bluuebunny/crossref_metadata_2025_split huggingface dataset:
Group 13 metal carbochalcogenoato complexes: Synthesis, X‐ray structure analysis, and reactions
Authors: Nakata Norio , Kato Shinzi , Niyomura Osamu , Ebihara Masahiro 
Published: November 2018

AbstractA series of alkali metal tetrakis(carbochalcogenoato)‐gallates and ‐indates M[M′(EOCR)4](solv.) (M = alkali metal; M′ = Ga, In; E = S, Se) and tris(carbodithioato)aluminum, ‐gallates and ‐indates M′ (SSCR)3(M′ = Al, Ga, In) were prepared by the reactions of alkali metal carbochalcogenate with metal trihalogenides (M′X3; M′ = Al, Ga, In; X = Cl, Br) and by those of piperidinium carbodithioates or carbodithioic and carboselenoic acids with M′X3, respectively. An X‐ray molecular structure analysis revealed that they have an acetone molecule as a crystal solvent. The reactions of the potassium complexes K[M′ (EOCR)4](H2O) (E = S, Se) with methanol and primary and secondary amines gave the corresponding methyl ester and amides in good yields, while the reactions with iodomethane and iodine gaveS‐ andSe‐methyl chalcogenoestersRCOEMe (E = S, Se) in good yields. Similar reactions of the tris(carbodithioato)gallates and ‐indates led to the correspondingO‐methyl thioesters, thioamides, andS‐methyl dithioesters in moderate to good yields. Oxidation of the tetrakis‐ and tris‐derivatives with iodine afforded the corresponding diacyl dichalcogenides (RCOE)2(E = S, Se) and di(carbothioyl) disulfides in quantitative yields. These reactions appeared to occur on the carbonyl or selenium atom of the tetrakis compounds and on the sulfide sulfur or thiocarbonyl carbon atom of the tris‐compounds, respectively. A possible mechanism for these I2‐oxidation reactions is discussed.
The arginine detection and cytotoxicity of fluorescent probes based on naphthalene derivatives
Authors: Shang Xuefang , Li Congshu , Li Jie , Chen Yanmei , Chen Hongli , Wang Tianyun 
Published: November 2018

AbstractFrom a biological point of view, Schiff base probes containing fluorescent groups are chemically modified to provide an effective method for the detection of amino acids. According to this method, three molecular probes containing Schiff base and hydroxyl group have been designed and synthesized. UV‐Vis and fluorescent data indicated that compound 2 showed strong sensitivity and high selectivity for arginine (Arg) among normal twenty kinds of amino acids. In addition, compound 2 displayed high combining ability with Arg and low cytotoxicity in MCF‐7 cell from 0 to 150 μg/mL. The above results showed the synthesized probes also can be used a biosensor for the Arg detection in vivo.
A model of cholinergic suppression of hippocampal ripples through disruption of balanced excitation/inhibition
Authors: Melonakos Eric D. , White John A. , Fernandez Fernando R. 
Published: November 2018

AbstractSharp wave‐ripples (140–220 Hz) are patterns of brain activity observed in the local field potential of the hippocampus which are present during memory consolidation. As rodents switch from memory consolidation to memory encoding behaviors, cholinergic inputs to the hippocampus from neurons in the medial septum‐diagonal band of Broca cause a marked reduction in ripple incidence. The mechanism for this disruption in ripple power is not fully understood. In isolated neurons, the major effect of cholinergic input on hippocampal neurons is depolarization of the membrane potential, which affects both hippocampal pyramidal neurons and inhibitory interneurons. Using an existing model of ripple‐frequency oscillations that includes both pyramidal neurons and interneurons, we investigated the mechanism whereby depolarizing inputs to these neurons can affect ripple power and frequency. We observed that ripple power and frequency are maintained, as long as inputs to pyramidal neurons and interneurons are balanced. Preferential drive to pyramidal neurons or interneurons, however, affects ripple power and can disrupt ripple oscillations by pushing ripple frequency higher or lower. Thus, an imbalance in drive to pyramidal neurons and interneurons provides a means whereby cholinergic input can suppress hippocampal ripples.
Two‐step technique of early adrenal artery ligation in open adrenalectomy of giant right adrenal pheochromocytomas: Three case reports
Authors: Ochi Atsuhiko , Fan Bo , Kimura Natsuo , Watanabe Hisaki , Toki Sari , Fukuokaya Wataru , Okada Daigo , Aikawa Koichi , Huang Tingwen , Suzuki Koichiro , Shiga Naoki , Kitagawa Yasuhide , Abe Hirokazu 
Published: November 2018

