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Summary Results of investigations on the occurrence of nerve fibres and endings in the synovial membrane of the knee and elbow joint in the cat are reported. The stratum synoviale contains only autonomic fibres, running in the adventitia of arteries.Free nerve endings are lacking in the stratum synoviale. Simple Pacinian corpuscles with an inner core are occasionally observed in the border zone between the stratum synoviale and fibrosum. The ultrastructure of these endorgans resembles that of Pacinian corpuscles in the hairless and hairy skin of the cat.  相似文献   
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The ORF2 gene of Gill-associated virus (GAV) of Penaeus monodon prawns resides 93 nucleotides downstream of the ORF1a-ORF1b gene and encodes a 144-amino-acid hydrophilic polypeptide (15,998 Da; pI, 9.75) containing 20 basic (14%) and 13 acidic (9%) residues and 19 prolines (13%). Antiserum to a synthetic ORF2 peptide or an Escherichia coli-expressed glutathione S-transferase-ORF2 fusion protein detected a 20-kDa protein in infected lymphoid organ and gill tissues in Western blots. The GAV ORF2 fusion protein antiserum also cross-reacted with the p20 nucleoprotein in virions of the closely related Yellow head virus. By immuno-gold electron microscopy, it was observed that the ORF2 peptide antibody localized to tubular GAV nucleocapsids, often at the ends or at lateral cross sections. As GAV appears to contain only two structural protein genes (ORF2 and ORF3), these data indicate that GAV differs from vertebrate nidoviruses in that the gene encoding the nucleocapsid protein is located upstream of the gene encoding the virion glycoproteins.  相似文献   
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Typical civilization diseases, such as type II diabetes, are common, complex in the underlying pathogenic mechanisms, heterogenous in the phenotype and multifactorial due to a wide variety of possible combinations of disease susceptibility or protective genes in different relevant tissues and negative or positive environmental factors. This is in sharp contrast to classical inherited diseases, such as Chorea Huntington, which are often caused by complete loss‐ or gain‐of‐function mutations in a single gene. The causative polymorphisms of susceptibility genes, however, are characterized by relative subtle alterations in the function of the corresponding gene product, which per se do not support the pathogenesis, by high frequency, high expenditure for their identification and rather low predictive value. Consequently, the reliable and early diagnosis of civilization diseases depends on the individual determination of all (or as many as possible) polymorphisms of each susceptibility gene together with the corresponding gene products and the metabolites emerging thereof.  相似文献   
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Extracellular vesicles (EVs) are abundant, lipid‐enclosed vectors that contain nucleic acids and proteins, they can be secreted from donor cells and freely circulate, and they can be engulfed by recipient cells thus enabling systemic communication between heterotypic cell types. However, genetic tools for labeling, isolating, and auditing cell type‐specific EVs in vivo, without prior in vitro manipulation, are lacking. We have used CRISPR‐Cas9‐mediated genome editing to generate mice bearing a CD63‐emGFPloxP/stop/loxP knock‐in cassette that enables the specific labeling of circulating CD63+ vesicles from any cell type when crossed with lineage‐specific Cre recombinase driver mice. As proof‐of‐principle, we have crossed these mice with Cdh5‐CreERT2 mice to generate CD63emGFP+ vasculature. Using these mice, we show that developing vasculature is marked with emerald GFP (emGFP) following tamoxifen administration to pregnant females. In adult mice, quiescent vasculature and angiogenic vasculature (in tumors) is also marked with emGFP. Moreover, whole plasma‐purified EVs contain a subpopulation of emGFP+ vesicles that are derived from the endothelium, co‐express additional EV (e.g., CD9 and CD81) and endothelial cell (e.g., CD105) markers, and they harbor specific miRNAs (e.g., miR‐126, miR‐30c, and miR‐125b). This new mouse strain should be a useful genetic tool for generating cell type‐specific, CD63+ EVs that freely circulate in serum and can subsequently be isolated and characterized using standard methodologies.  相似文献   
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Background

Although levels of iron are known to be increased in the brains of patients with Parkinson disease (PD), epidemiological evidence on a possible effect of iron blood levels on PD risk is inconclusive, with effects reported in opposite directions. Epidemiological studies suffer from problems of confounding and reverse causation, and mendelian randomization (MR) represents an alternative approach to provide unconfounded estimates of the effects of biomarkers on disease. We performed a MR study where genes known to modify iron levels were used as instruments to estimate the effect of iron on PD risk, based on estimates of the genetic effects on both iron and PD obtained from the largest sample meta-analyzed to date.

Methods and Findings

We used as instrumental variables three genetic variants influencing iron levels, HFE rs1800562, HFE rs1799945, and TMPRSS6 rs855791. Estimates of their effect on serum iron were based on a recent genome-wide meta-analysis of 21,567 individuals, while estimates of their effect on PD risk were obtained through meta-analysis of genome-wide and candidate gene studies with 20,809 PD cases and 88,892 controls. Separate MR estimates of the effect of iron on PD were obtained for each variant and pooled by meta-analysis. We investigated heterogeneity across the three estimates as an indication of possible pleiotropy and found no evidence of it. The combined MR estimate showed a statistically significant protective effect of iron, with a relative risk reduction for PD of 3% (95% CI 1%–6%; p = 0.001) per 10 µg/dl increase in serum iron.

Conclusions

Our study suggests that increased iron levels are causally associated with a decreased risk of developing PD. Further studies are needed to understand the pathophysiological mechanism of action of serum iron on PD risk before recommendations can be made. Please see later in the article for the Editors'' Summary  相似文献   
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Abstract

Larvae of 46 species of caddisfly from 14 of the 15 families present in New Zealand are described. A key to the families is included, and where possible there is a key to the spccies in each family. Information on larval habits and habitats, pupation, distribution, and life cycles is given. The classification of Trichoptera is discussed with particular reference to the New Zealand fauna. The origins of the New Zealand caddisflies are discussed, and the possibilities of Indo-Malaysian, Australian, and trans-Antarctic influences are considered. The distribution of some of the species is discussed in relation to paleogeography and present-day climatic features. Larvae described: HYDROPSYCHIDAEOrthopsyche fimbriata, O. thomasi, Aoteapsyche colonica, A. tepoka, A. raruraru, Diplectrona zealandensis; POLYCENTROPODIDAEPolyplectropus puerilis, Plectrocnemia maclachlani; PSYCHOMYIIDAEEcnomina zealandica; Philopotamidae — Dolophilodes (Hydrobiosella) stenocerca, D. (H.) mixta; Hydroptilidae — Oxyethira albiceps, Paroxyethira hendersoni; Kokiriidae — Kokiria miharo; Oeconesidae — Oeconesus maori, O. similis, Zelandopsyche ingens; Pycnocentrellidae — Pycnocentrella eruensis; Sericostomatidae — Pycnocentria funerea, P. evecta, P. sylvestris, Beraeoptera roria, Pycnocentrodes aeris, P. aureola, P. modesta, Confluens hamiltoni, Conuxia gunni, Olinga feredayi, O. jeanae; HELICOPHIDAEZelolessica cheira, Z. sp., Alloecentrella magnicornis; Chathamiidae — Philanisus plebeius; PHILORHEITHRIDAEPhilorheithrus agilis; Helicopsychidae — Helicopsyche zealandica, H. albescens, H. poutini, Rakiura vernale; LEPTOCERIDAETriplectides cephalotes, T. obsoleta, T. oreolimnetes, Hudsonema amabilis, H. aliena, Oecetis unicolor, O. iti.  相似文献   
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