Biomedical subjects

P Berthon

Publications and source records attributed to P Berthon.

At least 19 recordsLinked to original sources

PubMed1999

FGF7/KGF triggers cell transformation and invasion on immortalised human prostatic epithelial PNT1A cells.

Fibroblast growth factor 7 (FGF7/KGF) is synthesized exclusively by fibroblasts in normal tissues; it acts as a potent mitogen on epithelial cells, through interaction with the FGF7-specific receptor FGFR2/IIIb. To examine the importance of this growth factor both to prostate physiology and to prostate-cancer progression, we have tested the exogenous effect of FGF7. Thus, by mimicking the paracrine pathway (on proliferation, growth in soft agar and invasion) on the human prostatic epithelial cell line PNT1A positively checked for FGFR2/IIIb expression, FGF7 significantly enhanced cell proliferation at an optimal concentration of 7.5 x 10(-11) M, but no significant invasion or growth in soft agar were observed. To confirm FGF7 properties on human prostatic epithelial cells, we constitutively expressed FGF7 by transfecting PNT1A cells with FGF7-cDNA. The FGF7-transfected clones, PNT1A/ FGF7-T5 and PNT1A/FGF7-T6, were stable and expressed FGF7. Analysis of the FGF7-autocrine loop on the non-tumorigenic epithelial cells PNT1A showed acquired invasive potential in in vitro extracellular-matrix migration assays, specifically inhibited by an FGF7-neutralizing antibody, and over-expressed factors implicated in the migration process: the metalloproteinase MMP-1 and the plasminogen activator uPA. Taken together, these results demonstrate a role for FGF7 in triggering invasion of human prostatic epithelial cells. Furthermore, these FGF7-transfected clones exhibited functional and physiological differences from the original PNT1A cell line: anchorage-independent growth, growth in serum-free media and increased proliferation. These data confirm the oncogenic function of FGF7 in prostate progression potentially acting through paracrine and/or autocrine regulatory pathways.

Cell Division↗

PubMed1999

Upregulation of endothelin 1 and its precursor by IL-1beta, TNF-alpha, and TGF-beta in the PC3 human prostate cancer cell line.

Increasing evidence indicates that endothelin 1 (ET-1) is implicated in prostate tumour progression. However, data on ET-1 regulation in human prostate and prostate cancer cell lines are lacking. In this study, regulation of ET-1 and its precursor big ET-1, using PC3 cells, a human bone metastatic prostatic carcinoma cell line, was addressed. ET-1 and big ET-1 assays demonstrated greater secretion of both peptides in the presence of 10% fetal calf serum (FCS) as compared with 0.5% FCS. Incubation of PC3 cells in the absence and presence of various cytokines and growth factors known to be implicated in prostate stroma-epithelium interactions, revealed that IL-6, FGF7/KGF and FGF2/bFGF had no effect on ET-1 and big ET-1 secretion, whereas interleukin 1beta (IL-1beta), tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta) stimulated their secretion in a concentration-dependent manner. Binding experiments indicated the presence of specific ET-1 receptors in PC3 cells: Kdapp = 1.1 x 0.2 x 10(-10)M, Bmax = 2660 +/- 390 sites/cell. Data analysis demonstrated the presence of only the ETA receptor subtype in PC3 cells. In conclusion, our results indicate that the implication of ET-1 in prostate cancer is likely to be mediated via paracrine/autocrine control of cell factors.

Cytokines↗

PubMed1999

An experimental model of bulbar urethral stricture in rabbits using endoscopic radiofrequency coagulation.