IntroductionSurgical manipulation of a pheochromocytoma carries the risk of releasing catecholamines into bloodstream leading to severe intraoperative hypertension.Case presentationWe present three patients with right adrenal pheochromocytoma over 10 cm diameter: a 40‐year‐old woman, 63‐year‐old man, and 66‐year‐old woman. They were diagnosed by 123I‐MIBG scintigraphy and received preoperative antihypertensive treatment with 16 mg/day of doxazosin. Open adrenalectomy was performed with early right adrenal artery ligation between the inferior vena cava and ventral aorta (Step 1) as well as between the tumor and upper pole of the right kidney (Step 2). There was no severe intraoperative hypertension, and no recurrence was observed over 33 months, postoperatively.ConclusionEarly adrenal artery ligation may stop tumor blood supply and significantly reduce the catecholamine release. Our technique was thought to be safe and useful for preventing severe intraoperative hypertension in giant right adrenal pheochromocytoma.
Heart valve tissue‐derived hydrogels: Preparation and characterization of mitral valve chordae, aortic valve, and mitral valve gels
Authors: Wu Jinglei , Brazile Bryn , McMahan Sara R. , Liao Jun , Hong Yi 
Published: November 2018

AbstractHeart valve (HV) diseases are among the leading causes of death and continue to threaten public health worldwide. The current clinical options for HV replacement include mechanical and biological prostheses. However, an ongoing problem with current HV prostheses is their failure to integrate with the host tissue and their inability grow and remodel within the body. Tissue engineered heart valves (TEHVs) are a promising solution to these problems, as they are able to grow and remodel somatically with the rest of the body. Recently, decellularized HVs have demonstrated great potential as valve replacements because they are tissue specific, but recellularization is still a challenge due to the dense HV extracellular matrix (ECM) network. In this proof‐of‐concept work, we decellularized porcine mitral valve chordae, aortic valve leaflets, and mitral valve leaflets and processed them into injectable hydrogels that could accommodate any geometry. While the three valvular ECMs contained various amounts of collagen, they displayed similar glycosaminoglycan contents. The hydrogels had similar nanofibrous structures and gelation kinetics with various compressive strengths. When encapsulated with NIH 3 T3 fibroblasts, all the hydrogels supported cell survivals up to 7 days. Decellularized HV ECM hydrogels may show promising potential HV tissue engineering applications. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 1732–1740, 2019.
Leucine aminopeptidase 3 promotes migration and invasion of breast cancer cells through upregulation of fascin and matrix metalloproteinases‐2/9 expression
Authors: Fang Chunyan , Zhang Jian , Yang Hanlin , Peng Lili , Wang Kun , Wang Yanjie , Zhao Xin , Liu Huijie , Dou Chunhui , Shi Lihong , Zhao Chunling , Liang Shujuan , Li Daqi , Wang Xuejian 
Published: November 2018

