Publications by authors named "Kazuyuki Miyamoto"

23 Publications

  • Page 1 of 1

A novel mouse model of heatstroke accounting for ambient temperature and relative humidity.

J Intensive Care 2021 Apr 16;9(1):35. Epub 2021 Apr 16.

Department of Emergency, Critical Care and Disaster Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan.

Background: Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure.

Methods: Mildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS.

Results: The survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage.

Conclusions: We developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.
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http://dx.doi.org/10.1186/s40560-021-00546-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8052643PMC
April 2021

Hypovolemic shock induced by a large chest wall hematoma caused by a single rib fracture in an elderly patient.

Trauma Case Rep 2021 Apr 17;32:100459. Epub 2021 Mar 17.

Department of Emergency and Disaster Medicine, Showa University.

Displaced rib fractures can injure intercostal vessels leading to chest wall hematomas. As the bleeding occurs within the vessel, compression of the vessel wall helps in preventing further bleeding. Therefore, chest wall hematomas rarely result in shock. A thin 78-year-old man transferred to the emergency department with complaints of left dorsal pain due to an injury. He had a history of hypertension and aorta dissection. He arrived at the ED in a state of shock and presented with a large left dorsal wall mass. Subsequent imaging using computed tomography angiography revealed a large hyperdense hematoma at the left dorsal-flank wall along with rib fracture (11th intercostal artery). Moreover, a large fusiform aneurysm was detected from the abdominal aorta to the iliac arteries. Extravasation of the contrast agent was detected at the branch of the 11th intercostal artery, and hence, embolization was performed. The dermis, which comprises collagen and elastin fibers, plays an important role in vessel compression to prevent bleeding. The aortic media also comprises collagen and elastin fibers. Cell turnover, loss of collagen, and excessive elastolysis are associated with the formation of abdominal aortic aneurysms. The systemic degeneration of connecting tissue (collagen and elastin fiber) appears to be progress in patients with an aortic aneurysms and history of aortic dissection compared with other healthy older individuals. Physicians should be cognizant of the potential unexpected large hematoma complications if a risk of systemic connecting tissue degradation exists, as seen in patients with aortic aneurysm or aortic dissection.
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http://dx.doi.org/10.1016/j.tcr.2021.100459DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8010857PMC
April 2021

Diagnosis of neurofibromatosis type 1 after rupture of aneurysm and consequent fatal hemothorax.

Am J Emerg Med 2020 07 7;38(7):1543.e3-1543.e5. Epub 2020 Apr 7.

Department of Emergency and Disaster Medicine, Showa University, Fujigaoka Hospital, 1-30 Fujigaoka Aoba-ku, Yokohama 227-8501, Japan; Department of Emergency and Disaster Medicine, Showa University, 1-5-8 Hatanodai Shinagawa-ku, Tokyo 142-8666, Japan.

Patients with neurofibromatosis type 1 (NF1) can develop both benign and malignant tumors throughout their lives. A 49-year-old man was transferred to the emergency department with complaints of sudden right dorsal pain and respiratory discomfort. He was in shock on arrival. On finding significantly decreased permeability of the left lung field in chest X-ray, drainage was immediately performed. Subsequent computed tomography (CT; Lammert et al., 2005) angiography revealed the extravasation of contrast media from the deep carotid artery, a branch of subclavian artery. It suggested rupture of an aneurysm located at a rare site; the ruptured aneurysm penetrated the pleura, causing shock. The patient was resuscitated. Transcatheter arterial embolization (TAE; Evans et al., 2010) was successfully performed. Immediate drainage, resuscitation, and TAE 2 improved his condition. Most NF1 patients have café-au-lait macules; café-au-lait macules tend to fade with age. Importantly, café-au-lait macules, neurofibromas, and Lisch nodules were noticed at admission. NF1 patients are likely to have a malignant neoplasm when they are young. The patient had been diagnosed with thyroid cancer when he was young. As his deceased mother was an NF1 patient, we diagnosed him with NF1. Detailed patient history and early-stage examination led to the early diagnosis. NF1 should be considered as an early differential diagnosis to improve the outcome of patients in such cases.
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http://dx.doi.org/10.1016/j.ajem.2020.04.004DOI Listing
July 2020

The enhancement of CCL2 and CCL5 by human bone marrow-derived mesenchymal stem/stromal cells might contribute to inflammatory suppression and axonal extension after spinal cord injury.

