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1.
Food Chem ; 366: 130613, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34304136

RESUMO

A colorimetric and fluorescence dual-signal method based on sulfur quantum dots (SQDs) was established for determination of iron (II) (Fe2+) and H2O2 in foods. Due to the complexation of Fe2+ with SQD, Fe2+ can cause fluorescence quenching of SQDs, and the color of the mixed solution changed from light yellow to deep green. By use of Fenton reaction, H2O2 can restore the quenched fluorescence of SQDs, and the color of the mixture changed from green to colorless. The concentration of Fe2+ and H2O2 has a good linear relationship with the fluorescence intensity and absorbance in the range of 2.5-55 µM and 1.25-500 µM, and the detection limits were 1.41 µM and 0.54 µM, respectively. For determination of H2O2, the linear ranges were 1.17-1.97 mM and 0.867-1.50 mM, and the detection limits were 0.03 µM and 0.06 µM, respectively.

2.
Zhongguo Zhong Yao Za Zhi ; 46(12): 3116-3122, 2021 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-34467703

RESUMO

Screening suitable reference genes is the premise of quantitative Real-time PCR(qRT-PCR)for gene expression analysis. To provide stable reference genes for expression analysis of genes in Aconitum vilmorinianum, this study selected 19 candidate re-ference genes(ACT1, ACT2, ACT3, aTUB1, aTUB2, bTUB, 18S rRNA, UBQ, eIF2, eIF3, eIF4, eIF5, CYP, GAPDH1, GAPDH2, PP2A1, PP2A2, ACP, and EF1α) based on the transcriptome data of A. vilmorinianum. qRT-PCR was conducted to profile the expression of these genes in the root, stem, leaf, and flower of A. vilmorinianum. The Ct values showed that 18S rRNA with high expression level and GAPDH2 with large expression difference among organs were not suitable as the reference genes. NormFinder and geNorm showed similar results of the expression stability of the other candidate reference genes and demonstrated PP2A1, EF1α, and CYP as the highly stable ones. However, BestKeeper suggested EF1α, ACT3, and PP2A1 as the top stable genes. In view of the different results from different softwares, the geometric mean method was employed to analyze the expression stability of the candidate re-ference genes, the results of which indicated that PP2A1, EF1α, and ACT3 were the most stable. Based on the comprehensive analysis results of geNorm, NormFinder, BestKeeper, and geometric mean method, PP2A1 and EF1α presented the most stable expression in different organs of A. vilmorinianum. PP2A1 and EF1α were the superior reference genes for gene expression profiling in different organs of A. vilmorinianum.


Assuntos
Aconitum , Perfilação da Expressão Gênica , Genes de Plantas/genética , Reação em Cadeia da Polimerase em Tempo Real , Padrões de Referência , Reação em Cadeia da Polimerase Via Transcriptase Reversa
3.
Biomed Pharmacother ; 143: 112121, 2021 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-34474346

RESUMO

Obesity has been recognized as a major risk factor for the development of chronic cardiomyopathy, which is associated with increased cardiac inflammation, fibrosis, and apoptosis. We previously developed an anti-inflammatory compound C66, which prevented inflammatory diabetic complications via targeting JNK. In the present study, we have tested the hypothesis that C66 could prevent obesity-induced cardiomyopathy by suppressing JNK-mediated inflammation. High-fat diet (HFD)-induced obesity mouse model and palmitic acid (PA)-challenged H9c2 cells were used to develop inflammatory cardiomyopathy and evaluate the protective effects of C66. Our data demonstrate a protective effect of C66 against obesity-induced cardiac inflammation, cardiac hypertrophy, fibrosis, and dysfunction, overall providing cardio-protection. C66 administration attenuates HFD-induced myocardial inflammation by inhibiting NF-κB and JNK activation in mouse hearts. In vitro, C66 prevents PA-induced myocardial injury and apoptosis in H9c2 cells, accompanied with inhibition against PA-induced JNK/NF-κB activation and inflammation. The protective effect of C66 is attributed to its potential to inhibit JNK activation, which led to reduced pro-inflammatory cytokine production and reduced apoptosis in cardiomyocytes both in vitro and in vivo. In summary, C66 provides significant protection against obesity-induced cardiac dysfunction, mainly by inhibiting JNK activation and JNK-mediated inflammation. Our data indicate that inhibition of JNK is able to provide significant protection against obesity-induced cardiac dysfunction.

