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Giant cell arteritis is a potentially systemic disease of medium-sized and large caliber arteries, showing a preferential manifestation in the extracranial branches of the carotid artery. The diagnosis is oriented to clinical and histomorphological criteria which will be critically reviewed. Particular emphasis is placed on the differentiation from normal aging processes and from healing stages under steroid therapy. In addition, the advances in our understanding of the disease pathomechanism during the last 10 years will be briefly presented as the basis for the hitherto empiric steroid treatment.

Purpose: To assess the benefit and the effect of intraarterial lipiodol application on histological analysis of patients suspected of having HCC. To determine whether lipiodol marking leads to a better biopsy result and how lipiodol or a transarterial chemoembolization influences the histological diagnosis., Materials and Methods: Two groups of patients were examined. Group A included 14 patients highly suspected of having an HCC which had previously been unsuccessfully biopsied. A transarterial embolization with lipiodol was performed in these patients to mark intrahepatic tumors which could not otherwise be defined in unenhanced CT. A biopsy was then repeated. Group B included 22 patients undergoing therapy using transarterial chemoembolization (TACE). A biopsy was performed to support the diagnosis of a multifocal HCC before changing the therapy., Results: The transversal diameters of the biopsied tumors were similar in both groups (A: 22 mm; B: 21 mm). The length of percutaneous access was 71 mm in Group A and 88 mm in Group B. In eleven of 14 patients of Group A we confirmed the diagnosis of an HCC. Thirty-six procedures were necessary for this confirmation. In Group B we confirmed the diagnosis in 17 of 22 patients. In addition, we found typical histological modification due to hepatic cirrhosis and virus hepatitis. Lipiodol had no negative influence on the histological diagnosis., Conclusion: Applying lipiodol for marking and delineating HCC-suspicious liver tumors in cases of formerly negative histology seems to enhance the success of biopsy, confirming the diagnosis of an HCC.

The guidelines of the German Orthopaedic Societies regarding the treatment of lateral elbow epicondylitis were analysed on the ground of recently published reviews or randomised placebo-controlled trials (RCT). For the acute phase, reviews or RCTs failed to show a clinical effect beyond placebo if follow-up was extended over 6 weeks. For the chronic phase a current Cochrane review failed to identify any controlled trial regarding surgical procedures during the last decades. Without an adequate control group, it is not possible to draw any meaningful conclusions about the value of this modality of treatment. Therefore surgery is not indicated before repetitive low-energy extracorporeal shock wave therapy (ESWT) has been applied. This novel treatment, under strictly standardized conditions, showed effects beyond placebo in independent randomised placebo-controlled trials for follow-up periods of 3 and 6 months. To date there exists no evidence-based therapeutic algorithm for the treatment of acute and chronic tennis elbow. Even medium-term effects should be regarded as either a placebo effect or natural regression to the mean.

Atherogenesis is a disease of middle-sized and large caliber blood vessels that can be divided into three major phases. The initial lesions of early atherosclerosis are characterized by the adhesion and subendothelial emigration of blood-borne monocytes, which differentiate into macrophages and provide the morphological basis for the formation of foam cells and fatty streak lesions. These lesions are found in most children and teenagers in industrialized nations. The next key event in atherogenesis is the proliferation of smooth muscle cells within the intima and media, resulting in the gradual compromise of the vessel lumen. Myofibroblastic cells also contribute to lesion growth through the production of excessive amounts of extracellular matrix. Such lesions are clinically silent unless progression to the next phase continues: the lesions degenerate, forming a mostly necrotic "lipid core" consisting of extracellular lipid, cholesterol crystals, inflammatory cells and necrotic debris. A fibrous cap is formed which prevents the interaction of blood cells, particularly of platelets with the highly proaggregatory material found in the lipid core. However, continuous inflammatory activity and/or heightened mechanical stress (i.e. in hypertension) tends to weaken the fibrous caps. Eventually, plaque rupture ensues, platelets aggregate, and the lesions become clinically manifest in such dramatic events as myocardial infarction, stroke, or mesenteric ischemia. Research into lesion formation and progression is limited by the fact that lesions develop in silence over many decades and that animal models only incompletely model the situation in humans. Most currently debated concepts accept the "response to injury" hypothesis formulated by the late Russell Ross and the multifactorial nature of atherogenesis. The discussion today circles around the relative contributions of low density lipoproteins (oxidized or enzymatically modified LDL?), the immune response (adaptive or innate?), infectious agents (CMV, chlamydia pneumoniae?), and/or hereditary factors, to name only a few of the most widely debated concepts. Irrespective of the outcome of this pathomechanistic discussion, the knowledge of established risk factors (hypercholesterolemia, hypertension, diabetes, smoking, etc.) and protective interventions (lifestyle changes, physical exercise, "healthy" diets, effective dietary and pharmacological control of hyperglycemia, blood pressure or hyperlipidemia) has helped to define atherosclerosis as a "new entity" that has little to do with the archaic concept of a "degenerative" vessel disease.

Unlabelled: After angioplasty, restenosis remains the major drawback of the procedure with an incidence of between 20-40%. It is a matter of concern whether the cellular alterations start immediately after directional atherectomy (DA) and if they are dependent on the depth of the lesion., Method: Cellular alterations immediately after DA were investigated using peripheral atherectomy in normal vessels of 30 pigs (A. femoralis, A. carotis communis). DA was used to remove material. The arteries were assigned to two groups according to the depth of vessel injury. (Group 1: lesions to the intima; Group 2: lesions to the media.) 68 arteries with 41 intimal and 27 media lacerations were excised 4 to 24 hours later and processed for transmission electron microscopy, histology and immunohistochemistry., Results: Immediately after DA, thrombus formation at the site of the altered segment was found. A transient infiltration of polymorphonuclear leukocytes (PMN) occurred, especially if the media was lacerated, followed by the transformation of contractile smooth muscle cells (SMC) into the synthetic subtype. A marked myoproliferative response was found in Group 2 whereas only moderate tissue hyperplasia was seen in Group 1., Conclusion: The present data provides evidence that cellular alteration of the atherectomized vessel begins immediately after atherectomy. Subsequent to the initial temporary PMN infiltration, an activation of local SMC occurs at a very early stage. These effects and, in particular, a myoproliferative response were found lesions injured the internal elastic membrane, while only minor effects were seen when the lesion affected the intimal layer.