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P Delmas

Publications and source records attributed to P Delmas.

At least 37 records · Page 2Linked to original sources
PubMed2001

Early detection of bone metastases in a murine model using fluorescent human breast cancer cells: application to the use of the bisphosphonate zoledronic acid in the treatment of osteolytic lesions.

A very common metastatic site for human breast cancer is bone. The traditional bone metastasis model requires human MDA-MB-231 breast carcinoma cell inoculation into the left heart ventricle of nude mice. MDA-MB-231 cells usually develop osteolytic lesions 3-4 weeks after intracardiac inoculation in these animals. Here, we report a new approach to study the formation of bone metastasis in animals using breast carcinoma cells expressing the bioluminescent jellyfish protein (green fluorescent protein [GFP]). We first established a subclone of MDA-MB-231 cells by repeated in vivo passages in bone using the heart injection model. On stable transfection of this subclone with an expression vector for GFP and subsequent inoculation of GFP-expressing tumor cells (B02/GFP.2) in the mouse tail vein, B02/GFP.2 cells displayed a unique predilection for dissemination to bone. Externally fluorescence imaging of live animals allowed the detection of fluorescent bone metastases approximately 1 week before the occurrence of radiologically distinctive osteolytic lesions. The number, size, and intensity of fluorescent bone metastases increased progressively with time and was indicative of breast cancer cell progression within bone. Histological examination of fluorescent long bones from B02/GFP.2-bearing mice revealed the occurrence of profound bone destruction. Treatment of B02/GFP.2-bearing mice with the bisphosphonate zoledronic acid markedly inhibited the progression of established osteolytic lesions and the expansion of breast cancer cells within bone. Overall, this new bone metastasis model of breast cancer combining both fluorescence imaging and radiography should provide an invaluable tool to study the effectiveness of pharmaceutical agents that could suppress cancer colonization in bone.

Animals↗
PubMed2001

[Arterial anatomy of the facial nerve at the stylo-mastoid foramen].

OBJECTIVE: To provide specific informations about the arterial related anatomy of the trunk of the facial nerve from the stylomastoid foramen to its bifurcation. METHODS: Dissection of 30 facial nerves in fresh cadavers after arterial casting with red-colored latex. RESULTS: A great anatomic variability does exist. The facial nerve is most often in relation to the stylomastoid artery which arises from the posterior auricular artery. The stylomastoid artery originates sometimes from the occipital artery or from the external carotid artery. In 19 cases of 30 the stylomastoid artery passes medially to the nerve, and 11 cases laterally. CONCLUSION: During parotid surgery, the main trunk of the facial nerve may be difficult to identify because of a large-caliber stylomastoid artery which can mask it. Therefore it is preferable to dissect this artery with caution, remaining at distance from the dangerous.

Arteries↗
PubMed2000

GABAA receptor phosphorylation and functional modulation in cortical neurons by a protein kinase C-dependent pathway.

GABA(A) receptors are critical mediators of fast synaptic inhibition in the brain, and the predominant receptor subtype in the central nervous system is believed to be a pentamer composed of alpha, beta, and gamma subunits. Previous studies on recombinant receptors have shown that protein kinase C (PKC) and PKA directly phosphorylate intracellular serine residues within the receptor beta subunit and modulate receptor function. However, the relevance of this regulation for neuronal receptors remains poorly characterized. To address this critical issue, we have studied phosphorylation and functional modulation of GABA(A) receptors in cultured cortical neurons. Here we show that the neuronal beta3 subunit is basally phosphorylated on serine residues by a PKC-dependent pathway. PKC inhibitors abolish basal phosphorylation, increasing receptor activity, whereas activators of PKC enhance beta3 phosphorylation with a concomitant decrease in receptor activity. PKA activators were shown to increase the phosphorylation of the beta3 subunit only in the presence of PKC inhibitors. We also show that the main sites of phosphorylation within the neuronal beta3 subunit are likely to include Ser-408 and Ser-409, residues that are important for the functional modulation of beta3-containing recombinant receptors. Furthermore, PKC activation did not change the total number of GABA(A) receptors in the plasma membrane, suggesting that the effects of PKC activation are on the gating or conductance of the channel. Together, these results illustrate that cell-signaling pathways that activate PKC may have profound effects on the efficacy of synaptic inhibition by directly modulating GABA(A) receptor function.

