Schwangerschaft. Fehlgeburt. Geburt. Kindesmord

Ohne Zusammenfassung     

The value of stereotactic biopsy and percutaneous radiation in therapy of glioblastoma multiforme]

The concept of cytoreductive surgery in the treatment of glioblastoma multiforme is controversial. A retrospective study was carried out between 1986 and 1991 to analyze the results of stereotactic biopsy followed by supportive treatment (n = 49), incomplete radiation therapy (less than 40 Gy, n = 26), and complete radiation therapy (greater than or equal to 40 Gy, n = 58) and to compare with those of resection plus irradiation described in the literature. The patients treated with supportive care and an incomplete course of irradiation had a median survival of less than 8 weeks. For the patients who completed the radiation therapy the median survival was 32 weeks. In patients with midline shift the Karnofsky scores worsened more often during the course of radiation therapy, or therapy had to be terminated prematurely. The most important prognostic determinant was the patient's age. A comparison of survival rates in our series with those reported by other authors for patients who received tumor resection with subsequent irradiation yielded no significant difference. This would appear to cast doubt on the concept of cytoreductive surgery. The treatment of choice for patients with glioblastoma multiforme is at present radiation therapy. There is no question about the necessity of decompressive surgery whenever it is required to perform radiation therapy for severe space-occupying lesions and when it can be performed without causing new neurological deficits.     

Primitive neuroectodermal tumors after prophylactic central nervous system irradiation in children. Association with an activated K-ras gene.

Three patients had supratentorial malignant brain tumors 7 to 9 years after prophylactic central nervous system (CNS) treatment for acute lymphocytic leukemia or malignant T-cell lymphoma. Therapy was administered at the age of 3 to 8 years and included cranial irradiation (total dose, 1800 to 2400 cGy) and intrathecal methotrexate. The brain tumors had histologic and immunohistochemical features of primitive neuroectodermal tumors (PNET), including neuroblastic rosettes, rhythmic arrangement of tumor cells, and immunohistochemical expression of glial, and in one patient neuronal, marker proteins. Using polymerase chain reaction-mediated DNA amplification from paraffin-embedded tissues and subsequent DNA sequence analysis, an activating point mutation was detected in the K-ras protooncogene in one tumor. This mutation was a G to A transition in position 2 of codon 12, substituting aspartate (GAT) for glycine (GGT). This type of mutation has not been observed before in human brain tumors, but it is frequent in radiation-induced murine lymphomas. These observations suggest that PNET can be induced after completion of the embryonal and fetal development of the human CNS. Oncogene-activating point mutations may represent a pathogenetic mechanism involved in the genesis of radiation-induced brain tumors.     

Measured attenuation correction methods

Accurate attenuation correction is a prerequisite for the determination of exact local radioactivity concentrations in positron emission tomography. Attenuation correction factors range from 4–5 in brain studies to 50–100 in whole body measurements. This report gives an overview of the different methods of determining the attenuation correction factors by transmission measurements using an external positron emitting source. The long-lived generator nuclide⁶⁸Ge/⁶⁸Ga is commonly used for this purpose. The additional patient dose from the transmission source is usually a small fraction of the dose due to the subsequent emission measurement. Ring-shaped transmission sources as well as rotating point or line sources are employed in modern positron tomographs. By masking a rotating line or point source, random and scattered events in the transmission scans can be effectively suppressed. The problems of measured attenuation correction are discussed: transmission/emission mismatch, random and scattered event contamination, counting statistics, transmission/emission scatter compensation, transmission scan after administration of activity to the patient. By using a double masking technique simultaneous emission and transmission scans become feasible.This article was presented at the 1st EEC workshop on accuracy determination in PET, January 19–20th. 1989 Pisa, Italy (COMAC-BME Concerted Project Characterization and Standardization of PET Instrumentation)     

A novel active L1 retrotransposon subfamily in the mouse

Unlike human L1 retrotransposons, the 5' UTR of mouse L1 elements contains tandem repeats of approximately 200 bp in length called monomers. Multiple L1 subfamilies exist in the mouse which are distinguished by their monomer sequences. We previously described a young subfamily, called the T(F) subfamily, which contains approximately 1800 active elements among its 3000 full-length members. Here we characterize a novel subfamily of mouse L1 elements, G(F), which has unique monomer sequence and unusual patterns of monomer organization. A majority of these G(F) elements also have a unique length polymorphism in ORF1. Polymorphism analysis of G(F) elements in various mouse subspecies and laboratory strains revealed that, like T(F), the G(F) subfamily is young and expanding. About 1500 full-length G(F) elements exist in the diploid mouse genome and, based on the results of a cell culture assay, approximately 400 G(F) elements are potentially capable of retrotransposition. We also tested 14 A-type subfamily elements in the assay and estimate that about 900 active A elements may be present in the mouse genome. Thus, it is now known that there are three large active subfamilies of mouse L1s; T(F), A, and G(F), and that in total approximately 3000 full-length elements are potentially capable of active retrotransposition. This number is in great excess to the number of L1 elements thought to be active in the human genome.     

