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)

Quantitative determination of the nucleotides AMP, ADP, ATP, GTP, NAD, NADP, 2,3-DPG and the free amino acids Lys, His, Gly, Ala, Val, Met, Phe, Tyr, Pro, Thr, Ser, Glu, Asp in erythrocytes was carried out in early and late stages of myocardial infarction. It was found that in erythrocytes, in the early stage of myocardial infarction, the concentrations of AMP, NADP and 2,3-DPG increased, whereas those of ADP, ATP, GTP and NAD decreased. In the third week of the disease the concentrations of AMP, ADP, NADP, and especially 2,3-DPG remained high, while those of ATP and GTP shifted towards the control. The concentrations of His, Gly, Ala, Val, Met, Phe, Thr and Glu increased, while those of Tyr, Ser and Asp decreased in the first stage of myocardial infarction. At the later stage of the illness (21 days) the concentrations of free amino acids returned to normal.
Atherosclerosis
PMID:Myocardial infarction. Changes in the concentrations of high-energy compounds and free amino acids in erythrocytes. 733 15

We report a 39-year-old Japanese man with HDL and apoA-I deficiency as well as data from members of his family. Corneal opacity and a stomatocyte were found but not tonsillar hypertrophy, xanthomas, or splenomegaly. His serum HDL cholesterol, apoA-I, apoA-II, and LDL cholesterol levels were t mg/dL, < 3 mg/dL, 6 mg/dL, and 175 mg/dL, respectively. Plasma triglyceride, phospholipid, apoB, apoC-III, and apoE levels were all within normal limits. Lecithin:cholesterol acyltransferase activity was half of normal, while lipoprotein lipase and hepatic triglyceride lipase activities were within normal limits. ApoA-I deficiency was confirmed by combined isoelectric focusing and sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by an immunoblotting method. We surveyed the apoA-I gene of the patient and five of his family members by direct sequencing after amplification by polymerase chain reaction and found a codon 8 nonsense mutation (TGG --> TAG, Trp --> stop) in exon 3 of the apoA-I gene. The results of a pedigree analysis by DNA sequencing and restricted fragment length polymorphism (Sty I) were consistent with an autosomal codominant trait. Coronary angiography was performed to evaluate coronary atherosclerosis, but no significant luminal narrowing was detected. An intracoronary ultrasound study showed mild intimal hyperplasia in segment 6. In summary, this is a case of apoA-I deficiency without evidence of coronary heart disease.
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PMID:A new case of apoA-I deficiency showing codon 8 nonsense mutation of the apoA-I gene without evidence of coronary heart disease. 758 66

The lipid peroxidation product trans-4-hydroxy-2-nonenal (HNE) has been implicated in the covalent modification of low-density lipoproteins (LDL) thought to contribute to the over-accumulation of LDL in the arterial wall in the initial stages of atherosclerosis. Proposals for the exact structures of "early" protein side-chain modifications until now have been based on indirect evidence. In this paper, the structures of first-formed His- and Lys-based adducts were elucidated by correlating NMR spectral properties with those obtained on models with reduced chiral center content, in some cases following hydride reduction. In this manner, we could confirm unambiguously the structure of a HNE-His imidazole(N tau) Michael adduct, stabilized as a cyclic hemiacetal and isolated from a neutral aqueous 1:1 stoichiometry reaction mixture. In the case of Lys/amine reactivity, where an excess of amine is needed to avert HNE aldol condensation, the predominance of a 1:1 Michael adduct in homogeneous aqueous solution and a 1:2 Michael-Schiff base adduct under two-phase aqueous-organic conditions could be verified by isolation of the respective borohydride-reduced forms. The 1:2 adduct, shown to exist as the cyclic hemiaminal, could represent a stable lysine-based cross-link in certain protein microenvironments.
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PMID:Structural definition of early lysine and histidine adduction chemistry of 4-hydroxynonenal. 776 13

