bluuebunny/crossref_metadata_2025_split huggingface dataset:
Split agent‐based routing in interconnected networks
Authors: X. Mavromoustakis Constandinos , D. Karatza Helen 
Published: April 2004

AbstractAdaptive behaviour of swarm‐based agents (BT Technol. J. 1994; 12:104–113; AAMAS Conference '02, Melbourne, Australia, Month 1–2, 2002; Softcomput. J. 2001; 5(4):313–317.) is being studied in this paper with respect to network throughput for a certain amount of data traffic. Algorithmically complex problems like routing data packets in a network need to be faced with a dynamically adaptive approach such as agent‐based scheme. Particularly in interconnected networks where multiple networks are participating in order to figure a large‐scale network with different QoS levels and heterogeneity in the service of delay sensitive packets, routing algorithm must adopt in frequent network changes to anticipate such situations. Split agent‐based routing technique (SART) is a variant of swarm‐based routing (Adapt. Behav. 1997; 5:169–207; Proceedings of 2003 International Symposium on Performance Evaluation of Computer and Telecommunication Systems—SPECTS, Montreal, Canada, July 20–24, 2003; 240–247.) where agents are split after their departure to the next node on a hop‐by‐hop basis. Packets that are delay sensitive are marked as prioritized which agents recognize‐as being a part of a packet‐ and try to influence the two‐way routing tables. Thorough examination is made, for the performance of the proposed algorithm in the network and the QoS offered, taking into account a number of metrics. It is shown that the split agent routing scheme applied to interconnected networks offers a decentralized control in the network and an efficient way to increase overall performance and packet control reducing at the same time the packet loss concept. Copyright © 2004 John Wiley & Sons, Ltd.
Energy efficient broadcast routing in mobilead hocnetworks
Authors: Low Chor Ping , Yuen Chau 
Published: April 2004

AbstractIn this paper, we address the problem of broadcast routing in mobilead hocnetworks from the viewpoint of energy efficiency. In anad hocwireless network, each node runs on a local energy source which has a limited energy lifespan. Thus, energy conservation is a critical issue inad hocnetworks. One approach for energy conservation is to establish routes which require lowest total energy consumption. This optimization problem is referred as the minimum‐energy broadcast routing problem (MEBRP). In this paper, we propose new efficient algorithms for the construction of energy‐efficient trees for broadcast in mobilead hocnetworks. These algorithms exploit the broadcast nature of the wireless channel, and address the need for energy‐efficient operations. Empirical studies show that our algorithms are able to achieve better performance than algorithms that have been developed for MEBRP. Copyright © 2004 John Wiley & Sons, Ltd.
Improved insulin secretory function and reduced chemotactic properties after tissue culture of islets from type 1 diabetic patients
Authors: Lupi Roberto , Marselli Lorella , Dionisi Sabrina , Del Guerra Silvia , Boggi Ugo , Del Chiaro Marco , Lencioni Cristina , Bugliani Marco , Mosca Franco , Di Mario Umberto , Del Prato Stefano , Dotta Francesco , Marchetti Piero 
Published: April 2004

AbstractBackgroundType 1 diabetes results from the destruction of pancreatic beta‐cell as a consequence of an autoimmune process. To date, information on the properties of islets isolated from type 1 diabetic patients is very scant.MethodsSome immunological and functional properties of islets prepared from the pancreas of type 1 diabetic patients were studied shortly after the isolation and after a period of culture in euglycemic condition.ResultsCompared to control islets, freshly prepared type 1 diabetic islets released a significantly higher amount of cytokines (pg/mL) into the culture medium (TNF‐α: 112.9 ± 5.6 vs 75.6 ± 24.4; INF‐γ: 286.9 ± 26.9 vs 58.6 ± 6.2; IL‐10: 41.8 ± 4.3 vs 10.1 ± 3.2; TGF‐1 β: 294.0 ± 20.6 vs 45.1 ± 3.5); had a significantly higher chemotactic index (1.9 ± 0.2 vs 1.2 ± 0.1); showed reduced insulin release (% of insulin content) in response to glucose (2.8 ± 0.7 vs 5.3 ± 1.9), arginine (3.0 ± 0.6 vs 5.6 ± 1.0), and glibenclamide (2.9 ± 0.7 vs 5.4 ± 0.9); and exhibited decreased glucose oxidation capability and diminished mRNA expression of glucokinase, aldolase, pyruvate kinase, and mitochondrial glycerolphosphate dehydrogenase. Ten days after isolation, a normalization of cytokine release (TNF‐α: 55.7 ± 2.3; INF‐γ: 53.9 ± 4.3; IL‐10: 8.6 ± 0.7; TGF‐1 β: 60.7 ± 12.4) and chemotactic index (1.3 ± 0.2) were observed. Moreover, there was an improvement of insulin secretion (3.8 ± 0.3, 4.7 ± 0.6 and 3.5 ± 0.2 respectively in response to glucose, arginine, and glibenclamide) and glucose oxidation, and a partial recovery of the measured mRNA expressions.ConclusionsThese novel results, obtained with islets prepared from patients with type 1 diabetes, demonstrate that even after months after diabetes diagnosis, a period of culture of the islets in a more favorable environment has beneficial effects on the islet function. Copyright © 2004 John Wiley & Sons, Ltd.
Differentiating between effects of streptozotocin per se and subsequent hyperglycemia on renal function and metabolism in the streptozotocin‐diabetic rat model
Authors: Palm Fredrik , Ortsäter Henrik , Hansell Peter , Liss Per , Carlsson Per‐Ola 
Published: April 2004

