bluuebunny/crossref_metadata_2025_split huggingface dataset:
The heat shock protein 70 inhibitor VER155008 suppresses the expression of HSP27, HOP and HSP90β and the androgen receptor, induces apoptosis, and attenuates prostate cancer cell growth
Authors: Brünnert Daniela , Langer Clara , Zimmermann Luise , Bargou Ralf C. , Burchardt Martin , Chatterjee Manik , Stope Matthias B. 
Published: June 2019

AbstractHeat shock proteins (HSPs) are molecular chaperones that play a pivotal role in correct folding, stabilization and intracellular transport of many client proteins including those involved in oncogenesis. HSP70, which is frequently overexpressed in prostate cancer (PCa), has been shown to critically contribute to tumor cell survival, and might therefore represent a potential therapeutic target. We treated both the androgen receptor (AR)‐positive LNCaP and the AR‐negative PC‐3 cell lines with the pharmacologic HSP70 inhibitor VER155008. Although we observed antiproliferative effects and induction of apoptosis upon HSP70 inhibition, the apoptotic effect was more pronounced in AR‐positive LNCaP cells. In addition, VER155008 treatment induced G1 cell cycle arrest in LNCaP cells and decreased AR expression. Further analysis of the HSP system by Western blot analysis revealed that expression of HSP27, HOP and HSP90β was significantly inhibited by VER155008 treatment, whereas the HSP40, HSP60, and HSP90α expression remained unchanged. Taken together, VER155008 might serve as a novel therapeutic option in PCa patients independent of the AR expression status.
circRNA_0058097 promotes tension‐induced degeneration of endplate chondrocytes by regulating HDAC4 expression through sponge adsorption of miR‐365a‐5p
Authors: Xiao Liang , Ding Baiyang , Xu Shujuan , Gao Jianming , Yang Bijing , Wang Jing , Xu Hongguang 
Published: June 2019

AbstractExcessive mechanical tension can lead to the degeneration of endplate chondrocytes. The presence of tension‐sensitive circRNA_0058097 molecules has been detected in human endplate chondrocytes, where it was found to be a potential competing endogenous RNA. Indeed, inhibiting the expression of circRNA_0058097 effectively enhanced the stress resistance of endplate chondrocytes, suggesting that it may be an important trigger point for the degeneration of endplate cartilage. Through a series of experiments, we reveal that circRNA_0058097 can upregulate the expression of downstream target gene histone deacetylase 4 by sponge adsorption of miR‐365a‐5p, which promoted morphological changes of endplate chondrocytes, and increased extracellular matrix degradation and degeneration of endplate cartilage. Therefore, circRNA_0058097 may provide a new way to prevent and treat endplate cartilage degeneration.
Supramolecular gold(I) compounds with trithiocyanuric acid: Self‐assembly and luminescent properties
Authors: Tzeng Biing‐Chiau , Chiu Hsiu‐Hui , Chang Jia‐Hen , Lee Gene‐Hsiang 
Published: June 2019

Abstract[(N3S3)Au(AuPMe3)2]2 (1) and [(N3S3)Au(AuPEt3)2]2 (2) were prepared by treating AuCl(PMe3) or AuCl(PEt3) with H3N3S3 upon deprotonation by trimethylamine to give respective Au6 supermolecules. Using dppm(AuCl)2 instead of AuCl(PMe3) or AuCl(PEt3) to react with H3N3S3 in a similar reaction condition led to a rare heptanuclear supermolecule of [(N3S3)2Au7(dppm)4]Cl (3). It is noted that besides short intramolecular gold(I)⋯gold(I) distances, both compounds 1 and 2 also show intermolecular gold(I)⋯gold(I) distances of 3.067(1) and 3.241(1) Å, resulting in two‐dimensional and one‐dimensional polymeric gold(I) solid, respectively. In fact, compound 1 shows a similar two‐dimensional polymeric gold(I) solid to that of the reported [(N3S3)Au(AuPPhMe2)2]2 with an intermolecular gold(I)⋯gold(I) distance of 3.130(2) Å. Significantly, these intermolecular gold(I)⋯gold(I) distances are well correlated with their cone angles and emission energies. For example, intermolecular gold(I)⋯gold(I) distances increase in the order of 3.067(1) Å < 3.130(2) Å < 3.241(1) Å for PMe3 (118°), PPhMe2 (122°), and PEt3 (132°), and their emission energies also increase in the order of 542 nm < 530 nm < 504 nm, respectively. This work highlights a very good correlation between intermolecular aurophilic interactions and emission energies for a series of Au6 supermolecules, where the cone angle plays a vital role in the self‐assembly process as well. Finally, the emissions for 1–3 are tentatively assigned to the S → Au charge‐transfer transition, whereas they are most probably modified by gold(I)⋯gold(I) interactions.
Retracted: LncRNA HAND2‐AS1 exerts anti‐oncogenic effects on ovarian cancer via restoration of BCL2L11 as a sponge of microRNA‐340‐5p
Authors: Chen Jun , Lin Yang , Jia Yan , Xu Tianmin , Wu Fuju , Jin Yuemei 
Published: June 2019

