PubMed Health⌕ Search

Biomedical subjects

C Vetter

Publications and source records attributed to C Vetter.

At least 19 recordsLinked to original sources
PubMed2006

[MRI-based diagnosis of giant cell arteritis].

The giant cell arteritis and its symptoms are usually non-specific and accompanied with symptoms of polymyalgia rheumatica. As complications of the giant cell arteritis ischemia, infarction or rupture of the damaged vessel can occur. We report on a 56-year-old female patient, who suffered for one year about weight loss, tiredness and intolerance as well as symptoms of polymyalgia rheumatica. Gastroscopy and colonoscopy showed normal findings. In the context of the malignancy search we made a computer tomography and magnet resonance tomography. The data showed an enlargement and an enhancement of the aorta, which led us to the suspicion of a giant cell arteritis. We started immediately with a medical treatment. The biopsy of the arteries temporales supported histological the diagnosis.

Aortitis↗
PubMed2001

Comparative analysis of ras proto-oncogene mutations in selected mammalian tumors.

Point mutations within ras proto-oncogenes are frequently detected in human malignancies and in different types of experimentally induced tumors in animals. In contrast to findings in experimental animal models of carcinogenesis, little is known about the incidence of ras mutations in naturally occurring animal tumors. In the present study, we investigated whether point mutations, particularly within the mutational hot-spot codons 12, 13, and 61, occur at comparable frequencies in human malignancies and spontaneously occurring tumors in other mammalian species. Two hundred seventy-nine of the most frequent canine and feline neoplasms were analyzed for changes in mutational hot-spot regions of the N-, Ki-, and Ha-ras genes. DNA fragments from exons 1 and 2 of all three ras genes were amplified by polymerase chain reaction, and the presence of point mutations was assessed by single-strand conformation polymorphism analysis and direct sequencing of amplified products. Only one sample, a case of canine melanoma, exhibited an Ha-ras mutation. Thus, our data strongly suggested that ras mutations at the hot-spot loci are apparently very rare and do not play a major role in the pathogenesis of the spontaneously occurring canine and feline tumors investigated. These observations were in marked contrast to those in experimental rodent models of carcinogen-induced mammary and skin tumors that described a consistent association with Ha- or Ki-ras activation. The role of ras oncogene activation in related human malignancies therefore cannot be readily inferred from studies of experimental carcinogenesis in animal models.

Animals↗
PubMed2001

Intensity modulated proton therapy: a clinical example.

In this paper, we report on the clinical application of fully automated three-dimensional intensity modulated proton therapy, as applied to a 34-year-old patient presenting with a thoracic chordoma. Due to the anatomically challenging position of the lesion, a three-field technique was adopted in which fields incident through the lungs and heart, as well as beams directed directly at the spinal cord, could be avoided. A homogeneous target dose and sparing of the spinal cord was achieved through field patching and computer optimization of the 3D fluence of each field. Sensitivity of the resultant plan to delivery and calculational errors was determined through both the assessment of the potential effects of range and patient setup errors, and by the application of Monte Carlo dose calculation methods. Ionization chamber profile measurements and 2D dosimetry using a scintillator/CCD camera arrangement were performed to verify the calculated fields in water. Modeling of a 10% overshoot of proton range showed that the maximum dose to the spinal cord remained unchanged, but setup error analysis showed that dose homogeneity in the target volume could be sensitive to offsets in the AP direction. No significant difference between the MC and analytic dose calculations was found and the measured dosimetry for all fields was accurate to 3% for all measured points. Over the course of the treatment, a setup accuracy of +/-4 mm (2 s.d.) could be achieved, with a mean offset in the AP direction of 0.1 mm. Inhalation/exhalation CT scans indicated that organ motion in the region of the target volume was negligible. We conclude that 3D IMPT plans can be applied clinically and safely without modification to our existing delivery system. However, analysis of the calculated intensity matrices should be performed to assess the practicality, or otherwise, of the plan.

Adult↗
PubMed1997

Tumor necrosis factor alpha and interleukin 6 release induced by antibiotic killing of Pseudomonas aeruginosa and Staphylococcus aureus.

Using a recently described ex vivo model, tumor necrosis factor-alpha and interleukin-6 released by peripheral blood monocytes after killing of Pseudomonas aeruginosa and Staphylococcus aureus by ceftazidime, imipenem, and meropenem was measured. Cytokine release was highest with ceftazidime and lowest with imipenem for both bacteria (p < 0.05), although cytokine concentrations were much lower after killing of Staphylococcus aureus. Differences in cytokine release rates induced by various cell-wall active antibiotics have not yet been described for gram-positive organisms and should be studied further.

Anti-Bacterial Agents↗
PubMed1995

Effects of porcine growth hormone on pregnancy and fetal/neonatal development in the rat.

Porcine growth hormone was given subcutaneously twice daily to two groups of 20 females at dose levels of 0.5 and 2.5 IU/kg (1 and 5 IU/kg/day). A control group of 20 females was similarly treated with vehicle. The females were given either vehicle or porcine growth hormone from gestation day (GD) 6 through GD 21, for 10 females that were cesarean sectioned, or through lactation day (LD) 21, for 10 females scheduled for natural delivery. There were no deaths, abortions, or drug-related physical signs in any treatment group. Drug-related effects during gestation were limited to significant (p < or = 0.05) pharmacologically mediated increases in F0 maternal body weight gain during GD 6-20 in the 2.5-IU/kg group, approximately 24% above controls. During LD 0-21, there were significant (p < or = 0.05) dose-related increases in average maternal body weight gain in the 0.5- and 2.5IU/kg groups (72 and 200% above controls, respectively). Consistent with these findings, there were dose-dependent increases in maternal serum growth hormone and IGF-1 levels noted on GD 21 and LD 21 in both drug-treated groups. There were no drug-related effects on embryonal/fetal survival, GD 21 fetal body weight, placental weight, fetal femur length and width, or fetal morphology as determined by external, visceral, and skeletal examinations. There were no drug-related effects on F1 pup mortality, physical signs, body weight, biparietal diameter, liver weight, and femur length or width. These data suggest that subcutaneous administration of growth hormone to pregnant and lactating rats, at a dose that produces significant (p < or = 0.05) increases in maternal body weight gain and serum IGF-1 levels, has no apparent effect on embryonal/fetal development or preweaning growth.

Animals↗
PubMed1994

Effects of the class III antiarrhythmic, dofetilide (UK-68,798) on the heart rate of midgestation rat embryos, in vitro.

Gestation day 11 (GD11) and 14 (GD14) embryos were cultured for up to 4 hours in the presence of Dofetilide (0.01-0.50 microgram/ml), a potent Class III Antiarrhythmic which selectively inhibits the rapid component of the time dependent outward potassium current (IKr). Significant (P < or = 0.05) reductions in heart rate (HR) as measured over a 4 hour period were dose dependent and reversible. The sensitivity of the GD11 embryos was greater than GD14 embryos (14-64% decrease in HR vs. an 11-43% decrease in HR, respectively) at the same concentrations tested. These in vitro results support the hypothesis that the embryo-lethality of Class III Antiarrhythmics observed in vivo may be a class effect of the IKr subtype potassium channel blockers. The data suggest a possible mechanism of embryotoxicity is to lower embryonic HR resulting in subsequent hypoxia and death. Dofetilide's effects on GD11 HR were partially reversible by the sequential addition of Isoproterenol or Theophylline.

Animals↗