bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nevirapine patch testing in Thai human immunodeficiency virus infected patients with nevirapine drug hypersensitivity
Authors: Prasertvit Piyatida , Chareonyingwattana Angkana , Wattanakrai Penpun 
Published: August 2017

SummaryBackgroundAntiretroviral drug hypersensitivity in HIV patients is common. Publications have shown that Abacavir (ABC) patch testing is useful in confirming ABC hypersensitivity in 24–50% of cases with a 100% sensitivity of HLA‐B*5701 in patch test positive cases. However, Nevirapine (NVP) patch testing has not been reported.Objectives(1) To evaluate the usefulness and safety of NVP patch testing in Thai HIV patients with NVP hypersensitivity. (2) To assess the correlation of positive patch tests with HLA‐B*3505.Patients and methodsPatients were classified into two groups: (1) study group of 20 HIV NVP hypersensitivity patients and (2) control group of 15 volunteers without NVP hypersensitivity. Both groups were patch tested with purified and commercialized form of NVP in various vehicles.ResultsTwo HIV patients with NVP hypersensitivity were patch test positive. All controls tested negative. Three HIV patients were positive for HLA‐B*3505 and the two patients with positive patch testing were both HLA‐B*3505 positive.ConclusionsNVP patch testing in Thai HIV patients is safe and can be used to help confirm the association between NVP and hypersensitivity skin reactions. NVP patch test results significantly correlated with HLA‐B*3505. The sensitivity of HLA‐B*3505 for positive patch test was 100%.
Screening with doppler ultrasound for carotid artery stenosis in patients with stroke or transient ischaemic attack
Authors: Kristensen Tatiana , Hovind Peter , Iversen Helle K. , Andersen Ulrik B. 
Published: August 2017

SummaryIntroductionCarotid endarterectomy of symptomatic internal carotid artery stenosis in patients with stroke or transient ischaemic attack reduces the risk of recurrent stroke, particularly if performed within 2 weeks from the first event. We evaluated the efficiency of a screening programme based on Doppler ultrasound in patients hospitalized with stroke or transient ischaemic attack in the stroke centre at Rigshospitalet, Glostrup, Denmark, concerning timeliness of referral to the vascular surgeon and performance of carotid endarterectomy according to national recommendations.MethodsProspective study of a consecutive cohort of patients with transient ischaemic attack or stroke, referred for carotid Doppler ultrasound over a one‐year period.ResultsWe examined 1390 patients (1048 with stroke, 342 with transient ischaemic attack), 71% within 24 h and 93% within 4 days after admission. Carotid stenosis or occlusion was found in 171 patients (12·3%) and was hemisphere related in 78 patients (5·6%). Among these, 68 (87%) were referred to the vascular department, 94% within 4 days of admission. Carotid endarterectomy was performed in 16 patients, all within 14 days from admission, and was not declined in any patient due to procedural delay.ConclusionsIn a major Danish stroke centre, the national recommended time limit of 4 days in patients with stroke or transient ischaemic attack for screening for carotid stenosis was met in almost all patients. No patients were excluded from surgery as a result of a time limit of 14 days from admission to surgery being exceeded. Of all patients screened, 1·2% underwent carotid endarterectomy.
Simulation of aortopulmonary collateral flow in Fontan patients for use in prediction of interventional outcomes
Authors: Frieberg Petter , Sjöberg Pia , Revstedt Johan , Heiberg Einar , Liuba Petru , Carlsson Marcus 
Published: August 2017

SummaryPurposePatients with complex congenital heart disease may need to be converted to a Fontan circulation with systemic venous return surgically connected to the pulmonary circulation. These patients frequently form aortopulmonary collaterals (APC), that is arterial inflows to the pulmonary artery vascular tree. The aim of this study was to develop a method to calculate the effect of APC on the pulmonary flow distribution based on magnetic resonance imaging (MRI) measurements and computational fluid dynamics simulations in order to enable prediction of interventional outcomes in Fontan patients.MethodsPatient‐specific models of 11 patients were constructed in a 3D‐design software based on MRI segmentations. APC flow was quantified as the difference between pulmonary venous flow and pulmonary artery flow, measured by MRI. A method was developed to include the modulating effect of the APC flow by calculating the patient‐specific relative pulmonary vascular resistance. Simulations, including interventions with a Y‐graft replacement and a stent dilatation, were validated against MRI results.ResultsThe bias between simulated and MRI‐measured fraction of blood to the left lung was 2·9 ± 5·3%. Including the effects of the APC flow in the simulation (n = 6) reduced simulation error from 9·8 ± 7·0% to 5·2 ± 6·3%. Preliminary findings in two patients show that the effect of surgical and catheter interventions could be predicted using the demonstrated methods.ConclusionsThe work demonstrates a novel method to include APC flow in predictive simulations of Fontan hemodynamics. APC flow was found to have a significant contribution to the pulmonary flow distribution in Fontan patients.
Physiological measures in participants with chronic fatigue syndrome, multiple sclerosis and healthy controls following repeated exercise: a pilot study
Authors: Hodges L. D. , Nielsen T. , Baken D. 
Published: August 2017

