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1.
Mol Med Rep ; 23(1)2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33179076

RESUMO

At present, treatment options for thyroid carcinoma remain limited. The present study aimed to investigate the role of ZFAS1 in various major hallmarks of cancer and the underlying mechanisms in thyroid carcinoma cells. The interactions between long non­coding RNAs (lncRNAs), microRNAs (miRs) and target genes were predicted by bioinformatics and confirmed by performing dual­luciferase assays. The mRNA and protein expressions were determined by reverse transcription­quantitative PCR and western blotting. Cell invasion, migration, and viability were evaluated via Transwell, wound­healing and Cell Counting Kit­8 assays, respectively. The results demonstrated that lncRNA ZFAS1 expression was upregulated in thyroid carcinoma tissues, TT and SW579 cells, and was associated with the proliferation of these two cell lines. Notably, downregulation ZFAS1 reduced migration and invasion, and reversed the promotive effects of miR­302a­3p inhibitor on the proliferation, migration and invasion of TT and SW579 cells. Moreover, cyclin D1 (CCND1) is targeted by miR­302a­3p, and was regulated by ZFAS1. In addition, the downregulation of ZFAS1 not only reversed the promotive effects of miR­302a­3p inhibitor on CCND1 expression and the epithelial­mesenchymal transition (EMT) of TT and SW579 cells, but also targeted and increased the expression of miR­302a­3p, and further reduced the expression of CCND1, resulting in suppression of the proliferation, migration, invasion and EMT of thyroid carcinoma cells.

2.
J Biol Chem ; 2020 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-33208462

RESUMO

The TP53 gene is the most frequently mutated gene in human cancers, and the majority of TP53 mutations are missense mutations. As a result, these mutant p53 (mutp53) either directly lose wild-type p53 (wtp53) tumor suppressor function or exhibit a dominant negative effect over wtp53. In addition, some mutp53 have acquired new oncogenic function (gain of function). Therefore, targeting mutp53 for its degradation, may serve as a promising strategy for cancer prevention and therapy. Based on our previous finding that farnesylated DNAJA1 is a crucial chaperone in maintaining mutp53 stabilization, and by using an in silico approach, we built 3-D homology models of human DNAJA1 and mutp53R175H proteins, identified the interacting pocket in the DNAJA1-mutp53R175H complex, and found one critical druggable small molecule binding  site in the DNAJA1 glycine/phenylalanine rich region. We confirmed that the interacting pocket in the DNAJA1-mutp53R175H complex was crucial for stabilizing mutp53R175H using a site-directed mutagenesis approach. We further screened a drug-like library to identify a promising small molecule hit (GY1-22) against the interacting pocket in DNAJA1-mutp53R175H complex. The GY1-22 compound displayed an effective activity against DNAJA1-mutp53R175H complex. Treatment with GY1-22 significantly reduced mutp53 protein levels, enhanced Waf1p21 expression, suppressed cyclin D1 expression, and inhibited mutp53-driven pancreatic cancer growth both in vitro and in vivo. Together, our results indicate that the interacting pocket in the DNAJA1-mutp53R175H complex is critical for mutp53's stability and oncogenic function, and DNAJA1 is a robust therapeutic target for developing the efficient small molecule inhibitors against oncogenic mutp53.

3.
Cell Signal ; : 109839, 2020 Nov 16.
Artigo em Inglês | MEDLINE | ID: mdl-33212156

RESUMO

Orexin A (OXA) is a neuroprotective peptide that exerts protective effects on multiple physiological and pathological processes. Activation of autophagy is linked to the occurrence of cerebral ischemia-reperfusion injury (CIRI); however, its function remains incompletely understood. In this study, OXA was sought to exert its neuroprotective role by regulating autophagy in oxygen and glucose deprivation and reoxygenation (OGD/R) model and middle cerebral artery occlusion (MCAO) model of rats, and to elucidate the underlying molecular mechanisms. Acridine orange (AO) staining was used to evaluate autophagic vacuoles. Cell viability was measured by CCK8. The levels of p-ERK1/2, t-ERK1/2, p-mTOR, LC3B, Beclin 1, and p62 were evaluated by western blotting. Apoptosis rate was detected by Hoechst 33342 staining and Terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL). OXA treatment alleviated neuronal apoptosis and significantly inhibited autophagy activity. Mechanistically, OXA exerted its neuroprotective effects in vivo and in vitro by suppressing over-activated autophagy by modulating OX1R-mediated MAPK/ERK/mTOR pathway. The results of this study elucidate the roles of autophagy in CIRI and the mechanisms underlying the neuroprotective action of OXA. Our findings could facilitate the development of novel therapeutics for ischemic stroke.

