bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of the blood supply to the lingual surface of the mandible for reduction of bleeding during implant surgery
Authors: Tagaya Atsuko , Matsuda Yukiko , Nakajima Koh , Seki Kenji , Okano Tomohiro 
Published: March 2009

AbstractObjectives: The aim of this study was to assess the frequency of the foramina and their canals on the lingual surface of the mandible using computed tomography (CT), which was carried out for dental implant planning.Material and methods: First, the visibility of the lingual canals of the CT image was verified by dissecting five cadavers. CT images of 200 patients, who had decided on implant treatment, were used in this study. The visibility of the foramina and their canals on the lingual surface of the mandible were assessed.Results: The foramina were divided into two groups by the positions of the mandible, the medial lingual foramen and the lateral lingual foramen. At least one foramen was found in all patients. In the medial group, a higher level of mental spine was seen in 190 patients, the same level of mental spine was observed in 99 patients and a lower level of mental spine was observed in 114 patients. The lateral lingual foramina were found in 160/200 patients and 88/200 patients presented bilaterally. CT can predict the position and the size of the foramina and their canals on the lingual surface of the mandible. All the patients had more than one foramen in the middle of the lingual surface of the mandible on the CT image.Conclusion: The frequency of the lingual foramina in the medial region was 100% and that in the lateral region was 80%. It would also be useful to emphasize the significant variation in the precise location of these lingual foramina, and that these can only be visualized presurgically with volumetric imaging modalities, such as CT or Cone beam 3D systems.
Use of a new cross‐linked collagen membrane for the treatment of dehiscence‐type defects at titanium implants: a prospective, randomized‐controlled double‐blinded clinical multicenter study
Authors: Becker Jürgen , Al‐Nawas Bilal , Klein Marcus O. , Schliephake Hennig , Terheyden Hendrik , Schwarz Frank 
Published: March 2009

AbstractObjectives: The aim of the present randomized‐controlled double‐blinded clinical multicenter study was to assess the use of either a new cross‐linked (VN) or a native collagen membrane (BG) for the treatment of dehiscence‐type defects at titanium implants.Material and methods: A total of n=54 patients were recruited in four German university clinics. According to a parallel‐groups design, dehiscence‐type defects at titanium implants were filled with a natural bone mineral and randomly assigned to either VN or BG. Submerged sites were allowed to heal for 4 months. Primary (e.g., changes in defect length –ΔDL, quality of newly formed tissue [0–4] – TQ) and secondary parameters (e.g., membrane exposure, tissue conditions at dehisced sites) were consecutively recorded.Results: Four patients were excluded due to an early wound infection (VN:3; BG:1), and one patient was lost during follow‐up (VN). The mean ΔDL was 3.0 ± 2.5 mm in the VN, and 1.94 ± 2.13 mm in the BG group. The assessment of TQ revealed comparable mean values in both groups (VN: 3.05 ± 1.66, BG: 3.46 ± 1.48). A significant correlation between membrane exposure and inflammation of the adjacent soft tissue was observed in the VN group. In both groups, the mean DL and TQ values were not significantly different at either non‐exposed or exposed implant sites.Conclusion: The results of the present study have indicated that VN supported bone regeneration on a level non‐inferior to BG. However, in case of a premature membrane exposure, cross‐linking might impair soft‐tissue healing or may even cause wound infections.
Guided tissue regeneration with bioabsorbable barriers III 10‐year results in infrabony defects
Authors: Pretzl Bernadette , Kim Ti‐Sun , Steinbrenner Harald , Dörfer Christof , Himmer Katrin , Eickholz Peter 
Published: March 2009

