bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bioaccumulation and Health Risk Assessment of Heavy Metals in the Soil–Rice System in a Typical Seleniferous Area in Central China
Authors: Chang Chuanyu , Yin Runsheng , Zhang Hua , Yao Linjun 
Published: April 2019

Abstract
Heavy metals are rich in seleniferous areas; however, the bioaccumulation and health risk of heavy metals are poorly understood, given the fact that selenium (Se) can inhibit the phytotoxicity and bioavailability of many heavy metals. The present study investigated the bioaccumulation of heavy metals in the soil–rice system in the Enshi seleniferous area of central China. Soils were contaminated by Mo, Cu, As, Sb, Zn, Cd, Tl, and Hg caused by the weathering of Se-rich shales. Among these heavy metals, Cd and Mo had the highest bioavailability in soils. The bioavailable fractions of Cd and Mo accounted for 41.84 and 10.75% of the total Cd and Mo in soils, respectively. Correspondingly, much higher bioaccumulation factors (BAFs) of Cd (0.34) and Mo (0.46) were found in rice, compared with those of other heavy metals (Zn 0.16, Cu 0.05, Hg 0.04, and Sb 0.0002). For the first time—to our knowledge—we showed that the uptake of Hg, Cd, and Cu by rice could be inhibited by the presence of Se in the soil. The probable daily intake (PDI) of Se, Cd, Mo, Zn, and Cu through consumption of local rice was 252 ± 184, 314 ± 301, and 1774 ± 1326 μg/d; and 7.4 ± 1.68 and 0.87 ± 0.35 mg/d, respectively. The high hazard quotients (HQs) of Mo (1.97 ± 1.47) and Cd (5.22 ± 5.02) suggested a high risk of Cd and Mo for Enshi residents through consumption of rice. Environ Toxicol Chem 2019;38:1577–1584. © 2019 SETAC
Inflammation in mild cognitive impairment due to Parkinson's disease, Lewy body disease, and Alzheimer's disease
Authors: King Eleanor , O'Brien John , Donaghy Paul , Williams‐Gray Caroline H. , Lawson Rachael A. , Morris Christopher M. , Barnett Nicola , Olsen Kirsty , Martin‐Ruiz Carmen , Burn David , Yarnall Alison J. , Taylor John‐Paul , Duncan Gordan , Khoo Tien K. , Thomas Alan 
Published: April 2019

BackgroundInflammation appears to play a role in the progression of neurodegenerative diseases. However, little is known about inflammation during early stages of cognitive decline or whether this differs in different disease groups. We sought to investigate this by assessing the inflammatory profile in patients with Parkinson disease with the early stages of cognitive impairment (PD‐MCI), patients with prodromal Alzheimer disease (MCI‐AD), prodromal Lewy body disease (MCI‐LB), and controls.MethodsWe obtained venous blood samples from participants with PD‐MCI (n = 44), PD‐normal cognition (n = 112), MCI‐LB (n = 38), MCI‐AD (n = 21), and controls (n = 84). We measured 10 cytokines using Meso Scale Discovery V‐Plex Plus including interferon gamma, interleukin (IL)‐10, IL‐12p70, IL‐13, IL‐1beta, IL‐2, IL‐4, IL‐6, IL‐8, and tumour necrosis factor alpha. High‐sensitivity C‐reactive protein was measured.ResultsThere was a higher level of inflammation in patients with MCI‐AD and MCI‐LB compared with controls. PD noncognitively impaired had higher inflammatory markers than controls, but there was no difference between PD‐MCI and controls. There was a decrease in inflammatory markers with increasing motor severity based on the Unified Parkinson's Disease Rating Scale.ConclusionsInflammation may be involved in the onset of cognitive decline in patients with MCI‐AD and MCI‐LB but appears to be less prominent PD‐MCI albeit in a small data set. This suggests that anti‐inflammatory medications may have most benefit at the earliest stages of neurodegenerative diseases. For PD cases, this might be in advance of the development of MCI.
A survey on the prevalence of apathy in elderly people referred to specialized memory centers
Authors: Manera Valeria , Fabre Roxane , Stella Florindo , Loureiro Júlia Cunha , Agüera‐Ortiz Luis , López‐Álvarez Jorge , Hanon Cécile , Hoertel Nicolas , Aalten Pauline , Ramakers Inez , Zeghari Radia , Robert Philippe 
Published: April 2019

