bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gastric transcatheter chemoembolization can resolve advanced gastric cancer presenting with obstruction
Authors: Peng Dong , Qian Kun , Cheng Yuxi , Tao Wei , Zou Ying-Ying , Zhang Wei 
Published: October 2020

Abstract
Background Gastric transcatheter chemoembolization (GTC) is an interventional minimal invasive method, which has never been mentioned in the previous literature for advanced gastric cancer with obstruction. The purpose of this study was to evaluate its safety and efficacy in treating advanced gastric cancer with obstruction.MethodsAdvanced gastric cancer patients with obstruction who underwent GTC were retrospectively analysed from June 2017 to January 2020. Baseline information, peri-intervention data, and post-intervention follow-up information were collected. Clinical data obtained before and after the GTC were compared, and the survival of all patients was analysed.ResultForty-Two patients were included in this study. 42 (100%) patients achieved technical success, and 22 (52.4%) achieved clinical success. The median time of the GTC was 83 (30.0-180.0) minutes, and the median time of hospitalization after GTC was 3 (1-6) days. One patient experienced abdominal pain during and after GTC. Twenty (47.6%) of the 42 patients underwent gastrectomy after intervention. The pre-intervention gastric outlet obstruction scoring system(GOOSS) was 1 (0-1) and the post-intervention GOOSS was 2 (0-3) (p=0.000<0.05). The median follow-up time was 9.5 (3-35) months, and the overall survival time was 14 months. In the univariate survival analysis, a significant difference was observed between patients who did or did not undergo radical gastrectomy after GTC (p = 0.014<0.05).ConclusionsGTC is a safe and effective treatment, and furthermore, it could be an alternative method in treating advanced gastric cancer with obstruction.
Timing of surgery for benign periacetabular tumor: virtual finite element analysis and clinical verification on 39 cases
Authors: Yang Hongsheng , Zhang Wenli , Lang Yun , Fang Xiang , Hong Duan 
Published: October 2020

Abstract
BackgroundThe treatment of periacetabular tumor has always been met with great challenges, including the lack of a standard for the timing of surgery. The purposes of this study were to predict the risk for fracture by finite element analysis of benign periacetabular tumor; to guide the timing of operation; and to verify the practical application of this standard through clinical cases. MethodsBone defects in different areas of the acetabulum were constructed, and the fracture risk was predicted by finite element analysis. According to the results of finite element analysis and Enneking classification, the patients with benign periacetabular tumor were divided into the low fracture risk noninvasive lesion, low fracture risk invasive lesion, and high fracture risk groups. The grouping was used to guide the timing of operation. ResultsThis study included 39 patients who were followed-up for at least two years to verify the effectiveness of this program. The 12 patients in the low risk noninvasive lesion group that did not undergo operation showed no obvious pathological changes and no pathological fracture; there was no significant difference in the MSTS-93 score between the first and last visits (P > 0.05). The 7 patients in the low risk invasive lesion group were treated with adjuvant therapy before the operation; the MSTS-93 score was significantly lower on the first visit than on the last visit (P < 0.05). The 20 cases that had high risk for fracture underwent surgery after the diagnosis; of these, 13 patients achieved osseointegration of the graft bone and 7 patients had no prosthesis loosening, detachment, displacement or rupture after prosthesis replacement. The MSTS-93 score significantly improved from a preoperative value of 19.61 ± 7.32 to a final follow-up value of 26.28 ± 15.59 (P < 0.01). ConclusionsOur study confirmed that for benign periacetabular tumor, finite element analysis, combined with the nature of the tumor, can predict the risk for acetabular fracture and guide the appropriate timing and method of operation, thereby, enabling a safe therapeutic effect.
Inflammatory pseudotumor-like follicular dendritic cell sarcoma of the liver with hepatic lymphoma history: a case report and literature review
Authors: Zhang Erlei , Wang Wenqiang , Li Jian , Chen Dong , Huang Zhiyong 
Published: October 2020

