Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perturbations to the 1H and 31P chemical shifts of DNA resonances together with twenty-four intermolecular nuclear Overhauser effects show that the anthracycline antibiotic arugomycin intercalates between the basepairs of the hexamer duplex d(5'-GCATGC)2 at the 5'-CpA and 5'-TpG binding sites. In the complex two drug molecules are bound per duplex with full retention of the dyad symmetry. Arugomycin adopts a threaded binding orientation with chains of sugars positioned in both the major and minor groove of the helix simultaneously. The complex is stabilized by hydrogen bonding, electrostatic and van der Waals interactions principally in the major groove and involving substituents on the rigidly oriented bicycloamino-glucose sugar of the antibiotic. A specific hydrogen bond is identified between the C2'-hydroxyl and the guanine N7 at the intercalation site. Together, interactions in the major groove appear to account for the intercalation specificity of arugomycin that requires both a guanine and thymine at the intercalation site. We are unable to identify any sequence specific interactions between the minor groove and the arugarose sugar (S1) which binds only weakly, through van der Walls contacts, over the d(GCA).d(TGC) trinucleotide sequence. The data indicate that the sugar chains of arugomycin are flexible and play little part in the interaction of the antibiotic with DNA. The intensity of sequential internucleotide NOEs identifies the intercalation site as being assymmetric. A family of conformers computed using restrained energy minimisation and molecular dynamics indicate that basepair buckling is a feature of the anthracycline intercalation site that may serve to maximise intermolecular van der Waals interactions by wrapping the basepairs around the antibiotic chromophore.
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PMID:Anthracycline antibiotic arugomycin binds in both grooves of the DNA helix simultaneously: an NMR and molecular modelling study. 164 21

A 78-year-old white woman presented with a 1-month history of neck and right shoulder pain and a 12-day history of acute horizontal diplopia. On examination, bilateral sixth nerve pareses were present, right greater than left. On evaluation, the patient was noted to have normal fasting blood sugars, but moderately elevated blood sugars after a glucose load. A temporal artery biopsy was performed which was positive. Whether diabetic or arteritic, bilateral sixth nerve pareses resulted in our patient seeking medical attention. By considering temporal arteritis, it is possible that blindness was avoided.
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PMID:Bilateral sixth nerve pareses with temporal arteritis and diabetes. 294 76

Eight patients with giant cell arteritis (6 with Horton's disease and 2 with polymyalgia rheumatica) were investigated for abnormalities in glycoregulation, previously reported in Horton's disease, using oral glucose tolerance tests with measurement of insulinaemia and C-peptide response to glucagon to evaluate pancreatic function. The results were compared with those obtained in an age and weight matched population of patients with inflammatory syndromes of other origins. All patients with giant cell arteritis had abnormal glucose tolerance tests, with diabetes mellitus in 6 and impaired glucose tolerance in 2. Insulinaemias at all stages of the test, insulin response areas and basal C-peptide values were elevated; C-peptide response to glucagon was normal. Similar results were observed in patients with other inflammatory syndromes. It is concluded that glycoregulation disorders are not incidental in giant cell arteritis, that the normal pancreatic function seems to exclude immune pancreatic vasculitis, and that the abnormal glycoregulation is probably due to insulin-resistance. Since these abnormalities cannot be explained by the patients' advanced age alone, the part played by the inflammatory syndrome, which was common to both groups, is discussed. Its responsibility for inducing insulin-resistance may account for the fact that corticosteroids, which are rapidly effective against giant cell arteritis, normalise oral glucose tolerance tests.
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PMID:[Glycoregulation disorders in giant-cell arteritis]. 316 17