PLoS One 2020 10;15(3):e0230080. Epub 2020 Mar 10.

Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan.

Human bone marrow-derived mesenchymal stem/stromal cells (hMSCs) have shown potential in facilitating recovery from spinal cord injury (SCI) through communicating with microglia/macrophages (MG/MΦ). We here focused on chemokines as a candidate for the communication. Selected MG/MΦ-related chemokines were determined gene expression after SCI and further focused CCL2/CCR2 and CCL5/CCR5 to estimate role of the chemokines by hMSCs. Male C57/BL6 mice were subjected to spinal cord transection. Gene expression was assayed in the spinal cords following SCI for selected MG/MΦ-related chemokines and their receptors. hMSCs (5×105 cells) were then transplanted into parenchyma of the spinal cord, and the expressions of the Ccl2/Ccr2 and Ccl5/Ccr5 axes, inflammation, MG/MΦ-polarization, and axonal regeneration were evaluated to measure the influence of the hMSCs. Finally, mouse CCL5 was injected into the spinal cords. Acute increases in gene expression after SCI were observed for most chemokines, including Ccl2; chronic increases were observed for Ccl5. CCL2+-cells merged with NeuN+-neurons. CCR2+ immunoreactivity was principally observed in Ly-6G+/iNOS+-granulocytes on postoperative day (pod) 1, and CCL5+ and CCR5+ immunoreactivity overlapped with NeuN+-neurons and F4/80+-MG/MΦ on pod 14. The hMSC transplantation enhanced Ccl2 and Ccl5 and improved locomotor activity. The hMSC implantation did not alter the number of Ly-6G+/CCR2+ but decreased Il1, Elane, and Mpo on pod 3. Conversely, hMSC transplantation increased expression of Zc3h12a (encodes MCP-1-induced protein) on pod 14. Moreover, hMSC increased the Aif1, and two alternatively activated macrophage (AAM)-related genes, Arg1 and Chil3 (Ym1), as well as axonal regenerative markers, Dpysl2 and Gap43. Gene expression indicative of AAM polarization and axonal regeneration were partially recovered by CCL5 injection. These results suggest that hMSC implantation increases Ccl2 and Ccl5, improves locomotor activity, enhances MG/MΦ polarization to AAM, and increases the gene expression of axonal regenerative markers. These functions of hMSCs might be partially mediated by the CCL2/CCR2 and CCL5/CCR5 axes.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0230080PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064230PMC
June 2020

Molecular hydrogen in the treatment of acute and chronic neurological conditions: mechanisms of protection and routes of administration.

J Clin Biochem Nutr 2017 07 15;61(1):1-5. Epub 2017 Jun 15.

Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington, Rm 810A, Bldg 1 VAPSHCS/GRECC S-182, 1660 S, Columbian Way, Seattle, WA 98108, USA.

Oxidative stress caused by reactive oxygen species is considered a major mediator of tissue and cell injuries in various neuronal conditions, including neurological emergencies and neurodegenerative diseases. Molecular hydrogen is well characterized as a scavenger of hydroxyl radicals and peroxynitrite. Recently, the neuroprotective effects of treatment with molecular hydrogen have been reported in both basic and clinical settings. Here, we review the effects of hydrogen therapy in acute neuronal conditions and neurodegenerative diseases. Hydrogen therapy administered in drinking water may be useful for the prevention of neurodegenerative diseases and for reducing the symptoms of acute neuronal conditions.
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http://dx.doi.org/10.3164/jcbn.16-87DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5525017PMC
July 2017

Pituitary adenylate cyclase-activating polypeptide (PACAP) contributes to the proliferation of hematopoietic progenitor cells in murine bone marrow via PACAP-specific receptor.

