211 research outputs found
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çãšãè³æ翻蚳ãéèš³ã®é¢ã§ååãåŸãäœè€ç¶Ÿåæ°ã«æè¬ããããæ¬ç 究ã®ç¬¬1çš¿ã¯ã1998幎9æ3æ¥ïœ6æ¥ã«ãã¹ãã³ã§éå¬ãããã¢ã¡ãªã«æ¿æ²»åŠäŒã®äŒåã§çºè¡šããããAt a time when metropolitan governments have been weakened or dismant1ed, Tokyo Metropolitan Government (TMG) exemplifies the model of integrated metropolitan government. Yet. TMG is at a cross-roads. The 23 special wards (ku), administrative units of TMG, are demanding greater local autonomy. The central government seeks to devolve administrative and fiscal policy while retaining central authority. Efforts to bring about balanced growth and limit over concentration are meeting with limited success while the metropolis continues to expand outwards. As the millenium approaches, Tokyo finds itself constrained by the economic slump and associated fiscal strain. This paper reports on a case study of changing intergovernmental relations in Tokyo
Transcriptional Profiling of Aging in Human Muscle Reveals a Common Aging Signature
We analyzed expression of 81 normal muscle samples from humans of varying ages, and have identified a molecular profile for aging consisting of 250 age-regulated genes. This molecular profile correlates not only with chronological age but also with a measure of physiological age. We compared the transcriptional profile of muscle aging to previous transcriptional profiles of aging in the kidney and the brain, and found a common signature for aging in these diverse human tissues. The common aging signature consists of six genetic pathways; four pathways increase expression with age (genes in the extracellular matrix, genes involved in cell growth, genes encoding factors involved in complement activation, and genes encoding components of the cytosolic ribosome), while two pathways decrease expression with age (genes involved in chloride transport and genes encoding subunits of the mitochondrial electron transport chain). We also compared transcriptional profiles of aging in humans to those of the mouse and fly, and found that the electron transport chain pathway decreases expression with age in all three organisms, suggesting that this may be a public marker for aging across species
Exuberant fibroblast activity compromises lung function via ADAMTS4
© 2020, The Author(s), under exclusive licence to Springer Nature Limited. Severe respiratory infections can result in acute respiratory distress syndrome (ARDS)1. There are no effective pharmacological therapies that have been shown to improve outcomes for patients with ARDS. Although the host inflammatory response limits spread of and eventually clears the pathogen, immunopathology is a major contributor to tissue damage and ARDS1,2. Here we demonstrate that respiratory viral infection induces distinct fibroblast activation states, which we term extracellular matrix (ECM)-synthesizing, damage-responsive and interferon-responsive states. We provide evidence that excess activity of damage-responsive lung fibroblasts drives lethal immunopathology during severe influenza virus infection. By producing ECM-remodelling enzymesâin particular the ECM protease ADAMTS4âand inflammatory cytokines, damage-responsive fibroblasts modify the lung microenvironment to promote robust immune cell infiltration at the expense of lung function. In three cohorts of human participants, the levels of ADAMTS4 in the lower respiratory tract were associated with the severity of infection with seasonal or avian influenza virus. A therapeutic agent that targets the ECM protease activity of damage-responsive lung fibroblasts could provide a promising approach to preserving lung function and improving clinical outcomes following severe respiratory infections
Publisher Correction: Exuberant fibroblast activity compromises lung function via ADAMTS4 (Nature, (2020), 587, 7834, (466-471), 10.1038/s41586-020-2877-5)
© 2020, The Author(s), under exclusive licence to Springer Nature Limited. An amendment to this paper has been published and can be accessed via a link at the top of the paper
The Politics of Environmental Dispute Resolution
Also PCMA Working Paper #17.http://deepblue.lib.umich.edu/bitstream/2027.42/51148/1/380.pd
Minimally invasive versus open distal pancreatectomy (LEOPARD): Study protocol for a randomized controlled trial
Background: Observational cohort studies have suggested that minimally invasive distal pancreatectomy (MIDP) is associated with better short-term outcomes compared with open distal pancreatectomy (ODP), such as less intraoperative blood loss, lower morbidity, shorter length of hospital stay, and reduced total costs. Confounding by indication has probably influenced these findings, given that case-matched studies failed to confirm the superiority of MIDP. This accentuates the need for multicenter randomized controlled trials, which are currently lacking. We hypothesize that time to functional recovery is shorter after MIDP compared with ODP even in an enhanced recovery setting. Methods: LEOPARD is a randomized controlled, parallel-group, patient-blinded, multicenter, superiority trial in all 17 centers of the Dutch Pancreatic Cancer Group. A total of 102 patients with symptomatic benign, premalignant or malignant disease will be randomly allocated to undergo MIDP or ODP in an enhanced recovery setting. The primary outcome is time (days) to functional recovery, defined as all of the following: independently mobile at the preoperative level, sufficient pain control with oral medication alone, ability to maintain sufficient (i.e. >50%) daily required caloric intake, no intravenous fluid administration and no signs of infection. Secondary outcomes are operative and postoperative outcomes, including clinically relevant complications, mortality, quality of life and costs. Discussion: The LEOPARD trial is designed to investigate whether MIDP reduces the time to functional recovery compared with ODP in an enhanced recovery setting. Trial registration: Dutch Trial Register, NTR5188. Registered on 9 April 201
Colorectal cancer stages transcriptome analysis
Colorectal cancer (CRC) is the third most common cancer and the second leading cause of
cancer-related deaths in the United States. The purpose of this study was to evaluate the
gene expression differences in different stages of CRC. Gene expression data on 433 CRC
patient samples were obtained from The Cancer Genome Atlas (TCGA). Gene expression
differences were evaluated across CRC stages using linear regression. Genes with
p 0.001 in expression differences were evaluated further in principal component analysis
and genes with p 0.0001 were evaluated further in gene set enrichment analysis. A total of
377 patients with gene expression data in 20,532 genes were included in the final analysis.
The numbers of patients in stage I through IV were 59, 147, 116 and 55, respectively. NEK4
gene, which encodes for NIMA related kinase 4, was differentially expressed across the four
stages of CRC. The stage I patients had the highest expression of NEK4 genes, while the
stage IV patients had the lowest expressions (p = 9*10â6
). Ten other genes (RNF34,
HIST3H2BB, NUDT6, LRCh4, GLB1L, HIST2H4A, TMEM79, AMIGO2, C20orf135 and
SPSB3) had p value of 0.0001 in the differential expression analysis. Principal component
analysis indicated that the patients from the 4 clinical stages do not appear to have distinct
gene expression pattern. Network-based and pathway-based gene set enrichment analyses
showed that these 11 genes map to multiple pathways such as meiotic synapsis and packaging of telomere ends, etc. Ten of these 11 genes were linked to Gene Ontology terms
such as nucleosome, DNA packaging complex and protein-DNA interactions. The protein
complex-based gene set analysis showed that four genes were involved in H2AX complex
II. This study identified a small number of genes that might be associated with clinical stages
of CRC. Our analysis was not able to find a molecular basis for the current clinical staging
for CRC based on the gene expression patterns
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