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Notes: Abstract. The CO2-laser has a successful record in treatment of extensive, refractory vulvar condylomas and vulvar intraepithelial neoplasia. A prerequisite for optimal use of the laser is careful preoperative diagnosis and optimized surgical technique based upon the exact knowledge of the interaction process between laser radiation and tissue. Using a new CO2-laser scanning device, the Sharplan SwiftLase®, this in-vivo study analyses the effects of CO2-laser parameters [average power density (PD), beam size and exposure time] on vulvar skin to determine optimum laser settings. Our histomorphometric analyses reveal a minimal skin destruction (ablation depth 40 µm, extent of irreversible thermal damage 80 µm to 120 µm) after application of the CO2-laser energy with the SwiftLase® using a PD of 1000 W/cm2 with a beam size of 1 mm diameter. Previous CO2-laser application techniques required low PD (200 W/cm2 to 750 W/cm2) and a larger beam size (1.5 mm to 2 mm) moving over the epithelial surface as fast as possible to obtain a precise skin destruction. The SwiftLase® allows the laser beam to be moved slowly with a beam size of 1 mm and significantly higher PD (up to 5000 W/cm2). These advantageous application conditions guarantee precise, homogeneous vulvar skin treatments with minimal thermal damage to the surrounding normal skin. The SwiftLase® enables a less experienced colposcopists to perform vulvar CO2-laser surgery.

Notes: Abstract Background: In neonates and infants epicardial stimulation may be preferred to endocardial stimulation because of growth-associated lead problems and the risk of vascular complications associated with transvenous electrodes. This study analyzes the feasibility of atrioventricular implantation of a new epicardial lead using the video-assisted thoracic surgical (VATS) technique in an animal model. Methods: Bipolar steroid-eluting epicardial leads were implanted in seven young white pigs. In five animals bipolar atrial and ventricular pacing leads (n= 10) were inserted and fixed by the VATS technique, while two animals served as controls and underwent implantation through anterolateral thoracotomy. Surgical feasibility, pacing, and sensing thresholds of the leads as well as hemodynamic parameters during pacing were studied. Histological changes beneath the electrodes were evaluated 1 week after the implantation. Results: All animals survived the pacemaker lead implantation. One animal which underwent thoracotomy died because of irreversible ventricular fibrillation induced by rapid ventricular pacing. One animal in the VATS group exhibited intraoperative herniation of the heart through the pericardial window. All animals with left-sided VATS implantations demonstrated good individual pacing and sensing threshold values. The mean cardiac output was 1.6 times higher during AAI-mode pacing as compared to VVI-mode pacing at a heart rate of 140/min. One animal died postoperatively due to respiratory failure. No displacements of the pacemaker leads were observed in the survivors. Conclusion: While VATS-guided implantation of epicardial, atrial, and ventricular leads is feasible, technical improvements of the system are mandatory for safe clinical application.

Notes: Abstract Background: Unsuspected malignancy remains a problem for the laparoscopic surgeon. The aim of this study was to evaluate the risk of ovarian micrometastasis in patients with breast cancer who undergo laparoscopic oophorectomy. Methods: We analyzed 25 premenopausal women with breast cancer who underwent therapeutic laparoscopic oophorectomy. The patients were subdivided into the following two groups according to ovarian pathology: group A with and group B without breast carcinoma micrometastasis. We then reviewed the follow-up data for both groups, with special attention to metastasis of the abdominal wall. Results: Twelve of 44 ovaries removed by laparoscopy showed ovarian breast carcinoma micrometastasis. There were no predictive factors of micrometastasis. After a mean follow-up of 38.1 months (95% CI: 29.2–46.9 months), none of the patients with proven micrometastasis developed metastasis of the abdominal wall, and the 21 puncture sites were inconspicuous. Conclusions: Although 32% of patients may have unexpected ovarian micrometastasis, laparoscopic oophorectomy in patients with breast cancer remains a safe procedure.