BackgroundApathy is a pervasive neuropsychiatric syndrome in people with neurocognitive and psychiatric disorders. The diagnostic criteria for apathy (DCA) have been revised in 2018.ObjectivesEmploying the 2018 DCA, in the present study, we investigated in groups of elderly subjects suffering from different neuropsychiatric disorders (a) the apathy prevalence; (b) the most commonly affected apathy dimensions (behavior/cognition, emotion, and social interaction); (c) the sensitivity and specificity of those dimensions for apathy diagnosis; and (d) the concurrent validity of 2018 DCA compared with the 2009 DCA.MethodsThis multicenter survey included 166 subjects. Each center checked the presence of apathy in subjects belonging to the following DSM‐5 diagnoses: mild neurocognitive disorders (mild NCDs); major NCDs; affective disorders (Aff D); and subjective cognitive decline (SCD).ResultsThe frequency of apathy varied significantly based on the diagnostic groups (0% of subjects with apathy in the SCD group; 25% in the mild NCD group; 77% in the major NCD group; and 57% in the Aff. D group). All subjects with apathy fulfilled the criteria for the behavior/cognition dimension, 73.1% fulfilled the criteria for the emotion dimension, and 97.4% fulfilled the criteria for the social interaction dimension. Behavior/cognition showed the highest sensitivity, the copresence of emotion and social interaction the highest specificity. The concordance between the 2009 and the 2018 DCA indicated an almost perfect agreement.ConclusionsThese results are consistent with previous reports and confirm that the social interaction dimension added to the 2018 DCA is present in most of subjects with apathy referred to specialized memory centers.
Factors associated with misreporting in performance‐based financing in Burkina Faso: Implications for risk‐based verification
Authors: Kuunibe Naasegnibe , Lohmann Julia , Schleicher Michael , Koulidiati Jean‐Louis , Robyn Paul Jacob , Zigani Zambendé , Sanon Adama , De Allegri Manuela 
Published: April 2019

SummaryPerformance‐based financing (PBF) has been piloted in many low‐ and middle‐income countries (LMICs) as a strategy to improve access to and quality of health services. As a key component of PBF, quantity verification is carried out to ensure that reported data matches the actual number of services provided. However, cost concerns have led to a call for risk‐based verification. Existing evidence suggests misreporting is associated with factors such as complexity of indicators, high service volume, and accepted error margin. In contrast, evidence on the association of key facility characteristics with misreporting in PBF is scarce. We contributed to filling this gap in knowledge by combining administrative data from a large‐scale pilot PBF program in Burkina Faso with data from a health facility assessment in the context of an impact evaluation of the intervention. Our results showed the coexistence of both overreporting and underreporting and that misreporting varied by service indicator and health district. We also found that the number of clinical staff at the facility, the population size in the facility catchment area, and the distance between the facility and the district administration were associated with the probability of misreporting. We recommend further research of these factors in the move towards risk‐based verification. In addition, given that our analysis identified relevant associations, but could not explain them, we recommend further qualitative inquiry into verification processes.
Local Tumor Recurrence and Escape from Suppression of Bone Resorption With Denosumab Treatment in Two Adolescents With Giant Cell Tumors of Bone
Authors: Akel Umar , Robinson Marie‐Eve , Werier Joel , Rampersaud Raja , Rakhra Kawan , Johnston Donna , Konji Victor N , Ma Jinhui , Pagé Marika , Matzinger Mary Ann , Ward Leanne M 
Published: April 2019

