bluuebunny/crossref_metadata_2025_split huggingface dataset:
Henry George and Social Theory
Authors: Siemens Robert Peter 
Published: July 2006

Abstract. It was contended in Part 1 (in the January, 1995 issue) that Henry George should be recognized as an original American social theorist. He was a pioneering postmodern contributor to social theory who criticized the linear idea of progress and anticipated Durkheim's concept of the “collective consciousness.”He recognized the fateful consequences of the separation of political economy into “economics” and “sociology.” These include the loss of moral considerations from political economy, and the rise of a sociology that culminates in the proliferation of meaningless abstractions because it is premised on amoral economic assumptions. His theory of speculative land value as the cause of civilizations decline is recapitulated and shown in a larger context. The congruence between the concerns and conceptions of George and Weber is detailed.Part II concludes by tracing the tragic consequences for modern American social theory, from Spencer to Parsons, that result from confusing the value of commodities with the value of land, of private wealth with social value.
Child Welfare Allocations: State‐level Estimates of Effective Guarantees
Authors: Gensler Howard 
Published: July 2006

AbstractWelfare grants in the United States very from year to year and from state to state. Actual grants are very different from stated nominal levels of support for two reasons. First, grants are reduced for income. Second, not all qualified families receive welfare. Some do not apply. Others are discouraged, wrongly denied, or poorly counselled. The actual level of welfare support per child is estimated herein at the state level for single female household heads for each year from 1979 to 1990. A tobit estimation technique is employed to account for the probability of not receiving welfare when otherwise qualified.
C. E. Ayres's Reliance on T. H. Huxley: Did Darwin's Bulldog Bite?
Authors: Jones Lamar B. 
Published: July 2006

AbstractIn David Seckler's Thorstein Veblen and the Institutionalists, the proposition is advanced that “Ayres out‐Veblens Veblen and out Deweys Dewey”. This commonly held view of the intellectual orientation of the prominent American institutional economist, Clarence Edwin Ayres, places him as an intellectual descendent of philosopher John Dewey's pragmatism, and economist Thorstein B, Veblen's institutionalist economics. Certainly such an outlook is not incorrect, but it is also not adequate if one is to achieve an understanding of Ayres. A careful check of the indexes of Ayres's major works shows that his references preponderantly go not to Dewey and to Veblen, but to Adam Smith and Charles Darwin, Moreover, it is to the latter that Ayres turned in his effort to overturn the former. However, Ayres in interpreting Darwin relied not upon Dewey and Veblen, but rather upon Thomas Henry Huxley, the British physician turned scientist, who because of his outspoken advocacy of Darwin's evolutionary biology became known as “Darwin's bulldog.”
Emerging Social‐economic Institutions in the Venture Capital Industry:
Authors: Waddell Steven J. 
Published: July 2006

AbstractNine venture capital organizations which are taking equity positions with socially guided as well as financial goals are investigated. The organizations are presented as new entrants to ihe financial industry, and are placed in the context of community development financial institutions and social investment funds. Four emerging models are identified; socially guided venture capital networks, socially guided private funds, Specialized Small Business Development Corporations and equity Community Development Corporations. Forty nine deals of six of the organizations are analyzed for financial and social outcomes. The paper concludes that the private venture funds have the most promising future, and predicts the emergence of publicly offered venture capital funds that incorporate social goals.
Socioeconomic Conditions and Property Crime:
Authors: Allen Ralph C. 
Published: July 2006

Abstract.A comprehensive review of the crime literature indicates varying and often opposing hypotheses of relationships between property crime and socioeconomic conditions such as poverty, business cycle conditions, demographics, criminal justice system actions, and family structure. Employing measures of each of the hypothesized factors, time‐series models for robbery, burglary, and vehicle theft are estimated from yearly and national Uniform Crime Report (UCR) data for the period 1959 through 1992 and are used to test these hypotheses' current empirical relevance. The empirical findings selectively confirm the importance of macroeconomic stability and criminal justice system actions in reducing property crime activity. In contrast, decreases in absolute poverty and general income inequality are associated with increased criminal activity; and age demographics and family/community structure apparently have little impact on any of the analyzed property‐crime trends, A reduction in inflation apparently decreases property crimes.
Maynard Keynes: An Economist's Biography
Authors: Mini Piero V. 
Published: July 2006

