PubMed Health⌕ Search

Biomedical subjects

M Montana

Publications and source records attributed to M Montana.

At least 19 recordsLinked to original sources
PubMed2003

Polymorphonuclear leukocyte integrin pattern, at baseline and after activation, in type 2 diabetic subjects with macrovascular complications.

In vascular atherosclerotic disease and in diabetes mellitus few studies have evaluated the polymorphonuclear leukocyte (PMN) adhesion molecule pattern. In this study we examined the PMN integrin expression at baseline and after activation in controls and type 2 diabetic subjects with macrovascular complications (MVC). We enrolled 21 subjects with type 2 diabetes mellitus and macrovascular complications, localized in peripheral, coronary and cerebral sites. The patients had peripheral occlusive arterial disease, chronic cerebrovascular disease or coronary heart disease. We evaluated the expression of some PMN integrins (CD11a, CD11b, CD11c, CD18), using flow cytofluorimetry, at baseline and after in vitro activation with 4-phorbol-12-myristate-13 acetate. Type 2 diabetic subjects with MVC showed, compared to normals, an increase of CD11a and CD18 and a decrease of CD11b and CD11c. After activation, in PMN(s) of normal subjects, we found an increase in the expression of all adhesion molecules, while in PMNS of type 2 diabetic subjects with MVC we observed an increase of CD11b and CD11c and a decrease of CD11a. In type 2 diabetic patients with MVC the basal upregulation of CD11a and CD18 may be related to the PMN spontaneous activation, while the behavior of CD11b may depend on its self-consumption. After activation the CD11a modification may be due to its cleavage or to an altered integrin phosphorylation/dephosphorylation balance.

Aged↗
PubMed2002

Polymorphonuclear leukocyte membrane fluidity, at baseline and after in vitro activation, in obesity with or without diabetes mellitus.

We studied a group of 28 obese subjects (mean age 38.2+/-13.5 years, body mass index 35.0+/-5.6 kg/m2) with insulin resistance demonstrated employing an euglycemic hyperinsulinemic clamp, subdivided into a subgroup with normal glucose tolerance (NGT) and a subgroup with type 2 diabetes mellitus (DM). We examined the polymorphonuclear leukocyte (PMN) membrane fluidity at baseline and after activation with 4-phorbol 12-myristate 13-acetate (PMA) or N-formyl-methionyl-leucylphenylalanine (fMLP). At baseline, PMN membrane fluidity was significantly decreased in both subgroups compared to normals. In obese subjects with NGT no correlation was found between this PMN determinant and the parameters reflecting the insulin-resistance degree (glucose disposal [M] and metabolic clearance rate of glucose [MCR]), while in type 2 DM subjects the PMN membrane fluidity was correlated to M and MCR. After activation with PMA and fMLP, no variation in PMN membrane fluidity was observed in normals, while in obese subjects with NGT an early decrease was present only after fMLP activation, and in obese subjects with type 2 DM there was a constant and significant decrease of this PMN parameter after activation with PMA and fMLP. Our interest in the study of the PMN membrane fluidity emerges from its known role in PMN function, especially considering that PMN cells, together with monocytes, may be mediators of vascular damage.

Adult↗
PubMed2002

Haemorheological profile in metabolic Syndrome.

Metabolic Syndrome (MetS) has been defined as a clinical condition including impaired glucose tolerance or diabetes mellitus and/or insulin-resistance, associated with two or more of the following components: arterial hypertension, central obesity, dyslipidaemia, microalbuminuria. In a group of subjects with MetS we examined the macrohaemorheological profile, demonstrating a significant increase of blood, plasma and serum viscosity and a decrease of whole blood filterability. The results show that in these subjects a secondary hyperviscosity condition is present, but also that several significant correlations are present between the haemorheological variables and some aspects of MetS, especially those reflecting central obesity (waist to hip ratio) and insulin-resistance. The altered haemorheological profile likely contributes to explain the high cardiovascular risk present in MetS, but it may also participate, through its influence on haemodynamic pattern, in the pathogenesis of insulin-resistance.

