bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of smoking on platelet function of ticagrelor versus clopidogrel in minor stroke or transient ischaemic attack
Authors: Yang Y. , Chen W. , Meng X. , Liu L. , Wang Y. , Pan Y. , Wang Y. 
Published: February 2020

Background and purposeIt remains unclear whether smoking status has an impact on platelet reactivity and clinical outcomes of ticagrelor versus clopidogrel in patients with acute minor stroke or transient ischaemic attack (TIA).MethodsA subgroup analysis of a randomized controlled trial was conducted. Patients with minor stroke or TIA were randomized for treatment with ticagrelor plus aspirin or clopidogrel plus aspirin. Platelet reactivity was assessed by VerifyNow P2Y12 assay at baseline, 7 + 2 days and 90 ± 7 days. High on‐treatment platelet reactivity (HOPR) was defined as P2Y12 reaction units >208. Clinical outcomes included any stroke, composite clinical vascular events and bleeding events at 90 days. Patients who smoked one or more cigarettes per day for at least 1 year in their lives were defined as smokers.ResultsOf 675 patients enrolled in the trial, 370 patients (54.8%) were smokers. At 7 + 2 days, the proportion of HOPR in ticagrelor versus clopidogrel was significantly lower in smokers (5.2% vs. 21.8%) and non‐smokers (2.3% vs. 34.4%). There were marginal significant interactions between treatment groups and smoking status for the proportion of HOPR (P = 0.058). At 90 ± 7 days, there were significant interactions between treatment groups and smoking status for the risk of new stroke (smokers: 7.0% vs. 4.9%; hazard ratio, 1.57; 95% confidence interval, 0.65–3.79; P = 0.39; non‐smokers: 5.3% vs. 13.5%; hazard ratio, 0.39; 95% confidence interval, 0.17–0.91; P = 0.01; P for interaction = 0.02).ConclusionsAmong patients with minor stroke or TIA, ticagrelor was superior to clopidogrel in inhibiting platelet reactivity and reducing the risk of new stroke, particularly for non‐smokers.
Will coral reef sponges be winners in the Anthropocene?
Authors: Lesser Michael P. , Slattery Marc 
Published: February 2020

AbstractRecent observations have shown that increases in climate change‐related coral mortality cause changes in shallow coral reef community structure through phase shifts to alternative taxa. As a result, sponges have emerged as a potential candidate taxon to become a “winner,” and therefore a numerically and functionally dominant member of many coral reef communities. But, in order for this to occur, there must be sufficient trophic resources to support larger populations of these active filter‐feeding organisms. Globally, climate change is causing an increase in sea surface temperatures (SSTs) and a decrease in salinity, which can lead to an intensification in the stratification of shallow nearshore waters (0–200 m), that affects both the mixed layer depth (MLD) and the strength and duration of internal waves. Specifically, climate change‐driven increases in SSTs for tropical waters are predicted to cause increased stratification, and more stabilized surface waters. This causes a shallowing of the MLD which prevents nutrients from reaching the euphotic zone, and is predicted to decrease net primary production (NPP) up to 20% by the end of the century. Lower NPP would subsequently affect multiple trophic levels, including shallow benthic filter‐feeding communities, as the coupling between water column productivity and the benthos weakens. We argue here that sponge populations may actually be constrained, rather than promoted, by climate change due to decreases in their primary trophic resources, caused by bottom‐up forcing, secondary to physical changes in the water column (i.e., stratification and changes in the MLD resulting in lower nutrients and NPP). As a result, we predict sponge‐dominated tropical reefs will be rare, or short‐lived, if they occur at all into the future in the Anthropocene.
Brachio‐basilic upper arm transposition fistulas vs. prosthetic brachio‐axillary vascular access grafts—Which one is preferred for hemodialysis?
Authors: Tayebi Pouya , Kazemzadeh Gholamhossein , Modaghegh Mohammad Hadi Saeed , Kamyar Mohammad Mahdi , Ravari Hassan 
Published: February 2020

