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Biomedical subjects

G Monte

Publications and source records attributed to G Monte.

11 recordsLinked to original sources
PubMed1994

[Transfer of plasma cholesterol and atherosclerosis].

Transfer processes in plasma are determinant in cholesterol metabolism. In many species, including man, there is an alternative route for the disposal of cholesteryl esters (CE) in HDL via transfer to VLDL in exchange for triglycerides (TG), a process dependent on a hydrophobic 74 kDa glycoprotein called cholesteryl ester transfer protein (CETP). In vivo, cholesteryl esters transferred from HDL will contribute to LDL, to which VLDL is converted. Although the prevention of CE accumulation in HDL may enhance the ability of HDL to take up more cholesterol from tissues, high rates of transfer may also increase the risk for atheroma by increasing formation of atherogenic lipoproteins. Conversely, CE retained within HDL, if returned directly to the liver, would be expected to be beneficial. Moreover, in most conditions predisposing to atheroma, CETP activity is raised; whereas species with low or absent CETP activity are at low risk for atherosclerosis.

Animals↗
PubMed1993

[The pharmacological effects of certain compounds on lipoprotein(a)].

Lipoprotein(a) represents a cholesterol ester, LDL-like particle with apo B-100 linked to apo (a). Lp(a) is a fascinating subject of research because of its presumed association with atherosclerotic cardiovascular disease. The reported results do not encourage optimism. Drugs like niacin or fibrates when used alone have been attended by mixed results. Neither clofibrate nor bezafibrate, which reduce the VLDL concentration, affect LP(a) levels. Neither the ion-exchange resin cholestyramine, nor the HMG CoA reductase inhibitor lovastatin reduce the serum concentration of Lp(a). But, we must keep in mind that drugs used to lower plasma Lp(a) levels were designed for apo B and not apo B-apo(a) containing particles. Thus, it may be necessary to develop drugs specifically targeted to Lp(a).

Arteriosclerosis↗
PubMed1992

Use of low molecular weight heparin in pregnancy.

In a controlled study of 15 pregnant patients undergoing therapeutic termination of pregnancy, seven received subcutaneously 5,000 anti-FXa units of low molecular weight (LMW) heparin 15 and 3 h prior to the termination, and eight patients acted as controls. Paired maternal and fetal blood samples were taken (before or immediately after the termination) for assay of heparin activity by a chromogenic anti-FXa method sensitive to levels of 0.02 anti-FXa U/ml. LMW heparin was detected in all maternal samples of the test patients but was not detected in any of the fetal samples. The use of LMW heparin as a thromboprophylactic agent was then evaluated in 11 patients who were known to have a severe thromboembolic tendency, had suffered recurrent miscarriages and had responded poorly to conventional anticoagulation (oral anticoagulant, conventional heparin). All patients receiving LMW heparin in thromboprophylactic doses completed uneventful pregnancies and gave birth to healthy babies (three for the first time) without complication. Bone density scans performed in all patients shortly after the delivery showed normal mineral mass. We conclude that LMW heparin does not cross the placental barrier, and in addition offers satisfactory antithrombotic protection for both maternal and placental circulation. In addition, this study provides preliminary data from 11 patients suggesting LMWH may not give rise to maternal osteoporosis, a finding that now needs further investigation.

Abortion, Habitual↗
PubMed1992

Congenital thrombophilia among patients with venous thromboembolism.

During a 3-year period we studied 393 adult patients (382 of whom were unrelated) with a history of acute venous thromboembolism. A congenital deficiency state known to predispose to thrombosis was found in 27.2%. Of these, most were due to deficiencies of protein C (9.2%), protein S (7.6%), antithrombin III (5%) or to increased plasma PAI-1 concentration (3.1%) which, in the absence of any known factor that predisposes towards thrombosis, results in a diminished fibrinolytic activity. There was a characteristic pattern between the age of onset (mean 34 years) of thrombosis and individual protein deficiency. Thrombosis appeared spontaneously in 73% of cases with recurrence in 80%. In contrast, in the remaining unrelated patients, 138 (35.1%) in whom venous thromboembolism was secondary and occurred at a mean age of 43 years, and in the other 140 (35.6%) who suffered thromboembolism spontaneously at a later age (mean age 55), there was no permanent protein deficiency state or alteration in fibrinolytic activity and thrombosis recurrence was lower (53.6% and 20.7% respectively). Of the 393 patients, deep vein thrombosis was the most common manifestation; however, in congenital thrombophilia, thrombosis of visceral vessels and Raynaud's syndrome (6%) were also detected.

Acute Disease↗
PubMed1991

The influence of venous occlusion on the status of protein S.

In the present study the effect of perturbation of the vessel wall by venous occlusion on protein S release, was evaluated in 10 healthy male volunteers. A 9% (P less than 0.01) increase in free protein S and a 7% (NS) in total protein S over the baseline were observed 7 min after venous occlusion, whereas von Willebrand factor antigen (vWF:Ag)--a known release product of vascular endothelium--increased by 11% (P less than 0.01). In addition, the possibility of free protein S release from unstimulated platelets was investigated in pre- and post-occlusion samples incubated at room temperature for 24 h as whole blood or platelet-rich plasma. An increase in the mean free protein S was observed in the pre-occlusion samples which peaked after 4 h of incubation--121% at time 0 to 130% (P less than 0.05) of the normal pooled plasma whereas total protein S increased by only 4% (NS). In the post-occlusion samples, a similar peak in mean free protein S levels was observed after 12 h of incubation--132% at time 0 increased to 142% (P less than 0.01) of the normal human plasma pooled and the total protein S was increased by 8.55 (P less than 0.05). Small but significant increases in vWF:Ag levels were observed at 2 h and 6 h for the pre- and post-occlusion samples, respectively. No changes in C4b-binding protein were observed throughout the study. We conclude that, firstly, venous occlusion causes release of protein S in addition to vWF:Ag and, secondly, unstimulated platelets release protein S in addition to vWF:Ag.

Adolescent↗