bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional phosphoproteomic profiling of phosphorylation sites in membrane fractions of salt-stressed Arabidopsis thaliana
Authors: Hsu Jue-Liang , Wang Lan-Yu , Wang Shu-Ying , Lin Ching-Huang , Ho Kuo-Chieh , Shi Fong-Ku , Chang Ing-Feng 
Published: November 2009

AbstractBackgroundUnder conditions of salt stress, plants respond by initiating phosphorylation cascades. Many key phosphorylation events occur at the membrane. However, to date only limited sites have been identified that are phosphorylated in response to salt stress in plants.ResultsMembrane fractions from three-day and 200 mM salt-treated Arabidopsis suspension plants were isolated, followed by protease shaving and enrichment using Zirconium ion-charged magnetic beads, and tandem mass spectrometry analyses. From this isolation, 18 phosphorylation sites from 15Arabidopsisproteins were identified. A unique phosphorylation site in 14-3-3-interacting protein AHA1 was predominately identified in 200 mM salt-treated plants. We also identified some phosphorylation sites in aquaporins. A doubly phosphorylated peptide of PIP2;1 as well as a phosphopeptide containing a single phosphorylation site (Ser-283) and a phosphopeptide containing another site (Ser-286) of aquaporin PIP2;4 were identified respectively. These two sites appeared to be novel of which were not reported before. In addition, quantitative analyses of protein phosphorylation with either label-free or stable-isotope labeling were also employed in this study. The results indicated that level of phosphopeptides on five membrane proteins such as AHA1, STP1, Patellin-2, probable inactive receptor kinase (At3g02880), and probable purine permease 18 showed at least two-fold increase in comparison to control in response to 200 mM salt-stress.ConclusionIn this study, we successfully identified novel salt stress-responsive protein phosphorylation sites from membrane isolates of abiotic-stressed plants by membrane shaving followed by Zr4+-IMAC enrichment. The identified phosphorylation sites can be important in the salt stress response in plants.
Comparative analysis of Panicum streak virus and Maize streak virus diversity, recombination patterns and phylogeography
Authors: Varsani Arvind , Monjane Aderito L , Donaldson Lara , Oluwafemi Sunday , Zinga Innocent , Komba Ephrem K , Plakoutene Didier , Mandakombo Noella , Mboukoulida Joseph , Semballa Silla , Briddon Rob W , Markham Peter G , Lett Jean-Michel , Lefeuvre Pierre , Rybicki Edward P , Martin Darren P 
Published: November 2009

Abstract

Background

Panicum streak virus (PanSV; Family Geminiviridae; Genus Mastrevirus) is a close relative of Maize streak virus (MSV), the most serious viral threat to maize production in Africa. PanSV and MSV have the same leafhopper vector species, largely overlapping natural host ranges and similar geographical distributions across Africa and its associated Indian Ocean Islands. Unlike MSV, however, PanSV has no known economic relevance.

Results
Here we report on 16 new PanSV full genome sequences sampled throughout Africa and use these together with others in public databases to reveal that PanSV and MSV populations in general share very similar patterns of genetic exchange and geographically structured diversity. A potentially important difference between the species, however, is that the movement of MSV strains throughout Africa is apparently less constrained than that of PanSV strains. Interestingly the MSV-A strain which causes maize streak disease is apparently the most mobile of all the PanSV and MSV strains investigated.

Conclusion
We therefore hypothesize that the generally increased mobility of MSV relative to other closely related species such as PanSV, may have been an important evolutionary step in the eventual emergence of MSV-A as a serious agricultural pathogen.
The GenBank accession numbers for the sequences reported in this paper are GQ415386-GQ415401
FSL-1, a bacterial-derived toll-like receptor 2/6 agonist, enhances resistance to experimental HSV-2 infection
Authors: Rose William A , McGowin Chris L , Pyles Richard B 
Published: November 2009

Abstract

Background
Herpes simplex virus type 2 (HSV-2) is a leading cause of genital ulceration that can predispose individuals to an increased risk of acquiring other sexually transmitted infections. There are no approved HSV-2 vaccines and current suppressive therapies require daily compound administration that does not prevent all recurrences. A promising experimental strategy is the use of toll-like receptor (TLR) agonists to induce an innate immune response that provides resistance to HSV-2 infection. Previous studies showed that anti-herpetic activity varied based on origin of the agonists and activation of different TLR indicating that activity likely occurs through elaboration of a specific innate immune response. To test the hypothesis, we evaluated the ability of a bacterial-derived TLR2/6 agonist (FSL-1) to increase resistance to experimental genital HSV-2 infection.

