RTE demonstrated all testicular tumors as lesions with increased tissue stiffness. Because of its higher specificity, RTE can provide additional information in cases with indeterminate US findings.

Aims: Female stress urinary incontinence is thought to result from impairment of the connective tissue ''ligaments'' of the urethra. Surgical repair of female incontinence mainly involves ¢xation of the urethra to the pubic bone or other surrounding structures. In the present anatomical-radiological study, the anatomy of the connective tissue structures around the female urethra was investigated to determine the anatomical structures that support the urethra and the rhabdosphincter. Materials and Methods: The topography of the anterior compartment of the female pelvis was studied in serial sections and one anatomical preparation of 30 female fetuses and of six adult females. The pelves of 29 female fetuses were processed according to plastination histology technique. The pelves of the six adult specimens were processed according to sheet plastination technique. In addition, the anatomical ¢ndings were compared with MR images of 41 adult female volunteers. Results: The ventro-lateral aspect of the urethra remains free of ¢xating ligaments throughout its pelvic course. Ventro-laterally the urethra is enclosed by the ventral parts of the levator ani, its fasciae and a ventral urethral connective tissue bridge connecting both sides. Dorsally, the urethra is intimately connected to the wall of the vagina. Conclusions: The female urethra has no direct ligamentous ¢xation to the pubic bone. Urethral continence after pregnancy and childbirth may be explained by a widening of the hiatus of the levator ani or the anterior vaginal wall, resulting in overstretching of the ventral urethral connective tissue bridge or the disruption of the ¢xation between urethra and vagina. Neurourol. Urodynam. 25: 128^134, 2006. ß 2005 Wiley-Liss, Inc.

It is well known that prostate cancer (PCa) has a higher cell density than the surrounding normal tissue. This increased cell density leads to an alteration in tissue elasticity, which can be measured and displayed by sonographic-based elastography under real-time conditions. Real-time sonoelastography (RTE) has been proven capable to visualize PCa areas as "hard" lesions and therefore can be used for PCa detection and for targeted ultrasound-guided biopsy. Further applications such as the assessment of local extent of PCa should be considered. This overview describes the capabilities, advantages, and limitations of this new ultrasound technique for PCa diagnosis.

BackgroundMale sex is related to increased COVID-19 severity and fatality although confirmed infections are similarly distributed between men and women. The aim of this retrospective analysis was to investigate the impact of sex hormones on disease progression and immune activation in men with COVID-19.Patients and MethodsWe studied for effects of sex hormones on disease severity and immune activation in 377 patients (230 men, 147 women) with PCR-confirmed SARS-CoV-2 infections hospitalized at the Innsbruck University Hospital between February and December 2020.ResultsMen had more severe COVID-19 with concomitant higher immune system activation upon hospital admission when compared to women. Men with a severe course of infection had lower serum total testosterone (tT) levels whereas luteinizing hormone (LH) and estradiol (E2) levels were within the normal range. tT deficiency was associated with elevated CRP (rs = - 0.567, p < 0.001), IL-6 levels (rs = - 0.563, p < 0.001), lower cholesterol levels (rs = 0.407, p < 0.001) and an increased morbidity and mortality. Men with tT levels < 100 ng/dL had a more than eighteen-fold higher in-hospital mortality risk (OR 18.243 [95%CI 2.301 – 144.639], p = 0.006) compared to men with tT levels > 230 ng/dL. Moreover, while morbidity and mortality showed a positive correlation with E2 levels at admission, we detected a negative correlation with the tT/E2 ratio upon hospital admission.ConclusionHospitalized men with COVID-19 present with rather low testosterone levels linked to more advanced immune activation, severe clinical manifestations translating into an increased risk for ICU admission or death. The underlying mechanisms remain elusive but may include infection driven hypogonadism as well as inflammation mediated cholesterol reduction causing gonadotropin suppression and impaired androgen formation. Finally, in elderly late onset hypogonadism might also contribute to lower testosterone levels.

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