Publications by authors named "Katada R"

Pulmonary metastasis of ameloblastoma is a rare associated with the histopathologically plexiform types of ameloblastoma. In this report, we present an exceptionally rare case of pulmonary metastatic ameloblastoma without local recurrence, emerging 12 years post-initial resection. A female patient, initially diagnosed with mandibular desmoplastic ameloblastoma, revealed masses in both lung fields of the lung on chest radiography, while chest computed tomography revealed more than 10 nodules in both lungs.

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Background: Pneumoparotid is a rare disease associated with retrograde airflow into the ductal system. There is no established treatment for this disease, which has no known complications. Mouth puffing and playing wind instruments are known to be the causes of this disease.

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Abstract Background/purpose: The dentition shows individual characteristics and dental structures are stable with respect to postmortem decomposition, allowing the dentition to be used as an effective tool in forensic dentistry. We developed an automatic identification system using panoramic radiographs (PRs) with a deep learning method.

Materials And Methods: In total, 4966 PRs from 1663 individuals with various changes in image characteristics due to various dental treatments were collected.

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Cerebral edema following cerebral infarction can be severe and directly affect mortality and mobility. Exercise therapy after cerebral infarction is an effective therapeutic approach; however, the molecular mechanism remains unclear. Myokines such as interleukin-1 receptor antagonist (IL-1RA) are released during skeletal muscle contraction with effects on other organs.

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A case of delayed epistaxis from the mucosa behind the right side of the inferior nasal mucosa 11 days after orthognathic surgery by Le Fort I osteotomy is presented. The patient was a 31-year-old man who underwent orthognathic surgery under general anesthesia. No abnormal findings were found during or after the operation.

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Small bowel obstruction due to broad ligament hernia (BLH) is a rare type of internal hernia. Preoperative diagnosis is difficult, as clinical symptoms and imaging results are often nonspecific. BLH has a high risk of strangulation and requires surgery for the reduction of herniated bowels.

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Salivary gland hypofunction due to radiation therapy for head and neck cancer or Sjögren syndrome may cause various oral diseases, which can lead to a decline in the quality of life. Cell therapy using salivary gland stem cells is a promising method for restoring hypofunction. Herein, we show that salivary gland-like cells can be induced from epithelial tissues that were transdifferentiated from mouse embryonic fibroblasts (MEFs).

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Although stem cell aging leads to a decline in tissue homeostasis and regenerative capacity, it remains unclear whether salivary gland stem cell function changes during this process. However, the salivary glands are gradually replaced by connective tissue during aging. Here, we show a decline in the stem cell ability of CD133-positive stem/progenitor cells in the salivary glands of aged mice.

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Brain edema following brain infarction affects mobility and mortality. The mechanisms underlying this process remain to be elucidated. Animal studies have shown that aquaporin-4 (AQP4) expression in astrocytes increases after stroke, and its deletion significantly reduces brain swelling.

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Article Synopsis
  • Wischnewski spots, dark-brown-colored spots in the gastric mucosa, are often seen in hypothermia patients, but their formation mechanisms are unclear.
  • Research indicates that hypothermia may trigger gastric acid and pepsin secretion, as experiments showed that cold temperatures increase the mRNA expression of gastrin and enhance the activity of the H,K-ATPase pump.
  • These changes lead to increased acidity and pepsin levels in the stomach, which may cause small hemorrhages in the gastric mucosa, resulting in the appearance of Wischnewski spots during fatal hypothermia.
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Post-mortem detection of pathogenetic microorganisms in severe infectious death is significantly important for diagnosing the cause of death as well as for public health. However, it is difficult to recognize whether a microorganism detected from post-mortem materials is truly pathogenic or not. We report a case of severe soft tissue infection due to Streptococcus oralis subsp.

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was recently described as a novel species, and some strains are highly virulent. We detected in infected tissue sampled by necropsy. In order to characterize and confirm the virulence of this species, whole-genome sequencing of the pure cultured bacterium was performed.

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Ethanol increases brain aquaporin-4 (AQP4) expression after traumatic brain injury (TBI), leading to augment mortality and morbidity after TBI. AQP4 is regulated by sodium ion channels/transporters. Ethanol affects the ion channels/transporters.

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Aquaporin-4 (AQP4), the principal water channel in astrocytes, is involved in brain water movement, inflammation, and neuroexcitation. In this study, there was strong neuroprotection in mice lacking AQP4 in a model of global cerebral ischemia produced by transient, bilateral carotid artery occlusion (BCAO). Survival and neurological outcome were greatly improved in the AQP4(-/-) vs.

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Alcohol-induced osteonecrosis of the femoral head (ONFH) is observed in alcohol abusers and patients with alcoholic fatty liver disease. It has been reported that Toll-like receptor 4 (TLR4) signalling plays a crucial role in the pathogenesis of alcoholic fatty liver disease. We previously reported a corticosteroid-induced ONFH rat model, and suggested that TLR4 signalling contributes to the pathogenesis of ONFH.

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To identify lung findings specific to fatal hypothermia on postmortem computed tomography (CT) imaging. Whole body CT scans were performed followed by full autopsy to investigate causes of death. There were 13 fatal hypothermia cases (group A) and 118 with other causes of death (group B).

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The hip joint is one of the major structures in the human body and the resultant force acting through the hip joint is 300% of body weight. Therefore, weight bearing, as a cause of ischaemia, may contribute to the development of non-traumatic osteonecrosis of the femoral head (ONFH). However, it remains unclear whether weight bearing is related to the development of non-traumatic ONFH.

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Withdrawal from chronic alcohol cause the persistent molecular alteration, such as changes in the release of neurotransmitter and gene expression. The alterations are thought to increase in the risk of relapse. Recent studies suggest that the gene expression regulated by histone acetylation may play an important role in the dependence of abused drugs, including of ethanol.

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Osteonecrosis of the femoral head (ONFH), the pathogenesis of which remains unclear, has been observed in autoimmune disease patients treated with corticosteroids. Recently, it has been shown that anti-tripartite motif-containing 21 (TRIM21) autoantibodies, which are often present in patients with systemic lupus erythematosis and Sjögren's syndrome, inhibit the E3 ligase activity of TRIM21. TRIM21 negatively regulates nuclear factor-κB (NF-κB) and interferon regulatory factors (IRFs) 3 and 7, three downstream transcription factors, via toll-like receptor 4 signaling.

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Alcohol consumption augments brain edema by expression of brain aquaporin-4 after traumatic brain injury. However, how ethanol induces brain aquaporin-4 expression remains unclear. Aquaporin-4 can operate with some of ion channels and transporters.

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[Effects of alcohol consumption on traumatic brain injury].

Nihon Arukoru Yakubutsu Igakkai Zasshi

October 2011

It has been well known that alcohol consumption affects traumatic brain injury. The mechanism of detrimental effect of ethanol on traumatic brain injury has not been clarified. This review focused on the relationship among traumatic brain injury, ethanol and aquaporin-4.

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We previously reported that ethanol consumption affects morbidity and mortality after traumatic brain injury (TBI) by accelerating brain edema via oxidative stress after TBI. Aquaporin-4 (AQP4), a water channel, is involved in brain edema formation. In this study, we found that acute ethanol administration increased AQP4 expression after TBI, leading to severe brain edema in rats.

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