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M Parise

Publications and source records attributed to M Parise.

At least 19 recordsLinked to original sources
PubMed2001

Transfusion-transmitted malaria in the United States from 1963 through 1999.

BACKGROUND: Transfusion-transmitted malaria is uncommon in the United States. After the report of three cases of complicated Plasmodium falciparum infection acquired by transfusion, we reviewed all cases of transfusion-transmitted malaria reported to the Centers for Disease Control and Prevention (CDC) from 1963 through 1999. METHODS: Information on the patients was from surveillance reports sent to the CDC. Information about the implicated blood donors came from the National Malaria Surveillance System. To determine whether donors should have been excluded from donating blood, we compared their characteristics with the exclusion guidelines of the Food and Drug Administration and the American Association of Blood Banks. RESULTS: Of 93 cases of transfusion-transmitted malaria reported in 28 states, 33 (35 percent) were due to P. falciparum, 25 (27 percent) were due to P. vivax, 25 (27 percent) were due to P. malariae, 5 (5 percent) were due to P. ovale, 3 (3 percent) were mixed infections, and 2 (2 percent) were due to unidentified species. Ten of the 93 patients (11 percent) died. There were potentially 91 donors (in two cases, two patients received blood from the same donor), 67 of whom (74 percent) could be identified as infective. Of 64 implicated donors whose country of origin was reported, 38 (59 percent) were foreign born. Among those for whom complete information was available, 37 of 60 donors (62 percent) would have been excluded from donating according to current guidelines (in place since 1994), and 30 of 48 donors (62 percent) should have been excluded under the guidelines in place at the time of donation. CONCLUSIONS: Careful screening of donors according to the recommended exclusion guidelines remains the best way to prevent transfusion-transmitted malaria.

Blood Donors↗
PubMed1997

Clinical use of polysynaptic flexion reflexes in the management of spasticity with intrathecal baclofen.

The aim of this study was to evaluate the clinical usefulness of lower limb flexion reflexes (FR) in the assessment of spinal excitability responsible for spontaneous or induced spasms. FR were recorded on the short head of biceps femoris, after electrical stimulation of the ipsilateral sural nerve at the ankle, in 17 spastic patients selected for chronic intrathecal administration of baclofen. The results obtained before and after treatment were compared with clinical scores commonly used to assess spasticity (Ashworth and spasm scores). Before intrathecal baclofen 15/17 patients (88%) had pathologically enhanced flexor reflexes in the lower limbs, which were associated to clinical spasms. Reflex enhancement was accompanied in 47% of cases by abnormal decrease of reflex threshold. No significant correlation appeared between the magnitude or threshold of FR in control conditions and either the hypertonia (Ashworth scale) or the number of clinical spasms per unit of time. Intrathecal baclofen attenuated flexor reflex amplitude and increased reflex threshold in all patients. Our results suggest that FR investigate the intrinsic features of the spasms (threshold, intensity and duration) not assessed clinically, and that therefore the information gathered from FR recordings is not redundant with, and adds significantly to, that obtained by clinical scales. In our experience, FR recordings appeared to be a useful tool for quantifying the benefit of antispastic treatment and might be used as an ancillary indicator to determine the minimal effective dose of intrathecal baclofen.

Adult↗
PubMed1997

Somatosensory evoked potentials following functional posterior rhizotomy in spastic children.

Ten children with cerebral palsy and severe lower limb spasticity were treated by functional posterior rhizotomy (FPR). Somatosensory evoked potential recordings were performed preoperatively, intraoperatively (directly on the surface of the spinal cord) and 6 months after surgery, to evaluate the effects of FPR on lower limb somatosensory function. Before surgery, 7/10 patients showed abnormal cortical responses after tibial stimulation. In all patients, intraoperative recordings showed a reduction in the amplitude of segmental responses (N22) (50 +/- 25% of reference value) after the section of a mean 50% of L2-S2 dorsal rootlets. The modifications of segmental responses (N22) were maintained 6 months after surgery, whereas reduction of cortical responses (P39) did not reach the significance level when compared with preoperative recordings.

