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Biomedical subjects

A Picardi

Publications and source records attributed to A Picardi.

At least 73 records · Page 4Linked to original sources
PubMed1996

Tetrasomy 8 and t(1;11)(p32;q24) in acute myelo-monocytic leukemia with extensive leukemic cutaneous involvement.

We report a case of tetrasomy 8 in a patient suffering from acute myelomonocytic leukemia with extensive leukemic cutaneous infiltration. In all metaphases analyzed t( I;11)(p32;q24) was concomitantly observed. Similarly to other cases with tetrasomy 8, the patient showed monocytic involvement and poor response to chemotherapy. We conclude that this kind of cytogenetic aberration is associated with distinct morphologic and clinical features.

Aged↗
PubMed1996

A phase II study of VP-16, intermediate-dose Ara-C and carboplatin (VAC) in advanced acute myelogenous leukemia and blastic chronic myelogenous leukemia.

Thirty-one patients with either advanced AML (18) or blastic CML (13) were treated with an intensive timed sequential combination of VP-16 (100 mg/m2/day i.v., days 1-3 and 8-10), intermediate-dose Ara-C (500 mg/m2 i.v. over 1 h q 12 h, days 1-3 and 8-10) and carboplatin (150 mg/m2/day i.v. continuous infusion, days 1-3 and 8-10). CR rates were 9/18 (50%) for patients with AML and 9/13 (69%) for those with blastic CML, for an overall CR rate of 58%. Among patients with AML, CR rates for specific subgroups were: primary resistant disease 2/6; resistant relapse 1/5; second relapse 6/7. Ten patients were refractory to VAC and three (10%) died of complications during marrow hypoplasia. Median overall survival was 7 months, and median DFS of the 18 responders 4 months. The major toxicity was myelosuppression and infection. The VAC regimen has significant activity and acceptable toxicity in myelogenous leukemias. The very high response rate observed in blastic CML warrants further testing of carboplatin-based regimens in this poor-risk form of leukemia.

Adolescent↗
PubMed1996

A potential experimental model for the study of osteopenia in CCl4 liver cirrhotic rats.

In order to search for an experimental model to further investigate the osteopenia associated to liver cirrhosis (LC), this study has been focused on investigating the occurrence of bone disorders in male rats to which LC histologically confirmed was induced through the validated procedure of CCl4 inhalation. Length, anteroposterior and lateromedial diameters, densitometry, mechanical stress resistance, hydroxyproline (OHprol) and calcium and phosphate contents were measured in femurs from control (n = 10) and liver cirrhosis rats (n = 10). It has been found that femurs from liver cirrhosis rats showed a significant reduction (p < 0.01) in bone weight (0.254 +/- 0.003 vs 0.230 +/- 0.004 g/100 g b.w.), anteroposterior (4.08 +/- 0.06 vs 3.69 +/- 0.05 mm) and lateromedial (5.33 +/- 0.05 vs 5.08 +/- 0.04 mm, p < 0.05) diameters, resistance to mechanical stress (405.8 +/- 9.5 vs 332.5 +/- 9.1 N) and total densitometry (0.416 +/- 0.005 vs 0.381 +/- 0.004 g/cm2). However, no significant differences were observed in bone length, calcium, OHprol and phosphate (all expressed as mg/100 mg fresh bone tissue) contents. Therefore, the proteins matrix to mineral contents ratio was not altered. These results indicate that in this model of experimental liver cirrhosis there is osteopenia characterized by bone frailty and reduced thickness, and it could offer an experimental model to study bone changes associated to liver cirrhosis.

Animals↗
PubMed1995

In vitro purging with BCR-ABL antisense oligodeoxynucleotides does not prevent haematologic reconstitution after autologous bone marrow transplantation.

