bluuebunny/crossref_metadata_2025_split huggingface dataset:
Input and Output Characteristics of Collision Avoidance Behavior in the Frog <i>Rana catesbeiana</i>
Authors: Yamamoto Keisuke , Nakata Maki , Nakagawa Hideki 
Published: October 2003

Input and output characteristics of collision avoidance behavior in the bullfrog were examined using computer graphics to model a looming stimulus. The means of time-to-collision of avoidance behavior in response to looming visual stimuli approaching at a velocity of either 2 or 4 m/s were significantly different (t<sub>(141)</sub> = 7.93, p < 0.05). On the other hand, mean threshold sizes of visual stimuli triggering avoidance behavior were not significantly different in either case (t<sub>(201)</sub> = 0.54, p > 0.05). Furthermore, we showed that the mean threshold sizes changed in a predictable manner depending on the distance between the displayed stimulus and the animal. These results strongly suggest that the frog displays collision avoidance behavior when the visual angle of a looming object reaches a constant value (about 20°). The mean maximum velocities of the avoidance behavior in response to the two visual stimuli were not significantly different (t<sub>(198)</sub> = 1.44, p > 0.05). However, we found that the frog could control the velocity depending on the location of an approaching object in its dorsal visual field. Finally, we demonstrated that habituation significantly affected the mean probability of avoidance behavior occurrence (ANOVA, at 2 m/s, F<sub>(2,15)</sub> = 14.25; at 4 m/s, F<sub>(2,15)</sub> = 13.35, p < 0.05), but not those of time-to-collision, threshold size and maximum velocity (ANOVA, at 2 m/s, F<sub>(2,13)</sub> = 0.07, F<sub>(2,14)</sub> = 0.46 and F<sub>(2,14)</sub> = 0.70, respectively; at 4 m/s, F<sub>(2,15)</sub> = 0.50, F<sub>(2,14)</sub> = 0.68 and F<sub>(2,14)</sub> = 0.41, respectively, p > 0.05). Thus, frog collision avoidance behavior seems to have an all or none – like property.
Brain injury in children with sickle cell disease: Prevalence and etiology
Authors: Steen R. Grant , Xiong Xiaoping , Langston James W. , Helton Kathleen J. 
Published: October 2003

AbstractOur objective was to evaluate the relationship between brain injury by magnetic resonance imaging (MRI) and vasculopathy by magnetic resonance angiography (MRA) in children with hemoglobin SS, the most serious form of sickle cell disease. We reviewed imaging for all 146 SS patients imaged at St. Jude Children's Research Hospital since 1993. Standard MRI criteria were used to identify cystic infarction, leukoencephalopathy, encephalomalacia, or atrophy. Standard MRA criteria were used to identify arterial tortuousity (limited vasculopathy), and stenosis or occlusion (extensive vasculopathy). At an average age of 10 years, the estimated prevalence of infarction, ischemic damage, or atrophy in SS patients was 46%, and of vasculopathy was 64%. Only 28% of patients were normal by both modalities, and patients abnormal by MRA often were abnormal by MRI (p< 0.00001). Patients with cystic infarction had limited vasculopathy, whereas patients with encephalomalacia had stenosis or occlusion (p< 0.0001). Large arteries were affected in 31% of brain injury patients, whereas small arteries are inferred to be abnormal in up to 69% of patients with brain injury. The degree of vasculopathy is closely related to the degree of brain injury, implying that vasculopathy is prodromal to most forms of brain injury in hemoglobin SS.
CCR1 is an early and specific marker of Alzheimer's disease
Authors: Halks‐Miller Meredith , Schroeder Miriam L. , Haroutunian Vahram , Moenning Ursula , Rossi Michael , Achim Cristian , Purohit Dushyant , Mahmoudi Mithra , Horuk Richard 
Published: October 2003

