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Adrenal metastasis of renal cell carcinoma usually is an autopsy finding and seldom a clinical diagnosis. The incidence of ipsilateral suprarenal gland involvement also can be identified by histological examination of the organ with radical nephrectomy. The necessity of adrenalectomy performed in combination with nephrectomy is discussed. After a retrospective examination of our patients we discovered 8 adrenal metastases among 138 radical nephrectomies. Five patients who also had metastases in the lymph nodes (stages pN1 to pN2) died after an average of 26.4 months. Three patients without lymph node involvement are free of tumor. In these cases routine adrenalectomy must be regarded as a possible curative treatment.

BACKGROUND A “reawakening” of ontogenetic processes in the development of BPH is still in debate. Therefore, morphological analogies of fetal prostate stroma and nodular stromal proliferates in BPH were investigated. METHODS Fetal prostates (n = 30; weeks 12–40 of gestation) and stromal nodules of benign prostatic hyperplasia (n = 375 from autopsies, n = 100 from biopsies) were investigated by histo‐ and immunohistochemistry with special regard to cytoskeletal (alpha‐actin, desmin, myosin, and vimentin), neuronal (S‐100 protein), neuroendocrine (neuron‐specific enolase), leukocytic (CD3, CD20, and CD68) and vascular (CD34, BMA‐120, and factor VIII) antigens. RESULTS The developing fetal prostate stroma consists of immature mesenchymal cells up to week 17 of gestation, followed by fibroblastic and fibromuscular stromal cells up to week 25 of gestation and predominantly smooth‐muscular cells until the end of gestation. Stromal nodules occur as immature mesenchymal, fibroblastic, fibromuscular, and smooth‐muscular, suggestive of a maturational process. The fetal prostate stroma and the stromal nodules present, with an increasing degree of maturation, a similar vascular pattern and a similar occurrence of CD3 (T‐lymphocytes), CD20 (B‐lymphocytes), CD68 (macrophages), S‐100, and neuron‐specific enolase‐positive cells. CONCLUSIONS The data suggest that ontogenetic processes are recapitulated in the development of stromal nodules in benign prostatic hyperplasia, supporting the idea of a “reawakening” of fetal processes in BPH. Prostate 31:234–240, 1997. © 1997 Wiley‐Liss, Inc.

Background: The effects of blood flow restriction (training) may serve as a model of peripheral artery disease. In both conditions, circulating micro RNAs (miRNAs) are suggested to play a crucial role during exercise-induced arteriogenesis. We aimed to determine whether the profile of circulating miRNAs is altered after acute resistance training during blood flow restriction (BFR) as compared with unrestricted low- and high-volume training, and we hypothesized that miRNA that are relevant for arteriogenesis are affected after resistance training. Methods: Eighteen healthy volunteers (aged 25 ± 2 years) were enrolled in this three-arm, randomized-balanced crossover study. The arms were single bouts of leg flexion/extension resistance training at (1) 70% of the individual single-repetition maximum (1RM), (2) at 30% of the 1RM, and (3) at 30% of the 1RM with BFR (artificially applied by a cuff at 300 mm Hg). Before the first exercise intervention, the individual 1RM (N) and the blood flow velocity (m/s) used to validate the BFR application were determined. During each training intervention, load-associated outcomes (fatigue, heart rate, and exhaustion) were monitored. Acute effects (circulating miRNAs, lactate) were determined using pre-and post-intervention measurements. Results: All training interventions increased lactate concentration and heart rate (p < 0.001). The high-intensity intervention (HI) resulted in a higher lactate concentration than both lower-intensity training protocols with BFR (LI-BFR) and without (LI) (LI, p = 0.003; 30% LI-BFR, p = 0.008). The level of miR-143-3p was down-regulated by LI-BFR, and miR-139-5p, miR-143-3p, miR-195-5p, miR-197-3p, miR-30a-5p, and miR-10b-5p were up-regulated after HI. The lactate concentration and miR-143-3p expression showed a significant positive linear correlation (p = 0.009, r = 0.52). A partial correlation (intervention partialized) showed a systematic impact of the type of training (LI-BFR vs. HI) on the association (r = 0.35 remaining after partialization of training type). Conclusions: The strong effects of LI-BFR and HI on lactate- and arteriogenesis-associated miRNA-143-3p in young and healthy athletes are consistent with an important role of this particular miRNA in metabolic processes during (here) artificial blood flow restriction. BFR may be able to mimic the occlusion of a larger artery which leads to increased collateral flow, and it may therefore serve as an external stimulus of arteriogenesis.

Background: The vascular effects of training under blood flow restriction (BFR) in healthy persons can serve as a model for the exercise mechanism in lower extremity arterial disease (LEAD) patients. Both mechanisms are, inter alia, characterized by lower blood flow in the lower limbs. We aimed to describe and compare the underlying mechanism of exercise-induced effects of disease- and external application-BFR methods. Methods: We completed a narrative focus review after systematic literature research. We included only studies on healthy participants or those with LEAD. Both male and female adults were considered eligible. The target intervention was exercise with a reduced blood flow due to disease or external application. Results: We identified 416 publications. After the application of inclusion and exclusion criteria, 39 manuscripts were included in the vascular adaption part. Major mechanisms involving exercise-mediated benefits in treating LEAD included: inflammatory processes suppression, proinflammatory immune cells, improvement of endothelial function, remodeling of skeletal muscle, and additional vascularization (arteriogenesis). Mechanisms resulting from external BFR application included: increased release of anabolic growth factors, stimulated muscle protein synthesis, higher concentrations of heat shock proteins and nitric oxide synthase, lower levels in myostatin, and stimulation of S6K1. Conclusions: A main difference between the two comparators is the venous blood return, which is restricted in BFR but not in LEAD. Major similarities include the overall ischemic situation, the changes in microRNA (miRNA) expression, and the increased production of NOS with their associated arteriogenesis after training with BFR.

Results of cell kinetic analyses on transurethrally obtained material from urinary bladder are compared with parallel immunohistochemical tests on carcinoembryonic antigen (CEA) and tissue polypeptide antigen (TPA), performed on the same material. Labelling index increases from 1.4% in slight to 20% in marked urothelial atypia. CEA reaction in slight atypia is slight or moderate, slight, moderate or distinct in atypia, and moderate to distinct in carcinoma in situ. TPA always shows moderate to distinct reactions. Cell kinetically, urothelial carcinomas yield similar gradations. They were positive for CEA in 70% and for TPA in 100%. In GO and GI carcinomas, negative and slightly positive reactions predominate, poorly differentiated lesions yield predominantly distinct reactions. In all grades, TPA ranges from slight to distinctly positive. As in cell kinetic analyses, there is a relationship between differentiation grade and stage for CEA expression. This does not apply for TPA. The results permit us to draw conclusions on the different biological and histogenetical behavior of urothelial carcinomas. There are undoubtedly differences in the behavior of papillary-exophytical and solid invasive carcinomas in terms of both cell kinetics and immunohistochemistry.

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