Arthroscopic treatment of lateral epicondylitis: Indication, technique and early results

The purpose of this study is to present the results of the arthroscopic treatment of lateral epicondylitis. Twenty patients with lateral epicondylitis (mean age 42 years) were treated arthroscopically. The average duration of symptoms prior to surgery was 14 months. The arthroscopic joint inspection showed an intact capsule in seven patients (type-I lesion), in eight patients a linear capsule tear (type-II lesion) and in six patients a complete rupture of the capsule (type-III lesion). An associated intraarticular pathology was documented in eight patients. Within an average follow-up period of 1.8 years, local pain and function were documented and analyzed. Subjective pain at rest was reduced from 5.0 to 0.5 points, pain at daily living activities from 6.0 to 1.0 points and pain at athletic activities from 7.3 to 1.2 points in the VAS score. Function increased from 5.2 to an average value of 10.9 (max. 12 points). Patients returned back to work after 3.2 weeks. In conclusion, the arthroscopic release in patients with radial epicondylitis is a reproducible method with a marked postoperative increase in function within a short rehabilitation period.     

Indikation, OP-Technik und Ergebnisse des endoskopischen Releases der Plantarfaszie (ERPF)

Zusammenfassung Fragestellung Ziel der vorliegenden Untersuchung ist es, die Indikation, OP-Technik sowie die Ergebnisse des endoskopischen Releases der Plantarfaszie darzustellen. Material und Methode An 5 nicht fixierten Präparaten wurde eine biportale Technik zum endoskopischen Release der Plantarfaszie erprobt. Ziel war es hierbei zum einen, die Relation zwischen Plantarfaszie und plantarem Fersensporn zu evaluieren; zum anderen wurde eine Technik erprobt, bei welcher nur 50–70% der medialen Plantarfaszie vom Kalkaneus abgelöst wurde.Über einen Zeitraum von 5 Jahren wurde diese Technik bei 10 männlichen und 7 weiblichen Patienten mit dem klinischen Bild einer Plantarfasziitis durchgeführt. Das mittlere Alter der Patienten betrug 35 Jahre (24–56 Jahre). Alle Patienten durchliefen zunächst konservative Therapieversuche von zumindest 6 Monaten. Ergebnisse Bei den ersten 5 Patienten wurde der Eingriff unter Bildwandlerkontrolle durchgeführt; bei den weiteren Patienten erfolgte die Resektion ohne intraoperative BV-Kontrolle. Bei allen Patienten konnte der Eingriff wie geplant durchgeführt werden. Die endoskopischen Portale heilten ohne Probleme. Die OP-Zeit ist im Rahmen der Lernkurve mit Zeiten zwischen 21 und 74 Minuten (MW: 41 Minuten) noch länger als in der offenen Technik. Der Nachuntersuchungszeitraum betrug zwischen 4 und 48 Monate (MW: 18,5 Monate). Bei 13 der 17 Patienten kam es zu einer klinischen Verbesserung und sie würden den Eingriff erneut durchführen lassen. 7 Patienten zeigten ein gutes und 6 ein sehr gutes Ergebnis im Ogilvie-Harris-Score. Bei 2 Patienten war das initiale Ergebnis nicht zufriedenstellend. Die Ursache hier lag in einer ossären Übermüdungsreaktion des Kalkaneus. Diese Komplikation wurde durch Entlastung über 6 Wochen symptomastisch behandelt. Bei zwei weiteren Patienten stellten sich sekundäre Überlastungen am lateralen Fußrand ein. Im Rahmen der frühen Rehabilitationsphase war es wichtig, trotz des minimalinvasiven Vorgehens, eine vorsichtige Belastungssteigerung durchzuführen. Schlussfolgerung Die Technik des endoskopischen Releases der Plantarfaszie (ERPF) ist standardisiert und reproduzierbar durchführbar. Sie führt zu guten mittelfristigen Ergebnissen. Ein Stabilitätsverlust der plantaren Verspannung sollte jedoch unbedingt vermieden werden.     

