bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treatment Response to an Intensive Summer Treatment Program for Adolescents With ADHD
Authors: Sibley Margaret H. , Smith Bradley H. , Evans Steven W. , Pelham William E. , Gnagy Elizabeth M. 
Published: February 2012

Objective: There are presently almost no empirically validated treatments for adolescents with ADHD. However, in childhood, behavioral treatments for ADHD typically include behavioral parent training, classroom interventions, and intensive child-directed interventions. Method: The present investigation examines treatment gains following an 8-week intensive summer day treatment program for adolescents with ADHD (STP-A). Baseline measures of functioning and parent improvement ratings were obtained for 34 STP-A participants. Results: Parent ratings indicated that adolescents who attended the STP-A improved across all target domains. Across domains, 63.0% to 90.9% of adolescents improved during the STP-A. There was no evidence of iatrogenic effects during the STP-A. Correlates of treatment response included adolescent effort, oppositional-defiant behavior, and cognitive/scholastic functioning. Conclusion: Findings are discussed with regard to effective treatment delivery for adolescents with ADHD.
Natural killer cell degranulation capacity predicts early onset of the immune reconstitution inflammatory syndrome (IRIS) in HIV-infected patients with tuberculosis
Authors: Pean Polidy , Nerrienet Eric , Madec Yoann , Borand Laurence , Laureillard Didier , Fernandez Marcelo , Marcy Olivier , Sarin Chan , Phon Kerya , Taylor Sylvia , Pancino Gianfranco , Barré-Sinoussi Françoise , Scott-Algara Daniel 
Published: February 2012

Abstract
Immune reconstitution inflammatory syndrome (IRIS) is a common and potentially serious complication occurring in HIV-infected patients being treated for tuberculosis (TB) using combined antiretroviral treatment. A role of adaptive immunity has been suggested in the onset of IRIS, whereas the role of natural killer (NK) cells has not yet been explored. The present study sought to examine the involvement of NK cells in the onset of IRIS in HIV-infected patients with TB and to identify predictive markers of IRIS. A total of 128 HIV-infected patients with TB from the Cambodian Early versus Late Introduction of Antiretroviral Drugs (CAMELIA) trial were enrolled in Cambodia. Thirty-seven of the 128 patients developed IRIS. At inclusion, patients had low CD4 cell counts (27 cells/mm3) and high plasma viral load (5.76 and 5.50 log/mL in IRIS and non-IRIS patients, respectively). At baseline, NK-cell degranulation capacity was significantly higher in IRIS patients than in non-IRIS patients (9.6% vs 6.38%, P < .005). At IRIS onset, degranulation capacity did not differ between patients, whereas activating receptor expression was lower in IRIS patients. Patients with degranulation levels > 10.84% had a higher risk of IRIS (P = .002 by log-rank test). Degranulation level at baseline was the most important IRIS predictor (hazard ratio = 4.41; 95% confidence interval, 1.60-12.16). We conclude that NK-degranulation levels identify higher IRIS risk in HIV-infected patients with TB.
FOXO1 is a tumor suppressor in classical Hodgkin lymphoma
Authors: Xie Linka , Ushmorov Alexey , Leithäuser Frank , Guan Hanfeng , Steidl Christian , Färbinger Johanna , Pelzer Christin , Vogel Marion J. , Maier Harald J. , Gascoyne Randy D. , Möller Peter , Wirth Thomas 
Published: February 2012

