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Biomedical subjects

F Martin

Publications and source records attributed to F Martin.

At least 199 records · Page 11Linked to original sources
PubMed1997

[Screening for trisomy 21 by measuring nuchal translucency during the first trimester of pregnancy].

The purpose of the present literature review is to assess the screening value of trisomy 21 by measurement of fetal nuchal translucency (NT) thickness in the first trimester. NT is a subcutaneous translucency between the skin and the soft tissues overlying the cervical spine, which disappears in the second trimester. Ultrasound examination was used to image a sagittal section of the fetus to measure the maximum thickness of the subcutaneous translucency. NT is physiological for a measurement < 3 mm but the incidence of chromosomal abnormalities (essentially trisomies 21, 18 and 13) increases when NT > or = 3 mm. Differential diagnoses include cystic hygroma and fetal hydrops. For screening purposes, a cut-off threshold value of > or = 3 mm, with a standardized technique, gave a sensitivity > or = 50%, a false positive rate < 5% and a positive predictive value > 1%. In the chromosomally normal group, prognosis was good, but incidence of structural defects and fetal loss increased, with a sharp rise in these complications for fetal translucency thickness > or = 5 mm.

Anthropometry↗
PubMed1996

Expression of a 74-kDa nuclear factor 1 (NF1) protein is induced in mouse mammary gland involution. Involution-enhanced occupation of a twin NF1 binding element in the testosterone-repressed prostate message-2/clusterin promoter.

Testosterone repressed prostate message-2 (TRPM-2)/clusterin gene expression is rapidly induced in early involution of the mouse mammary gland, after weaning, and in the rat ventral prostate, after castration. A search for involution-enhanced DNaseI footprints in the proximal mouse TRPM-2/clusterin gene promoter led to the identification and characterization (by DNase I footprinting and EMSA) of a twin nuclear factor 1 (NF1) binding element at -356/-309, relative to the proposed transcription start site; nuclear extracts from 2-day involuting mouse mammary gland showed an enhanced footprint over the proximal NF1 element; extracts from involuting prostate showed enhanced occupancy of both NF1 binding elements. Subsequent EMSA and Western analysis led to the detection of a 74-kDa NF1 protein whose expression is triggered in early involution in the mouse mammary gland; such an induced protein is not found in the involuting rat ventral prostate. This protein was not found in lactation where three other NF1 proteins of 114, 68, and 46 kDa were detected. Reiteration of the epithelial cell apoptosis associated with early mammary gland involution, in vitro, in a primary cell culture system, triggered the appearance of the 74-kDa NF1. Overlaying the cells with laminin-rich extracellular matrix suppressed the apoptosis and the expression of the 74-kDa NF1 and, in the presence of lactogenic hormones, initiated milk protein gene expression and the expression of two of the lactation-associated NF1 proteins (68 and 46 kDa). This study, thus, identifies for the first time the occurrence of a switch in expression of different members of the family of NF1 transcription factors as mammary epithelial cells move from the differentiated to the involution/apoptotic state, and it is likely that the involution-specific 74-kDa NF1 accounts for the enhanced NF1 footprint detected on the TRPM-2/clusterin promoter with extracts of mouse mammary gland.

Animals↗
PubMed1996

Inhibition of insulin release by synthetic peptides shows that the H3 region at the C-terminal domain of syntaxin-1 is crucial for Ca(2+)- but not for guanosine 5'-[gamma-thio]triphosphate-induced secretion.

Recently, we have described the presence and possible role of syntaxin in pancreatic beta-cells by using monoclonal antibodies [F. Martin, F. Moya, L. M. Gutierrez, J.A. Reig, B. Soria (1995) Diabetologia 38, 860-863]. In order to characterize further the importance of specific domains of this protein, the functional role of a particular region of the syntaxin-1 molecule has now been investigated by using two synthetic peptides, SynA and SynB, corresponding to two portions of the H3 region at the C-terminal domain of the protein, residues 229-251 and 197-219 respectively. Functional experiments carried out in permeabilized pancreatic beta-cells demonstrate that these peptides inhibit Ca(2+)-dependent insulin release in a dose-dependent manner. This effect is specific because peptides of the same composition but random sequence do not show the same effect. In contrast with this inhibitory effect on Ca(2+)-induced secretion, both peptides increase basal release. However, under the same conditions, SynA and SynB do not affect guanosine 5'-[gamma-thio]triphosphate-induced insulin release. These results demonstrate that specific portions of the H3 region of syntaxin-1 are involved in critical protein-protein interactions specifically during Ca(2+)-induced insulin secretion.

