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Docosahexaenoic acid inhibits the phosphorylation of STAT3 and the growth and invasion of renal cancer cells.
Get PDF埼玉医科大学博士（医学）平成29年度Docosahexaenoic acid (DHA) has a variety of anti-tumor activities. The present study examined the anti-tumor activity of DHA in renal cancer cells and its underlying mechanisms of action. The effects of DHA on the viability and proliferation of the human renal cancer cell lines Caki-1 and 786-O were examined by an MTS assay and cell counting. In addition, cell cycle distribution and cell apoptosis were analyzed by flow cytometry and Annexin V staining, and modulation of cell mobility and invasiveness was assessed by wound healing and Matrigel invasion assays. Effects of DHA on intracellular signaling pathways were also analyzed by western blotting. It was observed that DHA significantly reduced the viability and proliferation of Caki-1 and 786-O cells (P<0.01). Specifically, there were increases in the sub-G1 and G2/M cell populations, as well as the percentages of cells exhibiting Annexin-positive and propidium-iodide-negative staining. In addition, the covered area in a wound and the number of cells invading through a Matrigel chamber decreased when Caki-1 or 786-O cells were treated with DHA. Phosphorylation of epidermal growth factor receptor was also upregulated following DHA treatment, while phosphorylation of signal transducer and activator of transcription 3 and Akt was downregulated. Collectively, these data suggest that DHA may be useful in the treatment of renal cell carcinoma
Comparison of Dopamine Transporter SPECT and 123I-MIBG Myocardial Scintigraphy to Assess Clinical Severity in Patients With Parkinson Disease.
Get PDF埼玉医科大学博士(医学)平成29年度The aim of our study was to evaluate the use of dopamine transporter (DAT) SPECT and I-MIBG myocardial scintigraphy to determine the clinical severity of Parkinson disease (PD), with a focus on motor impairments affecting activities of daily living (ADLs).Data for 65 consecutive PD patients who underwent both DAT and MIBG imaging were reviewed. Associations between imaging variables and Hoehn and Yahr (H&Y) staging or self-supportive care ratings were investigated. Univariate and multivariate regression analyses were performed to determine the factors associated with ADLs.After applying the exclusion criteria, 45 patients were analyzed (age, 73.1 ± 9.3 years; 23 males; H&Y stage 1: n = 12, stage 2: n = 14, stage 3: n = 10, stage 4: n = 5, and stage 5: n = 4; self-supportive care rating-dependent ADLs: n = 29). Dopamine transporter variables were significantly associated with the clinical severity of PD as assessed by H&Y staging, whereas MIBG variables were not. Dopamine transporter variables gradually decreased throughout progressive stages, whereas the MIBG variables changed only in the advanced stages. In a multivariate analysis including clinical and imaging variables, both lower DAT and MIBG uptakes were significantly associated with dependent ADL status (P = 0.028 and 0.034, respectively).In patients with PD, DAT SPECT and MIBG myocardial scintigraphy were associated with ADL status; DAT SPECT was a stronger indicator of severity than MIBG myocardial scintigraphy in the early and middle stages
Prevalence and molecular characteristics of defective mismatch repair epithelial ovarian cancer in a Japanese hospital-based population.
Get PDF埼玉医科大学博士(医学)平成30年度Background
The prevalence and molecular characteristics of defective mismatch repair epithelial ovarian cancers in the Japanese population have scarcely been investigated.
Methods
Immunohistochemistry for mismatch repair proteins (MLH1, MSH2, MSH6 and PMS2) was performed in formalin-fixed paraffin-embedded sections prepared from resected primary epithelial ovarian cancers in patients who underwent oophorectomy at our institution between April 2005 and September 2014. Genetic and/or epigenetic alterations of the mismatch repair genes were investigated in patients with loss of any mismatch repair proteins in the tumor.
