bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dyspepsia and gastric emptying in end-stage renal disease patients on hemodialysis
Authors: Salles Junior Luiz Derwal , Santos Paulo Roberto , dos Santos Armênio Aguiar , de Souza Marcellus Henrique Loiola Ponte 
Published: December 2013

Abstract

Background
Dyspepsia is common among end-stage renal disease (ESRD) patients and its association with delayed gastric emptying is not well established. We assessed the association of dyspepsia with gastric emptying time in ESRD patients undergoing hemodialysis (HD).

Methods
Dyspepsia was assessed through the Porto Alegre Dyspeptic Symptoms Questionnaire (PADYQ). PADYQ’s scores ≥ 6 classified participants as dyspeptic. The octanoic acid breath test using 13carbon was employed to assess the gastric emptying time. Based on the test, time in minutes to metabolize the first half of the 13carbon in the test meal (t1/2) was calculated. Association of dyspepsia with gastric emptying time was tested by the correlation between PADYQ scores and t1/2, and also by comparing t1/2 between dyspeptics and non-dyspeptics.

Results
There were 34 (68.0%) dyspeptic patients. Dyspepsia score was positively correlated with t1/2 (r = 0.366; p = 0.009). Dyspeptics had longer t1/2 compared to non-dyspeptics, respectively, 238.0 ± 92.9 versus 185.5 ± 45.5 minutes (p = 0.042).

Conclusions
Delayed gastric emptying was associated with dyspepsia. Prokinetic medications could have a role in preventing or relieving dyspeptic symptoms among HD patients. Future research in larger samples is necessary to confirm this association.
Eugenol triggers apoptosis in breast cancer cells through E2F1/survivin down-regulation
Authors: Al-Sharif Ibtehaj , Remmal Adnane , Aboussekhra Abdelilah 
Published: December 2013

Abstract

Background
Breast cancer is a major health problem that threatens the lives of millions of women worldwide each year. Most of the chemotherapeutic agents that are currently used to treat this complex disease are highly toxic with long-term side effects. Therefore, novel generation of anti-cancer drugs with higher efficiency and specificity are urgently needed.

Methods
Breast cancer cell lines were treated with eugenol and cytotoxicity was measured using the WST-1 reagent, while propidium iodide/annexinV associated with flow cytometry was utilized in order to determine the induced cell death pathway. The effect of eugenol on apoptotic and pro-carcinogenic proteins, both in vitro and in tumor xenografts was assessed by immunoblotting. While RT-PCR was used to determine eugenol effect on the E2F1 and survivin mRNA levels. In addition, we tested the effect of eugenol on cell proliferation using the real-time cell electronic sensing system.

Results
Eugenol at low dose (2 μM) has specific toxicity against different breast cancer cells. This killing effect was mediated mainly through inducing the internal apoptotic pathway and strong down-regulation of E2F1 and its downstream antiapoptosis target survivin, independently of the status of p53 and ERα. Eugenol inhibited also several other breast cancer related oncogenes, such as NF-κB and cyclin D1. Moreover, eugenol up-regulated the versatile cyclin-dependent kinase inhibitor p21WAF1 protein, and inhibited the proliferation of breast cancer cells in a p53-independent manner. Importantly, these anti-proliferative and pro-apoptotic effects were also observed in vivo in xenografted human breast tumors.

Conclusion
Eugenol exhibits anti-breast cancer properties both in vitro and in vivo, indicating that it could be used to consolidate the adjuvant treatment of breast cancer through targeting the E2F1/survivin pathway, especially for the less responsive triple-negative subtype of the disease.
Epigenetic silencing of glutaminase 2 in human liver and colon cancers
Authors: Zhang Jianbin , Wang Cheng , Chen Mingquan , Cao Jianping , Zhong Ying , Chen Liting , Shen Han-Ming , Xia Dajing 
Published: December 2013

Abstract

Background
Glutaminase 2 (Gls2) is a p53 target gene and is known to play an important role in energy metabolism. Gls2 has been reported to be downregulated in human hepatocellular carcinomas (HCC). However, the underlying mechanism responsible for its downregulation is still unclear. Here, we investigated Gls2 expression and its promoter methylation status in human liver and colon cancers.

