bluuebunny/crossref_metadata_2025_split huggingface dataset:
Shade Matching Assisted by Digital Photography and Computer Software
Authors: Schropp Lars 
Published: December 2008

Abstract Purpose: To evaluate the efficacy of digital photographs and graphic computer software for color matching compared to conventional visual matching. Materials and Methods: The shade of a tab from a shade guide (Vita 3D‐Master Guide) placed in a phantom head was matched to a second guide of the same type by nine observers. This was done for twelve selected shade tabs (tests). The shade‐matching procedure was performed visually in a simulated clinic environment and with digital photographs, and the time spent for both procedures was recorded. An alternative arrangement of the shade tabs was used in the digital photographs. In addition, a graphic software program was used for color analysis. Hue, chroma, and lightness values of the test tab and all tabs of the second guide were derived from the digital photographs. According to the CIE L*C*h* color system, the color differences between the test tab and tabs of the second guide were calculated. The shade guide tab that deviated least from the test tab was determined to be the match. Shade matching performance by means of graphic software was compared with the two visual methods and tested by Chi‐square tests (α= 0.05). Results: Eight of twelve test tabs (67%) were matched correctly by the computer software method. This was significantly better (p < 0.02) than the performance of the visual shade matching methods conducted in the simulated clinic (32% correct match) and with photographs (28% correct match). No correlation between time consumption for the visual shade matching methods and frequency of correct match was observed. Conclusions: Shade matching assisted by digital photographs and computer software was significantly more reliable than by conventional visual methods.
Effects of Six Surface Treatment Methods on the Surface Roughness of a Low‐Fusing and an Ultra Low‐Fusing Feldspathic Ceramic Material
Authors: Dalkiz Mehmet , Sipahi Cumhur , Beydemir Bedri 
Published: December 2008

Abstract Purpose: The purpose of this in vitro study was to determine the effects of six surface treatment methods on the surface roughness of two feldspathic ceramic materials. Materials and Methods: One hundred twenty metal discs were cast (Remanium CS). A low‐fusing feldspathic ceramic (Vita Omega 900) was fired onto 60 metal discs, and an ultra low‐fusing feldspathic ceramic (Finesse) was fired onto the other 60 metal discs. Six surface treatment methods were selected: (1) autoglazing (AUG), (2) overglazing (OVG), (3) polishing (POL), (4) fine diamond disc grinding + polishing + autoglazing (FDPA), (5) coarse diamond disc grinding + polishing + autoglazing (CDPA), (6) polishing + autoglazing (PA). Omega specimens were assigned to six experimental groups representing six surface treatment methods (Om‐AUG, Om‐OVG, Om‐POL, Om‐FDPA, Om‐CDPA, Om‐PA) (n = 10). Finesse specimens were also assigned to six experimental groups (Fn‐AUG, Fn‐OVG, Fn‐POL, Fn‐FDPA, Fn‐CDPA, Fn‐PA) (n = 10). Treated ceramic surfaces were examined by means of profilometry and transmission electron microscopy. Results: In Omega groups mean roughness values ranged as follows: group Om‐AUG = Om‐POL > Om‐OVG > Om‐CDPA = Om‐FDPA > Om‐PA (p < 0.001). No significant difference was found between groups Om‐AUG/Om‐POL and Om‐CDPA/Om‐FDPA (p > 0.05). In Finesse groups mean roughness values ranged as follows: Fn‐CDPA > Fn‐FDPA = Fn‐AUG = Fn‐POL = Fn‐OVG > Fn‐PA (p < 0.001). No significant difference was found between Fn‐FDPA, Fn‐AUG, Fn‐ POL and Fn‐OVG (p > 0.05). Conclusions: For both ceramic types, the smoothest surfaces were obtained with polishing prior to autoglazing. Diamond disc grinding prior to polishing and autoglazing (Fn‐FDPA, Fn‐CDPA) displayed the roughest surfaces in ultra low‐fusing ceramic (Finesse). Autoglazing alone and polishing displayed the roughest surfaces in low‐fusing ceramic material (Om‐AUG, Om‐POL).
Microtensile Bond Strength and Impact Energy of Fracture of CAD‐Veneered Zirconia Restorations
Authors: Aboushelib Moustafa N. , De Kler Marcel , Van Der Zel Jef M. , Feilzer Albert J. 
Published: December 2008

