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Biomedical subjects

N Frisina

Publications and source records attributed to N Frisina.

At least 19 recordsLinked to original sources
PubMed1999

Effects of lisinopril administration on blood bcl-2 concentrations in patients with immunoglobulin A nephropathy.

We evaluated blood concentrations of bcl-2, a proto-oncogene that can inhibit apoptotic phenomena, in a group of patients with immunoglobulin A (IgA) nephropathy. Concentrations of bcl-2 were higher in patients with proteinuria than in those without proteinuria. A 6-month course of 5 mg/day lisinopril given to subjects with proteinuria significantly reduced blood bcl-2 concentrations and caused a reduction in proteinuria. Therefore increased blood bcl-2 concentrations may be considered an index of risk in subjects with IgA nephropathy, and the positive effects of angiotensin-converting enzyme inhibitors on proteinuria in patients with IgA nephropathy may be attributed, at least in part, to their effect on the mechanisms that regulate apoptosis. This is of fundamental importance in resolving glomerular hypercellularity in the course of glomerulonephritis.

Adult↗
PubMed1999

Reduced bcl-2 concentrations in hypertensive patients after lisinopril or nifedipine administration.

In 30 patients with essential hypertension and 30 healthy control subjects, we evaluated blood concentrations of B cell leukemia-2 (bcl-2), a protooncogene that can reduce apoptosis. Bcl-2 concentrations were higher in hypertensive than in normotensive subjects. The increase in pressure due to a cold pressor test caused a further increase in blood bcl-2 concentrations, in both hypertensive and normotensive subjects. Treatment of hypertensive patients with hypotensive drugs caused a reduction in bcl-2 concentrations, which was more marked after administration of lisinopril than of nifedipine. The results suggest that concentrations of bcl-2 are increased in patients with hypertension, which could be an important factor in cell proliferation underlying posthypertensive vascular remodeling. Moreover, lisinopril and nifedipine appear to be capable of reducing bcl-2 concentrations, with potentially beneficial effects on vascular modifications in patients with hypertension.

Administration, Oral↗
PubMed1999

Does captopril have a direct pro-apoptotic effect?

The beneficial effect of ACE inhibitors on cardiovascular remodelling from hypertension and ischemic disease may be due to the effect of these drugs on the proliferation/cell death balance. We therefore investigated the effect of the addition of captopril in vitro, on the onset of apoptosis in human vascular myocytes, by using a propidium iodide fluorescence analysis and a morphological analysis using the acridine orange technique. Captopril (0.23 mM) caused an increase in apoptotic phenomena that was more than 3. 5-fold than in controls both at the 24th (7.7 vs. 2%) and the 48th h (10.1 vs. 3.8%). The addition of propranolol strengthened the effect on apoptosis. The induction of apoptotic phenomena may be a mechanism by which ACE inhibitors affect cardiovascular remodelling and it might also explain the favorable effect these drugs have on diseases such as IgA nephropathy and diabetic nephropathy.

Adrenergic beta-Antagonists↗
PubMed1998

Translocation (5;10)(q13;q26) in acute monoblastic leukemia.

We report a case of acute monoblastic leukemia [French-American-British (FAB) M5a] observed in a 38-year-old man and associated at diagnosis with a t(5;10)(q13;q26) found in cells from a bone marrow culture. The patient survived only 2 months after diagnosis. t(5;10) as a solitary chromosome abnormality has not been previously reported in M5a, and, in the case that we describe, it appears to be correlated with a poor prognosis.

Adult↗
PubMed1998

Normotensive offspring with non-dipper hypertensive parents have abnormal sleep pattern.

