PubMed Health⌕ Search

Biomedical subjects

D Jambou

Publications and source records attributed to D Jambou.

18 recordsLinked to original sources
PubMed2004

[Repeated thromboembolism during pregnancy with constitutional antithrombin deficiency].

We report the case of a twenty-three-year old woman with constitutional antithrombin deficiency, who had oral anticoagulation since she was four years old. During her first pregnancy, after the introduction of unfractionated heparin prophylactic therapy, she presented a first venous thromboembolism at nine weeks, and a second one with low-molecular-weight heparin therapy at nineteen weeks. Because of a severe antithombin deficiency, regular infusions of antithrombin concentrates were necessary until delivery to ensure effective anticoagulation by heparin. Patients with antithrombin deficiency have a very high risk of venous thromboses during the pregnancy and post-partum. We discuss the significant points of management for this period.

Adult↗
PubMed1999

Effects of low density and high density lipoproteins isolated from non-insulin dependent diabetic patients on prostaglandin secretion by mouse macrophage cell line P388D1.

We have previously shown that low-density (LDL) and high-density (HDL) lipoprotein from healthy subjects can promote in vitro prostaglandin (PG) release by murine macrophages. In this pilot study, we have measured PG production induced by lipoproteins of six diabetic patients with poor metabolic control, compared to five healthy controls. Plasma lipoprotein levels were similar in both groups. Lipoprotein fractions were purified by sequential ultracentrifugation. After lipoprotein incubation with cells, supernatants were extracted and PG quantified by HPLC. In presence of LDL, in control subjects, there was an increase in total PG production, mainly due to thromboxane B2 (TxB2). In diabetic patients, the secretion pattern was similar. In presence of HDL, in control subjects, total PG secretion was also increased, but it was balanced between TxB2 and prostacyclin. In diabetic patients, at low HDL concentration (10 mg/l) the secretion was mainly due to TxB2, while at higher HDL concentrations (100 mg/l). the secretion was balanced between TxB2 and prostacyclin. Comparison of means of areas under curve for the two groups studied showed that LDL increased all PG secretion in diabetic patients compared to controls (P < 0.05 for PGF2alpha), while HDL increased all PG secretion in controls compared to diabetic patients, except PGF2alpha. Our work suggests a key role of LDL in TxB2 secretion in diabetic patients, which is a major proaggregant and vasoconstrictive agent. There was also an increased secretion of all PG in diabetic patients.

Animals↗
PubMed1999

Fasting, postprandial, and post-methionine-load homocysteinaemia and methylenetetrahydrofolate reductase polymorphism in vascular disease.

Hyperhomocysteinaemia is an independent risk factor for cardiovascular disease. The C677T mutation of the methylenetetrahydrofolate reductase (MTHFR) is a common genetic cause of increased homocysteine (HCY) levels. Post-methionine-load HCY concentrations allow identification of certain cases of hyperhomocysteinaemia not demonstrated by fasting levels. This study investigated the relationship between MTHFR polymorphism and (1) fasting HCY levels (77 patients); (2) post-methionine HCY levels (54 patients); and (3) postprandial HCY concentrations (36 patients) in cardiovascular disease. As expected, mean fasting HCY value was higher in the +/+ patients. Moreover, patients who were homozygous for the mutation exhibited significantly increased mean post-methionine-load HCY; in contrast, literature results are conflicting. Mean postprandial HCY, which is not known to be increased in controls, was also increased in the (+/+) patients, although the difference did not reach statistical significance, probably owing to the small size of the sample. MTFHR polymorphism is known to be aggravated by a drop in circulating folate. Additional risk factors may be more prevalent in patients with cardiovascular disease.

Adolescent↗
PubMed1998

[Rapid decrease of serum endothelin-1 levels after treatment with ACE inhibitors in chronic cardiac failure].

