bluuebunny/crossref_metadata_2025_split huggingface dataset:
Investigating Body Image Disturbance in Anorexia Nervosa Using Novel Biometric Figure Rating Scales: A Pilot Study
Authors: Mölbert Simone C. , Thaler Anne , Streuber Stephan , Black Michael J. , Karnath Hans‐Otto , Zipfel Stephan , Mohler Betty , Giel Katrin E. 
Published: October 2017

AbstractThis study uses novel biometric figure rating scales (FRS) spanning body mass index (BMI) 13.8 to 32.2 kg/m2 and BMI 18 to 42 kg/m2. The aims of the study were (i) to compare FRS body weight dissatisfaction and perceptual distortion of women with anorexia nervosa (AN) to a community sample; (ii) how FRS parameters are associated with questionnaire body dissatisfaction, eating disorder symptoms and appearance comparison habits; and (iii) whether the weight spectrum of the FRS matters. Women with AN (n = 24) and a community sample of women (n = 104) selected their current and ideal body on the FRS and completed additional questionnaires. Women with AN accurately picked the body that aligned best with their actual weight in both FRS. Controls underestimated their BMI in the FRS 14–32 and were accurate in the FRS 18–42. In both FRS, women with AN desired a body close to their actual BMI and controls desired a thinner body. Our observations suggest that body image disturbance in AN is unlikely to be characterized by a visual perceptual disturbance, but rather by an idealization of underweight in conjunction with high body dissatisfaction. The weight spectrum of FRS can influence the accuracy of BMI estimation. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.
Detecting Eating Psychopathology in Female Athletes by Asking About Exercise: Use of the Compulsive Exercise Test
Authors: Plateau Carolyn R. , Arcelus Jon , Meyer Caroline 
Published: October 2017

AbstractThe present study assessed the suitability of the Compulsive Exercise Test (athlete version; CET‐A) for identifying female athletes with clinically significant features related to or comparable with eating psychopathology. Three hundred and sixty‐one female athletes (including 12 with a clinically diagnosed eating disorder) completed the Eating Disorders Examination Questionnaire and the CET‐A. Receiver operating curve analysis was employed to identify a cut‐off value on the CET‐A, which could indicate clinically significant features related to or comparable with eating psychopathology among female athletes. The analysis demonstrated that a CET‐A score of 10 successfully discriminated female athletes with a current eating disorder. The results suggest that the CET‐A may be a suitable tool for detecting eating psychopathology in female athletes. Additional longitudinal research is needed to evaluate the predictive value of the CET‐A. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.
Fast Ca2+ responses in astrocyte end‐feet and neurovascular coupling in mice
Authors: Lind Barbara Lykke , Jessen Sanne Barsballe , Lønstrup Micael , Joséphine Charlène , Bonvento Gilles , Lauritzen Martin 
Published: October 2017

AbstractCerebral blood flow (CBF) is regulated by the activity of neurons and astrocytes. Understanding how these cells control activity‐dependent increases in CBF is crucial to interpreting functional neuroimaging signals. The relative importance of neurons and astrocytes is debated, as are the functional implications of fast Ca2+ changes in astrocytes versus neurons. Here, we used two‐photon microscopy to assess Ca2+ changes in neuropil, astrocyte processes, and astrocyte end‐feet in response to whisker pad stimulation in mice. We also developed a pixel‐based analysis to improve the detection of rapid Ca2+ signals in the subcellular compartments of astrocytes. Fast Ca2+ responses were observed using both chemical and genetically encoded Ca2+ indicators in astrocyte end‐feet prior to dilation of arterioles and capillaries. A low dose of the NMDA receptor antagonist (5R,10s)‐(+)‐5‐methyl‐10,11‐dihydro‐5H‐dibenzo[a,d]cyclohepten‐5,10‐imine‐hydrogen‐maleate (MK801) attenuated fast Ca2+ responses in the neuropil and astrocyte processes, but not in astrocyte end‐feet, and the evoked CBF response was preserved. In addition, a low dose of 4,5,6,7‐tetrahydroisoxazolo[5,4‐c]pyridin‐3‐ol (THIP), an agonist for the extrasynaptic GABAA receptor (GABAAR), increased CBF responses and the fast Ca2+ response in astrocyte end‐feet but did not affect Ca2+ responses in astrocyte processes and neuropil. These results suggest that fast Ca2+ increases in the neuropil and astrocyte processes are not necessary for an evoked CBF response. In contrast, as local fast Ca2+ responses in astrocyte end‐feet are unaffected by MK801 but increase via GABAAR‐dependent mechanisms that also increased CBF responses, we hypothesize that the fast Ca2+ increases in end‐feet adjust CBF during synaptic activity.
Identifying disease foci from static and dynamic effective connectivity networks: Illustration in soldiers with trauma
Authors: Rangaprakash D. , Dretsch Michael N. , Venkataraman Archana , Katz Jeffrey S. , Denney Thomas S. , Deshpande Gopikrishna 
Published: October 2017

