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C Abreu

Publications and source records attributed to C Abreu.

14 recordsLinked to original sources
PubMed2005

Lack of association between androgen receptor polymorphisms and bone mineral density or physical function in older men.

Individuals whose androgen receptors have short polyglutamine tracts (resulting from CAG repeats) may have greater receptor signaling activity of the androgen receptor. We evaluated the association between bone mineral density (BMD) and CAG repeats in 91 older men with normal (control) and low femoral neck (EN) BMD (OP) or a history of femoral fracture (FX). Bioavailable testosterone (BioT) and physical performance, including composite score (EPESE) and physical activity (PASE), were also measured. Comparing FX, OP, and control subjects, we observed BMD Tscores of -2.16 +/- 1.08, -2.26 +/- 0.74, and -0.20 +/- 0.40 (p < 0.001); CAG repeat lengths of 21.9 +/- 2.7, 22.5 +/- 2.4, and 22.3 +/- 2.9 (p = 0.63); BioT levels of 2.29 +/- 1.25, 2.19 +/- 1.11, and 3.99 +/- 1.25 nmol/L (p < 0.001); EPESE scores of 8.0 +/- 3.0, 9.7 +/- 2.0, and 11.3 +/- 0.9 (p < 0.001); and PASE scores of 91 +/- 66, 122 +/- 66, and 200 +/- 55 (p < 0.001), respectively. There were no significant correlations between CAG repeats and BioT or physical performance. Men with osteoporosis or fracture had lower BioT, physical performance, and physical activity than controls. This study found no association between CA G repeats and FN BMD in older men with normal or low BMD or FX.

Aged↗
PubMed2001

Crenarchaeota and Euryarchaeota in temperate estuarine sediments.

AIMS: Application of molecular techniques to ecological studies has unveiled a wide diversity of micro-organisms in natural communities, previously unknown to microbial ecologists. New lineages of Archaea were retrieved from several non-extreme environments, showing that these micro-organisms are present in a large variety of ecosystems. The aim was therefore to assess the presence and diversity of Archaea in the sediments of the river Douro estuary (Portugal), relating the results obtained to ecological data. METHODS AND RESULTS: Total DNA was extracted from sediment samples obtained from an estuary deprived of vegetation, amplified by PCR and the resulting DNA fragments cloned. The archaeal origin of the cloned inserts was checked by Southern blot, dot blot or colony blot hybridization. Recombinant plasmids were further analysed by restriction with AvaII and selected for sequencing. Phylogenetic analyses of 14 sequences revealed the presence of members of the domain Archaea. Most of the sequences could be assigned to the kingdom Crenarchaeota. CONCLUSION: Most of these sequences were closely related to those obtained from non-extreme Crenarchaeota members previously retrieved from diverse ecosystems, such as freshwater and marine environments. SIGNIFICANCE AND IMPACT OF THE STUDY: The presence of archaeal 16S rDNA sequences in temperate estuarine sediments emerges as a valuable contribution to the understanding of the complexity of the ecosystem.

Cloning, Molecular↗
PubMed1999

Prostaglandins regulate the expression of fibroblast growth factor-2 in bone.

We examined the effect of PGs, particularly PGF2alpha, on basic fibroblast growth factor-2 (FGF-2) messenger RNA (mRNA) and protein in the rat osteoblastic cell line Py1a and in fetal rat calvariae. Py1a cells expressed multiple FGF-2 mRNA transcripts. PGF2alpha dose-dependently increased the 6-kb transcript at 6 h. The selective PGF2alpha agonist, fluprostenol (Flup), was more potent than PGF2alpha. Phorbol myristate acetate (10(-6) M) also increased a 6-kb mRNA at 6 h. By immunofluorescence microscopy, Flup increased perinuclear staining for FGF-2 protein at 6 h and nuclear labeling at 24 h. Immunogold labeling of calvariae revealed that treatment with Flup for 3 h caused a transition of FGF expression from matrix to cells and an increase in cytoplasmic labeling for FGF-2 protein in periosteal cells and in osteoblasts. After treatment with Flup for 24 h, nuclear labeling was marked in periosteal cells and in osteoblasts, and a further increase in cytoplasmic labeling for FGF-2 was noted in osteocytes, periosteal cells, and osteoblasts. We conclude that PGs can increase FGF-2 mRNA and protein in bone cells. Because the effect of Flup was mimicked by phorbol myristate acetate, we hypothesize that PGs' regulation of FGF-2 is mediated by a PGF2alpha-selective receptor acting through protein kinase C. Hence, effects of PGs on bone remodeling may be mediated, in part, by endogenous FGF-2.

