The First Class Appliance for rapid molar distalization.
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Biomedical subjects
Publications and source records attributed to A Fortini.
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In order to evaluate the involvement of endogenous opiates in the insulin disorders of polycystic ovary syndrome (PCOs) a total of 25 PCOs women and 11 normo-ovulatory controls were studied by comparing the effect of a chronic opioid blockade on beta-cells responsiveness to oral glucose load and to intravenous glucagon bolus. Each patient, studied on follicular phase, underwent to oral glucose tolerance test (OGTT), and, 2 days later, to a glucagon intravenous bolus (1 mg); these tests were then repeated after 6 weeks of naltrexone treatment (50 mg orally). Naltrexone treatment did not modify the insulin secretory patterns of control subjects, whereas the same therapy significantly reduced, in hyperinsulinemic PCOs women, the beta-cell hyperresponsiveness both to oral glucose load and to intravenous glucagon (p < 0.05 and p < 0.01, respectively), even if with different mean percent decrease (32% OGTT vs. 45% glucagon, p < 0.05). Moreover, normoinsulinemic PCOs patients showed a slight, but not significantly increase in the beta-cells response to OGTT after opioid blockade, whereas, in the same situation, the insulin release after glucagon bolus was significantly reduced (p < 0.01). Chronic opioid blockade did not modify gonadotropins, steroids and SHBG levels in either group. Our data show that naltrexone treatment is able to reduce the beta-cell response to a direct intravenous secretagogue stimulus in all PCOs patients, while only in hyperinsulinemic PCOs subjects the same treatment is effective in reducing the exaggerated insulin secretion after oral glucose load. The reason for such a discrepancy could be ascribed to a different effect of opioids on first- and second-phase insulin secretion, or, alternatively, to an involvement of other secretagogue factors, such as glucoincretins.
An increased sensitivity to painful stimuli and an abnormal cardiac autonomic function have previously been reported in patients with angina and angiographically normal coronary arteries, a syndrome that mainly affects postmenopausal women. In this study we compared both general sensitivity to pain, by evaluating time to forearm ischemic pain (FIP) provoked by sphygmomanometer cuff inflation, and cardiac autonomic function, by measuring heart rate variability (HRV), and QT and QT(c) intervals on 24-hour Holter recordings, in 25 postmenopausal women with angina and normal coronary arteries and in 22 healthy postmenopausal women. Compared with controls, patients had a reproducible strikingly lower time to FIP (149 +/- 121 vs 295 +/- 158 seconds, p <0.001), whereas there were no differences between the 2 groups in HRV variables and mean 24-hour QT and QT(c) intervals. HRV indexes, and QT and QT(c) intervals also showed similar circadian patterns. Thus, our data show that postmenopausal women with angina and normal coronary arteries have an enhanced sensitivity to systemic painful stimuli, but no detectable impairment in cardiac autonomic function compared with a well-matched control group of postmenopausal healthy women.
OBJECTIVE: To investigate the ability of GH to increase the steroidogenic response of the ovary to FSH in the early stage of human follicle development in vivo. DESIGN: Ovarian sensitivity to FSH and/or GH during the early follicular phase of the human menstrual cycle was evaluated in a prospective study. SETTING: Normal human volunteers in the Department of Obstetrics and Gynecology, Università Cattolica Sacro Cuore. PATIENT(S): Twenty-four normal patients with normo-ovulatory cycles and tubal factor infertility. INTERVENTION(S): Pure urinary FSH (75 IU) or saline were injected IV in the early follicular phase with or without a pretreatment with human GH (0.1 IU/kg IM for 3 days). MAIN OUTCOME MEASURE(S): Plasma levels of LH, FSH, E2, and T in samples collected for a period of 26 hours after saline or FSH IV injection. RESULT(S): Follicle-stimulating hormone injection increased E2 and E2:T stimulated area under the curve (AUC) with respect to saline administration. Moreover, the E2 secretion was increased significantly in the group treated with GH plus FSH as compared with that found in the group receiving FSH alone. Growth hormone itself was unable to increase any steroidogenic response by ovary in terms of both E2 and E2:T AUC values. CONCLUSION(S): The results of present study demonstrate in vivo a synergistic effect of GH on the FSH-induced follicular steroidogenesis, suggesting a potential relevance of GH in the reproductive biology.
