One-step hydrothermal preparation of Ta-doped ZnO nanorods for improving decolorization efficiency under visible light

In this work, Ta-doped ZnO (Ta-ZnO) nanomaterials were synthesized by the hydrothermal method at different temperatures (110, 150, and 170 °C) for the photodegradation of methylene blue (MB) under visible light. Ta doping significantly affects the crystal defects, optical properties, and MB photocatalytic efficiency of ZnO materials. The optical absorption edge of Ta-ZnO 150 was redshifted compared to undoped ZnO, correlating to bandgap narrowing (E_gTa–ZnO = 2.92 eV; E_gZnO = 3.07 eV), implying that Ta doped ZnO is capable of absorbing visible light. Besides, Ta-doping was the reason for enhanced blue light emission in the photoluminescence spectrum, which is related to the oxygen defect V⁰_O. It is also observed in the XPS spectra, where the percentage of oxygen in the oxygen-deficient regions (O_531.5 eV) of Ta-ZnO150 is higher than that of ZnO150. It is an important factor in enhancing ZnO''s photocatalytic efficiency. The MB degradation efficiency of Ta-doped ZnO reached the highest for Ta-ZnO 150 and was 2.5 times higher than ZnO under a halogen lamp (HL). Notably, the influence of hydrothermal temperature on the structural, morphological, and photoelectrochemical properties was discussed in detail. As a result, the optimal hydrothermal temperature for synthesizing the nanorod is 150 °C. Furthermore, photocatalytic experiments were also performed under simulated sunlight and natural sunlight. The nature of the photo-oxidative degradation of MB was also investigated.

The Ta doped ZnO nanorods (Ta-ZnO) were synthesized by a hydrothermal method at different temperatures (110, 150, and 170 °C) for the photodegradation of methylene blue (MB) under visible light.     

RGD肽类示踪剂及其PET显像在脑胶质瘤诊疗中的应用

细胞黏附因子整合素αvβ3在包括脑胶质瘤在内的多种肿瘤新生血管内皮细胞及细胞表面高表达,而在正常细胞表面低表达或不表达。精氨酸-甘氨酸-天冬氨酸（RGD）肽可特异性结合整合素αvβ3。放射性核素标记的RGD肽已成为脑胶质瘤靶向显像的研究热点,RGD PET显像在脑胶质瘤诊断和疗效监测中有一定的价值。基于此,笔者对RGD PET显像在脑胶质瘤诊疗中的应用进行综述。     

Tau as a biomarker of cognitive impairment and neuropsychiatric symptom in Alzheimer's disease

The A/T/N research framework has been proposed for the diagnosis and prognosis of Alzheimer''s disease (AD). However, the spatial distribution of ATN biomarkers and their relationship with cognitive impairment and neuropsychiatric symptoms (NPS) need further clarification in patients with AD. We scanned 83 AD patients and 38 cognitively normal controls who independently completed the mini‐mental state examination and Neuropsychiatric Inventory scales. Tau, Aβ, and hypometabolism spatial patterns were characterized using Statistical Parametric Mapping together with [18F]flortaucipir, [18F]florbetapir, and [18F]FDG positron emission tomography. Piecewise linear regression, two‐sample t‐tests, and support vector machine algorithms were used to explore the relationship between tau, Aβ, and hypometabolism and cognition, NPS, and AD diagnosis. The results showed that regions with tau deposition are region‐specific and mainly occurred in inferior temporal lobes in AD, which extensively overlaps with the hypometabolic regions. While the deposition regions of Aβ were unique and the regions affected by hypometabolism were widely distributed. Unlike Aβ, tau and hypometabolism build up monotonically with increasing cognitive impairment in the late stages of AD. In addition, NPS in AD were associated with tau deposition closely, followed by hypometabolism, but not with Aβ. Finally, hypometabolism and tau had higher accuracy in differentiating the AD patients from controls (accuracy = 0.88, accuracy = 0.85) than Aβ (accuracy = 0.81), and the combined three were the highest (accuracy = 0.95). These findings suggest tau pathology is superior over Aβ and glucose metabolism to identify cognitive impairment and NPS. Its results support tau accumulation can be used as a biomarker of clinical impairment in AD.     

