bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mangosteen Vinegar Rind from Garcinia mangostana Prevents High‐Fat Diet and Streptozotocin‐Induced Type II Diabetes Nephropathy and Apoptosis
Authors: Karim Naymul , Rahman Atiar , Chanudom Lanchakon , Thongsom Montakarn , Tangpong Jitbanjong 
Published: April 2019

AbstractType II diabetes (T2D) nephropathy, a major cause of end‐stage kidney disease, progresses and develops from oxidative stress. Natural polyphenols can protect the kidney from diabetic nephropathy exerting antioxidant activities. The present approach enumerates the reno‐protective and anti‐apoptotic effects of mangosteen vinegar rind (MVR, a phenolic aqueous extract) against high‐fat diet (5 g/day up to five weeks)‐/streptozotocin (single ip, dose 30 mg/kgBW)‐induced T2D nephropathy of albino mice. In vitro total phenolic content, 2,2'‐azino‐bis(3‐ethylbenzothiazoline‐6‐sulphonic acid) (ABTS) activity, 2,2‐diphenyl‐1‐picrylhydrazyl (DPPH) antioxidant capacity, and α‐amylase inhibition activity as antidiabetic assay of MVR were performed. In vivo mice body weight, oral glucose, and maltose tolerance test, metabolic parameters (plasma glucose, insulin level, omeostasis model assessment‐estimated insulin resistance), biochemical parameters (kidney hypertrophy, blood urea nitrogen, creatinine), oxidative stress parameters (malondialdehyde, superoxide dismutase, catalase) were estimated in an intervention study. Additionally, renal morphology and early apoptosis were observed following the H & E staining and TUNEL assay of the tissue frozen section. We found that the aqueous extract of MVR possesses potent in vitro antioxidative and antidiabetic activities. Animal intervention results showed that MVR 100, 200 mg/kgBW, and Glibenclamide 60 mg/kgBW treatments significantly improved (P < 0.05) the abovementioned parameters compared to the diabetic control group. Furthermore, treatments also significantly restored (P < 0.05) kidney histological alterations and reduced cellular apoptosis compared to the diabetic control group. These findings concluded that MVR treatments significantly modulated the glucose intolerance, metabolic alterations, and oxidative stress‐induced pathological alterations and cellular apoptosis of diabetic kidney.Practical ApplicationGarcinia mangostana, a polyphenol rich natural product, is obtained from the tropical rain forest area of Southeast Asian countries and processes diverse biological activities including antioxidant, anti‐proliferative, anti‐inflammatory, anti‐carcinogenic, and so on. This research first time focuses on the nephro‐protective and anti‐apoptotic effects of mangosteen vinegar rind (MVR) from the mangosteen fruit pericarp. Our study provides the efficient data to prove the beneficial effect of MVR as a dietary supplement for the prevention and management of diabetic nephropathy.
Sex‐biased disease dynamics increase extinction risk by impairing population recovery
Authors: Rosa G. M. , Bosch J. , Martel A. , Pasmans F. , Rebelo R. , Griffiths R. A. , Garner T. W. J. 
Published: April 2019

AbstractThe periodicity of life‐cycle events (phenology) modulates host availability to pathogens in a repeatable pattern. The effects of sexual differences in host phenology have been little explored in wildlife epidemiological studies. A recent series of ranavirosis outbreaks led to serious declines of Boscas’ newt populations at Serra da Estrela (Portugal). The peculiar phenology of this species, in which a large number of females remain in the aquatic habitat after the breeding season, turns it into a suitable model to test how sex‐biased mortality can affect host population persistence in the context of infectious diseases. We investigated how the phenology of Bosca's newt (i.e. biased number of females) mediated the impact of Ranavirus. We then evaluated the risk of extinction of the population under different scenarios of sex‐biased mortality using a population viability analysis. Two newt populations (one subject to yearly outbreaks and a comparative site where outbreaks have not been recorded) were tracked for trends over time following emergence of ranaviral disease, allowing us to assess the differential impact of the disease on both sexes. In addition to a significant decline in abundance of adult newts, our data suggest that phenology can affect disease dynamics indirectly, leading to reduction in females and a reversal of the sex ratio of the breeding population. Our models suggest that female‐biased mortality does not exacerbate Ranavirus‐driven population declines in the short‐term, but is likely to have a deleterious impact during the recovery process once the lethal effect of disease is removed from the system.
Photodynamic therapy: A targeted literature review focussing on outcomes and optimisation in solid organ transplant recipients
Authors: Lim Chloe M , Gordon Lynne 
Published: April 2019

