bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of SGLT2 inhibitors on fractures and bone mineral density in type 2 diabetes: An updated meta‐analysis
Authors: Li Xiaoyu , Li Ting , Cheng Ying , Lu Yunhong , Xue Mei , Xu Linxin , Liu Xiangyang , Yu Xiaochen , Sun Bei , Chen Liming 
Published: April 2019

AbstractBackgroundThe aim of the study is to update and determine the effects of sodium glucose cotransporter 2 (SGLT2) inhibitor therapy on fracture and bone mineral density (BMD) in patients with type 2 diabetes mellitus (T2DM).MethodsWe identified 27 eligible randomized controlled trials (RCTs) that compared the efficacy and safety of SGLT2 inhibitors to a placebo in 20 895 T2DM participants, with an average duration of 64.22 weeks. The relative risk (RR) of bone fracture and weighted mean difference (WMD) of changes in the BMD from baseline were determined to evaluate the risk of fracture. The degree of heterogeneity was evaluated by the I2 statistic, and publication bias was estimated using a funnel plot and Egger test.ResultsThe pooled RR was 1.02 (95% CI [0.81, 1.28]) with low heterogeneity, indicating that SGLT2 inhibitor treatment was not correlated with a higher risk of fracture. Additionally, no increased risk was found for patients with different ages, sexes, and levels of HbA1c and some biochemical indicators. Three trials with 1303 patients reported a change in the BMD from baseline. SGLT2 inhibitor treatment did not decrease the BMD at four skeletal sites (lumbar spine, femoral neck, total hip, and distal forearm), and the overall WMD was 0.08 (95% CI [−0.09, 0.26]). No significant publication bias was detected.ConclusionsNo increased risk for bone fracture was detected in patients with T2DM treated with SGLT2 inhibitors in this meta‐analysis. SGLT2 inhibitor therapy did not appear to affect bone health, but more long‐term detailed data are needed to validate this conclusion.
Changing landscapes of Southeast Asia and rodent‐borne diseases: decreased diversity but increased transmission risks
Authors: Morand Serge , Blasdell Kim , Bordes Frédéric , Buchy Philippe , Carcy Bernard , Chaisiri Kittipong , Chaval Yannick , Claude Julien , Cosson Jean‐François , Desquesnes Marc , Jittapalapong Sathaporn , Jiyipong Tawisa , Karnchanabanthoen Anamika , Pornpan Pumhom , Rolain Jean‐Marc , Tran Annelise 
Published: April 2019

AbstractThe reduction in biodiversity from land use change due to urbanization and agricultural intensification appears to be linked to major epidemiological changes in many human diseases. Increasing disease risks and the emergence of novel pathogens result from increased contact among wildlife, domesticated animals, and humans. We investigated the relationship between human alteration of the environment and the occurrence of generalist and synanthropic rodent species in relation to the diversity and prevalence of rodent‐borne pathogens in Southeast Asia, a hotspot of threatened and endangered species, and a foci of emerging infectious diseases. We used data from an extensive pathogen survey of rodents from seven sites in mainland Southeast Asia in conjunction with past and present land cover analyses. At low spatial resolutions, we found that rodent‐borne pathogen richness is negatively associated with increasing urbanization, characterized by increased habitat fragmentation, agriculture cover and deforestation. However, at a finer spatial resolution, we found that some major pathogens are favored by environmental characteristics associated with human alteration including irrigation, habitat fragmentation, and increased agricultural land cover. In addition, synanthropic rodents, many of which are important pathogen reservoirs, were associated with fragmented and human‐dominated landscapes, which may ultimately enhance the opportunities for zoonotic transmission and human infection by some pathogens.
Molecular identification of natural hybridization betweenMelastoma malabathricumandMelastoama beccarianumin Sarawak, Malaysia
Authors: Wu Renzhi , Zou Peishan , Tan Guangwen , Hu Zhenyang , Wang Yongqi , Ning Zulin , Wu Wei , Liu Ying , He Shaoyun , Zhou Renchao 
Published: April 2019

