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71.
Summary In inbred mice of a low leukemic strain, dd, urethan was proved to induce thymic lymphoma when it was repeatedly administered early in life. At the age of 135 to 150 days the incidence of the tumor was 6/23 in males and 12/24 in females. In 8 males (8/17) and 6 females (6/12) of mice macroscopically free of the tumor, the thymus revealed microscopically early neoplastic changes. Thus the cumulative incidence of both neoplastic and early neoplastic cases was 14/23 for males and 18/24 for females. The urethan-induced thymic lymphoma was similar, in both histological characteristics and histogenesis, to that induced by other agents. The early lymphomatous changes appeared as replenishment with immature lymphocytes in the cortex after depletion of cortical small lymphocytes. The changes preceding lymphoma were often found in one lobe only of the thymus.
With 7 Figures in the Text 相似文献
Zusammenfassung An Mäusen eines japanischen Inzuchtstammes (dd) ließ sich zeigen, daß Urethan ein Thymuslymphom hervorrufen kann, wenn es in den ersten Lebensmonaten wiederholt gegeben wird. Bei 6/23 Männchen und 12/24 Weibchen traten im Alter von 135–150 Tagen makroskopisch erkennbare Tumoren auf. Bei 8 Männchen (8/17) und 6 Weibchen (6/12) von den Tieren, die makroskopisch noch frei von Tumoren waren, zeigte der Thymus mikroskopisch frühneoplastische Veränderungen. Die Häufigkeit der neoplastischen und frühneoplastischen Fälle zusammen war also 14/23 bei den Männchen und 18/24 bei den Weibchen. Das Urethan-Lymphom des Thymus war hinsichtlich Histologie und Histogenese identisch mit den von anderen Agentien erzeugten Lymphomen. Die Frühveränderungen sahen aus wie eine regenerative Proliferation undifferenzierter Lymphocyten in der Rinde. Oft wurden sie nur in einem Thymuslappen beobachtet.
With 7 Figures in the Text 相似文献
72.
Relation of circulating interleukin-6 to left ventricular remodeling in patients with reperfused anterior myocardial infarction 总被引:3,自引:0,他引:3
Ohtsuka T Hamada M Inoue K Ohshima K Sujzuki J Matsunaka T Ogimoto A Hara Y Shigematsu Y Higaki J 《Clinical cardiology》2004,27(7):417-420
BACKGROUND: During the remodeling process after myocardial infarction (MI), the expression of proinflammatory cytokines is enhanced in the myocardium. However, only a few clinical studies have been conducted on cytokine involvement in left ventricular (LV) remodeling after MI. HYPOTHESIS: Circulating proinflammatory cytokines may be involved in LV remodeling in patients with reperfused MI. METHODS: We studied 25 patients with acute anterior MI who had undergone coronary reperfusion therapy, and 10 normal control subjects with no cardiac disease. In all patients, LV ejection fraction, end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were determined using left ventriculography at the acute phase and 6 months after onset. The delta EDVI and delta ESVI were calculated as the value of LV volume reduction, suggesting LV reverse remodeling. Serum levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha were measured using enzyme-linked immunosorbent assay. RESULTS: Serum levels of IL-6 and TNF-alpha at the acute phase were significantly higher in patients with MI than in control subjects (both p < 0.05). The IL-6 levels correlated well negatively with delta EDVI (r = 0.779, p = 0.039), whereas no correlation was found for TNF-alpha. According to multivariate analysis, IL-6 at the acute phase was a significant independent predictor for LV remodeling after reperfused MI (p = 0.007). CONCLUSIONS: Circulating IL-6 levels correlated closely with LV geometric changes during the remodeling process in patients with reperfused MI. Our study addresses the usefulness of another marker for LV remodeling after MI. 相似文献
73.
Comparison of micafungin and voriconazole as empirical antifungal therapies in febrile neutropenic patients with hematological disorders: a randomized controlled trial 下载免费PDF全文
74.