AbstractSquamous cell carcinoma incidence is 65‐ to 250‐fold in solid organ transplant recipients, BCC is 10‐fold and in Australia, rates of skin cancer in solid organ transplant recipients reach 70–82% prevalence within the first 20 years; hence, effective, evidence‐based treatment of early and precancerous lesions is an essential tool in dermatological patient care. Photodynamic therapy is used to treat a range of conditions including actinic keratoses, squamous cell carcinoma in situ, superficial basal cell carcinoma and nodular basal cell carcinoma. A literature review was undertaken to examine the outcomes of photodynamic therapy in solid organ transplant recipients and methods of optimising outcomes in solid organ transplant recipients. Study sizes were small and protocols varied widely, so meta‐analysis was not possible; however, photodynamic therapy appears to be an acceptable treatment for approved indications in solid organ transplant recipients in whom ongoing surveillance is maintained to ensure clearance and detect recurrence. Methods for improving efficacy were also reviewed for this population. Improved outcomes may be achieved by combining photodynamic therapy with other local methods such as 5‐fluorouracil or ablative fractional laser.
Keratinocyte cancer excisions in Australia: Who performs them and associated costs
Authors: Thompson Bridie S , Pandeya Nirmala , Olsen Catherine M , Dusingize Jean Claude , Green Adele C , Neale Rachel E , Whiteman David C 
Published: April 2019

AbstractBackground/ObjectiveTo describe the clinical settings in which keratinocyte cancers are excised in Queensland and describe the types of practitioners who excise them; to examine costs; and to identify predictors of hospital admission.MethodsWe used linked data for participants from the QSkin study (n = 43 794), including Medicare claims and Queensland hospital admissions relating to treatment episodes for incident keratinocyte cancers from July 2011 to June 2015. We used multinomial logistic regression to measure associations between demographic and clinical characteristics and treatment setting. The median costs of Medicare claims (AU$) were calculated.ResultsDuring 4 years of follow‐up, there were 18 479 skin cancer excision episodes among 8613 people. Most excisions took place in private clinical rooms (89.7%), the remainder in hospitals (7.9% private; 2.4% public). Compared with other anatomical sites, skin cancers on the nose, eyelid, ear, lip, finger or genitalia were more likely to be treated in hospitals than in private clinical rooms (public hospital OR 5.7; 95%CI 4.5–7.2; private hospital OR 8.3; 95%CI 7.3–9.4). Primary care practitioners excised 83% of keratinocyte cancers, followed by plastic surgeons (9%) and dermatologists (6%). The median Medicare benefit paid was $253 in private clinical rooms and $334 in private hospitals. Out‐of‐pocket payments by patients treated in private hospitals were fourfold higher than those in private clinical rooms ($351 vs $80).ConclusionsMost keratinocyte cancers are excised in primary care, although more than 10% of excisions occur in hospital settings.
Home‐based ‘exergaming’ was safe and significantly improved 6‐min walking distance in patients with prostate cancer: a single‐blinded randomised controlled trial
Authors: Villumsen Brigitta R. , Jorgensen Martin G. , Frystyk Jan , Hørdam Britta , Borre Michael 
Published: April 2019

