A new species and key to known species of the genus Conophymacris Willemse, 1933 (Orthoptera, Acridoidea, Catantopidae, Podisminae) from China.

A new species in the genus Conophymacris Willemse, 1933 from Yunnan, China is described. The new species Conophymacris reni sp. nov. is similar to C. jiulongensis Zheng et al., 2009, but differs from latter in width of vertex between eyes of male equal to 2.8 width of frontal ridge between antennae, epiproct of male width longer than length, cercus of male apical part not wider, tegmina extending over the hind margin of first abdominal tergum, hind tibia all red, epiphallus ancorae small, lower than anterior projection, lophi not acute, width of subgenital plate shorter than its length and hind margin with 1 tooth in female. Type specimens are deposited in the Natural Museum of Hebei University, Baoding, Hebei, China.

Intervention of Tyrosine Hydroxylase Expression Alters Joint Inflammation and Th17/Treg Imbalance in Collagen-Induced Arthritis.

BACKGROUND/AIMS: Neuroendocrine dysregulation has been associated with rheumatoid arthritis (RA). Tyrosine hydroxylase (TH), a rate-limiting enzyme for synthesis of neuroendocrine hormones such as epinephrine, is also expressed in T lymphocytes and regulates balance between helper T (Th) 17 cells and regulatory T (Treg) cells. Herein, we aimed to show that TH expression in joints alleviates joint inflammation and Th17/Treg imbalance in collagen-induced arthritis (CIA), an animal model of RA, and these effects may be implemented by the mechanism of epinephrine action on α1-adrenoreceptor (α1-AR) in T cells. METHODS: CIA was prepared by intradermal injection of collagen type II in tail base of DBA1/J mice. On the 33rd day post-immunization, lentiviral vectors encoding TH or TH shRNA were injected into ankle joints of CIA mice. Limb inflammation of the mice was assessed beginning from day 21 until day 69 post-immunization by measurement of limb swelling, erythema and rigidity. Th17 and Treg differentiation and function in ankle joints were assessed on day 69 post-immunization by test of the expression of Th17 transcriptional factor ROR-γt and the levels of proinflammatory cytokines interleukin (IL)-17 and IL-22 as well as the expression of Treg transcriptional factor Foxp3 and the levels of antiinflammatory cytokines transforming growth factor (TGF)-ß1 and IL-10. T cells were obtained from the spleen of mice that had been immunized with collagen type II 41 day earlier and treated with epinephrine or α1-AR agonist phenylephrine in vitro. Flow cytometry was used to analyze the percentages of CD25-IL-17+ cells and CD25+Foxp3+ cells in CD4+ T cells. RESULTS: TH gene overexpression in ankle joints of CIA mice reduced limb inflammation and Th17-related transcription factor expression and inflammatory cytokine production but increased Treg-related antiinflammatory cytokine production in the joints. In contrast, TH gene silence in ankle joints of CIA mice enhanced limb inflammation and Th17 cell activity but decreased Treg cell function in the joints. Epinephrine upregulated α1-AR expression in T cells derived from CIA mice. Both epinephrine and phenylephrine reduced CIA-induced Th17 transcription factor expression and inflammatory cytokine production but enhanced Treg antiinflammatory cytokine production in vitro. CONCLUSION: Upregulating TH expression in joints alleviates joint inflammation and Th17/Treg imbalance in CIA at least partially by enhancing epinephrine action on α1-AR in T cells.

Pannexin 1, a large-pore membrane channel, contributes to hypotonicity-induced ATP release in Schwann cells.

Pannexin 1 (Panx 1), as a large-pore membrane channel, is highly permeable to ATP and other signaling molecules. Previous studies have demonstrated the expression of Panx 1 in the nervous system, including astrocytes, microglia, and neurons. However, the distribution and function of Panx 1 in the peripheral nervous system are not clear. Blocking the function of Panx 1 pharmacologically (carbenoxolone and probenecid) or with small interfering RNA targeting pannexins can greatly reduce hypotonicity-induced ATP release. Treatment of Schwann cells with a Ras homolog family member (Rho) GTPase inhibitor and small interfering RNA targeting Rho or cytoskeleton disrupting agents, such as nocodazole or cytochalasin D, revealed that hypotonicity-induced ATP release depended on intracellular RhoA and the cytoskeleton. These findings suggest that Panx 1 participates in ATP release in Schwann cells by regulating RhoA and the cytoskeleton arrangement. This study was approved by the Animal Ethics Committee of Nantong University, China (No. S20180806-002) on August 5, 2018.

--A new species and a key to 10 species of the genus Lemba Huang, 1983 (Orthoptera: Catantopidae) from China.

A new species and a key to 10 species of the genus Lemba Huang, 1983, namely Lemba wushanensis sp. nov. is described in this paper from China. The new species is similar to L. sichuanensis Ma et al, 1994, but differs from the latter by the length of tegmen 2.7 times width in male, length of interspace of mesosternum 3.5 times width in male, posterior margin of epiproct straight; ancorae of epiphallus not inward tilt and vertical diameter 1.8 times subocular furrow in female. The type specimens are deposited in the Northwest Plateau Institute of Biology, Chinese Academy of Sciences, Xining, China.

Study on efficacy and safety of Huangqi Guizhi Wuwu decoction treatment for oxaliplatin induced peripheral neurotoxicity: A protocol for a randomized, controlled, double-blind, multicenter trial.

