bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dose‐dependent separation of the hypertrophic and myotoxic effects of the β2‐adrenergic receptor agonist clenbuterol in rat striated muscles
Authors: Burniston Jatin G. , Clark William A. , Tan Lip‐Bun , Goldspink David F. 
Published: January 2006

AbstractMuscle growth in response to large doses (milligrams per kilogram) of β2‐adrenergic receptor agonists has been reported consistently. However, such doses may also induce myocyte death in the heart and skeletal muscles and hence may not be safe doses for humans. We report the hypertrophic and myotoxic effects of different doses of clenbuterol. Rats were infused with clenbuterol (range, 1 μg to 1 mg.kg−1) for 14 days. Muscle protein content, myofiber cross‐sectional area, and myocyte death were then investigated. Infusions of ≥10 μg.kg−1.d−1 of clenbuterol significantly (P < 0.05) increased the protein content of the heart (12%–15%), soleus (12%), plantaris (18%–29%), and tibialis anterior (11%–22%) muscles, with concomitant myofiber hypertrophy. Larger doses (100 μg or 1 mg) induced significant (P < 0.05) myocyte death in the soleus (peak 0.2 ± 0.1% apoptosis), diaphragm (peak 0.15 ± 0.1% apoptosis), and plantaris (peak 0.3 ± 0.05% necrosis), and significantly increased the area fraction of collagen in the myocardium. These data show that the low dose of 10 μg.kg−1.d−1 can be used in rats to investigate the anabolic effects of clenbuterol in the absence of myocyte death. Muscle Nerve, 2006
An integer programming approach to routing in daisy networks
Authors: Becker Johanna , Csizmadia Zsolt , Galtier Jérôme , Laugier Alexandre , Szabó Jácint , Szegő László 
Published: January 2006

AbstractWe are concerned with routing problems arising in special kinds of SDH networks, called daisy networks. Beside the capacity constraints, some disjoint edge‐sets of the network, called arcs, are also prescribed. Our goal is to find a routing of the demands satisfying the capacities with the additional constraint that whenever a path (with value 1) enters an arc then it uses capacity 1 on all edges of that arc. We consider two types of arc‐systems and give algorithms and computational results of integer programming formulations. © 2006 Wiley Periodicals, Inc. NETWORKS, Vol. 47(2), 116–121 2006
Changes within maturing neurons limit axonal regeneration in the developing spinal cord
Authors: Blackmore Murray , Letourneau Paul C. 
Published: January 2006

AbstractEmbryonic birds and mammals display a remarkable ability to regenerate axons after spinal injury, but then lose this ability during a discrete developmental transition. To explain this transition, previous research has emphasized the emergence of myelin and other inhibitory factors in the environment of the spinal cord. However, research in other CNS tracts suggests an important role for neuron‐intrinsic limitations to axon regeneration. Here we re‐examine this issue quantitatively in the hindbrain‐spinal projection of the embryonic chick. Using heterochronic cocultures we show that maturation of the spinal cord environment causes a 55% reduction in axon regeneration, while maturation of hindbrain neurons causes a 90% reduction. We further show that young neurons transplanted in vivo into older spinal cord can regenerate axons into myelinated white matter, while older axons regenerate poorly and have reduced growth cone motility on a variety of growth‐permissive ligands in vitro, including laminin, L1, and N‐cadherin. Finally, we use video analysis of living growth cones to directly document an age‐dependent decline in the motility of brainstem axons. These data show that developmental changes in both the spinal cord environment and in brainstem neurons can reduce regeneration, but that the effect of the environment is only partial, while changes in neurons by themselves cause a nearly complete reduction in regeneration. We conclude that maturational events within neurons are a primary cause for the failure of axon regeneration in the spinal cord. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006
Cytoplasmic domain of protocadherin‐α enhances homophilic interactions and recognizes cytoskeletal elements
Authors: Triana‐Baltzer Gallen B. , Blank Martina 
Published: January 2006

