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1.
Biochem Pharmacol ; 202: 115107, 2022 May 25.
Artigo em Inglês | MEDLINE | ID: mdl-35643339

RESUMO

Osteoarthritis (OA) is a common and debilitating chronic joint disease, which is characterized by degeneration of articular cartilage and the aging of chondrocytes. Acid-sensitive ion channel 1a (ASIC1a) is a proton-activated cationic channel abundant in chondrocytes, which senses and regulates joint cavity pH. Our previous study demonstrated that ASIC1a was involved in acid-induced rat articular chondrocyte senescence, but the mechanistic basis remained unclear. In this study, we explored the mechanism of ASIC1a in chondrocyte senescence and OA. The results showed that senescence-related-ß-galactosidase, senescence-related markers (p53 and p21) and the autophagy-related protein Beclin-1 were found to be increased, but Lamin B1 was found to be reduced with acid (pH 6.0) treatment. These effects were inhibited by ASIC1a-specific blocker psalmotoxin-1 or ASIC1a-short hairpin RNA respectively in chondrocytes. Moreover, Silencing of Lamin B1 enhanced ASIC1a-mediated chondrocyte senescence, this effect was reversed by overexpression of Lamin B1, indicating that Lamin B1 was involved in ASIC1a-mediated chondrocyte senescence. Further, blockade of ASIC1a inhibits acid-induced autophagosomes and Beclin-1 protein expression, suggesting that ASIC1a is involved in acid-induced chondrocyte autophagy. Blocking autophagy with chloroquine inhibited Beclin-1 and increased Lamin B1 in acid-induced chondrocyte senescence. We further demonstrated that ASIC1a-mediated reduction of Lamin B1 expression was caused by autophagy pathway-dependent protein degradation. Finally, blocking ASIC1a protected cartilage tissue, restored Lamin B1 levels and inhibited chondrocyte senescence in a rat OA model. In summary, these findings suggest that ASIC1a may promote Lamin B1 degradation to mediate osteoarthritis chondrocyte senescence through the autophagy pathway.

2.
Endocrine ; 2022 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-35751776

RESUMO

The COVID-19 pandemic has posed a significant health threat globally. Timely and appropriate vaccination is a key step to reduce the morbidity and mortality from COVID-19. The clinical course of COVID-19 infection and the effects of COVID-19 vaccination are influenced by patients' health situations and involve a systemic physiological reaction. Just like an "endocrine phenotype" of COVID-19 infection, endocrine dysfunction after COVID-19 vaccination also acquired clinical concerns. In the present review, we briefly introduce the commonly available vaccines against SARS-CoV-2, summarize the influence of COVID-19 vaccines on the endocrine system, and explore the underlying pathogenic mechanisms.

3.
J Hazard Mater ; 430: 128511, 2022 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-35739688

RESUMO

The metabolic disorders are becoming an epidemic disease endangering public health in countries. Environmental factors are mainly reason for the growth of metabolic disorders. Previous research suggests that DNA methylation is a potential mechanism. Recently, it has been reported that DNA hydroxymethylation is also a stable marker of epigenetic reprogramming. Hence, the study aims to investigate whether DNA hydroxymehylation mediates early-life environmental stress-evoked metabolic disorder in adulthood. Mice were orally administered with arsenic (As), an environmental stressor, throughout pregnancy. We show that early-life As exposure induces glucose intolerance and hepatic lipid accumulation in adulthood. Early-life As exposure alters epigenetic reprogramming and expression of lipid metabolism-related genes including ß-oxidation-specific genes in adulthood. Of interest, early-life As exposure alters epigenetic reprogramming of hepatic lipid metabolism partially through reducing DNA hydroxymethylation modification of ß-oxidation-related genes in developing liver. Mechanistically, early-life As exposure suppresses ten-eleven translocation (TET) activity through downregulating isocitrate dehydrogenases (Idh) and reducing alpha-ketoglutarate (α-KG) content in the developing liver. In addition, early-life As exposure inhibits TET1 binding to CpG-rich fragments of ß-oxidation-related genes in developing liver. This study provide novel evidence that early-life environmental stress leads to later life metabolic disorders by altering hepatic DNA hydroxymethylation reprogramming.

