bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acteoside inhibits autophagic apoptosis of retinal ganglion cells to rescue glaucoma‐induced optic atrophy
Authors: Chen Qianbo , Xi Xiaoting , Zeng Yong , He Zhendan , Zhao Jianfeng , Li Yan 
Published: April 2019

AbstractBackgroundGlaucoma is the world's second biggest cause of blindness, and patients progressively lose their eyesight. The current clinical treatment for glaucoma involves controlling intraocular pressure with drugs or surgery; however, some patients still progressively lose their eyesight. This treatment is also similar to the treatment of traumatic optic neuropathy. Thus, saving retinal ganglion cells (RGCs) from apoptosis is essential.MethodsThe role of Acteoside on autophagy modulation in the 661 W cell line.ResultsIn this study, we first find that Acteoside inhibits autophagy, Rapamycin alleviates this inhibition and the PI3K inhibitor, 3‐MA or LY294002, synergistically promotes it. In a mechanistic study, we find that Optineurin (OPTN) mediates Acteoside regulation of autophagy. OPTN overexpression or knockdown activates or inhibits autophagy, respectively. OPTN is inhibited by autophagy inhibitors, such as Acteoside and 3‐MA and is promoted by the autophagy activator, Rapamycin. Meanwhile, PI3K and AKT are elevated by Acteoside and 3‐MA and inhibited by Rapamycin. Finally, we find that Acteoside inhibits apoptosis in parallel to autophagy and that this inhibition is also mediated by OPTN.ConclusionIn summary, we conclude that Acteoside inhibits autophagy‐induced apoptosis in RGCs through the OPTN and PI3K/AKT/mTOR pathway, and glaucoma patients may benefit from Acteoside treatment alone or in combination with other autophagy inhibitors.
Dendrobium candidum protects against diabetic kidney lesions through regulating vascular endothelial growth factor, Glucose Transporter 1, and connective tissue growth factor expression in rats
Authors: Chang Jingzhi , Zhou Yuanting , Cong Guobin , Guo Hui , Guo Yali , Lu Kun , Li Yi chuan , Tian Hua 
Published: April 2019

AbstractDiabetes mellitus (DM) remains a great health problem with approximate 30% of patients with DM eventually suffering from diabetic nephropathy. The search for exogenous protective factors has recently received wide attention. The current study aimed to investigate the protective effects of Dendrobium candidum (DC) on kidneys in diabetic rats. Initially, streptozotocin‐induced diabetic rats were established and randomly divided into the model group, DC group (0.2, 0.4, and 0.8 g/kg) and irbesartan group (17.5 mg/kg). The biochemical indexes, pathological changes, and the expressions of vascular endothelial growth factor (VEGF), GLUT‐1, and CTGF were examined. It was found that as compared with the model group, the kidney index, serum creatine, blood urea nitrogen, 24‐hour urine protein, and VEGF of DC treatment groups were significantly decreased, and pathological changes in kidney were improved in the DC groups and irbesartan group (
P < 0.05 for each parameter). The protein and messenger RNA levels of GLUT‐1 and CTGF in treatment groups were significantly lower than those in rats' renal cortex without treatment. Our data suggest that DC may protect the kidneys of diabetic rats via regulating expression of VEGF, GLUT‐1, and CTGF.
Association of 584C/T polymorphism in endothelial lipase gene with risk of coronary artery disease
Authors: Elnaggar Ismail Zaki , Hussein Samia , Amin Mohamed Ibrahem , Abdelaziz Eman Ahmed 
Published: April 2019

AbstractBackgroundCoronary artery disease (CAD) is one of the cardiovascular diseases, which is caused by a reduced amount of oxygen and blood that goes to the heart. CAD includes stable angina, unstable angina, myocardial infarction, and sudden cardiac death. It is a common cause of death in both men and women. The environmental and genetic factors are involved in the development of CAD. Multiple gene polymorphisms are risk factors of CAD.ObjectiveTo evaluate the association between EL 584C/T polymorphism, CAD risk, and lipid profile in an Egyptian population.MethodsThis is a case‐control study. The patients were classified into three groups: Group A: Control group, this group included 42 apparently healthy people. Group B: included 42 subjects diagnosed with previous myocardial infarction (MI). Group C: included 42 subjects diagnosed with unstable angina (UA).ResultsThe frequencies of TT and CT genotypes and T allele were higher in control healthy individuals than CAD patients. In addition, the risk of CAD was significantly lower in individuals carrying T allele (P = 0.001). Serum high‐density lipoprotein (HDL) levels were significantly higher in healthy individuals and CAD patients (MI and UA patients) carrying EL 584 T allele compared with those carrying CC genotype (P ≤  0.001). By multiple logistic regression, we found that the protective effect of T allele remained significant (P = 0.005) and it decreased the risk of CAD independent of plasma HDL levels.ConclusionThere was a significant difference between 584C/T polymorphism in the EL gene and CAD and HDL level. T‐allele carriers had a higher HDL level and were protected from CAD. T allele was significantly associated with the decreased risk of CAD independent of plasma HDL levels.
Protective effect of ulinastatin on hepatic ischemia reperfusion injury through autophagy activation in Chang liver cells
Authors: Zhao Yiming , Cai Huabo , Zhou Pengmin , Lin Shengping , Pan Yun , Liang Xiao 
Published: April 2019

