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Biomedical subjects

J Bernard

Publications and source records attributed to J Bernard.

At least 73 records · Page 4Linked to original sources
PubMed1998

Dual-energy X-ray absorptiometry in osteonecrosis of the femoral head.

UNLABELLED: Osteonecrosis of the hip classically produces a heterogeneous density in the femoral head, although the bone marrow ischemia extends down to the femoral neck and trochanters. Also, bone insufficiency fractures due to diffuse bone loss have been implicated in the genesis of osteonecrosis. OBJECTIVES: To use dual-energy X-ray absorptiometry to quantify the bone changes produced by osteonecrosis of the hip and to compare bone mineral density values in patients with osteonecrosis of the hip and in controls. METHODS: Bone mineral density was measured at the femoral neck (total femoral neck, Ward's triangle, and trochanter), femoral head and lumbar spine using dual-energy X-ray absorptiometry (DPX, L Lunar) in 22 patients with osteonecrosis of the hip and in 22 age- and sex-matched controls. RESULTS: In the patients with osteonecrosis, bone mineral density on the affected side was higher than on the opposite side at the femoral head (+18%), femoral neck (+7%), and Ward's triangle (+6%) and lower at the trochanter (-4%). These differences were most marked at the more advanced end of the osteonecrosis spectrum. As compared to age-specific normative values, the osteonecrosis patients had moderately decreased bone mineral density values at the lumbar spine (-0.53 +/- 1.1 SD or -6 +/- 1.5%) and at the femoral neck on the normal side (-0.9 +/- 1.4 SD or 12 +/- 1.8%). As compared to the controls, bone mineral density was significantly decreased at Ward's triangle (-25%; P: 0.04) and nonsignificantly decreased at the lumbar spine (-4.7%; P: 0.15) and at the femoral neck (-15%; P: 0.09).

Absorptiometry, Photon↗
PubMed1998

[Subacute intestinal obstruction due to bladder distension].

We report a case of subacute bowel obstruction due to a compression of the rectosigmoid junction by a chronically distended bladder, occurring in a 91-year-old male suffering from a long-standing diabetes mellitus and a prostatic adenoma. Radiographic, water-soluble contrast enema and pelvic CT features are reported.

Aged↗
PubMed1997

IL-13 induces CD34+ cells isolated from G-CSF mobilized blood to differentiate in vitro into potent antigen presenting cells.

Dendritic cells (DCs), which are antigen presenting cells of potential use in human antitumor vaccination trials, are presently the subject of intense investigation. Many recent studies have reported the possibility of generating ex vivo large numbers of DCs with high antigen presenting capacity by the culture of bone marrow or blood progenitors. In this study, we examined the differentiation into DCs of CD34+ progenitors isolated from the G-CSF mobilized blood of 3 healthy donors and 5 patients with breast cancer and cultured in the presence of GM-CSF + IL-13. The characteristics of the cells were compared to those of cells obtained in the presence of GM-CSF + TNF alpha. By day 15, one third of the bulk cells cultured with IL-13 were CD1a+/CD14- and strongly expressed CD1c, CD40, CD80 and HLA-DR. In contrast, cells obtained with TNF alpha expressed CD1a on one in three cells but with a considerably lower fluorescence intensity than on IL-13-cultured cells and strongly expressed CD14 on more than 50% of cells. CD1a+/CD14- cells emerged in IL-13 cultures at day 5, while in TNF alpha cultures CD14+ cells appeared before CD1a+ cells. Cells grown in the presence of IL-13 had an increased capacity to present antigens to autologous lymphocytes and to stimulate allogeneic T-lymphocytes. This effect was greater than that of cells grown in the presence of TNF alpha. These cells should therefore have greater effector potential in any therapeutic applications in humans.

Animals↗
PubMed1997

Ultrastructural changes in the nerve fiber population of anastomosed vagal and spinal accessory nerves in the sheep.

