bluuebunny/crossref_metadata_2025_split huggingface dataset:
Night eating syndrome: an overview
Authors: Milano Walter , De Rosa Michele , Milano Luca , Capasso Anna 
Published: September 2011

Abstract

Objectives
The purpose of this review is to outline the nosographic characteristics of NES and the most reliable ethiopathogenetic theories in relation to the most recent evidence in the literature.

Key findings
The night eating syndrome (NES) is a disorder occurring at the stated time, that does not meet the criteria for any specific eating disorder. NES is characterized by a reduced feeding during the day, evening hyperphagia accompanied by frequent nocturnal awakenings associated with conscious episodes of compulsive ingestion of food and abnormal circadian rhythms of food and other neuroendocrine factors. Frequently it is associated with obesity and depressed mood. We highlight the therapeutic possibilities of some drugs, especially selective serotonin re-uptake inhibitors (SSRIs), which reduce the hyperactivity of the serotonin transporter in NES and significantly improve the clinical picture of this disease.

Conclusions
Night eating syndrome is of importance clinically because of its association with obesity. The recognition and effective treatment of NES may be an increasingly important way to treat a subset of the obese population. Treatment of the syndrome, however, is still in its infancy. One clinical trial has reported efficacy with the SSRI sertraline. Other treatments, such as the anticonvulsant topiramate, phototherapy, and other SSRIs, may also offer future promise. Particularly useful would be studies involving brain scans (magnetic resonance imaging or single-photon emission computed tomography) of patients with NES compared with the healthy population, to investigate more thoroughly the possible alterations involved in the pathogenesis of NES.
Selfinjective quivers with potential and 2-representation-finite algebras
Authors: Herschend Martin , Iyama Osamu 
Published: September 2011

AbstractWe study quivers with potential (QPs) whose Jacobian algebras are finite-dimensional selfinjective. They are an analogue of the ‘good QPs’ studied by Bocklandt whose Jacobian algebras are 3-Calabi–Yau. We show that 2-representation-finite algebras are truncated Jacobian algebras of selfinjective QPs, which are factor algebras of Jacobian algebras by certain sets of arrows called cuts. We show that selfinjectivity of QPs is preserved under iterated mutation with respect to orbits of the Nakayama permutation. We give a sufficient condition for all truncated Jacobian algebras of a fixed QP to be derived equivalent. We introduce planar QPs which provide us with a rich source of selfinjective QPs.
A highly asymmetric direct aldol reaction catalyzed by chiral proline amide – thiourea bifunctional catalysts
Authors: Li Yun , Yang Qing-chuan , Xu Xiao-Ying , Zhou Yong , Bai Jian-fei , Wang Fei-ying , Wang Li-xin 
Published: September 2011

A series of chiral proline amide – thiourea bifunctional catalysts derived from l-proline and chiral diamine were prepared and successfully applied to highly enantioselective direct aldol reactions of cyclohexanone with various aldehydes in excellent yields (85%–97%), diastereoselectivities (anti/syn > 20:1) and enantioselectivities (up to 91% ee).
Asymmetric hydroamination catalyzed by in situ generated chiral amidate and ureate complexes of zirconium — Probing the role of the tether in ligand design
Authors: Payne Philippa R. , Bexrud Jason A. , Leitch David C. , Schafer Laurel L. 
Published: September 2011

Simple chiral proligands have been synthesized from inexpensive chiral starting materials. These amidate and ureate ligands support zirconium complexes that successfully catalyze intramolecular hydroamination with up to 26% ee. Several elements necessary for successful ligand design are highlighted and discussed. In particular, the strict control of metal geometry through multidentate tethered ligands is determined to be an essential aspect of future ligand development.
Possible Role of Visfatin in Hepatoma Progression and the Effects of Branched-Chain Amino Acids on Visfatin-Induced Proliferation in Human Hepatoma Cells
Authors: Ninomiya Soranobu , Shimizu Masahito , Imai Kenji , Takai Koji , Shiraki Makoto , Hara Takeshi , Tsurumi Hisashi , Ishizaki Sonoko , Moriwaki Hisataka 
Published: September 2011