AbstractObjective: Evaluation of the 10‐year results after GTR‐therapy of infrabony defects using two bioabsorbable barriers in a randomized‐controlled clinical trial.Material and Methods: In 15 patients with periodontitis, 15 pairs of infrabony defects were treated. For each patient, one defect received a polydioxanon (test: T) and the other received a polylactide acetyltributyl citrate (control: C) barrier by random assignment. At baseline, 12 and 120 ± 6 months after surgery, the clinical parameters and standardized radiographs were obtained.Results: Nine patients were available for the 120‐month re‐examinations. Twelve and 120 ± 6 months after therapy statistically significant (p0.004) vertical probing attachment level (PAL‐V) gain was found in both groups (T12: 3.9 ± 1.6 mm; T120: 2.4 ± 1.8 mm; C12: 4.0 ± 1.1 mm; C120: 2.4 ± 1.7 mm). From 12 to 120 months both groups experienced PAL‐V loss (T: 1.4 ± 1.5 mm, p=0.021; C: 1.6 ± 2.5 mm, p=0.09). After 120 month, two teeth were lost in the control group (one periapical lesion, and one due to unknown reason). The study failed to show statistically significant differences between both groups regarding PAL‐V gain 120 months after surgery.Conclusions: PAL‐V gain achieved after GTR therapy in infrabony defects using both bioabsorbable barriers was stable after 10 years in 15 of 22 defects (68%).
Uroprotective Effects of Curcumin in Cyclophosphamide‐Induced Haemorrhagic Cystitis Paradigm
Authors: Arafa Hossam M. M. 
Published: March 2009

Abstract:  The possible uroprotective effects of curcumin have been addressed in the current study. Haemorrhagic cystitis was induced by challenging male Swiss albino rats with a single dose of cyclophosphamide (150 mg/kg, i.p.). Curcumin (200 mg/kg, i.p.) was administered for 10 consecutive days followed by a single dose of cyclophosphamide. Haemorrhagic cystitis was well characterized morphologically and biochemically. The hallmark of this toxicity was marked congestion, oedema and extravasation in rat urinary bladder, as well as a marked desquamative damage to the urothelium and severe inflammation in the lamina propria. Leucocytic infiltration was also observed and determined by histopathological examination. Serum level of tumour necrosis factor‐alpha was notably elevated associated with apparent hypokalaemia and hyponatraemia. Bladder contents of adenosine triphosphate, reduced glutathione and glutathione‐S‐transferase activity were markedly reduced. Malondialdehyde level, myeloperoxidase activity and urinary nitrite‐nitrate levels, expressed as nitric oxide, were dramatically increased. Prior administration of curcumin ahead of cyclophosphamide challenge improved all the biochemical and histologic alterations induced by the cytotoxic drug. Based on these broad findings, it could be concluded that curcumin has proven uroprotective efficacy in this cyclophosphamide haemorrhagic cystitis model, possibly through modulating the release of inflammatory endocoids, namely tumour necrosis factor‐alpha and nitric oxide, improving the energy status and restoring the oxidant/antioxidant balance.
Comparative Evaluation of Adenosine Deaminase Activity in Cerebral Cortex and Hippocampus of Young and Adult Rats: Effect of Garlic Extract (Allium sativum L.) on Their Susceptibility to Heavy Metal Exposure
Authors: Bellé Luziane Potrich , De Bona Karine Santos , Abdalla Faida Husein , Pimentel Victor Camera , Pigatto Aline Schirmer , Moretto Maria Beatriz 
Published: March 2009