PURPOSE: The authors report on their device, the surgical image tracker, which provides automatic compensation for movements of the surgical image within the microscope field of view, during vitreoretinal procedures. METHODS: The authors developed a compact device acting as an automatic image tracker, based on video monitoring of the surgical image and translation of the operating microscope. Basic components are a standard color charge-coupled device camera and a specifically designed frame grabber for discrimination and tracking of the target image. Operation of the device is fully compatible with the usual pedal adjustments. RESULTS: Ready, fast, and correct automatic centering of the microscope field of view has been achieved successfully in all typical operating conditions. Video recording always is equally well centered. System operation also is effective with panoramic optics and diffuse illumination. CONCLUSION: The surgical image tracker appears to be a valuable tool to obtain well auto-centered surgical images, eliminating a bothersome task during vitreoretinal surgery.
We describe a case of a 26 year old patient affected by a rare syndrome characterized by hyperkalemia, arterial hypertension and normal glomerular filtration rate (Gordon's syndrome), probably due to a renal tubular defect in the reabsorption of sodium or chloride. The patient, who had hyperkalemia since the age of 4 years, was referred to our Centre because of hypertension not well controlled with antihypertensive treatment. After drug therapy wash-out, we confirmed the existence of hypertension (180/100 mm Hg; ambulatory BP monitoring: 24-h mean BP = 151/91 mm Hg; 7 am-11 pm = 157/95; 11 pm-7 am: 133/82) and blood and urine tests showed hyperkalemia (6.6 mEq/L), hyperchloremia (115 mEq/L), mild metabolic acidosis (pH = 7.35, HCO3 = 19 mEq/L), low levels of plasma renin activity ( < 0.2 ng/ml/h), slight increase of plasma (1.08 nM/L) and daily urine aldosterone (129 nM) and normal serum creatinine (1.1 mg/dl) and glomerular filtration rate (91 ml/min). These data allowed to exclude the presence of renal failure and hyporeninemic hypoaldosteronism, which are the most common diseases with hypertension and hyperkalemia, and suggested the diagnosis of Gordon's syndrome. After 1 month of treatment with chlorthalidone (12.5 mg o.i.d) we observed the normalization of BP (130/80 mm Hg; ambulatory BP monitoring: 24-h BP: 132/76 mm), serum potassium (5,1 mEq/L) and the other blood and urine tests. These results were confirmed 6 months later and at present the patient has good clinical conditions.
A total of 17 women affected by polycystic ovarian disease (PCOD) were studied to evaluate the involvement of endogenous opioids in the pathophysiology of the hyperinsulinism in PCOD by administering naltrexone, an oral opioid antagonist. An oral glucose tolerance test (OGTT) was performed at baseline (on day 5 of the cycle) and repeated after 6 weeks of naltrexone administration. Plasma glucose, insulin and connecting peptide (c-peptide) concentrations were evaluated in all samples. Based on their insulinaemic response to OGTT, patients were classified as hyperinsulinaemic or normoinsulinaemic. Naltrexone treatment significantly (P < 0.007) reduced the insulin response to OGTT in the hyperinsulinaemic group without affecting the c-peptide incremental area; in the normoinsulinaemic group there was a slight, but not significant, increase in both c-peptide and insulin incremental areas. The two groups showed similar c-peptide incremental areas after naltrexone treatment. There was no significant difference in the c-peptide:insulin incremental areas molar ratio between the two groups; after treatment, a significant increase in this ratio was observed in both groups. When we considered the data as an expression of the fractional hepatic extraction of insulin, we found a lower value for hyperinsulinaemic in comparison with normoinsulinaemic patients (not significant), and a significant (P < 0.01) improvement of this parameter in the hyperinsulinaemic group after naltrexone administration. In conclusion, we suggest that the contribution to hyperinsulinaemia in PCOD patients may be at least in part due to both increased pancreatic secretion and reduced hepatic removal of insulin. Chronic pharmacological inhibition of opioid tone could improve the insulin plasma concentration by acting chiefly on the liver metabolism of insulin in hyperinsulinaemic patients.
