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排序方式: 共有2944条查询结果,搜索用时 15 毫秒
1.
Wu Changwei W. Tsai Pei-Jung Chen Sharon Chia-Ju Li Chia-Wei Hsu Ai-Ling Wu Hong-Yi Ko Yu-Ting Hung Pai-Chuan Chang Chun-Yen Lin Ching-Po Lane Timothy J. Chen Chia-Yuen 《Sleep and biological rhythms》2019,17(4):423-431
Sleep and Biological Rhythms - Neurovascular coupling (NVC), the transient regional hyperemia following the evoked neuronal responses, is the basis of blood oxygenation level-dependent techniques... 相似文献
2.
James K. Nuñez Jin Chen Greg C. Pommier J. Zachery Cogan Joseph M. Replogle Carmen Adriaens Gokul N. Ramadoss Quanming Shi King L. Hung Avi J. Samelson Angela N. Pogson James Y.S. Kim Amanda Chung Manuel D. Leonetti Howard Y. Chang Martin Kampmann Bradley E. Bernstein Volker Hovestadt Jonathan S. Weissman 《Cell》2021,184(9):2503-2519.e17
3.
William J. Joiner Eliot B. Friedman Hsiao-Tung Hung Kyunghee Koh Mallory Sowcik Amita Sehgal Max B. Kelz 《PLoS genetics》2013,9(9)
A robust, bistable switch regulates the fluctuations between wakefulness and natural sleep as well as those between wakefulness and anesthetic-induced unresponsiveness. We previously provided experimental evidence for the existence of a behavioral barrier to transitions between these states of arousal, which we call neural inertia. Here we show that neural inertia is controlled by processes that contribute to sleep homeostasis and requires four genes involved in electrical excitability: Sh, sss, na and unc79. Although loss of function mutations in these genes can increase or decrease sensitivity to anesthesia induction, surprisingly, they all collapse neural inertia. These effects are genetically selective: neural inertia is not perturbed by loss-of-function mutations in all genes required for the sleep/wake cycle. These effects are also anatomically selective: sss acts in different neurons to influence arousal-promoting and arousal-suppressing processes underlying neural inertia. Supporting the idea that anesthesia and sleep share some, but not all, genetic and anatomical arousal-regulating pathways, we demonstrate that increasing homeostatic sleep drive widens the neural inertial barrier. We propose that processes selectively contributing to sleep homeostasis and neural inertia may be impaired in pathophysiological conditions such as coma and persistent vegetative states. 相似文献
4.
The granulocyte colony-stimulating factor receptor (G-CSFR) regulates the proliferation, differentiation and survival of neutrophilic progenitor cells. In these studies, we introduced mutant G-CSFRs with cytoplasmic domains truncated approximately every 30 amino acids from the C-terminus into interleukin-3 (IL-3)-dependent myeloid LGM-1 cells. The G-CSFR membrane proximal region containing the Box 2 homology sequence was determined to be critical for proliferative signaling, as well as for activation of Janus kinase (JAK2) and p44/42 mitogen-activated protein kinase (MAPK) following G-CSF stimulation. In the presence of increasing concentrations of JAK2 or p44/42 MAPK inhibitors, LGM-1 cells expressing the full-length G-CSFR exhibited a decreased capacity to proliferate in response to G-CSF. These results demonstrate that JAK2 and p44/42 MAPK activation is involved in proliferative signaling through the G-CSFR membrane proximal region containing the Box 2 homology sequence. 相似文献
5.
Mutations were induced in tissue-cultured wasabi (Wasabia japonica Matsumura) by treating in vitro-derived shoot tips with either γ-rays or X-rays at 0, 10, 20, 40 or 80 Gy. Doses of up to 40 Gy of either γ- or X-ray treatments
resulted in a survival rate of more than 60% in culture after 3 mo. The use of γ- or X-rays at doses between 10 Gy and 40 Gy
to induce mutation in W. japonica resulted in an alteration of the growth and allyl isothiocyanate (AITC) content of multiple shoots after 3 mo. in culture
on Murashige and Skoog medium containing 5 μM N6-benzyladenine (BA). Putative mutants from the 40 Gy treatments of either γ- or X-rays exhibited a reduction in shoot weight,
number, and height, whereas treatments of either γ-rays or X-rays at 10 Gy and 20 Gy doses showed no significant differences
in shoot growth. All shoots treated with 80 Gy were either necrotic or irregenerable, while those treated with 40 Gy produced
deformed leaves, from both types of ionizing radiation. Concentrations of AITC were measured by the use of gas chromatography-mass
spectrometry (GC-MS). The accumulation of AITC was shown to decrease when doses increased in both γ- and X-ray treatments,
compared with the controls. Positive responses were solely occurred at 18 mo. after transfer of in vitro rooted shoots to the shade house. The survival rate, rhizome weight and AITC content of plants derived from shoots treated
with 20 Gy or 40 Gy of either γ-rays or X-rays were significantly greater than those of the controls. 相似文献
6.
