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1.
Leuk Res ; 110: 106664, 2021 Jul 07.
Artigo em Inglês | MEDLINE | ID: mdl-34271293

RESUMO

The prognostic nutritional index (PNI), an indicator of nutritional status and systemic inflammation, is associated with survival in several types of lymphoma. The purpose of this study was to investigate the prognostic value of PNI in diffuse large B cell lymphoma (DLBCL). With three hundred and ten patients were enrolled, the median level of PNI was 45.90 (range 25.30-139.70). According to the receiver operating characteristic (ROC) curve, 44.85 was determined to be the best cutoff value to divide patients into two different groups. With a median follow-up of 33.3 months (range 3.5-118.5), compared with the high PNI group, the 3-year and adjusted 3-year progression-free survival (PFS) and overall survival (OS) were worse in the low PNI group (all P < 0.050). Multivariate Cox analysis suggested that low PNI was an independent risk factor for PFS (hazard ratio (HR) 2.196, 95 % CI 1.197-4.030, P = 0.011) and showed a tendency to predict inferior OS (HR 1.918, 95 % CI 0.932-3.948, P = 0.077). Furthermore, PNI combined with other significant prognostic factors to build a novel prognostic index, namely NPI, was more accurate than the National Comprehensive Cancer Network international prognostic index (NCCN-IPI) to predict worse PFS and had a similar effect on predicting OS. All these findings suggested that PNI, as a novel available biomarker, was of prognostic significance in DLBCL patients.

2.
Materials (Basel) ; 14(13)2021 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-34279295

RESUMO

Shotcrete is the primary material for tunnel support due to its early rapid hardening characteristics. During tunnel construction in a sulfate environment, the hardening law of concrete will be affected. In this study, samples were prepared at six different curing times and immersed in four different concentrations of sulfate solutions. A uniaxial test was conducted and analyzed to investigate the effect of sulfate attack on the mechanical properties of early aged shotcrete materials. Results indicated that waterlogged shotcrete does not have apparent cracks on the outside. The stress-strain curve or ultimate compressive strength of the samples showed that the effect of sulfate on shotcrete should be differentiated into chemical and physical sulfate attacks, according to the concentration of sulfate ions. The two parameters in the equation of the hardening behaviors of sulfate attack samples, ultimate compressive strength, and time constant, are related to sulfate concentration. The crack damage stress threshold of samples demonstrates that high-concentration sulfate corrosion leads to an impact on the durability of shotcrete.

3.
Artigo em Inglês | MEDLINE | ID: mdl-34279752

RESUMO

OBJECTIVES: We sought to distinguish area at risk from salvage myocardial zone and to predict left ventricle functional recovery in the convalescent stage by Texture Analysis (TA) of T2-Mapping. METHODS: One hundred and six patients diagnosed with AMI and treated with percutaneous coronary intervention (PCI) underwent acute cardiac magnetic resonance imaging (CMR) and 45 of whom had a subsequent CMR scan following recovery. Cine imaging, T2-Mapping, T2-weighted STIR imaging, and LGE imaging were performed. In the texture analysis, regions of interest (infarcted, salvageable, and remote) were drawn by two blinded, independent readers. RESULTS: Seven independent texture features on T2-Mapping were selected: Perc.50%, S(2,2)InvDfMom, S(2.-2)AngScMom, S(4,0)Entropy, 45dgrLngREmph, 45dgr_Fraction and 135dr_GLevNonU. Among them, the average value of 135dr_GLevNonU in the infarct zone, AAR zone, and the remote zone was: 61.96±26.03, 31.811±18.933 and 99.839±26.231, respectively. Additionally, 135dr_GLevNonU provided the highest area under the curve (AUC) from the receiver operating characteristic curve (ROC curve) for distinguishing AAR from the infarct zone in each subgroup (all patients, patients with MVO and)were 0.845 ± 0.052 0.855 ± 0.083 and 0.845 ± 0.066, respectively, and were more promise than T2-Mapping mean (p<0.001). The AUC for differentiating AAR from the remote zone is 0.942±0.041. Texture features are not associated with convalescent decreased strain, ejection fraction (EF) or left ventricle remodeling (LVR) in analysis (p>0.05). CONCLUSION: TA of T2-mapping can distinguish AAR from both the infarct zone and the remote myocardial zone without LGE imaging in reperfused AMI. However, these features are not able to predict patients' functional recovery in the convalescent stage.

