bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stimulation of MMP-11 (stromelysin-3) expression in mouse fibroblasts by cytokines, collagen and co-culture with human breast cancer cell lines
Authors: Selvey Saxon , Haupt Larisa M , Thompson Erik W , Matthaei Klaus I , Irving Michael G , Griffiths Lyn R 
Published: July 2004

Abstract
Background
Matrix metalloproteinases (MMPs) are central to degradation of the extracellular matrix and basement membrane during both normal and carcinogenic tissue remodeling. MT1-MMP (MMP-14) and stromelysin-3 (MMP-11) are two members of the MMP family of proteolytic enzymes that have been specifically implicated in breast cancer progression. Expressed in stromal fibroblasts adjacent to epithelial tumour cells, the mechanism of MT1-MMP and MMP-11 induction remains unknown.

Methods
To investigate possible mechanisms of induction, we examined the effects of a number of plausible regulatory agents and treatments that may physiologically influence MMP expression during tumour progression. Thus NIH3T3 and primary mouse embryonic fibroblasts (MEFs) were: a) treated with the cytokines IL-1β, IL-2, IL-6, IL-8 and TGF-β for 3, 6, 12, 24, and 48 hours; b) grown on collagens I, IV and V; c) treated with fibronectin, con-A and matrigel; and d) co-cultured with a range of HBC (human breast cancer) cell lines of varied invasive and metastatic potential.

Results
Competitive quantitative RT-PCR indicated that MMP-11 expression was stimulated to a level greater than 100%, by 48 hour treatments of IL-1β, IL-2, TGF-β, fibronectin and collagen V. No other substantial changes in expression of MMP-11 or MT1-MMP in either tested fibroblast culture, under any treatment conditions, were observed.

Conclusion
We have demonstrated significant MMP-11 stimulation in mouse fibroblasts using cytokines, matrix constituents and HBC cell lines, and also some inhibition of MT1-MMP. Our data suggest that the regulation of these genes in the complex stromal-epithelial interactions that occur in human breast carcinoma, is influenced by several mechanisms.
Ciprofibrate therapy in patients with hypertriglyceridemia and low high density lipoprotein (HDL)-cholesterol: greater reduction of non-HDL cholesterol in subjects with excess body weight (The CIPROAMLAT study)
Authors: Aguilar-Salinas Carlos A , Assis-Luores-Vale Andréia , Stockins Benjamín , Rengifo Hector Mario , Filho José Dondici , Neto Abrahão Afiune , Rabelo Lísia Marcílio , Torres Kerginaldo Paulo , de Oliveira José Egídio Paulo , Machado Carlos Alberto , Reyes Eliana , Saavedra Victor , Florenzano Fernando , Hernández Ma Victoria , Jiménez Sergio Hernandez , Ramírez Erika , Vazquez Cuauhtémoc , Salinas Saul , Hernández Ismael , Medel Octavio , Moreno Ricardo , Lugo Paula , Alvarado Ricardo , Mehta Roopa , Gutierrez Victor , Gómez Pérez Francisco J 
Published: July 2004

Abstract
Background
Hypertriglyceridemia in combination with low HDL cholesterol levels is a risk factor for cardiovascular disease. Our objective was to evaluate the efficacy of ciprofibrate for the treatment of this form of dyslipidemia and to identify factors associated with better treatment response.

Methods
Multicenter, international, open-label study. Four hundred and thirty seven patients were included. The plasma lipid levels at inclusion were fasting triglyceride concentrations between 1.6–3.9 mM/l and HDL cholesterol ≤ 1.05 mM/l for women and ≤ 0.9 mM/l for men. The LDL cholesterol was below 4.2 mM/l. All patients received ciprofibrate 100 mg/d. Efficacy and safety parameters were assessed at baseline and at the end of the treatment. The primary efficacy parameter of the study was percentage change in triglycerides from baseline.

Results
After 4 months, plasma triglyceride concentrations were decreased by 44% (p < 0.001). HDL cholesterol concentrations were increased by 10% (p < 0.001). Non-HDL cholesterol was decreased by 19%. A greater HDL cholesterol response was observed in lean patients (body mass index < 25 kg/m2) compared to the rest of the population (8.2 vs 19.7%, p < 0.001). In contrast, cases with excess body weight had a larger decrease in non-HDL cholesterol levels (-20.8 vs -10.8%, p < 0.001). There were no significant complications resulting from treatment with ciprofibrate.

