bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Acute Hypervolemic Fluid Infusion of Hydroxyethyl Starch and Gelatin on Hemostasis and Possible Mechanisms
Authors: Jin Shan-Liang , Yu Bu-Wei 
Published: October 2009

Objective: The purpose of this study was to investigate the effects of acute hypervolemic fluid infusion (AHFI) of 6% hydroxyethyl starch (HES) 130/0.4 or 4% succinylated gelatin (GEL) on hemostasis and the possible mechanisms. Methods: Thirty-six gastric cancer patients were randomized to receive AHFI of either HES, GEL or lactated Ringer’s (RL) solution at the rate of 30 mL·kg-1·h -1 from 20 minutes before to 40 minutes after induction of general anesthesia. Results: Group HES and GEL had significantly prolonged PT and aPTT, decreased VIII:C and vWF immediately after AHFI. Statistically prolonged reaction time and coagulation time, and decreased growth angle were seen immediately after HES infusion. Maximum amplitude decreased significantly in group HES and GEL immediately after and 4 hours after AHFI. Conclusion: Gelatin reduced clot quality associated with derangements of fibrin polymerization and HES 130/0.4 delayed initiation of sufficient thrombin generation to convert fibrinogen to fibrin and impaired platelet function.
Hyperhomocysteinemia and C677T MTHFR Genotype in Patients With Retinal Vein Thrombosis
Authors: Sottilotta Gianluca , Siboni Simona Maria , Latella Caterina , Oriana Vincenzo , Romeo Ermelinda , Santoro Rita , Consonni Dario , Trapani Lombardo Vincenzo 
Published: October 2009

Introduction: Elevated homocysteine (Hcy) is associated with the risk of deep vein thrombosis, pulmonary embolism, ischemic heart disease, and stroke. Several studies have suggested that hyperhomocysteinemia (HHcy) may predispose to retinal vein thrombosis (RVT) development. The aim of this study is to investigate the relationship between Hcy, C677T methylenetetrahydrofolate reductase (MTHFR) genotype, and RVT in patients compared with controls. Materials and Methods: We evaluated the Hcy plasma level of 3114 consecutive participants in 2 Italian centers during a 2-year period. Hyperhomocysteinemia was found in 99 patients and 136 healthy participants. Of the 99 patients, 20 had RVT with a high prevalence of HHcy in the RVT subgroup (20.2%). This result suggested a possible relationship between HHcy and RVT development. We investigated 105 consecutive patients with recent diagnosis of RVT, and we compared them with 226 healthy controls to evaluate whether HHcy may be a risk factor for RVT. Results: the prevalence of HHcy was higher in patients compared with controls (34.3% vs 14.2%; P < .001). The MTHFR C677T genotype was found in 69 of 105 (65.7%) patients with RVT (heterozygosity: 40 of 105 and homozygosity: 29 of 105). The control group showed the presence of MTHFR C677T genotype in 169 of 226 participants (74.8%; heterozygosity: 100 of 226 and homozygosity: 69 of 226) without difference between the 2 groups (P = .08). Conclusion: our study suggests that HHcy is a possible risk factor for RVT development, while no association was found between RVT and the C677T MTHFR genotype.
Polyploid evolution in Oryza officinalis complex of the genus Oryza
Authors: Wang Baosheng , Ding Zhuoya , Liu Wei , Pan Jin , Li Changbao , Ge Song , Zhang Daming 
Published: October 2009

Abstract

Background
Polyploidization is a prominent process in plant evolution, whereas the mechanism and tempo-spatial process remained poorly understood. Oryza officinalis complex, a polyploid complex in the genus Oryza, could exemplify the issues not only for it covering a variety of ploidy levels, but also for the pantropical geographic pattern of its polyploids in Asia, Africa, Australia and Americas, in which a pivotal genome, the C-genome, witnessed all the polyploidization process.

Results
Tracing the C-genome evolutionary history in Oryza officinalis complex, this study revealed the genomic relationships, polyploid forming and diverging times, and diploidization process, based on phylogeny, molecular-clock analyses and fluorescent in situ hybridization using genome-specific probes. Results showed that C-genome split with B-genome at ca. 4.8 Mya, followed by a series of speciation of C-genome diploids (ca. 1.8-0.9 Mya), which then partook in successive polyploidization events, forming CCDD tetraploids in ca. 0.9 Mya, and stepwise forming BBCC tetraploids between ca. 0.3-0.6 Mya. Inter-genomic translocations between B- and C-genomes were identified in BBCC tetraploid, O. punctata. Distinct FISH (fluorescent in situ hybridization) patterns among three CCDD species were visualized by C-genome-specific probes. B-genome was modified before forming the BBCC tetraploid, O. malampuzhaensis.