Animals↗
PubMed2000

Constitutive endocytosis of GABAA receptors by an association with the adaptin AP2 complex modulates inhibitory synaptic currents in hippocampal neurons.

Type A GABA receptors (GABA(A)) mediate the majority of fast synaptic inhibition in the brain and are believed to be predominantly composed of alpha, beta, and gamma subunits. Although changes in cell surface GABA(A) receptor number have been postulated to be of importance in modulating inhibitory synaptic transmission, little is currently known on the mechanism used by neurons to modify surface receptor levels at inhibitory synapses. To address this issue, we have studied the cell surface expression and maintenance of GABA(A) receptors. Here we show that constitutive internalization of GABA(A) receptors in hippocampal neurons and recombinant receptors expressed in A293 cells is mediated by clathrin-dependent endocytosis. Furthermore, we identify an interaction between the GABA(A) receptor beta and gamma subunits with the adaptin complex AP2, which is critical for the recruitment of integral membrane proteins into clathrin-coated pits. GABA(A) receptors also colocalize with AP2 in cultured hippocampal neurons. Finally, blocking clathrin-dependant endocytosis with a peptide that disrupts the association between amphiphysin and dynamin causes a large sustained increase in the amplitude of miniature IPSCs in cultured hippocampal neurons. These results suggest that GABA(A) receptors cycle between the synaptic membrane and intracellular sites, and their association with AP2 followed by recruitment into clathrin-coated pits represents an important mechanism in the postsynaptic modulation of inhibitory synaptic transmission.

Adaptor Protein Complex 2↗
PubMed2000

Muscarinic inhibition of calcium current and M current in Galpha q-deficient mice.

Activation of M(1) muscarinic acetylcholine receptors (M(1) mAChR) inhibits M-type potassium currents (I(K(M))) and N-type calcium currents (I(Ca)) in mammalian sympathetic ganglia. Previous antisense experiments suggested that, in rat superior cervical ganglion (SCG) neurons, both effects were partly mediated by the G-protein Galpha(q) (Delmas et al., 1998a; Haley et al., 1998a), but did not eliminate a contribution by other pertussis toxin (PTX)-insensitive G-proteins. We have tested this further using mice deficient in the Galpha(q) gene. PTX-insensitive M(1) mAChR inhibition of I(Ca) was strongly reduced in Galpha(q) -/- mouse SCG neurons and was fully restored by acute overexpression of Galpha(q). In contrast, M(1) mAChR inhibition of I(K(M)) persisted in Galpha(q)-/- mouse SCG cells. However, unlike rat SCG neurons, muscarinic inhibition of I(K(M)) was partly PTX-sensitive. Residual (PTX-insensitive) I(K(M)) inhibition was slightly reduced in Galpha(q) -/- neurons, and the remaining response was then suppressed by anti-Galpha(q/11) antibodies. Bradykinin (BK) also inhibits I(K(M)) in rat SCG neurons via a PTX-insensitive G-protein (G(q) and/or G(11); Jones et al., 1995). In mouse SCG neurons, I(K(M)) inhibition by BK was fully PTX-resistant. It was unchanged in Galpha(q) -/- mice but was abolished by anti-Galpha(q/11) antibody. We conclude that, in mouse SCG neurons (1) M(1) mAChR inhibition of I(Ca) is mediated principally by G(q), (2) M(1) mAChR inhibition of I(K(M)) is mediated partly by G(q), more substantially by G(11), and partly by a PTX-sensitive G-protein(s), and (3) BK-induced inhibition of I(K(M)) is mediated wholly by G(11).

Animals↗
PubMed2000

Bisphosphonates inhibit breast and prostate carcinoma cell invasion, an early event in the formation of bone metastases.