AbstractThe FOXO transcription factors control proliferation and apoptosis in different cell types. Their activity is regulated by posttranslational modifications, mainly by the PI3K-PKB pathway, which controls nuclear export and degradation. We show that FOXO1 is highly expressed in normal germinal center B cells as well as in non-Hodgkin lymphomas, including follicular lymphoma, diffuse large B-cell lymphoma, mucosa-associated lymphoid tissue non-Hodgkin lymphoma, B-cell chronic lymphocytic leukemia, and mantle cell lymphoma. In contrast, in 31 of 32 classical Hodgkin lymphoma (cHL) cases, Hodgkin and Reed-Sternberg cells were FOXO1 negative. Neoplastic cells of nodular lymphocyte-predominant Hodgkin lymphoma were negative in 14 of 20 cases. FOXO1 was down-regulated in cHL cell lines, whereas it was expressed in non-Hodgkin lymphoma cell lines at levels comparable with normal B cells. Ectopic expression of a constitutively active FOXO1 induced apoptosis in cHL cell lines and blocked proliferation, accompanied with cell-cycle arrest in the G0/G1 phase. We found that, in cHL cell lines, FOXO1 is inactivated by multiple mechanisms, including constitutive activation of AKT/PKB and MAPK/ERK kinases and up-regulation of microRNAs miR-96, miR-182, and miR-183. These results suggest that FOXO1 repression contributes to cHL lymphomagenesis.
Familial monoclonal gammopathy of undetermined significance and multiple myeloma: epidemiology, risk factors, and biological characteristics
Authors: Greenberg Alexandra J. , Rajkumar S. Vincent , Vachon Celine M. 
Published: February 2012

Abstract
Monoclonal gammopathy of undetermined significance (MGUS), a precursor to multiple myeloma (MM), is one of the most common premalignant conditions in the general population. The cause of MGUS is largely unknown. Recent studies show that there is an increased prevalence of MGUS in blood relatives of persons with lymphoproliferative and plasma cell proliferative disorders, suggesting presence of shared underlying genetic influences. In the past few years, additional studies have examined risk factors and biologic characteristics that may contribute to the increased prevalence of MGUS among relatives of probands with MGUS, MM, and other blood malignancies. This article reviews the known epidemiology and risk factors for familial MGUS and myeloma, the risk of lymphoproliferative disorders and other malignancies among blood-relatives of patients with MGUS and MM, and discusses future directions for research.
NHERF-2 maintains endothelial homeostasis
Authors: Bhattacharya Resham , Wang Enfeng , Dutta Shamit K. , Vohra Pawan K. , E Guangqi , Prakash Y. S. , Mukhopadhyay Debabrata 
Published: February 2012

AbstractThe Na+/H+ exchanger regulatory factor-2 (NHERF-2) is an integral component of almost all endothelial cells (ECs), yet its endothelial function is not known. Here, we found that NHERF-2, is a key regulator of endothelial homeostasis because NHERF-2–silenced ECs proliferate at a much higher rate even in the absence of mitogens such as VEGF compared with control ECs. We further show that the hyperproliferation phenotype of NHERF-2–silenced EC is because of an accelerated cell cycle that is probably caused by a combination of the following factors: increased cytoplasmic calcium, increased expression of c-Myc, increased expression of cyclin D1, and reduced expression of p27. Using an experimental mouse model of human hemangioma, we found that the endothelial neoplasms derived from NHERF-2–silenced cells were much larger in volume than those derived from control cells. Thus, NHERF-2 is a negative regulator of endothelial proliferation and may have important roles in endothelial homeostasis and vascular modeling.
Mutations affecting mRNA splicing define distinct clinical phenotypes and correlate with patient outcome in myelodysplastic syndromes
Authors: Damm Frederik , Kosmider Olivier , Gelsi-Boyer Véronique , Renneville Aline , Carbuccia Nadine , Hidalgo-Curtis Claire , Della Valle Véronique , Couronné Lucile , Scourzic Laurianne , Chesnais Virginie , Guerci-Bresler Agnes , Slama Bohrane , Beyne-Rauzy Odile , Schmidt-Tanguy Aline , Stamatoullas-Bastard Aspasia , Dreyfus François , Prébet Thomas , de Botton Stéphane , Vey Norbert , Morgan Michael A. , Cross Nicholas C. P. , Preudhomme Claude , Birnbaum Daniel , Bernard Olivier A. , Fontenay Michaela 
Published: February 2012