Abstract
BackgroundInflammatory pseudotumor (IPT)-like follicular dendritic cell (FDC) sarcoma of the liver is very rare and mostly occurs in females. Up to now, 19 cases were reported in the English literature. Surgical resection remains the preferred method for the management of this kind of tumor. Case presentationWe reported a case of a 47-year-old male patient who had hepatitis B virus infection history and presented with up-abdominal discomfort. He underwent liver resection of segment VII for hepatic non-hodgkin lymphoma (B-cell lymphoma) 19 years ago. Serum alpha fetoprotein was normal. Imaging studies revealed a well-circumscribed, solid mass in the right hepatic lobe and was diagnosed as HCC or hepatic lymphoma. Right hemihepatectomy was performed and the patient was disease free after a follow-up of 20 months. Histological feature showed a mixture of chronic inﬂammatory cells and variable amounts of spindle cells. Immunohistochemical studies demonstrated that all the tumor cells showed strong nuclear in situ labeling for EBV-encoded small RNAs (EBER) and strongly positive staining with CD21 and CD35. A diagnosis of hepatic IPT-like FDC sarcoma was rendered. The coexistence of IPT-like sarcoma and non-Hodgkin’s lymphoma in same patient is extremely rare. He remains disease-free more than 40 months after surgical resection.ConclusionTo our knowledge, this is the first report to demonstrate hepatic IPT-like FDC sarcoma in a patient with primary hepatic non-hodgkin lymphoma history. Complete surgical resection should be pursued.
Mulching measures improve soil moisture in rain-fed jujube orchard in the loess hilly region of China
Authors: Tang Min , Li Hongchen , Zhang Chao , Zhao Xining , Gao Xiaodong , Wu Pute 
Published: October 2020

Abstract
BackgroundWater shortage is the main bottleneck restricting the healthy and sustainable development of rain-fed jujube orchards in the loess hilly region of China. Given the functions of mulching on soil moisture conservation, evaporation reduction, and water use efficiency improvement, maize straw mulching (SM) and pruned jujube branch mulching (BM) were applied to rain-fed jujube orchards in this study. Soil moisture dynamics, soil water storage, water consumption, and soil moisture attenuation after typical rainfall under SM, BM, and clean tillage (CT) were systematically studied. Results(1) The 0-60 cm soil layer was the seasonal fluctuation layer of soil moisture under SM, BM, and CT in both the normal precipitation year and the dry year. The 0-60, 60-160, and 160-280 cm soil layers under CT all obtained the lowest soil moisture content in the three experimental years. The soil moisture content of each soil layer under SM and BM was higher than that under CT, and SM showed the most obvious effect of increasing soil moisture. (2) SM and BM showed significant soil water storage effect in all the jujube growth stages in both the normal precipitation year and the dry year, and SM had a better water storage effect than BM. (3) SM and BM reduced the water consumption amount in each jujube growth stage. SM reduced water consumption amount by 94.3, 60.8, and 121.3 mm compared with CT in the whole growth period of jujube in 2014, 2015, and 2016, respectively. The water consumption amount of BM decreased by 34.8 mm and 31.0 mm respectively compared with that of CT in the whole growth period in 2014 and 2015. (4) CT had the maximum soil moisture loss rate under continuous drought after rainfall. The soil moisture loss rate of CT was above 37.3% on the eleventh day after the typical rainfall in 2014, 2015, and 2016. With the extension of drought, the soil moisture loss rate under SM increased slowly, while it increased rapidly under CT. ConclusionThis study suggests that straw mulching is the best mulching measure for rain-fed jujube orchards, and the pruned jujube branches can also be used for in-situ mulching, which can also obtain a certain moisture conservation effect.
Identification of Mechanisms of Resistance to ALK Inhibitors. Next-generation sequencing-based liquid biopsy profiling: A step towards personalized treatment.
Authors: Sánchez-Herrero Estela , Serna-Blasco Roberto , Ivanchuk Vadym , García-Campelo Rosario , Dómine Manuel , Sánchez José Miguel , Massuti Bartomeu , Reguart Noemi , Camps Carlos , Sanz-Moreno Sandra , Calabuig-Fariñas Silvia , Jantus-Lewintre Eloísa , Arnal Magdalena , Fernández-Orth Dietmar , González-Rumayor Víctor , Calvo Virginia , Provencio Mariano , Romero Atocha 
Published: October 2020