OBJECTIVES: To develop an experimental model of endoscopic urethral stricture mimicking the human clinical situation. METHODS: Twenty-four New Zealand male rabbits were included. Eighteen animals (study group) underwent videourethroscopy with a pediatric resectoscope, and a 3 to 5-mm-long circumferential electrocoagulation of the bulbar urethra was performed, without postoperative urinary diversion. Six animals underwent the same procedure without application of electrocautery (control group). Each animal was assessed for urethral stricture on day 15 and day 30 by videourethroscopy and voiding cystogram. Among the study group, 8 animals were killed on day 15 and 10 on day 30 for histologic evaluation. All the control animals were killed on day 30 for histologic examination. RESULTS: Nine animals (50%) in the study group developed a significant bulbar stricture (reducing the lumen by more than 50%) at day 15. Histologic examination confirmed the presence of hyalin fibrosis mutilating the urethral wall. No spontaneous improvement of the stricture was observed on day 30. None of the controls developed urethral stricture, and histologic examination showed a normal urethra in each case. CONCLUSIONS: Endoscopic electrocoagulation of the urethral wall provides a reproducible model of stricture in the rabbit.

Animals↗

PubMed1999

(CAG)nCAA and GGN repeats in the human androgen receptor gene are not associated with prostate cancer in a French-German population.

Alleles of the CAG and the GGC repeat in the first exon of the human androgen receptor (AR) gene have been shown to be associated with the risk of (advanced) prostate cancer. These studies had been carried out in the United States. We have analysed these polymorphisms in a French-German collection of 105 controls, 132 sporadic cases, and a sample of prostate cancer families comprising 85 affected and 46 not affected family members. The allele distributions were very similar in all four groups and chi square statistics on contingency tables did not detect any significant differences. The relative risk (odds ratio, OR) were calculated using logistic regression and did not reach significance despite sufficient numbers of patients and controls. Typical results were OR = 1.007; 95% Confidence Interval (CI) 0.97-1.1, P = 0.87 for CAG as continuous variable and OR = 1.2 (95% CI 0.7-2.0), P = 0.47 for CAG classes < 22 and > = 22 repeats. Similar results were obtained for subgroups defined by age or Gleason score. We conclude that these polymorphisms can not be used as predictive parameters for prostate cancer in the French or German population.

Aged↗

PubMed1999

Thermal radiofrequency induced porcine ureteral stricture: a convenient endourologic model.

PURPOSE: To establish a reliable model of iatrogenic ureteral stricture mimicking the human clinical situation in order to experiment with new site-specific endourologic treatment concepts. MATERIALS AND METHODS: After cystoscopic insertion of a 7F right ureteral catheter, we induced external thermal radiofrequency injury to the right upper third ureter at low power setting (10 W) using an open surgical approach in 13 pigs. Three pigs considered as controls underwent the same procedure without application of electrocautery. All 16 animals were initially assessed at 8 days; 3 study animals and the 3 controls were followed for 6 weeks. RESULTS: No control animals had strictures. Significant upper third ureteral strictures with marked hydronephrosis where achieved in all study animals after a mean interval of 9 days, as evidenced by ultrasound examination and retrograde ureteropyelography. Endoscopic retrograde access to these strictures was always possible (mean length 1.4 cm.). Histologic examination displayed severe disorganization of the muscular layer by dense fibrosis composed of collagen bundles with few scattered fibroblasts. No spontaneous improvement of the stricture was observed in the 3 animals reassessed at 6 weeks. CONCLUSIONS: Externally applied radiofrequency energy to porcine ureter provides a reproducible model of fibrous stricture resembling its clinical counterparts.

Animals↗

PubMed1999

Ureteral gene transfer to porcine induced strictures using endourologic delivery of an adenoviral vector.

PURPOSE: Direct gene transfer to the ureter is an attractive approach to prevent restenosis after endourologic management of ureteral strictures. We therefore assessed the rationale for adenovirus-mediated gene transfer in the ureter in vitro and in vivo using a porcine model. MATERIALS AND METHODS: Primary cultures of porcine ureteral epithelial and stromal cells were infected with an adenoviral solution carrying a nucleus-targeted beta-Galactosidase (beta-Gal) reporter gene (6.5 10(8) pfu/ml.). In addition, in order to mimic the human clinical situation, we have devised a model of thermally-induced stricture in porcine ureter which produced tight fibrotic stenosis within 8 days. Using a purposely designed channelled balloon catheter prototype, these strictures were endoscopically dilated and then instilled with the same beta-Gal adenoviral construction. RESULTS: Application of recombinant adenovirus harboring a nucleus-targeted beta-Gal reporter gene to cultured porcine urothelial and stromal cells resulted in high transduction efficiency of up to 99% and 84% respectively. Seven days after infection, X-Gal staining of the strictured ureters demonstrated transfection up to 2 mm. depth within the fibrosis, confirmed by polymerase chain reaction (PCR) analysis. Adjacent and distal spread of the virus was excluded by histochemistry (X-Gal staining) and PCR. CONCLUSION: This data represents the first report of adenovirus-mediated gene transfer to the ureter. It remained site specific by endourologic retrograde clinically applicable techniques.