AbstractIntroductionThere is still controversy on the use of brachio‐basilic upper arm transposition fistula (BBAVF) and prosthetic brachio‐axillary vascular access grafts (BAPTFE) in patients with no suitable cephalic veins for creating an autogenous brachio‐cephalic fistula.MethodsIn a randomized controlled clinical trial, 60 hemodialysis patients who were not a suitable candidate for BCAVF were randomly assigned into two groups: BBAVF and BAPTFE. The patients were clinically followed up to 1 year and the patency rate and access‐related complications were compared between the two groups.FindingsAccess failure rate in the BBAVF and BAPTFE groups was 30.0% and 36.6%, respectively. The primary patency time was 232.73 ± 113.36 and 261.53 ± 147.37 days, respectively (P = 0.40). Thrombosis formation and infection were the two main causes for access failure, yet indicating no significant difference between the two groups (P > 0.05).DiscussionBBAVF and BAPTFE have comparable clinical outcomes in short‐term follow‐up. Therefore, BAPTFE can be used as an alternative vascular access for hemodialysis in patients who are not a suitable candidate for BBAVF.
Stevens‐Johnson syndrome and toxic epidermal necrolysis‐like reactions to checkpoint inhibitors: a systematic review
Authors: Maloney Nolan J. , Ravi Vignesh , Cheng Kyle , Bach Daniel Q. , Worswick Scott 
Published: February 2020

AbstractThe use of checkpoint inhibitors for treatment of advanced malignancies is increasing. Rashes, pruritus, and more rarely, reactions resembling Stevens‐Johnsons syndrome (SJS) or toxic epidermal necrolysis (TEN) may occur secondary to checkpoint inhibitors. To characterize existing literature on these reports, we queried the PubMed/MEDLINE database for cases of SJS or TEN associated with checkpoint inhibitors. We identified 18 cases of SJS or TEN‐like reactions to checkpoint inhibitors in the literature. There were 12 cases of SJS‐like rashes with median time to onset of 5.6 weeks (average of 8.9 weeks), of which five were delayed to week 8 or later from checkpoint inhibitor initiation. The five TEN‐like reactions had a median time to onset of 4 weeks (average of 5.38 weeks), of which two were delayed to week 6 or later. SJS/TEN‐like reactions to nivolumab (seven cases) had median onset time of 3 weeks, whereas five cases secondary to pembrolizumab had median onset time of 11 weeks. Seven cases in this study described prodromal rashes, which varied from localized papular rashes to generalized morbilliform rashes, prior to evolution into SJS or TEN‐like patterns. SJS‐like patterns generally improved well on systemic treatment/supportive care and no cases of death were identified, but mortality occurred in three of five patients with TEN‐like reactions. Dermatologists should consider the possibility for unique features of SJS/TEN in response to checkpoint inhibitors. Additional studies will be necessary to further characterize SJS/TEN‐like eruptions on checkpoint inhibitors and determine the optimal management of these cases.
The effect of boron and aluminum additions on the microstructure of arc‐melted boron carbide
Authors: Xiang Sisi , Yang Qirong , Lien Hsu‐Ming , Shial Keya , Gronske Eric , Haber Richard , Xie Kelvin Y. 
Published: February 2020

AbstractIn this work, B4C, B4C + 5 at.% Al, B4C + B, and B4C + B + 5 at.% Al were arc melted, and the resultant solid products were characterized. Results from x‐ray diffraction and scanning electron microscopy showed that adding Al alone in B4C did not result in Al doping; adding Al and B in B4C led to Al doping. Al‐doping also changed the surface energy of boron carbide in the liquid state, thus altered the wettability. Transmission electron microscopy revealed that stacking faults are more likely to form in the Al‐doped sample, especially in the regions where the Al concentration is high.
Transvenous lead extraction after heart transplantation: How to avoid abandoned lead fragments
Authors: Hahnel Fabian , Pecha Simon , Bernhardt Alexander , Barten Markus J. , Chung Da‐Un , Sinning Christoph , Willems Stephan , Reichenspurner Hermann , Hakmi Samer 
Published: February 2020

