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Biomedical subjects

G Anfossi

Publications and source records attributed to G Anfossi.

At least 55 records · Page 3Linked to original sources
PubMed1992

Insulin, at physiological concentrations, enhances the polymorphonuclear leukocyte chemotactic properties.

We investigated the influence of insulin on human polymorphonuclear leukocyte (PMN) chemotaxis induced by mediators in a microchamber assay. Insulin increased, with a dose-response relationship, chemotaxis induced by formyl-methionyl-leucyl-phenylalanine, calcium ionophore and phorbol-miristyl acetate (p = 0.0057, p = 0.0001 and p = 0.0215, respectively). The hormone effect was present also at the physiological concentration of 40 microU/ml. Our data show that insulin affects PMN activity in normal subjects and therefore support the hypothesis that insulin deficiency may be responsible for the impaired PMN function observed in diabetic patients in poor metabolic control.

Adult↗
PubMed1992

Studies on the effect of dopamine on the human platelet response.

1. The present study investigated the in vitro effect of dopamine on platelet responses in healthy subjects. 2. Dopamine concentrations over 5 mumol/L induced a primary aggregating response and a slight release of alpha-granule proteins, beta-thromboglobulin and platelet factor-4 in all subjects. In 25% of investigated subjects a delayed secondary aggregation was observed with dopamine concentrations over 100 mumol/L. 3. Low dopamine concentrations (5-7.5 nmol/L) increased the platelet sensitivity to other aggregating agents (adenosine diphosphate, collagen and sodium arachidonate). The effect of subaggregating concentrations of serotonin was potentiated by dopamine. 4. The effect of dopamine on platelet responses was prevented by low concentrations of alpha-adrenoceptor antagonists (phentolamine and yohimbine); antagonists of dopamine receptors (haloperidol and domperidone) were able to decrease the extent of the dopamine-induced secondary aggregating wave in the responders, but they failed to prevent the primary aggregation and the effects on platelet response to other aggregating agents. 5. The present data demonstrated that the effects of dopamine on human platelets are mainly mediated by interactions with alpha-adrenoceptors.

Adenosine Diphosphate↗
PubMed1992

A comparison of the predictive power for overall blood glucose control of a 'good' fasting level in type 2 diabetic patients on diet alone or with oral agents.

The European NIDDM Policy Group classifies both fasting and post-prandial blood glucose concentrations into 'good', 'acceptable', and 'poor' categories. The aim of the present study was to evaluate whether a 'good' fasting blood glucose concentration in Type 2 diabetic patients on diet or diet + oral hypoglycaemic agents is able to predict 'good' blood glucose values throughout the day, and therefore to discover whether or not it is necessary to perform blood glucose profiles in Type 2 diabetic patients when their fasting value is 'good'. Capillary blood glucose profiles (n = 417) were measured in 287 Type 2 diabetic patients, on diet alone (279 profiles), or on diet + tablets (138 profiles). We observed that 66% of profiles on diet and 44% of profiles on diet + tablets had only 'good' blood glucose concentrations (p less than 0.001). Eleven percent of profiles on diet and 30% of profiles on diet + tablets included 'poor' blood glucose concentrations (p less than 0.001). Despite matched fasting blood glucose concentrations (diet 5.69 +/- 0.04 (+/- SE) vs tablets 5.75 +/- 0.05 mmol l-1), levels were higher in the diet + tablet treated patients at all later time-points (p less than 0.01-0.001). HbA1c was significantly higher in tablet-treated patients than in patients on diet alone (6.6 +/- 0.1 vs 5.9 +/- 0.1%, p less than 0.001), and correlated with the mean blood glucose concentration (r = 0.43, p less than 0.001) but not with the fasting glucose concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1992

Moderate exercise increases platelet function in type I diabetic patients without severe angiopathy and in good control.