AbstractOverexpression of leucine aminopeptidase 3 (LAP3) is involved in proliferation, migration, and invasion of several tumor cells and plays a crucial role in tumor metastasis. However, the related mechanism remains unknown. In this study, we used MDA‐MB‐231 and MCF7 breast cancer cell lines to explore the role of LAP3 in the regulation of cancer cell migration and invasion by employing the natural LAP3 inhibitor bestatin and a lentivirus vector that overexpresses or knocks down LAP3. Bestatin inhibited tumor cell migration and invasion in a dose‐dependent manner. Western blot assay showed that bestatin and knockdown of LAP3 upregulated phosphorylation of Hsp27 and downregulated expression of fascin. Phosphorylation of Akt and expression of matrix metalloproteinase‐2/9 can also be downregulated. LAP3 overexpression showed the opposite results. Immunohistochemistry analysis was conducted to detect expression levels of LAP3 in breast cancer tissues. High LAP3 expression was correlated with the grade of malignancy. Findings of this study uncovered the molecular mechanism of LAP3 on breast cancer metastasis and indicated that LAP3 may act as a potential antimetastasis therapeutic target.
Lycium barbarum polysaccharides promoted proliferation and differentiation in osteoblasts
Authors: Zhang Huiying , Zheng Lei , Yuan Zhanpeng 
Published: November 2018

AbstractOsteoblasts have the capacity to differentiate into several different cell types, including adipocyte, chondrocyte, and muscle lineages. Therefore, osteoblast can be potentially applied in the treatment of bone diseases. The factors controlling osteoblast differentiation is complex. Recently, it has been reported that some natural products regulate the differentiation in osteoblasts and promote bone formation. Based on these findings, this study demonstrated that Lycium barbarum polysaccharides (LBP) could promote proliferation of osteoblast MC3T3‐E1 cells through 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay. Besides, expression of key proteins correlated with cellular proliferation such as proliferating cell nuclear antigen (PCNA) and Ki67 was enhanced in the presence of LBP. We also detected the increased expression of bone‐specific matrix proteins such as morphogenetic protein 2 (BMP2), bone Gla protein (BGP), osteopontin (OPN), and α‐1 type‐I collagen (COL1A1) when treated with LBP. This process was mediated by some signals, such as smad1, smad8, Runt‐related transcription factor 2 (RUNX2), and Osterix. Furthermore, RUNX2 silencing inhibited osteoblast differentiation by decreasing expression of bone‐specific matrix proteins. Collectively, we proposed a previously unidentified function of LBP in osteoblast differentiation, suggesting its potential clinical role in bone disease treatment.
BET inhibitors reduce cell size and induce reversible cell cycle arrest in AML
Authors: Zhang Susu , Zhao Yue , Heaster Tiffany M. , Fischer Melissa A. , Stengel Kristy R. , Zhou Xiaofan , Ramsey Haley , Zhou Ming‐Ming , Savona Michael R. , Skala Melissa C. , Hiebert Scott W. 
Published: November 2018

AbstractInhibitors of the bromodomain and extraterminal domain family (BETi) offer a new approach to treat hematological malignancies, with leukemias containing mixed lineage leukemia rearrangements being especially sensitive due to a reliance on the regulation of transcription elongation. We explored the mechanism of action of BETi in cells expressing the t(8;21), and show that these compounds reduced the size of acute myeloid leukemia cells, triggered a rapid but reversible G0/G1 arrest, and with time, cause cell death. Meta‐analysis of PRO‐seq data identified ribosomal genes, which are regulated by MYC, were downregulated within 3 hours of addition of the BETi. This reduction of MYC regulated metabolic genes coincided with the loss of mitochondrial respiration and large reductions in the glycolytic rate. In addition, gene expression analysis showed that transcription of BCL2 was rapidly affected by BETi but this did not cause dramatic increases in cell death. Cell cycle arrest, lowered metabolic activity, and reduced BCL2 levels suggested that a second compound was needed to push these cells over the apoptotic threshold. Indeed, low doses of the BCL2 inhibitor, venetoclax, in combination with the BETi was a potent combination in t(8;21) containing cells. Thus, BET inhibitors that affect MYC and BCL2 expression should be considered for combination therapy with venetoclax.
MicroRNA‐382 silencing induces a mitonuclear protein imbalance and activates the mitochondrial unfolded protein response in muscle cells
Authors: Dahlmans Dennis , Houzelle Alexandre , Andreux Pénélope , Wang Xu , Jörgensen Johanna A. , Moullan Norman , Daemen Sabine , Kersten Sander , Auwerx Johan , Hoeks Joris 
Published: November 2018

