Institution
Kumamoto University
Education•Kumamoto, Kumamoto, Japan•
About: Kumamoto University is a education organization based out in Kumamoto, Kumamoto, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 19602 authors who have published 35513 publications receiving 901260 citations. The organization is also known as: Kumamoto Daigaku.
Topics: Population, Cancer, Cell culture, Stem cell, Cellular differentiation
Papers published on a yearly basis
Papers
More filters
••
TL;DR: Extensive thin-section CT abnormalities indicative of fibroproliferative changes were independently predictive of poor prognosis in patients with a clinically early stage of ARDS.
Abstract: Purpose: To retrospectively evaluate whether the thin-section computed tomographic (CT) appearance has prognostic value for prediction of mortality, number of ventilator-free days (ie, days without mechanical ventilation), and 28-day risk of barotrauma in patients with a clinically early stage of acute respiratory distress syndrome (ARDS) from diverse causes. Materials and Methods: Institutional review board approval and informed consent were obtained. Two independent observers who were blinded to patient outcomes retrospectively evaluated the thin-section CT scans obtained within 7 days after clinical ARDS onset in 26 survivors and 18 nonsurvivors. Of 44 patients, there were 37 men and seven women (mean age ± standard deviation, 61.8 years ± 15.6). CT findings were graded on a scale of 1–6 that corresponded with consecutive pathologic phases: score of 1, normal attenuation; score of 2, ground-glass attenuation; score of 3, consolidation; score of 4, ground-glass attenuation associated with traction bronc...
169 citations
••
TL;DR: In this paper, the role of free radicals in the pathogenesis of virus infection and in viral mutation is discussed. But, the authors do not consider the effect of NO on the host's immune response.
Abstract: Oxygen radicals and nitric oxide (NO) are generated in excess in a diverse array of microbial infections. Emerging concepts in free radical biology are now shedding light on the pathogenesis of various diseases. Free-radical induced pathogenicity in virus infections is of great importance, because evidence suggests that NO and oxygen radicals such as superoxide are key molecules in the pathogenesis of various infectious diseases. Although oxygen radicals and NO have an antimicrobial effect on bacteria and protozoa, they have opposing effects in virus infections such as influenza virus pneumonia and several other neurotropic virus infections. A high output of NO from inducible NO synthase, occurring in a variety of virus infections, produces highly reactive nitrogen oxide species, such as peroxynitrite, via interaction with oxygen radicals and reactive oxygen intermediates. The production of these various reactive species confers the diverse biological functions of NO. The reactive nitrogen species cause oxidative tissue injury and mutagenesis through oxidation and nitration of various biomolecules. The unique biological properties of free radicals are further illustrated by recent evidence showing accelerated viral mutation by NO-induced oxidative stress. NO appears to affect a host's immune response, with immunopathological consequences. For example, NO is reported to suppress type 1 helper T cell-dependent immune responses during infections, leading to type 2 helper T cell-biased immunological host responses. NO-induced immunosuppression may thus contribute to the pathogenesis of virus infections and help expansion of quasispecies population of viral pathogens. This review describes the pathophysiological roles of free radicals in the pathogenesis of viral disease and in viral mutation as related to both nonspecific inflammatory responses and immunological host reactions modulated by NO.
169 citations
••
TL;DR: If trypsin activation (due to excessive stimulation of pancreatic acinar cells) exceeds the capacity of PSTI, a subsequent cascade of events leads to the activation of various proteases that damage cells, and this can be interpreted as the main causative event of pancreatitis onset.
Abstract: Trypsin activity is properly suppressed in the pancreatic acinar cells under normal conditions. A small amount of trypsinogen is converted to active trypsin and inactivated by pancreatic secretory trypsin inhibitor (PSTI), thereby preventing damage to pancreatic acinar cells as a first line of defense. However, if trypsin activation (due to excessive stimulation of pancreatic acinar cells) exceeds the capacity of PSTI, a subsequent cascade of events leads to the activation of various proteases that damage cells. This can be interpreted as the main causative event of pancreatitis onset. Trypsin produced in and secreted from the pancreatic acinar cells activates protease activated receptor-2 (PAR-2), which is present at high densities on the luminal surfaces of pancreatic acinar cells and duct cells. Results of PAR-2 activation are the production of cytokines and the regulation of exocrine function via a negative feedback loop. Thus, the actions of trypsin, trypsin inhibitor (PSTI), and trypsin receptor (PAR-2) in the pancreas are strongly interconnected.
