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J Guiramand

Publications and source records attributed to J Guiramand.

At least 19 recordsLinked to original sources
PubMed2006

[Pelvic posterior exenteration with immediate colo-rectal anastomosis: is it justified and feasible in advanced stage ovarian carcinoma?].

PURPOSE: The aim of this study is to show that the removal of the rectum is not an obstacle to implement an optimal surgery in advanced epithelial cancer of the ovary. MATERIAL AND METHODS: Retrospective study on a population of 44 women with advanced epithelial cancer of the ovary. The surgery was realized between January 95 and July 03, and all surgeries required a posterior exenteration. This treatment was completed by chemotherapy for 36 of them. RESULTS: The median survival of this population is 36.6 months. 6/44 patients (13.6%) had post-operative complications. The completion of chemotherapy started after an average of 5.2 weeks after surgery. All the assessable patients (43/44) have an anal satisfactory continence. CONCLUSION: The posterior exenteration, when it's necessary, for advanced epithelial cancer of the ovary must not be an obstacle to obtain an optimal surgery. Anal continence is respected and there are no more complications. This surgical act is safe for the management of this pathology without delaying the others therapeutics and allowing a satisfactory quality of life.

Adenocarcinoma↗
PubMed2005

Long term morbidity of neoadjuvant chemoradiation for pancreatic head adenocarcinoma.

PURPOSE: To report the long term risks of neoadjuvant chemoradiation (NCRT) after duodenopancreatectomy (DP) for adenocarcinoma of the head of pancreas. METHODS: Between January 1996 and December 2002, 26 patients with biopsy-proven adenocarcinoma of the head of pancreas were treated by this combination of therapies. RESULTS: Two patients had delayed NCRT-related small bowel infarction: one died from superior mesenteric artery stenosis 36 months after DP without recurrence at laparotomy; there was one limited infarction 16 months after DP. CONCLUSIONS: Long term vascular morbidity after NCRT is significant.

Adenocarcinoma↗
PubMed2005

[Major hepatectomy for metastasis of colorectal cancer improves survival in the elderly].

OBJECTIVE: Assessing impact of major liver resection (LR) for hepatic metastasis of colorectal cancer (HMCC) on post operative courses and long term survival in the elderly. PATIENTS AND METHOD: Thirty-three consecutive patients aged over 70 years-old were treated in our institution for up to 3 resectable metachronous HMCC. Fifteen patients had major LR (9 right hepatectomy, 3 extended right hepatectomy, 3 left hepatectomy) without pre or postoperative chemotherapy (group 1) and 18 patients were exclusively treated by chemotherapy (group 2) because of high ASA score (ASA 3) or patients refusal. RESULTS: No patients died of another cause that colorectal cancer disease during observation time. All patients of group 2 died during observation time. Post operative mortality and morbidity of group 1 were respectively 0% and 33%. Survival at 1 and 2 years of group 1-2 were respectively 73-50% (P=0,04) and 47-15% (P=0,05). Median survival of group 1 and 2 were respectively 22 and 12 months (P=0,03). CONCLUSIONS: Major LR for HMCC could be proposed regardless the age. High ASA score, multiple (more than 4) metastasis location, evolutive disease could justify an exclusive medical approach.

Age Factors↗
PubMed2004

Gastric duplication in an adult mimicking mucinous cystadenoma of the pancreas.

Gastric duplication cyst (GDC) in an adult can have several clinical presentations. A review of the literature showed previously reported cases of GDC presenting as pancreatic pseudocyst or with greatly raised concentrations of carbohydrate antigen 19-9 (CA 19-9). It is often difficult to discriminate GDC from pancreatic cystic tumour, in particular pancreatic mucinous cystadenoma, in which concentrations of carcinoembryonic antigen and CA 19-9 are classically raised. This report describes an adult case of GDC mimicking a mucinous cystadenoma of the pancreas. This is the first report of a simultaneous increase in carcinoembryonic antigen and CA 19-9 in GDC in the absence of malignancy. Although few cases of carcinoma arising from a GDC having been reported, the production of oncofetal antigens raises the problem of a precancerous condition in long standing intestinal duplications. In this situation surgical resection must be performed.