Abstract Purpose: With state‐of‐the‐art CAD/CAM technology, the fabrication of large and complex zirconia frameworks is just a click away. On the other hand, veneering of the frameworks is still operator‐dependent. The aim of this work was to evaluate CAD veneering of zirconia restorations in terms of zirconia veneer bond strength and impact energy of fracture in a step towards complete automation of the fabrication process. Materials and Methods: A new CAD/CAM system was used to fabricate a resin replica of the esthetic ceramic required to veneer a zirconia framework. The replica was seated on the zirconia framework and further processed using press‐on technology. The bond strength between zirconia and the CAD veneer was evaluated using microtensile bond strength test. The impact energy of fracture of the specimens was also investigated. Manually layered zirconia specimens served as a control (α= 0.05). Results: There was no significant difference in the microtensile bond strength between zirconia and either of the used veneers (39 MPa). Even though the impact energy of fracture of the CAD‐veneered and manually layered specimens was almost identical (0.13 J), the former demonstrated a cohesive fracture of the veneer, while the latter failed by delamination of the veneer ceramic. Conclusion: CAD veneering is a reliable method for veneering zirconia restorations.
Commentary: On the Integration of Strategic Management and Entrepreneurship: Views of a Contrarian
Authors: Meyer G. Dale 
Published: December 2008

“Nescire autem quid ante quam natus sis acciderit, id est semper esse puerum. Quid enim est aetas hominis, nisi ea memoria rerum veterum cum superiorum aetate contexitur? (To be ingorant of what occurred before you were born is to remain always a child. For what is the worth of human life, unless it be woven into the life of our ancestors by the records of history?)” —Cicero: Oratur ad M. Brutum A new generation now leads. President Barack Hussein Obama straddles what Tom Brokaw called the “greatest generation” and the Baby Boomers (b. 1946–1964). Academia is now populated by “Millenials” (b. 1980–2000) and increasingly led by Generation X (b. 1960–1980). This Commentary purposively intends to create deeper conversation about the origins and tendencies in the small but interesting academic discipline of entrepreneurship. I accept my role as an aging curmudgeon and hope that you will also. My intent is to surface several operative ideologies, reveal a few egoistic tendencies, and perfectly (quack, quack) predict the future of academic entrepreneurship. Please place this Commentary in your 2039 tickler file titled “foolhardy predictions from 2009.”
Reports of Police Calls for Service as a Risk Indicator for Intimate Partner Violence
Authors: Dichter Melissa E. , Rhodes Karin V. 
Published: December 2008

AbstractObjectives:  The purpose of this study was to evaluate the utility of asking female emergency department (ED) patients about police calls for service as a possible indicator of intimate partner violence (IPV).Methods:  Trained research assistants screened female, adult, English‐speaking patients presenting to an urban university ED 7am to midnight, 7 days per week during the 2006–2007 academic year. Patients were asked two commonly used IPV screening questions regarding past‐year experience with physical violence or threat by an intimate partner and whether or not the police had been called due to a fight between themselves and a male partner.Results:  Of the 4,984 patients screened, 3.9% screened positive for an IPV‐related police call in the past 12 months; more than one‐third (37.8%) of those screened negative for IPV on the traditional screening questions. The question about an IPV‐related police call for service identified an additional 74 cases of possible IPV, representing 1.5% of the overall sample or a 30.8% increase over those identified with the traditional IPV screening questions.Conclusions:  Adding an additional question regarding police calls to standard IPV screening could alert healthcare providers to possible IPV risk.
Hepatotoxicity Despite Early Administration of Intravenous N‐Acetylcysteine for Acute Acetaminophen Overdose
Authors: Doyon Suzanne , Klein‐Schwartz Wendy 
Published: December 2008

AbstractObjectives:  The objective was to evaluate the effectiveness of intravenous N‐acetylcysteine (IV NAC; 300 mg/kg over 21 hours) in early acute acetaminophen (APAP) overdose patients.Methods:  This observational case series included patients hospitalized between 2004 and 2007 for acute APAP overdoses and who were reported to a regional poison center. Inclusion criteria were plasma APAP concentrations on or above the treatment line on the Rumack‐Matthew nomogram, administration of IV NAC within 8 hours of ingestion, and follow‐up to known outcome. The hospital chart of each patient who received IV NAC for longer than the standard 21 hours was reviewed. Hepatotoxicity was defined as hepatic aminotransferase levels greater than 1,000 IU/L.Results:  Seventy‐seven patients met inclusion criteria and received at least 21 hours of IV NAC for an acute APAP overdose. Seven patients received antidotal therapy for greater than 21 hours. These patients tended to have ingested combination preparations, have very high initial plasma APAP concentrations, and had persistently elevated plasma concentrations during their hospital stay. Hepatotoxicity occurred in 4 patients (5.2%, 95% confidence interval [CI] = 0.2% to 10.1%), including 1 death and 1 liver transplantation.Conclusions:  Hepatotoxicity developed in 5.2% of cases, suggesting that the 21‐hour IV NAC regimen is suboptimal in some patients. In addition to high initial plasma APAP concentrations, APAP product formulation and persistently elevated plasma APAP concentrations were identified as factors possibly associated with developing hepatotoxicity. The authors propose a tailored approach to the discontinuation of IV NAC and point out the need for reevaluation of optimal doses and duration of therapy.
URG11 promotes gastric cancer growth and invasion by activation of β‐catenin signalling pathway
Authors: Du Rui , Xia Lin , Sun Shiren , Lian Zhaorui , Zou Xue , Gao Juan , Xie Huahong , Fan Rui , Song Jiugang , Li Xiaohua , Liu Jie , Fan Daiming 
Published: December 2008