AbstractChemokines are a diverse group of small proteins that effect cell signaling by binding to G‐protein–coupled, seven‐trans‐membrane receptors. Our group had found previously that the chemokine receptor CCR1 was present in neurons and dystrophic processes in a small sample of Alzheimer's disease cases. This expanded immunohistochemical study shows that the number of CCR1‐positive plaque‐like structures in the hippocampus and entorhinal cortex is highly correlated to dementia state as measured by the clinical dementia rating score. CCR1 immunoreactivity is found in dystrophic, neurofilament‐positive, synaptophysin‐negative neurites that are associated with senile plaques containing amyloid beta peptides of the 1‐42 species (Aβ42). CCR1 was not, however, associated with diffuse deposits of Aβ42. There was limited expression of CCR1 in neurofibrillary tangle‐bearing neuritic processes. Astrocytes and microglia were typically negative for CCR1. Human brains from age‐matched, nondemented individuals rarely displayed either CCR1 or Aβ42 immunoreactivity. Seven other types of dementing neurodegenerative diseases were examined, and all failed to demonstrate CCR1 immunopositivity unless Aβ42‐positive plaques were also present. Thus, neuronal CCR1 is not a generalized marker of neurodegeneration. Rather, it appears to be part of the neuroimmune response to Aβ42‐positive neuritic plaques.
Dually infected (HSV‐1/VZV) single neurons in human trigeminal ganglia
Authors: Theil Diethilde , Paripovic Igor , Derfuss Tobias , Herberger Simone , Strupp Michael , Arbusow Viktor , Brandt Thomas 
Published: October 2003

AbstractHuman trigeminal ganglia were tested by double fluorescence in situ hybridization for the presence and distribution of herpes simplex virus type 1 (HSV‐1) and varicella‐zoster virus (VZV) latency. Latency transcripts of both viruses were detected in common areas within the ganglia. Also, a few single neurons were shown to harbor HSV‐1 and VZV together. Ann Neurol 2003;54:678–681
Protective role of tuftsin fragment 1‐3 in an animal model of intracerebral hemorrhage
Authors: Wang Jian , Rogove Andrew D. , Tsirka Anna E. , Tsirka Stella E. 
Published: October 2003

AbstractIntracerebral hemorrhage (ICH) causes morbidity and mortality and commonly follows the reperfusion after an ischemic event. Tissue plasminogen activator (tPA), a fibrinolytic serine protease, is routinely given for the treatment of stroke. However, tPA also can promote neuronal death, suggesting that caution should be exercised when using it. Furthermore, tPA upon brain injury mediates microglial activation and modulates neuronal survival. To investigate the role of tPA and microglia during brain hemorrhage, we induced experimentally ICH by intracerebral injection of collagenase. Seven days after the introduction of ICH, it persisted in tPA‐deficient (tPA−/−) mice but is drastically reduced in size in wild‐type mice. Three weeks after ICH, there are still red blood cells in tPA−/− but not in wild‐type animals. Activated microglia persist around the injury site. When microglial activation is inhibited by tuftsin fragment 1‐3 macrophage/microglial inhibitory factor (MIF), the stroke injury volume is significantly reduced, and the neurobehavioral deficits exhibited by the mice are improved. Our results suggest that endogenous tPA assists in the clearance of intracerebral hemorrhage, presumably by affecting microglial activation, and MIF could be a valuable neuroprotective agent for the treatment of ICH. Ann Neurol 2003;54:655–664
The Dutch‐Belted rabbit: An alternative breed for developmental toxicity testing
Authors: Spence Stan 
Published: October 2003

AbstractBACKGROUND: Historical control data play a crucial role in the interpretation of observations made from developmental and reproductive toxicity studies. METHODS: In our effort to develop the Dutch‐Belted rabbit as an alternative breed of rabbit for testing of small molecule pharmaceuticals, data collected from 236 untreated pregnant Dutch Belted rabbits are summarized and compared to data collected from 350 untreated pregnant New Zealand White Rabbits. RESULTS: The data presented include mean maternal body weight and food consumption values, mean maternal hematological and serum biochemical values collected during gestation, maternal reproductive (laparotomy) parameters collected at cesarean section, and incidences of spontaneous fetal morphological alterations collected during 1999–2002. Due to their smaller size the use of this breed of rabbit would require approximately 40% less drug than studies conducted with New Zealand White rabbits. Because the Dutch‐Belted rabbit is pigmented this breed also offers the ability to test the potential effects of various xenobiotics on melanocyte development and to evaluate the potential sequela of drugs that have a propensity to bind melanin in the skin and pigmented retinal epithelium. CONCLUSIONS: Based on these data, the Dutch‐Belted rabbit is considered to be a practical alternative to use of the New Zealand White rabbit for these types of studies. Birth Defects Res B 68:439–448, 2003. © 2003 Wiley‐Liss, Inc.
An IQGAP‐like protein is involved in actin assembly together with Cdc42 in the sea urchin egg
Authors: Nishimura Yukako , Mabuchi Issei 
Published: October 2003