Neuronavigation Computerassistierte Neurochirurgie

The use of stereotactic methods for the resection of subcortical lesions is heavily advocated in clinical neurosurgery introducing the term "neuronavigation". Though being an unequivocally elegant technique for the localisation and delineation of pathological lesions in the central nervous system neuronavigation has not been validated by any prospective randomized controlled trial. The method is prone to significant errors as to the intraoperative localisation based upon preoperative three-dimensional images. The maximum error can be up to 2.6 cm depending on the extent of the so-called brain shift. In comparison classical frame based stereotaxy has a mean error of +/- 1 mm and remains the gold standard for the exact three-dimensional localisation of a given lesion. The value of neuronavigation is evident for small deep seated vascular lesions. For metastatic tumors or skull base tumors the usefulness is rather marginal because alternative therapies are available with proven and equivalent efficacy and reduced morbidity on one hand, and because of the anatomy of the tumor which makes neuronavigation unnecessary. For the currently most common application of neuronavigation, i.e. surgery of gliomas, no significant improvements of therapeutic results can be expected from neuronavigation. The biology of gliomas limits any mechanical approaches.     

Sentinel-Node-Biopsie beim Mammakarzinom

Die Sentinel-Lymphknotenbiopsie (Sentinel-Node-Biopsie, SNB) ist ein diagnostisches Verfahren beim Mammakarzinom, mit dem der Nodalstatus durch selektive Entnahme und Untersuchung des (der) Lymphknoten mit der höchsten Wahrscheinlichkeit für eine Metastasierung bestimmt wird. Hauptziel der Methode ist eine vollständige Erfassung der Patientinnen mit Lymphknotenmetastasen sowie die Vermeidung von Morbidität durch eine Axilladissektion bei nodalnegativen Frauen. Aufgrund der hohen Übereinstimmung zwischen dem histologischem Status des Sentinel-Nodes und dem definitiven Nodalstatus (ermittelt durch konventionelle Axilladissektion) stellt sich immer mehr die Frage, ob und unter welchen Bedingungen die SNB als Routineverfahren für das axilläre Staging gelten kann.     

Insulin-like growth factor system components in hyperparathyroidism and renal osteodystrophy

BACKGROUND: The insulin-like growth factor (IGF) system plays a key role in regulation of bone formation. In patients with renal osteodystrophy, an elevation of some IGF binding proteins (IGFBPs) has been described, but there is no study measuring serum levels of both IGF-I and IGF-II as well as IGFBP-1 to -6 in different forms of renal osteodystrophy and hyperparathyroidism. METHODS: In a cross-sectional study, we investigated 319 patients with mild (N = 29), moderate (N = 48), preuremic (N = 37), and end-stage renal failure (ESRF; N = 205). The ESRF group was treated by hemodialysis (HD; N = 148), peritoneal dialysis (PD; N = 27), or renal transplantation (RTX; N = 30). As controls without renal failure, we recruited age-matched healthy subjects (N = 87) and patients with primary hyperparathyroidism (pHPT; N = 25). Serum levels of total and free IGF-I, IGF-II, IGFBP-1 to -6, and biochemical bone markers including intact parathyroid hormone (PTH), bone alkaline phosphatase (B-ALP), and osteocalcin (OSC) were measured by specific immunometric assays. IGF system components and bone markers were correlated with clinical and bone histologic findings. Mean values +/- SEM are given. RESULTS: With declining renal function a significant increase was measured for IGFBP-1 (range 7- to 14-fold), IGFBP-2 (3- to 8-fold), IGFBP-3 (1.5- to 3-fold), IGFBP-4 (3- to 19-fold), and IGFBP-6 (8- to 25-fold), whereas IGFBP-5 levels tended to decrease (1.3- to 1. 6-fold). In contrast, serum levels of IGF-I, free IGF-I, and IGF-II remained constant in most patients. Compared with renal failure patients, pHPT patients showed a similar decline in IGFBP-5 levels and less elevated levels of IGFBP-1 (3.5-fold), IGFBP-2 (2-fold), IGFBP-3 (1.2-fold), and IGFBP-6 (4-fold) but no elevation of IGFBP-4 levels. In all subjects, free and total IGF-I levels showed significant negative correlations with IGFBP-1, IGFBP-2, and IGFBP-4 (that is, inhibitory IGF system components) and significant positive correlations with IGFBP-3 and IGFBP-5 (that is, stimulatory IGF system components). A positive correlation was observed between IGF-II and IGFBP-6. ESRF patients with mixed uremic bone disease and histologic evidence for osteopenia revealed significantly (P < 0.05) higher levels of IGFBP-2 and IGFBP-4 but lower IGFBP-5 levels. Histologic parameters of bone formation showed significant positive correlations with serum levels of IGF-I, IGF-II, and IGFBP-5. In contrast, IGFBP-2 and IGFBP-4 correlated positively with indices of bone loss. Moreover, dialysis patients with low bone turnover (N = 24) showed significantly (P < 0.05) lower levels of IGFBP-5, PTH, B-ALP, and OSC than patients with high bone turnover. CONCLUSION: Patients with primary and secondary hyperparathyroidism showed lower levels of the putative stimulatory IGFBP-5 but higher levels of IGFBP-1, -2, -3, and -6, whereas total IGF-I and IGF-II levels were not or only moderately increased. The marked increase in serum levels of IGFBP-4 appeared to be characteristic for chronic renal failure. IGFBP-5 correlated with biochemical markers and histologic indices of bone formation in renal osteodystrophy patients and was not influenced by renal function. Therefore, IGFBP-5 may gain significance as a serological marker for osteopenia and low bone turnover in long-term dialysis patients.