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1.
Adv Healthc Mater ; : e2100934, 2021 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-34648692

RESUMO

Tissue engineering techniques have enabled to replicate the geometrical architecture of native tissues but usually fail to reproduce their exact cellular arrangements during the fabricating process, while it's critical for manufacturing physiologically relevant tissues. To address this problem, we here report a "sewing-like" method of controlling cellular alignment during the fabricating process. By integrating the stretching step into the fabricating process, we are able to create a static mechanical environment which, in turn, would regulate the subsequent cellular alignment, elongation, and differentiation in the generated tissues. With this method, patterned cellular constructs can be fabricated with controlled cellular alignment. Moreover, our method shows a potent capability to fabricate physiologically relevant skeletal muscle constructs in vitro by mechanically inducing myoblast fusion and maturation. As a potential clinical application, aligned myofibers were directly fabricated onto injured muscles in vivo, which repair the damaged tissues effectively. This study shows that our "sewing-like" method can produce engineered tissues with precise control of cellular arrangements and more clinically viable functionalities. This article is protected by copyright. All rights reserved.

2.
J Environ Manage ; 301: 113816, 2021 Sep 24.
Artigo em Inglês | MEDLINE | ID: mdl-34571474

RESUMO

The Mongolian Plateau, home to the world's largest contiguous temperate grasslands, has been known for its vast steppe landscapes and legendary history of the Mongol Empire. However, like temperate grasslands elsewhere around the world, the Mongolian steppe landscapes have been severely degraded by increasing human activities during the past several decades. The main objective of this study was to assess the landscape and ecosystem changes in the Wulagai River Basin (WRB) in Inner Mongolia, where China's last intact steppe ecosystem reportedly resides. Using remote sensing data and landscape metrics, we found that, during 1979-2016, WRB lost about 55 % of wetlands, 76 % of shrublands, and 46 % of sandy-land vegetation, with its most dominant vegetation type shifting from meadow steppe to dry steppe for the first time in history. Human land uses continued to intensify: cropland expanded by about 40 %; impervious surface area increased by almost 34 times; and surface coal mining rampaged through the heartland, tearing up vegetation and sucking up water near and far. The WRB landscape became more diverse compositionally (increasing land cover types), more fragmented ecologically (habitat loss and isolation), and more complex geometrically (anthropogenic and natural landscape elements entangled). Damming, mining, and overgrazing were the major direct drivers for the observed environmental changes. Government-sponsored restoration programs have had positive ecological changes across China, but landscape destruction and fragmentation in the Wulagai River Basin have continued. This dire situation demands urgent government policy intervention and stakeholder-involved governance actions to promote the sustainability of this legendary landscape.

3.
Signal Transduct Target Ther ; 6(1): 308, 2021 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-34408131

RESUMO

Cytokine storm induced by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a major pathological feature of Coronavirus Disease 2019 (COVID-19) and a crucial determinant in COVID-19 prognosis. Understanding the mechanism underlying the SARS-CoV-2-induced cytokine storm is critical for COVID-19 control. Here, we identify that SARS-CoV-2 ORF3a and host hypoxia-inducible factor-1α (HIF-1α) play key roles in the virus infection and pro-inflammatory responses. RNA sequencing shows that HIF-1α signaling, immune response, and metabolism pathways are dysregulated in COVID-19 patients. Clinical analyses indicate that HIF-1α production, inflammatory responses, and high mortalities occurr in elderly patients. HIF-1α and pro-inflammatory cytokines are elicited in patients and infected cells. Interestingly, SARS-CoV-2 ORF3a induces mitochondrial damage and Mito-ROS production to promote HIF-1α expression, which subsequently facilitates SARS-CoV-2 infection and cytokines production. Notably, HIF-1α also broadly promotes the infection of other viruses. Collectively, during SARS-CoV-2 infection, ORF3a induces HIF-1α, which in turn aggravates viral infection and inflammatory responses. Therefore, HIF-1α plays an important role in promoting SARS-CoV-2 infection and inducing pro-inflammatory responses to COVID-19.


Assuntos
COVID-19/metabolismo , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Mitocôndrias/metabolismo , SARS-CoV-2/metabolismo , Transdução de Sinais , Proteínas Viroporinas/metabolismo , Células A549 , Animais , Chlorocebus aethiops , Células HEK293 , Células HeLa , Humanos , Mitocôndrias/patologia , RNA-Seq , Células THP-1 , Células Vero
5.
Nat Commun ; 12(1): 4664, 2021 08 02.
Artigo em Inglês | MEDLINE | ID: mdl-34341353

RESUMO

Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1ß and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses.