Adolescent↗
PubMed1995

Long-term clinical, electrophysiological and urodynamic effects of chronic intrathecal baclofen infusion for treatment of spinal spasticity.

Seventeen patients with severe disabling spinal spasticity were selected and treated by chronic intrathecal baclofen infusion using an implanted programmable pump. Nine patients were tetraparetic, seven were paraplegic and one paraparetic. Patients were regularly followed for 5 to 69 months (mean 37.5 months). The clinical efficacy of baclofen was estimated by means of evaluation of: hypertonia, spasms, pain and functional disability. All patients experienced significant amelioration of quality of life secondary to reduction of hypertonia, spasms and pain related to contractures. Neurogenic pain improved in 3 cases and remained unchanged in 3 others. In patients whose motor functions were partially preserved, various degrees of motor improvement were detected. Electrophysiological recordings of Polysynaptic flexion reflexes (FR) were obtained to control conditions, and under intrathecal baclofen, in order to quantify the spinal excitability responsible for spontaneous or induced spasms. Flexion reflex threshold was increased and amplitude proved to be very significantly reduced by chronic baclofen infusion in all our patients. Twelve patients with neurogenic bladder dysfunction were also evaluated by a clinically oriented questionnaire and by quantitative urodynamic recordings, before and after pump implantation. In patients with normal micturition, this was not changed by intrathecal baclofen. In patients with spastic bladder, intrathecal baclofen produced a decrease of detrusor hypertonia and hyperactivity in 50% of cases, with reduction of leakage and increase in functional bladder capacity.

Adolescent↗
PubMed1994

A P-selectin/CD62P monoclonal antibody (LYP-20), in tandem with flow cytometry, detects in vivo activated circulating rat platelets in severe vascular trauma.

P-selectin, also known as CD62P, GMP140 or PADGEM, is present in platelet alpha-granules and endothelial cell Weibel-Palade bodies and is very rapidly expressed on the surface of these cells on activation. In this study, an anti P-selectin monoclonal antibody (LYP20) was used, in tandem with flow cytometry, to identify activated platelets at the site of induced vascular trauma or in peripheral blood. Moreover, electron microscopy was performed to characterize sites of vascular trauma and quantify the number of adhering platelets. The same induced vascular trauma was observed to result into animals responding in 2 different ways (Group I, Group II) following the degree of platelet activation. Five rats, out of 14 with induced vascular trauma, had more than half of their circulating platelets expressing P-selectin when drawn at the site of the trauma (67.4% +/- 3.44) or in peripheral blood (78.5% +/- 2.5) (Group I). In the remaining 9 animals a much smaller proportion of circulating platelets expressed P-selectin when assayed from trauma sites (18% +/- 3.34) or in peripheral blood (18.0% +/- 4.30) (Group II). Enhanced P-selectin expression by circulating platelets in Group I, compared to Group II, appears to be linked to the degree of activated platelets adhering at sites of trauma (171 +/- 15 x 10(3) platelets versus 48 +/- 31 x 10(3) platelets per mm2). In the 5 control animals, that were not operated on, platelets expressing P-selectin when drawn at the site of a mock trauma (7.0% +/- 1.84) or in the peripheral blood (11.2% +/- 3.30) showed little activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Pressor reactivity to norepinephrine and angiotensin in salt-sensitive hypertensive patients.