ObjectivesTo explore the effects of 12 weeks of unsupervised home‐based ‘exergaming’ (i.e., technology‐driven exercise) compared to usual care on physical function, body composition, quality of life (QoL), and fatigue in patients with prostate cancer on androgen‐deprivation therapy (ADT).Patients and methodsIn an assessor‐blinded randomised controlled trial, 46 patients with prostate cancer (aged >65 years) with locally advanced or advanced stage disease undergoing ADT were randomised to 12 weeks of unsupervised home‐based exergaming or usual care from two hospitals in Denmark. The primary outcome of the study was 6‐min walking test (6MWT). Secondary outcomes were leg extensor power (LEP), body composition (lean‐ and fat‐mass), self‐reported physical functioning and global health status (European Organisation for Research and Treatment of Cancer quality of life questionnaire 30‐item core [EORTC QLQ‐C30]), QoL (Functional Assessment of Cancer Therapy – Prostate [FACT‐P]) and fatigue (FACT – fatigue [FACT‐F]).ResultsThere was significant improvement in the exergaming group compared to the usual care group in the primary outcome of 6MWT (mean difference: 21.5 m; 95% confidence interval ([CI]) 3.2–39.9; P = 0.023). There were no differences between the groups for LEP (P = 0.227), lean body mass (P = 0.100), fat body mass (P = 0.092), self‐reported physical functioning (P = 0.084) and global health status (P = 0.113), QoL (P = 0.614), and fatigue (P = 0.147).ConclusionUnsupervised home‐based exergaming for 12 weeks had an effect on the primary outcome of 6MWT in patients with prostate cancer receiving ADT. However, no significant effects were found in secondary outcomes. The exergaming intervention appeared safe and could be an alternative to traditional aerobic and resistance training in this patient group.
The cholecystokinin receptor agonist, CCK‐8, induces adiponectin production in rat white adipose tissue
Authors: Plaza Adrián , Merino Beatriz , Del Olmo Nuria , Ruiz‐Gayo Mariano 
Published: April 2019

Background and PurposeA cholecystokinin (CCK) system has been identified in white adipose tissue (WAT). Nevertheless, the endocrine actions of CCK on WAT remain unknown. Our goal was to investigate the role of CCK in regulating the production of adiponectin, an adipokine expressed in WAT, which is pivotal in preserving energy homeostasis.Experimental ApproachThe effect of the bioactive CCK fragment CCK‐8 on adiponectin production was studied both in vivo and in vitro. CCK‐8 effects were characterized in rats treated with selective CCK1 and CCK2 receptor antagonists as well as in pre‐adipocytes carrying the selective silencing of either CCK1 or CCK2 receptors. The influence of insulin on CCK‐8 responses was also analysed.Key ResultsIn WAT, CCK‐8 increased plasma adiponectin levels and the expression of the adiponectin gene (Adipoq). In pre‐adipocytes, CCK‐8 up‐regulated adiponectin production. CCK‐8 effects were abolished by L‐365,260, a selective CCK2 receptor antagonist. CCK2 receptor knockdown also abolished the effects of CCK‐8 in pre‐adipocytes. Moreover, in vitro CCK‐8 effects were blocked by triciribine, a specific inhibitor of protein kinase B (Akt) and by the PPARγ antagonist T0070907. Silencing the expression of the insulin receptor inhibited CCK‐8‐induced Adipoq expression in pre‐adipocytes. Furthermore, insulin potentiated the effect of CCK‐8.Conclusion and ImplicationsCCK‐8 stimulates adiponectin production in WAT by acting on CCK2 receptors, through a mechanism involving both Akt and PPARγ. Moreover, CCK‐8 actions are only observed in the presence of insulin. Our results could have translational value in the design of new insulin‐sensitizing therapies.
Indoleamine 2, 3‐dioxygenase 1 promoter hypomethylation is associated with poor prognosis in patients with esophageal cancer
Authors: Kiyozumi Yuki , Baba Yoshifumi , Okadome Kazuo , Yagi Taisuke , Ogata Yoko , Eto Kojiro , Hiyoshi Yukiharu , Ishimoto Takatsugu , Iwatsuki Masaaki , Iwagami Shiro , Miyamoto Yuji , Yoshida Naoya , Watanabe Masayuki , Baba Hideo 
Published: April 2019

