bluuebunny/crossref_metadata_2025_split huggingface dataset:
Therapeutic management of neonatal chylous ascites: report of a case and review of the literature
Authors: Karagol Belma Saygili , Zenciroglu Aysegul , Gokce Selim , Kundak Ahmet Afsin , Ipek Mehmet Sah 
Published: April 2010

AbstractCongenital chylous ascites is a rare condition seen in the neonatal period and the data on pathogenesis and treatment modalities are limited. In this article, we report a case of neonate with chylous ascites and review the therapeutic management procedures on chylous ascites in childhood. We present our experience in the diagnosis and treatment of this condition.Conclusion:  Medium‐chain triglycerides (MCT)‐based diet can be tried as a first option in chylous ascites treatment. In resistant or unresponsive cases, somatostatin along with TPN can have use in closing the lymphatic leakage or relieving the symptoms effectively and rapidly. Conventional regimens including enteral feeding with MCT‐based formula can then be re‐administered as a maintenance treatment after reduction of lymph flow with the use of total parenteral nutrition (TPN) and somatostatin infusion combination. Patient‐specific approach should be attempted for chylous ascites caused by various disorders and started as soon as possible.
GIP and GLP‐1, the two incretin hormones: Similarities and differences
Authors: Seino Yutaka , Fukushima Mitsuo , Yabe Daisuke 
Published: April 2010

AbstractGastric inhibitory polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1) are the two primary incretin hormones secreted from the intestine on ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. GIP and GLP‐1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP‐1 receptor (GLP‐1R), which belong to the G‐protein coupled receptor family. Receptor binding activates and increases the level of intracellular cyclic adenosine monophosphate in pancreatic β cells, thereby stimulating insulin secretion glucose‐dependently. In addition to their insulinotropic effects, GIP and GLP‐1 play critical roles in various biological processes in different tissues and organs that express GIPR and GLP‐1R, including the pancreas, fat, bone and the brain. Within the pancreas, GIP and GLP‐1 together promote β cell proliferation and inhibit apoptosis, thereby expanding pancreatic β cell mass, while GIP enhances postprandial glucagon response and GLP‐1 suppresses it. In adipose tissues, GIP but not GLP‐1 facilitates fat deposition. In bone, GIP promotes bone formation while GLP‐1 inhibits bone absorption. In the brain, both GIP and GLP‐1 are thought to be involved in memory formation as well as the control of appetite. In addition to these differences, secretion of GIP and GLP‐1 and their insulinotropic effects on β cells have been shown to differ in patients with type 2 diabetes compared to healthy subjects. We summarize here the similarities and differences of these two incretin hormones in secretion and metabolism, their insulinotropic action on pancreatic β cells, and their non‐insulinotropic effects, and discuss their potential in treatment of type 2 diabetes. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00022.x, 2010)
An extension of Buchberger’s criteria for Gröbner basis decision
Authors: Perry John 
Published: April 2010

AbstractTwo fundamental questions in the theory of Gröbner bases are decision (‘Is a basis G of a polynomial ideal a Gröbner basis?’) and transformation (‘If it is not, how do we transform it into a Gröbner basis?’) This paper considers the first question. It is well known that G is a Gröbner basis if and only if a certain set of polynomials (the S-polynomials) satisfy a certain property. In general there are m(m−1)/2 of these, where m is the number of polynomials in G, but criteria due to Buchberger and others often allow one to consider a smaller number. This paper presents two original results. The first is a new characterization theorem for Gröbner bases that makes use of a new criterion that extends Buchberger’s criteria. The second is the identification of a class of polynomial systems G for which the new criterion has dramatic impact, reducing the worst-case scenario from m(m−1)/2 S-polynomials to m−1.
Vaccination of Rabbits with an Alkylated Toxoid Rapidly Elicits Potent Neutralizing Antibodies against Botulinum Neurotoxin Serotype B
Authors: Held Daniel M. , Shurtleff Amy C. , Fields Scott , Green Christopher , Fong Julie , Jones Russell G. A. , Sesardic Dorothea , Buelow Roland , Burke Rae Lyn 
Published: April 2010

