bluuebunny/crossref_metadata_2025_split huggingface dataset:
Scaling the gas transfer velocity and hydraulic geometry in streams and small rivers
Authors: Raymond Peter A. , Zappa Christopher J. , Butman David , Bott Thomas L. , Potter Jody , Mulholland Patrick , Laursen Andrew E. , McDowell William H. , Newbold Denis 
Published: May 2012

Lay AbstractThe exchange of gasses between water and air is important to the budgets of carbon, nutrients, and pollutants. This exchange is driven, in part, by the turbulent energy at the air–water interface. Turbulent energy at the air–water interface scales with the gas transfer velocity (k), which can be measured in streams through various methods. We performed a metadata analysis of studies that have measured k in streams using direct gas tracer releases. We evaluated models that predict k based on stream morphology. We found that models that use slope and velocity to predict k perform reasonably well and are consistent with general theory. We also used the data set to provide new stream hydraulic equations that predict stream morphology (width, depth, velocity) based on discharge.
Genome wide expression profiling of the mesodiencephalic region identifies novel factors involved in early and late dopaminergic development
Authors: Chakrabarty Koushik , Von Oerthel Lars , Hellemons Anita , Clotman Frédéric , Espana Agnès , Groot Koerkamp Marian , Holstege Frank C. P. , Pasterkamp R. Jeroen , Smidt Marten P. 
Published: May 2012

Summary
Meso-diencephalic dopaminergic (mdDA) neurons are critical for motor control and cognitive functioning and their loss or dysfunction is associated with disorders such as Parkinson's disease (PD), schizophrenia and addiction. However, relatively little is known about the molecular mechanisms underlying mdDA neuron development and maintenance. Here, we determined the spatiotemporal map of genes involved in the development of mdDA neurons to gain further insight into their molecular programming. Genome-wide gene expression profiles of the developing ventral mesencephalon (VM) were compared at different developmental stages leading to the identification of novel regulatory roles of neuronal signaling through nicotinic acthylcholine receptors (Chrna6 and Chrnb3 subunits) and the identification of novel transcription factors (Oc2 and 3) involved in the generation of the mdDA neuronal field. We show here that Pitx3, in cooperation with Nurr1, is the critical component in the activation of the Chrna6 and Chrnb3 subunits in mdDA neurons. Furthermore, we provide evidence of two divergent regulatory pathways resulting in the expression of Chrna6 and Chrnb3 respectively.
Conditional over-expression of PITX1 causes skeletal muscle dystrophy in mice
Authors: Pandey Sachchida N. , Cabotage Jennifer , Shi Rongye , Dixit Manjusha , Sutherland Margret , Liu Jian , Muger Stephanie , Harper Scott Q. , Nagaraju Kanneboyina , Chen Yi-Wen 
Published: May 2012

Summary
Paired-like homeodomain transcription factor 1 (PITX1) was specifically up-regulated in patients with facioscapulohumeral muscular dystrophy (FSHD) by comparing the genome-wide mRNA expression profiles of 12 neuromuscular disorders. In addition, it is the only known direct transcriptional target of the double homeobox protein 4 (DUX4) of which aberrant expression has been shown to be the cause of FSHD. To test the hypothesis that up-regulation of PITX1 contributes to the skeletal muscle atrophy seen in patients with FSHD, we generated a tet-repressible muscle-specific Pitx1 transgenic mouse model in which expression of PITX1 in skeletal muscle can be controlled by oral administration of doxycycline. After PITX1 was over-expressed in the skeletal muscle for 5 weeks, the mice exhibited significant loss of body weight and muscle mass, decreased muscle strength, and reduction of muscle fiber diameters. Among the muscles examined, the tibialis anterior, gastrocnemius, quadricep, bicep, tricep and deltoid showed significant reduction of muscle mass, while the soleus, masseter and diaphragm muscles were not affected. The most prominent pathological change was the development of atrophic muscle fibers with mild necrosis and inflammatory infiltration. The affected myofibers stained heavily with NADH-TR with the strongest staining in angular-shaped atrophic fibers. Some of the atrophic fibers were also positive for embryonic myosin heavy chain using immunohistochemistry. Immunoblotting showed that the p53 was up-regulated in the muscles over-expressing PITX1. The results suggest that the up-regulation of PITX1 followed by activation of p53-dependent pathways may play a major role in the muscle atrophy developed in the mouse model.
CD81 and CD9 work independently as extracellular components upon fusion of sperm and oocyte
Authors: Ohnami Naoko , Nakamura Akihiro , Miyado Mami , Sato Masahiro , Kawano Natsuko , Yoshida Keiichi , Harada Yuichirou , Takezawa Youki , Kanai Seiya , Ono Chihiro , Takahashi Yuji , Kimura Ken , Shida Toshio , Miyado Kenji , Umezawa Akihiro 
Published: May 2012

