Biomedical subjects

S Turco

Publications and source records attributed to S Turco.

At least 37 records · Page 2Linked to original sources

PubMed1994

Isolation of virulence genes directing GPI synthesis by functional complementation of Leishmania.

Recent advances in molecular genetics of Leishmania parasites prompted us to develop methods of functional genetic complementation in Leishmania and apply them to the isolation of genes involved in the biosynthesis of the virulence determinant LPG, an abundant GPI-anchored polysaccharide. LPG1, the gene product identified by complementation of our R2D2 LPG- mutant, may be a glycosyltransferase responsible for the addition of galactofuranose to the nascent chain. As galactofuranose is not found in mammalian cells, inhibition of the addition of this sugar could be exploited for chemotherapy. Overall, the success of the functional complementation approach opens the way to the identification of a variety of genes involved in pathogenesis and parasitism.

Animals↗

PubMed1993

Comparison of left ventricular function in insulin- and non-insulin-dependent diabetes mellitus.

Diabetes mellitus has been reported to have controversial effects on left ventricular (LV) function in patients with no evidence of coronary artery disease. In this study, LV function at rest was evaluated in 2 groups of diabetic patients, with insulin-dependent (IDD; n = 16) and non-insulin-dependent (NIDD; n = 23) diabetes mellitus, with no evidence of coronary artery disease. All patients underwent an electrocardiographic stress test, and first-pass and equilibrium radionuclide angiography at rest and during supine exercise. Data in each group of diabetic patients were compared with those obtained from age- and sex-matched normal subjects. In both groups of diabetic patients plasma catecholamine levels were significantly greater than in control subjects. Ejection fraction at rest and during exercise did not differ between each group of diabetic patients and their respective control group. In patients with IDD, peak ejection rate (4 +/- 1 end-diastolic count/s) was significantly greater than in control subjects (2.6 +/- 0.1 end-diastolic count/s; p < 0.001); similarly, peak filling rate (4.3 +/- 1.0 end-diastolic count/s) was significantly greater than in controls (3.0 +/- 0.2 end-diastolic count/s; p < 0.001). Cardiac output and systemic vascular resistances did not differ between patients with IDD and control subjects. In contrast, patients with NIDD had significantly reduced cardiac output compared with that of control subjects (5.7 +/- 0.2 vs 5.9 +/- 0.2 liter/min; p < 0.01), and increased systemic vascular resistances (1,422 +/- 137 vs 1,314 +/- 68 dynes.s.cm-5; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Evaluation of an aseptic technique testing and challenge kit (ATTACK).

Currently, there is considerable discussion and concern about quality assurance when sterile pharmaceuticals are prepared by pharmacists and other health professionals. This study describes the utility of a kit made by Marsam Pharmaceutics Inc. in detecting microbial contamination during simulated drug transfers by syringe. Common microbial detection techniques were incorporated in a simple series of transfers intended to simulate actual use. Growth promotion studies were carried out using Trypticase Soy Broth initially in tubes and then in vials (as supplied in the kit). Three test organisms were employed (Staphylococcus epidermidis, Bacillus subtilis, and Candida albicans) and inoculated at three levels, < 1000, < 100, and < 10 CFU/mL. All studies demonstrated growth occurring in 100% of the trials in 8 days. Similar studies were initiated in stored media (32 month) to determine the effects of time on the ability of the medium to support growth. Growth promoting ability of 32 month old media showed no significant difference. 100% of the vials inoculated showed growth in 8 days. Once the growth promoting qualities of the medium and vials was established a kit was developed then a study to determine the effectiveness of the kit as used was undertaken. Kits were manipulated according to the directions for use by a trained individual, under aseptic conditions and by an untrained individual in an area described as less than desirable. No growth occurred in the vials of the 10 kits used to illustrate good technique and good environmental conditions with 30% (3 of 10) of the kits showing contamination when transfers by syringe were carried out in the less than desirable setting.(ABSTRACT TRUNCATED AT 250 WORDS)

Asepsis↗

PubMed1992

Weight reduction lowers blood pressure independently of salt restriction.

The existence of a link between obesity and hypertension is nowadays universally accepted; however, there are still some doubts about the fact that weight reduction induces a significant long-term decrease in blood pressure. This clinical trial aimed at evaluating the effects of marked weight loss (at least 30% of excess body weight) induced by a low-energy (600 Kcal), normal sodium diet in severely obese patients, on blood pressure at rest and during sympathetic stimulation. Eight of the 20 patients initially recruited for the study were able to reach the therapeutical goal and brought their body weight from 107 +/- 6 to 91 +/- 4 kg. Their blood pressure (BP) at rest was at the same time reduced from 137/81 +/- 5/4 to 122/74 +/- 4/4 mmHg. Also, blood pressure measured during three different stimuli (cold pressor test, handgrip and mental arithmetic test) was lowered by this nonpharmacological means. These effects are related solely to weight reduction, since no change in salt intake occurred, as demonstrated by measurements of the 24-h sodium excretion test (191 +/- 13 vs 185 +/- 10 mEq/24 h). In conclusion, these results support the hypothesis that a drastic weight loss, independently of salt restriction, significantly reduces BP at rest and during stimulation of the adrenergic nervous system.