The molecular mechanisms by which tumor cells metastasize to bone are likely to involve invasion, cell adhesion to bone, and the release of soluble mediators from tumor cells that stimulate osteoclast-mediated bone resorption. Bisphosphonates (BPs) are powerful inhibitors of the osteoclast activity and are, therefore, used in the treatment of patients with osteolytic metastases. However, an added beneficial effect of BPs may be direct antitumor activity. We previously reported that BPs inhibit breast and prostate carcinoma cell adhesion to bone (Boissier et al., Cancer Res., 57: 3890-3894, 1997). Here, we provided evidence that BP pretreatment of breast and prostate carcinoma cells inhibited tumor cell invasion in a dose-dependent manner. The order of potency for four BPs in inhibiting tumor cell invasion was: zoledronate > ibandronate > NE-10244 (active pyridinium analogue of risedronate) > clodronate. In addition, NE-58051 (the inactive pyridylpropylidene analogue of risedronate) had no inhibitory effect, whereas NE-10790 (a phosphonocarboxylate analogue of risedronate in which one of the phosphonate groups is substituted by a carboxyl group) inhibited tumor cell invasion to an extent similar to that observed with NE-10244, indicating that the inhibitory activity of BPs on tumor cells involved the R2 chain of the molecule. BPs did not induce apoptosis in tumor cells, nor did they inhibit tumor cell migration at concentrations that did inhibit tumor cell invasion. However, although BPs did not interfere with the production of matrix metalloproteinases (MMPs) by tumor cells, they inhibited their proteolytic activity. The inhibitory effect of BPs on MMP activity was completely reversed in the presence of an excess of zinc. In addition, NE-10790 did not inhibit MMP activity, suggesting that phosphonate groups of BPs are responsible for the chelation of zinc and the subsequent inhibition of MMP activity. In conclusion, our results provide evidence for a direct cellular effect of BPs in preventing tumor cell invasion and an inhibitory effect of BPs on the proteolytic activity of MMPs through zinc chelation. These results suggest, therefore, that BPs may be useful agents for the prophylactic treatment of patients with cancers that are known to preferentially metastasize to bone.

Antineoplastic Agents, Phytogenic↗
PubMed2000

Calcium channel gating and modulation by transmitters depend on cellular compartmentalization.

Voltage-gated Ca2+ channels participate in dendritic integration, yet functional properties of Ca2+ channels and mechanisms of their modulation by neurotransmitters in dendrites are unknown. Here we report how pharmacologically identified Ca2+ channels behave in different neural compartments. Whole-cell and cell-attached patch-clamp recordings were made on both cell bodies and electrically isolated dendrites of sympathetic neurons. We found not only that Ca2+ channel populations differentially contribute to somatic and dendritic currents but also that families of Ca2+ channels display gating properties and neurotransmitter modulation that depend on channel compartmentalization. By comparison with their somatic counterparts, dendritic N-type Ca2+ currents were hypersensitive to neurotransmitters and G proteins. Single-channel analysis showed that dendrites express a unique N-type channel that has enhanced interaction with Gbetagamma. Thus Ca2+ channels in dendrites seem to be specialized elements with unique regulatory mechanisms.

Animals↗
PubMed2000

Facial nerve: vascular-related anatomy at the stylomastoid foramen.

We dissected 30 facial nerves in fresh cadavers after arterial casting with red latex to provide specific information about the arterial-related anatomy of the trunk of the facial nerve from the stylomastoid foramen to its bifurcation. We found that a wide anatomic variability does exist. The trunk of the facial nerve was in proximity to the stylomastoid artery, which originated from the posterior auricular artery in 70% of the specimens (21/30), from the occipital artery in 20% (6/30), and directly from the external carotid artery in 10% (3/30). The stylomastoid artery passed medially to the trunk of the facial nerve in 63 of the specimens (19/30) and laterally in 37% (11/30). Among these 11 specimens, 8 were large-caliber stylomastoid arteries. During parotid surgery, the main trunk of the facial nerve may be difficult to identify, because a large-caliber stylomastoid artery can mask it. Therefore, it is important to dissect this artery with caution.

Facial Nerve↗
PubMed2000

Platelet-osteosarcoma cell interaction is mediated through a specific fibrinogen-binding sequence located within the N-terminal domain of thrombospondin 1.