4.
J Hazard Mater ; 436: 129242, 2022 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-35739761

RESUMO

Biochar (BC) is a biomass material that has a wide range of applications on the remediating heavy metals. In this experiment, we prepared BC (300 ºC, 500 ºC, and 700 ºC) and applied them to adsorb lead ions (Pb2+) to simulate BC treatment of Pb2+-contaminated soil. The retention capacity of BC for heavy metals was altered by means of bacterial culture, and the heavy metals released by BC can have toxicological effects on bacteria. This approach was used to assess the effects of long-term application of BC in heavily contaminated land with heavy metals on soil microorganisms. The results show that Escherichia coli survived in the medium containing lower doses of Pb2+-aged BC prepared at 300 ºC and 500 ºC (25 mg/L and 50 mg/L), depending on its ability of tolerating a certain amount of Pb2+. The addition of 100 mg/L Pb2+-aged BC prepared at 700 ºC not only significantly inhibited the growth of E. coli, but also promoted the release of citric acid from E. coli, which in turn triggered BC releasing more Pb2+. It is hoped that this will provide foundation to support the long-term application of BC in the remediation of heavy metal contaminated soils.

5.
Diagnostics (Basel) ; 12(6)2022 Jun 14.
Artigo em Inglês | MEDLINE | ID: mdl-35741271

RESUMO

This study aimed to assess the diagnostic values of peptidoglycan (PGN), lipopolysaccharide (LPS) and (1,3)-Beta-D-Glucan (BDG) in patients with suspected bloodstream infection. We collected 493 heparin anticoagulant samples from patients undergoing blood culture in Peking Union Medical College Hospital from November 2020 to March 2021. The PGN, LPS, and BDG in the plasma were detected using an automatic enzyme labeling analyzer, GLP-F300. The diagnostic efficacy for PGN, LPS, and BDG were assessed by calculating the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). This study validated that not only common bacteria and fungi, but also some rare bacteria and fungi, could be detected by testing the PGN, LPS, and BDG, in the plasma. The sensitivity, specificity, and total coincidence rate were 83.3%, 95.6%, and 94.5% for PGN; 77.9%, 95.1%, and 92.1% for LPS; and 83.8%, 96.9%, and 95.9% for BDG, respectively, which were consistent with the clinical diagnosis. The positive rates for PGN, LPS, and BDG and the multi-marker detection approach for PGN, LPS, and BDG individually were 11.16%, 17.65%, and 9.13%, and 32.86% significantly higher than that of the blood culture (p < 0.05). The AUC values for PGN, LPS, and BDG were 0.881 (0.814-0.948), 0.871 (0.816-0.925), and 0.897 (0.825-0.969), separately, which were higher than that of C-reactive protein (0.594 [0.530-0.659]) and procalcitonin (0.648 [0.587-0.708]). Plasma PGN, LPS, and BDG performs well in the early diagnosis of bloodstream infections caused by Gram-positive and Gram-negative bacterial and fungal pathogens.

6.
Front Pharmacol ; 13: 858118, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35721105

RESUMO

Inflammation and endothelial dysfunction play an essential role in heart failure (HF). Epidermal growth factor-like protein 7 (EGFL7) is upregulated during pathological hypoxia and exerts a protective role. However, it is unclear whether there is a link between abnormal EGFL7 expression and inflammation in overload stress-induced heart failure. Our results showed that EGFL7 transiently increased during the early 4 weeks of TAC and in hypertensive patients without heart failure. However, it decreased to the basal line in the heart tissue 8 weeks post-transverse aortic constriction (TAC) or hypertensive patients with heart failure. Knockdown of EGFL7 with siRNA in vivo accelerated cardiac dysfunction, fibrosis, and macrophage infiltration 4 weeks after TAC. Deletion of macrophages in siRNA-EGFL7-TAC mice rescued that pathological phenotype. In vitro research revealed the mechanism. PI3K γ /AKT/N FκB signaling in macrophages was activated by the supernatant from endothelial cells stimulated by siRNA-EGFL7+phenylephrine. More macrophages adhered to endothelial cells, but pretreatment of macrophages with PI3Kγ inhibitors decreased the adhesion of macrophages to endothelial cells. Ultimately, treatment with recombinant rmEGFL7 rescued cardiac dysfunction and macrophage infiltration in siRNA-EGFL7-TAC mice. In conclusion, EGFL7 is a potential inhibitor of macrophage adhesion to mouse aortic endothelial cells. The downregulation of EGFL7 combined with increased macrophage infiltration further promoted cardiac dysfunction under pressure overload stress. Mechanistically, EGFL7 reduced endothelial cell adhesion molecule expression and inhibited the PI3K γ /AKT/NF κ B signaling pathway in macrophages.