SummaryPurposeTo compare physiological responses of chronic fatigue syndrome (CFS/ME), multiple sclerosis (MS) and healthy controls (HC) following a 24‐h repeated exercise test.MethodsTen CFS, seven MS and 17 age‐ and gender‐matched healthy controls (10, CFS HC; and seven, MS HC) were recruited. Each participant completed a maximal incremental cycle exercise test on day 1 and again 24 h later. Heart rate (HR), blood pressure (BP), rating of perceived exertion (RPE), oxygen consumption (), carbon dioxide production and workload (WL) were recorded. Data analysis investigated these responses at anaerobic threshold (AT) and peak work rate (PWR).ResultsOn day 2, both CFS and MS had significantly reduced max workload compared to HC. On day 2, significant differences were apparent in WL between CFS and CFS HC (93 ± 37 W, 132 ± 42 W, P<0·042). CFS workload decreased on day 2, alongside a decrease in HR but with an increase in (ml kg min−1). This was in comparison with an increase in WL, HR and for CFS HC. MS demonstrated a decreased WL compared to MS HC on both days of the study (D1 81 ± 30 W, 116 ±30 W; D2 84 ± 29 W, 118 ± 36 W); however, patients with MS were able to achieve a higher WL on day 2 alongside MS HC.ConclusionThese results suggest that exercise exhibits a different physiological response in MS and CFS/ME, demonstrating repeated cardiovascular exercise testing as a valid measure for differentiating between fatigue conditions.
Like Father, Like Son: Inheriting and Bequeathing
Authors: Bethencourt Carlos , Kunze Lars 
Published: August 2017

Abstract
This paper incorporates indirect reciprocal behavior in the context of bequeathing decisions into an otherwise standard OLG model. We provide conditions for the existence of a unique steady state with operative bequests. Contrary to standard OLG models, we show that taking into account such behavioral interactions allows one to rationalize both an increasing and U-shaped pattern of the inheritance to GDP ratio over time, consistent with recent empirical evidence. Moreover, the model predicts a nonlinear (U-shaped) relationship between the size of an unfunded social security program and the long-run stock of per capita capital, which in turn provides a novel explanation of the inconclusive empirical findings on the relationship between social security, savings and long-run growth. Ricardian equivalence is shown to hold in a special case of the model.
3′‐Sialyllactose protects against osteoarthritic development by facilitating cartilage homeostasis
Authors: Jeon Jimin , Kang Li‐Jung , Lee Kwang Min , Cho Chanmi , Song Eun Kyung , Kim Wook , Park Tae Joo , Yang Siyoung 
Published: August 2017

Abstract3′‐Sialyllactose has specific physiological functions in a variety of tissues; however, its effects on osteoarthritic development remain unknown. Here, we demonstrated the function of 3′‐sialyllactose on osteoarthritic cartilage destruction. In vitro and ex vivo, biochemical and histological analysis demonstrated that 3′‐sialyllactose was sufficient to restore the synthesis of Col2a1 and accumulation of sulphated proteoglycan, a critical factor for cartilage regeneration in osteoarthritic development, and blocked the expression of Mmp3, Mmp13 and Cox2 induced by IL‐1β, IL‐6, IL‐17 and TNF‐α, which mediates cartilage degradation. Further, reporter gene assays revealed that the activity of Sox9 as a transcription factor for Col2a1 expression was accelerated by 3′‐sialyllactose, whereas the direct binding of NF‐κB to the Mmp3, Mmp13 and Cox2 promoters was reduced by 3′‐sialyllactose in IL‐1β‐treated chondrocytes. Additionally, IL‐1β induction of Erk phosphorylation and IκB degradation, representing a critical signal pathway for osteoarthritic development, was totally blocked by 3′‐sialyllactose in a dose‐dependent manner. In vivo, 3′‐sialyllactose protected against osteoarthritic cartilage destruction in an osteoarthritis mouse model induced by destabilization of the medial meniscus, as demonstrated by histopathological analysis. Our results strongly suggest that 3′‐sialyllactose may ameliorate osteoarthritic cartilage destruction by cartilage regeneration via promoting Col2a1 production and may inhibit cartilage degradation and inflammation by suppressing Mmp3, Mmp13 and Cox2 expression. The effects of 3′‐sialyllactose could be attributed in part to its regulation of Sox9 or NF‐κB and inhibition of Erk phosphorylation and IκB degradation. Taken together, these effects indicate that 3′‐sialyllactose merits consideration as a natural therapeutic agent for protecting against osteoarthritis.
Systemic administration of bone marrow‐derived cells leads to better uterine engraftment than use of uterine‐derived cells or local injection
Authors: Liu Ying , Tal Reshef , Pluchino Nicola , Mamillapalli Ramanaiah , Taylor Hugh S. 
Published: August 2017

