WordNet

lie at the top of; "Snow capped the mountains" (同)crest
a fruiting structure resembling an umbrella or a cone that forms the top of a stalked fleshy fungus such as a mushroom (同)pileus
restrict the number or amount of; "We had to cap the number of people we can accept into our club"
a tight-fitting headdress
a top (as for a bottle)
something serving as a cover or protection
a white insoluble fibrous protein formed by the action of thrombin on fibrinogen when blood clots; it forms a network that traps red cells and platelets

PrepTutorEJDIC

(縁のない)『帽子』,制帽 / (形・用途が)帽子に似たもの;万年筆のキャップ,時計の中ぶた,びんのふた,キノコのかさなど / (銃弾の)雷管;おもちゃのピストル玉 / 頂上,最高 / …‘に'帽子をかぶせる / …‘の'頂をおおう / 〈人が言った・した事〉‘の'上手(うわて)を行く,'を'しのぐ / …‘に'栄誉を与える
(凝固血液中の)線維素,フィブリン
Civil Air Patrol民間航空巡視員
circa

UpToDate Contents

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1. 小児の肺炎球菌性肺炎 pneumococcal pneumonia in children
2. 成人における肺炎球菌性肺炎 pneumococcal pneumonia in adults
3. 小児における肺炎随伴胸水および膿胸の疫学、臨床症状および評価 epidemiology clinical presentation and evaluation of parapneumonic effusion and empyema in children
4. 成人における嚥下性肺炎 aspiration pneumonia in adults
5. 特発性器質化肺炎 cryptogenic organizing pneumonia

English Journal

Sneddon syndrome presenting with unilateral third cranial nerve palsy.

Jiménez-Gallo D1, Albarrán-Planelles C, Linares-Barrios M, González-Fernández JA, Espinosa-Rosso R, Báez-Perea JM.Author information 1Departments of Dermatology (DJG, CAP, MLB), Neurology (RER), and Pathology (JMBP), Puerta del Mar University Hospital, Cadiz, Spain.Abstract: Sneddon syndrome is a rare systemic vasculopathy affecting the skin as livedo racemosa and the central nervous system as stroke. A 31-year-old man with a history of livedo racemosa presented with a partial left third nerve palsy. Skin biopsy showed signs of endotheliitis with obliteration of dermal blood vessels due to intimal proliferation and fibrin thrombi consistent with Sneddon syndrome. The patient was treated with platelet antiaggregant therapy with complete resolution of his third nerve palsy. Clinicians should be aware of Sneddon syndrome because prompt diagnosis and treatment may prevent potential morbidity and mortality.
Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society.J Neuroophthalmol.2014 Mar;34(1):50-2. doi: 10.1097/WNO.0b013e3182a3060d.
: Sneddon syndrome is a rare systemic vasculopathy affecting the skin as livedo racemosa and the central nervous system as stroke. A 31-year-old man with a history of livedo racemosa presented with a partial left third nerve palsy. Skin biopsy showed signs of endotheliitis with obliteration of derma
PMID 24051423

Has Our Understanding of Calcification in Human Coronary Atherosclerosis Progressed?

Otsuka F1, Sakakura K, Yahagi K, Joner M, Virmani R.Author information 1From CVPath Institute Inc, Gaithersburg, MD.AbstractCoronary artery calcification is a well-established predictor of future cardiac events; however, it is not a predictor of unstable plaque. The intimal calcification of the atherosclerotic plaques may begin with smooth muscle cell apoptosis and release of matrix vesicles and is almost always seen microscopically in pathological intimal thickening, which appears as microcalcification (≥0.5 μm, typically <15 μm in diameter). Calcification increases with macrophage infiltration into the lipid pool in early fibroatheroma where they undergo apoptosis and release matrix vesicles. The confluence of calcified areas involves extracellular matrix and the necrotic core, which can be identified by radiography as speckled (≤2 mm) or fragmented (>2, <5 mm) calcification. The calcification in thin-cap fibroatheromas and plaque rupture is generally less than what is observed in stable plaques and is usually speckled or fragmented. Fragmented calcification spreads into the surrounding collagen-rich matrix forming calcified sheets, the hallmarks of fibrocalcific plaques. The calcified sheets may break into nodules with fibrin deposition, and when accompanied by luminal protrusion, it is associated with thrombosis. Calcification is highest in fibrocalcific plaques followed by healed plaque rupture and is the least in erosion and pathological intimal thickening. The extent of calcification is greater in men than in women especially in the premenopausal period and is also greater in whites compared with blacks. The mechanisms of intimal calcification remain poorly understood in man. Calcification often occurs in the presence of apoptosis of smooth muscle cells and macrophages with matrix vesicles accompanied by expression of osteogenic markers within the vessel wall.
Arteriosclerosis, thrombosis, and vascular biology.Arterioscler Thromb Vasc Biol.2014 Feb 20. [Epub ahead of print]
Coronary artery calcification is a well-established predictor of future cardiac events; however, it is not a predictor of unstable plaque. The intimal calcification of the atherosclerotic plaques may begin with smooth muscle cell apoptosis and release of matrix vesicles and is almost always seen mic
PMID 24558104

Procoagulant platelets form an α-granule protein-covered "cap" on their surface that promotes their attachment to aggregates.

Abaeva AA1, Canault M, Kotova YN, Obydennyy SI, Yakimenko AO, Podoplelova NA, Kolyadko VN, Chambost H, Mazurov AV, Ataullakhanov FI, Nurden AT, Alessi MC, Panteleev MA.Author information 1From the Center for Theoretical Problems of Physicochemical Pharmacology, 119991 Moscow, Russia.AbstractStrongly activated "coated" platelets are characterized by increased phosphatidylserine (PS) surface expression, α-granule protein retention, and lack of active integrin αIIbβ3. To study how they are incorporated into thrombi despite a lack of free activated integrin, we investigated the structure, function, and formation of the α-granule protein "coat." Confocal microscopy revealed that fibrin(ogen) and thrombospondin colocalized as "cap," a single patch on the PS-positive platelet surface. In aggregates, the cap was located at the point of attachment of the PS-positive platelets. Without fibrin(ogen) retention, their ability to be incorporated in aggregates was drastically reduced. The surface fibrin(ogen) was strongly decreased in the presence of a fibrin polymerization inhibitor GPRP and also in platelets from a patient with dysfibrinogenemia and a fibrinogen polymerization defect. In contrast, a fibrinogen-clotting protease ancistron increased the amount of fibrin(ogen) and thrombospondin on the surface of the PS-positive platelets stimulated with collagen-related peptide. Transglutaminases are also involved in fibrin(ogen) retention. However, platelets from patients with factor XIII deficiency had normal retention, and a pan-transglutaminase inhibitor T101 had only a modest inhibitory effect. Fibrin(ogen) retention was normal in Bernard-Soulier syndrome and kindlin-3 deficiency, but not in Glanzmann thrombasthenia lacking the platelet pool of fibrinogen and αIIbβ3. These data show that the fibrin(ogen)-covered cap, predominantly formed as a result of fibrin polymerization, is a critical mechanism that allows coated (or rather "capped") platelets to become incorporated into thrombi despite their lack of active integrins.
The Journal of biological chemistry.J Biol Chem.2013 Oct 11;288(41):29621-32. doi: 10.1074/jbc.M113.474163. Epub 2013 Aug 30.
Strongly activated "coated" platelets are characterized by increased phosphatidylserine (PS) surface expression, α-granule protein retention, and lack of active integrin αIIbβ3. To study how they are incorporated into thrombi despite a lack of free activated integrin, we investigated the structur
PMID 23995838