Adenoviridae↗

PubMed1999

[Epidemiology of familial prostatic cancer: 4-year assessment of French studies].

OBJECTIVES: (1) To determine the frequency of familial (at least 2 cases) and hereditary forms of prostate cancer (CaP), (2) to define the results according to the patient's age at diagnosis, as various epidemiological studies have demonstrated a possible familial aggregation of CaP in about 15 to 25% of cases. Carter's familial segregation study (P.N.A.S. 1992, 89, 3367-71) showed that a genetic predisposition, with autosomal dominant transmission, could be responsible for 9% of all cases of prostate cancer. MATERIAL AND METHODS: We conducted a systematic genealogy study of patients suffering from newly diagnosed CaP or followed for known CaP in 3 French urological centres, by means of questionnaires completed by the patients. Subsequently, a national collection of families with at least 2 cases of CaP identified families with hereditary forms of CaP. Hereditary cases were considered to be those presenting at least: one CaP in three 1st degree relatives, or 3 cases over 3 generations in the same branch of the family (paternal or maternal), or finally 2 early cases before the age of 55 years. Statistical analysis used the univariate logistic regression test between family status and the medical centre or the patient's age at diagnosis. RESULTS: From July 1994 onwards, we included 801 patients (all stages combined) in the systematic study and 110 patients (13.7%) were excluded (refusal to participate, advanced age). For 691 of the families studied (Brest: 225, Nancy: 249, Paris St Louis: 217), we observed 32 (14.2%), 29 (11.6%), 37 (17.1%) of familial forms (mean: 14.2%) and 11 (4.9%), 6 (2.4%), 8 (3.7%) of hereditary forms (mean: 3.6%), respectively (no significant differences between centres). Analysis of the results according to age at diagnosis of CaP also showed a higher incidence of familial (significant difference) and hereditary forms (limit of significance) for CaP occurring at a younger age (before 65 years). The national collection collected a total of 624 familial forms of CaP, including 236 (37.8%) cases of hereditary forms; 115 families were informative for the genetic linkage study. CONCLUSION: These results confirm the data of earlier studies, revealing about 15 to 25% of familial forms of CaP and 5 to 10% of hereditary forms. Similarly, the systematic study confirmed the earlier onset of CaP in patients with a genetic predisposition. These data therefore encourage systematic questioning of patients for a family history of CaP in order to propose targeted screening of high-risk subjects in the families concerned and to intensify identification of hereditary forms in order to investigate the genes involved.

Aged↗

PubMed1999

[Genetic analysis of familial prostatic cancer: localization of a gene predisposing to prostatic cancer (PCaP) on chromosome 1q 42.2-43].

