Institution
Hyogo College of Medicine
Education•Nishinomiya, Hyôgo, Japan•
About: Hyogo College of Medicine is a education organization based out in Nishinomiya, Hyôgo, Japan. It is known for research contribution in the topics: Cancer & Transplantation. The organization has 5030 authors who have published 10629 publications receiving 258734 citations. The organization is also known as: Hyōgo ika daigaku.
Topics: Cancer, Transplantation, Population, Medicine, Survival rate
Papers published on a yearly basis
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TL;DR: It is concluded that indeed the 2275 putative CK2 sites (accounting for 20.9% of the whole phosphoproteome they belong to), or at least the great majority of these are generated by CK2.
176 citations
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TL;DR: To assess the in vivo essential role of ATF4, mice lacking ATF4 are generated by gene targeting and shown to have a variety of combinatorial diversity in gene regulation.
Abstract: Background: Activating transcription factor-4 (ATF4)—also termed CREB2, C/ATF, and TAXREB67—is a basic-leucine zipper (bZip) transcription factor that belongs to the ATF/CREB family. In addition to its own family members, ATF4 can also form heterodimers with other related but distinct bZIP proteins such as the C/EBP, AP-1 and Maf families, which may give rise to a variety of combinatorial diversity in gene regulation. In order to assess the in vivo essential role of ATF4, we have generated mice lacking ATF4 by gene targeting.
Results: ATF4-deficient mice exhibited severe microphthalmia. Although ATF4-deficient eyes revealed a normal gross lens structure up to embryonic day 14.5, later on the ATF4-deficient lens, degenerated due to apoptosis without the formation of lens secondary fibre cells. Retinal development was normal in the mutant mice. The lens-specific expression of ATF4 in the mutant mice led not only to the recovery of lens secondary fibres but also to the induction of hyperplasia of these fibres.
Conclusion: These results demonstrated that ATF4 is essential for the later stages of lens fibre cell differentiation.
176 citations
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TL;DR: The finding that P2X3 mRNA in ATF3‐ir neurons decreased significantly after injury indicates that axotomized neurons decreased the expression of P2x3 mRNA, despite the increase in P2 X3 mRNA relative to the total number of sensory ganglion neurons.
Abstract: The P2X(3) receptor is a ligand-gated cation channel activated by the binding of extracellular adenosine 5'-triphosphate (ATP), an agent that has been suggested to have a role in the nociceptive pathway after tissue and nerve injury. After peripheral nerve injury, both down regulation and up regulation of the P2X(3) receptor in sensory ganglion neurons have been observed. The purpose of this study was to examine the precise regulation of P2X(3) mRNA expression in primary sensory neurons after nerve injury. We used two nerve injury models in the rat, the transection of the tibial and common peroneal nerves and the transection of the infraorbital nerve, and observed dorsal root ganglion (DRG) and trigeminal ganglion neurons, respectively. P2X(3) mRNA in both neuron populations was detected by in situ hybridization with an oligonucleotide probe that was confirmed by Northern blot analysis. To identify axotomized neurons, we examined the expression of activating transcription factor 3 (ATF3), which is regarded as a neuronal-injury marker, using immunohistochemistry. In the DRG, the mean percentage of P2X(3) mRNA-labeled neurons relative to the total number of neurons increased from 32.7% in the naive rats to 42.7% at 3 days after injury. The mean percentage of P2X(3) mRNA-labeled neurons in ATF3 immunoreactive (ir) neurons was 29.5% at 3 postoperative days, which gradually decreased to 11.2% at 28 days after injury. In the trigeminal ganglion, the mean percentage of P2X(3) mRNA-labeled neurons was 36.9% at 3 days after injury, versus 26.0% in the naive rats. In the ATF3-ir neurons, the mean percentage of P2X(3) mRNA-labeled neurons was 25.3% at 1 postoperative day and was reduced to 6.1% at 28 postoperative days. The finding that P2X(3) mRNA in ATF3-ir neurons decreased significantly after injury indicates that axotomized neurons decreased the expression of P2X(3) mRNA, despite the increase in P2X(3) mRNA relative to the total number of sensory ganglion neurons. These data strongly suggest that P2X(3) mRNA expression increases in intact neurons and that P2X(3) mRNA in intact neurons may play a role in the pathomechanism of post-nerve injury in primary sensory neurons.