AbstractUpregulated gene 11 (URG11), a new gene upregulated by Heptatitis B Virus X protein (HBx), was previously shown to activate β‐catenin and promote hepatocellular growth and tumourigenesis. Although the oncogenic role of URG11 in the development of hepatocellular carcinoma has been well documented, its relevance to other human malignancies and the underlying molecular mechanisms remain largely unknown. Here we reported a novel function of URG11 to promote gastric cancer growth and metastasis. URG11 was found to be highly expressed in gastric cancer tissues compared with adjacent nontumourous ones by immunohistochemical staining and western blot. Knockdown of URG11 expression by small interfering RNA (siRNA) effectively attenuated the proliferation, anchorage‐independent growth, invasiveness and metastatic potential of gastric cancer cells. URG11 inhibition led to decreased expression of β‐catenin and its nuclear accumulation in gastric cancer cells and extensive costaining between URG11 and β‐catenin was observed in gastric cancer tissues. Transient transfection assays with the β‐catenin promoter showed that it was inhibited by URG11‐specific small inhibitory RNA. Moreover, suppression of endogenous URG11 expression results in decreased activation of β‐catenin/TCF and its downstream effector genes, cyclinD1 and membrane type 1 matrix metallopeptidase (MT1‐MMP), which are known to be involved in cell proliferation and invasion, respectively. Taken together, our data suggest that URG11 contributes to gastric cancer growth and metastasis at least partially through activation of β‐catenin signalling pathway. These findings also propose a promising target for gene therapy in gastric cancer.
The α1HCa2+channel subunit is expressed in mouse jejunal interstitial cells of Cajal and myocytes
Authors: Gibbons Simon J. , Strege Peter R. , Lei Sha , Roeder Jaime L. , Mazzone Amelia , Ou Yijun , Rich Adam , Farrugia Gianrico 
Published: December 2008

AbstractT‐type Ca2+currents have been detected in cells from the external muscular layers of gastrointestinal smooth muscles and appear to contribute to the generation of pacemaker potentials in interstitial cells of Cajal from those tissues. However, the Ca2+channel α subunit responsible for these currents has not been determined. We established that the α subunit of the α1HCa2+channel is expressed in single myocytes and interstitial cells of Cajal using reverse transcription and polymerase chain reaction from whole tissue, laser capture microdissected tissue and single cells isolated from the mouse jejunum. Whole‐cell voltage clamp recordings demonstrated that a nifedipine and Cd2+resistant, mibefradil‐sensitive current is present in myocytes dissociated from the jejunum. Electrical recordings from the circular muscle layer demonstrated that mibefradil reduced the frequency and initial rate of rise of the electrical slow wave. Gene targeted knockout of both alleles of thecacna1hgene, which encodes the α1HCa2+channel subunit, resulted in embryonic lethality because of death of the homozygous knockouts prior to E13.5 daysin utero. We conclude that a channel with the pharmacological and molecular characteristics of the α1HCa2+channel subunit is expressed in interstitial cells of Cajal and myocytes from the mouse jejunum, and that ionic conductances through the α1HCa2+channel contribute to the upstroke of the pacemaker potential. Furthermore, the survival of mice that do not express the α1HCa2+channel protein is dependent on the genetic background and targeting approach used to generate the knockout mice.
Minerval induces apoptosis in Jurkat and other cancer cells
Authors: Llado Victoria , Gutierrez Antonio , Martínez Jordi , Casas Jesús , Terés Silvia , Higuera Mónica , Galmés Antonio , Saus Carles , Besalduch Joan , Busquets Xavier , Escribá Pablo V. 
Published: December 2008