Sci Rep 2016 Feb 29;6:22373. Epub 2016 Feb 29.

Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa, Tokyo 142-8555, Japan.

Pituitary adenylate cyclase-activating polypeptide (PACAP, encoded by adcyap1) plays an important role in ectodermal development. However, the involvement of PACAP in the development of other germ layers is still unclear. This study assessed the expression of a PACAP-specific receptor (PAC1) gene and protein in mouse bone marrow (BM). Cells strongly expressing PAC1(+) were large in size, had oval nuclei, and merged with CD34(+) cells, suggesting that the former were hematopoietic progenitor cells (HPCs). Compared with wild-type mice, adcyap1(-/-) mice exhibited lower multiple potential progenitor cell populations and cell frequency in the S-phase of the cell cycle. Exogenous PACAP38 significantly increased the numbers of colony forming unit-granulocyte/macrophage progenitor cells (CFU-GM) with two peaks in semi-solid culture. PACAP also increased the expression of cyclinD1 and Ki67 mRNAs. These increases were completely and partially inhibited by the PACAP receptor antagonists, PACAP6-38 and VIP6-28, respectively. Little or no adcyap1 was expressed in BM and the number of CFU-GM colonies was similar in adcyap1(-/-) and wild-type mice. However, PACAP mRNA and protein were expressed in paravertebral sympathetic ganglia, which innervate tibial BM, and in the sympathetic fibers of BM cavity. These results suggested that sympathetic nerve innervation may be responsible for PACAP-regulated hematopoiesis in BM, mainly via PAC1.
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http://dx.doi.org/10.1038/srep22373DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772629PMC
February 2016

[Case of continuous trans-arterial calcium gluconate infusion using a direct arterial sphygmomanometry line that exhibited dramatic improvement of chemical burns on the fingers caused by hydrofluoric acid].

Chudoku Kenkyu 2014 Dec;27(4):343-7

Hydrofluoric acid (HFA) is commonly used and many injuries occur on the upper extremities following exposure to HFA. The use of calcium gluconate (CG) -containing gel or local injections of CG are widely used for the initial treatment of HFA exposure. However, severe pain continues in some cases despite the treatment. There was a report that trans-arterial CG infusion could improve HFA burns, however, such treatment is not an established clinical procedure. A 30-year-old male presented at our hospital with severe pain in his left thumb. He had been cleaning tiles with an HFA-containing detergent. We diagnosed him with a chemical burn due to HFA exposure. Local CG injections were tried several times, but his terrible pain continued. Therefore, a direct arterial sphygmomanometry line was inserted from the left radial artery, and continuous transarterial CG injection was performed. His terrible pain dramatically improved. Direct arterial sphygmomanometry systems are widely used in the critical care field to monitor the hemodynamics and ICU staffs are used to dealing with it. Moreover, continuous saline infusion prevents the tube obstruction. Continuous CG infusion from a direct arterial sphygmomanometry line is simple and safe way to administer CG in HFA burns.
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December 2014

PACAP38 suppresses cortical damage in mice with traumatic brain injury by enhancing antioxidant activity.

J Mol Neurosci 2014 Nov 8;54(3):370-9. Epub 2014 Jun 8.

Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan.

The production of reactive oxygen species (ROS) and the resulting oxidative stress in mice in response to a controlled cortical impact (CCI) are typical exacerbating factors associated with traumatic brain injury (TBI). Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38) is a multifunctional peptide that has been shown to exhibit neuroprotective effects in response to a diverse range of injuries to neuronal cells. We recently reported that PACAP38 might regulate oxidative stress in mice. The aim of the present study was to determine whether PACAP38 exerts neuroprotective effects by regulating oxidative stress in mice with TBI. Reactive oxidative metabolites (ROMs) and biological antioxidant potential (BAP) were measured in male C57Bl/6 mice before and 3, 4, and 24 h after CCI. PACAP38 was administered intravenously immediately following CCI, and immunostaining for the oxidative stress indicator nitrotyrosine (NT), and for neuronal death as an indicator of the area affected by TBI, was measured 24 h later. Western blot experiments to determine antioxidant activity [as indicated by superoxide dismutase-2 (SOD-2) and glutathione peroxidase 1 (GPx-1)] in the neocortical region were also performed 3 h post-CCI. Results showed that plasma BAP and ROM levels were dramatically increased 3 h after CCI. PACAP38 suppressed the extent of TBI and NT-positive regions 24 h after CCI, and increased SOD-2 and GPx-1 levels in both hemispheres. Taken together, these results suggest that increasing antioxidant might be involving in the neuroprotective effect of PACAP38 in mice subjected to a CCI.
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http://dx.doi.org/10.1007/s12031-014-0309-4DOI Listing
November 2014

