Piriformis syndrome--an attempt to understand its pathology.

OBJECTIVE: Gross anatomy of the hip rotators and histology of the sciatic nerves in adult cadavers were studied, aiming to the identification of possible pathologic changes related to the piriformis syndrome (PS). MATERIAL: 50 cadavers were dissected; in 17 cases with macroscopical findings the sciatic nerves were harvested (34 sciatic nerves; 17 cadavers). History of low back or leg pain was not available. METHOD: Site anatomy and additional findings at the harvesting sites were recorded, such as anatomical variations, adhesions, hematomas etc. All nerves were additionally microscopically analyzed. In cases with findings at the dissection, the contralateral unaffected nerves served as controls. All the dissected nerves were conserved in 10% formalin solution, embedded in paraffin, stained with Hematoxylin and Eosin (H&E) and immunolabeled with antibodies against Neurofilament (NF). RESULTS: Both the H&E staining as well as the performed immunohistochemistry showed, to a variable degree, significant alterations in the structure of the affected nerves compared to the controls. CONCLUSIONS: These findings both in the local anatomy and sciatic nerve correspond to lesions that are expected in PS. Nevertheless, since this was a cadaveric study, unassociated to a certain pain patient's history, results should be considered and interpreted as an indication of a sciatic nerve injury in PS.

Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.

The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause. A possible influence of the Insulin like Growth Factor 1 (IGF-1) might be of interest, since this protein is also synthesized in most pituitary adenomas. Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells. We analyzed a large group (103 patients) of unselected clinical pituitary adenoma samples. From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR. Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts. This result was obtained, when all pituitary adenoma samples were included in the statistical calculations, irrespective of their subclassification. Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.

Micromolar concentrations of 2-methoxyestradiol kill glioma cells by an apoptotic mechanism, without destroying their microtubule cytoskeleton.

The purpose of this study was to investigate the potential effects of 2-methoxyestradiol, a natural mammalian steroid, in glioma cells, since antiproliferative effects of this compound had been shown earlier in several leukemia and carcinoma cell lines. The effects of 0.2, 2 and 20 microM concentrations of 2-methoxyestradiol were measured in three malignant human glioma cell lines (U87MG, U138MG, LN405) and one malignant rat glioma cell line (RG-2) using a microtiter-tetrazolium (MTT) assay. In all cell lines, a significant reduction of the viable cell number by more then 75% occurred ( P < 0.05) for concentrations of 2 and 20 microM 2-methoxyestradiol after 6 days. A concentration of 0.2 microM had smaller effects (10-40% cell reduction), which were significant in two of the cell lines tested. The apoptotic nature of cell death was further analyzed in U87MG and RG-2 cells. Caspase-3 activity was significantly induced to levels between 3.4- and 23-fold after 4 days for the two higher 2-methoxyestradiol concentrations (P < 0.05). In the cell line RG-2 nuclear fragmentation was visible in many nuclei, following stains with Hoechst H33258. A round cell morphology occurred in most treated cells, which was not accompanied by a complete destruction of the microtubule network, as it can be observed with other microtubule targeting drugs.

Sudden progression of a glioblastoma in partial remission?

There are only sparse data on viral CNS infections in patients with malignant glioma. We report a case of fatal herpes encephalitis in a patient with glioblastoma in partial remission and provide a short review of the literature.

Nanomolar concentrations of epothilone D inhibit the proliferation of glioma cells and severely affect their tubulin cytoskeleton.