Abstract:  Adenosine plays an important neuromodulatory role in the central nervous system, and adenosine deaminase is an important enzyme in the degradation of adenine nucleotides. Methylmercury is the most prevalent form of mercury found in the environment. Methylmercury neurotoxicity has been correlated to the production of reactive oxygen species. In this study, its potential pathogenic effects were investigated in vitro in cerebral cortex and hippocampus of rats. We first observed that adenosine deaminase activity was higher in young rat brains when compared to the 60‐day‐old rats and was higher in hippocampus when compared to the cortex. Methylmercury (0.1, 1.0, 20 µM) inhibited adenosine deaminase activity in 7‐ and 60‐day‐old rats in a concentration‐dependent manner. We have demonstrated that methylmercury‐induced inhibition was antagonized by garlic alcoholic extract, but sodium selenate did not alter enzyme activity. In addition, glutathione and dithiothreitol restored the methylmercury‐induced decrease of adenosine deaminase activity. These results demonstrated that there are age‐related changes in adenosine deaminase activity and that thiol agents may contribute to the maintenance of adenosine deaminase activity and may be important in the neuromodulation of adenosine. Garlic alcoholic extract may be effective in reducing the effect of methylmercury‐induced adenosine deaminase, which may be due to its sulphur‐containing compounds.
The effects of human‐generated sound on fish
Authors: POPPER Arthur N. , HASTINGS Mardi C. 
Published: March 2009

AbstractThere is growing international concern about the effects of human‐generated sound on fish and other aquatic organisms. However, because of a striking paucity of well‐designed and controlled experimental data, very little is actually known about the effects of these sounds on fish. Findings suggest that human‐generated sounds, even from very high intensity sources, might have no effect in some cases or might result in effects that range from small and temporary shifts in behavior all the way to immediate death. At this point, however, it is nearly impossible to extrapolate from results with one sound source, one fish species, or even fish of one size to other sources, species, or fish sizes. The present paper briefly discusses the potential effects of sound on fish, describes some of the more recent well‐controlled experimental studies, and points out areas for future study that will be needed before a real understanding of the effects of sound on fish can be developed.
Equally Potent Inhibition of c-Src and Abl by Compounds that Recognize Inactive Kinase Conformations
Authors: Seeliger Markus A. , Ranjitkar Pratistha , Kasap Corynn , Shan Yibing , Shaw David E. , Shah Neil P. , Kuriyan John , Maly Dustin J. 
Published: March 2009

Abstract
Imatinib is an inhibitor of the Abl tyrosine kinase domain that is effective in the treatment of chronic myelogenic leukemia. Although imatinib binds tightly to the Abl kinase domain, its affinity for the closely related kinase domain of c-Src is at least 2,000-fold lower. Imatinib recognition requires a specific inactive conformation of the kinase domain, in which a conserved Asp-Phe-Gly (DFG) motif is flipped with respect to the active conformation. The inability of c-Src to readily adopt this flipped DFG conformation was thought to underlie the selectivity of imatinib for Abl over c-Src. Here, we present a series of inhibitors (DSA compounds) that are based on the core scaffold of imatinib but which bind with equally high potency to c-Src and Abl. The DSA compounds bind to c-Src in the DFG-flipped conformation, as confirmed by crystal structures and kinetic analysis. The origin of the high affinity of these compounds for c-Src is suggested by the fact that they also inhibit clinically relevant Abl variants bearing mutations in a structural element, the P-loop, that normally interacts with the phosphate groups of ATP but is folded over a substructure of imatinib in Abl. Importantly, several of the DSA compounds block the growth of Ba/F3 cells harboring imatinib-resistant BCR-ABL mutants, including the Thr315Ile “gatekeeper” mutation, but do not suppress the growth of parental Ba/F3 cells. [Cancer Res 2009;69(6):2384–92
A Phase II Study of Celecoxib in Combination with Paclitaxel, Carboplatin, and Radiotherapy for Patients with Inoperable Stage IIIA/B Non–Small Cell Lung Cancer
Authors: Mutter Robert , Lu Bo , Carbone David P. , Csiki Ildiko , Moretti Luigi , Johnson David H. , Morrow Jason D. , Sandler Alan B. , Shyr Yu , Ye Fei , Choy Hak 
Published: March 2009

