222 research outputs found

    McKeown esophagectomy with concomitant median arcuate ligament release in a case of esophageal cancer with celiac artery stenosis

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    [Background] The celiac artery stenosis due to compression by median arcuate ligament (MAL) has been reported in many cases of pancreaticoduodenectomy, but not in cases of esophagectomy. Recently, the celiac artery stenosis due to MAL or arteriosclerosis has been reported to be associated with the gastric tube necrosis or anastomotic leakage following Ivor–Lewis esophagectomy. Herein, we present the first reported case of esophageal cancer with celiac artery stenosis due to compression by the MAL successfully treated by McKeown esophagectomy and gastric tube reconstruction following prophylactic MAL release. [Case presentation] A 72-year-old female patient was referred to our department for esophagectomy. The patient had received two courses of neoadjuvant chemotherapy with 5-FU and cisplatin for T2N0M0 squamous cell carcinoma of the middle esophagus. Preoperative contrast-enhanced computed tomography (CECT) showed celiac artery stenosis due to compression by the MAL. The development of collateral arteries around the pancreatic head was observed without evidence of aneurysm formation. The patient reported no abdominal symptoms. After robot-assisted esophagectomy with mediastinal lymphadenectomy, gastric mobilization, supra-pancreatic lymphadenectomy, and preparation of the gastric tube were performed under laparotomy. Subsequently, the MAL was cut, and released to expose the celiac artery. Improved celiac artery blood flow was confirmed by decreased pulsatility index on intraoperative Doppler sonography. The operation was completed with the cervical esophagogastric anastomosis following cervical lymphadenectomy. Postoperative CECT on postoperative day 7 demonstrated increased celiac artery patency. The patient had an uncomplicated postoperative course thereafter. [Conclusions] Prophylactic MAL release may be considered in patients with celiac artery stenosis due to compression by the MAL on preoperative CECT for esophagectomy

    Investigation of superconductivity in Ce-doped (La,Pr)OBiS2 single crystals

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    Single crystals of Ce-doped (La,Pr)OBiS2 superconductors, multinary rare-earth elements substituted ROBiS2, were successfully grown. The grown crystals typically had a size of 1-2 mm and a plate-like shape with a well-developed c-plane. The c-axis lattice constants of the obtained (La,Ce,Pr)OBiS2 single crystals were approximately 13.6-13.7 A, and the superconducting transition temperature was 1.23-2.18 K. Valence fluctuations of Ce and Pr were detected through X-ray absorption spectroscopy analysis. In contrast to (Ce,Pr)OBiS2 and (La,Ce)OBiS2, the superconducting transition temperature of (La,Ce,Pr)OBiS2 increased with increasing concentrations of the tetravalent state at the R-site

    Thoracic epidural analgesia in a patient with von Hippel-Lindau disease

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    von Hippel-Lindau disease (VHLD) is an autosomal dominant disorder characterized by central nervous system hemangioblastomas and renal tumors. Here, we report a case of thoracic epidural placement in a 35-year-old woman with VHLD presenting for left open heminephrectomy for renal masses. We also reviewed the literature on this topic

    MARCH1 protects the lipid raft and tetraspanin web from MHCII proteotoxicity in dendritic cells

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    Dendritic cells (DCs) produce major histocompatibility complex II (MHCII) in large amounts to function as professional antigen presenting cells. Paradoxically, DCs also ubiquitinate and degrade MHCII in a constitutive manner. Mice deficient in the MHCII-ubiquitinating enzyme membrane-anchored RING-CH1, or the ubiquitin-acceptor lysine of MHCII, exhibit a substantial reduction in the number of regulatory T (Treg) cells, but the underlying mechanism was unclear. Here we report that ubiquitin-dependent MHCII turnover is critical to maintain homeostasis of lipid rafts and the tetraspanin web in DCs. Lack of MHCII ubiquitination results in the accumulation of excessive quantities of MHCII in the plasma membrane, and the resulting disruption to lipid rafts and the tetraspanin web leads to significant impairment in the ability of DCs to engage and activate thymocytes for Treg cell differentiation. Thus, ubiquitin-dependent MHCII turnover represents a novel quality-control mechanism by which DCs maintain homeostasis of membrane domains that support DC's Treg cell-selecting function

    Comparative study of the effect of neuromuscular electrical stimulation and oral administration of branched-chain amino acid on preventing sarcopenia in patients after living-donor liver transplantation: study protocol for an open-label randomized controlled trial

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    Background: Liver cirrhosis is the irreversible fibrosis of the liver and causes refractory ascites and hepatic encephalopathy, which might not respond to treatment. Living donor liver transplantation (LDLT) is an effective treatment for patients with cirrhosis. However, post-LDLT patients are prone to muscle atrophy and sarcopenia. Therefore, physiotherapy of post-LDLT patients is essential for preventing the progression of sarcopenia. Recently, rehabilitation using neuromuscular electrical stimulation (NMES) has been reported to be useful for preventing the progression of sarcopenia. Similarly, nutrition therapy is essential for post-LDLT patients because these patients frequently experience malnutrition. However, the effects of combined NMES and nutrition therapy on post-LDLT patients remain unknown. Methods/design: This open-label, randomized, parallel-group study will compare the effects of combined therapy with NMES and branched-chain amino acids (BCAA) with those of NMES alone in patients with decompensated cirrhosis after LDLT. After LDLT, 50 patients with decompensated cirrhosis will be randomly assigned to receive NMES with BCAA or NMES without BCAA. The duration of the intervention will be 3 months. To analyze the change in skeletal muscle mass, InBody 770 body composition and body water analysis and ultrasonography will be performed before LDLT and 4 weeks and 12 weeks post-LDLT. The primary endpoint is changes in the skeletal muscle mass from baseline to 3 months. Important secondary endpoints are the changes in the skeletal muscle mass from baseline to 1 month and changes in the quadriceps strength from baseline to 1 month. Discussion: The results of this study are expected to provide evidence regarding the effect of NMES combined with BCAA therapy on the skeletal muscle of post-LDLT patients. Trial registration: Japan Registry of Clinical Research jRCTs071190051. Registered on February 26, 2020
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