AbstractMinerval is an oleic acid synthetic analogue that impairs lung cancer (A549) cell proliferation upon modulation of the plasma membrane lipid structure and subsequent regulation of protein kinase C localization and activity. However, this mechanism does not fully explain the regression of tumours induced by this drug in animal models of cancer. Here we show that Minerval also induced apoptosis in Jurkat T‐lymphoblastic leukaemia and other cancer cells. Minerval inhibited proliferation of Jurkat cells, concomitant with a decrease of cyclin D3 and cdk2 (cyclin‐dependent kinase2). In addition, the changes that induced on Jurkat cell membrane organization caused clustering (capping) of the death receptor Fas (CD95), caspase‐8 activation and initiation of the extrinsic apoptosis pathway, which finally resulted in programmed cell death. The present results suggest that the intrinsic pathway (associated with caspase‐9 function) was activated downstream by caspase‐8. In a xenograft model of human leukaemia, Minerval also inhibited tumour progression and induced tumour cell death. Studies carried out in a wide variety of cancer cell types demonstrated that apoptosis was the main molecular mechanism triggered by Minerval. This is the first report on the pro‐apoptotic activity of Minerval, and in part explains the effectiveness of this non‐toxic anticancer drug and its wide spectrum against different types of cancer.
In GERD patients, mucosal repair associated genes are upregulated in non‐inflamed oesophageal epithelium
Authors: De Vries D. R. , Ter Linde J. J. M. , Van Herwaarden M. A. , Schwartz M. P. , Shephard P. , Geng M. M. , Smout A. J. P. M. , Samsom M. 
Published: December 2008

AbstractPrevious studies addressing the effects of acid reflux and PPI therapy on gene expression in oesophageal epithelium concentrated on inflamed tissue. We aimed to determine changes in gene expression in non‐inflamed oesophageal epithelium of GERD patients. Therefore, we included 20 GERD patients with pathological total 24‐hr acid exposure of 6–12% and SAP ≥ 95%. Ten patients discontinued PPI treatment (PPI‐), 10 took pantoprazole 40 mg bid (PPI+). Ten age/sex‐matched healthy controls were recruited. Biopsies were taken from non‐inflamed mucosa 6 cm and 16 cm proximal to the squamocolumnar junction (SCJ). Gene expression profiling of biopsies from 6 cm was performed on Human Genome U133 Plus 2.0 arrays (Affymetrix). Genes exhibiting a fold change >1.4 (t‐test P‐value < 1E– 4) were considered differentially expressed. Results were confirmed by real‐time RT‐PCR. In PPI‐ patients, 92 microarray probesets were deregulated. The majority of the corresponding genes were associated with cell–cell contacts, cytoskeletal reorganization and cellular motility, suggesting facilitation of a migratory phenotype. Genes encoding proteins with anti‐apoptotic or anti‐proliferative functions or stress‐protective functions were also deregulated. No probesets were deregulated in PPI+ patients. QPCR analysis of 20 selected genes confirmed most of the deregulations in PPI‐ patients, and showed several deregulated genes in PPI+ patients as well. In the biopsies taken at 16 cm QPCR revealed no deregulations of the selected genes. We conclude that upon acid exposure, oesophageal epithelial cells activate a process globally known as epithelial restitution: up‐regulation of anti‐apoptotic, anti‐oxidant and migration associated genes. Possibly this process helps maintaining barrier function.
Pharmacological induction of vascular extracellular superoxide dismutase expression in vivo
Authors: Oppermann Marc , Balz Vera , Adams Volker , Thao‐Vi Dao Vu , Bas Murat , Suvorava Tatsiana , Kojda Georg 
Published: December 2008

