bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mycotoxins Detection Based on Electrochemical Approaches
Authors: Dong Shaoqing , Yan Jixian , Zhou Shuang , Zhou Qing 
Published: August 2021

AbstractElectrochemical biosensors have attracted much attention in mycotoxin bioanalysis. In this review, three electrochemical biosensor technologies for mycotoxins were reviewed, including general electrochemistry, photoelectrochemistry, and electrochemiluminescence. Based on the classification of multiple electrochemical detection methods, the design schemes, recognition mechanism and probe materials were described in detail. Moreover, the characteristics and limitations of these electrochemical biosensors were summarized. The challenges and future trends of electrochemical biosensor development in mycotoxin bioanalysis were also briefly discussed in the end. This review is expected to provide some inspirations for point‐of‐care testing in electrochemical sensors for mycotoxins and further electrochemical analysis application.
Performance analysis for user selection‐based downlink non‐orthogonal multiple access system over generalized fading channels
Authors: Sharma Priyank , Kumar Atul , Bansal Matadeen 
Published: August 2021

AbstractIn this study, user selection‐based downlink power domain‐non‐orthogonal multiple access (NOMA) system is investigated over generalized fading channels, that is, η‐μ and κ‐μ fading channels. In particular, this system considers multiple users and out of which two users are selected to serve with NOMA principle in perfect channel state information scenario. The outage probability expressions of the system are derived with respect to the fixed target rate and the orthogonal multiple access (OMA) rate. In addition, the average sum‐rate and rate of paired users of the system are derived and compared with that of OMA. Further, the optimum power allocation coefficients are derived for the system to ensure fixed and dynamic rate requirements. The impact of imperfect successive interference cancelation on the system performance is discussed. The paper also investigates the effect of various parameters on the performance of the system. The extensive simulations show the accuracy of the derived expressions.
Typifications and notes on Hyptidinae (Lamiaceae) described by Pilger from Mato Grosso state, Brazil
Authors: Antar Guilherme Medeiros , Harley Raymond Mervyn , Soares Arthur de Souza , Buchoski Mônica Gomes , Pastore José Floriano Barêa , Sano Paulo Takeo 
Published: August 2021

AbstractThe subtribe Hyptidinae (Lamiaceae) is predominantly Neotropical with ca. 400 species, most diverse in the Cerrado domain, the Brazilian savanna. Mato Grosso state, located in the core of the Cerrado, owns a remarkable richness in the subtribe with 71 species recognized. Robert Pilger, who accompanied Hermann Meyer on an expedition to the state in 1898, collected about 700 angiosperm specimens that were mostly deposited in the Berlin Herbarium and many subsequently destroyed during the 2nd World War, with few if any duplicates surviving. Five species of Hyptidinae were described by Pilger based on these materials from Mato Grosso, subsequently were lectotypified by Epling, and later destroyed. They are: Hyptis helophila Pilg. (= H. petiolaris Pohl ex Benth.), H. indivisa Pilg. (= Cantinoa indivisa (Pilg.) Harley & J.F.B.Pastore), H. lasiocalyx Pilg. (= Cyanocephalus desertorum (Pilg.) Harley & J.F.B.Pastore), H. loeseneriana Pilg. and H. mattogrossensis Pilg. (= Hypenia macrosiphon (Briq.) Harley). To fix the application of these names, neotypes are here designated. Notes are also provided on the habitats and distribution of these species.
Geophysical mapping of hyporheic processes controlled by sedimentary architecture within compound bar deposits
Authors: McGarr Jeffery Tyler , Wallace Corey D. , Ntarlagiannis Dimitrios , Sturmer Daniel M. , Soltanian Mohamad Reza 
Published: August 2021