Adult↗

PubMed1991

Responses of serum insulin and blood pressure to cold and handgrip in obese patients.

A close correlation between body weight and blood pressure has been frequently observed in both clinical and epidemiological studies. The aim of this clinical trial was to evaluate whether, in obese patients, there is any relationship between blood pressure, at rest or during sympathetic stimulation, and blood glucose and serum insulin, both while fasting and during an oral glucose challenge. Twenty obese patients (age 26-65 years, body weight 97 +/- 16 kg, 11 normotensive and 9 hypertensive) entered the study. After a 4-week run-in period on an isocaloric diet with normal intake of sodium, blood pressure and heart rate were measured at rest and during sympathetic stimulation induced by cold and isometric testing. Responses of glucose and insulin to a standardized 75 g oral glucose tolerance test were also evaluated. The responses of glucose and insulin to glucose challenge were not statistically different in normotensive and hypertensive obese patients. Levels of insulin in the serum in the serum in the fasting state and during glucose load were significantly correlated with the response of blood pressure to cold and isometric exercise, but not to blood pressure at rest. The response of heart rate to cold was closely related to insulin only in the subgroup of normotensives. The present findings support the hypothesis that the sympathetic nervous system, which influences secretion of insulin and regulation of blood pressure, is involved in the pathophysiology of the association of obesity and hypertension.

Adult↗

PubMed1991

[Cardiac function (angiocardioscintigraphic evaluation) and plasma catecholamine levels in non-insulin-dependent diabetics].

Cardiac mortality is more frequent in diabetic patients than in normal subjects and particularly heart failure occurs 4-6 times more frequently in these patients than in normals also excluding diabetics with coronary artery disease (CAD). To study cardiac function, 20 patients with type II diabetes mellitus (11 M and 9 F, mean age 48 +/- 9 years), and 13 normal subjects (6 M and 7 F, mean age 48 +/- 13 years), were submitted to radionuclide ventriculography with technetium 99m to evaluate some indices of cardiac function at rest and during effort. The diabetic patients were on good metabolic control testified by a satisfactory fasting and post prandial glycaemia, absence of glycosuria in the last 3 monthly controls and a normal value of glycosylate haemoglobin; they had no vascular or neurological complications; CAD was excluded submitting these patients to a maximal effort ECG on an ergometer. The normal subjects were comparable to diabetic patients for age, sex, mean arterial pressure, body mass index and body surface area. At rest, stroke volume, peak filling rate, cardiac output, ejection fraction (EF), were significantly lower in diabetic patients than in normal subjects. Systemic vascular resistances (SVR) were higher in diabetics than in normal subjects (p less than 0.01). Mean EF during effort increased in both normals and diabetics but 30% of diabetic patients showed no increase in EF during effort (less than 5%). Preload, represented by end-diastolic volume or blood volume, did not differ in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Cardiac function and sympathetic activity in young diabetics.

This study was aimed at evaluating cardiac function, both systolic and diastolic, in young type 1 diabetics with a mean duration of the disease of 10.9 +/- 6 years and without evidence of cardiac autonomic neuropathy and micro- or macroangiopathy. Thirteen diabetics, with good metabolic control, and 10 normal matched subjects were studied by echocardiography at rest and by radionuclide ventriculography both at rest and during effort. The level of plasma catecholamines was also determined. The echocardiographic data were comparable in the two groups. Scintigraphic data showed an increased peak ejection and peak filling rate (P less than 0.001) in diabetics while the other indices of cardiac function were comparable. Norepinephrine (P less than 0.01) and epinephrine (P less than 0.001) were higher in diabetics. A hypothesis is formulated that the higher indices of flow velocities in type 1 diabetics are supported by a sympathetic overactivity.

Adult↗

PubMed1990

[Heart function (angioscintigraphic evaluation) and sympathetic tone in insulin-dependent diabetes mellitus].

Cardiac failure is a frequent feature in diabetic patients and it often causes their death. But how and when cardiac disease begins in this kind of patient is still debatable. For example, cardiac failure can be present even in the absence of atherosclerotic involvement of coronary arteries in young diabetics. The aims of our study were to evaluate the cardiac function and sympathetic tone of 16 young type 1 diabetic patients (8 M and 8 F, mean age: 27 years, SD +/- 5) in comparison with 10 normal subjects (4 M and 6 F, mean age: 30 years, SD +/- 7). Diabetic patients were choose from a large population because of the following features young age, absence of clinical and instrumental evidence of micro- or macroangiopathy, clinical evidence of diabetic autonomic neuropathy, proteinuria or arterial hypertension. They were in good metabolic control on daily insulin therapy of two or three administrations. Cardiac function was evaluated at rest and during submaximal exercise on a cycloergometer in supine position using radionuclide ventriculography with technetium 99m. Sympathetic tone was checked using the five clinical tests according to Ewing and the plasmatic level of catecholamines at rest was evaluated using high pressure chromatography. The ejection fraction, cardiac output, stroke volume of diabetics were comparable with those of normal subjects even in the presence of comparable systemic vascular resistance. The increase in ejection fraction during effort was normal. Only in one diabetic patient (incidentally the oldest one) did ejection fraction decrease (7%) during effort. The peak ejection and filling rates were significantly higher (p less than 0.001) in diabetic patients compared to those of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

[Hemodynamic adaptation in severe obesity with or without arterial hypertension].