Antimicrobial drugs may affect the normal gut microflora in a potentially harmful manner. The purpose of the present study was to ascertain whether any of several tests could detect drug influence on the intestinal flora of healthy subjects. Jejunal secretions and feces were cultivated aerobically and anaerobically, with measurement of fermentation gas production in tubes supplemented with glucose or lactulose; bacterial bile acid deconjugation was measured with the 14C-GCA test; and pulmonary H2 and CH4 excretion were measured with gas-solid chromatography after lactulose and glucose ingestion in 18 healthy subjects before and after peroral treatment with either penicillin, metronidazole, or doxycyclin. Bacterial numbers and fermentation gas production were unchanged after treatment, as was the bacterial bile acid deconjugating activity. Pulmonary H2 excretion after lactulose ingestion was significantly reduced after penicillin and metronidazole but not after doxycyclin treatment. Pulmonary CH4 disappeared after metronidazole but remained unchanged after penicillin and doxycyclin treatment. It is concluded that pulmonary H2 and CH4 measurement after lactulose ingestion may serve as a sensitive determinant for drug effects on the normal gut microflora.
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PMID:Influence of three antimicrobial agents--penicillin, metronidazole, and doxycyclin--on the intestinal microflora of healthy humans. 732 85

Since the insulin receptor substrate-1 (IRS-1) is the major substrate of the insulin receptor tyrosine kinase and has been shown to activate phosphatidylinositol (PI) 3-kinase and promote GLUT4 translocation, the IRS-1 gene is a potential candidate for development of non-insulin-dependent diabetes mellitus (NIDDM). In this study, we have identified IRS-1 gene polymorphisms, evaluated their frequencies in Japanese subjects, and analysed the contribution of these polymorphisms to the development of NIDDM. The entire coding region of the IRS-1 gene of 94 subjects (47 NIDDM and 47 control subjects) was screened by polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP) analysis. Seven SSCP polymorphisms were identified. These corresponded to two previously identified polymorphisms [Gly971 --> Arg (GGG --> AGG) and Ala804 (GCA --> GCG)] as well as five novel polymorphisms [Pro190 --> Arg (CCC --> CGC), Met209 --> Thr (ATG --> ACG), Ser809 --> Phe (TCT --> TTT), Leu142 (CTT --> CTC), and Gly625 (GGC --> GGT)]. Although the prevalence of each of these polymorphisms was not statistically different between NIDDM and control subjects, the prevalence of the four IRS-1 polymorphisms with an amino acid substitution together was significantly higher in NIDDM than in control subjects (23.4 vs 8.5%, p < 0.05), and two substitutions (Met 209 --> Thr and Ser809 --> Phe) were found only in NIDDM patients. Equilibrium glucose infusion rates during a euglycaemic clamp in NIDDM and control subjects with the IRS-1 polymorphisms decreased by 29.5 and 22.0%, respectively on the average when compared to those in comparable groups without polymorphisms, although they were not statistically significant. Thus, IRS-1 polymorphisms may contribute in part to the insulin resistance and development of NIDDM in Japanese subjects; however, they do not account for the major part of the decrease in insulin-stimulated glucose uptake which is observed in subjects with clinically apparent NIDDM.
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PMID:Molecular scanning of the insulin receptor substrate-1 (IRS-1) gene in Japanese patients with NIDDM: identification of five novel polymorphisms. 873 21

Mitochondrial FAD-linked glycerophosphate dehydrogenase (mGPDH) is thought to be an important factor for glucose sensing in pancreatic beta cells. To evaluate the significance of the mGPDH gene in the development of non-insulin-dependent diabetes mellitus (NIDDM), we set up primers and conditions for polymerase chain reaction (PCR) amplification of the coding exons and flanking regions. Screening of 100 Japanese NIDDM patients for mutations using the PCR-single strand conformation polymorphism (SSCP) method revealed four variants (ACA:Thr243-ACG:Thr243, CAT:His264-CGT:Arg264, GCA:Ala305-GCC:Ala305, GCA:Ala 306-TCA:Ser306). The His264-Arg264 variant was found in 36 patients, while the other variants were found in only one patient each. Neither the genotypic (chi 2 = 3.15, p = 0.21) nor the allelic (chi 2 = 2.27, p = 0.13) frequency of the His264-Arg264 mutation differed between 253 Japanese NIDDM patients and 157 non-diabetic subjects. In addition, in NIDDM patients, neither the treatment modality nor body mass index differed between those with and without this mutation. These results suggest that inherited defects at this locus do not make a major contribution to genetic susceptibility to NIDDM in the Japanese population.
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PMID:Detection of variants in the mitochondrial glycerophosphate dehydrogenase gene in Japanese NIDDM patients. 908 74