AbstractPentaerythritol tetranitrate (PETN) treatment reduces progression of atherosclerosis and endothelial dysfunction and decreases oxidation of low‐density lipoprotein (LDL) in rabbits. These effects are associated with decreased vascular superoxide production, but the underlying molecular mechanisms remain unknown. Previous studies demonstrated that endogenous nitric oxide could regulate the expression of extracellular superoxide dismutase (ecSOD) in conductance vessels in vivo. We investigated the effect of PETN and overexpression of endothelial nitric oxide synthase (eNOS++) on the expression and activity of ecSOD. C57BL/6 mice were randomized to receive placebo or increasing doses of PETN for 4 weeks and eNOS++ mice with a several fold higher endothelial‐specific eNOS expression were generated. The expression of ecSOD was determined in the lung and aortic tissue by real‐time PCR and Western blot. The ecSOD activity was measured using inhibition of cytochrome C reduction. There was no effect of PETN treatment or eNOS overexpression on ecSOD mRNA in the lung tissue, whereas ecSOD protein expression increased from 2.5‐fold to 3.6‐fold (P < 0.05) by 6 mg PETN/kg body weight (BW)/day and 60 mg PETN/kg BW/day, respectively. A similar increase was found in aortic homogenates. eNOS++ lung cytosols showed an increase of ecSOD protein level of 142 ± 10.5% as compared with transgene‐negative littermates (P < 0.05), which was abolished by Nω‐nitro‐L‐arginine treatment. In each animal group, the increase of ecSOD expression was paralleled by an increase of ecSOD activity. Increased expression and activity of microvascular ecSOD are likely induced by increased bioavailability of vascular nitric oxide. Up‐regulation of vascular ecSOD may contribute to the reported antioxidative and anti‐atherosclerotic effects of PETN.
Enforced expression of protein kinase C in skeletal muscle causes physical inactivity, fatty liver and insulin resistance in the brain
Authors: Hennige Anita M. , Heni Martin , Machann Jürgen , Staiger Harald , Sartorius Tina , Hoene Miriam , Lehmann Rainer , Weigert Cora , Peter Andreas , Bornemann Antje , Kroeber Stefan , Pujol Anna , Franckhauser Sylvie , Bosch Fatima , Schick Fritz , Lammers Reiner , Häring Hans‐Ulrich 
Published: December 2008

AbstractAmong the multitude of dysregulated signalling mechanisms that comprise insulin resistance in divergent organs, the primary events in the development of type 2 diabetes are not well established. As protein kinase C (PKC) activation is consistently present in skeletal muscle of obese and insulin resistant subjects, we generated a transgenic mouse model that overexpresses constitutively active PKC‐β2 in skeletal muscle to test whether activation of PKC is sufficient to cause an aversive whole‐body phenotype. Upon this genetic modification, increased serine phosphorylation in Irs1 was observed and followed by impaired 3H‐deoxy‐glucose uptake and muscle glycogen content, and transgenic mice exhibited insulin and glucose intolerance as they age. Muscle histochemistry revealed an increase in lipid deposition (intramyocellular lipids), and transgenic mice displayed impaired expression of transcriptional regulators of genes involved in fatty acid oxidation (peroxisome proliferator‐activated receptor‐γ, PGC‐1β, acyl‐CoA oxidase) and lipolysis (hormone‐sensitive lipase). In this regard, muscle of transgenic mice exhibited a reduced capacity to oxidize palmitate and contained less mitochondria as determined by citrate synthase activity. Moreover, the phenotype included a profound decrease in the daily running distance, intra‐abdominal and hepatic fat accumulation and impaired insulin action in the brain. Together, our data suggest that activation of a classical PKC in skeletal muscle as present in the pre‐diabetic state is sufficient to cause disturbances in whole‐body glucose and lipid metabolism followed by profound alterations in oxidative capacity, ectopic fat deposition and physical activity.
Polymorphisms in p53 and the p53 pathway: roles in cancer susceptibility and response to treatment
Authors: Hrstka Roman , Coates Philip J. , Vojtesek Borivoj 
Published: December 2008

IntroductionSNPs inTP53exons altering amino‐acid sequencePolymorphism inTP53intronsLinkage between the polymorphismsSilent mutations and SNPs inTP53Polymorphisms in other members of the p53 familyPolymorphisms in p53 target genesPolymorphisms in p53 response elementsConcluding remarksAbstractThe p53 tumour suppressor protein lies at the crossroads of multiple cellular response pathways that control the fate of the cell in response to endogenous or exogenous stresses and inactivation of the p53 tumour suppressor signalling pathway is seen in most human cancers. Such aberrant p53 activity may be caused by mutations in theTP53gene sequence producing truncated or inactive mutant proteins, or by aberrant production of other proteins that regulate p53 activity, such as gene amplification and overexpression of MDM2 or viral proteins that inhibit or degrade p53. Recent studies have also suggested that inherited genetic polymorphisms in the p53 pathway influence tumour formation, progression and/or response to therapy. In some cases, these variants are clearly associated with clinico‐pathological variables or prognosis of cancer, whereas in other cases the evidence is less conclusive. Here, we review the evidence that common polymorphisms in various aspects of p53 biology have important consequences for overall tumour susceptibility, clinico‐pathology and prognosis. We also suggest reasons for some of the reported discrepancies in the effects of common polymorphisms on tumourigenesis, which relate to the complexity of effects on tumour formation in combination with other oncogenic changes and other polymorphisms. It is likely that future studies of combinations of polymorphisms in the p53 pathway will be useful for predicting tumour susceptibility in the human population and may serve as predictive biomarkers of tumour response to standard therapies.