We treated a patient with chronic myeloid leukaemia in accelerated phase with autologous bone marrow transplantation. Before reinfusion, cells were purged in vitro with a 26-mer phosphorothioate antisense oligodeoxynucleotide specific for the B2A2 junction. Incubation with antisense oligodeoxynucleotides produced a 24 and 41% reduction of CFU-GM and CD34+ cells, respectively. However, an in vitro test previously performed as a screening for patient inclusion in this procedure, revealed a 38 and 75% reduction of colony formation after 24-h and 168-h incubation, respectively. The patient showed bone marrow engraftment 15 days after reinfusion and haematological reconstitution after 17 and 25 days for platelets and neutrophils, respectively. Using fluorescence in situ hybridization in interphase nuclei, we demonstrated the presence of a proportion of Ph-negative cells in repeated controls after the autograft. The patient is now in unmaintained complete haematological remission 9 months after the autograft.

Antigens, CD↗
PubMed1994

Noradrenergic and dopaminergic interrelation in schizophrenia.

Growth hormone (GH) and prolactin (PRL) responses to the acute administration of clonidine (150 micrograms) and apomorphine (0.5 mg) were investigated in parallel in 20 drug-free subchronic and chronic schizophrenic patients and in nine control subjects. Neither basal levels of the two hormones nor their mean responses to both stimuli differed significantly between the two groups. However, eight patients had blunted GH responses to clonidine and seven to apomorphine; only two patients showed blunted GH responses to both stimuli. The blunted GH response to apomorphine correlated with the chronicity of the disorder. A greater than normal GH response to clonidine stimulation was observed in paranoid patients. Significant correlations were observed between negative symptoms and GH responses to clonidine (negative), between negative symptoms and PRL responses to apomorphine (positive), and between positive symptoms and PRL responses to apomorphine (negative).

Adolescent↗
PubMed1993

Temporomandibular joint pain-dysfunction syndrome and bruxism: etiopathogenesis and treatment from a psychosomatic integrative viewpoint.

It is common opinion that temporomandibular joint pain-dysfunction (TMJPD) syndrome and bruxism have a major psychosomatic component. In this paper, we try to review these entities in an integrated manner, taking into account both medical and psychological aspects. Two etiological models have been developed: the structural model emphasizes the role played by malocclusion or alterations of the maxillomandibular relationship, while the functional model underscores the role of stress, emotional tension, and personality characteristics. In TMJPD and bruxist patients a careful physical and psychological examination has to be performed. The classical dental treatment is based on equilibration procedures, prostheses and drugs. Treatment strategy can also be based on psychotherapeutic and relaxation treatments; in this respect, the use of EMG biofeedback training has been subjected to intense study.

Bruxism↗
PubMed1992

Intravenous infusion of diarginylinsulin, an insulin analogue: effects on glucose turnover and lipid levels in insulin-treated type II diabetic patients.

Diarginylinsulin is an intermediate in the conversion of proinsulin to insulin and is usually present in small amounts in vivo in humans. This study was designed to evaluate the following in insulin-treated type II diabetic patients: (1) the feasibility of an overnight intravenous infusion of diarginylinsulin, as compared with an overnight intravenous infusion of short-acting insulin, and the degree of early morning glycemic control; and (2) the effects of diarginylinsulin and human insulin on hepatic glucose production (HGO) in the postabsorptive state and on the glucose turnover rate and peripheral insulin sensitivity during an euglycemic hyperinsulinemic clamp. Diarginylinsulin and regular human insulin maintained a comparable degree of normoglycemia during the night, without significant glucose increases in the morning. Free-diarginylinsulin and free-insulin concentrations were not significantly different, and (HGO) was 2.1 +/- 0.5 versus 2.1 +/- 0.4 mg/kg/min with diarginylinsulin and regular human insulin, respectively (NS). During the euglycemic clamp, glucose infusion rate per unit of diarginylinsulin or human insulin infused (M/I ratio) was similar, and HGO was equally suppressed with diarginylinsulin and regular human insulin. No significant differences were seen in NEFA and triglyceride levels. In conclusion, these results indicate that diarginylinsulin is as potent as regular human insulin; it is normalizes HGO in the postabsorptive state; and its hepatic and peripheral actions on glucose and lipids are comparable to those of human insulin during an euglycemic hyperinsulinemic clamp.