AbstractBackgroundMany patients awaiting heart transplantation (HTX) have a cardiac implantable electronic device (CIED). Lead removal is often still a part of the HTX procedure. Abandoned lead fragments carry a risk for infections and prohibit magnetic resonance imaging (MRI) imaging. This study evaluated the concept of an elective lead management algorithm after HTX.Methods and ResultsBetween 2009 and 2018, 102 consecutive patients with previously implanted CIED underwent HTX. Lead removal by manual traction during HTX was performed in 74 patients until December 2014. Afterward, treatment strategy was changed and 28 patients received elective lead extraction procedures in a hybrid operating room (OR) using specialized extraction tools. Total of 74 patients with 157 leads underwent lead extraction by manual traction during HTX. The mean lead age was 32.3 ± 38.7 months. Postoperative X‐ray revealed abandoned intravascular lead fragments in 31(41.9%) patients, resulting in a complete lead extraction rate of only 58.1%. The high rate of unsuccessful lead extractions led to the change in the extraction strategy in 2015. Since then, HTX was performed in 28 CIED patients. In those patients, 64 leads with a mean lead age of 53.8 ± 42.8 months were treated in an elective lead extraction procedure. No major or minor complications occurred during lead extraction. All leads could be removed completely, resulting in a procedural success rate of 100%.ConclusionOur results demonstrate that chronically implanted leads should be removed in an elective procedure, using appropriate extraction tools. This enables complete lead extraction, which reduces the infection risk in this patient population with the necessity for permanent immunosuppressive therapy and allows further MRI surveillance.
Cisplatin resistance in gastric cancer cells is involved with GPR30‐mediated epithelial‐mesenchymal transition
Authors: Wang Xiaofeng , Xu Zhiyuan , Sun Jiancheng , Lv Hang , Wang Yiping , Ni Yixiu , Chen Shangqi , Hu Can , Wang Lijing , Chen Wei , Cheng Xiangdong 
Published: February 2020

AbstractCisplatin is the major chemotherapeutic drug in gastric cancer, particularly in treating advanced gastric cancer. Tumour cells often develop resistance to chemotherapeutic drugs, which seriously affects the efficacy of chemotherapy. GPR30 is a novel oestrogen receptor that is involved in the invasion, metastasis and drug resistance of many tumours. Targeting GPR30 has been shown to increase the drug sensitivity of breast cancer cells. However, few studies have investigated the role of GPR30 in gastric cancer. Epithelial‐mesenchymal transition (EMT) has been shown to be associated with the development of chemotherapeutic drug resistance. In this study, we demonstrated that GPR30 is involved in cisplatin resistance by promoting EMT in gastric cancer. GPR30 knockdown resulted in increased sensitivity of different gastric cancer (GC) cells to cisplatin and alterations in the epithelial/mesenchymal markers. Furthermore, G15 significantly enhanced the cisplatin sensitivity of GC cells while G1 inhibited this phenomenon. In addition, EMT occurred when AGS and BGC‐823 were treated with cisplatin. Down‐regulation of GPR30 with G15 inhibited this transformation, while G1 promoted it. Taken together, these results revealed the role of GPR30 in the formation of cisplatin resistance, suggesting that targeting GPR30 signalling may be a potential strategy for improving the efficacy of chemotherapy in gastric cancer.
Activation of metabotropic glutamate receptor 4 regulates proliferation and neural differentiation in neural stem/progenitor cells of the rat subventricular zone and increases phosphatase and tensin homolog protein expression
Authors: Zhang Zhichao , Zheng Xiaoyan , Liu Yingfei , Luan Yan , Wang Li , Zhao Lingyu , Zhang Jianshui , Tian Yumei , Lu Haixia , Chen Xinlin , Liu Yong 
Published: February 2020