OBJECTIVES: To conduct genetic linkage analysis in order to localize predisposition genes for hereditary prostate cancer (CaP), as various epidemiological studies have demonstrated a family aggregation in 15 to 25% of cases, and the development of hereditary forms in 5 to 10% of cases of CaP. MATERIAL AND METHODS: A genetic study on 47 French and German families included 122 patients and 72 subjects considered to be healthy after PSA assay. This study was conducted by linkage analysis of 364 microsatellite markers distributed throughout the genome (on average every 10 cM). RESULTS: Parametric and nonparametric linkage analysis identified a locus on chromosome 1q 42.2-43, which could be with a gene predisposing to CaP (called PCaP). The primary site was confirmed by several markers, using 3 different genetic models. The maximum LOD score (probability of linkage between the locus and the disease) on two-point analysis was 2.7 for the D1S2785 marker. Parametric and nonparametric multipoint analysis provided an HLOD score and an NPL score of 2.2 and 3.1, respectively (with P = 0.001). Heterogeneity analysis with calculations of LOD scores by multipoint analysis estimated that up to 50% of hereditary CaPs were related to this locus, with a heterogeneity probability of 157/1. Analysis of a subgroup of 9/47 families characterized by early onset CaP (before the age of 60 years) confirmed the very high probability of localization of a predisposition gene at locus 1q42.2-43 for these families (multipoint LOD score and NPL score of 3.31 and 3.32, respectively; with P = 0.001). CONCLUSION: The identification of predisposition genes will eventually allow identification within certain families of those subjects who have inherited the genetic abnormality and who therefore present a high risk of CaP. It will then be possible to perform targeted screening of CaP in order to diagnose CaP as early as possible.

Adult↗

PubMed1998

Predisposing gene for early-onset prostate cancer, localized on chromosome 1q42.2-43.

There is genetic predisposition associated with >=10% of all cancer of the prostate (CaP). By means of a genomewide search on a selection of 47 French and German families, parametric and nonparametric linkage (NPL) analysis allowed identification of a locus, on chromosome 1q42.2-43, carrying a putative predisposing gene for CaP (PCaP). The primary localization was confirmed with several markers, by use of three different genetic models. We obtained a maximum two-point LOD score of 2.7 with marker D1S2785. Multipoint parametric and NPL analysis yielded maximum HLOD and NPL scores of 2.2 and 3.1, respectively, with an associated P value of . 001. Homogeneity analysis with multipoint LOD scores gave an estimate of the proportion of families with linkage to this locus of 50%, with a likelihood ratio of 157/1 in favor of heterogeneity. Furthermore, the 9/47 families with early-onset CaP at age <60 years gave multipoint LOD and NPL scores of 3.31 and 3.32, respectively, with P = .001.

Age of Onset↗

PubMed1998

Hereditary prostate cancer and other genetic predispositions to prostate cancer.

The incidence of prostate cancer (CaP) and its increase in the last 10 years vary both from country to country and according to the ethnic group, with the highest incidence reported for Afro-Americans and the lowest for Asian men. To date, only three risk factors have been established for CaP: age; familial aggregation of CaP, and ethnic origins. No dietary or environment-related cause has been established. However, some variations in endogenous genetic factors may help explain differences in risk among ethnic groups or geographic areas. Similarly, certain genetic polymorphisms of genes encoding for 5alpha-reductase, androgen receptor or vitamin D, have been associated with different levels of CaP risk, and could explain the variations observed between populations. Different studies support the view that familial CaP may truly be hereditary, and not due to a similar lifestyle. Thus, familial inheritance is a parameter that needs to be considered in recommending screening for high-risk families. Indeed, when 1, 2, and 3 first-degree relatives are affected, the relative risk of first-degree relatives of CaP patients may increase to 2, 5, and 11%, respectively. Some familial forms appear to be associated with transmission of a rare putative dominant gene with a high penetrance (88% at age 85), with the cumulative proportion of CaP attributable to this gene being more marked for younger patients (a 43 versus a 34% risk of CaP appearing before the age of 55 versus 70 years). Using this transmission model and linkage analysis, a predisposing locus on chromosome 1q24-25 (HPC-1) has been described. Moreover, recessive and X-linked transmission has been suggested, showing that a large proportion of familial CaP may not be due to segregation of a few major gene mutations, but rather to familial sharing of alleles at many loci, each contributing to a small increase in cancer risk. Candidate genes may be the same suppressor genes that are involved in other cancers and in sporadic CaP.

Aged↗

PubMed1998

Evaluation and clinical value of neuroendocrine differentiation in human prostatic tumors.

