Daughter cells inherit YAP localization from mother cells in early preimplantation embryos.

The first stage of cell differentiation during mouse development is the differentiation into the trophectoderm and inner cell mass, which occurs during the 8-32-cell stages of preimplantation embryos. This differentiation is regulated by the Hippo signaling pathway. At the 32-cell stage, embryos establish a position-dependent distribution of the Hippo pathway coactivator, Yes-associated protein 1 (YAP, encoded by Yap1). The outer and inner cells showed nuclear and cytoplasmic localization of YAP, respectively. However, the process by which embryos establish position-dependent YAP localization remains elusive. Here, we established a YAP-reporter mouse line, Yap1mScarlet , and examined YAP-mScarlet protein dynamics during the 8-32-cell stages using live imaging. During mitosis, YAP-mScarlet diffused throughout the cells. YAP-mScarlet dynamics in daughter cells varied depending on the cell division patterns. YAP-mScarlet localization in daughter cells at the completion of cell division coincided with that in mother cells. Experimental manipulation of YAP-mScarlet localization in mother cells also altered its localization in daughter cells upon completion of cell division. In daughter cells, YAP-mScarlet localization gradually changed to the final pattern. In some divisions during the 8-16-cell stages, the cytoplasmic YAP-mScarlet localization preceded cell internalization. These results suggest that cell position is not a primary determinant of YAP localization and that the Hippo signaling status of the mother cell is inherited by the daughter cells, which likely contributes to the stabilization of the cell fate specification process beyond cell division.

[A case of malignant lymphoma originating from paraureteral tissue].

A 53-year-old man was admitted with epigastric discomfort. Excretory pyelography demonstrated left non visualizing kidney. Computed tomography showed the dilatation of left renal pelvis and a mass along with a left lower ureter. Retrograde pyelography showed the stenosis of left lower ureter. Urine cytologies from both voided and upper urinary tract showed class I. Ureteroscopy revealed the normal ureteral mucosa, suggesting extrinsic obstruction of the ureter. The operation was performed under the diagnosis of retropelvic tumor. The tumor could be easily resected from the left ureter. The pathological diagnosis was follicular lymphoma. There was no prolificative accumulation on Gallium scintigraphy after the operation. The tumor was considered to have originated from paraureteral tissue.

[Clinical evaluation of the effect of tamsulosin hydrochloride and cernitin pollen extract on urinary disturbance associated with benign prostatic hyperplasia in a multicentered study].

We evaluated the clinical efficacy and safety of tamsulosin hydrochloride and cernitin pollen extract in 243 patients with urinary disturbance associated with benign prostatic hyperplasia. They were assigned randomly to 3 groups, oral tamsulosin hydrochloride, cernitin pollen extract and their combination were administered for 12 weeks. The international prostate symptom score, post-voided residual urine and uroflowmetrogram were obtained before and after treatment. The international prostate symptom score improved in each group and then the maximum flow rate and average flow rate also increased significantly in the tamsulosin hydrochloride-administered groups. In conclusion, the administration of only tamsulosin hydrochloride and the combination of tamsulosin hydrochloride and cernitin pollen extract seemed more effective then the administration of only cernitin pollen extract in the treatment of urinary disturbance associated with benign prostatic hyperplasia.