Biomedical subjects

Luisa Klotz

Publications and source records attributed to Luisa Klotz.

6 recordsLinked to original sources

PubMed2006

Higher sensitivity in the detection of inflammatory brain lesions in patients with clinically isolated syndromes suggestive of multiple sclerosis using high field MRI: an intraindividual comparison of 1.5 T with 3.0 T.

The purpose of this study was to determine the sensitivities in the detection of inflammatory lesions in patients with clinically isolated syndromes suggestive of multiple sclerosis at 3.0 T and 1.5 T. MR imaging of 40 patients at both field strengths was performed in separate sessions including contiguous axial slices of T2 turbo spin-echo (T2 TSE), fluid-attenuated-inversion-recovery (FLAIR) and pre- and postcontrast T1 spin-echo (T1 SE). Inflammatory lesions > 3 mm in size were counted and categorized according to their anatomic location. Lesion conspicuity was assessed on a five-point scale. At 3.0 T, 13% more white matter lesions could be identified on the FLAIR sequence and on the T2 TSE sequence. Compared to 1.5 T 7.5% more contrast-enhancing lesions were detected at 3.0 T. The higher detection rate at 3.0 T was significant for the infratentorial (p = 0.02) and juxtacortical (p < 0.01) region on the FLAIR as well as for the infratentorial (p = 0.03), juxtacortical (p = 0.02) and periventricular (p = 0.03) region on the T2 TSE sequence. The lesion conspicuity was significantly better at 3.0 T for FLAIR and T2 TSE sequences (p<0.01; p=0.01). In conclusion, high-field MRI at 3.0 T provides a significantly higher detection rate of inflammatory brain lesions especially in the infratentorial, juxtacortical and periventricular anatomic region.

Adolescent↗

PubMed2006

Imaging of inflammatory lesions at 3.0 Tesla in patients with clinically isolated syndromes suggestive of multiple sclerosis: a comparison of fluid-attenuated inversion recovery with T2 turbo spin-echo.

The aims of this study were to determine and compare the sensitivity of T2 turbo spin-echo (T2 TSE) and fluid-attenuated inversion recovery (FLAIR) sequences at 3.0 T in the detection of inflammatory lesions in patients with clinically isolated syndromes suggestive of multiple sclerosis. Forty-nine patients were examined with a 3.0 T MRI system using 5 mm axial sections of T2 TSE (2:19 min), FLAIR (4:00 min) and pre- and postcontrast T1 spin-echo sequences (3:37 min). Brain lesions were counted and categorized according to their anatomic location. Patients were classified according to Barkhof MRI criteria for FLAIR and T2 TSE sequences. The FLAIR sequence detected more lesions in every anatomic region except for the infratentorial region. The higher sensitivity was significant for the total number of lesions (p<0.01), the juxtacortical (p<0.01), and the periventricular (p=0.01) region. A 9% increase of infratentorial lesions using the T2 TSE sequence was not significant. The higher sensitivity using the FLAIR sequence resulted in one additional MRI criterion in nine patients, whereas the better detection of infratentorial lesions using the T2 TSE sequence resulted in additional MRI criteria in three patients. In conclusion, FLAIR provides the highest sensitivity when compared with the T2 TSE, although T2 TSE still has a diagnostic relevance in terms of MRI criteria classification.

Adolescent↗

PubMed2006

Hepatocellular neoplasms after intrahepatic transplantation of ovarian fragments into ovariectomized rats.

Intrahepatic transplantation of ovarian fragments in ovariectomized rats results in morphological abnormalities. The liver acini draining blood from ovarian grafts show alterations resembling chemically induced amphophilic hepatocellular preneoplasias. We investigated the long-term development of these estrogen-induced foci of altered hepatocytes (FAH). We divided 451 Lewis rats into one main group (MG) and 11 (7 female, 4 male) control groups and observed them for up to 30 months. MG animals were ovariectomized and received ovarian transplants into the right liver part. Different combinations of castration, transplantation of ovarian or testicular fragments, and administration of antiestrogenic toremifene were used in controls. In the MG, transplants showed signs of gonadotropic stimulation, and estrogen levels were strongly increased in the downstream liver acini. After 6 and 12 months, FAH developed in hepatocytes downstream of the transplants. After 18 months, 27% of the MG animals showed transformation of FAH into hepatocellular adenomas; this figure increased to 42% after 24 months (8/19), significantly outnumbering four spontaneous adenomas that developed between 18 and 30 months in 258 control animals. Hepatocellular carcinoma (HCC) appeared only in the MG. At 24 and 30 months, 18 HCCs developed; thus, 78% of MG animals showed at least one carcinoma. Administration of toremifene in ovariectomized and transplanted animals completely prevented hepatocarcinogenesis. Testicular grafts showed no influence on liver tissue. In conclusion, initially adaptive but preneoplastic alterations in hepatocytes downstream of intrahepatically transplanted ovarian fragments may transform into HCC, indicating a strong hepatocarcinogenic potential of high local levels of endogenous estrogens in the rat liver.