19. Klinisches Krebsregister eine ärztliche Leitstelle

Zusammenfassung Krebsbekämpfung ist eine Funktionskette der unterschiedlichen Fachdisziplinen, zu ihrer Koordination wird eine ärztliche Leitstelle - das klinische Krebsregister - benötigt. Mit Hilfe dieses klinischen Krebsregisters wird die Nachsorge garantiert, es werden alle prognoserelevanten Faktoren im Schicksalsablauf der Krebspatienten - das Pathogram - dokumentiert. Hierzu wurde eine patientenbezogene erweiterte Krebsbasisdokumentation der Chirurgie entwickelt.     

Digital planimetry for exact assessment of peri-articular ossification

PROBLEM: Currently, non-steroidal anti-inflammatory drugs (NSAID) and radiation have become established as methods of choice in the prevention of ectopic ossifications after total hip replacement. The most effective doses is still not known exact for both. Conventional classification systems only permit a rough distinction of ossifications, so they cannot be used for an exact quantitative measuring. Further, only a limited number of categories can be distinguished. We wanted to find out whether a quantitative measurement of ossifications can be realized, and if small differences in prophylactic effect can be detected in this way. METHOD: By computerized digitized planimetry, we measured ossifications of patients after total hip replacement on plain X-rays of the pelvis. We followed 57 patients for up to 2 years after operation. After marking the ossifications they were measured by drawing the outline with a magnifying glass-mouse. We checked all aspects of precision and reproducibility of the measurements and the comparability with an established classification method (Brooker). RESULTS: The digitized planimetry could be performed on all patients X-rays. It gave a much more differentiated picture compared to the method of Brooker. The method is simple and reproducible, but time consuming. CONCLUSIONS: Digitized planimetry allows a very exact measurement of ectopic bone formation. Compared to conventional classification systems, it differentiates more subtly. In limited, well controlled studies slight differences of prophylactic methods on ossifications can be evaluated. New developments in X-ray technology will make the handling of this method even easier.     

Cytochrome P450-generated metabolites derived from ω-3 fatty acids attenuate neovascularization

