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The widespread use of tris(1,3‐dichloro‐2‐propyl) phosphate (TDCIPP) as a flame retardant has led to its release to the environment. Thus, the toxicological effects of TDCIPP on humans and animals are of importance. For better understanding of its potential toxicities, TDCIPP (250, 500, or 650 mg/kg/day) or vehicle control was administrated orally to adult male Wistar‐Imamichi rats for 7 days. After the final administration of compounds, organ weights, histopathology, blood biochemistry, and hematology were examined. Hepatic toxicity was observed at doses ≥ 500 mg/kg/day of TDCIPP, and renal toxicity was observed at 650 mg/kg/day. The anti‐androgenic activity of TDCIPP was previously confirmed in vitro and in vivo, but weights of epididymis, an androgen‐dependent organ, were not affected by TDCIPP treatment in adults. Serum alkaline phosphatase activity was significantly decreased in all TDCIPP‐treated rats independent of dose. Hemoglobin concentration, hematocrit, red blood cell count, and reticulocyte count were decreased in all TDCIPP‐treated rats, but mean corpuscular volume, total iron‐binding capacity, and serum iron were normal, suggesting that renal anemia was caused by TDCIPP. Together with previous reports on effects of anti‐androgenic substances on red blood cell indices, anemia caused by TDCIPP could be due to its anti‐androgenic activity. These considerations will contribute to further assessment of the toxicity of the compound. Tris(1,3‐dichloro‐2‐propyl) phosphate (TDCIPP) was administrated orally to adult male Wistar‐Imamichi rats for 7 days. Serum ALP activity was significantly decreased in all TDCIPP‐treated rats independent of dose. Hemoglobin concentration, hematocrit, red blood cell count, and reticulocyte count were decreased by TDCIPP, suggesting that renal anemia is possibly caused by its anti‐androgenic activity. These considerations will contribute to further assessment of the toxicity of the compound. [ABSTRACT FROM AUTHOR]

Muse cells, a novel type of nontumorigenic pluripotent-like stem cells, reside in the bone marrow, skin, and adipose tissue and are collectable as cells positive for pluripotent surface marker SSEA-3. They are able to differentiate into cells representative of all three germ layers. The capacity of intravenously injected human bone marrow-derived Muse cells to repair an immunodeficient mouse model of liver fibrosis was evaluated in this study. The cells exhibited the ability to spontaneously differentiate into hepatoblast/hepatocyte lineage cells in vitro. They demonstrated a high migration capacity toward the serum and liver section of carbon tetrachloride-treated mice in vitro. In vivo, they specifically accumulated in the liver, but not in other organs except, to a lesser extent, in the lungs at 2 weeks after intravenous injection in the liver fibrosis model. After homing, Muse cells spontaneously differentiated in vivo into HepPar-1 (71.1 ± 15.2%), human albumin (54.3 ± 8.2%), and anti-trypsin (47.9 ± 4.6%)-positive cells without fusing with host hepatocytes, and expressed mature functional markers such as human CYP1A2 and human Glc-6-Pase at 8 weeks after injection. Recovery in serum, total bilirubin, and albumin and significant attenuation of fibrosis were recognized with statistical differences between the Muse cell-transplanted group and the control groups, which received the vehicle or the same number of a non-Muse cell population of MSCs (MSCs in which Muse cells were eliminated). Thus, unlike ESCs and iPSCs, Muse cells are unique in their efficient migration and integration into the damaged liver after intravenous injection, nontumorigenicity, and spontaneous differentiation into hepatocytes, rendering induction into hepatocytes prior to transplantation unnecessary. They may repair liver fibrosis by two simple steps: expansion after collection from the bone marrow and intravenous injection. A therapeutic strategy such as this is feasible and may provide significant advancements toward liver regeneration in patients with liver disease.

In general, the treatment methods for esophageal achalasia are largely classified into four groups, including drug therapy using nitrite or a calcium channel blocker, botulinum toxin injection, endoscopic therapy such as endoscopic balloon dilation, and surgery. Various studies have suggested that the most effective treatment of esophageal achalasia is surgical therapy. The basic concept of this surgical therapy has not changed since Heller proposed esophageal myotomy for the purpose of resolution of lower esophageal obstruction for the first time in 1913, but the most common approach has changed from open-chest surgery to laparoscopic surgery. Currently, the laparoscopic surgery has been the procedure of choice for the treatment of esophageal achalasia. During the process of the transition from open-chest surgery to laparotomy, to thoracoscopic surgery, and to laparoscopic surgery, the necessity of combining antireflux surgery has been recognized. There is some debate as to which type of antireflux surgery should be selected. The Toupet fundoplication may be the most effective in prevention of postoperative antireflux, but many medical institutions have selected the Dor fundoplication which covers the mucosal surface exposed by myotomy. Recently, a new endoscopic approach, peroral endoscopic myotomy (POEM), has received attention. Future studies should examine the long-term outcomes and whether POEM becomes the gold standard for the treatment of esophageal achalasia.