Methods
mRNA expression of Gls2 was determined in human liver and colon cancer cell lines and HCC tissues by real-time PCR and promoter methylation was analyzed by methylation-specific PCR (MSP) and validated by bisulfite genome sequencing (BGS). Cell growth was determined by colony formation assay and MTS assay. Statistical analysis was performed by Wilcoxon matched-pairs test or non-parametric t test.

Results
First, we observed reduced Gls2 mRNA level in a selected group of liver and colon cancer cell lines and in the cancerous tissues from 20 HCC and 5 human colon cancer patients in comparison to their non-cancerous counter parts. Importantly, the lower level of Gls2 in cancer cells was closely correlated to its promoter hypermethylation; and chemical demethylation treatment with 5-aza-2′-deoxycytidine (Aza) increased Gls2 mRNA level in both liver and colon cancer cells, indicating that direct epigenetic silencing suppressed Gls2 expression by methylation. Next, we further examined this correlation in human HCC tissues, and 60% of primary liver tumor tissues had higher DNA methylation levels when compared with adjacent non-tumor tissues. Detailed methylation analysis of 23 CpG sites at a 300-bp promoter region by bisulfite genomic sequencing confirmed its methylation. Finally, we examined the biological function of Gls2 and found that restoring Gls2 expression in cancer cells significantly inhibited cancer cell growth and colony formation ability through induction of cell cycle arrest.

Conclusions
We provide evidence showing that epigenetic silencing of Gls2 via promoter hypermethylation is common in human liver and colon cancers and Gls2 appears to be a functional tumor suppressor involved in the liver and colon tumorigenesis.
Rates and risk factors for drug resistance tuberculosis in Northeastern China
Authors: Liu Qiao , Zhu Limei , Shao Yan , Song Honghuan , Li Guoli , Zhou Yang , Shi Jinyan , Zhong Chongqiao , Chen Cheng , Lu Wei 
Published: December 2013

Abstract

Background
Drug-resistant tuberculosis (TB) has emerged as a major challenge toward TB control and prevention. In Lianyungang city, the extent and trend of drug resistant TB is not well known. The objective of the survey was to assess drug resistance pattern of MTB and risk factors for drug resistant TB, including multidrug resistance tuberculosis (MDR-TB) in this area.

Methods
We performed drug susceptibility testing on Mycobacterium tuberculosis (MTB) isolates with first- and second-line anti-tuberculosis drugs of 1012 culture positive TB cases by using the proportion method, who were consecutively enrolled from January 2011 to December 2012 in Lianyungang city, China. The patterns of drug resistance in MTB were investigated and multiple logistic regression analysis was performed to assess the risk factors for drug resistant TB.

Results
Among the 1012 strains tested, 308 (30.4%) strains were resistant to at least one first-line drug; the prevalence of MDR-TB was 88 (8.7%), 5 (0.5%) strains were found to be extensively drug-resistant tuberculosis (XDR-TB). Female gender was a risk factor for MDR-TB (adjusted odds ratio (aOR) 1.763, 95% CI (1.060-2.934). The aged 28–54 years was significantly associated with the risk of MDR-TB with an aOR: 2.224, 95% CI (1.158-4.273) when compared with those 65 years or older. Patients with previous treatment history had a more than 7-fold increased risk of MDR-TB, compared with those never previously treated.

Conclusions
The burden of drug resistant TB cases is sizeable, which highlights an urgent need to reinforce control, detection and treatment strategies for drug resistant TB.
Factors associated with HIV infection among children born to mothers on the prevention of mother to child transmission programme at Chitungwiza Hospital, Zimbabwe, 2008
Authors: Ngwende Stella , Gombe Notion T , Midzi Stanley , Tshimanga Mufuta , Shambira Gerald , Chadambuka Addmore 
Published: December 2013

Abstract

Background
Zimbabwe is one of the five countries worst affected by the HIV/AIDS pandemic with HIV infection contributing increasingly to childhood morbidity and mortality. Among the children born to HIV positive mothers participating in the PMTCT programme, 25% tested positive to HIV. We investigated factors associated with HIV infection among children born to mothers on the PMTCT programme.

Methods
A 1:1 unmatched case–control study was conducted at Chitungwiza Hospital, Zimbabwe, 2008. A case was defined as a child who tested HIV positive, born to a mother who had been on PMTCT programme. A control was a HIV negative child born to a mother who had been on PMTCT programme. An interviewer-administered questionnaire was used to collect data on demographic characteristics, risk factors associated with HIV infection and immunization status.