4.
Eur Heart J ; 2021 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-34506618

RESUMO

AIMS : This study aimed to assess the clinical characteristics and long-term survival outcome in patients with Takayasu's arteritis-associated pulmonary hypertension (TA-PH). METHODS AND RESULTS: We conducted a nationally representative cohort study of TA-PH using data from the National Rare Diseases Registry System of China. Patients with pulmonary artery involvement who fulfilled the diagnostic criteria of Takayasu's arteritis and pulmonary hypertension were included. The primary outcome was the time from diagnosis of TA-PH to the occurrence of all-cause death. Between January 2007 and January 2019, a total of 140 patients were included, with a mean age of 41.4 years at diagnosis, and a female predominance (81%). Patients with TA-PH had severely haemodynamic and functional impairments at diagnosis. Significant improvements have been found in N-terminal pro-B-type natriuretic peptide (NT-proBNP) and haemodynamic profiles in patients with TA-PH receiving drugs approved for pulmonary arterial hypertension. The overall 1-, 3-, and 5-year survival rates in TA-PH were 94.0%, 83.2%, and 77.2%, respectively. Predictors associated with an increased risk of all-cause death were syncope [adjusted hazard ratio (HR) 5.38 (95% confidence interval 1.77-16.34), P = 0.003], NT-proBNP level [adjusted HR 1.04 (1.03-1.06), P < 0.001], and mean right atrial pressure [adjusted HR 1.07 (1.01-1.13), P = 0.015]. CONCLUSION : Patients with TA-PH were predominantly female and had severely compromised haemodynamics. More than 80% of patients in our cohort survived for at least 3 years. Medical treatment was based on investigators' personal opinions, and no clear risk-to-benefit ratio can be derived from the presented data.

5.
Chem Biol Interact ; 348: 109648, 2021 Sep 08.
Artigo em Inglês | MEDLINE | ID: mdl-34506766

RESUMO

Allium chinense is a vegetable with nutrition and unique flavor, and it is used as traditional Chinese medicine. We previously reported that the active compound A-24 induces apoptosis and autophagy in p53 wild-type gastric cancer cells through the PI3K/Akt/mTOR pathway. Our present work indicates that A-24 also has a significant proliferation inhibition effect on p53-deficient KATO-III cells, and the p53 status did not affect A-24 induced migration inhibition, but negatively controlled the occurrence of autophagy. We also found that the accumulation of reactive oxygen species (ROS) mediated A-24 induced apoptosis is p53-independent. Besides, p-Akt was not downregulated by A-24 in p53-deficient gastric cancer cells. Taken together, our results indicate that A-24 induced apoptosis and autophagy via the ROS-PI3K/Akt/mTOR pathway in p53 wild-type gastric cancer cells and through the ROS-mTOR pathway in p53-deficient gastric cancer cells. Our study recommended A-24 as a promising future phytotherapeutic candidate for gastric cancer treatment.

