Huaxiang Liu

Electronic structure and optical properties of Sb-doped SnO2

The electronic structures and optical properties of pure and Sb-doped SnO2 are investigated by first-principles calculations based on the density functional theory. The calculation results show that the Fermi level of SnO2 is located in the band gap, and the maximum of the valence band and minimum of the conduction band are both located at Γ point (the Brillouin zone center), indicating that SnO2 is a direct band gap semiconductor. When one of the 16 Sn atoms in the SnO2 supercell is replaced by one Sb atom, the Fermi level moves into the conduction band and the compound displays metallic characteristics in electronic band structure. For the case of an Sb impurity coexisting with oxygen vacancies, the Fermi level is also located in the conduction band and the density of states near the Fermi level is increased comparing to that without oxygen vacancies. Moreover, some impurity bands depart from the top of the valence band, which narrows the band gap of the compound. With respect to the optical properties,...

Regulatory effect of nerve growth factor on release of substance P in cultured dorsal root ganglion neurons of rat.

To investigate the regulatory effects of nerve growth factor (NGF) on basal and capsaicin-induced release of neuropeptide substance P (SP) in primary cultured embryonic rat dorsal root ganglion (DRG) neurons. DRGs were dissected from 15-day-old embryonic Wistar rats. DRG neurons were dissociated and cultured, and then exposed to different concentrations of NGF (10 ng/mL, 30 ng/mL, or 100 ng/mL) for 72 h. The neurons cultured in media without NGF served as control. RT-PCR were used for detecting the mRNAs of SP and vanilloid receptor 1 (VR1) in the DRG neurons. The SP basal and capsaicin (100 nmol/L)-induced release in the culture were measured by radioimmunoassay (RIA). SP mRNA and VR1 mRNA expression increased in primary cultured DRG neurons in a dose-dependent manner of NGF. Both basal release and capsaicin-evoked release of SP increased in NGF-treated DRG neurons compared with in control group. The capsaicin-evoked release of SP also increased in a dose-dependent manner of NGF. NGF may promote both basal release and capsaicin-evoked release of SP. NGF might increase the sensitivity of nociceptors by increasing the SP mRNA or VR1 mRNA. 观察神经生长因子 (nerve growth factor, NGF) 对原代培养的背根神经节(dorsal root ganglion, DRG)神经元中 P 物质 (substance P, SP) 的基础释放量和辣椒素诱发释放量的调节效应。 将 15 天胚龄的 Wistar 大鼠 DRG 神经元培养于含有不同浓度 NGF 的 DMEM/F12 培养液中, 不含 NGF 的培养液培养的神经元作为对照。 72 小时后, 用RT-PCR检测神经元中 SP mRNA 和辣椒素受体(vanilloid receptor 1, VR1)mRNA 的表达, 用放射免疫分析 (radioimmunoassay, RIA) 法检测 SP 的基础释放量和辣椒素 (100 nmol/L) 刺激 10 min 后的诱发释放量。 SP mRNA 和VR1 mRNA 在 NGF 孵育的标本中表达增加, 并与孵育液中 NGF 的浓度呈剂量依赖关系。 SP 的基础释放量和辣椒素诱发释放量在 NGF 孵育的标本中均增加?而且诱发释放量与 NGF 的浓度呈剂量依赖关系。 NGF 使 DRG 神经元SP的基础释放量和诱发释放量增加, 表明 NGF 能增加初级传入神经元感受伤害刺激的敏感性, 该效应可能与SP 和VR1 的 mRNA 表达增加有关。

Effects of Exogenous Galanin on Neuropathic Pain State and Change of Galanin and Its Receptors in DRG and SDH after Sciatic Nerve-Pinch Injury in Rat

A large number of neuroanatomical, neurophysiologic, and neurochemical mechanisms are thought to contribute to the development and maintenance of neuropathic pain. However, mechanisms responsible for neuropathic pain have not been completely delineated. It has been demonstrated that neuropeptide galanin (Gal) is upregulated after injury in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) where it plays a predominantly antinociceptive role. In the present study, sciatic nerve-pinch injury rat model was used to determine the effects of exogenous Gal on the expression of the Gal and its receptors (GalR1, GalR2) in DRG and SDH, the alterations of pain behavior, nerve conduction velocity (NCV) and morphology of sciatic nerve. The results showed that exogenous Gal had antinociceptive effects in this nerve-pinch injury induced neuropathic pain animal model. It is very interesting that Gal, GalR1 and GalR2 change their expression greatly in DRG and SDH after nerve injury and intrathecal injection of exougenous Gal. Morphological investigation displays a serious damage after nerve-pinch injury and an amendatory regeneration after exogenous Gal treatment. These findings imply that Gal, via activation of GalR1 and/or GalR2, may have neuroprotective effects in reducing neuropathic pain behaviors and improving nerve regeneration after nerve injury.