Results
A total of 120 mothers were interviewed. Independent risk factors associated with HIV infection among children included maternal CD4 count of less than 200 during pregnancy [aOR = 7.1, 95% CI (2.6-17)], mixed feeding [aOR = 29, 95% CI (4.2-208)], being hospitalized since birth [aOR = 2.9, 95% CI (1.2-4.8)] whilst being exclusively breast fed for less than 6 months [aOR = 0.1 (95% CI 0.03-0.4)] was protective.

Conclusions
HIV infection among children increased if the mother’s CD4 count was ≤200 cells/μL and if the child was exposed to mixed feeding. Breastfeeding exclusively for less than six months was protective. We recommended exclusive breast feeding period for the first six months and stop breast feeding after 6 months if affordable, sustainable and safe.
Matrix forming characteristics of inner and outer human meniscus cells on 3D collagen scaffolds under normal and low oxygen tensions
Authors: Croutze Roger , Jomha Nadr , Uludag Hasan , Adesida Adetola 
Published: December 2013

Abstract

Background
Limited intrinsic healing potential of the meniscus and a strong correlation between meniscal injury and osteoarthritis have prompted investigation of surgical repair options, including the implantation of functional bioengineered constructs. Cell-based constructs appear promising, however the generation of meniscal constructs is complicated by the presence of diverse cell populations within this heterogeneous tissue and gaps in the information concerning their response to manipulation of oxygen tension during cell culture.

Methods
Four human lateral menisci were harvested from patients undergoing total knee replacement. Inner and outer meniscal fibrochondrocytes (MFCs) were expanded to passage 3 in growth medium supplemented with basic fibroblast growth factor (FGF-2), then embedded in porous collagen type I scaffolds and chondrogenically stimulated with transforming growth factor β3 (TGF-β3) under 21% (normal or normoxic) or 3% (hypoxic) oxygen tension for 21 days. Following scaffold culture, constructs were analyzed biochemically for glycosaminoglycan production, histologically for deposition of extracellular matrix (ECM), as well as at the molecular level for expression of characteristic mRNA transcripts.

Results
Constructs cultured under normal oxygen tension expressed higher levels of collagen type II (p = 0.05), aggrecan (p < 0.05) and cartilage oligomeric matrix protein, (COMP) (p < 0.05) compared to hypoxic expanded and cultured constructs. Accumulation of ECM rich in collagen type II and sulfated proteoglycan was evident in normoxic cultured scaffolds compared to those under low oxygen tension. There was no significant difference in expression of these genes between scaffolds seeded with MFCs isolated from inner or outer regions of the tissue following 21 days chondrogenic stimulation (p > 0.05).

Conclusions
Cells isolated from inner and outer regions of the human meniscus demonstrated equivalent differentiation potential toward chondrogenic phenotype and ECM production. Oxygen tension played a key role in modulating the redifferentiation of meniscal fibrochondrocytes on a 3D collagen scaffold in vitro.
BioSuper: A web tool for the superimposition of biomolecules and assemblies with rotational symmetry
Authors: Rueda Manuel , Orozco Modesto , Totrov Maxim , Abagyan Ruben 
Published: December 2013

Abstract

Background
Most of the proteins in the Protein Data Bank (PDB) are oligomeric complexes consisting of two or more subunits that associate by rotational or helical symmetries. Despite the myriad of superimposition tools in the literature, we could not find any able to account for rotational symmetry and display the graphical results in the web browser.

Results
BioSuper is a free web server that superimposes and calculates the root mean square deviation (RMSD) of protein complexes displaying rotational symmetry. To the best of our knowledge, BioSuper is the first tool of its kind that provides immediate interactive visualization of the graphical results in the browser, biomolecule generator capabilities, different levels of atom selection, sequence-dependent and structure-based superimposition types, and is the only web tool that takes into account the equivalence of atoms in side chains displaying symmetry ambiguity. BioSuper uses ICM program functionality as a core for the superimpositions and displays the results as text, HTML tables and 3D interactive molecular objects that can be visualized in the browser or in Android and iOS platforms with a free plugin.