AbstractThis study aimed to investigate the protective effect of ulinastatin in hepatic ischemia‐reperfusion progress, involving its association with the role of autophagy during hypoxia‐induced hypoxia‐reoxygenation injury in vitro. The model of hepatic hypoxia/reoxygenation (H/R) injury in Chang liver cells was established. After treatment with ulinastatin at the doses of 10, 100, and 1000 U/mL in H/R liver cells, the cell proliferation was significantly increased, morphological damage was reduced, and the cell apoptosis rate was decreased. The protein levels of antiapoptotic myeloid cell leukemia‐1 (Mcl‐1) and caspase‐3 were upregulated, and C‐PARP protein was downregulated. Meanwhile, ulinastatin led to an increase in the messenger RNA and protein levels of autophagy maker Unc‐like kinase 1 (ULK1), Beclin‐1, and microtubule‐associated protein 1 light chain 3 (LC‐3) and a decrease in p62. Then, 3‐methyladenine (3‐MA), an inhibitor of autophagy, made morphological damage and cell apoptosis worsen in ulinastatin‐treated H/R liver cells. And the expression levels of caspase‐3, C‐PARP, p62, Beclin‐1, and LC‐3, proteins were also reversed by 3‐MA. Taken together, our results demonstrate that ulinastatin inhibited the hepatic H/R injury in Chang liver cells, which was, to some extent, related to the autophagy activation.
Thyroid function following breast cancer chemotherapy: A systematic review
Authors: Mortezaee Keywan , Ahmadi Amirhossein , Haghi‐Aminjan Hamed , Khanlarkhani Neda , Salehi Ensieh , Shabani Nashtaei Maryam , Farhood Bagher , Najafi Masoud , Sahebkar Amirhossein 
Published: April 2019

AbstractBackgroundChemotherapy, as a systemic therapy, is one of the most effective modalities for cancer treatment. However, the use of chemotherapeutic drugs in patients with breast cancer can lead to thyroid dysfunction. This systematic review summarizes the available data on thyroid function following breast cancer chemotherapy.MethodsTo illuminate the thyroid toxicities induced by different chemotherapy regimens in patients with breast cancer, a systematic search was done in accordance with Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guideline in Scopus, Embase, PubMed and Web of Science electronic databases up to December 2018. On the basis of a set of prespecified inclusion and exclusion criteria, eight eligible articles providing data on thyroid function following chemotherapy in patients with breast cancer were included in the study.ResultsAccording to the obtained results, it was found that for most cases, the levels of triiodothyronine (T3), free T3 (FT3), thyroxin (T4) and free T4 (FT4) hormones decrease following breast cancer chemotherapy regimens used in these eligible studies. However, alteration of thyroid‐stimulating hormone (TSH) level after breast cancer chemotherapy was not clear.ConclusionThe findings showed that thyroid function and TSH hormone level can change in patients with breast cancer receiving different chemotherapy regimens.
LEM domain containing 1 promotes proliferation via activating the PI3K/Akt signaling pathway in gastric cancer
Authors: Li Qiang , Ge Yugang , Chen Xiaofeng , Wang Lu , Xia Yiwen , Xu Zhipeng , Li Zheng , Wang Weizhi , Yang Li , Zhang Diancai , Xu Zekuan 
Published: April 2019