Abstract
Background: Despite impressive and durable responses, patients treated with ALK inhibitors (ALK-Is) ultimately progress. We investigated potential resistance mechanisms in a series of ALK-positive non-small cell lung cancer (NSCLC) patients progressing on different types of ALK-Is.Methods: 26 plasma and 2 cerebrospinal fluid samples collected upon disease progression to an ALK-I, from 24 advanced ALK-positive NSCLC patients, were analyzed by next-generation sequencing (NGS). A tool to retrieve variants at the ALK locus was developed. Results: 61 somatic mutations were detected in 14 genes: TP53, ALK, PIK3CA, SMAD4, MAP2K1 (MEK1) FGFR2, FGFR3, BRAF, EGFR, IDH2, MYC, MET, CCND3 and CCND1. Overall, We identified at least one mutation in ALK locus in 10 (38.5%) plasma samples, being the G1269A and G1202R mutations the most prevalent among patients progressing to first- and second-generation ALK-I treatment, respectively. An exon 19 deletion in EGFR was identified in a patient showing primary resistance to ALK-I. Likewise, the G466V mutation in BRAF and the F129L mutation in MAP2K1 (MEK1) were identified as the underlying mechanism of resistance in three patients who gained no or little benefit from second-line treatment with an ALK-I. Putative ALK-I resistance mutations were also found in PIK3CA and IDH2. Finally, a c-MYC gain, along with a loss of CCND1 and a FGFR3, were detected in a patient progressing on a first-line treatment with crizotinib. Conclusions: NGS analysis of liquid biopsies upon disease progression identified putative ALK-I resistance mutations in most cases, being a valuable approach to devise therapeutic strategies upon ALK-I failure.
S-nitrosylation of CYR61 protein reduces triple-negative breast cancer metastasis ability
Authors: Jia Lee , Lu Yusheng , He Sudan , Xie Huanzhang , Zhong Chunlian , Yang Xingtian , Yu Suhong , Lian Shu , Li Yumei , Lin Guoxing , Zhang Chen 
Published: October 2020

Abstract
BackgroundTriple-negative breast cancer (TNBC) is the most difficult cancer to be treated. TNBC expresses high level of matricellular cysteine-rich protein CYR61/CCN1 that plays a key role in producing cancer metastases and is an important target for metastasis chemoprevention. Nitric oxide (NO) can covalently bind to the thiol group of cysteines (termed S-nitrosylation) resulting in regulation of the targeted protein functions. MethodsProtein S-nitrosylation were detected by biotin-switch assay and western blotting assay. CYR61 protein S-nitrosylated sites and 3D structure were determined by mass spectrometry and MODELLER software. Adhesion assay, cell morphology assay, wound healing assay and transwell invasion assay were used to evaluate effects of CYR61 S-nitrosylation on the cell metastatic ability. In vivo metastasis activity of CYR61 S-nitrosylation were tested by intravenous injection and mammary xenograft implantation mouse metastatic models.ResultsS-nitrosylation by GSNO of CYR61 reached a plateau quickly and was confirmed by spectroscopic analysis and biotin-switch assay. Mass-spectrometry proteomic analysis revealed that S-nitrosylation predominantly occurred at Cys100, Cys117, Cys229 and Cys239, resulting in CYR61 structure relaxed and unstable evidenced by protein structure modeling. S-nitrosylation of MDA-MB-231 cells, their CYR61-overexpressed and CYR61–silenced counterparts significantly attenuated the metastatic ability of these cells, including their ability of adhesion, mobility, invasion, and interplay with platelets, and made the adhered cells unattached. The attenuation in metastatic ability proportionally increased with the degree of S-nitrosylation to CYR61 naturally-expressed or genetically-manipulated cells, and was demonstrated in mice, where, S-nitrosylation of these cell lines not only inhibited their acute seeding to lungs after an intravenous injection, but also inhibited the late development of these cells into the metastatic nodes after mammary xenograft implantation. Furthermore, orthotopically-implanted MDA-MB-231 developed mammary tumors and later lung metastasis; whereas, the same cells with S-nitrosylation developed no tumor and metastasis at all. Conclusionwe present the first evidence that S-nitrosylation of CYR61 can significantly inhibit metastatic aggressiveness of the TNBC MDA-MB-231 cells. This conceptual creative study opens a new avenue to prevent the most aggressive TNBC from metastases by S-nitrosylation to CYR61.
A Combinatorial Strategy for Tageting Papillary Thyroid Carcinoma with MEK Inhibitor and SHP2 Inhibitor
Authors: Zhi Jingtai , Yi Jiaoyu , Hou Xiukun , Wang Wei , Yang Weiwei , Hu Linfei , Huang Jianfeng , Guo Shicheng , Ruan Xianhui , Zheng Xiangqian , Gao Ming 
Published: October 2020