175 citations
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TL;DR: Nivolumab met the primary endpoint as second- or third-line treatment for patients with MPM and showed promising efficacy with manageable toxicity and adverse events and treatment-related AEs.
Abstract: Purpose: Malignant pleural mesothelioma (MPM) is a rare and aggressive malignancy with poor prognosis. MPM patients who do not respond to standard first-line chemotherapy have limited treatment options. We evaluated the efficacy and safety of nivolumab, an immune checkpoint inhibitor, for the treatment of advanced or metastatic MPM. Patients and Methods: Japanese patients with unresectable, advanced, or metastatic MPM resistant or intolerant to ≤2 regimens of chemotherapy and ≥1 measurable lesion(s) were enrolled. Patients received nivolumab 240 mg intravenously every 2 weeks until progressive disease or unacceptable toxicity. The primary endpoint was objective response rate by central assessment according to the Modified Response Evaluation Criteria in Solid Tumors. Adverse events (AEs) and treatment-related AEs (TRAEs) were evaluated. Results: Thirty-four patients were enrolled between July 2016 and October 2016. Median follow-up was 16.8 (range: 1.8-20.2) months. Ten (29%, 95% confidence interval, 16.8-46.2) patients showed a centrally assessed objective response. The objective response rates were 26% (7/27), 67% (2/3), and 25% (1/4) patients for epithelioid, sarcomatoid, and biphasic histological subtypes, respectively. Median duration of response was 11.1 months with a 68% disease control rate. Median overall survival and progression-free survival were 17.3 and 6.1 months, respectively. The objective response rate was 40% with programmed death-ligand 1 (PD-L1) expression ≥1% and 8% with
175 citations
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TL;DR: This review will focus on inhalationalAnesthetic neuroprotection during cerebral ischemia and inhalational anesthetic preconditioning before ischemic brain injury and mechanisms underlying volatile anesthetic neuro protection and preconditionsing will be examined.
Abstract: This review will focus on inhalational anesthetic neuroprotection during cerebral ischemia and inhalational anesthetic preconditioning before ischemic brain injury. The limitations and challenges of past and current research in this area will be addressed before reviewing experimental and clinical studies evaluating the effects of inhalational anesthetics before and during cerebral ischemia. Mechanisms underlying volatile anesthetic neuroprotection and preconditioning will also be examined. Lastly, future directions for inhalational anesthetics and ischemic brain injury will be briefly discussed.
175 citations
Authors
Showing all 5043 results
Name | H-index | Papers | Citations |
---|---|---|---|
Shizuo Akira | 261 | 1308 | 320561 |
James G. Fujimoto | 165 | 1115 | 116451 |
Kiyoshi Takeda | 129 | 416 | 109817 |
David A. Brenner | 128 | 499 | 52756 |
Akira Yamamoto | 117 | 1999 | 74961 |
Osamu Takeuchi | 116 | 288 | 90116 |
Takaomi C. Saido | 90 | 352 | 27802 |
Taroh Kinoshita | 87 | 379 | 23714 |
Takenobu Kamada | 86 | 700 | 27535 |
Kazuhiko Nakagawa | 84 | 917 | 41018 |
Takashi Yamamoto | 84 | 1401 | 35169 |
Taro Kawai | 83 | 141 | 66916 |
Hiroo Imura | 83 | 781 | 29276 |
Kunio Matsumoto | 82 | 465 | 25131 |
Yukihiko Kitamura | 80 | 419 | 37965 |