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1.
Sci Rep ; 10(1): 4439, 2020 Mar 10.
Artigo em Inglês | MEDLINE | ID: mdl-32157148

RESUMO

The safety and efficacy of selective antegrade cerebral perfusion (SACP) in children undergoing aortic arch surgery are unclear. In this retrospective analysis, we compared moderate hypothermic circulatory arrest (MHCA; n = 61) plus SACP vs deep hypothermic circulatory arrest (DHCA; n = 53) in children undergoing aortic arch surgery during a period from January 2008 to December 2017. Demographic characteristics and the underlying anomalies were comparable between the two groups. The MHCA + SACP group had shorter cardiopulmonary bypass (CPB) time (146.9 ± 40.6 vs 189.6 ± 41.2 min for DHCA; p < 0.05) and higher nasopharyngeal temperature (26.0 ± 2.1 vs 18.9 ± 1.6 °C; p < 0.01). The MHCA + SACP group had lower rate of neurologic complications (3/61 vs 10/53 for DHCA; p < 0.05) but not complications in other organ systems. The MHCA + SACP group also had less 24-hour chest drainage (median, interquartile rage: 28.9, 12.6-150.0 vs 47.4, 15.2-145.0 ml/kg for DHCA; p < 0.05), shorter duration of postoperative mechanical ventilation (35.0, 15.4-80.3 vs 94.0, 42.0-144.0 h; p < 0.01), and shorter stay in intensive care unit (3.9, 3.0-7.0 vs 7.7, 5.0-15.0 d; p < 0.05). In regression analysis, in-hospital mortality was associated with longer CPB time. In conclusion, MHCA + SACP is associated with better short-term outcomes in children receiving aortic arch surgery under CPB.

2.
J Diabetes Res ; 2020: 9309768, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32051833

RESUMO

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease (ESRD), and therapeutic strategies for delaying its progression are limited. Loss of podocytes by apoptosis characterizes the early stages of DKD. To identify novel therapeutic options, we investigated the effects of Xuesaitong (XST), consisting of total saponins from Panax notoginseng, on podocyte apoptosis in streptozotocin- (STZ-) induced diabetic rats. XST (5 mg/kg·d) or Losartan (10 mg/kg·d) was given to diabetic rats for 12 weeks. Albuminuria, renal function markers, and renal histopathology morphological changes were examined. Podocyte apoptosis was determined by triple immunofluorescence labelling including a TUNEL assay, WT1, and DAPI. Renal expression of Nox4, miRNA-214, PTEN, PDK1, phosphorylated Akt, mTOR, and mTORC1 was detected. In diabetic rats, severe hyperglycaemia and albuminuria developed, and apoptotic podocytes were markedly increased in diabetic kidneys. However, XST attenuated albuminuria, mesangial expansion, podocyte apoptosis, and morphological changes of podocytes in diabetic rats. Decreased expression of PTEN, as well as increased expression of Nox4, miRNA-214, PDK1, phosphorylated Akt, mTOR, and mTORC1, was detected. These abnormalities were partially restored by XST treatment. Thus, XST ameliorated podocyte apoptosis partly through modulating the PTEN-PDK1-Akt-mTOR pathway. These novel findings might point the way to a natural therapeutic strategy for treating DKD.

3.
Nature ; 578(7796): 577-581, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-32076270

RESUMO

Hydrogen peroxide (H2O2) is a major reactive oxygen species in unicellular and multicellular organisms, and is produced extracellularly in response to external stresses and internal cues1-4. H2O2 enters cells through aquaporin membrane proteins and covalently modifies cytoplasmic proteins to regulate signalling and cellular processes. However, whether sensors for H2O2 also exist on the cell surface remains unknown. In plant cells, H2O2 triggers an influx of Ca2+ ions, which is thought to be involved in H2O2 sensing and signalling. Here, by using forward genetic screens based on Ca2+ imaging, we isolated hydrogen-peroxide-induced Ca2+ increases (hpca) mutants in Arabidopsis, and identified HPCA1 as a leucine-rich-repeat receptor kinase belonging to a previously uncharacterized subfamily that features two extra pairs of cysteine residues in the extracellular domain. HPCA1 is localized to the plasma membrane and is activated by H2O2 via covalent modification of extracellular cysteine residues, which leads to autophosphorylation of HPCA1. HPCA1 mediates H2O2-induced activation of Ca2+ channels in guard cells and is required for stomatal closure. Our findings help to identify how the perception of extracellular H2O2 is integrated with responses to various external stresses and internal cues in plants, and have implications for the design of crops with enhanced fitness.