BACKGROUND: The ultrastructure of the vagal and spinal accessory nerves was studied 1) in normal sheep and 2) in sheep in which an experimental crossed-nerve anastomosis had been made by sectioning the supranodose vagal and spinal accessory nerves, then suturing the distal end of the vagal nerve to the distal end of the spinal accessory nerve, and allowing time for regeneration to occur. This study was carried out in order to analyze the modifications liable to occur when this technique is used and to specify the origin and the nature of the fibers that colonize the spinal accessory nerve. METHODS: The study was performed in 4- to 5-month-old-sheep. After the surgical procedure, the animals were housed indoors during 1 year until their sacrifice by fixative perfusion. Then, nerve samples were dissected out, processed for electron microscopy, examined, and systematically photographed. After printing, the diameters of the nerve fibers were determined. RESULTS: In sheep, the ratios of nonmyelinated to myelinated fibers (NF/MF) in the infranodose and supranodose vagal nerve and accessory spinal nerve were 1.21, 1.67, and 3.21, respectively. In both parts of the vagal nerve, the myelinated fibers had a unimodal diameter distribution around a peak of 4 microns; whereas, in the spinal accessory nerve, they were distributed bimodally, and 53% had values of 15-18 microns. After making the above anastomosis, the centrifugal vagal fibers degenerated, and the NF/MF ratios increased in the centripetal infranodose vagal nerve, in the reinnervating supranodose vagal nerve, and in the reinnervated spinal accessory nerve (approximately 1.87, 1.72, and 6.04, respectively). In all of these nerves, the myelinated fibers had a unimodal distribution with a peak at 4 microns, as in the vagal nerve of normal sheep. CONCLUSIONS: These results reveal the large part taken by the nonmyelinated fibers in the nerve fiber population of the vagal nerve and support the vagal origin of the fibers reinnervating the spinal accessory nerve.

Accessory Nerve↗
PubMed1997

Cloning of human IL-12 p40 and p35 DNA into the Semliki Forest virus vector: expression of IL-12 in human tumor cells.

IL-12 can enhance the development of effective immune responses against tumors as well as against certain infectious agents. It is therefore a potential candidate for therapeutic use in cancer therapy and in the design of vaccines against several infectious diseases. Several studies have demonstrated that IL-12 could efficiently induce tumor regression in animal models. To investigate the antitumor effect of direct gene transfer of human IL-12 into tumors, human IL-12 p35 and p40 cDNAs were cloned into the Semliki Forest virus (SFV) vector pSFV1. In order to express the two subunits from the same vector, the p35 and the p40 cDNAs were cloned into pSFV1, each under the control of a subgenomic SFV promoter. Recombinant RNA produced by in vitro transcription of SFV-IL-12 construct, was packaged into SFV viral particles with the use of a non-packageable helper RNA. We show that human tumor cell lines infected in vitro in vivo with recombinant SFV-IL-12 viral particles secrete high levels of biologically active heterodimeric p35/p40 IL-12, as demonstrated using ELISA and biological assays.

Gene Expression↗
PubMed1997

An X-ray absorptiometry study of reflex sympathetic dystrophy syndrome.

X-ray absorptiometry (Lunar DPX) was performed before and after treatment to determine bone mineral content and density, as well as fat-free mass and body fat, in 28 males and 11 females with a mean age of 37 years who met Doury's criteria for reflex sympathetic dystrophy syndrome. Mean disease duration was eight months. Before treatment, as compared to the unaffected limb, bone mineral content was decreased by 8.8%, bone mineral density by 9.6%, and fat-free mass by 6.2%, whereas body fat was increased by 6%. These differences were largest in those patients with the longest disease durations. The severity of bone loss was not correlated with the outcome, the severity of roentgenographic lesions, or whether the patient was evaluated at the warm or cold stage of the disease process. Study parameters were unchanged after three months both in patients who were and were not improved. After nine to 12 months, increases in bone and fat-free mass were seen in those patients whose clinical manifestations had subsided.

Absorptiometry, Photon↗
PubMed1996

Involvement of the 12-lipoxygenase pathway of arachidonic acid metabolism in homosynaptic long-term depression of the rat hippocampus.

Low-frequency stimulation is associated with long-term depression (LTD) of synaptic efficacy in various brain structures. Like long-term potentiation (LTP), homosynaptic LTD in area CA1 of the hippocampus appears to require NMDA receptor activation, changes in postsynaptic calcium concentration and phospholipase A2 (PLA2) activation. Arachidonic acid (AA) is released after the activation of calcium-dependent phospholipases and free AA is rapidly metabolized to a family of bioactive products (the eicosanoids) which are thought to be both intracellular and extracellular messengers. In the present study, we investigated the involvement of the cyclooxygenase and lipoxygenase pathways of AA metabolism in the formation of homosynaptic LTD in the rat hippocampus. Stimulation at 1 Hz for 15 min was used to produce homosynaptic depression in area CA1 of hippocampal slices. LTD induction was partially blocked by bromophenacyl bromide (50-100 microM), a selective PLA2 inhibitor, and by the a nonselective lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA; 100 microM). In contrast, the specific cyclooxygenase blocker indomethacin (100 microM) did not significantly reduce hippocampal LTD. Since NDGA interferes with LTD formation, we examined whether specific inhibitors of 5- and 12-lipoxygenases were capable of blocking LTD expression. The 12-lipoxygenase inhibitor baicalein at a concentration of 50 microM reduced LTP formation when given in the bath, an effect that was less pronounced with the 5-lipoxygenase inhibitor AA-861. These data suggest that the activation of endogenous PLA2 and the formation of 12-lipoxygenase metabolites of AA may be important factors controlling the expression of hippocampal LTD.