AbstractHyporheic exchange influences water quality and controls numerous physical, chemical, and biological processes. Despite its importance, hyporheic exchange and the associated dynamics of solute mixing are often difficult to characterize due to spatial (e.g., sedimentary heterogeneity) and temporal (e.g., river stage fluctuation) variabilities. This study coupled geophysical techniques with physical and chemical sediment analyses to map sedimentary architecture and quantify its influence on hyporheic exchange dynamics within a compound bar deposit in a gravel‐dominated river system in southwestern Ohio. Electromagnetic induction (EMI) was used to quantify variability in electrical conductivity within the compound bar. EMI informed locations of electrode placement for time‐lapse electrical resistivity imaging (ERI) surveys, which were used to examine changes in electrical resistivity driven by hyporheic exchange. Both geophysical methods revealed a zone of high electrical conductivity in the center of the bar, identified as a fine‐grained cross‐bar channel fill. The zone acts as a baffle to flow, evidenced by stable electrical conditions measured by time‐lapse ERI over the study period. Large changes in electrical resistivity throughout the survey period indicate preferential flowpaths through higher permeability sands and gravels. Grain size analyses confirmed sedimentological interpretations of geophysical data. Loss on ignition and x‐ray fluorescence identified zones with higher organic matter content that are locations for potentially enhanced geochemical activity within the cross‐bar channel fill. Differences in the physical and geochemical characteristics of cross‐bar channel fills play an important role in hyporheic flow dynamics and nutrient processing within riverbed sediments. These findings enhance our understanding of the applications of geophysical methods in mapping riverbed heterogeneity and highlight the importance of accurately representing geomorphologic features and heterogeneity when studying hyporheic exchange processes.
International variation in childhood cancer mortality rates from 2001 to 2015: Comparison of trends in the International Cancer Benchmarking Partnership countries
Authors: Smith Lesley , Stiller Charles A. , Aitken Joanne F. , Hjalgrim Lisa L. , Johannesen Tom , Lahteenmaki Paivi , McCabe Martin G. , Phillips Robert , Pritchard‐Jones Kathy , Steliarova‐Foucher Eva , Winther Jeanette F. , Woods Ryan R. , Glaser Adam W. , Feltbower Richard G. 
Published: August 2021

AbstractDespite improved survival rates, cancer remains one of the most common causes of childhood death. The International Cancer Benchmarking Partnership (ICBP) showed variation in cancer survival for adults. We aimed to assess and compare trends over time in cancer mortality between children, adolescents and young adults (AYAs) and adults in the six countries involved in the ICBP: United Kingdom, Denmark, Australia, Canada, Norway and Sweden. Trends in mortality between 2001 and 2015 in the six original ICBP countries were examined. Age standardised mortality rates (ASR per million) were calculated for all cancers, leukaemia, malignant and benign central nervous system (CNS) tumours, and non‐CNS solid tumours. ASRs were reported for children (age 0‐14 years), AYAs aged 15 to 39 years and adults aged 40 years and above. Average annual percentage change (AAPC) in mortality rates per country were estimated using Joinpoint regression. For all cancers combined, significant temporal reductions were observed in all countries and all age groups. However, the overall AAPC was greater for children (−2.9; 95% confidence interval = −4.0 to −1.7) compared to AYAs (−1.8; −2.1 to −1.5) and adults aged >40 years (−1.5; −1.6 to −1.4). This pattern was mirrored for leukaemia, CNS tumours and non‐CNS solid tumours, with the difference being most pronounced for leukaemia: AAPC for children −4.6 (−6.1 to −3.1) vs AYAs −3.2 (−4.2 to −2.1) and over 40s −1.1 (−1.3 to −0.8). AAPCs varied between countries in children for all cancers except leukaemia, and in adults over 40 for all cancers combined, but not in subgroups. Improvements in cancer mortality rates in ICBP countries have been most marked among children aged 0 to 14 in comparison to 15 to 39 and over 40 year olds. This may reflect better care, including centralised service provision, treatment protocols and higher trial recruitment rates in children compared to older patients.
Fatty acid‐binding protein 5 limits the generation of Foxp3+ regulatory T cells through regulating plasmacytoid dendritic cell function in the tumor microenvironment
Authors: Kobayashi Shuhei , Wannakul Tunyanat , Sekino Kaname , Takahashi Yu , Kagawa Yoshiteru , Miyazaki Hirofumi , Umaru Banlanjo Abdulaziz , Yang Shuhan , Yamamoto Yui , Owada Yuji 
Published: August 2021

AbstractPlasmacytoid dendritic cells (pDCs) promote viral elimination by producing large amounts of Type I interferon. Recent studies have shown that pDCs regulate the pathogenesis of diverse inflammatory diseases, such as cancer. Fatty acid‐binding protein 5 (FABP5) is a cellular chaperone of long‐chain fatty acids that induce biological responses. Although the effects of FABP‐mediated lipid metabolism are well studied in various immune cells, its role in pDCs remains unclear. This study, which compares wild‐type and Fabp5−/− mice, provides the first evidence that FABP5‐mediated lipid metabolism regulates the commitment of pDCs to inflammatory vs tolerogenic gene expression patterns in the tumor microenvironment and in response to toll‐like receptor stimulation. Additionally, we demonstrated that FABP5 deficiency in pDCs affects the surrounding cellular environment, and that FABP5 expression in pDCs supports the appropriate generation of regulatory T cells (Tregs). Collectively, our findings reveal that pDC FABP5 acts as an important regulator of tumor immunity by controlling lipid metabolism.
Bidirectional Mendelian randomisation analysis of the relationship between circulating vitamin D concentration and colorectal cancer risk
Authors: He Yazhou , Zhang Xiaomeng , Timofeeva Maria , Farrington Susan M. , Li Xue , Xu Wei , Campbell Harry , Houlston Richard S. , Tomlinson Ian P. , Theodoratou Evropi , Dunlop Malcolm G. 
Published: August 2021

