bluuebunny/crossref_metadata_2025_split huggingface dataset:
Decoy cells and malignant cells coexisting in the urine from a transplant recipient with BK virus nephropathy and bladder adenocarcinoma
Authors: Galed‐Placed Ignacio , Valbuena‐Ruvira Luis 
Published: November 2010

AbstractThe search for decoy cells (DC) in urine is widely used as screening for BK virus (BKV) reactivation in transplant recipients. BKV cytopathic effect of DC must not be confused with high‐grade urothelial carcinoma. This report presents a case of coexistence of DC and malignant cells in the urine from a transplant recipient with BKV‐associated nephropathy (BKVN) and bladder adenocarcinoma.A 38‐year‐old female with type 1 diabetes mellitus and end‐stage renal disease underwent a simultaneous pancreas and kidney transplant. Four years post‐transplantation, BK virus studies were performed for renal dysfunction. Isolated DC and DC in casts were identified in urine. Also, the tests for BKV DNA were positive in serum and renal allograft biopsy. BKVN was treatment‐resistant and the patient returned to hemodialysis. A kidney transplant nephrectomy was performed 2 years later. The next urine cytology showed, in addition to DC, other distinct cells with nuclear atypia highly suggestive of malignancy. Some cells showed both, malignant and DC features. A bladder adenocarcinoma was diagnosed on biopsy and BKV proteins were demonstrated on tumor cells, supporting a possible role for BKV in the oncogenic pathway in this clinical setting.The presence of DC in the urine from a transplant recipient is the hallmark of BKV activation, but it does not exclude the existence of carcinoma. Furthermore, the presence of highly atypical cells should raise, not eliminate, the possibility of neoplastic transformation of the bladder. Diagn. Cytopathol. 2011. © 2010 Wiley Periodicals, Inc.
Contribution of postprandial glucose to excess hyperglycaemia in Asian type 2 diabetic patients using continuous glucose monitoring
Authors: Wang J.‐S. , Tu S.‐T. , Lee I.‐T. , Lin S.‐D. , Lin S.‐Y. , Su S.‐L. , Lee W.‐J. , Sheu Wayne H.‐H. 
Published: November 2010

AbstractBackgroundPrevious studies examining the contributions of fasting glucose (FG) and postprandial glucose (PPG) to glycated haemoglobin ($\hbox{HbA}_{{\rm 1c}}$) have yielded conflicting results. We aimed to clarify the contributions of PPG to hyperglycaemia in Asian type 2 diabetic patients using continuous glucose monitoring.MethodsContinuous glucose monitoring was conducted in 121 non‐insulin‐using type 2 diabetic outpatients, who were divided into five groups according to quintiles of $\hbox{HbA}_{{\rm 1c}}$ (ranging from 5.7 to 12.7%). Glucose area under the curve (AUC) above a glucose value of 5.5 mmol/L 24 or 4 h after meals was defined as $\hbox{AUC}_{{\rm total}}$. Glucose AUC above FG or preprandial glucose levels was defined as $\hbox{AUC}_{{\rm PPG}}$. The contribution of PPG to hyperglycaemia was calculated as ($\hbox{AUC}_{{\rm PPG}}$/$\hbox{AUC}_{{\rm total}}$) × 100%. The contribution of FG or preprandial glucose was calculated as [($\hbox{AUC}_{{\rm total}} -$ $\hbox{AUC}_{{\rm PPG}}$)/$\hbox{AUC}_{{\rm total}}$] × 100%.ResultsThe contribution of PPG to either 24‐h hyperglycaemia or 4‐h hyperglycaemia after meals was significantly higher than FG and preprandial glucose in the lowest quintile of $\hbox{HbA}_{{\rm 1c}}$ (both p < 0.001). However, no difference was observed in the other four quintiles. Peak PPG and glucose excursions were higher after breakfast than those after lunch and dinner (p < 0.01 for all comparisons).ConclusionsIn Asian patients with type 2 diabetes, PPG 24 and 4 h after meals was a predominant contributor to excess hyperglycaemia in well‐controlled patients and was equally important as FG or preprandial glucose in moderately to poorly controlled patients with mean $\hbox{HbA}_{{\rm 1c}}$ up to 10%. Copyright © 2010 John Wiley & Sons, Ltd.
Primer and interviews: Molecular mechanisms of morphological evolution
Authors: Kiefer Julie C. 
Published: November 2010

