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V Salle

Publications and source records attributed to V Salle.

17 recordsLinked to original sources
PubMed2005

[Incidence of cardiovascular events in giant cell arteritis: preliminary results of a prospective double cohort study (GRACG)].

UNLABELLED: Giant cell arteritis is the most frequent vasculitis. Cardiovascular events such as cerebrovascular accident or ischemic heart disease may occur in patients with giant cell arteritis. However, their real incidence, as well as their relative risk compared to the general population, remains unknown. PURPOSE: To assess in a prospective, double cohort study, the incidence of cardiovascular events in giant cell arteritis patients compared to controls, after controlling for cardiovascular risk factors. PATIENTS AND METHODS: We included on predefined criteria 432 newly diagnosed patients with giant cell arteritis, each assigned to sex- and age-matched controls randomly selected from the general population. Cardiovascular risk factors (high-blood pressure, diabetes, smoking, hypercholesterolemia and preexisting peripheral vascular disease) were collected at inclusion. During the 24-month follow-up, all cardiovascular events were collected. After stratification for cardiovascular risk factors, a log-rank test was performed to compare cases and controls. A parametric survival model was used for multivariate analysis. RESULTS: Cardiovascular events all combined were significantly increased in patients with giant cell arteritis (RR = 2.15 [1.21-3.81], P = 0.009), and were mainly associated with age (P = 0.0001), past history of cardiovascular disease (P = 0.023) but also with giant cell arteritis (P = 0.009). However, each subset of cerebrovascular accident (RR = 2.42 [0.84-7]) or ischemic heart disease (RR = 1.67 [0.72-3.89]) increased but did not significantly. CONCLUSION: Cardiovascular events incidence is increased in patients with giant cell arteritis, and prescription of preventive antiagregant treatment may be discussed.

Aged↗
PubMed2005

[Aetiological spectrum of hyperferritinemia].

UNLABELLED: Serum ferritin levels may be increased in many conditions: renal diseases, liver diseases, human immunodeficiency virus infection. The purpose of this study was to assess the aetiological spectrum of high serum ferritin levels in a 1200-bed university hospital, to compare our results with the data already published and to assess a potential association between aetiology and ferritin levels. PATIENTS AND METHODS: Patients with a serum ferritin level higher than 600 microg/l were retrospectively included between 15 November 2003 and 15 January 2004, and their medical records were reviewed. RESULTS: Ninety-eight patients (38 women and 60 men; median age: 59,5 years [19-92]) were recruited in departments of hepatology and gastroenterology (22%), haematology (14%) and internal medicine (18%). Diagnosis performed were: non-HIV systemic infections (23,8%), haematological diseases (16,1%), alcoholism (11,2%) and malignancies (9,8%). Dialysed chronic renal failure, liver diseases, haemochromatosis and systemic inflammatory diseases counted for 4.2 to 5.2% of cases. Serum ferritin level lied between 600 and 1000 microg/l for 50 patients, between 1000 and 1500 microg/l for 24, and over 1500 microg/l for 24. There was no significant difference between the three groups as regards the etiological distribution. DISCUSSION: In our study, chronic renal failure was not a major cause of high ferritin level: this is probably due to the current use of erythropoietin, which has decreased the use of blood transfusions. The two major aetiology of hyperferritinemia were non-HIV infections and malignancies.

Adult↗
PubMed2004

[Angioedema and angiotensin converting enzyme inhibitors: a report of 19 cases].