The effects of galanin on dorsal root ganglion neurons with high glucose treatment in vitro

The exposure of neurons to high glucose concentrations is considered a determinant of diabetic neuropathy. The extracellular high concentration of glucose can cause neuronal cellular damage. Galanin (Gal) not only plays a role in processing of sensory information but also participates in energy homeostasis and glucoregulation. However, the effects of Gal on dorsal root ganglion (DRG) neurons with high glucose are not clear. Using an in vitro model of high glucose-treated DRG neurons in culture, the effects of Gal on intracellular reactive oxygen species (ROS) expression, cell viability, apoptosis, expression of Gal and its receptors (GalR1 and GalR2) of DRG neurons were investigated. Neurons were dissociated from embryonic day 15 (E15) rat DRG and cultured for 48 h and then maintained in serum-free neurobasal medium containing high glucose (45 mmol/L) or normal glucose (25 mmol/L) for 24h. Mannitol (20 mmol/L) was also used to create a high osmotic pressure mimicking the high glucose condition. The results showed that high glucose caused a rapid increasing of intracellular ROS, decreases of cell viability, and upregulation of Gal and its mRNA. Exogenous Gal (1 μmol/L) inhibited the above effects caused by high glucose. Interestingly, high glucose caused downregulation of GalR1 and its mRNA and administration of exogenous Gal could further decrease their expression, whereas expression of GalR2 and its mRNA was not affected at different experimental conditions. The results of the present study indicate for the first time that Gal and its receptor system are involved in high glucose-induced DRG neuronal injury. The contribution of exogenous Gal on neuroprotection appears to be quite significant. These results provide rationale and experimental evidence for development and further studies of Gal on therapeutic strategy for improving diabetic neuropathy.

Neuregulin-1β regulates outgrowth of neurites and migration of neurofilament 200 neurons from dorsal root ganglial explants in vitro

Neuregulin-1β (NRG-1β) signaling has multiple functions in neurons. To assess NRG-1β on neurite outgrowth and neuronal migration in vitro, organotypic dorsal root ganglion (DRG) neuronal culture model was established. Neurite outgrowth and neuronal migration were evaluated using this culture model in the presence (5nmol/L, 10nmol/L, 20nmol/L) or absence of NRG-1β. Neurofilament 200 (NF-200)-immunoreactive (IR) neurons were determined as the migrating neurons. The number of nerve fiber bundles extended from DRG explant increased significantly in the presence of NRG-1β (5nmol/L, 23.0±2.2, P<0.05; 10nmol/L, 27.0±2.7, P<0.001; 20nmol/L, 30.8±3.7, P<0.001) as compared with that in the absence of NRG-1β (19.0±2.2). The number of neurons migrating from DRG explants increased significantly in the presence of NRG-1β (5nmol/L, 39.6±5.0, P<0.05; 10nmol/L, 54.6±6.7, P<0.001; 20nmol/L, 62.2±5.7, P<0.001) as compared with that in the absence of NRG-1β (31.6±4.0). Moreover, the increase of the number of nerve fiber bundles and the number of migrating NF-200-IR neurons was dose-dependent for NRG-1β addition. The data in this study imply that NRG-1β promotes neurite outgrowth and neuronal migration from DRG explants in vitro.

Insulin-Like Growth Factor-1 Regulates Neurite Outgrowth and Neuronal Migration From Organotypic Cultured Dorsal Root Ganglion

ABSTRACT Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor and plays an important role in promoting axonal growth from neurons. Whether IGF-1 could promote neurite outgrowth and neuronal migration of dorsal root ganglion (DRG) explants in vitro remains unknown. In the present study, organotypic rat DRG explant culture model was established. Using this unique culture system, outgrowth of neurites from the peripheral nerve attached to DRG explant and migration of neurons from DRG explant to the peripheral area were quantified in the presence (5 nmol/L, 10 nmol/L, 20 nmol/L) or absence of IGF-1. The number of nerve fiber bundles extended from DRG explant increased significantly in the presence of IGF-1 (5 nmol/L, 19.25 ± 3.11, p < .05; 10 nmol/L, 20.92 ± 2.31, p < .01; 20 nmol/L, 23.00 ± 4.09, p < .001) as compared with that in the absence of IGF-1 (16.58 ± 2.94). The number of neurons migrated from DRG explant increased significantly in the presence of IGF-1 (5 nmol/L, 104.08 ± 16.70, p < .05; 10 nmol/L, 115.25 ± 13.68, p < .001; 20 nmol/L, 138.75 ± 18.05, p < .001) as compared with that in the absence of IGF-1 (90.25 ± 8.53). These data implicated that IGF-1 could promote neurite outgrowth and neuronal migration from DRG explants in vitro.