4.
BMJ Open ; 11(6): e044322, 2021 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-34193481

RESUMO

OBJECTIVES: To determine the incidence and intensity of household impoverishment induced by cancer treatment in China. DESIGN: Average income and daily consumption per capita of the households and out-of-pocket payments for cancer care were estimated. Household impoverishment was determined by comparing per capita daily consumption against the Chinese poverty line (CPL, US$1.2) and the World Bank poverty line (WBPL, US$1.9) for 2015. Both pre-treatment and post-treatment consumptions were calculated assuming that the households would divert daily consumption money to pay for cancer treatment. PARTICIPANTS: Cancer patients diagnosed initially from 1 January 2015 to 31 December 2016 who had received cancer treatment subsequently. Those with multiple cancer diagnoses were excluded. DATA SOURCES: A household questionnaire survey was conducted on 2534 cancer patients selected from nine hospitals in seven provinces through two-stage cluster/convenience sampling. FINDINGS: 5.89% (CPL) to 12.94% (WBPL) households were impoverished after paying for cancer treatment. The adjusted OR (AOR) of post-treatment impoverishment was higher for older patients (AOR=2.666-4.187 for ≥50 years vs <50 years, p<0.001), those resided in central region (AOR=2.619 vs eastern, p<0.01) and those with lower income (AOR=0.024-0.187 in higher income households vs the lowest 20%, p<0.001). The patients without coverage from social health insurance had higher OR (AOR=1.880, p=0.040) of experiencing post-treatment household impoverishment than those enrolled with the insurance for urban employees. Cancer treatment is associated with an increase of 5.79% (CPL) and 12.45% (WBPL) in incidence of household impoverishment. The median annual consumption gap per capita underneath the poverty line accumulated by the impoverished households reached US$128 (CPL) or US$212 (WBPL). US$31 170 395 (CPL) or US$115 238 459 (WBPL) were needed to avoid household impoverishment induced by cancer treatment in China. CONCLUSIONS: The financial burden of cancer treatment imposes a significant risk of household impoverishment despite wide coverage of social health insurance in China.

5.
Artigo em Inglês | MEDLINE | ID: mdl-34197932

RESUMO

OBJECTIVES: China banned the use of colistin as animal growth promoter in April 2017. Herein, we report the prevalence of mcr-1 in the intestine of healthy humans and risk factors associated with mcr-1 carriage after the implementation of the ban. METHODS: We recruited 719 healthy volunteers from Shenzhen City from 1 March 2018 to 31 December 2019 to investigate the prevalence of mcr-1 in human intestine, and undertook a case-control study to ascertain the risk factors associated with the mcr-1-positive population. A further comparative study was conducted to identify differences between genetic characteristics of mcr-1-positive and mcr-1-negative Escherichia coli. RESULTS: Overall, 56 (7.8%, 95% CI 5.9%-10.0%, n = 719) individual faecal samples were positive for mcr-1, and prevalence of mcr-1 among individuals in 2019 (2.4%, 95% CI 8.7%-15.0%, 7/294) was significantly lower than that in 2018 (11.5%, 95% CI 1.0%-4.8%, 49/425) (p < 0.0001). After the colistin ban, animal-derived food (pork and chicken meat) was no longer a risk factor for mcr-1 carriage in human intestine, whereas a higher intake of fish and seafood (>75 g/day) and whole grains (>150 g/day) was associated with higher and lower risk of mcr-1 carriage, respectively (OR 2.175, 95% CI 1.047-4.517; OR 0.045, 95% CI 0.004-0.567). Compared with mcr-1-negative E. coli, the mcr-1-positive E. coli had different patterns of resistance genes and genetic heterogeneity. CONCLUSIONS: Our study implicates aquatic food as beeing associated with mcr-1 carriage in the healthy population, even after the ban on colistin. Dietary modification (e.g. whole grains) may help to combat mcr-1-positive bacterial colonization of the gut.