4.
Chem Asian J ; 2020 Feb 06.
Artigo em Inglês | MEDLINE | ID: mdl-32026606

RESUMO

Owing to the high specific capacity and energy density, metal oxides have become very promising electrodes for lithium-ion batteries (LIBs). However, poor electrical conductivity accompanied with inferior cycling stability resulting from large volume changes are the main obstacles to achieve a high reversible capacity and stable cyclability. Herein, a facile and general approach to fabricate SnO2 , Fe2 O3 and Fe2 O3 /SnO2 fibers is proposed. The appealing structural features are favorable for offering a shortened lithium-ion diffusion length, easy access for the electrolyte and reduced volume variation when used as anodes in LIBs. As a consequence, both single and hybrid oxides show satisfactory reversible capacities (1206 mAh g-1 for Fe2 O3 and 1481 mAh g-1 for Fe2 O3 /SnO2 after 200 cycles at 200 mA g-1 ) and long lifespans.

5.
Drug Des Devel Ther ; 14: 527-538, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32103895

RESUMO

Introduction: Epithelial-mesenchymal transition (EMT) may contribute to podocyte dysfunction in diabetic nephropathy (DN). Aiming to identify novel therapeutic options, we investigated the protective effects of Panax notoginseng (PN) on podocyte EMT in diabetic rats and explored its mechanisms. Methods: Diabetes was induced in rats with streptozotocin (STZ) by intraperitoneal injection at 55 mg/kg. Diabetic rats were randomly divided into three groups, namely, diabetic rats, diabetic rats treated with beraprost sodium (BPS) at 0.6 mg/kg/d or PN at 0.4 g/kg/d p.o., for 12 weeks. Urinary albumin/creatinine ratio (ACR), biochemical parameters, renal histopathology, and podocyte morphological changes were evaluated. Protein expression of EMT markers (desmin, α-SMA, and nephrin) as well as components of the Wnt/ß-catenin pathway (wnt1, ß-catenin, and snail) was detected by immunohistochemistry and Western blot, respectively. Results: In diabetic rats, severe hyperglycemia and albuminuria were detected. Moreover, mesangial expansion and podocyte foot process effacement were found markedly increased in diabetic kidneys. Increased protein expression of wnt1, ß-catenin, snail, desmin, and α-SMA, as well as decreased protein expression of nephrin was detected in diabetic kidneys. All these abnormalities found in DN rats were partially restored by PN treatment. Conclusion: PN ameliorated albuminuria and podocyte EMT in diabetic rats partly through inhibiting Wnt/ß-catenin signaling pathway. These findings provide experimental arguments for a novel therapeutic option in DN.

6.
Theranostics ; 10(4): 1649-1677, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32042328

RESUMO

Rationale: Autophagy in Schwann cells (SCs) is crucial for myelin debris degradation and clearance following peripheral nerve injury (PNI). Nerve growth factor (NGF) plays an important role in reconstructing peripheral nerve fibers and promoting axonal regeneration. However, it remains unclear if NGF effect in enhancing nerve regeneration is mediated through autophagic clearance of myelin debris in SCs. Methods: In vivo, free NGF solution plus with/without pharmacological inhibitors were administered to a rat sciatic nerve crush injury model. In vitro, the primary Schwann cells (SCs) and its cell line were cultured in normal medium containing NGF, their capable of swallowing or clearing degenerated myelin was evaluated through supplement of homogenized myelin fractions. Results: Administration of exogenous NGF could activate autophagy in dedifferentiated SCs, accelerate myelin debris clearance and phagocytosis, as well as promote axon and myelin regeneration at early stage of PNI. These NGF effects were effectively blocked by autophagy inhibitors. In addition, inhibition of the p75 kD neurotrophin receptor (p75NTR) signal or inactivation of the AMP-activated protein kinase (AMPK) also inhibited the NGF effect as well. Conclusions: NGF effect on promoting early nerve regeneration is closely associated with its accelerating autophagic clearance of myelin debris in SCs, which probably regulated by the p75NTR/AMPK/mTOR axis. Our studies thus provide strong support that NGF may serve as a powerful pharmacological therapy for peripheral nerve injuries.