AbstractA cohort of MDS patients was examined for mutations affecting 4 splice genes (SF3B1, SRSF2, ZRSR2, and U2AF35) and evaluated in the context of clinical and molecular markers. Splice gene mutations were detected in 95 of 221 patients. These mutations were mutually exclusive and less likely to occur in patients with complex cytogenetics or TP53 mutations. SF3B1mut patients presented with lower hemoglobin levels, increased WBC and platelet counts, and were more likely to have DNMT3A mutations. SRSF2mut patients clustered in RAEB-1 and RAEB-2 subtypes and exhibited pronounced thrombocytopenias. ZRSR2mut patients clustered in International Prognostic Scoring System intermediate-1 and intermediate-2 risk groups, had higher percentages of bone marrow blasts, and more often displayed isolated neutropenias. SRSF2 and ZRSR2 mutations were more common in TET2mut patients. U2AF35mut patients had an increased prevalence of chromosome 20 deletions and ASXL1 mutations. Multivariate analysis revealed an inferior overall survival and a higher AML transformation rate for the genotype ZRSR2mut/TET2wt (overall survival: hazard ratio = 3.3; 95% CI, 1.4-7.7; P = .006; AML transformation: hazard ratio = 3.6; 95% CI, 2-4.2; P = .026). Our results demonstrate that splice gene mutations are among the most frequent molecular aberrations in myelodysplastic syndrome, define distinct clinical phenotypes, and show preferential associations with mutations targeting transcriptional regulation.
Invasive fungal infection among hematopoietic stem cell transplantation patients with mechanical ventilation in the intensive care unit
Authors: Hung Chen-Yiu , Kao Kuo-Chin , Wang Po-Nan , Hu Han-Chung , Hsieh Meng-Jer , Fu Jui-Ying , Chang Chih-Hao , Li Li-Fu , Huang Chung-Chi , Tsai Ying-Huang , Yang Cheng-Ta 
Published: February 2012

Abstract

Background
Invasive fungal infection (IFI) is associated with high morbidity and high mortality in hematopoietic stem cell transplantation (HSCT) patientsThe purpose of this study was to assess the characteristics and outcomes of HSCT patients with IFIs who are undergoing MV at a single institution in Taiwan.

Methods
We performed an observational retrospective analysis of IFIs in HSCT patients undergoing mechanical ventilation (MV) in an intensive care unit (ICU) from the year 2000 to 2009. The characteristics of these HSCT patients and risk factors related to IFIs were evaluated. The status of discharge, length of ICU stay, date of death and cause of death were also recorded.

Results
There were 326 HSCT patients at the Linkou Chang-Gung Memorial Hospital (Taipei, Taiwan) during the study period. Sixty of these patients (18%) were transferred to the ICU and placed on mechanical ventilators. A total of 20 of these 60 patients (33%) had IFIs. Multivariate analysis indicated that independent risk factors for IFI were admission to an ICU more than 40 days after HSCT, graft versus host disease (GVHD), and high dose corticosteroid (p < 0.01 for all). The overall ICU mortality rate was 88% (53 of 60 patients), and was not significantly different for patients with IFIs (85%) and those without IFIs (90%, p = 0.676).

Conclusion
There was a high incidence of IFIs in HSCT patients requiring MV in the ICU in our study cohort. The independent risk factors for IFI are ICU admission more than 40 days after HSCT, GVHD, and use of high-dose corticosteroid.
L-Rhamnose induction of Aspergillus nidulans α-L-rhamnosidase genes is glucose repressed via a CreA-independent mechanism acting at the level of inducer uptake
Authors: Tamayo-Ramos Juan A , Flipphi Michel , Pardo Ester , Manzanares Paloma , Orejas Margarita 
Published: February 2012

Abstract

Background
Little is known about the structure and regulation of fungal α-L-rhamnosidase genes despite increasing interest in the biotechnological potential of the enzymes that they encode. Whilst the paradigmatic filamentous fungus Aspergillus nidulans growing on L-rhamnose produces an α-L-rhamnosidase suitable for oenological applications, at least eight genes encoding putative α-L-rhamnosidases have been found in its genome. In the current work we have identified the gene (rhaE) encoding the former activity, and characterization of its expression has revealed a novel regulatory mechanism. A shared pattern of expression has also been observed for a second α-L-rhamnosidase gene, (AN10277/rhaA).