PURPOSE: Inhibitors of angiotensin-converting enzyme are worldwide used and are a real progress for the treatment of systemic hypertension or cardiac failure and are a real progress. The most common adverse side effect is cough. Angioedema is a sudden and localized edema involving the deeper cutaneous and mucosa tissue lappers. 0.1-0.5% of patients treated by ACE inhibitors could develop angioedema. MATERIALS AND METHODS: We report a series of 19 cases, recruited in the Parmacovigilance Center of the University Hospital of Amiens from 1997 to 2003. RESULTS: All the patients had a facial swelling edema at initial presentation. Intestinal mucosa or preputial are misleading localisations. In 1/3 of cases, angioedema appeared after the first administration, in 1/3 of cases it appeared with a delay of 1-2 years. The oropharynx localisation with glottic involvement may need an airway intervention. One patient died from pulmonary distress at home. CONCLUSION: The pathophysiology is current unknown although there is increasing evidence for bradykinin accumulation involvement. The treatment by ACE inhibitors must be broken off; angiotensin II antagonists may be an alternative treatment, but has to be introduced carefully.

Adult↗
PubMed2004

Autoantibodies recognizing the 27 carboxy-terminal amino acids of calpastatin are associated with secondary Sjögren syndrome in systemic lupus erythematosus.

The objective of this study was to determine in systemic lupus erythematosus (SLE) the prevalence and clinical significance of anticalpastatin antibodies (ACAST), an autoantibody population previously detected in sera from patients with various connective tissue diseases. Eighty-four patients with SLE (mean age: 30 years at diagnosis, females 77) that fulfilled ACR criteria were included in the study retrospectively. Several clinical and biological data were collected. ACAST were detected by a solid-phase enzyme linked immunosorbent assay (ELISA) using as antigen a synthetic peptide corresponding to the 27 C-terminal amino acids of calpastatin (CAST-C27). The prevalence of ACAST-C27 was 13% (11/84) in SLE patients. No correlation was found between the presence of ACAST-C27 and clinical manifestations such as thrombosis and vasculitis. Furthermore, no correlation was observed with the presence ofantiphospholipid antibodies (APL). However, we found a statistically significant association between the presence of ACAST-C27 and that of secondary Sjögren syndrome (P = 0.01). The conclusion is ACAST-C27 are not associated with thrombosis in SLE patients. The association observed between ACAST-C27 and secondary Sjögren syndrome suggests that ACAST-C27 might be useful in discriminating a clinical subgroup of SLE patients.

Adolescent↗
PubMed2001

Autoantibodies to the 27 C-terminal amino acids of calpastatin are detected in a restricted set of connective tissue diseases and may be useful for diagnosis of rheumatoid arthritis in community cases of very early arthritis.

BACKGROUND: Calpastatin is the natural inhibitor of calpains, a protease that is overexpressed in rheumatoid synovial tissue and plays a key role in cartilage destruction. Autoantibodies to calpastatin (ACAST) were recently detected in rheumatoid arthritis (RA). Our aim was to determine their prevalence and their clinical significance. METHODS: ACAST were detected in a solid-phase enzyme-linked immunosorbent assay (ELISA) using a synthetic peptide corresponding to the 27 C-terminal amino acids of calpastatin (CAST-C27) as the antigen. All sera reacting with this peptide also bound to purified erythrocyte calpastatin in an ELISA and/or an immunoblot assay. The frequencies and clinical significance of ACAST-C27 were assessed in sera from a well-documented population of 102 community-recruited patients (76 females; mean age 50 yr) with RA that had been evolving for <5 yr (median 2 yr) (group 1), 109 healthy blood donors, 289 patients with non-RA rheumatic disease and 88 community cases of very early (median 4 months) arthritis, i.e. 58 RA and 30 non-RA patients (group 2). RESULTS: The sensitivity of ACAST-C27 for RA was 19.5% (20/102) in group 1 and 10.3% (6/58) in group 2. These antibodies were also found in patients with anti-double-stranded DNA-positive systemic lupus erythematosus (SLE) (15.5%) and patients with anti-Ro-positive Sjögren's syndrome (18.5%). However, they were not detected in cases of rheumatism resembling early RA, i.e. peripheral spondylarthropathies. ACAST-C27 were not detected in the 30 non-RA patients of group 2. They were predominantly of immunoglobulin isotype G3 and exclusively expressed lambda chains. Among ACAST-C27-positive sera, eight out of 20 (group 1) and four out of six (group 2) were negative for rheumatoid factor and anti-keratin antibodies/antiperinuclear factor. No relationship was found between ACAST-C27 and clinical, biological or radiological findings. CONCLUSION: ACAST-C27 are detected only in a restricted set of connective tissue diseases and therefore appear to be specific for RA when antibodies that are usually associated with SLE or primary Sjögren's syndrome are negative. Because of their presence in community cases of very early RA, particularly in some seronegative forms, ACAST-C27 may be useful in discriminating recent-onset RA from the more common non-RA rheumatic diseases, such as spondylarthropathies.