AbstractThe beauty of the developing embryo, and the awe that it inspires, lure many scientists into the field of developmental biology. What compels cells to divide, migrate, and morph into a being with a complex body plan? Evolutionary developmental biologists hold similar fascinations, with dynamics that take place on a grander timescale. How do phenotypic traits diverge over evolutionary time? This primer illustrates how a deep understanding of the basic principles that underlie developmental biology have changed how scientists think about the evolution of body form. The primer culminates in a conversation with David Stern, PhD, and Michael Shapiro, PhD, who discuss current topics in morphological evolution, why the field should be of interest to classic developmental biologists, and what lies ahead. Developmental Dynamics 239:3497–3505, 2010. © 2010 Wiley‐Liss, Inc.
Tissue‐ and development‐dependent expression of the small GTPase Arf6 in mice
Authors: Akiyama Masahiro , Zhou Miao , Sugimoto Rika , Hongu Tsunaki , Furuya Momoko , Funakoshi Yuji , Kato Mitsuyasu , Hasegawa Hiroshi , Kanaho Yasunori 
Published: November 2010

AbstractThe small GTPase Arf6 is a member of the Arf (ADP‐ribosylation factor) family. Although the function of Arf6 has been heavily studied at the cellular level, its physiological function at the whole animal level is largely unknown. In this study, we examined both the tissue distribution and developmental timing of Arf6 expression in wild type mice to obtain valuable information to speculate on the physiological function of Arf6. Western blot analysis using anti‐Arf6 antibody revealed that Arf6 was ubiquitously expressed with its developmental timing differing in a tissue‐specific manner. These results were supported by Arf6 mRNA in situ hybridization experiments, which showed that Arf6 was highly expressed in the polarized epithelial cells and embryonic mesenchymal cells of most tissues in a temporally dependent manner. Taken in toto, our results suggest that the expression of Arf6 in mouse tissues is precisely regulated in a development‐ and tissue‐dependent manner. Developmental Dynamics 239:3416–3435, 2010. © 2010 Wiley‐Liss, Inc.
Elevated risk of papillary thyroid cancer in Korean patients with Hashimoto's thyroiditis
Authors: Kim Kyung Won , Park Young Joo , Kim Eun Hye , Park So Yeon , Park Do Joong , Ahn Soon‐Hyun , Park Do Joon , Jang Hak C. , Cho Bo Youn 
Published: November 2010

AbstractBackground.Hashimoto's thyroiditis (HT) and higher levels of thyroid‐stimulating hormone (TSH) have been proposed as risk factors for papillary thyroid cancer (PTC), but this issue is still being debated. The purpose of this study was whether HT was related to the risk of PTC over TSH.Methods.We enrolled 1329 patients (1028 with PTC, 52 with follicular thyroid cancer, and 249 with benign disease) of 1490 patients who underwent thyroidectomy.Results.The TSH concentration was not different among patients with PTC or benign disease. Our study showed that men (odds ratio [OR] = 1.54; p = .049) and the presence of HT (OR = 2.96; p <.001) increased the risk of PTC. Moreover, HT was associated with multifocal cancer (p = .005) and smaller tumor size (p = .031), but it did not influence the extrathyroidal invasion or nodal metastasis.Conclusion.Clinicians who deal with thyroid nodules should pay particular attention to HT because it is a stronger predictor for PTC than other risk factors. © 2010 Wiley Periodicals, Inc. Head Neck, 2011
Cutaneous squamous cell carcinoma of the head and neck metastasizing to the parotid gland—A review of current recommendations
Authors: O'Hara James , Ferlito Alfio , Takes Robert P. , Rinaldo Alessandra , Strojan Primož , Shaha Ashok R. , Rodrigo Juan P. , Paleri Vinidh 
Published: November 2010