Adenoma, Liver Cell↗

PubMed2005

Proinflammatory stimulation and pioglitazone treatment regulate peroxisome proliferator-activated receptor gamma levels in peripheral blood mononuclear cells from healthy controls and multiple sclerosis patients.

The peroxisome proliferator-activated receptor gamma (PPAR-gamma) belongs to a receptor superfamily of ligand-activated transcription factors involved in the regulation of metabolism and inflammation. Oral administration of PPAR-gamma agonists ameliorates the clinical course and histopathological features in experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis (MS), and PPAR-gamma agonist treatment of PBMCs from MS patients suppresses PHA-induced cell proliferation and cytokine secretion. These effects are pronounced when cells are preincubated with the PPAR-gamma agonists and reexposed at the time of stimulation, indicating a sensitizing effect. To characterize the mechanisms underlying this sensitizing effect, we analyzed PPAR-gamma expression in PMBCs of MS patients and healthy controls. Surprisingly, MS patients exhibited decreased PPAR-gamma levels compared with controls. PHA stimulation of PBMCs from healthy controls resulted in a significant loss of PPAR-gamma, which was prevented by in vitro preincubation of the cells or in vivo by long-term oral medication with the PPAR-gamma agonist pioglitazone. Differences in PPAR-gamma expression were accompanied by changes in PPAR-gamma DNA-binding activity, as preincubation with pioglitazone increased DNA binding of PPAR-gamma. Additionally, preincubation decreased NF-kappaB DNA-binding activity to control levels, whereas the inhibitory protein IkappaBalpha was increased. In MS patients, pioglitazone-induced increase in PPAR-gamma DNA-binding activity and decrease in NF-kappaB DNA-binding activity was only observed in the absence of an acute MS relapse. These results suggest that the sensitizing effect observed in the preincubation experiments is mediated by prevention of inflammation-induced suppression of PPAR-gamma expression with consecutive increase in PPAR-gamma DNA-binding activity.

Adult↗

PubMed2005

Multiple system atrophy with macrosquare-wave jerks.

Macrosquare-wave jerks consist of high-amplitude saccadic intrusions occurring mainly during fixation that are observed in several disease entities, e.g., multiple sclerosis or parkinsonian syndromes, but very rarely in patients with multiple system atrophy. We present here a patient with multiple system atrophy exhibiting the oculomotor feature of macrosquare-wave jerks.

Electrooculography↗

PubMed2003

Noradrenaline induces expression of peroxisome proliferator activated receptor gamma (PPARgamma) in murine primary astrocytes and neurons.

Cerebral inflammatory events play an important part in the pathogenesis of Alzheimer's disease (AD). Agonists of the peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear hormone receptor that mediates anti-inflammatory actions of non-steroidal anti-inflammatory drugs (NSAIDs) and thiazolidinediones, have been therefore proposed as a potential treatment of AD. Experimental evidence suggests that cortical noradrenaline (NA) depletion due to degeneration of the locus ceruleus (LC) - a pathological hallmark of AD - plays a permissive role in the development of inflammation in AD. To study a possible relationship between NA depletion and PPARgamma-mediated suppression of inflammation we investigated the influence of NA on PPARgamma expression in murine primary cortical astrocytes and neurons. Incubation of astrocytes and neurons with 100 micro m NA resulted in an increase of PPARgamma mRNA as well as PPARgamma protein levels in both cell types. These effects were blocked by the beta-adrenergic antagonist propranolol but not by the alpha-adrenergic antagonist phentolamine, suggesting that they might be mediated by beta-adrenergic receptors. Our results indicate for the first time that PPARgamma expression can be modulated by the cAMP signalling pathway, and suggest that the anti-inflammatory effects of NA on brain cells may be partly mediated by increasing PPARgamma levels. Conversely, decreased NA due to LC cell death in AD may reduce endogenous PPARgamma expression and therefore potentiate neuroinflammatory processes.

Adrenergic beta-Agonists↗