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Article ; Online: Revisiting the canonical definition of heat hematoma: A rare case of postmortem subdural heat hematoma.

Wen, Shuheng / Unuma, Kana / Uemura, Koichi / Harada, Kazuki

2023 Volume 98, Page(s) 102563

Abstract: Heat hematoma is generally recognized as a postmortem heat-induced artifact in extradural spaces found in burned bodies. Conversely, subdural hematoma in charred bodies is more indicative of antemortem trauma. Here, we present a rare case of a subdural ... ...

Abstract	Heat hematoma is generally recognized as a postmortem heat-induced artifact in extradural spaces found in burned bodies. Conversely, subdural hematoma in charred bodies is more indicative of antemortem trauma. Here, we present a rare case of a subdural heat hematoma in forensic practice. The subdural hematoma was found in a charred body that was determined to be dead before the fire without findings of antemortem head injury. Furthermore, the detailed determination and formation mechanism of this subdural heat hematoma are discussed. With this rare case, we propose a reconsideration of the canonical definition of heat hematoma. This report envisions benefitting forensic pathologists facing similar cases.
MeSH term(s)	Humans ; Hot Temperature ; Hematoma, Subdural ; Autopsy ; Postmortem Changes ; Craniocerebral Trauma
Language	English
Publishing date	2023-07-13
Publishing country	England
Document type	Case Reports
ZDB-ID	2268721-X
ISSN	1878-7487 ; 1752-928X
ISSN (online)	1878-7487
ISSN	1752-928X
DOI	10.1016/j.jflm.2023.102563
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Article ; Online: Ectopic myogenesis and fibrosis accompany adipogenesis during thymic involution induced by repeated cocaine administration.

Unuma, Kana / Wen, Shuheng / Aki, Toshihiko / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 686, Page(s) 149201

Abstract: We have shown previously that daily cocaine administration for 7-14 days in rats resulted in the acceleration of thymic involution, which is, alike to age-related thymic involution, accompanied by ectopic adipogenesis. Here we show that the thymic ... ...

Abstract	We have shown previously that daily cocaine administration for 7-14 days in rats resulted in the acceleration of thymic involution, which is, alike to age-related thymic involution, accompanied by ectopic adipogenesis. Here we show that the thymic involution caused by repeated cocaine administration is accompanied by not only adipogenesis but also ectopic myogenesis and fibrosis. In accordance with fibrosis, we observed an increase of N-cadherin, a marker of mesenchymal cells, as well as a decrease of E-cadherin, an epithelial cell marker, in the thymus in response to cocaine administration, suggesting the occurrence of epithelial-to-mesenchymal transition (EMT). Levels of fibronectin was also increased in the thymus of cocaine group compared to control group. In addition, increases in the levels of the transcription factors for myogenic differentiation, myogenin, MYF5, and MYF6, were observed in the thymus administered cocaine for 14 days. These results indicate that the thymic involution induced by cocaine administration involves not only adipogenesis and fibrosis but also ectopic myogenesis, which is scarcely observed and rather pathological process during thymic involution.
MeSH term(s)	Rats ; Animals ; Adipogenesis ; Thymus Gland ; Cell Differentiation ; Epithelial Cells/pathology ; Fibrosis
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.149201
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Article ; Online: Two fatal cases due to inadvertent discharge of carbon dioxide fire suppressant: Intoxication or asphyxiation?

Wen, Shuheng / Unuma, Kana / Uemura, Koichi

Journal of forensic and legal medicine

2022 Volume 90, Page(s) 102390

Abstract: Carbon dioxide ( ... ...

Abstract	Carbon dioxide (CO
MeSH term(s)	Asphyxia/etiology ; Autopsy ; Carbon Dioxide ; Fires ; Humans
Chemical Substances	Carbon Dioxide (142M471B3J)
Language	English
Publishing date	2022-06-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2268721-X
ISSN	1878-7487 ; 1752-928X
ISSN (online)	1878-7487
ISSN	1752-928X
DOI	10.1016/j.jflm.2022.102390
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Article ; Online: Excessive N-acetylcysteine exaggerates glutathione redox homeostasis and apoptosis during acetaminophen exposure in Huh-7 human hepatoma cells.

Aki, Toshihiko / Tanaka, Hiroki / Funakoshi, Takeshi / Unuma, Kana / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 676, Page(s) 66–72

Abstract: Acetaminophen (APAP) hepatotoxicity is one of the biggest drawbacks of this relatively safe and widely used drug. In addition to its hepatotoxicity, APAP also cause comparable levels of toxicity on human hepatoma cells. Here we show activation of the ... ...

