Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcified carotid plaques are thought to be less likely to be symptomatic than non-calcified plaques. We present a patient with an unusual cerebral embolism that appeared as very high density on CT and was ascertained to derive from a calcified plaque. This 46-year-old male was admitted within 1 hr of sudden aphasia onset. The admission CT scan showed multiple high-intensity lesions that appeared like calcification. They were high intensity on MRI FLAIR images. MRA showed occlusion of the posterior trunk of the middle cerebral artery. As we considered cerebral embolism, the patient received heparin followed by warfarin. Routine MRA and DSA detected no abnormality, however, a carotid echogram showed a hyperechoic plaque at the left carotid bifurcation. As the NASCET method indicated 6.5% stenosis, carotid endarterectomy was not indicated. However, the thrombus at the bifurcation gradually enlarged despite adequate medical treatment (PT-INR 2.2 - 2.7) and we decided to surgically remove the calcified plaque, thought to be the embolus source. We removed the plaque content through a defect in the plaque membrane. Intraoperatively we found that the rapidly enlarging lesion was the plaque content rather than a thrombus. Pathologically, calcification was more dominant than atherosclerosis. His postoperative course was good and he required only aspirin. This case was peculiar in that the calcification mimicked a hyperdensity embolus and that the lesion derived from a calcified plaque which is usually stable. Repeat carotid ultrasonography is easy and useful when routine investigation fails to reveal the embolic source.
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PMID:[Artery-to-artery embolism due to ruptured calcified carotid plaque]. 1735 54

Aneurysms of the coronary arteries are extremely rare. The most common cause is atherosclerosis. Coronary aneurysms may be asymptomatic, or they may be complicated by thrombosis and rupture. We report a multiple coronary artery aneurysm that caused thrombosis in a patient, along with 22-month follow-up results with multi-slice spiral computerized tomography. A 43-year-old man was admitted to hospital with a diagnosis of acute inferior myocardial infarction. He underwent thrombolytic treatment with streptokinase. Cardiac catheterization revealed multiple large aneurysms of the proximal coronary arteries and intracoronary thrombosis in the midportion of the circumflex coronary artery. His multi-slice spiral computerized tomography revealed an organized thrombus in the CX coronary artery, no critical stenosis and no change in the coronary aneurysm after 22 months. The patient did not experience any problem during the 22-month follow-up period. In our opinion, middle diameter coronary artery aneurysms that are asymptomatic and not accompanied by critical stenosis can be followed up with medical treatment, and multi-slice spiral computerized tomography is a safe way to follow up these patients.
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PMID:Multiple coronary artery aneurysms that cause thrombosis: 22-month follow-up results with multi-slice spiral computerized tomography without surgery. 1747 87

Oxidatively modified low-density lipoprotein (oxLDL) is one of the major factors involved in the development of atherosclerosis. Because of the insolubility of apolipoprotein B-100 (apoB-100) and the heterogeneous nature of oxidative modification, modified structures of apoB-100 in oxLDL are poorly understood. We applied an on-Membrane sample preparation procedure for LC-MS/MS analysis of apoB-100 proteins in native and modified low-density lipoprotein (LDL) samples to eliminate lipid components in the LDLs followed by collection of tryptic digests of apoB-100. Compared with a commonly used in-gel digestion protocol, the sample preparation procedure using PVDF membrane greatly increased the recovery of tryptic peptides and resulted in improved sequence coverage in the final analysis, which lead to the identification of modified amino acid residues in copper-induced oxLDL. A histidine residue modified by 4-hydroxynonenal, a major lipid peroxidation product, as well as oxidized histidine and tryptophan residues were detected. LC-MS/MS in combination with the on-Membrane sample preparation procedure is a useful method to analyze highly hydrophobic proteins such as apoB-100.
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PMID:Analysis of modified apolipoprotein B-100 structures formed in oxidized low-density lipoprotein using LC-MS/MS. 1754 98

