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Biomedical subjects

N Andre

Publications and source records attributed to N Andre.

10 recordsLinked to original sources
PubMed2006

On-line monitoring of the buffer capacity of particleboard furnish by near-infrared spectroscopy.

This paper reports on a study of on-line monitoring of the buffer capacity of particleboard furnish using near-infrared (NIR) spectroscopy and multivariate analysis models (chemometrics). The buffer capacity of wood furnish is known to affect the quality of polymerization and the curing rates of urea-formaldehyde (UF) resins, which may affect the mechanical properties of manufactured panel. The first phase of the study consisted of building multivariate calibration and validation models from NIR spectroscopy data to predict the buffer capacity of particleboard furnish in a laboratory environment. During this phase, a spectrometer (Ocean Optics USB2000) operating in the 550-1100 nm spectral range was evaluated. The second phase of the study took place at a North American particleboard plant over several weeks. Several multivariate calibration models were constructed and tested on-line during a four-day test period. The on-line root mean square error of prediction (RMSEP) and the coefficient of variation (CV) for buffer capacity predictions ranged from 3.45 to 0.92 and 22.4% to 5.8%, respectively.

Journal Article↗
PubMed2005

Cassini magnetometer observations during Saturn orbit insertion.

Cassini's successful orbit insertion has provided the first examination of Saturn's magnetosphere in 23 years, revealing a dynamic plasma and magnetic environment on short and long time scales. There has been no noticeable change in the internal magnetic field, either in its strength or its near-alignment with the rotation axis. However, the external magnetic field is different compared with past spacecraft observations. The current sheet within the magnetosphere is thinner and more extended, and we observed small diamagnetic cavities and ion cyclotron waves of types that were not reported before.

Journal Article↗
PubMed2004

[Colorectal cancer: current treatment options].

Colorectal Cancer is one of the leading causes for cancer related death in the industrialized world. The 5 year overall survival is only 50 - 60 %, although 70 - 80% of the patients are potentially cured by surgical resection. During the last 10 years intensive clinical studies helped to establish the value of adjuvant therapy for colorectal cancer. The introduction of new chemotherapeutic agents like Irinotecan and Oxaliplatin, has led to a significant increase in tumor response and median survival in patients with colorectal carcinoma receiving adjuvant or palliative chemotherapy. In the later situation the sequential application of new combination therapies enables an overall survival of exceeding more than 20 month. In addition the targeted manipulation of molecular tumor mechanisms with new substances like monoclonal antibodies against the epidermal growth factor receptor or the vascular endothelial growth factor shows promising effects. Besides the encouraging improvement of treatment results the introduction of the new drugs has also led to more complexity within choice, strategy and conduction of specific therapies. This manuscript introduces actual treatment concepts and their impact on colorectal cancer.

Antibodies, Monoclonal↗
PubMed2000

Expression patterns of placenta growth factor in human melanocytic cell lines.

Expression patterns of the angiogenic placenta growth factor and its receptor neuropilin-1 were assessed in normal human melanocytes, SV40T-transformed melanocytes, and melanoma cells derived from primary and metastatic lesions. As determined by reverse transcription-polymerase chain reaction all primary and metastatic melanoma cell lines tested and SV40T-transformed melanocytes coexpressed two placenta growth factor splice variants (placenta growth factor-1 and -2) as well as neuropilin-1 mRNA. Placenta growth factor protein was detected in conditioned media derived from five of eight melanomas and from SV40T-transformed melanocytes. In contrast to melanoma cells, normal melanocytes did not express placenta growth factor mRNA at detectable levels and did not secrete placenta growth factor protein. By contrast, neuropilin-1 transcripts were detected in some of the normal melanocytes. Secretion of placenta growth factor by melanoma cells appeared to be constitutive because it was not affected by the addition of exogenous growth factors including insulin, epidermal growth factor, or basic fibroblast growth factor to culture media. Although melanoma cells expressed both, neuropilin-1 and flt-1, exogenous homodimeric placenta growth factor had no effect on melanoma cell growth. Similarly, placenta growth factor did not induce urokinase-type plasminogen activator production in these cells. These findings demonstrate that melanoma progression is accompanied by deregulated, constitutive placenta growth factor expression. Placenta growth factor, however, serves no apparent autocrine role in melanoma proliferation. Further studies are needed to define the relative contribution of placenta growth factor to the angiogenic properties of human melanomas.