Abstract.D. E. Moggridge's perhaps too exhaustive biography is examined and some questions are raised relative to Keynes'views on theory and their source, and his views on German reparations and whether Britain should have accepted the original provisions of the agreement providing for establishment of the World Bank and the International Monetary Fund.
In Conrad’s Footsteps: Critical Approaches to Africanist Travel Writing
Authors: Burroughs Robert 
Published: July 2006

AbstractTravel writing about Central Africa in English reverberates with the language of Joseph Conrad’sHeart of Darkness. This essay considers how that canonical text, in shaping twentieth‐century travellers’ understandings of Central Africa and the travel genre, also shapes literary critics’ understandings of the same subjects.
Prognostic Associations of Activated Mitogen-Activated Protein Kinase and Akt Pathways in Glioblastoma
Authors: Pelloski Christopher E. , Lin E , Zhang Li , Yung W.K. Alfred , Colman Howard , Liu Juinn-Lin , Woo Shaio Y. , Heimberger Amy B. , Suki Dima , Prados Michael , Chang Susan , Barker Fredrick G. , Fuller Gregory N. , Aldape Kenneth D. 
Published: July 2006

Abstract
Purpose: Activation of mitogen-activated protein kinase (MAPK) and members of the Akt pathway have been shown to promote cell proliferation, survival, and resistance to radiation. This study was conducted to determine whether any of these markers are associated with survival time and response to radiation in glioblastoma.
Experimental Design: The expression of phosphorylated (p-)Akt, mammalian target of rapamycin (p-mTOR), p-p70S6K, and p-MAPK were assessed by immunohistochemical staining in 268 cases of newly diagnosed glioblastoma. YKL-40, a prognostic marker previously examined in these tumors, was also included in the analysis. Expression data were tested for correlations with response to radiation therapy in 131 subtotally resected cases and overall survival (in all cases). Results were validated in an analysis of 60 patients enrolled in clinical trials at a second institution.
Results: Elevated p-MAPK expression was most strongly associated with poor response to radiotherapy, a finding corroborated in the validation cohort. For survival, higher expressions of p-mTOR, p-p70S6K, and p-MAPK were associated with worse outcome (all P &lt; 0.03). YKL-40 expression was associated with the expressions of p-MAPK, p-mTOR, and p-p70S6K (all P &lt; 0.02), with a trend toward association with p-Akt expression (P = 0.095). When known clinical variables were added to a multivariate analysis, only age, Karnofsky performance score, and p-MAPK expression emerged as independent prognostic factors.
Conclusions: p-MAPK and activated members of the Akt pathway are markers of outcome in glioblastoma. Elevated expression of p-MAPK is associated with increased radiation resistance and represents an independent prognostic factor in these tumors.
Clinical and Pharmacokinetic Study of Clofarabine in Chronic Lymphocytic Leukemia: Strategy for Treatment
Authors: Gandhi Varsha , Plunkett William , Bonate Peter L. , Du Min , Nowak Billie , Lerner Susan , Keating Michael J. 
Published: July 2006

AbstractPurpose: Based on its mechanistic similarity to fludarabine and cladribine and the success of these analogues for treatment of chronic lymphocytic leukemia (CLL), we hypothesized that clofarabine would be effective for indolent leukemias. The present study was conducted to determine the efficacy and cellular pharmacology during clinical trials of single-agent clofarabine in CLL.Experimental Design: Previously treated patients with relapsed/refractory CLL were eligible for this study. Clofarabine was infused over 1 hour daily for 5 days. Most patients received 3 or 4 mg/m2/d × 5 days, whereas the other two were treated with 15 mg/m2/d × 5 days. Clinical outcome and associated pharmacologic end points were assessed.Results: Myelosuppression limited the maximum tolerated dose of clofarabine to 3 mg/m2/d on this schedule. Cellular pharmacokinetic studies showed a median clofarabine triphosphate concentration in CLL lymphocytes of 1.5 μmol/L (range, 0.2-2.3 μmol/L; n = 9). In the majority of cases, &gt;50% of the analogue triphosphate was present 24 hours after infusion, indicating prolonged retention of the triphosphate in CLL cells. Although cytoreduction was observed, no patients achieved a response. In vitro clofarabine incubation of leukemic lymphocytes from 29 CLL patients showed that clofarabine monophosphate accumulated to a higher concentration compared with the triphosphate. Nonetheless, the triphosphate increased in a dose-dependent fashion and upon successive clofarabine infusions, suggesting benefit from greater doses given at less frequent intervals.Conclusion: Levels of clofarabine triphosphate at higher doses and prolonged maintenance of clofarabine triphosphate in leukemic lymphocytes provide a rationale to treat CLL in a weekly clofarabine schedule.
Complement-Induced Cell Death by Rituximab Depends on CD20 Expression Level and Acts Complementary to Antibody-Dependent Cellular Cytotoxicity
Authors: van Meerten Tom , van Rijn Rozemarijn S. , Hol Samantha , Hagenbeek Anton , Ebeling Saskia B. 
Published: July 2006