AbstractBrain connectivity studies report group differences in pairwise connection strengths. While informative, such results are difficult to interpret since our understanding of the brain relies on region‐based properties, rather than on connection information. Given that large disruptions in the brain are often caused by a few pivotal sources, we propose a novel framework to identify the sources of functional disruption from effective connectivity networks. Our approach integrates static and time‐varying effective connectivity modeling in a probabilistic framework, to identify aberrant foci and the corresponding aberrant connectomics network. Using resting‐state fMRI, we illustrate the utility of this novel approach in U.S. Army soldiers (N = 87) with posttraumatic stress disorder (PTSD), mild traumatic brain injury (mTBI) and combat controls. Additionally, we employed machine‐learning classification to identify those significant connectivity features that possessed high predictive ability. We identified three disrupted foci (middle frontal gyrus [MFG], insula, hippocampus), and an aberrant prefrontal‐subcortical‐parietal network of information flow. We found the MFG to be the pivotal focus of network disruption, with aberrant strength and temporal‐variability of effective connectivity to the insula, amygdala and hippocampus. These connectivities also possessed high predictive ability (giving a classification accuracy of 81%); and they exhibited significant associations with symptom severity and neurocognitive functioning. In summary, dysregulation originating in the MFG caused elevated and temporally less‐variable connectivity in subcortical regions, followed by a similar effect on parietal memory‐related regions. This mechanism likely contributes to the reduced control over traumatic memories leading to re‐experiencing, hyperarousal and flashbacks observed in soldiers with PTSD and mTBI.Hum Brain Mapp 39:264–287, 2018. ©2017 Wiley Periodicals, Inc.
Organic Synthesis: Wherefrom and Whither? (Some Very Personal Reflections)
Authors: Denmark Scott E. 
Published: October 2017

AbstractThis perspective represents a (highly personal) examination of the past, present and future of synthetic organic chemistry. The central thesis posits that the confluence of factors that led to the “Golden Age of Natural Product Synthesis” in the second half of the twentieth century can be traced back to the identification of the therapeutic potential of steroid hormones culminating in the introduction of oral contraceptives. The tremendous benefits of those activities to the development of organic synthesis as a vibrant discipline led to the exponential increase in strategies and methods and the ability to tackle, larger and larger molecules of greater and greater complexity. The existential challenge to the health of organic synthesis is whether a similarly dynamic future can be anticipated and if so, to what end and how. Musings on potential answers to those questions are presented.
Polypyrrole‐coated electrodes show thickness‐dependent stability in different conditions during 42‐day follow‐up in vitro
Authors: Alarautalahti V. , Hiltunen M. , Onnela N. , Nymark S. , Kellomäki M. , Hyttinen J. 
Published: October 2017

AbstractElectroconductive polypyrrole/dodecylbenzenesulphonate (PPy/DBS) has been proposed as novel electrode coating for biomedical applications. However, as yet, little is known about its long‐term stability in moist conditions. This study compares the stability of PPy/DBS‐coated platinum electrodes that are either dry‐stored, incubated, or both incubated and electrically stimulated. The electrical and material properties of three different coating thicknesses were monitored for 42 days. Initially, the PPy/DBS‐coating decreased the low frequency impedance of the platinum electrodes by 52% to 79%. The dry‐stored electrodes remained stable during the follow‐up, whereas the properties of all the incubated electrodes were altered in three stages with thickness‐dependent duration: stabilization, stable, and degradation. The coated electrodes would be applicable for short‐term, low‐frequency in vitro measurements of up to 14 days without electrical stimulation, and up to 7 days with stimulation. The coating thickness is bound to other coating properties, and should therefore be selected according to the specific target application. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 106B: 2202–2213, 2018.
Parathyroid Hormone Signaling in Osteocytes
Authors: Wein Marc N 
Published: October 2017

