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Biomedical subjects

S Martinelli

Publications and source records attributed to S Martinelli.

30 records · Page 2Linked to original sources
PubMed1986

Noninvasive determination of the anaerobic threshold in swimming.

The relationship between swimming velocity (V) and heart rate (HR) was determined in 60 swimmers. The athletes were asked to increase their work intensity progressively, from low to submaximal velocities; HRs were determined by a telemetric cardiofrequency meter. In all the athletes examined and for each style employed, the linearity of the V3-HR relationship was maintained up to a submaximal velocity (deflection velocity, Vd), beyond which the increase in work intensity exceeded the increase in HR. The test-retest correlation for Vd determined in nine pent-athletes was 0.99. Vd and anaerobic threshold (AT), determined through lactate measurements, were correlated in six swimmers (r = 0.84). Vd and average swimming velocities in a modern pentathlon swimming race (300 m free-style) were also correlated (n = 9, r = 0.91), thus suggesting that AT is critical in determining the speed in middle-distance swimming events.

Adult↗
PubMed1985

Further studies on the hypercoagulable state of patients with Cushing's syndrome.

Factors XII, XI, IX and VIII, plasminogen and alpha 2-antiplasmin levels were found to be increased in a group of patients affected by Cushing's syndrome. High activity of these coagulation factors could be due to their increased release and synthesis mediated by cortisol. A significant correlation between the main arterial pressure and either factor VIII antigen, ristocetin cofactor or factor XII activity was found. Moreover a similar correlation between factor XII activity and either factor VIII antigen or ristocetin cofactor was seen. In conclusion, the presence of a hypercoagulable state in Cushing's syndrome seems confirmed. Synergic release of factor XII and factor VIII from endothelium could be due to high blood vessel tone secondary to hypercorticism. Finally, decreased fibrinolytic activity was suspected according to plasminogen and alpha 2-antiplasmin increase.

Blood Coagulation Disorders↗
PubMed1985

Reduced hemoglobin concentration and red cell hemoglobinization in Italian marathon and ultramarathon runners.

Red blood cell indices, serum iron, and serum ferritin concentration were determined in 45 marathon runners, 56 ultramarathon runners, and 32 healthy sedentary controls. A significant reduction of hemoglobin concentration, hematocrit, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, mean corpuscular volume, serum iron, and serum ferritin were found in marathon runners compared to control subjects. The same variables were also reduced, but to a lesser extent, in the less trained ultramarathon runners. The decreased hemoglobin concentration demonstrated in the runners examined is related to both a reduced mean corpuscular hemoglobin concentration and a reduced hematocrit and may depend on a reduction of the body iron stores.

Adult↗
PubMed1985

Fibrinolytic study in plasma and ascitic fluid of cirrhotic patients before and after ascites concentration; reinfusion technique.

Management of cirrhosis with massive ascites involves particular difficulties. The introduction of a peritoneovenous shunt and reinfusion of concentrated ascitic fluid techniques allows increased diuresis and improves renal function. However, these procedures have frequently been associated with disseminated intravascular coagulation and/or activation of fibrinolysis. Factor VIII activity, antigen and ristocetin cofactor, plasminogen, antiplasmin, plasminogen activator activity and plasmin-antiplasmin complex were investigated both in the ascitic fluid and plasma of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicated that no hyperfibrinolysis was seen in the plasma of cirrhotic patients and that activation of fibrinolysis exists in ascites. Significantly higher levels of plasmin-antiplasmin complex and plasminogen activator activity were found in ascitic fluid than in plasma. In post-reinfusion much higher levels of all three Factor VIII components were observed in cirrhotic plasma than in normal plasma. In conclusion, activation of fibrinolysis could explain coagulation complications occurring after ascites reinfusion. Antifibrinolytic treatment could render the concentration-reinfusion technique more acceptable.

Adult↗
PubMed1985

Contact phase of coagulation in diabetes mellitus after aspirin administration.

The purpose of our study was to investigate the connection between platelets and the contact phase of coagulation. In 17 patients affected by diabetes mellitus we studied the behaviour of prekallikrein, factor XII and factor XI before and after aspirin administration. To evaluate the activity of aspirin we measured platelet production of thromboxane B2 using a radioimmunoassay. In our diabetic patients a hypercoagulable state was confirmed: PK, factor XII and XI levels were significantly higher as compared with normal controls. After aspirin administration a significant decrease of PK levels was found. After 7 days of aspirin administration and 7 days after stopping aspirin a modest but not significant improvement of factor XII and factor XI was observed. In conclusion, we believe that the contact phase of coagulation is another index of the hypercoagulable state in diabetes mellitus. In addition, the decrease of PK obtained by aspirin administration could support the possible connection between the contact phase of coagulation and platelets.

Aspirin↗
PubMed1984

The contact phase of blood coagulation and renin activation in essential hypertension before and after captopril.

The contact phase of blood coagulation in a group of patients suffering from essential hypertension was studied before and after captopril administration. The baseline levels of factor XII, factor XI and plasminogen were significantly higher than in normals and correlated with baseline diastolic blood pressure levels. On the contrary, plasma prekallikrein was not significantly different from normal. These results suggest the presence of a hypercoagulable state in essential hypertension. After captopril administration, factor XII, factor XI and prekallikrein rapidly decreased, perhaps as a consequence of the drug's effect on the vascular endothelial surface. There was no correlation between the changes of active and inactive renin and the changes of prekallikrein and plasminogen levels. Our data do not support the view that factor XII-plasma kallikrein or plasmin dependent pathways are involved in the activation of inactive renin in vivo. Captopril, by provoking rapid pressure changes, appears to be able to affect the clotting system.

Adult↗
PubMed1982

Kallikrein and prekallikrein levels in a large number of congenital clotting deficiencies and abnormalities.

Kallicrein (K) and prekallicrein (PK) were assayed in a large number of cases with congenitial clotting factor defects. Patients with factor XII deficiency were separated from other clotting abnormalities. The results were compared with a control group of normal subjects. We found significantly reduced PK activity levels in the factor XII deficient group. Although less evident, the reduction of PK activity in the group of other clotting defects was modest, however, not due to a factor VII defect. In our study we found that in the absence of factor XII, PK is not activated. Further studies will be necessary to show if PK activation is altered or reduced in other congenital clotting abnormalities.

Adolescent↗
PubMed1979

Allele specific, gene unspecific suppressors in Aspergillus nidulans.

Seven suppressor mutations have been isolated in Aspergillus nidulans by coreversion of alleles in physiologically unrelated genes namely, alX, sB, alcA, putative structural genes for allantoinase, sulphate permease and alcohol dehydrogenase respectively. The suppressors are allele specific, gene unspecific. Those described map in four loci, suaA, B, C, D. suaA and suaB are on linkage group III, suaC and suaD on VII. suaB111, suaD103 and suaD108 are semi-dominant in their suppression of alX4 and sB43, suaA101, suaA105 and suaC10. are recessive and have a pleiotropic effect on morphology. SuaC109 is cold sensitive for growth as is sua115, an unmapped mutation on linkage group III which is similar in morphology to suaC109. The two mutations, suaA101 and suaA105 have different spectra of suppression and morphologies. suaA105 weakly suppresses alX4 and sB43 whereas suaA101 strongly suppresses these and alcA125. suaD103 and suaD108 have the same spectrum of suppression. The properties of these suppressors are consistent with their being informational suppressors are consistent with their being informational suppressors of the nonsense type.

Alleles↗