Results
Amino acid sequence data for the oenological α-L-rhamnosidase were determined using MALDI-TOF mass spectrometry and correspond to the amino acid sequence deduced from AN7151 (rhaE). The cDNA of rhaE was expressed in Saccharomyces cerevisiae and yielded p NP-rhamnohydrolase activity. Phylogenetic analysis has revealed this eukaryotic α-L-rhamnosidase to be the first such enzyme found to be more closely related to bacterial rhamnosidases than other α-L-rhamnosidases of fungal origin. Northern analyses of diverse A. nidulans strains cultivated under different growth conditions indicate that rhaA and rhaE are induced by L-rhamnose and repressed by D-glucose as well as other carbon sources, some of which are considered to be non-repressive growth substrates. Interestingly, the transcriptional repression is independent of the wide domain carbon catabolite repressor CreA. Gene induction and glucose repression of these rha genes correlate with the uptake, or lack of it, of the inducing carbon source L-rhamnose, suggesting a prominent role for inducer exclusion in repression.

Conclusions
The A. nidulans rhaE gene encodes an α-L-rhamnosidase phylogenetically distant to those described in filamentous fungi, and its expression is regulated by a novel CreA-independent mechanism. The identification of rhaE and the characterization of its regulation will facilitate the design of strategies to overproduce the encoded enzyme - or homologs from other fungi - for industrial applications. Moreover, A. nidulans α-L-rhamnosidase encoding genes could serve as prototypes for fungal genes coding for plant cell wall degrading enzymes regulated by a novel mechanism of CCR.
Targeting different types of human meningioma and glioma cells using a novel adenoviral vector expressing GFP-TRAIL fusion protein from hTERT promoter
Authors: Li Jessica T , Bian Ka , Zhang Alan L , Kim Dong H , Ashley William W , Nath Rahul , McCutcheon Ian , Fang Bingliang , Murad Ferid 
Published: February 2012

Abstract

Objective
The objective of this study was to evaluate the anti-tumor effects of Ad/gTRAIL (an adenoviral vector in which expression of GFP and TRAIL is driven by a human telomerase reverse transcriptase promoter, hTERT) on malignant meningiomas and gliomas.

Background
Gliomas and meningiomas are the two most common types of human brain tumors. Currently there is no effective cure for recurrent malignant meningiomas or for gliomas. Ad/gTRAIL has been shown to be effective in killing selected lung, colon and breast cancer cells, but there have been no studies reporting its antitumor effects on malignant meningiomas. Therefore, we tested the antitumor effect of Ad/gTRAIL for the first time in human malignant meningioma and glioma cell lines, and in intracranial M6 and U87 xenografts.

Methods
Materials and Methods: Human malignant meningioma and glioma cells were infected with adenoviruses, Ad/gTRAIL and Ad/CMV-GFP. Cell viability was determined by proliferation assay. FACS analysis and quantification of TRAIL were used to measure apoptosis in these cells. We injected Ad/gTRAIL viruses in intracranial M6 and U87 xenografts, and measured the brain tumor volume, quantified apoptosis by TUNEL assay in the brain tumor tissue.

Results
Our studies demonstrate that in vitro/in vivo treatment with Ad/gTRAIL virus resulted in significant increase of TRAIL activity, and elicited a greater tumor cell apoptosis in malignant brain tumor cells as compared to treatment with the control, Ad/CMV-GFP virus without TRAIL activity.