Amino Acid Sequence↗
PubMed1996

The tissue-specific transcriptional regulation of the megakaryocytic glycoprotein IIb gene is controlled by interactions between a repressor and positive cis-acting elements.

Much information on regulation of the transcription of megakaryocytic genes stems from studies on the glycoprotein IIb (GPIIb) gene, an early and specific marker of this lineage. Transcriptional activity is controlled by the association of positive promoter elements corresponding to binding sites for the transcription factor GATA-1 and a member of the Ets family. In the present study, we show that these elements are not directly involved in the control of cell specificity. In contrast, we identified a sequence located between -170 and -73 that exhibited a repressor activity based on an analysis of the transcriptional activity of 5'-deleted GPIIb promoter fragments transfected in the nonhematopoietic HeLa cells. Further analysis of this repressor by substitution mutagenesis of the -139/-63 region showed that bases -120/-116 and -102/-93 were required for full repressor activity. The repressor is able to interact differentially with GPIIb promoter elements active in the megakaryocytic HEL, the erythroid K562, the monocytic U937, or the nonhematopoietic HeLa cell lines, indicating that it controls GPIIb gene tissue specificity. In addition, direct evidence for tissue-specific interaction between this repressor and the GPIIb -598/ -406 enhancer was obtained when these elements were set in the context of a heterologous SV40 promoter. Interestingly, the same repressor element controlling tissue specificity of the GPIIb gene may also control its temporal expression during megakaryocyte differentiation, based on recent evidence obtained by Fong and Santoro (J Biol Chem 269:18441, 1994). Finally, we found that the -120/-116 GPIIb sequence was part of a consensus motif shared by promoters of other megakaryocyte-specific genes, suggesting a common repressor mechanism.

Base Sequence↗
PubMed1996

Entry of polyunsaturated fatty acids into the brain: evidence that high-density lipoprotein-induced methylation of phosphatidylethanolamine and phospholipase A2 are involved.

The conversion of phosphatidylethanolamine (PE) into phosphatidylcholine (PC) by a sequence of three transmethylation reactions is shown to be stimulated by the apolipoprotein E-free subclass of high-density lipoprotein (HDL3) in isolated bovine brain capillary (BBC) membranes, HDL3-induced stimulation of BBC membranes pulsed with [methyl-14C]methionine causes a transient increase in each methylated phospholipid, i.e. phosphatidyl-N-monomethylethanolamine (PMME), phosphatidyl-NN-dimethylethanolamine (PDME) and PC. PC substrate arising from the activation of PE N-methyltransferase (PEMT) is hydrolysed by a phospholipase A2 (PLA2), as demonstrated by the accumulation of lysophosphatidylcholine (lyso-PC). When PE containing [14C]arachidonic acid in the sn-2 position ([14C]PAPE) is incorporated into BBC membranes, HDL3 stimulation induces the formation of PMME, PDME, PC and lyso-PC and the release of [14C]arachidonic acid, which correlates with the previous production of lyso-PC, suggesting that HDL3 stimulates a PLA2 that can release polyunsaturated fatty acids (PUFA). Both PEMT and PLA2 activities depend on a HDL3 concentration in the range 0-50 micrograms/ml and are strictly dependent on HDL3 binding, because HDL3 modified by tetranitromethane is no longer able to bind to specific receptors and to trigger PEMT and PLA2 activation. Moreover, HDL3 prelabelled with [14C]PAPE can stimulate PDME and lyso-PC synthesis in BBC membranes in the presence of S-adenosylmethionine, suggesting that HDL3 can supply BBC membranes in polyunsaturated PE and can activate enzymes involved in PE N-methylation and PUFA release. The results support the hypothesis of a close relationship between HDL3 binding, PE methylation and PUFA release, and suggest that the PC pool arising from PE could be used as a pathway for the supply of PUFA to the brain.

Animals↗
PubMed1996

T-Cell co-stimulation by the CD28 ligand B7 is involved in the immune response leading to rejection of a spontaneously regressive tumor.