Animals↗
PubMed1999

[Kaposi sarcoma associated with HIV infection].

Kaposi's sarcoma is the most common neoplasm in AIDS patients. In a 12-year period, 45 (8%) cases were diagnosed in 552 patients with AIDS. Epidemiological and clinical aspects are reviewed. The disease occurred predominantly in males and homosexuals. In 30 (67%) patients it was the first manifestation of AIDS. Skin and/or oral disease was the most frequent manifestation observed in our patients; 13 (29%) had visceral involvement. Previous or concommitant opportunistic diseases, systemic illness and severe immunosuppression were present in the majority of the patients. Opportunistic infections were the cause of death in 30 patients; in five others, Kaposi's sarcoma was responsible for death. Advances in antiretroviral therapy were of benefit for patients submitted to chemotherapy and may contribute to a reduction in morbidity with this neoplasm.

Adolescent↗
PubMed1996

Intact insulin-like growth factor binding protein-5 (IGFBP-5) associates with bone matrix and the soluble fragments of IGFBP-5 accumulated in culture medium of neonatal mouse calvariae by parathyroid hormone and prostaglandin E2-treatment.

We examined the distribution of insulin-like growth factor binding proteins (IGFBPs) in cultured neonatal mouse calvariae. IGFBP-3 and -4 were predominantly found in the conditioned medium. IGFBP-2 was partitioned between conditioned medium and bone and extracellular matrix (BECM), while intact (31-kDa) IGFBP-5 was most abundant in BECM extracts. After treatment with parathyroid hormone (PTH, 10(-8) M) or prostaglandin E2 (PGE2, 10(-6) M), immunoreactive IGFBP-5 accumulated in the conditioned medium in a 21-kDa form which did not bind IGF-I on Western ligand blots. PTH and PGE2 did not alter the level of steady-state IGFBP-5 mRNA, nor markedly stimulate IGFBP-5 synthesis in the calvariae, and thus accumulation of 21-kDa IGFBP-5 was largely due to release from BECM. This accumulation of truncated IGFBP-5 in the conditioned medium was not dependent on osteoclastic bone resorption, since it was not blocked by calcitonin or a bisphosphonate which inhibited PTH- and PGE2-stimulated 45Ca-release. The conditioned medium from PTH- or PGE2-treated cultures degraded recombinant human IGFBP-5 into lower molecular weight fragments. Addition of IGF-1 at 10(-8) M into the culture resulted in accumulation of native 31-kDa IGFBP-5. However, even in the presence of IGF-1, the native IGFBP-5 was degraded and the 21-kDa product accumulated in the culture medium. These results suggested a possible proteolytic mechanism for 21-kDa IGFBP-5 accumulation, responsive to PTH and PGE2. Aprotinin, leupeptin, cystatin, and bestatin did not inhibit the effects of PTH and PGE2 in the cultures. The localization of IGFBP-5 in BECM and its release and proteolysis induced by PTH and PGE2 could play a role in the local regulation of bone metabolism.

Animals↗
PubMed1996

Regulation of NFIL-6 and IL-6 expression by basic fibroblast growth factor in osteoblasts.

