Approximately 20 pelvic lymph nodes may serve as a guideline for a sufficient standard pelvic lymph node dissection. Lymphadenopathy in prostate cancer patients is not always a result of metastases but, rather, hyperplastic or regressive alterations. A preferential distribution of lymph node metastases along the left iliac vessels regardless of the primary tumor site in the prostate warrants further investigation.

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Objective To evaluate the extent of vascularization by assessing vascular surface density in renal cell carcinomas (RCCs) of different nuclear grades, and in normal renal cortex and medulla. Materials and methods Specimens of 79 RCCs of different nuclear grades (16 of G1, 42 of G2 and 21 of G3) were immunostained with the lectin Ulex europaeus agglutinin‐I (UEA I). The vascular surface density of tumour tissue was assessed stereologically using a test grid at ×400 magnification and compared to the values obtained in normal renal tissue. Results G3 tumours had a lower vascular surface density than had G1 and G2 RCCs and normal renal tissue of the cortex and medulla (P<0.001, respectively). G1 tumours had a significantly higher vessel density than had normal medullary parenchyma and G2 carcinomas (P<0.001). Vessel density was not significantly different among G1 tumours and cortical parenchyma in controls and among normal medullary tissue and G2 tumours. Statistical analysis showed that the vascular surface density was independent of tumour stage and size and the age and sex of the patients. Conclusion The degree of vascularization in RCCs decreased with their grade of differentiation, suggesting that the extent of neovascularization in tumour tissue reflects the relationship between tumour cell proliferation and vascular growth. The values of vascular surface density in normal renal tissue of the cortex and medulla partially overlapped with those obtained in tumour tissue.

For differentiation of melanoma in situ (MIS) from melanocytic hyperplasia (MH) in sun-damaged skin, several criteria have been proposed. To assess sensitivity and specificity of those criteria, we examined the epidermis adjacent to 50 consecutive basal cell carcinomas and 50 MISs in skin with significant solar elastosis. The most valuable criteria for the diagnosis of MIS, as opposed to MH, were presence of nests of melanocytes, irregular distribution of melanocytes, descent of melanocytes far down adnexal epithelial structures, irregular distribution of pigment, presence of melanocytes above the junction, a high number of melanocytes, pleomorphism of melanocytes, and atypical nuclei of melanocytes. Other criteria, e.g., collapse of cytoplasm around nuclei of melanocytes; flattening of rete ridges; differences in the area, shape, and contour of nuclei of melanocytes as assessed by nuclear morphometry; and presence of melanocytes stained by HMB-45 and Ki-67/MIB-1 monoclonal antibodies, were found to be of low or no value for differential diagnosis.

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Q Qu ua an nt ti it ta at ti iv ve e a an na al ly ys si is s o of f p pa ar re en nc ch hy ym ma al l a an nd d v va as sc cu ul la ar r a al lt te er ra at ti io on ns s i in n N NO O 2 2 --i in nd du uc ce ed d l lu un ng g i in nj ju ur ry y i in n r ra at ts s ABSTRACT: Nitrogen dioxide (NO 2 ), the oxidation product of nitric oxide (NO), is a reactive free radical forming gas, the inhalation of which has been reported to induce severe damage to distal airways. In order to quantify dose and time course of parenchymal and vascular damage, rats were exposed to 5, 10 and 20 ppm NO 2 for 3 and 25 days, followed by quantitative histology and morphometry of the lung.Histological investigations of the short-term exposed animals showed structural alterations extending from slight interstitial oedema after exposure to 5 ppm, to epithelial necrosis and interstitial inflammatory infiltration after exposure to 10 ppm, and an additional intra-alveolar oedema after 20 ppm. The pulmonary arteries disclosed no qualitative changes, such as muscularization of intra-acinar vessels. Long-term exposure to 10 ppm and 20 ppm NO 2 resulted in emphysema and slight centrilobular interstitial fibrosis. Morphometric analysis revealed the alveolar surface density to be significantly diminished after short-term exposure to 20 ppm NO 2 and long-term exposure to 10 and 20 ppm NO 2 . The medial thickness of pulmonary arteries was significantly increased after short-and long-term exposure to 20 ppm NO 2 and long-term exposure to 10 ppm NO 2 . In the 5 ppm short-and long-term exposure groups the pulmonary arterial medial thickness was significantly decreased compared to controls. Correlation analysis revealed a negative correlation between average medial thickness and alveolar surface density (coefficient of correlation: -0.56).We conclude that the extent of NO 2 -induced pulmonary parenchymal and vascular alterations are closely related and concentration-and time-dependent.

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