ABSTRACTOsteocytes are the most abundant cell type in bone and play a central role in orchestrating skeletal remodeling, in part by producing paracrine‐acting factors that in turn influence osteoblast and osteoclast activity. Recent evidence has indicated that osteocytes are crucial cellular targets of parathyroid hormone (PTH). Here, we will review the cellular and molecular mechanisms through which PTH influences osteocyte function. Two well‐studied PTH target genes in osteocytes are SOST and receptor activator of NF‐κB ligand (RANKL). The molecular mechanisms through which PTH regulates expression of these two crucial target genes will be discussed. Beyond SOST and RANKL, PTH/PTH‐related peptide (PTHrP) signaling in osteocytes may directly influence the way osteocytes remodel their perilacunar environment to influence bone homeostasis in a cell‐autonomous manner. Here, I will highlight novel, additional mechanisms used by PTH and PTHrP to modulate bone homeostasis through effects in osteocytes. © 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
ABIN1 inhibits HDAC1 ubiquitination and protects it from both proteasome‐ and lysozyme‐dependent degradation
Authors: Ma Yuhong , Yuan Sen , Tian Xuezhang , Lin Shanchuan , Wei Shangmou , Hu Tongtong , Chen Shiyou , Li Xueqing , Chen Shuliang , Wu Dongcheng , Wang Min , Guo Deyin 
Published: October 2017

AbstractABIN1, an important immune regulator, has been shown to be involved in various cellular functions, such as immunity, development, tissue homeostasis, and tumor progression. It inhibits TNF‐ and TLR‐induced NF‐κB signaling activation and the consequent gene expression. Despite its functional significance, the mechanism of ABIN1 in the regulation of various cellular functions remains unclear. In this study, we identified HDAC1, a key regulator of eukaryotic gene expression and many important cellular events, including cell proliferation, differentiation, cancer and immunity, as an interacting partner of ABIN1. The results showed that ABIN1 acted as a modulator to down‐regulate HDAC1 ubiquitination via three different linkages, thereby stabilizing HDAC1 by inhibiting its lysosomal and proteasomal degradation. Interestingly, the inhibitory function of ABIN1 required direct binding with HDAC1. Moreover, the level of p53, which was a tumor suppressor and a well‐studied substrate of HDAC1, was under the regulation of ABIN1 via the modulation of HDAC1 levels, suggesting that ABIN1 was physiologically significant in tumor progression. This study has revealed a new function of ABIN1 in mediating HDAC1 modification and stability.
In vitro and in vivo effect of PD‐1/PD‐L1 blockade on microglia/macrophage activation and T cell subset balance in cryptococcal meningitis
Authors: Che Yuan‐Mei , Zhang Yi , Li Ming , Li Xiao‐Peng , Zhang Lun‐Li 
Published: October 2017

AbstractThis study aimed to investigate the PD‐1/ PD‐L1 signaling pathway and its effects the activation of microglia/macrophage and balancing T cell subsets in cryptococcal meningitis (CM). A total of 126 CM patients and 126 healthy individuals were recruited for the study. The CM patients were treated with amphotericin B (AmB). Seventy five C57BL/6 mice were grouped into the normal control, CM model, CM + AmB, sham, and CM + PD‐1 antibodies (Ab) groups. CD4+ and CD8+ T cells as well as microglia/macrophages were analyzed by means of flow cytometry. Ionized calcium‐binding adaptor molecule 1 (Ibal) expression was detected using western blotting and immunohistochemistry techniques. And the expression of Rab5 and Rab11 were detected using an immunofluorescence assay. Both PD‐1 and PD‐L1 mRNA and protein expression among the mice in the study were evaluated by qRT‐PCR and western blotting methods. Compared to the CM model group, the CM + AmB and CM + PD‐1 Ab groups exhibited increased levels of Th1 cytokines and chemokines expression, and reduced levels of Th2 cytokines expressions. Elevated cell purity and viability of CD4+ T cell were recorded as well as increases in microglia, however, there were reductions in the number of CD8+ T cells. Depleted expressions of Ibal, Rab5, and Rab11 as well as reduced mRNA expressions of PD‐1 and PD‐L1 in CD4+, microglia, and macrophage cells. The findings suggested that suppression of the PD‐1/PD‐L1 signaling pathway restricts the proliferation of CM by down‐regulating the expressions of Th2 cells and suppressing microglia and macrophage activation.
Molecular modeling studies to explore the binding affinity of virtually screened inhibitor toward different aminoglycoside kinases from diverse MDR strains
Authors: Parulekar Rishikesh S. , Sonawane Kailas D. 
Published: October 2017