AbstractGastric cancer (GC) is one of the most common cancers worldwide and has especially high morbidity and mortality in China. LEM domain containing 1 (LEMD1), an important cancer‐testis antigen, has been reported to be overexpressed in various cancers and promotes the progression of cancers. However, the biological characteristics of LEMD1 remain to be explored in GC. The connection between LEMD1 expression and GC progression was analyzed by using The Cancer Genome Atlas datasets and our human microarray datasets. A Kaplan‐Meier plot was used to analyze the relationship between LEMD1 expression and prognosis. The expression of LEMD1 was analyzed by quantitative real‐time polymerase chain reaction and Western blot, and the proliferation ability of GC cells was analyzed by cell proliferation and colony formation assays and 5‐ethynyl‐2′‐deoxyuridine analysis. The cell cycle and apoptosis were analyzed by flow cytometry. Furthermore, subcutaneously implanted tumor models in nude mice were used to demonstrate the role of LEMD1 in promoting tumor proliferation in vivo. In this study, we demonstrated that the LEMD1 expression level was increased in GC tissues and cells compared with normal tissues and GES‐1. The in vivo and in vitro assays showed that LEMD1 promoted GC cell proliferation by regulating the cell cycle and apoptosis. Moreover, we showed that LEMD1 regulated cell proliferation by activating the phosphatidylinositol 3 kinase (PI3K) / protein kinase B (AKT) signaling pathway. Overall, the results of our study suggest that LEMD1 contributes to GC proliferation by regulating the cell cycle and apoptosis via activation of the PI3K/AKT signaling pathway. LEMD1 may act as a potential target for GC treatment.
1α,25(OH)2D3 alleviates high glucose–induced lipid accumulation in rat renal tubular epithelial cells by inhibiting SREBPs
Authors: Xu Miao , Jiang Fei , Li Bingyan , Zhang Zengli 
Published: April 2019

AbstractLipid accumulation is a vital event in the progression of diabetic nephropathy. 1,25‐Dihydroxyvitamin D3 (1α,25(OH)2D3) is considered to have a protective effect on diabetic nephropathy. However, it remains unclear whether 1α,25(OH)2D3 can inhibit lipid accumulation, and the potential mechanisms responsible for lipid metabolism are incompletely understood. In this study, we evaluated the effects of 1α,25(OH)2D3 on lipid metabolism in high glucose–exposed rat renal tubular epithelial NRK‐52E cells. Results indicated that high glucose–enhanced lipid accumulation in NRK‐52E cells and 1α,25(OH)2D3 can remarkably decrease high glucose–induced lipid accumulation. Western blot showed that 1α,25(OH)2D3 alleviated high glucose–induced upregulation of sterol regulatory element‐binding protein‐1c (SREBP‐1c) and SREBP2, along with their established target genes fatty acid synthase (FASN) and hydroxymethylglutaryl CoA reductases (HMGCR). Overall, these findings suggest that 1α,25(OH)2D3 downregulated the expressions of SREBPs to inhibit high glucose–induced lipid accumulation, which provides new sights into the protective effects of 1α,25(OH)2D3 on diabetic nephropathy.
Circular RNA circ_001350 regulates glioma cell proliferation, apoptosis, and metastatic properties by acting as a miRNA sponge
Authors: Liu Yang , Ma Chunjie , Qin Xiangying , Yu Haiming , Shen Lei , Jin Haifeng 
Published: April 2019

AbstractGlioma is an aggressive malignancy with increasing incidence and threatens people's health worldwide. Accumulating evidence revealed that circular RNAs (circRNAs) play important functions in cancers. A previous study demonstrated that circ_001350 was elevated in glioma tissue samples than nontumorous tissue specimens screened by high‐throughput microarray. The level of circ_001350 in glioma tissue specimens and cell lines was detected by quantitative real‐time polymerase chain reaction. The Fisher exact test was carried out to estimate the correlation of circ_001350 level with clinical characteristics. Cell proliferation, apoptosis, and motility abilities were detected using cell counting kit‐8, clonogenic, flow cytometry, and transwell experiments, respectively. The potential target of circ_001350 was identified by the luciferase assay. circ_001350 level was significantly enhanced in glioma tissue specimens and cells. Further, elevated expression of circ_001350 was closely linked to patients' clinical severity. Knockdown of circ_001350 could inhibit cell proliferation and metastatic properties and increase apoptotic cells. circ_001350 could directly bind to miR‐1236 and regulate its expression to exert oncogenic functions. Collectively, circ_001350 directly sponges miR‐1236, thus contributing to malignant progression of glioma.
Amelioration of muscle wasting by glucagon‐like peptide‐1 receptor agonist in muscle atrophy
Authors: Hong Yeonhee , Lee Jong Han , Jeong Kwang Won , Choi Cheol Soo , Jun Hee‐Sook 
Published: April 2019