AbstractIndoleamine 2, 3‐dioxygenase 1 (IDO1) is a primary enzyme that generates immunosuppressive metabolites. It plays a major role in tumor immunology and is a potential immune‐based therapeutic target. We have reported that IDO1 protein expression was associated with an unfavorable clinical outcome in esophageal cancer. Recently, it has been reported that IDO1 expression is regulated by methylation of the IDO1 promoter. Thus, the aim of this study was to examine the relationship between IDO1 expression, IDO1 promoter methylation, and clinicopathological features in esophageal cancer. We first confirmed changes in IDO1 expression levels in vitro by treating cells with 5‐azacytidine. We then evaluated the relationship between IDO1 expression levels, IDO1 promoter methylation (bisulfite pyrosequencing), and clinicopathological features using 40 frozen samples and 242 formalin‐fixed, paraffin‐embedded samples resected from esophageal cancer patients. We treated cell lines with 5‐azacytidine, and the resulting hypomethylation induced significantly higher IDO1 expression (P < .001). In frozen samples, IDO1 expression levels correlated inversely with IDO1 promoter methylation levels (R = −0.47, P = .0019). Furthermore, patients in the IDO1 promoter hypomethylation group (n = 67) had a poor prognosis compared with those in the IDO1 promoter hypermethylation group (n = 175) (overall survival, P = .011). Our results showed that IDO1 promoter hypomethylation regulated IDO1 expression and was associated with a poor prognosis in esophageal cancer patients.
Time Spent Gaming and Social Competence in Children: Reciprocal Effects Across Childhood
Authors: Hygen Beate W. , Belsky Jay , Stenseng Frode , Skalicka Vera , Kvande Marianne N. , Zahl‐Thanem Tonje , Wichstrøm Lars 
Published: April 2019

Electronic games are popular and many children spend much time on this activity. Here we investigate whether the quantity of time children spend on gaming is related to their social development, making this the first study to examine this relationship in children. We examine prospective relations between time spent gaming and social competence in a community sample of Norwegian 6 year olds (n = 873) followed up at ages 8, 10, and 12, controlling for socioeconomic status, body mass index, and time spent gaming together with friends. Results revealed that greater social competence at both 8 and 10 years predicted less gaming 2 years later and that more age‐10 gaming predicted less social competence at age 12 but only among girls.
Deep spatiotemporal LSTM network with temporal pattern feature for 3D human action recognition
Authors: Wu Yirui , Wei Lianglei , Duan Yucong 
Published: April 2019

AbstractWith the rapid development of RGB‐D cameras and pose estimation techniques, action recognition based on three‐dimensional skeleton data has gained significant attention in the artificial intelligence community. In this paper, we incorporate temporal pattern descriptors of joint positions with the currently popular long short‐term memory (LSTM)–based learning scheme to obtain accurate and robust action recognition. Considering that actions are essentially formed by small subactions, we first utilize a two‐dimensional wavelet transform to extract temporal pattern descriptors in the frequency domain for each subaction. Afterward, we design a novel LSTM structure to extract deep features, which model a long‐term spatiotemporal correlation between body parts. Since temporal pattern descriptors and LSTM deep features can be regarded as multimodal representations for actions, we fuse them with an autoencoder network to achieve a more effective feature descriptor for action recognition. Experimental results on three challenging data sets with several comparative methods demonstrate the effectiveness of the proposed method for three‐dimensional action recognition.
Training‐induced changes on quadriceps muscle oxygenation measured by near‐infrared spectroscopy in healthy subjects and in chronic obstructive pulmonary disease patients
Authors: Barberan‐Garcia Anael , Munoz Phillip A. , Gimeno‐Santos Elena , Burgos Felip , Torralba Yolanda , Gistau Concepción , Roca Josep , Rodriguez Diego A. 
Published: April 2019