Circadian Rhythm↗
PubMed1992

Indirect pathway of liver glycogen synthesis in humans is predominant and independent of beta-adrenergic mechanisms.

The relative contribution of the direct and indirect pathways to liver glycogen formation was assessed in humans by using a combined tracer-hepatic vein catheterization technique. An oral glucose load (75 g) labelled with 1-14C-glucose was administered to five subjects (control group) and 4.5 h later hepatic glycogen was flushed with glucagon and analysed to determine the randomization of 14C. The specific activity (SA) of the glycogen derived glucose (1-14C-glucose SA+recycled 14C-glucose SA) was 61 +/- 7% of the mean blood glucose SA of the interval 0-180 min after the oral glucose load. The relative values due to 1-14C-glucose and recycled 14C-glucose were 33 +/- 7 and 28 +/- 3%, respectively. The data indicate that the indirect pathway of glycogen formation is not only active in humans but contributes substantially (at least 50%) to liver glycogen formation. In order to investigate whether the basal adrenergic tone plays a role in the maintenance of the indirect pathway, the same protocol was also performed in a second group of subjects (n = 5) who received propranolol before the oral glucose load (propranolol group). The SA of the glycogen-derived glucose was considerably smaller than that of the control group (18 +/- 5 vs. 61 +/- 7%, P < 0.001), suggesting lesser glycogen formation. However, the ratio of 1-14C to recycled-14C in the glucose molecule was similar in the control (1.3 +/- 0.4) and propranolol group (1.9 +/- 1.2). We conclude that the basal adrenergic tone does not play any role in the operation of the indirect pathway of liver glycogen synthesis.

Adult↗
PubMed1988

Quantitation of forearm glucose and free fatty acid (FFA) disposal in normal subjects and type II diabetic patients: evidence against an essential role for FFA in the pathogenesis of insulin resistance.

This study was designed to quantitate glucose and FFA disposal by muscle tissue in patients with type II diabetes and to investigate the relationship between FFA metabolism and insulin resistance. The forearm perfusion technique was used in six normal subjects and two groups of normal weight diabetic patients, i.e. untreated (n = 8) and insulin-treated (n = 6). The latter received 2 weeks of intensive insulin therapy before the study. Plasma insulin levels were raised acutely [950-1110 pmol/L) (130-150 microU/mL)], while the blood glucose concentration was clamped at its basal value [4.9 +/- 0.1 (+/- SE) mmol/L in the normal subjects, 5.7 +/- 0.5 in the insulin-treated diabetic patients, and 5.5 +/- 0.3 in the untreated diabetic patients] by a variable glucose infusion. During the control period, arterial FFA concentrations were similar in the three groups, and they decreased to a comparable extent (less than 0.1 mmol/L) in response to insulin infusion. During the control period, the mean forearm FFA uptake was 2.5 +/- 0.5 mumol/L.min in the normal subjects, 2.9 +/- 0.5 in the insulin-treated patients, and 2.1 +/- 0.5 in the untreated diabetic patients. During the insulin infusion, FFA uptake was profoundly suppressed to similar levels in the normal subjects (0.9 +/- 0.1 mumol/L.min), the insulin-treated diabetic patients (1.1 +/- 0.3), and the untreated diabetic patients (0.9 +/- 0.1; P less than 0.001). Forearm glucose uptake was similar in the three groups during the control period. It increased during the insulin infusion, but the response in both diabetic groups was less than that in the normal subjects. The total amounts of glucose taken up by the forearm during the study period were 5.2 +/- 0.7, 2.6 +/- 0.5, and 2.1 +/- 0.6 mmol/L.min in the normal subjects, the insulin-treated diabetic patients, and the untreated diabetic patients, respectively (P less than 0.01). We conclude that 1) insulin-mediated glucose uptake by forearm skeletal muscle is markedly impaired in type II diabetes and improves only marginally after 2 weeks of intensive insulin therapy; 2) in contrast, no appreciable abnormality in forearm FFA metabolism is demonstrable in insulin-treated type II diabetic patients; and 3) FFA do not contribute to the insulin-treated skeletal muscle insulin resistance that occurs in patients with type II diabetes mellitus.

