bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of neuronal death induced by focally evoked limbic seizures in the C57BL/6 mouse
Authors: Araki Tomohiro , Simon Roger P. , Taki Waro , Lan Jing‐Quan , Henshall David C. 
Published: September 2002

AbstractResearch into the molecular mechanisms of epileptic brain injury is hampered by the resistance of key mouse strains to seizure‐induced neuronal death evoked by systemically administered excitotoxins such as kainic acid. Because C57BL/6 mice are extensively employed as the genetic background for transgenic/knockout modeling in cell death research but are seizure resistant, we sought to develop a seizure model in this strain characterized by injury to the hippocampal CA subfields. Adult male C57BL/6 mice underwent focally evoked seizures induced by intraamygdala microinjection of kainic acid. Kainic acid (KA) effectively elicited ipsilateral CA3 pyramidal neuronal death within a narrow dose range of 0.1–0.3 μg, with mortality <10%. With employment of the most consistent (0.3 μg) dose, seizures were terminated 15, 30, 60, or 90 min after KA by diazepam. Damage was largely restricted to the ipsilateral CA3 subfield of the hippocampus, but injury was also consistent within CA1, suggesting that this mouse model better reflects the hippocampal neuropathology of human temporal lobe epilepsy than does the rat, in which CA1 is typically spared. Confirming this CA1 injury as seizure specific and not a consequence of ischemia, we used laser‐Doppler flowmetry to determine that cerebral perfusion did not significantly change (97% to 118%) over control. Degenerating cells were >95% neuronal as determined by neuron‐specific nuclear protein (NeuN) counterstaining of terminal deoxynucleotidyl transferase‐mediated dUTP nick end‐labeled (TUNEL) brain sections. Furthermore, TUNEL‐positive cells often exhibited the morphological features of apoptosis, and small numbers were positive for cleaved caspase‐3. These data establish a mouse model of focally evoked seizures in the C57BL/6 strain associated with a restricted pattern of apoptotic neurodegeneration within the hippocampal subfields that may be applied to research into the molecular basis of neuronal death after seizures. © 2002 Wiley‐Liss, Inc.
Role of low‐affinity p75 receptor in nerve growth factor‐inducible growth arrest of PC12 cells
Authors: Ito Hisanori , Nomoto Hiroshi , Furukawa Shoei 
Published: September 2002

AbstractMutant PC12 cell clones (PC84 cells) were obtained by transfection with nerve growth factor (NGF) cDNA. These cells secreted active NGF, extended short processes, and proliferated faster than the parental PC12 cells. These features are of great interest because the parental PC12 cells cease proliferation and extend long processes when transfected with NGF cDNA. PC84 cells expressed a high level of acetylcholinesterase activity and neurofilament M, which indicates that PC84 cells were differentiated. The inhibition of TrkA by K252a diminished the short processes of PC84 cells but had no effect on their fast proliferation. The expression level of TrkA in PC84 cells was comparable to that in PC12 cells; whereas that of another NGF receptor, p75, was significantly lower. These data suggest that the decrease of p75 contributed to the continuous growth of PC84 cells, which was confirmed by suppressing p75 activity of PC12 cells with the antisense oligonucleotide of p75 or with anti‐p75 neutralizing antibody. The treated cells did not cease proliferation in the presence of NGF and extended short processes. Our results suggest that NGF signaling via TrkA affects the differentiation characteristics of PC12 cells but that an additional signaling via p75 is necessary for the growth arrest of the cells. © 2002 Wiley‐Liss, Inc.
Rationale and definition of the lateral extension of the inguinal lymphadenectomy for vulvar cancer derived from an embryological and anatomical study
Authors: Micheletti Leonardo , Levi Alessandro Cesare , Bogliatto Fabrizio , Preti Mario , Massobrio Marco 
Published: September 2002