BACKGROUND: Prostate cancer, like other solid tumors, is a rather heterogeneous entity. More than 50% of all malignant prostatic tumors contain neuroendocrine-like cells, which cannot be attributed to small cell prostatic carcinoma or carcinoid-like tumors, which represent only 1-2% of all prostatic malignancies. Several investigators have reported that histopathologic determination of neuroendocrine differentiation in prostate carcinomas may have prognostic implications, while others have not confirmed these results. However, on the basis of experimental data, neuroendocrine-like cells appear to be involved in the emergence of androgen-independent cells and could be a target for new prostate cancer therapeutic strategies. METHODS: The literature on the neuroendocrine phenotype of prostatic carcinoma is reviewed. This review summarizes most of the accumulated experimental and clinical data on the neuroendocrine phenotype in prostate cancer. We analyze the putative functions of neuroendocrine-like cells in prostate cancer progression and discuss the place of neuroendocrine phenotype biomarkers as diagnostic and prognostic factors in prostate cancer. RESULTS: The fact that focal, patchy and heterogeneous clusters of neuroendocrine-like cells are frequently identified in organ-confined prostatic carcinoma probably accounts for the various evaluations of the predictive value of neuroendocrine histological patterns for the clinical outcome at this stage of the disease. The amount of neuroendocrine cells required to produce a detectable elevation in plasma chromogranin A has not yet been determined, but it is correlated with the number of chromogranin A-positive neuroendocrine (NE) cells. Despite the obvious current limitations of the application of neuropeptides as a serological test, this overview will try to more accurately define the possible roles of specific neuropeptides as prostatic cancer markers in diagnostic and monitoring protocols. The plasma chromogranin A level, in comparison with neuron-specific enolase (NSE), chromogranin B (CBG), pancreastatin, or secretogranin levels, appears to be the most useful neuroendocrine marker for determination of neuroendocrine differentiation of advanced prostatic adenocarcinoma. CONCLUSIONS: Future studies on neuroendocrine should confirm whether neuroendocrine biomarkers, especially the chromogranin family of peptides, can be used as prognostic markers during the course of prostate cancer or for the selection of patients suitable for evaluation of new antineoplastic drugs known to be active against specific and aggressive subpopulations of tumor cells.

Biomarkers, Tumor↗

PubMed1997

Androgens are not a direct requirement for the proliferation of human prostatic epithelium in vitro.

The androgen receptor pathway is known to be a key regulator of growth in the normal and pathological prostate. However, the precise mechanisms of this signaling pathway with respect to the different cellular compartments of the prostate remain largely unknown. We have used a primary culture system to grow human prostatic epithelial cells of normal, benign, tumor and metastatic origin, as well as immortalized human prostatic epithelial cell lines, to demonstrate the absence of a direct or indirect effect of androgens on cellular proliferation in vitro. In parallel to this observed androgen independence for growth, all cell systems lost significant expression of androgen receptor, prostate-specific antigen and prostatic acid phosphatase. Since the androgen receptor is expressed in the epithelium in situ, our results suggest that the androgen effect on epithelial cells may be one of prostatic differentiation rather than proliferation, and that the androgen receptor/growth factor pathway acts through mesenchymal-epithelial interactions.

Acid Phosphatase↗

PubMed1997

Constitutive expression of FGF2/bFGF in non-tumorigenic human prostatic epithelial cells results in the acquisition of a partial neoplastic phenotype.

Fibroblast growth factor 2 (FGF2), also known as basic fibroblast growth factor (bFGF), belongs to the FGF family, which consists of at least 9 closely related members. FGF2 is a potent mitogen for fibroblasts derived from normal prostate and, to a lesser extent, for prostatic epithelial cells. Its role in the physiology of the normal prostate seems to be limited to stromal cells, whereas in prostate cancer FGF2 may also have an autocrine/paracrine effect on epithelial cells. In order to better understand the effects of FGF2 on the prostatic epithelium, especially its role in the progression of prostate cancer by establishing an autocrine-stimulation loop, we transfected FGF2 cDNA into a human prostatic epithelial cell line, PNT1A, immortalized with SV40 large-T antigen. This cell line is non-tumorigenic and expresses a high-affinity FGF2 receptor, FGFR1/flg. We characterized 3 independent FGF2-transfected clones and found that the establishment of an FGF2 autocrine loop on these cells led to (i) serum-independent growth, (ii) increased proliferation and (iii) anchorage-independent growth. Such results argue in favor of the possible action of FGF2 on progression of prostate cancer via an FGF2 autocrine loop on epithelial cells.