Conclusion
C-genome, shared by all polyploid species in the complex, had experienced different evolutionary history particularly after polyploidization, e.g., inter-genomic exchange in BBCC and genomic invasion in CCDD tetraploids. It diverged from B-genome at 4.8 Mya, then participated in the tetraploid formation spanning from 0.9 to 0.3 Mya, and spread into tropics of the disjunct continents by transcontinentally long-distance dispersal, instead of vicariance, as proposed by this study, given that the continental splitting was much earlier than the C-genome species radiation. We also find reliable evidence indicated that an extinct BB diploid species in Asia was presumptively the direct genomic donor of their sympatric tetraploids.
A comparative analysis of DNA barcode microarray feature size
Authors: Ammar Ron , Smith Andrew M , Heisler Lawrence E , Giaever Guri , Nislow Corey 
Published: October 2009

Abstract

Background
Microarrays are an invaluable tool in many modern genomic studies. It is generally perceived that decreasing the size of microarray features leads to arrays with higher resolution (due to greater feature density), but this increase in resolution can compromise sensitivity.

Results
We demonstrate that barcode microarrays with smaller features are equally capable of detecting variation in DNA barcode intensity when compared to larger feature sizes within a specific microarray platform. The barcodes used in this study are the well-characterized set derived from the Yeast KnockOut (YKO) collection used for screens of pooled yeast (Saccharomyces cerevisiae) deletion mutants. We treated these pools with the glycosylation inhibitor tunicamycin as a test compound. Three generations of barcode microarrays at 30, 8 and 5 μm features sizes independently identified the primary target of tunicamycin to be ALG7.

Conclusion
We show that the data obtained with 5 μm feature size is of comparable quality to the 30 μm size and propose that further shrinking of features could yield barcode microarrays with equal or greater resolving power and, more importantly, higher density.
A novel inhibitor of Chlamydophila pneumoniae protein kinase D (PknD) inhibits phosphorylation of CdsD and suppresses bacterial replication
Authors: Johnson Dustin L , Stone Chris B , Bulir David C , Coombes Brian K , Mahony James B 
Published: October 2009

AbstractBackgroundWe have shown previously thatChlamydophila pneumoniaecontains a dual-specific Ser/Thr protein kinase that phosphorylates CdsD, a structural component of the type III secretion apparatus. To further study the role of PknD in growth and development we sought to identify a PknD inhibitor to determine whether PknD activity is required for replication.ResultsUsing anin vitrokinase assay we screened 80 known eukaryotic protein kinase inhibitors for activity against PknD and identified a 3'-pyridyl oxindole compound that inhibited PknD autophosphorylation and phosphorylation of CdsD. The PknD inhibitor significantly retarded the growth rate ofC. pneumoniaeas evidenced by the presence of very small inclusions with a reduced number of bacteria as seen by electron microscopy. These inclusions contained the normal replicative forms including elementary bodies (EB), intermediate bodies (IB) and reticulate bodies (RB), but lacked persistent bodies (PB), indicating that induction of persistence was not the cause of reduced chlamydial growth. Blind passage ofC. pneumoniaegrown in the presence of this PknD inhibitor for 72 or 84 hr failed to produce inclusions, suggesting this compound blocks an essential step in the production of infectious chlamydial EB. The compound was not toxic to HeLa cells, did not block activation of the MEK/ERK pathway required for chlamydial invasion and did not block intracellular replication of eitherChlamydia trachomatisserovar D orSalmonella entericasv. Typhimurium suggesting that the inhibitory effect of the compound is specific forC. pneumoniae.ConclusionWe have identified a 3'-pyridyl oxindole compound that inhibits thein vitrokinase activity ofC. pneumoniaePknD and inhibits the growth and production of infectiousC. pneumoniaeprogeny in HeLa cells. Together, these results suggest that PknD may play a key role in the developmental cycle ofC. pneumoniae.
Inhibition of HIV-1 gene expression by Ciclopirox and Deferiprone, drugs that prevent hypusination of eukaryotic initiation factor 5A
Authors: Hoque Mainul , Hanauske-Abel Hartmut M , Palumbo Paul , Saxena Deepti , D'Alliessi Gandolfi Darlene , Park Myung Hee , Pe'ery Tsafi , Mathews Michael B 
Published: October 2009

Abstract

Background
Eukaryotic translation initiation factor eIF5A has been implicated in HIV-1 replication. This protein contains the apparently unique amino acid hypusine that is formed by the post-translational modification of a lysine residue catalyzed by deoxyhypusine synthase and deoxyhypusine hydroxylase (DOHH). DOHH activity is inhibited by two clinically used drugs, the topical fungicide ciclopirox and the systemic medicinal iron chelator deferiprone. Deferiprone has been reported to inhibit HIV-1 replication in tissue culture.

