the surface of each section and stained with haematoxylin and eosin (H&E). Five randomly positioned areas from the tumour and normal peripheral zone (PZ) were examined by light microscopy at × 200, then digitally photographed and analysed to obtain automatic CD. ADC values were determined from the MRI data using the H&E slides as a reference. ADC and CD values were measured in both malignant lesions and the PZ, and the correlation between ADC and CD assessed. RESULTS ADC values were lower ( OBJECTIVETo assess the relationship between the apparent diffusion coefficient (ADC) on magnetic resonance imaging (MRI) and cell density (CD) obtained from radical prostatectomy (RP) specimens. PATIENTS AND METHODSIn all, 36 patients with prostate cancer were recruited; T2-weighted and diffusionweighted MRI was obtained axially using a 3.0 T scanner. Patients then proceeded to RP; the prostate was whole-mounted and sectioned axially. Slices (3 µ m) were cut from

The accumulation of beta-amyloid (Ab) plaques and neurofibrillary tangles consisting of hyperphosphorylated tau protein are pathological features of Alzheimer's disease (AD) commonly modeled in mice using known human familial mutations; however, the loss of neurons also found to occur in AD is rarely observed in such models. The mechanism of neuron degeneration remains unclear but is of great interest as it is very likely an important factor for the onset of adverse memory deficits occurring in individuals with AD. The role of Ab in the neuronal degeneration is a matter of controversial debates. In the present study we investigated the impact of extracellular plaque Ab versus intraneuronal Ab on neuronal cell death. The thalamus and the frontal cortex of the APP/ PS1KI mouse model were chosen for stereological quantification representing regions with plaques only (thalamus) or plaques as well as intraneuronal Ab (frontal cortex). A loss of neurons was found in the frontal cortex at the age of 6 months coinciding with the decrease of intraneuronal immunoreactivity, suggesting that the neurons with early intraneuronal Ab accumulation were lost. Strikingly, no neuron loss was observed in the thalamus despite the development of abundant plaque pathology with levels comparable to the frontal cortex. This study suggests that plaques have no effect on neuron death whereas accumulation of intraneuronal Ab may be an early transient pathological event leading to neuron loss in AD.

Background: Therapy with vemurafenib, an inhibitor of mutated BRAF, yields a response rate of approximately 50% in patients with metastatic melanoma harboring a BRAF V600E mutation. As an adverse effect of vemurafenib, proliferative disorders of keratinocytes, including squamous cell carcinoma, have been described. Low concentration of vemurafenib as present in the epidermis were found to activate wild-type RAF, which, in combination with a preexisting RAS mutation, can promote keratinocyte proliferation. While activating BRAF mutations occur in approximately 50% of melanomas, they are even more frequently observed in melanocytic nevi.Observation: We present the case of a patient with dynamic changes of melanocytic nevi well documented by sequential digital dermoscopy during vemurafenib therapy. A variety of dermoscopic changes were observed. First, nevi involuted, and all of these originally showed a centrally elevated papillomatous and predominant globular pattern. Second, preexisting nevi increased in size, and pigmentation that rendered them atypical. Such lesions were flat and showed a predominant reticular pattern at baseline. Third, multiple new nevi occurred. One example of each of the latter 2 categories was excised and showed wild-type BRAF. Conclusion:Our findings of changing nevi in a patient treated with vemurafenib highlight the need for sequential skin examinations, including dermoscopy.

confirmed malignant areas and the normal PZ, using whole-mounted pathology specimens as a reference to delineate regions of interest (ROI). These variables included maximum enhancement index (MaxEI), time to MaxEI at 30 s, the initial and final slopes of signal intensity change, and the area under curve. A threshold value for each DCE variable was identified, and the sensitivity and specificity were obtained. RESULTSMalignant lesions had a 56% higher MaxEI than normal PZ and took half the time to reach MaxEI ( P < 0.001). Hence, at 30 s, cancer lesions have double the mean ( SD ) EI than normal PZ, of 2.22 (1.04) vs 1.04 (0.51), respectively. Tumours showed significant washout of contrast medium, which was reflected in the final slope of the curve being negative, as opposed to positive for normal PZ. The combined data of DCE variables, using a logistic regression test, gave a mean (95% confidence interval) sensitivity and specificity of 89 (81-96)% and 90 (83-97)%, respectively. CONCLUSIONThis technique provides good discrimination of malignant lesions that might enable accurate localisation of the lesion. It is a simple, semiquantitive, noninvasive method that reflects the unusual vascular characteristics of newly formed microvessels and the changes in the interstitium that occur in prostate cancer. KEYWORDS

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The MUC1 mucin [also known as episialin, epithelial membrane antigen (EMA) or polymorphic epithelial mucin (PEM)] is a component of the mucosal glycocalyx, contributing to anti-adhesive and protective cell functions. MUC1 has been shown in a variety of epithelial cell types in the reproductive tracts of males and females, but this is the first report of its expression in human testis and non-epithelial cells of the germ cell lineage. Analysing 65 testes with normal or impaired spermatogenesis, we identified MUC1 protein in maturing germ cells by immunohistochemistry using the monoclonal antibodies HMFG1, HMFG2 and SM3 binding to different glycosylation variants. MUC1 expression was confirmed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis on tissue extracts of human testis, and RT-PCR of selected germ cells after UV laser-assisted cell picking. MUC1 glycosylation variants were selectively distributed during normal spermatogenesis. Whereas HMFG1 labelled certain groups of pachytene spermatocytes, HMFG2 labelled only spermatids. Low glycosylated forms of MUC1 mucin, recognized by SM3, were not found. In contrast to its weak expression during normal spermatogenesis, the HMFG1 glycosylation variant accumulated markedly in all spermatocytes showing abnormal or arrested maturation. These results suggest a variable glycosylation of MUC1 mucin in differentiating germ cells, which is aberrant in pathological conditions.

Mondor’s disease of the penis has been reported after genital trauma such as stretching and torsion of the veins and can cause endothelial necrosis and thrombosis. We report a 35-year-old male with thrombosis of the penile superficial dorsal vein who did not respond to topical drug therapy. Surgical management, e.g. superficial vein resection, is the most effective therapy in refractory cases for relieving pain, diminishing skin induration and producing esthetically pleasing results.

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