bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vascular compliance in women with polycystic ovary syndrome treated with spironolactone
Authors: Muneyyirci‐Delale Ozgul , Co Sherilyne , Winer Nathaniel 
Published: September 2018

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age in the United States and has been associated with several diseases including cardiovascular disease, obesity, and glucose intolerance. In this study, systolic blood pressure, diastolic blood pressure, pulse pressure (vascular compliance), large artery elasticity, systemic vascular resistance (SVR), total vascular impedance (TVI), and body mass index (BMI) were measured before and after treatment with spironolactone in 10 women with PCOS. Systolic BP, diastolic BP, and BMI were similar prior to treatment and after treatment. Pulse pressure decreased slightly post‐treatment compared to pretreatment but not to significance (P = 0.07). The results show that after treatment with spironolactone, there was a statistically significant increase in large artery elasticity (P = 0.047), while there was a statistically significant decrease in SVR and TVI (P = 0.0005 and P = 0.03). This study indicates that treatment with spironolactone improves large artery elasticity and reduces systemic vascular resistance without any change in small artery elasticity.
A minimally invasive approach to induce myocardial infarction in mice without thoracotomy
Authors: Sun Quan , Wang Kang‐Kai , Pan Miao , Zhou Ji‐Peng , Qiu Xue‐Ting , Wang Zhen‐Yu , Yang Zhen , Chen Yan , Shen Hong , Gu Qi‐Lin , Fang Long‐Hou , Zhang Guo‐Gang , Bai Yong‐Ping 
Published: September 2018

AbstractAcute myocardial infarction (MI) is a leading cause of morbidity and mortality in the world. Traditional method to induce MI by left coronary artery (LCA) ligation is typically performed by an invasive approach that requires ventilation and thoracotomy, causing serious injuries in animals undergoing this surgery. We attempted to develop a minimally invasive method (MIM) to induce MI in mice. Under the guide of ultrasound, LCA ligation was performed in mice without ventilation and chest‐opening. Compared to sham mice, MIM induced MI in mice as determined by triphenyltetrazolium chloride staining and Masson staining. Mice with MIM surgery revealed the reductions of LVEF, LVFS, E/A and ascending aorta (AAO) blood flow, and the elevations of S‐T segment and serum cTn‐I levels at 24 post‐operative hours. The effects of MI induced by MIM were comparable to the effects of MI produced by traditional method in mice. Importantly, MIM increased the survival rates and caused less inflammation after the surgery of LCA ligation, compared to the surgery of traditional method. Further, MIM induced angiogenesis and apoptosis in ischaemic hearts from mice at postoperative 28 days as similarly as traditional method did. Finally, the MIM model was able to develop into the myocardial ischaemia/reperfusion model by using a balloon catheter with minor modifications. The MI model is able to be efficiently induced by a minimally invasive approach in mice without ventilation and chest‐opening. This new model is potentially to be used in studying ischaemia‐related heart diseases.
Mesenchymal stromal cell potency to treat acute kidney injury increased by ultrasound‐activated interferon‐γ/interleukin‐10 axis
Authors: Burks Scott R. , Nagle Matthew E. , Bresler Michele N. , Kim Saejeong J. , Star Robert A. , Frank Joseph A. 
Published: September 2018

AbstractMesenchymal stromal cell (MSC) therapies combined with renal pulsed focused ultrasound (pFUS) pretreatment increase MSC homing and improve cisplatin‐induced acute kidney injury (AKI) better than MSC alone. However, mechanisms underlying improved outcomes remain unknown. We hypothesize pFUS up‐regulates renal interferon‐γ (IFNγ) and stimulates MSC to produce interleukin‐10 (IL‐10) after migrating to kidneys. To demonstrate initially, MSC cultured with IFNγ up‐regulated IL‐10. More MSC‐derived IL‐10 was detected in kidneys when IFNγ‐stimulated MSC were infused and they improved AKI better than unstimulated MSC. Next, IFNγ‐knockout mice with AKI received pFUS+MSC, but MSC‐derived IL‐10 expression and AKI were similar to using MSC alone. AKI in wild‐type mice receiving pFUS and IL‐10‐deficient MSC was also unimproved compared to administering IL‐10‐deficient MSC alone. Indoleamine 2,3‐dioxygenase (IDO), an anti‐inflammatory enzyme up‐regulated in MSC by IFNγ, was up‐regulated during AKI, but was not further elevated in MSC from pFUS‐treated kidneys, suggesting that IDO is not involved in improved AKI healing by pFUS+MSC. These data suggest IFNγ is up‐regulated by pFUS and after i.v.‐infused MSC home to pFUS‐treated kidneys, IFNγ stimulates additional IL‐10 production by MSC to improve AKI. Analogous mechanisms of ultrasound‐treated tissue microenvironments stimulating therapeutic MSC may exist in other pathologies where adjuvant ultrasound techniques are successful.
The outer membrane protein Tp92 of Treponema pallidum induces human mononuclear cell death and IL‐8 secretion
Authors: Luo Xi , Zhang Xiaohong , Gan Lin , Zhou Chenglong , Zhao Tie , Zeng Tiebing , Liu Shuangquan , Xiao Yongjian , Yu Jian , Zhao Feijun 
Published: September 2018

