bluuebunny/crossref_metadata_2025_split huggingface dataset:
Display of lead‐binding proteins on Escherichia coli surface for lead bioremediation
Authors: Jia Xiaoqiang , Li Ying , Xu Tao , Wu Kang 
Published: August 2020

AbstractCell surface display of heavy metal‐binding proteins has been used to enhance the adsorption capacity of heavy metals and the engineered microbial cells can be potentially used for the bioremediation of heavy metals. In this study, the proteins PbrR, PbrR691, and PbrD from the Cupriavidus metallidurans strain CH34 were displayed on the extracellular membrane of Escherichia coli BL21 cells, with the N‐domain of ice‐nucleation protein as the anchor protein to achieve specific adsorption of lead ions (Pb2+) and bioremediation of lead in the soil. The localization of fusion proteins was confirmed by western blot analysis. We investigated the effects of fusion pattern, expression level, heavy metal concentration, and the presence of other heavy metal ions on the adsorption of Pb2+ by these engineered bacteria, and the optimal linker peptide (flexible linker) and inducer concentration (0.5 mM) were obtained. The engineered bacteria showed specific selectivity and strong adsorption capacity for Pb2+. The maximum Pb2+ adsorption capacity of strains displaying the three proteins (PbrR, PbrR691, and PbrD) were 942.1‐, 754.3‐, and 864.8‐μmol/g cell dry weight, respectively, which was the highest reported to date. The engineered E. coli bacteria were also applied to Pb2+‐contaminated soil and the detoxification effects were observed via the seed germination test and the growth of Nicotiana benthamiana in comparison with the control BL21, which provides the proof‐of‐concept for in situ remediations of Pb2+‐contaminated water or soil.
Two‐year outcomes after percutaneous coronary intervention with drug‐eluting stents or bare‐metal stents in elderly patients with coronary artery disease
Authors: Lafont Alexandre , Sinnaeve Peter R , Cuisset Thomas , Cook Stéphane , Sideris Giorgios , Kedev Sasko , Carrie Didier , Hovasse Thomas , Garot Philippe , El Mahmoud Rami , Spaulding Christian , Helft Gérard , Diaz Fernandez José F , Brugaletta Salvatore , Pinar‐Bermudez Eduardo , Ferre Josepa Mauri , Commeau Philippe , Teiger Emmanuel , Bogaerts Kris , Sabate Manel , Morice Marie Claude , Varenne Olivier ,   for the SENIOR investigators
Published: August 2020

AbstractObjectivesReport the results at 2 years of the patients included in the SENIOR trial.BackgroundPatients above 75 years of age represent a fast‐growing population in the cathlab. In the SENIOR trial, patients treated by percutaneous coronary intervention (PCI) with drug eluting stent (DES) and a short duration of P2Y12 inhibitor (1 and 6 months for stable and unstable coronary syndromes, respectively) compared with bare metal stents (BMS) was associated with a 29% reduction in the rate of all‐cause mortality, myocardial infarction (MI), stroke, and ischaemia‐driven target lesion revascularization (ID‐TLR) at 1 year. The results at 2 years are reported here.Methods and ResultsWe randomly assigned 1,200 patients (596[50%] to the DES group and 604[50%] to the BMS group). At 2 years, the composite endpoint of all‐cause mortality, MI, stroke and ID‐TLR had occurred in 116 (20%) patients in the DES group and 131 (22%) patients in the BMS group (RR 0.90 [95%CI 0.72–1.13], p = .37). IDTLR occurred in 14 (2%) patients in the DES group and 41 (7%) patients in the BMS group (RR 0.35 [95%CI 0.16–0.60], p = .0002). Major bleedings (BARC 3–5) occurred in 27(5%) patients in both groups (RR 1.00, [95%CI 0.58–1.75], p = .99). Stent thrombosis rates were low and similar between DES and BMS (0.8 vs 1.3%, (RR 0.52 [95%CI 0.01–1.95], p = .27).ConclusionAmong elderly PCI patients, a strategy combining a DES together with a short duration of DAPT is associated with a reduction in revascularization up to 2 years compared with BMS with very few late events and without any increased in bleeding complications or stent thrombosis.
Dipeptidyl peptidase‐4 inhibitor treatment and the risk of bullous pemphigoid and skin‐related adverse events: A systematic review and meta‐analysis of randomized controlled trials
Authors: Yang Wenjia , Cai Xiaoling , Zhang Simin , Han Xueyao , Ji Linong 
Published: August 2020