ABSTRACTGiant cell tumors of bone (GCTB) may be difficult to resect because of size or location. We describe two adolescents who were treated with denosumab and followed for tumoral and biochemical responses. Denosumab was effective in achieving sufficient regression to allow surgical resection and in preserving peritumor cortical bone. Reactivation of bone resorption markers was noted while the patients were receiving monthly denosumab. One patient suffered a local tumor recurrence. Denosumab was safe in enabling surgical resection of GCTB. However, the effect was transient, with an escape of resorption markers and tumor recurrence. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
Combined Collagen-Induced Arthritis and Organic Dust-Induced Airway Inflammation to Model Inflammatory Lung Disease in Rheumatoid Arthritis
Authors: Poole Jill A , Thiele Geoffrey M , Janike Katherine , Nelson Amy J , Duryee Michael J , Rentfro Kathryn , England Bryant R , Romberger Debra J , Carrington Joseph M , Wang Dong , Swanson Benjamin J , Klassen Lynell W , Mikuls Ted R 
Published: April 2019

ABSTRACT
Rheumatoid arthritis (RA) is characterized by extra-articular involvement including lung disease, yet the mechanisms linking the two conditions are poorly understood. The collagen-induced arthritis (CIA) model was combined with the organic dust extract (ODE) airway inflammatory model to assess bone/joint–lung inflammatory outcomes. DBA/1J mice were intranasally treated with saline or ODE daily for 5 weeks. CIA was induced on days 1 and 21. Treatment groups included sham (saline injection/saline inhalation), CIA (CIA/saline), ODE (saline/ODE), and CIA +  ODE (CIA/ODE). Arthritis inflammatory scores, bones, bronchoalveolar lavage fluid, lung tissues, and serum were assessed. In DBA/1J male mice, arthritis was increased in CIA +  ODE &gt;  CIA &gt;  ODE versus sham. Micro-computed tomography (µCT) demonstrated that loss of BMD and volume and deterioration of bone microarchitecture was greatest in CIA +  ODE. However, ODE-induced airway neutrophil influx and inflammatory cytokine/chemokine levels in lavage fluids were increased in ODE &gt;  CIA +  ODE versus sham. Activated lung CD11c+CD11b+ macrophages were increased in ODE &gt;  CIA +  ODE &gt;  CIA pattern, whereas lung hyaluronan, fibronectin, and amphiregulin levels were greatest in CIA +  ODE. Serum autoantibody and inflammatory marker concentrations varied among experimental groups. Compared with male mice, female mice showed less articular and pulmonary disease. The interaction of inhalation-induced airway inflammation and arthritis induction resulted in compartmentalized responses with the greatest degree of arthritis and bone loss in male mice with combined exposures. Data also support suppression of the lung inflammatory response, but increases in extracellular matrix protein deposition/interstitial disease in the setting of arthritis. This coexposure model could be exploited to better understand and treat RA–lung disease. © 2019 American Society for Bone and Mineral Research.
Upregulation of hsa_circ_0136666 contributes to breast cancer progression by sponging miR‐1299 and targeting CDK6
Authors: Liu Li‐Hong , Tian Qing‐Qing , Liu Juan , Zhou Yong , Yong Hongmei 
Published: April 2019