Hypertension and obesity are 2 common pathological conditions that have been directly related. The incidence of hypertension in an obese population is far greater than in otherwise normal people. Nevertheless, a causal relationship between the 2 disorders has not been established. But their coincidence in the same patient carries increased risk of cardiovascular morbidity and mortality. In the present study we have studied a group of normotensive obese patients (21 patients, Group A), a group of hypertensive obese patients (19 patients, Group B) and a group of normal subjects (11 patients, Group C) by radionuclide ventriculography with Tc 99m to visualize the different hemodynamic adaptation to these different conditions. Overweight causes an increased preload while hypertension causes an increased afterload. In response to the increase in preload the heart of obese patient undergoes eccentric hypertrophy; when an increase in afterload is present at the same time, the left ventricle develops concentric hypertrophy. We found an increased preload in both the obese groups (A and B) testified by increased blood volume and end diastolic volume. Heart rate was higher in the 2 populations of obese patients. As a result, cardiac output was significantly increased in Group A and B. But the stroke index is decreased in Group A and B with respect to Group C. The ejection fraction is reduced in Group A with respect to Group B and C. The contractility index (systolic blood pressure/end systolic volume) is higher in Group B in comparison with Group A. Thus, hypertensive obese patients seem to have a better cardiac performance respect to the normotensive obese patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Functionally thrombasthenic state in normal platelets following the administration of ticlopidine.

To elucidate the bleeding tendency that follows the administration of ticlopidine, we investigated the skin bleeding time and some ex vivo functions of platelets obtained from eight healthy volunteers before and 1 wk after daily administration of 500 mg of ticlopidine. We found the following: ticlopidine significantly (P less than 0.001) prolonged the skin bleeding time and impaired the binding of radiolabeled fibrinogen and von Willebrand Factor, the clot retraction and the aggregation of platelets in response to ADP, epinephrine, thrombin, ionophore A23187, collagen, or arachidonic acid. In contrast, the administration of this drug did not affect intraplatelet levels of cAMP, agglutination and binding of von Willebrand Factor in response to ristocetin, shape change in response to ADP, collagen, thrombin, or arachidonic acid, or binding of prostaglandin E1 to resting platelets. Secretion of ATP in response to ADP or epinephrine was completely inhibited, whereas secretion as well as thromboxane synthesis in response to high concentrations of collagen, arachidonic acid, calcium ionophore A23187, or thrombin was unaffected. Studies with monoclonal antibodies showed that the glycoprotein IIb-IIIa complex (the putative receptor for fibrinogen and von Willebrand Factor on the surface of platelets exposed to naturally occurring aggregating agents) was quantitatively unaffected by ticlopidine. This observation was further confirmed by densitometric scannings of Periodic Acid-Schiff-stained gels of platelet suspensions. The onset, as well as the cessation of the inhibitory effect of ticlopidine on platelets was very slow, and reached a maximum after a 3-5-d administration. In addition, ticlopidine appeared to be a much more potent inhibitor when administered to subjects than when added in vitro to platelets. Finally, abnormalities comparable to those found in volunteers taking ticlopidine were observed when platelets from untreated subjects were incubated in the plasma of ticlopidine-treated subjects. We conclude that ticlopidine induces a thrombasthenic state in normal platelets without affecting the glycoprotein IIb-IIIa complex quantitatively. Furthermore, our data suggest that one or more active metabolites rather than the native drug mediate the abnormalities of platelet function observed in ticlopidine-treated subjects.

Adenosine Triphosphate↗

PubMed1985

Increased retraction of fibrin clots by endothelial cells of infants of diabetic mothers.

Cultured endothelial cells (EC) from the umbilical veins of infants of non-diabetic mothers induced retraction of fibrin clots formed by addition of thrombin to cell-free plasma. Fibrin clot retraction activity increased with time, reaching a maximum within 24 hours and was inhibited at 4 degrees C or in the presence of EDTA. This retraction had many characteristics in common with that induced by platelets. EC obtained from the umbilical veins of infants of poorly controlled insulin dependent diabetic mothers (IDDM) showed similar patterns of retraction. However, compared to normals, these cells induced greater retraction. Since the retraction of fibrin clots is thought to promote the exposure of sub-endothelial layers and since such an exposure plays a major role in thrombogenesis, we suggest that retraction of fibrin clot by EC should be taken into account in evaluating pre-thrombotic states.

Cells, Cultured↗

PubMed1984