Adult↗
PubMed1986

Splanchnic and renal contribution to disposal of infused epinephrine in humans.

To evaluate the role of splanchnic and renal tissues in epinephrine disposal, we infused epinephrine (60 ng X kg-1 X min-1) into nine human volunteers during hepatic (n = 6) and/or renal (n = 4) vein catheterization. During the infusion plasma epinephrine rose higher in the artery (1,345 +/- 126 pg/ml) than in the hepatic (218 +/- 42 pg/ml) or renal vein (528 +/- 95 pg/ml). Splanchnic plasma flow increased by 43% (P less than 0.001), whereas renal plasma flow was unchanged. Net epinephrine uptake increased to a greater extent (3-fold) in the splanchnic area as compared with the kidney, amounting to 32 +/- 3% and 10 +/- 2% of the infused epinephrine load, respectively. The splanchnic epinephrine clearance also increased by 50-60%, while fractional extraction remained stable at 80-85%. Renal epinephrine clearance and extraction was not significantly altered, however. Epinephrine infusion caused splanchnic norepinephrine uptake to increase as well, partially because of the increased plasma flow. In contrast, the kidney showed net norepinephrine production throughout. We conclude that the splanchnic area plays a much more important role than the kidney in the disposal of circulating epinephrine. The great efficiency of splanchnic epinephrine removal is further enhanced by epinephrine-induced hemodynamic changes that also promote the splanchnic uptake of norepinephrine.

Adult↗
PubMedDate not supplied

Residual insulin secretion at diagnosis of type 1 diabetes is independently associated with both, age of onset and HLA genotype.

BACKGROUND: We investigated whether residual insulin secretion and metabolic derangement at diagnosis of type 1 diabetes (T1DM) are influenced by human leukocyte antigens (HLA) class II genes. METHODS: Eight hundred and seventy-one T1DM consecutive Caucasian patients were typed for HLA class II genes. In 300 of these patients, glycated haemoglobin, insulin requirement, baseline C-peptide and body mass index (BMI) Z-score were measured at clinical diagnosis. The effect of the HLA genotypes on the quantitative variables was investigated using multiple linear regression. The beta coefficient regression of the age at onset and HLA genotypes were standardized to compare their specific importance for C-peptide levels. RESULTS: The HLA genotypes were divided in high-, moderate- and low-risk categories. The frequency of high-risk genotype, DRB1*03-DQB1*0201/DRB1*04-DQB1*0302, decreased with increasing age of onset (p < 0.0001, chi(2) linear trend). The presence of the high-risk genotype was independently associated with lower C-peptide levels at diagnosis (p = 0.002). In the regression analysis of C-peptide levels, the standardized beta coefficient for age of onset and high risk compared to low-risk genotypes showed similar results (0.27 and 0.24 respectively). There was a positive association between age of onset and C-peptide (p < 0.0001) and a negative association between age of onset and insulin requirement (p < 0.0001). CONCLUSIONS: The degree of beta-cell destruction at diagnosis of T1DM is independently associated with both, age of onset and HLA genotypes, the two variables exert a similar quantitative effect on residual beta-cell function at diagnosis.

Adolescent↗
PubMedDate not supplied

Percutaneous transhepatic stenting by Wallstents of portal vein and bile duct stenoses caused by immunoblastic sarcoma in a liver transplantation.

Posttransplant lymphoproliferative disorders are infrequent tumors related to chronic immunosuppressive therapy. We present a liver transplant recipient who developed such a tumor in the porta hepatis that provoked obstruction of the entire portal triad. Treatment consisted of systemic chemotherapy, percutaneous dilatation, and placement of Wallstent endoprostheses across both biliary and portal vein stenoses. The patient died 3 weeks later of pneumonia and sepsis. At necropsy, the tumor was completely necrosed and the prostheses in both the common bile duct and the portal vein were patent.

Cholestasis↗