Adult↗
PubMed2002

Polymorphonuclear leukocyte integrin profile in diabetes mellitus.

We examined the polymorphonuclear leukocyte (PMN) integrin pattern in 45 diabetic subjects without macrovascular complications, including 21 subjects with type 1 and 24 with type 2 diabetes mellitus. The PMN adhesion molecules (CD11a, CD11b, CD11c, CD18) were evaluated using indirect immunofluorescence and a flow cytometer, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenyl-alanine (fMLP). At baseline, in diabetic subjects the phenotypical expression of CD11a and CD11b was significantly reduced and CD11c was increased, whereas CD18 was unchanged in comparison with normals. Considering type 1 and 2 diabetic subjects separately, CD11a was reduced and CD11c was increased in both subgroups, CD11b was decreased only in type 1 diabetics and CD18, decreased in type 1, was increased in type 2 subjects. After activation with PMA and fMLP, in normal subjects we observed a significant increase of all PMN adhesion molecules whereas in diabetic subjects only CD11c increased significantly with both activating agents, and CD11b increased only after PMA activation. In type 1 diabetic subjects only CD11c expression was increased, and in type 2 diabetic subjects an increase of CD11b (with PMA) and an increase of CD11c (with fMLP) were noted. In conclusion, we found in diabetic subjects of type 1 and 2 an altered behaviour pattern of PMN integrins both at baseline and, in particular, after in vitro activation. These data may help in explaining the role of PMN in the evolution of diabetic vascular complications.

Adult↗
PubMed2001

Granulocyte integrins before and after activation in acute ischaemic stroke.

We examined in 19 subjects with acute ischaemic stroke (AIS) the PMN integrin pattern (CD11a, CD11b, CD11c, CD18), using indirect immunofluorescence and adopting a flow cytometer, at baseline and during activation, prolonged for 5 and 15 min, with 4-phorbol 12-myristate 13-acetate (PMA). At baseline, an increase in the expression of CD11c and CD18 and a decrease in the CD11b were evident in AIS subjects compared to normals. After activation, we found in normals a constant and significant increase of all PMN adhesive molecules, while in AIS subjects, we found an increase in CD11b and CD18, a decrease in CD11a and no variation in CD11c. While the basal upregulation of CD11c and CD18 may depend on the PMN spontaneous activation or on the increase of cytokines, the decrease of CD11b may be due to its self-consumption. After activation, the decrease in CD11a noted in AIS may be related to its cleavage or to an altered integrin phosphorylation/dephosphorylation balance.

Acute Disease↗
PubMed2000

Polymorphonuclear leukocyte membrane fluidity before and after activation in subjects with insulin resistance.

The aim of this research was the evaluation of polymorphonuclear leukocyte (PMN) membrane fluidity in subjects with insulin resistance. Insulin sensitivity, in fact, may be influenced by plasma membrane fluidity. We enrolled 19 subjects with insulin resistance previously demonstrated during an euglycemic hyperinsulinemic clamp. PMN membrane fluidity was studied by labeling intact cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene and calculating the fluorescence polarization degree. The measurement was made before and after incubation of PMNs with two activating agents: 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). The baseline data showed a reduction of PMN membrane fluidity in subjects with insulin resistance. After PMN activation with PMA and fMLP, no significant variation in membrane fluidity was present in PMNs from normals, while in those from subjects with insulin resistance a slight decrease in PMN membrane fluidity was found only after activation with fMLP. The behavior of PMN membrane fluidity, before and after activation, distinguishes insulin-resistant subjects from normal controls, although the effect cannot be directly correlated with the degree of insulin resistance.

Adolescent↗
PubMed2000

Acute ischemic stroke : polymorphonuclear leukocyte membrane fluidity and cytosolic Ca(2+) concentration at baseline and after chemotactic activation.