The mechanisms responsible for increased blood pressure in response to a high dietary sodium intake in salt-sensitive patients with essential hypertension are only partially understood. The possibility that increased reactivity to pressor hormones might contribute to hypertension in these patients has not been adequately investigated. We studied 11 salt-sensitive and 15 salt-resistant patients with essential hypertension while they were ingesting a diet with 20 meq/day sodium for 9 days or one with 200 meq/day sodium for 14 days. During the last 4 days of each dietary regimen, they received 30 mg/day of slow-release nifedipine. Blood pressure response to increasing doses of norepinephrine and angiotensin II (Ang II) was studied at the end of each of four phases of the study. Salt-sensitive patients exhibited a greater blood pressure response to norepinephrine than salt-resistant patients, irrespective of the dietary sodium intake and whether we took into account the dose infused or the actual plasma levels of norepinephrine achieved during the infusion. The blood pressure response to Ang II, on the other hand, was greater in salt-sensitive than salt-resistant patients during low but not during high sodium intake. The blood levels of norepinephrine achieved during the infusion of this hormone were lower in salt-sensitive than in salt-resistant patients. These studies indicate that an increased reactivity to the pressor action of norepinephrine might contribute to the maintenance of hypertension in salt-sensitive patients. The increased reactivity appears to be specific for norepinephrine. In fact, we observed increased reactivity to Ang II during low but not during high sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Antiischaemic effect of defibrotide treatment in rat kidney.

The authors previously demonstrated the protective activity of defibrotide (a profibrinolytic and antithrombotic drug) on endothelial cells. In the present work they examine the efficacy of defibrotide in protecting rat kidney from ischaemic/reperfusion injury by studying the modifications of intrarenal adenine nucleotide levels. Right renal ischaemia of 60 min and reperfusion of 30 min were induced in adult male Wistar rats. Defibrotide was administered as a bolus through a catheter inserted into the left femoral vein 5 min before the beginning of ischaemia at the dose of 32 mg/kg and continuously infused during ischaemia/reperfusion through the same vein at the final dose of 32 mg/kg in 5 ml of saline at the rate of 3 ml/h. Rats treated with vehicle of the drug were used as controls. At the end of postischaemic reperfusion, the ischaemic and left kidneys were rapidly removed and frozen in liquid nitrogen. Tissue extracts were prepared, and their ATP, ADP, AMP, cAMP, NAD+, and NADH contents were determined by using luminescence methods. In controls, ATP intrarenal levels were significantly higher in the left kidney than in the ischaemic organ of the same rat (3405 +/- 320 vs. 378 +/- 36 nmol/g fresh tissue and mean +/- s.e.m. of 10 experiments). Defibrotide treatment significantly protected ischaemic kidneys from the drop in ATP intrarenal content (1465 +/- 147 vs. 3124 +/- 303 nmol/g fresh tissue measured in the left kidney).

Adenosine Diphosphate↗
PubMed1993

Possible role of defibrotide in endothelial cell protection.

Defibrotide is a single-stranded DNA fraction obtained from mammalian lung and is able to increase prostacyclin production by endothelial cells. It has profibrinolytic and antithrombotic properties, and we have successfully used it as an anti-ischaemic drug in many in-vivo experimental models. In fact, we showed that defibrotide treatment significantly protected rat heart, kidney and liver from ischaemia and postischaemic reperfusion injury. In rats treated with defibrotide, the functionality and metabolic activity of ischaemic organs were significantly protected from impairment as compared to controls treated only with the vehicle of the drug. In the present work we evaluated all our results, together with those of others, in order to hypothesize the mechanism of action of the drug. We postulated that the prominent function of defibrotide is to inhibit platelet and leukocyte adhesion to endothelial cells: this may depend on reduced cell activation possibly following drug interaction with adenosine receptors. Defibrotide could also favour endothelial-cell function through binding with haemoglobin: such binding permits oxygen release and preservation of endothelium-derived relaxing factor. Moreover, prostacyclin production by endothelial cells is responsible for many drug activities and also limits superoxide radical generation.

Adenine Nucleotides↗
PubMed1992

Cyclosporine-induced insulin release in rats is related to an increase in plasma lipid levels.