Approximately 20% of patients with osteosarcoma have metastatic disease in lungs or bones at diagnosis. The requirement of platelets in hematogenous dissemination of metastatic cells is now well established. Tumor cells interact with platelets and induce platelet aggregation. In this respect, metastatic potential of tumor cells correlates with their capacity to aggregate platelets in vitro. We have previously shown that thrombospondin 1 (TSP-1) is synthesized and expressed on the surface of MG-63 osteosarcoma cells and mediates platelet-osteosarcoma cell interaction. However, active sites mimicking the function of TSP-1 during platelet-osteosarcoma cell interaction are not known. In this study, a panel of antibodies directed against the N-terminal and C-terminal domains and type 1, type 2, and type 3 repeats of TSP-1 were first used to delineate the structural requirement for the binding of osteosarcoma cell surface-associated TSP-1 to platelets. A drastic inhibition of the platelet-aggregating activity of MG-63 cells was obtained in the presence of a monoclonal antibody directed against the N-terminal domain of TSP-1. Among a series of 16 synthetic peptides spanning the whole N-terminal domain of TSP-1, only synthetic peptide N12/I encompassing amino acid residues 151-164 of the N-terminal domain of TSP-1 inhibited the platelet-aggregating activity of MG-63 cells. Electron microscopy studies showed that peptide N12/I strongly inhibited platelet-osteosarcoma cell interaction. A polyclonal antibody directed against peptide N12/I specifically bound to the surface of MG-63 cells, recognized TSP-1 and drastically inhibited the platelet-aggregating activity of MG-63 cells. In addition, peptide N12/I specifically bound to fibrinogen and inhibited TSP-1/fibrinogen interaction. Overall, our results provide evidence that a fibrinogen-binding sequence located within the N-terminal domain of TSP-1 mediates the binding of osteosarcoma cell surface-associated TSP-1 to platelet-bound fibrinogen.

Amino Acid Sequence↗
PubMed2000

Mechanisms of action of bisphosphonates on tumor cells and prospects for use in the treatment of malignant osteolysis.

Malignant osteolysis is a common complication of many cancers, most notably breast cancer, prostate cancer, and multiple myeloma. Hypercalcemia, pain, and fractures are the main manifestations. Malignant osteolysis can be fatal or cause a rapid deterioration in quality of life. The underlying mechanism in tumor cem-mediated activation of osteoclasts, whose function is normally to resorb bone. It follows that pharmacological agents capable of inhibiting osteoclast activity, including bisphosphonates, are likely to be useful in the treatment of malignant osteolysis. Also, experimental evidence suggest that bisphosphonates act on the tumor cells themselves, either by inhibiting mechanisms involved in the development of bone metastasis (tumor invasion, adhesion of tumor cells to the bone matrix) or by inducing apoptosis of tumor cells. Many clinical trials have found bisphophonates to be effective in the treatment of complications due to malignant osteolysis. Based on these studies, bisphosphonates are now indicated to treat hypercalcemia and to prevent skeletal complications of metastatic breast cancer and myeloma, in a dosage of 1600 mg.d orally for clodronate or 90 mg every four weeks intravenously for pamidronate. Osteoclast inhibition is clearly the mechanism underlying the efficacy of bisphosphonates in these clinical trials. Recent clinical trials found that prophylactic bisphosphonates therapy in patients with nonmetastasic breast cancer decreased the incidence of bone metastases, thus supporting a direct effect of biphosphonates on tumor cells. However, conflicting experimental and clinical data have been reported, so that it remains uncertain whether bisphosphonates have anti-tumor effects in vivo in humans. Nevertheless, biphosphonates now have an undisputed place in the therapeutic armamentarium for cancer.

Animals↗
PubMed2000

[Hardiness, coping and quality of life of nurses working in intensive care units].

The goals of the study are two-folds: on the one hand, to examine the relations between hardiness, coping strategies and quality of life at work of french nurses working in the intensive care units; on the other hand, to examine the mediating effect of coping strategies between hardiness and quality of life at work. Data was collected using a self-administered questionnaire, anonymously filled by 137 nurses which represented 60% participation from the initial sample population. Maddi & Kobasa's theory (1984) of Hardiness is the foundation for the present study and Baron & Kenny's statistical model (1986) was used to determine the mediating effect of the coping strategies. Regression analysis demonstrated that positive reevaluation/problem solving strategies had a mediating effect between a sense of commitment, a sense of mastery and quality of life at work. These results prompted various propositions in order to improve nurses quality of life at work.

Adaptation, Psychological↗
PubMed2000

[Anterior hypospadias: Duplay or Mathieu?].