AbstractProper mitochondrial function plays a central role in cellular metabolism. Various diseases as well as aging are associated with diminished mitochondrial function. Previously, we identified 19 miRNAs putatively involved in the regulation of mitochondrial metabolism in skeletal muscle, a highly metabolically active tissue. In the current study, these 19 miRNAs were individually silenced in C2C12 myotubes using antisense oligonucleotides, followed by measurement of the expression of 27 genes known to play a major role in regulating mitochondrial metabolism. Based on the outcomes, we then focused on miR‐382‐5p and identified pathways affected by its silencing using microarrays, investigated protein expression, and studied cellular respiration. Silencing of miRNA‐382‐5p significantly increased the expression of several genes involved in mitochondrial dynamics and biogenesis. Conventional microarray analysis in C2C12 myotubes silenced for miRNA‐382‐5p revealed a collective downregulation of mitochondrial ribosomal proteins and respiratory chain proteins. This effect was accompanied by an imbalance between mitochondrial proteins encoded by the nuclear and mitochondrial DNA (1.35‐fold, p < 0.01) and an induction of HSP60 protein (1.31‐fold,
p < 0.05), indicating activation of the mitochondrial unfolded protein response (mtUPR). Furthermore, silencing of miR‐382‐5p reduced basal oxygen consumption rate by 14% (
p < 0.05) without affecting mitochondrial content, pointing towards a more efficient mitochondrial function as a result of improved mitochondrial quality control. Taken together, silencing of miR‐382‐5p induces a mitonuclear protein imbalance and activates the mtUPR in skeletal muscle, a phenomenon that was previously associated with improved longevity.
Inflammation and pericarditis: Are neutrophils actors behind the scenes?
Authors: Bonaventura Aldo , Montecucco Fabrizio 
Published: November 2018

AbstractThe morbidity of acute pericarditis is increasing over time impacting on patient quality of life. Recent clinical trials focused especially on clinical aspects, with a modest interest in pathophysiological mechanisms. This narrative review, based on papers in English language obtained via PubMed up to April 2018, aims at focusing on the role of the innate immunity in pericarditis and discussing future potential therapeutic strategies impacting on disease pathophysiology.In developed countries, most cases of pericarditis are referred to as idiopathic, although etiological causes have been described, with autoreactive/lymphocytic, malignant, and infectious ones as the most frequent causes. Apart the known impairment of the adaptive immunity, recently a large body evidence indicated the central role of the innate immune system in the pathogenesis of recurrent pericarditis, starting from similarities with autoinflammatory diseases. Accordingly, the “inflammasome” has been shown to behave as an important player in pericarditis development. Similarly, the beneficial effect of colchicine in recurrent pericarditis confirms that neutrophils are important effectors as colchicine, which can block neutrophil chemotaxis, interferes with neutrophil adhesion and recruitment to injured tissues and abrogate superoxide production. Anyway, the role of the adaptive immune system in pericarditis cannot be reduced to a black or white issue as mechanisms often overlap. Therefore, we believe that more efficient therapeutic strategies have to be investigated by targeting neutrophil‐derived mediators (such as metalloproteinases) and disentangling the strict interplay between neutrophils and platelets. In this view, some progress has been done by using the recombinant human interleukin‐1 receptor antagonist anakinra.
Inhibition of PI3K/Akt/NF‐κB signaling with leonurine for ameliorating the progression of osteoarthritis: In vitro and in vivo studies
Authors: Hu Zhi‐Chao , Gong Lan‐Fang , Li Xiao‐Bin , Fu Xin , Xuan Jiang‐Wei , Feng Zhen‐Hua , Ni Wen‐Fei 
Published: November 2018

