Publications by authors named "Razvan Tudor"

Obesity and osteoarthritis (OA) are increasingly prevalent conditions that are intricately linked, with each exacerbating the other's pathogenesis and worsening patient outcomes. This review explores the dual impact of obesity on OA, highlighting the role of excessive weight in aggravating joint degeneration and the limitations OA imposes on physical activity, which further perpetuates obesity. The role of muscle tissue, particularly the release of myokines during physical activity, is examined in the context of OA and obesity.

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Article Synopsis
  • Coronary aneurysms are defined as sections of a coronary artery that are significantly enlarged, with giant aneurysms being particularly large and lacking a clear consensus definition.
  • Atherosclerosis is a common cause in adults, while Kawasaki disease and Takayasu arteritis are key contributors in children, but complications from these aneurysms can lead to serious health issues like heart failure and arrhythmias.
  • Recent studies are investigating the molecular mechanisms behind these aneurysms, highlighting the roles of specific molecules like MMPs and inflammatory cytokines in causing arterial wall degradation and subsequent aneurysm formation.
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Hemophilia, which is a rare disease, results from congenital deficiencies of coagulation factors VIII and IX, respectively, leading to spontaneous bleeding into joints, resulting in hemophilic arthropathy (HA). HA involves complex processes, including synovial proliferation, angiogenesis, and tissue remodeling. Despite ongoing research, factors contributing to HA progression, especially in adults with severe HA experiencing joint pain, remain unclear.

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Navigating through antithrombotic therapy in patients with both hemophilia and cardiovascular pathology presents a complex scenario with inherent challenges and opportunities. The presence of hemophilia, characterized by impaired blood clotting, adds a layer of complexity to the management of cardiovascular conditions requiring antiplatelet therapy and anticoagulation. Striking a delicate balance between the necessity for antithrombotic treatment to prevent cardiovascular events and the heightened risk of severe bleeding in individuals with hemophilia demands a nuanced and carefully considered approach.

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Cardiovascular diseases, among which includes coronary artery disease, represent one of the most important causes of mortality and morbidity worldwide. Research aimed at determining the risk factors involved recognizes a group of "traditional" risk factors, but also more recent studies identified over 100 "novel" ones which may have a role in the disease. Among the latter is the thrombophilia profile of a patient, a pathology well-established for its involvement in venous thromboembolism, but with less studied implications in arterial thrombosis.

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Hemophilia patients have a deficiency in or dysfunction of clotting factors, which can lead to a bleeding tendency. However, paradoxically, some hemophilia patients may also be at an increased risk of developing thrombotic events such as deep vein thrombosis or pulmonary embolism. The pathophysiology of thrombosis in hemophilia patients is not fully understood, but it is thought to involve a complex interplay of various factors, including the severity of the hemophilia, the presence of other risk factors such as obesity, smoking, or the use of hormonal therapies, and the presence of certain genetic mutations that increase the risk of thrombosis.

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