AbstractTreponema pallidum is the pathogen that causes syphilis, a sexually transmitted disease; however, the pathogenic mechanism of this organism remains unclear. Tp92 is the only T. pallidum outer membrane protein that has structural features similar to the outer membrane proteins of other Gram‐negative bacteria, but the exact functions of this protein remain unknown. In the present study, we demonstrated that the recombinant Tp92 protein can induce human mononuclear cell death. Tp92 mediated the human monocytic cell line derived from an acute monicytic leukemia patient (THP‐1) cell death by recognizing CD14 and/or TLR2 on cell surfaces. After the stimulation of THP‐1 cells by the Tp92 protein, Tp92 may induce atypical pyroptosis of THP‐1 cells via the pro‐caspase‐1 pathway. Meanwhile, this protein caused the apoptosis of THP‐1 cells via the receptor‐interacting protein kinase 1/caspase‐8/aspase‐3 pathway. Tp92 reduced the number of monocytes among peripheral blood mononuclear cells. Interestingly, further research showed that Tp92 failed to increase the tumour necrosis factor‐α, interleukin (IL)‐1β, IL‐6, IL‐10, IL‐18 and monocyte chemotactic protein 1 (MCP)‐1 levels but slightly elevated the IL‐8 levels via the Nuclear Factor (NF)‐κB pathway in THP‐1 cells. The data suggest that Tp92 recognizes CD14 and TLR2, transfers the signal to a downstream pathway, and activates NF‐κB to mediate the production of IL‐8. This mechanism may help T. pallidum escape recognition and elimination by the host innate immune system.
Inhibition of XPO1 enhances cell death induced by ABT‐199 in acute myeloid leukaemia via Mcl‐1
Authors: Luedtke Daniel A. , Su Yongwei , Liu Shuang , Edwards Holly , Wang Yue , Lin Hai , Taub Jeffrey W. , Ge Yubin 
Published: September 2018

AbstractThe antiapoptotic Bcl‐2 family proteins play critical roles in resistance to chemotherapy in acute myeloid leukaemia (AML). The Bcl‐2‐selective inhibitor ABT‐199 (Venetoclax) shows promising antileukaemic activity against AML, though Mcl‐1 limits its antileukaemic activity. XPO1 is a nuclear exporter overexpressed in AML cells and its inhibition decreases Mcl‐1 levels in cancer cells. Thus, we hypothesized that the XPO1‐selective inhibitor KPT‐330 (Selinexor) can synergize with ABT‐199 to induce apoptosis in AML cells through down‐regulation of Mcl‐1. The combination of KPT‐330 and ABT‐199 was found to synergistically induce apoptosis in AML cell lines and primary patient samples and cooperatively inhibit colony formation capacity of primary AML cells. KPT‐330 treatment decreased Mcl‐1 protein after apoptosis initiation. However, binding of Bim to Mcl‐1 induced by ABT‐199 was abrogated by KPT‐330 at the same time as apoptosis initiation. KPT‐330 treatment increased binding of Bcl‐2 to Bim but was overcome by ABT‐199 treatment, demonstrating that KPT‐330 and ABT‐199 reciprocally overcome apoptosis resistance. Mcl‐1 knockdown and overexpression confirmed its critical role in the antileukaemic activity of the combination. In summary, KPT‐330 treatment, alone and in combination with ABT‐199, modulates Mcl‐1, which plays an important role in the antileukaemic activity of the combination.
Cardioprotective cytokine interleukin‐33 is up‐regulated by statins in human cardiac tissue
Authors: Pentz Richard , Kaun Christoph , Thaler Barbara , Stojkovic Stefan , Lenz Max , Krychtiuk Konstantin A. , Zuckermann Andreas , Huber Kurt , Wojta Johann , Hohensinner Philipp J. , Demyanets Svitlana 
Published: September 2018