Animals↗

PubMed1997

A 5-min running field test as a measurement of maximal aerobic velocity.

Based on a theoretical approach from world record running data, we have previously calculated that the most suitable duration for measuring maximal aerobic velocity (Vamax) by a field test was 5 min (Vamax(5)). The aim of this study was, therefore, to check this hypothesis on 48 men of various levels of physical fitness by comparing (Vmax(5)) with (Vamax) determined at the last step of a progressive treadmill exercise test when the subject felt exhausted (Vamax(t)) and during a test on a running track, behind a cyclist (following an established protocol) (Vamax(c)). For each test, (VO2max) was also measured by a direct method on a treadmill (VO2max(1)) and calculated by an equation for field tests (VO2max(5) and VO2max(c)). The Vamax(5) [17.1 (SD 2.2) km.h-1] and (Vamax(c)) [(18.2 (SD 2.4) km.h-1] were significantly higher than (Vamax(t)) [16.9 (SD 2.6) km.h-1; P < 0.001]. The (Vamax(t)) was strongly correlated with (Vamax(5)) (r = 0.94) and (Vamax(c)) (r = 0.95) (P < 0.001). The best identity and correlation between (Vamax(5)) and track performances were found in the runners (n = 9) with experience over a distance of 3,000 m. The VO2max(5) and (VO2max(c)) were higher than VO2max(t) (+ 5.0% and + 13.7%, respectively; P < 0.001) and VO2max(t) was highly correlated with Vamax(5) (r = 0.90; P < 0.001). These results suggest that the 5-min field test, easy to apply, provided precise information on Vamax and to a lesser degree on VO2max.

Adolescent↗

PubMed1997

Analysis of ovine IL-1 beta production in vivo and in vitro by enzyme immunoassay and immunohistochemistry.

A monoclonal antibody (mAb) specific for ovine IL-1 beta was produced and, in conjunction with a polyclonal rabbit antiserum, used to develop a sensitive enzyme immunoassay (EIA) for ovine interleukin 1 beta (IL-1 beta). The mAb neutralised the activity of recombinant ovine IL-1 beta (rOvIL-1 beta) and native OvIL-1 in an ovine thymocyte proliferation assay. However, it did not neutralise the biological activity of rOvIL-1 beta in the murine NOB1/CTLL assay. The mAb did not react with rOvIL-1 alpha, IL-2, IL-4, IL-8, tumor necrosis factor-alpha, gamma-interferon or recombinant human IL-1 beta in indirect EIA. Immunohistological staining of activated alveolar macrophages and frozen lymph node sections sections demonstrated that the mAb detected IL-1 beta secreted by ovine macrophages (CD11c-positive). The EIA was highly sensitive, detecting less than 50 pg ml-1 of rOvIL-1 beta and low levels of native IL-1 beta in supernatants from lipopolysaccharide-stimulated macrophages. The EIA did not detect heat-inactivated IL-1 beta.

Alkaline Phosphatase↗

PubMed1997

L-carnitine stimulation of mitochondrial oxidative phosphorylation rate in isolated rat skeletal muscle mitochondria.