AbstractAimsThis meta‐analysis aimed to evaluate the risk of developing bullous pemphigoid (BP) and other skin‐related adverse events (AEs) in patients with type 2 diabetes (T2DM) undergoing dipeptidyl peptidase‐4 inhibitor (DPP‐4i) treatment in randomized controlled trials (RCTs).MethodsIn this meta‐analysis, the MEDLINE, Embase, and Cochrane Central Register of Controlled Trials databases were searched for RCTs, which involve patients with T2DM reporting skin‐related AEs. RCTs that comparatively evaluated the effects of DPP‐4i treatment and placebo on patients with T2DM and reported skin‐related AEs were included in the analysis. The odds ratio (OR) and 95% confidence interval (CI) were calculated using the Peto's methods. The GRADE approach was used to rate the quality of evidence.ResultsA total of 46 randomized placebo‐controlled trials, including 3 trials with reports of BP (n = 38 011), that reported skin‐related AEs were included (n = 59 332). Compared to the placebo group, the risk of developing BP was significantly higher in the DPP‐4i treatment group (OR = 7.38, 95% CI 2.00‐27.25, I2 = 0%, P = .003; quality rating: very low). Additionally, DPP‐4i treatment was associated with an increased overall risk of developing skin‐related AEs (OR = 1.22, 95% CI 1.02‐1.46, I2 = 32%, P = .03; quality rating: moderate).ConclusionsThis meta‐analysis suggested that treatment with DPP‐4is, including sitagliptin, saxagliptin, and linagliptin, was associated with an increased risk of developing BP. Additionally, the risk of developing skin‐related AEs increased when all DPP‐4is were combined. Skin lesion, especially BP, should be monitored in patients with diabetes undergoing DPP‐4i treatment. Future studies should evaluate the susceptible population and develop strategies for early detection of skin‐related AEs.
Assessment of systemic genetic damage in pediatric inflammatory bowel disease
Authors: Baig Ayesha , Avlasevich Svetlana L. , Torous Dorothea K. , Bemis Jeffrey C. , Saubermann Lawrence J. , Lovell David P. , MacGregor James T. , Dertinger Stephen D. 
Published: August 2020

AbstractThe etiology of distal site cancers in inflammatory bowel disease (IBD) is not well understood and requires further study. We investigated whether pediatric IBD patients' blood cells exhibit elevated levels of genomic damage by measuring the frequency of mutant phenotype (CD59‐/CD55‐) reticulocytes (MUT RET) as a reporter of PIG‐A mutation, and the frequency of micronucleated reticulocytes (MN‐RET) as an indicator of chromosomal damage. IBD patients (n = 18 new‐onset disease, 46 established disease) were compared to age‐matched controls (constipation or irritable bowel syndrome patients from the same clinic, n = 30) and young healthy adults age 19–24 (n = 25). IBD patients showed no indication of elevated MUT RET relative to controls (mean ± SD = 3.1 ± 2.3 × 10−6 vs. 3.6 ± 5.6 x 10−6, respectively). In contrast, 59 IBD patients where %MN‐RET measurements were obtained, 10 exceeded the upper bound 90% tolerance interval derived from control subjects (i.e., 0.42%). Furthermore, each of the 10 IBD patients with elevated MN‐RET had established disease (10/42), none were new‐onset (0/17) (p = .049). Interestingly, each of the subjects with increased chromosomal damage was receiving anti‐TNF based monotherapy at the time blood was collected (10/10, 100%), whereas this therapy was less common (20/32, 63%) among patients that exhibited ≤0.42% MN‐RET (p = .040). The results clearly indicate the need for further work to understand whether the results presented herein are reproducible and if so, to elucidate the causative factor(s) responsible for elevated MN‐RET frequencies in some IBD patients.
Upcycling of polyethylene terephthalate plastic waste to microporous carbon structure for energy storage
Authors: Mirjalili Arash , Dong Bo , Pena Pedro , Ozkan Cengiz S. , Ozkan Mihrimah 
Published: August 2020