AbstractIn the early stage of ovarian cancer (OC), molecular biomarkers are critical for its diagnosis and treatment. Nevertheless, there is little research on the mechanism underlying tumorigenesis in OC. Herein, we aimed to explore whether long noncoding RNA (lncRNA) HAND2‐AS1 participated in the regulation of the cell proliferation, migration, and apoptosis of OC by regulating B‐cell lymphoma 2 like 11 (BCL2L11) and microRNA‐340‐5p (miR‐340‐5p). Differentially expressed lncRNAs in OC were screened by microarray‐based analysis. HAND2‐AS1, BCL2L11, and miR‐340‐5p expression was assessed in normal ovarian and OC tissues and human OC cell lines. Then, the relationships among HAND2‐AS1, BCL2L11, and miR‐340‐5p were explored. Ectopic expression and depletion experiments were applied to analyze the effects of HAND2‐AS1, miR‐340‐5p and BCL2L11 on migration, invasion, and proliferation of OC cells, as well as apoptosis. Lastly, the tumor xenograft in nude mice was conducted to test the tumorigenesis in vivo. In silico analysis displayed poor expression of HAND2‐AS1 in OC. HAND2‐AS1 specifically sponged with miR‐340‐5p which was found to directly target BCL2L11. Importantly, HAND2‐AS1 or BCL2L11 overexpression or miR‐340‐5p downregulation resulted in reduction of cell invasion and migration, together with decrease of cell proliferation and increase of cell apoptosis in OC. Besides, high‐expressed HAND2‐AS1 inhibited the tumorigenesis in nude mice. To sum up, these data suggests HAND2‐AS1 as an anti‐oncogene in OC through upregulation of BCL2L11 by competitively binding to miR‐340‐5p, which demonstrates that there are potential diagnosis and therapy values of HAND2‐AS1 in OC.
The novel non‐immunological role and underlying mechanisms of B7‐H3 in tumorigenesis
Authors: Zhou Xiangqi , Ouyang Shuhui , Li Jianjun , Huang Xin , Ai Xiaohong , Zeng Yixin , Lv Yuncheng , Cai Manbo 
Published: June 2019

AbstractB7 homolog 3 (B7‐H3) has been proven to be involved in tumorigenesis. An elucidation of its role and underlying mechanisms is essential to an understanding of tumorigenesis and the development of effective clinical applications. B7‐H3 is abnormally overexpressed in many types of cancer and is generally associated with a poor clinical prognosis. B7‐H3 inhibits the initiation of the "caspase cascade" by the Janus kinase/signal transducers and activators of transcription pathway to resist tumor cell apoptosis. B7‐H3 accelerates malignant proliferation by attacking the checkpoint mechanism of the tumor cell cycle through the phosphatidylinositol 3‐kinase and protein kinase B pathway. B7‐H3 reprograms the metabolism of glucose and lipids and transforms the metabolic flux of tumor cells to promote tumorigenesis. B7‐H3 induces abnormal angiogenesis by recruiting vascular endothelial growth factor and matrix metalloproteinase to tumor lesions. B7‐H3 strongly promotes tumorigenesis through antiapoptotic, pro‐proliferation, metabolism reprogramming, and pro‐angiogenesis.
Long noncoding RNA MAGI1‐IT1 regulates cardiac hypertrophy by modulating miR‐302e/DKK1/Wnt/beta‐catenin signaling pathway
Authors: Zhang Qinghua , Wang Fengshuang , Wang Fenghua , Wu Naishi 
Published: June 2019

