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- Büki, Andras, 1966-, et al.
(författare)
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A koponyasérülés által kiváltott axonkárosodás és kezelésének lehetóségei : [Therapeutic possibilities in axonal injury caused by head trauma]
- 2002
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Ingår i: Orvosi Hetilap. - : Akademiai Kiado Rt.. - 0030-6002 .- 1788-6120. ; 143:10, s. 499-503
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Forskningsöversikt (refereegranskat)abstract
- Traumatic brain injury is putting an extreme burden on societies all over the world. While surgical and neuro-intensive treatment is traditionally aimed at space occupying or focal lesions, traumatic brain injury is frequently associated with diffuse axonal injury, which significantly contributes to its morbidity and mortality. Current taught appreciates that diffuse axonal injury is a progressive event gradually evolving from focal alterations in axolemmal permeability and the underlying axonal ultrastructure to axonal disconnection, a process amenable of therapeutic interventions. This review is primarily focusing on the clinical/neuroradiological manifestation and our contemporary knowledge of the pathobiology of traumatically evoked (diffuse-) axonal injury with particular emphasize on recent- to date, primarily experimental-therapeutic approaches that in the future might offer potential aid to the head injured.
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| 2. |
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| 3. |
- Erós, N, et al.
(författare)
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[New aspects in the classification of cutaneous lymphomas]. : Szemléletváltozás a kután lymphomák klasszifikációjában.
- 2001
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Ingår i: Orvosi hetilap. - 0030-6002. ; 142:8, s. 393-8
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Tidskriftsartikel (refereegranskat)abstract
- Authors discuss the classification of primary cutaneous lymphomas created by the Cutaneous Lymphoma Study Group of the European Organization for Research and Treatment of Cancer (EORTC) in 1996, which is based on the clinical, histological, immunohistochemical and genetic features of cutaneous lymphomas. Unlike the previous histologic classifications it contains well-defined disease entities characterized by their clinical and histological picture, clinical outcome, behaviour and therapeutic response. This classification does not use the term of low grade or high grade lymphoma, but introduces the indolent, aggressive and provisional subgroups in the T-cell lymphomas, and indolent, intermediate and provisional subgroups in the B-cell group. Authors demonstrate the EORTC classification by their own cases calling the attention to the clinical and therapeutic difference between nodal and extranodal lymphomas, and discuss the up-to-date therapeutic possibilities.
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| 4. |
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| 5. |
- Kovács, Anikó, 1961, et al.
(författare)
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[Immunohistochemical study of P-cadherin in breast cancer]. : P-cadherin immunhisztokémiai vizsgálata emlórákokban.
- 2002
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Ingår i: Orvosi hetilap. - 0030-6002. ; 143:8, s. 405-9
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Tidskriftsartikel (refereegranskat)abstract
- Cell adhesion molecules play a significant role in the cellular connection of normal cells. The cadherins are believed to act as tumour suppressors, and their altered expression and function have been associated with tumour development.The authors examined the expression of a Ca++ dependent intercellular adhesion molecule, P-cadherin using an immunohistochemical method in 69 surgically resected breast carcinomas.P-cadherin was detected in 30 cases (43.5%, cytoplasmic and/or membrane staining). The expression of P-cadherin was independent of tumour size and lymph node status, but correlated with a high tumour grade (grade III). In contrast, expression of E-cadherin correlated with lower tumour grade (grade I-II). P-cadherin expression was not detected in invasive lobular carcinomas.In general, P-cadherin was expressed at a lower frequency compared to E-cadherin, alpha-, and beta-catenin. These results suggest that an inverse relationship may exist between E- and P-cadherin in relation to grade, and that the expression of P-cadherin may be a marker of aggressiveness.
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| 9. |
- Sándor, János, et al.
(författare)
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A subduralis vérzés miatt kezelt betegek halálozását befolyásoló tényezók : [Predictors of lethal outcome in subdural haemorrhage]
- 2003
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Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 56:11-12, s. 386-395
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Tidskriftsartikel (refereegranskat)abstract
- Background: Subdural haemorrhage (SDH) is of high public health importance because of its frequency, high case fatality ratio (CFR) and the young age of affected population. Despite the fact that the effectivity of guideline based treatment has been improved in the last decade, the Hungarian praxis shows variable compliance for recommendations.Objectives: The study aimed to describe the heterogeneity of the treatment effectivity (by geographically identifying the populations provided with appropriate or non-optimal level care), to determine the relationship between the institutional proxies quality and the results of treatment for SDH by linking the proxies properties to the patients' records.Methods: The institutions' protocols were assessed by a self-completed questionnaire in 1997. The participating hospitals treated 79% of the Hungarian patients with SDH. The Hungarian hospital discharge data in 1997-1999 were the source of patient specific data. The risk factors of lethal outcome were investigated by logistic regression analysis.Results: High proportion of patients had been treated in hospital with low compliance for guidelines. The non-permanent access to neurosurgical service and CT facility, the lack of intracranial pressure monitoring and the respiration support provided out of intensive care units worsened the survival of subjects. It was quantified that the full compliance could have diminished the case fatality ratio by 15-20%. The ratio of extreme county level CFRs exceeded 2.36 and extrapolating the effectivity observed in the county with lowest lethality, the Hungarian CFR would have been reduced by 21% among patients with SDH main diagnosis. (The interpretation of findings is limited by the lack of differentiation between acute and chronic cases and of direct categorisation of severity for subdural haemorrhage in the official hospital discharge records).Discussion: The study results urge the increase of compliance for evidence based guidelines, since despite of some validity issues, it was demonstrated that the deviation from recommended practice is reflected in the disadvantageous outcome.
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| 10. |
- Stadler, Krisztian, et al.
(författare)
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Aminoguanidin-kezeles pozitiv hatasa a peroxinitrit-termelodesre es szivhipertrofiara streptozotocinnal indukalt diabeteses patkanyokban
- 2004
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Ingår i: Orvosi Hetilap. - 0030-6002. ; 145:49, s. 2491-2496
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Tidskriftsartikel (refereegranskat)abstract
- The effect and possible mechanisms of action of aminoguanidine (a preferential iNOS inhibitor) has been studied on cardiovascular damages and overproduction of reactive nitrogen species in streptozotocin-induced diabetic rats. MATERIALS AND METHODS: 40 rats were divided into five groups (control and diabetic, with or without aminoguanidine treatment, diabetic with insulin treatment) and oxidative stress parameters were examined. Tissue nitric oxide levels were determined by EPR spectroscopy, while peroxynitrite generation by a chemiluminescence method. Cardiac hypertrophy, blood metabolic parameters (blood glucose, HbA1c, fructosamine), as well as tissue protein carbonyl levels were also determined. RESULTS: Diabetic animals showed increased nitric oxide and peroxynitrite generation in the aorta along with a significant hypertrophy and protein carbonylation of the cardiac tissue. Both aminoguanidine and insulin treatment suppressed high levels of nitric oxide and peroxynitrite in the vasculature, but only aminoguanidine was able to prevent hypertrophic alterations and to reduce protein carbonylation in the heart. CONCLUSIONS: The results show that (1) aminoguanidine reduces nitric oxide production and prevents cardiac hypertrophy, (2) insulin therapy improves carbohydrate metabolism, reduces nitrosative stress but has no effect on cardiac hypertrophy. Cardiac hypertrophy in diabetes is strongly correlated with non-enzymatic glycation. Aminoguanidine prevented hypertrophy by blocking the formation of advanced glycation end products rather than via other mechanisms.
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