6.
Aging (Albany NY) ; 13(17): 21610-21627, 2021 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-34507301

RESUMO

Sepsis is the leading cause of death in hospital intensive care units. In light of recent studies showing that variations in N6-methyladenosine (m6A) levels in different RNA transcripts influence inflammatory responses, we evaluated the m6A profiles of rat aortic mRNAs and lncRNAs after lipopolysaccharide (LPS)-induced sepsis. LC-MS-based mRNA modification analysis showed that global m6A levels were significantly decreased in aortic tissue of rats injected intraperitoneally with LPS. This finding was consistent with downregulated expression of METTL3 and WTAP, two members of the m6A writer complex, in LPS-exposed aortas. Microarray analysis of m6A methylation indicated that 40 transcripts (31 mRNAs and 9 lncRNAs) were hypermethylated, while 223 transcripts (156 mRNAs and 67 lncRNAs) were hypomethylated, in aortic tissue from LPS-treated rats. On GO and KEGG analyses, 'complement and coagulation cascades', 'transient receptor potential channels', and 'organic anion transmembrane transporter activity' were the major biological processes modulated by the differentially m6A methylated mRNAs. In turn, competing endogenous RNA network analysis suggested that decreased m6A levels in lncRNA-XR_343955 may affect the inflammatory response through the cell adhesion molecule pathway. Our data suggest that therapeutic modulation of the cellular m6A machinery may be useful to preserve vascular integrity and function during sepsis.

7.
Neuroimage Clin ; 32: 102786, 2021 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-34500428

RESUMO

The aim of this study was to assess, in the context of cerebral small vessel disease (CSVD), whether cardiovascular risk factors and white matter hyperintensities (WMHs) were associated with brain tissue susceptibility as measured by quantitative susceptibility mapping (QSM). Given that CSVD is diagnosed by the presence of lacunar strokes, periventricular and deep WMHs, increased perivascular spaces, and microbleeds, we expected that QSM could capture changes in brain tissue due to underlying CSVD pathology. We compared a cohort of 101 HIV-infected individuals (mean age ± SD = 53.2 ± 10.9 years) with mild to moderate cardiovascular risk scores, as measured by the Reynolds risk score, to 102 age-matched controls (mean age (SD) = 50.3 (15.7) years) with similar Reynolds scores. We performed brain MRI to assess CSVD burden by acquiring 3D T1-MPRAGE, 3D FLAIR, 2D T2-TSE, and mGRE for QSM. We found that signs of CSVD are significantly higher in individuals with HIV-infection compared to controls and that WMH volumes are significantly correlated with age and cardiovascular risk scores. Regional QSM was associated with cardiovascular risk factors, age, sex, and WMH volumes but not HIV status. These results suggest that QSM may be an early imaging marker reflective of alterations in brain microcirculation.

8.
J Neuroimaging ; 2021 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-34480496

RESUMO

BACKGROUND AND PURPOSE: The objective ofthis study was to demonstrate a global cerebrospinal fluid (CSF) method for a consistent and automated zero referencing of brain quantitative susceptibility mapping (QSM). METHODS: Whole brain CSF mask was automatically segmented by thresholding the gradient echo transverse relaxation ( R 2 ∗ ) map, and regularization was employed to enforce uniform susceptibility distribution within the CSF volume in the field-to-susceptibility inversion. This global CSF regularization method was compared with a prior ventricular CSF regularization. Both reconstruction methods were compared in a repeatability study of 12 healthy subjects using t-test on susceptibility measurements, and in patient studies of 17 multiple sclerosis (MS) and 10 Parkinson's disease (PD) patients using Wilcoxon rank-sum test on radiological scores. RESULTS: In scan-rescan experiments, global CSF regularization provided more consistent CSF volume as well as higher repeatability of QSM measurements than ventricular CSF regularization with a smaller bias: -2.7 parts per billion (ppb) versus -0.13 ppb (t-test p<0.05) and a narrower 95% limits of agreement: [-7.25, 6.99] ppb versus [-16.60, 11.19 ppb] (f-test p<0.05). In PD and MS patients, global CSF regularization reduced smoothly varying shadow artifacts and significantly improved the QSM quality score (p<0.001). CONCLUSIONS: The proposed whole brain CSF method for QSM zero referencing improves repeatability and image quality of brain QSM compared to the ventricular CSF method.

9.
J Am Chem Soc ; 2021 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-34491051

RESUMO

An iron-catalyzed C-H functionalization of simple monosubstituted allenes is reported. An efficient protocol for this process was made possible by the use of a newly developed electron-rich and sterically hindered cationic cyclopentadienyliron dicarbonyl complex as the catalyst and N-sulfonyl hemiaminal ether reagents as precursors to iminium ion electrophiles. Under optimized conditions, the use of a mild, functional-group-tolerant base enabled the conversion of a range of monoalkyl allenes to their allenylic sulfonamido 1,1-disubstituted derivatives, a previously unreported and contrasteric regiochemical outcome for the C-H functionalization of electronically unbiased and directing-group-free allenes.