AbstractNeural stem/progenitor cells (NSPCs) persist in the mammalian subventricular zone throughout life, where they can be activated in response to physiological and pathophysiological stimuli. A recent study indicates metabotropic glutamate receptor 4 (mGluR4) is involved in regulating NSPCs behaviors. Therefore, defining mGluR4 function in NSPCs is necessary for determining novel strategies to enhance the intrinsic potential for brain regeneration after injuries. In this study, mGluR4 was functionally expressed in SVZ‐derived NSPCs from male Sprague‐Dawley rats, in which the cyclic adenosine monophosphate concentration was reduced after treatment with the mGluR4‐specific agonist VU0155041. Additionally, lateral ventricle injection of VU0155041 significantly decreased 5‐bromo‐2'‐deoxyuridine (BrdU)+ and Ki67+ cells, while increased Doublecortin (DCX)/BrdU double‐positive cells in SVZ. In cultured NSPCs, mGluR4 activation decreased the ratio of BrdU+ cells, G2/M‐phase cells, and inhibited Cyclin D1 expression, whereas it increased neuron‐specific class III β‐tubulin (Tuj1) expression and the number of Tuj1, DCX, and PSA‐NCAM‐positive cells. However, pharmacological blocking mGluR4 with the antagonist MSOP or knockdown of mGluR4 abolished the effects of VU0155041 on NSPCs proliferation and neuronal differentiation. Further investigation demonstrated that VU0155041 treatment down‐regulated AKT phosphorylation and up‐regulated expression of the phosphatase and tensin homolog protein (PTEN) in NSPCs culture. Moreover VU0155041‐induced proliferating inhibition and neuronal differentiating amplification in NSPCs were significantly hampered by VO‐OHpic, a PTEN inhibitor. We conclude that activation of mGluR4 in SVZ‐derived NSPCs suppresses proliferation and enhances their neuronal differentiation, and regulation of PTEN may be involved as a potential intracellular target of mGluR4 signal.
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Cover Image for this issue: https://doi.org/10.1111/jnc.15052.
Long‐term use of dienogest for the treatment of primary and secondary dysmenorrhea
Authors: Osuga Yutaka , Hayashi Koichi , Kanda Shingo 
Published: February 2020

AbstractAimTo investigate the safety and efficacy of dienogest (DNG), a progestational 19‐norsteroid, administered for 52 weeks in patients with primary and secondary dysmenorrhea.MethodsA total of 147 patients with dysmenorrhea received 1 mg of DNG orally each day for 52 weeks. The dose could be increased to 2 mg/day at or after Week 12 according to the investigator's determination. The primary safety endpoint was evaluation of adverse events, and the secondary safety endpoint was evaluation of adverse drug reactions. The number of days and severity of genital bleeding were assessed according to records in the patients' diary. Lower abdominal pain and/or low back pain because of dysmenorrhea were assessed according to the dysmenorrhea score.ResultsThe most frequent adverse drug reaction was irregular uterine bleeding (94.6%). Most subjects completed the 52‐week administration. Genital bleeding was more likely to occur in subjects with secondary dysmenorrhea than in those with primary dysmenorrhea, and in subjects with “uterine myoma or adenomyosis” than in those with “endometriosis alone.” In any of the categorizations, there tended to be fewer days with genital bleeding as the treatment period increased in length, and most of the genital bleeding cases were mild. The change from baseline in the dysmenorrhea score (mean ± standard deviation [SD]) was −3.7 ± 1.6 at Week 24 of treatment and −4.0 ± 1.3 at Week 52.ConclusionThis study showed favorable tolerability of the long‐term use of DNG to patients with dysmenorrhea and a sustainable pain relief effect.
Kidney Health for Everyone Everywhere—From Prevention to Detection and Equitable Access to Care
Authors: Li Philip Kam‐Tao , Garcia‐Garcia Guillermo , Lui Siu‐Fai , Andreoli Sharon , Fung Winston Wing‐Shing , Hradsky Anne , Kumaraswami Latha , Liakopoulos Vassilios , Rakhimova Ziyoda , Saadi Gamal , Strani Luisa , Ulasi Ifeoma , Kalantar‐Zadeh Kamyar ,   for the World Kidney Day Steering Committee
Published: February 2020