Optical-transition properties of the Nd3+ ion in Gd0.8La0.2VO4 crystal

Nd:Gd0.8La0.2VO4 has been investigated as a Nd-doped laser crystal belonging to the zircon structural family. The optical absorption and emission properties have been characterized for the Nd3+ ion in Nd:Gd0.8La0.2VO4 crystal. It results in a good fit when the Judd–Ofelt theory of parity-forbidden electric-dipole transitions of rare earth ions on noncentrosymmetric sites is applied to the crystal. Based on the Judd–Ofelt theory, the following spectral parameters have been obtained: the phenomenological parameters Ωt (t=2, 4, and 6), the radiative lifetime, the fluorescence branching ratios and the quantum efficiency. The stimulated emission cross section σe for the 1.06 μm transition of Nd3+ in the crystal has been determined from fluorescence measurements. In comparison with those of other laser crystals, these results indicated that Nd:Gd0.8La0.2VO4 is a promising efficient laser material.

Expression level of the growth factor progranulin is related with development of systemic lupus erythematosus

BackgroundThis study is to investigate the expression of progranulin (PGRN) in systemic lupus erythematosus (SLE) patients and the effect of glucocorticoid (GC) treatment on its expression.MethodsThirty newly diagnosed severe SLE patients and 30 healthy subjects were enrolled in this study. The serum levels of PGRN and the inflammatory factors of SLE were detected by ELISA and the mRNA expression of these proteins were detected by real-time PCR.ResultsThe serum levels of PGRN, IL-6, PR3, TNFR, TNF-α and anti-dsDNA antibody in SLE patients were increased significantly compared with healthy controls (P < 0.05). The relative expression of PGRN mRNA was increased by 4.88-fold in pre-treatment SLE patients compared with controls (P < 0.05). After prednisone treatment, the serum levels of PGRN decreased significantly, and the relative expression of PGRN mRNA was decreased by 1.34-fold compared with the untreated controls (P < 0.01). Moreover, Serum concentration of PGRN was correlated with serum levels of IL-6, TNF-α, TNFR and anti-dsDNA antibody in both pre-treatment and post-treatment SLE patients.ConclusionsPGRN is up-regulated in the SLE patients and is correlated with pro-inflammatory cytokines and anti-dsDNA antibody. Glucocorticoids can down-regulate the expression of PGRN in SLE patients.Virtual slideshttp://www.diagnosticpathology.diagnomx.eu/vs/1562484036905973

The effects of galanin on neuropathic pain in streptozotocin-induced diabetic rats.

Diabetic neuropathy is a common complication associated with diabetes and is frequently painful. However, mechanisms responsible for diabetic neuropathic pain are still unclear. Experimental evidence has shown that the galanin and its receptor are involved in pain sensitization. The objective of the present study was to investigate the role of galanin and its receptor antagonist or agonist on neuropathic pain in streptozotocin-induced diabetic rats. The expression of galanin, galanin receptors 1 and 2 in dorsal root ganglion (DRG) and spinal dorsal horn (SDH) in diabetic rats were detected by Western blot assay. The effects of galanin, galanin receptor antagonist M35, galanin receptor 1 agonist M617, and galanin receptor 2 agonist AR-M1896 on neuropathic pain were evaluated by mechanical stimuli. The results showed that (1) the diabetic rats showed a significant mechanical hyperalgesia between 4 and 12weeks; (2) galanin receptor 1 expression decreased in SDH in diabetic rats; (3) galanin receptor 2 expression decreased in DRG and SDH in diabetic rats; (4) intrathecal administration of exogenous galanin attenuated diabetic neuropathic pain, this effect could be blocked by pre-treatment with galanin receptor antagonist M35; and (5) intrathecal administration of galanin receptor 1 agonist M617, but not galanin receptor 2 agonist AR-M1896, attenuated diabetic neuropathic pain. These results imply that galanin acts through receptor 1, but not galanin receptor 2, to exert analgesic effect in diabetic neuropathic pain and is one of the potential therapeutic targets on diabetic neuropathic pain sensitization.

Neuronal phenotype and tyrosine kinase receptor expression in cocultures of dorsal root ganglion and skeletal muscle cells.

The neuropeptide‐immunoreactive (IR) and neurofilament‐IR neurons are two major phenotypical classes in dorsal root ganglion (DRG). Tyrosine kinase receptor (Trk)A, TrkB, and TrkC are three members of the Trk family which may be relevant to neuronal phenotypes. Whether target skeletal muscle cells generate their expression remains unclear. Neurons containing substance P (SP), calcitonin gene‐related peptide (CGRP), neurofilament 200 (NF‐200), TrkA, TrkB, and TrkC were quantified using immunohistochemistry in rat DRG neuronal cultures and cocultures of DRG neurons and skeletal muscle cells. The percentage of NF‐200 and TrkC‐expressing neurons in cocultures of DRG neurons and skeletal muscle cells was significantly higher, 26.86% ± 3.17% (NF‐200) and 27.74% ± 3.63% (TrkC) compared with 20.92% ± 1.98% (NF‐200) and 16.70% ± 3.68% (TrkC) in DRG cultures; whereas the percentage of SP, CGRP, TrkA, and TrkB‐expressing neurons was not changed significantly by the addition of target skeletal muscle cells. Thus, target skeletal muscle cells may influence neurofilament‐phenotype and TrkC receptor but not neuropeptide‐phenotype and TrkA and TrkB receptors. Anat Rec, 2009.