10.
Int J Mol Sci ; 22(17)2021 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-34502300

RESUMO

Folate depletion causes chromosomal instability by increasing DNA strand breakage, uracil misincorporation, and defective repair. Folate mediated one-carbon metabolism has been suggested to play a key role in the carcinogenesis and progression of hepatocellular carcinoma (HCC) through influencing DNA integrity. Methylenetetrahydrofolate reductase (MTHFR) is the enzyme catalyzing the irreversible conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate that can control folate cofactor distributions and modulate the partitioning of intracellular one-carbon moieties. The association between MTHFR polymorphisms and HCC risk is inconsistent and remains controversial in populational studies. We aimed to establish an in vitro cell model of liver origin to elucidate the interactions between MTHFR function, folate status, and chromosome stability. In the present study, we (1) examined MTHFR expression in HCC patients; (2) established cell models of liver origin with stabilized inhibition of MTHFR using small hairpin RNA delivered by a lentiviral vector, and (3) investigated the impacts of reduced MTHFR and folate status on cell cycle, methyl group homeostasis, nucleotide biosynthesis, and DNA stability, all of which are pathways involved in DNA integrity and repair and are critical in human tumorigenesis. By analyzing the TCGA/GTEx datasets available within GEPIA2, we discovered that HCC cancer patients with higher MTHFR had a worse survival rate. The shRNA of MTHFR (shMTHFR) resulted in decreased MTHFR gene expression, MTHFR protein, and enzymatic activity in human hepatoma cell HepG2. shMTHFR tended to decrease intracellular S-adenosylmethionine (SAM) contents but folate depletion similarly decreased SAM in wildtype (WT), negative control (Neg), and shMTHFR cells, indicating that in cells of liver origin, shMTHFR does not exacerbate the methyl group supply in folate depletion. shMTHFR caused cell accumulations in the G2/M, and cell population in the G2/M was inversely correlated with MTHFR gene level (r = -0.81, p < 0.0001), MTHFR protein expression (r = -0.8; p = 0.01), and MTHFR enzyme activity (r = -0.842; p = 0.005). Folate depletion resulted in G2/M cell cycle arrest in WT and Neg but not in shMTHFR cells, indicating that shMTHFR does not exacerbate folate depletion-induced G2/M cell cycle arrest. In addition, shMTHFR promoted the expression and translocation of nuclei thymidine synthetic enzyme complex SHMT1/DHFR/TYMS and assisted folate-dependent de novo nucleotide biosynthesis under folate restriction. Finally, shMTHFR promoted nuclear MLH1/p53 expression under folate deficiency and further reduced micronuclei formation and DNA uracil misincorporation under folate deficiency. In conclusion, shMTHFR in HepG2 induces cell cycle arrest in G2/M that may promote nucleotide supply and assist cell defense against folate depletion-induced chromosome segregation and uracil misincorporation in the DNA. This study provided insight into the significant impact of MTHFR function on chromosome stability of hepatic tissues. Data from the present study may shed light on the potential regulatory mechanism by which MTHFR modulates the risk for hepatic malignancies.