Abstract
Purpose: Cyclooxygenase (COX)-2 up-regulation plays an important role in the pathogenesis of lung cancer. Selective COX-2 inhibitors have promoted chemosensitivity and radiosensitivity of tumor cells in preclinical trials.
Experimental Design: In a single-institution phase II study, we sought to determine the effectiveness of concurrent chemoradiation given with celecoxib and examined biomarkers to predict response to COX-2 inhibition.
Results: Seventeen patients with stage IIIA or IIIB non–small cell lung cancer (NSCLC) were enrolled in the study. All received 400 mg celecoxib twice daily continuously while on trial in addition to concurrent chemoradiation therapy with paclitaxel and carboplatin. Celecoxib was continued until disease progression. The overall objective response rate was 42.9%, and the median overall survival time was 203 days. In contrast to nonresponders, those patients with complete and partial responses had a significant decrease in the level of urinary 11α-hydroxy-9,15-dioxo-2,3,4,5-tetranor-prostane-1,20-dioic acid (PGE-M), the major metabolite of prostaglandin E2, after 1 week of celecoxib administration. Patients with very high levels of PGE-M before initiation of therapy also responded poorly to therapy. Serum vascular endothelial growth factor levels did not predict response or survival.
Conclusion: The trial was terminated because it did not meet the predetermined goal of 80% overall response rate. In unselected patients, the addition of celecoxib to concurrent chemoradiotherapy with inoperable stage IIIA/B NSCLC does not improve survival. Urinary PGE-M is a promising biomarker for predicting response to COX-2 inhibition in NSCLC.
Interaction between BCL2 and Interleukin-10 Gene Polymorphisms Alter Outcomes of Diffuse Large B-Cell Lymphoma following Rituximab Plus CHOP Chemotherapy
Authors: Park Yeon Hee , Sohn Sang Kyun , Kim Jong Gwang , Lee Myung-Hoon , Song Hong Suk , Kim Min Kyoung , Jung Joo Seop , Lee Je-Joong , Kim Hyeoung Joon , Kim Dong Hwan 
Published: March 2009

Abstract
Purpose: Rituximab may overcome bcl-2-mediated chemoresistance through the inhibition of interleukin-10 (IL-10)-mediated loops, thus down-regulating bcl-2 expression. We examined the effects of genetic variation in BCL2/IL10 gene loops on treatment outcomes of diffuse large B-cell lymphoma when treated with either CHOP or rituximab plus CHOP (R-CHOP) chemotherapy.
Experimental Design: Four genotypes were tested including BCL2 -938 C&gt;A (rs2279115), +21 A&gt;G (rs1801018), IL10 -819 T&gt;C (rs1800871), and -592 A&gt;C (rs1800872) in patients receiving either R-CHOP (n = 125) or CHOP (n = 110).
Results: IL10 SNPs, -819 TT/TC or -592 AA/AC genotypes correlated with improved CHOP response rates (P = 0.04). Neither polymorphism separately influenced the failure-free survival (FFS) or overall survival in patients, but the IL10 haplotype was associated with treatment outcomes after R-CHOP for FFS (P = 0.03) or progression (P = 0.007), whereas the -938 AA BCL2 genotype significantly affected overall survival (P = 0.04). An interactive effect between BCL2 and IL10 SNPs was significant in the group with both -938 AA BCL2 genotype and 1 to 2 copies of CC IL10 haplotype. This group showed a better FFS (P = 0.01) and a lower probability of progression (P = 0.004) compared with other genotype groups when treated with R-CHOP chemotherapy.
Conclusions: These data indicated that R-CHOP chemotherapy resistance in diffuse large B-cell lymphoma may involve interactions between the BCL2 and IL10 genes.
Novel Dithiolethione-Modified Nonsteroidal Anti-Inflammatory Drugs in Human Hepatoma HepG2 and Colon LS180 Cells
Authors: Bass Sara E. , Sienkiewicz Pawel , MacDonald Christopher J. , Cheng Robert Y.S. , Sparatore Anna , Del Soldato Piero , Roberts David D. , Moody Terry W. , Wink David A. , Yeh Grace Chao 
Published: March 2009

