The distribution of the reaction product of a staining method for adenosine triphosphatase (ATPase) in rat small intestine, kidney, and liver was studied with electron microscopy. Several procedures were tried but the best results were obtained from tissue that had been quenched in liquid nitrogen, sectioned at 25 µ in a cryostat, fixed for 30 to 90 minutes at 4°C in formalin-sucrose buffered to pH 7.2, incubated with substrate, and then osmicated and prepared for electron microscopy in the usual way. This procedure enabled the localization of mitochondrial ATPase to be studied. In tissue fixed in small blocks in osmium tetroxide for 3 minutes prior to incubation with substrate, good preservation was noted, and the reaction product for ATPase was localized on the cell membrane and nuclei. The reaction product was present in abundant amount in the nuclei, and particularly within nucleoli, of all tissues studied. Because the histochemical localization of nuclear enzymes poses numerous interpretative problems at the present time, the significance of this nuclear localization is uncertain. Cell (plasma) membranes were the site of localization, especially at areas where it has been proposed that active transport mechanisms may occur, namely, on the microvilli of intestinal epithelium, endothelial lining of capillaries, glomerular epithelial cell membranes, basal infoldings of the cell membrane of renal tubules, on the microvilli of bile canaliculi, and on the microvilli of proximal convoluted tubular epithelial cells. ATPase localization on the cristae mitochondriales was also demonstrated.

The isolated frog lens epithelium can be maintained intact in both appearance and electrical properties for more than 24 hours. The mean resting membrane potential was -80 mV and the cells were depolarized by both high potassium and low calcium Ringer's solution in a manner very similar to that of the whole lens. The epithelial cells were found to be well coupled using both electrical and dye-injection techniques. Electrical coupling was measured using separate current-injection and voltage-measuring electrodes and the relationship between the induced voltage and distance from the current-passing electrode could be well fitted by a Bessel Function solution to the cable equation. The values obtained from the fit for the membrane and internal resistances were 1.95 omega m2 and 25 omega m, respectively. Exposure to octanol (500 microM) or low external Ca2+ (less than 1 microM) failed to disrupt significantly the intercellular flow of current. There was evidence to suggest that raised intracellular calcium does, however, uncouple the cells. Dye coupling was investigated by microinjecting Lucifer Yellow CH into single epithelial cells. Diffusion into surrounding cells was rapid and, in control medium, occurred in a radially symmetrical manner. In contrast to the electrical coupling data, dye transfer appeared to be blocked by exposure to 500 microM octanol and was severely restricted on perfusing with low external calcium. Differences between the electrical and dye-coupling experiments indicate either that there are two types of junction within the cell and only the larger type, permeable to Lucifer Yellow, is capable of being uncoupled or that there is only one large type of junction which can be partially closed by uncoupling agents.

SUMMARYThe efflux of 36C1-from perifused rat lenses consisted of two components: a fast (extracellular) component and a slow (cellular) component. The 36CI-efflux rate constant of the cellular component was 5-7 x 10-3 min-'. The 36Cl-efflux was sensitive to changes in lens potential induced by treatment with high-K+ solutions. The decrease in the 36Cl-efflux rate constant caused by high-K+ solutions was consistent with the Goldman model, indicating that, under normal conditions, the majority of the 36C1-efflux is by diffusion. The 36iCl-efflux rate constant corresponds to a Cl-permeability of 1-3 x 10-8 m s-'. The Cl-channel inhibitor anthracene-9-carboxylate (A-9-C), however, caused a relatively small reduction in the efflux rate constant. The anion-exchange inhibitor 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonate (SITS) has little effect on the 36C1-efflux under control conditions. Intracellular acidification, induced by pre-treatment with NH4+, leads to a rapid stimulation of 38C1-efflux. This increased 36Cl-efflux is blocked by SITS. Thus, it appears that at low intracellular pH (pHi), a normally quiescent, SITS-sensitive, anion-exchange mechanism is activated. The possible role of this exchange mechanism in regulating pH, is discussed.

Introduction Multi‐parametric magnetic resonance imaging of the prostate is crucial in detecting prostate cancer (CaP) and staging local disease. The Prostate Imaging Reporting and Data System (PIRADS) scoring system is used to assess and classify lesions and enables communication between clinicians and radiologists. This study aimed to assess the accuracy of PIRADSv2 in detecting CaP using histopathology specimens within our local service. Methods This retrospective study included 192 patients between September 2016 and May 2019. All had mpMRI prostate examinations prior to biopsy or prostatectomy. Lesions on MRI were assigned a PIRADS score and comparison made with histopathology results. Gleason score ≥7 was considered as clinically significant prostate cancer (csCaP). We calculated accuracy, sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) for detecting all CaP and csCaP. Results In the PIRADS 3 group, 32% were Gleason 6 and 32% were Gleason 7 lesions. In the PIRADS 4 group, 37% were Gleason 6 and 41% were Gleason ≥7. For PIRADS 5 lesions, 32% were Gleason 6 and 68% were Gleason ≥7. For all CaP, sensitivity was 84.7%, specificity 54.6%, PPV 82.3% and NPV 58.8%. For csCaP Gleason ≥7, PIRADS cut‐off ≥3 had sensitivity, specificity, PPV and NPV of 95.7%, 39.3%, 47.5% and 94.1%, respectively, and cut‐off ≥4 had sensitivity, specificity, PPV and NPV of 84.3%, 53.3%, 50.9% and 85.5%. Conclusions This study confirms PIRADS has high accuracy, sensitivity and NPV for detecting all CaP and csCaP. A high NPV may obviate need for biopsy in low‐risk patients.

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