AbstractPlastic pollution and its harmful effects on the earth ecosystem, which inevitably affect quality of life, have brought attention to the frontiers of research society. Among plastics, polyethylene terephthalate (PET) is used on a massive scale in various sectors of industry, including the automobile, textile, and packaging. Utilizing an electrospinning fiber production technique, we have successfully upcycled PET waste bottle into electrochemical active carbon material that functions as a double‐layer supercapacitor substance. Our detailed electrochemical and analytical characterization revealed that the generated carbon substance is a mixture of amorphous carbon and reduced graphene oxide with relatively high surface area. The electrochemical characterization of the as‐prepared material consisting of cyclic voltammetry, galvanostatic cycling with potential limitations, and electrochemical impedance spectroscopy analyses revealed that the generated medium has combined characteristics of both double‐layer and redox reaction pseudo‐capacitance with self‐strengthening effect along cycling. We believe that the proposed process is scalable with environmental and economic advantages and this study could present opportunities for future research and development.
Mast Cells Induce Ductular Reaction Mimicking Liver Injury in Mice Through Mast Cell–Derived Transforming Growth Factor Beta 1 Signaling: [RETRACTED]
Authors: Kyritsi Konstantina , Kennedy Lindsey , Meadows Vik , Hargrove Laura , Demieville Jennifer , Pham Linh , Sybenga Amelia , Kundu Debjyoti , Cerritos Karla , Meng Fanyin , Alpini Gianfranco , Francis Heather 
Published: August 2020

Background and Aims
Following liver injury, mast cells (MCs) migrate into the liver and are activated in patients with cholestasis. Inhibition of MC mediators decreases ductular reaction (DR) and liver fibrosis. Transforming growth factor beta 1 (TGF‐β1) contributes to fibrosis and promotes liver disease. Our aim was to demonstrate that reintroduction of MCs induces cholestatic injury through TGF‐β1.

Approach and Results
Wild‐type, KitW‐sh
(MC‐deficient), and multidrug resistance transporter 2/ABC transporter B family member 2 knockout mice lacking l‐histidine decarboxylase were injected with vehicle or PKH26‐tagged murine MCs pretreated with 0.01% dimethyl sulfoxide (DMSO) or the TGF‐β1 receptor inhibitor (TGF‐βRi), LY2109761 (10 μM) 3 days before sacrifice. Hepatic damage was assessed by hematoxylin and eosin (H&E) and serum chemistry. Injected MCs were detected in liver, spleen, and lung by immunofluorescence (IF). DR was measured by cytokeratin 19 (CK‐19) immunohistochemistry and F4/80 staining coupled with real‐time quantitative PCR (qPCR) for interleukin (IL)‐1β, IL‐33, and F4/80; biliary senescence was evaluated by IF or qPCR for p16, p18, and p21. Fibrosis was evaluated by sirius red/fast green staining and IF for synaptophysin 9 (SYP‐9), desmin, and alpha smooth muscle actin (α‐SMA). TGF‐β1 secretion/expression was measured by enzyme immunoassay and qPCR. Angiogenesis was detected by IF for von Willebrand factor and vascular endothelial growth factor C qPCR. In vitro, MC‐TGF‐β1 expression/secretion were measured after TGF‐βRi treatment; conditioned medium was collected. Cholangiocytes and hepatic stellate cells (HSCs) were treated with MC‐conditioned medium, and biliary proliferation/senescence was measured by 3‐(4,5‐dimethylthiazol‐2‐yl)‐5‐(3‐carboxymethoxyphenyl)‐2‐(4‐sulfophenyl)‐2H‐tetrazolium and qPCR; HSC activation evaluated for α‐SMA, SYP‐9, and collagen type‐1a expression. MC injection recapitulates cholestatic liver injury characterized by increased DR, fibrosis/TGF‐β1 secretion, and angiogenesis. Injection of MC‐TGF‐βRi reversed these parameters. In vitro, MCs induce biliary proliferation/senescence and HSC activation that was reversed with MCs lacking TGF‐β1.

Conclusions
Our study demonstrates that reintroduction of MCs mimics cholestatic liver injury and that MC‐derived TGF‐β1 may be a target in chronic cholestatic liver disease.
Tacrolimus Impairs Kupffer Cell Capacity to Control Bacteremia: Why Transplant Recipients Are Susceptible to Infection
Authors: Deppermann Carsten , Peiseler Moritz , Zindel Joel , Zbytnuik Lori , Lee Woo‐Yong , Pasini Elisa , Baciu Cristina , Matelski John , Lee Yun , Kumar Deepali , Humar Atul , Surewaard Bas , Kubes Paul , Bhat Mamatha 
Published: August 2020

Background and Aims
Kupffer cells (KCs) are the resident intravascular phagocyte population of the liver and critical to the capture and killing of bacteria. Calcineurin/nuclear factor of activated T cells (NFAT) inhibitors (CNIs) such as tacrolimus are used to prevent rejection in solid organ transplant recipients. Although their effect on lymphocytes has been studied extensively, there are limited experimental data about if and how CNIs shape innate immunity, and whether this contributes to the higher rates of infection observed in patients taking CNIs.