Assuntos
COVID-19/metabolismo , Proteínas do Nucleocapsídeo de Coronavírus/metabolismo , Inflamassomos/metabolismo , Inflamação/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , SARS-CoV-2/metabolismo , Animais , COVID-19/virologia , Células Cultivadas , Citocinas/metabolismo , Células HEK293 , Humanos , Inflamassomos/genética , Lesão Pulmonar/genética , Lesão Pulmonar/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Fosfoproteínas/metabolismo , Ligação Proteica , SARS-CoV-2/fisiologia , Células THP-1
6.
Nat Commun ; 12(1): 4667, 2021 08 03.
Artigo em Inglês | MEDLINE | ID: mdl-34344898

RESUMO

Urbanization and climate change are together exacerbating water scarcity-where water demand exceeds availability-for the world's cities. We quantify global urban water scarcity in 2016 and 2050 under four socioeconomic and climate change scenarios, and explored potential solutions. Here we show the global urban population facing water scarcity is projected to increase from 933 million (one third of global urban population) in 2016 to 1.693-2.373 billion people (one third to nearly half of global urban population) in 2050, with India projected to be most severely affected in terms of growth in water-scarce urban population (increase of 153-422 million people). The number of large cities exposed to water scarcity is projected to increase from 193 to 193-284, including 10-20 megacities. More than two thirds of water-scarce cities can relieve water scarcity by infrastructure investment, but the potentially significant environmental trade-offs associated with large-scale water scarcity solutions must be guarded against.

7.
Nat Commun ; 12(1): 5026, 2021 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-34408158

RESUMO

Nationwide prospective surveillance of all-age patients with acute respiratory infections was conducted in China between 2009‒2019. Here we report the etiological and epidemiological features of the 231,107 eligible patients enrolled in this analysis. Children <5 years old and school-age children have the highest viral positivity rate (46.9%) and bacterial positivity rate (30.9%). Influenza virus, respiratory syncytial virus and human rhinovirus are the three leading viral pathogens with proportions of 28.5%, 16.8% and 16.7%, and Streptococcus pneumoniae, Mycoplasma pneumoniae and Klebsiella pneumoniae are the three leading bacterial pathogens (29.9%, 18.6% and 15.8%). Negative interactions between viruses and positive interactions between viral and bacterial pathogens are common. A Join-Point analysis reveals the age-specific positivity rate and how this varied for individual pathogens. These data indicate that differential priorities for diagnosis, prevention and control should be highlighted in terms of acute respiratory tract infection patients' demography, geographic locations and season of illness in China.


Assuntos
Bactérias/isolamento & purificação , Infecções Bacterianas/microbiologia , Infecções Respiratórias/microbiologia , Infecções Respiratórias/virologia , Viroses/virologia , Vírus/isolamento & purificação , Adolescente , Adulto , Bactérias/classificação , Bactérias/genética , Infecções Bacterianas/epidemiologia , Criança , Pré-Escolar , China/epidemiologia , Feminino , Humanos , Lactente , Masculino , Estudos Prospectivos , Infecções Respiratórias/epidemiologia , Estações do Ano , Viroses/epidemiologia , Vírus/classificação , Vírus/genética , Adulto Jovem
8.
FEBS Lett ; 595(19): 2463-2478, 2021 10.
Artigo em Inglês | MEDLINE | ID: mdl-34407203

RESUMO

The activation of the NLRP3 inflammasome plays a crucial role in the innate immune response. During cell division, NLRP3 inflammasome activation must be strictly controlled. In this study, we discover that the anaphase-promoting complex subunit 10 (APC10), a substrate recognition protein of the anaphase-promoting complex/cyclosome (APC/C), is a critical mediator of NLRP3 inflammasome activation. During interphase, APC10 interacts with NLRP3 to promote NLRP3 inflammasome activation, whereas during mitosis, APC10 disassociates from the NLRP3 inflammasome to repress inflammatory responses. This study reveals a distinct mechanism by which APC10 serves as a switch for NLRP3 inflammasome activation during the cell cycle.