OBJECTIVE: The aim of this study was to investigate whether a 45-min moderate exercise, performed postprandially with a timing that partially prevented the risk of hypoglycemia, was able to modify platelet function in patients affected by insulin-dependent (type I) diabetes mellitus without severe late complications and in a good metabolic control. RESEARCH DESIGN AND METHODS: We submitted 6 male type I diabetic patients (27.2 +/- 3.4 yr; body mass index, 21.4 +/- 0.6 kg/m2; HbA1c, 7.6 +/- 0.9%) on a daily three-insulin injection regimen, without severe late complications of diabetes, to a 45-min moderate exercise (about 50% of maximal oxygen consumption) with a cycle ergometer, beginning 180 min after breakfast and 195 min after a subcutaneous shot of regular insulin. Serial venous blood samples were conducted to measure plasma glucose, free insulin, counterregulatory hormones (glucagon, growth hormone, cortisol, and catecholamines), platelet sensitivity to ADP, platelet activating factor and collagen, and plasma concentrations of the platelet-specific protein beta-thromboglobulin (a marker of the platelet release reaction in vivo). RESULTS: Exercise was accompanied by a decrease of plasma glucose (from 5.9 +/- 1.2 to 4.6 +/- 1 mmol/L, P = 0.067) and free insulin (from 180 +/- 36 to 114 +/- 30 pmol/L, P = 0.003), and by a significant increase of growth hormone (from 5 +/- 1 to 15 +/- 4 micrograms/L, P = 0.045), cortisol (from 240 +/- 30 to 406 +/- 69 nmol/L, P = 0.018), epinephrine (from 1005 +/- 240 to 5143 +/- 1753 pmol/L, P = 0.077), and norepinephrine (from 5.04 +/- 1.08 to 13.48 +/- 2.98 nmol/L, P = 0.009). Platelet sensitivity to the agonists and plasma concentrations of beta-thromboglobulin increased during the exercise period. In particular, ADP ED50 reached during exercise 61 +/- 16% of basal values (P = 0.048), platelet activating factor ED50 reached 73 +/- 11% (P = 0.043), and collagen ED50 reached 68 +/- 9% (P = 0.008). beta-Thromboglobulin rose from 24 +/- 2 to 32 +/- 3 micrograms/L (P = 0.007). CONCLUSIONS: Moderate exercise enhances platelet function in type I diabetic patients without severe angiopathy and in a good metabolic control.

Adenosine Diphosphate↗
PubMed1991

Occurrence of low blood glucose concentrations during the afternoon in type 2 (non-insulin-dependent) diabetic patients on oral hypoglycaemic agents: importance of blood glucose monitoring.

The European NIDDM Policy Group states that the lowest target for good control of Type 2 (non-insulin-dependent) diabetic patients is a blood glucose level 4.4 mmol/l, both fasting and postprandially. The aim of this study is to evaluate the occurrence and temporal distribution of values under this target in the clinical records of 463 Type 2 diabetic patients, treated by diet or diet and oral hypoglycaemic agents, monitored for at least 2 years. The protocol includes blood glucose measurements after overnight fasting (08.00 hours), 120-150 min after breakfast (11.00 hours) and 120 and 240 min after lunch (14.00 and 16.00 hours). At least one blood glucose concentration of less than 4.4 mmol/l was presented by 42% of the patients. The only difference between patients showing and not showing glycaemic levels under this target was the higher percentage on oral hypoglycaemic agents in the first group (68.4% vs 56.9%, p = 0.016). We considered 299 blood glucose profiles containing at least one value of less than 4.4 mmol/l, observing that a) 46.9% of profiles from patients treated by diet alone and 68.7% of profiles from patients treated both by diet and oral hypoglycaemic agents presented the lowest blood glucose concentration at 16.00 hours (p = 0.002). b) No correlation existed between fasting blood glucose and values at 16.00 hours in profiles from diet-treated patients, whereas a negative correlation was present in patients on diet and oral hypoglycaemic agents, indicating that an excess of oral agents, administered to correct fasting hyperglycaemia, was the cause of the low glycaemic values in the afternoon.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Phenothiazines inhibit collagen-induced thromboxane B2 synthesis and increase forskolin anti-aggregating effects in human platelets.