AbstractBackgroundThe animal model with streptozotocin (STZ)‐induced diabetes mellitus is associated with progressive renal disturbances. The aim of this study was to differentiate between toxic effects of STZ and the effect of hyperglycemia. Previous studies have been limited to investigating the influence of STZ on glomerular filtration rate (GFR), albuminuria and renal morphology. The present study presents a new approach when transplanting β‐cells to cure the STZ‐treated animals and extends the evaluation to include both renal function and oxygen metabolism.MethodsAnimals were allocated to three groups: control animals, STZ‐diabetic animals and animals rendered diabetic with an injection of STZ, followed by immediate syngeneic transplantation of ∼1000 pancreatic islets into the splenic parenchyma. This latter procedure reversed the hyperglycemia induced by STZ. Renal function was evaluated from GFR and urinary albumin and protein leakage, while regional renal blood flow was determined using a laser‐Doppler technique and oxygen tension measured with Clark‐type electrodes.ResultsIn diabetic animals, GFR increased, renal oxygen tension decreased and renal hypertrophy occurred, along with urinary leakage of protein, including albumin. Early transplantation of pancreatic islets to STZ‐treated animals prevented the development of all these changes, except for proteinuria. However, an analysis of urinary protein content revealed that albuminuria was preventable by islet transplantation.ConclusionsWe conclude that the urinary protein leakage in this animal model is at least partly due to direct toxic effects of STZ, whereas the other renal changes investigated in this study are due to the long‐term diabetic condition. Copyright © 2004 John Wiley & Sons, Ltd.
A trial of a relapse prevention strategy in women with bulimia nervosa who respond to cognitive‐behavior therapy
Authors: Mitchell James E. , Agras W. Stewart , Wilson G. Terence , Halmi Katherine , Kraemer Helena , Crow Scott 
Published: April 2004

AbstractObjectiveThis study examines a relapse prevention strategy for bulimia nervosa (BN). Subjects in a multicenter BN treatment trial who initially achieved abstinence after a course of cognitive‐behavioral therapy (CBT) were told to recontact the clinic if they had a recurrence of symptoms or feared such a reoccurrence so that they could receive additional therapy visits.MethodAt the end of CBT, subjects whose scores on the Eating Disorders Examination indicated that they were abstinent from binge eating and purging, and therefore considered to be treated successfully, were assigned randomly to follow‐up only or to a crisis intervention model. With the crisis intervention model, subjects would receive additional visits if needed.ResultsNone of the 30 subjects who relapsed during the follow‐up sought additional treatment visits.DiscussionSimply telling patients with BN who appear to have been successfully treated to come back if they have additional problems, or fear that they are developing such problems, may be an ineffective relapse prevention technique. Alternative strategies, such as planned return visits or phone calls, should be considered as alternative relapse prevention strategies. © 2004 by Wiley Periodicals, Inc. Int J Eat Disord 35: 549–555, 2004.
Lesional RhoA+ cell numbers are suppressed by anti‐inflammatory, cyclooxygenase‐inhibiting treatment following subacute spinal cord injury
Authors: Schwab Jan M. , Conrad Sabine , Elbert Tina , Trautmann Katrin , Meyermann Richard , Schluesener Hermann J. 
Published: April 2004