7.
J Med Chem ; 63(3): 1216-1232, 2020 Feb 13.
Artigo em Inglês | MEDLINE | ID: mdl-31895569

RESUMO

Several epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors have been developed and approved by Food and Drug Administration for the treatment of non-small-cell lung cancers, but their efficacy can be compromised by acquired drug resistance conferred by EGFR-mutant variants. Here, we described the discovery of a novel E3 ligase von Hippel-Lindau-recruiting EGFR degrader, MS39 (compound 6), and a first-in-class E3 ligase cereblon-recruiting EGFR degrader, MS154 (compound 10), using the proteolysis targeting chimera technology. These compounds potently induced the degradation of mutant but not wild-type EGFR in an E3 ligase-dependent manner in cancer cell lines and effectively suppressed the growth of lung cancer cells compared with the corresponding negative controls. The global proteomic analyses revealed that the compounds were highly selective for EGFR. Furthermore, both compounds were bioavailable in mouse pharmacokinetic studies, and compound 6 is the first EGFR degrader suitable for in vivo efficacy studies. Overall, we provide a set of well-characterized chemical tools to the research community.

8.
Oxid Med Cell Longev ; 2020: 9741369, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31998447

RESUMO

Spinal cord injury (SCI) is a devastating disease that may lead to lifelong disability. Thus, seeking for valid drugs that are beneficial to promoting axonal regrowth and elongation after SCI has gained wide attention. Metformin, a glucose-lowering agent, has been demonstrated to play roles in various central nervous system (CNS) disorders. However, the potential protective effect of metformin on nerve regeneration after SCI is still unclear. In this study, we found that the administration of metformin improved functional recovery after SCI through reducing neuronal cell apoptosis and repairing neurites by stabilizing microtubules via PI3K/Akt signaling pathway. Inhibiting the PI3K/Akt pathway with LY294002 partly reversed the therapeutic effects of metformin on SCI in vitro and vivo. Furthermore, metformin treatment weakened the excessive activation of oxidative stress and improved the mitochondrial function by activating the nuclear factor erythroid-related factor 2 (Nrf2) transcription and binding to the antioxidant response element (ARE). Moreover, treatment with Nrf2 inhibitor ML385 partially abolished its antioxidant effect. We also found that the Nrf2 transcription was partially reduced by LY294002 in vitro. Taken together, these results revealed that the role of metformin in nerve regeneration after SCI was probably related to stabilization of microtubules and inhibition of the excessive activation of Akt-mediated Nrf2/ARE pathway-regulated oxidative stress and mitochondrial dysfunction. Overall, our present study suggests that metformin administration may provide a potential therapy for SCI.

9.
J Clin Ultrasound ; 2019 Dec 13.
Artigo em Inglês | MEDLINE | ID: mdl-31833078

RESUMO

PURPOSE: The aim of this study was to investigate myocardial dysfunction and mechanical abnormalities in young patients with Graves' disease before therapy, using two-dimensional speckle tracking echocardiography. METHODS: We performed a comprehensive transthoracic echocardiographic examination, including segmental and global radial strain, and time-to-peak radial strain, in 47 young patients with hyperthyroidism and 34 healthy adults. The time-to-peak radial strain was corrected by RR interval. The variables derived from radial myocardial deformation by the six-basal, six-mid, and six-apical segmental model were compared to investigate the difference of the myocardial function between the two groups. RESULTS: Early diastolic mitral inflow velocity, E/A ratio, early diastolic mitral annular velocity, and e'/a' ratio were lower in patients with Graves' disease than in controls. The left ventricular end-diastolic volume, left ventricular end-systolic volume, stroke volume, cardiac output, heart rate, late diastolic mitral inflow velocity, and late diastolic mitral annular velocity were slightly higher in patients than in controls. Radial strain, global radial strain, and corrected time-to-peak radial strain were lower in the patient group. CONCLUSIONS: The decreased radial strain, global radial strain, and corrected time-to-peak radial strain in young patients with newly diagnosed hyperthyroidism due to Graves' disease could serve as an early sign of subclinical cardiac involvement.

