Abnormal Doppler ultrasound signals were detected in 44 of 47 patients with primary malignant tumors of the liver, kidney, adrenal gland, or pancreas (94%). Two different signal types were noted: a high-velocity signal (n = 38) with Doppler shifts exceeding 3 kHz (at an insonating frequency of 3 MHz) and a very low-impedance signal (n = 9) demonstrating little systolic-diastolic variation. In three patients, both types were present. In 19 patients, histologic (n = 12) and/or angiographic (n = 16) correlation was available. Among 13 patients with angiographic studies and signals over 3 kHz, arteriovenous shunting was demonstrated in six. The ratio of the systolic to diastolic Doppler shift is a function of vascular impedance. This systolic/diastolic index was less than 3 in eight patients with histologic correlation. All eight had prominent vascular spaces, and the flow in such thin-walled, endothelium-lined spaces would account for the low-impedance signals. Of nine patients with systolic/diastolic indexes of 3 or less and angiographic correlation, three had marked and four had moderate tumor staining.

Meiotic recombination generates crossovers between homologous chromosomes that are essential for genome haploidization. The synaptonemal complex is a ‘zipper'-like protein assembly that synapses homologue pairs together and provides the structural framework for processing recombination sites into crossovers. Humans show individual differences in the number of crossovers generated across the genome. Recently, an anonymous gene variant in C14ORF39/SIX6OS1 was identified that influences the recombination rate in humans. Here we show that C14ORF39/SIX6OS1 encodes a component of the central element of the synaptonemal complex. Yeast two-hybrid analysis reveals that SIX6OS1 interacts with the well-established protein synaptonemal complex central element 1 (SYCE1). Mice lacking SIX6OS1 are defective in chromosome synapsis at meiotic prophase I, which provokes an arrest at the pachytene-like stage and results in infertility. In accordance with its role as a modifier of the human recombination rate, SIX6OS1 is essential for the appropriate processing of intermediate recombination nodules before crossover formation.

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Diffusion in breast lesions follows a non-Gaussian distribution. MK enables differentiation and characterisation of breast lesions, providing new insights into microstructural complexity. To confirm these results, further investigation in a broader sample should be performed.

The ubiquitin proteasome system regulates meiotic recombination in yeast through its association with the synaptonemal complex, a ‘zipper’-like structure that holds homologous chromosome pairs in synapsis during meiotic prophase I. In mammals, the proteasome activator subunit PA200 targets acetylated histones for degradation during somatic DNA double strand break repair and during histone replacement during spermiogenesis. We investigated the role of the testis-specific proteasomal subunit α4s (PSMA8) during spermatogenesis, and found that PSMA8 was localized to and dependent on the central region of the synaptonemal complex. Accordingly, synapsis-deficient mice show delocalization of PSMA8. Moreover, though Psma8 -deficient mice are proficient in meiotic homologous recombination, there are alterations in the proteostasis of several key meiotic players that, in addition to the known substrate acetylated histones, have been shown by a proteomic approach to interact with PSMA8, such as SYCP3, SYCP1, CDK1 and TRIP13. These alterations lead to an accumulation of spermatocytes in metaphase I and II which either enter massively into apoptosis or give rise to a low number of aberrant round spermatids that apoptose before histone replacement takes place.