4.
Sci Rep ; 10(1): 16222, 2020 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-33004842

RESUMO

Internet addiction (IA) is common among adolescents and significantly determined by sociocultural and economic factors. The aim of this study was to compare the prevalence of IA among adolescents between Macau and mainland China and also examine its association with quality of life. A total of 2892 secondary school students were included. Standardized instruments were used to measure IA, depressive symptoms and quality of life. The overall prevalence of IA was 23.7%, with 32.5% in Macau and 19.8% in mainland China. Students in Macau were more likely to suffer from IA than those in mainland China (OR = 2.15, p < 0.001). Correlates of IA included being in higher school grades, poor academic performance, and more severe depressive symptoms. Students with IA reported lower quality of life in physical, psychological, social, and environmental domains. IA is common among Chinese adolescents, particularly in Macau. Considering the negative impact of IA on health and quality of life, regular screening and effective interventions should be undertaken for young Internet users.

5.
Pest Manag Sci ; 2020 Oct 09.
Artigo em Inglês | MEDLINE | ID: mdl-33034948

RESUMO

BACKGROUND: The two-spotted spider mite Tetranychus urticae is a polyphagous and cosmopolitan pest that has developed high resistance to abamectin, making it difficult to control. Although 'target resistance' related to glutamate-gated chloride channel mutations was found in T. urticae field populations in China, other resistance mechanisms appear to be involved. Here, we conducted genome-wide transcriptome profiling using RNA-sequencing of two abamectin-resistant populations (NB-ZJ and SY-BJ) and one susceptible strain (Lab-SS) to identify differentially expressed genes that might contribute to the resistance of T. urticae to abamectin in China. RESULTS: Our experiments showed that abamectin resistance was synergized by piperonyl butoxide (PBO) and triphenyl phosphate (TPP), with synergistic ratios (SR) of 2.95-fold and 2.21-fold for PBO and 3.55-fold and 2.84-fold for TPP in NB-ZJ and SY-BJ populations, respectively. Transcriptome data and quantitative real-time PCR (qRT-PCR) revealed that seven detoxification enzyme genes were overexpressed in the two resistant populations. Furthermore, functional analysis by RNA interference (RNAi) indicated that the mortality caused by abamectin was significantly increased by the separate silencing of the P450 genes CYP389C10, CYP392D8, CYP392A11, and CYP392A12. CONCLUSION: qRT-PCR expression and RNAi data suggest that the overexpression of P450 genes CYP389C10, CYP392D8, CYP392A11, and CYP392A12 may be involved in the abamectin-resistance of field populations of T. urticae in China. This knowledge could facilitate the elucidation of resistance mechanisms and the development of resistance management of T. urticae field populations.

6.
Sci Rep ; 10(1): 16705, 2020 10 07.
Artigo em Inglês | MEDLINE | ID: mdl-33028907

RESUMO

The Yunnan province has one of the most serious outbreaks of the plague epidemic in China. Small mammals and fleas are risk factors for the occurrence of plague in commensal plague foci. Understanding the relationship between fleas and small mammals will help control fleas and prevent the onset of the plague. Four hundred and twenty-one small mammals, belonging to 9 species, were captured. Of these, 170 small mammals (40.4%) were found infested with fleas. A total of 992 parasitic fleas (including 5 species) were collected. The number of Leptopsylla segnis and Xenopsylla cheopis accounted for 91.03% (903/992). The final multiple hurdle negative binomial regression model showed that when compared with Rattus tanezumi, the probability of flea infestation with Mus musculus as well as other host species decreased by 58% and 99%, respectively, while the number of flea infestations of the other host species increased by 4.71 folds. The probability of flea prevalence in adult hosts increased by 74%, while the number of fleas decreased by 76%. The number of flea infestations in small male mammals increased by 62%. The number of fleas in small mammals weighing more than 59 g has been multiplied by about 4. R. tanezumi is the predominant species in households in the west Yunnan province, while L.segnis and X. cheopis were dominant parasitic fleas. There is a strong relationship between the abundance of fleas and the characteristics of small mammals (e.g. Species, age, sex, and body weight).