Modification of biomolecules by reactive aldehydes is believed to play a role in biological processes, including aging, atherosclerosis, and Alzheimer's disease. Here, the modification of cytochrome c promoted by trans, trans-2,4-decadienal (DDE) was investigated. Matrix-assisted laser desorption/ionization time-of-flight experiments indicated increases in the molecular weight of cytochrome c, consistent with the formation of DDE adducts. Our data show that the protein modification was time-, pH-, and DDE concentration-dependent, leading to the formation of at least six adducts after 2 h of incubation at pH 7.4. Electrospray ionization quantitative TOF mass spectrometry analysis of tryptic digests indicated that His-33, Lys-39, Lys-72, and Lys-100 were modified by DDE. These adducts could have significant effects considering that His-33, Lys-72, and Lys-100 are present in clusters of basic amino acid residues, which are believed to participate in the interaction of cytochrome c with cardiolipin in the inner mitochondrial membrane and cytochrome c oxidase. A blue shift in the cytochrome c Soret band from 409 to 406 nm was also observed after DDE reaction, indicating heme crevice opening and displacement of heme sixth ligand (Met-80) coordination in modified protein. The covalent modifications in cytochrome c could play a role in mitochondrial dysfunction associated with oxidative stress.
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PMID:Covalent modification of cytochrome c exposed to trans,trans-2,4-decadienal. 1765 62

We describe a 49-year old male Nigerian with HIV infection who presented in our institution with aorto-iliac arterial occlusive disease and progressive severe ischaemic changes of the lower extremity. His preoperative CD4 count was 43 cells / microlitre. He underwent a successful intra-peritoneal aorto-femoral bypass. This report illustrates that vascular reconstruction in an HIV infected patient can be successfully performed with minimal morbidity despite a high risk factor for major infection. The histological finding was in keeping with an accelerated atherosclerosis resulting from HIV infection.
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PMID:Aorto-femoral bypass in the HIV infected patient. 1772 18

We present a case of purpura associated with concomitant ingestion of cilostazol, aspirin and grapefruit juice. A 79-year-old man with atherosclerosis obliterans, taking cilostazol and aspirin, complained of purpura. Interview by a pharmacist revealed that he had been taking grapefruit juice for a month. His purpura disappeared upon cessation of grapefruit juice, although his medication was not altered. The most probable cause of his purpura is an increase in the blood level of cilostazol because of the inhibition of cilostazol metabolism by components of grapefruit juice. Aspirin may possibly have potentiated the risk of purpura. Grapefruit juice should be avoided in patients taking cilostazol, especially in patients being concomitantly treated with other anticoagulants.
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PMID:Possible case of potentiation of the antiplatelet effect of cilostazol by grapefruit juice. 1787 11

We report the case of a 32-year-old man who presented at the emergency department with severe chest pressure, left arm pain, and dizziness. These symptoms were described as intermittent, occurring after exercise and at rest. He had undergone several stress tests during the past 8 years, but no objective evidence of ischemia was produced. His history of hyperlipidemia and increasing frequency of symptoms prompted us to perform coronary angiography, which showed a single coronary artery with an ostium at the right sinus of Valsalva. The vessel had an initial, mixed common trunk that gave rise to both the right coronary artery proper and to the left coronary artery. The left main trunk followed a prepulmonic course. The anatomic features were eventually confirmed by computed tomographic angiography. The left main stem had a fixed 50% to 60% area narrowing, at baseline study. A treadmill stress myocardial perfusion study showed no evidence of ischemia. The patient was referred to a 2nd facility, where intravascular ultrasonography, at baseline, revealed 63% left main narrowing without evidence of atherosclerosis. Acetylcholine provocation demonstrated worsening of the stenosis to about 80%, with reproduction of angina and ST-segment depression, which indicated that medical management of spasm might provide symptomatic relief.
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PMID:Single coronary artery with prepulmonic coursing left main coronary artery manifesting as prinzmetal's angina. 1817 28

