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Biomedical subjects

J Wirsching

Publications and source records attributed to J Wirsching.

10 recordsLinked to original sources
PubMed2005

Homocysteine levels, haemostatic risk factors and patency rates after endovascular treatment of the common iliac arteries.

OBJECTIVES: To investigate the impact of clinical risk factors, plasma homocysteine and haemostatic variables on the results after endovascular treatment of symptomatic atherosclerosis of the common iliac artery. DESIGN: Prospective observational study. SETTING: University hospital. PATIENTS AND METHOD: The study included 139 technically successful interventions in 103 patients. Technical success was defined as < or = 30% residual stenosis as seen on the post treatment angiogram. Blood samples for analyses of fasting plasma values of homocysteine, fibrinogen, D-dimer, activated protein C resistance were drawn upon admission. Median follow-up for all procedures was 22 months (range 0-55 months). Patency was defined as freedom from > or = 50% restenosis or reocclusion. RESULTS: The technical success rate for all procedures was 93%. The 1-year cumulative primary patency rate based on intention to treat was 85%. Multivariate analysis revealed a significant independent association between patency rates and levels of fibrinogen and homocysteine and the nature of the lesion treated (stenosis vs. occlusion). CONCLUSION: The aetiology of restenoses and reocclusions is probably multifactorial. Procoagulant activity, the nature of the lesion treated and homocysteine levels within and above the upper range of normal limits are important risk factors for failure after endovascular treatment of the common iliac arteries.

Adult↗
PubMed2004

Homocysteine levels, haemostatic risk factors and patency rates after endovascular treatment of the above-knee femoro-popliteal artery.

OBJECTIVES: To investigate the relationship between plasma homocysteine and other haemostatic variables and restenoses or reocclusions after endovascular treatment of symptomatic atherosclerosis of the above-knee femoro-popliteal artery. DESIGN: Prospective observational study. SETTING: University hospital. PATIENTS AND METHODS: The study included 103 patients (116 limbs), treated with subintimal angioplasty in 58 cases (50%) and with intraluminal PTA in 58 (50%): 39 (34%) patients were treated for critical limb ischaemia. Blood samples for analyses of fasting plasma values of homocysteine, fibrinogen, D-dimer, activated protein C resistance were drawn upon admission. Median follow-up for all procedures was 11 months (range 0-42 months). Outcome events (arterial patency) were defined as > or =50% restenosis or reocclusion in the treated arterial segment. Patency rates were estimated with the product limit method and Kaplan-Meier curves. Variables found to be related significantly to patency were included in multivariate analysis performed with the Cox proportional hazard model. RESULTS: The 1-year cumulative primary patency rate for all procedures was 48%. One-year limb salvage rate in cases of critical ischaemia was 74%. Multivariate analysis demonstrated significant independent associations between patency rates and plasma D-dimer, diabetes mellitus, the nature of the lesion treated (stenosis vs. occlusion) and antithrombotic therapy with aspirin after the procedure. Plasma levels of homocysteine, fibrinogen or activated protein C resistance were not associated with patency rates. Homocysteine levels were higher in patients with critical limb ischaemia than those with intermittent claudication. CONCLUSIONS: Early restenosis or reocclusion after endovascular intervention of lesions in the above-knee femoro-popliteal artery was more frequent following treatment of occlusion (versus stenosis), for patients with diabetes, patients with elevated D-dimer and those without antithrombotic therapy after the procedure. Plasma homocysteine did not appear to influence the outcome of endovascular intervention.

Aged↗
PubMed2001

Thiosugars. VIII. Preparation of new 4'-thio-L-lyxo pyrimidine nucleoside analogues.

Reaction of 1-O-acetyl-2,3,5-tri-O-benzyl-4-thio-L-lyxofuranose with silylated pyrimidine bases and subsequent deprotection with boron tribromide led to 4'-thio-L-lyxo pyrimidine nucleosides. The 5-bromo-6-methyl derivative was prepared from methyl 2,3,5-tri-O-acetyl-4-thio-L-lyxofuranoside. Deacetylation was performed with sodium methoxide. The anomers were separated by HPLC and their configurations assigned by NMR spectroscopy and X-ray structural analyses. The biological activity of the nucleosides was tested.