Wijelath ES Rahman S Namekata M Murray J Nishimura T Mostafavi-Pour Z Patel Y Suda Y Humphries MJ Sobel M 《Circulation research》2006,99(8):853-860
We describe extracellular interactions between fibronectin (Fn) and vascular endothelial growth factor (VEGF) that influence integrin-growth factor receptor crosstalk and cellular responses. In previous work, we found that VEGF bound specifically to fibronectin (Fn) but not vitronectin or collagens. Herein we report that VEGF binds to the heparin-II domain of Fn and that the cell-binding and VEGF-binding domains of Fn, when physically linked, are necessary and sufficient to promote VEGF-induced endothelial cell proliferation, migration, and Erk activation. Using recombinant Fn domains, the C-terminal heparin-II domain of Fn (type III repeats 13 to 14) was identified as a key VEGF-binding site. Mutation of the heparin-binding residues on FnIII(13-14) abolished VEGF binding, and peptides corresponding to the heparin-binding sequences in FnIII(13-14) inhibited VEGF binding to Fn. Fn fragments containing both the alpha5beta1 integrin-binding domain (III 9 to 10) and the VEGF-binding domain (III 13 to 14) significantly enhanced VEGF-induced EC migration and proliferation and induced strong phosphorylation of the VEGF receptor and Erk. Neither the cell-binding or VEGF-binding fragment of Fn alone had comparable VEGF-promoting effects. These results suggest that the mechanism of VEGF/Fn synergism is mediated extracellularly by the formation of a novel VEGF/Fn complex requiring both the cell-binding and VEGF-binding domains linked in a single molecular unit. These data also highlight a new function for the Fn C-terminal heparin-binding domain that may have important implications for angiogenesis and tumor growth. 相似文献
75.
Shinjiro Hoshino Takayuki Hosoi Masataka Shiraki Hajime Orimo Yasuyoshi Ouchi Satoshi Inoue 《Geriatrics & Gerontology International》2003,3(2):101-105
Background: Estrogen deficiency in postmenopausal women causes an increased production of proinflammatory cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α. These cytokines are associated with an increase of bone turnover and an acceleration of bone loss. Tumor necrosis factor-α is known to promote osteoclastogenesis via TNFR1, one of the tumor necrosis factor receptors (TNFR). Therefore, the purpose of the present report was to investigate the association of TNFR1 gene polymorphism with bone mineral density (BMD) in postmenopausal Japanese women.
Methods: The question of whether a polymorphism of the TNFR1 gene would correlate with osteoporosis in 320 unrelated healthy postmenopausal women in Japan, was investigated. A single nucleotide polymorphism (SNP) located at Pro12 (CCA to CCG) in exon 1 of TNFR1 was utilized.
Results: The subjects were categorized into three genotypes: AA, AG, and GG. The frequency of each genotype was 72.2%, 23.8%, and 4.0%, respectively. The association of this polymorphism with BMD of the lumbar spine and total body, and several bone metabolic markers was then examined. Concerning the TNFR1 gene, the AA group had significantly low total body BMD, compared with the AG + GG group (Z score; 0.285 vs 0.568; P = 0.03), although BMD of the lumbar spine was not statistically different.
Conclusion: These results suggest an association between this SNP of the TNFR1 gene and BMD, and an involvement of TNFR1 in postmenopausal osteoporosis among Japanese. 相似文献
Methods: The question of whether a polymorphism of the TNFR1 gene would correlate with osteoporosis in 320 unrelated healthy postmenopausal women in Japan, was investigated. A single nucleotide polymorphism (SNP) located at Pro12 (CCA to CCG) in exon 1 of TNFR1 was utilized.
Results: The subjects were categorized into three genotypes: AA, AG, and GG. The frequency of each genotype was 72.2%, 23.8%, and 4.0%, respectively. The association of this polymorphism with BMD of the lumbar spine and total body, and several bone metabolic markers was then examined. Concerning the TNFR1 gene, the AA group had significantly low total body BMD, compared with the AG + GG group (Z score; 0.285 vs 0.568; P = 0.03), although BMD of the lumbar spine was not statistically different.
Conclusion: These results suggest an association between this SNP of the TNFR1 gene and BMD, and an involvement of TNFR1 in postmenopausal osteoporosis among Japanese. 相似文献
76.
Nakayama Nobuaki Uemura Hayato Uchida Yoshihito Imai Yukinori Tomiya Tomoaki Terai Shuji Yoshiji Hitoshi Genda Takuya Ido Akio Inoue Kazuaki Kato Naoya Sakaida Isao Shimizu Masahito Takikawa Yasuhiro Abe Masanori Abe Ryuzo Chayama Kazuaki Hasegawa Kiyoshi Inui Ayano Kasahara Mureo Ohira Hiromasa Tanaka Atsushi Takikawa Hajime Mochida Satoshi 《Journal of gastroenterology》2021,56(12):1092-1106
Journal of Gastroenterology - The significance of the 2018 Japanese diagnostic criteria for acute-on-chronic liver failure (ACLF) has not yet been evaluated. A nationwide survey was performed for... 相似文献
77.
