A Case of Paraplegia Treated with Cerebrospinal Fluid Drainage and Permissive Hypertension after Graft Replacement of the Ascending Aorta and the Total Aortic Arch for Acute Aortic Dissection Stanford Type A

Paraplegia after an operation for acute aortic dissection Stanford type A (AADA) is fairly uncommon, and there is no consensus about optimal treatment. We present a case in which cerebrospinal fluid drainage (CSFD) and permissive hypertension were used for treatment of paraplegia. When the patient showed complete bilateral paraplegia after operation for AADA, we immediately began CSFD and maintained mean arterial blood pressure at over 90 mmHg. His neurological deficit gradually recovered, and he was eventually able to walk without support. The combination of CSFD and permissive hypertension could be a first-line emergent treatment for postoperative paraplegia after AADA surgery

Characterization of the neurovascular pathology in CADASIL : a model for subcortical vascular dementia

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is one of the most common forms of hereditary vascular dementia (VaD). Characterised by early-onset strokes and cognitive impairment in the absence of vascular risk factors, CADASIL is an ideal model to understand the pathophysiology of VaD. Pathogenic mutations in the NOTCH3 gene, which encodes a single-pass transmembrane cell surface receptor expressed predominantly in vascular smooth muscle cells (VSMC), cause severe vascular alterations including VSMC degeneration, hyalinosis, deposition of CADASIL-specific granular osmiophilic material (GOM) and white matter (WM) changes. While these changes have been well-described, their causative mechanism or difference between sporadic VaD is poorly understood. The aim of the project was to quantitatively characterise various aspects of cerebral pathology of CADASIL in order to reveal the pathological basis of CADASIL phenotypes, especially of cognitive dysfunction. Firstly, we assessed vascular and perivascular changes in CADASIL brain areas and found significant vessel wall thickening and perivascular space enlargement, even compared to sporadic VaD. Secondly, by using immunogold electron microscopy, NOTCH3 extracellular domain (N3ECD) was located within GOM in the wall of cerebral arteries/arterioles/capillaries, establishing at least one component of GOM and its wide-spread existence in the vasculature. This study also suggested the possible existence of intracellular N3ECD accumulation and involvement of inflammatory response in the pathogenesis of CADASIL. Finally, we provide neuronal density data from the hippocampal formation in CADASIL brains to identify the neural substrates of VaD in CADASIL. Overall, the number of neurons in CA1, CA2 and entorhinal cortex was relatively spared in CADASIL while pyramidal neuronal subpopulation, as shown by SMI32 immunoreactivity, was slightly decreased. In addition, SMI32 staining revealed extensive chronic damage to WM tracts, especially those in the frontal-parietal area. These data suggest that vascular dysfunction and inflammation result in frontal disconnection, which could underlie cognitive impairment in CADASIL patients.EThOS - Electronic Theses Online ServiceNewcastle UniversityGBUnited Kingdo

THE CHARACTERISTICS OF BACKWARD WALKING AND BACKWARD RUNNING IN PRIMARY SCHOOL CHILDREN

The purpose of this study is to identify the characteristics of both backward walking (BW) and backward running (BR) and show the differences between two kinds of movements according to age. One 'hundred and four primary school children and varsity 20 students participated in this study. The SUbjects were divided into four groups. 15-meters-long lane was used in this experiment. All video pictures were manually digitized on Sony Motion Analyzer (SMC-70G). Cycles of motion in BW &BR were analyzed. The walking velocity didn't increase so with age in BW-test, but the results of BR-test revealed that running velocity increased with age. Step length was increased with age in each test. Step frequency of BR didn't increase with age. Step frequency in BW didn't increase with age. We categorized the form using examples from Miyamaru's procedure. BW was categorized to 5 patterns, and BR divided to 6 patterns