7.
Front Genet ; 13: 878063, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35646082

RESUMO

Objective: This study aims to characterize the abnormal changes in placental DNA methylation associated with conotruncal heart defects (CTDs) and the level of methylation as epigenetic biomarkers for CTDs detection. Methods: This was a prospective study involving 28 fetuses diagnosed with CTDs in the second trimester at Beijing Anzhen Hospital between September 2020 and June 2021. These cases were classified into four groups based on their subtypes. 12 normal fetuses were used as controls. Placental tissue was obtained after inducing labor in fetuses. To identify differential methylation sites (DMSs) and regions (DMRs) in cases vs. controls, an Infinium Human Methylation 850 k bead chip was used. Differential methylation was assessed by comparing the ß-values for individual CpG loci. Based on the p-value (<0.05), the most discriminating CpG sites were identified. The area under the receiver-operating-characteristics curve (AUC) was used to determine the predictive accuracy of CpG loci with significant methylation changes for CTDs. The function of genes was assessed through KEGG enrichment analysis, Gene Ontology (GO) analysis, and KEGG pathway analysis. Results: In comparison to the control group, the DNA methylation of the placental tissue is significantly different in fetuses with CTDs. We identified the most significantly different methylated loci and they demonstrated excellent individual predictive accuracy for CTDs detection with AUC >0.9 in cases compared with controls. HOXD9, CNN1, NOTCH1, and ECE1 were identified as CTDs-detection candidate genes. Conclusion Our study established the abnormal changes in placental methylation associated with CTDs and potential epigenetic biomarkers for CTDs detection.

8.
Front Oncol ; 12: 723089, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35646701

RESUMO

Objective: To investigate the value of diffusion-weighted imaging (DWI) combined with the hepatobiliary phase (HBP) Gd-BOPTA enhancement in differentiating intrahepatic mass-forming cholangiocarcinoma (IMCC) from atypical liver abscess. Materials and Methods: A retrospective analysis was performed on 43 patients with IMCCs (IMCC group) and 25 patients with atypical liver abscesses (liver abscess group). The DWI signal, the absolute value of the contrast noise ratio (│CNR│) at the HBP, and visibility were analyzed. Results: A relatively high DWI signal and a relatively high peripheral signal were presented in 29 patients (67.5%) in the IMCC group, and a relatively high DWI signal was displayed in 15 patients (60.0%) in the atypical abscess group with a relatively high peripheral signal in only one (6.7%) patient and a relatively high central signal in 14 (93.3%, 14/15). A significant (P<0.001) difference existed in the pattern of signal between the two groups of patients. On T2WI, IMCC was mainly manifested by homogeneous signal (53.5%), whereas atypical liver abscesses were mainly manifested by heterogeneous signal and relatively high central signal (32%, and 64%), with a significant difference (P<0.001) in T2WI imaging presentation between the two groups. On the HBP imaging, there was a statistically significant difference in peripheral │CNR│ (P< 0.001) and visibility between two groups. The sensitivity of the HBP imaging was significantly (P=0.002) higher than that of DWI. The sensitivity and accuracy of DWI combined with enhanced HBP imaging were significantly (P=0.002 and P<0.001) higher than those of either HBP imaging or DWI alone. Conclusion: Intrahepatic mass-forming cholangiocarcinoma and atypical liver abscesses exhibit different imaging signals, and combination of DWI and hepatobiliary-phase enhanced imaging has higher sensitivity and accuracy than either technique in differentiating intrahepatic mass-forming cholangiocarcinoma from atypical liver abscesses.