7.
Artigo em Inglês | MEDLINE | ID: mdl-33009612

RESUMO

To better understand the cardiopulmonary alterations associated with personal exposed PM2.5-bound heavy meals, we conducted a cross-sectional study in 2018 on 54 general residents. For each subject, PM2.5 exposure filter was collected by a low-volume sampler for 24 h; blood and urine samples were collected subsequently. Heavy metals in PM2.5, blood, and urine samples were determined by inductively coupled plasma mass spectrometry method. PM2.5-bound Mn, Cd, Sb, Pb, and Ni levels were 20.5, 9.27, 9.59, 28.3, and 16.9 ng/m3, respectively. The distribution of these metals followed the order: Pb (33.47%) > Mn (24.24%) > Ni (19.99%) > Sb (11.34%) > Cd (10.96%). The distribution of heavy meals in PM2.5, blood, and urine differed from each other. PM2.5-bound Cd, Pb levels were positively correlated with blood Cd, Pb levels (r = 0.323, r = 0.334, p < 0.05), respectively. PM2.5-bound Cd level was significantly higher in smoking group than non-smoking group (28.8 vs. 7.27 ng/m3, p < 0.01), same as Sb level (12.0 vs. 9.34 ng/m3, p < 0.01). Cd and Pb exposure might interact with cardiovascular function through autonomic regulation. No significant correlation was observed between metal exposure and pulmonary function. In conclusion, our data suggested that personal exposure to specific PM2.5-bound heavy metals might interact with profound cardiovascular alterations.

8.
Birth Defects Res ; 2020 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-33030311

RESUMO

Mutations in the transforming growth factor ß-binding protein-like domain 5 (TB5) region of FBN1 can lead to autosomal acromelic dysplasia and Marfan syndrome, which are two diseases with apparently opposite phenotypes. We identified six patients with acromelic dysplasia carrying either the previously reported mutations c.5284G > A (p.Gly1762Ser) and c.5096A > G (p.Tyr1699Cys) or the novel mutation c.5260G > A (p.Gly1754Ser). A systematic review of patients with mutations in the FBN1-TB5 region showed that acromelic dysplasia is caused only by in-frame amino acid substitutions. In contrast, truncating mutations in the FBN1-TB5 have been reported only in Marfan syndrome. Acromelic dysplasia subtypes that share symptoms with Marfan syndrome are associated with FBN1-TB5 disulfide disruptions, which are also commonly found in Marfan syndrome. These results suggest that the type and location of mutations in the FBN1-TB5 region determine the clinical spectrum of fibrillinopathy.

