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51.
Hyperlipidemia stimulates the extracellular release of the nuclear high mobility group box 1 protein
Our aim was to evaluate the effect of hyperlipidemia on the activation of endogenous alarmin, the high mobility group box
1 (HMGB1) protein, related to systemic inflammation associated with the progression of experimental atherosclerosis and to
establish whether statin treatment regulates the HMGB1 signaling pathway. Hyperlipidemia was induced in vivo in golden Syrian
hamsters and in monocyte cell culture (U937) by feeding the animals with a high-fat Western diet and by exposing the cells
to hyperlipidemic serum. Blood samples, heart, lung and cells were harvested for biochemical, morphological, Western blot,
quantitative polymerase chain reaction and enzyme-linked immunosorbent assay analyses. The data revealed that, in the atherosclerotic
animal model, the protein HMGB1 and its gene expression were increased and that fluvastatin treatment significantly reduced
the release of HMGB1 into the extracellular space. The cell culture experiments demonstrated the relocation of HMGB1 protein
from the nucleus to cytoplasm under hyperlipidemic stress. The high level of detected HMGB1 correlated positively with the
up-regulation of the advanced glycation end product receptors (RAGE) in the lung tissue from hyperlipidemic animals. During
hyperlipidemic stress, the AKT signaling pathway could be activated by HMGB1-RAGE interaction. These results support the existence
of a direct correlation between experimentally induced hyperlipidemia and the extracellular release of HMGB1 protein; this
might be controlled by statin treatment. Moreover, the data suggest new potentials for statin therapy, with improved effects
on patients with systemic inflammation induced by hyperlipidemia. 相似文献
52.
Dziegiel P Dolilńska-Krajewska B Dumańska M Wecławek J Jeleń M Podhorska-Okołów M Jagoda E Fic M Zabel M 《Folia histochemica et cytobiologica / Polish Academy of Sciences, Polish Histochemical and Cytochemical Society》2007,45(1):21-25
Langerhans cell histiocytoses (LCH) represent rare diseases of unclear etiology and pathogenesis. Most of the cases include children, 1 to 15 years of age, and various organs are involved (bones, skin, liver, lymph nodes, bone marrow and other). The diagnosis of LCH used to be established by biopsy of the inflamed tissue and demonstration of expression of markers specific for Langerhans cells: CD1a and langerin. The diagnosis can be ultimately confirmed by demonstration of Birbeck's granules in the electron microscopy. The present study was aimed at immunocytochemical demonstration, in the examined LCH material (skin, bones, lymph nodes), of the specific antigen expression and at comparing it with the presence of Birbeck's granules. In the examined 11 cases co-expression of CD1a with langerin and with the presence of Birbeck's granules was noted. Also in all examined biopsies the expression of S-100 protein on inflammatory cells was found. The results corroborate the usefulness of immunocytochemical studies on CD 1 a and langerin expression in diagnosis of LCH. 相似文献
53.
Pierluca Coiro Luminita Stoenica Ulf Strauss Anja Ursula Br?uer 《The Journal of biological chemistry》2014,289(36):24956-24970
The transmembrane protein plasticity-related genes 3 and 5 (PRG3 and PRG5) increase filopodial formation in various cell lines, independently of Cdc42. However, information on the effects of PRG5 during neuronal development is sparse. Here, we present several lines of evidence for the involvement of PRG5 in the genesis and stabilization of dendritic spines. First, PRG5 was strongly expressed during mouse brain development from embryonic day 14 (E14), peaked around the time of birth, and remained stable at least until early adult stages (i.e. P30). Second, on a subcellular level, PRG5 expression shifted from an equal distribution along all neurites toward accumulation only along dendrites during hippocampal development in vitro. Third, overexpression of PRG5 in immature hippocampal neurons induced formation of spine-like structures ahead of time. Proper amino acid sequences in the extracellular domains (D1 to D3) of PRG5 were a prerequisite for trafficking and induction of spine-like structures, as shown by mutation analysis. Fourth, at stages when spines are present, knockdown of PRG5 reduced the number but not the length of protrusions. This was accompanied by a decrease in the number of excitatory synapses and, consequently, by a reduction of miniature excitatory postsynaptic current frequencies, although miniature excitatory postsynaptic current amplitudes remained similar. In turn, overexpressing PRG5 in mature neurons not only increased Homer-positive spine numbers but also augmented spine head diameters. Mechanistically, PRG5 interacts with phosphorylated phosphatidylinositols, phospholipids involved in dendritic spine formation by different lipid-protein assays. Taken together, our data propose that PRG5 promotes spine formation. 相似文献
54.