Approach and Results
Here, we investigated the impact of tacrolimus treatment on innate immunity and, more specifically, on the capability of Kupffer cells (KCs) to fight infections. Retrospective analysis of data of >2,700 liver transplant recipients showed that taking calcineurin inhibitors such as tacrolimus significantly increased the likelihood of Staphylococcus aureus infection. Using a mouse model of acute methicillin‐resistant S. aureus (MRSA) bacteremia, most bacteria were sequestered in the liver and we found that bacteria were more likely to disseminate and kill the host in tacrolimus‐treated mice. Using imaging, we unveiled the mechanism underlying this observation: the reduced capability of KCs to capture, phagocytose, and destroy bacteria in tacrolimus‐treated animals. Furthermore, in a gene expression analysis of infected KCs, the triggering receptor expressed on myeloid cells 1 (TREM1) pathway was the one with the most significant down‐regulation after tacrolimus treatment. TREM1 inhibition likewise inhibited KC bacteria capture. TREM1 levels on neutrophils as well as the overall neutrophil response after infection were unaffected by tacrolimus treatment.

Conclusions
Our results indicate that tacrolimus treatment has a significant impact directly on KCs and on TREM1, thereby compromising their capacity to fend off infections.
High‐efficiency methane capture by living fungi and dried fungal hyphae (necromass)
Authors: Liew Feng Jin , Schilling Jonathan S. 
Published: August 2020

AbstractFungi can hasten microbial degradation of hydrophobic compounds by enhancing capture and dissolution into biofilms. For methane (CH4) released from natural soils and agricultural systems, prokaryotes are ultimately responsible for oxidation and degradation; however, in many cases Henry's law of gas dissolution, not oxidation, is rate‐limiting. Given that fungi can improve capture and bioremediation of other hydrophobic compounds (e.g., toluene), we tested fungi for CH4 capture. We used a batch system of CH4–flooded vials to screen candidate fungi. We found 79% removal efficiency by Ganoderma lucidum relative to activated carbon. In a follow‐up, we found comparable efficiency in other Ganoderma species (G. applanatum, G. meredithae). However, these efficiency gains by Ganoderma species could not be sustained when inoculated wood substrates were placed in “live” soils. Substrates colonized naturally, without preinoculations, performed similarly to those deployed with (native) test strains, likely because inoculated fungi were outcompeted and displaced by native colonizers. Instead of rescreening using more combative fungi, we tested an alternative way to present fungi with high single‐strain efficiencies for filtration: in dried form as dead biomass (necromass). In dried biomass trials, dried G. lucidum biomass performed better than when testing living biomass, again with the highest strain‐specific removal efficiencies (84% of activated carbon). These results demonstrate the potential for G. lucidum, commonly used in biomaterial production, in a variety of indoor and outdoor biofiltration scenarios. It also implies an overlooked, potentially large role for fungi and their soil necromass in capturing and reducing CH4 emissions from soils in nature.
Increased protein propionylation contributes to mitochondrial dysfunction in liver cells and fibroblasts, but not in myotubes
Authors: Lagerwaard Bart , Pougovkina Olga , Bekebrede Anna F. , te Brinke Heleen , Wanders Ronald J.A. , Nieuwenhuizen Arie G. , Keijer Jaap , de Boer Vincent C. J. 
Published: August 2020

AbstractPost‐translational protein modifications derived from metabolic intermediates, such as acyl‐CoAs, have been shown to regulate mitochondrial function. Patients with a genetic defect in the propionyl‐CoA carboxylase (PCC) gene clinically present symptoms related to mitochondrial disorders and are characterised by decreased mitochondrial respiration. Since propionyl‐CoA accumulates in PCC deficient patients and protein propionylation can be driven by the level of propionyl‐CoA, we hypothesised that protein propionylation could play a role in the pathology of the disease. Indeed, we identified increased protein propionylation due to pathologic propionyl‐CoA accumulation in patient‐derived fibroblasts and this was accompanied by defective mitochondrial respiration, as was shown by a decrease in complex I‐driven respiration. To mimic pathological protein propionylation levels, we exposed cultured fibroblasts, Fao liver cells and C2C12 muscle myotubes to propionate levels that are typically found in these patients. This induced a global increase in protein propionylation and histone protein propionylation and was also accompanied by a decrease in mitochondrial respiration in liver and fibroblasts. However, in C2C12 myotubes propionate exposure did not decrease mitochondrial respiration, possibly due to differences in propionyl‐CoA metabolism as compared to the liver. Therefore, protein propionylation could contribute to the pathology in these patients, especially in the liver, and could therefore be an interesting target to pursue in the treatment of this metabolic disease.
Deforming to Best Practice: Key considerations for deformable image registration in radiotherapy
Authors: Barber Jeffrey , Yuen Johnson , Jameson Michael , Schmidt Laurel , Sykes Jonathan , Gray Alison , Hardcastle Nicholas , Choong Callie , Poder Joel , Walker Amy , Yeo Adam , Archibald‐Heeren Ben , Harrison Kristie , Haworth Annette , Thwaites David 
Published: August 2020