6.
Mol Oncol ; 2021 Jul 04.
Artigo em Inglês | MEDLINE | ID: mdl-34218518

RESUMO

Cancer-associated fibroblasts (CAFs) are a heterogenous cell population within the tumor microenvironment, and play an important role in tumor development. By regulating the heterogeneity of CAFs, transforming growth factor ß (TGFß) influences tumor development. Here, we explored oncogenes regulated by TGFß1 that are also involved in signaling pathways and interactions within the tumor microenvironment. We analyzed sequencing data of The Cancer Genome Atlas (TCGA) and our own previously established RNA microarray data (GSE53625), as well as esophageal squamous cell carcinoma (ESCC) cell lines with or without TGFß1 stimulation. We then focused on laminin subunit gamma 1 (LAMC1), which was overexpressed in ESCC cells, affecting patient prognosis, and could be upregulated by TGFß1 through the synergistic activation of SMAD family member 4 (SMAD4) and SP1. LAMC1 directly promoted the proliferation and migration of tumor cells, mainly via Akt-NFκB-MMP9/14 signaling. Additionally, LAMC1 promoted CXCL1 secretion, which stimulated the formation of inflammatory CAFs (iCAFs) through CXCR2-pSTAT3. Inflammatory CAFs promoted tumor progression. In summary, we identified the dual mechanism by which the upregulation of LAMC1 by TGFß in tumor cells not only promotes ESCC proliferation and migration, but also indirectly induces carcinogenesis by stimulating CXCL1 secretion to promote the formation of iCAFs. This finding suggests that LAMC1 could be a potential therapeutic target and prognostic marker for ESCC.

7.
Cancer Med ; 2021 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-34213079

RESUMO

BACKGROUND: Long non-coding RNA (lncRNA) HULC (highly upregulated in liver cancer) is considered as an oncogenic factor for various malignant tumors. This study aimed to reveal the role of lncRNA HULC in the malignant behavior of glioblastoma (GBM) by exploring its effects on the epithelial-mesenchymal transition (EMT) and vasculogenic mimicry (VM) of human GBM. MATERIALS AND METHODS: The contents of VM in 27 GBM samples were assessed by immunohistochemistry-histology and their association with progress-free survival (PFS) was analyzed. Human GBM SHG44 and U87 cells were manipulated to establish stable lncRNA HULC overexpressing and silencing cells by lentivirus-based technology. The effects of altered lncRNA HULC on vasculogenic tubular formation, invasion, and EMT process in GBM cells were tested in vitro and the growth of implanted GBM tumors and their EMT process were examined in vivo. RESULTS: The numbers of VM were positively associated with disease progression, but negatively with PFS periods of GBM patients. Compared with the control vec cells, lncRNA HULC overexpression significantly increased the tubular formation, invasion, and EMT process of both SHG44 and U87 cells, accompanied by promoting the growth of implanted GBM tumors and EMT process in mice. LncRNA HULC silencing had opposite effects on the tubular formation, invasion, and EMT process as well as tumor growth of GBM cells. CONCLUSION: LncRNA HULC stimulates the EMT process and VM in human GBM, and may be a therapeutic target for intervention of GBM.