AbstractStem cells are recruited to the uterus where they differentiate into endometrial cells and have been suggested as potential therapy for uterine injury such as Asherman's syndrome. However, it is unknown whether local intrauterine injection may result in better stem cell engraftment of the uterus compared with systemic administration, and whether uterine‐derived cells (UDCs) may confer an advantage over BM‐derived cells (BMDCs). Mice underwent local injury to a single uterine horn. Green fluorescent protein (GFP)‐expressing BMDCs, UDCs or saline (control) were injected either intravenously or locally (uterine lumen) into wild‐type recipients. Two or 3 weeks post‐transplant, uterine tissues were collected for fluorescence‐activated cell sorting (FACS) and immunohistochemistry/immunofluorescence studies. Mice injected intravenously with BMDCs or UDCs had increased GFP+ cells recruitment to the non‐injured or injured uterus compared to those injected locally. No significant differences were noted in GFP+ cell recruitment to the injured versus non‐injured horn. In addition, systemic injection of BMDCs led to greater recruitment of GFP+ cells at 2 weeks and 3 weeks compared with UDCs. Immunohistochemical staining demonstrated that GFP+ cells were found in stroma but not in epithelium or blood vessels. Immunofluorescence analysis revealed that GFP+ cells were mostly CD45‐negative, and negative for CD31 and cytokeratin, confirming their stromal identity. In conclusion, the systemic route of administration results in better recruitment of BMDCs or UDCs to the injured uterus than local injection. In addition, BMDCs recruitment to the uterus is greater than UDCs. These findings inform the development of stem cell‐based therapies targeting the uterus.
A novel mutation of adenomatous polyposis coli (APC) gene results in the formation of supernumerary teeth
Authors: Yu Fang , Cai Wenping , Jiang Beizhan , Xu Laijun , Liu Shangfeng , Zhao Shouliang 
Published: August 2017

AbstractSupernumerary teeth are teeth that are present in addition to normal teeth. Although several hypotheses and some molecular signalling pathways explain the formation of supernumerary teeth, but their exact disease pathogenesis is unknown. To study the molecular mechanisms of supernumerary tooth‐related syndrome (Gardner syndrome), a deeper understanding of the aetiology of supernumerary teeth and the associated syndrome is needed, with the goal of inhibiting disease inheritance via prenatal diagnosis. We recruited a Chinese family with Gardner syndrome. Haematoxylin and eosin staining of supernumerary teeth and colonic polyp lesion biopsies revealed that these patients exhibited significant pathological characteristics. APC gene mutations were detected by PCR and direct sequencing. We revealed the pathological pathway involved in human supernumerary tooth development and the mouse tooth germ development expression profile by RNA sequencing (RNA‐seq). Sequencing analysis revealed that an APC gene mutation in exon 15, namely 4292‐4293‐Del GA, caused Gardner syndrome in this family. This mutation not only initiated the various manifestations typical of Gardner syndrome but also resulted in odontoma and supernumerary teeth in this case. Furthermore, RNA‐seq analysis of human supernumerary teeth suggests that the APC gene is the key gene involved in the development of supernumerary teeth in humans. The mouse tooth germ development expression profile shows that the APC gene plays an important role in tooth germ development. We identified a new mutation in the APC gene that results in supernumerary teeth in association with Gardner syndrome. This information may shed light on the molecular pathogenesis of supernumerary teeth. Gene‐based diagnosis and gene therapy for supernumerary teeth may become available in the future, and our study provides a high‐resolution reference for treating other syndromes associated with supernumerary teeth.
Adaptive changes of telocytes in the urinary bladder of patients affected by neurogenic detrusor overactivity
Authors: Traini Chiara , Fausssone‐Pellegrini Maria‐Simonetta , Guasti Daniele , Del Popolo Giulio , Frizzi Jacopo , Serni Sergio , Vannucchi Maria‐Giuliana 
Published: August 2017