Abstract
Obesity and related metabolic abnormalities, including adipocytokine dysbalance, are risk factors for hepatocellular carcinoma (HCC). Visfatin, an adipocytokine that is highly expressed in visceral fat, is suggested to play a role in the progression of human malignancies. Branched-chain amino acids (BCAA) reduce the incidence of HCC in obese patients with liver cirrhosis and prevent obesity-related liver carcinogenesis in mice. In this study, we investigated the possible role of visfatin on HCC progression and the effects of BCAA on visfatin-induced proliferation of HCC cells. In patients with HCCs, serum visfatin levels were significantly correlated with stage progression and tumor enlargement. Visfatin preferentially stimulated the proliferation of HepG2, Hep3B, and HuH7 human HCC cells compared with Hc normal hepatocytes. Visfatin phosphorylated extracellular signal–regulated kinase (ERK), Akt, and GSK-3β proteins in HepG2 cells. LY294002 [a phosphoinositide-3-kinase (PI3K) inhibitor], PD98059 [a MAP/ERK 1 kinase (MEK1) inhibitor], CHIR99021 (a GSK-3β inhibitor), and BCAA significantly inhibited visfatin-induced proliferation in HepG2 cells. BCAA also inhibited phosphorylation of GSK-3β, increased cellular levels of p21CIP1, caused cell-cycle arrest in G0/G1 phase, and induced apoptosis in HCC cells in the presence of visfatin. These findings suggest that visfatin plays a critical role in the proliferation of HCC cells and may be associated with the progression of this malignancy. In addition, BCAA might inhibit obesity-related liver carcinogenesis by targeting and, possibly, by overcoming the stimulatory effects of visfatin. Cancer Prev Res; 4(12); 2092–100. ©2011 AACR.
Adhesion molecule periplakin is involved in cellular movement and attachment in pharyngeal squamous cancer cells
Authors: Tonoike Yurie , Matsushita Kazuyuki , Tomonaga Takeshi , Katada Koji , Tanaka Nobuko , Shimada Hideaki , Nakatani Yukio , Okamoto Yoshitaka , Nomura Fumio 
Published: September 2011

AbstractBackgroundWe previously reported that periplakin (PPL) is downregulated in human esophageal cancer tissues compared to the adjacent non-cancer epithelium. Thus PPL could be a useful marker for detection of early esophageal cancer and evaluation of tumor progression, but largely remains unknown in this field. To investigate PPL involvement in carcinogenesis, tumor progression, cellular movement or attachment activity, siRNAs against PPL were transfected into pharyngeal squamous cancer cell lines and their effects on cellular behaviours were examined.ResultsPPL knockdown appeared to decrease tumor cell growth together with G2/M phase accumulation in cells attached to a culture dish. However, the extent of cell growth suppression, evaluated by the number of cells attached to the culture dish, was too distinctive to be explained only by cell cycle delay. Importantly, PPL knockdown suppressed cellular movement and attachment to the culture dish accompanied by decreased pAktSer473 phosphorylation. Additionally, LY294002, a PI3K inhibitor that dephosphorylates pAktSer473, significantly suppressed D562 cell migration. Thus PPL potentially engages in cellular movement al least partly via the PI3K/Akt axis.ConclusionsPPL knockdown is related to reduced cellular movement and attachment activity in association with PI3K/Akt axis suppression, rather than malignant progression in pharyngeal cancer cells.
Novel mutations of TCOF1 gene in European patients with treacher Collins syndrome
Authors: Conte Chiara , D'Apice Maria Rosaria , Rinaldi Fabrizio , Gambardella Stefano , Sangiuolo Federica , Novelli Giuseppe 
Published: September 2011

Abstract

Background
Treacher Collins syndrome (TCS) is one of the most severe autosomal dominant congenital disorders of craniofacial development and shows variable phenotypic expression. TCS is extremely rare, occurring with an incidence of 1 in 50.000 live births. The TCS distinguishing characteristics are represented by down slanting palpebral fissures, coloboma of the eyelid, micrognathia, microtia and other deformity of the ears, hypoplastic zygomatic arches, and macrostomia. Conductive hearing loss and cleft palate are often present. TCS results from mutations in the TCOF1 gene located on chromosome 5, which encodes a serine/alanine-rich nucleolar phospho-protein called Treacle. However, alterations in the TCOF1 gene have been implicated in only 81-93% of TCS cases.