We studied the modifications of plasma lipid levels induced by cyclosporine (CsA), streptozocin (STZ) or both drugs in rats. Male Wistar rats (RT1y) were administered i.p. with CsA or STZ or both at the dosage of 15 mg/kg daily for 8 days and were sacrificed on day 9. Total lipid, triglyceride and total cholesterol plasma levels were measured. The plasma total lipid content was significantly increased in CsA-treated and in CsA + STZ-treated rats with respect to controls (662 +/- 29 and 632 +/- 32, respectively, vs 472 +/- 27 mg/dl). The triglyceride content was significantly higher in CsA-treated and in CsA + STZ-treated animals than in controls (137 +/- 8.7 and 188 +/- 14.1, respectively, vs 79 +/- 7.7 mg/dl). The total cholesterol level was not significantly different in CsA- and STZ-treated rats with respect to controls. CsA-treated and STZ-treated rats concomitantly revealed a significant impairment of glucose tolerance. In fact, 150 min after orogastric administration of 350 mg glucose, glycaemia was significantly more elevated in treated animals than in controls. We conclude that the increase in lipid levels induced by CsA treatment could be related to drug-induced damage to the pancreas islets, as shown by the early insulin release and fatty tissue degeneration.

Animals↗
PubMed1992

Effect of dietary sodium intake on intracellular calcium in lymphocytes of salt-sensitive hypertensive patients.

High dietary Na+ raises mean arterial pressure (MAP) by more than 10% in salt-sensitive (SS) patients with essential hypertension. To test whether the rise in MAP in these patients is caused by a Na(+)-linked increase in [Ca2+]i in vascular smooth muscle cells, we measured [Ca2+]i in the lymphocytes of 14 patients with essential hypertension kept on a Na+ intake of 20 mEq/day for 9 days, and 200-mEq/day for 14 days. Nifedipine gastrointestinal transport system (GITS) (30 mg/day) was given during the last 4 days of each diet. We isolated lymphocytes on Ficoll-Hypaque gradient and measured [Ca2+]i levels using Fura-2 fluorescent dye. During low Na+ intake, there was no difference in MAP (102 +/- 3.5 v 93 +/- 3.8 mm Hg) and in lymphocytes [Ca2+]i (80 +/- 3.0 v 87 +/- 5.4 nmol/L) between the seven salt-sensitive and the seven salt-resistant patients. During high Na+ intake, MAP (92 +/- 2.8 mm Hg) and [Ca2+]i (85 +/- 6.8 nmol/L) did not change in salt-resistant patients. On the contrary, MAP (115 +/- 3.4 mm Hg) and [Ca2+]i (130 +/- 11.1 nmol/L) increased significantly (P less than .01) in the salt-sensitive patients. Nifedipine did not significantly alter MAP and [Ca2+]i in both groups of patients during low Na+ and in salt-resistant patients during high Na+ intake. On the contrary, during high Na+ intake, nifedipine decreased significantly (P less than .01) both MAP (104 +/- 2.4 mm Hg) and [Ca2+]i (89 +/- 5.7 nmol/L) in salt-sensitive patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Meningioma of the olfactory groove and breast neoplasms: report of 2 cases].

Two cases of olfactory groove meningiomas are presented in patients with breast cancer. Predominance of breast cancer and meningiomas in the age decades of the forties and the fifties, presence of steroid hormones receptors in both and prevalence of meningiomas in women are referred as significant correlations. Examination of the breast of women with meningiomas is recommended. Tomographic images are sometimes atypical, and a surgical intervention may be necessary.

Brain Neoplasms↗
PubMed1991

Protection of rat heart from damage due to ischemia-reperfusion during procurement and grafting by defibrotide.