The purpose of this study was to investigate the potential effects of epothilones (EPOs), a new class of microtubule stabilizing cytotoxic drugs, on glioma cells in vitro. The effects of 1, 10 and 100 nM concentrations of EPO D in four malignant human glioma cell lines were measured using a microtiter-tetrazolium assay. Besides the cell lines U87MG, U138MG and LN405, one cell line was used, which had been derived from a recurrent and therapy-resistant glioblastoma in our laboratory. In addition, changes of the cell morphology were followed by light microscopy and changes in the microtubule and actin cytoskeleton were visualized by a confocal laser microscope. In all four human glioma cell lines, 10 and 100 nM concentrations of the drug, applied for 96 h, lead to a highly significant decrease in the viable cell number (p < 0.001). A mean reduction of the viable cell number between 30% and 40% (60% and 90%) was observed for a drug concentration of 10 nM (100 nM). A round cell morphology occured in most EPO treated cells and the organized network of microtubules was shrunk in these round cells. The tubulin immunostaining now appeared amorphous and was restricted to small perinuclear regions. Large actin filaments also disappeared, but actin staining was present in the whole cytosplasm. These results prove that EPOs have antiproliferative effects in glioma cells and affect their tubulin cytoskeleton, as it was previously observed in several types of carcinoma cells.

Pineal epidermoid coinciding with pineocytoma.

Tumours of the pineal region are uncommon. We report on a 62-year-old male presenting with Parinaud's syndrome and aqueduct stenosis caused by a cystic tumour in the pineal region. During surgery, adjacent to the cystic tumour, a second smaller tumour was identified, which was clearly separate from the first tumour and from the pineal gland. Histological examination disclosed the cystic tumour as an epidermoid cyst, whereas the second tumour demonstrated histological and immunohistochemical features of a pineocytoma. The unique finding of two different types of tumours in the pineal region is evaluated with regard to the histogenesis of epidermoid cysts and pineocytomas.

Promoter mutations are no major cause of PTTG overexpression in pituitary adenomas.

OBJECTIVE: The pituitary tumour transforming gene (PTTG) was proven to cause transformation of NIH3T3 fibroblasts, which produce tumours when transplanted into immunodeficient mice. PTTG is overexpressed in about 90% of pituitary adenomas. The reason for its overexpression is still unclear. DESIGN: Because promoter mutations may play a role for an altered regulation of PTTG transcription in the pituitary adenomas, we analysed two promoter regions which were characterized previously as functionally important. PATIENTS: Twenty-five patients of both sexes with pituitary adenomas, mainly null-cell adenomas, were included in this study. MEASUREMENTS: Both DNA regions were amplified from paraffin sections by PCR and analysed for small deletions or insertions on polyacrylamide gels in all patients. In 16 cases both DNA regions were sequenced to detect base substitutions. RESULTS: No deletions/insertions and no tumour-specific substitutions were found. In three homopolymeric regions a polymorphism was detected, which also occurred in control sequences. In addition, these tracts showed some degree of length instability. CONCLUSIONS: Promoter mutations do not play a major role for the enhanced PTTG transcription in pituitary adenomas. Therefore, DNA-binding proteins, hypomethylation or other epigenetic factors may be responsible for PTTG overexpression.

Parental variables associated with bulimia nervosa.

The present study examined daughter and parent variables associated with bulimia nervosa, including attitudes about body image, eating and dieting histories, and self-esteem. Subjects were female undergraduates (bulimic, subclinical bulimic, and normal) their parents. Daughters differed in bodymass, with bulimics largest, followed by subclinicals, and finally controls. After daughter's bodymass was covaried, daughters differed in the expected direction on eating and body measures and perceived pressure from mothers to lose weight. Bulimic and subclinical daughters also perceived their mothers, more than their fathers, to pressure them to lose weight. After parents' bodymass was controlled, parents did not differ in eating behavior, dieting and weight history, self-esteem, body importance, or body image (self). Parents also did not differ in their perceptions of their daughters' bodies or the pressure exerted upon their daughters to lose weight after daughter's body-mass was covaried.

Bulimia and interpersonal relationships: an extension of a longitudinal study.

We examined changes in bulimia in female college students and changes in the relationship between bulimia and satisfaction with interpersonal relationships. We extended data collected from a 19-month time period in a previous study to a 31-month time period. Bulimics, subclinical bulimics, and normals showed a leveling off of the previous decline in bulimic symptoms assessed at the 19-month testing. There were strong negative correlations between the Bulimia Test and ratings of satisfaction with male interpersonal relationships, but the correlations were not significant for satisfaction with female relationships.