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Objective: In this study anxiety and depressive disorders were evaluated in patients admitted to an emergency department (ED) or to a medical department (MD). Methods: The General Health Questionnaire-30 (GHQ-30) [...]

Abstract Objective--To determine the circulating levels of nerve growth factor (NGF), neuropeptide Y (NPY), and vasoactive intestinal peptide (VIP) in systemic sclerosis (SSc), and to correlate these levels with clinical [...]

Background:Quantitative measurement of circulating D‐dimer, a product of fibrin degradation, has been shown to be a very useful diagnostic tool in the management of patients with suspected deep vein thrombosis and/or pulmonary embolism. Whether D‐dimer can play a similar role in the diagnostic approach to patients with suspected cerebral vein thrombosis (CVT) remains controversial.Methods:Studies evaluating the diagnostic accuracy of the D‐dimer test in the diagnosis of CVT were systematically searched for in the MEDLINE and EMBASE databases (up to July 2011). Weighted mean sensitivity and specificity with 95% confidence intervals (CIs) were calculated with a bivariate random‐effects regression approach.Results:Fourteen studies, for a total of 1134 patients, were included. D‐dimer accuracy was good, with a resulting weighted mean sensitivity of 93.9% (95% CI 87.5–97.1) and weighted mean specificity of 89.7% (95% CI 86.5–92.2), calculated with a bivariate approach. Potential risk factors for false‐negative D‐dimer results included isolated headache, longer duration of symptoms, and limited sinus involvement.Conclusions:Our findings suggest that D‐dimer may be a useful diagnostic tool in the management of patients with suspected CVT. Future prospective studies are warranted to confirm our preliminary findings.

To report 4 cases of autosomal recessive hereditary neuropathy associated with novel mutations in the periaxin gene (PRX) with a review of the literature. Periaxin protein is required for the maintenance of peripheral nerve myelin. Patients with PRXmutations have early-onset autosomal recessive demyelinating Charcot-Marie-Tooth disease (CMT4F) or Déjèrine-Sottas neuropathy (DSN). Only 12 different mutations have been described thus far.

Duchenne muscular dystrophy (DMD) is a lethal X-linked recessive muscle disease due to defect on the gene encoding dystrophin. The lack of a functional dystrophin in muscles results in the fragility of the muscle fiber membrane with progressive muscle weakness and premature death. There is no cure for DMD and current treatment options focus primarily on respiratory assistance, comfort care, and delaying the loss of ambulation. Recent works support the idea that stem cells can contribute to muscle repair as well as to replenishment of the satellite cell pool. Here we tested the safety of autologous transplantation of muscle-derived CD133+ cells in eight boys with Duchenne muscular dystrophy in a 7-month, double-blind phase I clinical trial. Stem cell safety was tested by measuring muscle strength and evaluating muscle structures with MRI and histological analysis. Timed cardiac and pulmonary function tests were secondary outcome measures. No local or systemic side effects were observed in all treated DMD patients. Treated patients had an increased ratio of capillary per muscle fibers with a switch from slow to fast myosin-positive myofibers.

We report here that chlorpromazine, a first generation antipsychotic drug, inhibits anionic amino acid transport mediated by system X−AG(EAAT transporters) in cultured human fibroblasts. With 30 µM chlorpromazine, transport inhibition is detectable after 3 h of treatment, maximal after 48 h (>60%), and referable to a decrease in Vmax. Chlorpromazine effect is not dependent upon changes of membrane potential and is selective for system X−AGsince transport systems A and y+are not affected. Among antipsychotic drugs, the inhibitory effect of chlorpromazine is shared by two dibenzodiazepines, clozapine and olanzapine, while other compounds, such as risperidon, zuclopentixol, sertindol and haloperidol, are not effective. Transport inhibition by clozapine and olanzapine, but not by chlorpromazine, is reversible, suggesting that the mechanisms involved are distinct. These results indicate that a subset of antipsychotic drugs inhibits EAAT transporters in non-nervous tissues and prompt further investigation on possible alterations of glutamate transport in peripheral tissues of schizophrenic patients.We report here that chlorpromazine, a first generation antipsychotic drug, inhibits anionic amino acid transport mediated by system X−AG(EAAT transporters) in cultured human fibroblasts. With 30 µM chlorpromazine, transport inhibition is detectable after 3 h of treatment, maximal after 48 h (>60%), and referable to a decrease in Vmax. Chlorpromazine effect is not dependent upon changes of membrane potential and is selective for system X−AGsince transport systems A and y+are not affected. Among antipsychotic drugs, the inhibitory effect of chlorpromazine is shared by two dibenzodiazepines, clozapine and olanzapine, while other compounds, such as risperidon, zuclopentixol, sertindol and haloperidol, are not effective. Transport inhibition by clozapine and olanzapine, but not by chlorpromazine, is reversible, suggesting that the mechanisms involved are distinct. These results indicate that a subset of antipsychotic drugs inhibits EAAT transporters in non-nervous tissues and prompt further investigation on possible alterations of glutamate transport in peripheral tissues of schizophrenic patients.