AbstractInterleukin (IL)‐33 is a member of the IL‐1 family and is able to act cardioprotective. The aim of this study was to investigate the regulation of IL‐33 by 3‐hydroxy‐3‐methylglutaryl‐coenzyme‐A (HMG‐CoA) reductase inhibitors (statins) and bisphosphonates (BPs) in human cardiac tissue. The lipophilic fluvastatin, simvastatin, atorvastatin, and lovastatin as well as the nitrogenous BPs alendronate and ibandronate, but not hydrophilic pravastatin increased IL‐33 mRNA and intracellular IL‐33 protein levels in both human adult cardiac myocytes (HACM) and fibroblasts (HACF). Additionally, fluvastatin reduced soluble ST2 secretion from HACM. IL‐33 was also up‐regulated by the general inhibitor of prenylation perillic acid, a RhoA kinase inhibitor Y‐27632, and by latrunculin B, but statin‐induced IL‐33 expression was inhibited by mevalonate, geranylgeranyl pyrophosphate (GGPP) and RhoA activator U‐46619. The IL‐33 promoter was 2.3‐fold more accessible in statin‐treated HACM compared to untreated cells (P = 0.037). In explanted hearts of statin‐treated patients IL‐33 protein was up‐regulated as compared with the hearts of non‐statin‐treated patients (P = 0.048). As IL‐33 was previously shown to exert cardioprotective effects, one could speculate that such up‐regulation of IL‐33 expression in human cardiac cells, which might happen mainly through protein geranylgeranylation, could be a novel mechanism contributing to known cardioprotective effects of statins and BPs.
Functional protection against cardiac diseases depends on ATP‐sensitive potassium channels
Authors: Ye Peng , Zhu Yan‐Rong , Gu Yue , Zhang  Dai‐Min , Chen Shao‐Liang 
Published: September 2018

AbstractATP‐sensitive potassium channels (KATP) channels are widely distributed in various tissues, including pancreatic beta cells, muscle tissue and brain tissue. KATP channels play an important role in cardioprotection in physiological/pathological situations. KATP channels are inhibited by an increase in the intracellular ATP concentration and are stimulated by an increase in the intracellular MgADP concentration. Activation of KATP channels decreases ischaemia/reperfusion injury, protects cardiomyocytes from heart failure, and reduces the occurrence of arrhythmias. KATP channels are involved in various signalling pathways, and their participation in protective processes is regulated by endogenous signalling molecules, such as nitric oxide and hydrogen sulphide. KATP channels may act as a new drug target to fight against cardiovascular disease in the development of related drugs in the future. This review highlights the potential mechanisms correlated with the protective role of KATP channels and their therapeutic value in cardiovascular diseases.
Oral health‐related quality of life and standard of treatment in aggressive periodontitis patients more than 5 years after therapy
Authors: Bäumer Amelie , Kappesz Dieter , Ozga Ann‐Kathrin , Mertens Christian , Eickholz Peter , Pretzl Bernadette 
Published: September 2018

AbstractObjectivesTo assess OHRQoL in patients with aggressive periodontitis (AgP) after periodontal treatment using the Oral Health Impact Profile‐49 (OHIP‐49) and compare to patients’ dental status.Material and methodsMore than 5 years after therapy, 71 patients were examined and answered the OHIP‐questionnaire. The dental and periodontal status were assessed according to the SSO (Swiss Dental Society) criteria. Descriptive statistics were performed with SPSS, correlation analysis and tests for differences using R 3.2.2.ResultsMore than 90% of all patients showed no probing depths (PD) >5 mm, a bleeding on probing (BOP) index below 35%, and a sufficient function. Four patients showed no visible plaque, PDs ≤ 3 mm, a BOP below 10%, and an optimum function. Non‐smoking and compliant patients exhibited a more favourable status.The OHIP‐49 added up to 24.9 points, representing a comparatively high satisfaction of AgP‐patients with their oral status. The subscale which most patients reported impairment in was “functional limitation.” A correlation between quality standard and the OHIP‐49G could only be shown in the psychological disability subscale.ConclusionAfter treatment, a moderate to high quality level can be retained over more than 5 years. Most patients are satisfied with their oral health. Correlations between the objective and subjective view could not be found, apart from the subscale “psychological disability.”
Omega‐3 polyunsaturated fatty acids exert anti‐oxidant effects through the nuclear factor (erythroid‐derived 2)‐related factor 2 pathway in immortalized mouse Schwann cells
Authors: Tatsumi Yasuaki , Kato Ayako , Sango Kazunori , Himeno Tatsuhito , Kondo Masaki , Kato Yoshiro , Kamiya Hideki , Nakamura Jiro , Kato Koichi 
Published: September 2018