OBJECTIVE: The Mathieu urethroplasty is considered to be the reference operation for the treatment of anterior hypospadias. The vertical incision of the urethral groove, described by Snodgrass, has extended the field of indications for urethroplasty by tubularisation of the urethral plate (Duplay principle), by allowing it to be applied in almost every case of anterior hypospadias, The objective of this study was to compare results of Mathieu urethroplasty and Duplay urethroplasty for the treatment of anterior hypospadias. MATERIALS AND METHODS: 50 Mathieu urethroplasties and 50 Duplay urethroplasties were performed by the same operator over the same period (1996 to 1999). All urethral sutures were performed by inverted running sutures. Urine drainage was ensured by Foley catheter for 48 hours. For Duplay operations, the urethral plate was incised longitudinally in 17 out of 50 cases. Foreskin reconstruction was performed 41 out of 100 cases. RESULTS: The follow-up is 6 months to 4 years. Three children (6%) in each group had to be reoperated because of urethral complications (fistula, meatal stricture, urethroplasty dehiscence). CONCLUSION: Our results confirm those published in the literature. Duplay and Mathieu urethroplasties provide equivalent results in terms of the urethra. The appearance of the urinary meatus appears to be more satisfactory after Duplay urethroplasty. The Snodgrass modification allows tubularisation of the urethral plate to be performed even when it is narrow. Cover of the urethroplasty by a foreskin subcutaneous connective tissue pedicled flap reduces the fistula rate of Duplay urethroplasty to the same value as that observed after Mathieu urethroplasty, although it classically used to be higher.

Child↗
PubMed1999

Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell.

The potassium M current was originally identified in sympathetic ganglion cells, and analogous currents have been reported in some central neurons and also in some neural cell lines. It has recently been suggested that the M channel in sympathetic neurons comprises a heteromultimer of KCNQ2 and KCNQ3 (Wang et al., 1998) but it is unclear whether all other M-like currents are generated by these channels. Here we report that the M-like current previously described in NG108-15 mouse neuroblastoma x rat glioma cells has two components, "fast" and "slow", that may be differentiated kinetically and pharmacologically. We provide evidence from PCR analysis and expression studies to indicate that these two components are mediated by two distinct molecular species of K(+) channel: the fast component resembles that in sympathetic ganglia and is probably carried by KCNQ2/3 channels, whereas the slow component appears to be carried by merg1a channels. Thus, the channels generating M-like currents in different cells may be heterogeneous in molecular composition.

Animals↗
PubMed1999

betagamma dimers derived from Go and Gi proteins contribute different components of adrenergic inhibition of Ca2+ channels in rat sympathetic neurones.

1. Using perforated-patch recordings, we have examined the part played by endogenous G-protein subunits in the alpha2-adrenoceptor-mediated inhibition of N-type Ca2+ currents in sympathetic neurones. 2. Two components of ICa inhibition by noradrenaline were recorded: a prominent, high affinity and voltage-dependent pertussis toxin (PTX)-sensitive pathway and a minor, low affinity and mostly voltage-insensitive PTX-resistant pathway. 3. PTX-sensitive inhibition was reduced by microinjection of antibodies against either GalphaoA,B or Galphai1,2. The voltage-dependent fraction of inhibition was reduced by anti-Galphao but not by anti-Galphai antibody. 4. Antisense depletion of GalphaoA led to a marked reduction of noradrenaline-induced inhibition and voltage dependence. By contrast, Galphai depletion attenuated noradrenergic modulation without affecting the voltage dependence. 5. Expression of the betagamma-binding agents beta-adrenergic receptor kinase 1 (C-terminus, betaARK1C-ter) or Galphai1 with a Cys3 to Ser mutation partially prevented noradrenergic inhibition while alpha-transducin abolished it. Residual inhibition was mostly voltage independent in cells expressing betaARK1C-ter but was strongly reversed by depolarization in Galphai1 Cys3Ser-expressing cells. 6. Expression of the PTX-resistant Galphai1 Cys351Ile mutant in cells treated with PTX restored alpha2-adrenoceptor inhibition. This restored inhibition was weakly reversed by depolarization. Both the degree and voltage dependence of inhibition were correlated with the level of expression of the Galphai1 Cys351Ile subunit. 7. Our findings identify betagamma dimers associated with GalphaoA and Galphai as mediators of the PTX-sensitive alpha2-adrenoceptor-mediated inhibition of N-type Ca2+ channels. Different betagamma combinations may account for the differential voltage-dependent effects of Go and Gi on ICa.