11.
Epilepsia ; 2021 Sep 12.
Artigo em Inglês | MEDLINE | ID: mdl-34510417

RESUMO

OBJECTIVE: China has the largest population of patients with epilepsy worldwide, which imposes a heavy burden on the public and health care systems. Several epidemiological surveys on epilepsy have been performed in China. Although these surveys grossly describe the prevalence and gap in treatment of epilepsy, the status of epilepsy centers is unclear. The number of epilepsy centers has increased substantially in recent decades. Therefore, a nationwide investigation of the scale and distribution, personnel, equipment, and epilepsy care capacity of each epilepsy center is of great value. METHODS: In 2017-2018, a multicenter cross-sectional survey was performed by the Commission on Standardized Development of Epilepsy Centers, China Association Against Epilepsy in 31 provinces, autonomous regions, and municipalities. The survey consisted of 74 questions divided into four sections: (1) overview, (2) personnel, (3) essential equipment and facilities, and (4) epilepsy care service capacity. The questions ranged from January 1, 2016 to December 31, 2016. The data were analyzed using descriptive statistics. RESULTS: There were 358 epilepsy centers for the 1.38 billion national population in 2016. Three quarters were in the eastern and western regions, and >90% were in tertiary hospitals. There were 9688 doctors engaged in epilepsy care, and 4.8% of doctors and electrophysiological physicians/technicians passed the national test for electroencephalography technical accreditation. A total of 9667 patients underwent resective surgeries in 2016. There were 888 vagus nerve stimulation procedures and 275 deep brain stimulation procedures. SIGNIFICANCE: This study is the first unique survey of epilepsy centers in China. Despite their rapid development, epilepsy centers cannot meet patients' needs at this stage. The results provide data-based evidence for the formulation of policies related to epilepsy service planning.

12.
Adv Mater ; : e2103262, 2021 Sep 12.
Artigo em Inglês | MEDLINE | ID: mdl-34510573

RESUMO

A plasmonic nanolaser architecture that can produce white-light emission is reported. A laser device is designed based on a mixed dye solution used as gain material sandwiched between two aluminum nanoparticle (NP) square lattices of different periodicities. The (±1, 0) and (±1, ±1) band-edge surface lattice resonance (SLR) modes of one NP lattice and the (±1, 0) band-edge mode of the other NP lattice function as nanocavity modes for red, blue, and green lasing respectively. From a single aluminum NP lattice, simultaneous red and blue lasing is realized from a binary dye solution, and the relative intensities of the two colors are controlled by the volume ratio of the dyes. Also, a laser device is constructed by sandwiching dye solutions between two Al NP lattices with different periodicities, which enables red-green and blue-green lasing. With a combination of three dyes as liquid gain, red, green, and blue lasing for a white-light emission profile is realized.

13.
Cancer Med ; 2021 Sep 12.
Artigo em Inglês | MEDLINE | ID: mdl-34510798

RESUMO

BACKGROUND: Computed tomography (CT)-detected extramural venous invasion (EMVI) has been identified as an independent factor that can be used for risk stratification and prediction of prognosis in patients with gastric cancer (GC). Overall survival (OS) is identified as the most important prognostic indicator for GC patients. However, the molecular mechanism of EMVI development and its potential relationship with OS in GC are not fully understood. In this radiogenomics-based study, we sought to investigate the molecular mechanism underlying CT-detected EMVI in patients with GC, and aimed to construct a genomic signature based on EMVI-related genes with the goal of using this signature to predict the OS. MATERIALS AND METHODS: Whole mRNA genome sequencing of frozen tumor samples from 13 locally advanced GC patients was performed to identify EMVI-related genes. EMVI-prognostic hub genes were selected based on overlapping EMVI-related differentially expressed genes and OS-related genes, using a training cohort of 176 GC patients who were included in The Cancer Genome Atlas database. Another 174 GC patients from this database comprised the external validation cohort. A risk stratification model using a seven-gene signature was constructed through the use of a least absolute shrinkage and selection operator Cox regression model. RESULTS: Patients with high risk score showed significantly reduced OS (training cohort, p = 1.143e-04; validation cohort, p = 2.429e-02). Risk score was an independent predictor of OS in multivariate Cox regression analyses (training cohort, HR = 2.758; 95% CI: 1.825-4.169; validation cohort, HR = 2.173; 95% CI: 1.347-3.505; p < 0.001 for both). Gene functions/pathways of the seven-gene signature mainly included cell proliferation, cell adhesion, regulation of metal ion transport, and epithelial to mesenchymal transition. CONCLUSIONS: A CT-detected EMVI-related gene model could be used to predict the prognosis in GC patients, potentially providing clinicians with additional information regarding appropriate therapeutic strategy and medical decision-making.