Ocular neovascularization, including age-related macular degeneration (AMD), is a primary cause of blindness in individuals of industrialized countries. With a projected increase in the prevalence of these blinding neovascular diseases, there is an urgent need for new pharmacological interventions for their treatment or prevention. Increasing evidence has implicated eicosanoid-like metabolites of long-chain polyunsaturated fatty acids (LCPUFAs) in the regulation of neovascular disease. In particular, metabolites generated by the cytochrome P450 (CYP)–epoxygenase pathway have been shown to be potent modulators of angiogenesis, making this pathway a reasonable previously unidentified target for intervention in neovascular ocular disease. Here we show that dietary supplementation with ω-3 LCPUFAs promotes regression of choroidal neovessels in a well-characterized mouse model of neovascular AMD. Leukocyte recruitment and adhesion molecule expression in choroidal neovascular lesions were down-regulated in mice fed ω-3 LCPUFAs. The serum of these mice showed increased levels of anti-inflammatory eicosanoids derived from eicosapentaenoic acid and docosahexaenoic acid. 17,18-epoxyeicosatetraenoic acid and 19,20-epoxydocosapentaenoic acid, the major CYP-generated metabolites of these primary ω-3 LCPUFAs, were identified as key lipid mediators of disease resolution. We conclude that CYP-derived bioactive lipid metabolites from ω-3 LCPUFAs are potent inhibitors of intraocular neovascular disease and show promising therapeutic potential for resolution of neovascular AMD.Angiogenesis plays a central role in many diseases, including age-related macular degeneration (AMD), a leading cause of blindness. Advanced AMD exists in two forms, “atrophic” and “neovascular,” which are defined by the absence or presence of choroidal neovascularization (CNV), respectively (1). Neovascular AMD is characterized by the formation of abnormal blood vessels that grow from the choroidal vasculature, through breaks in Bruch’s membrane, toward the outer retina (1). These vessels generally are immature in nature and leak fluid below or within the retina (2). Although growth factors are thought to play an important role in the late stage of neovascular AMD progression, they likely do not contribute to the underlying cause of the disease. The current standard of care for individuals with neovascular AMD is based on the targeting of VEGF, which promotes both angiogenesis and vascular permeability (3). However, although VEGF-targeted therapy attenuates angiogenesis and vascular permeability, it does not lead to complete vascular regression or disease resolution (3).The ω-3 and ω-6 long-chain polyunsaturated fatty acids (LCPUFAs) are two classes of dietary lipids that are essential fatty acids and have opposing physiological effects. The ω-6 LCPUFA, arachidonic acid (AA), and its cytochrome P450 (CYP)-generated metabolites (epoxyeicosatrienoic acids, EETs) recently have attracted much attention as a result of increasing evidence that they play a role in cancer as well as in cardiovascular disease (4–9). EETs are part of the VEGF-activated signaling cascade leading to angiogenesis (10) and promote tumor growth and metastasis (11). The major dietary ω-3 LCPUFAs are docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), which are highly enriched in the central nervous system including the retina (12). The ω-3 LCPUFAs have antithrombotic, antiangiogenic, and anti-inflammatory properties, and they compete with ω-6 LCPUFAs as substrates for synthesis of downstream metabolites by CYP enzymes, cyclooxygenases (COX), and lipoxygenases (LOX) (6, 13–15). Moreover, dietary enrichment with ω-3 LCPUFAs has been shown to protect against pathological angiogenesis-associated cancer and retinopathy (2, 16–19). Of the three main pathways (COX, LOX, and CYP) involved in eicosanoid biosynthesis, the lipid mediators derived from the CYP branch are the most susceptible to changes in dietary fatty acid composition (20–23). The ω-3 double bond that distinguishes DHA and EPA from their ω-6 counterparts provides a preferred epoxidation site for specific CYP family members (20, 22). In fact, most CYP isoforms can metabolize EPA and DHA with significantly higher catalytic efficiency than AA, making them uniquely susceptible to variations in the availability of these lipids (19–22). CYP epoxygenases target the ω-3 double bond, resulting in an accumulation of 17,18-epoxyeicosatetraenoic acid (17,18-EEQ) derived from EPA and 19,20-epoxydocosapentaenoic acid (19,20-EDP) from DHA (20, 22). Very recently, it was recognized that19,20-EDP inhibits angiogenesis, tumor growth, and metastasis (24). Thus, it appears that the CYP–epoxygenase pathway has the capacity to produce proangiogenic metabolites from ω-6 LCPUFAs (10, 11) and antiangiogenic metabolites from ω-3 LCPUFAs (24). This unique feature of the CYP enzymes may provide a previously unidentified mechanistic link between the ω-6/ω-3 ratio of dietary LCPUFAs and pathological angiogenesis; however, their roles in ocular angiogenesis have been largely unexplored to date.We now show that dietary enrichment with ω-3 LCPUFAs suppresses CNV, vascular leakage, and immune cell recruitment to the lesion site in a mouse model of laser-induced CNV. We characterized the CYP-dependent pathway by which dietary ω-3 LCPUFAs promote resolution of choroidal neovessels in this model and identified CYP-generated metabolites 17,18-EEQ and 19,20-EDP as mediators of disease resolution. Furthermore, we show that expression of adhesion molecules at the CNV site was down-regulated in association with inhibition of leukocyte recruitment in mice receiving ω-3 LCPUFAs.     

Oxygen consumption through metabolism and photodynamic reactions in cells cultured on microbeads

Oxygen consumption by cultured cells, through metabolism and photosensitization reactions, has been calculated theoretically. From this result, we have derived the partial oxygen pressure PO2 in the perfusion medium flowing across sensitized cultured cells during photodynamic experiments. The PO2 variations in the perfusate during light irradiation are related to the rate of oxygen consumption through photoreactions, and to the number of cells killed per mole of oxygen consumed through metabolic processes. After irradiation, the reduced metabolic oxygen consumption yields information on the cell death rate, and on the photodynamic cell killing efficiency. The aim of this paper is to present an experimental set-up and the corresponding theoretical model that allows us to control the photodynamic efficiency for a given cell-sensitizer pair, under well defined and controlled conditions of irradiation and oxygen supply. To demonstrate the usefulness of the methodology described, CHO cells cultured on microbeads were sensitized with pheophorbide a and irradiated with different light fluence rates. The results obtained, i.e. oxygen consumption of about 0.1 microM s(-1) m(-3) under a light fluence rate of 1 W m(-2), 10(5) cells killed per mole of oxygen consumed and a decay rate of about 1 h(-1) of living cells after irradiation, are in good agreement with the theoretical predictions and with previously published data.     