9.
PLoS Pathog ; 17(7): e1008603, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-34310658

RESUMO

Dengue virus (DENV) is a mosquito-borne pathogen that causes a spectrum of diseases including life-threatening dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Vascular leakage is a common clinical crisis in DHF/DSS patients and highly associated with increased endothelial permeability. The presence of vascular leakage causes hypotension, circulatory failure, and disseminated intravascular coagulation as the disease progresses of DHF/DSS patients, which can lead to the death of patients. However, the mechanisms by which DENV infection caused the vascular leakage are not fully understood. This study reveals a distinct mechanism by which DENV induces endothelial permeability and vascular leakage in human endothelial cells and mice tissues. We initially show that DENV2 promotes the matrix metalloproteinase-9 (MMP-9) expression and secretion in DHF patients' sera, peripheral blood mononuclear cells (PBMCs), and macrophages. This study further reveals that DENV non-structural protein 1 (NS1) induces MMP-9 expression through activating the nuclear factor κB (NF-κB) signaling pathway. Additionally, NS1 facilitates the MMP-9 enzymatic activity, which alters the adhesion and tight junction and vascular leakage in human endothelial cells and mouse tissues. Moreover, NS1 recruits MMP-9 to interact with ß-catenin and Zona occludens protein-1/2 (ZO-1 and ZO-2) and to degrade the important adhesion and tight junction proteins, thereby inducing endothelial hyperpermeability and vascular leakage in human endothelial cells and mouse tissues. Thus, we reveal that DENV NS1 and MMP-9 cooperatively induce vascular leakage by impairing endothelial cell adhesion and tight junction, and suggest that MMP-9 may serve as a potential target for the treatment of hypovolemia in DSS/DHF patients.

10.
Virulence ; 12(1): 1795-1807, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34282707

RESUMO

Zika virus (ZIKV) infection can cause severe neurological disorders, including Guillain-Barre syndrome and meningoencephalitis in adults and microcephaly in fetuses. Here, we reveal that laminin receptor 1 (LAMR1) is a novel host resistance factor against ZIKV infection. Mechanistically, we found that LAMR1 binds to ZIKV envelope (E) protein via its intracellular region and attenuates E protein ubiquitination through recruiting the deubiquitinase eukaryotic translation initiation factor 3 subunit 5 (EIF3S5). We further found that the conserved G282 residue of E protein is essential for its interaction with LAMR1. Moreover, a G282A substitution abolished the binding of E protein to LAMR1 and inhibited LAMR1-mediated E protein deubiquitination. Together, our results indicated that LAMR1 represses ZIKV infection through binding to E protein and attenuating its ubiquitination.

11.
ACS Sens ; 6(7): 2593-2604, 2021 07 23.
Artigo em Inglês | MEDLINE | ID: mdl-34253023

RESUMO

Among basic taste sensations, bitter taste is vital to the survival of mammals due to its indispensable role in toxin prediction or identification, so the identification of bitter compounds is of great value in the pharmaceutical and food industry. Recently, bitter taste receptor (T2Rs)-based biosensors have been developed for specific bitter detection. However, the taste biosensors based on taste cells/tissues suffer from simple function, low sensitivity, low content, and limited parameters. Here, to establish a high-content, highly sensitive, and multifunctional taste biosensor, we developed a multifunctional hybrid integrated cardiomyocyte biosensor (HICB) for bitter detection. Due to the expression of bitter taste receptors in cardiomyocytes, the HICB can recognize the specific bitter agonists by synchronously recording the extracellular field potential (EFP) and mechanical beating (MB) signals from the cultured cardiomyocytes in vitro. Multiple feature parameters were defined and extracted from the electromechanical signals of cardiomyocytes to analyze the specific responses to four typical bitter compounds. The radar map, heat map, and principal component analysis (PCA) were used to visualize and classify the specific responses. Moreover, bitter-induced cardiotoxicity also was chronically evaluated, and these bitter compounds presented an inhibition effect on the electrophysiological and contractile activities of cardiomyocytes. This high-content HICB offers an alternative platform for both bitter detection and cardiotoxicity assessment, showing promising applications in the fields of taste detection and toxicity screening.