Fluorine-18 fluorodeoxyglucose positron emission tomography ((18)FDG PET) plays a major role in the management of oncology patients. Owing to the singular properties of the glucose tracer, many patients suffering from non-malignant diseases such as inflammatory or infectious diseases may also derive clinical benefit from the appropriate use of metabolic imaging. Large vessel vasculitides such as giant cell arteritis and Takayasu arteritis are other examples that may potentially extend the field of (18)FDG PET indications. The purpose of the present article is to assess the feasibility of metabolic imaging in vasculitis on the basis of the current literature data. In particular, the clinical context and the (18)FDG imaging patterns seen in patients with large vessel vasculitis are analysed in order to identify potential indications for metabolic imaging.
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PMID:Imaging of large vessel vasculitis with (18)FDG PET: illusion or reality? A critical review of the literature data. 1512 14

Corticosteroid treatment should start directly after suspected diagnosis. The diagnosis should be confirmed within the next 5 days by histology or ultrasound. Clinical assessment includes auscultation of the axillary arteries in the search for large-vessel giant cell arteritis. Angiography, magnetic resonance angiography, positron emission tomography, or ultrasound can confirm the diagnosis of large-vessel giant cell arteritis. The initial prednisolone dose is 40 to 70 mg/d. It should be reduced in weekly steps of 5 to 10 mg until 20 mg/d, and by 2.5 mg until 10 mg/d. Dose reduction is 1 mg/mo below 10 mg/d, depending on symptoms and erythrocyte sedimentation rate or C-reactive protein. Patients with ophthalmologic complications receive three to four daily infusions of 250 mg of methylprednisolone for 3 days. Low-dose aspirin reduces the risk of ophthalmologic and cardiovascular complications. The benefit of methotrexate as a corticosteroid-sparing agent is controversial. Corticosteroid treatment requires monitoring of glucose, blood and eye pressure, and adequate prevention of osteoporosis.
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PMID:Current diagnosis and treatment of temporal arteritis. 1653 89

This case report describes a patient who presented with severe anemia, monoclonal gammopathy, a high erythrocyte sedimentation rate and significant weight loss. These features were highly suggestive of multiple myeloma. Bone marrow aspiration was negative for myeloma on two occasions. A positron emission tomography (PET) scan showed extensive 2-flourodeoxy-glucose uptake in the vascular tree consistent with arteritis. A temporal artery biopsy established the diagnosis of giant cell arteritis (GCA). There were no typical symptoms of GCA, such as headache, visual disturbance, or polymyalgia rheumatica. The patient was treated with steroids, which resulted in the resolution of anemia, monoclonal gammapathy, and other symptoms.
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PMID:Giant cell arteritis mimicking multiple myeloma; diagnosed by PET scan. 1719 11

Giant cell arteritis (GCA) is a relatively infrequent disorder that is underdiagnosed and little appraised in the field of general cardiology. However, it is important to be familiar with the clinical picture of this disease, especially because of the risk of developing fatal aortic aneurysms. If the disease is suspected after a thorough history and clinical examination combined with laboratory investigation, the diagnosis can be confirmed with (18)F-2-deoxy-glucose positron emission tomographic (FDG-PET) imaging. Early recognition of giant cell arteritis followed by prompt treatment with glucocorticosteroids will decrease the risk of developing large-vessel complications. (Neth Heart J 2009;17:281-3.).
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PMID:Giant cell arteritis as a cardiovascular entity. 1978 95


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