Adult↗
PubMed2003

Long-term results of preoperative radiotherapy for 113 cases of UT3 and UT4 rectal cancer: a need for long-term follow-up.

PURPOSE: Eighty percent of local recurrence after resection of rectal adenocarcinoma classically occurs within two years of surgery. Pretherapeutic staging is frequently limited to clinical examination, although the accuracy of endoanal ultrasonography has been demonstrated. The aim of this study was to report the long-term results of preoperative radiation therapy and resection of pretherapeutic endoanal ultrasonography-staged T3 and T4 rectal adenocarcinoma. METHODS: This retrospective review analyzed a series of 113 patients who underwent radiation therapy followed by surgery. All patients underwent an endoanal ultrasonography. Median follow-up was 75 months. RESULTS: Fifty-seven percent of patients were pT3 or T4. Thirty-six percent had involvement of lymph nodes. Five-year rates of survival, local recurrence-free survival, and disease-free survival were 79, 73, and 68 percent, respectively. Ten-year rates were 65, 63, and 62 percent, respectively. Median time to detection of local recurrence was 39 months. Eight of ten local recurrences occurred after two years of follow-up. Eight of ten patients with local recurrence had pretherapeutic endoanal ultrasonography-staged N+ tumors. CONCLUSION: These results appear to justify a follow-up program for patients with pretherapeutic endoanal ultrasonography-staged N+ tumor. However, a minimum of seven years of follow-up is needed to obtain an accurate assessment of results.

Adenocarcinoma↗
PubMed2001

An endogenous adrenoceptor ligand potentiates excitatory synaptic transmission in cultured hippocampal neurons.

Noradrenergic inputs modulate hippocampal function via distinct receptors. In hippocampal neuronal cultures, mRNA expression of adrenoceptor subtypes is maintained from 1 day in vitro (DIV) to 22 DIV. Noradrenaline dose-dependently stimulates phosphoinositide (PI) breakdown in both immature and mature cultures through the activation of alpha1 receptors. At 22 DIV, basal PI breakdown depends on excitatory synaptic activity since it is decreased by tetrodotoxin or glutamate receptor antagonists. At 22 DIV, a similar decrease of basal PI breakdown is also observed with alpha1, alpha2 or beta adrenoceptor antagonists. These effects are not additive with that produced by tetrodotoxin. Adrenergic antagonists also strongly reduce spontaneous excitatory post-synaptic currents (sEPSC) as evidenced by whole cell recording. Therefore, in hippocampal cultures, excitatory transmission is modulated by a tonic activation of adrenoceptors probably produced by an endogenous ligand. Indeed, (i) the depletion of catecholamine pools by reserpine also decreases both basal PI metabolism and sEPSC; (ii) hippocampal neurons possess both tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase mRNAs, encoding enzymes required for catecholamine synthesis; and (iii) some hippocampal neurons show TH-immunoreactivity. TH-positive cells are also detected in E18 hippocampal sections. Thus, cultured hippocampal neurons synthesize and release an adrenergic-like ligand, which tonically potentiates excitatory synaptic transmission in mature cultures.

Adrenergic Uptake Inhibitors↗
PubMed2001

A bizarre giant leiomyoma.

We report the clinical and imaging features of a huge deep leiomyoma of the rectus abdominis treated surgically in an 84-year-old man. Hypotheses are put forward to elucidate the etiology of this enigmatic localization, apparently the first described in the literature.

Abdominal Neoplasms↗
PubMed1999

Potentiation of glutamatergic agonist-induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation.