Conclusions
Ciprofibrate is efficacious for the correction of hypertriglyceridemia / low HDL cholesterol. A greater decrease in non-HDL cholesterol was found among cases with excess body weight. The mechanism of action of ciprofibrate may be influenced by the pathophysiology of the disorder being treated.
Multi-component based cross correlation beat detection in electrocardiogram analysis
Authors: Last Thorsten , Nugent Chris D , Owens Frank J 
Published: July 2004

Abstract
Background
The first stage in computerised processing of the electrocardiogram is beat detection. This involves identifying all cardiac cycles and locating the position of the beginning and end of each of the identifiable waveform components. The accuracy at which beat detection is performed has significant impact on the overall classification performance, hence efforts are still being made to improve this process.

Methods
A new beat detection approach is proposed based on the fundamentals of cross correlation and compared with two benchmarking approaches of non-syntactic and cross correlation beat detection. The new approach can be considered to be a multi-component based variant of traditional cross correlation where each of the individual inter-wave components are sought in isolation as opposed to being sought in one complete process. Each of three techniques were compared based on their performance in detecting the P wave, QRS complex and T wave in addition to onset and offset markers for 3000 cardiac cycles.

Results
Results indicated that the approach of multi-component based cross correlation exceeded the performance of the two benchmarking techniques by firstly correctly detecting more cardiac cycles and secondly provided the most accurate marker insertion in 7 out of the 8 categories tested.

Conclusion
The main benefit of the multi-component based cross correlation algorithm is seen to be firstly its ability to successfully detect cardiac cycles and secondly the accurate insertion of the beat markers based on pre-defined values as opposed to performing individual gradient searches for wave onsets and offsets following fiducial point location.
Low fasting low high-density lipoprotein and postprandial lipemia
Authors: Kolovou Genovefa D , Anagnostopoulou Katherine K , Pilatis Nektarios , Kafaltis Nikolaos , Sorodila Konstandina , Psarros Eleftherios , Cokkinos Dennis V 
Published: July 2004

Abstract
Background
Low levels of high density lipoprotein (HDL) cholesterol and disturbed postprandial lipemia are associated with coronary heart disease. In the present study, we evaluated the variation of triglyceride (TG) postprandially in respect to serum HDL cholesterol levels.

Results
Fifty two Greek men were divided into 2 main groups: a) the low HDL group (HDL < 40 mg/dl), and b) the control group. Both groups were further matched according to fasting TG (matched-low HDL, and matched-control groups). The fasting TG concentrations were higher in the low HDL group compared to controls (p = 0.002). The low HDL group had significantly higher TG at 4, 6 and 8 h postprandially compared to the controls (p = 0.006, p = 0.002, and p < 0.001, respectively). The matched-low HDL group revealed higher TG only at 8 h postprandially (p = 0.017) compared to the matched-control group. ROC analysis showed that fasting TG ≥ 121 mg/dl have 100% sensitivity and 81% specificity for an abnormal TG response (auc = 0.962, p < 0.001).

Conclusions
The delayed TG clearance postprandially seems to result in low HDL cholesterol even in subjects with low fasting TG. The fasting TG > 121 mg/dl are predictable for abnormal response to fatty meal.
Quality of life and emotional distress in advanced prostate cancer survivors undergoing chemotherapy
Authors: Trask Peter C 
Published: July 2004

AbstractProstate cancer continues to occur in over 230,000 men each year. Although the majority of these will be diagnosed in the early stages, there remains a proportion who will either be diagnosed in late stage disease or develop progressive disease. In patients with advanced disease, research has recently focused on using chemotherapy for symptom management and palliation. Given that the focus is not on cure, the effect of chemotherapy on quality of life is of utmost importance. The present article will 1) summarize the current chemotherapeutic studies that have included a quality of life component, with a particular focus on pain and fatigue, 2) discuss the issue of distress in advanced prostate cancer patients treated with chemotherapy, and 3) suggest future research directions.From the studies that have investigated quality of life, it appears that several chemotherapeutic agents reduce pain and fatigue, although the development of fatigue is often the dose-limiting factor of some agents. The assessment of overall quality of life has occurred in several studies, however, an examination into the impact of chemotherapy on functional status and interpersonal relationships has not been studied. Finally, in contrast to the numerous studies in early stage prostate cancer patients, the presence and effect of distress in chemotherapy-treated prostate patients has not been examined. As such, increased attention is needed to quality of life during phase I-III chemotherapy trials.
A unique dedifferentiated tumor of the retroperitoneum
Authors: Karmali Shahzeer , Benediktson Halligrimur , Temple Walley , Bathe Oliver F 
Published: July 2004

Abstract
Background
Dedifferentiated liposarcomas represent heterogeneous tumors with lipomatous and nonlipomatous elements starkly juxtaposed. It is thought that the high grade nonlipomatous elements of the tumor portend a worse prognosis.