9.
Microbiol Spectr ; : e0212421, 2022 Jun 06.
Artigo em Inglês | MEDLINE | ID: mdl-35658572

RESUMO

Limosilactobacillus reuteri plays an important role in regulating intestinal functions and maintaining barrier integrity in animals. In this study, Limosilactobacillus reuteri strain SLZX19-12 was isolated from the fecal microbiota of Tibetan pigs, and it was found that this strain is sensitive to common antibiotics and has strong resistance to stress. Upon being administered by gavage at different doses, including low, medium, and high doses, for 14 days, Limosilactobacillus reuteri SLZX19-12 may enhance the intestinal barrier. After administration of a high dose of SLZX19-12, mice were challenged with Salmonella enterica serovar Typhimurium SL1344. Infection with Salmonella Typhimurium SL1344 led to disordered colonic microbiotas, colonic inflammation through the S100A8/S100A9-NF-κB pathway and potential apoptosis, and translocation of pathogens to parenteral visceral organs in mice. However, the mice pretreated with Limosilactobacillus reuteri SLZX19-12 showed lower loads of Salmonella in visceral organs, less colonic inflammation, and higher barrier integrity. More importantly, the administration of strain SLZX19-12 resulted in a more stable microbiota structure of the colon, in which the abundance of Alloprevotella was greatly enhanced. Therefore, this study suggests that Limosilactobacillus reuteri SLZX19-12 can protect the colon from infection by enhancing the stability of gut microbiota and barrier integrity and reducing inflammation. IMPORTANCE The use of antibiotics to treat bacterial infections leads to a series of side effects. As an alternative method, the biocontrol strategy, which uses probiotics to suppress pathogens, is considered a potential way to deal with bacterial infections in gut. However, there are few probiotics that are currently safe and can protect against infection. In this study, Limosilactobacillus reuteri strain SLZX19-12 was obtained from Tibetan pigs, which have higher resistance to infection. This strain is sensitive to conventional antibiotics, secretes a wide spectrum of enzymes, and also promotes the intestinal barrier function in mice. In addition, Limosilactobacillus reuteri SLZX19-12 can promote the stability of the gut microbiota to avoid or alleviate the occurrence or development of foodborne infections.

10.
Cell Cycle ; : 1-11, 2022 Jun 06.
Artigo em Inglês | MEDLINE | ID: mdl-35659445

RESUMO

The mammary gland of mammals possesses the specific function of synthesizing, secreting, and delivering milk. Notably, mammary epithelial cells are considered to be central to control the expansion and remodeling of mammary gland into a milk-secretory organ. And the biological function of mammary gland is mainly regulated by the endocrine system, especially for estrogen. G protein-coupled receptor 30 (GPR30), an estrogen membrane receptor, mediates estrogen-induced functions of physiology and pathophysiology. However, the relationship between estrogen/GPR30 signaling and proliferation of goat mammary epithelial cells (gMECs) is still unclear. Herein, estrogen promoted cell proliferation than control, as evidence by upregulation of cell numbers, BrdU-positive cell counts, and cell viability. Of note, these activities were all obviously reduced by treatment with GPR30 antagonist G15, yet GPR30 agonist G1 increased cell proliferation than control. Further, GPR30 silencing inhibited cell proliferation than negative control. This inhibition was accompanied by a G2/M phase arrest and downregulation of cell cycle regulators. Meanwhile, estrogen increased the phosphorylation of ERK1/2 and AKT. Further, the protein level of p-ERK1/2 and p-AKT was enhanced by GPR30 agonist G1 but inhibited by GPR30 antagonist G15 and GPR30 silencing. Importantly, MEK inhibitor and PI3K inhibitor decreased the expression of cell cycle regulators, and repressed estrogen-induced and G1-driven promotion of cell proliferation, suggesting that estrogen regulated cell proliferation of gMECs through mechanisms involving cell cycle, dependent of GPR30 and MEK/ERK and PI3K/AKT signaling pathway. This may provide a strong theoretical basis for researching estrogen sustained-release drugs promoting breast development and improving lactation performance.Abbreviations: gMECs, goat mammary epithelial cells; E2, 17ß-estradiol; GPR30, G protein-coupled receptor 30; shRNA, small hairpin RNA; CDK, cyclin-dependent kinase; PI3K, phosphatidylinositol 3-kinase; AKT, proteinkinase B; MAPK, mitogen-activated protein kinase; MEK, mitogen-activated protein kinase kinase; ERK1/2, extracellular signal-regulated kinase 1/2.

11.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 53(3): 414-420, 2022 May.
Artigo em Chinês | MEDLINE | ID: mdl-35642148