Acetophenones↗
PubMed1996

Developmental changes in depolarization-mediated AMPA receptor modifications and potassium-induced long-term potentiation.

In the present study, we examined the KCl-induced increase in [3H] amino-3-hydroxy-5-methylisoxazole-4-propionate ([3H]AMPA) binding in telencephalic synaptoneurosomes and potentiation of synaptic transmission (KLTP) in hippocampal slices during development in rats. As previously reported, KCI-induced depolarization of telencephalic synaptoneurosomes resulted in a 40 +/- 5% increase in [3H]AMPA binding to membrane fractions in adult rats (3 months old). KCI-induced increase in [3H]AMPA binding was reduced to 24 +/- 5% and 15 +/- 5% at postnatal days (PND) 25-30 and PND 15-20 respectively, and was only 6 +/- 5% at PND 5-10. KLTP in area CA1 of hippocampus was most pronounced in adult slices (40 +/- 5%), and was reduced to 30 +/- 5% in slices prepared from PND 25-30 animals; KCI-induced LTP was absent in CA1 hippocampal slices prepared from PND 5-10 animals (3 +/- 5%). The decrease in KCI-induced changes in AMPA receptor binding in young animals was also associated with an altered capacity of the bee venom peptide, mellitin (a phospholipase A2 (PLA2) activator), to increase [3H]AMPA binding in synaptoneurosomes. The smaller effect of mellitin on [3H]AMPA binding in young animals was not due to a decreased ability of this peptide to release [3H]arachidonate from synaptoneuro-somes. The parallel modifications in the extent of depolarization-induced change in AMPA receptor binding and excitatory synaptic transmission during development further support the hypothesis that alterations in AMPA receptor properties may play a critical role in synaptic plasticity.

Age Factors↗
PubMed1996

Repair of the in vitro HIV-1-induced immunosuppression and blockade of the generation of functional suppressive CD8 cells by anti-alpha interferon and anti-Tat antibodies.

The acute human immunodeficiency virus type 1 (HIV-1) infection of activated peripheral blood mononuclear cells (PBMCs) from normal donors results in inhibition of cell proliferation and generation of functional suppressive T cells. Cultured HIV-1 infected PBMCs but not uninfected PBMCs, following irradiation, can inhibit the proliferation of antigen-activated autologous T cells in a dose-dependent way. CD8+ cell subpopulation is responsible for this inhibition. The presence of anti-alpha interferon (IFN alpha) and anti-Tat antibodies in the culture medium counteracts the HIV-1-induced immunosuppression and prevents the generation of suppressive T cells by these PBMCs. The reported data should have major implications for strategies of AIDS treatment which, in association with antiviral drugs, aim at targetting immune disorders.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Phase I/II trial of autologous activated macrophages in advanced colorectal cancer.

Autologous activated macrophage (AAM) therapy is an adoptive cellular therapy based on ex vivo differentiation and activation of autologous peripheral blood monocytes. This study was undertaken to evaluate the tolerance, efficiency and biological effects of AAMs in chemoresistant progressive colorectal cancers. From January 1993 to May 1995, 15 patients were treated. Mononuclear cells were collected six times by weekly apheresis, cultured for 7 days, and activated with interferon-gamma. AAMs were then separated by elutriation and re-infused intravenously, with a mean total of 7.95 x 10(9) macrophages per patient. Clinical tolerance was good: toxicity consisted only of a World Health Organisation grade 2 fever after 28% of the infusions. Responses were not seen in the 14 evaluable patients, as expected with very bulky tumours: in 11, the tumours continued to progress, but disease was stabilised in 3 patients who experienced progression-free survival for 14, 12 and 12 weeks, respectively.

Aged↗
PubMed1996

Dynamics of virus versus host interaction in children with human immunodeficiency virus type 1 infection.