Status of systemic oxidative stress during therapeutic hypothermia in patients with post-cardiac arrest syndrome.

Oxid Med Cell Longev 2013 26;2013:562429. Epub 2013 Aug 26.

Department of Emergency and Critical Care Medicine, Showa University Fujigaoka Hospital, Aoba-ku, Yokohama, Kanagawa 227-8501, Japan.

Therapeutic hypothermia (TH) is thought to be due to the downregulation of free radical production, although the details of this process remain unclear. Here, we investigate changes in oxidative stress and endogenous biological antioxidant potential during TH in patients with post-cardiac arrest syndrome (PCAS). Nineteen PCAS patients were enrolled in the study. Brain temperature was decreased to the target temperature of 33°C, and it was maintained for 24 h. Patients were rewarmed slowly (0.1°C/h, <1°C/day). The generation of reactive oxygen metabolites (ROMs) was evaluated in plasma samples by d-ROM test. Plasma antioxidant capacity was measured by the biological antioxidant potential (BAP) test. Levels of d-ROMs and BAP levels during the hypothermic stage (33°C) were suppressed significantly compared with pre-TH induction levels (P < 0.05), while both d-ROM and BAP levels increased with rewarming (33-36°C) and were correlated with brain temperature. Clinical monitoring of oxidative stress and antioxidant potential is useful for evaluating the redox state of patients undergoing TH after PCAS. Additional therapy to support the antioxidant potential in the rewarming stage following TH may reduce some of the observed side effects associated with the use of TH.
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http://dx.doi.org/10.1155/2013/562429DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770059PMC
February 2014

The anti-inflammatory property of human bone marrow-derived mesenchymal stem/stromal cells is preserved in late-passage cultures.

J Neuroimmunol 2013 Oct 6;263(1-2):55-63. Epub 2013 Aug 6.

Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.

Human mesenchymal stem/stromal cells (hMSCs) have been reported to improve neural damage via anti-inflammation and multi-differentiation abilities. Here, we investigated immunosuppression effects of hMSCs by mixed-culturing with interferon-γ (IFNγ) stimulated BV-2 mouse microglial cells. We show that hMSCs decreased nitrite oxide (NO) production from BV-2 cells in cell density dependent manner. Aged hMSCs and peroxisome proliferator-activated receptor-γ (PPARγ) knockdown hMSCs decreased differentiation abilities but maintained NO suppressive function. We finally confirmed NO suppression activities of hMSCs in IFNγ-stimulated primary microglia/macrophages. It suggested that hMSCs significantly modified NO production in activated phagocytes and it might be preserved in late passage cultures.
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http://dx.doi.org/10.1016/j.jneuroim.2013.07.018DOI Listing
October 2013

Edaravone increases regional cerebral blood flow after traumatic brain injury in mice.

Acta Neurochir Suppl 2013 ;118:103-9

Department of Anatomy, Showa University School of Medicine, Shinagawa-Ku, Tokyo, Japan.