We investigated the modulation by growth factors of phospholipase C (PLC)-linked glutamate receptors during in vitro development of hippocampal cultures. In defined medium, glial cells represent between 3 and 14% of total cell number. When we added basic fibroblast growth factor (bFGF) 2 h after plating, we found: (i) a neuroprotection from naturally occurring death for up to 5 days; (ii) a proliferation of glial cells from day 3; and (iii) a potentiation of quisqualate (QA)-induced inositol phosphate (IP) formation from 1 to 10 days in vitro (DIV) and 1S, 3R-amino-cyclopentane-1,3-dicarboxylate (ACPD) response from 3 to 10 DIV. The antimitotic cytosine-beta,D-arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection. Under these conditions, the early potentiation of the QA response (1-3 DIV) was not changed, while the ACPD and late QA response potentiations were prevented (5-10 DIV). Epidermal growth factor was not neuroprotective but it induced both glial cell proliferation and late QA or ACPD potentiation. Surprisingly, the early bFGF-potentiated QA-induced IP response was blocked by 6, 7-dinitro-quinoxaline-2,3-dione (DNQX), suggesting the participation of ionotropic (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (KA) receptors. The delayed bFGF-potentiated ACPD-induced IP response is inhibited by (S)-alpha-methyl-4-carboxyphenylglycine (MCPG), indicating possible activation of glial metabotropic receptors. These results suggest that, in hippocampal cultures, bFGF modulates AMPA and metabotropic glutamate receptors linked to the IP cascade, possibly in relation to the regulation of neuronal survival and glial cell proliferation, respectively.

Animals↗
PubMed1998

Synthesis and biological activity of glutamic acid derivatives.

In order to develop new specific glutamate analogues at metabotropic glutamate receptors, Diels-Alder, 1-4 ionic and radical reactions were performed starting from (2S)-4-methyleneglutamic acid. Preliminary pharmacological evaluation by measuring IP accumulation using rat forebrain synaptoneurosomes has shown that (2S)-4-(2-phthalimidoethyl)glutamic acid (3a), (2S)-4-(4-phthalimidobutyl)glutamic acid (3b) and 1-[(S)-2-amino-2-carboxyethyl]-3,4-dimethylcyclohex-3-ene-1-carbox ylic acid (8) presented moderate antagonist activities.

Animals↗
PubMed1996

Cadmium rapidly and irreversibly blocks presynaptic phospholipase C-linked metabotropic glutamate receptors.

Calcium ions (Cd2+) inhibit inositol phosphate (IP) formation elicited by glutamate (GLU) or K+ ions, without affecting carbachol (Carb)-induced IP response in 8-day-old rat forebrain synaptoneurosomes and synaptosomes. On the contrary, Cd2+ was almost ineffective in blocking GLU- and K(+)-responses in hippocampal neurones in culture. The mechanism of Cd2+ inhibition was thus examined in synaptoneurosomes. Extensive washing of synaptoneurosomes pretreated for 1, 5, 15, or 30 min by 100 microM Cd2+ did not modify the inhibitory effect of Cd2+ on GLU-, K(+)- and A23187-evoked IP formation or its lack of effect on Carb response. The later addition of a high affinity Cd2+ chelator (100 microM), N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) also did not reverse the inhibitory effect. TPEN, however, penetrates into synaptoneurosomes and efficiently displaces Cd2+ from the Fura-2-Cd2+ complex as shown by Fura-2 fluorescence recordings. TPEN is not easily removed from the intracellular space, as demonstrated by its ability to still block Cd(2+)-induced Fura-2 fluorescence increase after extensive washing. Pretreatment of synaptoneurosomes by this chelator did not prevent Cd2+ inhibition of GLU-induced IP formation. These data indicate that Cd2+ ions rapidly, irreversibly and extracellularly inhibit GLU-elicited IP formation in synaptoneurosomes or synaptosomes, but not in hippocampal neurones in culture. It is speculated that Cd2+ ions could allow one to distinguish the activity of presynaptic metabotropic glutamate receptors (mGLURs) linked to phosphoinositide metabolism from that of mGLURs located postsynaptically.

Animals↗
PubMed1996

A modulation of glutamate-induced phosphoinositide breakdown by intracellular pH changes.