AbstractBackgroundSkeletal muscle atrophy is defined as a reduction of muscle mass caused by excessive protein degradation. However, the development of therapeutic interventions is still in an early stage. Although glucagon‐like peptide‐1 receptor (GLP‐1R) agonists, such as exendin‐4 (Ex‐4) and dulaglutide, are widely used for the treatment of diabetes, their effects on muscle pathology are unknown. In this study, we investigated the therapeutic potential of GLP‐1R agonist for muscle wasting and the mechanisms involved.MethodsMouse C2C12 myotubes were used to evaluate the in vitro effects of Ex‐4 in the presence or absence of dexamethasone (Dex) on the regulation of the expression of muscle atrophic factors and the underlying mechanisms using various pharmacological inhibitors. In addition, we investigated the in vivo therapeutic effect of Ex‐4 in a Dex‐induced mouse muscle atrophy model (20 mg/kg/day i.p.) followed by injection of Ex‐4 (100 ng/day i.p.) for 12 days and chronic kidney disease (CKD)‐induced muscle atrophy model. Furthermore, we evaluated the effect of a long‐acting GLP‐1R agonist by treatment of dulaglutide (1 mg/kg/week s.c.) for 3 weeks, in DBA/2J‐mdx mice, a Duchenne muscular dystrophy model.ResultsEx‐4 suppressed the expression of myostatin (MSTN) and muscle atrophic factors such as F‐box only protein 32 (atrogin‐1) and muscle RING‐finger protein‐1 (MuRF‐1) in Dex‐treated C2C12 myotubes. The suppression effect was via protein kinase A and protein kinase B signalling pathways through GLP‐1R. In addition, Ex‐4 treatment inhibited glucocorticoid receptor (GR) translocation by up‐regulating the proteins of GR inhibitory complexes. In a Dex‐induced muscle atrophy model, Ex‐4 ameliorated muscle atrophy by suppressing muscle atrophic factors and enhancing myogenic factors (MyoG and MyoD), leading to increased muscle mass and function. In the CKD muscle atrophy model, Ex‐4 also increased muscle mass, myofiber size, and muscle function. In addition, treatment with a long‐acting GLP‐1R agonist, dulaglutide, recovered muscle mass and function in DBA/2J‐mdx mice.ConclusionsGLP‐1R agonists ameliorate muscle wasting by suppressing MSTN and muscle atrophic factors and enhancing myogenic factors through GLP‐1R‐mediated signalling pathways. These novel findings suggest that activating GLP‐1R signalling may be useful for the treatment of atrophy‐related muscular diseases.
A cross‐sectional study of stool form (using Bristol stool chart) in an urban South Indian population
Authors: Srinivas Melpakkam , Srinivasan Vijaya , Jain Mayank , Rani Shanthi Coimbatore Subramanian , Mohan Viswanathan , Jayanthi Venkataraman 
Published: April 2019

BackgroundThere is paucity of data on Bristol stool form (BSF) in healthy South Indian residents.AimTo determine the BSF types and associated factors in an urban bowel health noncomplainant population.MethodsThis cross‐sectional study, performed using a self‐administered questionnaire among adult Chennai residents, compared BSF types by gender for various factors (age, occupation, bowel frequency, and defecation‐related abdominal pain). BSF types 1/2 and 6/7 were grouped as hard and loose stools, respectively. The statistical tests used were proportion test, χ2, and Kruskal–Wallis tests (P < 0.05 deemed significant).ResultsThe study cohort of 1402 subjects included 748 (53.3%) men and a third each of professionals, semiprofessionals, and “non‐office goers” (homemakers, retirees, students, and unemployed). A total of 97% had daily bowel movement, and 8.5% reported defecation associated abdominal pain. The BSF types in decreasing prevalence were: Type 3 (35.6%), Type 4 (32.5%), Types 1 or 2 (20.5%), Type 5 (6.9%), and Types 6 or 7 (4.5%). On gender comparison, significantly more men passed hard (P = 0.03) or loose stools (P = 0.001), while more women passed Type 3 (P = 0.0002). Loose stools in men were associated with abdominal pain (P = 0.0035). Women passing hard or loose stool types were slightly older (median age in 30s vs. 20s in Types 3–5) and had reduced stool frequency (P = 0.026: hard; P = 0.006: loose).ConclusionsThis South Indian noncomplainant cohort's most common stool types were BSF Types 3 and 4, with few gender variations in extreme stool types.
Recent advances in understanding the molecular genetic basis of mitochondrial disease
Authors: Thompson Kyle , Collier Jack J. , Glasgow Ruth I. C. , Robertson Fiona M. , Pyle Angela , Blakely Emma L. , Alston Charlotte L. , Oláhová Monika , McFarland Robert , Taylor Robert W. 
Published: April 2019