Results
Ciclopirox and deferiprone blocked HIV-1 replication in PBMCs. To examine the underlying mechanisms, we investigated the action of the drugs on eIF5A modification and HIV-1 gene expression in model systems. At early times after drug exposure, both drugs inhibited substrate binding to DOHH and prevented the formation of mature eIF5A. Viral gene expression from HIV-1 molecular clones was suppressed at the RNA level independently of all viral genes. The inhibition was specific for the viral promoter and occurred at the level of HIV-1 transcription initiation. Partial knockdown of eIF5A-1 by siRNA led to inhibition of HIV-1 gene expression that was non-additive with drug action. These data support the importance of eIF5A and hypusine formation in HIV-1 gene expression.

Conclusion
At clinically relevant concentrations, two widely used drugs blocked HIV-1 replication ex vivo. They specifically inhibited expression from the HIV-1 promoter at the level of transcription initiation. Both drugs interfered with the hydroxylation step in the hypusine modification of eIF5A. These results have profound implications for the potential therapeutic use of these drugs as antiretrovirals and for the development of optimized analogs.
Pancreatic ampullary carcinoma with neck metastases: a case report
Authors: Aksoy Murat , Sumer Aziz , Sari Serkan , Mete Ozgur , Salmaslioglu Artur , Erbil Yesim 
Published: October 2009

Abstract

Background
An 18-year-old Turkish woman was referred with a 6-week history of rapidly enlarging cervical mass at the left side.

Case report
She was diagnosed of ampullary carcinoma for which pancreatoduodenectomy was performed 14 months ago. In our patient with a history of malignancy, a rapidly enlarging neck mass was considered a metastasis to the neck. Tumor resection was performed. Histopathological examination revealed the metastasis of the precedent ampullary adenocarcinoma.

Conclusion
Surgery does not improve survival for advanced metastatic ampullary cancer however, it can be mandatory in specific conditions as our patient.
Daunorubicin Versus Mitoxantrone Versus Idarubicin As Induction and Consolidation Chemotherapy for Adults With Acute Myeloid Leukemia: The EORTC and GIMEMA Groups Study AML-10
Authors: Mandelli Franco , Vignetti Marco , Suciu Stefan , Stasi Roberto , Petti Maria-Concetta , Meloni Giovanna , Muus Petra , Marmont Filippo , Marie Jean-Pierre , Labar Boris , Thomas Xavier , Di Raimondo Francesco , Willemze Roel , Liso Vincenzo , Ferrara Felicetto , Baila Liliana , Fazi Paola , Zittoun Robert , Amadori Sergio , de Witte Theo 
Published: October 2009

Purpose To compare the antitumor efficacy of three different anthracyclines in combination with cytarabine and etoposide in adult patients with newly diagnosed acute myeloid leukemia (AML). Patients and Methods We randomly assigned 2,157 patients (age range, 15 to 60 years) to receive intensive induction-consolidation chemotherapy containing either daunorubicin, idarubicin, or mitoxantrone. After achieving complete remission (CR), patients were assigned to undergo either allogeneic or autologous stem-cell transplantation (SCT), depending on the availability of a sibling donor. Results The overall CR rate (69%) was similar in the three groups. Autologous SCT was performed in 37% of cases in the daunorubicin arm versus only 29% and 31% in mitoxantrone and idarubicin, respectively (P < .001). However, the disease-free survival (DFS) and survival from CR were significantly shorter in the daunorubicin arm: the 5-year DFS was 29% versus 37% and 37% in mitoxantrone and idarubicin, respectively. The proportion of patients who underwent allogeneic SCT (22%) was equivalent in the three treatment groups, and the outcome was similar as well: the 5-year overall survival rates were 34%, 34%, and 31%, respectively. Conclusion In adult patients with AML who do not receive an allogeneic SCT, the use of mitoxantrone or idarubicin instead of daunorubicin enhances the long-term efficacy of chemotherapy.
Local Excision Alone Without Irradiation for Ductal Carcinoma In Situ of the Breast: A Trial of the Eastern Cooperative Oncology Group
Authors: Hughes Lorie L. , Wang Molin , Page David L. , Gray Robert , Solin Lawrence J. , Davidson Nancy E. , Lowen Mary Ann , Ingle James N. , Recht Abram , Wood William C. 
Published: October 2009