Chlamydophila pneumoniae is a gram-negative obligate intracellular bacterial pathogen that causes pneumonia and bronchitis and may contribute to atherosclerosis. The developmental cycle of C. pneumoniae includes a morphological transition from an infectious extracellular elementary body (EB) to a noninfectious intracellular reticulate body (RB) that divides by binary fission. The C. pneumoniae genome encodes a type III secretion (T3S) apparatus that may be used to infect eukaryotic cells and to evade the host immune response. In the present study, Cpn0712 (CdsD), Cpn0704 (CdsQ), and Cpn0826 (CdsL), three C. pneumoniae genes encoding yersiniae T3S YscD, YscQ, and YscL homologs, respectively, were cloned and expressed as histidine- and glutathione S-transferase (GST)-tagged proteins in Escherichia coli. Purified recombinant proteins were used to raise hyper-immune polyclonal antiserum and were used in GST pull-down and copurification assays to identify protein-protein interactions. CdsD was detected in both EB and RB lysates by Western blot analyses, and immunofluorescent staining demonstrated the presence of CdsD within inclusions. Triton X-114 solubilization and phase separation of chlamydial EB proteins indicated that CdsD partitions with cytoplasmic proteins, suggesting it is not an integral membrane protein. GST pull-down assays indicated that recombinant CdsD interacts with CdsQ and CdsL, and copurification assays with chlamydial lysates confirmed that native CdsD interacts with CdsQ and CdsL. To the best of our knowledge, this is the first report demonstrating interactions between YscD, YscQ, and YscL homologs of bacterial T3S systems. These novel protein interactions may play important roles in the assembly or function of the chlamydial T3S apparatus.
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PMID:Interactions between CdsD, CdsQ, and CdsL, three putative Chlamydophila pneumoniae type III secretion proteins. 1828

Matrix metalloproteinase-2 (MMP-2) is an attractive target for the diagnosis of cancer and atherosclerosis in nuclear imaging. A cyclic decapeptide, cCTTHWGFTLC (cCTT), has been used as the mother compound for the development of MMP-2-imaging agents with high potency and selectivity. Most of radiolabeled derivatives of cCTT currently developed for in vivo studies of MMP-2, however, suffer from low accumulation in the target tissues, such as tumors. For enhanced in vivo stability and tissue penetration, we designed a linear beta-tetrapeptide analog, H-beta 3-Phe-beta-Ala-beta 3-Trp-beta 3-His-OH (1), to mimic cCTT. The component beta-amino acids were prepared by reduction of N-protected alpha-amino acid methyl esters to the alcohols, followed by conversion into the cyanides, and subsequent hydrolysis. Compound 1 was obtained from these beta-amino acids by the conventional solution method. In MMP-2 inhibition assay, compound 1 displayed desirably significant inhibition, which was comparable to cCTT. These findings suggest that compound 1 may serve as a mother compound in the design and development of in vivo MMP-2-imaging agents.
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PMID:Synthesis of a beta-tetrapeptide analog as a mother compound for the development of matrix metalloproteinase-2-imaging agents. 1831 Sep 33

Karl Rokitansky (1804-1878) was the first to put forward a theory on pathogenesis of atherosclerosis. His "thrombogenic" theory is included in his famous three-volume Manual of Pathological Anatomy. In its first edition issued in 1844 he describes the disease under the heading Excessive formation of plaques on the interior of vessels. He does not use the term "atherosclerosis", speaking simply about a process. The description is merely macroscopic, based predominantly on lesions of the aorta. The process starts as thickening--hypertrophy and plaque formation of the vascular inner layer. The apposed pseudomembrane is composed of foreign substance of blood origin--fibrin. The pseudomembrane eventually develops into either an atheromatous process or ossification. Rokitansky accurately describes an atheromatous plaque with its lipid-rich interior, including its complications, however, he misregards plaque calcification for ossification. Although Rokitansky is aware that the disease may cause both narrowing and dilatation of a vessel, he claims that outcomes of the disease are unknown. In the third edition of Rokitansky's textbook issued 12 years later there are already included histological drawings of the aortic intimal and medial lesions.
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PMID:[Rokitansky on atherosclerosis]. 1833 31


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