AbstractOsteoarthritis (OA) is characterized as the degeneration and destruction of articular cartilage. In recent decades, leonurine (LN), the main active component in medical and edible dual purpose plant Herba Leonuri, has been shown associated with potent anti‐inflammatory effects in several diseases. In the current study, we examined the protective effects of LN in the inhibition of OA development as well as its underlying mechanism both in vitro and in vivo experiments. In vitro, interleukin‐1 beta (IL‐1β) induced over‐production of prostaglandin E2, nitric oxide, inducible nitric oxide synthase, cyclooxygenase‐2, interleukin‐6 and tumor necrosis factor alpha were all inhibited significantly by the pretreatment of LN at a dose‐dependent manner (5, 10, and 20 µM). Moreover, the expression of thrombospondin motifs 5 (ADAMTS5) and metalloproteinase 13 (MMP13) was downregulated by LN. All these changes led to the IL‐1β induced degradation of extracellular matrix. Mechanistically, the LN suppressed IL‐1β induced activation of the PI3K/Akt/NF‐κB signaling pathway cascades. Meanwhile, it was also demonstrated in our molecular docking studies that LN had strong binding abilities to PI3K. In addition, LN was observed exerting protective effects in a surgical induced model of OA. To sum up, this study indicated LN could be applied as a promising therapeutic agent in the treatment of OA.
Between an ugly truth and a perfect lie: Wiping off fearful memories using beta‐adrenergic receptors antagonists
Authors: AlOkda Abdelrahman M. , Nasr Mostafa M. , Amin Shaimaa N. 
Published: November 2018

AbstractPsychiatric disorders such as anxiety, phobias, and post‐traumatic stress disorder are considered of high global prevalence. Currently, a therapeutic approach to treat these disorders using beta‐blockers, which antagonize the beta‐adrenergic receptors (B1, B2, and B3) is being studied. This approach claims that beta‐blockers, such as propranolol, inhibit fear memory reconsolidation. However, there are several studies refuting such claims by discrediting their experimental design and pointing out both the drugs pharmacokinetic properties and confounding factors. In this review, we explore the different effects of central beta‐adrenergic agonists and antagonists on the fear memory consolidation providing mixed‐evidence, limitations, and future directions.
Activation of Pyk2 by CaM kinase II in cultured hypothalamic neurons and gonadotroph cells
Authors: Okitsu‐Sakurayama Shiho , Higa‐Nakamine Sayomi , Torihara Hidetsugu , Takahashi Hana , Higashiyama Shigeki , Yamamoto Hideyuki 
Published: November 2018

AbstractGonadotropin‐releasing hormone (GnRH) is secreted from hypothalamic GnRH neurons and stimulates a GnRH receptor in gonadotroph cells and GnRH neurons. The GnRH receptor belongs to the G‐protein‐coupled receptors, and stimulation of the GnRH receptor activates extracellular signal‐regulated protein kinase (ERK). We reported previously that the δ2 isoform of Ca2+/calmodulin‐dependent protein kinase II (CaM kinase IIδ2) was involved in GnRH‐induced ERK activation in cultured GnRH neurons (GT1–7 cells). Recently, we found that GnRH treatment of GT1–7 cells activated proline‐rich tyrosine kinase 2 (Pyk2), and Pyk2 was involved in ERK activation. In the current study, we examined the possibility that CaM kinase IIδ2 might activate Pyk2. Knockdown of CaM kinase IIδ2 and KN93, an inhibitor of CaM kinases, inhibited the GnRH‐induced activation of Pyk2. In the case of cultured gonadotroph cells (αT3‐1 cells), knockdown of CaM kinase IIβ’e inhibited GnRH‐induced Pyk2 activation. In addition, our inhibitor studies indicated that Pyk2 and CaM kinase II were involved in the GnRH‐induced shedding of proHB‐EGF in GT1–7 cells. These results suggested that CaM kinase II activated the ERK pathway through Pyk2 activation and HB‐EGF production in response to GnRH.
Licochalcone A attenuates abdominal aortic aneurysm induced by angiotensin II via regulating the miR‐181b/SIRT1/HO‐1 signaling
Authors: Hou Xuhui , Yang Songbai , Zheng Yan 
Published: November 2018