The objective of this study was to determine whether abnormal microstructure of sleep in non-dipper hypertensive patients was present in their offspring. Subjects included 11 normotensive offspring of non-dipper hypertensive parents (FH + ND), 6 of dipper hypertensive parents (FH + D) and 5 of normotensive parents (Controls). We measured blood pressure beat-to-beat by Finapres and all stages of sleep by polysomnographically recording simultaneously during spontaneous nocturnal sleep. We analysed blood pressure pattern for 4-min long random periods while the subjects were awake and during all stages of sleep; sleep efficiency (SE), sleep latency (SL), delta-sleep latency (delta-SL), REM sleep latency (REM-SL), Stage 1, Stage 2, Stage 3, Stage 4 and REM duration and percentage values, and microstructural aspects of sleep (arousal and microarousal temporization and features). FH + D and controls showed a fall in blood pressure greater than 10% in all stages of NREM sleep and in the FH + ND blood pressure fall in less than 10% of waking values in all NREM stages. REM sleep and heart rate were similar in the three groups during all stages of sleep. FH + ND showed the same number of arousals but more microarousals than FH + D and controls (p < 0.0001). Microarousals induced several stage shifts through lighter sleep. For this reason, FH + ND spent more time in stage 2 than FH + D and controls. In conclusion, offspring of non-dipper hypertension parents showed a greater number of microarousals than the other two groups.

Adult↗
PubMed1998

Reduced blood bcl-2 protein concentration in patients on hemodialysis.

The concentrations of bcl-2 protein that can block programmed cellular death in various cell lines were evaluated in blood samples from 10 uremic patients on hemodialysis, 10 uremics not yet on hemodialysis, and in 10 healthy controls. The bcl-2 protein variations (in uremics on dialysis) were ascertained in patients during the dialysis session. Oxidative stress was evaluated in all groups by assaying the products of intraerythrocytic lipoperoxidation. Dialyzed and nondialyzed uremic patients had higher bcl-2 protein concentrations than healthy subjects. Dialysis causes a significant reduction in the concentrations of bcl-2 protein which becomes statistically significant during the 3rd hour. In both groups of uremic patients a positive correlation was found between bcl-2 protein and products of lipoperoxidation.

Aged↗
PubMed1997

Renal failure from mitochondrial cytopathies.

Mitochondrial cytopathies are metabolic diseases, expressing mutations in nuclear DNA, punctiform mutations or depletions in mitochondrial DNA. These genetic lesions alter mitochondrial oxidative phosphorylation, with a reduction in energy produced for cell activity. Renal disease may be the first sign of mitochondrial cytopathy, or it may appear together with neurological and neuromuscular signs. Fanconi's syndrome, a benign sign of renal tubulopathy, is particularly frequent in newborns with mitochondrial cytopathy, whereas tubulointerstitial nephropathy, which affects infants and adults, is more serious because it develops into terminal uremia. Findings of hyperlactatemia and reduced enzymatic activity on the respiratory chain in tissue biopsies are of diagnostic significance in mitochondrial cytopathy. A breakthrough is being made in our understanding of genetic alterations in mitochondrial DNA, and with future therapy, the kidney, a target organ, may be safeguarded.

Adult↗
PubMed1997

Cold pressor test raises serum concentrations of ICAM-1, VCAM-1, and E-selectin in normotensive and hypertensive patients.

In patients with essential hypertension, elevated soluble E-selectin (sE-selectin) levels may indicate endothelial cell injury or activation. We therefore sought to ascertain whether arterial blood pressure increased by the cold pressor test can modify serum concentrations of sE-selectin and other soluble forms of adhesion molecules, such as soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), or the expression of any adhesion molecules in circulating monocytes and lymphocytes. Our findings show that levels of sE-selectin, sVCAM-1, and sICAM-1 are higher in patients with essential hypertension than in normotensive subjects (sICAM-1, 380 +/- 52 versus 262 +/- 96 ng/mL, P<.05; sVCAM-1, 720 +/- 52 versus 625 +/- 38 ng/mL, P<.05; and sE-selectin, 75 +/- 21 versus 61 +/- 22 ng/mL, P<.05). Furthermore, in normotensive and hypertensive patients, the cold pressor test caused an increase in serum concentrations of sICAM-1, sVCAM-1, and sE-selectin, but it did not cause changes in the expression of adhesion molecules in circulating monocytes and lymphocytes. High arterial blood pressure may therefore increase the production of serum adhesion molecules, probably through endothelial activation.

Blood Pressure↗
PubMed1996

Frequency domain of heart rate and blood pressure variability in essential hypertensive patients during sleep: differences between dippers and non-dippers.