RESUMO

Objective: To investigate the expression and role of programmed death ligand-1 (PD-L1) in a mouse model of necrotizing enterocolitis (NEC). Methods: A total of 20 wild-type C57 BL/6 J mice were randomly assigned to the control and the model groups. Mice in the control group were breastfed, while mice in the model group were given lipopolysaccharide, formula feeding, hypoxia, and cold stimulation for NEC induction. Then, the intestines of the mice were collected in order to assess the pathological changes through HE staining, to examine PD-L1 expression and localization with immunofluorescence co-localization, and to evaluate intestinal PD-L1 expression with Western blot. Peripheral blood was collected for flow cytometry to examine leukocyte subpopulations and their PD-L1 expression. On the other hand, 14 PD-L1 (+/+) mice and 14 PD-L1 (-/-) mice were randomly divided into their respective genotype control groups and model groups. The same induction method as was already mentioned was adopted for the model groups. The intestines of the mice were collected for HE staining to evaluate the pathological change and peripheral blood was collected to examine the expression of inflammatory factors. Results: The NEC mouse model was successfully constructed. PD-L1 was widely expressed in enterocytes and inflammatory cells in the mouse intestines and in T cells, monocytes, and neutrophils in peripheral blood. The expression of PD-L1 in NEC mouse intestines increased in comparison with that of the control group. In the peripheral blood of NEC mice, the proportion of T cells and monocytes and their PD-L1 expression showed no significant changes compared with those of the control group, while the proportion of neutrophils and their PD-L1 expression increased by about 140% and 150%, respectively, in comparison with those of the control group ( P<0.05). According to the results of the PD-L1 gene mouse experiment, the control groups of PD-L1 (+/+) mice and PD-L1 (-/-) mice showed no significant difference in their intestinal conditions and serum inflammatory factor levels, while the PD-L1 (-/-) NEC mouse had worse intestinal pathological changes and increased mean pathological scores compared with those of PD-L1 (+/+) NEC mouse ( P<0.05). In addition, serum interleukin (IL)-10 in PD-L1 (-/-) NEC mouse decreased by about 44% compared with that of PD-L1 (+/+) NEC mice, and chemokine (C-X-C motif) ligand 1/IL-6/IL-1ß all increased by more than 25% (all P<0.05). Conclusion: PD-L1 is widely expressed in inflammatory cells and enterocytes in mice. Knocking out PD-L1 aggravates the degree of NEC inflammation and intestinal pathological changes. PD-L1 plays a protective role by reducing inflammation in the pathogenesis of NEC, the mechanism of which may be related to the regulation of neutrophils/enterocytes.


Assuntos
Antígeno B7-H1 , Enterocolite Necrosante , Animais , Antígeno B7-H1/genética , Modelos Animais de Doenças , Enterocolite Necrosante/genética , Enterocolite Necrosante/metabolismo , Enterocolite Necrosante/patologia , Inflamação , Interleucina-1beta , Camundongos , Camundongos Endogâmicos C57BL
12.
Front Plant Sci ; 13: 870949, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35668809

RESUMO

Urticeae s.l., a tribe of Urticaceae well-known for their stinging trichomes, consists of more than 10 genera and approximately 220 species. Relationships within this tribe remain poorly known due to the limited molecular and taxonomic sampling in previous studies, and chloroplast genome (CP genome/plastome) evolution is still largely unaddressed. To address these concerns, we used genome skimming data-CP genome and nuclear ribosomal DNA (18S-ITS1-5.8S-ITS2-26S); 106 accessions-for the very first time to attempt resolving the recalcitrant relationships and to explore chloroplast structural evolution across the group. Furthermore, we assembled a taxon rich two-locus dataset of trnL-F spacer and ITS sequences across 291 accessions to complement our genome skimming dataset. We found that Urticeae plastomes exhibit the tetrad structure typical of angiosperms, with sizes ranging from 145 to 161 kb and encoding a set of 110-112 unique genes. The studied plastomes have also undergone several structural variations, including inverted repeat (IR) expansions and contractions, inversion of the trnN-GUU gene, losses of the rps19 gene, and the rpl2 intron, and the proliferation of multiple repeat types; 11 hypervariable regions were also identified. Our phylogenomic analyses largely resolved major relationships across tribe Urticeae, supporting the monophyly of the tribe and most of its genera except for Laportea, Urera, and Urtica, which were recovered as polyphyletic with strong support. Our analyses also resolved with strong support several previously contentious branches: (1) Girardinia as a sister to the Dendrocnide-Discocnide-Laportea-Nanocnide-Zhengyia-Urtica-Hesperocnide clade and (2) Poikilospermum as sister to the recently transcribed Urera sensu stricto. Analyses of the taxon-rich, two-locus dataset showed lower support but was largely congruent with results from the CP genome and nuclear ribosomal DNA dataset. Collectively, our study highlights the power of genome skimming data to ameliorate phylogenetic resolution and provides new insights into phylogenetic relationships and chloroplast structural evolution in Urticeae.