AbstractWe isolated a gene homologous to human cdc42 (ucdc42) from a sea urchin cDNA library. The GTPγS‐bound UCdc42 induced actin assembly in sea urchin egg extract. Proteins that are involved in this actin assembly system were searched using UCdc42‐bound agarose beads. A 180‐kDa protein (p180), which showed a homology to human IQGAPs, bound to the GTPγS‐UCdc42 beads. Immunodepletion of p180 from the sea urchin egg extract abolished this actin assembly on the UCdc42 beads. Immunofluorescent localization of p180 was similar to that of the actin cytoskeleton in the egg cortex and it was concentrated in the cleavage furrow during cytokinesis. A possible role of p180 in actin assembly is discussed. Cell Motil. Cytoskeleton 56:207–218, 2003. © 2003 Wiley‐Liss, Inc.
A phase II study of gemcitabine and docetaxel therapy in patients with advanced urothelial carcinoma
Authors: Gitlitz Barbara J. , Baker Carole , Chapman Yvonne , Allen Heather J. , Bosserman Linda D. , Patel Ravi , Sanchez James D. , Shapiro Richard M. , Figlin Robert A. 
Published: October 2003

AbstractBACKGROUNDThe objectives of the current study were to evaluate the safety and efficacy of gemcitabine plus docetaxel in patients with unresectable (Stage T4 or ≥ N1) metastatic or locally advanced transitional cell carcinoma (TCC) of the urothelial tract.METHODSA total of 27 patients were enrolled in the current multisite study, which was performed within the University of California‐Los Angeles Community Oncology Research Network. The first 10 patients in the study received 800 mg/m2 of gemcitabine intravenously on Days 1, 8, and 15 of a 28‐day treatment cycle. In addition, on Day 1, the first 10 patients received 80 mg/m2 of docetaxel intravenously after completion of the gemcitabine infusion. Because of dose‐limiting toxicity (neutropenia), the initial dose of docetaxel was reduced to 60 mg/m2 for the remaining patients who entered the study (n = 17 patients).RESULTSNeutropenia was the most common adverse event that occurred in patients at the Grade 3 level (in 10 of 27 patients; 37.0%) and the Grade 4 level (in 6 of 27 patients; 22.2%). There were no other adverse events at the Grade 4 toxicity level. Twenty‐five of 27 patients (92.6%) completed more than 1 cycle of combination therapy and were evaluated for antitumor responses. The frequency of objective clinical responses was 33.3% (9 of 27 patients). Complete responses to therapy were observed in 2 of 27 patients (7.4%), and partial responses were observed in 7 of 27 patients (25.9%). The median duration of response was 20 weeks (range, 12+ weeks to 152 weeks). The median survival duration was 52 weeks (range, 12 weeks to 160+ weeks). Four of 27 patients (14.8%) remained alive at the time of the current data analysis.CONCLUSIONSThe results of the current study suggested that combination therapy with gemcitabine and docetaxel was an effective treatment for patients with unresectable (Stage T4 or ≥ N1) metastatic or locally advanced TCC of the urothelial tract. Gemcitabine plus docetaxel appeared to be tolerated well, and treatment‐related toxicities were limited to hematologic toxicities. Because cisplatin‐containing regimens are contraindicated for patients with impaired renal function, the gemcitabine plus docetaxel combination may prove to be an effective and well tolerated treatment option for these patients. Cancer 2003. © 2003 American Cancer Society.
A phase II trial of temozolomide in patients with unresectable or metastatic soft tissue sarcoma
Authors: Talbot Susan M. , Keohan Mary Louise , Hesdorffer Mary , Orrico Russell , Bagiella Emilia , Troxel Andrea B. , Taub Robert N. 
Published: October 2003