AbstractEpidemiological evidence is consistent with a protective effect of vitamin D against colorectal cancer (CRC), but the observed strong associations are open to confounders and potential reverse causation. Previous Mendelian randomisation (MR) studies were limited by poor genetic instruments and inadequate statistical power. Moreover, whether genetically higher CRC risk can influence vitamin D level, namely the reverse causation, still remains unknown. Herein, we report the first bidirectional MR study. We employed 110 newly identified genetic variants as proxies for vitamin D to obtain unconfounded effect estimates on CRC risk in 26 397 CRC cases and 41 481 controls of European ancestry. To test for reserve causation, we estimated effects of 115 CRC‐risk variants on vitamin D level among 417 580 participants from the UK Biobank. The causal association was estimated using the random‐effect inverse‐variance weighted (IVW) method. We found no significant causal effect of vitamin D on CRC risk [IVW estimate odds ratio: 0.97, 95% confidence interval (CI) = 0.88‐1.07, P = .565]. Similarly, no significant reverse causal association was identified between genetically increased CRC risk and vitamin D levels (IVW estimate β: −0.002, 95% CI = −0.008 to 0.004, P = .543). Stratified analysis by tumour sites did not identify significant causal associations in either direction between vitamin D and colon or rectal cancer. Despite the improved statistical power of this study, we found no evidence of causal association of either direction between circulating vitamin D and CRC risk. Significant associations reported by observational studies may be primarily driven by unidentified confounders.
Circulating C‐reactive protein increases lung cancer risk: Results from a prospective cohort of UK Biobank
Authors: Ji Mengmeng , Du Lingbin , Ma Zhimin , Xie Junxing , Huang Yanqian , Wei Xiaoxia , Jiang Xiangxiang , Xu Jing , Yin Rong , Wang Yuzhuo , Dai Juncheng , Jin Guangfu , Xu Lin , Zhu Chen , Hu Zhibin , Ma Hongxia , Zhu Meng , Shen Hongbing 
Published: August 2021

AbstractChronic inflammation has been associated with the development of lung cancer. In this study, we examined the association between C‐reactive protein (CRP) and lung cancer in a prospective cohort study and used Mendelian randomization (MR) to clarify the causality. We included 420 977 participants from the UK Biobank (UKB) in the analyses; 1892 thereof were diagnosed with lung cancer during the follow‐up. Hazards ratios (HRs) of CRP concentrations were estimated by Cox proportional hazard models and two approaches of MR analysis were performed. Besides, we added CRP concentrations to epidemiological model of lung cancer to evaluate its prediagnostic role through time‐dependent receiver operating characteristic curve analysis. Elevated CRP levels were associated with a 22% increased lung cancer risk per 1 SD increase (HR = 1.22, 95% confidence interval [CI] = 1.18‐1.26). Positive associations were observed in small cell lung cancer (HR = 1.21, 95% CI = 1.10‐1.33), lung adenocarcinoma (HR = 1.17, 95% CI = 1.11‐1.23) and lung squamous cell carcinoma (HR = 1.22, 95% CI = 1.14‐1.31). No genetical association of circulating CRP levels and lung cancer risk was observed in MR analysis. When added to a risk model of lung cancer, CRP improved the performance of model as long as 8 years among current smokers (basic model: C‐statistic = 0.78 [95% CI = 0.75‐0.80]; CRP model: C‐statistic = 0.79 [95% CI = 0.76‐0.81]; Pnonadjusted = .003, Padjusted = .014). Our results did not support the causal association of circulating CRP with lung cancer risk. However, circulating CRP could be a prediagnostic marker of lung cancer as long as 8 years in advance for current smokers.
A PHARMacist led Initiative for the Management of Hydroxyurea Therapy in Pediatric Sickle Cell Anemia patients attending a Multidisciplinary Tertiary Hemoglobinopathy Clinic: A retrospective cohort study (PHARMIT‐SCA)
Authors: Barton Amanda , Defoe Kimberly , Jupp Jennifer , Dersch‐Mills Deonne , Ghosh Sunita , Leaker Michael 
Published: August 2021