We studied the efficacy of defibrotide, a prostacyclin-stimulating agent, in preventing ischemia reperfusion injury in Wistar rat heart by using three experimental models: (1) hearts from donors were perfused with the drug (32 mg/kg/hr) during 15, 30, 45, and 60 min of cold ischemia following 5, 10, and 15 min of warm ischemia; (2) hearts from donors treated with the drug were cold-stored for 12 or 24 hr; and (3) procured hearts perfused with the drug were isografted, after 30 or 60 min of warm ischemia, in recipient rats treated daily with defibrotide. Hearts perfused with saline and/or vehicle of the drug were used as controls. At the end of established ischemia times, and after 30 min, and 2, 4, 7 and 14 days from transplantation, hearts were rapidly cooled in liquid nitrogen. ATP, ADP, AMP, cAMP contents, and NAD+/NADH ratios were evaluated in prepared tissue extracts. Cardiac ATP and ADP levels and NAD+/NADH ratios were significantly higher in defibrotide-treated organs than in controls. Isografted defibrotide-treated hearts were also significantly preserved, with respect to controls, from the loss of ATP levels until rejection occurred. Our results demonstrate the protective activity of the drug against the myocardial metabolic damage due to ischemia-reperfusion.

Adenosine Diphosphate↗
PubMed1991

rT3 metabolism in patients with nephrotic syndrome and normal GFR compared with normal subjects.

To evaluate reverse 3,3',5'-triiodothyronine (rT3) metabolism in nephrotic syndrome, serum rT3 kinetic studies from 10 nephrotics (mean urinary protein losses 7.0 g/day) with normal glomerular filtration rates (GFR; creatinine clearance 107 ml/min) were compared with 9 normal healthy subjects. Serum disappearance data were analyzed in a three-pool model, including rapidly (liver and kidney) and slowly (muscle, skin, and brain) equilibrating pools exchanging with serum, with all losses from the rapidly equilibrating pool. Serum free thyroxine (T4), determined by equilibrium dialysis, and parathyroid hormone levels were unaltered; total T4, T3, and rT3, and free rT3, albumin, and transferrin levels were significantly decreased; and free fractions of T4 and rT3 and thyroid-stimulating hormone (TSH) levels were increased. Despite reduced rT3 binding in serum, fractional transfer rates from serum to extravascular sites and serum clearance rates of total rT3 were unaltered. Free hormone clearance, serum appearance, and maximum hormone production rates were decreased. Total hormone transfer rates between serum and tissue pools and rT3 mass in serum and both tissue pools were reduced. Binding in the slowly equilibrating pool was decreased, and binding in both rapidly and slowly equilibrating pools was correlated with the free fraction of rT3 (r = -0.79, P = 0.007, and r = -0.70, P less than 0.025, respectively), with a shift of rT3 from the slow to the rapid pool. These findings suggest that binding of rT3 and T4 to serum carrier proteins is reduced, the transfer process for rT3 from serum to extravascular sites is decreased by factors in addition to reduced serum binding, degradation of rT3 is impaired, and decreased slow-pool binding may reflect reduced rT3 binding to serum-derived proteins in interstitial fluid. Furthermore, rT3 production rates are reduced, despite normal serum free T4 levels, accounting for low serum free rT3 concentrations. Total rT3 levels are decreased because of decrements in both serum binding and production rates.

Adult↗
PubMed1991

Abnormal renal hemodynamics in black salt-sensitive patients with hypertension.

African-Americans with essential hypertension are more prone to the development of renal failure and are frequently salt-sensitive as well. Because alterations of intrarenal hemodynamics are important in the progression of renal disease and because salt-sensitive animal models with hypertension manifest a greater propensity to develop glomerulosclerosis in association with a rise in glomerular capillary pressure, we tested whether the renal hemodynamic adaptation to high dietary Na+ intake differs in salt-sensitive and salt-resistant hypertensive patients. We studied 17 black and nine white patients with essential hypertension who were placed on a low Na+ diet (20 meq/day) for 9 days, followed by a high Na+ diet (200 meq/day) for 14 days. During the last 4 days of each diet regimen, they received 30 mg/day of slow-release nifedipine. Eleven blacks were salt-sensitive, and all whites were salt-resistant. During the low Na+ diet period, salt-sensitive and salt-resistant patients had similar mean arterial pressure, glomerular filtration rate, effective renal plasma flow, and filtration fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