beta aminopropionitrile/التهاب

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Effects of beta-aminopropionitrile after posterior penetrating injury in the rabbit.

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Beta-aminopropionitrile, an inhibitor of collagen cross-linking, effectively limited the degree of posttraumatic vitreous proliferation in rabbits three weeks after double perforating injury. Light microscopic examination of the sites of perforating injury after five weeks showed minimal

The effects of beta-aminopropionitrile on colonic anastomosis in rats.

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Wound contraction is a clinically important biological process because it frequently results in contractures, strictures, and stenosis. If collagen synthesis could be altered to minimize the contracture, then the outcome could be improved. Lathyrism produces poorly cross-linked collagen in healing

Substance P blocks β-aminopropionitrile-induced aortic injury through modulation of M2 monocyte-skewed monocytopoiesis

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Aortic injuries, including aortic aneurysms and dissections, are fatal vascular diseases with distinct histopathological features in the aortic tissue such as inflammation-induced endothelial dysfunction, infiltration of immune cells, and breakdown of the extracellular matrix. Few treatments are

CCR2 Positron Emission Tomography for the Assessment of Abdominal Aortic Aneurysm Inflammation and Rupture Prediction.

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BACKGROUND

The monocyte chemoattractant protein-1/CCR2 (chemokine receptor 2) axis plays an important role in abdominal aortic aneurysm (AAA) pathogenesis, with effects on disease progression and anatomic stability. We assessed the expression of CCR2 in a rodent model and human

IL-5 overexpression attenuates aortic dissection by reducing inflammation and smooth muscle cell apoptosis.

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As an inflammation-related cytokine, interleukin (IL)-5 has been reported to be involved in the development of cardiovascular diseases, such as chronic heart failure and atherosclerosis. However, the role of IL-5 in acute aortic dissection (AAD) has barely been

CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function.

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Acute aortic dissection is one of the most lethal cardiovascular disease. The major histopathological feature of AAD is medial degradation, especially breakdown of elastin and collagen. However, the underlying mechanism remains a mystery. Platelets expressed CD40 Ligand (CD40L) is recently

Intermittent Hypoxia Alleviates β-Aminopropionitrile Monofumarate Induced Thoracic Aortic Dissection in C57BL/6 Mice.

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Thoracic aortic dissection (TAD) has a high mortality rate. Intermittent hypoxia (IH) triggers both harmful and beneficial effects in numerous physiological systems. The effects of IH on TAD development were explored in a mouse

Involvement of B cells in the pathophysiology of β-aminopropionitrile-induced thoracic aortic dissection in mice.

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Thoracic aortic dissection (TAD) is a life-threatening disease that is characterized by an inflammatory response. Innate and cellular immunity has long been known to be involved in TAD, but the role of humoral immunity in the pathophysiology of TAD remains unknown. We administered the lysyl oxidase

Azelnidipine suppresses the progression of aortic aneurysm in wild mice model through anti-inflammatory effects.

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BACKGROUND Although systemic hypertension is closely associated with aortic aneurysm (AA) formation, there are many patients with AA without hypertension. In these patients, an inflammation-mediated progression of aneurysmal disease is likely responsible for AA growth and eventual rupture.

A Novel Finding: Macrophages Involved in Inflammation Participate in Acute Aortic Dissection Complicated with Acute Lung Injury.

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BACKGROUND Little is known about the pathogenesis of acute lung injury (ALI) complicated with acute aortic dissection (AAD). OBJECTIVE We aim to investigate the roles of macrophages-derived matrix metalloproteinase 9 (MMP9) in the development of ALI complicated with AAD and factors involved in the

Targeting Mitochondrial Fission as a Potential Therapeutic for Abdominal Aortic Aneurysm.

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Angiotensin II is a potential contributor to the development of abdominal aortic aneurysm (AAA). In aortic vascular smooth muscle cells, exposure to angiotensin II induces mitochondrial fission via dynamin-related protein 1 (Drp1). However, pathophysiological relevance of mitochondrial

Hypoxia-inducible factor 1-regulated lysyl oxidase is involved in Staphylococcus aureus abscess formation.

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Hypoxia-inducible factor 1 (HIF-1) is the key transcription factor involved in the adaptation of mammals to hypoxia and plays a crucial role in cancer angiogenesis. Recent evidence suggests a leading role for HIF-1 in various inflammatory and infectious diseases. Here we describe the role of HIF-1

Pharmacology of fibrosis and tissue injury.

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Methods controlling tissue fibrosis are classified into those specifically inhibiting various metabolic aspects of collagen selectively in the injured tissue (ascorbic acid deficiency, effect of agent chelating Fe(2+), proline analogs, lathyrogens). The most promising method seems to be the blocking

Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation.

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OBJECTIVE We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of

Therapeutic Effect of Rapamycin on Aortic Dissection in Mice.

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Aortic dissection (AD) is a serious clinical condition that is unpredictable and frequently results in fatal outcome. Although rapamycin, an inhibitor of mechanistic target of rapamycin (mTOR), has been reported to be effective in preventing aortopathies in mouse models, its mode of action has yet

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