AbstractHybridization is very common in flowering plants and it plays a significant role in plant evolution and adaptation.MelastomaL. (Melastomataceae) comprises about 80–90 species in tropical Asia and Oceania, among which 41 species occur in Borneo. Natural hybridization is frequently reported inMelastomain China, but so far there have been no confirmed cases of hybridization in Southeast Asia (including Borneo), where most species occur. Here, we identified a case of natural hybridization betweenMelastoma malabathricumL. andMelastoma beccarianumCogn. in Sarawak, Malaysia, by using sequence data of three nuclear genes and one chloroplast intergenic spacer.Melastoma malabathricumis the most widespread species of this genus, occurring in almost the whole range of this genus, whileM. beccarianumis a local species endemic to northern Borneo. Our results showed that natural hybridization and introgression occur betweenM. malabathricumandM. beccarianum, and the introgression was asymmetrical, mainly fromM. malabathricumtoM. beccarianum. As adaptive traits can be transferred by introgression, our study suggests that natural hybridization should be a significant mechanism for the evolution and adaptation ofMelastomain Southeast Asia. However, introgression from the common speciesM. malabathricumto the relatively rare speciesM. beccarianummay cause the decline ofM. beccarianum, incurring conservation concern. With a large number of species ofMelastomaand almost year‐around flowering in Southeast Asia, more cases of natural hybridization are expected to be found and identified in near future.
Temporal and spatial variation in distribution of fish environmental DNA in England’s largest lake
Authors: Lawson Handley Lori , Read Daniel S. , Winfield Ian J. , Kimbell Helen , Johnson Harriet , Li Jianlong , Hahn Christoph , Blackman Rosetta , Wilcox Rose , Donnelly Rob , Szitenberg Amir , Hänfling Bernd 
Published: April 2019

AbstractEnvironmental DNA offers great potential as a biodiversity monitoring tool. Previous work has demonstrated that eDNA metabarcoding provides reliable information for lake fish monitoring, but important questions remain about temporal and spatial repeatability, which is critical for understanding the ecology of eDNA and developing effective sampling strategies. Here, we carried out comprehensive spatial sampling of England's largest lake, Windermere, during summer and winter to (1) examine repeatability of the method, (2) compare eDNA results with contemporary gill‐net survey data, (3) test the hypothesis of greater spatial structure of eDNA in summer compared to winter due to differences in water mixing between seasons, and (4) compare the effectiveness of shore and offshore sampling for species detection. We find broad consistency between the results from three sampling events in terms of species detection and abundance, with eDNA detecting more species than established methods and being significantly correlated with rank abundance determined by long‐term data. As predicted, spatial structure was much greater in the summer, reflecting less mixing of eDNA than in the winter. For example Arctic charr, a deep‐water species, was only detected in deep, midlake samples in the summer, while littoral or benthic species such as minnow and stickleback were more frequently detected in shore samples. By contrast in winter, the eDNA of these species was more uniformly distributed. This has important implications for design of sampling campaigns, for example, deep‐water species could be missed and littoral/benthic species overrepresented by focusing exclusively on shoreline samples collected in the summer.
Post‐wildfire sediment cascades: A modeling framework linking debris flow generation and network‐scale sediment routing
Authors: Murphy Brendan P. , Czuba Jonathan A. , Belmont Patrick 
Published: April 2019

AbstractWildfires represent one of the largest disturbances in watersheds of the Intermountain West. Yet, we lack models capable of predicting post‐wildfire impacts on downstream ecosystems and infrastructure. Here we present a novel modeling framework that links new and existing models to simulate the post‐wildfire sediment cascade, including spatially explicit predictions of debris flows, storage of debris flow sediment within valleys, delivery of debris flow sediment to active channels, and the downstream routing of sediment through river networks. We apply the model to sediment dynamics in Clear Creek watershed following the 2010 Twitchell Canyon Fire in the Tushar Mountains of southern Utah. The debris flow generation model performed well, correctly predicting 19 out of 20 debris flows from the largest catchments, with only four false positives and two false negatives at observed rainfall intensities. In total, the model predicts the occurrence of 160 post‐wildfire debris flows across the Clear Creek watershed, generating more than 650 000 m3 of sediment. Our new storage and delivery model predicts the vast majority of this sediment is stored within valleys, and only 13% is delivered to the river network. The sediment routing model identifies numerous sediment bottlenecks within the network, which alter transport dynamics and may be hotspots for aggradation and aquatic habitat alteration. The volume of sediment exported from the watershed after seven years of simulation totals 17% of that delivered, or 2% of the total generated debris flow sediment. In the case of the Twitchell Canyon Fire, this highlights that significant post‐wildfire sediment volumes can be stored in valleys (87%) and within the stream network (11%). Finally, we discuss useful insights that can be gleaned from the model framework, as well as the limitations and need for more monitoring and theory development in order to better constrain essential inputs, process rates, and morphodynamics. © 2019 John Wiley & Sons, Ltd.
Modeling and simulation of batteries and development of an energy storage system based in Riyadh, Saudi Arabia
Authors: Khan Salah Ud‐Din , Almutairi Zeyad Ammar 
Published: April 2019