Abstract
Background: Pharmacologic targeting of components of MAPK/ERK pathway in thyroid carcinoma is often limited due to the development of adaptive resistance. However, the detailed mechanism for MEK inhibitor (MEKi) resistance is not fully understood in papillary thyroid carcinoma (PTC). Methods: RNA-seq was performed in MEKi-resistant PTC cell lines (K1, BCPAP, TPC-1 and KTC-1) to investigate the intrinsic mechanism of drug resistance. Colony formation assay, cell viability assay, cell cycle analysis and various murine models, including xenograft model, long-term MEKi-treated model, and transgenic model were conducted to evaluate the treatment effect of combination therapy (SHP099 and selumetinib). Results: Multiple receptor tyrosine kinases (RTKs) signaling pathways as well as Src-homology 2 domain-containing phosphatase 2 (SHP2) were activated in MEKi-resistant cells. Given the physiological role of SHP2 as the downstream of many RTKs, we first found that blockage of SHP2 abrogated MEKi resistance in thyroid cancer. Interestingly, we also found MEKi in combination with SHP2 inhibitor remarkably suppress rebound of MEK/ERK pathway compared to that of MEKi treatment alone, which significantly improved antitumor effects of MEKi. Various murine models confirmed the synergistic suppression on PTC in mice treated with both inhibitors. Conclusion: SHP2 blockade by SHP099 in combination with selumetinib is a promising therapeutic approach for advanced thyroid cancer.
Ferroptosis Involved in the Progression of Hepatocellular Carcinoma Through Circ0097009/miR-1261/SLC7A11 Axis
Authors: Lyu Ning , Zeng Yan , Kong Yanan , Chen Qifeng , Deng Haijing , Gao Guanfeng , Tang Hailin , Zhao Ming 
Published: October 2020

Abstract
Background: Circular RNAs (circRNAs) is a class of non-coding RNAs and have been demonstrated to play important roles in tumorigenesis. Nevertheless, how circRNAs regulate the progression of hepatocellular cancer (HCC) remains unclear.Methods: CircRNA microarrays was performed in HCC tissues to screen circRNAs that are extinct expressed. Quantitative real-time PCR (qRT-PCR) was conducted in HCC cell lines, and tissues and circ0097009 were found to be significantly up-regulated. Then, we explored the functions of circ0097009 in HCC by a series of experiments including cell proliferation, invasion and mouse xenograft assay. Additionally, luciferase assay and RNA immunoprecipitation (RIP) assay was used to explore the interactions of circ0097009, miRNA-1261 and SLC7A11 (a key regulator in cancer cell ferroptosis) in HCC.Results: Microarray analysis and qRT-PCR verified a circRNA circ0097009, which was significantly up-regulated in HCC tissues and cell lines. Knockdown of circ0097009 inhibited proliferation and invasion in HCC. Luciferase reporter assays showed that circ0097009 and SLC7A11 directly bind to miR-1261. Subsequent experiments showed that circ0097009 and SLC7A11 regulated the expression of each other by sponging miR-1261.Conclusions: Circ0097009 act as a competing endogenous RNA (ceRNA) to regulate SLC7A11 expression, a key regulator in cancer cell ferroptosis through sponging miR-1261 in HCC. Circ0097009 may be used as a diagnostic biomarker and potential target for HCC therapy.
Involvement and Targeted Intervention of Mortalin-Regulated Proteome Phosphorylated-Modification in Hepatocellular Carcinoma
Authors: Yang Ye , Jin Ming , Dai Yi , Shan Wenqi , Chen Shuai , Cai Rong , Yang Haojun , Tang Liming , Li Lei 
Published: October 2020

Abstract
BackgroundAngiogenesis and sorafenib resistance are the main obstacles to the treatment of advanced/recurrent hepatocellular carcinoma (HCC).MethodsThree HCC cell lines, HepG2 and Hep3B, and sorafenib-resistant HuH7, and xenografts in nude mice were used as experimental models. A cohort of 126 HCC patients and a cohort of 34 advanced recurrent HCC patients receiving sorafenib therapy were used to indicate the clinical significance.ResultsMortalin regulated the phosphorylated-modification of cancer associated proteome, causing the angiogenesis and sorafenib resistance in HCC cells. For one of the molecular mechanisms, via regulating the PI-3K/Akt, mortalin activated the VEGF/VEGFR2 and β-Catenin/Bcl-XL/anti-apoptosis signaling. Treatment the sorafenib resistant xenografts with sorafenib combining with mortalin knockdown facilitated the sorafenib-inhibited tumor growth and angiogenesis, and enhanced the apoptosis. Mortalin was a potential risk factor of HCC, predicting poor prognosis and sorafenib resistance. We finally revealed that, caffeic acid (CaA, C9H8O4) could bind to and induce the ubiquitination degradation of mortalin, leading to the inhibition of PI-3K/Akt, VEGF/VEGFR2, and β-Catenin/Bcl-XL/anti-apoptosis signal pathways.ConclusionsMortalin, which regulated the phosphorylated-modification of cancer associated proteome, caused angiogenesis and sorafenib resistance, and was a competitive risk factor of HCC. CaA could be recognized as a novel chemical inhibitor, targeting mortalin in HCC.
Combined Inhibition of AURKA and HSF1 Suppresses the Cell Proliferation and Promotes Cell Apoptosis of Hepatocellular Carcinoma by Activating Endoplasmic Reticulum Stress
Authors: Shen Zetian , Yin Li , Zhou Han , Ji Xiaoqin , Jiang Changchen , Zhu Xixu , He Xia 
Published: October 2020