Case Presentation
A 19.8 kg heterogeneous retroperitoneal tumor was successfully and completely resected. Because of its extent, no additional treatment modalities were practicable. The tumor soon recurred. The recurrent tumor differed from the primary tumor in that it was more homogeneous, consisting mainly of nonlipogenic, calcific tissue.

Conclusions
Dedifferentiated liposarcomas are known to have a very high recurrence rate. The biological behavior of dedifferentiated liposarcomas is likely dictated by the most aggressive element of these heterogeneous tumors.
How can Health Behavior Theory be made more useful for intervention research?
Authors: Jeffery Robert W 
Published: July 2004

Abstract
Background
The present paper expresses the author's views about the practical utility of Health Behavior Theory for health behavior intervention research. The views are skeptical and perhaps even a bit exaggerated. They are, however, also based on 20-plus years of in-the-trenches research focused on improving health behavior practice through research.

Discussion
The author's research has been theoretically driven and has involved measurement of varying variables considered to be important theoretical mediators and moderators of health behavior. Regretfully, much of this work has found these variables wanting in basic scientific merit. Health Behavior Theory as we have known it over the last 25 years or so has been dominated by conceptualizations of behavior change processes that highlight cognitive decision-making. Although much of health behavior practice targets what people do rather than what they think, the logic of focusing on thoughts is that what people think about is the key to what they will do in the future, and that interventions that can measure and harness those processes will succeed to a greater extent than those that do not. Unfortunately, in the author's experience, the premise of cognitive theories has fallen short empirically in a number of ways. The cognitive schemata favored by most health behavior theories are difficult to measure, they do not predict behavioral outcomes very well, there is little evidence that they cause behavior, and they are hard to change directly.

Summary
It is suggested that health behavior researchers reconsider their use of these theories in favor of models whose variables are more accessible to observation and experimental manipulation and that most importantly have strong empirical support.
Antisecretory factor expression is regulated by inflammatory mediators and influences the severity of experimental autoimmune encephalomyelitis
Authors: Davidson Todd S , Hickey William F 
Published: July 2004

AbstractAntisecretory factor (ASF) was originally identified as a potent inhibitor of intestinal fluid secretion induced by a number of enterotoxins. In addition to its involvement in intestinal fluid secretion, ASF modulates the proliferation of memory/effector T cells and is expressed by cells of the immune system. This report describes the role of ASF in modulating immune responses and assesses the regulation of ASF during an in vivo immunological reaction. ASF expression was redistributed during adoptively transferred experimental autoimmune encephalomyelitis (EAE), and in response to other inflammatory stimuli. Administration of the anti-ASF antibody TLD-1A8A increased the clinical severity and duration of the disease. Consistent with these findings, addition of TLD-1A8A to T cell proliferation assays resulted in up-regulation of the proinflammatory cytokines IL-18 and IL-6 and in down-regulation of IL-10. Furthermore, we identified cytokines that regulated the expression of ASF at both the mRNA and protein level. ASF, therefore, appears to play a previously unappreciated and potentially important role in the regulation of immune responses.
Plasminogen activator inhibitor-2 (PAI-2) in eosinophilic leukocytes
Authors: Swartz Jonathan M , Byström Jonas , Dyer Kimberly D , Nitto Takeaki , Wynn Thomas A , Rosenberg Helene F 
Published: July 2004