AbstractCell adhesion molecules of the protocadherin‐α (pcdh‐α), ‐β, and ‐γ families have been proposed to be synaptic specifiers. Pcdh‐α and ‐γ family members localize in part to synapses, and deletion of all pcdh‐γs in mouse affects synaptogenesis. Little is known, however, about the binding specificities and intracellular signaling of protocadherins. Using heterologous expression of tagged constructs, immunostaining, and biotinylation of surface components followed by Western blots we demonstrate that pcdh‐αs undergo homophilic interactions that are significantly enhanced by the cytoplasmic domain. Pcdh‐αs cloned from chick ciliary ganglion have one of two cytoplasmic constant regions (A‐ and B‐types). Screening a yeast two‐hybrid library of ciliary ganglion cDNA with the A‐type domain yielded a fragment of neurofilament M (NFM); screening with B‐type domain yielded a fragment of the actin‐bundling protein fascin. Cotransfection of HEK cells with the constructs indicated that the NFM and A‐type fragments codistributed as did the fascin and B‐type fragments, and the latter could be coimmunoprecipitated. Antibody‐induced clustering of full‐length pcdh‐αs on the surface of transfected HEK cells induced coclustering of the interacting NFM fragment. Native full‐length NFM in tissue extracts bound specifically to the A‐type domain on beads, while native full‐length fascin in tissue extracts specifically coimmunoprecipitated with pcdh‐α. Immunostaining neurons demonstrated codistribution of full‐length pcdh‐α with both NFM and actin filaments. These findings suggest cytoskeletal links for pcdh‐αs and identify candidate targets. They also demonstrate homophilic interactions for pcdh‐αs as described for classical cadherins. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006
Genome‐wideP‐element screen forDrosophilasynaptogenesis mutants
Authors: Liebl Faith L.W. , Werner Kristen M. , Sheng Qi , Karr Julie E. , McCabe Brian D. , Featherstone David E. 
Published: January 2006

AbstractA molecular understanding of synaptogenesis is a critical step toward the goal of understanding how brains “wire themselves up,” and then “rewire” during development and experience. Recent genomic and molecular advances have made it possible to study synaptogenesis on a genomic scale. Here, we describe the results of a screen for genes involved in formation and development of the glutamatergicDrosophilaneuromuscular junction (NMJ). We screened 2185P‐element transposon mutants representing insertions in ≈16% of the entireDrosophilagenome. We first identified recessive lethal mutants, based on the hypothesis that mutations causing severe disruptions in synaptogenesis are likely to be lethal. Two hundred twenty (10%) of all insertions were homozygous lethal. Two hundred five (93%) of these lethal mutants developed at least through late embryogenesis and formed neuromusculature. We examined embryonic/larval NMJs in 202 of these homozygous mutants using immunocytochemistry and confocal microscopy. We identified and classified 88 mutants with altered NMJ morphology. Insertion loci in these mutants encode several different types of proteins, including ATP‐ and GTPases, cytoskeletal regulators, cell adhesion molecules, kinases, phosphatases, RNA regulators, regulators of protein formation, transcription factors, and transporters. Thirteen percent of insertions are in genes that encode proteins of novel or unknown function. Complementation tests and RT‐PCR assays suggest that approximately 51% of the insertion lines carry background mutations. Our results reveal that synaptogenesis requires the coordinated action of many different types of proteins—perhaps as much as 44% of the entire genome—and that transposon mutageneses carry important caveats that must be respected when interpreting results generated using this method. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006
Kinesin‐2 differentially regulates the anterograde axonal transports of acetylcholinesterase and choline acetyltransferase in Drosophila
Authors: Baqri Rehan , Charan Rakshita , Schimmelpfeng Kristina , Chavan Swati , Ray Krishanu 
Published: January 2006

AbstractCholine acetyltransferase (ChAT) and acetylcholinesterase (AChE) are involved in acetylcholine synthesis and degradation at pre‐ and postsynaptic compartments, respectively. Here we show that their anterograde transport in Drosophila larval ganglion is microtubule‐dependent and occurs in two different time profiles. AChE transport is constitutive while that of ChAT occurs in a brief pulse during third instar larva stage. Mutations in the kinesin‐2 motor subunit Klp64D and separate siRNA‐mediated knock‐outs of all the three kinesin‐2 subunits disrupt the ChAT and AChE transports, and these antigens accumulate in discrete nonoverlapping punctae in neuronal cell bodies and axons. Quantification analysis further showed that mutations in Klp64D could independently affect the anterograde transport of AChE even before that of ChAT. Finally, ChAT and AChE were coimmunoprecipitated with the kinesin‐2 subunits but not with each other. Altogether, these suggest that kinesin‐2 independently transports AChE and ChAT within the same axon. It also implies that cargo availability could regulate the rate and frequency of transports by kinesin motors. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006
Second and third malignant solid tumor in a girl with ovarian Sertoli–Leydig tumor
Authors: Panagiotou John P. , Polychronopoulou Sophia , Sofou Kalliopi , VanVliet‐Constantinidou Catherine , Papandreou Evangelos , Haidas Stavros 
Published: January 2006