AbstractCardiac hypertrophy (CH) is an adaptive cardiac response to overload whose decompensation eventually leads to heart failure or sudden death. Recently, accumulating studies have indicated the implication of long noncoding RNAs (lncRNAs) in CH progression. MAGI1‐IT1 is a newly‐identified lncRNA that is highly associated with CH, while its specific role in CH progression remains masked. In this study, we uncovered that MAGI1‐IT1 was distinctly downregulated in angiotensin (Ang) II‐induced hypertrophic H9c2 cells. Also, MAGI1‐IT1 overexpression in Ang II‐treated H9c2 cells strikingly abolished the enlarged surface area and the enhanced levels of hypertrophic markers such as ANP, BNP, and β‐MHC. Mechanically, we found MAGI1‐IT1 sponged miR‐302e which was identified as a hypertrophy‐facilitator here, and that miR‐302e upregulation countervailed the inhibition of MAGI1‐IT1 overexpression on hypertrophic cells. Moreover, it was confirmed that MAGI1‐IT1 boosted DKK1 expression by absorbing miR‐302e. Subsequently, we also illustrated that MAGI1‐IT1 inactivated Wnt/beta‐catenin signaling through a DKK1‐dependent pathway. Finally, both the DKK1 inhibition and LiCI (Wnt activator) supplement abrogated the hypertrophy‐suppressive impact of MAGI1‐IT1 on Ang II‐simulated hypertrophic H9c2 cells. Jointly, our findings disclosed that MAGI1‐IT1 functioned as a negative regulator in CH through inactivating Wnt/beta‐catenin pathway via targeting miR‐302e/DKK1 axis, revealing a novel road for CH treatment.
Mice with myocyte deletion of vitamin D receptor have sarcopenia and impaired muscle function
Authors: Girgis Christian M. , Cha Kuan Minn , So Benjamin , Tsang Michael , Chen Jennifer , Houweling Peter J. , Schindeler Aaron , Stokes Rebecca , Swarbrick Michael M. , Evesson Frances J. , Cooper Sandra T. , Gunton Jenny E. 
Published: June 2019

AbstractBackgroundIt has long been recognized that vitamin D deficiency is associated with muscle weakness and falls. Vitamin D receptor (VDR) is present at very low levels in normal muscle. Whether vitamin D plays a direct role in muscle function is unknown and is a subject of hot debate. Myocyte‐specific deletion of VDR would provide a strategy to answer this question.MethodsMyocyte‐specific vitamin D receptor (mVDR) null mice were generated by crossing human skeletal actin‐Cre mice with floxed VDR mice. The effects of gene deletion on the muscle phenotype were studied in terms of body tissue composition, muscle tissue histology, and gene expression by real‐time PCR.ResultsUnlike whole‐body VDR knockout mice, mVDR mice showed a normal body size. The mVDR showed a distinct muscle phenotype featuring reduced proportional lean mass (70% vs. 78% of lean mass), reduced voluntary wheel‐running distance (22% decrease, P = 0.009), reduced average running speed, and reduced grip strength (7–16% reduction depending on age at testing). With their decreased voluntary exercise, and decreased lean mass, mVDR have increased proportional fat mass at 20% compared with 13%.Surprisingly, their muscle fibres showed slightly increased diameter, as well as the presence of angular fibres and central nuclei suggesting ongoing remodelling. There were, however, no clear changes in fibre type and there was no increase in muscle fibrosis. VDR is a transcriptional regulator, and changes in the expression of candidate genes was examined in RNA extracted from skeletal muscle. Alterations were seen in myogenic gene expression, and there was decreased expression of cell cycle genes cyclin D1, D2, and D3 and cyclin‐dependent kinases Cdk‐2 and Cdk‐4. Expression of calcium handling genes sarcoplasmic/endoplasmic reticulum calcium ATPases (SERCA) Serca2b and Serca3 was decreased and Calbindin mRNA was lower in mVDR muscle.ConclusionsThis study demonstrates that vitamin D signalling is needed for myocyte function. Despite the low level of VDR protein normally found muscle, deleting myocyte VDR had important effects on muscle size and strength. Maintenance of normal vitamin D signalling is a useful strategy to prevent loss of muscle function and size.
Descriptive studies on the tongue of two micro‐mammals inhabiting the Egyptian fauna; the Nile grass rat (Arvicanthis niloticus) and the Egyptian long‐eared hedgehog (Hemiechinus auritus)
Authors: Massoud Diaa , Abumandour Mohamed M. A. 
Published: June 2019