Circulating endothelin-1, a very strong peptide vasoconstrictor first discovered in 1988, is raised in cardiac failure. This increase contributes to the deleterious effects of cardiac failure. Although specific anti-endothelin drugs are under development in this condition, the effects of more commonly used drugs on circulating endothelin-1 levels are not well known. The aim of this study was to evaluate the effects of ACE inhibitor therapy on plasma endothelin-1 levels in cardiac failure. The plasma endothelin-1 levels were measured in 24 patients (stages III and IV of the NYHA classification), before and after treatment with angiotensin converting enzyme inhibitor (Captopril: test doses, then 75 mg/day). A control group of 10 paired patients was used to shake off the effects of bed rest and hospital salt-free diet. The initial endothelin-1 levels were high but equivalent in the control and study groups: 9.13 +/- 1.87 fmol/mL vs 8.98 +/- 1.92 fmol/mL. Plasma endothelin-1 decreased significantly in the study group 72 hours after beginning ACE inhibitor therapy (7.44 +/- 1.95, p < 0.02) but remained higher than normal (p < 0.01), whereas the values in the control group remained the same. This study demonstrates a decreases in plasma endothelin-1 levels 72 hours after onset of ACE inhibitor therapy in patients with stable severe cardiac failure. This results, already suggested by many experimental studies and certain ancillary clinical trials, could explain some of the beneficial effects of ACE inhibitors in this condition.

Adult↗
PubMed1997

[Cerebral vascular complication of hyperhomocysteinemia. Controlling thromboembolic complications with folates].

BACKGROUND: Young patients who experience cardiovascular events may have raised levels of homocysteine. There may be several causes for this hyperhomocysteinemia. CASE REPORT: Cerebrovascular disease occurred in a 40-year-old female smoker with hyperhomocysteinemia. This patient subsequently had several episodes of thromboembolism involving the brain and lower limb arteries. Prothrombin concentration was difficult to control with antivitamin K anticoagulants. Investigations to identify a genetic cause of hyperhomocysteinemia revealed that she was homozygous for the C677T mutation on the methylenetetrahydrofolate reductase gene. There was no G1691A mutation of the factor V gene, a risk factor for familial thrombosis. Supplementation with folic acid successfully halted episodes of thromboembolism (follow-up 2 years) and prothrombin levels stabilized under treatment. DISCUSSION: The C677T mutation, which is common in the general population (15.7%), cannot explain the effect of folate supplementation alone. Other mutations affecting homocysteine metabolism could have a potentializing effect on vascular events.

Adult↗
PubMed1997

Evaluation of the ABX Cobas Vega automated hematology analyzer and comparison with the Coulter STKS.

An evaluation of the new automated hematology analyzer was performed in comparison with the Coulter STKS on 1,694 blood samples coming from the different departments of Nice University Hospital. The Cobas Vega showed very satisfactory results in terms of repeatability, reproducibility and linearity. Correlation with the STKS was excellent with the exception of the following parameters: red blood cell distribution index and the absolute values for eosinophils and basophils. Two qualities were particularly appreciable: absence of leukocyte carryover, and stability of the complete blood count and leukocyte differential count over a long period. Analysis of qualitative flags showed that the overall blood smear review rate was 47% for the Cobas Vega, not forgetting that optical microscopy detects 37% of all abnormalities. The STKS's review rate was 49.5%. Flags commonly concerned the granulocytic lineage, 61% for the STKS and 48% for the Vega, with a false positive rate of 43.4% for the STKS compared with 22% for the Vega. The opposite phenomenon was observed with the flag for atypical lymphocytes which represented 11% of flags for the STKS and 25.6% for the Vega, with a false positive rate of 25.5% for the STKS and 34% for the Cobas Vega. This may be explained by the fact that lymphocyte abnormalities sometimes generated "granulocytic" flags on the STKS. Studies of the false negative rate carried out using light microscopy on 505 blood samples without flags on either system, detected the presence of a slight myelemia, and a few hyperbasophilic lymphocytes or plasmocytes in 18.6% of all cases. Finally, the Cobas Vega's practicality was greatly appreciated and there was no trouble with breakdowns throughout the whole period of its use.