SUMMARYThe global burden of chronic kidney disease (CKD) is increasing with a projection of becoming the fifth leading cause of years of life lost globally by 2040. CKD is a major cause of catastrophic health expenditure. The costs of dialysis and transplantation consume up to 3% of the entire annual healthcare budget in high‐income countries. Crucially, however, both the onset and progression of CKD is potentially preventable. In 2020, the World Kidney Day campaign highlights the importance of preventive interventions—be it primary, i.e. to prevent de novo CKD, or secondary or tertiary, i.e. prevention of worsening early CKD or progression of more advanced CKD to end‐stage kidney disease, respectively. Primary prevention should focus on the modification of CKD risk factors and address the structural abnormalities of the kidney and urinary tracts, and exposure to environmental risk factors and nephrotoxins. In persons with pre‐existing kidney disease, secondary prevention, including blood pressure optimization, glycemic control and avoiding high‐protein high‐sodium diet should be the main goal of education and clinical interventions. In patients with moderate to advanced CKD, the management of comorbidities such as uremia and cardiovascular disease along with low‐protein diet are among the recommended preventative interventions to avoid or delay dialysis or kidney transplantation. Whereas national policies and strategies for noncommunicable diseases may exist in a country, specific policies directed toward education and awareness about CKD screening, prevention and treatment are often lacking. There is an urgent need to increase awareness for preventive measures throughout populations, professionals and policy makers.
Antidepressant Usage in Haemodialysis Patients: Evidence of Sub‐Optimal Practice Patterns
Authors: Guirguis Ayman , Chilcot Joseph , Almond Michael , Davenport Andrew , Wellsted David , Farrington Ken 
Published: February 2020

SUMMARYBackgroundDepression is common in patients on haemodialysis and associated with adverse outcomes. Antidepressant use is widespread though evidence of efficacy is limited.ObjectivesTo study antidepressant management practices in patients on haemodialysis with reference to NICE guidelines on management of depression in adults with chronic physical health problems.DesignProspective, multicentre, longitudinal cohort study with 6–15 month follow‐up.ParticipantsPatients on haemodialysis established on antidepressant medication.MeasurementsBaseline assessment of mood was undertaken using Beck Depression Inventory (BDI‐II). Demographic, clinical and medication data were also collected. Changes in clinical and life circumstances and medication during follow‐up were recorded. At follow‐up, BDI‐II was reassessed and diagnostic psychiatric assessment undertaken.ResultsForty‐one patients were studied. General practitioners were the main prescribers (68%). Ten agents were in use, the commonest being Citalopram (39%). Doses were often suboptimal. At baseline, 30 patients had high BDI‐II scores (≥16) and 22 remained high at follow‐up. Eleven had BDI‐II < 16 at baseline. In five, this increased on follow‐up to ≥16. Sixteen patients (39%) had no medication review during follow‐up, 14 (34%) had a dose review, and 11 (27%) a medication change. On psychiatric assessment at follow‐up, eight patients had current major depressive disorder (MDD), seven recurrent and 20 evidence of past MDD. Six displayed no evidence of ever having MDD.ConclusionsAntidepressant management in patients on haemodialysis reflected poor drug selection, overprescription, under‐dosing and inadequate follow‐up suggesting sub‐optimal adherence to NICE guidelines. Most patients had high depression scores at follow‐up. Antidepressant use in haemodialysis requires reappraisal.
Induction of SIRT1 by melatonin improves alcohol‐mediated oxidative liver injury by disrupting the CRBN‐YY1‐CYP2E1 signaling pathway
Authors: Lee Sung‐Eun , Koh Hong , Joo Dong Jin , Nedumaran Balachandar , Jeon Hwang‐Ju , Park Chul‐Seung , Harris Robert A. , Kim Yong Deuk 
Published: February 2020