Assuntos
Técnicas Biossensoriais , Paladar , Animais , Cardiotoxicidade , Miócitos Cardíacos , Receptores Acoplados a Proteínas G
12.
Transl Oncol ; 14(10): 101168, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34252743

RESUMO

Genomic aberrations (GAs) in fibroblast growth factor receptors (FGFRs) are involved in the pathogenesis of intrahepatic cholangiocarcinoma (ICC), and clinical trials have shown efficacy of FGFR inhibitors in treating ICC patients with FGFR GAs such as FGFR2 rearrangement. To clarify the FGFRs GA profile and corresponding clinicopathological features in Chinese patients with ICC, a total of 257 cases were identified. Fourteen cases (5.45%) were positive for FGFR2 rearrangement. Further analysis on the 110 FGFR2 rearrangement negative cases showed that 13 patients present additional FGFRs GAs, including FGFR3 rearrangement (2.73%), and FGFRs mutations. When compared with patients without FGFRs GAs, those with FGFR2 or FGFR3 rearrangement presented more under the age of 58 years, female sex, HBsAb positivity, CD10 expression, and PD-L1 expression. The clinical characteristics between patients with FGFRs mutation and those without FGFRs GAs were similar, with the exception that cases with FGFRs mutation have more hepatolithiasis. We concluded that FGFR rearrangement is associated with unique clinical phenotypes in ICC.

13.
Virol Sin ; 2021 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-34224109

RESUMO

Human adenovirus type 55 (HAdV-B55) is a re-emergent acute respiratory disease pathogen that causes adult community-acquired pneumonia (CAP). Previous studies have shown that the receptor of HAdV-B14, which genome is highly similar with HAdV-B55, is human Desmoglein 2 (DSG2). However, whether the receptor of HAdV-B55 is DSG2 is undetermined because there are three amino acid mutations in the fiber gene between HAdV-B14 and HAdV-B55. Here, firstly we found the 3T3 cells, a mouse embryo fibroblast rodent cell line which does not express human DSG2, were able to be infected by HAdV-B55 after transfected with pcDNA3.1-DSG2, while normal 3T3 cells were still unsusceptible to HAdV-B55 infection. Next, A549 cells with hDSG2 knock-down by siRNA were hard to be infected by HAdV-B3/-B14/-B55, while the control siRNA group was still able to be infected by all these types of HAdVs. Finally, immunofluorescence confocal microscopy indicated visually that Cy3-conjugated HAdV-B55 viruses entered A549 cells by binding to DSG2 protein. Therefore, DSG2 is a major receptor of HAdV-B55 causing adult CAP. Our finding is important for better understanding of interactions between adenoviruses and host cells and may shed light on the development of new drugs that can interfere with these processes as well as for the development of potent prophylactic vaccines.

14.
J Virol ; 95(16): e0061721, 2021 07 26.
Artigo em Inglês | MEDLINE | ID: mdl-34105996

RESUMO

The current pandemic of COVID-19 is caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The SARS-CoV-2 spike protein receptor-binding domain (RBD) is the critical determinant of viral tropism and infectivity. To investigate whether naturally occurring RBD mutations during the early transmission phase have altered the receptor binding affinity and infectivity, we first analyzed in silico the binding dynamics between SARS-CoV-2 RBD mutants and the human angiotensin-converting enzyme 2 (ACE2) receptor. Among 32,123 genomes of SARS-CoV-2 isolates (December 2019 through March 2020), 302 nonsynonymous RBD mutants were identified and clustered into 96 mutant types. The six dominant mutations were analyzed applying molecular dynamics simulations (MDS). The mutant type V367F continuously circulating worldwide displayed higher binding affinity to human ACE2 due to the enhanced structural stabilization of the RBD beta-sheet scaffold. The MDS also indicated that it would be difficult for bat SARS-like CoV to infect humans. However, the pangolin CoV is potentially infectious to humans. The increased infectivity of V367 mutants was further validated by performing receptor-ligand binding enzyme-linked immunosorbent assay (ELISA), surface plasmon resonance, and pseudotyped virus assays. Phylogenetic analysis of the genomes of V367F mutants showed that during the early transmission phase, most V367F mutants clustered more closely with the SARS-CoV-2 prototype strain than the dual-mutation variants (V367F+D614G), which may derivate from recombination. The analysis of critical RBD mutations provides further insights into the evolutionary trajectory of early SARS-CoV-2 variants of zoonotic origin under negative selection pressure and supports the continuing surveillance of spike mutations to aid in the development of new COVID-19 drugs and vaccines. IMPORTANCE A novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused the pandemic of COVID-19. The origin of SARS-CoV-2 was associated with zoonotic infections. The spike protein receptor-binding domain (RBD) is identified as the critical determinant of viral tropism and infectivity. Thus, whether mutations in the RBD of the circulating SARS-CoV-2 isolates have altered the receptor binding affinity and made them more infectious has been the research hot spot. Given that SARS-CoV-2 is a novel coronavirus, the significance of our research is in identifying and validating the RBD mutant types emerging during the early transmission phase and increasing human angiotensin-converting enzyme 2 (ACE2) receptor binding affinity and infectivity. Our study provides insights into the evolutionary trajectory of early SARS-CoV-2 variants of zoonotic origin. The continuing surveillance of RBD mutations with increased human ACE2 affinity in human or other animals is critical to the development of new COVID-19 drugs and vaccines against these variants during the sustained COVID-19 pandemic.