9.
Plant Dis ; 2020 Oct 13.
Artigo em Inglês | MEDLINE | ID: mdl-33048597

RESUMO

Crape jasmine (Tabernaemontana divaricata) is a popular flowering shrub widely grown in southern China. Its leaves and roots are used in Chinese traditional medicine. In December, 2019, powdery mildew symptoms were observed on five crape jasmine shrubs on the campus of Shenzhen Polytechnic (22°35'N; 113°56'E), in Guangdong province. Approximately 45% of leaves were infected. Symptoms initially appeared as circular to irregular white patches on the leaf petiole, and subsequently coalesced to develop into abundant hyphal growth on both sides of the leaves, which soon wilted. Hyphae were septate, branched, with simple kidney-shaped to moderately lobed appressoria. Conidia formed singly, ellipsoid-ovoid to subcylindrical, 27-37 × 14-20 µm (mean 32±2.5 × 17±1.6 µm), with a length/width ratio varying from 1.3 to 2.4. Conidiophores were erect, unbranched, consisted of two cells, 60 to 84 µm long (mean 73±4 µm), and with straight to severely kinked cylindrical foot-cells at the base, 29-35 × 3-7 µm (mean 32±3 × 6±2 µm). Chasmothecia were not observed on sampled plants. These morphological characteristics were typical to the conidial stage of the genus Erysiphe (Braun and Cook, 2012). For molecular identification, genomic DNA was extracted from conidia washed from infected leaves and using Fungal DNA Kit (Omega Bio-tek Inc., Guangzhou, China). Semi-nested PCR amplification of the internal transcribed spacer (ITS) region of rDNA was conducted by using primer sets P3 (Kusaba et al., 1995)/ITS5 and ITS5/ITS4 (White et al., 1990) for the first and second reactions, respectively. BLASTn analysis of the obtained 719 bp sequence (GenBank Accession No. MT802112) showed 99.7% identity with those of E. elevata (KY660910, MH985631, MK253282). On the basis of morphological and molecular analyses, the fungus was identified as Erysiphe elevata. To confirm pathogenicity, infected leaves were gently pressed onto healthy leaves of three healthy plants in separate pots, and three noninoculated plants were used as controls. All plants were maintained in a greenhouse at 25 ℃, and relative humidity of 50 to 65%. After 11 days, similar disease symptoms were observed on the inoculated plants while no symptoms developed on control plants. The fungus observed on the inoculated shrubs was identical morphologically to that o the original infected leaves. E. elevata is a common powdery mildew species infecting Catalpa spp. (Cook et al., 2006), Plumeria rubra (Wu et al., 2019; Yeh et al., 2019) and Eucalyptus camaldulensis (Meeboon and Takamatsu, 2017). However, no powdery mildew were found on P. rubra nearby. To our knowledge, this is the first report of this fungus infecting T. divaricata.

10.
Chem Commun (Camb) ; 56(83): 12570-12573, 2020 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-32940298

RESUMO

The first ring-opening addition of a benzylic C(sp3)-H bond to azabenzonorbornadienes is demonstrated. The reaction proceeded under the catalytic system of [Cp*CoI2(CO)], AgSbF6 and Fe(OAc)2 in PhOMe. The methodology showed a good substrate scope with up to 96% yield. The relative configuration of the product was determined as cis-configuration by X-ray crystallography.

11.
Theranostics ; 10(19): 8721-8743, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32754274

RESUMO

Over the past few decades, substantial evidence has convincingly revealed the existence of cancer stem cells (CSCs) as a minor subpopulation in cancers, contributing to an aberrantly high degree of cellular heterogeneity within the tumor. CSCs are functionally defined by their abilities of self-renewal and differentiation, often in response to cues from their microenvironment. Biological phenotypes of CSCs are regulated by the integrated transcriptional, post-transcriptional, metabolic, and epigenetic regulatory networks. CSCs contribute to tumor progression, therapeutic resistance, and disease recurrence through their sustained proliferation, invasion into normal tissue, promotion of angiogenesis, evasion of the immune system, and resistance to conventional anticancer therapies. Therefore, elucidation of the molecular mechanisms that drive cancer stem cell maintenance, plasticity, and therapeutic resistance will enhance our ability to improve the effectiveness of targeted therapies for CSCs. In this review, we highlight the key features and mechanisms that regulate CSC function in tumor initiation, progression, and therapy resistance. We discuss factors for CSC therapeutic resistance, such as quiescence, induction of epithelial-to-mesenchymal transition (EMT), and resistance to DNA damage-induced cell death. We evaluate therapeutic approaches for eliminating therapy-resistant CSC subpopulations, including anticancer drugs that target key CSC signaling pathways and cell surface markers, viral therapies, the awakening of quiescent CSCs, and immunotherapy. We also assess the impact of new technologies, such as single-cell sequencing and CRISPR-Cas9 screening, on the investigation of the biological properties of CSCs. Moreover, challenges remain to be addressed in the coming years, including experimental approaches for investigating CSCs and obstacles in therapeutic targeting of CSCs.

12.
Dalton Trans ; 49(35): 12441-12449, 2020 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-32852016

RESUMO

An Ni-Zn battery is a distinguished member in the family of closed Zn-based batteries due to its ideal power density and voltage. However, when it is employed as a power supply for electric vehicles, its defects in terms of specific capacitance and energy density become obvious. Herein, to resolve this problem, a hybrid battery system was created through a combination of Ni-Zn and Zn-air batteries at the cell level. In a hybrid battery system, oxygen vacancy rich NiO with S,N co-modified mesoporous carbon as a matrix was used as the cathode material. This cathode material showed a high specific capacitance of 202.1 mA h g-1 at 1.0 A g-1. When the current density reduces to 20 A g-1, this value decreases to 130.2 mA h g-1, which implies that 64.4% of specific capacitance was retained. It also exhibits excellent OER and ORR activities. For the hybrid battery system, when the discharge process was carried out at 1 mA cm-2, there were two voltage plateaus at 1.72 and 1.12 V, which originated from Ni-Zn and Zn-air, respectively. In this case, its specific capacitance and energy density reaches 800.3 mA h g-1 and 961 W h kg-1, respectively. The hybrid battery also possesses perfect stability during multi-cycle charge-discharge tests. The construction of this hybrid battery system develops a new road to prepare a power supply device with high performance.