AbstractUrinary bladder activity involves central and autonomic nervous systems and bladder wall. Studies on the pathogenesis of voiding disorders such as the neurogenic detrusor overactivity (NDO) due to suprasacral spinal cord lesions have emphasized the importance of an abnormal handling of the afferent signals from urothelium and lamina propria (LP). In the LP (and detrusor), three types of telocytes (TC) are present and form a 3D‐network. TC are stromal cells able to form the scaffold that contains and organizes the connective components, to serve as guide for tissue (re)‐modelling, to produce trophic and/or regulatory molecules, to share privileged contacts with the immune cells. Specimens of full thickness bladder wall from NDO patients were collected with the aim to investigate possible changes of the three TC types using histology, immunohistochemistry and transmission electron microscopy. The results show that NDO causes several morphological TC changes without cell loss or network interruption. With the exception of those underlying the urothelium, all the TC display signs of activation (increase in Caveolin1 and caveolae, αSMA and thin filaments, Calreticulin and amount of cisternae of the rough endoplasmic reticulum, CD34, euchromatic nuclei and large nucleoli). In all the specimens, a cell infiltrate, mainly consisting in plasma cells located in the vicinity or taking contacts with the TC, is present. In conclusion, our findings show that NDO causes significant changes of all the TC. Notably, these changes can be interpreted as TC adaptability to the pathological condition likely preserving each of their peculiar functions.
The mechanism of acute fasting‐induced antidepressant‐like effects in mice
Authors: Cui Ranji , Fan Jie , Ge Tongtong , Tang Linda , Li Bingjin 
Published: August 2017

AbstractAcute fasting induced antidepressant‐like effects. However, the exact brain region and mechanism of these actions are still largely unknown. Therefore, in this study the antidepressant‐like effects of acute fasting on c‐Fos expression and BDNF levels were investigated. Consistent with our previous findings, immobility time was remarkably shortened by 9 hrs fasting in the forced swimming test. Furthermore, these antidepressant‐like effects of 9 fasting were inhibited by a 5‐HT2A/2C receptor agonist (±)‐1‐(2, 5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane hydrochloride (DOI), and the effect of DOI was blocked by pretreatment with a selective 5‐HT2A receptor antagonist ketanserin. Immunohistochemical study has shown that c‐Fos level was significantly increased by 9 hrs fasting in prefrontal cortex but not hippocampus and habenular. Fasting‐induced c‐Fos expression was further enhanced by DOI in prefrontal cortex, and these enhancements were inhibited by ketanserin. The increased BDNF levels by fasting were markedly inhibited by DOI in frontal cortex and hippocampus, and these effects of DOI on BDNF levels were also blocked by ketanserin. These findings suggest that the antidepressant‐like effects of acute fasting may be exerted via 5‐HT2A receptor and particularly sensitive to neural activity in the prefrontal cortex. Furthermore, these antidepressant‐like effects are also mediated by CREB and BDNF pathway in hippocampus and frontal cortex. Therefore, fasting may be potentially helpful against depression.
Ectodysplasin A regulates epithelial barrier function through sonic hedgehog signalling pathway
Authors: Li Sanming , Zhou Jing , Zhang Liying , Li Juan , Yu Jingwen , Ning Ke , Qu Yangluowa , He Hui , Chen Yongxiong , Reinach Peter S. , Liu Chia‐Yang , Liu Zuguo , Li Wei 
Published: August 2017