ABSTRACT

New Zealand White (NZW) rabbits were immunized with several different nontoxic botulinum neurotoxin serotype B (BoNT/B) preparations in an effort to optimize the production of a rapid and highly potent, effective neutralizing antibody response. The immunogens included a recombinant heavy chain (rHc) protein produced in
Escherichia coli
, a commercially available formaldehyde-inactivated toxoid, and an alkylated toxoid produced by urea-iodoacetamide inactivation of the purified active toxin. All three immunogens elicited an antibody response to BoNT/B, detected by enzyme-linked immunosorbent assay (ELISA) and by toxin neutralization assay, by the use of two distinct mouse toxin challenge models. The induction period and the ultimate potency of the observed immune response varied for each immunogen, and the ELISA titer was not reliably predictive of the potency of toxin neutralization. The kinetics of the BoNT/B-specific binding immune response were nearly identical for the formaldehyde toxoid and alkylated toxoid immunogens, but immunization with the alkylated toxoid generated an approximately 10-fold higher neutralization potency that endured throughout the study, and after just 49 days, each milliliter of serum was capable of neutralizing 10
7
50% lethal doses of the toxin. Overall, the immunization of rabbits with alkylated BoNT/B toxoid appears to have induced a neutralizing immune response more rapid and more potent than the responses generated by vaccination with formaldehyde toxoid or rHc preparations.
Microsatellite Typing To Trace
Aspergillus flavus
Infections in a Hematology Unit
Authors: Hadrich Inès , Makni Fattouma , Ayadi Ali , Ranque Stéphane 
Published: April 2010

ABSTRACT

Assessing the relatedness of strains isolated from patients and their environment is instrumental in documenting the source of preventable health care-associated life-threatening
Aspergillus flavus
human infection clusters. The present study aimed at identifying and selecting suitable microsatellite markers for
A. flavus
typing. This typing scheme was then applied to investigate the
A. flavus
epidemiology within a hematology unit in Sfax, Tunisia. Use of a combination of five markers made it possible to discern clusters of isolates and to substantiate the genetic diversity of
A. flavus
within clusters. Isolates from Tunisia and Marseille, France, displayed distinct haplotypes, indicating a highly significant geographical structuring of
A. flavus
. The typing of clinical and environmental
A. flavus
isolates in a hematology unit provided insights into its hospital epidemiology. From a heterogeneous genetic background, a cluster indicative of a clonal propagation episode within the unit could be identified. In two patients with invasive aspergillosis, the same genotype was found in clinical and environmental isolates, indicating hospital-acquired colonization and infection. In further studies, this novel microsatellite typing scheme might be instrumental in illuminating important epidemiological issues about
A. flavus
population genetics or epidemiology, including tracing the sources and routes of transmission.
Long-Term Control of HIV-1 in Hemophiliacs Carrying Slow-Progressing Allele HLA-B*5101
Authors: Kawashima Yuka , Kuse Nozomi , Gatanaga Hiroyuki , Naruto Takuya , Fujiwara Mamoru , Dohki Sachi , Akahoshi Tomohiro , Maenaka Katsumi , Goulder Philip , Oka Shinichi , Takiguchi Masafumi 
Published: April 2010

ABSTRACTHLA-B*51 alleles are reported to be associated with slow disease progression to AIDS, but the mechanism underlying this association is still unclear. In the present study, we analyzed the effect of HLA-B*5101 on clinical outcome for Japanese hemophiliacs who had been infected with HIV-1 before 1985 and had been recruited in 1998 for this study. HLA-B*5101+hemophiliacs exhibited significantly slow progression. The analysis of HLA-B*5101-restricted HIV-1-specific cytotoxic T-lymphocyte (CTL) responses to 4 HLA-B*-restricted epitopes in 10 antiretroviral-therapy (ART)-free HLA-B*5101+hemophiliacs showed that the frequency of Pol283-8-specific CD8+T cells was inversely correlated with the viral load, whereas the frequencies of CD8+T cells specific for 3 other epitopes were positively correlated with the viral load. The HLA-B*5101+hemophiliacs whose HIV-1 replication had been controlled for approximately 25 years had HIV-1 possessing the wild-type Pol283-8 sequence or the Pol283-8V mutant, which does not critically affect T-cell recognition, whereas other HLA-B*5101+hemophiliacs had HIV-1 with escape mutations in this epitope. The results suggest that the control of HIV-1 over approximately 25 years in HLA-B*5101-positive hemophiliacs is associated with a Pol283-8-specific CD8+T-cell response and that lack of control of HIV-1 is associated with the appearance of Pol283-8-specific escape mutants.
Evaluation of Cellular Determinants Required for
In Vitro
Xenotropic Murine Leukemia Virus-Related Virus Entry into Human Prostate Cancer and Noncancerous Cells
Authors: Bhosle Sushma , Suppiah Suganthi , Molinaro Ross , Liang Yuying , Arnold Rebecca , Diehl William , Makarova Natalia , Blackwell Jerry , Petros John , Liotta Dennis , Hunter Eric , Ly Hinh 
Published: April 2010