Methods
In this study, the entire coding regions of the TCOF1 gene, including newly described exons 6A and 16A, were sequenced in 46 unrelated subjects suspected of TCS clinical indication.

Results
Fifteen mutations were reported, including twelve novel and three already described in 14 sporadic patients and in 3 familial cases. Moreover, seven novel polymorphisms were also described. Most of the mutations characterised were microdeletions spanning one or more nucleotides, in addition to an insertion of one nucleotide in exon 18 and a stop mutation. The deletions and the insertion described cause a premature termination of translation, resulting in a truncated protein.

Conclusion
This study confirms that almost all the TCOF1 pathogenic mutations fall in the coding region and lead to an aberrant protein.
Cyclin D1, Id1 and EMT in breast cancer
Authors: Tobin Nicholas P , Sims Andrew H , Lundgren Katja L , Lehn Sophie , Landberg Göran 
Published: September 2011

Abstract

Background
Cyclin D1 is a well-characterised cell cycle regulator with established oncogenic capabilities. Despite these properties, studies report contrasting links to tumour aggressiveness. It has previously been shown that silencing cyclin D1 increases the migratory capacity of MDA-MB-231 breast cancer cells with concomitant increase in 'inhibitor of differentiation 1' (ID1) gene expression. Id1 is known to be associated with more invasive features of cancer and with the epithelial-mesenchymal transition (EMT). Here, we sought to determine if the increase in cell motility following cyclin D1 silencing was mediated by Id1 and enhanced EMT-features. To further substantiate these findings we aimed to delineate the link between CCND1, ID1 and EMT, as well as clinical properties in primary breast cancer.

Methods
Protein and gene expression of ID1, CCND1 and EMT markers were determined in MDA-MB-231 and ZR75 cells by western blot and qPCR. Cell migration and promoter occupancy were monitored by transwell and ChIP assays, respectively. Gene expression was analysed from publicly available datasets.

Results
The increase in cell migration following cyclin D1 silencing in MDA-MB-231 cells was abolished by Id1 siRNA treatment and we observed cyclin D1 occupancy of the Id1 promoter region. Moreover, ID1 and SNAI2 gene expression was increased following cyclin D1 knock-down, an effect reversed with Id1 siRNA treatment. Similar migratory and SNAI2 increases were noted for the ER-positive ZR75-1 cell line, but in an Id1-independent manner. In a meta-analysis of 1107 breast cancer samples, CCND1
low/ID1
high tumours displayed increased expression of EMT markers and were associated with reduced recurrence free survival. Finally, a greater percentage of CCND1
low/ID1
high tumours were found in the EMT-like 'claudin-low' subtype of breast cancer than in other subtypes.

Conclusions
These results indicate that increased migration of MDA-MB-231 cells following cyclin D1 silencing can be mediated by Id1 and is linked to an increase in EMT markers. Moreover, we have confirmed a relationship between cyclin D1, Id1 and EMT in primary breast cancer, supporting our in vitro findings that low cyclin D1 expression can be linked to aggressive features in subgroups of breast cancer.
Postcode Lotteries in Public Health - The NHS Health Checks Programme in North West London
Authors: Graley Clare EM , May Katherine F , McCoy David C 
Published: September 2011

AbstractBackgroundPostcode lotteries in health refer to differences in health care between different geographic areas. These have been previously associated with clinical services. However there has been little documentation of postcode lotteries relating to preventative health care services. This paper describes a postcode lottery effect in relation to the NHS Health Checks Programme (a national cardiovascular screening programme in England) in eight PCTs in the North West sector of London.MethodsA descriptive cross-sectional analysis of the Health Checks Programme was carried out in eight PCTs in North West London using a structured data-collecting instrument.ResultsThe analysis found variation in the implementation of the national Health Checks Programme in terms of: the screening approach taken; the allocated budget (which varied from £69,000 to £1.4 million per 100,000 eligible population); payment rates made to providers of Health Checks; tools used to identify and measure risk of cardiovascular disease and diabetes; monitoring and evaluation; and preventative services available following the health check.ConclusionsThis study identifies a postcode lottery effect related to a national public health programme. Although it is important to allow enough flexibility in the design of the Health Checks Programme so that it fits in with local factors, aspects of the programme may benefit from greater standardisation or stronger national guidance.
Medical interns' knowledge and training regarding urethral catheter insertion and insertion-related urethral injury in male patients
Authors: Manalo Manuel , Lapitan Marie Carmela M , Buckley Brian S 
Published: September 2011