AbstractBACKGROUNDThe objective of this study was to assess the efficacy and toxicity of the imidazotetrazine derivative temozolomide for patients with unresectable or metastatic soft tissue sarcoma.METHODSTwenty‐five of 26 patients were eligible and assessable for toxicity and response. Temozolomide was administered twice daily on a 12‐hour schedule for 5 days as an oral bolus dose of 200 mg/m2 followed by 9 doses of 90 mg/m2 every 4 weeks.RESULTSThere were 2 partial responses, 2 mixed responses, and 3 patients with stable disease that lasted > 6 months, for an overall objective response rate of 8%. At a median follow‐up of 13.2 months, the median progression‐free survival and the median overall survival were 2.0 months (95% confidence interval [95% CI], 1.7–2.3) and 13.2 months (95% CI, 4.7–31.1), respectively. All responding patients had leiomyosarcoma of uterine or nonuterine origin; and, in a subset analysis of these patients, the objective response rate was 18% (2 of 11 patients), with disease stabilization occurring in 3 of 11 patients (27%). For this subgroup, at a median follow‐up of 24.4 months, the median progression‐free survival and the median overall survival were 3.9 months (95% CI, 1.9–21.9) and 30.8 months (lower‐bound 95% CI, 7.8), respectively. There were no treatment‐related deaths or National Cancer Institute Grade 4 toxicities. Grade 3 toxicities included nausea, anemia, fatigue, elevated alkaline phosphatase levels and nonneutropenic fever (1 patient each).CONCLUSIONSTemozolomide at the dose schedule employed in the current study was tolerated well and had modest activity against previously treated unresectable or metastatic leiomyosarcoma of both uterine and nonuterine origin. Cancer 2003. © 2003 American Cancer Society.
Vinblastine and estramustine phosphate in metastatic renal cell carcinoma
Authors: Haas Naomi B. , Giantonio Bruce J. , Litwin Samuel , Minniti Carl J. , Fox Stephen , Yeslow Gwen , Reilly Robert , Nahum Kenneth , Greenberg Richard , Halbherr Theresa , Hudes Gary R. 
Published: October 2003

AbstractBACKGROUNDIt is well known that metastatic renal cell carcinoma (RCC) exhibits constitutive resistance to chemotherapeutic agents. Antimicrotubule agents such as vinblastine are associated with low but reproducible response rates (approximately 12%) in patients with RCC. Estramustine has been shown to potentiate the antimicrotubule effects of vinblastine. The authors sought to increase the activity of vinblastine in RCC through the addition of estramustine.METHODSTwenty‐one patients with metastatic RCC not previously treated with chemotherapy received oral estramustine phosphate, 600 mg/m2, on Days 1, 2, and 3 weekly for 6 weeks, and intravenous vinblastine, 4 mg/m2 on Day 2 weekly for 6 weeks, repeated every 8 weeks. Twenty‐one patients received 31 cycles of therapy.RESULTSTwo patients experienced Grade 3 and 4 hematologic toxicity, and three patients had Grade 3 nonhematologic toxicity consisting of neurologic toxicity, hepatic toxicity, or angioneurotic edema. One patient had a partial response with decreased liver metastases for 48 weeks; 9 patients had stable disease, for a median duration of 14 weeks (range, 11–31 weeks); and 11 patients demonstrated disease progression. The median overall time to progression was 8 weeks and the median overall survival period was 24 weeks.CONCLUSIONSAlthough well tolerated, the combination of oral estramustine phosphate with vinblastine administered on this schedule had minimal activity in patients with metastatic RCC. Cancer 2003. © 2003 American Cancer Society.
Metastasis of esophageal carcinoma to the brain
Authors: Weinberg Jeffrey S. , Suki Dima , Hanbali Fadi , Cohen Zvi R. , Lenzi Renato , Sawaya Raymond 
Published: October 2003

AbstractBACKGROUNDEsophageal carcinoma rarely metastasizes to the brain. The objectives of the current study were to assess the frequency of brain metastasis from an esophageal primary tumor, to determine correlates of survival, and to describe treatment modalities and their outcomes.METHODSBetween June, 1993 and July, 2001, 1588 patients with a primary esophageal carcinoma registered at The University of Texas M. D. Anderson Cancer Center; of those, 27 patients (1.7%) had a diagnosis of brain metastasis. The authors collected demographic and clinical data and performed a statistical analysis.RESULTSThe median age at the time patients were diagnosed with brain metastasis was 62 years. Tumor histologies were adenocarcinoma in 22 patients (82%), unclassified carcinoma in 3 patients (11%), and squamous cell carcinoma in 2 patients (7%). Twenty patients (74%) experienced symptoms related to the brain metastasis. The metastases were treated with whole‐brain radiation therapy (WBRT) alone in 15 patients (56%), and 10 patients (37%) underwent surgical resection, 4 of whom (15%) also received WBRT. Two patients (7%) underwent stereotactic radiosurgery. The median survival for the entire cohort after diagnosis of the primary tumor was 12.6 months (95% confidence interval [CI], 2.17–22.5 months), and the median survival after the diagnosis of brain metastasis was 3.8 months (95% CI, 1.1–6.5 months). The longest median survival observed after the diagnosis of brain metastasis (9.6 months) occurred in patients with a single brain lesion who underwent resection and received WBRT. There was a trend toward worse survival in patients with liver metastases and patients in recursive partitioning analysis (RPA) Class II–III versus RPA Class I (P= 0.10 for both; multivariate Cox proportional hazards model analysis).CONCLUSIONSApproximately 2% of patients with esophageal carcinoma had a diagnosis of brain metastasis. Improved outcome was associated with single brain lesions in patients who underwent surgery and received WBRT. Known liver metastasis and higher RPA scores were associated with a poorer survival trend. Cancer 2003. © 2003 American Cancer Society.
Cancer‐related fatigue
Authors: Stasi Roberto , Abriani Luca , Beccaglia Patrizia , Terzoli Edmondo , Amadori Sergio 
Published: October 2003