AbstractInhibition of the small GTPase RhoA or its downstream target Rho‐associated coiled kinase (ROCK) has been shown to promote axon regeneration and to improve functional recovery following spinal cord injury (SCI) in the adult rat. RhoA has also been implicated in delayed secondary injury pathophysiology, such as free radical formation and loss of endothelial integrity leading to edema formation. In the present report, we have analyzed the effect of the central nervous system (CNS) permissive, putatively neuroprotective, anti‐inflammatory cyclooxygenase‐1/‐2 (COX‐1/‐2) inhibitor indomethacin in CNS effective dosage (2 mg/kg/day) on lesional RhoA expression following subacute spinal cord injury. In control rats receiving vehicle alone, RhoA+ cells accumulate at the lesion site (Th8). At day 3 following SCI, the RhoA+ cellular composition is composed prevailingly of microglia/macrophages and polymononuclear granulocytes, but few reactive astrocytes. In contrast, in the verum group, lesional numbers of RhoA cells were reduced by indomethacin treatment by more than 60% (P < 0.0001). Inflammation‐dependent RhoA expression accessible by cyclooxygenase inhibition proposes an immune‐related mechanism. Our results identify COX blockers as candidates for a safe, synergistic, adjuvant treatment option in combination with cell‐specific approaches to Rho inactivation, effectively minimizing the pool of RhoA+ cells at the lesion site following SCI. © 2004 Wiley‐Liss, Inc.
Ensheathing cell cultures from the olfactory bulb and mucosa
Authors: Jani Harsha R. , Raisman Geoffrey 
Published: April 2004

AbstractTransplantation of cells cultured from the nerve layers of the adult rat olfactory bulb has been shown to repair CNS tract injuries. The precise cellular composition of the culture appears to be important for this effect. Comparison was made of tissue cultured from the adult rat olfactory mucosa with that from the olfactory bulb. Both yielded mixtures of p75 immunoreactive cells and fibronectin immunoreactive cells. In sequential observations over 21 days in culture, the population of p75‐expressing cells was maintained and continued to proliferate for longer in the samples from the olfactory mucosa. For derivation of cells for transplantation, the mucosa can be accessed without the need for intracranial surgery. © 2004 Wiley‐Liss, Inc.
Laminin‐induced aggregation of the inwardly rectifying potassium channel, Kir4.1, and the water‐permeable channel, AQP4, via a dystroglycan‐containing complex in astrocytes
Authors: Guadagno Eric , Moukhles Hakima 
Published: April 2004

AbstractDystroglycan (DG) is part of a multiprotein complex that links the extracellular matrix to the actin cytoskeleton of muscle fibers and that is involved in aggregating acetylcholine receptors at the neuromuscular junction. This complex is also expressed in regions of the central nervous system where it is localized to both neuronal and glial cells. DG and the inwardly rectifying potassium channels, Kir4.1, are concentrated at the interface of astroglia and small blood vessels. These channels are involved in siphoning potassium released into the extracellular space after neuronal excitation. This raises the possibility that DG may be involved in targeting Kir4.1 channels to specific domains of astroglia. To address this question, we used mixed hippocampal cultures to investigate the distribution of DG, syntrophin, dystrobrevin, and Kir4.1 channels, as well as aquaporin‐permeable water channels, AQP4. These proteins exhibit a similar distribution pattern and form aggregates in astrocytes cultured on laminin. Both DG and syntrophin colocalize with Kir4.1 channel aggregates in astrocytes. Similarly, DG colocalizes with AQP4 channel aggregates. Quantitative studies show a significant increase of Kir4.1 and AQP4 channel aggregates in astrocytes cultured in the presence of laminin when compared with those in the absence of laminin. These findings show that laminin has a role in Kir4.1 and AQP4 channel aggregation and suggest that this may be mediated via a dystroglycan‐containing complex. This study reveals a novel functional role for DG in brain including K+ buffering and water homeostasis. © 2004 Wiley‐Liss, Inc.
Facile dissociation of BS coordination bonds in [2,6‐bis(ethylthiomethyl)phenyl]diethylborane by an SN2‐type mechanism
Authors: Toyota Shinji , Uemitsu Nobuhide , Ōki Michinori 
Published: April 2004