Conclusions
BioSuper is a fast and functional tool that allows for pairwise superimposition of proteins and assemblies displaying rotational symmetry. The web server was created after our own frustration when attempting to superimpose flexible oligomers. We strongly believe that its user-friendly and functional design will be of great interest for structural and computational biologists who need to superimpose oligomeric proteins (or any protein). BioSuper web server is freely available to all users at http://ablab.ucsd.edu/BioSuper.
Effects of miR-193a and sorafenib on hepatocellular carcinoma cells
Authors: Salvi Alessandro , Conde Isabel , Abeni Edoardo , Arici Bruna , Grossi Ilaria , Specchia Claudia , Portolani Nazario , Barlati Sergio , De Petro Giuseppina 
Published: December 2013

AbstractBackgroundHepatocellular carcinoma (HCC) is a challenging malignancy of global importance, it is the third most common cause of cancer-related mortality worldwide. In the last years the multikinase inhibitor sorafenib has been used for advanced HCC, but some patients do not benefit from this therapy; thus, novel therapeutic options based on molecular approaches are urgently needed. microRNAs are short non coding RNAs involved in several physiological and pathological conditions including HCC and increasing evidence describes miRs as good tools for the molecular targeted therapies in HCC. The purpose of this study was to identify novel approaches to sensitize the HCC cells to sorafenib by microRNAs targeting urokinase-type plasminogen activator (uPA).MethodsThe miR-193a was validated as negative regulator of urokinase-type plasminogen activator (uPA) in 2 HCC undifferentiated cell lines by transient transfection of miR and anti-miR molecules. The molecular interaction between miR-193a and uPA mRNA target was verified by luciferase reporter assay. The miR-193a expression level was evaluated by stem-loop real time PCR in tumoral tissues from 39 HCC patients. The HCC cells were co-treated with sorafenib and miR-193a and the effects on cellular proliferation, apoptosis were tested. The effect of sorafenib on c-met expression levels was assessed by western blotting.ResultsThe miR-193a has resulted a negative regulator of uPA in both the HCC cell lines tested. The miR-193a expression has resulted dysregulated in tumoral tissues from 39 HCC patients. We found miR-193a down-regulation in HCC respect to peritumoral (PT) tissues and more in the cirrhotic HCCs than in non-cirrhotic ones. Transfection of HA22T/VGH HCC cells with miR-193a decreased proliferation and increased apoptosis, and combined treatment with miR-193a and sorafenib led to further proliferation inhibition.ConclusionsOur results present new advances in the post-transcriptional miR-mediated mechanisms of uPA and they suggest a new strategy to impair the aggressive behavior of HCC cells. Our findings could be helpful to explore novel approaches for multi-target and multi-agent therapies of the HCC.
Annealing temperature effect on self-assembled Au droplets on Si (111)
Authors: Sui Mao , Li Ming-Yu , Kim Eun-Soo , Lee Jihoon 
Published: December 2013

Abstract
We investigate the effect of annealing temperature on self-assembled Au droplets on Si (111). The annealing temperature is systematically varied while fixing other growth parameters such as deposition amount and annealing duration clearly to observe the annealing temperature effect. Self-assembled Au droplets are fabricated by annealing from 50°C to 850°C with 2-nm Au deposition for 30 s. With increased annealing temperatures, Au droplets show gradually increased height and diameter while the density of droplets progressively decreases. Self-assembled Au droplets with fine uniformity can be fabricated between 550°C and 800°C. While Au droplets become much larger with increased deposition amount, the extended annealing duration only mildly affects droplet size and density. The results are systematically analyzed with cross-sectional line profiles, Fourier filter transform power spectra, height histogram, surface area ratio, and size and density plots. This study can provide an aid point for the fabrication of nanowires on Si (111).
Involvement of interleukin-1β in the autophagic process of microglia: relevance to Alzheimer’s disease
Authors: François Arnaud , Terro Faraj , Janet Thierry , Bilan Agnès Rioux , Paccalin Marc , Page Guylène 
Published: December 2013

Abstract

Background
Autophagy is a major pathway of protein and organelle degradation in the lysosome. Autophagy exists at basal constitutive level and can be induced as a defense mechanism under stress conditions. Molecular relationships between autophagy and inflammation at the periphery were recently evidenced, highlighting a role of autophagy in the regulation of inflammation. Impairment of autophagy (with accumulation of autophagic vacuoles) and substantial inflammation are found in neurodegenerative diseases such as Alzheimer’s Disease (AD). However, the links between autophagy and inflammation in AD remain to be determined.

