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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) ;srt2:(1990-1999);srt2:(1999);lar1:(oru)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) > (1990-1999) > (1999) > Örebro universitet

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1.
  • Sriplakich, S., et al. (författare)
  • Epidermal growth factor receptor expression : predictive value for the outcome after cystectomy for bladder cancer?
  • 1999
  • Ingår i: BJU International. - Oxon, United Kingdom : Blackwell Publishing. - 1464-4096 .- 1464-410X. ; 83:4, s. 498-503
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To determine whether epidermal growth factor receptor (EGFR) immunostaining of tumour cells is associated with cancer-specific death after cystectomy for locally advanced bladder cancer.Patients and Methods: The hospital records of all patients treated with cystectomy for urothelial cancer of the urinary bladder between 1967 and 1992 were reviewed retrospectively. The paraffin-embedded specimens obtained before treatment from 173 patients were processed for immunohistochemical staining, using the monoclonal antibody NCL-EGFR (Novocastra, UK). EGFR immunostaining was considered positive if membrane staining was found in at > or = 20% of tumour cells in one or more fields at > or = 200 (area 0.59 mm2).Results: Most patients (149) received preoperative irradiation and one had neoadjuvant chemotherapy. The mean observation time was 81.3 months; 63 patients (36%) had tumour recurrence within 1-80 months (mean 18.3). Positive EGFR immunostaining was found in 100 patients (58%). The proportion of T2-4 tumours was higher in those EGFR-positive than in those EGFR-negative. Proportional-hazards analysis revealed that clinical stage was significantly associated with cancer-specific death, but EGFR expression was not.Conclusion: Although positive immunostaining for EGFR was more frequent in higher stages of locally advanced bladder cancer, this variable was not an independent predictor of outcome after cystectomy.
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2.
  • Mikhail, W. E., et al. (författare)
  • Complex cemented revision using polished stem and morselized allograft. Minimum 5-years' follow-up
  • 1999
  • Ingår i: Archives of Orthopaedic and Trauma Surgery. - New York, USA : Springer-Verlag New York. - 0936-8051 .- 1434-3916. ; 119:5-6, s. 288-291
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to evaluate the results of complex hip revision using a cemented, collarless and polished femoral stem design (CPT, Zimmer, Warsaw, In.) within a tightly impacted morselized allograft. We have now been using the impaction grafting technique in combination with the CPT stem (Zimmer) for 10 years in complex cases of severe bone loss. In this study we have elected to report only those patients who have been revised at least once before revision using the impaction grafting technique. All the patients in the study group have a minimum follow-up of 5 years after the impaction grafting revision. In total, 43 consecutive hips in 40 patients, 22 men and 18 women, with a follow-up time of between 5 and 7 years are included in the study. The complications related to the revised hip consist of three early dislocations managed by closed reduction. Two patients suffered from periprosthetic fracture, both managed with plate osteosynthesis. Two cementless sockets were revised due to aseptic socket loosening. The Endoklinik rating of preoperative bone loss for the revised hips was 2 in 13 hips, 3 in 23 hips, and 4 in 7 hips. During the first year 29 stems subsided 2-4 mm within the cement mantle. In 8 cases, a subsidence of 5-9 mm was measured. The subsidence was nonprogressive, and no subsidence occurred after the 1st year. The Charnley, D'Aubigne, Postel scoring (maximum 6 points) for pain improved from 2.2 points preoperatively to 4.4 postoperatively, function from 2.3 to 4.3, and movement from 2.3 to 4.1. In conclusion, the concept of impaction grafting in THR revision in our study has so far proven to be successful with good clinical results at 5 years despite the relatively high early subsidence of the femoral component.
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3.