AbstractBackgroundThe pharmacological treatment of choice for sickle cell anemia (SCA) is hydroxyurea (HU). The therapeutic effect of HU is believed to be dose‐dependent and titration to maximum tolerated dose (MTD) is the standard of care. Clinical pharmacists took an active role in managing HU therapy through patient assessment and prescribing as part of a multidisciplinary team in a pediatric Hemoglobinopathy Clinic.ObjectivesTo identify the proportion of pediatric patients with SCA achieving MTD within 6 months of initiating HU therapy with traditional or pharmacist‐led management. Secondary objectives included quantifying and characterizing pharmacist interventions, and comparing the rate of dose change, dose assessments secondary to laboratory visits and number of acute care visits between cohorts in the 6 months post therapy initiation.MethodsFor this retrospective single center cohort study, 46 patients with SCA on treatment for six consecutive months between January 3, 2013 and February 28, 2019 were included and analyzed. Both groups were allocated 23 patients. Data were collected using electronic and paper medical records. SPSS version 25 was used for all statistical analyses. A P‐value <.05 was used for statistical significance.ResultsMean HU dose at 6 months was significantly higher in the pharmacist cohort (19.1 vs 22.2, P = .038). No patients achieved MTD in either cohort. More acute care visits occurred in the traditional cohort (20 vs 6, P = .01), and dose assessments secondary to laboratory visits occurred more in the pharmacist cohort (1 vs 3 per patient, P = .002). Pharmacists completed 82 follow‐ups and 175 interventions. Most follow‐ups were by phone (53.7%) to assess HU therapy for dose assessments secondary to laboratory visits (58.5%). Thirty‐eight percent of pharmacist interventions were related to HU dose and medication adherence was assessed in 76.8% of follow‐ups.ConclusionPharmacist‐led HU dose management resulted in a significantly higher mean dose of HU at 6 months, more frequent dose assessments secondary to laboratory work, and a reduced number of acute care visits.
Antidotal effect of dihydroxyacetone against phosphine poisoning in mice
Authors: Niknahad Hossein , Heidari Reza , Hashemi Asieh , Jamshidzadeh Akram , Rashedinia Marzieh 
Published: August 2021

AbstractPhosphine (PH3) is widely used as an insecticide and rodenticide. On the contrary, many cases of PH3 poisoning have been reported worldwide. Unfortunately, there is no specific antidote against PH3 toxicity. Disruption of mitochondrial function and energy metabolism is a well‐known mechanism of PH3 cytotoxicity. Dihydroxyacetone (DHA) is an adenosine triphosphate supplying agent which significantly improves mitochondrial function. The current study was designed to evaluate DHA's effect on inhalational PH3 poisoning in an animal model. DHA was injected into BALB/c mice before and/or after the start of the PH3 inhalation. The cytochrome c oxidase activity was assessed in the animals' brain, heart, and liver exposed to PH3 (for 15, 30, and 60 min, with and without the antidote). The LC50 of PH3 was calculated to be 18.02 (15.42–20.55) ppm over 2 h of exposure. Pretreatment of DHA (1 or 2 g/kg) increased the LC50 of PH3 by about 1.6‐ or 3‐fold, respectively. Posttreatment with DHA (2 g/kg) increased the LC50 of PH3 by about 1.4‐fold. PH3 inhibited the activity of cytochrome c oxidase in the assessed organs. It was found that DHA treatment restored mitochondrial cytochrome c oxidase activity. These findings suggested that DHA could be an effective antidote for PH3 poisoning.
Molecular dynamics simulation of Toxin‐Antitoxin (TA) system in Acinetobacter baumannii to explore the novel mechanism for inhibition of cell wall biosynthesis: Zeta Toxin as an effective therapeutic target
Authors: Karthika Alagesan , Ramachandran Balajee , Chitra Jeyarajpandian , Prabhu Dhamodharan , Rajamanikandan Sundaraj , Veerapandiyan Malaisamy , Jeyakanthan Jeyaraman 
Published: August 2021