Abstract

Background
Improper catheterization can lead to urethral injury. Yet research from four continents suggests training of junior doctors in catheterization is insufficient. European research suggests a majority of catheterization related morbidities occur when the procedure is performed by interns.

Methods
To assess the knowledge and practices of medical interns relating to urethral catheterization and iatrogenic urethral injury secondary to traumatic catheter insertion, a questionnaire survey was conducted of all first year medical interns at a tertiary national university hospital in the Philippines. The questionnaire contained 17 items covering 4 areas: methods of training in catheterization and level of experience; perceived adequacy of training; theoretical knowledge of catheterization; the mechanisms of catheter-related urethral injury.

Results
225/240 interns (94%) completed the survey (130 (57.8%) female). 125 (55.6%) responded that they had adequate theoretical training and 150 (66.7%) adequate practical training. All had performed more than 10 catheterizations and 204 (90%) were supervised when they first performed catheterization. Despite relatively high levels of experience and confidence, deficits were identified in detailed knowledge of correct catheterization procedures and of risks associated with urethral injury.

Conclusions
More thorough training of incoming medical interns in urinary catheterization may help to reduce the risk of complications and injury. Training should be universal and thought given to its timing within the curriculum. Training should include step by step instruction in the process, emphasis on history taking and awareness of factors associated with increased risk of urethral injury.
Drosophila insulin and target of rapamycin (TOR) pathways regulate GSK3 beta activity to control Myc stability and determine Myc expression in vivo
Authors: Parisi Federica , Riccardo Sara , Daniel Margaret , Saqcena Mahesh , Kundu Nandini , Pession Annalisa , Grifoni Daniela , Stocker Hugo , Tabak Esteban , Bellosta Paola 
Published: September 2011

Abstract

Background
Genetic studies in Drosophila melanogaster reveal an important role for Myc in controlling growth. Similar studies have also shown how components of the insulin and target of rapamycin (TOR) pathways are key regulators of growth. Despite a few suggestions that Myc transcriptional activity lies downstream of these pathways, a molecular mechanism linking these signaling pathways to Myc has not been clearly described. Using biochemical and genetic approaches we tried to identify novel mechanisms that control Myc activity upon activation of insulin and TOR signaling pathways.

Results
Our biochemical studies show that insulin induces Myc protein accumulation in Drosophila S2 cells, which correlates with a decrease in the activity of glycogen synthase kinase 3-beta (GSK3β ) a kinase that is responsible for Myc protein degradation. Induction of Myc by insulin is inhibited by the presence of the TOR inhibitor rapamycin, suggesting that insulin-induced Myc protein accumulation depends on the activation of TOR complex 1. Treatment with amino acids that directly activate the TOR pathway results in Myc protein accumulation, which also depends on the ability of S6K kinase to inhibit GSK3β activity. Myc upregulation by insulin and TOR pathways is a mechanism conserved in cells from the wing imaginal disc, where expression of Dp110 and Rheb also induces Myc protein accumulation, while inhibition of insulin and TOR pathways result in the opposite effect. Our functional analysis, aimed at quantifying the relative contribution of Myc to ommatidial growth downstream of insulin and TOR pathways, revealed that Myc activity is necessary to sustain the proliferation of cells from the ommatidia upon Dp110 expression, while its contribution downstream of TOR is significant to control the size of the ommatidia.