10.
Cancer Discov ; 2019 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-31810986

RESUMO

TANK binding kinase 1 (TBK1) is an important kinase involved in the innate immune response. Here we discover that TBK1 is hyperactivated by von Hippel-Lindau (VHL) loss or hypoxia in cancer cells. Tumors from patients with kidney cancer with VHL loss display elevated TBK1 phosphorylation. Loss of TBK1 via genetic ablation, pharmacologic inhibition, or a new cereblon-based proteolysis targeting chimera specifically inhibits VHL-deficient kidney cancer cell growth, while leaving VHL wild-type cells intact. TBK1 depletion also significantly blunts kidney tumorigenesis in an orthotopic xenograft model in vivo. Mechanistically, TBK1 hydroxylation on Proline 48 triggers VHL as well as the phosphatase PPM1B binding that leads to decreased TBK1 phosphorylation. We identify that TBK1 phosphorylates p62/SQSTM1 on Ser366, which is essential for p62 stability and kidney cancer cell proliferation. Our results establish that TBK1, distinct from its role in innate immune signaling, is a synthetic lethal target in cancer with VHL loss. SIGNIFICANCE: The mechanisms that lead to TBK1 activation in cancer and whether this activation is connected to its role in innate immunity remain unclear. Here, we discover that TBK1, distinct from its role in innate immunity, is activated by VHL loss or hypoxia in cancer.See related commentary by Bakouny and Barbie, p. 348.

11.
Life Sci ; 239: 117035, 2019 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-31697952

RESUMO

AIMS: The purpose of this study was to investigate the role of long non-coding RNA taurine-upregulated gene 1 (TUG1) in colon cancer (Cc) and related molecular mechanisms. MATERIALS AND METHODS: RT-qPCR, Western blot and immunohistochemistry were used to detect the expression of related proteins. BrdU and Transwell assays were used to detect cell proliferation and invasion, respectively. Immunofluorescence was used to detect the expression of Vimentin. KEY FINDINGS: TUG1 expression was up-regulated in CaCO-2, SW620 and HT-29 cells, while miR-26a-5p was down-regulated. Bioinformatics analysis showed that miR-26a-5p was the target of TUG1, and the targeting relationship was further confirmed by dual-luciferase report analysis. Besides, matrix metalloproteinases-14 (MMP-14) was a target of mir-26a-5p. Knockdown of TUG1 by shRNA (sh-TUG1) inhibited MMP-14 expression. Functional analysis showed that sh-TUG1 significantly inhibited Cc cell proliferation, invasion and epithelial-mesenchymal transformation (EMT). Notably, miR-26a-5p inhibitor reversed the promotion of Cc caused by sh-TUG1. Mechanically, the overexpression of TUG1 significantly up-regulated the levels of MMP-14, VEGF, p-p38 mitogen-activated protein kinase (p-p38 MAPK) and p-HSP27 (heat shock protein 27), and promoted the proliferation, invasion and EMT of Cc cells. However, MAPK pathway inhibitor SB203580 has shown the opposite effect. Additionally, animal studies have shown that sh-TUG1 inhibited tumor growth and motility in vivo in the same way. SIGNIFICANCE: This study demonstrated that TUG1 accelerates the development of colon cancer by regulating miR-26a-5p/MMP14/p38 MAPK/Hsp27 axis in vitro and in vivo. Therefore, TUG1 provides a new direction for the treatment of Cc.


Assuntos
Carcinogênese/genética , Neoplasias do Colo/genética , Proteínas de Choque Térmico/biossíntese , Sistema de Sinalização das MAP Quinases/genética , Metaloproteinase 14 da Matriz/biossíntese , MicroRNAs/biossíntese , Chaperonas Moleculares/biossíntese , RNA Longo não Codificante/genética , Animais , Linhagem Celular Tumoral , Neoplasias do Colo/patologia , Biologia Computacional , Transição Epitelial-Mesenquimal/genética , Proteínas de Choque Térmico/genética , Humanos , Masculino , Metaloproteinase 14 da Matriz/genética , Camundongos , Camundongos Endogâmicos BALB C , MicroRNAs/genética , Chaperonas Moleculares/genética , Regulação para Cima
12.
Brain Behav ; 9(12): e01462, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31701661

