External Gauge Invariance and Anomaly in BS Vertices and Boundstates

A systematic method is given for obtaining consistent approximations to the Schwinger-Dyson(SD) and Bethe-Salpeter(BS) equations which maintain the external gauge invariance. We show that for any order of approximation to the SD equation there is a corresponding approximation to the BS equations such that the solutions to those equations satisfy the Ward-Takahashi identities of the external gauge symmetry. This formulation also clarifies the way how we can calculate the Green functions of current operators in a consistent manner with the gauge invariance and the axial anomaly. We show which type of diagrams for the $\pi^0\rightarrow\gamma\gamma$ amplitude using the pion BS amplitude give result consistent with the low-energy theorem. An interesting phenomenon is observed in the ladder approximation that the low energy theorem is saturated by the zeroth order terms in the external momenta of the pseudoscalar BS amplitude and the vector vertex functions.Comment: 30 pages, plain TeX (using `phyzzx' macro), 17 Postscript Figures are included as uuencoded files (need `epsf.tex'), KUNS-1236, HE(TH) 93/1

MiRNAs in Cancer

There are many layers of complexity involving the processes through which somatic cells transform into malignant cancers. Historically, cancer was considered to be a disease primarily caused by gene mutations, however it is now well established that the dysregulated expression of the genes leading to the tumorigenic phenotype involves not only mutations but also epigenetic changes. To understand the process of malignant transformation, it is thus important to determine the specific genes targeted by both types of changes. The studies in this thesis have focused on miRNA expression and its dysregulation in various malignancies and the subsequent role of such dysregulation in tumor pathogenesis. The work includes an analysis of the functional consequences of miRNA alterations in three distinct malignancies, (1) chronic lymphocytic leukemia (CLL), (2) Squamous cell carcinoma (SCC) and (3) Basal cell carcinoma (BCC). Furthermore, acute lymphoblastic leukemia (ALL) was used as a model to describe the role of miRNAs in anticancer treatment. Moreover, we analyzed the effect of the anticancer drug dexamethasone on miRNA expressions and the impact of manipulation of miRNA levels on drug efficacy. In the CLL study, we demonstrated that the frequently deleted DLEU2 gene functions as a regulatory host gene for two miRNAs, miR-15a and miR16-1, which negatively regulate the cell cycle by direct targeting G1 cyclins D1 and E1 at the post-transcriptional level, and which, when expressed at high levels in cell line models, lead to the inhibition of colony formation ability. In addition, we demonstrated that the oncoprotein Myc negatively regulates DLEU2 transcription by targeting the DLEU2 promoter. These results suggest that the loss of DLEU2 may be an important pathogenic factor in CLL development. Our studies on two non-melanoma-skin cancers, SCC and BCC, identified the preferential loss of expression of a skin-specific miRNA, miR-203, in these tumors. Our results further indicate a function of miR-203 in cell cycle regulation, migration and invasion, through the post-transcriptional targeting of the oncogenes c-JUN and c-MYC, and ultimately leading to an inappropriate inactivation of Hedgehog pathway. Finally, in the ALL study we demonstrated dexamethasone mediated global down-regulation of miRNAs, in particular the rapid downregulation of MIR17HG which occurred following direct binding of the glucocorticoid receptor protein to the MIR17HG promoter. The subsequent repression of miR-17 expression aids in dexamethasone cytotoxicity of ALL cells, possibly through de-repression of miR-17 mediated targeting of the anti-apoptotic protein Bim. Analysis of primary B-ALL tumor samples also demonstrated that the cytotoxic efficacy of dexamethasone is associated with its ability to regulate miR-17 levels. Collectively, these results provide new evidence, not only on the function and importance of microRNAs in tumor pathogenesis, but also suggest the possibility of miRNA targeting to improve the efficacy of existing therapies

Comparison of Total Laparoscopic Hysterectomy with Abdominal Total Hysterectomy in Patients with Benign Disease: A Retrospective Cohort Study

Background: The present study aimed to determine whether total laparoscopic hysterectomy (TLH) is being implemented safely and appropriately compared with abdominal total hysterectomy (ATH) in our hospital. Methods: We retrospectively reviewed clinical records of 102 patients who underwent total hysterectomy for benign gynecological disease at Japanese Red Cross Yamaguchi Hospital from January 2017 to August 2018. We examined periods of hospital stay, operation time, blood loss, weight of the uterus, frequency of perioperative complications, and the duration from the first visit to the date of surgery. P < 0.05 was considered to be statistically significant indicated statistical significance. Results: TLH and ATH were performed in 55 (53%) and 47 (46%) cases, respectively. The TLH group had significantly longer total operation time [133 (82-205) min vs. 87 (57-155) min, P < 0.0001], lesser blood loss [5 (5-35) g vs. 100 (10-820) g, P < 0.0001], shorter hospital stay [7 (5-14) days vs. 10 (9-26) days, P < 0.0001], and lighter uterine weight [206 (27-658) g vs. 554 (79-2284) g, P < 0.0001] than the ATH group. The frequency of perioperative complications did not differ between the two groups (3.5% vs. 8.0%, P = 0.4103). Conclusion: TLH had a longer operation time and a lesser excised uterine weight, but it had less intraoperative blood loss, shorter hospital stay, and no difference in perioperative complication frequency when compared with ATH

Regional changes of fractional anisotropy with normal aging using Statistical Parametric Mapping (SPM)