1. The aim of the present study was to investigate the effects of phenothiazine compounds chlorpromazine and trifluoperazine on human platelet response to collagen and sodium arachidonate. 2. The results demonstrated that phenothiazines inhibit collagen-induced platelet aggregation and thromboxane B2 synthesis in a dose-dependent way and increase the antiaggregating properties of forskolin. 3. Phenothiazines at high concentrations decreased the platelet aggregation in response to arachidonate, without a significant reduction of thromboxane B2 production. 4. The data provides evidence that phenothiazine effects could involve calmodulin-dependent enzymatic activities.

Adult↗
PubMed1991

Effects of diltiazem on thromboxane B2 production from platelet-rich plasma and whole blood.

The present study evaluated the effects of the calcium-channel blocking agent diltiazem on platelet aggregation and on synthesis of thromboxane B2 (the stable metabolite of thromboxane A2) from platelet-rich plasma (PRP) and whole blood samples. Our results showed that diltiazem inhibits collagen- and thrombin-induced platelet aggregation and TXB2 production from PRP. Since no significant interference with conversion of arachidonate to thromboxane A2 was demonstrated, inhibition of phospholipase A2 activity may be the prevailing mechanism of the diltiazem effect. The drug demonstrated a dose-related inhibitory activity on TXB2 synthesis from whole blood samples during spontaneous clotting or following stimulation with collagen or thrombin. The present results give further evidences for an antiplatelet activity of diltiazem and support the hypothesis that inhibition of platelet function contributes to the therapeutic efficacy of this drug in the treatment of cardiovascular diseases.

Adult↗
PubMed1991

Calcium-channel blocking agents verapamil and diltiazem are inhibitors of vasopressin-induced human platelet activation.

1. This study investigated the influences of calcium-channel blocking agents verapamil and diltiazem on platelet responses induced by arginine vasopressin (AVP) and lysine vasopressin (LVP). 2. The substances inhibited platelet aggregation induced by both low and high AVP concentrations, LVP and adrenaline plus AVP. IC50 values of each drug are lower than those determined for ADP- and collagen-elicited aggregation. Verapamil and diltiazem also decreased AVP-induced thromboxane B2 synthesis. 3. Other series of experiments showed that the addition of ethyleneglycol-bis-(beta-amino-ethyl ether) N, N'-tetra-acetic acid to platelet-rich plasma samples also prevented the platelet response to vasopressin polypeptides. 4. Our data provide evidence that the effects of verapamil and diltiazem on vasopressin-induced platelet responses may be directly related to inhibition of extracellular calcium entry.

Adult↗
PubMed1990

Studies on inhibition of human platelet response by diltiazem.

1. Aim of the present investigation was to investigate the effects of calcium blocking agent diltiazem on human platelet response to aggregating agents. 2. Results showed that diltiazem inhibits platelet aggregation induced by ADP, arginine vasopressin, adrenaline, collagen, Na arachidonate, thrombin and phorbol ester PMA in a dose-dependent way. 3. Diltiazem decreased also beta-thromboglobulin release and Thromboxane B2 production from stimulated platelets. 4. Intraplatelet cyclic AMP levels were not modified by the substance. 5. Data provide evidence that the modulation of human platelet function by diltiazem could be also related to inhibition of protein kinase C.

Adult↗
PubMed1990

Arginine vasopressin release from human platelets after irreversible aggregation.

1. The release of arginine vasopressin from human platelets was investigated in platelet-rich plasma after irreversible aggregation induced by adenosine 5'-pyrophosphate, collagen, sodium arachidonate, thrombin and adrenaline in vitro. 2. Arginine vasopressin levels were significantly higher in the supernatant from stimulated platelet-rich plasma than from unstimulated samples, reaching 3.5 X 10(-12) (range 1.6-12.5 X 10(-12) mol/l in the absence of an aggregating agent, 8.8 X 10(-12) (range 4.2-17.5 X 10(-12) mol/l after adenosine 5'-pyrophosphate, 13.7 X 10(-12) (2.2-63.2 X 10(-12) mol/l after collagen, 7.8 X 10(-12) (2.2-14.6 X 10(-12) mol/l after sodium arachidonate, 7.8 X 10(-12) (2.2-16.3 X 10(-12) mol/l after thrombin and 12.2 X 10(-12) (4.8-32.1 X 10(-12) mol/l after adrenaline. 3. An arginine vasopressin level of 18 X 10(12) mol/l, which can be achieved physiologically, increased the sensitivity of platelets to adenosine 5'-pyrophosphate and collagen in vitro; the same concentration of arginine vasopressin caused a potentiation of the effect of catecholamines on the response of platelets to sodium arachidonate. 4. These results indicate that intraplatelet arginine vasopressin is released during aggregation and suggest that a local release of arginine vasopressin could occur after complete platelet aggregation in vivo.