AbstractAims/IntroductionRecent studies advocate that omega‐3 polyunsaturated fatty acids (ω‐3 PUFAs) have direct anti‐oxidative and anti‐inflammatory effects in the vasculature; however, the role of ω‐3 PUFAs in Schwann cells remains undetermined.Materials and methodsImmortalized mouse Schwann (IMS32) cells were incubated with the ω‐3 PUFAs docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). The messenger ribonucleic acid levels of several anti‐oxidant enzymes (heme oxygenase‐1 [Ho‐1], nicotinamide adenine dinucleotide [phosphate] H quinone oxidoreductase 1, catalase, superoxide dismutase and glutathione peroxidase) were identified using real‐time reverse transcription polymerase chain reaction. Ho‐1 and nicotinamide adenine dinucleotide [phosphate] H quinone oxidoreductase 1 protein levels were evaluated using Western blotting. Nuclear factor (erythroid‐derived 2)‐related factor 2 (Nrf2) of the nuclear fraction was also quantified using western blotting. Catalase activity and glutathione content were determined by colorimetric assay kits. Nrf2 promoter‐luciferase activity was evaluated by a dual luciferase assay system.ResultsTreatment with tert‐butyl hydroperoxide decreased cell viability dose‐dependently. DHA or EPA pretreatment significantly alleviated tert‐butyl hydroperoxide‐induced cytotoxicity. DHA or EPA increased the messenger ribonucleic acid levels of Ho‐1, nicotinamide adenine dinucleotide (phosphate) H quinone oxidoreductase 1 and catalase dose‐dependently. Ho‐1 protein level, catalase activity, Nrf2 promoter‐luciferase activity and intracellular glutathione content were significantly increased by DHA and EPA.ConclusionsThese findings show that DHA and EPA can induce Ho‐1 and catalase through Nrf2, thus protecting Schwann cells against oxidative stress. ω‐3 PUFAs appear to exert their neuroprotective effect by increasing defense mechanisms against oxidative stress in diabetic neuropathies.
Extrinsic and intrinsic constraints interact to drive extra‐pair paternities in the Alpine marmot
Authors: Bichet Coraline , Lepetit David , Cohas Aurélie 
Published: September 2018

AbstractTo reproduce, animals have to form pairs and large variations in the degree of mate switching are observed. Extrinsic and intrinsic factors can constrain individual's mate switching. Among intrinsic factors, genes involved in pair‐bonding, such as Avpr‐1a, receive increasing attention. The length of microsatellites present in the regulatory region of Avpr‐1a determines the neural densities and distributions of the vasopressin receptors known to impact pair‐bonding behaviours. For the first time, we investigated whether and how the genetic makeup at Avpr‐1a, an intrinsic factor, and the social context, an extrinsic factor, experienced by wild Alpine marmot (Marmota marmota) females affect the proportion of extra‐pair young. This proportion was positively correlated with the length of their Avpr‐1a regulatory region but only when the social constraints were relaxed, that is when mature male subordinates were present. When ignoring the interactive effect between the length of their Avpr‐1a regulatory region and the social constraints, the genetic makeup at Avpr‐1a was not associated with the proportion of extra‐pair young. Under natural conditions, the genetic regulation of pair‐bonding could be hidden by extrinsic factors constraining mate choice.
Single‐operator cholangioscopy for the treatment of concomitant gallbladder stones and secondary common bile duct stones
Authors: Liu Dan‐qing , Zhang Hang , Xiao Le , Zhang Bing‐yin , Liu Wei‐hui 
Published: September 2018