脂蟾毒配基对人胃癌BGC-823细胞系细胞生长的干预效应

目的：观察中药蟾酥主要成分之一——脂蟾毒配基对体外培养人胃癌BGC-823细胞系细胞生长的干预及其与细胞色素C和半胱氨酸天冬氨酸蛋白酶3活化的关系。 方法：实验于2004—09／2005—12在北京大学医学部细胞生物学系实验室完成。体外培养人胃癌BGC-823细胞系，脂蟾毒配基各组加入不同浓度的脂蟾毒配基（先用二甲基亚砜溶解，再经RPMI-1640培养液稀释至终浓度。细胞增殖及增殖抑制实验、细胞核形态观察及核DNA含量测定实验中脂蟾毒配基浓度分别为0．1，1，10μmol／L；细胞周期分布实验、细胞凋亡率实验、线粒体膜电位实验中脂蟾毒配基浓度分别为0，1,2．5，5μmol／L）。空白对照组加入RPMI-1640培养液。盐酸阿克拉霉素组加入5μmoL／L盐酸阿克拉霉素。采用酸性磷酸酶法检测细胞增殖抑制作用；细胞荧光分光光度仪观察细胞核形态及核DNA含量测定；流式细胞仪检测细胞周期、细胞凋亡率及其线粒体膜电位变化；Western blot检测与细胞凋亡相关基因蛋白表达的变化。 结果：①经0．1，1，10μmol／L脂蟾毒配基分别作用24，48，72h后，细胞生长显著抑制，脂蟾毒配基对癌细胞的生长抑制百分率与剂量、时间呈正相关，其IC50分别为3．9，2．0，1．5μmol／L。②随脂蟾毒配基作用浓度和时间的延长，癌细胞核荧光强度减弱，细胞核DNA含量明显降低。③0．1，1μmol／L脂螗毒配基作用24～48h后癌细胞阻滞在S期，5μmol／L脂蟾毒配基作用72h时，细胞阻滞在G2＋M期；盐酸阿克拉霉素与癌细胞作用24～48h，细胞阻滞在S期，作用72h时细胞阻滞在G2＋M期。④脂蟾毒配基作用后，细胞凋亡率明显高于对照组。⑤脂蟾毒配基引起细胞线粒体膜电位下降，释放人胞质中的细胞色素C增多，促进半胱氨酸天冬氨酸蛋白酶3蛋白活化，抑制Bel-2蚤白表达，诱导细胞凋亡。 结论：体外实验条件下，脂蟾毒配基抑制人胃癌BGC-823细胞生长并诱导细胞发生凋亡，其诱导凋亡作用机制与线粒体通路有关。     

中西医结合治疗喘息性支气管炎40例临床观察

目的:观察中西医结合治疗喘息性支气管炎的临床疗效。方法:60例喘息性支气管炎患儿随机分为两组,其中对照组20例采用西医治疗,治疗组40例采用中西医结合治疗。结果:对照组治疗后总有效率为75.0%,治疗组治疗后总有效率为95.0%,两组患者治疗后疗效比较有显著性差异(P<0.05)。结论:中西医结合治疗喘息性支气管炎疗效显著,值得在临床上推广应用。     

Efficacy and safety of warm acupuncture in the treatment of ankylosing spondylitis: A protocol for systematic review and meta-analysis

Background:Ankylosing spondylitis refers to a type of autoimmune disease, which is commonly characterized by joint pain and stiffness, since the disease progression can exhibit joint deformity and other activities limited symptoms. Has significantly impacts on people''s work and life. Warm acupuncture as a traditional Chinese therapy, showing several advantages (eg, safety, economy, and less side effects), has been extensively used to treat ankylosing spondylitis. However, its curative effect is supported by limited evidence. Accordingly, the present study aims to comprehensively assess the reliability of warm acupuncture in ankylosing spondylitis treatment.Methods:Randomized controlled trials were searched from the Chinese Biomedical Literature Database, Chongqing VIP Database for Chinese Technical Periodicals, China National Knowledge Infrastructure, Wanfang, Web of Science, Cochrane Library, PubMed, and EMBASE, regardless of their publication status. The deadline was November 6th, 2020. Two experienced researchers adopted RevMan V.5.3 software for literature selection, data collection, data analysis, and synthesis, respectively. In addition, the quality of the trials involved in this study was measured with the Cochrane Bias risk assessment tool, regardless of language or publication status.Results:The protocol will be used to assess the efficacy and safety of warm acupuncture in ankylosing spondylitis treatment.Conclusion:This review reliably evidences whether warm acupuncture is a reliable method for the intervention of ankylosing spondylitis.INPLASY registration number:INPLASY2020110096.     

Proposition de délinéation des volumes cibles tumoraux et sélection des aires ganglionnaires des cancers de la glande parotide

Salivary glands tumours are uncommon tumours showing a large diversity of histological types. This article presents a synthesis of patterns and paths of invasion of parotid glands tumours in order to propose an approach of the delineation of primary tumour clinical target volumes and of the selection of lymph nodes target volumes. This article does not discuss treatment indications but defines clinical target volumes to treat if radiotherapy is indicated. Postoperative situation being the most frequent, the delineation of primary tumour clinical target volume is based on an anatomical approach.     

Manic fringe inhibits tumor growth by suppressing Notch3 degradation in lung cancer

Notch signaling plays an essential role in development as well as cancer. We have previously shown that Notch3 is important for lung cancer growth and survival. Notch receptors are activated through the interaction with their ligands, resulting in proteolytic cleavage of the receptors. This interaction is modulated by Fringe, a family of fucose-specific β1,3 N-acetylglucosaminyltransferases that modify the extracellular subunit of Notch receptors. Studies in developmental models showed that Fringe enhances Notch’s response to Delta ligands at the expense of Jagged ligands. We observed that Manic Fringe expression is down-regulated in lung cancer. Since Jagged1, a known ligand for Notch3, is often over-expressed in lung cancer, we hypothesized that Fringe negatively regulates Notch3 activation. In this study, we show that re-expression of Manic Fringe down-regulates Notch3 target genes HES1 and HeyL and reduces tumor phenotype in vitro and in vivo. The mechanism for this phenomenon appears to be related to modulation of Notch3 protein stability. Proteasome inhibition reverses Manic Fringe-induced protein turnover. Taken together, our data provide the first evidence that Manic Fringe functions as a tumor suppressor in the lung and that the mechanism of its anti-tumor activity is mediated by inhibition of Notch3 activation.