  • Bejerot, Susanne, 1955-, et al. (författare)
  • Low prevalence of smoking among patients with obsessive-compulsive disorder
  • 1999
  • Ingår i: Comprehensive Psychiatry. - Philadelphia, USA : Saunders Elsevier. - 0010-440X .- 1532-8384. ; 40:4, s. 268-272
  • Tidskriftsartikel (refereegranskat)abstract
    • Tobacco smoking is common among psychiatric patients, especially among those with schizophrenia, where the prevalence is extremely high, 74% to 88%, compared with 45% to 70% in patients with other psychiatric diagnoses. Patients with anxiety disorders are less well investigated in this respect, particularly obsessive-compulsive disorder (OCD) patients. Eighty-three psychiatric outpatients with OCD and 110 members of the Swedish OCD Association responded to questions concerning their smoking habits. Among OCD patients, 14% were current smokers (compared with 25% in the general population of Sweden), 72% had never smoked, and 11 previous smokers had stopped, mostly without any difficulties. Since a decreased smoking rate among OCD subjects was confirmed, the smoking prevalences in schizophrenia and OCD, respectively, seem to represent either end of a continuum, and OCD may also differ significantly from other anxiety disorders in this respect. Possible implications of this finding for the purported frontal lobe dysregulation in OCD are discussed.
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4.
  • Büki, Andras, 1966-, et al. (författare)
  • Initial Clinical Experience with a Combined Pulsed Holmium-Neodymium-YAG Laser in Minimally Invasive Neurosurgery*
  • 1999
  • Ingår i: Minimally Invasive Neurosurgery. - : Thieme Medical Publishers. - 0946-7211 .- 1439-2291. ; 42:1, s. 35-40
  • Tidskriftsartikel (refereegranskat)abstract
    • Various biophysical features of the laser beam have already been utilized in clinical neurosurgery. However, the application of this therapeutic modality has by no means been overexploited. The history of laser application in neurosurgery has shown that there is no universal laser system capable of performing all surgical tasks in a suitable manner. The best results in traditional neurosurgery were achieved with instruments combining various wavelengths, such as the CO2 and neodymium-YAG lasers. A pulsed holmium-YAG and neodymium-YAG (Ho:YAG and Nd:YAG) combined laser have been recently developed to meet the special requirements of minimally invasive neurosurgery. The system consists of a compact double-crystal single-head solid-state laser system generating 2 different wavelengths (Ho:YAG 2.08 microns and Nd:YAG 1.05 microns), selected for their capabilities of efficient coagulation and ablation. The two wavelengths are coupled into a common flexible optical fiber, which allows endoscopic application. The wavelengths can act simultaneously or separately without any interchange of the instruments. The system was employed first for experimental and subsequently for clinical purposes, primarily for endoscopic operations. In this work the initial clinical experience is reported. The excellent haemostatic properties of the Nd:YAG laser and the ablative properties of the Ho:YAG laser were confirmed. It was concluded that simultaneous application of the two laser modalities within one flexible fiber offers new perspectives in tissue handling in endoscopic neurosurgery and as in open microsurgery.
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5.
  • Büki, Andras, 1966-, et al. (författare)
  • Moderate Posttraumatic Hypothermia Decreases Early Calpain-Mediated Proteolysis and Concomitant Cytoskeletal Compromise in Traumatic Axonal Injury
  • 1999
  • Ingår i: Experimental Neurology. - : Academic Press. - 0014-4886 .- 1090-2430. ; 159:1, s. 319-328
  • Tidskriftsartikel (refereegranskat)abstract
    • Traumatic brain injury (TBI) in animals and man generates widespread axonal injury characterized by focal axolemmal permeability changes, induction of calpain-mediated proteolysis, and neurofilament side-arm modification associated with neurofilament compaction (NFC) evolving to axonal disconnection. Recent observations have suggested that moderate hypothermia is neuroprotective in several models of TBI. Nevertheless, the pathway by which hypothermia prevents traumatic axonal injury (TAI) is still a matter of debate. The present study was conducted to evaluate the effects of moderate, early posttraumatic hypothermia on calpain-mediated spectrin proteolysis (CMSP), implicated in the pathogenesis of TAI. Using moderate (32 degrees C) hypothermia of 90 min duration without rewarming, the density of CMSP immunoreactive/damaged axons was quantified via LM analysis in vulnerable brain stem fiber tracts of hypothermic and normothermic rats subjected to impact acceleration TBI (90 min postinjury survival). To assess the influence of posthypothermic rewarming, a second group of animals was subjected to 90 min of hypothermia followed by 90 min of rewarming to normothermic levels when CMSP was analyzed to detect if any purported CMSP prevention persisted (180 min postinjury survival). Additionally, to determine if this protection translated into comparable cytoskeletal protection in the same foci showing decreased CMSP, antibodies targeting altered/compacted NF subunits were also employed. Moderate hypothermia applied in the acute postinjury period drastically reduced the number of damaged axons displaying CMSP at both time points and significantly reduced NFC immunoreactivity at 180 min postinjury. These results suggest that the neuroprotective effects of hypothermia in TBI are associated with the inhibition of axonal/cytoskeletal damage. 