AbstractWe report a Sertoli–Leydig cell (SLC) tumor of the right ovary in a 10‐year‐old girl, which was dealt with surgical removal. Three months after resection, she presented with a new episode of acute abdomen because of an abdominal mass, which histologically was compatible with an undifferentiated embryonal rhabdomyosarcoma. Chemotherapy, according to SIOP‐??? 89 protocol, was administered additionally to radiotherapy (3,960 cGy). Three years after completing treatment, the patient developed a painful swelling at her left upper arm. The diagnosis was Ewing sarcoma of the humerus, which was confirmed by identification of the typical 11; 22 translocation on cytogenetic and molecular analysis of the tumor tissue. The patient died 14 months from Ewing diagnosis due to progressive disease. Pediatr Blood Cancer © 2006 Wiley‐Liss, Inc.
Optic pathway gliomas
Authors: Jahraus Christopher D. , Tarbell Nancy J. 
Published: January 2006

AbstractOptic pathway gliomas represent approximately 5% of all pediatric intracranial tumors. While these tumors are most frequently low grade astrocytomas, they follow a highly variable clinical course, and accordingly, there is much debate regarding their optimal management. Their propensity to occur in very young children and infants further complicates selection of therapy. Historically, surgery and radiotherapy have played a primary role in management, however, in the last 15 years, chemotherapy has evolved into the first‐line treatment of choice. Nonetheless, chemotherapy frequently fails, but serves to delay implementation of radiotherapy or surgery until the child has progressed neuropsychologically. An overall favorable prognosis for this tumor emphasizes the need for careful selection of therapy. Herein, we review the major features of optic pathway glioma, including epidemiology, pathology, therapeutic interventions, outcome, and treatment sequelae. Pediatr Blood Cancer © 2006 Wiley‐Liss, Inc.
Pediatric primary leptomeningeal lymphoma treated without cranial radiotherapy
Authors: Taga Takashi , Sakaue Yuko , Anzai Yuko , Takeuchi Yoshihiro , Ohta Shigeru 
Published: January 2006

AbstractWe report a case of primary leptomenigeal lymphoma (PLML) in an 11‐year‐old boy presenting with headache, vomiting, and diplopia. The patient was treated on an advanced non‐Hodgkin lymphoma protocol with systemic/intrathecal chemotherapy without cranial radiotherapy. He remains in complete remission 33 months after treatment. Pediatr Blood Cancer © 2006 Wiley‐Liss, Inc.
Weighing the risks of G‐CSF administration, leukopheresis, and standard marrow harvest: Ethical and safety considerations for normal pediatric hematopoietic cell donors
Authors: Pulsipher Michael A. , Nagler Arnon , Iannone Robert , Nelson Robert M. 
Published: January 2006

AbstractBackgroundGranulocyte colony stimulating factor (G‐CSF) is used for collection of hematopoietic cells in most adult and a smaller but significant percentage of pediatric normal donor harvests. Short and long‐term risks of G‐CSF administration and leukopheresis are not well understood in the pediatric population.ProcedureLiterature review including observations from the IBMTR, NMDP, EBMT, German Donor Registry, and the authors' work.ResultsG‐CSF causes temporary discomfort in a minority of younger donors. Rare serious side effects of G‐CSF have yet to be reported in children. To date, an increase in hematological malignancies after short‐term G‐CSF use has not been detected in adult donors and no cases have been reported in children. Reported complications of leukopheresis in children are rare and minor, but donors <20 kg may be exposed to allogeneic blood products. Pediatric aged donors vary widely in their ability to assent or consent to the risks of a donation procedure. There are key regulations and ethical imperitives, which must be addressed in deciding which donation procedures are appropriate for minors.ConclusionsWhile short term administration of G‐CSF and leukopheresis appear to be safe and effective procedures when used to assist in collection of a hematopoietic cell graft from a normal pediatric donor, institutions adding or substituting one or both of these procedures for standard marrow donation must decide whether the donor should be considered a research subject, and if so, whether the new procedures are a minor increase over minimal risk. Because these procedures are being performed on and off study at many pediatric centers, a comprehensive study addressing donor safety could help clarify risks of rare adverse events. Pediatr Blood Cancer 2006, 46:422–433. © 2006 Wiley‐Liss, Inc.
Topotecan and cyclophosphamide in patients with refractory or relapsed Ewing tumors
Authors: Hunold Andrea , Weddeling Nicole , Paulussen Michael , Ranft Andreas , Liebscher Caren , Jürgens Herbert 
Published: January 2006