AbstractThe title organoboron complex undergoes dissociation of the intramolecular B–S coordination bond much faster than the corresponding mono ethylthiomethyl complex as revealed by the dynamic NMR study. The facile dissociation is attributable to an SN2‐type mechanism, where the uncoordinated ligand assists the dissociation of the coordinated ligand in the transition state. This mechanism is supported by the initio calculations of a model reaction system. © 2004 Wiley Periodicals, Inc. Heteroatom Chem 15:241–245, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/hc.20005
Novel conversion of 6H‐1,3,5‐oxathiazine S‐oxides into 3H‐1,2,4‐dithiazoles by treating with Lawesson's reagent
Authors: Rafiqul Islam Md. , Shimada Kazuaki , Aoyagi Shigenobu , Fujisawa Yoriko , Takikawa Yuji 
Published: April 2004

AbstractTreatment of 6H‐1,3,5‐oxathiazine S‐oxides by Lawesson's reagent (LR) at high temperature furnished 3H‐1,2,4‐dithiazoles in moderate to good yields. Deoxygenation of 6H‐1,3,5‐oxathiazine S‐oxides was performed by LR in the presence of EtOH. © 2004 Wiley Periodicals, Inc. Heteroatom Chem 15:208–215, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/hc.20011
Synthesis of new potential chelating agents: Catechol–bisphosphonate conjugates for metal intoxication therapy
Authors: Xu Guangyu , Yang Chunhao , Liu Bo , Wu Xihan , Xie Yuyuan 
Published: April 2004

AbstractIn a quest for better chelating therapy drugs for the treatment of intoxication by Fe, Al, or actinides, three new series of bisphosphonates conjugated with catechol were synthesized. © 2004 Wiley Periodicals, Inc. Heteroatom Chem 15:251–257, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/hc.20013
Developmental expression of glutamate transporters and glutamate dehydrogenase in astrocytes of the postnatal rat hippocampus
Authors: Kugler Peter , Schleyer Verena 
Published: April 2004

AbstractGlutamate is the major excitatory transmitter in the CNS and plays distinct roles in a number of developmental events. Its extracellular concentration, which mediates these activities, is regulated by glutamate transporters in glial cells and neurons. In the present study, we have used nonradioactive in situ hybridization, immunocytochemistry, and immunoblotting to show the cellular and regional expression of the high‐affinity glutamate transporters GLAST (EAAT1) and generic GLT1 (EAAT2; glial form of GLT1) in the rat hippocampus during postnatal development (P1–60). The results of transporter expression were compared with the localization and activity pattern of glutamate dehydrogenase (GDH), an important glutamate‐metabolizing enzyme. The study showed that both transporters and GDH were demonstrable at P1 (day of birth). The expression of GLAST (detected by in situ hybridization and immunocytochemistry) in the early postnatal development was higher than GLT1. Thereafter, the expression of both transporters increased, showing adult levels at between P20 and P30 (detected by in situ hybridization and immunoblotting). At these time points, the expression of GLT1 appeared to be significantly higher than the GLAST expression. GLT1 and GLAST proteins were demonstrable only in astrocytes. The increase of GDH activities (steepest increase from P5–P8), which were localized preferentially in astrocytes, was in agreement with the increase of transporter expression, preferentially with that of GLT1. These observations suggest that the extent of glutamate transporter expression and of glutamate‐metabolizing GDH activity in astrocytes is intimately correlated with the formation of glutamatergic synapses in the developing hippocampus. © 2004 Wiley‐Liss, Inc.
Genetic abnormalities in plasma DNA of patients with lung cancer and other respiratory diseases
Authors: Khan Sarah , Coulson Judy M. , Woll Penella J. 
Published: April 2004

