Wireless internet architecture and testbed for wineglass

One of the most challenging issues in the area of mobile communication is the deployment of IPbased wireless multimedia networks in public and business environments. The public branch may involve public mobile networks, like UMTS as 3G system, while the business branch introduces local radio access networks by means of W-LANs. Conventional mobile networks realise mobile specific functionality, e.g. mobility management or authentication and accounting, by implementing appropriate mechanisms in specific switching nodes (e.g. SGSN in GPRS). In order to exploit the full potential of IP networking solutions a replacement of these mechanisms by IP-based solutions might be appropriate. In addition current and innovative future services in mobile environments require at least soft-guaranteed, differentiated QoS. Therefore the WINE GLASS project investigates and implements enhanced IP-based techniques supporting mobility and QoS in a wireless Internet architecture. As a means to verify the applicability of the implemented solutions, location-aware services deploying both IP-mobility and QoS mechanisms will be implemented and demonstratedPeer ReviewedPostprint (published version

Predictive role of node-rads score in patients with prostate cancer candidates for radical prostatectomy with extended lymph node dissection: comparative analysis with validated nomograms

Background and objectives: The Reporting and Data System (RADS) have been used in the attempts to standardize the results of oncological scans in different scenarios, such as lymph nodes, adding configuration criteria to size determination. We analyze the predictive value of preoperative Node-RADS determination at imaging for pelvic lymph node (PLN) involvement in cases of prostate cancer (PC) considered for radical prostatectomy (RP) with extended lymph node dissection (eLND) and we compare it with validate predictive nomograms (MSKCC, Briganti and Gandaglia). Methods: 150 patients with a histological diagnosis of PC (high risk or intermediate with an estimated risk for pN+ higher than 5% using the Briganti or 7% using the Gandaglia nomogram) submitted for RP with an ePLND from 2018 and 2021 were retrospectively examined. Node-RADS determination was performed in all cases using the preoperative magnetic resonance (MR), performed by a radiologist blinded for pathologic results and compared with the MSKCC, Briganti 2012, Gandaglia 2017 and Gandaglia 2019 nomograms. Results: PLN involvement at final pathology (pN+) was found in 36/150 (24.0%) of cases and the mean percentage of positive LNs in pN+ cases was 15.90 ± 13.40. The mean number of PLNs removed at RP was similar (p = 0.188) between pN0 (23.9 ± 8.0) and pN+ (25.3 ± 8.0) cases. Considering a Node RADS 4-5 positive and a Node RADS 1-2 negative, the PPV was 100% and the NPV was 79.6%. A Node RADS score 4-5 showed a lower sensitivity (0.167 versus 0.972, 1.000, 0.971, 0.960 respectively), a higher specificity (1.000 versus 0.079, 0.096, 0.138, 0.186 respectively) and a similar AUC (0.583 versus 0.591, 0.581, 0.574, 0.597 respectively) when compared to MSKCC, Briganti 2012, Gandaglia 2017 and Gandaglia 2019 nomograms. Conclusions: Our evaluation suggests that Node RADS score, combining configuration criteria to size determination could improve specificity in terms of pathologic PLN prediction but a very low sensitivity has been also described

Influence of operative time and blood loss on surgical margins and functional outcomes for laparoscopic versus robotic-assisted radical prostatectomy: a prospective analysis