Methods
Vaginal application of FSL-1 at selected doses and times was evaluated to identify potential increased resistance to genital HSV-2 infection in the mouse model. The FSL-1 induced cytokine profile was quantified using kinetically collected vaginal lavages. Additionally, cytokine elaboration and organ weights were evaluated after single or multiple FSL-1 doses to establish a preliminary safety profile. Human vaginal EC cultures were used to confirm the mouse model outcomes.

Results
The results showed that vaginally-applied FSL-1 created an environment resistant to a 25-fold higher HSV-2 challenge dose. Mechanistically, vaginal FSL-1 application led to transient elaboration of cytokines linked to anti-herpetic innate immune responses. No gross local or peripheral immunotoxicity was observed even after multiple dosing. FSL-1 also created an anti-herpetic environment in cultures of human vaginal epithelial cells (EC).

Conclusion
The results showed, for the first time, that the bacterial-derived TLR2/6 agonist FSL-1 induced significant resistance to HSV-2 infection when applied in mice or human vaginal EC cultures. Cytokine evaluation illustrated that anti-herpetic activity correlated with induction of a specific profile. The identified anti-herpetic profile provides an invaluable resource for the future design of novel compounds to reduce genital HSV-2 transmission and improves understanding of the complex innate immune response to potential pathogens elicited by the vaginal mucosa.
Pediatric chylolymphatic mesenteric cyst - a separate entity from cystic lymphangioma: a case series
Authors: Rattan Kamal Nayan , Nair Vimoj J , Pathak Manish , Kumar Sanjay 
Published: November 2009

Abstract

Introduction
Chylolymphatic mesenteric cysts are rare entities with variable presentations and this has surgical implications in the pediatric age group.

Case presentation
We carried out a retrospective analysis of the clinical and histopathological records of pediatric patients diagnosed and treated for chylolymphatic mesenteric cysts at our institute from 1998 to 2008. Eight patients met the histopathological criteria of chylolymphatic mesenteric cyst. These patients were in the age range 18 months to 10 years with a mean age of 4.5 years. Of these eight patients, four presented with an abdominal lump, and two each with abdominal pain and acute intestinal obstruction. On clinical examination, five out of the eight patients had a palpable abdominal mass. Laparotomy and complete excision of the cyst along with the involved gut was performed in all patients. There were no postoperative complications or any recurrence during the follow-up period which ranged from 4 months to 8 years.

Conclusion
Although very rare, chylolymphatic mesenteric cyst should be kept in mind as one of the differential diagnoses of cystic masses of the abdomen including cystic lymphangioma. Ultrasonography and computed tomography suggest the diagnosis but histopathological examination is required for confirmation. Complete excision of the cyst yields excellent results.
Human herpes virus 8 replication during disseminated tuberculosis in a man with human immunodeficiency virus: a case report
Authors: Inoubli Sarra , Toutous-Trellu Laurence , Cathomas Gieri , Oksenhendler Eric , Hirschel Bernard , El Amari Emmanuelle Boffi 
Published: November 2009

Abstract

Introduction
Human herpes virus 8 (HHV-8) is mainly responsible for the development of Kaposi's sarcoma and multicentric Castleman's disease in immunocompromised patients with untreated human immunodeficiency virus. Positive viral loads have been described in cases of Kaposi's sarcoma and multicentric Castleman's disease, with higher values found in the latter. We describe the case of a patient with HIV in whom a high level of HHV-8 replication was detected and who contracted an opportunistic disease other than multicentric Castleman's disease or Kaposi's sarcoma.