ABSTRACT

The newly identified retrovirus—the xenotropic murine leukemia virus-related virus (XMRV)—has recently been shown to be strongly associated with familial prostate cancer in humans (A. Urisman et al., PLoS Pathog.
2:
e25, 2006). While that study showed evidence of XMRV infection exclusively in the prostatic stromal fibroblasts, a recent study found XMRV protein antigens mainly in malignant prostate epithelial cells (R. Schlaberg et al., Proc. Natl. Acad. Sci. U. S. A.
106:
16351-16356, 2009). To help elucidate the mechanisms behind XMRV infection, we show that prostatic fibroblast cells express Xpr1, a known receptor of XMRV, but its expression is absent in other cell lines of the prostate (i.e., epithelial and stromal smooth muscle cells). We also show that certain amino acid residues located within the predicted extracellular loop (ECL3 and ECL4) sequences of Xpr1 are required for efficient XMRV entry. Although we found strong evidence to support XMRV infection of prostatic fibroblast cell lines via Xpr1, we learned that XMRV was indeed capable of infecting cells that did not necessarily express Xpr1, such as those of the prostatic epithelial and smooth muscle origins. Further studies suggest that the expression of Xpr1 and certain genotypes of the
RNASEL
gene, which could restrict XMRV infection, may play important roles in defining XMRV tropisms in certain cell types. Collectively, our data reveal important cellular determinants required for XMRV entry into different human prostate cells
in vitro
, which may provide important insights into the possible role of XMRV as an etiologic agent in human prostate cancer.
Integrin α4β7 Is Downregulated on the Surfaces of Simian Immunodeficiency Virus SIVmac239-Infected Cells
Authors: Budde Melisa L. , Lhost Jennifer J. , Dudley Dawn M. , Rakasz Eva G. , O'Connor David H. 
Published: April 2010

ABSTRACT

Simian immunodeficiency virus (SIV) and human immunodeficiency virus (HIV) infection results in an early and enduring depletion of intestinal CD4
+
T cells. SIV and HIV bind integrin α4β7, thereby facilitating infection of lymphocytes that home to the gut-associated lymphoid tissue (GALT). Using an ex vivo flow cytometry assay, we found that SIVmac239-infected cells expressed significantly lower levels of integrin α4β7 than did uninfected cells. This finding suggested a potential viral effect on integrin α4β7 expression. Using an
in vitro
model, we confirmed that integrin α4β7 was downregulated on the surfaces of SIVmac239-infected cells. Further, modulation of integrin α4β7 was dependent on
de novo
synthesis of viral proteins, but neither cell death, the release of a soluble factor, nor a change in activation state was involved. Downregulation of integrin α4β7 may have an unappreciated role in the CD4 depletion of the mucosal-associated lymphoid compartments, susceptibility to superinfection, and/or immune evasion.
Genome-Scale Phylogenetic Analyses of Chikungunya Virus Reveal Independent Emergences of Recent Epidemics and Various Evolutionary Rates
Authors: Volk Sara M. , Chen Rubing , Tsetsarkin Konstantin A. , Adams A. Paige , Garcia Tzintzuni I. , Sall Amadou A. , Nasar Farooq , Schuh Amy J. , Holmes Edward C. , Higgs Stephen , Maharaj Payal D. , Brault Aaron C. , Weaver Scott C. 
Published: April 2010