AbstractCutaneous squamous cell carcinoma (SCC) of the head and neck may metastasize in up to 5% of patients, with the parotid lymph nodes the most frequent site for spread. Metastases frequently show delayed presentation after the primary cancer had been treated. The optimum treatment should be surgery followed by adjuvant radiotherapy, with an appropriate parotidectomy, and preservation of the facial nerve if not involved by tumor and treatment to the neck. In a clinically N0 neck, levels I to III should be cleared for facial primaries, levels II to III for anterior scalp and external ear primaries, and levels II to V for posterior scalp primaries. Approximate 5‐year disease‐specific survival (DSS) after treatment was 70% to 75%. Patients with immunosuppression, in particular transplant recipients, are at high risk of developing aggressive metastatic cutaneous SCC. Modifications of the staging systems have demonstrated the prognostic benefits of accurately staging parotid and/or neck nodal disease. © 2010 Wiley Periodicals, Inc. Head Neck, 2010
Nonsurgical management of oropharyngeal, laryngeal, and hypopharyngeal cancer: The Fox Chase Cancer Center experience
Authors: Andrews Genevieve , Lango Miriam , Cohen Roger , Feigenberg Steven , Burtness Barbara , Mehra Ranee , Ahmed Sidrah , Nicolaou Nicos , Gaughan John , Ridge John A. 
Published: November 2010

AbstractBackground.Oropharyngeal, laryngeal, and hypopharyngeal cancer treatment has changed at our institution, but survival outcomes have not been evaluated.Methods.We approached the evaluation by a retrospective single‐institution cohort study.Results.Review of 180 patient records from 1993 to 2004 revealed that the number of patients with oropharyngeal cancer treated nearly doubled, whereas the number of patients with laryngeal and hypopharyngeal cancers declined (p = .006). Since 2000, concurrent chemotherapeutic regimens rather than radiation alone became the dominant treatment approach, with associated improvements in recurrence‐free and overall survival (p = .009 and p = .006, respectively). Stratification by tumor site, however, revealed the survival of patients with oropharyngeal cancer improved markedly, whereas the survival of patients with laryngeal cancer did not change. In the multivariate analysis, T classification (p = .0001) and chemotherapy use (p = .0001) were associated with improved survival. The recurrence‐free survival of nonsmokers was better than that for former or current smokers (p = .01), but was accounted for by earlier T classification on presentation in the multivariate analysis (p = .0001). The predominant initial site of failure remained at the primary site for oropharyngeal cancer (14 of 17 relapses or 82%), but not laryngeal cancer (3 of 7 relapses or 42%). As a result, an increasing number of patients with recurrent oropharyngeal cancer, and a decreasing number of recurrent laryngeal cancer patients were evaluated for salvage surgery. Patients with oropharyngeal recurrences, however, were less likely to undergo surgery with curative intent (p = .02) and were less likely to achieve locoregional control after disease recurrence.Conclusions.The survival of patients with oropharyngeal and hypopharyngeal cancers treated at our institution has improved over the last 15 years, which is likely related to changes in treatment and tumor biology. The improvement was not observed in patients with laryngeal cancer. A subset of patients with oropharyngeal cancer remain subject to local failure and disease‐related death. © 2010 Wiley Periodicals, Inc. Head Neck 33:1433–1440, 2010
Energy partitioning scheme based on self‐consistent method for subsystems: Populational space approach
Authors: De Silva Piotr , Korchowiec Jacek 
Published: November 2010