AbstractThe current study aimed to describe the anatomical features of the tongues of two micro‐mammals common in the Egyptian fauna; the Nile grass rat (Arvicathis niloticus), and the Egyptian long‐eared hedgehog (Hemiechinus auritus). The tongues of five adult individuals of each species were excised and processed histologically, histochemically, and morphometrically. Statistical analysis comparing the relative tongue length in both species showed that there was a significant difference, which may correlate with the difference in feeding preferences. Grossly, the Nile grass rat has a dorsal lingual prominence with bifurcated apex while, the long‐eared hedgehog has a median slight elevation with rounded apex. Numerous forms of mechanical and gustatory papillae are scattered along the lingual dorsal epithelium. The histochemical detection of keratin by Holland's trichrome stain showed an intense expression in the case of A. niloticus and mild expression in H. auritus. The framework of the tongue (entoglossum) is supported by either a core of cartilage in H. auritus or bone in A. niloticus which incorporated in the lingual root. The lingual glands also showed marked variation, the Nile grass rat exhibit dense populations of mucous‐secreting glands and lesser populations of serous‐secreting glands, the contrary is true in H. auritus. In conclusion, the micro and macro‐anatomical features of the tongues of both species showed adaptive changes to accommodate the feeding lifestyle. Such type of studies using mammals from different phylogenetic traits and almost have different feeding preferences provide answers to many research questions related to tongue evolution among mammalian vertebrates.
Widespread changes in sexual behaviour in eastern and southern Africa: Challenges to achieving global HIV targets? Longitudinal analyses of nationally representative surveys
Authors: Schaefer Robin , Gregson Simon , Benedikt Clemens 
Published: June 2019

AbstractIntroductionSexual behaviour change contributed to reductions in HIV incidence in eastern and southern Africa between 1990 and 2010. More recently, there are indications that non‐regular partnerships have increased. However, the effect of these increases on population‐level risks for HIV and other sexually transmitted infections could have been reduced by simultaneous increases in condom use. We describe recent trends in sexual behaviour and condom use within the region and assess their combined effects on population levels of sexual risk.MethodsNationally representative Demographic and Health Survey data on sexually active males and females (15 to 49 years) were used for 11 eastern and southern African countries (≥3 surveys for each country; 1999 to 2016) to describe trends in sexual behaviour (multiple, non‐regular, and casual sexual partnerships; condom use; age at first sex). Logistic regressions tested for statistical significance of changes. Analyses were stratified by sex.ResultsRecent increases in multiple, non‐regular, and/or casual partnerships can be found for males in 10 countries and, for females, in nine countries; five countries exhibited recent decreases in age of sexual debut. Reduction in sex without condoms with non‐regular partners was observed in six countries for males and eight for females. Changes in the proportion of the overall population reporting condomless sex with non‐regular partners varied between countries, with declines in six countries and increases in three.ConclusionsExtensive change in sexual behaviour occurred across eastern and southern Africa during the period of scale‐up of antiretroviral therapy programmes. This includes increasing multiple and non‐regular partnerships, but their potential effects on population‐level sexual risks were often offset by parallel increases in condom use. Strengthening condom programmes and reintegrating communication about behavioural dimensions into combination prevention programmes could help countries to meet international targets for reductions in HIV incidence.
The effectiveness of correcting abnormal metabolic profiles
Authors: Clayton Peter Theodore 
Published: June 2019

AbstractInborn errors of metabolism cause disease because of accumulation of a metabolite before the blocked step or deficiency of an essential metabolite downstream of the block. Treatments can be directed at reducing the levels of a toxic metabolite or correcting a metabolite deficiency. Many disorders have been treated successfully first in a single patient because we can measure the metabolites and adjust treatment to get them as close as possible to the normal range. Examples are drawn from Komrower's description of treatment of homocystinuria and the author's trials of treatment in bile acid synthesis disorders (3β‐hydroxy‐Δ5‐C27‐steroid dehydrogenase deficiency and Δ4‐3‐oxosteroid 5β‐reductase deficiency), neurotransmitter amine disorders (aromatic L‐amino acid decarboxylase [AADC] and tyrosine hydroxylase deficiencies), and vitamin B6 disorders (pyridox(am)ine phosphate oxidase deficiency and pyridoxine‐dependent epilepsy [ALDH7A1 deficiency]). Sometimes follow‐up shows there are milder and more severe forms of the disease and even variable clinical manifestations but by measuring the metabolites we can adjust the treatment to get the metabolites into the normal range. Biochemical measurements are not subject to placebo effects and will also show if the disorder is improving spontaneously. The hypothesis that can then be tested for clinical outcome is whether getting metabolite(s) into a target range leads to an improvement in an outcome parameter such as abnormal liver function tests, hypokinesia, epilepsy control etc. The metabolite‐guided approach to treatment is an example of personalized medicine and is a better way of determining efficacy for disorders of variable severity than a randomized controlled clinical trial.
Residue behaviours, dissipation kinetics and dietary risk assessment of pyaclostrobin, cyazofamid and its metabolite in grape
Authors: Pang Nannan , Dou Xinyu , Hu Jiye 
Published: June 2019