Assuntos
Substituição de Aminoácidos , Enzima de Conversão de Angiotensina 2/genética , COVID-19/transmissão , Mutação , SARS-CoV-2/genética , Glicoproteína da Espícula de Coronavírus/genética , Enzima de Conversão de Angiotensina 2/química , Enzima de Conversão de Angiotensina 2/metabolismo , Sítios de Ligação , COVID-19/patologia , COVID-19/virologia , Expressão Gênica , Interações Hospedeiro-Patógeno/genética , Humanos , Cinética , Simulação de Dinâmica Molecular , Fenilalanina/química , Fenilalanina/metabolismo , Filogenia , Ligação Proteica , Conformação Proteica em alfa-Hélice , Conformação Proteica em Folha beta , Domínios e Motivos de Interação entre Proteínas , SARS-CoV-2/classificação , SARS-CoV-2/metabolismo , SARS-CoV-2/patogenicidade , Glicoproteína da Espícula de Coronavírus/química , Glicoproteína da Espícula de Coronavírus/metabolismo , Termodinâmica , Valina/química , Valina/metabolismo , Virulência , Ligação Viral
15.
Clin Lab ; 67(6)2021 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-34107622

RESUMO

BACKGROUND: Pancreatic cancer (PC) is one of the most lethal malignant tumors with no valid biomarkers for early diagnosis. We evaluated the value of PD-1, PD-L1, PD-L2, CD28, B7-1, and B7-H5 for diagnosing PC. METHODS: We measured serum soluble PD-1, PD-L1, PD-L2, CD28, B7-1, and B7-H5, and serum carbohydrate antigen (CA)19-9 levels in 87 patients with PC, 27 patients with benign pancreatic disease, and 20 healthy volunteers. We evaluated the diagnostic value of CA19-9, PD-1, PD-L1, PD-L2, CD28, B7-1, B7-H5. RESULTS: Patients with PC had significantly higher serum CA19-9, PD-L1, PD-L2, and B7-H5. Combined detection (CA19-9 + PD-L1 + PD-L2 + B7-H5) had much higher sensitivity than single CA19-9 detection. CONCLUSIONS: Serum soluble PD-L1, PD-L2, and B7-H5 might be novel potential biomarkers for diagnosing PC; their combination with serum CA19-9 might improve diagnostic sensitivity and specificity.


Assuntos
Antígeno B7-H1 , Neoplasias Pancreáticas , Biomarcadores Tumorais , Antígeno CA-19-9 , Humanos , Neoplasias Pancreáticas/diagnóstico , Prognóstico , Sensibilidade e Especificidade
16.
Hepatol Commun ; 5(5): 830-845, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-34027272