AbstractPlasminogen activator inhibitor-2 (PAI-2) as a potential eosinophil protein was inferred from our gene microarray study of mouse eosinophilopoiesis. Here, we detect 47 kDa intracellular and ∼60 kDa secretory forms of PAI-2 in purified human eosinophil extracts. PAI-2 is present at variable concentrations in eosinophil lysates, ranging from 30 to 444 ng/106 cells, with a mean of 182 ng/106 cells from 10 normal donors, which is the highest per-cell concentration among all leukocyte subtypes evaluated. Enzymatic assay confirmed that eosinophil-derived PAI-2 is biologically active and inhibits activation of its preferred substrate, urokinase. Immunohistochemical and immunogold staining demonstrated PAI-2 localization in eosinophil-specific granules. Immunoreactive PAI-2 was detected in extracellular deposits in and around the eosinophil-enriched granuloma tissue encapsulating the parasitic egg in livers of wild-type mice infected with the helminthic parasite Schistosoma mansoni. Among the possibilities, we consider a role for eosinophil-derived PAI-2 in inflammation and remodeling associated with parasitic infection as well as allergic airways disease, respiratory virus infection, and host responses to tumors and metastasis in vivo.
MC-3 receptor and the inflammatory mechanisms activated in acute myocardial infarct
Authors: Getting Stephen J , Di Filippo Clara , Christian Helen C , Lam Connie W , Rossi Francesco , D'Amico Michele , Perretti Mauro 
Published: July 2004

AbstractInvestigation of the mechanisms activated by endogenous inhibitory pathways can lead to identification of novel targets for cardiovascular inflammatory pathologies. Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model. In resting conditions, mouse and rat heart extracts expressed MC3-R mRNA and protein, without changes following ischemia-reperfusion. At the cellular level heart macrophages, but not fibroblasts or cardiomyocytes, expressed this receptor, as demonstrated by immunogold labeling. In vivo, administration of the melanocortin agonist MTII (10 μg per mouse equivalent to 9.3 nmol) 30 min prior to ischemia (25 min) attenuated mouse heart 2 h reperfusion injury by ∼40%, an effect prevented by the mixed MC3/4-R antagonist SHU9119 but not by the selective MC4-R antagonist HS204. Similar results were obtained when the compound was given at the beginning of the reperfusion period. Importantly, delayed myocardial damage as measured 24 h post-reperfusion was equally protected by administration of 10 μg MTII. The focus on MC3-R was also substantiated by analysis of the recessive yellow (e/e) mouse, bearing a mutated (inactive) MC1-R, in which MTII was fully protective. Myocardial protection was associated with reduced markers of systemic and local inflammation, including cytokine contents (interleukin-1 and KC) and myeloperoxidase activity. In conclusion, this study has highlighted a previously unrecognized protective role for MC3-R activation on acute and delayed heart reperfusion injury. These data may open new avenues for therapeutic intervention against heart and possibly other organ ischemia-reperfusion injury.
Insulin-like growth factor-I stimulates IL-10 production in human T cells
Authors: Kooijman Ron , Coppens Astrid 
Published: July 2004

AbstractThere is vast body of evidence that the insulin-like growth factor (IGF)-I exerts immunomodulatory effects in vitro and in vivo. In vitro studies indicate that stimulatory effects of IGF-I may be exerted through augmentation of inflammatory cytokine production. To further explore the immunomodulatory effects of IGF-I through regulation of cytokine production, we tested the in vitro effects of IGF-I on the secretion of inflammatory T helper cell type 1 (Th1) and Th2 cytokines by human peripheral blood mononuclear cells (PBMC). To this end, PBMC were stimulated with the T cell mitogen phytohemagglutinin (PHA), and cytokines in the culture media were assessed after 18, 42, 66, and 80 h of culture. We found that IGF-I stimulated the secretion of the Th2 cytokine interleukin (IL)-10 by 40–70% in PHA-stimulated PBMC. In addition, we observed a small stimulatory effect (15%) on the secretion of another Th2 cytokine IL-4. The secretion of IL-2, IL-5, IL-6, interferon-γ, and the inflammatory cytokines IL-1β, IL-8, and tumor necrosis factor α was not or was hardly affected. IL-10 secretion was also stimulated in purified T cells, and we established that IGF-I also stimulated IL-10 mRNA expression by 100–150%. The monocyte-activating bacterial cell-wall product lipopolysaccharide induced IL-10 production in PBMC, but this was not affected by IGF-I. As IL-10 predominantly exerts anti-inflammatory actions and suppresses Th1-dependent immune responses, our results indicate that IGF-I may exert inhibitory actions on inflammatory and Th1-mediated cellular immune responses through stimulation of IL-10 production in T cells.
Polymorphonuclear leukocytes from patients with severe sepsis have lost the ability to degrade fibrin via u-PA
Authors: Moir E , Greaves M , Adey G D , Bennett B 
Published: July 2004

