Publications by authors named "Tsubasa Hatakeyama"

Introduction: We report a case of bladder eversion through a vesicovaginal fistula (VVF) in an elderly patient with severe pelvic organ prolapse (POP).

Case Presentation: A 90-year-old woman presented with a sensation of prolapse and urinary leakage. She was diagnosed with complete uterine prolapse and bladder mucosal ectropion through a VVF, with renal dysfunction due to bilateral hydronephrosis.

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Introduction: We present a patient with bladder pain syndrome (BPS) who underwent repeated bladder hydrodistentions.

Case Presentation: A female patient visited our department because of refractory bladder pain. She was diagnosed with BPS; she had only mucosal bleeding after distention.

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Introduction: We investigated the subsequent trends in age and antithrombotic therapy in patients who underwent transurethral resection of bladder tumor (TURBT) and examined the rate of perioperative complications.

Methods: Medical records of patients who underwent TURBT were retrospectively analyzed. We arbitrarily divided the observation years into three periods (I: 2007-2013, II: 2014-2018, and III: 2019-2023) to compare the trends in age and frequency of perioperative complications after TURBT between patients taking and those not taking antithrombotic drugs.

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We investigated the influence of sarcopenia on treatment outcomes in elderly patients receiving medical therapy for lower urinary tract symptoms (LUTS). We included male patients with LUTS aged ≥ 75 years who had not changed their medication for 1 year. Current conditions were estimated using IPSS, overactive bladder symptoms score (OABSS), and screening tool for sarcopenia (SARC-F).

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Objective: Detrusor underactivity (DU) is a common cause of lower urinary tract symptoms (LUTS). To date, no consensus has been reached on the urodynamic criteria for defining DU. We previously proposed the area under the curve of the Watts factor (WF-AUC) as a new parameter for diagnosing DU.

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Article Synopsis
  • A 49-year-old man diagnosed with fulminant myocarditis experienced severe heart issues and ultimately did not recover, despite advanced medical support.
  • His condition deteriorated, leading to complications like sepsis and gastrointestinal bleeding, resulting in his death 27 days later.
  • Autopsy revealed widespread myocardial calcification, with calcification affecting every heart cell in the left ventricle, linking the condition to poor outcomes.
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Introduction: We present a case of ischemic priapism caused by self intracavernous injection of tadalafil.

Case Presentation: A 77-year-old man developed priapism due to self-injection of tadalafil into the corpus cavernosum. He presented to our hospital 2 days after the development of priapism and severe penile pain.

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Lipolysis-stimulated lipoprotein receptor (LSR) is a novel molecule present at tricellular contacts which recruits tricellulin (TRIC), a molecular component of tricellular tight junctions (tTJs). LSR and TRIC are colocalized with the bicellular tight junction (bTJ) protein claudin (CLDN)-1-based tight junction strands at tricellular corners. Knockdown of LSR in normal epithelial cells affects tTJ formation and the epithelial barrier function.

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Lipolysis-stimulated lipoprotein receptor (LSR) is a unique molecule of tricellular contacts of normal and cancer cells. We investigated how the loss of LSR induced cell migration, invasion and proliferation in endometrial cancer cell line Sawano. mRNAs of amphiregulin (AREG) and TEA domain family member 1 (TEAD1) were markedly upregulated by siRNA-LSR.

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Junctional adhesion molecule-A (JAM-A), which belongs to the IgG superfamily, is a tight junction molecule associated with epithelial and endothelial barrier function. Overexpression of JAM-A is also closely associated with invasion and metastasis of cancers such as breast cancer, lung cancer and pancreatic cancer. However, little is known about the mechanism in overexpression of JAM-A in head and neck squamous cell carcinoma (HNSCC).

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Lipolysis-stimulated lipoprotein receptor (LSR) has been identified as a novel molecular constituent of tricellular contacts that have a barrier function for the cellular sheet. LSR recruits tricellulin (TRIC), which is the first molecular component of tricellular tight junctions. Knockdown of LSR increases cell motility and invasion of certain cancer cells.

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