BACKGROUND AND PURPOSE: Several reports have considered the role of systemic leukocytes in acute ischemic stroke (AIS). Initially, greater attention was focused on the leukocyte count and subsequently on their adhesiveness, aggregation, rheology, and activation. The aim of this study was the evaluation of certain polymorphonuclear leukocyte (PMN) parameters, reflecting their rheology and activation, in subjects with AIS. METHODS: In a group of 19 subjects with AIS and in a control group of 18 subjects with asymptomatic vascular atherosclerotic disease, we evaluated the PMN membrane fluidity and cytosolic Ca(2+) concentration at baseline and after in vitro chemotactic activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). RESULTS: From the obtained data, it is evident that at baseline only PMN membrane fluidity distinguishes control subjects from AIS subjects. After PMN activation with PMA and fMLP, prolonged for 5 and 15 minutes, we found an increase in PMN cytosolic Ca(2+) concentration and a decrease in PMN membrane fluidity only in subjects with AIS. CONCLUSIONS: These findings emphasize that in subjects with AIS a functional alteration of systemic PMN cells is clearly expressed during chemotactic activation, although the mechanism of this abnormality is not yet explained.

Acute Disease↗
PubMed1999

Diabetes mellitus: polymorphonuclear leukocyte (PMN) filtration parameters and PMN membrane fluidity after chemotactic activation.

The goal of this research was to determine leukocyte rheology at baseline and after chemotactic activation in type I and type II diabetics. In 19 normal subjects, 21 type I diabetics, and 16 type II diabetics at baseline and after in vitro chemotactic activation (prolonged for 5 and 15 minutes) with two stimulating agents (4-phorbol 12-myristate 13-acetate [PMA] and N-formyl-methionyl-leucyl-phenylalanine [fMLP]), we evaluated polymorphonuclear (PMN) filtration parameters (using a St. George filtrometer [Carri-Med, Dorking, UK] and considering the initial relative flow rate [IRFR] and the concentration of clogging particles [CP]) and PMN membrane fluidity (obtained by marking PMNs with the fluorescent probe 1-(4-[trimethylamino]phenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). At baseline, there was a difference between normals and type I and II diabetics for PMN membrane fluidity only. After activation in normals and diabetics of both types, a significant variation was present in PMN filtration parameters (IRFR and CP) at both 5 and 15 minutes. In normals, no variation was present in PMN membrane fluidity after activation with PMA or fMLP. After PMN activation, only in type I diabetics was a significant decrease in PMN membrane fluidity present at both 5 and 15 minutes. After PMN activation with either PMA or fMLP in comparison to basal values, only the mean variation (delta%) of the IRFR was significantly different between normals, type I diabetics, and type II diabetics at both 5 and 15 minutes. From the data obtained, it is evident that after activation, the PMN filtration pattern shows a specific behavior in diabetics of both types, while PMN membrane fluidity changes only in type I diabetics. The latter finding may be the basis of a metabolic pattern present in PMNs of this type, revealed after in vitro activation.

Adolescent↗
PubMed1999

Leukocyte rheology before and after chemotactic activation in some venous diseases.