Case presentation
A 25-year-old man of West African origin with HIV complained of asthenia, weight loss, fever, and abdominal pain. Physical examination revealed that the patient had adenopathies and hepatosplenomegaly, but no skin or mucosal lesions were seen. Our first presumptive diagnosis was disseminated tuberculosis. However, since the cultures (sputum, bronchoalveolar lavage, blood, urine and lymph node biopsies) for mycobacteria were negative, the diagnosis was expanded to include multicentric Castleman's disease which was supported by high HHV-8 viral loads in the patient's blood: 196,000 copies/ml in whole blood, 39,400 copies/ml in plasma and 260 copies/10E5 in peripheral blood mononuclear cells. However, the histology and positive polymerase chain reaction assay for Mycobacterium tuberculosis complex of a second lymph node biopsy enabled us to conclude that the patient had disseminated tuberculosis and we started the patient on antituberculosis treatment.
We analyzed the HHV-8 deoxyribonucleic acid in two other plasma samples (one from six months earlier and the other was 10 days after the positive test) and both yielded negative results. A search for latent and lytic HHV-8 antibodies confirmed that the patient was seropositive for HHV-8 before this episode.

Conclusion
We describe the case of a patient with HIV who tested positive for asymptomatic HHV-8 replication during an opportunistic disease suggestive of multicentric Castleman's disease. The initial analysis was nullified by the diagnosis of a disease that was unrelated to HHV-8. This case report underlines the need to clarify the full clinical meaning and implication of a positive HHV-8 viral load in patients with AIDS. The diagnosis of multicentric Castleman's disease needs to be studied further to determine its sensitivity and specificity. Finally, when faced with the dilemma of urgently starting chemotherapy on a patient whose condition is deteriorating and whose clinical presentation suggests multicentric Castleman's disease, high HHV-8 viral loads should be interpreted with caution and histological analysis of lymph nodes or liver biopsies should be obtained first.
Congenital hydrocephalus in an Egyptian baby with trisomy 18: a case report
Authors: Metwalley Kotb A , Farghalley Hekma S , Abd-Elsayed Alaa A 
Published: November 2009

Abstract

Introduction
Trisomy 18 is the second most common autosomal trisomy after Down syndrome (trisomy 21). A variety of anomalies of the central nervous system are observed in cases of trisomy 18. The association between trisomy 18 and congenital hydrocephalus is very rare.

Case presentation
A 4-month-old male Egyptian baby boy was referred to Assiut University hospital for evaluation of his large-sized head. The initial clinical examination revealed facial dysmorphism including a prominent wide forehead, wide anterior fontanel, bushy eyebrows, synophrosis, small palpebral fissures, ocular hypertelorism, high arched palate, depressed nasal bridge, low-set ears, micrognathia, bilateral clenched hands with over lapping fingers, rocker-bottom feet and penile hypospadius. A computed tomography scan of the patient's head showed a dilatation of all the ventricular systems of the brain that suggested hydrocephalus. A chromosome analysis of his peripheral blood confirmed a trisomy of chromosome 18 (47, XX+18). The hydrocephalus was treated with a ventriculoperitoneal shunt because of the abnormal increase in his head circumference. He was discharged home on nasogastric feeds at the age of 5 months. Despite the advice of the medical team, his parents did not bring him for further follow up. He died at the age of 7 months due to a sudden cardiorespiratory arrest at home.

Conclusion
Microcephaly is not mandatory for the diagnosis of trisomy 18 syndrome because some cases of trisomy 18 can be associated with other anomalies of the central nervous system, including hydrocephalus. There is no proven explanation for this association, and the management of hydrocephalus in such a situation is not different from the usual course of management.
Insights in to the pathogenesis of axial spondyloarthropathy based on gene expression profiles
Authors: Sharma Srilakshmi M , Choi Dongseok , Planck Stephen R , Harrington Christina A , Austin Carrie R , Lewis Jinnell A , Diebel Tessa N , Martin Tammy M , Smith Justine R , Rosenbaum James T 
Published: November 2009

Abstract
Introduction
Axial spondyloarthropathy (SpA) is a group of inflammatory diseases, with ankylosing spondylitis as the prototype. SpA affects the axial skeleton, entheses, joints and, at times, the eyes. This study tested the hypothesis that SpA is characterized by a distinct pattern of gene expression in peripheral blood of affected individuals compared with healthy controls.