AbstractBACKGROUNDGrape is an important fruit consumed either fresh or processed, therefore, fungicide misuse of grape has become an issue of global food safety and human health. Pyraclostrobin, and cyazofamid have been applied to grape frequently.RESULTSHere a simple QuEChERS (quick, easy, cheap, effective, rugged, and safe) liquid chromatography mass spectrometry technique has been developed and validated for the determination of pyraclostrobin, cyazofamid and its metabolite CCIM in open field grape samples. The recoveries of these three in the range of 0.01 to 5 mg kg−1 (n = 5) ranged from 73.1% to 97.9%. The relative standard deviations (RSDs) were below 12% for all cases. The limits of quantitation of each analyte was 0.005 mg kg−1, which was lower than maximum residue limits of not only pyraclostrobin but also cyazofamid. Not only dissipation kinetics but also residue determination was obtained in grape for those three pesticides. Furthermore, their half‐lives in grapes were 10.7–30.1 days, recommending the pre‐harvest intervals for these three of 14 days. The calculated hazard quotient and acute hazard index lower than 100% illustrated the safety of intake of grape for the Chinese population for not only long‐term but also short‐term dietary risk assessment.CONSLUSIONSThe less than 30 day half‐life illustrated that pyraclostrobin and cyazofamid could degrade relatively easily in the environment. The long‐term and short‐term dietary risk assessment also illustrated the intake safety of these three. Thus, a 14 day pre‐harvest interval was safe and recommended. The results of this study contributed to environmental protection, food safety and human health. © 2019 Society of Chemical Industry
Fruits of wild and semi‐domesticated Diospyros tree species have contrasting phenological, metabolic, and antioxidant activity profiles
Authors: Ramírez‐Briones Ernesto , Rodríguez Macías Ramón , Casarrubias Castillo Kena , del Río Rosa E , Martínez‐Gallardo Norma , Tiessen Axel , Ordaz‐Ortiz José , Cervantes‐Hernández Felipe , Délano‐Frier John Paul , Zañudo‐Hernández Julia 
Published: June 2019

AbstractBACKGROUNDIn contrast to commercial Diospyros species, Mesoamerican fruit‐producing species are scarcely known, particularly wild species that might harbor desirable traits suitable for breeding. Thus, metabolomic, chemical, and antioxidant profiles of fruits harvested from cultivated Diospyros digyna and wild Diospyros rekoi trees during consecutive winter seasons were obtained. Fruits were harvested in habitats having marked differences in soil quality, climate, and luminosity.RESULTSD. digyna fruits were larger and less acid than D. rekoi fruits, whereas antioxidant activity tended to be higher in D. rekoi fruits. Phenolic, flavonoid, and sugar contents also varied significantly between species. Metabolomic analysis allowed the pre‐identification of 519 and 1665 metabolites in negative and positive electrospray ionization (ESI) modes, respectively. Principal component analysis of the positive ESI data explained 51.8% of the variance and indicated clear metabolomic differences between D. rekoi and D. digyna fruits that were confirmed by direct‐injection ESI mass spectrometry profiles. Twenty‐one discriminating metabolites were detected in fruits of both species; D. digyna fruits differentially accumulated lysophospholipids, whereas discriminating metabolites in D. rekoi fruits were chemically more diverse than those in D. digyna fruits.CONCLUSIONDomesticated D. digyna fruits have improved physicochemical fruit traits compared with wild D. rekoi fruits, including larger size and lower acidity. The metabolomic and chemical composition of their respective fruits were also significantly different, which in D. rekoi was manifested as a notable season‐dependent increase in antioxidant capacity. Therefore, wild D. rekoi can be considered as an important genetic resource for the improvement of commercial Diospyros fruit quality. © 2019 Society of Chemical Industry