OBJECTIVE: To describe the clinical experience of our Centre in the assessment of antihypertensive therapy with 24-hour ambulatory blood pressure monitoring (ABPM). DESIGN AND PATIENTS: We retrospectively studied all the 241 out-patients on antihypertensive therapy submitted to ABPM (SpaceLabs 90207, USA) between March 1992 and March 1993 for clinical purposes. We evaluated: 1) the clinical indications for the test; 2) the modifications of drug treatment suggested by the ABPM results; 3) the referring physicians' acceptance of these suggestions; 4) the changes of office BP measured before and 3-6 months after ABPM. RESULTS: 1) The indications for ABPM were: resistant or poorly controlled hypertension (n = 170-71%); suspected "white coat effect" (n = 51-21%); assessment of symptoms (n = 20-8%). 2) The analysis of ABPM suggested to modify drug treatment in 51% of the patients; a "white-coat effect" was found in 18% of the patients. 3) The ABPM suggestions about treatment were accepted by the referring physicians in 89% of the patients. 4) Office BP decreased from 163 +/- 18/99 +/- 9 mm Hg (before ABPM) to 151 +/- 13/91 +/- 7 (3-6 months after ABPM), (p < 0.001). CONCLUSIONS: The use of ABPM in our Centre, which is based on specific clinical indications, provided indications to modify the drug treatment in a high percentage of patients.
This study evaluated the effects of medium-term once daily administration of fosinopril (20 mg) on BP profile and on BP response to exercise in patients with mild to moderate hypertension. Twenty patients (14 males and 6 females; 25-57 years of age), after a six week drug wash-out phase, underwent 24h ambulatory BP monitoring (ABPM) (Spacelabs 90207) and, the day after, maximal bicycle exercise testing. Patients then received a once daily treatment with fosinopril and ABPM and exercise testing were repeated 45-60 days later. Fosinopril decreased average 24h SBP and DBP (-13.5 mmHg and -9.7 mmHg, respectively, P < 0.002); a significant BP reduction was observed both in day and in nighttime, without alteration in diurnal BP profile. The antihypertensive effect was still evident 24h after dosing. Trough to peak ratio was 0.58 +/- 0.16. Fosinopril induced a reduction of SBP and DBP during exercise testing (-20 and -11 mmHg at baseline; -17 and -8 mmHg at peak exercise; -24 and -14 mmHg at the sixth minute of recovery; P < 0.002), with a slight prolongation of exercise time (+46 seconds, P = 0.041). These results indicate that fosinopril at a once daily dose of 20 mg provides a sustained 24h BP reduction associated with BP reduction during physical exercise. These effects have been obtained without altering diurnal BP profile, without excessive hypotension at the time of maximal antihypertensive effect and with a slight improvement of exercise tolerance.
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OBJECTIVE: To investigate the existence of a different sensitivity of ovaries to follicle-stimulating hormone (FSH) during the follicular phase of the human menstrual cycle and in patients with polycystic ovarian syndrome (PCOS). DESIGN: Thirty-four normal subjects and 13 patients with PCOS were treated intravenously by FSH (75 or 225 IU) or saline at different stages of follicular phase. MAIN OUTCOME MEASURES: Plasma levels of luteinizing hormone (LH), FSH, estradiol (E2), and testosterone (T) in samples collected for a period of 26 hours after the injection. RESULTS: In patients at the early stages of follicular phase (baseline E2 < 50 pg/mL), FSH increased in dose-dependent manner E2 and E2:T-stimulated area under curve (AUC) in respect to saline experiments. In PCOS subjects, saline E2, and E2:T-stimulated AUC were significantly lower than normal women. Follicle-stimulating hormone (75 IU) dramatically increased these values, and no difference was seen in respect to 75 and 225 IU FSH-treated controls. In patients with E2 baseline plasma levels > 50 pg/mL, FSH (75 or 225 IU) failed to increase both E2 and E2:T-stimulated AUC in comparison with saline studies. CONCLUSIONS: Early stages of follicular phase in normal and polycystic ovaries are the most responsive to the elevation of circulating FSH levels, whereas the ovarian sensitivity spontaneously decreases as follicular maturation enhances.
Ovarian and adrenal production of androgens was evaluated in 18 patients with polycystic ovary syndrome (PCOS) by administering a combination of short-term dexamethasone (DEX) and long-term gonadotropin-releasing hormone agonist (GnRH-A). At day 6 of the cycle, blood samples were collected at 7 A.M. (basal) and 11 P.M. At midnight, 2 mg DEX was given orally, and blood samples were collected at 7 A.M. the following day (DEX1). Blood samples were obtained for 6 weeks at the same time after administration of a potent GnRH-A (400 micrograms/day given subcutaneously). Eight normal subjects served as controls. The amounts of androgens and 17-hydroxyprogesterone (17-OHP) suppressed by using DEX (adrenal-source suppression) and GnRH-A (ovarian-source suppression) were greater in PCOS patients than in controls. We differentiated PCOS patients as having a normal or an exaggerated response to DEX or GnRH-A administration; threshold values were considered average +2SD of the suppressed androgen amounts of controls. Three patients had an exaggerated response to GnRH-A treatment for androstenedione, testosterone and 17-OHP, while DEX inhibition was similar to controls. The remaining 15 patients had an exaggerated response to DEX for all three androgens; seven also had an exaggerated response to GnRH-A. Thus, the combination of GnRH-A and DEX permitted us to selectively study and identify adrenal and ovarian sources of hyperandrogenemia.