Cell variants from experimental tumors may lose their tumorigenicity or give rise to tumors that regress after a short period of progression in immunocompetent syngeneic animals. Rejection of these tumor cells is often T-cell-dependent. It has recently been reported that, besides the specific signal delivered through the clonogenic receptor, T-cell activation requires a co-stimulatory signal, delivered through its CD28 receptor by B7-1 and/or B7-2 molecules expressed at the surface of the antigen-presenting cells. CTLA4Ig, a fusion molecule that specifically inhibits B7-1 and B7-2 binding to their receptors of T cells, was used to investigate the role of B7 in the spontaneous regression of the tumors induced in syngeneic rats by REGb cells, a regressor cell line established from a chemically induced colon carcinoma. When rats received either 1 or 3 CTLA4Ig injections, REGb tumors grew 3 or 7 times larger than in control animals, respectively. However, in most animals, single or repeated CTLA4Ig injections delayed rather than suppressed REGb tumor rejection. Antibodies to CTLA4Ig appeared in treated rats and could explain this transient effect. Neither REGb cells nor freshly isolated MHC class-II+ antigen-presenting cells infiltrating REGb tumors expressed B7, establishing that the target of CTLA4Ig was not located inside the tumor. In contrast, MHC class-II+ B7+ accessory cells were found in the tissue, rather than the tumor itself, was the site of tumor-antigen presentation to tumor-specific T cells. These results establish the role of B7/CD28 co-stimulation pathway in the control of a spontaneously regressive tumor.

Abatacept↗
PubMed1996

Colon-cancer cell variants producing regressive tumors in syngeneic rats, unlike variants yielding progressive tumors, attach to interstitial collagens through integrin alpha2beta1.

Nine clones of tumor cells, derived from a single rat colon carcinoma, were analyzed for their adhesive properties and in vivo growth patterns. Four clones (denoted REG) gave rise to regressively growing tumors. Cells from the 4 REG clones attached significantly better to collagen types I and III than did cells from the 5 clones (denoted PRO) which grew progressively in vivo. In contrast, REG and PRO clones did not differ in their attachment to collagen type IV, laminin or fibronectin. The attachment of REG cells to collagen was dependent on Mg2+, but not Ca2+. Monospecific rabbit IgG to rat integrin beta 1-chain inhibited REG cell attachment to collagen, demonstrating involvement of a beta 1 integrin in this process. PRO and REG cells expressed an underglycosylated beta 1 chain (Mr approximately 105,000) that was somewhat smaller than beta 1-chains described previously on rat fibroblasts and hepatocytes (Mr approximately 115,000). Monoclonal IgG to rat integrin alpha 2 beta 1, but not to alpha 1 beta 1, readily inhibited REG cell attachment to collagen, demonstrating the involvement of integrin alpha 2 beta 1. However, beta 1 and alpha 2 integrin subunits were found in purified glycoproteins from both PRO and REG cells. This suggests that alpha 2 beta 1 integrin is expressed by both cell variants, but is functional as a collagen receptor on REG cells only. In this system of tumor-cell variants, the clear-cut differences in attachment to interstitial collagens of the 9 clones suggest a possible relationship between this attachment and the capacity to induce progressive or regressive tumors.

Amino Acid Sequence↗
PubMed1996

Cloning and and characterization of hydrophobins-encoding cDNAs from the ectomycorrhizal basdiomycete Pisolithus tinctorius.

Major alterations of fungal gene expression are induced by the development of ectomycorrhiza, a symbiosis between tree roots and filamentous fungi. Several cDNAs corresponding to highly expressed transcripts of the Basidomycete Pisolithus tinctorius (Pt) were isolated from symbiotic tissues. Two of these abundant transcripts (hydPt-1 and hydPt-2) encoded polypeptides belonging to the hydrophobin (Hyd) family, a group of small cysteine-rich fungal proteins involved im morphogenesis and plant-fungus interactions. As shown for other Hyd, the hydPt-1 and hydPt-2 mRNAs were barely detectable in mycelium grown in liquid culture and highly accumulated in aerial hyphae. In addition, these transcripts were also abundant in eucalyptus globulus-Pt ectomycorrhiza in early stages of differentiation, during the colonisation of roots.

Amino Acid Sequence↗
PubMed1996

Coupling protein design and in vitro selection strategies: improving specificity and affinity of a designed beta-protein IL-6 antagonist.