RESUMO

OBJECTIVE: To explore the predictive value of serum creatinine (Cr) to cystatin C (CysC) ratio in neurocritically ill patients. METHODS: We conducted a retrospectively observational study of adult patients admitted to a neurocritical care unit (NCU) between Jan 2013 and Jan 2017. Patients were excluded if <18 years old, required neurocritical care <72 hr, did operation during hospitalization, had premorbid disability or acute kidney injury (AKI) at admission. The Cr/CysC ratio was obtained at NCU admission. Primary end points were short-term (30-day) mortality and long-term (6-month) poor outcome, with the latter defined as modified Rankin Scale (mRS) of 4-6. RESULTS: Of 538 eligible patients, the etiology included acute ischemic stroke (N = 193, 35.9%), intracranial hemorrhage (N = 116, 21.6%), encephalitis and/or meningitis (N = 85, 15.8%), and others (N = 144, 26.7%). Serum Cr/CysC ratio was significantly correlated with body mass index (BMI) (r = .161, p < .001), the length of NCU stay (r = -.161, p < .001), duration of mechanical ventilation (r = -.138, p = .001), and risk of tracheotomy (r = -.095, p = .028). During follow-up, 88 (16.4%), patients died within 30 days and 307 (57.1%) patients achieved good outcome at 6 months. In multivariate logistic regression analysis, we identified serum Cr/CysC ratio as an independent predictor of long-term functional outcome (OR: 0.989, 95% CI: 0.980-0.998, p = .015) but not 30-day mortality (p = .513). CONCLUSIONS: Serum Cr/CysC ratio at admission could be used as a predictor of long-term poor prognosis in neurocritically ill patients.

13.
Asian J Urol ; 6(4): 312-320, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31768316

RESUMO

The microphthalmia (MiT) subfamily of transcription factors includes TFE3, TFEB, TFEC, and MITF. In the 2016 World Health Organization classification, MiT family translocation renal cell carcinoma (tRCC) including Xp11 tRCC and t(6;11) RCC, was newly defined as an RCC subtype. Xp11 and t(6;11) RCC are characterized by the rearrangement of the MiT transcription factors TFE3 and TFEB, respectively. Recent studies identified the fusion partner-dependent clinicopathological and immunohistochemical features in TFE3-rearranged RCC. Furthermore, RCC with TFEB amplification, melanotic MiT family translocation neoplasms, was identified may as a unique subtype of MiT family associated renal neoplasms, along with MITF associated RCC. In this review, we will collect available literature of these newly-described RCCs, analyze their clinicopathological and immunohistochemical features, and summarize their molecular and genetic evidences. We expect this review would be beneficial for the understanding of these rare subtypes of RCCs, and eventually promote clinical management strategies.

14.
Nat Commun ; 10(1): 5177, 2019 11 15.
Artigo em Inglês | MEDLINE | ID: mdl-31729379

RESUMO

Protein hydroxylation affects protein stability, activity, and interactome, therefore contributing to various diseases including cancers. However, the transiency of the hydroxylation reaction hinders the identification of hydroxylase substrates. By developing an enzyme-substrate trapping strategy coupled with TAP-TAG or orthogonal GST- purification followed by mass spectrometry, we identify adenylosuccinate lyase (ADSL) as an EglN2 hydroxylase substrate in triple negative breast cancer (TNBC). ADSL expression is higher in TNBC than other breast cancer subtypes or normal breast tissues. ADSL knockout impairs TNBC cell proliferation and invasiveness in vitro and in vivo. An integrated transcriptomics and metabolomics analysis reveals that ADSL activates the oncogenic cMYC pathway by regulating cMYC protein level via a mechanism requiring ADSL proline 24 hydroxylation. Hydroxylation-proficient ADSL, by affecting adenosine levels, represses the expression of the long non-coding RNA MIR22HG, thus upregulating cMYC protein level. Our findings highlight the role of ADSL hydroxylation in controlling cMYC and TNBC tumorigenesis.

15.
J Med Chem ; 62(23): 10897-10911, 2019 Dec 12.
Artigo em Inglês | MEDLINE | ID: mdl-31730343

RESUMO

MEK1 and MEK2 (also known as MAP2K1 and MAP2K2) are the "gatekeepers" of the ERK signaling output with redundant roles in controlling ERK activity. Numerous inhibitors targeting MEK1/2 have been developed including three FDA-approved drugs. However, acquired resistance to MEK1/2 inhibitors has been observed in patients, and new therapeutic strategies are needed to overcome the resistance. Here, we report a first-in-class degrader of MEK1/2, MS432 (23), which potently and selectively degraded MEK1 and MEK2 in a VHL E3 ligase- and proteasome-dependent manner and suppressed ERK phosphorylation in cells. It inhibited colorectal cancer and melanoma cell proliferation much more effectively than its negative control MS432N (24), and its effect was phenocopied by MEK1/2 knockdown. Compound 23 was highly selective for MEK1/2 in global proteomic profiling studies. It was also bioavailable in mice and can be used for in vivo efficacy studies. We provide two well-characterized chemical tools to the biomedical community.