Conclusions
Our study presents novel evidence that Myc activity acts downstream of insulin and TOR pathways to control growth in Drosophila. At the biochemical level we found that both these pathways converge at GSK3β to control Myc protein stability, while our genetic analysis shows that insulin and TOR pathways have different requirements for Myc activity during development of the eye, suggesting that Myc might be differentially induced by these pathways during growth or proliferation of cells that make up the ommatidia.
Autoimmune cholangitis mimicking a klatskin tumor: a case report
Authors: Shingina Alexandra , Owen David , Zwirewich Charles , Salh Baljinder 
Published: September 2011

Abstract

Introduction
Autoimmune cholangitis remains an elusive manifestation of immunoglobulin G4-associated systemic disease most commonly encountered in patients with autoimmune pancreatitis. No strict diagnostic criteria have been described to date and diagnosis mainly relies on a combination of clinical and histopathologic findings. It is hence even more challenging to diagnose autoimmune cholangitis in patients with late or atypical presentations, such as without concomitant pancreatic involvement. Early diagnosis of this rare disorder can significantly improve outcomes considering high rates of surgical intervention, as well as high relapse rates in the absence of steroid treatment. To the best of our knowledge the literature is quite sparse on cases with atypical presentations of autoimmune cholangitis.

Case presentation
We report a case of a previously healthy 65-year-old man of Middle-Eastern origin, with a history of pancreatic insufficiency of unknown etiology, evaluated for elevated liver function tests found incidentally on a routine physical examination. Imaging studies revealed an atrophic pancreas and biliary duct dilatation consistent with obstruction. Subsequent endoscopic retrograde cholangiopancreatography showed a bile duct narrowing pattern suggestive of cholangiocarcinoma, but brushings failed to reveal malignant cells. Our patient proceeded to undergo surgical resection. Histological examination of the resected mass revealed lymphoplasmacytic infiltrate with no malignant features. Our patient returned three months later with persistently high liver function tests and no evidence of biliary obstruction on imaging. A presumptive diagnosis of autoimmune cholangitis was made and our patient's symptoms resolved after a short course of an oral steroid regimen. Post factum staining of the resection specimen revealed an immunoglobulin G4 antibody positive immune cell infiltrate, consistent with the proposed diagnosis.

Conclusion
Our case thus highlights the importance of clinician awareness of the autoimmune spectrum of biliary pathologies when confronted with atypical clinical presentations, the paucity of diagnostic measures and the benefit from long-term steroid and/or immunosuppressive treatment.
Stable accumulation of p67phox at the phagosomal membrane and ROS production within the phagosome
Authors: Tlili Asma , Erard Marie , Faure Marie-Cécile , Baudin Xavier , Piolot Tristan , Dupré-Crochet Sophie , Nüße Oliver 
Published: September 2011

ABSTRACT
Production of ROS by the leukocyte NADPH oxidase is essential for the destruction of pathogenic bacteria inside phagosomes. The enzyme is a complex of cytosolic and membranous subunits that need to assemble upon activation. Biochemical data suggest that the complex is renewed continuously during activity. Furthermore, it is generally assumed that complex assembly and activity occur in parallel. However, information about the oxidase assembly in individual phagosomes in live cells is scarce. We studied the dynamic behavior of the crucial cytosolic NADPH oxidase component p67phox during phagocytosis by videomicroscopy. p67phox is involved in the regulation of electron flow from NADPH to oxygen, leading to superoxide radical formation inside the phagosome. p67phox-citrine, expressed in myeloid PLB-985 cells, accumulated at the phagosomal membrane during phagocytosis of yeast particles. Using photobleaching techniques (FRAP, FLIP), we demonstrated that p67phox-citrine diffused freely in this phagosomal membrane, but the phagosomal pool of p67phox-citrine did not exchange with the cytosolic pool. This result suggests that once assembled in the NADPH oxidase complex, p67phox is stable in this complex. Furthermore, the time of the presence of p67phox-citrine at the phagosome increased substantially in the presence of complement in the opsonizing serum compared with decomplemented serum. PI(3)P also accumulated around phagosomes for twice as long in the presence of complement. The presence of p67phox-citrine was correlated with the duration of phagosomal ROS production in different opsonization conditions. These data support the critical role of p67phox for ROS production on the level of individual phagosomes.