RESUMO

We aimed to identify a microRNA (miRNA)-E3 ubiquitin ligase regulatory network for protein substrates enriched in cell death pathways and investigate the underlying molecular mechanisms in alcohol-associated hepatitis (AH). An miRNA-E3 ubiquitin ligase regulatory network for protein substrates enriched in cell death pathways was constructed using integrated bioinformatics analysis. Differentially expressed hub miRNAs (GSE59492) and their validated miRNA target genes (GSE28619) were identified in the liver of patients with AH compared with healthy controls. Liver samples from patients with AH and healthy individuals and mice exposed to Gao-binge (acute on chronic) ethanol were used for experimental validation. Using hub miRNAs identified by weighted correlation network analysis, a miRNA-E3 ubiquitin ligase regulatory network was established based on 17 miRNAs and 7 E3 ligase genes targeted by these miRNAs that were down-regulated in AH. Among the miRNAs in this regulatory network, miR-150-5p was the only miRNA regulating the E3 ligase cytokine-inducible SH2 containing protein (CISH), the E3 ligase that regulates the largest number of substrates among all E3 ligase family members. Therefore, the CISH regulatory pathway for ubiquitinated substrates was selected for subsequent experimental validation. Consistent with the bioinformatics analysis results, expression of miR-150-5p was markedly increased, while CISH was decreased, in the livers of patients with AH and mice exposed to Gao-binge ethanol. Moreover, ubiquitination of Fas-associated protein with death domain, a predicted CISH substrate involved in the regulation of programmed cell death, was reduced in livers from mice after Gao-binge ethanol. Conclusion: Identification of the miRNA-E3 ubiquitin ligase regulatory network for protein substrates enriched in the cell death pathways provides insights into the molecular mechanisms contributing to hepatocyte death in AH.

17.
Environ Sci Pollut Res Int ; 28(37): 51511-51529, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-33982261

RESUMO

Revealing the hazard features of forfeiting areal ranges for nonidentical scenarios of shifting climatic conditions is pivotal for the conformation of reptiles to climatic warming. Taking 115 reptiles in China as an example, the indefiniteness and danger of shrinking geographical range for the reptiles under stochastic and nonrandom scenarios of moving climatic situations were inspected via exploiting the scenarios of shifting climatic status associated with the representative concentration pathways, Monte Carlo simulation, and the classifications scheme based on the fuzzy set. For non-stochastic states of altering climatic elements, the richness of 115 reptiles improved in certain sites of northeastern, and western China and dropped in several areas of northern, eastern, central China, and southeastern China: roughly 59-74 reptiles forfeiting less than 20% of their present ranges, roughly 25-34 reptiles narrowing less than 20-40% of their present areal ranges, and roughly 105-111 reptiles inhabited more than 80% of their overall areal ranges. For the random status of shifting climatic elements, the count of reptiles that forfeited the various extent of the present or entire areal ranges descended with raising the eventuality; with a possibility of over 0.6, the count of reptiles that minified less than 20%, 20-40%, 40-60%, 60-80% and over 80% of the present ranges was roughly 28-49, 5-10, 1-3, 0-1 and 13-18, separately; the count of reptiles that inhabited below 20%, 20-40%, 40-60%, 60-80% and more than 80% of the entire real ranges was roughly 0-1, 5-6, 1-5, 0-2 and 35-36, separately. About 30% of 115 reptiles would face disappearance danger in response to moving climate conditions in the absence of adaption steps, and the conformation measures were indispensable for the reptiles that shrunk their areas.


Assuntos
Mudança Climática , Répteis , Animais , China
18.
Environ Sci Technol ; 55(12): 7808-7817, 2021 06 15.
Artigo em Inglês | MEDLINE | ID: mdl-33904720

RESUMO

Rising CO2 concentration and temperatures in urban areas are now well-known, but the potential of an emerging oxygen crisis in the world's large cities has so far attracted little attention from the science community. Here, we investigated the oxygen balance and its related risks in 391 global large cities (with a population of more than 1 million people) using the oxygen index (OI), which is the ratio of oxygen consumption to oxygen production. Our results show that the global urban areas, occupying only 3.8% of the global land surface, accounted for 39% (14.3 ± 1.5 Gt/yr) of the global terrestrial oxygen consumption during 2001-2015. We estimated that 75% of cities with a population more than 5 million had an OI of greater than 100. Also, cities with larger OI values were correlated with more frequent heatwaves and severe water withdrawals. In addition, cities with excessively large OI values would likely experience severe hypoxia in extremely calm weather. Thus, mitigation measures should be adopted to reduce the urban OI in order to build healthier and more sustainable cities.