AbstractEctodysplasin A (Eda), a member of the tumour necrosis factor superfamily, plays an important role in ectodermal organ development. An EDA mutation underlies the most common of ectodermal dysplasias, that is X‐linked hypohidrotic ectodermal dysplasia (XLHED) in humans. Even though it lacks a developmental function, the role of Eda during the postnatal stage remains elusive. In this study, we found tight junctional proteins ZO‐1 and claudin‐1 expression is largely reduced in epidermal, corneal and lung epithelia in Eda mutant Tabby mice at different postnatal ages. These declines are associated with tail ulceration, corneal pannus formation and lung infection. Furthermore, topical application of recombinant Eda protein markedly mitigated corneal barrier dysfunction. Using cultures of a human corneal epithelial cell line and Tabby mouse skin tissue explants, Eda up‐regulated expression of ZO‐1 and claudin‐1 through activation of the sonic hedgehog signalling pathway. We conclude that EDA gene expression contributes to the maintenance of epithelial barrier function. Such insight may help efforts to identify novel strategies for improving management of XLHED disease manifestations in a clinical setting.
Down‐regulation of miR‐10a‐5p in synoviocytes contributes to TBX5‐controlled joint inflammation
Authors: Hussain Nazim , Zhu Wenhua , Jiang Congshan , Xu Jing , Wu Xiaoying , Geng Manman , Hussain Safdar , Cai Yongsong , Xu Ke , Xu Peng , Han Yan , Sun Jian , Meng Liesu , Lu Shemin 
Published: August 2017

AbstractMicroRNAs are considered to play critical roles in the pathogenesis of human inflammatory arthritis, including rheumatoid arthritis (RA). The purpose of this study was to determine the relationship between miR‐10a‐5p and TBX5 in synoviocytes and evaluate their contribution to joint inflammation. The expression of miR‐10a‐5p and TBX5 in the synovium of RA and human synovial sarcoma cell line SW982 stimulated by IL‐1β was determined by RT‐qPCR and Western blotting. The direct interaction between miR‐10a‐5p and TBX5 3′UTR was determined by dual‐luciferase reporter assay in HeLa cells. Mimics and inhibitors of miR‐10a‐5p were transfected into SW982 cells. TBX5 was overexpressed by plasmid transfection or knocked down by RNAi. Proinflammatory cytokines and TLR3 and MMP13 expressions were determined by RT‐qPCR and Western blotting. Down‐regulated expression of miR‐10a‐5p and up‐regulation of TBX5 in human patients with RA were found compared to patients with OA. IL‐1β could reduce miR‐10a‐5p and increase TBX5 expression in SW982 cells in vitro. The direct target relationship between miR‐10a‐5p and 3′UTR of TBX5 was confirmed by luciferase reporter assay. Alterations of miR‐10‐5p after transfection with its mimic and inhibitor caused the related depression and re‐expression of TBX5 and inflammatory factors in SW982 cells. Overexpression of TBX5 after pCMV3‐TBX5 plasmid transfection significantly promoted the production of TLR3, MMP13 and various inflammatory cytokines, while this effect was rescued after knocking down of TBX5 with its specific siRNA. We conclude that miR‐10a‐5p in a relation with TBX5 regulates joint inflammation in arthritis, which would serve as a diagnostic and therapeutic target for RA treatment.
Serum lipid levels in patients with periodontal disease: A meta‐analysis and meta‐regression
Authors: Nepomuceno Rafael , Pigossi Suzane C. , Finoti Livia S. , Orrico Silvana R. P. , Cirelli Joni A. , Barros Silvana P. , Offenbacher Steven , Scarel‐Caminaga Raquel M. 
Published: August 2017

AbstractAimSeveral papers have considered the potential relationship between periodontitis and lipid parameters. The present systematic review, meta‐analysis and meta‐regression studies focused on investigating whether serum lipid parameter levels were elevated in patients with periodontal disease (PD; without altered systemic conditions) in comparison with periodontally healthy subjects.Materials and MethodsEligible studies were those with data about serum lipid parameter levels in non‐smoking subjects with and without chronic periodontitis, who are generally healthy and not taking any medication for dyslipidaemia. Mean differences and 95% confidence intervals for total cholesterol, triglycerides, low‐density lipoprotein (LDL) cholesterol and high‐density lipoprotein (HDL) cholesterol were obtained from all the selected studies.ResultsA total of 19 publications were included for meta‐analysis. Participants with chronic periodontitis presented significantly higher serum levels of LDL and triglycerides (p = .003 and p < .0001, respectively). The total cholesterol was higher in the PD group, but without significant difference in comparison with healthy participants. Significantly (p = .0005) lower HDL serum levels were found in patients with chronic periodontitis than in healthy subjects.ConclusionsEven considering the limitations of this meta‐analysis, it is suggested that PD is significantly associated with reduction in HDL and elevation of LDL and triglyceride concentrations. This analysis supports the rationale that periodontal disease is associated with lipid metabolic control.