Abstract
Purpose: The use of the CD20-specific antibody rituximab has greatly improved the response to treatment of CD20+ follicular lymphoma. Despite the success of rituximab, resistance has been reported and prognostic markers to predict individual response are lacking. The level of CD20 expression on tumors has been related to response, but results of several studies are contradictory and no clear relationship could be established. Complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) are thought to be important effector mechanisms, but the exact mechanism of rituximab-mediated cell kill is still unknown. Importantly, no data have been reported on the combined contribution of CDC and ADCC.
Experimental Design: We have developed a system of clonally related CEM-CD20 cells by retroviral transfer of the human CD20 cDNA (n = 90). This set of cells, with the CD20 molecule as the only variable, was used to study the importance of CD20 expression level on rituximab-mediated CDC, ADCC, and the combination.
Results: We show a sigmoidal correlation of CD20 expression level and rituximab-mediated killing via CDC but not ADCC. On both high and low CD20-expressing cells, all CD20 molecules were translocated into lipid rafts after rituximab binding. Furthermore, CDC and ADCC act simultaneously and CDC-resistant cells are sensitive to ADCC and vice versa.
Conclusions: These findings suggest that CDC depends on CD20 expression level and that both CDC and ADCC act complementary. These data give new insights into novel strategies to improve the efficacy of CD20-specific antibodies for the treatment of CD20+ tumors.
Effect of the Second-Generation Vascular Disrupting Agent OXi4503 on Tumor Vascularity
Authors: Salmon Howard W. , Siemann Dietmar W. 
Published: July 2006

Abstract
Purpose: As first-generation small-molecule vascular disrupting agents (VDA) have begun to enter clinical trials, second-generation agents are under active development. One such agent is the combretastatin A4 disodium phosphate (CA4P) analogue OXi4503 (CA1P).
Experimental Design: C3H/HeJ mice bearing KHT sarcomas were treated with CA4P and OXi4503 and the effect on tumor vasculature was determined by evaluating the extent of vascular shutdown (Hoechst-33342 vessel staining) and tumor perfusion inhibition (dynamic contrast-enhanced magnetic resonance imaging). Dynamic contrast-enhanced magnetic resonance imaging and tumor necrosis end points also were used to examine the pathophysiologic tumor effects following repeated exposures to these agents.
Results: Single doses of either agent (CA4P, 100 mg/kg; OXi4503, 25 mg/kg) resulted in an 80% to 90% reduction in tumor perfusion 4 hours after treatment. Whereas recovery in tumor perfusion was observed 48 hours posttreatment, this recovery was significantly slower in mice treated with OXi4503. Tumors re-treated with either VDA 72 hours after the first drug exposure showed a similar reduction and recovery in tumor perfusion. Histologic evidence showed the presence of a smaller viable rim after exposure to OXi4503 than that observed after CA4P treatment. Furthermore, the extent of recovery of tumor necrosis 72 hours after drug treatment was less for OXi4053.
Conclusions: The present studies show that the second-generation VDA OXi4503 possesses significant antivascular effects in solid tumors. Importantly, the vasculature of tumors of mice that had received an initial dose this agent was as responsive to a subsequent treatment.
Natural and Synthetic Progestins Accelerate 7,12-Dimethylbenz[a]Anthracene-Initiated Mammary Tumors and Increase Angiogenesis in Sprague-Dawley Rats
Authors: Benakanakere Indira , Besch-Williford Cynthia , Schnell Jennifer , Brandt Sandra , Ellersieck Mark R. , Molinolo Alfredo , Hyder Salman M. 
Published: July 2006