Animals↗
PubMed1999

Harlequin fetus: a case report.

We report a case of harlequin fetus. This very rare cutaneous malformation is a severe form of congenital ichthyosis. This disorder is due to an inborn error of epidermal keratinization. Malformations of ears, nose, and hypoplasia of fingers or nails are seen. This affection is most often lethal.

Biopsy↗
PubMed1999

Does the endoscopic incision of ureteroceles reduce the indications for partial nephrectomy?

OBJECTIVE: To determine whether the endoscopic incision of ureteroceles reduces the indications for partial nephrectomy. PATIENTS AND METHODS: Between 1987 and 1996, endoscopic incision was used as the first-line treatment of 18 children (13 boys, five girls, aged 8 days to 6 months) with a duplex-system ureterocele diagnosed antenatally (15) or in the first weeks of life during the course of a urinary infection (three). Of the 19 ureteroceles (one bilateral), four were intravesical and 15 ectopic, according to the American Academy of Paediatrics classification. Vesico-ureteric reflux into the inferior pole of the kidney was present in 10 children, seven of whom had an ectopic ureterocele. A functioning upper pole was detected by intravenous pyelography (IVP) in half the intravesical and in a third of the ectopic ureteroceles. RESULTS: Endoscopic incision resulted in decompression and reduction of dilatation in 16 cases; three with inferior pole reflux resolved on control cystography, whilst in seven with an ectopic ureterocele, reflux into the upper urinary tract was induced by endoscopic incision. In three children with an ectopic ureterocele, renal function had improved at 3 months, as assessed by IVP. Endoscopic incision was the only treatment for half the intravesical and six of 15 ectopic ureteroceles. Overall, nephrectomy was required in four of 18 patients (three partial nephrectomies for persistent dilatation and one total nephrectomy). Five nonfunctioning, undilated upper poles with no reflux were left in place. Nine vesico-ureteric reimplantations for persistent or induced reflux were carried out using the Cohen technique. CONCLUSION: Endoscopic incision can allow the deferral of nephrectomy, facilitate lower urinary tract reconstruction and reduce the indications for partial nephrectomy, if it is accepted that a nonfunctioning, undilated renal pole with no reflux can safely be left in place.

Electrocoagulation↗
PubMed1999

Aberrant gene expression in epithelial cells of mixed odontogenic tumors.

Comparative investigations of odontogenic cells in normally forming teeth and tumors may provide insights into the mechanisms of the differentiation process. The present study is devoted to late phenotypic markers of ameloblast and odontoblast cells, i.e., proteins involved in biomineralization. The in situ expression of amelogenins, keratins, collagens type III and IV, vimentin, fibronectin, osteonectin, and osteocalcin was performed on normal and tumor odontogenic human cells. The pattern of protein expression showed some similarities between ameloblasts and odontoblasts present in normally developing human teeth and cells present in neoplastic tissues of ameloblastic fibroma, ameloblastic fibro-odontomas, and complex odontomas. Amelogenins (for ameloblasts) and osteocalcin (for odontoblasts) were detected in cells with well-organized enamel and dentin, respectively. In contrast, "mixed" cells located in epithelial zones of mixed odontogenic tumors co-expressed amelogenins and osteocalcin, as shown by immunostaining. The presence of osteocalcin transcripts was also demonstrated by in situ hybridization in these cells. Keratins and vimentin were detected in the same epithelial zones. Tumor epithelial cells were associated with various amounts of polymorphic matrix (amelogenin- and osteocalcin-immunoreactive), depending on the types of mixed tumors. No osteocalcin labeling was found in epithelial tumors. This study confirms that the differentiation of normal and tumor odontogenic cells is accompanied by the expression of some common molecules. Furthermore, the gene products present in normal mesenchymal cells were also shown in odontogenic tumor epithelium. These data may be related to a tumor-specific overexpression of the corresponding genes transcribed at an undetectable level during normal development and/or to an epithelial-mesenchymal transition proposed to occur during normal root formation. A plausible explanation for the results is that the odontogenic tumor epithelial cells are recapitulating genetic programs expressed during normal odontogenesis, but the tumor cells demonstrate abnormal expression patterns for these genes.

Ameloblastoma↗