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)

Under examination there were alcoholics aged 25 to 45 years, 44 of whom later died. At lifetime the addicts showed various clinical syndromes of acute vascular disorders, such as, hemorrhages to the brain matter, subarachnoidal hemorrhages, subdural hematomas, general disturbances of the cerebral circulation, as well as alcoholic cardiopathies. On postmortem examination both acute and chronic vascular disorders were revealed. The acute disorders manifested themselves in a pronounced plethora of the brain, the meninges and the internal organs; disturbances of the vascular wall permeability, and hemorrhages (large and small) to the brain, the subarachnoidal and subdural space and to the internal organs. In chronic vascular disorders, cerebrovascular fibrosis and atherosclerosis of the cerebral vessels, the aorta and the coronary arteries as well as residua of large and small hemorrhages sustained were recorded.
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PMID:[Cerebrovascular disorders in alcoholics (clinico-morphologic study)]. 723 67

We report a 37-year-old man with cerebral infarction due to meningovascular neurosyphilis. He developed right hemiplegia and motor aphasia preceded by left retroorbital pain lasting a month. Bilateral tonic pupils were also observed. Magnetic resonance imaging (MRI) disclosed cerebral infarction in the distribution of perforating branches of the left middle cerebral artery. Abnormal enhancement was absent in the meninges on T1-weighted MRI examination. SPECT study with I-123 iodoamphetamine showed decreased perfusion in the area of the left middle cerebral artery on early phase. A delayed SPECT 4 hour later demonstrated redistribution of the cerebral blood flow in the area of its cortical branches. On cerebral angiograms, marked stenoses were disclosed at the supraclinoid segments of the bilateral internal carotid arteries as well as the M1 segment of the left middle cerebral artery. These stenoses were associated with increased collateral circulations on the left side. Atherosclerosis was not apparent, on angiography. The cerebrospinal fluid (CSF) showed pleocytosis and positive TPHA. The CSF/serum ratio of TPHA was 1/16. Oligoclonal IgG band was present in the CSF. CSF IgG index was elevated. These findings were consistent with meningovascular neurosyphilis. Causes of angiitis other than syphilis were excluded. A test for antibodies against human immunodeficiency virus was negative. The clinical course of his recovery was similar to that in patients with atherosclerotic thrombosis. The stenosis of the right internal carotid artery demonstrated by angiography could not be expected from the clinical manifestations and SPECT study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral internal carotid artery stenoses in a patient with meningovascular neurosyphilis]. 826

Retention of teeth into advanced age makes caries and periodontitis lifelong concerns. Dental caries occurs when acidic metabolites of oral streptococci dissolve enamel and dentin. Dissolution progresses to cavitation and, if untreated, to bacterial invasion of dental pulp, whereby oral bacteria access the bloodstream. Oral organisms have been linked to infections of the endocardium, meninges, mediastinum, vertebrae, hepatobiliary system, and prosthetic joints. Periodontitis is a pathogen-specific, lytic inflammatory reaction to dental plaque that degrades the tooth attachment. Periodontal disease is more severe and less readily controlled in people with diabetes; impaired glycemic control may exacerbate host response. Aspiration of oropharyngeal (including periodontal) pathogens is the dominant cause of nursing home-acquired pneumonia; factors reflecting poor oral health strongly correlate with increased risk of developing aspiration pneumonia. Bloodborne periodontopathic organisms may play a role in atherosclerosis. Daily oral hygiene practice and receipt of regular dental care are cost-effective means for minimizing morbidity of oral infections and their nonoral sequelae.
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PMID:Infectious complications of dental and periodontal diseases in the elderly population. 1295 53

Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the conversion of methylamine to formaldehyde. This enzyme is located on the surface of the cytoplasmic membrane and in the cytosol of vascular endothelial cells, smooth muscle cells, and adipocytes. Increased SSAO activity has been found in patients with diabetes mellitus, chronic heart failure, and multiple types of cerebral infarcts and is associated with obesity. Increased SSAO-mediated deamination may contribute to protein deposition, the formation of plaques, and inflammation, and thus may be involved in the pathophysiology of chronic vascular and neurological disorders, such as diabetic complications, atherosclerosis, and Alzheimer's disease. In the present study, we demonstrate the induction of cross-linkage of formaldehyde with the lysine moiety of peptides and proteins. Formaldehyde-protein adducts were reduced with sodium cyanoborohydride, hydrolyzed in hydrochloric acid, and the amino acids in the hydrolysates were derivatized with fluorenylmethyl chloroformate and then identified with high-performance liquid chromatography. We further demonstrate that incubation of methylamine in the presence of SSAO-rich tissues, e.g., human brain meninges, results in formaldehyde-protein cross-linkage of particulate bound proteins as well as of soluble proteins. This cross-linkage can be completely blocked by a selective inhibitor of SSAO. Our data support the hypothesis that the SSAO-induced production of formaldehyde may be involved in the alteration of protein structure, which may subsequently cause protein deposition associated with chronic pathological disorders.
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PMID:Protein cross-linkage induced by formaldehyde derived from semicarbazide-sensitive amine oxidase-mediated deamination of methylamine. 1512 65