SummaryAimWe hypothesize that training‐induced changes in muscle oxygen saturation (StO2) assessed by near‐infrared spectroscopy (NIRS) during constant work rate cycling exercise (CWRE) may be a useful marker of the effects of training at ‘vastus medialis’ of the quadriceps in patients with chronic obstructive pulmonary disease (COPD).MethodsIncremental exercise [peak oxygen uptake (VO2)] and CWRE at 70% pretraining peak VO2, before and after 8‐w training, were done in 10 healthy age‐matched subjects (H) [80% men, 65(11) years, FEV1 105(14)%] and 16 COPD patients [94% men, 70(5) years, FEV1 46(11) %] encompassing the entire spectrum of disease severity, recruited in the outpatient clinics. NIRS was used to assess StO2 in the ‘vastus medialis’ of the left quadriceps.ResultsPretraining CWRE decreased StO2 (P<0·05) and generated marked StO2 rebound (P<0·001) after unloading in the two groups. After training, VO2 peak increased in H [253(204) ml min−1] (P<0·01) and in COPD [180(183) ml·min−1] (P = 0·01) and blood lactate fell [−4·4 (2·7) and −1·6(2·3) mmol·m−1] (P<0·05 each). Training generated a further fall in StO2 during CWRE [−10(12)% and −10(10)%, P<0·05] and increased StO2 rebound after unloading [8(7)% and 5(9)%, P<0·05] in both groups.ConclusionEndurance training further decreased StO2 during CWRE, similarly in both groups, likely due to training‐induced enhancement of muscle O2 transfer and utilization. Training‐induced StO2 fall during CWRE may be useful individual marker for non‐invasive assessment of enhanced muscle aerobic post‐training function.
ERα is required for suppressing OCT4‐induced proliferation of breast cancer cells via DNMT1/ISL1/ERK axis
Authors: Jin Xiangshu , Li Yanru , Guo Yantong , Jia Yiyang , Qu Huinan , Lu Yan , Song Peiye , Zhang Xiaoli , Shao Yijia , Qi Da , Xu Wenhong , Quan Chengshi 
Published: April 2019

AbstractObjectivePOU5F1 (OCT4) is implicated in cancer stem cell self‐renewal. Currently, some studies have shown that OCT4 has a dual function in suppressing or promoting cancer progression. However, the precise molecular mechanism of OCT4 in breast cancer progression remains unclear.Materials and MethodsRT‐PCR and Western blot were utilized to investigate OCT4 expression in breast cancer tissues and cells. Cell proliferation assays and mouse models were applied to determine the effects of OCT4 on breast cancer cell proliferation. DNMT1 inhibitors, ChIP, CoIP, IHC and ERα inhibitors were used to explore the molecular mechanism of OCT4 in breast cancer.ResultsOCT4 was down‐regulated in breast cancer tissues, and the overexpression of OCT4 promoted MDA‐MB‐231 cell proliferation and inhibited the proliferation of MCF‐7 cells in vitro and in vivo, respectively. Two DNMT1 inhibitors (5‐aza‐dC and zebularine) suppressed OCT4‐induced MDA‐MB‐231 cell proliferation through Ras/Raf1/ERK inactivation by targeting ISL1, which is the downstream of DNMT1. In contrast, OCT4 interacted with ERα, decreased DNMT1 expression and inactivated the Ras/Raf1/ERK signalling pathway in MCF‐7 cells. Moreover, ERα inhibitor (AZD9496) reversed the suppression of OCT4‐induced proliferation in MCF‐7 cells via the activation of ERK signalling pathway.ConclusionsOCT4 is dependent on ERα to suppress the proliferation of breast cancer cells through DNMT1/ISL1/ERK axis.
Sex differences in preformed panel‐reactive antibody levels and outcomes in patients undergoing heart transplantation
Authors: Magnussen Christina , Ruebsamen Nicole , Ojeda Francisco M. , Rybczynski Meike , Kobashigawa Jon , Reichenspurner Hermann , Bernhardt Alexander M. , Schnabel Renate B. 
Published: April 2019