We determined whether basic fibroblast growth factor (bFGF) regulated the expression of IL-6 and NFIL-6 in osteoblasts. In mouse osteoblastic MC3T3-E1 cells, bFGF (10(-8) M) increased NFIL-6 mRNA 2-fold at 30 minutes and 3-fold at 2 h. IL-6 mRNA was increased by bFGF 10(-8) M after 1 h. IL-6 protein was detectable in control cultures but was significantly increased by bFGF (10(-8) M) at 4 h. Immunofluorescence analysis of MC3T3-E1 cells showed primarily cytoplasmic and perinuclear NFIL-6 staining in control cultures while bFGF-treated cells showed increased NFIL-6 staining at 2 and 4 h. Western blotting revealed that bFGF increased NFIL-6 protein at 2 h. In calvarial mouse osteoblasts, bFGF 10(-8) M induced IL-6 mRNA as early as 1 h and significantly increased IL-6 protein levels as early as 2 h. In conclusion, bFGF stimulates IL-6 and NFIL-6 mRNA in osteoblasts. The increase in NFIL-6 mRNA was associated with increased NFIL-6 protein. The increase in IL-6 mRNA was also associated with increased IL-6 protein. We propose that activations of NFIL-6 and IL-6 may be important mediators of the effects of bFGF on bone cells.

Animals↗
PubMed1996

Signal transduction by basic fibroblast growth factor in rat osteoblastic Py1a cells.

Basic fibroblast growth factor (bFGF) is a potent mitogen for bone. In this study, we utilized the clonal rat osteoblastic cell line, Py1a, to examine signal transduction by bFGF and to determine the role of mitogen activated protein kinases (MAPK) and induction of c-fos mRNA in the mitogenic response to bFGF. Stimulation of [3H]thymidine incorporation (TDR) into DNA by bFGF was determined in the presence of phorbol myristate acetate of (PMA) to down-regulate the protein kinase C (PKC) pathway, genistein, an inhibitor of tyrosine kinase and H-7, a PKC inhibitor, bFGF 10(-8) M and PMA 10(-7) M increased TDR by 242 and 245%, respectively. Treatment with bFGF or PMA for 5 or 30 minutes increased tyrosine phosphorylation of multiple proteins, and immunoblotting with MAPK-specific antibody revealed that two of these bands were the 42 and 44 kD isoforms of MAPK. PMA and bFGF induced c-fos mRNA expression at 30 minutes. Genistein at 10 micrograms/ml blocked the mitogenic effect of bFGF and partially inhibited the mitogenic effect of PMA. Genistein at 100 micrograms/ml also blocked both bFGF- and PMA-induced increases in c-fos mRNA. A 24 h pretreatment with PMA at 10(-7) M inhibited the mitogenic response, tyrosine phosphorylation of MAPK, and induction of c-fos mRNA subsequent to the addition of PMA, but not bFGF. H-7 at 50 microM blocked bFGF-induced mitogenesis and c-fos induction, but did not inhibit bFGF-induced tyrosine phosphorylation of MAPK. In this study, we show that the signaling pathway of bFGF and PMA are similar in that they both induce tyrosine phosphorylation of MAP kinases and activate c-fos. However, the signaling pathways ultimately diverge in that once the PKC pathway is down-regulated by PMA pretreatment or blocked by the PKC inhibitor H-7, tyrosine phosphorylation of MAP kinase, c-fos induction, and the mitogenic effect of PMA is blocked. In contrast, down-regulation of the PKC pathway inhibits c-fos and the mitogenic response to bFGF, but not bFGF's effects on tyrosine phosphorylation of MAP kinase.

Analysis of Variance↗
PubMed1995

Transcriptional regulation of the collagenase gene by basic fibroblast growth factor in osteoblastic MC3T3-E1 cells.