8.
Ying Yong Sheng Tai Xue Bao ; 32(6): 2249-2258, 2021 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-34212631

RESUMO

Soil heterogeneity is at a high level in the karst areas, which resulted from the complex habitat. On the one hand, plants have some adaptive strategies to such special habitats by forming certain morphological and physiological characteristics, which result in higher diversity of functional traits. One the other hand, plants improve the physical and chemical properties of soil through a series of life activities. The interactions between plants and soil drive ecosystem structure and function and its responses to global climate change. Here, we summarized the characteristics of soil hete-rogeneity in the karst areas, and reviewed the response of plant functional traits to soil and the feedback of plants to soil. It revealed the coupling mechanism between plants and soil in karst eco-system. We provided a future outlook, including future research contents and directions based on the current research status in this field, which aimed to provide theoretical reference for maintaining the structural and functional stability of fragile karst ecosystems.


Assuntos
Ecossistema , Solo , Plantas , Microbiologia do Solo
9.
Bioengineered ; 12(1): 3201-3218, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34224308

RESUMO

Preterm birth (PTB) is an immune-inflammatory disease that needs to be resolved. This study aimed to identify the role of interleukin-27 (IL-27), an immunomodulatory factor, in PTB and its associated mechanisms. Here, we analyzed the high-throughput of samples data from the maternal-fetal interface to the peripheral circulation obtained from public databases and reported that the elevated IL-27 was involved with the onset of PTB. Further bioinformatics analyses (e.g. GeneMANIA and GSEA) revealed that IL-27 overexpression in the peripheral circulation as well as maternal-fetal interface is related to the activation of the immune-inflammatory process represented by IFN-γ signaling, etc. In addition, IL-27 and immune infiltration correlation analysis demonstrated that IL-27 mediates this immune-inflammatory imbalance, plausibly mainly through monocyte-macrophage and neutrophils. This finding was further validated by analyzing additional datasets. Overall, this is the first study to elaborate on the role of IL-27-mediated immuno-inflammation in PTB from the perspective of bioinformatics, which may provide a novel strategy for the prevention and treatment of PTB.

10.
Nat Commun ; 12(1): 3785, 2021 06 18.
Artigo em Inglês | MEDLINE | ID: mdl-34145257

RESUMO

Primary small cell carcinoma of the esophagus (PSCCE) is a lethal neuroendocrine carcinoma. Previous studies proposed a genetic similarity between PSCCE and esophageal squamous cell carcinoma (ESCC) but provided little evidence for differences in clinical course and neuroendocrine differentiation. We perform whole-exome sequencing, RNA sequencing and immunohistochemistry profiling on 46 PSCCE cases. Integrated analyses enable the discovery of multiple mechanisms of RB1 disruption in 98% (45/46) of cases. The transcriptomic landscape of PSCCE closely resembles small cell lung cancer (SCLC) but differs from ESCC or esophageal adenocarcinoma (EAC). Distinct gene expression patterns regulated by ASCL1 and NEUROD1 define two molecular subtypes, PSCCE-A and PSCCE-N, which are highly similar to SCLC subtypes. A T cell excluded phenotype is widely observed in PSCCE. In conclusion, PSCCE has genomic alterations, transcriptome features and molecular subtyping highly similar to SCLC but distinct from ESCC or EAC. These observations are relevant to oncogenesis mechanisms and therapeutic vulnerability.


Assuntos
Adenocarcinoma/genética , Carcinoma de Células Pequenas/genética , Neoplasias Esofágicas/genética , Carcinoma de Células Escamosas do Esôfago/genética , Neoplasias Pulmonares/genética , Proteínas de Ligação a Retinoblastoma/genética , Carcinoma de Pequenas Células do Pulmão/genética , Ubiquitina-Proteína Ligases/genética , Adenocarcinoma/patologia , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Carcinoma de Células Pequenas/patologia , Neoplasias Esofágicas/patologia , Carcinoma de Células Escamosas do Esôfago/patologia , Esôfago/patologia , Perfilação da Expressão Gênica , Humanos , Neoplasias Pulmonares/patologia , Análise de Sequência de RNA , Carcinoma de Pequenas Células do Pulmão/patologia
11.
Cancer Med ; 10(13): 4575-4586, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-34076339