Methods
High-density, human GeneChip® probe arrays were used to profile mRNA of peripheral blood cells from 18 subjects with SpA and 25 normal individuals. Samples were processed as two separate sets at different times (11 SpA + 12 control subjects in primary set (Set 1); 7 SpA+ 13 control subjects in the validation set (Set 2)). Blood samples were taken at a time when patients were not receiving systemic immunomodulatory therapy. Differential expression was defined as a 1.5-fold change with a q value < 5%. Gene ontology and pathway information were also studied.

Results
Signals from 134 probe sets (representing 95 known and 12 unknown gene transcripts) were consistently different from controls in both Sets 1 and 2. Included among these were transcripts for a group of 20 genes, such as interleukin-1 (IL-1) receptors 1 and 2, Nod-like receptor family, pyrin domain containing 2 (NLRP2), secretory leukocyte peptidase inhibitor (SLPI), secreted protein acidic and rich in cysteine (SPARC), and triggering receptor expressed on myeloid cells 1 (TREM-1) that are clearly related to the immune or inflammatory response and a group of 4 transcripts that have a strong role in bone remodeling.

Conclusions
Our observations are the first to implicate SPARC, SLPI, and NLRP2, a component of the innate immune system, in the pathogenesis of SpA. Our results also indicate a possible role for IL-1 and its receptors in SpA. In accord with the bone pathology component of SpA, we also found that expression levels of transcripts reflecting bone remodeling factors are also distinguishable in peripheral blood from patients with SpA versus controls. These results confirm some previously identified biomarkers implicated in the pathogenesis of SpA and also point to novel mediators in this disease.
Altered serotonin physiology in human breast cancers favors paradoxical growth and cell survival
Authors: Pai Vaibhav P , Marshall Aaron M , Hernandez Laura L , Buckley Arthur R , Horseman Nelson D 
Published: November 2009

AbstractIntroductionThe breast microenvironment can either retard or accelerate the events associated with progression of latent cancers. However, the actions of local physiological mediators in the context of breast cancers are poorly understood. Serotonin (5-HT) is a critical local regulator of epithelial homeostasis in the breast and other organs. Herein, we report complex alterations in the intrinsic mammary gland serotonin system of human breast cancers.MethodsSerotonin biosynthetic capacity was analyzed in human breast tumor tissue microarrays using immunohistochemistry for tryptophan hydroxylase 1 (TPH1). Serotonin receptors (5-HT1-7) were analyzed in human breast tumors using the Oncomine database. Serotonin receptor expression, signal transduction, and 5-HT effects on breast cancer cell phenotype were compared in non-transformed and transformed human breast cells.ResultsIn the context of the normal mammary gland, 5-HT acts as a physiological regulator of lactation and involution, in part by favoring growth arrest and cell death. This tightly regulated 5-HT system is subverted in multiple ways in human breast cancers. Specifically, TPH1 expression undergoes a non-linear change during progression, with increased expression during malignant progression. Correspondingly, the tightly regulated pattern of 5-HT receptors becomes dysregulated in human breast cancer cells, resulting in both ectopic expression of some isoforms and suppression of others. The receptor expression change is accompanied by altered downstream signaling of 5-HT receptors in human breast cancer cells, resulting in resistance to 5-HT-induced apoptosis, and stimulated proliferation.ConclusionsOur data constitutes the first report of direct involvement of 5-HT in human breast cancer. Increased 5-HT biosynthetic capacity accompanied by multiple changes in 5-HT receptor expression and signaling favor malignant progression of human breast cancer cells (for example, stimulated proliferation, inappropriate cell survival). This occurs through uncoupling of serotonin from the homeostatic regulatory mechanisms of the normal mammary epithelium. The findings open a new avenue for identification of diagnostic and prognostic markers, and valuable new therapeutic targets for managing breast cancer.
Mutations of E3 Ubiquitin Ligase Cbl Family Members Constitute a Novel Common Pathogenic Lesion in Myeloid Malignancies
Authors: Makishima Hideki , Cazzolli Heather , Szpurka Hadrian , Dunbar Andrew , Tiu Ramon , Huh Jungwon , Muramatsu Hideki , O'Keefe Christine , Hsi Eric , Paquette Ronald L. , Kojima Seiji , List Alan F. , Sekeres Mikkael A. , McDevitt Michael A. , Maciejewski Jaroslaw P. 
Published: November 2009