AbstractAntibiotic resistance to aminoglycoside group of antibiotics mainly occurs by aminoglycoside kinases (AKs). Thus, targeting AKs from different multidrug resistant (MDR) strains could result into inhibition of AK enzymes and ultimately the resistance. Therefore, the present study aims to target one of these AKs that is APH(3')‐Ia from Acinetobacter baumannii through structure based virtual screening (SBVS) and test the binding affinity of the most stable virtually screened inhibitor with AKs from Mycobacterium tuberculosis, Acinetobacter baumannii, Enterococcus gallinarum, and Escherichia coli. SBVS investigated ZINC71575479 as a most stable inhibitor with −8.92 kcal/mol of binding energy and 0.66 µM of inhibition constant. Molecular docking results revealed that the ZINC71575479 can efficiently bind to nucleotide triphosphate (NTP) binding site of different AKs which is a known drug target site. Sequence analysis study of different AKs showed no significant similarity for active site residues; however structure superimposition study showed conserved NTP‐binding domain. Molecular dynamics (MD) simulations showed stable behavior of all docked complexes with notable conformational stability of salt bridges at NTP‐binding site of different AKs. Binding energy calculations revealed the interactions between key residues from NTP‐ binding domain of different AKs with ZINC71575479. In order to validate the MD simulations and binding energy results, crystal structure complexed with tyrphostin AG1478 a known inhibitor of AKs was kept as control. Thus, this work demonstrates the binding efficiency of ZINC71575479 toward different AKs for circumventing aminoglycoside resistance and opens avenues for the development of new antibiotics that can target diverse MDR strains with aminoglycoside resistance.
Retracted: Prognostic significance of long non‐coding RNA MALAT1 for predicting the recurrence and metastasis of gallbladder cancer and its effect on cell proliferation, migration, invasion, and apoptosis
Authors: Sun Ke‐Ke , Hu Ping‐Ping , Xu Feng 
Published: October 2017

AbstractThe objective of this study is to explore the role of MALAT1 as a molecular indicator in predicting the recurrence, metastasis, and prognosis of gallbladder cancer (GBC) and its effect on the proliferation, invasion, migration, and apoptosis of GBC cells in vitro. GBC tissues and adjacent normal tissues were collected from 102 patients. MALAT1 short hairpin RNA (shRNA) plasmids were first constructed to transfect the GBC‐SD cells. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) was applied to detect MALAT1 expression. CCK‐8 assay, flow cytometry, and Transwell assay were applied to testify the cell proliferation, cell cycle, apoptosis, invasion, and migration. A receiver operating characteristic (ROC) curve was used to evaluate the values of MALAT1 in GBC recurrence, metastasis, and prognosis. COX regression analysis was applied to analyze the independent influencing factors of GBC patients’ survival status. ROC curve results showed that the MALAT1 expression could be a predictor of the GBC recurrence, metastasis, and prognosis. According to the COX regression analysis, MALAT1 expression, tumor size, and TNM stage were independent influencing factors of GBC patients’ survival condition. Compared with the GBC‐SD cells transfected with empty plasmids, those transfected with MALAT1 shRNA plasmids showed higher apoptosis rates, weakened proliferation, migration, and invasion. In conclusion, our findings demonstrate that lncRNA MALAT1 can be considered as an indicator for evaluating the recurrence, metastasis, and prognosis of GBC patients. We also demonstrate how the overexpression of MALAT1 confers an oncogenic function in GBC.
Protective effects of PPAR‐γ against pregnancy‐induced hypertension by differential ETR expression in rat models
Authors: Wu Ying , Ruan Yan , Shen Lin , Gong Qing 
Published: October 2017

AbstractThis study aims to investigate the effects of PPAR‐γ on rats with pregnancy‐induced hypertension (PIH) by regulating endothelin receptor (ETR). A total of 60 pregnant Wistar rats were selected, and 50 rats were used to establish endotoxin induced PIH rat models. Rats were equally assigned into PIH‐NS, PIH‐5 mg/kg RM, PIH‐10 mg/kg RM, PIH‐100 mg/kg ETR, and PIH‐200 mg/kg ETR groups, and the rest 10 rats were assigned to a the control group. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and Western blotting were used for determining mRNA and protein expressions of PPAR‐γ and ETAR, respectively. Protein expression of ET‐1 was detected by immunohistochemistry. Results show that On the 22nd day of pregnancy, compared with the PIH‐NS group, SBP decreased in other groups, and platelet concentration increased most significantly in the PIH‐10 mg/kg RM and PIH‐200 mg/kg ETR groups. Compared with the control, PIH‐10 mg/kg RM and PIH‐200 mg/kg ETR groups, the increase in the expression of ET‐1 and ETAR was most significant in the PIH‐NS group. Compared with the control and PIH‐10 mg/kg RM groups, expression of PPAR‐γ was lower in the PIH‐NS, PIH‐5 mg/kg RM, PIH‐100 mg/kg ETR, and PIH‐200 mg/kg ETR groups. Compared with the PIH‐NS, PIH‐100 mg/kg ETR and PIH‐200 mg/kg ETR groups, PPAR‐γ expression was significantly higher in the PIH‐5 mg/kg RM group (all P < 0.05). Based on our findings, we conclude that PPAR‐γ activation inhibits ETR expression and reduces the effect of ET‐1 on vascular contraction thereby delaying PIH progression.
miR‐302a‐3p regulates RANKL expression in human mandibular osteoblast‐like cells
Authors: Irwandi Rizky A. , Khonsuphap Pakchisa , Limlawan Pirawish , Vacharaksa Anjalee 
Published: October 2017

