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Physical contact between melanocytes and keratinocytes is a prerequisite for melanosome transfer to occur, but cellular signals induced during or after contact are not fully understood. Herein, it is shown that interactions between melanocyte and keratinocyte plasma membranes induced a transient intracellular calcium signal in keratinocytes that was required for pigment transfer. This intracellular calcium signal occurred due to release of calcium from intracellular stores. Pigment transfer observed in melanocyte–keratinocyte co‐cultures was inhibited when intracellular calcium in keratinocytes was chelated. We propose that a ‘ligand‐receptor’ type interaction exists between melanocytes and keratinocytes that triggers intracellular calcium signalling in keratinocytes and mediates melanin transfer.  相似文献   
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Bashir G  Shakeel S  Wani T  Kakru DK 《Mycopathologia》2004,158(3):289-291
Pulmonary pseudallescheriasis in an immunocompetent patient without a pre-existing cavity or cyst is a rare phenomenon. We report a case of invasive pulmonary pseudallescheriasis in a lobectomised patient treated for tuberculosis. Filamentous fungi with pyriform conidia were seen in the bronchoalveolar lavage fluid .The fungus was identified as Pseudallescheria boydii on culture.  相似文献   
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We studied the prooxidant and cytotoxic action of thiols N-acetylcystein (NAC) and glutathione (GSH) combined with vitamin Bl2b. The synergism of action of the thiols and Bl2b resulted in human carcinoma cell damage was found. It was shown that GSH and NAC in physiological doses combined with Bl2b caused the initiation of apoptosis. It was established that prooxidant action of the thiols combined with vitamin Bl2b, i. e. generation and accumulation of hydrogen peroxide in culture medium, led to intracellular oxidative stress and injury of cell redox system. These effects were completely abolished by nonthiol antioxidants catalase and pyruvate. The chelators of iron phenanthroline and deferoxamine did not suppress the H2O2 accumulation in culture medium but significantly inhibited the cell death induced by the thiols combined with Bl2b. Therefore, the thiols GSH and NAC widely used as antioxidants, in combination with vitamin Bl2b show prooxidant characteristics and induce, with the participation of intracellular iron, apoptotic HEp-2 cell death.  相似文献   
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We investigated the mechanism of synaptic suppression by P2Y receptors in mixed hippocampal cultures wherein networked neurons exhibit synchronized Ca2+ oscillations (SCO) due to spontaneous glutamatergic synaptic transmission. Pharmacological studies suggested that SCO suppression was mediated by P2Y2/P2Y4 receptors. Immunostaining studies and characterization of ATP/UTP-stimulated Ca2+ responses in solitary neurons and astrocytes revealed that the SCO attenuation was effectuated by astrocytes. We demonstrate that nitric oxide released from activated astrocytes causes synaptic suppression by inhibiting neurotransmitter release. Physiological concentrations of ATP and UTP evoked NO production in astrocytes. SCO suppression was considerably diminished by removal of extracellular NO by membrane-impermeable scavenger c-PTIO or by pretreatment of cells with nitric oxide synthase inhibitor L-NAME. The nitric oxide donor DETA/NO effectively suppressed the SCO. ATP/UTP inhibited KCl-induced exocytosis at presynaptic terminals in an NO-dependent manner. In the absence of exogenously added ATP/UTP, both the NO scavenger and NOS inhibitor enhanced the frequency of SCO, implying that astrocytes release NO during spontaneous synaptic activity and exert a suppressive effect. We report for the first time that under physiological conditions astrocytes use NO as a messenger molecule to modulate the synaptic strength in the networked neurons.  相似文献   
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Hypoxia ischemia (HI)-related brain injury is the major cause of long-term morbidity in neonates. One characteristic hallmark of neonatal HI is the development of reactive astrogliosis in the hippocampus. However, the impact of reactive astrogliosis in hippocampal damage after neonatal HI is not fully understood. In the current study, we investigated the role of Na+/H+ exchanger isoform 1 (NHE1) protein in mouse reactive hippocampal astrocyte function in an in vitro ischemia model (oxygen/glucose deprivation and reoxygenation, OGD/REOX). 2 h OGD significantly increased NHE1 protein expression and NHE1-mediated H+ efflux in hippocampal astrocytes. NHE1 activity remained stimulated during 1–5 h REOX and returned to the basal level at 24 h REOX. NHE1 activation in hippocampal astrocytes resulted in intracellular Na+ and Ca2+ overload. The latter was mediated by reversal of Na+/Ca2+ exchange. Hippocampal astrocytes also exhibited a robust release of gliotransmitters (glutamate and pro-inflammatory cytokines IL-6 and TNFα) during 1–24 h REOX. Interestingly, inhibition of NHE1 activity with its potent inhibitor HOE 642 not only reduced Na+ overload but also gliotransmitter release from hippocampal astrocytes. The noncompetitive excitatory amino acid transporter inhibitor TBOA showed a similar effect on blocking the glutamate release. Taken together, we concluded that NHE1 plays an essential role in maintaining H+ homeostasis in hippocampal astrocytes. Over-stimulation of NHE1 activity following in vitro ischemia disrupts Na+ and Ca2+ homeostasis, which reduces Na+-dependent glutamate uptake and promotes release of glutamate and cytokines from reactive astrocytes. Therefore, blocking sustained NHE1 activation in reactive astrocytes may provide neuroprotection following HI.  相似文献   
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Prooxidant and cytotoxic effects of thiols N-acetylcysteine (NAC) and glutathione (GSH) were studied in combinations with vitamin B12b. Both GSH and NAC at physiological doses when combined with B12b were shown to cause initiation of apoptosis. It was established that the prooxidant action of NAC (or GSH) combined with B12b, i.e., generation and accumulation of hydrogen peroxide in culture medium, led to intractellular oxidative stress and cell redox imbalance. These effects are completely prevented by nonthiol antioxidants catalase and pyruvate. The chelators of iron phenanthroline and deferoxamine do not suppress the H2O2 accumulation in culture medium, but inhibit cell death induced by NAC combined with B12b or by GSH combined with B12b. Therefore, the thiols GSH or NAC in combination with vitamin B12b reveal prooxidant properties and induce, with participation of intracellular iron, apoptotic HEp-2 cell death.  相似文献   
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A total of 1,030 patients, 40.2% men and 59.8% women, identified during the period of October 1998 to November 2002 as having cutaneous leishmaniasis (CL), were studied; 1,431 lesions were identified in the 1,030 patients. One lesion was present in 80.7% of the patients. The size of the lesions (longest axis) was 13.6 mm (standard, 12.1 mm; range 3-150 mm). Most of the lesions were of the papular type (51.2%), although several atypical clinical presentations of CL were observed. The duration of the disease ranged between 1 and 72 mo (mean duration, 10.8 mo). The clinical suspicion of CL was confirmed by the observation of amastigotes on lesion tissue samples stained by Giemsa. The test was positive in 851 of 1,030 patients (82.6%). Intralesional meglumine antimonate solution (85 mg Sb/ml, 0.2-1 ml, depending on the size of the lesion) weekly until complete cure or up to 20 wk was used for first-line therapy of 890 patients (86.4%). We found that this regimen of intralesional Sb has an efficacy of 97.2% with a low relapse rate of 3.9% and no serious adverse side effects.  相似文献   
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