14.
Cancer Biomark ; 2021 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-34511486

RESUMO

BACKGROUND: Effective biomarkers for prediction of recurrence of lung adenocarcinoma cancer (LADC) patients are needed to determine treatment strategies post-surgery to improve outcome. OBJECTIVE: This study evaluates the efficacy of carboxypeptidase E (CPE) mRNA including its splice isoforms, CPE-ΔN, as a biomarker for predicting recurrence in adenocarcinoma patients. METHODS: RNA was extracted from resected tumors from 86 patients with different stages of non-small cell LADC. cDNA was synthesized and qRT-PCR carried out to determine the copy numbers of CPE/CPE-ΔN mRNA. Patients were followed for 7 years post-tumor resection to determine recurrence and death. RESULTS: ROC curve analysis showed the overall AUC for CPE/CPE-ΔN copy number was 0.563 in predicting recurrence and 0.563 in predicting death. Kaplan-Meier survival analysis showed statistical difference (p= 0.018), indicating that patients with high CPE/CPE-ΔN copy numbers had a shorter time of disease-free survival and also shorter time to death (p= 0.035). Subgroup analyses showed that association of disease-free survival time with CPE/CPE-ΔN copy number was stronger among stage I and II LADC patients (p= 0.047). CONCLUSIONS: CPE/CPE-ΔN mRNA is a potentially useful biomarker for predicting recurrence and death in LADC patients, especially in identifying patients at high risk of recurrence at early stages I and II.

15.
Neurochem Res ; 2021 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-34515922

RESUMO

Accumulated evidence has demonstrated causative links between neuropathic pain (NP) and immune-mediated inflammatory disorders. However, the role of inflammasome-induced pyroptosis in NP remains elusive. Melatonin possesses a well-documented analgesic action in various pain models. The current study aimed to test our hypothesis that melatonin regulated pyroptosis to alleviate NP by inhibiting NF-κB/NLRP3-dependent signaling. A rat model of spinal nerve ligation (SNL) was established to explore the potential association between melatonin and pyroptosis. Behavioral experiments revealed that SNL provoked severe allodynia which was suppressed by the administration of melatonin, a caspase-1 inhibitor (VX-765), or an NF-κB inhibitor (BAY 11-7085). SNL significantly up-regulated the inflammatory cytokines associated with the excessive activation of NLRP3 components and NF-κB signaling, as well as a marked pyroptosis activation. These effects were partially inhibited by melatonin, VX-765 or BAY 11-7085, and when melatonin and inhibitors were added together, the effect was enhanced. In conclusion, melatonin has potent analgesic and anti-inflammatory effects in SNL models through preventing pyroptosis via the NF-κB/NLRP3 inflammasome signaling pathway.

16.
Neoplasia ; 23(10): 1037-1047, 2021 Sep 09.
Artigo em Inglês | MEDLINE | ID: mdl-34509929

RESUMO

The E3 ubiquitin ligase adaptor Speckle-type POZ protein (SPOP) plays an important tumour suppressor role in prostate cancers (PCa), with mutation rate up to 15%. However, how SPOP mutations regulate prostate tumorigenesis remains elusive. Here, we report the identification of cell division cycle associated 5 (CDCA5) as a SPOP substrate. We found that SPOP interacts with CDCA5 and promotes its polyubiquitin degradation in a degron-dependent manner. This effect was greatly impaired by introducing PCa associated SPOP mutations. Importantly, we found that CDCA5 was essential for PCa cells to survive and proliferate. CDCA5 depletion in PCa cells led to cessation of proliferation, G2M arrest, severe sister chromatid aggregation disturbance, and apoptosis. we also found that CDCA5 knockdown decreased the protein expression of p-GSK3ß, increased the activity of caspase-3, caspase-9, and the Bax/Bcl-2 ratio. Besides, we confirmed that CDCA5 interrupted cancer cell behavior via the AKT pathway. In contrast, silencing SPOP or overexpressing CDCA5 increased cell proliferation. Consistently, depleting SPOP along with CDCA5, or overexpressing CDCA5 along with SPOP also caused the growth of cells repressed. Consistent with the functional role of CDCA5, the mRNA and protein levels of CDCA5 were significantly increased in PCa, compared to normal tissues, and its high expression was associated with more severe lymph node metastasis, higher Gleason score, and poorer prognosis. Together, our data showed that SPOP plays a crucial role in inhibiting tumorigenesis and partly achieved this by promoting the degradation of oncoprotein CDCA5.