13.
Foods ; 11(12)2022 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-35741985

RESUMO

Purple non-heading Chinese cabbage is one of the most popular vegetables, and is rich in various health-beneficial anthocyanins. Research related to genes associated with anthocyanin biosynthesis in non-heading Chinese cabbage is important. This study performed integrative transcriptome and metabolome analysis in the purple non-heading Chinese cabbage wild type (WT) and its green mutant to elucidate the formation of purple leaves. The anthocyanin level was higher in purple than in green plants, while the contents of chlorophyll and carotenoid were higher in the green mutant than in the purple WT. Twenty-five anthocyanins were identified in purple and green cultivars; eleven anthocyanin metabolites were identified specifically in the purple plants. RNA-seq analysis indicated that 27 anthocyanin biosynthetic genes and 83 transcription factors were significantly differentially expressed between the WT and its mutant, most of them with higher expression in the purple than green non-heading Chinese cabbage. Transcriptome and metabolome analyses showed that UGT75C1 catalyzing the formation of pelargonidin-3,5-O-diglucoside and cyanidin-3,5-O-diglucoside may play a critical role in purple leaf formation in non-heading Chinese cabbage. Therefore, these results provide crucial information for elucidating the formation of purple leaves in non-heading Chinese cabbage.

14.
Int J Mol Sci ; 23(12)2022 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-35743224

RESUMO

Dendrobium sinense, an endemic medicinal herb in Hainan Island, is rich in bibenzyls. However, the key rate-limited enzyme involved in bibenzyl biosynthesis has yet to be identified in D. sinense. In this study, to explore whether there is a significant difference between the D. sinense tissues, the total contents of bibenzyls were determined in roots, pseudobulbs, and leaves. The results indicated that roots had higher bibenzyl content than pseudobulbs and leaves. Subsequently, transcriptomic sequencings were conducted to excavate the genes encoding type III polyketide synthase (PKS). A total of six D. sinense PKS (DsPKS) genes were identified according to gene function annotation. Phylogenetic analysis classified the type III DsPKS genes into three groups. Importantly, the c93636.graph_c0 was clustered into bibenzyl synthase (BBS) group, named as D. sinense BBS (DsBBS). The expression analysis by FPKM and RT-qPCR indicated that DsBBS showed the highest expression levels in roots, displaying a positive correlation with bibenzyl contents in different tissues. Thus, the recombinant DsBBS-HisTag protein was constructed and expressed to study its catalytic activity. The molecular weight of the recombinant protein was verified to be approximately 45 kDa. Enzyme activity analysis indicated that the recombinant DsBBS-HisTag protein could use 4-coumaryol-CoA and malonyl-CoA as substrates for resveratrol production in vitro. The Vmax of the recombinant protein for the resveratrol production was 0.88 ± 0.07 pmol s-1 mg-1. These results improve our understanding with respect to the process of bibenzyl biosynthesis in D. sinense.

15.
Ying Yong Sheng Tai Xue Bao ; 33(6): 1511-1517, 2022 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-35729127

RESUMO

To select the tree species assembly model for improving the productivity in south subtropical plantations, we carried out an experiment following a random block design with eight native tree species across a richness gradient of 1, 2, 4, and 6 species. The effects of tree species diversity and species mixing with different functional identities on the young tree growth were investigated in the 5th year of the experiment. The results showed that tree growth was not positively correlated with tree species richness. The growth of fast-growing tree species (Pinus massoniana and Mytilaria laosensis) in the monoculture was 2.5-4.5 times of the valuable broadleaved tree species (Castanopsis hystrix and Erythrophleum fordii) monoculture. Tree growth was significantly increased by 51.5%-132.8% in the conifer and broadleaved tree species mixing plantations and in the fast-growing and nitrogen fixation tree species mixing plantations, when two tree species or four tree species were mixed. There was no significant difference in tree growth among different tree species mixed types, when six tree species were mixed. The contents of soil nitrogen, phosphorus and organic matter were the main factors affecting tree growth. The results indicated that young tree growth could be improved through the selecting conifer and broadleaved tree species mixing, fast-growing and nitrogen fixation tree species mixing in south subtropical plantations.


Assuntos
Pinus , Árvores , China , Nitrogênio/análise , Fósforo , Solo
16.
BMC Med ; 20(1): 207, 2022 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-35710548