13.
Oncol Rep ; 44(3): 897-908, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32705278

RESUMO

Renal cell carcinoma (RCC) is not sensitive to conventional radiotherapy and chemotherapy, and the effectiveness rate of molecular targeted therapy is low. Therefore, it is urgent to identify new treatment methods. Recently, adoptive T­cell therapy has provided a new option for cancer treatment. Furthermore, low­dose chemotherapy not only has no evident side effects and inhibitory effects on the human immune system, but can also enhance the immune activity of some effector cells. Therefore, it is surmised that the combination of different mechanisms of chemotherapy and immunotherapy could be a new treatment concept. In the present study, the effects of low­dose chemotherapy combined with T cells in the treatment of renal cell carcinoma were explored using cytotoxicity assays, enzyme­linked immunosorbent assay (ELISA), western blot analysis and flow cytometric analysis. The results revealed that low­dose chemotherapy and T cells had synergistic effects on tumor cell elimination in vitro. The transforming growth factor (TGF)­ß signaling pathway may be involved in the inhibition of T­cell functions. The targeted inhibition of TGF­ß signals may be a promising therapeutic strategy for the treatment of renal cancer. The present results provided a novel strategy for the combination of low­dose chemotherapy and T cells to enhance the therapeutic efficacy of RCC treatment.

14.
J Mol Cell Biol ; 2020 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-32722796

RESUMO

p53 is a key tumor suppressor, and loss of p53 function is frequently a prerequisite for cancer development. The p53 gene is the most frequently mutated gene in human cancers; p53 mutations occur in > 50% of all human cancers and in almost every type of human cancers. Most of p53 mutations in cancers are missense mutations, which produce the full-length mutant p53 (mutp53) protein with only one amino acid difference from wild-type p53 protein. In addition to loss of the tumor suppressive function of wild-type p53, many mutp53 proteins acquire new oncogenic activities independently of wild-type p53 to promote cancer progression, termed gain-of-function (GOF). Mutp53 protein often accumulates to very high levels in cancer cells, which is critical for its GOF. Given the high mutation frequency of the p53 gene and the GOF activities of mutp53 in cancer, therapies targeting mutp53 have attracted great interest. Further understanding the mechanisms underlying mutp53 protein accumulation and GOF will help develop effective therapies treating human cancers containing mutp53. In this review, we summarize the recent advances in the studies on mutp53 regulation and GOF as well as therapies targeting mutp53 in human cancers.