Summary
When a sperm and oocyte unite into one cell upon fertilization, membranous fusion between the sperm and oocyte occurs. In mice, Izumo1 and a tetraspanin molecule CD9 are required for sperm-oocyte fusion as one of the oocyte factors, and another tetraspanin molecule CD81 is also thought to involve in this process. Since these two tetraspanins often form a complex upon cell-cell interaction, it is probable that such a complex is also formed in sperm-oocyte interaction; however, this possibility is still under debate among researchers. Here we assessed this problem using mouse oocytes. Immunocytochemical analysis demonstrated that both CD9 and CD81 were widely distributed outside the oocyte cell membrane, but these molecules were separate, forming bilayers, confirmed by immunobiochemical analysis. Electron-microscopic analysis revealed the presence of CD9- or CD81-incorporated extracellular structures in those bilayers. Finally, microinjection of in vitro-synthesized RNA showed that CD9 reversed a fusion defect in CD81-deficient oocytes in addition to CD9-deficient oocytes, but CD81 failed in both oocytes. These results suggest that both CD9 and CD81 independently work upon sperm-oocyte fusion as extracellular components.
Ground-level Concentration of Ozone in Ambient Air in Chittagong (Bangladesh) City
Authors: Begum BA , Saroar G , Nasiruddin M , Biswas SK 
Published: May 2012

The distribution of the ground-level ozone concentration in Chittagong city was continuously monitored at air monitoring station in Chittagong city during period of December 2006 to December 2007. The results of this study have revealed that the ground-level ozone concentration in Chittagong city varied from season to season. The highest ground-level ozone concentration was found in winter. The groundlevel ozone concentration has also a clear diurnal cycle - with higher values in the daytime and notably becomes zero at night depending on season. Meteorological conditions are known to influence the formation and dispersion of ground-level ozone concentration. At temperature lower than 20°C, the concentration of ozone becomes high where as at high temperature (> 30°C), the concentration becomes low. It has also been found that at low wind speed, the ozone concentration is high and at high wind speed, the concentration becomes low due to dispersion. The results also establish that the during the study periods, the ozone concentration was below the Bangladesh National Ambient Air Quality Standard (BNAAQS) of 80 ppb (annual average). DOI: http://dx.doi.org/10.3329/bjsir.v47i1.10729 Bangladesh J. Sci. Ind. Res. 47(1), 83-88, 2012
Antibiotic resistant patterns of bacterial isolates from ready-to-eat (RTE) street vended fresh vegetables and fruits in Dhaka City
Authors: Ali Mohammad , Khan Mr , Saha Mihir Lal 
Published: May 2012

Key words: Enteric bacteria; lactose fermenter; non-lactose fermenter; antibiotic resistanceDOI: http://dx.doi.org/10.3329/bjsr.v24i2.10769 Bangladesh J. Sci. Res. 24(2):127-134, 2011 (December)
Principes de détermination de la peine, politiques publiques et modération en matière de recours à l’incarcération : la rupture du Canada avec son histoire
Authors: Doob Anthony N. 
Published: May 2012

Bien que le Canada n’ait jamais réussi à atteindre une grande cohérence en matière de détermination de la peine, pendant plus d’un siècle, les taux d’incarcérations y sont demeurés constants, alors que d’autres pays, notamment les États-Unis, ont vu leurs niveaux d’emprisonnement augmenter considérablement. Une explication partielle de cette stabilité réside dans la tradition canadienne de scepticisme à l’égard des bénéfices de l’emprisonnement – une position qui fut jusqu’en 2006 partagée par les gouvernements fédéraux libéraux et conservateurs. Toutefois, les juges chargés de prononcer les peines n’ont jamais reçu de directives claires du Parlement sur les objectifs qui devraient être concrètement associés aux décisions portant sur les sentences. Les politiques de détermination de la peine basées sur des principes clairs ont connu un rapide déclin à partir de 2006 avec l’introduction par les Conservateurs de nombreux projets de lois pénales modifiant l’économie de la punition. Dans son ensemble, cette activité législative représente l’antithèse d’une réforme de la justice pénale réfléchie et fondée sur des principes. En 1999, Jean-Paul Brodeur décrivait les valeurs qui sous-tendaient les politiques de détermination de la peine comme « rien de moins qu’une catastrophe morale ». Il ne fait aucun doute sur la manière dont il aurait qualifié la période qui s’est amorcée en 2006.
Principled sentencing, politics, and restraint in the use of imprisonment: Canada’s break with its history
Authors: Doob Anthony N. 
Published: May 2012