Abstract
Objective: This study aims to investigate the anti-tumor effect of combined inhibition of aurora kinase A (AURKA) and heat shock transcription factor 1 (HSF1) for hepatocellular carcinoma (HCC) and the underlying mechanism.Methods: The expression of AURKA and HSF1 in HCC tissues and cell lines were detected by Immunohistochemistry (IHC), qRT-PCR and Western blot. Then, AURKA was downregulated in HepG2 cells by lentivirus-induced RNA interfere. Cell viability, invasion, migration and apoptosis were examined by CCK8, clone formation, transwell assays and flow cytometry analysis. The expression of proteins related to cell cycle, apoptosis and endoplasmic reticulum stress (ERS) were detected by Western blot. The tumor in vivo growth was measured on nude mice model. Histopathological examination was performed with HE staining.Results: AURKA and HSF1 were highly expressed in HCC tissues and cells, as well as negative related with prognosis. Knockdown of AURKA significantly inhibited the colony formation and migration of HCC cells. Besides, AURKA inhibitor (Danusertib) significantly reduced the proliferation and migration of HCC cells, and promoted cell apoptosis. Combined inhibition of AURKA and HSF1 induced cell apoptosis of HCC cells and increased the expression of ERS-associated proteins including p-eIF2α, ATF4 and CHOP in vitro. Additionally, combined inhibition of AURKA and HSF1 displayed an excellent antitumor activity on HCC model with relative low cytotoxicity.Conclusion: Combined inhibition of AURKA and HSF1 display excellent anti-tumor effect on HCC by activating endoplasmic reticulum stress, suggesting that AURKA and HSF1 can served as potential targets for HCC treatment.
Piecewise Sparse Approximation via Threshold P_OMP with Application to Surface Reconstruction
Authors: Zhong Yijun , Li Chongjun 
Published: October 2020

Abstract
Sparse signal representations have gained extensive study in recent years. In applications, there are large amounts of signals that are structured. Motivated by signal decomposition and scattered data reconstruction applications, we consider a particular type of structured signals which can be represented by a union of several sparse vectors. We define this type of signal as piecewise sparse signals. To find a piecewise sparse representation of a signal, we propose a thresholding version of piecewise orthogonal matching pursuit(TP OMP), which aims to overcome the disadvantages of P_OMP. We also establish the connection of piecewise sparsity and sampling over a union of subspaces. We evaluate the performance of the proposed greedy programs through simulations on surface reconstruction.
“They’re Not Doing Enough.”: Women’s Experiences with Opioids and Naloxone in Toronto
Authors: MacLeod Emilie , Tajbakhsh Iren , Hamilton-Wright Sarah , Laliberte Nancy , Wiese Jessica , Matheson Flora I 
Published: October 2020

Abstract
BACKGROUND: Amid increasing opioid overdose deaths in Canada, there is currently a need for up-to-date research on Canadian women’s experiences with opioids and their recently down-scheduled antidote, naloxone. Studies on Canadian take-home naloxone programs are promising, but research on perspectives outside these programs is limited. As the first qualitative study since the inception of the 2010’s opioid crisis to focus on Canadian women’s experiences and perspectives, our objective was to address these knowledge gaps and to identify resulting flaws in current policies, responses, and practices.METHODS: We conducted semi-structured, qualitative interviews from January to April 2018 with 10 women with experience of opioid use. They were recruited through the study’s community health partner in Toronto. They provided demographic information, experiences with opioids and naloxone, and their views on the Canadian government’s responses to the opioid crisis. Interviews were transcribed verbatim and inductive thematic analysis was conducted to determine major themes within the data.RESULTS: Participants who had used illicit opioids since the Canadian government’s down-scheduling of naloxone in 2016 were much more knowledgeable about naloxone than participants who had only used opioids prior. The portability, dosage form, and effects of naloxone are important considerations for women who use opioids. Social alienation, violence, and isolation affect the wellbeing of women who use opioids. The Canadian government’s response to the opioid crisis was perceived as neglectful and inadequate. Participants demonstrated differing needs and views on ideal harm reduction approaches, despite facing similar structural issues surrounding stigma, addiction management, and housing.CONCLUSIONS: Participants experienced with naloxone use found it to be useful in preventing fatal overdose, however many of their needs with regards to physical, mental, and social health, housing, harm reduction, and access to opioid treatment remained unmet.