15.
Parasit Vectors ; 13(1): 314, 2020 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-32552779

RESUMO

BACKGROUND: Malaria caused by Plasmodium spp. is still a major threat to public health globally. The various approaches to developing new antimalarial agents rely on the understanding of the complex regulatory mechanisms of dynamic gene expression in the life-cycle of these malaria parasites. The nuclear members of the evolutionarily conserved actin-related protein nuclear (ARP) superfamily are the major components of nucleosome remodelling complexes. In the human malaria parasite Plasmodium falciparum, bioinformatics analysis has predicted three ARP orthologues: PfArp1, PfArp4 and PfArp6. However, little is known about the biological functions of putative PfArp4. In this study, we aimed to investigate the function and the underlying mechanisms of PfArp4 gene regulation. METHODS: A conditional gene knockdown approach was adopted by incorporating the glucosamine-inducible glmS ribozyme sequence into the 3' UTR of the PfArp4 and PfArp6 genes. The transgenic parasites PfArp4-Ty1-Ribo, PfArp6-Ty1-Ribo and pL6-PfArp4-Ty1::PfArp6-HA were generated by the CRISPR-Cas9 technique. The knockdown effect in the transgenic parasite was measured by growth curve assay and western blot (WB) analysis. The direct interaction between PfArp4 and PfArp6 was validated by co-IFA and co-IP assays. The euchromatic gene expression mediated through H2A.Z (histone H2A variant) deposition and H3K9ac modification at promoters and regulated by PfArp4, was determined by RNA-seq and ChIP-seq. RESULTS: The inducible knockdown of PfArp4 inhibited blood-stage development of P. falciparum. PfArp4 and PfArp6 were colocalized in the nucleus of P. falciparum parasites. PfArp4 gene knockdown altered the global transcriptome. PfArp4 protein colocalized with the histone variant H2A.Z and euchromatic marker H3K9ac in intergenic regions. The inducible downregulation of PfArp4 resulted in the depletion of H2A.Z and lower H3K9ac levels at the upstream regions of eukaryotic genes, thereby repressing the transcriptional abundance of H2A.Z-dependent genes. CONCLUSIONS: Our findings suggest that PfArp4 regulates the cell cycle by controlling H2A.Z deposition and affecting centromere function, contributing to the understanding the complex epigenetic regulation of gene expression and the development of P. falciparum.

16.
J Appl Physiol (1985) ; 129(1): 36-46, 2020 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-32407240

RESUMO

Skeletal muscle atrophy is associated with disease, aging, and disuse. Hindlimb unloading (HU) in animals provides an experimental model to study muscle atrophy. A comprehensive time course for how HU affects biomarkers of protein synthesis and degradation acutely and chronically and the associated resistance to an anabolic stimulus following disuse remain undocumented. Sixteen-week-old C57BL/6 mice underwent 0, 1, 12, 24, 72, 168, or 336 h of HU. Following 336 h of HU, mice were reloaded for 1, 24, or 72 h. Another group of mice underwent 120 h of HU, were fasted or refed, and were then compared with similar condition control animals (CTL). Protein content and phosphorylation of biomarkers of protein synthesis, degradation, and autophagy were assessed in the soleus muscle. Gastrocnemius, soleus, and plantaris muscles atrophied within 120 h of HU. Protein synthesis trended toward decrease following 24 h of HU. p70S6K phosphorylation and protein synthesis increased with reloading. Following HU, changes in MAFbx and DEPTOR expression and DEPTOR phosphorylation were consistent with development of a catabolic state. DEPTOR expression recovered following reloading. Animals that underwent 120 h of HU exhibited attenuation of refeeding-induced p70S6K phosphorylation compared with CTL counterparts. Following 120 h of HU, protein synthesis, eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) phosphorylation, and DEPTOR, MAFbx, and Sestrin1 expression indicated a catabolic state. Following 120 h of HU, autophagy markers, including p62 expression, REDD1 expression, LC3 ratio, and Unc-51-like autophagy-activating kinase 1 (ULK1) phosphorylation, indicated impaired autophagy. HU promotes a deleterious balance between protein synthesis and degradation. The time course herein provides scientists information about when the associated biomarkers become affected.NEW & NOTEWORTHY Hindlimb unloading causes significant skeletal muscle atrophy by adversely affecting the balance between protein synthesis and breakdown. This study demonstrates a more complete time course for changes in biomarkers associated with protein synthesis and breakdown and investigates the associated anabolic resistance to an anabolic stimulus following hindlimb unloading. These data in concert with information from other studies provide a basis for designing future experiments to optimally interrogate a desired cellular biomarker or pathway.