AbstractPurpose: Synthetic progestins are widely used therapeutically; however, there is controversy regarding their proliferative effects. We used a rat 7,12-dimethylbenz[a]anthracene (DMBA)–induced mammary tumor model to test the hypothesis that progestins increase angiogenesis and as a result decrease the latency period and increase the multiplicity of mammary tumors.Experimental Design: Medroxyprogesterone acetate (MPA) pellets were implanted 2, 4, or 6 weeks after DMBA exposure; RU-486 was given 3 days before MPA. Experiments were concluded 70 days after DMBA administration.Results: MPA exposure 4 or 6 weeks after DMBA reduced the latency period for appearance of tumors in a dose-dependent manner and increased tumor incidence. Administration of MPA 2 weeks after DMBA administration reduced tumor incidence and was protective. Progesterone did not reduce the latency period but significantly increased tumor incidence. RU-486 delayed the latency period and decreased tumor incidence in animals exposed to MPA at 4 weeks after DMBA treatment, indicating that the progesterone receptor may be partially responsible for transmission of proliferative signals. RU-486 also delayed the latency period but failed to reduce overall tumor incidence when animals were exposed to MPA at 6 weeks after DMBA treatment, indicating that other factors may also control MPA-induced acceleration. Whereas MPA-accelerated tumors were both intraductal and tubular, progesterone-accelerated and/or DMBA-induced tumors were tubular. Progestin treatment increased vascular endothelial growth factor expression within tumors in a ligand- and cell type–dependent manner and increased angiogenesis in correlation with vascular endothelial growth factor expression. No mammary tumors or progesterone receptor were detected in DMBA-treated ovariectomized rats regardless of progestin administration.Conclusions: We propose that progestins can accelerate the development of mammary tumors and that antiangiogenic agents and/or the use of antiprogestins that can reduce tumor incidence might be a viable therapeutic option for treatment of progestin-accelerated tumors. The model described here is a potentially useful preclinical model for rapidly screening such compounds.
Nitric oxide–releasing aspirin and indomethacin are potent inhibitors against colon cancer in azoxymethane-treated rats: effects on molecular targets
Authors: Rao Chinthalapally V. , Reddy Bandaru S. , Steele Vernon E. , Wang C-X , Liu Xiaoping , Ouyang Nengtai , Patlolla Jagan M.R. , Simi Barbara , Kopelovich Levy , Rigas Basil 
Published: July 2006

Abstract
Nitric oxide–releasing nonsteroidal anti-inflammatory drugs (NO-NSAID) are promising chemoprevention agents; unlike conventional NSAIDs, they seem free of appreciable adverse effects, while they retain beneficial activities of their parent compounds. Their effect on colon carcinogenesis using carcinoma formation as an end point is unknown. We assessed the chemopreventive properties of NO-indomethacin (NCX 530) and NO-aspirin (NCX 4016) against azoxymethane-induced colon cancer. Seven-week-old male F344 rats were fed control diet, and 1 week later, rats received two weekly s.c. injections of azoxymethane (15 mg/kg body weight). Two weeks after azoxymethane treatment, rats (48 per group) were fed experimental diets containing NO-indomethacin (0, 40, or 80 ppm), or NO-aspirin (1,500 or 3,000 ppm), representing 40% and 80% of the maximum tolerated dose. All rats were killed 48 weeks after azoxymethane treatment and assessed for colon tumor efficacy and molecular changes in colonic tumors and normally appearing colonic mucosa of different dietary groups. Our results suggest that NO-indomethacin at 40 and 80 ppm and NO-aspirin at 3,000 ppm significantly suppressed both tumor incidence (P &lt; 0.01) and multiplicity (P &lt; 0.001). The degree of inhibition was more pronounced with NO-indomethacin at both dose levels (72% and 76% inhibition) than with NO-aspirin (43% and 67%). NO-indomethacin at 40 and 80 ppm and NO-aspirin at 3,000 ppm significantly inhibited the colon tumors' (P &lt; 0.01 to P &lt; 0.001) total cyclooxygenase (COX), including COX-2 activity (52–75% inhibition) and formation of prostaglandin E2 (PGE2), PGF2α, and 6-keto-PGF1α, and TxB2 from arachidonic acid (53–77% inhibition). Nitric oxide synthase 2 (NOS-2) activity and β-catenin expression were suppressed in animals given NO-NSAID. In colonic crypts and tumors of animals fed these two NO-NSAIDs, there was a significant decrease in proliferating cell nuclear antigen labeling when compared with animals fed the control diet. The results of this study provide strong evidence that NO-NSAIDs possess strong inhibitory effect against colon carcinogenesis; their effect is associated with suppression of COX and NOS-2 activities and β-catenin levels in colon tumors. These results pave the way for the rational design of human clinical trials. [Mol Cancer Ther 2006;5(6):1530–8]
Therapeutic potential of antisense oligodeoxynucleotides to down-regulate thymidylate synthase in mesothelioma
Authors: Flynn Janet , Berg Randal W. , Wong Tracy , van Aken Marijke , Vincent Mark D. , Fukushima Masakazu , Koropatnick James 
Published: July 2006

