Pier Mannuccio Mannucci

ORCID: 0000-0002-1915-3897
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About
Contact & Profiles
Research Areas
  • Hemophilia Treatment and Research
  • Platelet Disorders and Treatments
  • Blood Coagulation and Thrombosis Mechanisms
  • Venous Thromboembolism Diagnosis and Management
  • Blood groups and transfusion
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Atrial Fibrillation Management and Outcomes
  • Heparin-Induced Thrombocytopenia and Thrombosis
  • Complement system in diseases
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Blood properties and coagulation
  • Antiplatelet Therapy and Cardiovascular Diseases
  • Hemostasis and retained surgical items
  • Chronic Myeloid Leukemia Treatments
  • Health Systems, Economic Evaluations, Quality of Life
  • Liver Disease and Transplantation
  • Pharmaceutical Practices and Patient Outcomes
  • Air Quality and Health Impacts
  • Blood disorders and treatments
  • Cancer-related gene regulation
  • Hepatitis C virus research
  • Liver Disease Diagnosis and Treatment
  • Climate Change and Health Impacts
  • Chronic Disease Management Strategies
  • Acute Myocardial Infarction Research

University of Milan
2016-2025

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2016-2025

Ospedale Maggiore
2014-2024

Istituti di Ricovero e Cura a Carattere Scientifico
2014-2024

Mario Negri Institute for Pharmacological Research
2002-2023

Regione Lombardia
2023

Lombardia Informatica (Italy)
2023

ORCID
2023

University Hospital Foundation
2019

Ospedale L. Bonomo
1997-2017

Air pollution has wide-ranging and deleterious effects on human health is a major issue for the global community. The Global Burden of Disease study described worldwide impact air with as many 3.1 million 52.8 all-cause all-age deaths being attributable to ambient in year 2010.1 Moreover, ranked ninth among modifiable disease risk factors, listed above other commonly recognized such low physical activity, high-sodium diet, high cholesterol, drug use. Finally, accounts 3.1%...

10.1093/eurheartj/ehu458 article EN European Heart Journal 2014-12-09

The role played by coagulation defects in the occurrence of bleeding cirrhosis is still unclear. This partly due to lack tests that truly reflect balance procoagulant and anticoagulant factors vivo. Conventional such as prothrombin time activated partial thromboplastin are inadequate explore physiological mechanism regulating thrombin, because they do not allow full activation main factor, protein C, whose levels considerably reduced cirrhosis. We used a thrombin generation test investigate...

10.1002/hep.20569 article EN Hepatology 2005-02-22

Idiopathic cerebral-vein thrombosis can cause serious neurologic disability. We evaluated risk factors for this disorder, including genetic (mutations in the genes encoding factor V and prothrombin) nongenetic (such as use of oral contraceptive agents).

10.1056/nejm199806183382502 article EN New England Journal of Medicine 1998-06-18

In a randomized double-blind cross-over trial we gave either 1-deamino-8-D-arginine vasopressin or placebo to 12 patients with uremia, hemorrhagic tendencies, and prolonged bleeding times. After infusion, all had shortened times, the effect lasting for at least four hours in most cases. Platelet count, platelet cyclic AMP levels, retention on glass beads, plasma fibronectin, serum thromboxane B2 residual prothrombin, hematocrit, osmolarity were unchanged after vasopressin. A consistent...

10.1056/nejm198301063080102 article EN New England Journal of Medicine 1983-01-06

Based upon the World Health Organisation report of a Joint Organisation/International Society on Thrombosis and Haemostasis Meeting held in Geneva, 6-8 November 1995. Published with permission Organisation. Rapporteur; 2ISTH Secretariat, 6WHO Secretariat

10.1055/s-0038-1650638 article EN Thrombosis and Haemostasis 1996-01-01

BACKGROUND The blood coagulation system is activated in the acute phase of unstable angina and myocardial infarction. However, it remains unclear whether augmented function hemostatic mechanism serves only as a marker thrombotic episode or hypercoagulable state persists for prolonged period after clinical stabilization. METHODS AND RESULTS We prospectively measured plasma concentrations prothrombin fragment 1 + 2 (F1 2) fibrinopeptide A (FPA) consecutive patients presenting with (n = 81)...

10.1161/01.cir.90.1.61 article EN Circulation 1994-07-01

Point mutations in the factor V gene (factor Leiden) and prothrombin (the substitution of A for G at position 20210) are most common causes inherited thrombophilia. Whether or not Leiden increases risk recurrent deep venous thrombosis is controversial, there no information on recurrence among carriers both mutations.

10.1056/nejm199909093411104 article EN New England Journal of Medicine 1999-09-09

The form of von Willebrand's disease characterized by a qualitative abnormality Factor VIII/von Willebrand factor (FVIII/vWF) in plasma has been designated as Type II. We have now identified 20 persons from five families whose qualitatively abnormal FVIII/vWF shows heightened responsiveness to ristocetin. classified this the IIB and reclassified IIA previously described II, which interaction with platelets is decreased or absent presence enhanced reactivity was evident studies...

10.1056/nejm198005083021902 article EN New England Journal of Medicine 1980-05-08
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