ABSTRACT

Chikungunya virus
(CHIKV), a mosquito-borne alphavirus, has traditionally circulated in Africa and Asia, causing human febrile illness accompanied by severe, chronic joint pain. In Africa, epidemic emergence of CHIKV involves the transition from an enzootic, sylvatic cycle involving arboreal mosquito vectors and nonhuman primates, into an urban cycle where peridomestic mosquitoes transmit among humans. In Asia, however, CHIKV appears to circulate only in the endemic, urban cycle. Recently, CHIKV emerged into the Indian Ocean and the Indian subcontinent to cause major epidemics. To examine patterns of CHIKV evolution and the origins of these outbreaks, as well as to examine whether evolutionary rates that vary between enzootic and epidemic transmission, we sequenced the genomes of 40 CHIKV strains and performed a phylogenetic analysis representing the most comprehensive study of its kind to date. We inferred that extant CHIKV strains evolved from an ancestor that existed within the last 500 years and that some geographic overlap exists between two main enzootic lineages previously thought to be geographically separated within Africa. We estimated that CHIKV was introduced from Africa into Asia 70 to 90 years ago. The recent Indian Ocean and Indian subcontinent epidemics appear to have emerged independently from the mainland of East Africa. This finding underscores the importance of surveillance to rapidly detect and control African outbreaks before exportation can occur. Significantly higher rates of nucleotide substitution appear to occur during urban than during enzootic transmission. These results suggest fundamental differences in transmission modes and/or dynamics in these two transmission cycles.
Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity
Authors: Lousberg Erin L. , Fraser Cara K. , Tovey Michael G. , Diener Kerrilyn R. , Hayball John D. 
Published: April 2010

ABSTRACT
Type I interferons (IFNs) are considered to be important mediators of innate immunity due to their inherent antiviral activity, ability to drive the transcription of a number of genes involved in viral clearance, and their role in the initiation of innate and adaptive immune responses. Due to the central role of type I IFNs, we sought to determine their importance in the generation of immunity to a recombinant vaccine vector fowlpox virus (FPV). In analyzing the role of type I IFNs in immunity to FPV, we show that they are critical to the secretion of a number of innate and proinflammatory cytokines, including type I IFNs themselves as well as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-α), IL-6, and IL-1β, and that deficiency leads to enhanced virus-mediated antigen expression. Interestingly, however, type I IFNs were not required for adaptive immune responses to recombinant FPV even though plasmacytoid dendritic cells (pDCs), the primary producers of type I IFNs, have been shown to be requisite for this to occur. Furthermore, we provide evidence that the importance of pDCs may lie in their ability to capture and present virally derived antigen to T cells rather than in their capacity as professional type I IFN-producing cells.
Small Noncoding RNAs Encoded within the Bovine Herpesvirus 1 Latency-Related Gene Can Reduce Steady-State Levels of Infected Cell Protein 0 (bICP0)
Authors: Jaber Tareq , Workman Aspen , Jones Clinton 
Published: April 2010

ABSTRACT
Following acute infection in mucosal epithelium, bovine herpes virus 1 (BHV-1) establishes lifelong latency in sensory neurons within trigeminal ganglia. The latency-related RNA (LR-RNA) is abundantly expressed in sensory neurons of latently infected calves. Expression of LR proteins is necessary for the latency reactivation cycle because a mutant virus that does not express LR proteins is unable to reactivate from latency after dexamethasone treatment. LR-RNA sequences also inhibit bICP0 expression, productive infection, and cell growth. However, it is unclear how LR-RNA mediates these functions. In this study, we identified a 463-bp region within the LR gene (the XbaI-PstI [XP] fragment) that inhibited bICP0 protein and RNA expression in transiently transfected mouse neuroblastoma cells. Small noncoding RNAs (sncRNAs) encoded within the XP fragment (20 to 90 nucleotides in length) were detected in transiently transfected mouse neuroblastoma cells. Two families of sncRNAs were cloned from this region, and each family was predicted to contain a mature microRNA (miRNA). Both miRNAs were predicted to base pair with bICP0 mRNA sequences, suggesting that they reduce bICP0 levels. To test this prediction, sequences encompassing the respective sncRNAs and mature miRNAs were synthesized and cloned into a small interfering RNA expression vector. Both sncRNA families and their respective miRNAs inhibited bICP0 protein expression in mouse neuroblastoma cells and productive infection in bovine cells. In trigeminal ganglia of latently infected calves, an sncRNA that migrated between nucleotides 20 and 25 hybridized to the XP fragment. During dexamethasone-induced reactivation from latency, XP-specific sncRNA levels were reduced, suggesting that these sncRNAs support the establishment and maintenance of lifelong latency in cattle.
Microcatheter contrast injections during intra-arterial thrombolysis increase intracranial hemorrhage risk
Authors: Khatri Rakesh , Khatri Pooja , Khoury Jane , Broderick Joseph , Carrozzella Janice , Tomsick Thomas 
Published: April 2010