OBJECTIVE: To investigate the relationship between insulin and adrenal androgens in patients with polycystic ovarian disease (PCOD). DESIGN: Patients with PCOD and a group of volunteers who attended the department during a period of 6 months were studied. SETTING: Department of Gynaecology and Obstetrics, Università Cattolica del Sacro Cuore, Roma, Italy. PARTICIPANTS: Healthy women with ovulatory cycles (hospital personnel, n = 8) and women affected by PCOD (n = 32) were studied on day 5 to 6 of their follicular phase. INTERVENTIONS: All women had an oral glucose tolerance test (OGTT) (75 g) on day 5 to 6 of the cycle. Then plasma samples were collected at 7.00 A.M.; at 11.00 P.M., 2 mg of dexamethasone (DEX) were orally administered with blood samples collected the day after at 7.00 A.M. (effect of DEX). Then adenocorticotropic hormone (ACTH, Synacten; Ciba-Geigy, Varese, Italy) 250 micrograms was injected intravenously (IV) and samples collected 60 minutes later (effect of ACTH). MAIN OUTCOME MEASURES: Plasma glucose and insulin concentration were assayed on OGTT samples collected at time 0, 30, 60, 90, 120, 180, and 240 minutes after glucose ingestion. Data are expressed as area under the curve. Cortisol, 17 alpha-hydroxyprogesterone (17-OHP), testosterone (T), androstenedione (A), and dehydroepiandrosterone sulphate (DHEAS) plasma levels were evaluated on the samples collected before and after DEX or ACTH administration. Data are expressed as absolute concentrations and percent increase in respect to values before the treatment. RESULTS: According to the OGTT response, 21 patients were classified as hyperinsulinemic and 11 as normoinsulinemic. The ideal body weight was greater in hyperinsulinemic patients. No differences in baseline hormone levels were found between the two groups. Only sex hormone binding globulin levels were significantly greater in normoinsulinemic patients (P less than 0.05). Also, the plasma concentration of all steroids after DEX were similar in both groups. Intravenous injection of ACTH significantly increased plasma androgens levels. Cortisol, DHEAS, and T enhancement did not differ in normoinsulinemic and hyperinsulinemic patients, whereas significantly greater A (P less than 0.01) and 17-OHP (P less than 0.05) plasma concentrations were observed after ACTH injection in hyperinsulinemic when compared with normoinsulinemic PCOD subjects. Control group after IV ACTH showed an increase of A and 17-OHP similar to those found in normoinsulinemic PCOD group. CONCLUSIONS: These data suggest that insulin could be involved in the androgen production by adrenal gland and it could influence the responsiveness of adrenal to its trophic hormones.
Conflicting data have been reported about the impaired sensitivity to the inhibitory effect of prostacyclin (PGI2) in platelets from patients with diabetes. In the present paper we investigated binding of and sensitivity to PGI2 of platelets from insulin dependent (IDDM) (n = 9), non insulin dependent (NIDDM) (n = 8) diabetics and two groups of ten healthy subjects of equivalent age in relation to platelet lipidic content. Platelet sensitivity to PGI2 (PGI2 IC50) was found not significantly changed in diabetics as compared to controls; similarly, no significant differences of the number of high affinity receptors for PGI2 in platelets from patients with IDDM and NIDDM were observed. Platelet sensitivity to PGI2 and PGI2 receptors were found to be significantly related to platelet cholesterol content (r = 0.89, p less than 0.001 and r = -0.80, p less than 0.001 respectively). In conclusion platelet PGI2 receptor changes are not detectable in diabetics in good metabolic control, but could take place when platelet lipid composition is altered.