AbstractBackground and ObjectivesThe objective of the present study was to define the location of the most lateral superficial inguinal node lying along the inguinal ligament, through an embryological and anatomotopographical study, in order to rationalize the lateral extension of the groin lymphadenectomy in vulvar cancer.MethodsSections of the upper portion of the femoral triangle belonging to three human fetuses, whose crown‐rump (CR) length ranged from 70 to 310 mm, corresponding to a developmental age of 11 and 35 weeks, were studied. In addition, for an objective topographical evaluation of the disposition of the superficial inguinal lymph nodes, adult cadavers photographs of dissected Scarpa's triangle, reported in anatomical atlases, were analyzed.ResultsBoth the embryological investigation and the anatomotopographical evaluation on cadavers photographs demonstrate that the most lateral superficial inguinal lymph node does not rise above the medial margin of the sartorius muscle, nor far lateral to the point where the superficial circumflex iliac vessels cross the inguinal ligament.ConclusionsOn the basis of the present study, the authors believe that the superficial circumflex iliac vessels could represent the lateral surgical landmark, easily detectable, at which the inguinal lymphadenectomy should cease. Therefore, there is no need to extend the lateral excision to the anterior superior iliac spine. Finally, leaving the fatty tissue laterally to these vessels, some lymphatic channels could be preserved, decreasing the incidence and the entity of wound seroma and lymphedema. J. Surg. Oncol. 2002;81:19–24. © 2002 Wiley‐Liss, Inc.
Desmopressin inhibits lung and lymph node metastasis in a mouse mammary carcinoma model of surgical manipulation
Authors: Giron Santiago , Tejera Agueda M. , Ripoll Giselle V. , Gomez Daniel E. , Alonso Daniel F. 
Published: September 2002

AbstractBackground and ObjectivesDesmopressin (DDAVP) is a synthetic derivative of vasopressin with hemostatic and fibrinolytic properties that has been used during surgery in patients with bleeding disorders. Our aim was to investigate the effect of DDAVP on lung and lymph node metastatic cell colonization using a preclinical mouse mammary carcinoma model of subcutaneous tumor manipulation and surgical excision.MethodsFemale BALB/c mice bearing the highly aggressive F3II mammary carcinoma were subjected to repeated manipulations of primary tumors (0.5 kg/cm2 during 2 min), followed (or not) by surgical excision. DDAVP was administered intravenously 30 min before and 24 h after each manipulation or surgery, at a dose of 2 μg/kg. At the end of the experiment, mice were sacrificed and necropsied.ResultsTumor manipulation induced dissemination to the axillary nodes and increased up to 6‐fold the number of metastatic lung nodules. Perioperative treatment with DDAVP dramatically reduced regional metastasis. The incidence of lymph node involvement in manipulated animals was 12% with DDAVP and 87% without treatment (P < 0.02). Histopathological analysis of axillary nodes from DDAVP‐treated animals showed sinusal histiocytosis and no evidence of cancer cells. Metastatic lung nodules were also reduced about 65% in animals treated with DDAVP (P = 0.026).ConclusionsOur results suggest a potential clinical application of DDAVP in the management of breast cancer, as well as other aggressive solid tumors. DDAVP may be useful to reduce the risk of metastatic cell colonization both during and after surgical manipulation. J. Surg. Oncol. 2002;81:38–44. © 2002 Wiley‐Liss, Inc.
Review of the clinical, histological, and molecular aspects of pancreatic endocrine neoplasms
Authors: Gumbs A.A. , Moore P.S. , Falconi M. , Bassi C. , Beghelli S. , Modlin I. , Scarpa A. 
Published: September 2002

AbstractPancreatic endocrine neoplasms (PENs) are rare tumors, and little is known about their genetic and chromosomal alterations. Elucidation of the molecular events involved in PEN carcinogenesis has been hindered by the fact that PENs have been considered a single disease entity. The emergence of novel molecular characterization strategies has, however, made it apparent that these lesions exhibit diverse molecular fingerprints, which will facilitate the precise delineation of PEN prognosis, histopathology, and carcinogenesis. J. Surg. Oncol. 2002;81:45–53. © 2002 Wiley‐Liss, Inc.
Biliary carcinoembryonic antigen in the diagnosis of occult hepatic metastases from colorectal cancer
Authors: Li Destri Giovanni , Curreri Roberto , Lanteri Raffaele , Gagliano Giuseppe , Rodolico Margherita , Di Cataldo Antonio , Puleo Stefano 
Published: September 2002

AbstractBackground and ObjectivesTwenty five percent of patients who undergo radical surgical treatment for colorectal cancer have occult hepatic metastases that become evident during the follow‐up period. We evaluated whether biliary carcinoembryonic antigen (CEA) measurements could be used in these patients to diagnose occult hepatic metastases.MethodsThree groups of patients were enrolled in the study. The first group consisted of patients treated for lithiasis of the common bile duct, the second group was affected by colorectal cancer and evident hepatic metastases, and the third group of patients underwent radical surgical treatment for colorectal cancer but had no evident hepatic metastases.ResultsIn the first study group, mean biliary CEA level was 0.52 ng/mL (normal value: 0–5 ng/mL) (diagnostic accuracy: 100%), 83.3 ng/mL in the second group (diagnostic accuracy: 91%) and 3.9 ng/mL in the third group. We registered only one false‐positive result in the third group, whereas biliary CEA level was above normal values in the three patients in whom hepatic metastases developed (diagnostic accuracy: 89.5%).ConclusionsThis study suggests that biliary CEA determination could represent an important method to select patients affected by occult hepatic metastases for inclusion in appropriate treatment protocols. J. Surg. Oncol. 2002;81:8–11. © 2002 Wiley‐Liss, Inc.
Are the axillary lymph nodes treated by standard tangent breast fields?
Authors: McCormick Beryl , Botnick Marc , Hunt Margie , Petrek Jeanne 
Published: September 2002