Abstract
Purpose: Nonsteroidal anti-inflammatory drugs (NSAID) are promising chemopreventive agents against colon and other cancers. However, the molecular basis mediated by NSAIDs for chemoprevention has not been fully elucidated. Environmental carcinogens induce DNA mutation and cellular transformation; therefore, we examined the effect of NSAIDs on carcinogenesis mediated by the aryl hydrocarbon receptor signaling pathway. In this study, we investigated the activities of a new class of NSAIDs containing dithiolethione moieties (S-NSAID) on both arms of carcinogenesis.
Experimental Design: We investigated the effects of the S-NSAIDs, S-diclofenac and S-sulindac, on carcinogen activation and detoxification mechanisms in human hepatoma HepG2 and human colonic adenocarcinoma LS180 cells.
Results: We found that S-diclofenac and S-sulindac inhibited the activity and expression of the carcinogen activating enzymes, cytochromes P-450 (CYP) CYP1A1, CYP1B1, and CYP1A2. Inhibition was mediated by transcriptional regulation of the aryl hydrocarbon receptor (AhR) pathway. The S-NSAIDs down-regulated carcinogen-induced expression of CYP1A1 heterogeneous nuclear RNA, a measure of transcription rate. Both compounds blocked carcinogen-activated AhR from binding to the xenobiotic responsive element as shown by chromatin immunoprecipitation. S-diclofenac and S-sulindac inhibited carcinogen-induced CYP enzyme activity through direct inhibition as well as through decreased transcriptional activation of the AhR. S-sulindac induced expression of several carcinogen detoxification enzymes of the glutathione cycle including glutathione S-transferase A2, glutamate cysteine ligase catalytic subunit, glutamate cysteine ligase modifier subunit, and glutathione reductase.
Conclusions: These results indicate that S-diclofenac and S-sulindac may serve as effective chemoprevention agents by favorably balancing the equation of carcinogen activation and detoxification mechanisms.
Quantitative Ultrasound Characterization of Responses to Radiotherapy in Cancer Mouse Models
Authors: Vlad Roxana M. , Brand Sebastian , Giles Anoja , Kolios Michael C. , Czarnota Gregory J. 
Published: March 2009

Abstract
Purpose: Currently, no imaging modality is used routinely to assess tumor responses to radiotherapy within hours to days after the delivery of treatment. In this study, we show the application of quantitative ultrasound methods to characterize tumor responses to cancer radiotherapy in vivo, as early as 24 hours after treatment administration.
Experimental Design: Three mouse models of head and neck cancer were exposed to radiation doses of 0, 2, 4, and 8 Gray. Data were collected with an ultrasound scanner using frequencies of 10 to 30 MHz. Ultrasound estimates calculated from normalized power spectra and parametric images (spatial maps of local estimates of ultrasound parameters) were used as indicators of response.
Results: Two of the mouse models (FaDu and C666-1) exhibited large hyperechoic regions at 24 hours after radiotherapy. The ultrasound integrated backscatter increased by 6.5 to 8.2 dB (P &lt; 0.001) and the spectral slopes increased from 0.77 to 0.90 dB/MHz for the C666-1 tumors and from 0.54 to 0.78 dB/MHz for the FaDu tumors (P &lt; 0.05), in these regions compared with preirradiated tumors. The hyperechoic regions in the ultrasound images corresponded in histology to areas of cell death. Parametric images could discern the tumor regions that responded to treatment. The other cancer mouse model (Hep-2) was resistant to radiotherapy.
Conclusions: The results indicate that cell structural changes after radiotherapy have a significant influence on ultrasound spectral parameters. This provides a foundation for future investigations regarding the use of ultrasound in cancer patients to individualize treatments noninvasively based on their responses to specific interventions.
Apo2L/TRAIL Inhibits Tumor Growth and Bone Destruction in a Murine Model of Multiple Myeloma
Authors: Labrinidis Agatha , Diamond Peter , Martin Sally , Hay Shelley , Liapis Vasilios , Zinonos Irene , Sims Natalie A. , Atkins Gerald J. , Vincent Cristina , Ponomarev Vladimir , Findlay David M. , Zannettino Andrew C.W. , Evdokiou Andreas 
Published: March 2009

