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RADIATION DAMAGE IN THE HUMAN BODY ACUTE RADIATION SYNDROME AND MULTIPLE ORGAN FAILURE
AKASHI, MAKOTO,TAMURA, TAIJI,TOMINAGA, TAKAKO,ABE, KENICHI,HACHIYA, MISAO,NAKAYAMA, FUMIAKI Korean Nuclear Society 2006 Nuclear Engineering and Technology Vol.38 No.3
Whole-body exposure to high-dose radiation causes injury involving multiple organs that depends on their sensitivity to radiation. This acute radiation syndrome (ARS) is caused by a brief exposure of a major part of the body to radiation at a relatively high dose rate. ARS is characterized by an initial prodromal stage, a latent symptom-free period, a critical or manifestation phase that usually takes one of four forms (three forms): hematologic, gastrointestinal, or cardiovascular and neurological (neurovascular), depending upon the exposure dose, and a recovery phase or death. One of the most important factors in treating victims exposed to radiation is the estimation of the exposure dose. When high-dose exposure is considered, initial dose estimation must be performed in order to make strategy decisions for treatment as soon as possible. Dose estimation can be based on onset and severity of prodromal symptoms, decline in absolute lymphocyte count post exposure, and chromosomal analysis of peripheral blood lymphocytes. Moreover, dose assessment on the basis of calculation from reconstruction of the radiation event may be required. Experience of a criticality accident occurring in 1999 at Tokai-mura, Japan, showed that ARS led to multiple organ failure (MOF). This article will review ARS and discuss the possible mechanisms of MOF developing from ARS.
Mitsuo Tokuhara,Masaaki Shimatani,Kazunari Tominaga,Hiroko Nakahira,Takuya Ohtsu,Katsuyasu Kouda,Makoto Naganuma 대한소화기내시경학회 2023 Clinical Endoscopy Vol.56 No.5
Background/Aims: Endoscopic resection of all colorectal adenomatous lesions with a low complication rate, simplicity, and negativeresiduals is challenging. Hence, we developed a new method called “non-injection resection using bipolar soft coagulation mode(NIRBS)” method, adapted for colorectal lesions. In addition, we evaluated the effectiveness of this method. Methods: We performed NIRBS throughout a 12-month period for all colorectal lesions which snare resection was acceptable withoutcancerous lesions infiltrating deeper than the submucosal layer. Results: A total of 746 resected lesions were included in the study, with a 4.5 mm mean size (range, 1–35 mm). The major pathologicalbreakdowns were as follows: 64.3% (480/746) were adenomas, and 5.0% (37/746) were intraepithelial adenocarcinomas (Tis lesions). Noresiduals were observed in any of the 37 Tis lesions (mean size, 15.3 mm). Adverse events included bleeding (0.4%) but no perforation. Conclusions: NIRBS allowed the resection of multiple lesions with simplicity because of the non-injection and without perforating dueto the minimal burn effect of the bipolar snare set in the soft coagulation mode. Therefore, NIRBS can be used to resect adenomatouslesions easily, including Tis lesions, from small to large lesions without leaving residuals.
Jang, Yongwoo,Lee, Sung Hoon,Lee, Byeongjun,Jung, Seungmoon,Khalid, Arshi,Uchida, Kunitoshi,Tominaga, Makoto,Jeon, Daejong,Oh, Uhtaek Society for Neuroscience 2015 The Journal of neuroscience Vol.35 No.34
<P>Bipolar disorder (BD) is a psychiatric disease that causes mood swings between manic and depressed states. Although genetic linkage studies have shown an association between BD and TRPM2, a Ca<SUP>2+</SUP>-permeable cation channel, the nature of this association is unknown. Here, we show that D543E, a mutation of <I>Trpm2</I> that is frequently found in BD patients, induces loss of function. <I>Trpm2</I>-deficient mice exhibited BD-related behavior such as increased anxiety and decreased social responses, along with disrupted EEG functional connectivity. Moreover, the administration of amphetamine in wild-type mice evoked a notable increase in open-field activity that was reversed by the administration of lithium. However, the anti-manic action of lithium was not observed in the <I>Trpm2</I><SUP>−/−</SUP> mice. The brains of <I>Trpm2</I><SUP>−/−</SUP> mice showed a marked increase in phosphorylated glycogen synthase kinase-3 (GSK-3), a key element in BD-like behavior and a target of lithium. In contrast, activation of TRPM2 induced the dephosphorylation of GSK-3 via calcineurin, a Ca<SUP>2+</SUP>-dependent phosphatase. Importantly, the overexpression of the D543E mutant failed to induce the dephosphorylation of GSK-3. Therefore, we conclude that the genetic dysfunction of <I>Trpm2</I> causes uncontrolled phosphorylation of GSK-3, which may lead to the pathology of BD. Our findings explain the long-sought etiologic mechanism underlying the genetic link between <I>Trpm2</I> mutation and BD.</P><P><B>SIGNIFICANCE STATEMENT</B> Bipolar disorder (BD) is a mental disorder that causes changes in mood and the etiology is still unknown. TRPM2 is highly associated with BD; however, its involvement in the etiology of BD is still unknown. We show here that TRPM2 plays a central role in causing the pathology of BD. We found that D543E, a mutation of <I>Trpm2</I> frequently found in BD patients, induces the loss of function. <I>Trpm2</I>-deficient mice exhibited mood disturbances and impairments in social cognition. TRPM2 actively regulates the phosphorylation of GSK-3, which is a main target of lithium, a primary medicine for treating BD. Therefore, abnormal regulation of GSK-3 by hypoactive TRPM2 mutants accounts for the pathology of BD, providing the possible link between BD and TRPM2.</P>