METHODS: Autonomic nervous function was evaluated by means of power spectral analysis of heart rate and blood pressure variability in dipper (n = 10) and non-dipper (n = 9) essential hypertensive subjects during sleep. The non-dipper subjects were defined as those in whom the nocturnal decrease in blood pressure was < 10% of the daytime blood pressure. We measured beat-to-beat blood pressure by using a Finapres device and all stages of sleep by simultaneous polysomnographic recording during spontaneous nocturnal sleep. We analysed the pattern of changes in blood pressure for random periods of 4 min duration while the patient was awake and during all stages of sleep. For each period (waking, stages 2, 3 and 4 of sleep) a segment of 256 stationary data points was analysed. In the frequency domain, the spectral characteristics of the stationary segments were estimatred by fast Fourier transformation over three frequency bands: low frequency (0.025-0.07 Hz), mid-frequency (0.07-0.14 Hz) and high frequency (0.14-0.35 Hz). RESULTS: Pulse-interval power spectral analysis did not reveal any difference between dippers and non-dippers during waking. In dipper patients, the low-frequency pulse interval (LFPI) decreased during sleep whereas the high-frequency pulse interval increased; the mid-frequency systolic blood pressure and diastolic blood pressure (DBP) decreased significantly and the high-frequency DBP increased during sleep. In non-dipper patients, the LFPI increased from wakefulness to stages 2 and 3 of sleep and the high-frequency pulse interval decreased during sleep; the mid-frequency systolic blood pressure and DBP increased in stage 4 sleep and the high-frequency DBP decreased during sleep. CONCLUSIONS: These findings indicate that non-dipper hypertensive subjects are characterized by increased LFPI and mid-frequency blood pressure during sleep compared with dipper subjects. This alteration in the autonomic nervous function may explain the non-dipper phenomenon in essential hypertension.

Journal Article↗
PubMed1995

No changes of peripheral insulin resistance in polycystic ovary syndrome after long-term reduction of endogenous androgens with leuprolide.

The aim of this study was to investigate the relationship between plasma insulin levels, peripheral insulin sensitivity and androgen secretion in ten patients with polycystic ovary syndrome and in six obese women as compared with six normal-weight control subjects. During a euglycemic-hyper-insulinemic clamp no significant change of testosterone, androstenedione or dehydroepiandrosterone sulfate plasma levels was observed in the two groups of patients or in the control subjects; insulin sensitivity was clearly reduced and was similar in polycystic ovary patients and in obese women, in spite of the different plasma androgen levels. A long-term (5 months) androgen suppression with the gonadotropin-releasing hormone agonist leuprolide was not able to improve significantly the insulin sensitivity. These results demonstrate that the short-term hyperinsulinemia achieved with the clamp technique does not affect androgen secretion and that insulin resistance, measured with the same technique, is not influenced by long-term suppression of plasma androgen levels in polycystic ovary syndrome.

Adult↗
PubMed1995

Sleep structure in essential hypertensive patients: differences between dippers and non-dippers.

The objective of this study was to determine whether the macrostructure and microstructure of sleep were altered in non-dipper essential hypertensive patients. Patients included 9 non-dipper essential hypertensive patients and 10 dippers. We measured blood pressure beat-to-beat by Finapres and all stages of sleep by polysomnografically recording simultaneously during spontaneous nocturnal sleep. We analysed blood pressure pattern for 4-min long random periods while the patients were awake and during all stages of sleep; sleep-efficiency (SE), sleep-latency (SL), delta sleep-latency (delta-SL), REM sleep-latency (REM-SL), St. 1, St.2, St.3, St.4 and REM duration and percentage (%) values, and microstructural aspects of sleep (arousal and microarousal temporisation and features). Dipper patients showed a fall in blood pressure (BP) greater than 10% in all stages of NREM sleep; in the non-dipper patients BP fell by less than 10% of waking values in all NREM stages. REM sleep as well as HR were similar in both groups during all stages of sleep. Non-dippers showed the same number of arousals but more microarousals than dippers (p < 0.001). During and after microarousals BP and HR increased in non-dippers, but showed light variation in dippers. Microarousals induced several stage shifts towards lighter sleep. For this reason non-dippers spent less time in stage 4 than dippers (p < 0.001). In conclusion, non-dipper essential hypertensive patients are a subset of patients with central sympathetic hyperactivity responsible for quantitative and qualitative alteration of sleep.

Adult↗