The influence of intracellular pH (pHi) changes on the formation of inositol phosphate metabolites (IPs) produced by glutamatergic stimulation was studied in 8-day-old rat brain synaptoneurosomes. For this purpose pHi was measured using 2',7'-bis-(2-carboxyl)-5,6-carboxyfluorescein (BCECF) fluorimetric assay in parallel with the basal and receptor-mediated formations of inositol monophosphate (IP1) and inositol bisphosphate (IP2). We found that glutamate (1 mM), which induces a transient acidification (delta pH = -0.05), produces an identical accumulation of IP1 and IP2. K+ (30 mM), which provokes an alkalinization of the internal medium (delta pH = +0.22), mainly leads to the formation of IP1 metabolites. Paired combinations of glutamate with 1, 5 and 10 mM NH4+ finally result in an alkalinization of the intrasynaptoneurosomal medium. These combinations produce a strong decrease of the IP2 level concomitant with an increase of the IP1 formation, compared to the levels of IP1 and IP2 evoked by glutamate alone. The total amount of IPs (IP1 + IP2) produced by these combinations is not different from that obtained with glutamate alone. Paired combinations of carbachol with NH4+ produce an identical alkalinization to that produced by NH4+ alone. These combinations produce an increased IP1 accumulation, while the IP2 formation is slightly decreased. When the internal medium is acidified by diminishing the external concentration of Na+, the ratio IP1/IP2 produced after metabotropic glutamate receptor (mGluR) activation is shifted to lower values, while it is not affected for the muscarinic stimulation. These data suggest that the mGluR-associated pathway in synaptoneurosomes is sensitive to pHi shifts, while the muscarinic receptor-associated pathway is less altered when pHi is manipulated. It may be proposed that pH-sensitive inositol phosphate dephosphorylating systems, i.e. phosphatases, are associated with mGluRs in this preparation.

Animals↗
PubMed1995

Alternative splicing of the dopamine D2 receptor directs specificity of coupling to G-proteins.

Two isoforms of the dopamine D2 receptor have been characterized, D2L (long) and D2S (short), generated by alternative splicing from the same gene. They differ by an in-frame insert of 29 amino acids specific to D2L within the putative third intracytoplasmic loop of the receptor. We have previously demonstrated (Montmayeur, J.-P., Guiramand, J., and Borelli, E. (1993) Mol. Endocrinol. 7, 161-170) that D2S and D2L, although presenting very similar pharmacological profiles, couple differently to the alpha-subunit of guanine nucleotide-binding regulatory proteins (G-proteins). In particular, D2L, but not D2S, requires the presence of the alpha-subunit of the inhibitory G-protein (G alpha i2) to elicit greater inhibition of adenylyl cyclase activity. The insert present in D2L must therefore confer the specificity of interaction with G alpha i2. Thus, we introduced substitution mutations within the D2L insert. These mutant receptors were expressed in JEG3 cells, a G alpha i2-deficient cell line, scoring for those presenting an increased inhibition of adenylyl cyclase by dopamine. Our analysis identified two mutants, S259/262A and D249V, with these properties. These results clearly show that the insert present in D2L plays a critical role in the selectivity for the G-proteins interacting with the receptor.

Adenylyl Cyclase Inhibitors↗
PubMed1993

Effect of thiol reagents on phosphoinositide hydrolysis in rat brain synaptoneurosomes.

Some divalent ions, such as Cd2+ and Zn2+, are able to stimulate phosphoinositide (PI) breakdown and to inhibit receptor-mediated PI metabolism. These ions are also known to react with the free -SH groups of proteins. This prompted us to investigate the effects of more potent sulphydryl reagents, Hg2+ and p-chloromercuric benzosulphonic acid (PCMBS), on the inositol phosphate (IP) accumulation triggered by the neuroactive substances: glutamate, carbachol and K+, using synaptoneurosomes from 8-day-old rat forebrains. Hg2+ and PCMBS, depending on their concentration, had two distinct effects on IP accumulation: at low doses, Hg2+ (from 1 to 10 microM) and PCMBS (0.1 mM) by themselves stimulated PI breakdown, inhibited glutamate-elicited IP accumulation and had additive effects with respect to carbachol-induced IP stimulation. At higher doses, Hg2+ (from 0.01 to 1 mM) inhibited both basal and neuroactive substance-stimulated IP accumulation. PCMBS (1 mM), provoked only an inhibition of the agonist-stimulated IP formation. Monitoring membrane potential and intracellular Ca2+ with the fluorescent dyes diSC2(5) and fura2, respectively, indicated that these mercurials could strongly depolarize the synaptoneurosomal membrane and produce a Ca2+ influx dependent on extracellular Ca2+. The stimulatory effects of low concentrations of mercurials on PI turnover could be linked to the depolarization they provoke and the subsequent Ca2+ rise, which in turn is known to stimulate some phospholipase C enzymes. The inhibitory effects observed at high concentrations might be due to a loss of activity of proteins involved in PI breakdown, as all receptor-mediated IP accumulations were inhibited.