AbstractReceptor activator of nuclear factor kappa‐B ligand (RANKL) is important substance during osteoclastogenesis that resulted in alveolar bone loss of periodontitis. MicroRNAs (miRNAs) regulate gene expression in several biological processes including osteoclastogenesis. We investigated the function of microRNA‐302a‐3p (miR‐302a‐3p) to regulate receptor activator of nuclear factor kappa‐B ligand (RANKL) expression in human mandibular osteoblast‐like cells (HMOBs). HMOBs were incubated with prostaglandin E2 (PGE2) to mimic inflammation, or with PGE2 and interferon gamma (IFNγ) to mimic homeostasis. MicroRNA (miRNA) profiles related to RANKL expression were demonstrated by PCR array, and miR‐302a‐3p was identified. Using TargetScanHuman 7.0, a target of miR‐302a‐3p was predicted. To confirm its function, miR‐302a‐3p was overexpressed, or silenced, by transfection with miR‐302a‐3p mimic, or inhibitor, respectively. Level of miR‐302a‐3p and RANKL mRNA was assessed by qRT‐PCR. Soluble RANKL (sRANKL), and membrane‐bound RANKL (mRANKL) were measured by ELISA and by Western blot, respectively. When PGE2 stimulated RANKL in HMOBs, miR‐302a‐3p was lower than baseline level. However, upregulation of miR‐302a‐3p is observed when IFNγ suppressed RANKL expression in PGE2‐stimulated HMOBs. miR‐302a‐3p was predicted to target PRKACB mRNA encoding the catalytic subunit in cAMP/PKA pathway. Overexpression of miR‐302a‐3p could decrease RANKL expression during PGE2 stimulation. In contrast, silencing of miR‐302a‐3p by its inhibitor increased RANKL expression in PGE2‐IFNγ conditioned HMOBs. miR‐302a‐3p regulates RANKL expression in HMOBs within PGE2‐IFNγ regulatory network.
Gene therapy for neuropathic pain induced by spared nerve injury with naked plasmid encoding hepatocyte growth factor
Authors: Hu Chunsheng , Lu Yuxin , Cheng Xiaochen , Cui Yufang , Wu Zuze , Zhang Qinglin 
Published: October 2017

AbstractBackgroundNeuropathic pain (NP) is a refractory disease in the clinic with a tremendous impact on the quality of life of patients. Gene therapy is a potential strategy for the management of NP. In the present study, we examined the analgesic effect and mechanism of hepatocyte growth factor (HGF) in vitro and in vivo.MethodsWe examined the proinflammatroy gene changes in lipopolysaccharide (LPS)‐induced microglia BV2 cells with a quantitative real‐time polymerase chain reaction of interleukin (IL)‐1β, IL‐6, tumor necrosis factor (TNF)‐α and inducible nitric oxide synthase (iNOS). Mechanical stimulation tests were performed five times at 5‐min intervals to assess pain thresholds using Von Frey Hair in mice following spared nerve injury (SNI). The glial cell activation of spinal cord was examined by western blotting. Statistical significance was determined by a Tukey's test and a paired t‐test.ResultsWe found that recombinant human HGF protein suppressed LPS‐induced BV2 cell activation in vitro, marked by the down‐regulation of IL‐1β, IL‐6, TNF‐α and iNOS expression, as well as decrease of nitric oxide production. Moreover, intrathecal injection of naked plasmid encoding HGF gene (pUDK‐HGF) significantly attenuated SNI‐induced pain behaviors in mice by direct inhibition of spinal cord microglia and astrocyte activation.ConclusionsThe results of the present study indicate that pUDK‐HGF can reduce cytotoxicity products released from activated glial cells, which may provide a promising therapeutic strategy for treating NP.