AbstractCircular RNAs (circRNAs) can participate in multiple cancers, including breast cancer. Increasing circRNAs are recognized in various cancers because of the high‐throughput sequencing. However, the potential physiological effect of hsa_circ_0136666 in breast cancer progression is unknown. In our study, the biological role of hsa_circ_0136666 in breast cancer development was studied. It was displayed that hsa_circ_0136666 was greatly increased in breast cancer. In addition, overexpression of hsa_circ_0136666 was able to promote Michigan Cancer Foundation‐7 (MCF7) and BT474 cell proliferation and triggered cell cycle in G2/M phase. microRNA plays critical role in tumor development and they can act as direct targets of circRNAs. miR‐1299 has been implicated as a famous tumor suppressor in many cancers. Here, miR‐1299 was predicted as the target of hsa_circ_0136666. Meanwhile, its Upregulation repressed breast cancer proliferation, migration and invasion capacity, which could be reversed by the increase of hsa_circ_0136666. Furthermore, Cyclin‐dependent kinase 6 (CDK6) was speculated as the downstream target of miR‐1299. In MCF7 and BT474 cells, CDK6 was greatly overexpressed and it was shown that CDK6 contributed a lot to breast cancer progression. Subsequently, it was implied that hsa_circ_0136666 could modulate CDK6 levels positively in vitro. In conclusion, it was revealed that Upregulation of hsa_circ_0136666 promoted breast cancer progression by sponging miR‐1299 and targeting CDK6.
Silencing of microRNA‐27a facilitates autophagy and apoptosis of melanoma cells through the activation of the SYK‐dependent mTOR signaling pathway
Authors: Tang Hua , Xu Xiaopeng , Xiao Weirong , Liao Yangying , Xiao Xiao , Li Lan , Li Ke , Jia Xiaomin , Feng Hao 
Published: April 2019

AbstractMelanoma is considered as an aggressive neoplastic transformation and featured with high metastatic potential. Although some studies have provided targets for novel therapeutic interventions, clinical development of targeted drugs for melanoma still remains obscure. Therefore, this study aims to identify the role of microRNA‐27a (miR‐27a) in autophagy and apoptosis of melanoma cells in regulating spleen tyrosine kinase (SYK)‐mediated the mammalian target of rapamycin (mTOR) signaling pathway. A microarray‐based analysis was made to screen differentially expressed genes and predict target miRNA. Melanoma specimens were collected with pigmented nevus as a control. Melanoma cell line Mel‐RM was treated with miR‐27a inhibitor or pcDNA‐SYK to prove their effects on autophagy and apoptosis of melanoma cells. The volume change and tumor mass of nude mice in each group were detected by the tumorigenesis assay. Microarray‐based analysis results showed that SYK was lowly expressed in melanoma cells and may be regulated by miR‐27a. Besides, miR‐27a expression was increased whereas SYK expression was decreased in melanoma tissues. Meanwhile, miR‐27a was positively correlated with tumor stage and lymph node metastasis of melanoma tissues. Furthermore, miR‐27a targeted SYK and silencing of miR‐27a or overexpression of SYK cells promoted autophagy and apoptosis of melanoma cells and reduced their tumorigenic ability in vivo. In conclusion, this study proves that silencing of miR‐27a facilitates autophagy and apoptosis of melanoma cells by upregulating SYK expression and activating the mTOR signaling pathway. The finding offers new ideas for the clinical development of melanoma.
lncRNA TINCR participates in ALA‐PDT‐induced apoptosis and autophagy in cutaneous squamous cell carcinoma
Authors: Zhou Wu , Zhang Shoumin , Li Jianguo , Li Zhenlu , Wang Yuping , Li Xueli 
Published: April 2019

AbstractThis study aims to investigate whether terminal differentiation‐induced ncRNA (TINCR) has an effect on apoptosis and autophagy induced by ALA‐PDT in cutaneous squamous cell carcinoma (CSCC). A431 cells were treated with 5‐aminolevulinic acid (ALA) solution at different concentrations and for different duration time. A431 cell viability was detected by Cell Counting Kit‐8 (CCK‐8) assay, relative TINCR messenger RNA expression was detected by quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). A431 cell apoptosis was examined by flow cytometry. Relative apoptosis/autophagy‐related protein expression was analyzed by Western blot analysis. The effect of TINCR on cell autophagy was detected by RFP‐LC3 immunofluorescence assay. Reactive oxygen species concentration was detected by 2′,7′‐dichlorodihydrofluorescein diacetate (DCFH‐DA) fluorescent probe. Relative expressions of ERK1/2 and specificity protein 3 (Sp3) in A43 cells were detected by Western blot analysis and qRT‐PCR. Sp3 binding sites were analyzed by ChIP‐qPCR. The relative transcription activity was measured with luciferase reporter assay. ALA‐PDT treatment at 3.2 mmol/L for 120 minutes significantly promoted TINCR expression in CSCC A431 cells, and TINCR promoted ALA‐PDT‐induced apoptosis and cell autophagy. Furthermore, ALA‐PDT promoted TINCR expression through ERK1/2‐SP3 pathway. Sp3 promoted TINCR transcription by binding TINCR promoters. Our data indicated that TINCR involves in ALA‐PDT‐induced apoptosis and autophagy in CSCC.
RETRACTED: Identification of Nrf2/STAT3 axis in induction of apoptosis through sub‐G1 cell cycle arrest mechanism in HT‐29 colon cancer cells
Authors: Tajmohammadi Issa , Mohammadian Jamal , Sabzichi Mehdi , Mahmuodi Shiva , Ramezani Mina , Aghajani Marjan , Ramezani Fatemeh 
Published: April 2019