AbstractFibrin persistence in the vasculature is an important complication of sepsis that can often lead to mortality. We have previously established that polymorphonuclear leukocytes (PMN) from healthy individuals have the capacity to degrade fibrin via urokinase-type plaminogen activator (u-PA). We have also demonstrated an increase in u-PA antigen in the plasma of patients suffering from septic shock. In this study, we investigate the hypothesis that PMN from patients with sepsis have lost their fibrinolytic ability and that this might contribute to the persistence of fibrin deposits We show here that PMN from these patients do not express any u-PA activity, despite retaining some u-PA antigen. Additionally, thrombi prepared from the whole blood of the patients exhibit reduced endogenous lysis compared with those from healthy individuals. These data indicate that loss of fibrinolytic activity from PMN may be a contributing factor in fibrin persistence in the microvasculature in sepsis.
Comparison of the Efficacy, Toxicity, and Pharmacokinetics of a Uracil/Tegafur (UFT) Plus Oral Leucovorin (LV) Regimen Between Japanese and American Patients With Advanced Colorectal Cancer: Joint United States and Japan Study of UFT/LV
Authors: Shirao K. , Hoff P.M. , Ohtsu A. , Loehrer P.J. , Hyodo I. , Wadler S. , Wadleigh R.G. , O'Dwyer P.J. , Muro K. , Yamada Y. , Boku N. , Nagashima F. , Abbruzzese J.L. 
Published: July 2004

Purpose To compare the efficacy, toxicities, and pharmacokinetics of an oral regimen consisting of uracil/tegafur (UFT) and leucovorin (LV) between Japanese patients and patients in the United States with previously untreated metastatic colorectal cancer. Patients and Methods Forty-four Japanese patients and 45 patients in the United States were enrolled in concurrent nonrandomized phase II trials. UFT 300 mg/m2/d and leucovorin 75 mg/d were administered orally for 28 days followed by a 7-day rest period. The total daily dose of each drug was divided into three equal doses. Treatment was repeated every 5 weeks until disease progression. Blood samples for the pharmacokinetic study were obtained after the initial dose on day 1 of the first course. Results The response rate for the Japanese patients and the patients in the United States was 36.4% (95% CI, 22.4% to 52.2%) and 34.1% (95% CI, 20.5% to 49.9%), respectively. The only major toxicity was diarrhea, and other toxicities were mild in both populations. The incidence of grade 3 or higher diarrhea in the Japanese and Americans was 9% and 22%, respectively. Although the area under the curve and maximum concentration of fluorouracil were found to be slightly higher in the Japanese patients than the patients in the United States, and area under the curve–adjusted body surface area appeared to be comparable between the two groups. Conclusion The efficacy and pharmacokinetic parameters of UFT and LV are comparable in Japanese and American patients; however, a difference in toxicity profile, specifically diarrhea, was noted. This oral regimen of UFT and LV is considered to have similar activity against metastatic colorectal cancer and to have acceptable toxicity in patients in both countries.
Pattern of Care at the End of Life: Does Age Make a Difference in What Happens to Women With Breast Cancer?
Authors: Gagnon Bruno , Mayo Nancy E. , Hanley James , MacDonald Neil 
Published: July 2004

Purpose In the last 40 years, palliative care has become the standard of care at the end of life. However, there are limited data about the degree of access to such care at the population level. Methods Using administrative databases, a care-oriented profile score was created to describe the care received during the last 6 months of life for 2,291 women who were dying of breast cancer in the province of Quebec, Canada, during the years 1992 to 1998. The care received was described through indicators of care that would reflect a palliative care philosophy. An ordinal score was developed for comparisons among age groups of women using a proportional odds ordinal regression model. Results We found that only 6.9% of women died at home, while 69.6% of them died in acute care beds. While most women (75%) had few indicators indicating provision of palliative care during the last 6 months of life, younger women (< 50 years) were even less likely (odds ratio, 0.70; 95% CI, 0.54 to 0.90) to receive such care compared with middle aged women (50 to 59 years; serving as the reference group), while older women (> 70 years) were more likely (odds ratio, 1.85; 95% CI, 1.49 to 2.29). Conclusion Our study indicates that a sizeable proportion of women terminally ill from breast cancer do not have access to palliative care—an issue that health care policy makers may wish to explore further.