AbstractBackground and ObjectivesWith the increasing use of sentinel lymph node biopsy, a growing proportion of women with early‐stage invasive breast cancer are undergoing breast conserving surgery without a formal axillary lymph node dissection. A frequent question raised is whether the level I‐II axillary lymph nodes are treated with standard breast tangent fields. In an attempt to answer this question, surgical clips placed at the time of the level I‐II axillary lymph node dissection were used as a surrogate for the location of the nodes and the simulator films for tangent fields of 45 patients were analyzed.MethodsStudy criteria were as follows: five or more clips placed in the axilla, and all clips and the humeral head visualized on the medial tangent film. Clips were scored as “in” or “out” of the tangent field, as defined by the delineator wires. All technical parameters were analyzed to determine whether any reproducible techniques would consistently include all of the clips and, hypothetically, the axillary nodes at levels I and II.ResultsAll clips were included in the medial tangent breast radiation field in only 38% (17 of 45) of cases.ConclusionsThe standard, two‐field tangent breast fields do not reliably encompass the all level I‐II axillary lymph nodes as defined by this study, but some of the nodes were treated in all 45 cases. J. Surg. Oncol. 2002;81:12–16. © 2002 Wiley‐Liss, Inc.
Synthesis of 1‐amino‐2‐methylindoline by Raschig process: Parallel reactions, modeling, and optimization
Authors: Elkhatib M. , Peyrot L. , Metz R. , Tenu R. , Elomar F. , Delalu H. 
Published: September 2002

AbstractThe reaction between chloramine and 2‐methylindoline was studied at pH 12.89, T = 40°C, and for different initial concentrations of reactants. The interaction includes two concurrent bimolecular mechanisms leading to 1‐amino‐2‐methylindoline and 2‐methylindole. The rate laws were determined at the first moments of the reaction by using a differential method. By considering the totality of the reactions that occur in the medium, an appropriate mathematical model was developed. It permits to follow the evolution of the system over time and to calculate the final yields of reaction products. An optimization in terms of the initial contents of 2‐methylindoline and chloramine was performed. It indicated that the maximum yield of 1‐amino‐2‐methylindoline does not exceed 56%. The results show the limit of the Raschig process for the synthesis of indolic hydrazines in aqueous medium. © 2002 Wiley Periodicals, Inc. Int J Chem Kinet 34: 575–584, 2002
Palladium(II) complexes of aliphatic amines and their oxidation by chloramine‐T in perchloric acid medium
Authors: Grover Neeti , Kambo Neelu , Upadhyay Santosh K. 
Published: September 2002

AbstractThe formation of palladium(II) complexes with aliphatic amines and their oxidation by chloramine‐T in perchloric acid medium has been studied. The spectrophotometric studies showed the formation of 1:1 and 1:2 complexes between palladium(II) and amine in absence of HClO4. An increase in [HClO4] in reaction mixture suppresses the complex formation and in presence of [HClO4] ∼10−3 mol dm−3 only a 1:1 complex between palladium(II) and amine has been observed. The effect of Cl− on the complex formation has also been studied.Palladium(II)‐catalyzed oxidation of these amines by chloramine‐T showed a first‐order dependence of rate with respect to each—oxidant, substrate, catalyst, and H+. The mechanism consistent with kinetic data for the oxidation process has been proposed in absence as well as in presence of initial [Cl−]. © 2002 Wiley Periodicals, Inc. Int J Chem Kinet 34: 603–612, 2002
Kinetics and mechanism of oxidation of aurate(I) by peroxydisulphate in aqueous hydrochloric acid
Authors: Babshet R. M. , Gokavi G. S. 
Published: September 2002

