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Massimiliano Bianchi

Publications and source records attributed to Massimiliano Bianchi.

7 recordsLinked to original sources

[Heart failure and cholelithiasis].

We previously found an high incidence of gallstone or cholecystectomy for lithiasis in patients affected by heart failure (52.1% up to 58.6%). As in general population the incidence of this disease is up to 38%, we tried to explain our findings.

Aged↗

Evidence that the metabotropic glutamate receptor 5 antagonist MPEP may act as an inhibitor of the norepinephrine transporter in vitro and in vivo.

The mechanisms through which blockade of metabotropic glutamate receptors 5 (mGluR5) results in anxiolytic and antidepressant effects are currently unknown. In the present study, we therefore hypothesized that the anxiolytic- and antidepressant-like profile of the noncompetitive mGluR5 receptor antagonist 2-ethyl-6-(phenylethynyl)-pyridine (MPEP) may be mediated by inhibition of the norepinephrine transporter (NET). Accordingly, we first examined the potency of MPEP to bind to or inhibit uptake at the NET as well as the dopamine and serotonin transporters (DAT and SERT, respectively). We also examined the simultaneous in vivo effects of MPEP and desipramine (DMI) on both NE-like oxidation current in the amygdala (AMY) and cell firing in the locus coeruleus (LC) by means of differential pulse voltammetry (DPV) coupled with electrophysiology. MPEP completely displaced the binding of [3H]-nisoxetine on human NET with a pKi of 6.63 +/- 0.02. In addition, MPEP was able to inhibit [3H]-NE uptake in LLCPK cells expressing human NET, with a pIC50 of 5.55 +/- 0.09. In vivo DPV data revealed that both MPEP (30 mg/kg i.p.) and DMI (10 mg/kg i.p.) significantly increased NE-like voltammetric responses levels in the AMY, whereas both compounds also significantly decreased cell firing monitored concomitantly from the second microelectrode in the LC. Collectively, the results of the present study provide potential new mechanisms through which MPEP exerts its anxiolytic and antidepressant effects.

Action Potentials↗

Cytoskeletal changes in the hippocampus following restraint stress: role of serotonin and microtubules.

The aetiology of depression is associated with depletion in central levels of serotonin (5-HT). Hence, a major effect of antidepressant drugs is to increase synaptic 5-HT levels. Stressful conditions have also been shown to affect neuronal plasticity and 5-HT neurotransmission in the hippocampus. Neuronal plasticity, which is typically referred to as a structural adaptation of neurons to functional requirements, requires more dynamic forms of microtubules (cytoskeletal component). The alpha-tubulin, which is the major component of microtubules, can be postranslationally modified and both the tyrosinated (tyr-tub) and acetylated (acet-tub) forms are considered markers of more dynamic or more stable microtubules, respectively. The aim of the present work was to investigate the expression of tyr-tub and acet-tub in the hippocampus of rats submitted to either acute (6 h for 1 day) or sub-chronic (6 h for 4 days every day) restraint stress. In addition, ex vivo hippocampal 5-HT levels were monitored by differential pulse voltammetry to analyse the influence of both stress conditions upon 5-HT levels. Our results showed that the expression of tyr-tub in the hippocampus was significantly decreased to 70 +/- 7% following sub-chronic restraint stress (P < 0.01). In contrast, acute and sub-chronic restraint stress increased the hippocampal expression of acet-tub to 139 +/- 11% and 145 +/- 11% of control, respectively. Finally, 5-HT levels were significantly increased (P < 0.05) to 142 +/- 15% and 135 +/- 11% following acute and sub-chronic restraint stress, respectively. The stress-induced cytoskeletal changes observed in the present study suggest that the microtubular network is a potential new pathway that may increase our understanding of stress-related events.

Animals↗

[Paget-Schroetter disease: clinical and therapeutic considerations].

A case of subclavian-axillary vein thrombosis prompted us to review the recent literature on the subject. Paget-Shroetter disease is an uncommon disease, which is still associated with high early and late morbidity rates and the prevention of which requires early diagnosis and treatment. The importance of trauma (in the form of physical strain) in determining the symptoms of the disease is universally accepted. We observed subclavian-axillary vein thrombosis in a young 22-year-old athlete who complained of unexpected onset of pain in the left armpit, spreading to the arm and to the shoulder on the same side, functional impotence of the upper arm and swelling of the hand and forearm, and engorgement of the vessels in the arm, shoulder and clavipectoral region, which in the course of time developed the characteristics of a collateral circulation. The patient underwent phlebography which documented lack of opacification of the axillo-subclavian axis and showed the presence of a collateral circulation with dilation of the vein of the shoulder and arm. We first attempted to dissolve the thrombus by locoregional infusion of urochinase and later started anticoagulative therapy with an intravenous infusion of heparin (10,000 IU/h after a bolus of 500 units). Because of the poor result of thrombolysis and anticoagulative therapy and the progressive worsening of the disease, the patient underwent surgery to restore the continuity of the venous axis. The surgical procedure was performed through a skin incision along the upper edge of the collar-bone. This was dissected and the two stumps were well separated to allow a clear view of the subclavian vein. Phlebotomy, thrombectomy and reconstruction of the venous axis with an expanded polytetrafluoroethylene patch were performed. The postoperative course was uneventful and the patient underwent phlebography again on postoperative day 8, which demonstrated complete patency of the subclavian vein, and was discharged on postoperative day 20 on oral anticoagulative therapy.