Traumatic brain injury (TBI) is a major cause of preventable death and serious morbidity, with subsequent low cerebral blood flow (CBF) considered to be associated with poor prognosis. In the present study, we demonstrated the effect of the free radical scavenger edaravone on regional CBF (rCBF) after TBI. Male mice (C57/BL6) were subjected to TBI using a controlled cortical impactor device. Immediately after TBI, the animals were intravenously administered 3.0 mg/kg of edaravone or a vehicle saline solution. Two-dimensional rCBF images were acquired before and 24 h post-TBI, and were quantified in the ipsilateral and contralateral hemispheres (n = 5 animals per group). CBF in the vehicle-treated animals decreased broadly over the ipsilateral hemisphere, with the region of low rCBF spreading from the frontal cortex to the occipital lobe. The zone of lowest rCBF matched that of the contusion area. The mean rCBF at 24 h for a defined elliptical region between the bregma and lambda was 73.7 ± 5.8 %. In comparison, the reduction of rCBF in edaravone-treated animals was significantly attenuated (93.4 ± 5.7 %, p < 0.05). The edaravone-treated animals also exhibited higher rCBF in the contralateral hemisphere compared with that seen in -vehicle-treated animals. It is suggested that edaravone reduces neuronal damage by scavenging reactive oxygen species (ROS) and by maintaining intact the autoregulation of the cerebral vasculature.
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http://dx.doi.org/10.1007/978-3-7091-1434-6_18DOI Listing
August 2013

Establishment and characterization of primary adult microglial culture in mice.

Acta Neurochir Suppl 2013 ;118:49-54

Department of Anatomy, Showa University School of Medicine, Shinagawa-Ku, Tokyo, Japan.

Microglial cells account for approximately 12-15 % of the cells in the central nervous system (CNS). Microglial cells are polarized by pathological stimuli such as cytokines, chemokines, and growth factors, and play important roles in the deterioration and repair of the CNS. Here, we established cultures of primary microglial cells isolated from the brains of adult C57/BL6 mice using Percoll density gradients. The cells were cultured and stained with antibodies against CD11b, glial fibrillary acidic protein, myelin basic protein and NeuN to determine microglial, astroglial, oligodendroglial, and neuronal cells respectively. Moreover, the cells were exposed to interferon-γ (IFNγ) plus interleukin-1β (IL-1β) or IL-4 for 24 h to demonstrate the activating phenotypes with inducible nitric oxide synthase (iNOS), Ym1, and Iba-1 immunoblotting. At least 95 % of the cultured cells were CD11b-positive and -negative for astroglial, neuronal, and oligodendrocyte markers. IFNγ plus IL-1β treatment resulted in classical activation, which was represented by an increase in iNOS. The cells also displayed alternative activation, which increased Ym1 when treated with IL-4. The present study indicates that the microglial cells isolated as described here are a useful tool for elucidating adult microglial function.
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http://dx.doi.org/10.1007/978-3-7091-1434-6_8DOI Listing
August 2013

Therapeutic time window for edaravone treatment of traumatic brain injury in mice.

Biomed Res Int 2013 10;2013:379206. Epub 2013 Apr 10.

Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.

Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also determined the temporal profile of reactive oxygen species (ROS) production, oxidative stress, and neuronal death. Male C57Bl/6 mice were subjected to a controlled cortical impact (CCI). Edaravone (3.0 mg/kg), or vehicle, was administered intravenously at 0, 3, or 6 hours following CCI. The production of superoxide radicals (O2 (∙-)) as a marker of ROS, of nitrotyrosine (NT) as an indicator of oxidative stress, and neuronal death were measured for 24 hours following CCI. Superoxide radical production was clearly evident 3 hours after CCI, with oxidative stress and neuronal cell death becoming apparent after 6 hours. Edaravone administration after CCI resulted in a significant reduction in the injury volume and oxidative stress, particularly at the 3-hour time point. Moreover, the greatest decrease in O2 (∙-) levels was observed when edaravone was administered 3 hours following CCI. These findings suggest that edaravone could prove clinically useful to ameliorate the devastating effects of TBI.
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http://dx.doi.org/10.1155/2013/379206DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3654699PMC
December 2013

Accumulation of autofluorescent storage material in brain is accelerated by ischemia in chloride channel 3 gene-deficient mice.

J Neurosci Res 2012 Nov 30;90(11):2163-72. Epub 2012 Jul 30.

Department of Anatomy, Showa University School of Medicine, Tokyo, Japan.

