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ApoE-KO mice are characterized by endothelial dysfunction and increased vasoconstrictor response. Previously, we have shown that chronic Ang-(1-7) treatment ameliorates endothelial dysfunction in apoE-KO. However, the impact of Ang-(1-7) on vasoconstrictor response to AngII is unknown. To examine the role of Ang-(1-7) in vascular resistance in atherosclerosis, apoE-KO and wild type (WT) mice fed on western diet were treated via osmotic minipumps either with Ang-(1-7) (82μg/kg/hr) or saline for 6 weeks. Vascular resistance was tested in isolated perfused kidneys. AngII induced renal pressor response was significantly increased in apoE-KO compared to WT mice. Remarkably, chronic Ang-(1-7) treatment attenuated AngII induced pressor response in apoE-KO mice. Accordingly, in apoE-KO, phospho-MLC20, a marker of enhanced contractility was increased in preglomerular vessels compared to WT and reduced after Ang-(1-7) treatment. To examine the underlying cause, we measured reactive oxygen species (ROS) production and changes in NADP(H) expression levels. In apoE-KO mice, p47phox was increased (1.5-fold; P<0.05) compared to WT and reduced after chronic Ang-(1-7) treatment. Concordantly, urinary isoprostane-8 excretion and H2O2 generation were significantly decreased in Ang-(1-7) treated apoE-KO mice. ROS is known to activate the MAPK p38. Moreover, p38 has shown to modulate pressor response. To test the role of p38 in our model, we measured p38 activity and renal pressor response to AngII in the presence of SB203580, a specific p38 inhibitor. Thus, in preglomerular vessels of apoE-KO, the phospho-p38 / p38 ratio was increased compared to WT. Chronic Ang-(1-7) treatment restored this ratio almost to WT levels (2.8±0.5 vs. 1.0±0.1 vs. 1.3±0.2 P<0.05). Administration of SB203580 (5μmol/L) reduced renal pressor response to AngII in apoE-KO but not in Ang-(1-7) treated mice. Hence, chronic inhibition of p38 with BIRB796 (30mg/kg) attenuated the increased pressor response to AngII in apoE-KO mice. In summary, p38 plays a crucial role in regulating renal vascular resistance in apoE-KO mice. Moreover, Ang-(1-7) attenuates pressor response to AngII by reducing p38 activity. Thus, this study revealed a new pathway how Ang-(1-7) modulates vascular function. [ABSTRACT FROM AUTHOR]

Transverse testicular ectopia is a condition in which a testicle crosses the midline and descends through the contralateral inguinal canal, with both testes in the same scrotal compartment. It is reported to be present in about 2% of persons who present with non-palpable testicles. Most transverse testicular ectopia patients undergo orchiopexy in early childhood; however, in rare cases, they are diagnosed in adulthood upon detection of testicular tumors.A 40-year-old man visited our hospital complaining of right abdominal pain. His right testis was palpable in the right scrotum; however, the left scrotal compartment seemed empty and there was a painful mass on the upper part of the right scrotal compartment. Computed tomography showed that both spermatic cords traversed through the right inguinal canal, and transverse testicular ectopia was diagnosed. Ultrasonography showed absent left testicular circulation on the upper part of the right scrotum. Upon diagnosis of left testicular torsion, emergency surgery was conducted. In the right scrotum, there was a normal right testicle, and a necrotic left testicle which was twisted 180 degrees on its axis, towards the cranial side. Histopathology of the excised left testicle revealed an incidental seminoma, pT1. Tumor markers following surgery were negative, and there was no evidence of recurrence observed with two years and five months of follow-up.Non-palpable testicular torsion may also be a transverse testicular ectopia. Therefore, it is necessary to consider malignant tumors based on the patient's age.

A 54-year-old woman was admitted to our hospital complaining of gross hematuria and difficulty urinating. Cystoscopy revealed a tumor 4 cm in size with calcification on top of the bladder. After diagnosis of urachal carcinoma by transurethral resection of the bladder, partial cystectomy with en bloc resection of the median umbilical ligament and pelvic lymphadenectomy was performed. Pathological diagnosis confirmed urachal carcinoma, pT3b, ly1, v0, pN1, RM0. TS-1 and cisplatin chemotherapy (TS-1 at 100 mg/day on days 1-21, CDDP at 60 mg/m 2 on day 8) was administered. On day 13, the patient was admitted because of consciousness disorder (Glasgow Coma Scale E2V1M4). Hyponatremia (Na 109 mEq/l) and renal excretion of sodium were present and the patient was diagnosed with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by chemotherapy. Serum sodium level and her consciousness level gradually improved after administration of 3% saline. SIADH caused by chemotherapy containing cisplatin is a relatively rare, but potentially serious adverse effect that requires close attention.