4-Chloromercuribenzenesulfonate↗
PubMed1993

Preferential coupling between dopamine D2 receptors and G-proteins.

The D2 dopamine receptor, an inhibitor of adenylyl cyclase, belongs to the family of seven transmembrane domain G-protein-coupled receptors. This receptor is encoded by two mRNAs produced from the same gene by alternative splicing, here referred to as D2L and D2S. The resultant proteins are identical except for an insertion of 29 amino acids in the putative third intracytoplasmic domain. This domain has been shown to be important for the coupling of this family of receptors to G-proteins. We have previously shown that there is differential inhibition of the adenylyl cyclase activity when these two receptors are produced in JEG3 cells; D2S is more efficient than D2L. To understand the molecular basis of such differential activity, we analyzed the G-proteins expressed in these cells. Here we show that G alpha i2 is absent in this cell line. Moreover, it is possible to restore the same inhibitory activity obtained by D2S when an expression vector encoding this alpha-subunit is cotransfected with D2L. In addition, transfections of the two receptors in a recipient cell line containing the three G alpha i subtypes confirm that the two receptors behave similarly. We conclude that the 29-amino acid insertion present in D2L allows it to interact specifically with G alpha i2. These data suggest that in vivo the function of activated D2 receptors is exerted by specific interactions with Gi-protein subtypes.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Dithiotreitol specifically inhibits metabotropic responses of glutamate and depolarizing agents in rat brain synaptoneurosomes.

Dithiotreitol (DTT), a sulfhydryl reducing agent inhibits in a dose-dependent manner the inositol phosphates (IPs) accumulation responses evoked by glutamate and potassium without affecting that of carbachol in rat forebrain synaptoneurosomes. Furthermore, DTT neither provokes a depolarization of the membrane, nor increases the internal calcium concentration. Depolarization and internal calcium rise are known to stimulate IPs production. Moreover, DTT does not modify the depolarizing effect and the calcium rise elicited by glutamate and potassium. In addition, the antioxidant compounds 2-aminoethylisothiouronium bromide (AET) and ascorbic acid have no effect on the basal and stimulated IPs accumulation. Thus, it is concluded that: (1) two distinct transduction pathways exist, one stimulated by glutamate and depolarizing agents and the other one by cholinergic agonists; (2) DTT produces its inhibition by reducing disulfide bridges likely at the level of proteins of the phosphoinositide transduction mechanism.

Animals↗
PubMed1992

Binding properties of 3-[125I]iodophencyclidine, a new radioligand for N-methyl-D-aspartate-gated ionic channels.

The binding properties of the 125I-labeled phencyclidine derivative N-[1-(3-[125I]iodophenyl)cyclohexyl]piperidine (3-[125I]iodo-PCP), a new ligand of the N-methyl-D-aspartate (NMDA)-gated ionic channel, were investigated. Association and dissociation kinetic curves of 3-[125I]iodo-PCP with rat brain homogenates were well described by two components. About 32% of the binding was of fast association and fast dissociation, and the remaining binding was of slow association and slow dissociation. Saturation curves of 3-[125I]iodo-PCP also were well described using two binding sites: one of a high affinity (KDH = 15.8 +/- 2.3 nM) and the other of a low affinity (KDL = 250 +/- 40 nM). 3-Iodo-PCP inhibited the binding of 3-[125I]iodo-PCP with inhibition curves that were well fitted by a two-site model. The binding constants (KiH, BmaxH; KiL, BmaxL) so obtained were close to those obtained in saturation experiments. Ligands of NMDA-gated ionic channels also inhibited the binding of 3-[125I]iodo-PCP with two constants, KiH and KiL. There was a very good correlation (r = 0.987) between the affinities of these ligands to bind to NMDA-gated ionic channels and their potencies to inhibit the binding of 3-[125I]iodo-PCP with a high affinity. Moreover, the regional distribution of the high-affinity binding of 3-[125I]-iodo-PCP paralleled that of tritiated N-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP). In contrast to that of [3H] TCP, the binding of 3-[125I]iodo-PCP to well-washed rat brain membranes was fast and insensitive to glutamate and glycine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