Bien que le Canada n’ait jamais réussi à atteindre une grande cohérence en matière de détermination de la peine, pendant plus d’un siècle, les taux d’incarcérations y sont demeurés constants, alors que d’autres pays, notamment les États-Unis, ont vu leurs niveaux d’emprisonnement augmenter considérablement. Une explication partielle de cette stabilité réside dans la tradition canadienne de scepticisme à l’égard des bénéfices de l’emprisonnement – une position qui fut jusqu’en 2006 partagée par les gouvernements fédéraux libéraux et conservateurs. Toutefois, les juges chargés de prononcer les peines n’ont jamais reçu de directives claires du Parlement sur les objectifs qui devraient être concrètement associés aux décisions portant sur les sentences. Les politiques de détermination de la peine basées sur des principes clairs ont connu un rapide déclin à partir de 2006 avec l’introduction par les Conservateurs de nombreux projets de lois pénales modifiant l’économie de la punition. Dans son ensemble, cette activité législative représente l’antithèse d’une réforme de la justice pénale réfléchie et fondée sur des principes. En 1999, Jean-Paul Brodeur décrivait les valeurs qui sous-tendaient les politiques de détermination de la peine comme « rien de moins qu’une catastrophe morale ». Il ne fait aucun doute sur la manière dont il aurait qualifié la période qui s’est amorcée en 2006.
Réflexion autour de la banalité du mal inspirée d’une conversation avec Jean-Paul Brodeur
Authors: Tanner Samuel 
Published: May 2012

Si la notoriété de Jean-Paul Brodeur est en grande partie due à ses recherches sur la police, il est un autre domaine, plus méconnu du grand public, qui le passionnait et le fascinait, à savoir les formes extrêmes de violence, dont le génocide et le crime contre l’humanité. Dans le cadre de cet article, je prolonge un dialogue que nous avions entamé avec Jean-Paul à propos du concept de banalité du mal, développé par Hannah Arendt. En particulier et à partir des contextes yougoslave et rwandais, je propose une extension de cette notion appliquée non pas tant ici aux fonctionnaires et bureaucrates, tels qu’ils constituaient le centre d’attention de la philosophie, alors concentrée sur l’Holocauste, mais bien plutôt des exécuteurs de terrain. Cette réflexion préliminaire révèle que la notion de banalité du mal peut être déclinée en quatre formes caractérisant la participation des exécuteurs ; soit la banalité de la similitude, de la familiarité, de l’idée et enfin de répétition.
Some thoughts on the banality of evil, inspired by a conversation with Jean-Paul Brodeur
Authors: Tanner Samuel 
Published: May 2012

Si la notoriété de Jean-Paul Brodeur est en grande partie due à ses recherches sur la police, il est un autre domaine, plus méconnu du grand public, qui le passionnait et le fascinait, à savoir les formes extrêmes de violence, dont le génocide et le crime contre l’humanité. Dans le cadre de cet article, je prolonge un dialogue que nous avions entamé avec Jean-Paul à propos du concept de banalité du mal, développé par Hannah Arendt. En particulier et à partir des contextes yougoslave et rwandais, je propose une extension de cette notion appliquée non pas tant ici aux fonctionnaires et bureaucrates, tels qu’ils constituaient le centre d’attention de la philosophie, alors concentrée sur l’Holocauste, mais bien plutôt des exécuteurs de terrain. Cette réflexion préliminaire révèle que la notion de banalité du mal peut être déclinée en quatre formes caractérisant la participation des exécuteurs ; soit la banalité de la similitude, de la familiarité, de l’idée et enfin de répétition.
Transcriptional Regulation of Murine IL-33 by TLR and Non-TLR Agonists
Authors: Polumuri Swamy Kumar , Jayakar Gift Gunaraj , Shirey Kari Ann , Roberts Zachary J. , Perkins Darren J. , Pitha Paula M. , Vogel Stefanie N. 
Published: May 2012