Methods
Here, we examined the inflammatory reaction and autophagy in murine tri-cultures of neurons, astrocytes, and microglia. Tri-cultures were exposed to various inflammatory stresses (lipopolysaccharide (LPS), amyloid peptide (Aβ42) with or without cytokines) for 48 hours. Furthermore, the relationships between inflammation and autophagy were also analyzed in astrocyte- and microglia-enriched cultures. Data for multiple variable comparisons were analyzed by a one-way ANOVA followed by a Newman-keuls’ test.

Results
Aβ42 induced a low inflammation without accumulation of acidic vesicles contrary to moderate or severe inflammation induced by LPS or the cytokine cocktail (IL-1β, TNF-α, and IL-6) or IL-1β alone which led to co-localization of p62 and LC3, two markers of autophagy, with acidic vesicles stained with Lyso-ID Red dye. Moreover, the study reveals a major role of IL-1β in the induction of autophagy in tri-cultures in the presence or absence of Aβ42. However, the vulnerability of the autophagic process in purified microglia to IL-1β was prevented by Aβ42.

Conclusion
These findings show a close relationship between inflammation and autophagy, in particular a major role of IL-1β in the induction of the microglial autophagy which could be the case in AD. New therapeutic strategies could target inflammasome and autophagy in microglia to maintain its role in the amyloid immunosurveillance.
Efficacy and safety of acupuncture for chronic dizziness: study protocol for a randomized controlled trial
Authors: Xue Zhe , Liu Cun-Zhi , Shi Guang-Xia , Liu Yan , Li Zhao-Xin , Zhang Zhen-Hua , Wang Lin-Peng 
Published: December 2013

Abstract

Background
Dizziness is one of the most challenging symptoms in medicine. No medication for dizziness in current use has well-established curative or prophylactic value or is suitable for long-term palliative use. Unconventional remedies, such as acupuncture, should be considered and scientifically evaluated. However, there has been relatively little evidence in randomized controlled clinical trials on acupuncture to treat chronic dizziness. The aim of our study is to evaluate the efficacy and safety of acupuncture in patients with dizziness.

Methods/Design
This trial is a randomized, single-blind, controlled study. A total of 80 participants will be randomly assigned to two treatment groups receiving acupuncture and sham acupuncture treatment, respectively, for 4 weeks. The primary outcome measures are the Dizziness Handicap Inventory (DHI) and the Vertigo Symptom Scale (VSS). Treatment will be conducted over a period of 4 weeks, at a frequency of two sessions per week. The assessment is at baseline (before treatment initiation), 4 weeks after the first acupuncture session, and 8 weeks after the first acupuncture session.

Discussion
The results from this study will provide clinical evidence on the efficacy and safety of acupuncture in patients with chronic dizziness.

Trial registration
International Standard Randomized Controlled Trial Number Register: ISRCTN52695239
A complicated case of pachydermoperiostosis with spondyloarthritides: a case report
Authors: Zhang Qing , Shen Min , Yang Bo , Yu Keyi 
Published: December 2013

Abstract

Introduction
Pachydermoperiostosis is a rare, hereditary disease commonly presenting with digital clubbing, pachydermia and periosteal hypertrophy. Therapeutic options for pachydermoperiostosis are few because of the unknown pathogenesis. Here, we report the complicated case of a patient with pachydermoperiostosis combined with spondyloarthritides, who was refractory to steroids and tumor necrosis factor alpha antagonists. We treated this patient with zoledronic acid and performed an arthroscopic synovectomy, with a satisfactory outcome. To the best of our knowledge, this is the first report in English on the combination of zoledronic acid administration and synovectomy for the treatment of a patient with pachydermoperiostosis and spondyloarthritides.

Case presentation
An 18-year-old Han Chinese man was diagnosed with pachydermoperiostosis in the presence of digital clubbing, periostitis and swollen limbs. Combined spondyloarthritides was also considered based on his lower back pain, lower limbs synovitis, bilateral sacroiliac sclerosis and a positive test for human leukocyte antigen B27, as well as immunoglobulin A nephropathy. He was refractory to steroids and tumor necrosis factor alpha antagonists, but treated with intravenous zoledronic acid and an arthroscopic synovectomy, with a satisfactory outcome.

Conclusion
This is a rare, complicated case of pachydermoperiostosis with spondyloarthritides. Combination therapy of zoledronic acid administration with synovectomy is a novel, convenient and effective option for patients with pachydermoperiostosis with remarkable synovitis.