12:639574. Epub 2021 Apr 12.

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin, China.

Idiopathic pulmonary fibrosis is a progressive lung disease with high mortality and limited therapy that is characterized by epithelial cell damage and fibroblast activation. Ellagic acid is a natural polyphenol compound widely found in fruits and nuts that has multiple pharmacological activities. In this study, we explored the potential effects and mechanisms of Ellagic acid on pulmonary fibrosis and . studies showed that Ellagic acid significantly alleviated bleomycin (BLM)-induced pulmonary fibrosis in mice. experiments indicated that Ellagic acid could suppress Wnt signaling and attenuate Wnt3a-induced myofibroblast activation and the phosphorylation of Erk2 and Akt. Further studies showed that Ellagic acid could induce autophagy formation in myofibroblasts mainly by suppressing mTOR signaling and promoting apoptosis of myofibroblasts. experiments revealed that Ellagic acid significantly inhibited myofibroblast activation and promoted autophagy formation. Taken together, our results show that Ellagic acid effectively attenuates BLM-induced pulmonary fibrosis in mice by suppressing myofibroblast activation and promoting autophagy and apoptosis of myofibroblasts by inhibiting the Wnt signaling pathway.
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http://dx.doi.org/10.3389/fphar.2021.639574DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8072668PMC
April 2021

Compound FC-10696 Inhibits Egress of Marburg Virus.

Antimicrob Agents Chemother 2021 06 17;65(7):e0008621. Epub 2021 Jun 17.

University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Marburg virus (MARV) VP40 protein (mVP40) directs egress and spread of MARV, in part, by recruiting specific host WW domain-containing proteins via its conserved PPxY late (L) domain motif to facilitate efficient virus-cell separation. We reported previously that small-molecule compounds targeting the viral PPxY/host WW domain interaction inhibited VP40-mediated egress and spread. Here, we report on the antiviral potency of novel compound FC-10696, which emerged from extensive structure-activity relationship (SAR) of a previously described series of PPxY inhibitors. We show that FC-10696 inhibits egress of mVP40 virus-like particles (VLPs) and egress of authentic MARV from HeLa cells and primary human macrophages. Moreover, FC-10696 treated-mice displayed delayed onset of weight loss and clinical signs and significantly lower viral loads compared to controls, with 14% of animals surviving 21 days following a lethal MARV challenge. Thus, FC-10696 represents a first-in-class, host-oriented inhibitor effectively targeting late stages of the MARV life cycle.
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http://dx.doi.org/10.1128/AAC.00086-21DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8218653PMC
June 2021

Intracarotid Transplantation of Skin-Derived Precursor Schwann Cells Promotes Functional Recovery After Acute Ischemic Stroke in Rats.

Front Neurol 2021 4;12:613547. Epub 2021 Feb 4.

Department of Neurology, Affiliated Hospital of Nantong University, Nantong, China.

Skin-derived Precursor Schwann cells (SKP-SCs) have been reported to provide neuroprotection for the injured and dysmyelinated nervous system. However, little is known about SKP-SCs on acute ischemic stroke (AIS). We aimed to explore the efficacy and the potential mechanism of action of SKP-SCs on AIS in a rat ischemic stroke model. Adult male Sprague-Dawley rats were subjected to a middle cerebral artery occlusion (MCAO) for 1.5 h on Day 0 and subsequently received an intracarotid injection of 2 × 10 green fluorescent protein (GFP) -labeled SKP-SCs or phosphate buffered saline (PBS) during reperfusion. Neurological function was assessed by behavioral tests on Days 1, 4, 7, 14, and 28. In a satellite cohort, rat brains were harvested and infarct volume was measured with 2,3,5-triphenyltetrazolium chloride (TTC) staining on Days 1 and 7, and migration and survival of SKP-SCs in the brain were traced by monitoring green fluorescence at 6 and12 h on Day 0, and on Days 1, 4, 7, 14, and 28. Histopathology and immunofluorescence staining were used to analyze the morphology, survival and apoptosis of neurons. Additionally, in an SKP-SC co-culture model using fetal rat primary cortical neurons underwent oxygen glucose deprivation/reoxygenation (OGD/R), Western blot was used to detect the expression of apoptosis indicators including activated caspase-3, Bax, and Bcl-2. TUNEL staining was used to count apoptotic cells. Intracarotid transplantation of SKP-SCs effectively migrated to the periinfarct area and survived for at least 4 weeks. Transplanted SKP-SCs inhibited neuronal apoptosis, reduced infarct volume, and improved neurological recovery in the MCAO rats. Moreover, data showed that SKP-SCs treatment inhibited OGD/R-induced neuronal apoptosis and promoted survival of the cultured primary cortical neurons. Intracarotid transplantation of SKP-SCs promoted functional recovery in the rat AIS model and possesses the potential to be further developed as a novel therapy to treat ischemic stroke in humans.
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http://dx.doi.org/10.3389/fneur.2021.613547DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7902026PMC
February 2021

Association between an increase in blood urea nitrogen at 24 h and worse outcomes in COVID-19 pneumonia.

Ren Fail 2021 12;43(1):347-350

Department of Critical Care Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, People's Republic of China.

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http://dx.doi.org/10.1080/0886022X.2021.1879855DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7889150PMC
December 2021

A valuable strategy to improve ferroelectric performance significantly metallic ion doping in the lattice nodes of metal-organic frameworks.

Chem Commun (Camb) 2021 Mar;57(20):2515-2518

Inner Mongolia Key Laboratory of Chemistry and Physics of Rare Earth Materials, School of Chemistry and Chemical Engineering, Inner Mongolia University, Hohhot, 010021, P. R. China.

Metal-organic frameworks (MOFs) with polar space groups in crystallography represent a class of potential molecular-based ferroelectrics; however, the rational design and enhancement of the performance of MOF-based ferroelectrics is a great challenge. In this work, a series of mixed-metal MOFs deriving from Mg2+ ions doped into the lattice nodes of the parent-MOF (Ni-MOF) are synthesized by an in situ solvothermal method. Taking advantage of Mg2+ ions doped in the Ni-MOF, the doped-MOFs (Mg/Ni-MOFs) appear to have a significant lattice distortion and noteworthy dipole asymmetry in the crystals. It is found that the obtained doped-MOFs show a significant enhancement of ferroelectricity compared with that of the parent-MOF. This study opens up a new landscape to explore possibilities for controlling ferroelectric performance in MOF-based ferroelectrics.
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http://dx.doi.org/10.1039/d0cc08217aDOI Listing
March 2021
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