Adenosine Diphosphate↗
PubMed1990

Desensitization of the platelet aggregation response to adrenaline during insulin-induced hypoglycaemia in man.

The aim of the present study was to investigate the influence of insulin-induced hypoglycaemia on platelet sensitivity to adrenaline and non-adrenergic agonists in man. Twenty-five healthy male subjects volunteered for the study. To evaluate the effects on platelets of different insulin-adrenaline interrelationships, two experimental models were used. In the first, hypoglycaemia was induced by a 60-min IV infusion of human insulin at the rate of 64 mU m-2 min-1, whereas in the other the same insulin dose was administered as an IV bolus (3.84 U m-2). Throughout the studies, plasma glucose, insulin, and adrenaline were measured together with platelet sensitivity to adrenaline, ADP, platelet activating factor, collagen, and sodium arachidonate. In both studies, hypoglycaemia induced a reduction of platelet sensitivity to adrenaline (p = 0.006 in infusion and p = 0.045 in injection study). In particular, maximal aggregation to adrenaline fell from 47.9 +/- 9.9 (+/- SE) to 31.1 +/- 11.3% at the hypoglycaemic nadir in the infusion study, and from 64.6 +/- 8.2 to 34.6 +/- 10.3% at the hypoglycaemic nadir in the injection study. In the injection study an increase of platelet sensitivity to ADP (p = 0.05), platelet activating factor (p = 0.018), sodium arachidonate (p = 0.035), and collagen (p = 0.027) was also found, in agreement with observations already published using the infusion protocol. Thus, insulin-induced hypoglycaemia increases platelet sensitivity to non-adrenergic agonists and decreases platelet response to adrenaline.

Adenosine Diphosphate↗
PubMed1990

Sodium taurocholate affects prostacyclin constitutive production by cultured human vascular endothelial cells.

The prostaglandin system is impaired in cholestasis; bile salts, which are a specific biochemical feature of this condition, have been shown to affect functional properties of cells and tissues, and, in some cases, their action is mediated through an alteration of prostaglandin pathway. Endothelium is a privileged site for the production and the action of arachidonate metabolites-prostacyclin in particular. To determine the effects of bile salts on the properties of vascular endothelium, cultured human endothelial cells were studied. Cholic acid sodium salt was seen to induce a direct injury on endothelial cells, as was demonstrated by a massive dismission of the intracellular radiolabel chromium 51. In the absence of detectable toxic effect, sodium taurocholate caused a significant depression of prostacyclin constitutive production from human endothelial cells. The action of sodium taurocholate was related to its concentration and to the time of exposure, and the alteration of prostacyclin production was found to be reversible. Conversely, the generation of thromboxane A2 was not influenced by this bile salt, which may suggest a specific action of sodium taurocholate on arachidonic acid metabolism. These findings indicate that bile salts may directly alter some functional properties of cultured human endothelial cells and may provide a basis for explaining some generalized manifestations that are observed in pathologic conditions characterized by cholemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

G1/S transition in normal human T-lymphocytes requires the nuclear protein encoded by c-myb.