Angiogenesis Inducing Agents↗
PubMed1999

Serum levels of vascular endothelial growth factor and basic fibroblast growth factor in patients with soft-tissue sarcoma.

PURPOSE: Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) have been suggested to be important mediators for tumor-induced angiogenesis. We measured serum VEGF and bFGF levels from patients with soft-tissue sarcomas and correlated serum VEGF and bFGF levels with tumor status at surgery and histological grading. MATERIALS AND METHODS: A group of 18 healthy controls and 85 patients with soft-tissue sarcoma were enrolled in this study. The patients were classified according to tumor status at surgery. Serum levels of VEGF and bFGF were also correlated with histological grading. VEGF and bFGF levels were determined by enzyme-linked immunosorbent assay (Quantikine R&D Systems). RESULTS: Serum VEGF and bFGF levels were significantly elevated in the patient group (VEGF: 580pg/ml, bFbF: 21pg/ml, P = 0.0001). The highest concentrations of serum VEGF and bFGF were found in patients with macroscopic tumor lesions or G3 histology. Serum VEGF levels showed a statistically significant correlation with tumor status and grading (P = 0.006 for tumor status, P = 0.0001 for grading). CONCLUSIONS: This study reveals that elevated preoperative serum VEGF and bFGF levels can be detected in the majority of patients with soft-tissue sarcoma. The significant correlation with tumor mass and histological grading suggests that a consecutive monitoring of VEGF and bFGF in the serum of patients with soft-tissue sarcoma might be a valuable marker for tumor follow-up.

Biomarkers, Tumor↗
PubMed1995

Characterisation of cyclooxygenase 1 and 2 expression in mouse resident peritoneal macrophages in vitro; interactions of non steroidal anti-inflammatory drugs with COX2.

Resident peritoneal macrophages exposed to inflammatory stimuli (zymosan, lipopolysaccharide (LPS)) represent a widely used model for studying arachidonic acid metabolism and for screening of prostaglandin (PG) synthesis inhibitors. In the present study, cyclooxygenase 1 (COX1) was shown constitutively expressed in mouse adherent and non-adherent macrophages whereas expression of COX2 was observed only in adherent cells, even when cultured in minimal conditions (Ca-, Mg- and serum-free medium). The COX2 expression was amplified by arachidonic acid cascade stimulating agents (Ca, Mg, zymosan) and by LPS in a time-dependant manner; PGE2 by itself amplified LPS-induced COX2 expression. In well-defined experimental conditions of COX2 expression (LPS-stimulated adherent macrophages), we studied specific interactions of some representative anti-inflammatory drugs with COX2 enzymatic activity and expression. By contrast with dexamethasone, which reduced PGE2 release together with a strong reduction of COX2 expression (protein and mRNA), non steroidal anti-inflammatory drugs (NSAIDs) reduced PGE2 synthesis without any effect at the COX2 mRNA level. This reduction of PGE2 production by NSAIDs resulted from either an exclusive enzymatic inhibition (aspirin, NS398, 6-Methoxy naphtyl acetic acid) or an enzymatic inhibition associated with a slight decrease of COX2 protein level (indomethacin). For paracetamol and salicylic acid, two weak inhibitors of COX enzymatic activity, reduction of PGE2 synthesis appeared to be related to reduced level of COX2. These findings show that the macrophage can be used as a cellular model to study specifically COX1 and COX2. In this cell type, COX2 expression is dependent on adhesion, enhanced by stimulation of arachidonic acid metabolism, and auto amplified by PGE2. Furthermore, the results indicate that known NSAIDs differ in their interaction with cyclooxygenase, being able to inhibit either COX2 enzymatic activity, and/or COX2 expression. However, further studies are required to determine the mechanism and the role of COX2 expression during inflammation in vivo, and to define more precisely the best target for new potent and safe NSAIDs.

Animals↗