OBJECTIVE: to evaluate leukocyte rheology, polymorphonuclear leukocyte (PMN) membrane fluidity and cytosolic Ca2+ concentration in subjects with post-phlebitic leg syndrome (PPS) and acute deep-venous leg thrombosis (DVT). SUBJECTS: twenty-two subjects with leg PPS and 14 subjects with leg DVT. METHODS: we evaluated the leukocyte filtration (unfractionated, mononuclear cells (MN) and PMN), the PMN membrane fluidity and the PMN cytosolic Ca2+ concentration. Subsequently, we evaluated the same PMN variables after in vitro chemotactic activation with 4-phorbol 12-myristate 13-acetate (PMA) and N -formyl-methionyl-leucyl-phenylalanine (fMLP). RESULTS: at baseline we observed a significant difference in the filtration variables of unfractionated and MN cells and in PMN cytosolic Ca2+ concentration. After activation, in normal subjects and subjects with PPS and DVT, a significant variation in PMN filtration at 5 and 15 minutes was evident. In normal subjects, no variation was present in PMN membrane fluidity or cytosolic Ca2+ concentration after activation. In subjects with PPS and DVT, we found a decrease in PMN membrane fluidity and an increase in PMN cytosolic Ca2+ concentration. After PMN activation (at 5 and 15 min) Delta% of IRFR distinguished normal subjects from subjects with PPS and DVT, while no difference was found in Delta% of membrane fluidity or cytosolic Ca2+ concentration. CONCLUSIONS: there is a functional alteration of leukocytes in these patients whose mechanisms are not yet clear.

Calcium↗
PubMed1999

Hydrocortisone levels in the urine and blood of horses treated with ACTH.

An investigation was undertaken to demonstrate whether therapeutic treatment with ACTH raises hydrocortisone (cortisol) levels in horse urine above the limit (1000 ng/ml) established by the International Conference of Racing Authorities with the aim of controlling the abuse of cortisol and ACTH in equine sports. ACTH (200 iu) was administered i.m. to 3 Thoroughbred horses; urine and blood samples were collected at intervals afterwards and analysed by an immunoenzymatic system (ELISA) and HPLC-MS. To ascertain post exercise cortisol levels in untreated horses, 101 urine and 103 serum samples were taken from horses immediately after racing and analysed by ELISA. The peak urine level of cortisol, detected 8 h after ACTH administration, was around 600 ng/ml using either ELISA or HPLC-MS. The peak serum cortisol concentration was found to be around 250 ng/ml by ELISA, but consistently less by HPLC-MS. Mean cortisol levels in post race horses were 135.1+/-72.1 ng/ml in urine and 90.1+/-41.7 ng/ml in serum. High levels of the metabolite 20beta-dihydrocortisol in urine and the cortisol precursor 11beta-desoxycortisol in serum were found. The latter showed high cross-reactivity with cortisol on ELISA. In our experiment, treatment with ACTH 200 iu i.m. did not raise urinary cortisol levels above the 1000 ng/ml threshold proposed by the ICRA.

Adrenocorticotropic Hormone↗
PubMed1999

Chronic renal failure: leukocyte rheology and polymorphonuclear cytosolic Ca2+ concentration.

In a group of subjects with chronic renal failure (CRF), we evaluated the leukocyte rheological activity, expressed as the filtration rate, the polymorphonuclear (PMN) membrane fluidity and the PMN cytosolic Ca2+ content. Using the St. George's Filtrometer, we determined the filtration rate of unfractionated, mononuclear and PMN leukocytes. Using the fluorescent probe 1.4-(trimethylamino)-phenyl-4-phenyl-hexatriene (TMA-DPH), we examined the PMN membrane fluidity and, using the Fura 2-AM, the PMN cytosolic Ca2+ content. From the results obtained, it is evident that only the initial relative flow rate of unfractionated leukocytes was significantly reduced in subjects with CRF, while the filtration parameters of mononuclear and PMN cells did not distinguish normals from CRF subjects. No variation was evident for the PMN membrane fluidity, while the PMN cytosolic Ca2+ content was significantly increased in CRF subjects. In these subjects no correlation was found between leukocyte filtration parameters, PMN membrane fluidity, PMN cytosolic Ca2+ content and plasma parameters (blood urea nitrogen and serum creatinine), reflecting the degree of the CRF. In conclusion, in CRF subjects the abnormality of the leukocyte flow properties was restricted to the initial flow rate of unfractionated leukocytes, whereas the increase of PMN cytosolic Ca2+ content might be attributed to PMN activation.

Calcium↗