Correlation of chromosomal aberrations and sister chromatid exchanges in individual CHO cells pre-labelled with BrdU and treated with DNaseI or X-rays

PURPOSE: To analyse the correlation between chromosomal aberrations and sister-chromatid exchanges (SCE) in cells treated in G1 phase with X-rays or DNaseI. MATERIALS AND METHODS: Chinese hamster ovary (CHO) cells were labelled with 5'-bromodeoxyuridine (BrdU) for one round of replication and irradiated in G1 phase with 1.2, 2.4, 3.6 and 4.8 Gy X-rays or treated by electroporation with 1000, 2000, 3000 and 4000 units DNaseI per 800 microl electroporation buffer. Using a computer-aided metaphase relocation system first post-treatment mitoses were analysed for SCE and chromosomal aberrations allowing a precise investigation of correlation between both phenomena. RESULTS: A better correlation between aberrations and SCE was observed for DNaseI than for X-rays. X-rays induced more SCE than expected on the basis of aberrations, whereas the frequencies of SCE induced by DNaseI can mainly be accounted for by chromosomal aberrations. DISCUSSION: The results obtained with X-rays support an earlier observation that radiation induces both "true" SCE that are not related to chromosomal aberrations and result from radiation damage to BrdU, and "false" SCE that result from exchange-type aberrations. The high frequency of aberrations observed in cells treated with DNaseI and the good correlation between aberrations and SCE suggests that the endonuclease induces mainly "false" SCE.     

Inducible NOS inhibition, eicosapentaenoic acid supplementation, and angiotensin II-induced renal damage

BACKGROUND: Cytochrome P450(CYP)-dependent hydroxylation and epoxygenation metabolites of arachidonic acid (AA) influence renal vascular tone, salt excretion, and inflammation. Transgenic rats over expressing both human renin and angiotensinogen genes (dTGR) feature angiotensin II (Ang II)-induced organ damage, increased expression of inducible nitric oxide synthase (iNOS), decreased AA hydroxylation, and epoxygenation. As nitric oxide production via iNOS can inhibit CYP AA metabolism, we tested the hypothesis that by blocking iNOS or by supplementing eicosapentanoic acid (EPA), which can serve as an alternative CYP substrate, Ang II-induced vasculopathy could be ameliorated. METHODS: We treated dTGR with the iNOS inhibitor L-N(6)-(1-iminoethyl) lysine (L-NIL), EPA, and the combination of both treatments from week 4 to 7. RESULTS: Immunohistochemistry showed that L-NIL and EPA reduced glomerular iNOS toward control levels. L-NIL-treated dTGR showed cardiac hypertrophy and albuminuria similar to untreated dTGR. EPA and the combination of EPA + L-NIL, ameliorated organ damage without lowering blood pressure. EPA and EPA + L-NIL reduced cardiac hypertrophy, albuminuria, renal fibronectin expression, and infiltration of monocytes/macrophages, compared to L-NIL and untreated dTGR. Reactive oxygen species were detected in glomeruli of untreated and L-NIL-treated dTGR, but was reduced in the EPA groups. EPA treatment reduced activator protein-1 (AP-1) activation and partially inhibited nuclear factor-kappaB (NF-kappaB) activity in kidneys of dTGR. CONCLUSION: These results demonstrate that iNOS inhibition does not protect against Ang II-induced end-organ damage, while EPA treatment does. Our electromobility shift assay experiments revealed that EPA protection may involve inhibition of AP-1- and NF-kappaB-dependent pathways.