AbstractMalignant mesothelioma is an aggressive tumor of the serosal surfaces of the lungs, heart, and abdomen. Survival rates are poor and effective treatments are not available. However, recent therapeutic regimens targeting thymidylate synthase (TS) in malignant mesothelioma patients have shown promise. We have reported the use of an antisense oligodeoxynucleotide targeting TS mRNA (antisense TS ODN 83) to inhibit growth of human tumor cells. To test the potential for antisense targeting of TS mRNA in treatment of malignant mesothelioma, we assessed and compared the effects of antisense TS ODN 83 on three human malignant mesothelioma cell lines (211H, H2052, and H28) and human nonmalignant mesothelioma cells (HT29 colorectal adenocarcinoma, HeLa cervical carcinoma, and MCF7 breast tumor cell lines). We report that ODN 83 applied as a single agent effectively reduced TS mRNA and protein in malignant mesothelioma cell lines. Furthermore, it inhibited malignant mesothelioma growth significantly more effectively than it inhibited growth of nonmalignant mesothelioma human tumor cell lines: a difference in susceptibility was not observed in response to treatment with TS protein-targeting drugs. In malignant mesothelioma cells, antisense TS both induced apoptotic cell death and reduced proliferation. In nonmalignant mesothelioma cells, only reduced proliferation was observed. Thus, antisense TS-mediated induction of apoptosis may be the basis for the high malignant mesothelioma sensitivity to antisense targeting of TS. Further preclinical and clinical study of TS antisense oligodeoxynucleotides, alone and in combination with TS-targeting chemotherapy drugs, in mesothelioma is warranted. [Mol Cancer Ther 2006;5(6):1423–33]
Spatiotemporal Structures and Mechanisms of the Tropospheric Biennial Oscillation in the Indo-Pacific Warm Ocean Regions*
Authors: Li Tim , Liu Ping , Fu X. , Wang B. , Meehl Gerald A. 
Published: July 2006

Abstract
The observed structure and seasonal evolution characteristics of the tropospheric biennial oscillation (TBO) in the warm ocean areas of the Indo-Pacific region are explored using a seasonal-sequence EOF analysis approach. The major convective activity centers associated with the TBO appear in the southeast Indian Ocean (SEIO) and western North Pacific (WNP), accompanied by anticyclonic (or cyclonic) circulation patterns with a first-baroclinic-mode structure. The convection and circulation anomalies have distinctive life cycles in the SEIO and WNP: the former have a peak phase in northern fall and the latter persist from northern winter to subsequent summer.
The mechanisms of the TBO in this region are investigated with a hybrid coupled GCM. Numerical results show that air–sea interaction in the warm ocean alone can support TBO variability that has many observed characteristics. Key processes involved in the TBO include the WNP monsoon variability and associated cross-equatorial flows, convective activity over Southeast Asia/the Maritime Continent and associated anomalous Walker circulation, and ocean dynamic responses to anomalous wind stress curl in the western Pacific. The coupled model experiment demonstrates that the essential element of the TBO in this region arises from the monsoon–warm ocean interaction.
A possible connection between the TBO and ENSO variability is further studied in another model that excludes the delayed oscillator dynamics. The key in causing the biennial variability of ENSO arises from teleconnections between the tropical Pacific and Indian Oceans, with three “atmospheric bridges”: 1) the north–south teleconnection that connects the WNP monsoon and the SEIO, 2) the east–west teleconnection that connects the Indian Ocean and the Pacific cold tongue, and 3) the El Niño–WNP monsoon teleconnection.