16.
PLoS One ; 14(10): e0223456, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31600260

RESUMO

Expression of the Alzheimer's disease associated polypeptide Aß42 and the human polypeptide hormon islet amyloid polypeptide (hIAPP) and the prohormone precursor (hproIAPP) in neurons of Drosophila melanogaster leads to the formation of protein aggregates in the fat body tissue surrounding the brain. We determined the structure of these membrane-encircled protein aggregates using transmission electron microscopy (TEM) and observed the dissolution of protein aggregates after starvation. Electron tomography (ET) as an extension of transmission electron microscopy revealed that these aggregates were comprised of granular subunits having a diameter of 20 nm aligned into highly ordered structures in all three dimensions. The three dimensional (3D) lattice of hIAPP granules were constructed of two unit cells, a body centered tetragonal (BCT) and a triclinic unit cell. A 5-fold twinned structure was observed consisting of the cyclic twinning of the BCT and triclinic unit cells. The interaction between the two nearest hIAPP granules in both unit cells is not only governed by the van der Waals forces and the dipole-dipole interaction but potentially also by filament-like structures that can connect the nearest neighbors. Hence, our 3D structural analysis provides novel insight into the aggregation process of hIAPP in the fat body tissue of Drosophila melanogaster.

17.
J Neurochem ; 2019 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-31602651

RESUMO

In recent years, many studies have focused on autophagy, an evolutionarily conserved mechanism that relies on lysosomes to achieve cellular metabolic requirements and organelle turnover, and revealed its important role in animal models of traumatic injury. Autophagy is a double-edged sword. Appropriate levels of autophagy can promote the removal of abnormal proteins or damaged organelles, while hyperactivated autophagy can induce autophagic apoptosis. However, recent studies suggest that autophagic flux seems to be blocked after traumatic brain injury (TBI), which contributes to the apoptosis of brain cells. In this study, valproic acid (VPA), which was clinically used for epilepsy treatment, was used to treat TBI. The Morris water maze test, hematoxylin & eosin staining and Nissl staining were first conducted to confirm that VPA treatment had a therapeutic effect on mice after TBI. Western blotting, enzyme-linked immunosorbent assay and immunofluorescence staining were then performed to reveal that VPA treatment reversed TBI-induced blockade of autophagic flux, which was accompanied by a reduced inflammatory response. In addition, the variations in activation and phenotypic polarization of microglia were observed after VPA treatment. Nevertheless, the use of the autophagy inhibitor 3-methyladenine partially abolished VPA-induced neuroprotection and the regulation of microglial function after TBI, resulting in the deterioration of the central nervous system microenvironment and neurological function. Collectively, VPA treatment reversed the TBI-induced blockade of autophagic flux in the mouse brain cortex, subsequently inhibiting brain cell apoptosis and affecting microglial function to achieve the promotion of functional recovery in mice after TBI.

18.
J Org Chem ; 84(17): 10701-10709, 2019 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-31364358

RESUMO

Superelectrophilic-initiated direct C-H functionalization of thiophenes at the ß-position was developed. A series of trans-stereospecific [2,1-a]-IF-thiophene-fused cyclic compounds (4) with saddle-shaped structure were prepared in 17-30% yields through a one-pot superelectrophilic Friedel-Crafts reaction of dihydroindenofluorene with thiophene derivatives. From the crystal packing analyses of 4a, its skeleton shows both strong intermolecular π-π stacking and C-H···π stacking. Furthermore, the ring-dependent photophysical properties of 4 were confirmed by UV-vis absorption and photoluminescence spectroscopy as well as through the study of their fluorescence quantum yield.

19.
MycoKeys ; 56: 1-11, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31327928

RESUMO

Three new species isolated from sugarcane rhizosphere in China, namely Conlariumbaiseense sp. nov., C.nanningense sp. nov., and C.sacchari sp. nov., are described and illustrated. Molecular evidence (phylogenetic analysis of combined LSU, SSU, ITS and RPB2 sequence data) and phenotypical characters support their independent status from related and similar species. The new species, as dark spetate endophytes, inhabit sugarcane rhizosphere and can form a symbiosis with sugarcane.

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