AbstractThe detection of tumour‐associated genetic alterations in plasma DNA has been proposed as a simple method for the early diagnosis of lung cancer and for identifying individuals at high risk of lung cancer who might be included in screening or chemoprevention programmes. To evaluate the practicality of this approach, we screened a panel of 16 plasma DNA markers in a lung cancer population to identify those with the highest genetic alteration rate. These were then used to study plasma DNA in 206 hospital outpatients with lung cancer and other respiratory diseases. Plasma and lymphocyte DNA were isolated from blood samples collected from hospital outpatients. Polymerase chain reaction was carried out with 16 microsatellite markers covering chromosomal regions 3p, 8p, 9p, 13q and 17p, using DNA from 32 lung cancer patients. The 3 markers most commonly affected were selected for use in a larger study of 86 lung cancer patients and 120 patients with other respiratory diseases. In the pilot study, 3 primer pairs (D3S1300, D3S1560, D8S201) together detected genetic alterations in plasma DNA in 60% of lung cancer patients. In the larger study, significantly higher genetic alteration rates were observed in lung cancer patients than in patients with other respiratory diseases for the two markers D3S1560 and D8S201. The overall genetic alteration rate was 69% in the lung cancer patients and 42% in the patients with other respiratory diseases (p < 0.001). Analysis of plasma and lymphocyte DNA to detect genetic alterations typical of lung cancer is possible in large studies. The genetic alteration rate we found in lung cancer patients was comparable with other studies. Although the genetic alteration rate was significantly higher in the lung cancer than the respiratory disease patients, it did not have good positive predictive value in this population. Longitudinal studies are required to determine whether genetic changes in plasma DNA of non‐cancer patients indicate a high risk of later lung cancer. © 2004 Wiley‐Liss, Inc.
The variant E233G of the RAD51D gene could be a low‐penetrance allele in high‐risk breast cancer families without BRCA1/2 mutations
Authors: Rodríguez‐López Raquel , Osorio Ana , Ribas Gloria , Pollán Marina , Sánchez‐Pulido Luis , de la Hoya Miguel , Ruibal Álvaro , Zamora Pilar , Arias Jose Ignacio , Salazar Raquel , Vega Ana , Martínez Jose Ignacio , Esteban‐Cardeñosa Eva , Alonso Carmen , Letón Rocío , Urioste Azcorra Miguel , Miner Cristina , Armengod M. Eugenia , Carracedo Angel , González‐Sarmiento Rogelio , Caldés Trinidad , Díez Orland , Benítez Javier 
Published: April 2004

AbstractSix SNPs have been detected in the DNA repair genes RAD51C and RAD51D, not previously characterized. The novel variant E233G in RAD51D is more highly represented in high‐risk, site‐specific, familial breast cancer cases that are not associated with the BRCA1/2 genes, with a frequency of 5.74% (n = 174) compared to a control population (n = 567) and another subset of breast cancer patients (n = 765) with a prevalence of around 2% only (comparison to controls, OR = 2.6, 95% CI 1.12–6.03; p < 0.021). We found that the immunohistochemical profile detected in available tumors from these patients differs slightly from those described in non‐BRCA1/2 tumors. Finally, the structural prediction of the putative functional consequence of this change indicates that it can diminish protein stability and structure. This suggests a role for E233G as a low‐penetrance susceptibility gene in the specific subgroup of high‐risk familial breast cancer cases that are not related to BRCA1/2. © 2004 Wiley‐Liss, Inc.
Evaluation of circulating thyroid‐specific transcripts as markers of thyroid cancer relapse
Authors: Barzon Luisa , Boscaro Marco , Pacenti Monia , Taccaliti Augusto , Palù Giorgio 
Published: April 2004

AbstractCirculating thyroid‐specific transcripts have been suggested as potential molecular markers of residual or recurrent thyroid cancer. We assessed the accuracy of real‐time RT‐PCR‐based detection of a panel of thyroid‐specific markers, including TG, TPO, TSHR, NIS and PDS, in comparison with serum TG measurements in a series of 55 patients operated for differentiated thyroid cancer (DTC). Serum TG levels were higher in patients with residual thyroid tissue or metastatic cancer than in disease‐free patients during thyroid hormone suppressive therapy (THST) and after stimulation with rhTSH (P < 0.05). Recombinant hTSH increased serum TG values in patients with tumor relapse (P < 0.05), but not in disease‐free patients. This assay showed high specificity and good sensitivity in detecting tumor relapse (accuracy under THST = 81.4%; after rhTSH stimulation = 90.9%). TPO and TSHR mRNA, either under THST or after rhTSH, showed a significant correlation with disease status for molecular assays. Qualitative analysis of baseline and stimulated TG, NIS and PDS mRNA showed high sensitivity but low specificity in the prediction of thyroid cancer recurrence or metastases (accuracy under THST = 51%, 43% and 54%, respectively), whereas TPO and TSHR mRNA assays had higher specificity but low sensitivity, with accuracy under THST of 67% and 61%, respectively, that improved when these tests were combined. Our findings indicate that serum TG assay after TSH stimulation is the most accurate test for monitoring DTC. Combined measurements of TPO and TSHR mRNA levels during THST may represent a specific test for early detection of DTC relapse. © 2004 Wiley‐Liss, Inc.