AbstractIn this study, a renewable energy powered energy storage and utilization system is designed and modeled. The main objective of the study involves developing a theoretical‐simulation model for a coupled energy storage unit suitable for Saudi Arabia's climate conditions. The study commenced with the selection of the batteries most appropriate for a representative location in Riyadh, Kingdom of Saudi Arabia (KSA). Various parameters associated with performance and economic assessments of batteries were calculated via simulation. Photovoltaic (PV) panels were used as a renewable energy source. Feasibility studies of the PV panels were performed by considering the working conditions in the KSA. Finally, an integrated system composed of a PV system, a battery, and an end‐user was designed. A technical and economic model was developed for the coupled PV based energy storage and utilization unit. The simulation results obtained from the integrated system confirmed the suitability of practical demonstration (prototype) in the selected location. The current findings suggested the development of a working prototype of the theoretically proven energy storage system. This study paves the path to develop a method to conduct a feasible study of various other renewable energy‐driven storage systems.
Cholangiocyte‐Derived Exosomal Long Noncoding RNA H19 Promotes Hepatic Stellate Cell Activation and Cholestatic Liver Fibrosis
Authors: Liu Runping , Li Xiaojiaoyang , Zhu Weiwei , Wang Yanyan , Zhao Derrick , Wang Xuan , Gurley Emily C. , Liang Guang , Chen Weidong , Lai Guanhua , Pandak William M. , Robert Lippman H. , Bajaj Jasmohan S. , Hylemon Phillip B. , Zhou Huiping 
Published: April 2019

Activation of hepatic stellate cells (HSCs) represents the primary driving force to promote the progression of chronic cholestatic liver diseases. We previously reported that cholangiocyte‐derived exosomal long noncoding RNA‐H19 (lncRNA‐H19) plays a critical role in promoting cholestatic liver injury. However, it remains unclear whether cholangiocyte‐derived lncRNA‐H19 regulates HSC activation, which is the major focus of this study. Both bile duct ligation (BDL) and Mdr2 knockout (Mdr2‐/‐) mouse models were used. Wild‐type and H19maternalΔExon1/+ (H19KO) mice were subjected to BDL. Mdr2‐/‐H19maternalΔExon1/+ (DKO) mice were generated. Exosomes isolated from cultured mouse and human cholangiocytes or mouse serum were used for in vivo transplantation and in vitro studies. Fluorescence‐labeled exosomes and flow cytometry were used to monitor exosome uptake by hepatic cells. Collagen gel contraction and bromodeoxyuridine assays were used to determine the effect of exosomal‐H19 on HSC activation and proliferation. Mouse and human primary sclerosing cholangitis (PSC)/primary biliary cholangitis (PBC) liver samples were analyzed by real‐time PCR, western blot analysis, histology, and immunohistochemistry. The results demonstrated that hepatic H19 level was closely correlated with the severity of liver fibrosis in both mouse models and human patients with PSC and PBC. H19 deficiency significantly protected mice from liver fibrosis in BDL and Mdr2‐/‐ mice. Transplanted cholangiocyte‐derived H19‐enriched exosomes were rapidly and preferentially taken up by HSCs and HSC‐derived fibroblasts, and promoted liver fibrosis in BDL‐H19KO mice and DKO mice. H19‐enriched exosomes enhanced transdifferentiation of cultured mouse primary HSCs and promoted proliferation and matrix formation in HSC‐derived fibroblasts. Conclusion: Cholangiocyte‐derived exosomal H19 plays a critical role in the progression of cholestatic liver fibrosis by promoting HSC differentiation and activation and represents a potential diagnostic biomarker and therapeutic target for cholangiopathies.
A multicenter retrospective comparison of induction chemoimmunotherapy regimens on outcomes in transplant‐eligible patients with previously untreated mantle cell lymphoma
Authors: Ng Zi Yun , Bishton Mark , Ritchie David , Campbell Robert , Gilbertson Michael , Hill Kate , Ratnasingam Sumita , Schwarer Anthony , Manos Kate , Shorten Sophie , Ng Melissa , Nelson Niles , Xin Liu , De Mel Widanalage Sanjay , Sunny Tenny , Purtill Duncan , Poon Michelle , Johnston Anna , Cochrane Tara , Lee Hui‐Peng , Hapgood Greg , Tam Constantine , Opat Stephen , Hawkes Eliza , Seymour John , Cheah Chan Yoon 
Published: April 2019