Autoanalysis↗
PubMed1993

Effect of human native low-density and high-density lipoproteins on prostaglandin production by mouse macrophage cell line P388D1: possible implications in pathogenesis of atherosclerosis.

Macrophages have been shown to play a key-role in the development of atherosclerotic lesions. Monocyte attraction and activation in the arterial wall lead to foam cell formation, cholesterol accumulation and secretion of inflammation mediators. Among macrophage secretions, prostacyclin and thromboxane are prostaglandins involved in the regulation of coagulation and vascular permeability. In this study, we have evaluated the effects of human native low-density and high-density lipoproteins on macrophage prostaglandin production (P388D1 mouse cell line). Lipoprotein fractions were purified from venous blood of healthy volunteers by sequential ultracentrifugation. After lipoprotein incubation with cells, supernatants were extracted and prostaglandins quantified by high-performance liquid chromatography. Our technique allows the determination of the main classes of prostaglandins. In the presence of low-density lipoproteins, time-course study showed an increase in total prostaglandin production within 10 min (50 times basal secretion level). This increase was dose-dependent. A steady-state was obtained at 20 mg protein LDL/1. Stimulation of thromboxane B2 and prostacyclin was predominant, with a main effect on the proaggregant thromboxane. Production of the proinflammatory PGF2 alpha and the immunoregulatory PGE2 was lower. In the presence of high-density lipoproteins, P388D1 cells also increased their total prostaglandin secretion at 30 min, in a dose-dependent manner. This increase was directly related to a stimulation of prostacyclin, with no significant effect on thromboxane. Our results demonstrate that normal low-density lipoproteins can stimulate macrophage prostaglandin secretions, with putative deleterious effects on the arterial wall, in particular thrombus formation. On the other hand, high-density lipoproteins, by mainly stimulating prostacyclin, could theoretically have a beneficial influence.

Animals↗
PubMed1993

[Mediators of the vascular endothelium as markers of myocardial ischemia and reperfusion].

Myocardial ischaemia may occur during spasm or thrombosis of the coronary arteries. The vascular endothelium plays an essential role in the lesions observed during ischaemia and myocardial reperfusion by the intermediary of the numerous endothelium-derived vasoactive factors. These include the "endothelium-derived relaxing factors" (EDRFs) nitrous oxide, prostacyclin, which are vasodilators and platelet antiaggregants ant the "endothelium-derived contracting factors" (EDCFs), endothelin, PGH2, oxygen-free radicals which are vasoconstrictive. The endothelial cells also produce the platelet activating factor and factors essential for coagulation. The metabolism and biological properties of these different mediators are reviewed. During the phenomena of myocardial ischemia-reperfusion, endothelial regulation is activated by tissue hypoxia and reduction of coronary flow and perfusion pressure. This regulation also depends on the functional state of the arteries (macroscopically normal or pathological). These vasomotor phenomena are associated with the effects of platelet aggregation and myocardial accumulation of neutrophil polynuclear blood cells. During the second phase of reperfusion cellular lesions are produced by the generation of cytotoxic oxygen-free radicals. Assays of mediators present a clinical interest when the modalities of sampling have been fixed (systemic blood samples or during cardiac catheterisation, sites of sampling, choice of timing of sampling with respect to the biological half lives of the mediators). Determining a correlation between the in vitro biological effects on those in isolated organs and clinical data has become possible with the improvement in techniques of sampling and the increasing collaboration between biologists and clinicians.

Endothelins↗
PubMed1991

In vitro and in vivo ciprofloxacin pharmacokinetics in human neutrophils.