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6.
  • Büki, Andras, 1966-, et al. (författare)
  • Peptidergic innervation of human cerebral blood vessels and saccular aneurysms
  • 1999
  • Ingår i: Acta Neuropathologica. - : Springer. - 0001-6322 .- 1432-0533. ; 98:4, s. 383-388
  • Tidskriftsartikel (refereegranskat)abstract
    • Peptidergic innervation of the human cerebral vasculature has not yet been described in detail and its role in the maintenance of cerebral autoregulation still needs to be established. Similarly, few data exist on the innervation of vascular malformations. The aim of this study was to clarify the peptidergic innervation patterns of human cerebral arteries of various sizes, and, for the first time, that of saccular aneurysms. Light microscopic study of whole-mount preparations of human cerebral arteries and aneurysm sacs resected either during tumor removal or after neck-clipping were carried out by means of silver-intensified light microscopic immunocytochemistry visualizing neuropeptide-Y, calcitonin gene-related peptide and substance P immunoreactivity. Systematic morphological investigations confirmed the presence of longitudinal fiber bundles on the adventitia and a network-like deeper peptidergic system at the adventitia-media border, while in smaller pial and intraparenchymal vessels, only sparse longitudinal immunopositive axons could be detected. The innervation pattern was totally absent in the wall of saccular aneurysms with the complete disappearance of peptidergic nerve fibers in some areas. To the best of our knowledge neither the disappearance of this network on small pial and intraparenchymal vessels, nor the absence of an innervation pattern in saccular aneurysms have been described before. Nonhomogeneous peptidergic innervation of the human cerebral vascular tree might be one of the factors responsible for the distinct autoregulatory properties of the capacitance and resistance vessels. Malfunction of this vasoregulatory system might lead to the impairment of autoregulation during pathological conditions such as subarachnoid hemorrhage. 
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7.
  • Büki, Andras, 1966-, et al. (författare)
  • Postinjury cyclosporin a administration limits axonal damage and disconnection in traumatic brain injury
  • 1999
  • Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 16:6, s. 511-521
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent observations concerning presumed calcium-induced mitochondrial damage and focal intraaxonal proteolysis in the pathogenesis of traumatic axonal injury (TAI) have opened new perspectives for therapeutic intervention. Studies from our laboratory demonstrated that cyclosporin A (CsA), a potent inhibitor of Ca2+-induced mitochondrial damage, administered 30 min prior to traumatic brain injury preserved mitochondrial integrity in those axonal foci destined to undergo delayed disconnection. We attributed this neuroprotection to the inhibition by CsA of mitochondrial permeability transition (MPT). Additional experiments proved that CsA pretreatment also significantly reduced calcium-induced, calpain-mediated spectrin proteolysis (CMSP) and neurofilament compaction (NFC), pivotal events in the pathogenesis of axonal failure and disconnection. Given these provocative findings the goal of the current study was to evaluate the potential of CsA to inhibit calcium-induced axonal damage in a more clinically relevant postinjury treatment paradigm. To this end, cyclosporin A was administered intrathecally to Sprague Dawley rats 30 min following impact acceleration traumatic brain injury. The first group of animals were sacrificed 120 min postinjury and the density of CMSP and NFC immunoreactive damaged axonal segments of CsA-treated and vehicle-treated injured animals were quantitatively analyzed. A second group of CsA- versus vehicle-treated rats was sacrificed at 24 h postinjury to compare the density of damaged axons displaying beta amyloid precursor protein (APP) immunoreactivity, a signature protein of axonal perturbation and disconnection. Postinjury CsA administration resulted in a significant decrease (>60%) in CMSP/NFC immunoreactivity in corticospinal tracts and medial longitudinal fasciculi. A similar decrease was detected in the density of APP immunoreactive damaged axons, indicating an attenuation of axonal disconnection at 24 h postinjury in CsA-treated animals. These results once again suggest that the maintenance of the functional integrity of the mitochondria can prevent TAI, presumably via the preservation of the local energy homeostasis of the axon. Moreover and perhaps more importantly, these studies also demonstrate the efficacy of CsA administration when given in the early posttraumatic period. Collectively, our findings suggest that a therapeutic window exists for the use of drugs targeting mitochondria and energy regulation in traumatic brain injury.