We propose artificial neural networks (ANN) for ambulatory ECG arrhythmic event classification, and we compare them with some traditional classifiers (TC). Among them, the one based on the median method (heuristic algorithm) was chosen and taken as a quality reference in this study, while a back propagation based classifier, designed as an autoassociator for its peculiar capability of rejecting unknown patterns, was examined. Two tests were performed: the first to discriminate normal vs ventricular beats and the second to distinguish among three classes of arrhythmic events. The results show that the ANN approach is more reliable than the traditional classifiers in discriminating among many classes of arrhythmic events: 98% by ANN vs 99% by a TC for correctly classified normal beats, 98% by ANN vs 96% by TC for correctly classified ventricular ectopic beats, 96% by ANN vs 59% by TC for correctly classified supraventricular ectopic beats, and 83% by ANN vs 86% by median method for correctly classified aberrated atrial premature beats. This paper also tackles the problem of the management of classification uncertainty. Two concurrent uncertainty criteria have been introduced, to reduce the classification error of the unknown ventricular and supraventricular arrhythmic beats respectively. The error in ventricular beats case was kept close to 0% in average and for supraventricular beats was kept at 35% in average. So we can state that the ANN approach is powerful in classifying beats represented in the training set and that it manages the uncertainty in such a way as to reduce, in any case, the global error percentage.

The present study was carried out in order to determine whether insulin-induced hypoglycemia exerts its stimulatory effect on plasma concentrations of arginine vasopressin (AVP) by interacting with a serotonergic, a GABA-ergic or an opioid pathway. For this purpose, the effect of the serotonergic antagonist metergoline (10 mg/day for 4 days po), the GABA-ergic agonist sodium valproate (600 mg in three divided doses po) and the opioid-receptor blocker naloxone (10 mg in a iv bolus) on the AVP response during an insulin (0.15 lU/kg bw) tolerance test (ITT) was evaluated in three groups of 6 normal men each. In all men, control ITTs were performed without drug treatments. Basal and ITT-stimulated AVP secretion was not modified by drug administration, suggesting that serotonergic, GABAergic and naloxone-sensitive opioid receptors are not involved in the regulation of AVP secretion in response to insulin-induced hypoglycemia.

Ambulatory blood pressure (BP) monitoring has been extensively utilized, so far, for studying BP profile and hypotensive treatment in arterial hypertension. In this paper, preliminary data will be reported from a clinical study on the possible contribution of the combined ECG and BP monitoring in clarifying mechanisms of dizziness in patients with multiple or complex cardiovascular problems. Results are shown of three patients with ischaemia, arrhythmias and/or episodes of hypotension, and of three patients with borderline hypertension and marked fluctuations of BP.

Ambulatory monitoring of the intra arterial blood pressure (IBP), through the Selyg-Oxford System, has been used so far primarily for studies on hypertension. Aim of our study is to explore the possibility of obtaining from IBP indications useful to extend its field of application. The study will investigate: 1) the usefulness of the continuous monitoring of the systolic time intervals (STI), measured from IBP as ventricular performance indicators, 2) the increasing of specificity of the ECG allowed by the simultaneous beat by beat estimate of the STI's, 3) the possibility of achieving the same information from non invasive peripheral pressure transducers.In this paper we are presenting the results obtained from the combined analysis of the STI's, ECG and IBP in a first series of 13 patients, selected out of 50 on the basis of the highest number of episodes of IBP variations, to allow the evaluation of the algorithms performances in severe conditions.

