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Biomedical subjects

J Collette

Publications and source records attributed to J Collette.

At least 37 records · Page 2Linked to original sources

Neuron-specific enolase as a marker of in vitro neuronal damage. Part II: Investigation of the astrocyte protective effect against kainate-induced neurotoxicity.

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte-poor mixed rat hippocampal cultures were submitted to various concentrations of kainate. At each kainate concentration, the amount of NSE released by neurons was significantly greater in astrocyte-poor than in astrocyte-rich cultures (p < 0.05). This protective effect was not observed when neuronal survival was tested on astrocyte-poor cultures in astrocyte-conditioned culture medium with or without 10(-4) M kainate. In conclusion, astrocytes significantly attenuate kainate toxicity on hippocampal neurons, and this effect is not mediated by a diffusible factor.

Animals↗

Insulin-like growth factor II in two human colon-carcinoma cell lines: gene structure and expression, and protein secretion.

Abnormal expression and structural modification of the IGF-II gene in correlation with high IGF-II production have recently been described in human colorectal tumors in comparison with normal adjacent tissues. Here, we have studied IGF-II in 2 human colon-carcinoma cell lines, HT29 and COLO 320DM. RFLP analyses revealed no apparent alteration at the IGF-II locus in these 2 cell lines. HT29 cells weakly expressed IGF-II mRNA in comparison with the high over-expression previously observed in some colorectal tumors, and only the 4.8-kb mRNA species was present. In addition, the serum-free medium conditioned by HT29 cells contained high IGF-II levels (approx. 900 ng/10(8) cells), as measured in a specific IGF-II radioimmunoassay (RIA). After chromatography on Bio-Gel P-60, we observed that 64% of the total IGF-II secreted by HT29 cells were present as a high-molecular-weight form of about 17 kDa. In contrast, no detectable expression of the IGF-II gene was observed in COLO 320DM cells, and low IGF-II levels were secreted by these cells in the serum-free medium, with only 9% total IGF-II represented by the large species.

Carcinoma↗

Tumor IGF-II content in a patient with a colon adenocarcinoma correlates with abnormal expression of the gene.

We have recently reported abnormal insulin-like growth factor-II (IGF-II) mRNA levels in a number of human colorectal adenocarcinomas. Using an IGF-II radioimmunoassay, we have now detected high levels of both 10-kDa and 7.5-kDa IGF-II species (2,370 ng/g) in a right colon tumor showing a 800-fold IGF-II gene over-expression in comparison to the normal adjacent tissue. The higher-molecular-mass form represents 74% of the total immunoreactive IGF-II detected in the tumor. This form appears to be less reactive in the radioreceptor assay than in the radioimmunoassay. The insulin-like growth factor-I (IGF-I) concentration in the tumor is low. The patient's pre-operative serum IGF-II level is not increased and the proportion of the 10-kDa species is normal. In addition, the IGF-II/IGF-I ratio is 3 in the serum and 308 in the tumor. Our results show that the very high IGF-II level produced by the tumor does not influence the seric concentration of the growth factor.

Adenocarcinoma↗

Stimulatory effect of oestradiol-17 beta and tamoxifen on gross cystic disease fluid protein 15,000 production and mRNA levels in T47D human breast cancer cells.

Oestradiol-17 beta and tamoxifen regulate the synthesis of a gross cystic disease fluid protein (GCDFP-15) in T47D human breast cancer cells. Dose-response curves of GCDFP-15 mRNA contents and GCDFP-15 levels in culture media and cells versus hormone or antihormone concentration have been established. Production of GCDFP-15 was increased by oestradiol-17 beta, tamoxifen and 4-OH tamoxifen. The effect of tamoxifen and 4-OH tamoxifen was greater than the effect of oestradiol-17 beta. Moreover, oestradiol-17 beta and 4-OH tamoxifen acted synergystically in enhancing GCDFP-15 release. The strong oestrogenic effect of the antioestrogen tamoxifen in regulating GCDFP-15 may reflect an unusual interaction between the tamoxifen-oestrogen receptor complex and the DNA oestrogen-responsive elements. As oestrogen control of GCDFP-15 depends also on the cell line studied, investigation of GCDFP-15 could extend our knowledge of the possible mechanism of action of oestrogens or antioestrogens.

Base Sequence↗

Effects of a hydrosoluble bacterial extract from Escherichia coli (OM-89) on cytokine production by peripheral blood mononuclear cells from healthy subjects and patients with rheumatoid arthritis.

