Biomedical subjects
J Constans
Publications and source records attributed to J Constans.
[Association of vitiligo and laryngeal carcinoma: a case report].
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[Clinicobiological study of 100 symptomatic patients with factor V Leiden mutation].
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Proton magnetic resonance spectroscopy (1H-MRS) of the thalamus in schizophrenia.
This study applied (1)H-MRS in the thalamus of schizophrenic patients and healthy subjects. There were no differences in the metabolite ratios (NAA/Cr, Cho/Cr or mI/Cr) between the two groups. Relationships were noted between NAA/Cr and age in patients with a trend toward this correlation in controls, suggesting an effect of age on the metabolism of the thalamus.
GM, KM immunoglobulin allotypes and other serum genetic markers (HP, GC, PI, and TF) among South American populations living at different altitudes (Jujuy Province, Argentina): admixture estimates.
A total of 154 individuals belonging to three populations located at different altitude levels in northwest Argentina (San Salvador de Jujuy, 1,200 m; Tilcara, 2,500 m; Abra Pampa, 3,500 m) were studied for the GM, KM, HP, GC, PI and TF genetic systems. Individuals were selected on the basis of ethnocultural affiliation. Gene frequency values were found to be comparable to those reported for other South American populations. The populations studied showed a close genetic identity and an absence of interpopulation heterogeneity. Distribution of the GM phenotypes and haplotypes corresponds to historical data on human settlements in Jujuy Province. The presence of some alleles and the anthropological significance of the allele distribution are discussed, as are the effects of the admixture with Africans and Spaniards. The genetic pattern appears to be the result of a varying admixture due to the genetic isolation in populations located at various altitude levels.
Inhibition of tissue factor synthesis by disruption of ERK kinases and PKC signaling pathways in human vascular SMCs.
Tissue Factor (TF), the receptor for plasma VII/VIIa and the initiator of blood coagulation, is inducible in vascular smooth muscle cells (SMCs) by growth factors and bacterial lysopolysaccharides (LPS) and is expressed in vivo after vascular injury. As TF expression is a determinant of the thrombogenicity of vascular lesions, we investigated the signal pathways involved in this process. Human vascular SMCs were obtained from normal arteries and made quiescent by serum deprivation. Baseline TF antigen and activity were up-regulated by various agonists: fetal calf serum (FCS), LPS, and platelet derived growth factor (PDGF) being the most effective but with different kinetics. TF expression induced by LPS was transient with a maximum 6 h after stimulation and returned to baseline levels after 24 h whereas TF expression induced by serum or PDGF was sustained for at least 24 h. Rapid and transient activation of Extracellular signal-Regulated Kinase (ERK) was observed after stimulation by PDGF and FCS, but not by LPS. The role of ERK, Ras and protein kinase C activities were investigated using specific inhibitors, PD 98059, manumycin A and calphostin C respectively. For TF induction by LPS, PKC activity was required and the ERK/Ras pathway was not involved. In contrast, the effect of PDGF was strictly ERK and Ras dependent, but partially prevented by PKC inhibitors. TF induction by FCS was ERK dependent but partially Ras and PKC dependent. In conclusion, TF expression appears to be a non-specific response of SMCs to numerous stimuli through multiple signal pathways which differ according to the inducing agent.
[Upper extremity deep venous thrombosis. 40 hospitalized patients].
Deep venous thrombosis is 50 times less frequent in upper than in lower limbs. Data remain poor in the literature. Forty consecutive patients (24 males, 16 females, mean age: 54.5 years) were retrospectively analysed from 161 subjects who underwent venous explorations of the upper extremity for a 3.5 year period in the same center. Diagnosis of thrombosis was made by duplex ultrasonography (n =37) or phlebography (n =3). Main clinical manifestations were edema (n =36) and pain (n =29). Location of thrombosis was humeral (n =1), axillary (n =2), or sub-clavian (n =37, 2 bilateral). The majority of thrombosis (n =29) were secondary to cancer and venous catheter (n =19, 15 implanted ports), to central catheter alone (n =3) or cancer alone (n =7). The 11 others were associated with thoracic outlet syndrome (n =6) or apparent primary thrombosis (n =5). Thrombophilia was identified in 6 out of these 11. During follow up [mean of 9 months (0,5-36)], two patients developed pulmonary embolism, 14 a post-thrombotic syndrome and 16 patients died. Initial therapy included heparin (n =36) or fibrinolysis (n =4). Upper extremity deep venous thrombosis are mostly associated with cancers and venous catheters. Thrombophilia is frequent in the other cases. Heparin followed by oral anticoagulation is the optimal therapy whose duration depends upon underlying condition. Fibrinolysis has not been useful for preventing post-thrombotic syndrome in our study.
[Hypocalcemia in a patient treated with estramustine].
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Endothelial dysfunction during acute methionine load in hyperhomocysteinaemic patients.
Hyperhomocysteinaemia has been associated with arterial and venous thrombosis possibly by causing damage to the endothelium. We hypothesised that an oral load in methionine, that increases plasma homocysteine, would also result in an increase in biological markers of endothelial or platelet dysfunction. Then we investigated two groups of patients with arterial or venous occlusive disease: 17 with hyperhomocysteinemia and 12 without hyperhomocysteinemia. We measured in both groups plasma soluble thrombomodulin, von Willebrand factor, P-selectin and tissue factor plasma inhibitor before and 6 hours after a load with 100 mg/kg oral methionine. Methionine load resulted in a significant increase in von Willebrand factor in both groups (P<0.02), suggesting that endothelial dysfunction occurs during the load.