PurposeTo determine the risk of ipsilateral breast events in patients with ductal carcinoma in situ (DCIS) treated with local excision without irradiation.Patients and MethodsPatients with either low- or intermediate-grade DCIS measuring 2.5 cm or smaller, or high-grade DCIS measuring 1 cm or smaller who had microscopic margin widths of 3 mm or wider and no residual calcifications on postoperative mammograms were eligible for a prospective trial conducted from 1997 to 2002 by the Eastern Cooperative Oncology Group and North Central Cancer Treatment Group. Patients entered in 2000 and later could take tamoxifen if they wished. Median age at last surgery for the entire population was 60 years (range, 28 to 88 years), and median tumor sizes in the two strata were 6 mm and 5 mm, respectively.ResultsWith a median follow-up of 6.2 years, the 5-year rate of ipsilateral breast events in the 565 eligible patients in the low/intermediate grade stratum was 6.1% (95% CI, 4.1% to 8.2%). With a median follow-up of 6.7 years, this incidence for the 105 eligible patients in the high-grade stratum was 15.3% (95% CI, 8.2% to 22.5%).ConclusionRigorously evaluated and selected patients with low- to intermediate-grade DCIS with margins 3 mm or wider had an acceptably low rate of ipsilateral breast events at 5 years after excision without irradiation. Patients with high-grade lesions had a much higher rate, suggesting that excision alone is inadequate treatment. Further follow-up is necessary to document long-term results.
Histone Deacetylase Inhibitors in Cancer Therapy
Authors: Lane Andrew A. , Chabner Bruce A. 
Published: October 2009

Purpose Epigenetic processes are implicated in cancer causation and progression. The acetylation status of histones regulates access of transcription factors to DNA and influences levels of gene expression. Histone deacetylase (HDAC) activity diminishes acetylation of histones, causing compaction of the DNA/histone complex. This compaction blocks gene transcription and inhibits differentiation, providing a rationale for developing HDAC inhibitors. Methods In this review, we explore the biology of the HDAC enzymes, summarize the pharmacologic properties of HDAC inhibitors, and examine results of selected clinical trials. We consider the potential of these inhibitors in combination therapy with targeted drugs and with cytotoxic chemotherapy. Results HDAC inhibitors promote growth arrest, differentiation, and apoptosis of tumor cells, with minimal effects on normal tissue. In addition to decompaction of the histone/DNA complex, HDAC inhibition also affects acetylation status and function of nonhistone proteins. HDAC inhibitors have demonstrated antitumor activity in clinical trials, and one drug of this class, vorinostat, is US Food and Drug Administration approved for the treatment of cutaneous T-cell lymphoma. Other inhibitors in advanced stages of clinical development, including depsipeptide and MGCD0103, differ from vorinostat in structure and isoenzyme specificity, and have shown activity against lymphoma, leukemia, and solid tumors. Promising preclinical activity in combination with cytotoxics, inhibitors of heat shock protein 90, and inhibitors of proteasome function have led to combination therapy trials. Conclusion HDAC inhibitors are an important emerging therapy with single-agent activity against multiple cancers, and have significant potential in combination use.
Phase II Study of Flavopiridol in Relapsed Chronic Lymphocytic Leukemia Demonstrating High Response Rates in Genetically High-Risk Disease
Authors: Lin Thomas S. , Ruppert Amy S. , Johnson Amy J. , Fischer Beth , Heerema Nyla A. , Andritsos Leslie A. , Blum Kristie A. , Flynn Joseph M. , Jones Jeffrey A. , Hu Weihong , Moran Mollie E. , Mitchell Sarah M. , Smith Lisa L. , Wagner Amy J. , Raymond Chelsey A. , Schaaf Larry J. , Phelps Mitch A. , Villalona-Calero Miguel A. , Grever Michael R. , Byrd John C. 
Published: October 2009