OM-89 is a bacterial extract from escherichia coli, proposed as an immunomodulating drug for the treatment of rheumatoid arthritis (RA). Since immunological mechanisms may play a role in its action, the immunological effects of OM-89 were evaluated in vitro on peripheral blood mononuclear cells (PBMC) derived from healthy subjects and RA patients. Results indicated that in the absence of OM-89, production of the monokines interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) is increased, while that of the lymphokines interleukin-2 (IL-2) and interferon-gamma (IFN-gamma is decreased by phytohemagglutinin (PHA)-stimulated PBMC from RA patients as compared with PBMC from healthy subjects. In the presence of PHA, OM-89 enhanced the production of IL-1 beta, TNF-alpha, IL-2, and IFN-gamma. IL-1 beta and IL-2 curves obtained using increasing amounts of OM-89 did not differ depending on the source of PBMC. By contrast, in the presence of increasing amounts of OM-89, TNF-alpha secretion significantly higher and IFN-gamma secretion significantly lower with PBMC from RA patients compared to PBMC from healthy subjects. These data indicate that OM-89 acts on monocytes and T cells directly and/or indirectly and suggest a possible clinical activity by OM-89 in RA relative to its immunological properties.

Adjuvants, Immunologic↗

Placental alkaline phosphatase in developing normal and abnormal gonads and in germ-cell tumours.

The evolution of the gonads during intra-uterine development has been followed by immunohistochemical demonstration of placental-like alkaline phosphatase (PLAP) at the germ-cell level. PLAP immunopositivity was restricted to the limited period when germ cells were not surrounded by granulosa or Sertoli cells. Abnormal fetuses or neonates presenting with chromosomal anomalies frequently had disorganized gonads where germ cells retained their membrane PLAP immunopositivity. This abnormal immunopositivity is similar to that expressed by abnormal germ cells in testicular in situ carcinoma, in gonadoblastoma (case of 45,XO/46,XY mosaic) and in seminoma. The pattern of positivity for other germ-cell tumours was highly variable. We suggest that in abnormal gonads, dysgenetic or neoplastic, an early embryonic property is retained by abnormal germ cells. Its importance in the process of neoplastic induction remains to be defined.

Adolescent↗

Dual photon absorptiometry of lumbar spine in west European (Belgian) postmenopausal females: normal range and fracture threshold.

Bone mineral content (BMC) and bone mineral density (BMD) of lumbar spine have been measured in 695 healthy postmenopausal and 64 type I osteoporotic Belgian, Caucasian females. Bone loss is strongly correlated to time elapse from menopause (Tm) with a maximum rate of bone loss during the first five years of menopause. BMC (gHA) = 461 + 0.662 ln Tm -0.481 (ln Tm)2 and BMD (gHA/cm2) = 0.91 + 0.00711 ln Tm - 0.00846 (ln Tm)2 (in both cases p less than 0.001 and Tm expressed in months of menopause). After 20 years of menopause, 50 to 60% of normal women have vertebral BMC and BMD values below the 90th percentile of women with vertebral fractures and, thus, might be considered to have asymptomatic osteoporosis. We conclude that prevention of postmenopausal osteoporosis should be initiated as soon as possible after the onset of menopause and that bone density screening should be extended in elderly in order to detect and allow treatment of asymptomatic "densitometric" osteoporosis.

Absorptiometry, Photon↗

Radioimmunoassay for human type II collagen.

Human articular cartilage type II collagen (h coll.II) was purified and used to develop a radioimmunoassay. The sequential saturation procedure allowed a sensitivity of 3 ng/tube. The intra and between assay coefficients of variation were less than 10 and 20% respectively in the linear part of the curve. The assay was highly specific for native human articular type II collagen. There was no cross-reactivity with other constituents of cartilage: human proteoglycans, fibronectin, laminin and hyaluronic acid did not interfere with the assay. No cross-reactivity existed with bovine collagen types I, III, IV. However, native collagens from human placenta (I, III, IV, V, VI), rat and calf skin type I collagens and bovine type II collagen produced a weak cross-reaction only at high doses. Concerning the latter, inhibition curves were not parallel. Parallelism of inhibition curves were observed for dilution of type II collagen, produced by human chondrocytes in three-dimensional culture. All of these characteristics indicate that radioimmunoassy of type II collagen is a very sensitive and specific method available for the study and quantification of type II collagen in in vitro experimental conditions.