AbstractImage registration is a process that underlies many new techniques in radiation oncology – from multimodal imaging and contour propagation in treatment planning to dose accumulation throughout treatment. Deformable image registration (DIR) is a subset of image registration subject to high levels of complexity in process and validation. A need for local guidance to assist in high‐quality utilisation and best practice was identified within the Australian community, leading to collaborative activity and workshops. This report communicates the current limitations and best practice advice from early adopters to help guide those implementing DIR in the clinic at this early stage. They are based on the state of image registration applications in radiotherapy in Australia and New Zealand (ANZ), and consensus discussions made at the ‘Deforming to Best Practice’ workshops in 2018. The current status of clinical application use cases is presented, including multimodal imaging, automatic segmentation, adaptive radiotherapy, retreatment, dose accumulation and response assessment, along with uptake, accuracy and limitations. Key areas of concern and preliminary suggestions for commissioning, quality assurance, education and training, and the use of automation are also reported. Many questions remain, and the radiotherapy community will benefit from continued research in this area. However, DIR is available to clinics and this report is intended to aid departments using or about to use DIR tools now.
De Novo Development of Distal Jejunal and Duodenal Adenomas After 41 Months of Teduglutide Treatment in a Patient With Short‐Bowel Syndrome: A Case Report
Authors: Pevny Sophie , Pape Ulrich‐Frank , Elezkurtaj Sefer , Rieger Anja , Jürgensen Christian , Blüthner Elisabeth , Jochum Christoph , Tacke Frank , Maasberg Sebastian 
Published: August 2020

AbstractThe glucagon‐like peptide‐2 (GLP‐2) analogue teduglutide is a medical treatment option for patients with short‐bowel syndrome–associated chronic intestinal failure. Because studies in mice have shown that GLP‐2 analogues may promote the growth of colonic neoplasms, surveillance colonoscopies before and during teduglutide therapy were recommended. The occurrence of small‐intestinal neoplasms has not been reported so far, except for a recent report about de novo development of hamartomatous duodenal polyps. We report a case of de novo development of small‐intestinal premalignant adenomatous polyps in both bulbar duodenum and distal jejunum in a patient treated with teduglutide for 41 months. Therefore, additional endoscopic surveillance of the upper gastrointestinal tract may be advised during teduglutide therapy for early detection and removal of potential small‐bowel adenomas.
Survival of Patients With Short‐Bowel Syndrome on Home Parenteral Nutrition: A Prospective Cohort Study
Authors: Noelting Jessica , Gramlich Leah , Whittaker Scott , Armstrong David , Marliss Errol , Jurewitsch Brian , Raman Matreyi , Duerksen Donald R. , Stevenson Danielle , Lou Wendy , Saha Sudipta , Allard Johane P. 
Published: August 2020

AbstractBackgroundSurvival of patients with short‐bowel syndrome (SBS) receiving home parenteral nutrition (HPN) and associated factors have not been reported recently in North America. The objective of this study was to determine the long‐term survival of adult patients with SBS as the primary indication for HPN and assess factors that may affect survival by using the Canadian HPN Registry.MethodsThis is a retrospective analysis of prospectively collected data extracted from the HPN registry, prior to approval of teduglutide in Canada. Using only incident cases, survival probabilities were estimated by using the Kaplan‐Meier method for both full‐cohort and nonmalignant SBS. Log‐rank test was also used to test the differences in survival distributions between subgroups in the univariate analysis. To identify potential variables that are affecting survival distribution of patients for the multivariable analysis, Least Absolute Shrinkage and Selection Operator and stepwise selection procedure were used.ResultsThere were 321 patients with a known duration receiving HPN (total, 2287 years), of whom 218 were entered into the registry within 1 year of initiation of HPN. Of 218 incident cases, 22 had active malignancy, along with SBS, and their survival time was significantly lower than those with nonmalignant SBS (P‐value < .0001). The 5‐year survival of nonmalignant‐SBS patients was 81.9%. In this subgroup, there was no significant association between patients’ survival and known intestinal anatomy, age, or sex.ConclusionPatients with nonmalignant SBS who receive HPN have a 5‐year survival of >80%. Known intestinal anatomical factors did not affect survival.