17.
Org Lett ; 2021 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-34519513

RESUMO

This work describes an electrochemically promoted nickel-catalyzed deoxygenative thiolation of alcohols and ketones under mild conditions. Excellent substrate tolerance and good chemical yields can be achieved by graphene/nickel foam electrodes in an undivided cell. Further study to gain mechanistic insight into this electrochemical cross-coupling has been carried out.

18.
J Plant Physiol ; 266: 153510, 2021 Sep 03.
Artigo em Inglês | MEDLINE | ID: mdl-34521019

RESUMO

Source sink balance is one of the major determinants of carbon partitioning in plants. However, its effects on photosynthesis in fruit trees are largely unknown. In this work, the effects of low sink demand on net photosynthetic rate (Pn) and chlorophyll fluorescence after fruit removal (-fruit) in peach (Prunus persica (L.) Batsch cv. 'Zaojiubao') trees were investigated. The stepwise energy flow through photosystem II (PSII) at the reaction center (RC) was analyzed with quantitative analyses of fluorescence transient, also called JIP-test. We found that Pn was significantly lower and closely correlated to the leaf stomatal conductance (Gs) of -fruit trees than that of fruit retained (+fruit) trees. Leaf temperature (Tleaf) of -fruit trees was remarkably higher than that of +fruit trees. Day-time-period assays of chlorophyll (Chl) fluorescence revealed that, in the leaves of -fruit trees, the fluorescence parameters, such as NPQ (non-photochemical quenching coefficient) and ΦD0 (maximum quantum yield of non-photochemical de-excitation), decreased in the morning and recovered to the normal level in the afternoon, whereas other parameters, such as ΦE0 (quantum yield for electron transport at t = 0), Ψ0 (probability that a trapped exciton moves an electron to QA pool), F0 (minimum fluorescence, when all PSII RCs are open) and Wk (relative variable fluorescence at 300 µs of the chlorophyll fluorescence transient), did not. These results suggest that OEC complex and QA pool were irreversibly affected by low sink demand, whereas light harvest antenna and PSII potential efficiency retained a strong ability to recover.

19.
Artigo em Inglês | MEDLINE | ID: mdl-34524142

RESUMO

ABSTRACT: "Where there is a will, there is a way." It is never easy to make progress and development but with full dedication and firm commitment, many aspirations can still be realized. We would like to share with the readers the story of how we develop our division of orbital diseases and surgery from scratch to strengths over a period of 2 decades at the Department of Ophthalmology of Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, China.

20.
Biomaterials ; 277: 121108, 2021 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-34478929

RESUMO

Rare monogenic disorders are a group of single-gene-mutated diseases that have a low incidence rate (less than 0.5‰) and eventually lead to patient disability and even death. Due to the relatively low number of people affected, these diseases typically fail to attract a great deal of commercial investment and research interest, and the affected patients thus have unmet medical needs. Advances in genomics biology, gene editing, and gene delivery can now offer potentially effective options for treating rare monogenic diseases. Herein, we review the application of gene therapy strategies (traditional gene therapy and gene editing) against various rare monogenic diseases with nuclear or mitochondrial gene mutations, including eye, central nervous system, pulmonary, systemic, and blood cell diseases. We summarize their pathologic features, address the barriers to gene delivery for these diseases, discuss available therapies in the clinic and in clinical trials, and sum up in-development gene delivery systems for various rare monogenic disorders. Finally, we elaborate the possible directions and outlook of gene therapy for rare monogenic disorders.

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