169 citations
••
TL;DR: In this paper, the authors compared high-resolution computed tomography (CT) findings between 10 survivors and 21 nonsurvivors of acute interstitial pneumonia and evaluated whether the CT findings were predictive of patients' response to treatment.
Abstract: This study compared high-resolution computed tomography (CT) findings between 10 survivors and 21 nonsurvivors of acute interstitial pneumonia and evaluated whether the CT findings were predictive of patients' response to treatment. The survivor and nonsurvivor groups with pathologically or clinically diagnosed acute interstitial pneumonia were similar in age, sex, disease duration, and lung injury score. Retrospective, subjective evaluations of the CT scans were conducted by two independent observers without knowledge of patient outcomes. CT findings were graded on a one to six scale corresponding to consecutive pathologic phases as follows: areas of (1) normal attenuation, (2) ground-glass attenuation, (3) consolidation, (4) ground-glass attenuation associated with traction bronchiolectasis or bronchiectasis, (5) consolidation associated with traction bronchiolectasis or bronchiectasis, and (6) honeycombing. An overall score was obtained by quantifying the extent of each abnormality in three lung zones in each lung. The extent of ground-glass attenuation or consolidation associated with traction bronchiolectasis or bronchiectasis was less in survivors than nonsurvivors (p = 0.004 and p = 0.009, respectively). Architectural distortion was less frequent, and ground-glass attenuation or consolidation without traction bronchiolectasis or bronchiectasis was more extensive in survivors than in nonsurvivors (p = 0.007, p = 0.002, and p = 0.029, respectively). Overall CT scores of survivors were significantly lower than those of nonsurvivors (p = 0.0003). A CT score of less than 245 had an 80% positive and a 90% negative predictive value for survival. There was good interobserver agreement in the assessment of the CT findings (Kappa 0.75). The results indicate that CT assessment is potentially helpful in predicting patient prognosis in acute interstitial pneumonia regardless of the degree of physiologic abnormality.
169 citations
•
TL;DR: In co-cultures of normal mouse bone marrow cells with fibroblast cell lines prepared from the lungs of the op/op mice, a defective differentiation of monocytes into macrophages was confirmed, supporting previous evidence that the fibro Blast cell lines of the mutant mouse failed to produce functional macrophage colony-stimulating factor (M-CSF/CSF-1).
Abstract: Examination of the op/op mouse disclosed marked reduction and abnormal differentiation of osteoclasts in the bones and of tissue-specific macrophages in various visceral organs and tissues. Most of these macrophages were immature as judged by ultrastructural criteria. In co-cultures of normal mouse bone marrow cells with fibroblast cell lines prepared from the lungs of the op/op mice, a defective differentiation of monocytes into macrophages was confirmed, supporting previous evidence that the fibroblast cell lines of the mutant mouse failed to produce functional macrophage colony-stimulating factor (M-CSF/CSF-1). In such co-cultures, however, a small number of macrophages apparently mature under the influence of granulocyte/macrophage colony-stimulating factor (GM-CSF) produced by the op/op fibroblast cell lines. In the mutant mice, the numbers of macrophages in the uterine wall and ovaries were severely reduced. Compared with the tissues of normal littermates, those of the mutants contained about 60% fewer macrophages in many tissues. This suggests that an M-CSF-independent population of macrophages is derived from granulocyte/macrophage-colony-forming cells (GM-CFC) or earlier hematopoietic progenitors.
169 citations
Authors
Showing all 19645 results
Name | H-index | Papers | Citations |
---|---|---|---|
Fred H. Gage | 216 | 967 | 185732 |
George D. Yancopoulos | 158 | 496 | 93955 |
Kenji Kangawa | 153 | 1117 | 110059 |
Tasuku Honjo | 141 | 712 | 88428 |
Hideo Yagita | 137 | 946 | 70623 |
Masashi Yanagisawa | 130 | 524 | 83631 |
Kazuwa Nakao | 128 | 1041 | 70812 |
Kouji Matsushima | 124 | 590 | 56995 |
Thomas E. Mallouk | 122 | 549 | 52593 |
Toshio Hirano | 120 | 401 | 55721 |
Eisuke Nishida | 112 | 349 | 45918 |
Hiroaki Shimokawa | 111 | 949 | 48822 |
Bernd Bukau | 111 | 271 | 38446 |
Kazuo Tsubota | 105 | 1379 | 48991 |
Toshio Suda | 104 | 580 | 41069 |