Cartilage, Articular↗

Relationship between whole plasma calcitonin levels, calcitonin secretory capacity, and plasma levels of estrone in healthy women and postmenopausal osteoporotics.

The exact role of calcitonin (CT) in the pathogenesis of postmenopausal osteoporosis remains unknown. Whole plasma calcitonin (iCT) basal levels, metabolic clearance rate (MCR), and production rate (PR) of CT were measured in 9 premenopausal and 16 postmenopausal women, including 11 osteoporotics (OP). Basal iCT levels were statistically lower in postmenopausal women than in the premenopausal group (P less than 0.01) and strongly correlated (r = 0.72; P less than 0.001) with estrone circulating levels (E1). MCR were similar in all groups. PR were similar in eugonadal women between 22 (mean +/- SD = 30.9 +/- 9.9 micrograms/d) and 37 yr (mean +/- SD = 25.5 +/- 11.1 micrograms/d) premenopausal women. In healthy postmenopausal women PR were reduced, but not significantly (mean +/- SD = 19.5 +/- 6.95 micrograms/d), whereas osteoporotic patients presented a highly significant reduction of CT PR (mean +/- SD = 9.8 +/- 4 micrograms/d) (P less than 0.01). Because there is a strong relationship between E1 and PR (r = 0.64; P less than 0.001), CT secretory capacity appears to be modulated by estrogen circulating levels. This modulation leads to a menopause-related decrease in iCT. In osteoporotics, an independent impairment of CT production drastically lowers PR and basal iCT levels. CT might be one of the determining factors in the pathogenesis of postmenopausal osteoporosis.

Adult↗

Epithelial membrane antigen (EMA) distribution in various biological fluids.

Different human biological fluids, namely breast cyst fluids (five), milks (four), sera (five), were submitted to molecular sieving chromatography on Sepharose CL6B. Global protein contents of the eluted fractions were estimated by the Bradford method. Epithelial membrane antigen (EMA) was assayed by two different ELISA techniques using polyclonal and monoclonal antibodies. Various molecular species reacting with EMA (15) were found in the chromatographies with molecular weights ranging from 35 to 1500 kd. But the total amount of antigens detected using polyclonal or monoclonal antibodies was quite similar. Moreover no significant difference was found between the sera from two lactating women and the sera from three women with adenocarcinoma with respect to the molecular distribution of different molecular species of EMA.

Adenocarcinoma↗

Biological and clinical assessment of a new bisphosphonate, (chloro-4 phenyl) thiomethylene bisphosphonate, in the treatment of Paget's disease of bone.

Several Biophosphonates have been used as therapeutic agents for Paget's bone disease. (Chloro-4 phenyl)thiomethylene-bisphosphonate (CIPsMBP) has recently been shown to have significant antiosteoclastic activity while an affect of CIPsMBP on mineralization was only observed at high doses. We tested this drug for 6 months in 23 pagetic patients distributed in three groups. Gr 1 (n = 5) receiving 200 mg/day showed a decrease of serum alkaline phosphatase (SAP) to 42 +/- 4% (p less than 0.01) of initial value (100%) while hydroxyprolinuria/creatinuria ratio (OH/Cr) dropped to 69 +/- 8% of baseline. In 4 patients receiving 400 mg/day, SAP improved to 48 +/- 9% of initial value (p less than 0.01) and OH/Cr to 40 +/- 3% (p less than 0.01). In the last group (n = 14) receiving 200 mg/day for 3 months, and 400 mg/day thereafter up to the 6th month SAP decreased to 53 +/- 4% and OH/Cr to 62 +/- 6% of initial value (p less than 0.01). Clinical improvement was significant from the first month of treatment. No resistance (mean decrease of SAP lower than 30%) was recorded and no radiological or clinical evidence of mineralization defect appeared. The clinical and biological tolerance was excellent throughout the study.

Aged↗

Immunohistochemical demonstration of placental alkaline phosphatase in various states of testicular development and in germ cell tumours.

Immunohistochemical localization of placental alkaline phosphatase (PlAP) has been performed on eighty-two samples of normal (embryonic, fetal, infantile or adult), cryptorchid or tumorous testicular tissue. The isoenzyme could be demonstrated at the cell membrane of primitive, embryonic germ cells but not in other normal tissues. In-situ carcinomas and seminomas were positively stained in 93% and 94% of cases respectively. The percentage of positivity decreased with tumour differentiation. It is suggested that PlAP is a marker of primitive germ cells and that it reappears in germ cell neoplasms by gene derepression.

Alkaline Phosphatase↗