AbstractPurpose: Multiple myeloma is an incurable disease, for which the development of new therapeutic approaches is required. Here, we report on the efficacy of recombinant soluble Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to inhibit tumor progression and bone destruction in a xenogeneic model of human multiple myeloma.Experimental Design: We established a mouse model of myeloma, in which Apo2L/TRAIL-sensitive RPMI-8226 or KMS-11 cells, tagged with a triple reporter gene construct (NES-HSV-TK/GFP/Luc), were transplanted directly into the tibial marrow cavity of nude mice. Tumor burden was monitored progressively by bioluminescence imaging and the development of myeloma-induced osteolysis was measured using high resolution in vivo micro-computed tomography.Results: Tumor burden increased progressively in the tibial marrow cavity of mice transplanted with Apo2L/TRAIL-sensitive RPMI-8226 or KMS-11 cells associated with extensive osteolysis directly in the area of cancer cell transplantation. Treatment of mice with recombinant soluble Apo2L/TRAIL reduced myeloma burden in the bone marrow cavity and significantly protected against myeloma-induced osteolysis. The protective effects of Apo2L/TRAIL treatment on bone were mediated by the direct apoptotic actions of Apo2L/TRAIL on myeloma cells within the bone microenvironment.Conclusions: This is the first in vivo study that investigates the efficacy of recombinant Apo2L/TRAIL on myeloma burden within the bone microenvironment and associated myeloma-induced bone destruction. Our findings that recombinant soluble Apo2L/TRAIL reduces myeloma burden within the bone microenvironment and protects the bone from myeloma-induced bone destruction argue against an inhibitory role of osteoprotegerin in Apo2L/TRAIL-induced apoptosis in vivo and highlight the need to clinically evaluate Apo2L/TRAIL in patients with multiple myeloma.
Single-Molecule Detection of Epidermal Growth Factor Receptor Mutations in Plasma by Microfluidics Digital PCR in Non–Small Cell Lung Cancer Patients
Authors: Yung Tony K.F. , Chan K.C. Allen , Mok Tony S.K. , Tong Joanna , To Ka-Fai , Lo Y.M. Dennis 
Published: March 2009

Abstract
Purpose: We aim to develop a digital PCR-based method for the quantitative detection of the two common epidermal growth factor receptor (EGFR) mutations (in-frame deletion at exon 19 and L858R at exon 21) in the plasma and tumor tissues of patients suffering from non-small cell lung cancers. These two mutations account for &gt;85% of clinically important EGFR mutations associated with responsiveness to tyrosine kinase inhibitors.
Experimental Design: DNA samples were analyzed using a microfluidics system that simultaneously performed 9,180 PCRs at nanoliter scale. A single-mutant DNA molecule in a clinical specimen could be detected and the quantities of mutant and wild-type sequences were precisely determined.
Results: Exon 19 deletion and L858R mutation were detectable in 6 (17%) and 9 (26%) of 35 pretreatment plasma samples, respectively. When compared with the sequencing results of the tumor samples, the sensitivity and specificity of plasma EGFR mutation analysis were 92% and 100%, respectively. The plasma concentration of the mutant sequences correlated well with the clinical response. Decreased concentration was observed in all patients with partial or complete clinical remission, whereas persistence of mutation was observed in a patient with cancer progression. In one patient, tyrosine kinase inhibitor was stopped after an initial response and the tumor-associated EGFR mutation reemerged 4 weeks after stopping treatment.
Conclusion: The sensitive detection and accurate quantification of low abundance EGFR mutations in tumor tissues and plasma by microfluidics digital PCR would be useful for predicting treatment response, monitoring disease progression and early detection of treatment failure associated with acquired drug resistance.