Conclusions
We showed for the first time that adenovirus Ad/gTRAIL had significant antitumor effects against high grade malignant meningiomas as well as gliomas. Although more work needs to be done, our data suggests that Ad/gTRAIL has the potential to be useful as a tool against malignant brain tumors.
Formation mechanism of SiGe nanorod arrays by combining nanosphere lithography and Au-assisted chemical etching
Authors: Lai Chih-Chung , Lee Yun-Ju , Yeh Ping-Hung , Lee Sheng-Wei 
Published: February 2012

Abstract
The formation mechanism of SiGe nanorod (NR) arrays fabricated by combining nanosphere lithography and Au-assisted chemical etching has been investigated. By precisely controlling the etching rate and time, the lengths of SiGe NRs can be tuned from 300 nm to 1μm. The morphologies of SiGe NRs were found to change dramatically by varying the etching temperatures. We propose a mechanism involving a locally temperature-sensitive redox reaction to explain this strong temperature dependence of the morphologies of SiGe NRs. At a lower etching temperature, both corrosion reaction and Au-assisted etching process were kinetically impeded, whereas at a higher temperature, Au-assisted anisotropic etching dominated the formation of SiGe NRs. With transmission electron microscopy and scanning electron microscopy analyses, this study provides a beneficial scheme to design and fabricate low-dimensional SiGe-based nanostructures for possible applications.
5, 8, 11, 14-eicosatetraynoic acid suppresses CCL2/MCP-1 expression in IFN-γ-stimulated astrocytes by increasing MAPK phosphatase-1 mRNA stability
Authors: Lee Jee Hoon , Kim Hyunmi , Woo Joo Hong , Joe Eun-hye , Jou Ilo 
Published: February 2012

Abstract

Background
The peroxisome proliferator-activated receptor (PPAR)-α activator, 5,8,11,14-eicosatetraynoic acid (ETYA), is an arachidonic acid analog. It is reported to inhibit up-regulation of pro-inflammatory genes; however, its underlying mechanism of action is largely unknown. In the present study, we focused on the inhibitory action of ETYA on the expression of the chemokine, CCL2/MCP-1, which plays a key role in the initiation and progression of inflammation.

Methods
To determine the effect of ETYA, primary cultured rat astrocytes and microglia were stimulated with IFN-γ in the presence of ETYA and then, expression of CCL2/MCP-1 and MAPK phosphatase (MKP-1) were determined using RT-PCR and ELISA. MKP-1 mRNA stability was evaluated by treating actinomycin D. The effect of MKP-1 and human antigen R (HuR) was analyzed by using specific siRNA transfection system. The localization of HuR was analyzed by immunocytochemistry and subcellular fractionation experiment.

Results
We found that ETYA suppressed CCL2/MCP-1 transcription and secretion of CCL2/MCP-1 protein through up-regulation of MKP-1mRNA levels, resulting in suppression of c-Jun N-terminal kinase (JNK) phosphorylation and activator protein 1 (AP1) activity in IFN-γ-stimulated brain glial cells. Moreover, these effects of ETYA were independent of PPAR-α. Experiments using actinomycin D revealed that the ETYA-induced increase in MKP-1 mRNA levels reflected an increase in transcript stability. Knockdown experiments using small interfering RNA demonstrated that this increase in MKP-1 mRNA stability depended on HuR, an RNA-binding protein known to promote enhanced mRNA stability. Furthermore, ETYA-induced, HuR-mediated mRNA stabilization resulted from HuR-MKP-1 nucleocytoplasmic translocation, which served to protect MKP-1 mRNA from the mRNA degradation machinery.