AbstractThe reaction between Au(I), generated by reaction of thallium(I) with Au(III), and peroxydisulphate was studied in 5 mol dm−3 hydrochloric acid. The reaction proceeds with the formation of an ion‐pair between peroxydisulphate and chloride ion as the Michealis–Menten plot was linear with intercept. The ion‐pair thus formed oxidizes AuCl2− in a slow two‐electron transfer step without any formation of free radicals. The ion‐pair formation constant and the rate constant for the slow step were determined as 113 ± 20 dm−3 mol−1 and 5.0 ± 1.0 × 10−2 dm3 mol−1 s−1, respectively. The reaction was retarded by hydrogen ion, and formation of unreactive protonated form of the reductant, HAuCl2, causes the rate inhibition. From the hydrogen ion dependence of the reaction rate, the protonation constant was calculated to be as 0.6 ± 0.1 dm3 mol−1. The activation parameters were determined and the values support the proposed mechanism. © 2002 Wiley Periodicals, Inc. Int J Chem Kinet 34: 589–594, 2002
Genetic analyses of mouse skin tumor progression susceptibility using SENCAR inbred derived strains
Authors: Stern Mariana C. , Benavides Fernando , LaCava Margaret , Conti Claudio J. 
Published: September 2002

AbstractSusceptibility to tumor development varies among individuals in the human population. This variability can also be found among different strains of mice, particularly in the mouse skin chemical carcinogenesis model. The genetic mechanisms underlying mouse skin tumor susceptibility are not fully understood. The SENCAR stock has been found to be the most sensitive mice for skin carcinogenesis studies; however, little is known about the genes underlying tumor susceptibility, particularly, those involved in tumor progression. Experiments with the SSIN/Sprd mice, an inbred strain derived from the outbred SENCAR stock, suggested that papilloma development, tumor promotion, and their conversion into squamous cell carcinomas (SCCs), progression, are regulated by different genes. In the highly sensitive SSIN/Sprd mice, papillomas rarely progress to SCC. Using crosses between the outbred SENCAR and the SSIN/Sprd mice, we previously determined that papilloma progression in the SENCAR stock could be controlled by at least one autosomal dominant gene. However, the outbred nature of the SENCAR stock precluded us from extending those findings. More recently, another inbred strain was developed from the outbred SENCAR stock, the SENCARB/Pt. These mice have similar tumor promotion sensitivity to the SSIN/Sprd but in contrast, have high papilloma progression susceptibility, similar to the outbred original stock. In the present study, we generated F1, F2, and backcross hybrids between the SSIN/Sprd and SENCARB/Pt mice to determine a possible model for tumor progression susceptibility and to map the putative tumor susceptibility genes. Our tumor data suggests that papilloma progression susceptibility in the SENCAR mouse skin model could be genetically determined by one susceptibility gene. Our preliminary linkage analysis failed to identify one strong susceptibility locus to confirm this but provided some evidence for at least one possible susceptibility locus in mouse chromosome 14. © 2002 Wiley‐Liss, Inc.
Follistatin overexpression in rodent liver tumors: A possible mechanism to overcome activin growth control
Authors: Rossmanith Walter , Chabicovsky Monika , Grasl‐Kraupp Bettina , Peter Barbara , Schausberger Elisabeth , Schulte‐Hermann Rolf 
Published: September 2002

AbstractThe activin‐follistatin system is a potent growth regulatory system of liver tissue homeostasis. Activin A inhibits hepatocellular DNA synthesis and induces cell death. Follistatin binds activin and sequesters it from the signaling pathway. Consistently, follistatin has been reported to act as an inducer of DNA synthesis in the liver. Using RNase protection analysis, we studied the expression of follistatin in rat and mouse liver tumors as a possible mechanism to overcome activin growth control. Approximately 40% of the tumors (nine of 24 each), most of them hepatocellular carcinomas, displayed increased levels of follistatin mRNA when compared to tumor‐surrounding liver tissue. The degree of overexpression was highly variable but independent of the carcinogen treatment that animals had received. It was also independent from the histological stage of malignancy and further found in rat liver adenomas. Follistatin expression was also observed in cell lines derived from human hepatocellular carcinomas. Overexpression of follistatin may represent a unique strategy of hepatic tumors to overcome the inhibitory action of a growth factor, activin, by decreasing its local bioavailability. © 2002 Wiley‐Liss, Inc.
CCND1‐ and ERBB2‐gene deregulation and PTEN mutation analyses in invasive lobular carcinoma of the breast
Authors: Mercapide Javier , Zhang Shi Yu , Fan Xing , Furió‐Bacete Vicente , Schneider José , Osa Íñigo López de la , Patchefsky Arthur S. , Klein‐Szanto Andrés J. P. , Castresana Javier S. 
Published: September 2002

