Background and Purpose-Intracranial fusiform aneurysms can be divided into 2 clinically different subtypes: acute dissecting aneurysms and chronic fusiform or dolichoectatic aneurysms. Of these 2, the natural history and growth mechanism of chronic fusiform aneurysms remains unknown. Methods-A consecutive series of 16 patients with chronic fusiform aneurysms was studied retrospectively to clarify patient clinical and neuroradiological features. Aneurysm tissues were obtained from 8 cases and were examined to identify histological features that could correspond to the radiological findings. Results-Four histological features were found: (1) fragmentation of internal elastic lamina (IEL), (2) neoangiogenesis within the thickened intima, (3) intramural hemorrhage (IMH) and thrombus formation, and (4) repetitive intramural hemorrhages from the newly formed vessels within thrombus. IEL fragmentation was found in all cases, which suggests that this change may be one of the earliest processes of aneurysm formation. MRI or CT detected IMH, and marked contrast enhancement of the inside of the aneurysm wall (CEI) on MRI corresponded well with intimal thickening. Eight of 9 symptomatic cases but none of 7 asymptomatic cases presented with both radiological features. Conclusions-Data suggest that chronic fusiform aneurysms are progressive lesions that start with IEL fragmentation.Formation of IMH seems to be a critical event necessary for lesions to become symptomatic and progress, and this can be monitored on MRI. Knowledge of this possible mechanism of progression and corresponding MRI characteristics could help determine timing of surgical intervention. (Stroke. 2000;31:896-900.)

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Abstract. Despite the prognostic importance of mitotic count as one of the components of the Bloom -Richardson grade [3], several studies [2, 9, 10] have found that pathologists' agreement on the mitotic grade is fairly modest. Collecting a set of more than 4,200 candidate mitotic figures, we evaluate pathologists' agreement on individual figures, and train a computerized system for mitosis detection, comparing its performance to the classifications of three pathologists. The system's and the pathologists' classifications are based on evaluation of digital micrographs of hematoxylin and eosin stained breast tissue. On figures where the majority of pathologists agree on a classification, we compare the performance of the trained system to that of the individual pathologists. We find that the level of agreement of the pathologists ranges from slight to moderate, with strong biases, and that the system performs competitively in rating the ground truth set. This study is a step towards automatic mitosis count to accelerate a pathologist's work and improve reproducibility.

prolonged steroid therapy may play a major role in accelerating atherosclerosis, which can result in aortic aneurysmal enlargement, possibly together with primary aortic wall involvement and/or vasculitic damage in patients with SLE.

AAV ANCA-associated vasculitis ACR American College of Rheumatology ADA adalimumab ANCA anti-neutrophil cytoplasmic antibody AZA azathioprine bDMARDs biologic disease-modifying anti-rheumatic drugs c-ANCA cytoplasmic ANCA CG cryoglobulin CHCC Chapel Hill Consensus Conference Cr creatinine CT computed tomography CRP C-reactive protein CyA cyclosporine CV cryoglobulinemic vasculitis CY cyclophosphamide DMARDs disease-modifying anti-rheumatic drugs * a The aorta and its primary branches corresond to the aorta (ascending, arch, thoracic descending, abdominal descending), primary branches of the aorta (including the coronary artery), and pulmonary artery. * b Multiple lesions are defined as those that involve two or more of the above arteries or sites or two or more segments of the aorta. * c Hypertrophic lesions are detected by ultrasonography (macaroni sign of the common carotid artery), contrast-enhanced CT, contrastenhanced MRI (circumferential contrast enhancement of the arterial wall), and PET-CT (circumferential FDG uptake of the arterial wall). * d Stenotic lesions and dilated lesions are detected by chest radiography (wave-like deformation of the descending aorta), CT angiography, MR angiography, echocardiography (aortic insufficiency), and angiography. They are accompanied by dilatation of the ascending aorta and frequently also by aortic insufficiency. In the chronic stage, circumferential calcification of the arterial wall is visualized by CT, and the development of collateral circulation is detected by CT angiography and MR angiography Points of attention in imaging diagnosis: Contrast-enhanced CT is performed in the late phase of contrast enhancement. CT angiography is performed in the early phase of contrast enhancement with 3-dimensional image processing. Angiography is usually performed when other procedures such as endovascular treatment and coronary artery angiography or left ventriculography are simultaneously intended. C. Conditions to be included in the differential diagnoses of Takayasu arteritis Arteriosclerosis, congenital vascular anomaly, inflammatory abdominal aortic aneurysm, infectious aneurysm, syphilitic mesaortitis, giant cell arteritis (temporal arteritis), vascular Behçet's disease, IgG4-related diseases. Definite: At least 1 of the items in A + any of the conditions in B are observed, and conditions in C can be excluded.

