Background : We determined if the α1-adrenergic receptor (AR) antagonist naftopidil, the phosphodiesterase 5 (PDE5) inhibitor tadalafil, or the combination inhibited cold stress-induced detrusor overactivity in bladder outlet obstructed rats. We also investigated the role of resiniferatoxin (RTX)-sensitive nerves in detrusor overactivity.
Methods : The urethras of 10-week-old female Sprague-Dawley rats were loosely ligated to create a partial bladder outlet obstruction. After 4 weeks, at room temperature (RT, 27℃), the rats were randomly assigned to receive an intraperitoneal infusion of vehicle control (n＝11), 0.15mg/kg-body weight naftopidil (n＝7), 0.5mg/kg-body weight tadalafil (n＝7), or the combination of naftopidil and tadalafil (n＝11). The treated rats were then exposed to low temperature (LT, 4℃) for cystometry. Other rats were subcutaneously injected with 0.3mg/kg RTX (n＝8), and then two days later underwent cystometric investigations. The number of calcitonin generelated peptide (CGRP)-positive neurons was examined by immunohistochemistry.
Results : After transfer from RT to LT, the vehicle-, naftopidil-, and tadalafil-treated rats had decreased voiding intervals and bladder capacity. These decreases were inhibited by the combined naftopidil-tadalafil treated rats. RTX caused similar cystometric decreases as the combination-treated rats. The number of the CGRP-positive afferent nerves in the RTX-treated rats was significantly reduced.
Conclusion : The combination of an α1-AR antagonist and a PDE5 inhibitor mitigated the cold stress-induced detrusor overactivity in bladder outlet obstructed rats. RTX treatment also inhibited the cold stress responses while reducing the presence of CGRP in afferent nerves. α1-AR antagonists and PDE5 inhibitors could act efficiently, and may affect RTX-sensitive nerves, to reduce cold stress-induced detrusor overactivity.

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Lysophosphatidylethanolamines (LPEs) are hydrolysis metabolites of polyunsaturated fatty acids and alkenyl group-rich phosphatidylethanolamine (PE). It was reported that LPE functions as a lipid mediator in vivo and it is involved in an inflammatory process of chronic autoimmune disease. LPE is present in not only cells but also serum, but the pathophysiological role and metabolic details of serum LPE are not known. In this study, characterization of the serum LPE species in autoimmune pancreatitis (AIP) was performed by mass spectrometry. Serum samples from patients with AIP (n＝7) and healthy subjects (n＝9) were examined for fatty acid compositions using gas chromatography mass spectrometry. LPE species were analyzed using matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Blood lipid tests, cholesterol and triglyceride were almost in the criteria range in patients with AIP. Serum arachidonic acid (C20 : 4) levels were higher in patients with AIP than in healthy subjects, but eicosapentaenoic acid (C20 : 5) and docosahexaenoic acid (C22 : 6) concentrations were not significantly different. In patients with AIP, serum total LPE levels were lower than those in healthy subjects, and LPE 20 : 4 levels were positively correlated with LPE 20 : 5 and LPE 22 : 6 levels. LPE p16 : 0 (plasmalogen-type) level was negatively correlated with LPE 20 : 4, LPE 20 : 5 and LPE 22 : 6 levels. This study showed that though serum lipids and the fatty acid compositions of patients with AIP resembled healthy subjects, serum LPE level of patients were significantly low and some serum LPE species fluctuated in a correlated way.

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The concept of physiological pituitary gland hypertrophy is well recognized in settings of increased physiological needs, such as pregnancy and puberty. However, it is very uncommon for it to transform into a neoplastic pituitary lesion in the form of a functioning or non-functioning pituitary adenoma. In this case report, we present a 24-year-old woman with an initial diagnosis in adolescence of physiological pituitary hypertrophy following neuroradiological evaluation of her persistent headache, who developed a neoplastic symptomatic prolactinoma 9 years later. She underwent endoscopic endonasal tumor excision, which was uneventful with no intraoperative complications. The present case study revealed the possibility that adolescent physiological pituitary gland hypertrophy can develop into prolactinoma. Hence, patients with symptomatic physiological pituitary gland enlargement should have long-term follow-up using clinical, laboratory, and neuroradiology evaluations.

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We report a case of right adrenal cortical carcinoma with tumor thrombus in the inferior vena cava (IVC), which was safely resected.
A 50-year-old woman was referred to our hospital for investigation of a right adrenal tumor, 13cm in diameter, with extension to the IVC. Preparing an artificial heart-lung machine, radical surgery, including resection of the tumor, part of the right liver lobe, and tumor thrombus in the IVC was performed. Surgery was safely performed without the aid of cardiopulmonary bypass. This was because we used intraoperative transesophageal echocardiographic evaluation, which was able to confirm whether tumor invasion extended into the right atrium, and to detect the resection range of the IVC. Surgical resection was completed as usual without complications ; the postoperative course was uneventful and the patient was discharged on postoperative day 16 with asymptomatic pulmonary thromboembolism. The patient was treated with mitotane (o,p'-DDD), which resulted in necrosis of the adrenocortical tumor. The patient was alive 9 months after surgery.

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