Atsushi Miyamoto Atsuko Kurosaki Shuhei Moriguchi Yui Takahashi Kazumasa Ogawa Kyoko Murase Shigeo Hanada Hironori Uruga Hisashi Takaya Nasa Morokawa Takeshi Fujii Junichi Hoshino Kazuma Kishi 《Respiratory investigation》2019,57(2):140-149
Background
This study aimed to determine the radiologic predictors and clarify the clinical features related to survival in patients with combined pulmonary fibrosis and emphysema (CPFE) and lung cancer.Methods
We retrospectively reviewed the medical chart data and high-resolution computed tomography (HRCT) findings for 81 consecutive patients with CPFE and 92 primary lung cancers (70 men, 11 women; mean age, 70.9 years). We selected 8 axial HRCT images per patient, and visually determined the normal lung, modified Goddard, and fibrosis scores. Multivariate analysis was performed using the Cox proportional hazards regression model.Results
The major clinical features were a high smoking index of 54.8 pack-years and idiopathic pulmonary fibrosis (n = 44). The major lung cancer profile was a peripherally located squamous cell carcinoma (n = 40) or adenocarcinoma (n = 31) adjacent to emphysema in the upper/middle lobe (n = 27) or fibrosis in the lower lobe (n = 26). The median total normal lung, modified Goddard, and fibrosis scores were 10, 8, and 8, respectively. TNM Classification of malignant tumors (TNM) stage I, II, III, and IV was noted in 37, 7, 26, and 22 patients, respectively. Acute exacerbation occurred in 20 patients. Multivariate analysis showed that a higher normal lung score and TNM stage were independent radiologic and clinical predictors of poor survival at the time of diagnosis of lung cancer.Conclusions
A markedly reduced area of normal lung on HRCT was a relevant radiologic predictor of survival. 相似文献78.
79.
We have investigated the potential of neurotropic microbes to invade the central nervous system (CNS) via the peripheral nervous system. Herpes simplex virus type 1 (HSV-1) strain KH6 and herpes simplex virus type 2 (HSV-2) strain 186 were found to infect chemosensory neurons in the vomeronasal organ (the pheromone detector) following intranasal inoculation of mice. HSV-1 strain KH6 infection was further transmitted to the accessory olfactory bulb (first relay), the medial amygdala (second relay), and the bed nucleus of the stria terminalis and the ventromedial hypothalamus (third relay). HSV-1 strain KH6 also targeted the olfactory and trigeminal systems. HSV-2 strain 186 predominantly attacked the brainstem including the trigeminal system. While both viruses did not induce apoptosis in infected chemosensory neurons, they did in infected brain tissue. These results suggest that neurotropic viruses can invade the brain by infecting vomeronasal chemosensory neurons and that the restrained induction of apoptosis in the infected neurons may facilitate viral transmission to the CNS. 相似文献
80.
Mitsuhashi N Tanaka Y Kubo S Ogawa S Hayashi C Uchino H Shimizu T Watada H Kawasumi M Onuma T Kawamori R 《Endocrine journal》2004,51(6):545-550
The aim of this study was to investigate the effect of cilostazol, a cAMP phosphodiesterase inhibitor, on carotid artery intima-media thickness (IMT) and on the incidence of cardiovascular events in Japanese subjects with type 2 diabetes. A total of 62 type 2 diabetic subjects were allocated equally to the cilostazol treatment group (n = 31) and the control group (n = 31). Carotid IMT was evaluated before and after treatment using B-mode ultrasonography. After the study period (mean +/- SD: 2.6 +/- 0.17 years), carotid IMT showed a significantly greater increase in the control group than in the cilostazol group (0.12 +/- 0.14 mm vs. 0.04 +/- 0.02 mm, p < 0.05). In the control group, 1 out of 31 patients suffered from symptomatic cerebral infarction and 1 had angina pectoris during the observation period. On the other hand, no subject in the cilostazol group developed cardiovascular events during the study period. At baseline, the diabetic patients given cilostazol had a significantly lower HbA1c level than the control subjects, but the other atherosclerotic risk factors (BMI, blood pressure, and serum lipids) and the duration of diabetes did not differ between the two groups. These results indicate that cilostazol therapy can attenuate the increase of carotid artery IMT in Japanese subjects with type 2 diabetes. 相似文献