Adult↗
PubMed1996

Temporary ex vivo inhibition of the expression of the human oncogene HER2 (NEU) by a triple helix-forming oligonucleotide.

A 28-base phosphodiester triple helix-forming oligonucleotide, mostly G and A containing, targeted to a polypurine tract interrupted by a purine-pyrimidine inversion, situated upstream from the TATA box of the promoter of the human HER2 gene, was conceived by computer modeling. The "energetically best choice" was oligo 28(C), which formed the triple helix in vitro, as proved by gel retardation and Fourier transform infrared spectroscopy. When administered as a complex with lipofectin, fluorescence confocal microscopy and electrophoresis confirmed the delivery and persistence of this unprotected oligonucleotide inside MCF7 (breast cancer) cells. At a concentration of 2 microM, the oligonucleotide reduced within 6 h the HER2 mRNA level to 42% (Northern blot) but did not interfere with the transcription of a housekeeping gene, glyceraldehyde-3-phosphate dehydrogenase. During the first day of administration at 0.22 microM, it lowered to 59% the HER2 protein in treated, as compared to nontreated, cells (ELISA). The effect was sequence specific when compared to that of five different negative controls, and it was target selective when compared to the expression of a related, nontargeted protein, the epidermal growth factor receptor. By day 2, the inhibitory effect was overcome by replenishment reactions.

Base Sequence↗
PubMed1994

Proliferative responses of epithelial cells to 8-bromo-cyclic AMP and to a phorbol ester change during breast pathogenesis.

We have explored the relationship of changes in proliferative responses of human mammary epithelial cells to a phorbol ester (TPA) and to 8-Br-cAMP, which modulate the activities of protein kinases A and C (PKA and PKC), with breast tumour progression. Treatment with TPA had no effect on nontumorigenic cell lines established from human fibrocystic biopsies and apparently normal tissue around a tumour. In contrast, TPA strongly inhibited the proliferation of numerous human tumorigenic breast cell lines. Treatment with 8-Br-cAMP decreased the proliferation of all studied nontumorigenic and tumorigenic cell lines. We have also studied the effect of TPA and 8-Br-cAMP on growth of epithelial cells in short-term culture obtained from surgical human mammary biopsies with different states of breast disease. Both drugs enhanced growth of normal breast cells but had no significant effects on cells from biopsies with benign breast disease. In contrast, all examined cultures from breast cancer biopsies were strongly inhibited by 8-Br-cAMP. Otherwise, TPA had an inhibitory effect only in the case of invasive ductal carcinoma of grade III. Malignant Ha-ras-transformation of nontumorigenic TPA-insensitive breast HBL-100 cells induced an inhibitory effect of TPA. In addition, a TPA-insensitive MCF7 clone was much less tumorigenic in athymic mice than the parental strain shown to be inhibited by TPA. These data suggest that the two intracellular transduction pathways change at different stages of breast pathogenesis. Alterations in the PKA pathway are early events and are probably important to cell immortalization but do not necessarily lead to malignant development. In contrast, changes in PKC pathway are rather later events associated with advanced malignant transformation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

[Growth factors of cultured epithelial cells of breast diseases and breast carcinoma].