Conclusion
ETYA induces MKP-1 through HuR at the post-transcriptional level in a receptor-independent manner. The mechanism revealed here suggests eicosanoids as potential therapeutic modulators of inflammation that act through a novel target.
Krüppel-like factor 4 (KLF4) promotes the survival of natural killer cells and maintains the number of conventional dendritic cells in the spleen
Authors: Shik Park Chun , Lee Ping-Hsien , Yamada Takeshi , Burns Audrea , Shen Ye , Puppi Monica , Lacorazza H Daniel 
Published: February 2012

ABSTRACT
The development and survival of NK cells rely on a complex, spatiotemporal gene expression pattern regulated by specific transcription factors in NK cells and tissue-specific microenvironments supported by hematopoietic cells. Here, we show that somatic deletion of the KLF4 gene, using inducible and lineage-specific cre-transgenic mice, leads to a significant reduction of NK cells (NK1.1+ TCR-β−) in the blood and spleen but not in the BM, liver, or LNs. Functional and immunophenotypic analyses revealed increased apoptosis of CD27+/− CD11b+ NK cells in the spleen of KLF4-deficient mice, although remaining NK cells were able to lyse tumor target cells and produce IFN-γ. A normal recovery of adoptively transferred KLF4-deficient NK cells in WT hosts suggested that the survival defect was not intrinsic of NK cells. However, BM chimeras using KLF4-deficient mice as donors indicated that reduced survival of NK cells depended on BM-derived hematopoietic cells in the spleen. The number of CD11chi DCs, which are known to support NK cell survival, was reduced significantly in the spleen of KLF4-deficient mice, likely a result of a lower number of precDC progenitor cells in this tissue. Taken together, our data suggest that the pluripotency-associated gene KLF4 is required for the maintenance of DCs in the spleen and consequently, survival of differentiated NK cells in this tissue.
Apoptosis signaling in influenza virus propagation, innate host defense, and lung injury
Authors: Herold Susanne , Ludwig Stephan , Pleschka Stephan , Wolff Thorsten 
Published: February 2012

Abstract
A review of mechanisms of apoptosis induction in influenza virus-infected cells, and the impact of apoptotic signaling on viral propagation, immune responses, and tissue injury.
Programmed cell death is a crucial cellular response frequently observed in IV-infected tissue. This article reviews the current knowledge on the molecular virus–host interactions that induce apoptosis pathways in an IV-infected cell and the functional implications of these cellular signaling events on viral propagation at distinct steps during the viral replication cycle. Furthermore, it summarizes the role of IV-induced apoptosis pathways in equilibrating the hostˈs antiviral immune response between effective viral clearance and development of severe apoptotic lung injury.
Jobs encompassing prolonged sitting in cramped positions and risk of venous thromboembolism: cohort study
Authors: Suadicani Poul , Hannerz Harald , Bach Elsa , Gyntelberg Finn 
Published: February 2012

Objectives There is mounting evidence that prolonged cramped sitting in connection with long-lasting air travel increases the risk of deep vein thrombosis of the legs and pulmonary embolism, i.e. venous thromboembolism (VTE). Prolonged cramped sitting may occur even in various jobs unrelated to air travel, and, theoretically, be associated with an increased risk of VTE. The issue is unsettled. Design A dynamic cohort study (open for both entry and departure) in Danish national registers 1997–2006. Participants 20–59-year-old manual workers. The cohort consisted of an exposed group with job functions basically characterised as sedentary ( n= 105,564) and a control group with more dynamic work ( n = 283,966). Setting Denmark. Main outcome measures Deaths and hospital contacts due to pulmonary embolism and deep vein thrombosis. Results Compared with occupations characterized by dynamic physical activity, the group encompassing those who would potentially be exposed to prolonged sitting in ergonomically adverse positions, had a significantly higher risk of pulmonary embolism ( n = 77, relative risk 1.28; 95% CI 0.97–1.67, P = 0.04 in one-sided test). With respect to deep vein thrombosis they had a slightly but not significantly higher risk ( n =256, relative risk 1.09; 95% CI 0.94–1.26, P = 0.12). Conclusion Despite the crude method used allowing for no control of individual risk factors, occupations encompassing longer and shorter periods of sitting in potentially adverse ergonomic positions, i.e. cramped sitting, had a higher risk of VTE, than a socioeconomically comparable group with more dynamic physical work demands.