Abstract	Acetaminophen (APAP) hepatotoxicity is one of the biggest drawbacks of this relatively safe and widely used drug. In addition to its hepatotoxicity, APAP also cause comparable levels of toxicity on human hepatoma cells. Here we show activation of the intrinsic caspase-9/3 pathway of apoptosis followed by gasdermin E (GSDME) cleavage and subsequent ballooning in APAP (10 mM, 72 h)-treated Huh-7 human hepatocarcinoma cells. N-acetylcysteine (NAC), an antioxidant currently used as an antidote for APAP overdose, does not alleviate APAP toxicity in Huh-7 cells; NAC overdose (10 mM) rather aggravates APAP toxicity. NAC overdose not only aggravates cell death, but also decreases the cellular GSH/GSSG ratio, an indicator of redox homeostasis of glutathione. These results show for the first time that APAP-induced apoptosis in hepatoma cells is followed by secondary necrosis via the caspase-3/GSDME pathway. NAC overdose (10 mM) not only worsens the glutathione redox status, but also accelerates this pathway.
MeSH term(s)	Humans ; Acetylcysteine/metabolism ; Acetaminophen/toxicity ; Carcinoma, Hepatocellular/pathology ; Chemical and Drug Induced Liver Injury/pathology ; Glutathione/metabolism ; Liver Neoplasms/pathology ; Apoptosis ; Oxidation-Reduction ; Homeostasis ; Liver/metabolism
Chemical Substances	Acetylcysteine (WYQ7N0BPYC) ; Acetaminophen (362O9ITL9D) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2023-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.07.023
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Article ; Online: Cocaine induces vascular smooth muscle cells proliferation via DRP1-mediated mitochondrial fission and PI3K/HIF-1α signaling.

Wen, Shuheng / Unuma, Kana / Funakoshi, Takeshi / Aki, Toshihiko / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 676, Page(s) 30–35

Abstract: Long-term cocaine abuse is associated with cardiovascular and pulmonary vascular complications. The vascular toxicity of cocaine can lead to vascular remodeling characterized by excessive proliferation of vascular smooth muscle cells. Though hypoxia- ... ...

Abstract	Long-term cocaine abuse is associated with cardiovascular and pulmonary vascular complications. The vascular toxicity of cocaine can lead to vascular remodeling characterized by excessive proliferation of vascular smooth muscle cells. Though hypoxia-inducible factor (HIF) signaling and mitochondrial fission have been suggested to play essential roles in the pathogenesis of hypoxia-induced vascular remodeling, pathogenetic mechanism for cocaine-related vascular remodeling remains to be elucidated. In this study, we explore the effect of cocaine on the proliferation of vascular smooth muscle cells by in vitro experiments. The findings indicated that the cocaine-induced vascular smooth muscle cell hyperproliferation is achieved by enhancing DRP1-mediated mitochondrial fission and activating PI3K/HIF-1α signaling. Current findings suggested that mitochondrial fission would play a pivotal role in cocaine-related vascular remodeling and would be helpful in understanding the vascular toxicity of cocaine.
MeSH term(s)	Humans ; Phosphatidylinositol 3-Kinases/pharmacology ; Vascular Remodeling ; Cell Proliferation ; Muscle, Smooth, Vascular ; Mitochondrial Dynamics ; Cocaine/toxicity ; Hypoxia/complications ; Hypoxia-Inducible Factor 1, alpha Subunit ; Myocytes, Smooth Muscle ; Cells, Cultured
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Cocaine (I5Y540LHVR) ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2023-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.07.020
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Zs.A 116: Show issues

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Article ; Online: Aristolochic acid induces an inflammatory response with prostaglandin E2 production and apoptosis in NRK-52E proximal tubular cells.

Komatsu, Miyu / Funakoshi, Takeshi / Aki, Toshihiko / Unuma, Kana / Uemura, Koichi

Toxicology letters

2023 Volume 378, Page(s) 39–50

Abstract: Aristolochic acid nephropathy (AAN) is a type of drug-induced nephropathy in which ingestion of aristolochic acid (AA) causes acute kidney injury, with progressive renal fibrosis and upper urothelial carcinoma. Although the pathological features of AAN ... ...