The minibody is a designed small beta-protein conceived to enable the construction of large libraries of minimal discontinuous epitopes displayed on the surface of filamentous phage. The 61 residue molecule consists of three strands from each of the two beta-sheets of the variable domain of immunoglobulins packed face to face, along with the exposed H1 and H2 hypervariable regions. We have previously shown that from a minibody repertoire of more than 50 million molecules displayed on phage, we were able to select a minibody with micromolar affinity for human interleukin-6 that behaves as a selective cytokine antagonist. The minibody exposes a surface composed of two constrained loops, which provides the possibility of improving IL-6 binding and specificity by swapping the hypervariable regions, followed by further selection. We established experimental conditions for "stringent" selection such as monovalent phage display, competitive selection and epitope masking. Here, we show that by virtue of the optimization/selection process, we have isolated a minibody with improved antagonistic potency and greater specificity. Furthermore, using hIL-6 mutants carrying amino acid substitutions in distinct surface sites it was possible to carefully define the cytokine region that binds the minibody.

Amino Acid Sequence↗
PubMed1996

Eucalypt alpha-tubulin: cDNA cloning and increased level of transcripts in ectomycorrhizal root system.

Because symbionts are experiencing major morphological changes during ectomycorrhiza development, the expression of genes encoding cytoskeletal proteins is likely altered. To test this contention, we have cloned and characterized in a alpha-tubulin cDNA (EgTubA1) from Eucalyptus globulus. A poorly-aggressive isolate (No. 270) of the ectomycorrhizal basidiomycete Pisolithus tinctorius caused no changes in root transcript levels of EgTubA1, whereas a drastic up-regulation in its expression was observed between 3 to 4 days after contact with the aggressive isolate 441. This enhanced alpha-tubulin expression coincided with the increase lateral root formation induced by fungal colonisation. The changes in alpha-tubulin expression support a role for cytoskeleton components in ectomycorrhiza development.

Amino Acid Sequence↗
PubMed1996

Malignant fibrous histiocytoma of the mandible.

We report a case of MFH of the mandible in a 16-year-old girl. The mandible is a rare location of MFH of bone, with only 21 cases described in the literature. Clinical, pathologic, and radiologic features are discussed, with special emphasis on the unusual pathologic and radiographic features.

Adolescent↗
PubMed1996

High expression of NKR-P1 is not an absolute requirement for natural killer activity in BDIX rats.

NKR-P1 has been identified as a triggering structure selectively expressed on rat natural killer (NK) cells and adherent lymphokine-activated killer (A-LAK) cells. In vivo treatment with anti-NKR-P1 monoclonal antibody (mAb 3.2.3) was shown to induce complete inhibition of NK cytotoxicity and elimination of LAK cell precursors in Lewis and Fisher rat strains. We investigated the effects of mAb 3.2.3 in a colon tumor model in BDIX rats. Inoculation of animals with mAb 3.2.3 even at very high doses induced a strong but incomplete inhibition of NK cytotoxicity in nylon-wool-non-adherent spleen and peripheral blood cells. Generation of adherent A-LAK cells from their spleen precursors was also strongly by not fully inhibited. We also investigated the effect of treatment with mAb 3.2.3 on the tumorigenicity of the NK-sensitive REGb cell line. When subcutaneously inoculated in syngeneic animals, REGb cells induce tumors that first grow for 2 weeks, then spontaneously regress and disappear. In contrast with previous results using anti-asialoGM1, no significant difference in tumor growth was observed between rats treated with mAB 3.2.3 and control animals, even with a long-term treatment. In vitro, mAb 3.2.3 exhibited the same incomplete efficiency. Nylon-wool-non-adherent spleen cells treated with mAb 3.2.3 plus complement were completely free of 3.2.3(bright) cells, but retained a substantial NK activity and generated LAK cells after culture with IL-2. After an overnight incubation in standard medium of 3.2.3-depleted spleen cells, 3.2.3(bright) cells were partially recovered and the NK cytotoxic activity, as well as the generation of LAK cells, was significantly enhanced. These results suggest that a strong expression of NKR-P1 is not required for BDIX mononuclear cells to exhibit NK function and generate LAK cells under IL-2 activation.

Animals↗
PubMed1996

Meiotic segregation and recombination of the intergenic spacer of the ribosomal DNA in the ectomycorrhizal basidiomycete Laccaria bicolor.