AbstractBackground and AimThis study aims to assess the clinical validity and safety of single‐operator cholangioscopy system (SOCS) for the treatment of concomitant gallbladder stones and secondary common bile duct (CBD) stones.MethodsThis retrospective study included 10 consecutive patients who had small‐sized stones (< 1 cm) in both the gallbladder and CBD; the patients underwent SOCS treatment from June 2016 to December 2016. The clinical validity of this minimally invasive surgery was determined by the operation success rate, stone removal rate, postoperative hospital stay, hospitalization cost, and contrast images before and after the operation. The clinical safety was evaluated by perioperative complications and outcomes, gallbladder stone recurrence, and gallbladder contractility function.ResultsBoth the technique success rate and the stone removal rate when using SOCS was 100%. There were no serious complications that occurred during the operation; three patients developed acute cholecystitis, and four patients underwent hyperamylasemia after the surgery. The average postoperative hospital stay was 5.8 ± 1.32 days, and the average hospitalization cost was 7466 ± 566.1 dollars. In the follow‐up period, which ranged from 3 to 8 months, there was no stone residuals or recurrences in the gallbladder and CBD, and no patient showed a recurrence of biliary colic. In addition, the gallbladder contractility function was proven to be normal within 3 to 6 months after the operation.ConclusionsSOCS could successfully manage concomitant gallbladder stones and secondary CBD stones and precisely protect normal biliary function.
Variability of the cortisol awakening response and morning salivary oxytocin in late adolescence
Authors: Van Dam Jago M. , Garrett Amy J. , Schneider Luke A. , Buisman‐Pijlman Femke T. A. , Short Michelle A. , Hodyl Nicolette A. , Edwards Hannah K. , Goldsworthy Mitchell R. , Pitcher Julia B. 
Published: September 2018

Exogenously administered oxytocin interacts with the hypothalamic‐pituitary‐adrenal (HPA) axis to modulate endogenous cortisol levels, suggesting a synergistic role for these two hormones in the response to stress, cognitive performance and the development of psycho‐behavioural disorders. The cortisol awakening response (CAR) is considered a reliable measure of HPA axis function in humans. However, the CAR appears to vary considerably from day to day and may be strongly influenced by the anticipated demands of the day ahead. The level of variation intrinsic to the CAR is unclear because few studies have examined the CAR in the absence of daily environmental variation. It is not known whether oxytocin has a similar or complementary awakening response. Therefore, over three consecutive days, we examined 12 adolescents (aged 15‐17 years) in a highly‐controlled sleep laboratory. Saliva was collected on days 4‐6 of a 9‐day laboratory visit. Cortisol and oxytocin levels were determined by an enzyme‐linked immunosorbent assay from saliva sampled at 0, 15, 30 and 45 minutes, and 8 and 12 hours post‐awakening. CAR magnitude varied between days and was associated with sleep duration and pre‐awakening sleep stage. Conversely, oxytocin levels dropped dramatically in the first 15 minutes post‐awakening and were highly consistent across participants and days. Older participants had higher awakening oxytocin concentrations. Although cortisol increases and oxytocin rapidly declines upon awakening, their diurnal variation does not appear to be related at basal, peripheral levels, consistent with a previous finding that exogenously administered oxytocin only modulates cortisol under conditions of stress.
Associations among two vitamin D receptor (VDR) gene polymorphisms (ApaI and TaqI) in acne vulgaris: A pilot susceptibility study
Authors: Swelam Mervat M. , El‐Barbary Rasha A. H. , Saudi Wael M. , Fathi Marwa S. , Soliman Dina A. , Abd Elrehem Heba H. 
Published: September 2018

AbstractBackgroundAcne vulgaris (AV) pathogenesis is multifactorial. Vitamin D (VitD) plays an important role in sebocytes' differentiation and function. Most VitD functions are mediated by the nuclear VitD receptor (VDR) following binding of its biologically active form (1,25 dihydroxyvitamin D3). Genetic variations in VDR gene may cause significant receptor dysfunction and have been found to be associated with many inflammatory skin diseases. Two adjacent single nucleotide polymorphisms of VDR, ApaI (rs7975232) and TaqI (rs731236), were commonly studied.ObjectiveTo evaluate the association between VDR ApaI and TaqI gene polymorphism and AV.MethodsThis case control study included 30 Egyptian acne patients who attended Dermatology Outpatient Clinic of Al‐Zahraa University and Misr University for Science and Technology Hospitals. Thirty age‐ and sex‐matched healthy individuals participated as controls. VDR gene ApaI and TaqI polymorphisms were examined by polymerase chain reaction restriction fragment length polymorphism. Serum 25(OH)D was measured in all participants.ResultsPatients had significant decrease in ApaI A allele and AATT combined genotype (60%, 3.3%) than controls (78.3%, 20%), respectively, and significant increase in TaqI tt genotype and t allele (46.7%, 63.3%) than controls (13.3%, 41.7%), respectively. Patients showed significantly lower serum 25(OH)D3 concentration than controls.ConclusionPolymorphisms of ApaI and TaqI may have a role in the pathogenesis of AV as A allele and AATT combined genotype could be considered protective against acne development and tt genotype and t allele may increase the risk of AV development. VitD deficiency can be considered as a risk factor for AV development.