A 50-year-old man was admitted to our hospital, because of weakness in his right leg. On admission, he had generalized hyperreflexia and positive Babinski signs bilaterally. After admission, weakness in his left leg and confusion developed. A cerebrospinal fluid examination revealed increases in cell counts and protein but was negative for malignant cells. Blood chemistry was normal except for elevated LDH. A bone marrow biopsy yielded lymphoma cells. Successive T2-weighted cranial MRI showed a progressively expanding high signal area in the right parieto-occipital lobe. His confusional state improved after chemotherapy; however, two months later another cranial CT showed multiple enhanced mass lesions. The patient died 20 months after the onset of illness. Postmortem examination revealed widespread intravascular aggregates of malignant lymphomatous cells in the cerebrum, lungs and kidney, as well as multiple infarcts without atherosclerosis in the cerebrum. These pathological findings are compatible with those of intravascular malignant lymphomatosis. In addition, extravascularly expanding tumor cells formed multiple nodular lesions in the cerebral hemisphere. An immunohistochemical study showed that the tumor cells were positive for B-cell marker L26. Intracranial lymphomatous mass lesion rarely occurs in cases of intravascular malignant lymphomatosis. In the present case, tumor cells were presumably restricted to intravascular spaces, occluded them and resulted in ischemic lesions in the cerebrum in the early phase, but they expanded extravascularly and developed mass lesions in the terminal stages. In conclusion, intravascular malignant lymphomatosis is considered to be phenotypes of malignant lymphoma. This is the first case of intravascular malignant lymphomatosis associated with intracranial lymphomatous mass lesions in Japan.
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PMID:[An autopsy case of intravascular malignant lymphomatosis with intracranial lymphomatous mass lesions]. 778 Dec 32

It has been proposed that plasma low-density lipoprotein (LDL) undergoes oxidative modification before it can give rise to foam cells in atherosclerosis. Oxidation of LDL generates a variety of reactive aldehyde products including 4-hydroxy-2-nonenal (HNE), which may covalently attach to the LDL apolipoproteins. We here present direct evidence that HNE derivatization of LDL forms Michael addition-type adducts of HNE with histidine and lysine residues of apolipoprotein B-100 (apoB) and also demonstrate the utility of an antibody specific to the HNE adducts generated in the LDL treated with HNE or oxidatively modified by Cu2+ or cultured endothelial cells. HNE adducts present in the LDL that had been treated with HNE were attested to be Michael addition-type adducts on the basis of the fact that incubation of LDL with 1 mM HNE (2 h, 37 degrees C) resulted primarily in the formation of Michael addition-type HNE-histidine (39.9 mol/mol of LDL) and HNE-lysine (19.3 mol/mol of LDL) adducts. An enzyme-linked immunosorbent assay (ELISA) and an SDS-polyacrylamide gel electrophoresis (SDS-PAGE)/immunoblot analysis of HNE-modified LDL demonstrated that these HNE adducts were detectable with the HNE-specific antibody affinity-purified with the Michael adduct (HNE-histidine) as a ligand. The following lines of evidence indicated the presence of Michael addition-type HNE adducts in the oxidatively modified LDL in vitro: (i) Amino acid analysis of LDL that had been treated with Cu2+ (24 h, 37 degrees C) demonstrated the presence of a Michael addition-type HNE-histidine adduct (7-9 mol/mol of LDL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Michael addition-type 4-hydroxy-2-nonenal adducts in modified low-density lipoproteins: markers for atherosclerosis. 791 71

The patient was a 26-year-old man with Cushing's disease who underwent transsphenoidal microscopic surgery for a pituitary microadenoma. His postoperative course was uneventful, but he died suddenly five years after the operation. At autopsy, a ruptured dissecting aneurysm with marked atherosclerosis was observed in the aorta. In the pituitary, a small focus of adrenocorticotropic hormone (ACTH) producing adenoma, possibly residual adenoma, was detected and Crooke's degeneration was observed in the non-tumorous pituitary gland. But immunohistochemical patterns of pituitary hormones in the non-tumorous pituitary gland were normal and the adrenal cortex was unremarkable. In the hypothalamus, corticotropin-releasing hormone immunoreactivity was not detected and arginine vasopressin was sporadically positive. Considering these findings, this patient may have developed subclinical hypercortisolism due to the residual adenoma at the time of autopsy, despite clinical remission. Cushing's syndrome is considered to be a risk factor dissecting aneurysm, and in this case the metabolic changes in Cushing's disease may have influenced the development of the dissecting aneurysm. Periodic cardiovascular re-evaluations should therefore be performed when there is clinical remission of Cushing's syndrome.
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PMID:A case of ruptured dissecting aneurysm 5 years after pituitary microsurgical treatment of Cushing's disease: autopsy findings in the hypothalamic-pituitary-adrenal axis. 795 28