RESUMO

BACKGROUND: Osteoarthritis (OA) is a worldwide public health concern, mainly afflicting older adults. Although the etiology of OA remains unclear, environmental factors are increasingly considered as non-negligible risk factors. This study aims to evaluate the associations of urinary metals with OA risk and the mediated effect of biological aging. METHODS: Nine urinary metal concentrations were detected among 12,584 U.S. adults based on the National Health and Nutrition Examination Survey (NHANES), including barium (Ba), cadmium (Cd), cobalt (Co), cesium (Cs), molybdenum (Mo), lead (Pb), antimony (Sb), thallium (Tl), and uranium (Tu). Multivariable logistic regression and weighted quantile sum (WQS) regression were used to explore the associations of single metal and mixed metals with OA risk, respectively. Furthermore, biological aging was measured from different perspectives, including cell senescence (telomere length) and whole-body aging (phenotypic age and biological age). Mediation analyses were conducted to investigate the mediated effects of aging on the associations of metals with OA risk. RESULTS: In the single-exposure model, Cd, Co, and Cs were identified to be positively associated with OA risk, with odds ratios (OR) ranging from 1.48 to 1.64 (all P < 0.05). Mixed-exposure analyses showed consistent associations (OR 1.23, 95%CI 1.10 to 1.37) and highlighted that Cd, Co, and Cs were responsible for the outcomes. Additionally, Cd, Co, Cs, Pb, and Tl were positively associated with biological aging markers, while all biological aging markers had significant associations with OA risk. Further mediation analyses showed that the associations of single metal (mainly Cd and Cs) and mixed metals with OA risk parallelly mediated by the above biological aging markers, with the proportion of mediation ranging from 16.89 to 69.39% (all P < 0.05). Moreover, such associations were also serially mediated through telomere length-biological age path and telomere length-phenotypic age path (the proportion of mediation: 4.17-11.67%), indicating that metals accelerated cell senescence to lead to whole-body aging and finally aggravated OA progress. CONCLUSIONS: These findings suggested that exposure to metals increased OA risk, which was possibly and partly mediated by biological aging.


Assuntos
Cádmio , Osteoartrite , Idoso , Envelhecimento , Biomarcadores , Exposição Ambiental , Humanos , Chumbo/análise , Chumbo/toxicidade , Inquéritos Nutricionais , Osteoartrite/epidemiologia
17.
Artigo em Inglês | MEDLINE | ID: mdl-35738895

RESUMO

BACKGROUND: The aetiology of diabetes is complex with limited treatment strategies. Growing animal studies have shown that targeted antiageing can improve the outcomes of diabetes. However, population evidence is limited. This study aims to evaluate the associations of biological ageing with all-cause and cause-specific mortality among people with diabetes. METHODS: A total of 5278 people with diabetes from the National Health and Nutrition Examination Survey 1999-2014 were included. Biological ageing was measured from different perspectives, including phenotypic age, biological age, telomere length and klotho concentration. Phenotypic/biological age acceleration was the residual resulting from a linear model when regressing phenotypic/biological age on chronological age. Cox proportional hazards models were used to examine the relationships between ageing and all-cause, cardiovascular disease (CVD), and cancer mortality. RESULTS: Over median follow-up for 7.3 years, 1355 diabetics died. There was a positive and linear association of mortality with phenotypic age acceleration (HRall-cause 1.04; HRCVD 1.04; HRcancer 1.04, p<0.001) and biological age acceleration (HRall-cause 1.03; HRCVD 1.04; HRcancer 1.03, p<0.001). Telomere length was inversely associated with all-cause mortality (tertile (T)3 vs T1: HR 0.67, p<0.05). The concentration of klotho had a U-shaped relationship with mortality (T2 vs T1: HRall-cause 0.62; HRCVD 0.48; HRcancer 0.47, p<0.05). Further, stratified analysis by age and sex found that the associations of ageing-related markers with mortality were more significant in the aged and female subgroup. CONCLUSIONS: Biological ageing was positively associated with mortality among people with diabetes, indicating therapies targeting antiageing could be encouraged to halt the progression of diabetes.

18.
Neural Plast ; 2022: 2847672, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35677839

RESUMO

Background: Helicobacter pylori (H. pylori) infection is closely associated with depression and development of neuroinflammation. The aim of this study is to explore the relationship between H. pylori, depression, and circulating levels of ghrelin. Methods: Mice were randomly divided into three groups: healthy control group (gavaged sterile saline and injected with saline, n = 8); H. pylori+saline group (gavaged H. pylori and injected with saline, n = 8); and H. pylori+rapa group (gavaged H. pylori and injected with rapamycin, n = 8). Open field test (OFT), sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST) were used for anxiety and depressive behavior test. Western blotting was utilized to assess mTOR, p-mTOR, and GSMD expression, and serum ghrelin levels were estimated using ELISA. Results: In the OFT, the control mice moved more and exhibited a increase in crossing number relative to the H. pylori+saline mice (all P < 0.05). Increased quantity of fecal boli can be indicative of increased anxiety and emotionality of the subject animal. H. pylori+saline mice exhibited an increase in fecal boli when compared to control mice and H. pylori+rapa mice (P < 0.05). H. pylori infected mice decreasing the expression of ghrelin. The protein levels of p-mTOR/mTOR in the gastric antrum mTOR signaling activation and low-level ghrelin in H. pylori-infect mice compared to those in control mice (all P <0.001). Compared with single H. pylori infection, mTOR inhibitors increased the ghrelin secretion of H. pylori infection to a certain extent (P < 0.05). The protein levels of GSDMD expression significantly increase in hippocampus of H. pylori-infected mice (P < 0.001). Rapamycin treatment inhibited expression of GSDMD in H. pylori-infected mice (P < 0.05). Conclusions: H. pylori infection is associated with increased expression of mTOR and decreased circulating levels of ghrelin. Elevated pyroptosis in the brain and anxiety- and depressed-like behaviors occur when ghrelin levels are suppressed.