Several alterations in hypothalamo–pituitary–thyroid (HPT) function have been described in diabetes mellitus and have been attributed to metabolic decompensation. The present study was performed in order to establish whether residual endogenous insulin secretion in patients with insulin-dependent diabetes mellitus (IDDM) may play a role in the control of HPT function.

A new database of cardiovascular signals has recently been developed at the CNR Institute of Clinical Physiology in a study based on patients admitted to the Coronary Care Unit for suspected ischaemic heart disease (IHD), who underwent both ECG effort stress test and echo or radionuclide diagnostic imaging procedures associated with pharmacological test of myocardial ischaemia. During stress testing, in addition to 12-lead ECG, arterial, blood pressure and respiration signals are measured non-invasively and recorded. Signals and representative image frames at baseline and during ischaemia are stored in the database, which is planned to include 50 cases, annotated beat by beat and archived on CD-ROM. Each case also contains resting ECG and a comprehensive patient clinical record; if possible Holier ECG and coronary arteriography frames.

The current role of ECG and signal monitoring in the diagnosis of Ischaemic Heart Disease is outlined in relation to imaging techniques giving accurate information on myocardial anatomy and function. ECG monitoring during stress testing remains the first step non-invasive method providing pathophysiological information. Long term continuous monitoring of the ECG and of other signals (e.g. arterial blood pressure and respiration) is commonly used to control patients with suspected or ascertained IHD. Progress of technology and of signal processing methods are driving the exploitation of signal information for diagnosis, prognosis and therapy control of ischaemic patients.

In order to test the possible effects of lysine vasopressin (LVP) on basal and TRH stimulated TSH and PRL release, an iv bolus of LVP (0.06 lU/kg bw) was injected alone or just before TRH (20 or 400 µg iv) in 18 normal male subjects. The administration of LVP modified neither the basal secretion of TSH and PRL nor the TSH and PRL release induced by 20 or 400 µg TRH. These data suggest that in humans, vasopressin is not involved in the control of TSH and PRL release at the anterior pituitary level.

Glucocorticoids are known to reduce both ACTH and arginine vasopressin responses to insulin-induced hypoglycemia in normal men. The present study was undertaken in order to establish whether glucocorticoids are capable of modifying the oxytocin (OT) response to hypoglycemia. For this purpose, 8 normal men (28–33 yr) were tested with insulin (0.15 IU/kg in an iv bolus) [insulin tolerance test (ITT)] with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin). Eight different subjects (29–35 yr) were tested with dexamethasone alone. The administration of dexamethasone (2 or 4 mg) alone changed neither ACTH nor OT concentrations in the plasma during the next hour. Insulin produced similar hypoglycemic responses, regardless of dexamethasone treatment. ACTH levels rose significantly in response to insulin-induced hypoglycemia, with a mean peak response at 45 min (p<0.01 vs baseline). Two and four mg dexamethasone produced similar significant reductions of the ACTH response to hypoglycemia (p<0.02 at 45 min, p<0.05 at 30 and 60 min vs ITT). In the ITT, OT levels rose significantly in response to hypoglycemia, with a mean peak response at 45 min (p<0.01 vs basal value). The pretreatment with 2 or 4 mg dexamethasone reduced in a similar manner the hypoglycemia-induced OT rise (p<0.05 at 30 and 45 min vs ITT). These findings show a partial inhibition by dexamethasone of the OT response to hypoglycemia. In view of the possible hyperglycemic effects of OT at least in pathological conditions, such as diabetes mellitus, the inhibition by glucocorticoids of OT secretion may be supposed to play a role in the regulation of glucose homeostasis.

Abstract. The present study was undertaken in order to establish whether muscarinic cholinergic receptors are involved in the anomalous GH response to GnRH in men with insulin-dependent diabetes mellitus and in male patients with major depression. For this purpose, 16 male diabetics, 18 depressed men and 9 normal controls were tested with GnRH (25 µg iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before GnRH). Additional experiments with TRH (200 µg iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. The administration of GnRH stimulated GH release in 12 out of the 16 diabetics and in 8 out of the 18 depressed patients, but not in the normal controls. Control and diabetic non-responders to GnRH did not respond to TRH. In contrast, all diabetic responders to GnRH, except 2, showed paradoxical GH responses to TRH. All depressed responders to GnRH and 3 of the non-responders, were responsive to TRH. The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression.