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81.
Immunogold labelling of the cytoplasmic estradiol receptor in resting porcine endometrium 总被引:2,自引:0,他引:2
Summary Serial sections of resting porcine endometrium were analyzed with the monoclonal antibody 13H2 using goat antimouse IgG/5 nm gold as secondary reagent or with either polyclonal antibodies from goat #402 or the rat monoclonal antibody H222, both in combination with protein G/12 nm gold. A modestly higher labelling of nuclei than of cytoplasm was seen only with the monoclonal antibody H222. Polyclonal #402 and monoclonal 13H2 showed fewer attachments over nuclear than over cytoplasmic areas. The highest densities of attachment and of predominantly cytoplasmic labelling were obtained with the monoclonal antibody 13H2. The results confirm the earlier assumption of a restricted accessiblity of estradiol receptor in the cytoplasm of resting cells for immunoreagents. 相似文献
82.
83.
Summary The development of acellular extrinsic fiber cementum (AEFC) has never before been studied in human teeth. We have therefore examined the initiation of AEFC in the form of a collagenous fiber fringe and its attachment to the underlying dentinal matrix, in precisely selected, erupting human premolars with roots developed to 50%–60% of their final length. Freshly extracted teeth were prefixed in Karnovsky's fixative, decalcified in EDTA and subdivided into about 10 blocks each, cut from the mesial and distal root surfaces, vertical to and along the root axis. The blocks were postfixed in osmium tetroxide, embedded in Epon and cut for light- and electron-microscopic investigation. Starting at the advancing edge of the root, within a region extending about 1 mm coronal to this edge, fibroblast-like cells were seen closely covering the external root surface. Along the first 100 m from the root edge, these cells extended cytoplasmic processes and contacted the dentinal collagen fibrils. Between these cells and the dentinal matrix, new collagen fibrils and very short collagen fibers gradually developed. Within the second 100 m from the root edge, this resulted in the formation of a cell-fiber fringe network. Newly formed fibers of the fringe were directly attached to the non-mineralized matrix containing dentinal collagen fibrils and could be distinguished from the latter by differences in fibril orientation. During the process of dentin mineralization, the transitional zone between the fiber-fringe base and the dentinal matrix, i.e., the future dentino-cemental junction, also mineralized. It is suggested that this fiber fringe is the base of AEFC, which later increases in thickness by fiber extension and subsequent mineralization.Abbreviations
AEFC
acellular extrinsic fiber cementum
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AIFC
acellular intrinsic fiber cementum
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CIFC
cellular intrinsic fiber cementum
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CMSC
cellular mixed stratified cementum
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ARE
advancing root edge
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CP
cytoplasmic process
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D
dentin
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DCJ
dentinocemental junction
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E
enamel
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EBL
external basal lamina
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EC
epithelial cell
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EDTA
ethylene diaminetetraacetic acid
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ERM
epithelial rests of Malassez
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FF
fiber fringe
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HRS
Hertwig's epithelial root sheath
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IBL
internal basal lamina
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MD
mineralized dentin
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NMD
non-mineralized dentin
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OB
odontoblast
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PD
predentin
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PL
periodontal ligament 相似文献
84.
85.
E Devinoy C Hubert E Schaerer L M Houdebine J P Kraehenbuhl 《Nucleic acids research》1988,16(16):8180
86.
Hui Liu Xiang Li Matthew D. Dun Sam Faulkner Chen Chen Jiang Hubert Hondermarck 《Proteomics》2020,20(10)
Pancreatic cancer has a dismal prognosis and to date there are no targeted therapies for this malignancy. Using shotgun proteomics, the mRNA binding protein cold shock domain containing E1 (CSDE1), also called upstream‐of‐N‐Ras, is detected in pancreatic cancer cell lines but not in normal pancreatic epithelial cells. The expression of CSDE1 in pancreatic cancer cells is confirmed by Western blotting and immunohistochemistry of human pancreatic tumors. In vitro functional assays show that siRNA downregulation of CSDE1 or gene knockout using CRISPR‐Cas9 significantly reduce the invasiveness of pancreatic cancer cells. Together, this study reveals that CSDE1 is overexpressed in pancreatic cancer and is a potential therapeutic target to inhibit pancreatic cancer cell invasion. 相似文献
87.
Júlia R. de Rezende Thomas B. P. Oldenburg Tetyana Korin William D. L. Richardson Milovan Fustic Carolyn M. Aitken Bernard F. J. Bowler Angela Sherry Alexander Grigoryan Gerrit Voordouw Stephen R. Larter Ian M. Head Casey R. J. Hubert 《Environmental microbiology》2020,22(8):3049-3065
Most of the oil in low temperature, non-uplifted reservoirs is biodegraded due to millions of years of microbial activity, including via methanogenesis from crude oil. To evaluate stimulating additional methanogenesis in already heavily biodegraded oil reservoirs, oil sands samples were amended with nutrients and electron acceptors, but oil sands bitumen was the only organic substrate. Methane production was monitored for over 3000 days. Methanogenesis was observed in duplicate microcosms that were unamended, amended with sulfate or that were initially oxic, however methanogenesis was not observed in nitrate-amended controls. The highest rate of methane production was 0.15 μmol CH4 g−1 oil d−1, orders of magnitude lower than other reports of methanogenesis from lighter crude oils. Methanogenic Archaea and several potential syntrophic bacterial partners were detected following the incubations. GC–MS and FTICR–MS revealed no significant bitumen alteration for any specific compound or compound class, suggesting that the very slow methanogenesis observed was coupled to bitumen biodegradation in an unspecific manner. After 3000 days, methanogenic communities were amended with benzoate resulting in methanogenesis rates that were 110-fold greater. This suggests that oil-to-methane conversion is limited by the recalcitrant nature of oil sands bitumen, not the microbial communities resident in heavy oil reservoirs. 相似文献
88.
Maxime Olmos Mark R. Payne Marie Nevoux Etienne Prvost Grald Chaput Hubert Du Pontavice Jrme Guitton Timothy Sheehan Katherine Mills Etienne Rivot 《Global Change Biology》2020,26(3):1319-1337
A major challenge in understanding the response of populations to climate change is to separate the effects of local drivers acting independently on specific populations, from the effects of global drivers that impact multiple populations simultaneously and thereby synchronize their dynamics. We investigated the environmental drivers and the demographic mechanisms of the widespread decline in marine survival rates of Atlantic salmon (Salmo salar) over the last four decades. We developed a hierarchical Bayesian life cycle model to quantify the spatial synchrony in the marine survival of 13 large groups of populations (called stock units, SU) from two continental stock groups (CSG) in North America (NA) and Southern Europe (SE) over the period 1971–2014. We found strong coherence in the temporal variation in postsmolt marine survival among the 13 SU of NA and SE. A common North Atlantic trend explains 37% of the temporal variability of the survivals for the 13 SU and declines by a factor of 1.8 over the 1971–2014 time series. Synchrony in survival trends is stronger between SU within each CSG. The common trends at the scale of NA and SE capture 60% and 42% of the total variance of temporal variations, respectively. Temporal variations of the postsmolt survival are best explained by the temporal variations of sea surface temperature (SST, negative correlation) and net primary production indices (PP, positive correlation) encountered by salmon in common domains during their marine migration. Specifically, in the Labrador Sea/Grand Banks for populations from NA, 26% and 24% of variance is captured by SST and PP, respectively and in the Norwegian Sea for populations from SE, 21% and 12% of variance is captured by SST and PP, respectively. The findings support the hypothesis of a response of salmon populations to large climate‐induced changes in the North Atlantic simultaneously impacting populations from distant continental habitats. 相似文献
89.
Evelyn Walenta Ariane R. Pessentheiner Helmut J. Pelzmann Alexander Deutsch Madeleine Goeritzer Dagmar Kratky Hubert Hackl Da Young Oh Andreas Prokesch Juliane G. Bogner-Strauss 《PloS one》2013,8(11)
Our knowledge about adipocyte metabolism and development is steadily growing, yet many players are still undefined. Here, we show that α/β-hydrolase domain containing protein 15 (Abhd15) is a direct and functional target gene of peroxisome proliferator-activated receptor gamma (PPARγ), the master regulator of adipogenesis. In line, Abhd15 is mainly expressed in brown and white adipose tissue and strongly upregulated during adipogenesis in various murine and human cell lines. Stable knockdown of Abhd15 in 3T3-L1 cells evokes a striking differentiation defect, as evidenced by low lipid accumulation and decreased expression of adipocyte marker genes. In preconfluent cells, knockdown of Abhd15 leads to impaired proliferation, which is caused by apoptosis, as we see an increased SubG1 peak, caspase 3/7 activity, and BAX protein expression as well as a reduction in anti-apoptotic BCL-2 protein. Furthermore, apoptosis-inducing amounts of palmitic acid evoke a massive increase of Abhd15 expression, proposing an apoptosis-protecting role for ABHD15. On the other hand, in mature adipocytes physiological (i.e. non-apoptotic) concentrations of palmitic acid down-regulate Abhd15 expression. Accordingly, we found that the expression of Abhd15 in adipose tissue is reduced in physiological situations with high free fatty acid levels, like high-fat diet, fasting, and aging as well as in genetically obese mice. Collectively, our results position ABHD15 as an essential component in the development of adipocytes as well as in apoptosis, thereby connecting two substantial factors in the regulation of adipocyte number and size. Together with its intricate regulation by free fatty acids, ABHD15 might be an intriguing new target in obesity and diabetes research. 相似文献
90.
Hubert Kolb Kathrin Lückemeyer Tim Heise Christian Herder Nanette C. Schloot Wolfgang Koenig Lutz Heinemann Stephan Martin 《PloS one》2013,8(8)