To investigate the dynamic interplay between human immunodeficiency virus type I (HIV-1) replication and the extent of immune destruction in HIV-1-infected children, virus burden in lymphoid tissues (LN) and peripheral blood was compared with changes in LN architecture and cytokine levels constitutively expressed in LN. In agreement with results of a preliminary study, the plasma HIV-1 RNA level correlated with the amount of provirus in LN. However, the level was also associated with a degree of destruction of lymphoid follicular architecture and an alteration of immune cytokine expression. Expression of interleukin (IL)-4 was higher in LN with higher virus replication. Reduction of plasma viremia was associated with an increase in IL-2 mRNA levels in LN. These findings suggest that measurable virus burden in the peripheral blood is not a simple reflection of viral replication in LN but is also influenced by the extent of progressive immune destruction.

Child↗
PubMed1996

Electrocardiographic changes and halofantrine plasma level during acute falciparum malaria.

The aim of this study was 1) to assess the incidence of electrocardiographic changes after treatment with halofantrine and 2) to study the relationship between these changes and plasma levels of halofantrine and its main metabolite, N-desbutyl-halofantrine. Thirty-four male patients with uncomplicated falciparum malaria were enrolled in this study. Halofantrine was administered on two separate days at a total oral dosage of 24 mg/kg/day in three doses over a 12-hr period. The interval between the two treatments was seven days. Twelve-lead electrocardiography (ECG) was performed to measure the QT interval (QTc), ambulatory ECG monitoring was done to detect ventricular arrhythmia, signal-averaged ECG was performed to detect late ventricular potentials, and blood tests were performed to determine plasma concentrations of halofantrine and N-desbutyl-halofantrine. Maximum QTc was observed at 12 hr after both the first (P < 0.0002) and second treatments (P < 0.03). Signal-averaged ECG revealed late potentials in four cases (72 hr after the first treatment in one case and 24 hr after the second treatment in three cases). Ventricular arrhythmia was not observed. Significantly higher plasma concentrations of halofantrine were observed 2 hr after the second treatment. At this time, both the time effect and time interaction were significant (P < 0.008 and P < 0.02, respectively). The QTc interval was significantly correlated with the plasma halofantrine level (r = 0.41, P < 0.01) but not with the plasma N-desbutyl-halofantrine level (r = 0.30, not significant). In three cases, late ventricular potentials were associated with a maximum concentration of halofantrine. Our findings indicate that electrocardiographic changes are dose-dependent and that a second treatment at the same dosage may be hazardous.

Acute Disease↗
PubMed1996

[Electrocardiographic changes due to halofantrine in the treatment of malaria: therapeutic implications].

Electrocardiographic changes and their relationship with profiles of halofantrine (H) and desbutylhalofantrine (DBH) were assessed in a prospective study of 34 male patients with an uncomplicated falciparum malaria. H. was delivered in a one day in three intakes, 24 mg/kg/day. Seven days later the same regimen was administered. This study included a twelve-lead-electrocardiogram (to measure QTc interval), an ambulatory ECG monitoring a signal-averaged-electrocardiogram (to detect late ventricular potentials), and a kinetic-time profile of H. and DBH with high performance liquid chromatography. Data were obtained as follows: day 1 just prior to drug intake, 6 hours (H6), 12 hours (H12) after to drug delivery on day 1 and 8. There after on days 2, 3, 4, 9, 10, 11. Ambulatory ECG monitoring was recorded on day 1 and 8. QTc lengthening was noted in 10 patients with a mean QTc interval of 451 msec (range: 440-469 msec). Maximum QTc interval was obtained at H12 on day 1 (p < 0.0002) and 8 (p < 0.03). Signal-averaged electrocardiogram performed in 8 cases disclosed late potential in 4 cases (day 4: one case, day 9: 3 cases). No ventricular arrhythmia was observed on day 1 and 8. Plasma concentration time profile of H. showed a significant increase at day 8 H12 with a time effect (p < 0.0008) and a significant time-intake interaction (p < 0.02). QTc interval was significantly correlated with H. plasma level (p < 0.01) but not with D.B.H.. Late potentials were associated in 3 cases with a maximum plasma concentration level of H. These data showed that H. is potentially deleterious with a cardiac toxicity which appears dose-related, particularly during the second cure. Following this study, new prescription rules has been proposed before H. therapy.

Adult↗
PubMed1996

[History of congenital thrombocytic hemorrhagic dystrophy].

This historical review of the Bernard-Soulier syndrome relates: (1) the first description of the disease; (2) the main data of the research from 1948 to 1982 which led to the discovery of the molecular abnormality (lack or qualitative abnormality of the platelet glycoprotein Ib) responsible for the functional disorder (defective platelet adhesion to the vascular subendothelium) which nowadays defines the disorder.

Bernard-Soulier Syndrome↗