AbstractThe majority of bacteria and archaea contains Toxin‐Antitoxin system (TA) that codes for the stable Toxin and unstable Antitoxin components forming a complex. The Antitoxin inhibits the catalytic activities of the Toxin. In general, the Antitoxin will be degraded by the proteases leading to the Toxin activation that subsequently targets essential cellular processes, including transcription, translation, replication, cell division, and cell wall biosynthesis. The Zeta Toxin‐Epsilon Antitoxin system in ESKAPE pathogen stabilizes the resistance plasmid and promotes pathogenicity. The known TA system in Acinetobacter baumannii are known to be involved in the replication and translation, however, the mechanism of Zeta Toxin‐Epsilon Antitoxin in cell wall biosynthesis remains unknown. In the present study, molecular docking and molecular dynamic (MD) simulations were employed to demonstrate whether Zeta Toxin can impair cell wall synthesis in A. baumannii. Further, the degradation mechanism of Antitoxin in the presence and absence of adenosine triphosphate (ATP) molecules are explained through MD simulation. The result reveals that the cleavage of Antitoxin could be possible with the presence of ATP by displaying its response from 20 ns, whereas the Zeta Toxin/Epsilon was unstable after 90 ns. The obtained results demonstrate that Zeta Toxin is “temporarily favorable” for ATP to undergo phosphorylation at UNAG kinase through the substrate tunneling process. The study further evidenced that phosphorylated UNAG prevents the binding of MurA, the enzyme that catalyzes the initial step of bacterial peptidoglycan biosynthesis. Therefore, the present study explores the binding mechanism of Zeta Toxin/Epsilon Antitoxin, which could be beneficial for preventing cell wall biosynthesis as well as for unveiling the alternative treatment options to antibiotics.
Diagnostic criteria for cancer cachexia: reduced food intake and inflammation predict weight loss and survival in an international, multi‐cohort analysis
Authors: Martin Lisa , Muscaritoli Maurizio , Bourdel‐Marchasson Isabelle , Kubrak Catherine , Laird Barry , Gagnon Bruno , Chasen Martin , Gioulbasanis Ioannis , Wallengren Ola , Voss Anne C. , Goldwasser Francois , Jagoe R. Thomas , Deans Chris , Bozzetti Federico , Strasser Florian , Thoresen Lene , Kazemi Sean , Baracos Vickie , Senesse Pierre 
Published: August 2021

AbstractBackgroundCancer‐associated weight loss (WL) associates with increased mortality. International consensus suggests that WL is driven by a variable combination of reduced food intake and/or altered metabolism, the latter often represented by the inflammatory biomarker C‐reactive protein (CRP). We aggregated data from Canadian and European research studies to evaluate the associations of reduced food intake and CRP with cancer‐associated WL (primary endpoint) and overall survival (OS, secondary endpoint).MethodsThe data set included a total of 12,253 patients at risk for cancer‐associated WL. Patient‐reported WL history (% in 6 months) and food intake (normal, moderately, or severely reduced) were measured in all patients; CRP (mg/L) and OS were measured in N = 4960 and N = 9952 patients, respectively. All measures were from a baseline assessment. Clinical variables potentially associated with WL and overall survival (OS) including age, sex, cancer diagnosis, disease stage, and performance status were evaluated using multinomial logistic regression MLR and Cox proportional hazards models, respectively.ResultsPatients had a mean weight change of −7.3% (±7.1), which was categorized as: ±2.4% (stable weight; 30.4%), 2.5–5.9% (19.7%), 6.0–10.0% (23.2%), 11.0–14.9% (12.0%), ≥15.0% (14.6%). Normal food intake, moderately, and severely reduced food intake occurred in 37.9%, 42.8%, and 19.4%, respectively. In MLR, severe WL (≥15%) (vs. stable weight) was more likely (P < 0.0001) if food intake was moderately [OR 6.28, 95% confidence interval (CI 5.28–7.47)] or severely reduced [OR 18.98 (95% CI 15.30–23.56)]. In subset analysis, adjusted for food intake, CRP was independently associated (P < 0.0001) with ≥15% WL [CRP 10–100 mg/L: OR 2.00, (95% CI 1.58–2.53)] and [CRP > 100 mg/L: OR 2.30 (95% CI 1.62–3.26)]. Diagnosis, stage, and performance status, but not age or sex, were significantly associated with WL. Median OS was 9.9 months (95% CI 9.5–10.3), with median follow‐up of 39.7 months (95% CI 38.8–40.6). Moderately and severely reduced food intake and CRP independently predicted OS (P < 0.0001).ConclusionsModelling WL as the dependent variable is an approach that can help to identify clinical features and biomarkers associated with WL. Here, we identify criterion values for food intake impairment and CRP that may improve the diagnosis and classification of cancer‐associated cachexia.