Early in vitro investigations have shown that ciprofloxacin is concentrated within human neutrophils (polymorphonuclear leukocytes [PMNs]) at between 3 and 11 times the extracellular concentration. The elution of ciprofloxacin from cells is relatively rapid when the extracellular concentration is reduced. In order to estimate the in vivo intracellular penetration of ciprofloxacin and to determine its intracellular pharmacokinetics, PMNs were recovered from blood samples drawn from healthy volunteers at different times during a 24-h period after they were given a 750-mg oral dose. High-performance liquid chromatographic determination of ciprofloxacin in serum and cells showed that the intracellular/serum ratio was 3.7 at 1.5 h (maximum concentration of drug in serum), 5.7 at 12 h, and 20 at 24 h. The area under the curve ratio was 3.73. The mean elimination half-lives of ciprofloxacin were 3.7 and 6.2 h in serum and PMNs, respectively. These data show that in vivo findings are in agreement with in vitro findings. The large uptake of ciprofloxacin by PMNs combined with a prolonged intracellular half-life described under the conditions of human therapy should provide the basis for the use of ciprofloxacin in infections caused by susceptible intracellular bacteria.

Adult↗
PubMed1990

HLA DR and DQ expression on human retinal pigment epithelial cells in vitro.

In a previous immunohistopathological study, we demonstrated a deviant expression of class II antigens on the uveal pigment epithelial cells of patients with proliferative diabetic retinopathy. The mechanisms triggering this abnormal expression by epithelial cells are not well known, and we tried to induce this phenomenon on primary cultures of human retinal pigment epithelial (RPE) cells. Confluent RPE-cell monolayers were supplemented with several biological or chemical reagents [recombinant interferon gamma, phytohemagglutinin A-P (PHA-P), phorbol-myristate acetate (PMA), recombinant interleukin-2, fibroblast growth factor (FGF), Insulin], to investigate their ability to induce HLA DR and DQ expression. On days 1, 3 and 5 after stimulation, the cells were incubated with monoclonal antibodies directed against human class II antigens: all reagents used failed to induce class II antigen: all reagents used failed to induce class II antigen expression. However, on day 7, we demonstrated the presence of numerous positive HLA DR and HLA DQ cells stimulated by gamma interferon, the percentages being closely related to the dose of this lymphokine. These findings, together with those of other investigators and our previous work on uveal pigmented epithelial cells in diabetic patients, may shed light on the exact implication of RPE in many poorly documented ocular diseases.

Aged↗
PubMed1990

Effect of N-acetyl-aspartyl-glutamate (Naaga) on in-vitro leukotriene synthesis by macrophage cell line P388D1.

The magnesium salt of N acetyl-aspartyl glutamic acid (Naaga), used in ophthalmic allergies, is a synthetic dipeptide analogue of a natural peptide found in mammalian brains. It has been shown in vitro that Naaga inhibits complement activation, mast-cell degranulation and leukotriene anaphylactic release. In order to verify Naaga's action on leukotriene production, we used the macrophage cell line P388D1 activated by calcium ionophore A23187. Leukotriene determination was performed by high-performance liquid chromatography. It was found that Naaga inhibits 15 to 80% macrophage eicosanoid secretion (10(-9) M to 10(-2) M), acting mainly on LTC4-D4-E4 synthesis. Naaga was as potent as the leukotriene inhibitor nordihydroguaiaretic acid and as dexamethasone in this model. This inhibition of leukotriene secretion could partially explain the in-vivo antiallergic effects of Naaga.

Animals↗
PubMed1990

Cytotoxicity studies in ophthalmology.