AbstractWe investigated the role of stattic as an adjuvant molecule to increase the cytotoxicity of 5‐fluorouracil (5‐FU) through specific inhibition of molecular targets, signal transducer and activator of transcription 3 (STAT3) and nuclear factor erythroid 2–related factor 2 (Nrf2) in HT‐29 colon cancer cells. Cytotoxicity and apoptotic effects were investigated by methylthiazolyldiphenyl‐​tetrazolium bromide assay and flow cytometry analysis, respectively. Real‐time polymerase chain reaction was applied to assess the messenger RNA (mRNA) level of STAT3, Nrf2, and apoptotic genes including Bax, Bcl‐xl, and Bcl‐2. The antitumor effect of 5‐FU in combination with stattic induced synergistic effect in HT‐29 cells with combination indexes (CIs) 0.49. Flow cytometric results related to apoptotic confirmed that there was up to 40% increase in the population of apoptotic cells in HT‐29 colon cancer cells incubated with 5‐FU and stattic compared with control groups. Our data from gene expression determined a substantial diminish in the mRNA levels of the Nrf2 and antiapoptotic gene Bcl‐2 along with a noticeable increase in the level of the proapoptotic Bax in HT‐29 colon cells that underwent cotreatment with 5‐FU and stattic (P < 0.05). Moreover, the results exhibited that stattic can be used as adjuvant chemotherapy besides the 5‐FU. This therapeutic approach in colon cancer could mediate 5‐FU chemoresistance via modulating therapeutic targets (ie, STAT3 and Nrf2 pathways) and decreased 5‐FU‐related adverse effects.
Long noncoding RNA HOXA‐AS2 regulates the expression of SCN3A by sponging miR‐106a in breast cancer
Authors: Wu Jie , Li Maolan , Zhang Yijian 
Published: April 2019

AbstractBreast cancer is the most commonly diagnosed cancer that affects women worldwide. This study aimed to investigate the competing endogenous RNAs (ceRNAs) mechanism in breast cancer. Microarray data were downloaded from the University of California Santa Cruz (UCSC) Xena database. The limma package was used to screen the differentially expressed messenger RNAs (DEMs) and differentially expressed long noncoding RNAs (DELs). Subsequently, functional analysis was performed using DAVID tool. After constructing the protein‐protein interaction (PPI) network, we identified the major gene modules using the Cytoscape software. Univariate survival analysis in the survival package was performed. Finally, the ceRNA regulatory network was constructed to identify the critical genes. A total of 1380 DEMs and 345 DELs were identified in breast cancer samples compared with normal samples. Functional enrichment analysis showed that DEMs were mainly involved in cell division, and cell cycle. We screened four major gene modules and identified the hub nodes in these functional modules. Several DEMs (including FABP7, C4BPA, and LAMB3) and three long noncoding RNAs (lncRNAs) (LINC00092, SLC26A4.AS1, and COLCA1) exhibited significant correlation with patients' survival outcomes. In the ceRNA network, the lncRNA HOXA‐AS2 regulated the expression level of SCN3A by interacting with hsa‐miR‐106a‐5p. Thus, our study investigated the ceRNA mechanism in breast cancer. The results showed that lncRNA HOXA‐AS2 might modulate the expression of SCN3A by sponging miR‐106a in breast cancer.
Radiosynthesis, radiochemical, and biological characterization of 177Lu‐labeled diethylenetriamine penta‐acetic acid
Authors: Akbar Muhammad U. , Bokhari Tanveer H. , Ahmad Muhammad R. , Zia Khalid M. , Roohi Samina , Ayub Nimra , Sohaib Muhammad 
Published: April 2019