AbstractThe refinement of the previously proposed energy partitioning scheme, self‐consistent charge and configuration method for subsystems (Korchowiec and Uchimaru, J Chem Phys 2000, 112, 1623), is proposed. Our new realization takes rigorously into account all the interactions between subsystems and guarantees proper symmetry of the intermediate wavefunctions. In addition, the scheme is supplemented with natural orbitals for chemical valence to trace the charge reorganization during polarization and charge transfer steps. The water dimer and ammonia borane are used to illustrate the proposed formalism. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2011
HB‐EGF synthesis and release induced by cholesterol depletion of human epidermal keratinocytes is controlled by extracellular atp and involves both p38 and ERK1/2 signaling pathways
Authors: Giltaire Séverine , Lambert Sylviane , Poumay Yves 
Published: November 2010

AbstractThe heparin‐binding EGF‐like growth factor (HB‐EGF) is an autocrine/paracrine keratinocyte growth factor, which binds to the epidermal growth factor (EGF) receptor family and plays a critical role during the re‐epithelialization of cutaneous wound by stimulating the keratinocytes proliferation and migration. In this study, cellular stressing condition in autocrine cultures of human keratinocytes was induced by cholesterol depletion using methyl‐beta‐cyclodextrin (MβCD). MβCD treatment induces the expression and the release of HB‐EGF. By analysis of the culture media, large amounts of cellular ATP were measured particularly after 1 h of MβCD treatment. To investigate whether ATP contributes to the expression of HB‐EGF, the nonhydrolyzable ATP analogue, ATP‐γ‐S, was used to mimic the extracellular ATP released. We report that keratinocytes stimulated with ATP‐γ‐S induce HB‐EGF expression and activate EGFR and ERK1/2. Using an antagonist of P2 purinergic receptors, we demonstrate that HB‐EGF synthesis induced by lipid rafts disruption is dependent on ATP interaction with P2 purinergic receptors. Moreover, our data suggest that both MAPKs p38 and ERK1/2 are involved together or independently in the regulation of HB‐EGF gene expression. These findings provide new insight into the signaling pathway by which HB‐EGF is expressed after lipid rafts disruption. In summary, after lipid raft disruption, keratinocytes release large amount of extracellular ATP. ATP induces HB‐EGF synthesis and release by interacting with the P2 purinergic receptor and through p38 and ERK1/2 signaling in response to a challenging environment. A release of ATP acts as an early stress response in keratinocytes. J. Cell. Physiol. 226: 1651–1659, 2011. © 2011 Wiley‐Liss, Inc.
Lipopolysaccharide activated phosphatidylcholine‐specific phospholipase C and induced IL‐8 and MCP‐1 production in vascular endothelial cells
Authors: Zhang Lu , Li Hai Ying , Li Hui , Zhao Jing , Su Le , Zhang Yun , Zhang Shang Li , Miao Jun Ying 
Published: November 2010

AbstractSecretion of proinflammatory cytokines by lipopolysaccharide (LPS) activated vascular endothelial cells (VECs) contributes substantially to the pathogenesis of several inflammatory diseases such as atherosclerosis and septic shock. However, the mechanisms involved in this process are not well understood. Here, we investigated the role of phosphatidylcholine‐specific phospholipase C (PC‐PLC) in LPS‐induced IL‐8 and MCP‐1 production in VECs. The results showed that LPS elevated the level of PC‐PLC and the production of IL‐8 and MCP‐1 in Human umbilical vein vascular endothelial cells (HUVECs). Blocking the function of PC‐PLC by exploiting the neutralization antibody of PC‐PLC or tricyclodecan‐9‐yl‐xanthogenate (D609), an inhibitor of PC‐PLC, significantly inhibited LPS‐induced production of IL‐8 and MCP‐1 in HUVECs. Furthermore, the in vivo experimental results showed that the levels of PC‐PLC, IL‐8, and MCP‐1 in the aortic endothelium and serum were increased in mice injected with LPS. The increased levels of these molecules were also inhibited by the treatment with D609. The data suggested that blocking PC‐PLC function significantly inhibited LPS‐induced IL‐8 and MCP‐1 production in cultured HUVECs and in vivo. PC‐PLC might be a potential target for therapy in inflammation associated‐diseases such as atherosclerosis. J. Cell. Physiol. 226: 1694–1701, 2011. © 2010 Wiley‐Liss, Inc.
Morphology and ultrastructure of the nephridial system of Hypania invalida (Grube, 1860) (Annelida, Polychaeta, Ampharetidae)
Authors: Kremer Philipp , Fiege Dieter , Wehe Thomas 
Published: November 2010