Purpose Patients with chronic lymphocytic leukemia (CLL) with high-risk genomic features achieve poor outcomes with traditional therapies. A phase I study of a pharmacokinetically derived schedule of flavopiridol suggested promising activity in CLL, irrespective of high-risk features. Given the relevance of these findings to treating genetically high-risk CLL, a prospective confirmatory study was initiated. Patients and Methods Patients with relapsed CLL were treated with single-agent flavopiridol, with subsequent addition of dexamethasone to suppress cytokine release syndrome (CRS). High-risk genomic features were prospectively assessed for response to therapy. Results Sixty-four patients were enrolled. Median age was 60 years, median number of prior therapies was four, and all patients had received prior purine analog therapy. If patients tolerated treatment during week 1, dose escalation occurred during week 2. Dose escalation did not occur in four patients, as a result of severe tumor lysis syndrome; three of these patients required hemodialysis. Thirty-four patients (53%) achieved response, including 30 partial responses (PRs; 47%), three nodular PRs (5%), and one complete response (1.6%). A majority of high-risk patients responded; 12 (57%) of 21 patients with del(17p13.1) and 14 (50%) of 28 patients with del(11q22.3) responded irrespective of lymph node size. Median progression-free survival among responders was 10 to 12 months across all cytogenetic risk groups. Reducing the number of weekly treatments per cycle from four to three and adding prophylactic dexamethasone, which abrogated interleukin-6 release and CRS (P ≤ .01), resulted in improved tolerability and treatment delivery. Conclusion Flavopiridol achieves significant clinical activity in patients with relapsed CLL, including those with high-risk genomic features and bulky lymphadenopathy. Subsequent clinical trials should use the amended treatment schedule developed herein and prophylactic corticosteroids.
Prognostic Acceptance and the Well-Being of Patients Receiving Palliative Care for Cancer
Authors: Thompson Genevieve N. , Chochinov Harvey M. , Wilson Keith G. , McPherson Christine J. , Chary Srini , O'Shea Fiona M. , Kuhl David R. , Fainsinger Robin L. , Gagnon Pierre R. , Macmillan Karen A. 
Published: October 2009

Purpose To identify the impact of prognostic acceptance/nonacceptance on the physical, psychological, and existential well-being of patients with advanced cancer. Patients and Methods A Canadian multicenter prospective national survey was conducted of patients diagnosed with advanced cancer with an estimated survival duration of 6 months or less (n = 381) receiving palliative care services. Results Of the total number of participants, 74% reported accepting their situation and 8.6% reported accepting with “moderate” to “extreme” difficulty. More participants with acceptance difficulties than without acceptance difficulties met diagnostic criteria for a depressive or anxiety disorder (χ2 = 8.67; P < .01). Nonacceptors were younger (t = 4.13; P < .000), had more than high school education (χ2 = 4.69; P < .05), and had smaller social networks (t = 2.53; P < .05) than Acceptors. Of the Nonacceptors, 42% described their experience as one of “moderate” to “extreme” suffering compared with 24.1% of Acceptors (χ2 = 5.28; P < .05). More than one third (37.5%) of Nonacceptors reported feeling hopeless compared with 8.6% who had no difficulty accepting (χ2 = 24.76; P < .000). Qualitatively, participants described active and passive coping strategies that helped them accept what was happening to them, as well as barriers that made it difficult to come to terms with their current situation. Conclusion The challenge of coming to terms with a terminal prognosis is a complex interplay between one's basic personality, the availability of social support, and one's spiritual and existential views on life. Nonacceptance appears to be highly associated with feelings of hopelessness, a sense of suffering, depression, and anxiety, along with difficulties in terms of social–relational concerns.
Physician Referral for Fertility Preservation in Oncology Patients: A National Study of Practice Behaviors
Authors: Quinn Gwendolyn P. , Vadaparampil Susan T. , Lee Ji-Hyun , Jacobsen Paul B. , Bepler Gerold , Lancaster Johnathan , Keefe David L. , Albrecht Terrance L. 
Published: October 2009

Purpose Cancer survival rates are improving, and the focus is moving toward quality survival. Fertility is a key aspect of quality of life for cancer patients of childbearing age. Although cancer treatment may impair fertility, some patients may benefit from referral to a specialist before treatment. However, the majority of studies examining patient recall of discussion and referral for fertility preservation (FP) show that less than half receive this information. This study examined the referral practices of oncologists in the United States. Methods This study examined oncologists' referral practice patterns for FP among US physicians using the American Medical Association Physician Masterfile database. A 53-item survey was administered via mail and Internet to a stratified random sample of US physicians. Results Forty-seven percent of respondents routinely refer cancer patients of childbearing age to a reproductive endocrinologist. Referrals were more likely among female physicians (P = .004), those with favorable attitudes (P = .043), and those whose patients routinely ask about FP (odds ratio = 2.09; 95% CI, 1.31 to 3.33). Conclusion Less than half of US physicians are following the guidelines from the American Society of Clinical Oncology, which suggest that all patients of childbearing age should be informed about FP.