[Atherosclerosis. Congress of the European Atherosclerosis Society (EAS), Athens (Greece), 26-29 May 1999].
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[Multiple arterial aneurysms].
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[Secondary aortoduodenal fistulas: report of 7 cases].
PURPOSE: Aortoduodenal fistulas are the most frequent aortoenteric fistulas. They may be primary (occurring after aneurysms of the native aorta) or secondary (occurring after aortic prosthesis). Aortoduodenal fistulas are a rare complication of aortic prostheses. They may be caused by prosthesis infection or due to inadequate prosthesis. METHODS: We report seven observations that emphasize issues pertaining to either diagnosis or therapy. RESULTS: The delay of occurrence is variable, with a mean of 3 years as reported in the literature. Clinical picture includes upper digestive tract hemorrhage, sometimes fever, abdominal pain or mass. Though difficult, diagnosis can be achieved through gastric endoscopy or CT-scan. Additional diagnostic procedures are often not useful and should not be numerous. Surgical procedures help guide the diagnosis and constitute the main part of the treatment with suture of the duodenum and vascular prosthesis. According to previous works, our observations including prolonged follow-up of the patients suggest that the best vascular treatment is extra-anatomic axillo-bifemoral bypass, while simple suture and prosthesis replacement lead to poor results. CONCLUSION: Mortality related to aortodigestive fistulas is high (five out of seven patients in the present study) and requires prevention, including more particularly delicate surgery and antibiotic therapy in case of any episode of infection. Aortoduodenal fistulas must be suspected whenever a patient with aortic prosthesis has digestive bleeding or unexplained fever.
Selenium and HIV infection.
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Three months supplementation of hyperhomocysteinaemic patients with folic acid and vitamin B6 improves biological markers of endothelial dysfunction.
Hyperhomocysteinaemia is a risk factor for premature atherosclerosis and venous thromboembolic disease. Supplementation with folic acid and vitamin B6 has been shown to decrease plasma homocysteine but data fail to assess an effect on the progression of vascular disease. We measured plasma homocysteine and two markers of endothelial injury (plasma soluble thrombomodulin and von Willebrand factor) at baseline and after 3 months of treatment with folic acid and vitamin B6. After this treatment there was a significant decrease in fasting soluble thrombomodulin (-15 ng/ml, 95%CI 5-22.2). Von Willebrand factor was significantly raised after methionine load at baseline but did not significantly rise after supplementation.
[Inflammatory arteriopathy of the arms in the course of Horton disease. Report of six cases].
We report 6 cases of upper limb involvement in giant cell arteritis; upper limb involvement revealed the disease in 4 cases and clinical symptoms were present in 5 (upper limb pain, Raynaud's phenomenon). Upper limb pulses were not palpable and blood pressure unmeasurable in all. Duplex ultrasonography found signs of inflammatory arteriopathy in 4 cases (hypoechogenous halo of the arterial wall and acceleration of flow velocity). Arteriography was performed in 5 cases and showed long and regular stenoses. In the last case, arteriography was not done because the duplex exploration gave an easier diagnosis. With this technique, the diagnosis of upper limb involvement, frequent in autopsy series of giant cell arteritis, might be made more often. Corticosteroid therapy is indicated and surgery should be discussed only in emergency situations.
Antiprothrombin autoantibodies and portal vein thrombosis without antiphospholipid antibodies.
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Effects of heparin and related sulfated polysaccharides on tissue factor expression induced by mitogenic and non-mitogenic factors in human vascular smooth muscle cells.
Smooth muscle cells (SMCs) of the intima are generally quiescent and non proliferative. Their proliferation due to different stimulations occurs in myointimal hyperplasia and is regularly present in atherogenesis or after transluminal angioplasty leading to vascular occlusive stenosis. In the course of these pathologies, the Tissue Factor (TF) synthesis was upregulated and rapidly expressed at the membrane of the SMCs. Heparin is known to inhibit SMCs proliferation induced by FCS. We evaluated the inhibitory effect of heparin on the expression of TF induced by various mitogenic (FCS, PDGF-BB and EGF) and non-mitogenic (bacterial LPS) agents. Inhibition by heparin of SMCs proliferation induced by the same agonists was also determined. Quiescent human vascular SMCs from normal adult arteries were treated for 1 h by heparin and related sulfated polysaccharides before stimulation by the agonists. All the agonists up-regulated the expression of TF antigen and activity. TF expression induced by the growth factors was inhibited by heparin (IC 50: 10-30 microg/ml), and other sulfated polysaccharides (IC 50: 1-5 microg/ml). SMCs proliferation, late activation of the extracellular signal-regulated kinases (ERK1/2), and PKC activity were inhibited by heparin (IC 50: 30-50 microg/ml) in SMCs stimulated by FCS but not in SMCs treated by PDGF or EGF. In contrast, heparin had no effect on LPS-induced TF expression nor on LPS-induced PKC activation. These results indicate that, besides its well known effect on SMC proliferation, heparin displays an inhibitory effect on cell mediated blood clotting processes through regulation of the TF expression.