AbstractBackgroundSex differences in panel‐reactive antibody (PRA) levels in heart transplant recipients and their association with transplant‐related outcomes are mostly unknown.MethodsIn 20 181 (24.7% women) first‐time heart transplant recipients included from July 2004 to March 2015 in the prospective Organ Procurement and Transplantation Network (OPTN), we studied sex differences in most recent (mr) and peak (p)PRA and outcomes (graft failure, rejection, cardiac allograft vasculopathy [CAV], retransplantation, and mortality). Median follow‐up (all‐cause mortality) was 6 years. Analyses are based on OPTN data (March 6, 2017).ResultsMrPRA levels were associated with all‐cause mortality (hazard ratio, 95% confidence interval: class I 1.03, 1.01‐1.04, P < 0.001) and acute rejection (class II 1.08, 1.03‐1.14, P = 0.0044). PPRA levels were associated with all‐cause mortality (class I 1.02, 1.00‐1.04, P = 0.015) and CAV (class II 1.03, 1.01‐1.06, P = 0.020). Sex interactions were seen for the association of pPRA and graft failure with a higher risk in women, and for pPRA and CAV with a higher risk in men.ConclusionsPRA were associated with different transplant‐related outcomes in both sexes. However, women with elevated pPRA were shown to be at higher risk for graft failure, whereas higher levels of pPRA were more hazardous for men in developing CAV.
From embryonic stem cells to induced pluripotent stem cells—Ready for clinical therapy?
Authors: Hu Jing , Wang Jimei 
Published: April 2019

AbstractEmbryonic stem cells and induced pluripotent stem cells have increasingly important roles in many different fields of research and medicine. Major areas of impact include improved in vitro disease models, drug screening, and the development of cell‐based clinical therapies. Here, we review the generation and uses of embryonic stem cells compared to induced pluripotent stem cells and discuss their advantages and limitations. We also evaluate the feasibility of clinical therapies and the future prospects for induced pluripotent cell‐based treatments.
Altered Rb, p16, and p53 expression is specific for porocarcinoma relative to poroma
Authors: Zahn Joseph , Chan May P. , Wang Grace , Patel Rajiv M. , Andea Aleodor A. , Bresler Scott C. , Harms Paul W. 
Published: April 2019

AbstractBackgroundPorocarcinomas are rare aggressive carcinomas that harbor tumor suppressor mutations and must be distinguished from benign entities such as poromas.MethodsTo determine whether altered expression of these genes was diagnostically informative, we examined p53, Rb, and p16 staining patterns in 15 poromas and 16 porocarcinomas.ResultsPoromas consistently displayed diffuse strong expression of Rb in all but one case that displayed focal loss (1/15, 7%), and no evidence of aberrancy in p53 or p16. Porocarcinomas displayed diffuse or focal loss of Rb expression in 9/16 (56%) cases, diffuse loss or overexpression of p53 in 8/15 (53%), and diffuse loss or overexpression of p16 in 6/14 (43%). Diffuse aberrancy in p53 and Rb expression correlated with tumor mutations in TP53 and RB1, respectively, whereas focal Rb loss was associated with wild type RB1. Diffuse p16 overexpression correlated with Rb loss rather than CDKN2A mutation. For porocarcinomas with all three stains evaluable, 10/13 (77%) displayed aberrancy in at least one marker.ConclusionsOur findings suggest that altered p53, p16, and/or Rb expression is relatively specific to porocarcinoma in comparison with poroma. Technical limitations of this panel, including possible focal Rb loss, must be kept in mind, especially in limited samples.