Abstract	Aristolochic acid nephropathy (AAN) is a type of drug-induced nephropathy in which ingestion of aristolochic acid (AA) causes acute kidney injury, with progressive renal fibrosis and upper urothelial carcinoma. Although the pathological features of AAN have been reported to involve significant cell degeneration and loss in the proximal tubules, the details of the toxic mechanism in the acute phase of the disease remain unclear. This study investigates the cell death pathway and intracellular metabolic kinetics of AA exposure in rat NRK-52E proximal tubular cells. AA exposure induces dose- and time-dependent apoptotic cell death in NRK-52E cells. We examined the inflammatory response to further investigate the mechanism of AA-induced toxicity. AA exposure increased the gene expression of inflammatory cytokines IL-6 and TNF-α, suggesting that AA exposure induces inflammation. Furthermore, analysis of lipid mediators by LC-MS revealed increases in intra- and extra-cellular arachidonic acid and prostaglandin E2 (PGE2). To investigate the relationship between the AA-induced increase in PGE2 production and cell death, celecoxib, an inhibitor of cyclooxygenase-2 (COX-2), which is involved in the production of PGE2, was administered, and a marked inhibition of AA-induced cell death was observed. These results suggest that exposure to AA induces concentration- and time-dependent apoptosis in NRK-52E cells, which is attributed to inflammatory responses mediated by COX-2 and PGE2.
MeSH term(s)	Rats ; Animals ; Dinoprostone/metabolism ; Kidney Tubules/metabolism ; Cell Line ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Carcinoma, Transitional Cell/metabolism ; Carcinoma, Transitional Cell/pathology ; Urinary Bladder Neoplasms/pathology ; Apoptosis/physiology ; Aristolochic Acids/toxicity ; Kidney Diseases/chemically induced
Chemical Substances	Dinoprostone (K7Q1JQR04M) ; aristolochic acid I (94218WFP5T) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Aristolochic Acids
Language	English
Publishing date	2023-03-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	433788-8
ISSN	1879-3169 ; 0378-4274
ISSN (online)	1879-3169
ISSN	0378-4274
DOI	10.1016/j.toxlet.2023.02.009
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Article: The Role of Peroxiredoxins in the Regulation of Sepsis.

Aki, Toshihiko / Unuma, Kana / Uemura, Koichi

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 1

Abstract: Oxidative stress, a result of a disturbance in redox homeostasis, is considered to be one of the main aggravating events in the pathogenesis of immune disorders. Peroxiredoxins (Prdxs) are an enzyme family that catalyzes the reduction of peroxides, ... ...

Abstract	Oxidative stress, a result of a disturbance in redox homeostasis, is considered to be one of the main aggravating events in the pathogenesis of immune disorders. Peroxiredoxins (Prdxs) are an enzyme family that catalyzes the reduction of peroxides, including hydrogen peroxide, lipid peroxides, and nitrogen peroxides. Although the maintenance of cellular redox homeostasis through Prdxs is essential for surviving in adverse environments, Prdxs also participate in the regulation of cellular signal transduction by modulating the activities of a panel of molecules involved in the signal transduction process. Although Prdxs were discovered as intracellular anti-oxidative enzymes, recent research has revealed that Prdxs also play important roles in the extracellular milieu. Indeed, Prdxs have been shown to have the capacity to activate immune cells through ligation with innate immune receptors such as toll-like receptors (TLRs). In this review, we will summarize the intracellular as well as extracellular roles of Prdxs for and against the pathogenesis of inflammatory disorders including sepsis, hemorrhagic shock, and drug-induced liver injury.
Language	English
Publishing date	2022-01-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11010126
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Article ; Online: Inverse regulation of GSDMD and GSDME gene expression during LPS-induced pyroptosis in RAW264.7 macrophage cells.

Aki, Toshihiko / Funakoshi, Takeshi / Unuma, Kana / Uemura, Koichi

Apoptosis : an international journal on programmed cell death

2022 Volume 27, Issue 1-2, Page(s) 14–21

Abstract: GSDMD and GSDME, members of the gasdermin protein family, are involved in the formation of plasma membrane channels contributing to cell rupture during a certain type of necrosis called pyroptosis. GSDMD is activated in response to immunological ... ...