AbstractMantle cell lymphoma (MCL) is an uncommon and typically aggressive form of lymphoma. Although often initially chemosensitive, relapse is common. Several induction and conditioning regimens are used in transplant‐eligible patients, and the optimal approach remains unknown. We performed an international, retrospective study of transplant‐eligible patients to assess impact of induction chemoimmunotherapy and conditioning regimens on clinical outcomes. We identified 228 patients meeting inclusion criteria. Baseline characteristics were similar among the induction groups except for some variation in age. The type of induction chemoimmunotherapy received did not influence overall response rates (ORRs) (0.43), progression‐free survival (PFS) (P > .67), or overall survival (OS) (P > .35) on multivariate analysis (PFS and OS). Delivery of autologous stem cell transplant (ASCT) was associated with favorable PFS and OS (0.01) on univariate analysis only; this benefit was not seen on multivariate analysis—PFS (0.36) and OS (0.21). Compared with busulfan and melphalan (BuMel), the use of the carmustine, etoposide, cytarabine, melphalan (BEAM)–conditioning regimen was associated with inferior PFS (HR = 2.0 [95% CI 1.1‐3.6], 0.02) but not OS (HR = 1.1 [95% CI 0.5‐2.3], 0.81) on univariate analysis only. Within the limits of a retrospective study and modest power for some comparisons, type of induction therapy did not influence ORR, PFS, or OS for transplant‐eligible patients with MCL. International efforts are required to perform randomized clinical trials evaluating chemoimmunotherapy induction regimens.
Impact of 2016 WHO diagnosis of early and overt primary myelofibrosis on presentation and outcome of 232 patients treated with ruxolitinib
Authors: Palandri Francesca , Palumbo Giuseppe A. , Abruzzese Elisabetta , Iurlo Alessandra , Polverelli Nicola , Elli Elena , Bonifacio Massimiliano , Bergamaschi Micaela , Martino Bruno , Tiribelli Mario , Benevolo Giulia , Tieghi Alessia , Sgherza Nicola , Isidori Alessandro , Binotto Gianni , Crugnola Monica , Heidel Florian , Cavazzini Francesco , Bosi Costanza , Auteri Giuseppe , Cattaneo Daniele , Foà Robin , Lemoli Roberto M. , Cuneo Antonio , Krampera Mauro , Bartoletti Daniela , Cavo Michele , Vianelli Nicola , Breccia Massimo , Latagliata Roberto 
Published: April 2019

AbstractThe 2016 WHO criteria identified early primary myelofibrosis (PMF) as an individual entity with milder clinical features and better outcome compared with overt PMF. Here, we compared early and overt PMF patients treated with ruxolitinib in terms of baseline clinical/laboratory characteristics, response, and toxicity to treatment. We observed that early‐PMF patients achieve better and more stable spleen and symptoms responses, with significantly lower rates of hematological toxicities. No differences in overall and leukemia‐free survival were detected between the two cohorts. The application of 2016 WHO criteria is crucial to identify those PMF patients who deserve a stricter monitoring during treatment.
Transplantation of miR‐219 overexpressed human endometrial stem cells encapsulated in fibrin hydrogel in spinal cord injury
Authors: Jalali Monfared Marzie , Nasirinezhad Farinaz , Ebrahimi‐Barough Somayeh , Hasanzade Gholamreza , Saberi Hooshang , Tavangar Seyed Mohammad , Asadpour Shiva , Aryan Leila , Barabadi Zahra , Ai Jafar 
Published: April 2019