Primary cultures of non-malignant human breast tissues, benign mastopathies and breast carcinomas were raised in defined culture conditions and characterized for in vitro cell proliferation. Although some mastopathies had estradiol receptors they did not respond to hormone treatment. Epidermal growth factor (EGF) was capable of stimulating the 3 types of primary culture. In contrast, dexamethasone, insulin and transferrin stimulated only the proliferation of some benign mastopathies and carcinoma cells. Cholera toxin increased the cell growth of normal tissues and mastopathies but not of carcinoma in primary cultures. Taken together, these results show that epithelial cells from mastopathies differ from one another; some are similar to non-malignant cells, whereas others are comparable to tumor cells.

Breast Diseases↗
PubMedDate not supplied

Primary cultures of human benign mastopathies and mammary carcinomas; growth factor requirements.

Primary cultures of non malignant human breast tissues, benign mastopathies and breast carcinoma were performed in defined culture conditions. Epithelial cells from these primary cultures were characterized for mammary epithelial cell specific markers, for in vitro cell proliferation, for steroid receptors and hormone sensitivity (estradiol, progesterone and prolactin) and for EGF sensitivity. We show that although some mastopathies have estradiol and progesterone receptors, they did not respond to hormone treatment. Human prolactin had no effect on the proliferation of one mastopathy but stimulates the cell growth of another fibrocystic mastopathy. EGF was capable of stimulating the three types of primary cultures. As regards growth characteristics, steroid hormone receptors and prolactin sensitivity, phenotypes of mastopathy cells differ from each other; some are similar to non malignant cells, whereas others are comparable to tumor cells.

Adenocarcinoma↗
PubMedDate not supplied

Steroid hormone receptors and tumorigenicity of sublines from breast tumor metastatic MDA-MB 231 cell line.

Ten cell sublines the MDA-MB 231 human breast cell line were analyzed for their phenotypic diversity: morphology, karyotype, growth rate, clonogenicity in semisolid medium, tumorigenicity in nude mice, number and affinity of nuclear receptors for oestradiol, progesterone and glucocorticoids. Karyotypic analysis showed different aneuploidies from 50 to 120 chromosomes and variable chromosomal rearrangements in the analyzed subclones. All except two of the ten subclones were tumorigenic when injected subcutaneously or intraperitoneally into nude mice. Although the parental cell line has no receptor, all except two of the tested subclones contained various amounts of high affinity oestradiol and progesterone receptors ranging from 3,000 to 33,000 per cell. Seven subclones contained either high affinity oestradiol or progesterone receptors in nuclei. The diversity found in different subclones derived from one breast carcinoma cell line might represent variabilities acquired and selected continuously in culture.

Aneuploidy↗
PubMedDate not supplied

Phenotypes of human epithelial cell lines immortalized from benign mastopathies.

We have cultured cells from normal and benign mastopathy tissues under conditions favoring epithelial cell proliferation. However, such primary cells rapidly lose their ability to grow in vitro. Immortal lines were established after transfection with SV 40 T gene and several cell clones isolated from Normal Breast Adjacent to a tumor (NBAT 32 T2 to T7) and two benign mastopathies (NPM 21 T1 to T14 and NPM 14 T4). This immortalization of epithelial cells reduced the doubling time of cultured cells and increased the densities of the cultured cell populations. Among there cell lines we have characterized five clones and found differences in a number of aspects. Southern blot analysis showed that the SV 40 T gene was stably integrated in the genome of all the established cell lines. Two of the clones (NPM 21 T2 and NPM 21 T4) were nearly diploid showing a high degree of stability. Two other clones (NPM 14 T4 and NPM 21 T1) had near-tetraploid karyotypes, although quite heterogeneous. Comparison of the ultrastructural phenotypes shows that the two near-diploid cell lines were more differentiated than the two others. Estradiol receptors measured by Scatchard analysis and by transactivation of vitellogenin promotor were absent from all the cell lines. Progesterone receptors measured by Scatchard analysis of hormone binding were present in the NPM 14 T4 and NBAT 32 T4 cell lines. The NPM 21 T1 cell line did not contain such steroid receptors. These cell lines are persistent in long-term culture, thus providing a useful in vitro model system for studying factors involved in the proliferation and the transformation of human mammary epithelial cells.

Breast↗