S.C. Hung N.I. Ghali D.L. Venton G.C. Le Breton 《Prostaglandins & other lipid mediators》1982,24(2):195-206
The effects of prostaglandin F2α on human blood platelet function were investigated. PGF2α at 15 μM completely blocked platelet aggregation induced by 500 μM arachidonic acid or 3 μM U46619 but had no effect on aggregatin induced by 7.5 μM ADP. A similar specificity of action was not obtained with either PGI2 or PGE2. Thus concentrations of PGI2 (3 nM) or PGE2 (20 μ M) which inhibited U46619-induced aggregation by 100% also blocked ADP-stimulated aggregation.The inhibitory properties of PGF2α were not related to increases in platelet cAMP, since direct measurement of intracellular cAMP revealed that 15 μ M PGF2α produced no substantial change in cAMP levels. This finding was in direct contrast to results obtained using either PGI2 or PGE2. Both PGI2 (3 nM) and PGE2 (20 μ M) induced significant increases in platelet cAMP levels.The possibility that PGF2α directly interacts at the platelet TXA2/PGH2 receptor was investigated by measuring [3H]PGF2α binding to isolated platelet membranes. It was found that [3H] PGF2α binding reached equilibrium within 30 min at room temperature and could be 90% displaced by addition of 1000 fold excess of unlabelled PGF2α. Furthermore, when 1000 fold excess of either the TXA2/PGH2 “mimetic” U46619 or the TXA2/PGH2 antagonist 13-azaprostanoic acid was added, specific [3H] PGF2α binding was displaced by 95% and 85% respectively. In contrast, the same molar excess of 6-keto-PGF1α, azo analog 1, or TXB2, caused displacement of only 15%, 20% or 25% of the [3H] PGF2α binding. Scatchard analysis indicated that [3H] PGF2α has two binding sites; i.e., a high affinity binding site with an apparent Kd of 50 nM and a low affinity binding site with apparent Kd of 320 nM. These results suggest that the selective inhibition by PGF2α of AA or U46619-induced aggregation may be mediated through interaction at the platelet TXA2/PGH2 receptor. 相似文献
7.
T.‐H. Yen Y. Chen J.‐F. Fu C.‐H. Weng Y.‐C. Tian C.‐C. Hung J.‐L. Lin C.‐W. Yang 《Cell proliferation》2010,43(3):287-296
Objectives: Myofibroblasts are a vital component of stroma of many malignant neoplasms, but it is not yet established whether stromal myofibroblasts also exist in benign tumours such as oncocytoma of the kidney. Materials and methods: Histomorphological and immunohistochemical analysis of 16 renal oncocytomas diagnosed at Chang Gung Memorial Hospital, Taiwan, has been performed. Results: Renal oncocytomas were composed of oncocytes, large cells with granular eosinophilic cytoplasm, arranged mostly in sheets, in tubulocystic or combined pattern. Few oncocytes appeared to be undergoing proliferation or apoptosis. MIB‐1 and active caspase 3 indices were low, but higher in tumour than in surrounding non‐tumour parenchyma (MIB‐1: 0.93 ± 0.09 versus 0.46 ± 0.07, P < 0.001 and active caspase 3: 0.76 ± 0.08 versus 0.41 ± 0.09, P < 0.001). Wnt/β‐catenin signalling was not implicated in this neoplasm, as there was no loss of E‐cadherin membranous localization or expression of intranuclear β‐catenin in the cells. Clumps of oncocytes were stained with periodic acid Schiff and had collagen I‐, collagen III‐ and fibronectin‐positive, but desmin‐ and human caldesmon‐negative stromas. Importantly, α‐smooth muscle actin (SMA)‐immunostaining established the myofibroblastic nature of many of the stromal cells. Some of the myofibroblasts were also positive for MIB‐1, indicating a proliferative role for them in the stroma. Conclusions: Renal oncocytomas were composed of two independent compartments: benign oncocytes and pronounced fibrotic stroma, which consisted of proliferating myofibroblasts (SMA‐ and MIB‐1‐positive) which were associated with excessive deposition of extracellular matrix (periodic acid Schiff‐component, collagen I‐, collagen III‐ and fibronectin‐positive, and desmin‐ and human caldesmon‐negative). 相似文献
8.
9.
The recent development of third generation sequencing (TGS) generates much longer reads than second generation sequencing (SGS) and thus provides a chance to solve problems that are difficult to study through SGS alone. However, higher raw read error rates are an intrinsic drawback in most TGS technologies. Here we present a computational method, LSC, to perform error correction of TGS long reads (LR) by SGS short reads (SR). Aiming to reduce the error rate in homopolymer runs in the main TGS platform, the PacBio® RS, LSC applies a homopolymer compression (HC) transformation strategy to increase the sensitivity of SR-LR alignment without scarifying alignment accuracy. We applied LSC to 100,000 PacBio long reads from human brain cerebellum RNA-seq data and 64 million single-end 75 bp reads from human brain RNA-seq data. The results show LSC can correct PacBio long reads to reduce the error rate by more than 3 folds. The improved accuracy greatly benefits many downstream analyses, such as directional gene isoform detection in RNA-seq study. Compared with another hybrid correction tool, LSC can achieve over double the sensitivity and similar specificity. 相似文献
10.
Ai‐Xin Song Chen‐Jie Zhou Xiao Guan Kong‐Hung Sze Hong‐Yu Hu 《Protein science : a publication of the Protein Society》2010,19(5):1104-1109
DC‐UbP/UBTD2 is a ubiquitin (Ub) domain‐containing protein first identified from dendritic cells, and is implicated in ubiquitination pathway. The solution structure and backbone dynamics of the C‐terminal Ub‐like (UbL) domain were elucidated in our previous work. To further understand the biological function of DC‐UbP, we then solved the solution structure of the N‐terminal domain of DC‐UbP (DC‐UbP_N) and studied its Ub binding properties by NMR techniques. The results show that DC‐UbP_N holds a novel structural fold and acts as a Ub‐binding domain (UBD) but with low affinity. This implies that the DC‐UbP protein, composing of a combination of both UbL and UBD domains, might play an important role in regulating protein ubiquitination and delivery of ubiquitinated substrates in eukaryotic cells. 相似文献