AbstractOligodendrocyte (OL) loss and demyelination occur after spinal cord injury (SCI). Stimulation of remyelination through transplantation of myelinating cells may be effective in improving function. For the repair strategy to be successful, the selection of a suitable cell and maintaining cell growth when cells are injected directly to the site of injury is important. In addition to selecting the type of cell, fibrin hydrogel was used as a suitable tissue engineering scaffold for this purpose. To test the relationship between myelination and functional improvement, the human endometrial stem cells (hEnSCs) were differentiated toward oligodendrocyte progenitor cells (OPCs) using overexpression of miR‐219. Adult female Wistar rats were used to induce SCI by using a compression model and were randomly assigned to the following four experimental groups: SCI, Vehicle, hEnSC, and OPC. Ten days after injury, miR‐219 overexpressed hEnSC‐derived OPCs encapsulated in fibrin hydrogel, as an injectable scaffold, were injected to the injury site. In this study, with a focus on promoting functional recovery after SCI, the Basso‐Beattie‐Bresnahan test was performed to evaluate the recovery of motor function every week for 10 weeks and the histological assay was then performed. Results showed that the rate of motor function recovery was significantly higher in OPC group compared to SCI and vehicle groups but no marked differences were found between OPC and hEnSC groups, although, the rate of myelination in the OPC group was significantly higher than the other groups. These results demonstrated that remyelination was not the cause of recovery of motor function.
siRNA‐mediated silencing of PAI‐1 gene acts as a promoter over the recanalization of endothelial progenitor cells in rats with venous thrombosis
Authors: Li Hang , Zhang Bo , Lu Shan , Ji De‐Gang , Ding Meng , Ye Yan‐Shuo , Sun Da‐Jun 
Published: April 2019

AbstractWith the changing lifestyle, venous thrombosis (VT) is becoming increasingly prevalent and poses a burden on the health economy. Endothelial progenitor cells (EPCs) are recruited into resolving VT. We aimed to investigate the effect of plasminogen activator inhibitor 1 (PAI‐1) silencing on the recanalization of VT in rat EPCs. EPCs and VT rat models were cultured and treated with negative control‐siRNA vector and PAI‐1‐siRNA vector, respectively. 4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, wound‐healing test, and Matrigel‐induced tubular experiment were performed to detect the ability of cell proliferation, migration, and EPCs lumen formation. Immunohistochemistry was used to observe the recanalization of thrombus. The messenger RNA (mRNA) and protein expression of PAI‐1 and vascular endothelial growth factor (VEGF) were determined by reverse transcription quantitative polymerase chain reaction and Western blot analysis. PAI‐1‐siRNA enhances the luminal formation ability of EPCs and significantly promotes EPCs homing. In response to PAI‐1 gene silencing, tissues from inferior vena cava displayed reduced mRNA and protein expression of PAI‐1, increased VEGF expression as well as promoted lumen‐like structures. PAI‐1 gene silencing can promote the recanalization of VT by enhancement of the luminal formation ability of rats’ EPCs.
Inflammatory cytokines associated with cancer growth induce mitochondria and cytoskeleton alterations in cardiomyocytes
Authors: Buoncervello Maria , Maccari Sonia , Ascione Barbara , Gambardella Lucrezia , Marconi Matteo , Spada Massimo , Macchia Daniele , Stati Tonino , Patrizio Mario , Malorni Walter , Matarrese Paola , Marano Giuseppe , Gabriele Lucia 
Published: April 2019

AbstractCardiac dysfunction is often observed in patients with cancer also representing a serious problem limiting chemotherapeutic intervention and even patient survival. In view of the recently established role of the immune system in the control of cancer growth, the present work has been undertaken to investigate the effects of a panel of the most important inflammatory cytokines on the integrity and function of mitochondria, as well as of the cytoskeleton, two key elements in the functioning of cardiomyocytes. Either mitochondria features or actomyosin cytoskeleton organization of in vitro‐cultured cardiomyocytes treated with different inflammatory cytokines were analyzed. In addition, to investigate the interplay between tumor growth and cardiac function in an in vivo system, immunocompetent female mice were inoculated with cancer cells and treated with the chemotherapeutic drug doxorubicin at a dosing schedule able to suppress tumor growth without inducing cardiac alterations. Analyses carried out in cardiomyocytes treated with the inflammatory cytokines, such as tumor necrosis factor α (TNF‐α), interferon γ (IFN‐γ), interleukin 6 (IL‐6), IL‐8, and IL‐1β revealed severe phenotypic changes, for example, of contractile cytoskeletal elements, mitochondrial membrane potential, mitochondrial reactive oxygen species production and mitochondria network organization. Accordingly, in immunocompetent mice, the tumor growth was accompanied by increased levels of the inflammatory cytokines TNF‐α, IFN‐γ, IL‐6, and IL‐8, either in serum or in the heart tissue, together with a significant reduction of ventricular systolic function. The alterations of mitochondria and of microfilament system of cardiomyocytes, due to the systemic inflammation associated with cancer growth, could be responsible for remote cardiac injury and impairment of systolic function observed in vivo.