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The clinical and pathological concept of thromboangiitis obliterans (TAO, Buerger's disease) is still controversial. While the clinical criteria of TAO are relatively well defined, the etiology is unknown and its diagnosis based on pathology is confusing, since there is no consensus on the precise pathological criteria for TAO. To investigate the morphological features that differentiate TAO from arteriosclerosis obliterans (ASO) or thromboembolism, and to clarify the morphological independence of TAO, we studied 94 amputated specimens of lower extremities, including 31 specimens from patients with a clinical diagnosis of TAO and 31 autopsy specimens as control cases. It was revealed that most of the classic morphological features described by Buerger and others are not helpful when considered independently in the differential diagnosis, except for intact internal elastic lamina. In addition, findings of intimal inflammation, intact media and absence of medial calcification were demonstrated to be common in both TAO and thromboembolism. Statistical analysis in the present study, the most comprehensive thus far, showed that novel findings of onion-like-shaped recanalizing vessels in the occluded arteries, adventitial fibrosis without medial fibrosis, swelling of the endothelium of the vasa vasorum and edema beneath the external elastic lamina were characteristic of TAO and would be helpful in a differential diagnosis. When a combination of these morphological features is present, diagnosis of a presumed overlap of TAO and ASO in the same site of the vessel concerned is possible. Furthermore, comparison of statistical evaluations based on morphological features performed in various diagnostic groups implies that the clinical diagnosis of TAO is currently underestimated because the results of the analysis of morphological features of specimens in which TAO was suspected or specimens selected on the basis of a broad and nonspecific definition of TAO were surprisingly similar to the results in strictly defined TAO cases. Our findings suggest that injury and regeneration of minute vessels such as recanalizing vessels and vasa vasorum play a part in the pathogenesis of TAO.

!Objective: Small cell ovarian carcinomas (SCOC) are differentiated into two types: hypercalcaemic (SCOCHT) and pulmonary (SCOCPT). Unfortunately, little is known about pulmonary-type small cell ovarian carcinoma. Study Design: We carried out a systematic analysis of all available reports in the literature on individual cases of SCOCHT and SCOCPT. Results: We found that patients with SCOCPT were significantly older than those with SCOCHT. Vimentin and chromogranin detection by immunohistochemistry allow good differentiation between the two types. Interestingly, SCOCPT but not SCOCHT was found to be associated with other benign and malignant ovarian tumours in about 44 % of cases. Although the percentage of R0/R1 resections was high (~74%), survival was poor; even in patients with disease limited to the ovaries (stage Ia and Ib) the recurrence rate was 40 %. Chemotherapy with etoposide or anthracyclines could be useful. Conclusion: Taking the limitations of our study such as its retrospective nature into account and based on the results from studies of small cell carcinomas originating from other tumour sites, we conclude that treatment of SCOCPT should be based on the therapies used to treat other small cell carcinomas. Surgery is appropriate, especially in very early stages of disease, but chemotherapy should not be omitted. Newer concepts such as treatment with somatostatin analogues could help to control symptoms and stabilise some slow-growing tumours. Zusammenfassung