Assuntos
Infecções por Helicobacter , Helicobacter pylori , Animais , Ansiedade/tratamento farmacológico , Grelina , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Camundongos , Sirolimo/farmacologia , Serina-Treonina Quinases TOR
19.
Front Pharmacol ; 13: 907108, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35694252

RESUMO

Membranous nephropathy (MN) is the most common cause of nephrotic syndrome among adults, which is the leading glomerular disease that recurs after kidney transplantation. Treatment for MN remained controversial and challenging, partly owing to absence of sensitive and specific biomarkers and effective therapy for prediction and diagnosis of disease activity. MN starts with the formation and deposition of circulating immune complexes on the outer area in the glomerular basement membrane, leading to complement activation. The identification of autoantibodies against the phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing protein 7A (THSD7A) antigens illuminated a distinct pathophysiological rationale for MN treatments. Nowadays, detection of serum anti-PLA2R antibodies and deposited glomerular PLA2R antigen can be routinely applied to MN. Anti-PLA2R antibodies exhibited much high specificity and sensitivity. Measurement of PLA2R in immune complex deposition allows for the diagnosis of PLA2R-associated MN in patients with renal biopsies. In the review, we critically summarized newer diagnosis biomarkers including PLA2R and THSD7A tests and novel promising therapies by using traditional Chinese medicines such as Astragalus membranaceus, Tripterygium wilfordii, and Astragaloside IV for the treatment of MN patients. We also described unresolved questions and future challenges to reveal the diagnosis and treatments of MN. These unprecedented breakthroughs were quickly translated to clinical diagnosis and management. Considerable advances of detection methods played a critical role in diagnosis and monitoring of treatment.

20.
Arthritis Res Ther ; 24(1): 142, 2022 Jun 14.
Artigo em Inglês | MEDLINE | ID: mdl-35701843

RESUMO

BACKGROUND: Systemic lupus erythematosus (SLE) can cause placental dysfunctions, which may result in pregnancy complications. Long noncoding RNAs (lncRNAs) are actively involved in the regulation of immune responses during pregnancy. The present study aimed to determine the lncRNA expression profiles in placentas from women with SLE to gain new insights into the underlying molecular mechanisms in SLE pregnancies. METHODS: RNA sequencing (RNA-seq) analysis was performed to identify SLE-dysregulated lncRNAs and mRNAs in placentas from women with SLE and normal full-term (NT) pregnancies. Bioinformatics analysis was conducted to predict the biological functions of these SLE-dysregulated lncRNAs and mRNAs. RESULTS: RNA-seq analysis identified 52 dysregulated lncRNAs in SLE placentas, including 37 that were upregulated and 15 downregulated. Additional 130 SLE-dysregulated mRNAs were discovered, including 122 upregulated and 8 downregulated. Bioinformatics analysis revealed that SLE-dysregulated genes were associated with biological functions and gene networks, such as regulation of type I interferon-mediated signaling pathway, response to hypoxia, regulation of MAPK (mitogen-activated protein kinase) cascade, response to steroid hormone, complement and coagulation cascades, and Th1 and Th2 cell differentiation. CONCLUSIONS: This is the first report of the lncRNA profiles in placentas from SLE pregnancies. These results suggest that the aberrant expression and the potential regulatory function of lncRNAs in placentas may play comprehensive roles in the pathogenesis of SLE pregnancies. SLE-dysregulated lncRNAs may potentially serve as biomarkers for SLE.


Assuntos
Lúpus Eritematoso Sistêmico , RNA Longo não Codificante , Feminino , Perfilação da Expressão Gênica/métodos , Redes Reguladoras de Genes , Humanos , Placenta/metabolismo , Placenta/patologia , Gravidez , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , RNA Mensageiro/genética
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