AbstractBecause of the relatively low incidence of lobular breast carcinoma, there are very few studies on the molecular characteristics of this breast cancer. In an attempt to improve its characterization, we investigated in a large collection of invasive lobular carcinomas (ILCs) the status of markers known to be involved in the better‐studied invasive ductal carcinomas (IDC). In the current study we disposed of 80 well‐characterized ILC cases. Gene amplification of cyclin D1 (CCND1) and c‐erbB2‐encoding gene (ERBB2) and expression of their gene products were studied by differential polymerase chain reaction (PCR) and immunohistochemistry, respectively. A comprehensive point mutation study of the phosphatase and tensin homolog tumor suppressor gene (PTEN) was pursued by single strand conformation polymorphism (SSCP)/sequencing analysis. The CCND1 gene was rarely amplified in ILC in spite of showing overexpression of the protein in 41% of tumors. Hence, unlike IDC, increase in gene dosage did not account for the protein excess. PTEN mutations were detected in ILC (truncating mutations) in around 2% of the tumors. Unlike IDC, ILC did not display ERBB2 overexpression and expression of the transcription factor E2F1 correlated inversely with tumor grade. The observed discrepancy in the pattern of the human oncogenes CCND1 and ERBB2, which are involved in the process of carcinogenesis of ductal tumors, appears to suggest a different molecular basis for development and progression of ILC. © 2002 Wiley‐Liss, Inc.
Evidence of increased Id‐1 expression and its role in cell proliferation in nasopharyngeal carcinoma cells
Authors: Wang Xianghong , Xu Kexin , Ling Ming Tat , Wong Y. C. , Feng Hui Chen , Nicholls John , Tsao S. W. 
Published: September 2002

AbstractInhibitor of differentiation or DNA binding (Id‐1), a helix‐loop‐helix transcription factor, has recently been shown to inactivate the retinoblastoma (RB)/p16INK4a pathway through down‐regulation of p16INK4a and increasing phosphorylation of RB in certain cell types. Nasopharyngeal carcinoma (NPC) is a common cancer in Hong Kong, and inactivation of the tumor suppressor RB at transcription level is a rare event in NPC. The objective of this study was to investigate the role of Id‐1 in NPC cell proliferation and its expression in NPC samples. An NPC cell line, CNE1, was transfected with a retroviral vector containing a full‐length Id‐1 cDNA, and six stable transfectant clones were isolated with differential Id‐1 expression levels. The effect of ectopic Id‐1 expression on serum‐independent cell growth, cell‐cycle distribution, and expression of proteins associated with RB pathway was studied. The Id‐1 expression in five NPC samples was also investigated using immunohistochemistry. Ectopic Id‐1 expression in CNE1 cells resulted in an increase in serum‐independent cell growth, percentage of cells in S phase, and phosphorylation of RB and cyclin‐dependent kinase 2 proteins. In addition, immunohistochemical studies on NPC samples showed that expression of Id‐1 was present in NPC cells but absent in normal tissues. This study demonstrates that Id‐1 plays an important role in cell proliferation in NPC cells, and our results provide evidence for the first time of the significance of Id‐1 expression in NPC cells and suggest a possible role of Id‐1 expression in the inactivation of RB and development of NPC. © 2002 Wiley‐Liss, Inc.
Time‐to‐market, window of opportunity, and salvageability of a new product development
Authors: Messica A. , Mehrez A. 
Published: September 2002

AbstractThe time‐to‐market in the presence of a window of opportunity is analyzed using ;a probabilistic model, i.e. a model where the completion time of new product development is a random variable characterized by a gamma distribution. Two cases are considered: the first, a case where the discounted return‐on‐investment exceeds the return expected from a conservative investment—e.g. investment in bonds—termed ‘the profitable case’; and the second, a case where the discounted return‐on‐investment just balances the cost of new product development, termed ‘the salvageable case’. The model constructed is focused on the financial aspects of new product development. It allows a decision‐maker to monitor, as well as terminate, a project based on its expected value (at any time prior to completion) by computing the mean time‐to‐market that provides profit, investment salvage, or loss. The mean time‐to‐market computed by the model may be compared with that estimated by the technology development team for decision‐making purposes. Finally, in the presence of a window of opportunity and for the specific cases analyzed, we recommend to always keep the expenditure rate lower than the expected return rate. This will provide the decision‐maker a salvageable exit opportunity if project termination is decided. Copyright © 2002 John Wiley & Sons, Ltd.