AbstractAlcoholic liver disease is the most prevalent chronic liver disease. Melatonin is known to control many vital processes. Here, we explored a novel molecular mechanism by which melatonin‐induced SIRT1 signaling protects against alcohol‐mediated oxidative stress and liver injury. Gene expression profiles and metabolic changes were measured in liver specimens of mice and human subjects. Expression levels of Cb1r, Crbn, Btg2, Yy1, pro‐inflammatory cytokines, and Cyp2e1 were significantly enhanced in chronic alcohol‐challenged mice and human subjects. Levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatic CYP2E1 protein, and reactive oxygen species (ROS) were elevated in alcohol‐fed WT mice but not in Cb1r antagonist‐treated, Crbn null, or Yy1‐silenced mice. Importantly, alcohol‐induced Yy1 and Cyp2e1 expression, ROS amount, and liver injury were markedly diminished by melatonin treatment and the transduction of Sirt1 in mice, whereas this phenomenon was prominently ablated by silencing of Sirt1. Notably, SIRT1 physically interacted with YY1 and attenuated YY1 occupancy on the Cyp2e1 gene promoter. Melatonin‐SIRT1 signaling ameliorates alcohol‐induced oxidative liver injury by disrupting the CRBN‐YY1‐CYP2E1 signaling pathway. The manipulation of CRBN‐YY1‐CYP2E1 signaling network by the melatonin‐SIRT1 pathway highlights a novel entry point for treating alcoholic liver disease.
The impact of ABO blood type on the prevalence of portal vein thrombosis in patients with advanced chronic liver disease
Authors: Scheiner Bernhard , Northup Patrick G. , Gruber Anselm B. , Semmler Georg , Leitner Gerda , Quehenberger Peter , Thaler Johannes , Ay Cihan , Trauner Michael , Reiberger Thomas , Lisman Ton , Mandorfer Mattias 
Published: February 2020

AbstractBackground and aimsNon‐O blood type (BT) is a risk factor for thromboses, which has been attributed to its effects on von Willebrand factor (VWF)/factor VIII (FVIII) levels. Although high VWF/FVIII may be risk factors for portal vein thrombosis (PVT) in patients with advanced chronic liver disease (ACLD), the impact of BT on PVT is unknown. We aimed to assess (I) whether non‐O‐BT is a risk factor for PVT and (II) whether non‐O‐BT impacts VWF/factor VIII in patients with ACLD.MethodsRetrospective analysis comprising two cohorts: (I) “US” including all adult liver transplantations in the US in the MELD era and (II) “Vienna” comprising patients with a hepatic venous pressure gradient (HVPG) ≥6 mmHg.Results(I) The “US cohort” included 84 947 patients (non‐O: 55.43%). The prevalence of PVT at the time of listing (4.37% vs 4.56%; P = .1762) and at liver transplantation (9.56% vs 9.33%; P = .2546) was similar in patients with O‐ and non‐O‐BT. (II) 411 patients were included in the “Vienna cohort” (non‐O: 64%). Mean HVPG was 18(9) mmHg and 90% had an HVPG ≥10 mmHg. Patients with non‐O‐BT had slightly increased VWF levels (318(164)% vs 309(176)%; P = .048; increase of 23.8%‐23.9% in adjusted analyses), but this difference was driven by patients with less advanced disease. However, non‐O‐BT explained only 1% of the variation in VWF and had no effect on FVIII.ConclusionsAlthough non‐O‐BT impacts VWF in patients with early stage ACLD, its contribution to VWF variation is considerably smaller than in the general population. Moreover, non‐O‐BT had no impact on FVIII. These findings may explain the absence of an association between non‐O‐BT and PVT in patients with advanced cirrhosis.