Abstract	GSDMD and GSDME, members of the gasdermin protein family, are involved in the formation of plasma membrane channels contributing to cell rupture during a certain type of necrosis called pyroptosis. GSDMD is activated in response to immunological stimulation such as lipopolysaccharides (LPS) treatment while GSDME is mainly involved in drug-induced tumor cell death. Here we show that the expression of the GSDMD gene increases significantly during LPS-induced pyroptosis in RAW264.7 murine macrophage cells. In contrast, GSDME expression is decreased in the same cells. The increasing effect of LPS on GSDMD expression was observed only when the cells were cultured in high glucose (4.5 g/l) medium, suggesting that glucose availability is important for this effect. The effect of LPS on GSDMD expression is abolished by 2-deoxyglucose (2DG), confirming that glycolysis plays crucial roles in the increasing effect of LPS. Small interference RNA-mediated knock down of GSDMD or overexpression of GSDME causes LPS-induced pyroptosis to take place through GSDME rather than through GSDMD. Taken together, LPS regulates GSDMD and GSDME expression in opposite directions through, at least in part, its effect on glycolysis. This transcriptional regulation may contribute to the execution of pyroptosis in a GSDMD-dependent manner.
MeSH term(s)	Animals ; Apoptosis ; Gene Expression ; Lipopolysaccharides/pharmacology ; Macrophages/metabolism ; Mice ; Pyroptosis/genetics
Chemical Substances	Lipopolysaccharides
Language	English
Publishing date	2022-01-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-022-01708-1
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Zs.A 5178: Show issues

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Article ; Online: Role of Mitochondrial Dynamics in Cocaine's Neurotoxicity.

Wen, Shuheng / Aki, Toshihiko / Funakoshi, Takeshi / Unuma, Kana / Uemura, Koichi

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: The dynamic balance of mitochondrial fission and fusion maintains mitochondrial homeostasis and optimal function. It is indispensable for cells such as neurons, which rely on the finely tuned mitochondria to carry out their normal physiological ... ...

Abstract	The dynamic balance of mitochondrial fission and fusion maintains mitochondrial homeostasis and optimal function. It is indispensable for cells such as neurons, which rely on the finely tuned mitochondria to carry out their normal physiological activities. The potent psychostimulant cocaine impairs mitochondria as one way it exerts its neurotoxicity, wherein the disturbances in mitochondrial dynamics have been suggested to play an essential role. In this review, we summarize the neurotoxicity of cocaine and the role of mitochondrial dynamics in cellular physiology. Subsequently, we introduce current findings that link disturbed neuronal mitochondrial dynamics with cocaine exposure. Finally, the possible role and potential therapeutic value of mitochondrial dynamics in cocaine neurotoxicity are discussed.
MeSH term(s)	Cocaine/metabolism ; Cocaine/toxicity ; Homeostasis ; Mitochondria ; Mitochondrial Dynamics/physiology ; Neurons/metabolism
Chemical Substances	Cocaine (I5Y540LHVR)
Language	English
Publishing date	2022-05-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105418
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Article ; Online: Increased fatty acid synthesis and disturbed lipid metabolism in Neuro2a cells after repeated cocaine exposure: A preliminary study.

Nomura, Moeka / Wen, Shuheng / Unuma, Kana / Funakoshi, Takeshi / Aki, Toshihiko / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 695, Page(s) 149438

Abstract: Chronic use of cocaine prompts neurodegeneration and neuroinflammation. Lipids play pivotal roles in neuronal function and pathology. Although evidence correlates cocaine use with the alteration of lipid metabolism in blood and brain, the precise ... ...

Abstract	Chronic use of cocaine prompts neurodegeneration and neuroinflammation. Lipids play pivotal roles in neuronal function and pathology. Although evidence correlates cocaine use with the alteration of lipid metabolism in blood and brain, the precise mechanism remains to be elucidated. In this study, we explore the effect of cocaine on neuronal fatty acid profiles in vitro. Neuro2a cells following seven days of repeated exposure to cocaine (0, 600, 800, 1000 μM) showed apoptosis-irrelevant cell death, dysregulated autophagy, activation of atypical endoplasmic reticulum stress response, increased saturated and unsaturated fatty acid synthesis, and disrupted lipid metabolism. These preliminary findings indicated the association between lipid metabolism and cocaine-induced neurotoxicity, which should be beneficial for understanding the neurotoxicity of cocaine.
MeSH term(s)	Lipid Metabolism ; Fatty Acids/metabolism ; Apoptosis ; Lipogenesis ; Cocaine/toxicity ; Endoplasmic Reticulum Stress
Chemical Substances	Fatty Acids ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2023-12-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.149438
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