Administration, Oral↗

[Report of a case of Gardner's syndrome: clinical and epidemiologic considerations and review of the literature].

Familial adenomatous polyposis is a hereditary clinical syndrome characterised by the presence of numerous adenomatous polyps of the colon and rectum and by lesions in other organs. The disease affects various different tissues and characteristically presents a variable biological and clinical behaviour. Colon polyps are precancerous lesions and the certainty of their malignant evolution within the 3rd-4th decades of life is now practically an established, extensively documented fact. Recently, new methods of genetic screening, prevention and early diagnosis and, as a result, more advanced treatment protocols have been introduced in clinical practice, thus offering young patients diagnosed as suffering from familial adenomatous polyposis better prospects and a better quality of life. The patient in our case came in for medical observation for abdominal pain experienced close to the scar of a previous appendectomy and for the presence of an abdominal tumefaction on the same side. Initially the patient underwent surgical resection of the growth that proved to be a desmoid tumour of the abdominal wall. The results of the pathology examination and the patients' long-term disease and family history led to a presumptive diagnosis of familial adenomatous polyposis, which was then confirmed by the appropriate instrumental examinations. Genetic tests on the patient's relatives yielded the same diagnosis in some of them. On the basis of our personal experience and a thorough review of the literature we can safely state that no medical treatment currently available is capable of reducing, let alone definitively eliminating colon polyps. To date, then, the therapeutic options most commonly adopted are colectomy with ileo-rectal anastomosis and total conservative proctocolectomy with an ano-ileal pouch anastomosis. These two types of surgical procedures yield different results in terms of functional capability and oncological radicality with their respective repercussions on the patient's quality of life. The choice of the most appropriate surgical procedure is made on the basis of a series of parameters such as age, site of the polyps, number of polyps, degree of cell atypia of the polyps, and patient willingness to undergo regular check-ups. The current tendency advocated by the various authors is to perform a total colectomy as soon as possible.

Adolescent↗

[Treatment of acute biliary pancreatitis: our experience].

The results of endoscopic and surgical treatment in 21 patients affected by acute biliary pancreatitis are reported. All patients were managed according to the same protocol. Once the diagnosis was formulated (pain, serum amylase, ultrasonography, cholestasis and/or cholangitis) and the severity evaluated (Ranson's criteria, glucose and urea levels), the 21 patients underwent endoscopic retrograde cholangiopanctratography--within 24 hours in 8 patients (predicted severe disease) or within 72 hours in 13 patients (predicted mild disease). Endoscopic sphincterotomy was performed in 18 patients with stones in the common bile duct and was successful in 94.5% (17 patients: 3 patients underwent more than one session to confirm or achieve clearance of the duct). The morbidity rate associated with endoscopic sphincterotomy was 16% (3 patients: 2 haemorrhages, 1 perforation). There were no deaths. Cholecystectomy was performed in 16 patients within 2-9 weeks of the initial attack of acute biliary pancreatitis. There were 3 minor complications (respiratory, laparotomy, urinary infection), no major intraoperative or postoperative morbidity, and no mortality. Acute biliary pancreatitis is still associated with significant morbidity and mortality, but can be managed safely with combined medical, endoscopic and surgical treatment.

Acute Disease↗

Refractory generalized edema: an infrequent complication of long-term pergolide treatment for Parkinson disease.

Generalized edema is the result of increased interstitial fluid volume due to altered Starling forces or capillary endothelial damage. The authors present a patient with severe Parkinson disease who presented with increasing dyspnea, bilateral pleural effusion, and peripheral edema that was refractory to diuretics. Common causes of the severe loss of fluid into the extravascular space were ruled out and pergolide was suspected. Upon discontinuation of pergolide therapy, all signs of fluid retention resolved. This report emphasizes that pergolide should be considered a cause of otherwise unexplained generalized edema in patients with Parkinson disease on this therapy.

Aged↗