Ocular tissues and cells are more and more in direct contact not only with drugs but also with biomaterials, such as contact lenses, intraocular implants, corneal shields, and the cell reactivity study is an indispensable step before any clinical and human utilization. The cell toxicity may be direct, by cell membrane damaging, metabolic disturbance, or indirect by mitosis or cell differentiation blocking. In order to evaluate the unwanted effects, cell cultures are performed according to the drug or to the biomaterial to be tested: conjunctival and corneal epithelial cells, lens epithelium, ciliary processes epithelium... In this report, the cytotoxicity of three substances were evaluated on corneal cultured cells: Benzalkonium chloride (BAK), an ophthalmic preservative; Novesine (Oxybuprocaine + BAK), local anaesthetic; Neosynephrine (Phenylephrine chlorydrate), a commonly used mydriatic in ocular surgery. Results of cell counting (cell viability) are given according to curves and histograms (percentage of dead cells depending on time and doses). These data are discussed according to the different mechanisms of action of the three drugs BAK and Oxybuprocaine were found to exert a more direct cell toxicity whereas phenylephrine chloride acted indirectly by causing the sloughing of the cell monolayer.

Anesthetics, Local↗
PubMed1990

[Influence of some antibiotics on eicosanoid production by human macrophages in vitro].

Non antibacterial effects of antibiotics are presently investigated by several authors. They estimate the effects of different molecules on polynuclear chemotaxis, cytokine production or macrophage activity. In this experiment we have studied the effects of two betalactams, two macrolides, a fluoroquinolone and a tetracycline on eicosanoïd production by stimulated human macrophages in vitro. All evaluated antibiotics are able to modify the prostaglandin and/or leukotriene production. Taking into account the immunomodulative and inflammatory properties of the eicosanoids, the variation of their production could be relevant in clinical practice.

Anti-Bacterial Agents↗
PubMed1989

[Effects of antibiotics on the production of prostaglandins by macrophages in vitro].

Many reports have pointed out a relationship between antibiotics and immunity. It has been shown that antibiotics are able to modify polynuclear chemotactism, bacteria phagocytosis by macrophages, lymphocyte proliferation and the production of various cytokines (interleukins I, II...). On the other hand, the immunoregulatory activity of metabolites of arachidonic acid is proposed to explain, in part, these properties. For example it is well established that PGE2 has a negative retro control on Interleukin production by monocytes. Moreover eicosanoids are probably involved in the inflammatory and vasoactive reactions during the septic shock syndrome observed frequently during phagocytosis and bacterial lysis of Gram negative bacteria. Thus it seems interesting to evaluate the antibiotics activity on eicosanoid monocyte production. We have studied the influence of ciprofloxacin, ofloxacin, pefloxacin, imipenem, doxycycline, clindamycin and cefadroxil at various concentrations on eicosanoid production by A 13187 calcium ionophore activated mouse peritoneal macrophages (P 388 D1). The analyzed prostaglandins are: 6 keto (PGI2), PGE1, PGE2, F2 alpha, A2, B2, TxB2 et PG D2. All the antibiotics tested show either an inhibiting or a stimulating action on eicosanoid production. These immunomodulatory and pro-inflammatory effects must be considered, together with anti-infectious activity before the prescription of an antibiotic.

Animals↗
PubMedDate not supplied

[Immunopathologic study of retinal detachment with vitreo-retinal proliferation].

Immunopathological studies were performed on biopsies or autopsies of pars plana samples from patients with retinal detachment, with or without vitreo-retinal proliferation. Immunoglobulins and complement deposits have been found in vitreo retinal proliferation, together with a deviant expression of HLA-DR and DQ antigens by pigmented epithelial cells of the ciliary body. Gamma interferon is able to induce this expression in vitro, and the inducing effect of this lymphokine and other mediators has been tested on pigment epithelium cultures. Cultured pigment epithelial cells expressed HLA-DR and DQ antigens after being stimulated by very low doses of gamma interferon. The precise target of this immune reaction is still impossible to determine, but its consequences could be the release of growth factors as FGF, which has been found at very high levels in pigmented and non pigmented cells of pars plana and ciliary processes. Our work asserts the existence of auto-immune phenomena in retinal detachment with vitreo-retinal proliferation as well as in proliferative diabetic retinopathy, their exact involvement remaining to determine.

HLA-DQ Antigens↗