Autofluorescent storage material (ASM) is an aging pigment that accumulates during the normal course of senescence. Although the role of ASM has yet to be fully elucidated, ASM has been implicated in age-related neurodegeneration. In this study, we determined the level of ASM in chloride channel 3 (ClC-3) gene-deficient (KO) mice both in response to aging and following mild global ischemia. To understand the mechanism of action of the ASM, mice subjected to ischemia were treated with the cyclooxygenase (COX) inhibitor indomethacin or with the noncompetitive glutamate receptor antagonist MK-801. ClC-3 KO mice displayed age-related neurodegeneration of the neocortex as well as the hippocampus. The cortical layers in particular granular layers became thinner with aging. ASM accumulated in the brains of ClC-3 KO mice was increased seven- to 50-fold over that observed in the corresponding regions of their wild-type littermates. Young wild-type mice survived longer than age-matched ClC-3 KO mice after permanent global ischemia. However, in the case of older animals, the survival curves were similar. The ASM also increased four- to fivefold 10 days after mild global ischemia, an effect that was suppressed by treatment with indomethacin and MK-801. These results suggest that temporary ischemia might trigger a process similar to aging in the brain, mimicking the effect of age-related neurodegenerative diseases.
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http://dx.doi.org/10.1002/jnr.23110DOI Listing
November 2012

[Aggressive endoscopic removal of bezoars effective for the treatment of acute poisoning].

Chudoku Kenkyu 2012 Jun;25(2):113-6

Department of Emergency and Critical Care Medicine, Showa University.

A 37-year-old female presented with acute chlorpromazine and phenobarbital poisoning. Contrast enhanced abdominal CT on admission revealed a high density area at the gastric fundus and residual drugs were suspected. Activated charcoal and cathartics were administered following the gastric lavage under the intubation. As the plasma concentration of phenobarbital was high, urinary alkalinization and crystalloid infusion were carried out to reduce it. However, at 3 days after admission, the plasma concentration level had increased and the consciousness disturbance and respiratory depression continued. Abdominal CT was performed again and bezoars formation was suspected. Endoscopy was carried out to remove the bezoars. After the removal, the plasma concentration level significantly decreased. Her consciousness disturbance and respiratory depression also improved and high density area at the gastric fundus disappeared. Acute endoscopy is seldom advocated in cases of drug overdose. However, aggressive endoscopic removal should be considered in the case of acute poisoning of drugs with form bezoars.
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June 2012

[The correlation between the intraoperative flow of coronary artery bypass grafts and the patency of grafts at midterm follow-up].

Kyobu Geka 2012 Jun;65(6):433-9

Department of Cardiovascular Surgery, Japanese Red Cross, Japan.

We evaluated the correlation between the intraoperative flow of coronary artery bypass grafting (CABG) and the patency of grafts at midterm follow-up. When internal mammary arteries were used as grafts, there was no correlation between graft flow rate and graft patency rate. On the other hand, when saphenous vein was used, the greater graft flow was associated with better graft patency. Receiver operator characteristic( ROC) analysis identified the optimum threshold for the intraoperative flow rate to predict the patency at midterm follow-up as 23 ml/min (sensitivity 78%, specificity 71%). The difference in the correlation( of flow rate with patency rate) between the 2 graft types was attributed to the difference of physiological reaction of each type of grafts.
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June 2012

[Evaluation of preoperative intraaortic balloon pumping for high risk off-pump coronary artery bypass grafting].

Kyobu Geka 2011 Nov;64(12):1043-6: discussion 1047-9

Department of Cardiovascular Surgery, Red Cross Fukuoka Hospital, Fukuoka, Japan.