The aim of this study was to clarify the inheritance of the nuclear ribosomal DNA (rDNA) in the ectomycorrhizal basidiomycete Laccaria bicolor S238N in order to resolve inter- and within-strain relationships in forest ecosystems. PCR amplification of the intergenic spacer (IGS) was carried out in the dikaryotic mycelium and its haploid progeny. In the dikaryotic mycelium, multiple amplification products were produced for the 25s/5s (IGS1) and 5s/17s (IGS2) intergenic spacers. The 4.5- and 4.0-kb fragments of IGS2 (haplotypes alpha and beta, respectively) were observed to occur in a 1:1 ratio within the haploid progeny as a result of divergent IGS haplotypes in the two separate nuclei. Recombinant monokaryons having both types of IGS2 occurred at a low frequency (6.5%; 60 kb per centimorgan) during meiosis. Haplotypes alpha and beta of IGS1 cross-hybridized forming heteroduplexes during the PCR temperature cycle. The two IGS1 haplotypes differed only by the repeat number of a TA2C3 motif and co-segregated with the IGS2 haplotypes. Heteroduplex formation and IGS polymorphism provide information that is helpful in distinguishing between introduced exotic L. bicolor S238N and indigenous populations of Laccaria spp. in forest ecosystems.

Agaricales↗
PubMed1996

Role of stromal myofibroblasts infiltrating colon cancer in tumor invasion.

In the normal colon, myofibroblasts are closely apposed to colonocytes where they deposit type IV collagen, the main basement membrane component. In colon carcinomas, this epithelial-mesenchymal association is physically disrupted, leading to the production of an abnormal, type IV collagen defective, basement membrane. Tumor-infiltrating myofibroblasts are migratory cells that accumulate at the invasive front of the colorectal carcinomas. They produce lytic enzymes able to degrade the basement membrane surrounding tumor glands. They also participate in the synthesis of the extracellular matrix components of the tumor stroma, which could subsequently alter the adhesive and migratory properties of the epithelial colon cancer cells. These results suggest that tumor-infiltrating myofibroblasts play a role in the invasion and metastasis of colorectal tumor cells.

Animals↗
PubMed1996

Oral budesonide as maintenance treatment for Crohn's disease: a placebo-controlled, dose-ranging study. Canadian Inflammatory Bowel Disease Study Group.

BACKGROUND & AIMS: Budesonide is a corticosteroid with high topical anti-inflammatory activity and low systemic activity due to rapid hepatic metabolism. The efficacy and safety of an oral controlled-release preparation of budesonide for maintenance of remission was evaluated in patients with ileal or ileocecal Crohn's disease. METHODS: In a double-blind, multicenter trial, 105 patients were randomly assigned to receive placebo or budesonide at doses of 3 or 6 mg daily for 1 year. The primary outcome measure was relapse defined by a Crohn's Disease Activity Index score of > 150 and a minimum increase of 60 points. RESULTS: Patients receiving 6 mg of budesonide had a median time to relapse or discontinuation of therapy of 178 days compared with 124 days in those receiving 3 mg of budesonide and 39 days in those receiving placebo. However, at 1 year, the rate of relapse in the group receiving 6 mg of budesonide was similar to the rates in the 3-mg and placebo groups. Basal plasma cortisol levels and incidence of corticosteroid-associated effects were similar in the three groups. CONCLUSIONS: Oral controlled-release budesonide (6 mg/day) was well tolerated and prolonged remission in Crohn's disease of the ileum and proximal colon, but this effect was not sustained at 1-year follow-up.

Administration, Oral↗
PubMed1996

The effect of lorazepam on memory and event-related potentials in heavy and light social drinkers.

To investigate the effects of heavy social drinking on sober cognitive processing, event-related potentials were recorded from 13 heavy social drinkers and 13 light social drinkers in the presence and absence of a pharmacological challenge (i.e., lorazepam). Event-related potentials were elicited by a task requiring continuous recognition memory for visually presented words. The heavy social drinkers exhibited shorter P2 latencies than the light social drinkers and decreased P300 latencies to correctly identified "old" words (i.e., words presented previously in the task) versus "new" words. Lorazepam increased motor reaction time to correctly identified old words and produced a deficit in recognition memory only in the light social drinkers. Light social drinkers had an increased P300 latency and a larger P300 amplitude to new words in the lorazepam treatment. The differences in cognitive functioning evident between heavy and light social drinkers were reflected in event-related potential deviations and appear to indicate a tolerance in heavy social drinkers to the effects of lorazepam.

Adult↗