AbstractBackgroundThe prognosis of Ewing tumor (ET) patients has significantly improved to cure rates approximating 70%. The prognosis in relapse, however, is poor. Promising response rates have recently been reported for the combination of topotecan (TOPO) and cyclophosphamide (CYC) encouraging wider application of this combination in patients with relapsed ETs. This report summarizes the experience of patients treated with TOPO/CYC for recurrent or refractory disease within the German ET trials.ProcedureFifty‐four patients aged 3.2–49.5 (median: 17.4) years received TOPO (0.75 mg/m2/day, days 1–5) and CYC (250 mg/m2/day, days 1–5) following first (40) or second (6) relapse or progression under first‐line therapy (8).ResultsA median of 3 (range: 1–11) TOPO/CYC courses were given. Sixteen patients (32.6%) showed partial response (PR), 13/49 (26.5%) had stable disease (SD), 14/49 (28.6%) progressed, 2/49 (4.1%) showed a mixed response (MR). In 4 patients response was not documented, 5/54 patients with complete initial resection at the diagnosis of relapse were excluded from the response analysis. At completion of relapse therapy, 24/54 patients had entered complete (19) or partial (5) remission, 2 had SD, 26 showed progression, information was unavailable in 2 patients. Of the 19 relapse patients achieving complete response (CR), 10 maintained remission (52.6%). At the time of evaluation, after a median follow‐up for survivors of 23.1 (range: 7.8–59.8) months from the event prompting TOPO/CYC treatment, 14/54 patients (25.9%) were in continuous complete (13) or partial (1) remission. Overall survival (OAS) after 1 year was 0.61 (95%‐CI 0.47–0.74).ConclusionTOPO/CYC is active in relapsed ETs and warrants further evaluation. Pediatric Blood Cancer 2006;47:795–800. © 2006 Wiley‐Liss, Inc.
Langerhans cell histiocytosis infiltration into pancreas and kidney
Authors: Goyal Richa , Das Ashim , Nijhawan Raje , Bansal Deepak , Marwaha Ram Kumar 
Published: January 2006

AbstractAn 18‐month‐old male presented with a swelling of the neck for 2 months. A presumptive diagnosis of Langerhans cell histiocytosis (LCH) was made on fine needle aspiration cytology from the lymph node. The child received chemotherapy. He remained well for around 10 months, when he represented with loose stools, cough, and respiratory distress. His condition deteriorated over a few hours culminating in death. A partial autopsy revealed LCH infiltration in liver, pancreas, and kidneys along with bronchopneumonia. The pancreatic and renal infiltration by LCH is extremely rare. Pediatr Blood Cancer 2007;49:748–750. © 2006 Wiley‐Liss, Inc.
Evaluation of persistent pulmonary infiltrates in pediatric oncology patients
Authors: Armenian Saro H. , La Via William V. , Siegel Stuart E. , Mascarenhas Leo 
Published: January 2006

AbstractPurposeTo evaluate the role of bronchoalveolar lavage (BAL), computed‐tomography‐guided biopsy (CTB), and open lung biopsy (OLB) in the management of persistent pulmonary infiltrates in pediatric oncology patients.MethodsRetrospective review of clinical records of pediatric oncology patients who underwent BAL, CTB, and OLB over a 7‐year period. Data was compared across the three procedures using chi‐square analysis. Logistic regression was used to adjust potential confounding variables for diagnostic yield.ResultsThere were 113 consecutive patients who underwent 140 separate procedures during their hospitalization. Thirty (26%) patients had a previous BMT. BALs were more likely to occur as the first line of investigation (98% vs. 47%, 45%; P < 0.01) and in patients with diffuse infiltrates (64% vs. 6%, 26%; P < 0.01) when compared to CTB and OLB, respectively. OLBs were performed less frequently in neutropenic patients (26% vs. 53%, 54%; P < 0.05), more often led to change in management directly because of procedure (61% vs. 12%, 33%; P < 0.01), and had higher diagnostic yield (61% vs. 24%, 36%; P < 0.01) when compared to CTB and BAL, respectively. Diagnostic yield of OLB was significantly higher regardless of diffuse or focal nature of infiltrate. Major adverse events after a procedure were not significantly different across the three procedures. Logistic regression demonstrated that having an OLB was independently associated with identifying the cause of pulmonary infiltrate.ConclusionOLB appears to be safe, has the best diagnostic yield, and leads to change in management more often than CTB or BAL in pediatric oncology patients with persistent pulmonary infiltrates. Pediatr Blood Cancer 2007;48:165–172. © 2006 Wiley‐Liss, Inc.
Effective treatment of kaposiform hemangioendotheliomas associated with Kasabach–Merritt phenomenon using four‐drug regimen
Authors: Hauer Julia , Graubner Ulrike , Konstantopoulos Nikos , Schmidt Susanne , Pfluger Thomas , Schmid Irene 
Published: January 2006