Purpose Acquired somatic uniparental disomy (UPD) is commonly observed in myelodysplastic syndromes (MDS), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes harboring mutations. Recurrent UPD11q led to identification of homozygous mutations in c-Cbl, an E3 ubiquitin ligase involved in attenuation of proliferative signals transduced by activated receptor tyrosine kinases. We examined the role and frequency of Cbl gene family mutations in MPN and related conditions. Methods We applied high-density SNP-A karyotyping to identify loss of heterozygosity of 11q in 442 patients with MDS, MDS/MPN, MPN, sAML evolved from these conditions, and primary AML. We sequenced c-Cbl, Cbl-b, and Cbl-c in patients with or without corresponding UPD or deletions and correlated mutational status with clinical features and outcomes. Results We identified c-Cbl mutations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML blast crisis and juvenile myelomonocytic leukemia (JMML). Most mutations were homozygous and affected c-Cbl; mutations in Cbl-b were also found in patients with similar clinical features. Patients with Cbl family mutations showed poor prognosis, with a median survival of 5 months. Pathomorphologic features included monocytosis, monocytoid blasts, aberrant expression of phosphoSTAT5, and c-kit overexpression. Serial studies showed acquisition of c-Cbl mutations during malignant evolution. Conclusion Mutations in the Cbl family RING finger domain or linker sequence constitute important pathogenic lesions associated with not only preleukemic CMML, JMML, and other MPN, but also progression to AML, suggesting that impairment of degradation of activated tyrosine kinases constitutes an important cancer mechanism.
Aortic Stiffness Increases Upon Receipt of Anthracycline Chemotherapy
Authors: Chaosuwannakit Narumol , D'Agostino Ralph , Hamilton Craig A. , Lane Kimberly S. , Ntim William O. , Lawrence Julia , Melin Susan A. , Ellis Leslie R. , Torti Frank M. , Little William C. , Hundley W. Gregory 
Published: November 2009

Purpose Cancer survivors exposed to anthracyclines experience an increased risk of cardiovascular (CV) events. We hypothesized that anthracycline use may increase aortic stiffness, a known predictor of CV events. Patients and Methods We performed a prospective, case-control study involving 53 patients: 40 individuals who received an anthracycline for the treatment of breast cancer, lymphoma, or leukemia (cases), and 13 age- and sex-matched controls. Each participant underwent phase-contrast cardiovascular magnetic resonance measures of pulse wave velocity (PWV) and aortic distensibility (AoD) in the thoracic aorta at baseline, and 4 months after initiation of chemotherapy. Four one-way analyses of covariance models were fit in which factors known to influence thoracic aortic stiffness were included as covariates in the models. Results At the 4-month follow-up visit, aortic stiffness remained similar to baseline in the control participants. However, in the participants receiving anthracyclines, aortic stiffness increased markedly (relative to baseline), as evidenced by a decrease in AoD (P < .0001) and an increase in PWV (P < .0001). These changes in aortic stiffness persisted after accounting for age, sex, cardiac output, administered cardioactive medications, and underlying clinical conditions known to influence aortic stiffness, such as hypertension or diabetes (P < .0001). Conclusion A significant increase in aortic stiffness occurs within 4 months of exposure to an anthracycline which was not seen in an untreated control group. These results indicate that previously regarded cardiotoxic cancer therapy adversely increases thoracic aortic stiffness, a known independent predictor of adverse cardiovascular events.