We present a computerized method for the semi-automatic detection of contours in ultrasound images.The novelty of our study is the introduction of a fast and efficient image function relating to parametric active contour models.This new function is a combination of the gray-level information and first-order statistical features,called standard deviation parameters.In a comprehensive study,the developed algorithm and the efficiency of segmentation were first tested for synthetic images.Tests were also performed on breast and liver ultrasound images.The proposed method was compared with the watershed approach to show its efficiency.The performance of the segmentation was estimated using the area error rate.Using the standard deviation textural feature and a 5×5 kernel,our curve evolution was able to produce results close to the minimal area error rate(namely 8.88% for breast images and 10.82% for liver images).The image resolution was evaluated using the contrast-to-gradient method.The experiments showed promising segmentation results. 相似文献
55.
Musculoskeletal-related pain is one of the most disabling health conditions affecting more than one third of the adult population worldwide. Pain from various mechanisms and origins is currently underdiagnosed and undertreated. The complexity of molecular mechanisms correlating pain and the progression of musculoskeletal diseases is not yet fully understood. Molecular biomarkers for objective evaluation and treatment follow-up are needed as a step towards targeted treatment of pain as a symptom or as a disease. Stem cell therapy is already under investigation for the treatment of different types of musculoskeletal-related pain. Mesenchymal stem cell-based therapies are already being tested in various clinical trials that use musculoskeletal system-related pain as the primary or secondary endpoint. Genetically engineered stem cells, as well as induced pluripotent stem cells, offer promising novel perspectives for pain treatment. It is possible that a more focused approach and reassessment of therapeutic goals will contribute to the overall efficacy, as well as to the clinical acceptance of regenerative medicine therapies. This article briefly describes the principal types of musculoskeletal-related pain and reviews the stem cell-based therapies that have been specifically designed for its treatment. 相似文献
56.
57.
58.
Alexandra Grubman Maria Kaparakis Jérôme Viala Cody Allison Luminita Badea Abdulgader Karrar Ivo G. Boneca Lionel Le Bourhis Shane Reeve Ian A. Smith Elizabeth L. Hartland Dana J. Philpott Richard L. Ferrero 《Cellular microbiology》2010,12(5):626-639
The cytosolic innate immune molecule, NOD1, recognizes peptidoglycan (PG) delivered to epithelial cells via the Helicobacter pylori cag pathogenicity island (cagPAI), and has been implicated in host defence against cagPAI+H. pylori bacteria. To further clarify the role of NOD1 in host defence, we investigated NOD1‐dependent regulation of human β‐defensins (DEFBs) in two epithelial cell lines. Our findings identify that NOD1 activation, via either cagPAI+ bacteria or internalized PG, was required for DEFB4 and DEFB103 expression in HEK293 cells. To investigate cell type‐specific induction of DEFB4 and DEFB103, we generated stable NOD1‘knockdown’ (KD) and control AGS cells. Reporter gene assay and RT‐PCR analyses revealed that only DEFB4 was induced in an NOD1‐/cagPAI‐dependent fashion in AGS cells. Moreover, culture supernatants from AGS control, but not AGS NOD1 KD cells, stimulated with cagPAI+H. pylori, significantly reduced H. pylori bacterial numbers. siRNA studies confirmed that human β‐defensin 2 (hBD‐2), but not hBD‐3, contributes to the antimicrobial activity of AGS cell supernatants against H. pylori. This study demonstrates, for the first time, the involvement of NOD1 and hBD‐2 in direct killing of H. pylori bacteria by epithelial cells and confirms the importance of NOD1 in host defence mechanisms against cagPAI+H. pylori infection. 相似文献
59.
Adenylate cyclase (AC) was localized ultracytochemically in certain tissues of the regenerating planarian Dugesia lugubris. Studies were carried out from one hour after injury up to the 5th day of regeneration. It was found that the greatest amount of active AC appears during the initial hours of regeneration in the membranes of the muscle cells near the wound, in the epithelial cells surrounding the wound, and in rhabdite-forming cells and neoblasts. 相似文献
60.
Corinna Sawallisch Kerstin Berh?rster Andrea Disanza Sara Mantoani Michael Kintscher Luminita Stoenica Alexander Dityatev Sabrina Sieber Stefan Kindler Fabio Morellini Michaela Schweizer Tobias M. Boeckers Martin Korte Giorgio Scita Hans-J��rgen Kreienkamp 《The Journal of biological chemistry》2009,284(14):9225-9236