Uncoupling protein 2 (UCP2) is a member of the mitochondrial transporter superfamily that is expressed in many tissues, including immune cells. UCP2 prevents oxidative stress by reducing reactive oxygen species. Using UCP2-deficient mice, it was shown that UCP2 is involved in the regulation of insulin secretion, in the resistance to infection, and in atherosclerosis. Here, we investigated the role of UCP2 in experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis. Immunized C57BL/6J UCP2-deficient mice showed a slightly delayed onset during experimental autoimmune encephalomyelitis (13.0 +/- 0.6 versus 11.5 +/- 0.8 in wild-type controls) and developed significantly higher disease scores than littermate controls (maximum disease score of 2.9 +/- 0.2 versus 1.7 +/- 0.2, P = 0.001). Higher levels of infiltrating T cells into the spinal cord meninges and parenchyma were observed. The T-cell proliferative response to the specific antigen was increased in UCP2-deficient mice compared with littermate controls, and CD4 cells of UCP2 knockout mice produced significantly higher levels of pro-inflammatory cytokines, eg, tumor necrosis factor-alpha and interleukin-2, resulting from a Th1 response. Mice lacking UCP2 also developed a higher B-cell response. Concomitantly, CD4 and CD8 cells of the UCP2-deficient mice showed increased production of reactive oxygen species. These results suggest a protective function of UCP2 in chronic inflammatory diseases such as multiple sclerosis.
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PMID:Uncoupling protein 2 has protective function during experimental autoimmune encephalomyelitis. 1665 23

Highly active antiretroviral treatment (HAART) has had a significant impact on survival of individuals with acquired immunodeficiency syndrome (AIDS); however, with the longer life-span of patients with AIDS, there is increasing prevalence of AIDS dementia complex (ADC) and other non-AIDS-defining illness, and cardiovascular diseases (CVD) are also common. The influence of these varied disease processes on HIV-1 DNA concentration in brain tissues has not been thoroughly assessed in the post-HAART era. The purpose of the current study is to clarify the impacts of ADC and other complications of HIV disease on the viral load in the brains in AIDS patients with post-HARRT. We examined autopsy specimens from the brains of thirteen patients who died from complications of AIDS with quantitative polymerase chain reaction (QPCR). All but one patient had received HAART prior to death since 1995. Two patients died with severe CVD, multiple cerebrovascular atherosclerosis (CVA) throughout the brain and five patients died with ADC. Six patients had no ADC/CVA. A QPCR was used to measure the presence of HIV-1 DNA in six brain tissues (meninges, frontal grey matter, frontal white matter, temporal subcortex, cerebellum and basal ganglia). In the post-HARRT era, for non-ADC/CVA patients, HIV-1 DNA concentration in brain tissues was statistically higher than that in patients with ADC. In a new finding, two patients who suffered from severe CVD, especially CVA, also had high concentrations of HIV-1 in brain compartments not showing ADC related changes. To our knowledge, this is the first report of a relationship between the CVA and HIV-1 viral burden in brain. The current observations suggest that HAART-resistant HIV reservoirs may survive within ADC lesions of the brain as well as the macrophage rich atherosclerosis, which needs to be confirmed by more AIDS cases with CVA.
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PMID:High level HIV-1 DNA concentrations in brain tissues differentiate patients with post-HAART AIDS dementia complex or cardiovascular disease from those with AIDS. 1964 70

CASE DESCRIPTION A 2.5-year-old 12-kg (26.4-lb) castrated male Miniature American Shepherd was referred because of a 3-week history of a localized crusted skin lesion on the digital pad of digit 3 of the right hind limb. CLINICAL FINDINGS Skin lesions were noted on the digital pads of the right hind limb. Serum biochemical analyses indicated severe hypercholesterolemia and hypertriglyceridemia. Ultrasonography of the terminal portion of the aorta and other major arterial vessels revealed substantial arteriosclerotic change. TREATMENT AND OUTCOME Medical treatments included administration of atorvastatin calcium, a low-fat diet, and omega-3 fatty acids to reduce serum lipids concentration; clopidogrel to prevent thrombosis; pentoxifylline to improve microcirculatory blood flow; clomipramine hydrochloride and trazodone hydrochloride to help with the behavioral problems; and gabapentin to help with pain management and behavioral problems. Surgical management included amputation of the initial digit involved, then eventually the entire initial limb involved. The response to treatment was poor, and euthanasia was elected. Postmortem findings revealed severe, widespread, and chronic intimal atherosclerosis; mild, widespread, and degenerative changes in the cerebral cortex; and edema and vascular congestion in the meninges. CLINICAL RELEVANCE To the authors' knowledge, this was the first report of skin necrosis secondary to atherosclerosis in a dog. Although the incidence of atherosclerosis has been considered very low in dogs, it should be investigated in dogs with severe hyperlipidemia. Primary hyperlipidemia has not been previously described in Miniature American Shepherd dogs but was the suspected underlying metabolic disorder.
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PMID:Ischemic necrosis of the digits and hyperlipidemia associated with atherosclerosis in a Miniature American Shepherd. 2996 46