Notes: Summary Lasers provide the endoscopic surgeon with a sophisticated tool for high precision cutting, destruction of tissue and coagulation. The laser allows efficient and time-saving operating techniques. Various laser systems emitting at different wavelenghts are available. The absorption of the laser is determined by the tissue properties, such as water content or pigmentation, and varies strongly with the wavelength. Each laser offers advantages for the treatment of specific disorders. Further data from clinical studies are required to evaluate whether the advantages found in experimental studies are of significance in clinical use.

Notes: Abstract The cellular nature of the giant eosinophilic cells of tuber and of the cells comprising subependymal giant cell astrocytoma (SEGA) in tuberous sclerosis (TS) remains unclear. To assess the characteristics of these lesions, 13 tubers and 6 SEGA were immunohistochemically studied with glial and neuron-associated antigens. In addition to conventional ultrastructure, 6 tubers and 8 SEGA were fibrillary acidic protein (GFAP) and somatostatin. Eosinophilic giant cells of tubers were positive for vimentin (100%), GFAP (77%) and S-100 protein (92%); such cells were also found to a various extent to be reactive for neuron-associated antigens, including neurofilament (NF) proteins (38%) or class III β-tubulin (77%). SEGA also showed variable immunoreactivity for GFAP (50%) or for S-100 protein (100%); NF epitopes, class III β-tubulin, and calbindin 28-kD were expressed in 2 (33%), 5 (83%) and 4 (67%) cases, respectively. Cytoplasmic staining for somatostatin (50%), met-enkephalin (50%), 6-hydroxytryptamine (33%), β-endorphin (33%) and neuropeptide Y (17%) was noted in SEGA, but not in tubers. Ultrastructurally, the giant cells of tubers and the cells of SEGA contained numerous intermediate filaments, frequent lysosomes and occasional rectangular or rhomboid membrane-bound crystalloids exhibiting lamellar periodicity and structural transition to lysosomes. Some SEGA cells showed features suggestive of neuronal differentiation, including stacks of rough endoplasmic reticulum, occasional microtubules and a few dense-core granules. Furthermore, in one case of tuber, a process of a single large cell was seen to be engaged in synapse formation. Intermediate filaments within a few cells of both lesions were decorated by gold particle-labeled GFAP antiserum. Within the tumor cells of SEGA, irregular, non-membrane-bound, electron-lucent areas often contained somatostatin-immunoreactive particles, whereas the latter could not be detected in tuber. The present study provides further evidence of divergent glioneuronal differentiation, both in the giant cells of tubers and the cells of SEGA. The findings of similar cells at different sites, including the subependymal zone, white matter (“heterotopias”), and cortex indirectly supports the idea that these lesions of TS result from a migration abnormality.

Notes: Abstract The cellular nature of the giant eosinophilic cells of tuber and of the cells comprising subependymal giant cell astrocytoma (SEGA) in tuberous sclerosis (TS) remains unclear. To assess the characteristics of these lesions, 13 tubers and 6 SEGA were immunohistochemically studied with glial and neuron-associated antigens. In addition to conventional ultrastructure, 6 tubers and 8 SEGA were subjected to immunoelectron microscopic study for glial fibrillary acidic protein (GFAP) and somatostatin. Eosinophilic giant cells of tubers were positive for vimentin (100%), GFAP (77%) and S-100 protein (92%); such cells were also found to a various extent to be reactive for neuron-associated antigens, including neurofilament (NF) proteins (38%) or class III β-tubulin (77%). SEGA also showed variable immunoreactivity for GFAP (50%) or for S-100 protein (100%); NF epitopes, class III b-tubulin, and calbindin 28-kD were expressed in 2 (33%), 5 (83%) and 4 (67%) cases, respectively. Cytoplasmic staining for somatostatin (50%), met-enkephalin (50%), 5-hydroxytryptamine (33%), β-endorphin (33%) and neuropeptide Y (17%) was noted in SEGA, but not in tubers. Ultrastructurally, the giant cells of tubers and the cells of SEGA contained numerous intermediate filaments, frequent lysosomes and occasional rectangular or rhomboid membrane-bound crystalloids exhibiting lamellar periodicity and structural transition to lysosomes. Some SEGA cells showed features suggestive of neuronal differentiation, including stacks of rough endoplasmic reticulum, occasional microtubules and a few dense-core granules. Furthermore, in one case of tuber, a process of a single large cell was seen to be engaged in synapse formation. Intermediate filaments within a few cells of both lesions were decorated by gold particle-labeled GFAP antiserum. Within the tumor cells of SEGA, irregular, non-membrane-bound, electron-lucent areas often contained somatostatin-immunoreactive particles, whereas the latter could not be detected in tuber. The present study provides further evidence of divergent glioneuronal differentiation, both in the giant cells of tubers and the cells of SEGA. The findings of similar cells at different sites, including the subependymal zone, white matter ("heterotopias"), and cortex indirectly supports the idea that these lesions of TS result from a migration abnormality.