RESUMO

BACKGROUND: Cancer is a major concern for children and adolescents worldwide. This study aims to report on cancer incidence patterns at age 0-19 years in 2011-2015 and their trends in 2000-2015. METHODS: We collected data on malignancies in population of 0-19 years submitted by high-quality population-based cancer registries in China. Age-standardized rates by world standard population (WSR) and annual percent change (APC) were calculated. RESULTS: In total, 215 cancer registries from 30 provinces contributed datasets during 2011-2015. Twenty-two registries provided continuous data for trend analysis from 2000 to 2015. In total 16,954 malignancies occurred in 177,416,582 person-years. WSRs were 93.32 and 96.03 per million person-years in children aged 0-14 and 0-19 years. Incidence rates were higher in boys than in girls and were higher in urban area than in rural area. In children aged 0-14 years, the top three common diagnostic groups were leukemia, central nervous system (CNS) tumors, and lymphomas in both sexes. In adolescents aged 15-19 years, the top three common diagnostic groups were leukemia, epithelial tumors and melanoma, and CNS tumors in boys and epithelial tumors and melanoma, leukemia, and germ cell and gonadal tumors in girls. WSRs for cancers in 0-19 years of age increased significantly in boys from 2000 to 2005 (APC = 5.3%, 95% CI: 2.3%-8.3%) and in girls from 2000 to 2015 (APC = 1.2%, 95% CI: 0.1%-2.4%). CONCLUSIONS: Cancer incidence in children and adolescents is on the rise in China. The observed age, sex, and geographical variations in cancer incidence should be used to inform targeted prevention and control policies.

12.
Nat Commun ; 12(1): 3803, 2021 06 21.
Artigo em Inglês | MEDLINE | ID: mdl-34155197

RESUMO

The adenomatous polyposis coli (APC) is a frequently mutated tumour suppressor gene in cancers. However, whether APC is regulated at the epitranscriptomic level remains elusive. In this study, we analysed TCGA data and separated 200 paired oesophageal squamous cell carcinoma (ESCC) specimens and their adjacent normal tissues and demonstrated that methyltransferase-like 3 (METTL3) is highly expressed in tumour tissues. m6A-RNA immunoprecipitation sequencing revealed that METTL3 upregulates the m6A modification of APC, which recruits YTHDF for APC mRNA degradation. Reduced APC expression increases the expression of ß-catenin and ß-catenin-mediated cyclin D1, c-Myc, and PKM2 expression, thereby leading to enhanced aerobic glycolysis, ESCC cell proliferation, and tumour formation in mice. In addition, downregulated APC expression correlates with upregulated METTL3 expression in human ESCC specimens and poor prognosis in ESCC patients. Our findings reveal a mechanism by which the Wnt/ß-catenin pathway is upregulated in ESCC via METTL3/YTHDF-coupled epitranscriptomal downregulation of APC.


Assuntos
Adenosina/análogos & derivados , Proteínas do Citoesqueleto/genética , Metiltransferases/metabolismo , Proteínas de Ligação a RNA/metabolismo , Adenosina/metabolismo , Animais , Carcinogênese , Proliferação de Células , Proteínas do Citoesqueleto/metabolismo , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/metabolismo , Neoplasias Esofágicas/patologia , Carcinoma de Células Escamosas do Esôfago/genética , Carcinoma de Células Escamosas do Esôfago/metabolismo , Carcinoma de Células Escamosas do Esôfago/patologia , Regulação Neoplásica da Expressão Gênica , Humanos , Metiltransferases/genética , Camundongos , Prognóstico , RNA Mensageiro/metabolismo , Efeito Warburg em Oncologia , Via de Sinalização Wnt , beta Catenina/genética , beta Catenina/metabolismo
13.
JAMA Oncol ; 2021 Jun 24.
Artigo em Inglês | MEDLINE | ID: mdl-34165501