Exposure of peripheral blood mononuclear cells (PBMC) to an 18-base c-myb antisense oligomer before mitogen or antigen stimulation resulted in almost complete inhibition of c-myb messenger RNA and protein synthesis and blockade of T lymphocyte proliferation. Expression of early and late activation markers, interleukin-2 receptor and transferrin receptor, respectively, by PBMC was unaffected by antisense oligomer exposure as was the expression of c-myc messenger RNA. In contrast, histone H3 messenger RNA levels and DNA content were selectively decreased. These results suggest that c-myb protein deprivation does not perturb T lymphocyte activation or early molecular events that may prepare the cell for subsequent proliferation. Rather, it appears to specifically block cells in late G1 or early S phase of the cell cycle.

Cell Division↗
PubMed1989

Insulin influences the renin-angiotensin-aldosterone system in humans.

This study investigates whether insulin influences the renin-angiotensin-aldosterone system in humans. Six healthy male volunteers were placed on a 30-minute euglycemic insulin clamp at 160 microU/mL; euglycemia was maintained also in the following 60 minutes by means of appropriate dextrose infusion. Throughout the study, plasma renin activity, angiotensin II, aldosterone, and factors involved in the regulation of the renin-angiotensin-aldosterone system were measured: catecholamines, angiotensin-converting enzyme, sodium, and potassium. A significant increase of plasma renin activity and angiotensin II was observed, and a decrease of aldosterone was also detected. These changes can be ascribed to the effects of the rapid insulin-induced plasma potassium decrease on plasma renin activity and aldosterone secretion because they did not occur in a control clamp study with a potassium infusion.

Adult↗
PubMed1989

Influence of propranolol on platelet aggregation and thromboxane B2 production from platelet-rich plasma and whole blood.

The beta-adrenoceptor antagonist propranolol is used in the therapy of hypertension and ischemic heart disease. The aim of our study was to evaluate the effects of this drug on platelet aggregation and on synthesis of thromboxane B2 (the stable metabolite of Thromboxane A2) from platelet rich plasma (PRP), whole blood samples and during spontaneous clotting. The results indicate that propranolol at concentrations near the therapeutic range, significantly inhibit collagen and thrombin-induced platelet aggregation and TxB2 synthesis from PRP. Furthermore the drug demonstrates inhibitory activity on B-TG release and TxB2 production from whole blood samples and on spontaneous clotting. The results suggest that some benefits of propranolol in the treatment of patients with coronary artery disease or cardiovascular conditions associated with platelet hyperaggregability may also be related to interference with platelet activation "in vivo" and with TxA2 generation.

Adult↗
PubMed1989

An oligomer complementary to c-myb-encoded mRNA inhibits proliferation of human myeloid leukemia cell lines.

To study the role of the protooncogene c-myb in regulating myeloid leukemia cell proliferation and differentiation, we exposed cells of the human leukemia lines HL-60, ML-3, KG-1, and KG-1a to an oligodeoxynucleotide complementary to an 18-base-pair (bp) sequence of c-myb-encoded mRNA. This treatment resulted in a significant decrease in cell proliferation in all of the lines, which was most marked in HL-60 cells. After 5 days in culture, in several separate experiments with different oligomer preparations, 75% growth inhibition was observed in c-myb antisense treated cells in comparison to untreated HL-60 cells. Two c-myb antisense oligomers of identical length with either 2- or 4-bp mismatches had no effect on cell growth nor did an 18-bp c-myb sense or myeloperoxidase antisense oligomer. The effect of a c-myc antisense oligomer (18 bp) on the growth of HL-60, KG-1, and KG-1a cells was also studied. This oligomer had much less inhibitory effect on cell proliferation than did the c-myb antisense sequence. Interestingly, although c-myc antisense treatment induced maturation of HL-60 cells while it inhibited cell proliferation, such an effect was not noted in c-myb antisense treated cells. These studies indicate that the nuclear protein encoded by the c-myb protooncogene is required for maintenance of proliferation in certain leukemia cell lines. In compared to c-myc protein suggest that, at least in HL-60 cells, c-myc amplification or N-ras activation may not be sufficient to maintain the leukemic growth in the absence of c-myb protein. These findings support the hypothesis that development and maintenance of a malignant phenotype requires a multiplicity of interrelated genetic events.

Cell Differentiation↗