Abstract
IL-33, a member of the IL-1 family of cytokines, is produced by many cell types, including macrophages, yet its regulation is largely unknown. Treatment of primary murine macrophages with a panel of TLR (e.g., TLR2, TLR3, TLR4, and TLR9) agonists and non-TLR (e.g., MDA5, RIG-I) agonists revealed a pattern of gene and protein expression consistent with a role for IFN regulatory factor-3 (IRF-3) in the expression of IL-33. Accordingly, induction of IL-33 mRNA was attenuated in IRF-3−/− macrophages and TBK-1−/− mouse embryonic fibroblasts. Despite the fact that all IL-33 agonists were IRF-3 dependent, LPS-induced IL-33 mRNA was fully inducible in IFN-β−/− macrophages, indicating that IL-33 is not dependent on IFN-β as an intermediate. Epinephrine and Bordetella pertussis adenylate cyclase toxin (ACT), cAMP-activating agents, activate CREB and greatly synergize with LPS to induce IL-33 mRNA in macrophages. Both LPS-induced and ACT/LPS-enhanced expression of IL-33 mRNA was partially, but significantly, inhibited by the protein kinase A inhibitor H-89 but not by tyrosine kinase or protein kinase C inhibitors. Two IL-33 mRNA species derived from two alternative promoters encode full-length IL-33; however, the shorter “A” species is preferentially induced by all IL-33–inducing agonists except Newcastle disease virus, a RIG-I agonist that induced expression of both “A” and “B” transcripts. Together, these studies greatly extend what is currently known about the regulation of IL-33 induction in macrophages stimulated by bacterial and viral agonists that engage distinct innate immune signaling pathways.
α-1 Antitrypsin Promotes Semimature, IL-10–Producing and Readily Migrating Tolerogenic Dendritic Cells
Authors: Ozeri Eyal , Mizrahi Mark , Shahaf Galit , Lewis Eli C. 
Published: May 2012

Abstract
Tolerogenic IL-10–positive CCR7-positive dendritic cells (DC) promote T regulatory (Treg) cell differentiation upon CCR7-dependent migration to draining lymph nodes (DLN). Indeed, in human DC deficiencies, Treg levels are low. α-1 antitrypsin (AAT) has been shown to reduce inflammatory markers, promote a semimature LPS-induced DC phenotype, facilitate Treg expansion, and protect pancreatic islets from alloimmune and autoimmune responses in mice. However, the mechanism behind these activities of AAT is poorly understood. In this study, we examine interactions among DC, CD4+ T cells, and AAT in vitro and in vivo. IL-1β/IFN-γ–mediated DC maturation and effect on Treg development were examined using OT-II cells and human AAT (0.5 mg/ml). CCL19/21-dependent migration of isolated DC and resident islet DC was assessed, and CCR7 surface levels were examined. Migration toward DLN was evaluated by FITC skin painting, transgenic GFP skin tissue grafting, and footpad DC injection. AAT-treated stimulated DC displayed reduced MHC class II, CD40, CD86, and IL-6, but produced more IL-10 and maintained inducible CCR7. Upon exposure of CD4+ T cells to OVA-loaded AAT-treated DC, 2.7-fold more Foxp3+ Treg cells were obtained. AAT-treated cells displayed enhanced chemokine-dependent migration and low surface CD40. Under AAT treatment (60 mg/kg), DLN contained twice more fluorescence after FITC skin painting and twice more donor DC after footpad injection, whereas migrating DC expressed less CD40, MHC class II, and CD86. Intracellular DC IL-10 was 2-fold higher in the AAT group. Taken together, these results suggest that inducible functional CCR7 is maintained during AAT-mediated anti-inflammatory conditions. Further studies are required to elucidate the mechanism behind the favorable tolerogenic activities of AAT.
BLIMP-1 and STAT3 Counterregulate MicroRNA-21 during Plasma Cell Differentiation
Authors: Barnes Nicholas A. , Stephenson Sophie , Cocco Mario , Tooze Reuben M. , Doody Gina M. 
Published: May 2012