RESUMO

Importance: The role of postoperative radiotherapy (PORT) has not been well defined in resected pIIIA-N2 non-small cell lung cancer (NSCLC). Objective: To evaluate the effect of PORT using modern techniques on survival and safety in patients with pIIIA-N2 NSCLC after complete resection and adjuvant chemotherapy. Design, Setting, and Participants: The PORT-C randomized clinical trial was conducted in 394 patients with pIIIA-N2 NSCLC treated with complete resection and 4 cycles of platinum-based chemotherapy between January 2009 and December 2017. Data were analyzed between March 2019 and December 2020. Interventions: Patients were randomized equally into the PORT arm (n = 202) or the observation arm (n = 192). The total dose of PORT was 50 Gy. Main Outcomes and Measures: The primary end point was disease-free survival (DFS). Secondary end points included overall survival (OS), locoregional recurrence-free survival (LRFS), distant metastasis-free survival, and toxic effects. Results: In total, 394 patients were enrolled and 364 were eligible, with a median (range) age of 55 (25-70) years. There were 202 (55.5%) male and 162 (44.5%) female patients. The median follow-up was 46.0 (95% CI, 41.9-51.4) months, and 230 DFS events were reported. There were 184 patients in the PORT arm and 180 patients in the observation arm. The 3-year DFS rates were 40.5% with PORT vs 32.7% with observation (median, 22.1 vs 18.6 months), and the difference in DFS was not statistically significant without adjustment (hazard ratio [HR], 0.84; 95% CI, 0.65-1.09; P = .20), though it was significant with preplanned yet exploratory analysis (stratified analysis by the number of detected lymph nodes and positive lymph nodes, HR, 0.75; log-rank P = .04). The 3-year OS rates were 78.3% vs 82.8% (HR, 1.02; P = .93), and LRFS was 66.5% vs 59.7% (HR, 0.71; 95% CI, 0.51-0.97; P = .03), respectively. For 310 per-protocol patients (140 with PORT and 170 with observation), PORT significantly improved DFS (42.8% vs 30.6%; HR, 0.75; 95% CI, 0.57-1.00; P = .05) but not OS (HR, 0.83; 95% CI, 0.53-1.30; P = .41). The 3-year local recurrence only rates were 9.5% and 18.3% in the 2 arms, respectively (Fine-Gray HR, 0.55; Gray test P = .04). No radiotherapy-related grade 4 or 5 adverse event was observed. Conclusions and Relevance: In this phase 3 randomized clinical trial of patients with pIIIA-N2 NSCLC after complete resection and adjuvant chemotherapy, PORT did not improve DFS. Further studies exploring patients who might best benefit from PORT are needed. Trial Registration: ClinicalTrials.gov Identifier: NCT00880971.

14.
Cancer Commun (Lond) ; 2021 Jun 19.
Artigo em Inglês | MEDLINE | ID: mdl-34146456

RESUMO

BACKGROUND: Risk-stratified endoscopic screening (RSES), which offers endoscopy to those with a high risk of esophageal cancer, has the potential to increase effectiveness and reduce endoscopic demands compared with the universal screening strategy (i.e., endoscopic screening for all targets without risk prediction). Evidence of RSES in high-risk areas of China is limited. This study aimed to estimate whether RSES based on a 22-score esophageal squamous cell carcinoma (ESCC) risk prediction model could optimize the universal endoscopic screening strategy for ESCC screening in high-risk areas of China. METHODS: Eight epidemiological variables in the ESCC risk prediction model were collected retrospectively from 26,618 individuals aged 40-69 from three high-risk areas of China who underwent endoscopic screening between May 2015 and July 2017. The model's performance was estimated using the area under the curve (AUC). Participants were categorized into a high-risk group and a low-risk group with a cutoff score having sensitivities of both ESCC and severe dysplasia and above (SDA) at more than 90.0%. RESULTS: The ESCC risk prediction model had an AUC of 0.80 (95% confidence interval: 0.75-0.84) in this external population. We found that a score of 8 (ranging from 0 to 22) had a sensitivity of 94.2% for ESCC and 92.5% for SDA. The RSES strategy using this threshold score would allow 50.6% of endoscopies to be avoided and save approximately US$ 0.59 million compared to universal endoscopic screening among 26,618 participants. In addition, a higher prevalence of SDA (1.7% vs. 0.9%), a lower number need to screen (60 vs. 111), and a lower average cost per detected SDA (US$ 3.22 thousand vs. US$ 5.45 thousand) could have been obtained by the RSES strategy. CONCLUSIONS: The RSES strategy based on individual risk has the potential to optimize the universal endoscopic screening strategy in ESCC high-risk areas of China.