Notes: Abstract Subependymal giant cell astrocytoma (SEGA) is the most common neoplastic process involving the brain in patients with tuberous sclerosis complex (TSC). Morphologically, these tumors exhibit a wide range of cytoarchitecture with spindle and epithelioid cells resembling astrocytes, and also large, occasionally giant cells, some of which have a distinctly ganglion-like appearance. Unresolved questions regarding SEGAs center on: (a) their cytogenesis, i.e., whether they are derived from single or multiple precursors; and (b) their differentiating capacity along glial or neuronal lines. We sought to determine whether SEGAs represent truly mixed tumors or whether they consist of a single population of cells with a capacity for divergent differentiation. Twenty SEGAs were assessed for immunophenotypic features of either neuronal or glial differentiation or both. Only tumors from patients with a clinically confirmed diagnosis of TSC were included. Immunoreactivity for glial fibrillary acidic protein (GFAP) and/or S-100 protein was considered indicative of a glial phenotype, whereas the presence of neuronal differentiation was assessed by staining for cytoskeletal proteins [neurofilament epitopes, class III β-tubulin, microtubule-associated protein 2 (MAP2), synaptophysin], neurosecretory substances [serotonin, cholecystokinin, β-endorphin, substance P, somatostatin, met-enkephalin, neuropeptide Y, vasoactive intestinal polypeptide (VIP)], and for the 28-kDa neuron-associated calcium binding protein calbindin. Of the tumors examined, 18 exhibited both glial and neuronal epitopes, the staining pattern being variable. In 19 tumors, the constituent spindle, polygonal and giant or ganglion-like cells showed variable immunoreactivity for GFAP and S-100 protein, both within the cell body and processes. Neuron-associated cytoskeletal proteins were present in 18 cases. Class III β-tubulin immunoreactivity was demonstrated in 17 tumors, both within the bodies of all three cell types and to varying degrees within their processes. Neurofilament protein and calbindin staining was present in 8 tumors, with reactivity for the former being distributed in a phosphorylation-dependent manner. MAP2 was detected in a few cells of two tumors. Immunoreactivity for neuropeptides was observed in 17 lesions. Somatostatin and met-enkephalin staining was noted in 10 tumors (50%), being present particularly within polygonal cells. Neuropeptide Y, serotonin and β-endorphin reactivity was found in 6 (30%), 5 (25%), and 4 tumors (20%), respectively; β-endorphin was lacking in giant cells, whereas neuropeptide Y and serotonin were seen within their cell bodies. Substance P and VIP were evident in only occasional polygonal cells of 2 (10%) and 1 tumor (5%), respectively. Stains for cholecystokinin were negative. The observation of immunoreactivity for both glial- and neuron-associated epitopes within tumor cells of the same morphology suggests that SEGAs represent proliferations of cell lineages with the capacity to undergo divergent glioneuronal as well as neuroendocrine differentiation to a greater extent than do other mixed glial-neuronal neoplasms.