AbstractThe excretory organs of the freshwater polychaete Hypania invalida have been examined using scanning and transmission electron microscopy. Three pairs of macroscopically and ultrastructurally different nephridia are present in the thorax. Intersegmental septa in the thorax are absent, with the exception of a single diaphragm between second and third chaetiger. The first pair of nephridia is anterior to this septum, the second pair crosses the septum, with the nephrostomes anterior and the ducts and the nephridiopori posterior to it, and the third pair of nephridia is entirely posterior to the diaphragm. The first two pairs of nephridia have ciliated nephrostomes of moderate size and long nephridial ducts that extend the length of the thorax. In contrast, the third pair is characterized by short ducts and very prominent nephrostomes. Macroscopically, seven different sections of nephridial duct cells can be distinguished along the length of the first two pairs of nephridia, whereas, on an ultrastructural basis, only six different regions can be identified. Only two regions of different duct cells can be recognized in the third pair of nephridia. Cells of the two anterior pairs of nephridia show typical characteristics of transport epithelia and most likely function as excretory organs. In contrast, the duct cells of the third pair are not that much differentiated and might primarily be responsible for the release of sexual products, as sperm was observed passing through these ducts. Podocyte‐like cells were observed to accompany nephridial ducts. J. Morphol., 2011. © 2010 Wiley‐Liss, Inc.
Serum insulin‐like system alterations in patients with spinocerebellar ataxia type 3
Authors: Saute Jonas Alex Morales , da Silva Andrew Chaves Feitosa , Muller Alexandre Pastoris , Hansel Gisele , de Mello Alexandre Silva , Maeda Fábio , Vedolin Leonardo , Saraiva‐Pereira Maria Luiza , Souza Diogo Onofre , Arpa Javier , Torres‐Aleman Ignacio , Portela Luis Valmor Cruz , Jardim Laura Bannach 
Published: November 2010

AbstractSpinocerebellar ataxias (SCAs) constitute a group of autosomal dominant neurodegenerative disorders with no current treatment. The insulin/insulin‐like growth factor 1 (IGF‐1) system (IIS) has been shown to play a role in the neurological dysfunction of SCAs and other polyglutamine disorders. We aimed to study the biomarker profile of serum IIS components in SCA3. We performed a case–control study with 46 SCA3 patients and 42 healthy individuals evaluating the peripheral IIS profile (insulin, IGF‐1, IGFBP1 and 3) and the correlation with clinical, molecular, and neuroimaging findings. SCA3 patients presented lower insulin and IGFBP3 levels and higher insulin sensitivity (HOMA2), free IGF‐I, and IGFBP1 levels when compared with controls. IGFBP‐1 levels were directly associated with CAG expanded repeat length; IGF‐1 was associated with the volumetries of specific brainstem regions on magnetic resonance imaging (MRI). Insulin levels and sensitivity were related to age at onset of symptoms. Our findings indicate an involvement of IIS components in SCA3 neurobiology and IGFBP‐1 as a potential biomarker of the disease. © 2010 Movement Disorder Society
Epoetin alfa increases frataxin production in Friedreich's ataxia without affecting hematocrit
Authors: Saccà Francesco , Piro Raffaele , De Michele Giuseppe , Acquaviva Fabio , Antenora Antonella , Carlomagno Guido , Cocozza Sergio , Denaro Alessandra , Guacci Anna , Marsili Angela , Perrotta Gaetano , Puorro Giorgia , Cittadini Antonio , Filla Alessandro 
Published: November 2010