15.
Artigo em Inglês | MEDLINE | ID: mdl-34076819

RESUMO

Controlling the emission of urban passenger transport modes has become one of the most important tasks of governing urban air pollution. Most strategies only focused on carbon emission, whereas neglecting the influences of other pollutants (CO, HC, NOx, PM2.5), especially for upstream emissions from electricity generation caused by the electricity consumed during the operation of electrified transport modes. Based on the multinomial logit model (MNL), this study firstly calculated and evaluated the emission reduction effects brought about by the implementation of targeted emission taxes on different transport modes from the perspective of whole fuel cycle. Taking Jiangning District as an example, our research found that the policy implementing targeted emission tax for different transport modes can not only bring reduce 13.104 tons of CO, 0.327 tons of HC, 0.568 tons of NOx, and 0.140 tons of PM2.5, but also 26,726.82 (euro) of eco-environmental benefits for the treatment of air pollution. Our study can provide useful insights for shifting the structure of urban passenger transport modes, especially promoting the transfer of private cars to the urban green transport systems, to alleviate urban air pollution by formulating effective emission reduction strategies.

16.
BMC Cancer ; 21(1): 690, 2021 Jun 10.
Artigo em Inglês | MEDLINE | ID: mdl-34112140

RESUMO

BACKGROUND: Published findings suggest sex differences in lung cancer risk and a potential role for sex steroid hormones. Our aim was to perform a meta-analysis to investigate the effects of sex steroid hormone exposure specifically on the risk of lung cancer in women. METHODS: The PubMed, MEDLINE, Web of Science, and EMBASE databases were searched. The pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) for female lung cancer risk associated with sex steroid hormones were calculated overall and by study design, publication year, population, and smoking status. Sensitivity analysis, publication bias, and subgroup analysis were performed. RESULTS: Forty-eight studies published between 1987 and 2019 were included in the study with a total of 31,592 female lung cancer cases and 1,416,320 subjects without lung cancer. Overall, higher levels of sex steroid hormones, both endogenous (OR: 0.92, 95% CI: 0.87-0.98) and exogenous (OR: 0.86, 95% CI: 0.80-0.93), significantly decreased the risk of female lung cancer by 10% (OR: 0.90, 95% CI: 0.86-0.95). The risk of lung cancer decreased more significantly with a higher level of sex steroid hormones in non-smoking women (OR: 0.88, 95% CI: 0.78-0.99) than in smoking women (OR: 0.98, 95% CI: 0.77-1.03), especially in Asia women (OR: 0.84, 95% CI: 0.74-0.96). CONCLUSIONS: Our meta-analysis reveals an association between higher levels of sex steroid hormone exposure and the decreased risk of female lung cancer. Surveillance of sex steroid hormones might be used for identifying populations at high risk for lung cancer, especially among non-smoking women.