Abstract
During cellular differentiation, mRNA transcription and translation require precise coordination. The mechanisms controlling this are not well defined. IL-21 is an important regulator of plasma cell differentiation, and it controls the master regulator of plasma cell differentiation, B lymphocyte-induced maturation protein-1 (BLIMP-1), via STAT3 and IRF4. Among the other targets of STAT3 is microRNA-21 (miR-21). miR-21 is the most frequently deregulated microRNA in malignancy, including B cell lymphomas, and it has oncogenic potential downstream of STAT3. However, the regulation and function of miR-21 during plasma cell differentiation are not characterized. In contrast to the induction of miR-21 observed in response to STAT3 activation in other systems, we demonstrate that miR-21 is repressed during IL-21–driven plasma cell differentiation. We explored the molecular basis for this repression and identify primary miR-21 transcription as a direct target of BLIMP-1–dependent repression, despite continued STAT3 activation and phospho-STAT3 binding to the primary miR-21 promoter. Thus, STAT3 and BLIMP-1 constitute an incoherent feed-forward loop downstream of IL-21 that can coordinate microRNA with mRNA expression during plasma cell differentiation.
B and T Lymphocyte Attenuator Mediates Inhibition of Tumor-Reactive CD8+ T Cells in Patients After Allogeneic Stem Cell Transplantation
Authors: Hobo Willemijn , Norde Wieger J. , Schaap Nicolaas , Fredrix Hanny , Maas Frans , Schellens Karen , Falkenburg J. H. Frederik , Korman Alan J. , Olive Daniel , van der Voort Robbert , Dolstra Harry 
Published: May 2012

Abstract
Allogeneic stem cell transplantation (allo-SCT) can cure hematological malignancies by inducing alloreactive T cell responses targeting minor histocompatibility antigens (MiHA) expressed on malignant cells. Despite induction of robust MiHA-specific T cell responses and long-term persistence of alloreactive memory T cells specific for the tumor, often these T cells fail to respond efficiently to tumor relapse. Previously, we demonstrated the involvement of the coinhibitory receptor programmed death-1 (PD-1) in suppressing MiHA-specific CD8+ T cell immunity. In this study, we investigated whether B and T lymphocyte attenuator (BTLA) plays a similar role in functional impairment of MiHA-specific T cells after allo-SCT. In addition to PD-1, we observed higher BTLA expression on MiHA-specific CD8+ T cells compared with that of the total population of CD8+ effector-memory T cells. In addition, BTLA’s ligand, herpes virus entry mediator (HVEM), was found constitutively expressed by myeloid leukemia, B cell lymphoma, and multiple myeloma cells. Interference with the BTLA–HVEM pathway, using a BTLA blocking Ab, augmented proliferation of BTLA+PD-1+ MiHA-specific CD8+ T cells by HVEM-expressing dendritic cells. Notably, we demonstrated that blocking of BTLA or PD-1 enhanced ex vivo proliferation of MiHA-specific CD8+ T cells in respectively 7 and 9 of 11 allo-SCT patients. Notably, in 3 of 11 patients, the effect of BTLA blockade was more prominent than that of PD-1 blockade. Furthermore, these expanded MiHA-specific CD8+ T cells competently produced effector cytokines and degranulated upon Ag reencounter. Together, these results demonstrate that BTLA–HVEM interactions impair MiHA-specific T cell functionality, providing a rationale for interfering with BTLA signaling in post-stem cell transplantation therapies.
Cathelicidin-Related Antimicrobial Peptide Is Required for Effective Lung Mucosal Immunity in Gram-Negative Bacterial Pneumonia
Authors: Kovach Melissa A. , Ballinger Megan N. , Newstead Michael W. , Zeng Xianying , Bhan Urvashi , Yu Fu-shin , Moore Bethany B. , Gallo Richard L. , Standiford Theodore J. 
Published: May 2012

Abstract
Cathelicidins are a family of endogenous antimicrobial peptides that exert diverse immune functions, including both direct bacterial killing and immunomodulatory effects. In this study, we examined the contribution of the murine cathelicidin, cathelicidin-related antimicrobial peptide (CRAMP), to innate mucosal immunity in a mouse model of Gram-negative pneumonia. CRAMP expression is induced in the lung in response to infection with Klebsiella pneumoniae. Mice deficient in the gene encoding CRAMP (Cnlp−/−) demonstrate impaired lung bacterial clearance, increased bacterial dissemination, and reduced survival in response to intratracheal K. pneumoniae administration. Neutrophil influx into the alveolar space during K. pneumoniae infection was delayed early but increased by 48 h in CRAMP-deficient mice, which was associated with enhanced expression of inflammatory cytokines and increased lung injury. Bone marrow chimera experiments indicated that CRAMP derived from bone marrow cells rather than structural cells was responsible for antimicrobial effects in the lung. Additionally, CRAMP exerted bactericidal activity against K. pneumoniae in vitro. Similar defects in lung bacterial clearance and delayed early neutrophil influx were observed in CRAMP-deficient mice infected with Pseudomonas aeruginosa, although this did not result in increased bacterial dissemination, increased lung injury, or changes in lethality. Taken together, our findings demonstrate that CRAMP is an important contributor to effective host mucosal immunity in the lung in response to Gram-negative bacterial pneumonia.