Apoptosis and necrosis are two distinctly different forms of cell death and both occur in the human heart. In contrast to necrosis, apoptosis is not associated with inflammation and there are two reasons for this. The apoptotic cell does not swell or rupture prior to its being engulfed by either a macrophage or even a neighboring like cell. And the phagocytosis occurs with unusual rapidity. Apoptosis, also thought of as cell suicide, is a tidy way of removing cells no longer useful, in essence a form of selective deletion. These features make apoptosis a valuable component of morphogenesis, mediation of hormonal and immunological responses, and the homeostatic balance between hypertrophy and atrophy or involution. In the human heart apoptosis has been found in the sinus node of patients with the long QT syndrome. It most likely participates in the important postnatal morphogenesis of the sinus node, AV (atrioventricular) node and His bundle. Apoptosis may also participate in the genesis and pathophysiology of cardiomyopathy, paroxysmal arrhythmias or conduction disturbances (some of which may be responsible for sudden death), focal fibromuscular dysplasia of small coronary arteries, hereditary medial degeneration of the tunica media of coronary arteries, and arrhythmogenic right ventricular dysplasia. The possible role of apoptosis in numerous other changes in the human heart merit future investigation, among them being the pathogenesis of atherosclerosis and mechanisms of ageing in the myocardium.
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PMID:Normal and abnormal consequences of apoptosis in the human heart: from postnatal morphogenesis to paroxysmal arrhythmias. 797 66

Apoptosis and necrosis are two distinctly different forms of cell death, and both occur in the human heart. In contrast to necrosis, apoptosis is not associated with inflammation for two reasons. First, the apoptotic cell does not swell or rupture before it is engulfed by either a macrophage or even a neighboring like cell. Second, the phagocytosis occurs with unusual rapidity. Apoptosis, also thought of as cell suicide, is a tidy way of removing cells no longer useful, in essence a form of selective deletion. These features make apoptosis a valuable component of morphogenesis, mediation of hormonal and immunologic responses, and the homeostatic balance between hypertrophy and atrophy or involution. In the human heart apoptosis has been found in the sinus node of patients with the long QT syndrome. It most likely participates in the important postnatal morphogenesis of the sinus node, AV node, and His bundle. Apoptosis may also participate in the genesis and pathophysiology of cardiomyopathy, paroxysmal arrhythmias, or conduction disturbances (some of which may be responsible for sudden death), focal fibromuscular dysplasia of small coronary arteries, hereditary medial degeneration of the tunica media of coronary arteries, and arrhythmogenic right ventricular dysplasia. The possible role apoptosis in numerous other changes in the human heart, among them the pathogenesis of atherosclerosis and mechanisms of aging in the myocardium, merits future investigation.
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PMID:Normal and abnormal consequences of apoptosis in the human heart. From postnatal morphogenesis to paroxysmal arrhythmias. 802 44

Histochemical (= HIS) methods (haematoxylin-eosin, luxol fast blue, chromotrope aniline blue) and various immunohistochemical (= IH) markers (myoglobin, desmin, fibrinogen, complement C5b-9) were applied in parallel to test the efficiency, specificity and sensitivity for the recognition of early ischemic myocardial damage. The whole series was subgrouped into cardiac deaths (N = 35) and controls (N = 13). Cardiac deaths were sub-divided into 3 groups: 1. infarction visible in gross examination (N = 15), 2. coronary thrombosis without infarction (N = 11), 3. stenosing coronary atherosclerosis without infarction (N = 9). The control group (group 4) consisted of unnatural deaths with presumed short agonal periods (N = 13). Group 1 cases usually exhibited extended coagulation necrosis of the diffuse type and the contraction type in combination (1 exception). Group 2 showed mainly a patchy type of coagulation necrosis and contained 1 cases where all methods failed to react and 3 more cases where only the HIS methods failed to react. Group 3 and 4 were associated with a disseminated type of single and/or grouped fibre necrosis. In addition, the average reaction strengths showed a decrease from group 1 to group 4 which was more pronounced in the HIS reactions compared with the IH reactions. One case in group 1 showing negative IH reactions cannot be explained. Positive IH reactions observed in a few cases in group 2 contrasting with negative HIS reactions would indicate a greater sensitivity of this methodology and this interpretation also applies to groups 3 and 4. From pathophysiological considerations, the positive cases in groups 3 and 4 can be well explained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The application of selected histochemical and immunohistochemical markers and procedures to the diagnosis of early myocardial damage. 811 91

A 65-year-old male presented with a descending aortic dissection. His past history was remarkable for severe blunt chest trauma 26 years prior to presentation. Operative and pathologic findings included a posttraumatic pseudoaneurysm of the thoracic aorta and an aortic dissection that originated from the orifice of the pseudoaneurysm. The ductal fovea, the mouth of the pseudoaneurysm, is an area that may be more susceptible to accelerated atherosclerosis and the complications of atherosclerosis including aortic dissection.
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PMID:Descending aortic dissection originating from a juxtaductal traumatic aneurysm: technical considerations. 814 46


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