17.
Sci Rep ; 11(1): 12587, 2021 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-34131250

RESUMO

Glioblastoma multiforme (GBM) is a life-threatening brain tumor. This study aimed to identify potential targets of the long noncoding RNA (lncRNA) HULC that promoted the progression of GBM. Two U87 cell lines were constructed: HULC-siRNA and negative control (NC). Quantitative real-time PCR (qRT-PCR) was performed to validate the transfection efficiency of HULC silencing vector. Mass spectrometry (MS) was used to generate proteomic profiles for the two cell lines. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to distinguish HULC-related genes and pathway mapping. Colony formation, Transwell, and wound-healing assays were used to investigate the functional effects of HULC knockdown on GBM. We identified 112 up-regulated proteins and 24 down-regulated proteins from a total of 4360 quantified proteins. GO enrichment illustrated that these proteins were mainly involved in organelle structure, catalysis, cell movement, and material metabolism. KEGG pathway analysis indicated that some of these proteins were significantly enriched in tight junction, metabolic pathways, and arachidonic acid metabolism. In vitro experiments demonstrated that HULC knockdown inhibited GBM cell proliferation, invasion, and migration. Our KEGG analyses revealed that PLA2G4A was a shared protein in several enriched pathways. HULC silencing significantly down-regulated the expression of PLA2G4A. Knockdown of HULC changed the proteomic characteristics of GBM and altered the behaviors of GBM cells. Specifically, we identified PLA2G4A as an HULC target in GBM. This study provides a new perspective on the mechanisms and potential drug targets of GBM treatment.

18.
Mol Med Rep ; 24(2)2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34132380

RESUMO

Epithelial ovarian cancer (EOC), a gynecological tumor, is associated with high mortality. MicroRNAs (miRs) serve a crucial role in EOC; however, the mechanisms underlying the effect of miRNA­193a­5p in EOC are not completely understood. Therefore, the present study aimed to investigate the expression levels of miR­193a­5p in serum samples of patients with EOC and to determine the role of miR­193a­5p in EOC. Reverse transcription­quantitative PCR was used to analyze the expression levels of miR­193a­5p in serum samples of patients with EOC and EOC cell lines. The effects of miR­193a­5p and RB binding protein 6, ubiquitin ligase (RBBP6) on the biological functions of EOC were determined by conducting a series of in vitro cell function experiments. The results indicated that the expression levels of miR­193a­5p were significantly decreased in serum samples obtained from patients with EOC and EOC cell lines compared with healthy individuals and normal cells, respectively. Further investigations indicated that RBBP6 was a target gene of miR­193a­5p. The expression levels of RBBP6 were significantly increased in patients with EOC compared with healthy individuals. In addition, in vitro analysis suggested that miR­193a­5p mimic significantly decreased SKOV3 cell proliferation, migration and invasion, and promoted SKOV3 cell apoptosis compared with the control and mimic­negative control groups. In addition, RBBP6 overexpression reversed miR­193a­5p mimic­mediated effects. In conclusion, the results of the present study suggested that downregulated expression levels of miR­193a­5p may serve an inhibitory role in EOC by inhibiting cell proliferation and metastasis, and promoting apoptosis.

20.
Cancer Cell ; 2021 Jun 22.
Artigo em Inglês | MEDLINE | ID: mdl-34171264

RESUMO

Activating mutations in HER2 (ERBB2) drive the growth of a subset of breast and other cancers and tend to co-occur with HER3 (ERBB3) missense mutations. The HER2 tyrosine kinase inhibitor neratinib has shown clinical activity against HER2-mutant tumors. To characterize the role of HER3 mutations in HER2-mutant tumors, we integrate computational structural modeling with biochemical and cell biological analyses. Computational modeling predicts that the frequent HER3E928G kinase domain mutation enhances the affinity of HER2/HER3 and reduces binding of HER2 to its inhibitor neratinib. Co-expression of mutant HER2/HER3 enhances HER2/HER3 co-immunoprecipitation and ligand-independent activation of HER2/HER3 and PI3K/AKT, resulting in enhanced growth, invasiveness, and resistance to HER2-targeted therapies, which can be reversed by combined treatment with PI3Kα inhibitors. Our results provide a mechanistic rationale for the evolutionary selection of co-occurring HER2/HER3 mutations and the recent clinical observations that HER3 mutations are associated with a poor response to neratinib in HER2-mutant cancers.

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