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8.
  • Büki, Andras, 1966-, et al. (författare)
  • The role of calpail-mediated spectrin proteolysis in traumatically induced axonal injury
  • 1999
  • Ingår i: Journal of Neuropathology and Experimental Neurology. - : American Association of Neuropathologists. - 0022-3069 .- 1554-6578. ; 58:4, s. 365-375
  • Tidskriftsartikel (refereegranskat)abstract
    • In animals and man, traumatic brain injury (TBI) results in axonal injury (AI) that contributes to morbidity and mortality. Such injured axons show progressive change leading to axonal disconnection. Although several theories implicate calcium in the pathogenesis of AI, experimental studies have failed to confirm its pivotal role. To explore the contribution of Ca2+-induced proteolysis to axonal injury, this study was undertaken in an animal model of TBI employing antibodies targeting both calpain-mediated spectrin proteolysis (CMSP) and focal neurofilament compaction (NFC), a marker of intra-axonal cytoskeletal perturbation, at 15-120 minutes (min) postinjury. Light microscopy (LM) revealed that TBI consistently evoked focal, intra-axonal CMSP that was spatially and temporally correlated with NFC. These changes were seen at 15 min postinjury with significantly increasing number of axons demonstrating CMSP immunoreactivity over time postinjury. Electron microscopy (EM) demonstrated that at 15 min postinjury CMSP was confined primarily to the subaxolemmal network. With increasing survival (30-120 min) CMSP filled the axoplasm proper. These findings provide the first direct evidence for focal CMSP in the pathogenesis of generalized/diffuse AI. Importantly, they also reveal an initial subaxolemmal involvement prior to induction of a more widespread axoplasmic change indicating a spatial-temporal compartmentalization of the calcium-induced proteolytic process that may be amenable to rapid therapeutic intervention. 
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9.
  • Degens, Hans, et al. (författare)
  • Post-operative effects on insulin resistance and specific tension of single skeletal muscle fibres
  • 1999
  • Ingår i: Clinical Science. - : Lippincott Williams & Wilkins. - 0143-5221 .- 1470-8736. ; 97:4, s. 449-455
  • Tidskriftsartikel (refereegranskat)abstract
    • Surgery and accidental trauma are associated with a transient period of insulin resistance, substrate catabolism and muscle weakness. In the present study, we evaluated the changes in the force-generating capacity of chemically skinned single muscle fibresfollowing abdominal surgery. Biopsies of the m. vastus lateralis were obtained in three patients 1 day before and 3 or 6 days after surgery. Part of the biopsy was frozen for histochemical analysis of the fibre cross-sectional area (FCSA) and myofibrillar protein content, and another part was used for single-fibre contractile measurements. All patients developed insulin resistance following surgery. The maximum velocity of unloaded shortening of single muscle fibres did not change following surgery. The FCSA did not decrease after surgery, as determined either from histochemical sections or from singlefibres measured at a fixed sarcomere length of 2.76+/-0.09 microm (mean+/-S.D.). Further, the force-generating capacity of the single fibres, measured as maximal Ca(2+)-activated force (P(0)) or as P(0) normalized to FCSA (specific tension), remained unchanged, as did the myofibrillar protein content of the muscle. In conclusion, the muscle weakness associated with post-operative insulin resistance is not related to a decreased specifictension or a loss of myofibrillar proteins. Other potential cellular mechanisms underlying post-operative weakness are discussed.
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10.
  • Ekman, Inger, et al. (författare)
  • Outpatient care programmes for the elderly
  • 1999
  • Ingår i: European Heart Journal. - London, United Kingdom : W. B. Saunders Co. Ltd.. - 0195-668X .- 1522-9645. ; 20:5, s. 393-4
  • Tidskriftsartikel (refereegranskat)
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