AbstractBACKGROUNDAlthough fatigue is one of the most common complaints of patients with cancer, it went unrecognized or overlooked for many years, until clinicians achieved better control over the more acute symptoms of nausea, emesis, and pain. A number of treatment‐related and disease‐related factors may contribute to the development of fatigue, but its physiologic basis remains poorly understood, and many proposed interventions have not been studied systematically. The lack of a standard of care for the assessment or treatment of fatigue in patients with cancer has limited research in this field. A critical appraisal of these issues is presented in this review.METHODSThe published literature was reviewed for definition, prevalence, causes, and means of managing cancer‐related fatigue (CRF).RESULTSFatigue was reportedly present at the time of diagnosis in approximately 50–75% of cancer patients. The prevalence of CRF increased to 80–96% in patients undergoing chemotherapy and to 60–93% in patients receiving radiotherapy. Two tested interventions that showed consistent effects to alleviate CRF were treatment of cancer‐related anemia with erythropoietin agents (recombinant human erythropoietin and darbepotin α) and aerobic exercise.CONCLUSIONSSeveral lines of research are needed to bridge the specific gaps in the current knowledge of CRF. These involve the pathophysiology of the symptom, the validation of diagnostic criteria, and specific therapeutic interventions. Current practice guidelines are based on a combination of research and expert clinical judgment and should be used to guide care with the expectation that they will evolve to incorporate the results of studies currently underway. Cancer 2003. © 2003 American Cancer Society.
Rieger‐Christ KM, Mourtzinos A, Lee PJ, et al. Identification of fibroblast growth factor receptor 3 mutations in urine sediment DNA samples complements cytology in bladder tumor detection. Cancer. (2003) 98(4):737–44.
Authors: Rieger‐Christ Kimberly M , Medina Arthur , Lee Peter J 
Published: October 2003

AbstractThe original article to which this Erratum refers was published in Cancer (2003) 98(4) 737–44
Cripto‐1 overexpression leads to enhanced invasiveness and resistance to anoikis in human MCF‐7 breast cancer cells
Authors: Normanno Nicola , Luca Antonella De , Bianco Caterina , Maiello Monica R. , Carriero Maria V. , Rehman Aasia , Wechselberger Christian , Arra Claudio , Strizzi Luigi , Sanicola Michele , Salomon David S. 
Published: October 2003

AbstractCripto‐1 (CR‐1) is an epidermal growth factor (EGF)‐CFC protein that has been shown to signal through nodal/Alk‐4, PI3K/Akt, and/or ras/raf/MEK/MAPK pathways in mammalian cells, and that is frequently expressed in human primary breast carcinomas. In the present study, the human estrogen receptor positive, MCF‐7 breast cancer cell line, that expresses low levels of endogenous CR‐1, was transfected with a CR‐1 expression vector. MCF‐7 CR‐1 cells expressed high levels of a 25 kDa recombinant CR‐1 protein that was not detected in MCF‐7 cells transfected with a control vector (MCF‐7 neo). Overexpression of CR‐1 did not induce an estrogen independent phenotype in MCF‐7 cells. In fact, MCF‐7 CR‐1 cells showed a response to exogenous estrogens that was similar to MCF‐7 neo cells, and failed to grow in immunosuppressed mice in absence of estrogen stimulation. However, MCF‐7 CR‐1 cells showed a rate of proliferation in serum free conditions, and an ability to form colonies in soft‐agar that were higher as compared with MCF‐7 neo cells. More importantly, overexpression of CR‐1 enhanced the resistance to anoikis and the invasion ability of MCF‐7 cells. MCF‐7 CR‐1 cells showed levels of activation of both Akt and Smad‐2 that were significantly higher as compared with MCF‐7 neo. These findings suggest that CR‐1 overexpression might be associated with the progression towards a more aggressive phenotype in breast carcinoma, through the activation of both Akt and Smad‐2 signalling pathways. J. Cell. Physiol. 198: 31–39, 2004. © 2003 Wiley‐Liss, Inc.