Recent studies have shown that Basic Fibroblast Growth Factor increases bone resorption and increases interstitial collagenase mRNA and protein in osteoblasts. We examined the effect of bFGF on a 1.8-kb fragment of the rabbit collagenase promoter linked to a chloramphenicol acetyl transferase CAT construct stably transfected into mouse osteoblastic MC3T3-E1 cells. Treatment with bFGF (10(-8)M) for 24 h caused a 3-fold increase in collagenase-CAT activity. CAT activity in a construct without the collagenase promoter was not regulated by 48 h treatment with bFGF (10(-8)M). Neither indomethacin nor staurosporine blocked the effect of bFGF on collagenase-CAT activity in these cells. However, the stimulatory effect of bFGF on collagenase-CAT activity was inhibited by genistein and herbimycin A, which are tyrosine kinase inhibitors. These data show for the first time that bFGF transcriptionally regulates collagenase gene expression in osteoblasts through a protein tyrosine kinase-dependent pathway.

3T3 Cells↗
PubMed1995

Basic fibroblast growth factor regulates IGF-I binding proteins in the clonal osteoblastic cell line MC3T3-E1.

In previous studies, we reported that basic fibroblast growth factor (bFGF) regulates insulin-like growth factor messenger RNAs and protein levels in the osteoblastic MC3T3-E1 cells. In the present study, we examined the expression of insulin-like growth factor binding proteins (IGFBPs) in MC3T3-E1 cells and determined whether bFGF altered IGFBP mRNAs and protein levels. Since previous studies suggested that IGFBPs can inhibit DNA synthesis stimulated by IGF-I, we wondered whether the mitogenic effect of bFGF was altered by exogenous IGFBP-3. Confluent MC3T3-E1 cells were serum-deprived for 24 h and then treated with bFGF for 6-24 h. In control cultures, MC3T3-E1 cells expressed the mRNAs for IGF-I, IGF-II, and IGFBP-2, 4, 5, and 6 but not IGFBP-1 or 3. A 24 h treatment with bFGF at 10(-8) M decreased IGF-I mRNA by 97%, IGF-II mRNA by 73%, IGFBP-2 by 64%, IGFBP-4 by 73%, IGFBP-5 by 95%, and IGFBP-6 by 65%. The inhibitory effect of bFGF on IGF-I and IGFBP mRNA levels was not altered by aphidicolin, an inhibitor of cell replication. bFGF 10 nM decreased IGF-I levels determined by radioimmunoassay after acidification by 45% and 72% at 24 and 48 h, respectively. Western ligand blot for IGF binding proteins revealed that MC3T3-E1 cells expressed IGFBPs of 24, 30, and 34 kD. Treatment with bFGF 10(-8) M decreased the levels of the 24 and 30 kD band at 24 h but increased the 34 kD band.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed1995

Transcriptional induction of prostaglandin G/H synthase-2 by basic fibroblast growth factor.

In serum-free mouse osteoblastic MC3T3-E1 cells, basic fibroblastic growth factor (bFGF) induced mRNA and protein for prostaglandin G/H synthase-2 (PGHS-2), the major enzyme in arachidonic acid (AA) conversion to prostaglandins. mRNA accumulation peaked at 1 h with bFGF 1 nM. In cells stably transfected with a 371-bp PGHS-2 promoter-luciferase reporter, bFGF stimulated luciferase activity, which peaked at 2-3 h with bFGF 1-10 nM. In the presence of exogenous AA, bFGF stimulated PGE2 production, which paralleled luciferase activity. In serum-free neonatal mouse calvarial cultures, bFGF stimulated PGE2 production in the absence of exogenous AA. bFGF stimulated PGHS-2 mRNA accumulation, which peaked at 2-4 h and then decreased; there were later mRNA elevations at 48 and 96 h that were inhibited by indomethacin. In both MC3T3-E1 cells and neonatal calvariae, bFGF produced smaller and slower increases in PGHS-1 mRNA levels than for PGHS-2. bFGF stimulated bone resorption in mouse calvariae with a maximal increase of 80% at 1 nM. Stimulation was partially inhibited by nonsteroidal anti-inflammatory drugs. We conclude that bFGF rapidly stimulates PGE2 production in osteoblasts, largely through transcriptional regulation of PGHS-2, and that prostaglandins mediate some of bFGF's effects on bone resorption.