In order to test the hypothesis that endogenous opiates are at least partially responsible for hyperinsulinaemia in patients with polycystic ovarian disease (PCOD), the effect of naloxone (an opiate receptor blocker) on the insulin response to oral glucose load (OGTT) was studied in 20 women with PCOD and 17 control subjects at days 5-8 of their follicular phase. After fasting overnight for 10-12 h, each woman received an i.v. bolus injection (2 mg) of naloxone or an equal volume of saline infusion followed by a constant infusion of naloxone or saline solution at a rate of 8 ml/h (1 mg/h of naloxone) for 5 h. OGTT (75 g) was performed 1 h after the bolus injection. The naloxone study was performed 48 h after the saline study. Naloxone did not modify the insulin response to OGTT in either group. When the data were related to the insulin response, in PCOD hyperinsulinaemic patients, naloxone significantly reduced (P less than 0.02) the insulin response to OGTT without any change in glycaemic response curves. In control and PCOD normoinsulinaemic patients, naloxone did not change significantly either the glycaemia or the insulin levels after OGTT. No change of gonadotrophin and steroid secretion was found in any patient receiving naloxone. In conclusion, endogenous opiates may play a significant role in hyperinsulinaemia in PCOD.
Fifty-four hyperandrogenized women were studied to evaluate the importance of the adrenal or ovarian contribution to androgen secretion. Forty-six had the polycystic ovarian (PCOD) syndrome. Eight normal women represented a control group. The endocrine study was performed during the follicular phase. The plasma samples were collected at 7.00 am (A1) and at 11.00 pm (A3). Dexamethasone 2 mg was administered orally at 11.30 pm and blood samples were collected the day after, at 7.00 am (B). The adrenocorticotropic hormone (ACTH) was injected, 250 micrograms i.v. and samples were collected after 60 min. Cortisol dehydroepiandrosterone-sulfate (DHEAS), androstenedione, testosterone and 17-hydroxyprogesterone (17OHP) were measured. The hyperandrogenized patients had A1 androgen levels higher than the controls (p less than 0.01). 17OHP and androstenedione A3 values showed a cortisol-related decrease. After dexamethasone, androgen levels, since DHEAS, were normalized in all patients. We found that baseline androgen levels and circadian and dexamethasone-inhibited amounts were strongly correlated (p less than 0.01). The ACTH test revealed five cases of enzymatic adrenal deficiencies. Moreover, the amplitude of the response of 17OHP and androstenedione to ACTH is predictable in relation to both circadian and dexamethasone-inhibited amounts (p less than 0.01). In conclusion, our study confirms and makes quantifiable the importance of the adrenal contribution to androgen secretion in hyperandrogenized patients. The ACTH test is important for detecting the presence of mild enzymatic adrenal defects.
To investigate whether magnetic resonance imaging (NMR) can detect alterations in LV contractility during myocardial ischemia, ten patients aged 32-72 with coronary artery disease underwent ECG gated NMR performed at 0.5 Tesla after intravenous infusion of high dose dipyridamole (DP) (0.7 mg/Kg) over 5 minutes. LV contraction in planes similar to echo short axis projection was imaged under condition, 3' and 15-20' after infusion of DP by fast multiphasic imaging (FMI), multiple angulated cine-NMR sequence with a temporal resolution of 50 m/sec. Entity and size of perfusion defects after DP were determined by Tc 99m MIBI myocardial scintigraphy. In all patients changes in LV contractility appeared at NMR in the same site of perfusion impairments revealed with MIBI. In 8 patients the alterations lasted even more than 20' after the first NMR scan. NMR provides the opportunity of performing long-lasting assessment of ventricular wall contractility and enables to exactly localize the site and extension of kinetic changes as well as their time of onset and time duration.
The aim of the present study was to investigate the ventilatory anaerobic threshold in patients with exercise-induced myocardial ischemia. Ventilatory volumes and gas exchanges were measured during treadmill stress testing in 36 patients (11 with previous myocardial infarction) with electrocardiographic criteria of myocardial ischemia during the test and in 23 healthy, untrained control subjects of equivalent age. The anaerobic threshold was detected in 32 of 36 patients (89%) and in 22 of 23 control subjects (96%). The anaerobic threshold was significantly lower in patients than in control subjects (13.5 +/- 1.9 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). In the 21 patients without previous myocardial infarction, the anaerobic threshold was also significantly lower than in the control subjects (13.9 +/- 1.6 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). Among the 21 patients without previous myocardial infarction, the 12 with a low ischemic threshold, which occurred during the first three steps of the modified Bruce protocol, had an anaerobic threshold significantly lower than the other nine patients (13.1 +/- 1.5 versus 14.9 +/- 1.0 ml/kg per minute VO2, p less than 0.01). However, even in the patients with a moderate to high ischemic threshold, the anaerobic threshold was significantly lower than in the control subjects (p less than 0.001). These data show that the anaerobic threshold can be measured in the great majority of patients with exercise-induced myocardial ischemia. The low anaerobic threshold level indicates a relevant functional impairment in these patients.