Assuntos
Oxigênio , Tempo (Meteorologia) , Cidades , Humanos , Risco
19.
PLoS Negl Trop Dis ; 15(4): e0009362, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33891593

RESUMO

Zika virus (ZIKV) is a kind of flavivirus emerged in French Polynesia and Brazil, and has led to a worldwide public health concern since 2016. ZIKV infection causes various neurological conditions, which are associated with fetus brain development or peripheral and central nervous systems (PNS/CNS) functional problems. To date, no vaccine or any specific antiviral therapy against ZIKV infection are available. It urgently needs efforts to explore the underlying molecular mechanisms of ZIKV-induced neural pathogenesis. ZIKV favorably infects neural and glial cells specifically astrocytes, consequently dysregulating gene expression and pathways with impairment of process neural cells. In this study, we applied a model for ZIKV replication in mouse primary astrocytes (MPAs) and profiled temporal alterations in the host transcriptomes upon ZIKV infection. Among the RNA-sequencing data of 27,812 genes, we examined 710 genes were significantly differentially expressed by ZIKV, which lead to dysregulation of numerous functions including neurons development and migration, glial cells differentiation, myelinations, astrocytes projection, neurogenesis, and brain development, along with multiple pathways including Hippo signaling pathway, tight junction, PI3K-Akt signaling pathway, and focal adhesion. Furthermore, we confirmed the dysregulation of the selected genes in MPAs and human astroglioma U251 cells. We found that PTBP1, LIF, GHR, and PTBP3 were upregulated while EDNRB and MBP were downregulated upon ZIKV infection. The current study highlights the ZIKV-mediated potential genes associated with neurodevelopment or related diseases.


Assuntos
Astrócitos/metabolismo , Astrócitos/virologia , Encéfalo/patologia , Neurogênese/genética , Zika virus/patogenicidade , Animais , Astrócitos/patologia , Linhagem Celular , Expressão Gênica , Humanos , Camundongos , Camundongos Endogâmicos C57BL , Fosfatidilinositol 3-Quinases/metabolismo , Análise de Sequência de RNA , Transdução de Sinais , Transcriptoma , Regulação para Cima , Replicação Viral , Zika virus/fisiologia
20.
J Orthop Surg Res ; 16(1): 260, 2021 Apr 14.
Artigo em Inglês | MEDLINE | ID: mdl-33853620

RESUMO

OBJECTIVE: This study was aimed to utilize a modified anterior drawer test (MADT) to detect the anterior cruciate ligament (ACL) ruptures and investigate its accuracy compares with three traditional tests. METHODS: Four hundred patients were prospectively enrolled between January 2015 and September 2017 preoperatively to undergo knee arthroscopic surgeries. The MADT, anterior drawer test, Lachman test, and pivot shift test were used in the outpatient clinical setting and were compared statistically for their accuracy in terms of ACL ruptures, with arthroscopic findings as the gold standard. RESULTS: The prevalence of ACL ruptures in this study was 37.0%. The MADT demonstrated the highest sensitivity (0.89) and accuracy (0.92) among the four tests and had comparable specificity (0.94) and a positive predictive value (0.90) compared with the anterior drawer test, Lachman test, and pivot shift test. The diagnostic odds ratio (DOR) of MADT was 122.92, with other test values of no more than 55.45. The area under the receiver operating characteristic curve (AUC) for the MADT was 0.92 ± 0.01, with a significant difference compared with that for the anterior drawer test (z = 17.00, p < 0.001), Lachman test (z = 9.66, p = 0.002), and pivot shift test (z = 16.39, p < 0.001). The interobserver reproducibility of the MADT was good, with a kappa coefficient of 0.86. When diagnosing partial tears of ACL, the MADT was significantly more sensitive than the anterior drawer test (p < 0.001), Lachman test (p = 0.026), and pivot shift test (p = 0.013). The MADT showed similar sensitivity in detecting anteromedial and posterolateral bundle tears (p = 0.113) and no difference in diagnosing acute and chronic ACL ruptures (χ2 = 1.682, p = 0.195). CONCLUSIONS: The MADT is also an alternative diagnostic test to detect ACL tear, which is equally superior to the anterior drawer test, Lachman test, and pivot shifting test. It could improve the diagnosis of ACL ruptures combined with other clinical information including injury history, clinical examination, and radiological findings. LEVELS OF EVIDENCE: Level II/observational diagnostic studies TRIAL REGISTRATION: Chinese Clinical Trial Registry. ChiCTR1900022945 /retrospectively registered.


Assuntos
Lesões do Ligamento Cruzado Anterior/diagnóstico , Técnicas e Procedimentos Diagnósticos , Ortopedia/métodos , Exame Físico/métodos , Ruptura/diagnóstico , Adulto , Feminino , Humanos , Masculino , Adulto Jovem
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