Introduction: The aim of this article was to analyze whether operative time and blood loss during radical prostatectomy (RP) can significantly influence surgical margins (SM) status and post-operative functional outcomes. Material and methods: We prospectively analyzed prostate cancer (PC) patients undergoing RP, using robot-assisted (RARP) or laparoscopic (LRP) procedures. Blood loss was defined using the variation in hemoglobin (Hb, g/dl) values from the day before surgery and no later than 4 hours after surgery. Results: From a whole population of 413 cases considered for RP, 67% underwent LRP and 33.0% RARP. Positive SM (SM+) were found in 33.9% of cases. Mean surgical operative time was 172.3 ±76 min (range 49-485), whereas blood loss was 2.3 ±1.2 g/dl (range 0.3-7.6). Operative time and blood loss at RP were not significantly correlated (r = -0.028275; p = 0.684). SM+ rates significantly (p = 0.002) varied by operative time; a higher SM+ rate was found in cases with an operative time <120 min (41.2%) and >240 min (53.4%). The risk of SM+ significantly increased 1.70 and 1.94 times in cases with an operative time <120 min and >240 min, respectively, independently to the surgical approach. The rate of erectile disfunction (ED) varied from 22.4% to 60.3% between <120 min and >240 min procedures (p = 0.001). According to blood loss, SM+ rates slightly but significantly (p = 0.032) varied; a higher rate of SM+ was found in cases with a Hb variation between 2-4 g/dl (35.9%). Conclusions: Independently to the surgical approach, operative time, more than blood loss at RP, represents a significant variable able to influence SM status and post-operative ED

Successful treatment of epilepsy with serotonin reuptake inhibitors: proposed mechanism

The widely used antidepressants Specific Serotonin Reuptake Inhibitors (SSRI) have been tried with success as anticonvulsants in cases of nonsymptomatic epilepsy. This attempt was performed on the basis of experimental data suggesting the involvement of impairments of the serotonin system in the genesis of epilepsy. This overview summarizes the clinical data and presents biochemical and neurochemical evidences suggesting the mechanism of the therapeutic effects of SSRI in nonsymptomatic epilepsy. In particular, studies on blood-borne neutral amino acids and platelet serotonin transporter (SERT) in epileptics suggest: (a) That a decreased brain availability of tryptophan may be related to some types of epilepsy. (b) That reduction of the density of SERT may be a homeostatic reaction in the brain following epileptic seizures. The possibility that derangements in the brain serotonin system may be involved in the generation of epileptic seizures has been discussed since long time ago [1]. Over the years, this possibility has been tested in animal models, among which the GEPR (genetically prone rat) model [2, 3]. Even more importantly, links between noradrenaline and serotonin deficiencies and the epileptic human brain have been found [3]. This theory is at odds with the initial suggestions that monoamine uptake blocking antidepressants are convulsants [4\u20136]. The lack of contradiction of this circumstance and the noradrenaline/serotonin theory in epilepsy has been discussed at length by Jobe and Browning [3]. The main point discussed is that doses much above the antidepressant therapeutic range are those leading to convulsions, thus eliminating the possibility that potentiation of the amine function may be the basis for the proconvulsant effect. The core of the theory discussed by Jobe and Browning [3] is that epilepsy and affective illnesses have a common background. In their view, the two illnesses have different intrinsic fabricators, i.e. neuronal circuits which actually initiate and sustain dysfunctional episodes. However, they share common exterior defensive shields which are made up of circuits using noradrenaline and serotonin and protect the system from a deranged function of the intrinsic fabricators. This may lead to either the epileptic pathology or affective disorders, such as depression, according to the particular fabricator involved. These ideas have been tested by those authors in the genetically epilepsy prone rat model GEPR. The idea that serotonin could be involved in epileptogenesis was already present in the early 1990s [7\u201310]. Even much earlier works had shown in animal models that 5-hydroxytryptophan, a serotonin precursor, has an antiepileptic effect [e.g. 11, 12]. Our group thus set out at that time to test in a clinical trial whether potentiation of the brain serotoninergic system could be helpful in patients with drug refractory epilepsy. Fluoxetine was initially added to ongoing treatments with carbamazepine or carbamazepine/phenobarbital and later this was repeated with cytalopram in another group of patients. Later over the years, we tested in epileptic patients and in controls the blood levels of the serotonin precursor tryptophan and of the neutral amino acids able to compete for the same carrier for the passage of the blood\u2013brain barrier (BBB). In addition, we studied the status of the serotonin transporter (SERT) of the venous blood platelets in epileptic patients vs. controls. In the present overview we try and discuss the overall picture emerging from these approaches. The results do not contradict the theoretical framework proposed by Jobe and Browning [3]