17.
Med Sci Monit ; 26: e921058, 2020 Apr 12.
Artigo em Inglês | MEDLINE | ID: mdl-32279065

RESUMO

BACKGROUND This study analyzed the distribution of Rh serological phenotype in people living in Hangzhou, China, and assessed the necessity of its routine clinical detection and homotypic infusion. MATERIAL AND METHODS Blood donors and patients who might need blood transfusion were enrolled into the study, and ABO and 5 major Rh serological antigens (C, c, D, E, and e) were routinely detected. The consistent ABO and Rh serological phenotype blood was transfused between the blood donors and recipients. Irregular antibodies were screened and identified in patients before the blood transfusion. Then, the transfusion adverse effects were monitored and compared with the previous data in the hospital. RESULTS The phenotypic frequencies of Rh blood groups were D>C>E>c>e. The CCDee was the most common phenotype and CcdEe was the least common. The detection rate of unexpected antibodies gradually increased, while the unexpected antibodies slowly decreased in the Rh system. There was a correlation between the isotypic infusion of 5 Rh antigens and the detection rate of antibodies in the Rh system (R=0.845). The adverse effects of blood transfusion declined from 19.95% in 2011 with just homotypic ABO infusion to 3.098% in 2019 with the transfusion of homotypic ABO and the 5 major Rh serological antigens. CONCLUSIONS The consistency of the transfusion with ABO and 5 significant Rh serological antigens could prevent and decrease the high frequency production of isoantibodies, which is of vital importance in reducing the incidence rate of adverse effects in patients receiving transfusions.


Assuntos
Tipagem e Reações Cruzadas Sanguíneas , Transfusão de Sangue , Sistema do Grupo Sanguíneo Rh-Hr/sangue , Reação Transfusional , Sistema ABO de Grupos Sanguíneos/sangue , Doadores de Sangue , China , Feminino , Humanos , Masculino , Fenótipo
18.
Dig Dis Sci ; 65(11): 3238-3243, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32239376

RESUMO

INTRODUCTION: Nonalcoholic fatty liver disease (NAFLD) is the leading cause of liver disease worldwide. Nonalcoholic steatohepatitis (NASH), is a more severe type of NAFLD. Exercise improves NASH, by reversing steatosis, and may arrest fibrosis. However, the mechanisms underlying these interactions are unknown. AMP-activated protein kinase (AMPK) is a fuel-sensing enzyme that is activated by energy stress. Mammalian target of rapamycin in complex 1 (mTORC1) is a nutrient sensor that regulates protein synthesis. In NASH, AMPK activity is low and mTORC1 is high. In healthy persons, exercise activates AMPK and suppresses mTORC1. We examined the effects of exercise on hepatic ribosomal protein S6 phosphorylation, a downstream target of AMPK and mTORC1 in patients with NASH. METHODS: Three subjects with biopsy-proven NASH underwent a structured, 20-week aerobic exercise intervention, five-days a week for 30-min at a moderate intensity (40-55% of VO2max). Immunofluorescence staining for rpS6 phosphorylation in hepatic tissue was quantified by ImageJ software. RESULTS: Following 20-weeks of aerobic exercise, rpS6 levels were significantly attenuated (3.9 ± 1.9 pre-exercise vs. 1.4 +/0.4 post-exercise, p = 0.04). CONCLUSIONS: These findings suggest exercise modulates the AMPK/mTORC1 pathway in patients with NASH and may guide the design of future studies into the mechanism of how exercise improves NASH and possibly reverses fibrosis.

19.
Org Biomol Chem ; 2020 Apr 22.
Artigo em Inglês | MEDLINE | ID: mdl-32319504

RESUMO

A metal-free direct oxidative dehydrogenation approach for the synthesis of azobenzenes from hydrazobenzenes has been developed by using TEMPO as an organocatalyst for the first time. The reaction proceeded in open air under mild reaction conditions. A wide range of hydrazobenzenes readily undergo dehydrogenation to give the corresponding azobenzenes in excellent yields.

20.
J Affect Disord ; 268: 20-27, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-32158003

RESUMO

BACKGROUNDS: Depression in children and adolescents is usually under-recognized. The findings of epidemiological studies on depressive symptoms in primary school students are inconsistent across studies. This study reports a systematic review and meta-analysis on the prevalence of depressive symptoms in primary school students in China. METHODS: Literature search was performed in both international (PubMed, PsycINFO, EMBASE) and Chinese (China National Knowledge Internet, WANFANG Data and Chinese Biological Medical Literature) databases. The random-effects model was used to analyze data. RESULTS: Twenty-seven studies involving 42,374 subjects were included. The pooled prevalence of depressive symptoms in Chinese primary school students was 17.2% (95% CI: 14.3%-20.5%). Subgroup analyses found that the prevalence significantly varied between geographic regions, with western China reporting the highest prevalence. Meta-regression analyses found that year of survey and study quality were significantly associated with the prevalence of depressive symptoms. CONCLUSIONS: Given the high prevalence of depressive symptoms and its negative health outcomes, preventive measures, regular screening and effective treatments need to be implemented for this population.

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