L-carnitine effects on mitochondrial adenosine triphosphate (ATP) production rate were investigated in mitochondria isolated from rat extensor digitorum longus (EDL) muscle. Kinetic parameters, apparent Michaelis constant for free adenosine diphosphate (ADP) (K(m)) and apparent maximal ATP production rate (Vmax), were determined in absence and presence of L-carnitine. Although the K(m) remained unchanged in response to L-carnitine addition when pyruvate + malate was oxidized, the affinity of isolated mitochondria towards ADP was decreased when pyruvate + palmitoylcarnitine + malate was used as substrate. As a result of L-carnitine addition, a slight non-significant (P < 0.07) increase in Vmax was observed with pyruvate + malate while the increase reached the level of significance with pyruvate + palmitoylcarnitine + malate. Moreover, a positive correlation was obtained when mitochondrial ATP production rate was plotted against the difference between values measured with and without L-carnitine. Our data suggest that addition of L-carnitine to isolated rat skeletal muscle mitochondria can stimulate mitochondrial oxidative phosphorylation rate under conditions where the inhibitory effect of acetyl-CoA accumulation on pyruvate dehydrogenase complex activity is optimized. A change in the control of mitochondrial ATP flux by pyruvate dehydrogenase (PDH) complex might also occur with increasing mitochondrial ATP production rate, reinforcing the L-carnitine effects.

Adenosine Triphosphate↗

PubMed1997

Maximal aerobic velocity measured by the 5-min running field test on two different fitness level groups.

The aim of the study was to verify the validity and the accuracy of the 5-min running field test (5RFT) relatively to the classical treadmill test. Two groups of subjects were tested, the first one being made of sub-elite runners (G1, n = 18) and the second one of athletes of other individual or collective disciplines (G2, n = 23). To check the field technique, maximal aerobic velocity (vamax) and an approached VO2max calculated from vamax during the 5RFT were compared with the corresponding values directly determined during a treadmill test. vamax obtained on treadmill (vamax(t)) or during a 5RFT (vamax(5)) were significantly higher in G1 than in G2 (+3.7 km.h-1 and +3.6 km.h-1 among the test). In each group, the difference between vamax(t) and vamax(5) was not significant (19.4 +/- 1.0 vs 19.5 +/- 0.9 km.h-1 in G1; 15.7 +/- 2.2 vs 15.9 +/- 1.2 km.h-1 in G2). A significant correlation was found between vamax(t) and vamax(5) (slope = 0.92; r = 0.86 in G1; slope = 0.71; r = 0.84 in G2). In each group, the approached VO2max(5) was significantly higher than VO2max(t) (respectively 67.8 +/- 2.9 vs 63.7 +/- 3.5 in G1; 54.8 +/- 3.9 vs 52.0 +/- 3.2 ml.min-1.kg-1 in G2. Weak but significant correlations were found between VO2(t) and vamax(5) (r = 0.69 and r = 0.56 respectively in G1 and G2). In conclusion, the 5RFT allows to measure vamax accurately whatever the physical fitness of the subjects but more closely in runners than in non-runners. The low correlation between VO2max(t) and vamax(5) for both groups indicates that a vamax running field test is specific and cannot evaluate VO2max with reasonable accuracy whatever the group, runners or non-runners.

Adult↗

PubMed1996

Ruminant cluster CD14.

Following the analysis of flow cytometry data on ovine and bovine cells and immunoprecipitation, immunohistochemistry and competitive binding studies, a cluster of three monoclonal antibodies (mAbs) (VPM65, VPM66 and VPM67) appeared to be specific for the ruminant CD14 (Gupta, V.K., McConnell, I., Dalziel, R.G. and Hopkins, J., 1996. Identification of the sheep homologue of the monocyte cell surface molecule-CD14. Vet. Immunol. Immunopathol. in press; Hopkins, J. and Gupta, V.K., 1996. Characterization of 3rd Worshop monoclonal antibodies specific for sheep macrophages/monocytes. Vet. Immunol. Immunopathol., 52:329-339). According to flow cytometry results from human CD14-transfected COS-7 cells and from bovine peripheral blood mononuclear cells, another mAb (CC-G33), not submitted to the Workshop, recognised a bovine CD14 epitope which is conserved in the human CD14 (Sopp, P., Kwong, L.S. and Howard, C.J., 1996. Identification of bovine CD14. Vet. Immunol. Immunopathol., 52: 323-328).

Animals↗