Results
There were 305 patients with a median age of 54 years (range, 18–83 years). Loss of expression in the ovarian tumor of one or more mismatch repair proteins was observed in 3 of the 305 patients (0.98%): 2 patients MLH1/PMS2 loss and 1 patient showed MSH2/MSH6 loss. Genetic testing of these three patients failed to reveal any pathogenic germline mutations of MLH1 or MSH2. One patient with MLH1/PMS2 loss showed hypermethylation of the promoter region of MLH1. Somatic mutations were found in each of the alleles of MLH1 (c.545dupG and deletion of exons 2–19) in the other patient with MLH1/PMS2 loss. In the patient with MSH2/MSH6 loss, two somatic mutations were detected in MSH2 (c.229_230delAG and c.1861C>T), although we could not determine whether these mutations were biallelic or not.
Conclusions
The prevalence of defective mismatch repair epithelial ovarian cancer in the Japanese hospital-based population was extremely low. Molecular mechanism involved in such defective mismatch repair ovarian cancers seems to be epigenetic events through MLH1 promotor hypermethylation or somatically mutated mismatch repair genes without germline mismatch repair mutation
Multiple simultaneous intracerebral hemorrhages: Clinical presentations and risk factors.
Get PDF埼玉医科大学博士(医学)平成30年度OBJECTIVE:
Multiple simultaneous intracerebral hemorrhages (MSICH) are a rare clinical entity. The mechanism and risk factors have yet to be elucidated. The purpose of this study was to clarify clinical presentations and risk factors of MSICH compared with solitary intracerebral hemorrhages (ICH).
PATIENTS AND METHODS:
Medical records of 313 consecutive patients with ICH admitted to our institution between April 2011 and September 2014 were retrospectively reviewed. Seventeen cases of MSICH were identified, and 10 clinical and neuroimaging variables were compared between MSICH cases and solitary ICH cases using the unpaired t-test, chi-square test, and multiple logistic regression analysis.
RESULTS:
There were significant differences in size between larger hematomas (mean 59.2±69.1mL) and smaller hematomas (mean 1.7±2.1mL) in patients with MSICH (p=0.001). Larger hematoma volume was the only independent risk factor for MSICH in multiple logistic regression analysis (OR=1.012, 95%CI 1.004-1.021, p=0.004).
CONCLUSIONS:
Patients with MSICH have clinical characteristics and outcomes similar to patients with solitary ICH. They present with two significantly different hematoma sizes, both of which are significantly larger than patients with solitary ICH, suggesting that a larger hematoma can trigger smaller hematomas. A future prospective study with a larger number of patients will explore the precise mechanism of this rare entity
Early postoperative hyperlactatemia in elective neurosurgical patients: A retrospective study
Get PDF埼玉医科大学博士(医学)平成30年
Demeanor of rivaroxaban in activated/inactivated FXa.
Get PDF埼玉医科大学博士（医学）平成29年度Activated factor X (FXa) plays an important role in thrombin generation and inflammation. Factor X is not converted constitutively to FXa, but only after intrinsic clotting factors are activated and/or cellular injury occurs. Although rivaroxaban is one of direct FXa inhibitors, its function in the inactivated coagulation cascade is unclear. In human umbilical vein endothelial cells that natively express protease-activated receptor-1 and -2, high dose rivaroxaban did not alter gene transcripts including pro-inflammatory genes in DNA microarray. Upon FXa stimulation, the expressions of pro-inflammatory genes such as monocyte chemoattractant protein-1 (MCP-1), intracellular adhesion molecule-1, and interleukin-8 were maximally increased at 4 h after stimulation, and were suppressed by rivaroxaban. To confirm these results, quantitative polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA) for MCP-1 were performed. FXa evoked the expression of MCP-1 maximally at 4 h after stimulation, whereas MCP-1 displayed a different temporal activation in ELISA. Interestingly, rivaroxaban inhibited both time courses of MCP-1 expression. These results suggest that rivaroxaban may not influence gene modulation in the inactivated coagulation state, but can attenuate the endothelial damage evoked by FXa and pro-inflammatory cytokine genes