AbstractMitochondrial disease is hugely diverse with respect to associated clinical presentations and underlying genetic causes, with pathogenic variants in over 300 disease genes currently described. Approximately half of these have been discovered in the last decade due to the increasingly widespread application of next generation sequencing technologies, in particular unbiased, whole exome—and latterly, whole genome sequencing. These technologies allow more genetic data to be collected from patients with mitochondrial disorders, continually improving the diagnostic success rate in a clinical setting. Despite these significant advances, some patients still remain without a definitive genetic diagnosis. Large datasets containing many variants of unknown significance have become a major challenge with next generation sequencing strategies and these require significant functional validation to confirm pathogenicity. This interface between diagnostics and research is critical in continuing to expand the list of known pathogenic variants and concomitantly enhance our knowledge of mitochondrial biology. The increasing use of whole exome sequencing, whole genome sequencing and other “omics” techniques such as transcriptomics and proteomics will generate even more data and allow further interrogation and validation of genetic causes, including those outside of coding regions. This will improve diagnostic yields still further and emphasizes the integral role that functional assessment of variant causality plays in this process—the overarching focus of this review.
Entrepreneurial motivation: A review of the literature and an agenda for future research
Authors: Murnieks Charles Y. , Klotz Anthony C. , Shepherd Dean A. 
Published: April 2019

SummaryGiven the substantial impact that new ventures have on the global economy, understanding what motivates entrepreneurs is of both practical and theoretical importance. Although research on the nature, causes, and consequences of entrepreneurial motivation has grown rapidly, it has evolved in distinct theoretical silos that tend to isolate motives based on the phase of business development (e.g., initiation, growth, and exit) rather than acknowledge that individuals often traverse all these phases and experience multiple types of motivation throughout their entrepreneurial journey. To advance the study of motivation in the fields of entrepreneurship and organizational behavior and provide a means through which these advancements can contribute to our understanding of how motivation drives the start‐up, growth, and exiting of businesses, we organize and review the extant literature on entrepreneurial motives based on the phases of the new venture process. In doing so, this article develops a roadmap of the current state of entrepreneurial motivation research and its nomological network and provides suggestions to guide future research in extending our understanding of motivation in the entrepreneurship domain as well as in traditional organizational settings.
Effects of a rotational UV‐C irradiation system and packaging on the shelf life of fresh pistachio
Authors: Hosseini Fereshteh‐Sadat , Akhavan Hamid‐Reza , Maghsoudi Hossein , Hajimohammadi‐Farimani Reza , Balvardi Mohammad 
Published: April 2019

AbstractBACKGROUNDIn this study, fresh pistachio was exposed to UV‐C irradiation (2.1 and 4.5 kJ m−2) in a rotating cylindrical system with seven germicidal UV‐C lamps and immediately packed in perforated and non‐perforated polyethylene terephthalate (PET). The fruit were evaluated for weight loss, total phenolic content, enzyme activities, color indices (L*, a*, b* and browning index), and microbial counts during 35 days of storage at 4 °C.RESULTSUV‐C treatment caused a significant decrease (P < 0.05) in the weight loss of fresh pistachios compared to the control. The activity of catalase and peroxidase enzymes was significantly higher (P < 0.05) in irradiated samples packed in non‐perforated PET in comparison to those of untreated samples. Irradiation did not inhibit the activity of polyphenol oxidase in treated samples, although a slight decrease in polyphenol oxidase activity was observed in irradiated samples compared to control. The fruit treated with 2.1 kJ m−2 of UV‐C and the control packed in non‐perforated PET were lighter (L*), redder (a*), and less yellow (b*) compared to 4.5 kJ m−2 treated samples. Furthermore, a dose of 4.5 kJ m−2 UV‐C significantly decreased sensory attributes of fresh pistachios compared to the other irradiation level and control.CONCLUSIONUV‐C irradiation at a dose of 2.1 kJ m−2 and packing in non‐perforated PET are recommended for fresh pistachio preservation based on the physicochemical, microbial, and sensory parameters. © 2019 Society of Chemical Industry