Acetylation↗
PubMed2000

Thiosugars. Part 5: synthesis and biological activity of 1-(4-thio-L-arabinofuranosyl)-5-halopyrimidine nucleosides.

1-O-Acetyl-2,3,5-tri-O-benzyl-4-thio-L-arabinofuranoside (6) was transformed in two steps into the 1-(4-thio-L-arabinofuranosyl)-5-halopyrimidine nucleosides 10, 11 and 12, obtained as anomeric mixtures which were separable in the case of 10 and 11. No in vitro antiviral activity against HIV-1 and HIV-2. TK+ and TK- VZV and CMV has been found for 10, 11 and 12.

Antiviral Agents↗
PubMed2000

Preparation of selenoanhydro- and telluroanhydroglycofuranosides and some corresponding nucleosides.

Methyl 2,3-anhydro-alpha-D-ribofuranoside (3a) was transformed into methyl 2-seleno-2,5-anhydro-alpha-D-arabinofuranoside (5a) and methyl 3-seleno-3,5-anhydro-alpha-D-xylofuranoside (6a) in two steps via the reaction of the C-5 mesylate of 3a, methyl 2,3-anhydro-5-O-mesyl-alpha-D-ribofuranoside (4a), with sodium hydrogen selenide. The corresponding beta anomer of 3a yielded methyl 3-seleno-3,5-anhydro-beta-D-xylofuranoside as the main product and only traces of methyl 2-seleno-2,5-anhydro-beta-D-arabinofuranoside. Sodium hydrogen telluride transformed 4a into methyl 2-telluro-2,5-anhydro-alpha-D-arabinofuranoside. Starting from 5a we prepared 1-(2-seleno-2,5-anhydro-alpha-D-arabinofuranosyl)uracil and the analogous thymidine nucleoside. Compound 6a could not be transformed into nucleosides.

Carbohydrate Sequence↗
PubMed1999

Endovascular treatment of abdominal aortic aneurysms in Norway: the first 100 patients.

OBJECTIVES: to present the first 100 consecutive endograft implantations for abdominal aortic aneurysms (AAAs) in Norway. DESIGN: retrospective study of 100 consecutive graft implantations, performed at five University Hospitals during 1995 to 1997. MATERIAL: one hundred patients with a median age of 70 years were included. In all patients the Vanguard modular system (Boston Scientific Corp.) was used. Ninety-four of the 100 patients were treated under regional anaesthesia. A completion angiography was done to evaluate the position of the graft and whether endoleaks were present. RESULTS: two patients died within 30 days, one due to cardiac insufficiency and another due to haemorrhage during the procedure. There were four early conversions to open repair. At discharge eight patients had an endoleak, while retrograde flow into the aneurysmal sac was observed in four patients. During the follow-up period one conversion to open repair became necessary due to graft migration. Four late leaks were all repaired successfully using endovascular techniques. Five cases of retrograde filling were detected and embolisation with coils was performed in two cases, while three were observed. Seven graft-limb occlusions occurred during the follow-up period and four of these required treatment. CONCLUSIONS: endovascular AAA repair should be regarded as an experimental treatment, although the short term results are promising. Close follow-up of patients with CT scans or arteriography is necessary.

Aged↗
PubMed1995

The human plakoglobin gene localizes on chromosome 17q21 and is subjected to loss of heterozygosity in breast and ovarian cancers.

The gene encoding human plakoglobin was mapped to chromosome 17q12-q22. An intragenic restriction fragment length polymorphism was used to localize the plakoglobin gene distal to locus KRT10 and proximal to the marker D17S858. The plakoglobin gene colocalizes with the polymorphic 17q21 marker UM8 on the same cosmid insert. This subregion of chromosome 17 is known to be particularly subjected to genetic alterations in sporadic breast and ovarian tumors. We show loss of heterozygosity of the plakoglobin gene in breast and ovarian tumors. We have identified a low-frequency polymorphism in the plakoglobin coding sequence which results in an arginine to histidine substitution at amino acid position 142 of the protein, as well as a silent mutation at nucleotide position 332 of the coding sequence. This polymorphism allowed us to demonstrate an allelic association of plakoglobin with predisposition to familial breast and ovarian cancers. Our results, together with the present knowledge about the biological function of plakoglobin, suggest that plakoglobin might represent a putative tumor suppressor gene for breast and ovarian cancers.

Amino Acid Sequence↗