AbstractDiethylenetriamine penta‐acetic acid (DTPA), when complexed with a gamma (γ)‐emitter radioisotope like 99mTc, is used for renal function diagnosis and many other diagnostic applications. The main aim of this study was to develop a novel and versatile single‐step methodology for the synthesis of a new 177Lu‐labeled radiopharmaceutical with high radiochemical yield, which can be used for diagnostic purposes and therapeutic purposes also. The single and well‐defined 177Lu‐DTPA complex was radiochemically characterized by paper chromatography, thin‐layer chromatography, high‐performance liquid chromatography, and electrophoresis techniques. Dependence of the labeling yield of 177Lu‐DTPA complex on different factors was studied in detail. Biological evaluation was also performed in a normal rabbit by developing images under a γ camera at various time intervals. More than 99% labeling yield was obtained by reacting DTPA with 177Lu at specific conditions (pH 7.0, 15 minutes reaction time at 100 °C). 177Lu‐DTPA complex showed high stability both at room temperature and in vitro. Biodistribution studies in normal mice indicated the fractional renal uptake of intravenously administered 177Lu‐DTPA complex, which reached in the kidneys within 2‐3 minutes. Scintigraphy showed rapid clearance from the body. Based on these results, we propose that 177Lu‐DTPA complex might be used as an ideal candidate for functional evaluation of kidneys and the urinary tract, especially when needed to be transported to long‐range consumer sites, because of its suitable half‐life.
GLP‐1 induces alpha cell proliferation and overrides leptin suppression induced by negative energy balance in vagotomized rats
Authors: Morais Tiago , Patrício Barbara , Pereira Sofia Silva , Andrade Sara , Carreira Marcos , Casanueva Felipe F. , Monteiro Mariana P. 
Published: April 2019

AbstractGlucagon‐like peptide‐1 (GLP‐1) influences energy balance by exerting effects on food intake and glucose metabolism, through mechanisms that are partially dependent on the vagal pathway. The aim of this study was to characterize the effects of chronic GLP‐1 stimulation on energy homeostasis and glucose metabolism in the absence of vagal innervationTruncal vagotomized (VGX) and sham operated rats (SHAM) received an intraperitoneal GLP‐1 infusion (3.5 pmol/kg/min) trough mini‐osmotic pumps. To dissect the effects derived from vagal denervation on food intake, an additional group was included consisting of sham operated rats that were PAIR FED to VGX. Food intake and body weight were recorded throughout the experimental period, while the percentage of white and brown adipose tissue, fasting glucose, insulin, gastro‐intestinal hormonal profile, hypothalamic, and BAT gene expression were assessed at endpoint.VGX rats had significantly lower food intake, body weight gain, and leptin levels when compared with SHAM rats. Despite having similar body weight, PAIR‐FED rats had lower fasting leptin, insulin and insulin resistance, while having higher ghrelin levels than VGX. GLP‐1 infusion did not influence food intake or body weight, but was associated with lower leptin levels in VGX and lower pancreatic α‐cells ki‐67 staining in SHAM.Concluding, this study corroborates that the vagus nerve may modulate whole body energy homeostasis by acting in peripheral signals. Our data suggest that in the absence of vagal or parasympathetic tonus, GLP‐1 mediated inhibition of cell proliferation markers in α‐cells is prevented, meanwhile leptin suppression, associated with a negative energy balance, is partially overridden.