AbstractObjective of the study was to test the efficacy, safety, and tolerability of two single doses of Epoetin alfa in patients with Friedreich's ataxia. Ten patients were treated subcutaneously with 600 IU/kg for the first dose, and 3 months later with 1200 IU/kg. Epoetin alfa had no acute effect on frataxin, whereas a delayed and sustained increase in frataxin was evident at 3 months after the first dose (+35%; P < 0.05), and up to 6 months after the second dose (+54%; P < 0.001). The treatment was well tolerated and did not affect hematocrit, cardiac function, and neurological scale. Single high dose of Epoetin alfa can produce a considerably larger and sustained effect when compared with low doses and repeated administration schemes previously adopted. In addition, no hemoglobin increase was observed, and none of our patients required phlebotomy, indicating lack of erythropoietic effect of single high dose of erythropoietin. © 2010 Movement Disorder Society
LMP1 antagonizes WNT/β‐catenin signalling through inhibition of WTX and promotes nasopharyngeal dysplasia but not tumourigenesis in LMP1B95‐8 transgenic mice
Authors: QingLing Zhang , LiNa Yu , Li Liu , Shuang Wang , YuFang Yang , Yi Ding , Divakaran Jeevan , Xin Li , YanQing Ding 
Published: November 2010

AbstractLatent membrane protein 1 (LMP1) of Epstein–Barr virus (EBV) can induce cell transformation and tumourigenesis, but the mechanism is not understood. Previous studies have suggested that LMP1 acts through up‐regulation of cellular proliferation pathways including the Wnt/β‐catenin pathway, in which β‐catenin is the central effector. Increased levels of β‐catenin coupled with a decrease in E‐cadherin lead to reduced cell adhesion. This pathway is antagonized by WTX (Wilms' tumour gene on the X chromosome), which can promote the ubiquitination and degradation of β‐catenin. In the present study, we established L2/LMP1B95 − 8/EGFP transgenic mice to investigate the in vivo role of LMP1. Down‐regulation of WTX and E‐cadherin was accompanied by increased expression of β‐catenin in these mice. Even though invasive tumours did not develop, dysplasia was seen in the nasopharynx and oropharynx epithelium of these transgenic mice. Analysis of LMP1+, WTX+, and LMP1 siRNA silenced HNE‐1 cell lines demonstrated that WTX could exert a dominant role in LMP1‐mediated WNT/β‐catenin pathway regulation. This study indicates that LMP1 antagonizes the WNT/β‐catenin pathway by inhibiting WTX, and this reduction in WTX is associated with epithelial dysplasia via regulation of the WNT/β‐catenin pathway molecules E‐cadherin and β‐catenin. Further studies are required for a better understanding of the relationship between LMP1‐mediated antagonization of the WNT/β‐catenin pathway and tumourigenesis. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Saint Siluan warning signs of cancer in children: Impact of education in rural South Africa
Authors: Poyiadjis Stelios , Wainwright Linda , Naidu Gita , Mackinnon Diane , Poole Janet 
Published: November 2010

AbstractTwo thirds of children with cancer never reach a specialist centre for treatment in South Africa. The majority of those who present have advanced disease. A campaign was undertaken to educate the public and the primary health workers on the Saint Siluan early warning signs of cancer in children. There was a statistically significant increase in the number of new patients referred in the 6 years following the campaign (P = 0.001), but did not succeed in achieving the referral of patients at earlier stages of disease. This list of the warning signs appears to be useful in promoting awareness of cancer. Pediatr Blood Cancer 2011;56:314–316. © 2010 Wiley‐Liss, Inc.