Background and purposeCombined analysis of the Interventional Management of Stroke I and II trials demonstrated a significant association between microcatheter contrast injections and both intracranial hemorrhage (ICH) and contrast extravasation following combined intravenous (IV) and intra-arterial (IA) thrombolysis. The reliability of these observations was tested in our local registry of IA cases.Design/methodsTreatment angiograms and post-procedure CTs of patients treated with combined IV/IA or IA only recombinant tissue plasminogen activator for ICA-T, M1 or M2 occlusions (n=77) were reviewed. The number of microcatheter injections (MCIs) within/distal to the target occlusion was assigned for every case. The association of MCIs to total ICH, total parenchymal hematoma (PH1+PH2) and PH2 after adjusting for significant covariates was tested.ResultsMCIs were used in 21 (27%) cases (range MCI 0–6). Any ICH occurred in 38 (49%) cases, including eight (10%) PH1s and eight (10%) PH2s. The use of MCIs was associated with increased PH (p=0.04), PH2 (p=0.07) and total ICH (p=0.03). MCIs were associated with increased contrast extravasation (CEx) (p=0.02). ICH was observed in all CEx cases (n=5, 100% vs 46% non-CEx; p=0.03), and four (80%) CEx cases developed PH2s (p<0.01). MCIs remained associated with total ICH after adjustment for significant covariates of Thromolysis in Cerebral Infarction score, glucose level and presence of atrial fibrillation (OR 3.60; 95% CI 1.12 to 11.49, p=0.03). MCI use was the only significantly associated covariate for total PHs.ConclusionsMCI use was associated with ICH and with clinically significant PHs in this cohort, providing further evidence that MCIs be reduced during IA thrombolysis.
The Transcriptional Coregulator RIP140 Represses E2F1 Activity and Discriminates Breast Cancer Subtypes
Authors: Docquier Aurélie , Harmand Pierre-Olivier , Fritsch Samuel , Chanrion Maïa , Darbon Jean-Marie , Cavaillès Vincent 
Published: April 2010

Abstract
Purpose: Receptor-interacting protein of 140 kDa (RIP140) is a transcriptional cofactor for nuclear receptors involved in reproduction and energy homeostasis. Our aim was to investigate its role in the regulation of E2F1 activity and target genes both in breast cancer cell lines and in tumor biopsies.
Experimental Design: Glutathione S-transferase pull-down assays, coimmunoprecipitation experiments, and chromatin immunoprecipitation analysis were used to evidence interaction between RIP140 and E2F1. The effects of RIP140 expression on E2F1 activity were determined using transient transfection and quantification of E2F target mRNAs by quantitative real-time PCR. The effect on cell cycle was assessed by fluorescence-activated cell sorting analysis on cells overexpressing green fluorescent protein–tagged RIP140. A tumor microarray data set was used to investigate the expression of RIP140 and E2F1 target genes in 170 breast cancer patients.
Results: We first evidenced the complex interaction between RIP140 and E2F1 and showed that RIP140 represses E2F1 transactivation on various transiently transfected E2F target promoters and inhibits the expression of several E2F1 target genes (such as CCNE1 and CCNB2). In agreement with a role for RIP140 in the control of E2F activity, we show that increasing RIP140 levels results in a reduction in the proportion of cells in S phase in various human cell lines. Finally, analysis of human breast cancers shows that low RIP140 mRNA expression was associated with high E2F1 target gene levels and basal-like tumors.
Conclusion: This study shows that RIP140 is a regulator of the E2F pathway, which discriminates luminal- and basal-like tumors, emphasizing the importance of these regulations for a clinical cancer phenotype. Clin Cancer Res; 16(11); 2959–70. ©2010 AACR.