Animals↗
PubMed1994

Expression and regulation of basic fibroblast growth factor mRNA levels in mouse osteoblastic MC3T3-E1 cells.

Basic fibroblast growth factor (bFGF) is a potent mitogen for bone cells and is a constituent of the bone matrix. We have found that osteoblastic MC3T3-E1 cells expressed bFGF mRNA transcript of 4.5 kilobases (kb). We examined factors that regulate the expression of bFGF mRNA and protein in MC3T3-E1 cells. Treatment of MC3T3-E1 cells with bFGF (10 nM) for 4-48 h induced another 7-kb bFGF transcript at 4 h. Treatment of MC3T3-E1 cells with TGF beta (10 ng/ml) also induced the 7-kb transcript of bFGF mRNA. In contrast, heparin, parathyroid hormone, and interleukin-1 had no effect on bFGF mRNA. Western blot analyses revealed that MC3T3-E1 cells produced a 24-kDa bFGF protein, which was increased by TGF beta. Immunofluorescence showed that bFGF protein was localized to the cytoplasm in serum-deprived MC3T3-E1 cells. Treatment of these cultures with medium containing fetal calf serum or TGF beta caused increased cytoplasmic staining for bFGF and marked shape change. Furthermore, in the cells treated with TGF beta there was both nuclear and cytoplasmic staining for the protein. These data demonstrate that bFGF mRNA and protein are expressed in osteoblastic cells and are regulated by treatment with TGF beta and bFGF. Production of bFGF may be important as an autocrine and paracrine mediator of bone cell replication, differentiation, and function.

Animals↗
PubMed1993

Basic fibroblast growth factor inhibits type I collagen gene expression in osteoblastic MC3T3-E1 cells.

We examined the effect of basic fibroblast growth factor (bFGF) on alpha 1(I) procollagen mRNA levels, alpha 1(I) collagen gene transcription, and alpha 1(I) collagen promoter activity in osteoblastic MC3T3-E1 cells. Cells were stably transfected with ColCAT 3.6, containing 3521 base pairs of alpha 1(I) collagen promoter DNA, fused to the CAT reporter gene, or an upstream deletion mutant of ColCAT 3.6 designated ColCAT 2.3. After 48 h, bFGF (0.1-10 nM) inhibited the incorporation of [3H]proline into collagenase-digestible protein (CDP). Indomethacin did not alter the inhibitory effect of bFGF on CDP labeling. Aphidicolin, an inhibitor of DNA synthesis, did not block the inhibitory effect of bFGF on CDP. bFGF (1-10 nM) decreased alpha 1(I) procollagen mRNA levels, with maximal inhibition, nearly 99% of control, caused by 10 nM bFGF. After 48 h, bFGF (1 nM) reduced alpha 1(I) procollagen gene transcription by about 92%. ColCAT 3.6 activity was inhibited with 0.1-10 nM bFGF and was maximally repressed by about 83% with 10 nM bFGF. In contrast, bFGF (1 and 10 nM) caused a stimulation of ColCAT 2.3 activity. These data show that bFGF inhibits collagen synthesis by a transcriptional mechanism and the alpha 1(I) collagen promoter contains DNA sequences which mediate bFGF inhibition of type I collagen gene expression in bone.

3T3 Cells↗
PubMedDate not supplied

Update on the use of cefotaxime for pediatric meningitis in Portugal.

We treated 256 children who had identified bacterial meningitis with cefotaxime. Causative organisms were: Neisseria meningitidis in 108 cases, Streptococcus pneumoniae in 61, Haemophilus influenzae in 60, enteric Gram-negative bacilli in 21, and Staphylococcus spp. in six. Daily doses of cefotaxime were 150-200 mg/kg. A total of 240 patients (93.7%) were cured. In the cured patients, sterilization of cerebrospinal fluid was obtained in the first 72 h of treatment in 214 (80.0%). Cefotaxime is an effective and safe drug for the treatment of childhood bacterial meningitis.

Adolescent↗