We evaluated the effect of preoperative intraaortic balloon pumping (IABP) support in high risk patients undergoing off-pump coronary artery bypass grafting (OPCAB). Between November 1999 and December 2010, 65 high-risk patients underwent OPCAB with the support of IABP inserted preoperatively. High risks were considered as (1) left main coronary artery stem stenosis > or = 75%, (2) unstable angina requiring intravenous nitrates and heparin, (3) preoperative left ventricular ejection fraction < or = 30%, (4) bilateral carotid artery stenosis > or = 75%. There were no hospital deaths or cerebrovascular complications. During operations, hemodynamics was stable with the support of low dose catecholamines, and no patient needed conversion to on-pump coronary artery bypass grafting. All patients were able to be weaned from IABP within 3 days (mean 5.7 hours) after the operation and were extubated within 4 days (mean 11.5 hours) after the operation. One patient had a peripheral embolism which might be related to insertion of IABP (1.5%). Preoperative IABP in high-risk patients undergoing OPCAB was considered to be useful and safe.
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November 2011

[Application of hyperbaric oxygen therapy for post-cardiac arrest syndrome].

Nihon Rinsho 2011 Apr;69(4):648-52

Department of Emergency and Critical Care Medicine, Showa University.

Therapeutic mechanisms of hyperbaric oxygen therapy (HBOT) are based on elevation of both the partial pressure of oxygen and hydrostatic pressure. It has been reported that HBOT supply much amount of oxygen and might prevent from brain tissue after global ischemia in patients with post-cardiac arrest syndrome(PCAS). On the other hand, high levels of oxygen produce reactive oxygen species(ROS). ROS occurs secondary brain damage after ischemia. The clinical evidence of HBOT has not been established. In this paper, we review some reports about the advantages and disadvantages of HBOT after global ischemia with PCAS.
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April 2011

Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury.

J Neuroinflammation 2010 Jul 26;7:41. Epub 2010 Jul 26.

Department of Emergency and Critical Care Medicine, Showa University School of Medicine, Shinagawa-Ku, Tokyo 142-8555, Japan.

Background: We hypothesized that gp91phox (NOX2), a subunit of NADPH oxidase, generates superoxide anion (O2-) and has a major causative role in traumatic brain injury (TBI). To evaluate the functional role of gp91phox and reactive oxygen species (ROS) on TBI, we carried out controlled cortical impact in gp91phox knockout mice (gp91phox-/-). We also used a microglial cell line to determine the activated cell phenotype that contributes to gp91phox generation.

Methods: Unilateral TBI was induced in gp91phox-/- and wild-type (Wt) mice (C57/B6J) (25-30 g). The expression and roles of gp91phox after TBI were investigated using immunoblotting and staining techniques. Levels of O2- and peroxynitrite were determined in situ in the mouse brain. The activated phenotype in microglia that expressed gp91phox was determined in a microglial cell line, BV-2, in the presence of IFNgamma or IL-4.

Results: Gp91phox expression increased mainly in amoeboid-shaped microglial cells of the ipsilateral hemisphere of Wt mice after TBI. The contusion area, number of TUNEL-positive cells, and amount of O2- and peroxynitrite metabolites produced were less in gp91phox-/- mice than in Wt. In the presence of IFNgamma, BV-2 cells had increased inducible nitric oxide synthase and nitric oxide levels, consistent with a classical activated phenotype, and drastically increased expression of gp91phox.

Conclusions: Classical activated microglia promote ROS formation through gp91phox and have an important role in brain damage following TBI. Modulating gp91phox and gp91phox -derived ROS may provide a new therapeutic strategy in combating post-traumatic brain injury.
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http://dx.doi.org/10.1186/1742-2094-7-41DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917406PMC
July 2010

Regulation of oxidative stress by pituitary adenylate cyclase-activating polypeptide (PACAP) mediated by PACAP receptor.

J Mol Neurosci 2010 Nov 13;42(3):397-403. Epub 2010 Apr 13.

Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a multifunctional peptide that has been shown to be neuroprotective following a diverse range of cell injuries. Although several mechanisms regulating this effect have been reported, no direct evidence has linked PACAP to the regulation of oxidative stress, despite the fact that oxidative stress is a factor in the injury progression that occurs in most models. In the present study, we investigated the plasma oxidative metabolite and anti-oxidation potential levels of PACAP-deficient mice, as well as those of wild-type animals treated with PACAP38. These were assayed by the determination of Reactive Oxidative Metabolites (d-ROMs) and the Biological Anti-oxidant Potential (BAP) using the Free Radical Electron Evaluator system. We also investigated the direct radical scavenging potency of PACAP38 and the functional role of its receptor in the regulation of oxidative stress by PACAP, by using vasoactive intestinal peptide (VIP) and the PACAP receptor antagonist, PACAP6-38. Although younger PACAP null mice displayed no significant effect, greater d-ROMs and lower BAP values were recorded in older animals than in their wild-type littermates. Intravenous injection of PACAP38 in wild-type mice decreased the plasma d-ROMs and BAP values in a dose-dependent manner. These effects were not reproduced using VIP and were abolished by co-treatment with PACAP38 and the PAC1R antagonist PACAP6-38. Taken together, these results suggest that PACAP plays an important role in the physiological regulation of oxidative stress.
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http://dx.doi.org/10.1007/s12031-010-9350-0DOI Listing
November 2010

Synthesis of super hard Ni-B/diamond composite coatings by wet processes.

Chem Commun (Camb) 2010 Jan 11;46(3):442-4. Epub 2009 Nov 11.

Department of Chemistry and Material Science, Tokyo Institute of Technology, 2-12-1, S1-44, Ookayama, Meguro-ku, Tokyo 152-8552, Japan.

Ni-B/diamond composite coatings were prepared using electrophoretic deposition and electroless deposition methods, leading to extremely high hardness which is comparable to hard coatings prepared by dry processes.
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http://dx.doi.org/10.1039/b914242hDOI Listing
January 2010

Cardiac tamponade due to spontaneous rupture of large coronary artery aneurysm.

Asian Cardiovasc Thorac Ann 2006 Oct;14(5):422-4

Department of Cardiovascular Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.

A 70-year-old woman admitted with chest pain went into shock due to cardiac tamponade; 1000 mL of blood was drained from her pericardium. Enhanced computed tomography showed massive pericardial effusion and a coronary artery aneurysm in front of the main pulmonary artery. Coronary angiography revealed a coronary artery-pulmonary artery fistula and 3 giant saccular coronary artery aneurysms. Emergency surgical repair was successful.
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http://dx.doi.org/10.1177/021849230601400516DOI Listing
October 2006

The low resistance strategy for the perioperative management of the Norwood procedure.

Ann Thorac Surg 2004 Mar;77(3):908-12

Department of Cardiovascular Surgery, Fukuoka Children's Hospital, Japan.

Background: Postoperative course of the Norwood procedure is fragile because of an unstable pulmonary to systemic blood flow ratio caused by fluctuation of systemic and pulmonary vascular resistance.

Methods: Twenty-seven patients with hypoplastic left heart syndrome who underwent the Norwood procedure from June 1998 to February 2002 were managed with the following low-resistance strategy. Intraoperative high-flow and low-resistance cardiopulmonary bypass was achieved with total avoidance of circulatory arrest and a large dose of chlorpromazine. In weaning from the bypass, pulmonary vascular resistance was maximally decreased by inspired oxygen fraction (100%), inhaled nitric oxide (20 ppm), and nitroglycerin (2 to 4 microg/kg/min). Then pulmonary blood flow was determined by adjusting the systemic to pulmonary shunt. Postoperatively, with continuous infusion of chlorpromazine and nitroglycerin as a systemic and pulmonary vasodilator, the inspired oxygen fraction and inhaled nitric oxide were tapered as the arterial oxygen saturation improved.

Results: In most patients, inhaled nitrous oxide and inspired oxygen fraction were weaned within 3 days. The postoperative course was stable with minimum changes in circulatory and respiratory status for the survivors. Patients were extubated on a median of 6 postoperative days. Early mortality was 11.1% (3 of 27), and none of the patients died of hemodynamic deterioration.

Conclusions: The low resistance strategy is a simple and useful method for perioperative management of the Norwood procedure, minimizing fluctuation in both pulmonary and systemic vascular resistance and maintaining stable circulatory and respiratory status.
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http://dx.doi.org/10.1016/j.athoracsur.2003.09.025DOI Listing
March 2004