A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis

International audienceIntrauterine hypoperfusion/ischemia is one of the major causes of intrauterine/fetal growth restriction, preterm birth, and low birth weight. Most studies of this phenomenon have been performed in either models with severe intrauterine ischemia or models with gradient degree of intrauterine hypoperfusion. No study has been performed in a model on uniform mild intrauterine hypoperfusion (MIUH). Two models have been used for studies of MIUH: a model based on suture ligation of either side of the arterial arcade formed with the uterine and ovarian arteries, and a transient model based on clipping the bilateral ovarian arteries and aorta having patency. Those two rodent models of MIUH have some limitations, e.g., not all fetuses are subjected to MIUH, depending on their position in the uterine horn. In our MIUH model, all fetuses are subjected to a comparable level of intrauterine hypoperfusion. MIUH was achieved by mild stenosis of all four arteries feeding the uterus, i.e., the bilateral uterine and ovarian arteries. Arterial stenosis was induced by metal microcoils wrapped around the feeding arteries. Producing arterial stenosis with microcoils allowed us to control, optimize, and reproduce decreased blood flow with very little inter-animal variability and a low mortality rate, thus enabling accurate evaluation. When microcoils with an inner diameter of 0.24 mm were used, the blood flow in both the placenta and fetus was mildly decreased (approximately 30% from the pre-stenosis level in the placenta). The offspring of our MIUH model clearly demonstrates long-lasting alterations in neurological, neuroanatomical and behavioral test results

A Study on Boards of Education Voluntarily Established : Case of Sakai City

Board of Education Law of 1948 prescribed that all prefectures and 5 big cities should establish the school board and that cities but for these big cities, towns, and words could establish the school board voluntarily. In this paper, I try to make the following questions, which has been unanswered, clear by investigating the case of Sakai City. 1) Why did they establish the school board voluntarily ? 2) What did the school board do ? Sakai City was the biggest of these cities and the activity of its school board was characterized by making its own curriculum in addition to the national curriculum

A study on school board voluntarily established (4) : Case of Aioi City and Miki Town

Under School Board Law of 1948. which kept it voluntary formunicipalities for all prefectures and 5 big cities to establish school board, 21 cities, 16 towns, 9 villages chose to do it. This was partly because same of these municipalities were subjected to the strong direction given by Military Government Regional (or District) Team, and partly because others had their own special motivation to do it. 2 Municipalties in Hyogo prefecture established their school boards to settle the problem of school closing and school construction. In Aioi City, the order, is usd by Military Government, of closing the technical high school raised the residents, movement against it. By establishing school board residents expected to get the authority to decide whether to close it or not, and in fact they did get it and the school was not closed. In Miki Town, in which there was a conflict around the problem of where to construct a junior high school which was supposed to be established under the school education law, school board played the role of conflict solving body

Two-Photon AMPK and ATP Imaging Reveals Metabolic Recovery in Mouse Rod Photoreceptor Cells

The title of publisher's version: Two-photon AMPK and ATP imaging reveals the bias between rods and cones in glycolysis utility.In vertebrates, retinal rod and cone photoreceptor cells rely significantly on glycolysis. Lactate released from photoreceptor cells fuels neighboring retinal pigment epithelium cells and Müller glial cells through oxidative phosphorylation. To understand this highly heterogeneous metabolic environment around photoreceptor cells, single-cell analysis is needed. Here, we visualized cellular AMP-activated protein kinase (AMPK) activity and ATP levels in the retina by two-photon microscopy. Transgenic mice expressing a hyBRET-AMPK biosensor were used for measuring the AMPK activity. GO-ATeam2 transgenic mice were used for measuring the ATP level. Temporal metabolic responses were successfully detected in the live retinal explants upon drug perfusion. A glycolysis inhibitor, 2-deoxy-d-glucose (2-DG), activated AMPK and reduced ATP. These effects were clearly stronger in rods than in cones. Notably, rod AMPK and ATP started to recover at 30 min from the onset of 2-DG perfusion. Consistent with these findings, ex vivo electroretinogram recordings showed a transient slowdown in rod dim flash responses during a 60-min 2-DG perfusion, whereas cone responses were not affected. Based on these results, we propose that cones surrounded by highly glycolytic rods become less dependent on glycolysis, and rods also become less dependent on glycolysis within 60 min upon the glycolysis inhibition

Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases

IL-32 is a newly described cytokine in the human found to be an in vitro inducer of tumor necrosis factor alpha (TNFα). We examined the in vivo relationship between IL-32 and TNFα, and the pathologic role of IL-32 in the TNFα-related diseases – arthritis and colitis. We demonstrated by quantitative PCR assay that IL-32 mRNA was expressed in the lymphoid tissues, and in stimulated peripheral T cells, monocytes, and B cells. Activated T cells were important for IL-32 mRNA expression in monocytes and B cells. Interestingly, TNFα reciprocally induced IL-32 mRNA expression in T cells, monocyte-derived dendritic cells, and synovial fibroblasts. Moreover, IL-32 mRNA expression was prominent in the synovial tissues of rheumatoid arthritis patients, especially in synovial-infiltrated lymphocytes by in situ hybridization. To examine the in vivo relationship of IL-32 and TNFα, we prepared an overexpression model mouse of human IL-32β (BM-hIL-32) by bone marrow transplantation. Splenocytes of BM-hIL-32 mice showed increased expression and secretion of TNFα, IL-1β, and IL-6 especially in response to lipopolysaccharide stimulation. Moreover, serum TNFα concentration showed a clear increase in BM-hIL-32 mice. Cell-sorting analysis of splenocytes showed that the expression of TNFα was increased in resting F4/80(+ )macrophages, and the expression of TNFα, IL-1β and IL-6 was increased in lipopolysaccharide-stimulated F4/80(+ )macrophages and CD11c(+ )dendritic cells. In fact, BM-hIL-32 mice showed exacerbation of collagen-antibody-induced arthritis and trinitrobenzen sulfonic acid-induced colitis. In addition, the transfer of hIL-32β-producing CD4(+ )T cells significantly exacerbated collagen-induced arthritis, and a TNFα blockade cancelled the exacerbating effects of hIL-32β. We therefore conclude that IL-32 is closely associated with TNFα, and contributes to the exacerbation of TNFα-related inflammatory arthritis and colitis

Insight into single cell cloning in serum-free media

Chinese hamster ovary (CHO) cells have been used as host cells for the manufacturing of therapeutic recombinant proteins over the past decade. It is thought that the development of high performance cell lines, which satisfy both productivity and regulatory expectations, is one of the key success drivers to establish good manufacturing processes. The cell line for the clinical and commercial productions should be derived from a single progenitor or clone, and so the single cell cloning is an essential step during the cell line development. Recently serum-free media have been widely applied for this step. But under such conditions, the cloning efficiency varies significantly among the clones. This might be because the serum-free conditions can be stressful for the CHO cells exposed to such an unexpected cloning process. In this study, we performed re-cloning from two pre-cloned cell lines to evaluate the impact of serum-free cloning on the resulting cell line characteristics; various parameters such as cell growth, productivity, fed-batch culture performance, product quality and cell stability were evaluated. As a result, most of the clones showed exactly the same performance before and after the cloning process, but some clones did not. The detail of these results will be presented and also the proper evaluation to be needed during cell line development, especially after the single cell isolation, will be discusse

Neuronal densities and vascular pathology in the hippocampal formation in CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common form of hereditary cerebral small vessel disease. Previous neuroimaging studies have suggested loss of hippocampal volume is a pathway for cognitive impairment in CADASIL. We used unbiased stereological methods to estimate SMI32-positive and total numbers and volumes of neurons in the hippocampal formation of 12 patients with CADASIL and similar age controls (young controls) and older controls. We found densities of SMI32-positive neurons in the entorhinal cortex, layer V, and cornu ammonis CA2 regions were reduced by 26%-50% in patients with CADASIL compared with young controls (p = CADASIL. These changes were not explained by any hippocampal infarct or vascular pathology or glial changes. Our results suggest notable loss of subsets of projection neurons within the hippocampal formation that may contribute to certain memory deficits in CADASIL, which is purely a vascular disease. It is likely that the severe arteriopathy leads to white matter damage which disconnects corticocortical and subcortical-cortical networks including the hippocampal formation. (C) 2020 The Authors. Published by ELSEVIER