Objective :There has been reports on the usefulness of diffusion tensor imaging (DTI) about age-or disease-related degradation. DTI is generally evaluated by the region of interest (ROI) methodology. In this study, we applied a statistical way using Statistical Parametric Mapping (SPM) to assess normal aging by DTI and compared results of these two methods. Methods : Ten young and ten senior normal volunteers were examined. On SPM, tensor images were changed into normalized tensor images. They were compared between the two groups by t-test. Results : In the senior group, fractional anisotropy (FA) values were higher on the basal ganglia, cingulated gyrus and other cortical gray matter, lower in the corona radiata, internal capsule, centrum semiovale and corpus callosum by using SPM. In the ROI method, the results were almost compatible except in the brain periphery. Conclusions : Aging changes on water diffusion anisotropy was clearly shown by SPM method which would be useful to evaluate change of water diffusion anisotropy without operator bias even in clinical setting instead of ROI measurement

Axial Anomaly and Transition Form Factors

We investigate the properties of the amplitude induced by the anomaly. In a relatively high energy region those amplitudes are constructed by the vector meson poles and the anomaly terms, in which the anomaly terms can be essentially evaluated by the triangle quark graph. We pay our attention to the anomaly term and make intensive analysis of the existing experimental data, i.e., the electromagnetic $\pi^0$ and $\omega$ transition form factors. Our result shows that it is essential to use the constituent quark mass instead of the current quark mass in evaluating the anomaly term from the triangle graph.Comment: LaTeX, 14 pages + 4 figures, (figures are included as uuencoded files), KUNS-1210 HE(TH) 93/0

Re-evaluation of Urinary Trypsin Inhibitor on Pregnancy Course in Patients with Threatened Preterm Delivery : A Single-Center Retrospective Study

Background: We evaluated the necessity of urinary trypsin inhibitor for patients with threatened premature labor. Methods: We enrolled 146 women with singleton pregnancies who were treated for threatened premature labor as inpatients. The uterine cervical length of each patient was ? 25 mm at 22?35 weeks of gestation on transvaginal ultrasonography. The patients were divided into two groups: the urinary trypsin inhibitor group (91 patients treated with urinary trypsin inhibitor daily) or non-urinary trypsin inhibitor group (55 patients not treated with urinary trypsin inhibitor). The childbirth outcomes were retrospectively assessed. Results: The median cervical length measured on the day of admission was almost similar between the urinary trypsin inhibitor and non-urinary trypsin inhibitor groups. Depending on the symptoms of uterine contractions, we determined whether ritodrine hydrochloride and/or magnesium sulfate would be appropriate for treatment. The median gestational week at birth was 38 weeks in the urinary trypsin inhibitor group, and no obvious differences were observed when compared with the non-urinary trypsin inhibitor group. With regard to birth weight, no significant difference was found between the two groups (urinary trypsin inhibitor group, 2776 g; non-urinary trypsin inhibitor group, 2800 g). Conclusion: Our data showed no significant beneficial effects of urinary trypsin inhibitor in the maternal course and delivery outcomes

Parkinson\u27s disease showing progressive conduction aphasia

Patients with Parkinson\u27s disease (PD) may develop progressive dementia late in their clinical course. Dementia in PD is mostly related to neuropathological findings of extensive Lewy bodies (LBs), with or without the coexistence of Alzheimer\u27s disease (AD) pathology. Aphasia has been reported in patients with LB diseases with AD pathology; however, there have been no reports of typical PD patients developing progressive aphasia during their clinical course. We describe a female PD patient who later developed progressive conduction aphasia characterized by phonemic paraphasia and disturbance in repetition of short sentences without disturbance in writing or auditory comprehension. No episodes of fluctuations of attention, memory complaints, or planning errors were observed. She experienced episodes of visual hallucination. Her low scores on the Mini-Mental State Examination suggested impairment of orientation and attention, and her scores on Raven\u27s Coloured Progressive Matrices test indicated impaired visuospatial functions. However, her cognitive deficits were not sufficiently severe to impair her daily life. Brain magnetic resonance images revealed atrophy of the left superior temporal gyrus and widening of the left sylvian fissure. [18F]-fluorodeoxyglucose positron emission tomography revealed glucose hypometabolism in the left cerebral hemisphere. These findings may be related to conduction aphasia. During the progression of PD lesions, the brainstem LB is assumed to take an upward course, extend to the limbic system, and then extend to the neocortex. Conduction aphasia observed in our patient may be associated with an unusual progression of the LB pathology from the brainstem to the left temporoparietal lobe. © 2011 Springer-Verlag

Jiadifenolide induces the expression of cellular communication network factor (CCN) genes, and CCN2 exhibits neurotrophic activity in neuronal precursor cells derived from human induced pluripotent stem cells

Jiadifenolide has been reported to have neurotrophin-like activity in primary rat cortical neurons, and also possesses neurotrophic effects in neuronal precursor cells derived from human induced pluripotent stem cells (hiPSCs), as we have previously reported. However, the molecular mechanisms by which jiadifenolide exerts its neurotrophic effects in rat and human neurons are unknown. Thus, we aimed to investigate the molecular mechanisms and pathways by which jiadifenolide promotes neurotrophic effects. Here, we found that jiadifenolide activated cellular communication network factor (CCN) signaling pathways by up-regulating mRNA level expression of CCN genes in human neuronal cells. We also found that CCN2 (also known as connective tissue growth factor, CTGF) protein promotes neurotrophic effects through activation of the p44/42 mitogen-activated protein kinase signaling pathway. This is the first discovery which links neurotrophic activity with CCN signaling