AbstractWe report a case of a 6‐month‐old girl suffering from a kaposiform hemangioendothelioma of the chest wall, associated with Kasabach–Merritt phenomenon. Despite rapid intervention with cortisone and interferon alpha the tumor led to a life‐threatening clinical condition with progressive growth and consumption coagulopathy under therapy. Because therapy for kaposiform hemangioendotheliomas with a single anti‐angiogenic or anti‐proliferative agent has not been reported to be very successful, we administered vincristine, combined with cyclophosphamide, actinomycin D, and methotrexate in a critically ill patient. After six cycles of the applied four‐drug regiment, the infant was in remission, which has been maintained for 5 months since stopping therapy. Pediatr Blood Cancer 2007;49:852–854. © 2006 Wiley‐Liss, Inc.
Temporary diabetes mellitus secondary to a primary pancreatic Burkitt lymphoma
Authors: Meier Constance , Kapellen Thomas , Tröbs Ralph B. , Hirsch Wolfgang , Parwaresch Reto , Kiess Wieland , Körholz Dieter 
Published: January 2006

AbstractPrimary pancreatic lymphoma (PPL) is a rare form of extranodal lymphoma. So far, only in adults has a coincidence with diabetes mellitus (DM) been described. We report a nearly 9‐year‐old German boy presenting with a Burkitt lymphoma associated with a temporary insulin‐dependent DM and exocrine insufficiency of the pancreas. After the patient went into remission, a spontaneous recovery of the endocrine pancreatic function was observed. On immunophenotyping, the lymphoma cells revealed expression of FasL suggesting a potentially apoptotic effect on pancreatic tissue. Beta cell impairment may have been caused by FasL resembling autoimmune diabetes. Pediatr Blood Cancer © 2006 Wiley‐Liss, Inc.
Complementary and alternative medicine in pediatric oncology: Availability and institutional policies in Canada—a report from the Children's Oncology Group
Authors: Johnston Donna L. , Nagel Kim , O'Halloran Claire , Sencer Susan F. , Kelly Kara M. , Friebert Sarah , Hilden Joanne M. , Friedman Debra L. 
Published: January 2006

AbstractComplementary and alternative medicine (CAM) is used frequently by pediatric oncology patients. A survey exploring the institutional practices and policies surrounding CAM use in pediatric oncology patients was completed by 17 pediatric hematology/oncology centers in Canada. We found that CAM was offered in only 18% of the institutions, but 94% of the communities. Only 6% of oncology divisions made direct referrals to community CAM providers, and only 20% of the centers had policies regarding use of CAM therapies for their patients. Despite published widespread use of CAM therapies, our study demonstrates that institutional CAM resources and policies on CAM are present in much lower proportions. Pediatr Blood Cancer © 2006 Wiley‐Liss, Inc.
Increased oxidation and degradation of cytosolic proteins in alcohol‐exposed mouse liver and hepatoma cells
Authors: Kim Bong‐Jo , Hood Brian L. , Aragon Richard A. , Hardwick James P. , Conrads Thomas P. , Veenstra Timothy D. , Song Byoung J. 
Published: January 2006

AbstractWe recently developed a sensitive method using biotin‐N‐maleimide (biotin‐NM) as a probe to positively identify oxidized mitochondrial proteins. In this study, biotin‐NM was used to identify oxidized cytosolic proteins in alcohol‐fed mouse livers. Alcohol treatment for 6 wk elevated the levels of CYP2E1 and nitrotyrosine, a marker of oxidative stress. Markedly increased levels of oxidized proteins were detected in alcohol‐fed mouse livers compared to pair‐fed controls. The biotin‐NM‐labeled oxidized proteins from alcohol‐exposed mouse livers were subsequently purified with streptavidin‐agarose and resolved on 2‐DE. More than 90 silver‐stained protein spots that displayed differential intensities on 2‐D gels were identified by MS. Peptide sequence analysis revealed that many enzymes or proteins involved in stress response, chaperone activity, intermediary metabolism, and antioxidant defense systems such as peroxiredoxin were oxidized after alcohol treatment. Smaller fragments of many proteins were repeatedly detected only in alcohol‐fed mice, indicating that many oxidized proteins after alcohol exposure were degraded. Immunoblot results showed that the level of oxidized peroxiredoxin (inactivated) was markedly increased in the alcohol‐exposed mouse livers and ethanol‐sensitive hepatoma cells compared to the corresponding controls. Our results may explain the underlying mechanism for cellular dysfunction and increased susceptibility to other toxic agents following alcohol‐mediated oxidative stress.