AbstractLicochalcone A (LA), a chalcone derived from liquorice, exhibits multiple biological activities, including anti‐oxidation and anti‐inflammation. This study aimed to investigate the role and underlying mechanism of LA in the abdominal aortic aneurysm (AAA). AAA model was established by continuous infusion of 1000 ng/kg/min of angiotensin II (AngII) in ApoE
‐/‐ mice for 4 weeks. At 7 days before AngII administration, 5 mg/kg/day or 10 mg/kg/day of LA was intraperitoneally administered to mice and continued for 4 weeks. The characteristics and quantification of AAAs were determined in situ. Real‐time PCR or western blot was used to measure mRNA or protein levels of matrix metalloproteinase 2 and matrix metalloproteinase 9; pro‐inflammatory cytokines tumor necrosis factor‐α, interleukin‐1β, and interleukin‐6; apoptosis‐related proteins Bax, Bcl‐2, and active caspase‐3; miR‐181b; Sirtuin 1 (SIRT1); and heme oxygenase‐1 (HO‐1). Mouse‐aorta‐origin vascular smooth muscle (MOVAS) cells were used to confirm the involved pathways in vitro. We found LA administration dose‐dependently reduced the incidence of AngII‐induced AAA, aneurysm diameter enlargement, elastin degradation, matrix metalloproteinase production, pro‐inflammatory cytokines and miR‐181b expression, and vascular smooth muscle cell apoptosis. It elevated SIRT1 and HO‐1 expression that was suppressed by AngII. AngII enhanced miR‐181b but reduced SIRT1 and HO‐1 expression in MOVAS cells. In AngII‐stimulated MOVAS cells, downregulation of miR‐181b significantly upregulated the expression of SIRT1 and HO‐1, the effect of which was abrogated by SIRT1 siRNA. Collectively, LA could attenuate AngII‐induced AAA by modulating the miR‐181b/SIRT1/HO‐1 signaling. LA might be a potential medical therapy for small AAA.
Four long noncoding RNAs as potential prognostic biomarkers for hepatocellular carcinoma
Authors: Wang Jianchu , Pu Jian , Yao Tianwei , Lu Xiaojie , Deng Yibin 
Published: November 2018

AbstractThe study aimed to identify the long noncoding RNAs (lncRNAs) biomarkers for occurrence and prognosis of patients with hepatocellular carcinoma (HCC), and simultaneously to investigate the potential role of lncRNAs in the oncogenesis of HCC. The lncRNAs expression data and the corresponding clinical information of HCC samples were extracted from The Cancer Genome Atlas (TCGA) database. The differentially expressed genes and lncRNAs were identified and the correlation networks were constructed. In this study, we identified 212 differentially expressed lncRNAs and 7,577 differentially expressed genes between liver HCC tumor tissues and normal tissue samples. And then, combining with clinical information, a total of 11 lncRNAs and 162 genes as HCC biomarkers were identified by comprehensive bioinformatics analysis. Further, through coexpress network analysis, we confirmed four lncRNAs (lncRNA_ANKRD10.IT1, lncRNA_CTD.2583A14.8, lncRNA_RP11.404P21.3, and lncRNA_RP11.488L18.10), which can serve as prognostic biomarkers for HCC. The four lncRNAs identified in this study may serve as a potential therapy target for HCC.