BACKGROUND: Oxaliplatin can cause severe peripheral neurotoxicity, which is an important reason for clinical oxaliplatin reduction and cessation of treatment. Oxaliplatin induced peripheral neurotoxicity (OIPN) can cause paresthesia and dysesthesia, even affect the quality life of patients. So far, there are no recognized and effective measures to prevent OIPN. Huangqi Guizhi Wuwu decoction is a classical prescription of ancient Chinese medicine recorded in "the synopsis of the Golden Chamber," which can be used in the treatment of various neurotoxicity. However, there is a lack of large-scale and high-quality clinical studies on the prevention of OIPN by Huangqi Guizhi Wuwu decoction. The purpose of this study is to evaluate the efficacy and safety of Huangqi Guizhi Wuwu decoction on preventing OIPN. METHODS/DESIGN: This study is a randomized, controlled, double-blind, and multicenter clinical trial. Three hundred sixty patients will be randomly assigned into Huangqi Guizhi Wuwu decoction group and Huangqi Guizhi Wuwu decoction mimetic agent group. Patients will receive chemotherapy with FOLFOX of 8 cycles of 3 weeks with Traditional Chinese Medicine (TCM) for 6 months and 1-year follow-up. The primary outcome measure is the differences in the incidence of chronic neurotoxicity of grade 2 and above during and after treatment. The secondary outcome measure is the improvement in other symptoms associated with chemotherapy. Four methods will be used to evaluate the efficacy of neurotoxicity, including oxaliplatin specific toxicity grading standard (Levi classification); CTCAE4.02 version; EORTC QLQ-CIPN20 scale, EORTC QLQ C30 scale, and EORTC QLQ-CR29 scale are used at the same time; Electromyography. DISCUSSION: This study will provide objective evidences to evaluate the efficacy and safety of Huangqi Guizhi Wuwu Decoction on preventing OIPN. TRIAL REGISTRATION: Clinical Trials.gov (Identifier: NCT04261920).

Acetylcholine suppresses microglial inflammatory response via α7nAChR to protect hippocampal neurons.

Neuroinflammation is principally linked to glial function and has been demonstrated to participate in the pathogenesis of Alzheimer's disease, a neurodegenerative disorder characterized by beta-amyloid ccumulation and neurotransmission disruption. Previous findings suggest acetylcholine exerts anti-inflammatory and neuroprotective properties in several neurodegenerative disorders. However, the underlying mechanisms remain elusive. Here evaluation of the influence of acetylcholine on neuroinflammation and neurodegeneration in Alzheimer's disease is reported and further neuroprotective mechanisms are investigated. Investigation of microglia in lipopolysaccharide-induced hippocampal neuronal toxicity employed α7nAChR gene silencing and demonstrated that both the anti-inflammatory and neuroprotective effects of acetylcholine rely on α7nAChR pathways. As expected, in neuron-microglia co-cultures lipopolysaccharide induced an increase in expression of pro-inflammatory factors, including inducible nitric oxide synthase, interleukin-1α, and tumor necrosis factor-α, and decreased expression of neurotrophic factors such as insulin-like growth factor-1, and neuronal apoptosis. Acetylcholine protects against lipopolysaccharide-elicited neuronal injury by inhibiting the microglial inflammatory response and promoting microglial neurotrophic factor production via the action of α7nAChR on microglia. These findings establish that ACh activates α7nAChR in microglia, which in turn protects hippocampal neurons.

2-Hydroxy-3-methylanthraquinone inhibits lung carcinoma cells through modulation of IL-6-induced JAK2/STAT3 pathway.

BACKGROUND: 2-hydroxy-3-methylanthraquinone (HMA), an anthraquinone monomer in traditional Chinese medicine Hedyotis diffusa, has been reported to inhibit the growth of several types of cancer, but its effect on lung cancer has not been adequately investigated. HYPOTHESIS/PURPOSE: This study aimed to test the hypothesis that HMA inhibit the growth, migration, and invasion of lung cancer cells in part via downregulation of interleukin (IL)-6-induced JAK2/STAT3 pathway. METHODS: Growth and apoptosis of lung cancer cells were quantitated by CCK-8 assay and Annexin V-FITC/PI flow cytometric analysis, respectively. Migration and invasion of A549 cells were determined by wound-healing assay and transwell invasion assay, respectively. The effect of HMA on cytokines expression in A549 cells was evaluated by the cytokine antibody array assay. Gene expression and protein levels of related molecular markers were quantitated by real time-PCR and Western blot analysis, respectively. RESULTS: HMA significantly inhibited IL-6-stimulated growth and colony formation of A549 cells, increased the number of apoptotic cells, and inhibited invasion associated with downregulation of expression of IL-6-induced MMP-1, MMP-2, and MMP-9 genes. IL-6 increased the levels of tyrosine phosphorylation of JAK2 and STAT3 in A549 cells, which was reversed by HMA treatment. In addition, HMA reduced the expression of a series of inflammation-related cytokines in A549 cells supernatant, including IL-6, G-CSF, IL-6R, IL-8, MCP-1, RANTES, TNF-α. CONCLUSION: These results suggest that HMA may inhibit the growth and invasion of lung cancer cells in part via downregulation of IL-6-induced JAK2/STAT3 pathway.

[Acetylcholine suppresses microglial inflammatory response in rats via acting on microglial α7nAChR].

Microglia are the main immune cells in the central nervous system. In the present study, the mechanism for acetylcholine (ACh) inhibiting microglial inflammatory response was investigated. Primary culture of microglia was isolated from cerebral cortex of Sprague-Dawley (SD) rats. Lipopolysaccharide (LPS) was used to activate the microglia to induce inflammatory response, and then the microglia were treated with ACh for 24 h. Protein expressions of several inflammatory factors, insulin-like growth factor 1 (IGF-1) and α7 nicotinic acetylcholine receptor (α7nAChR) were detected by Western blot. Release of inflammatory factors and IGF-1 into media was detected by ELISA. After α7nAChR gene silence was achieved by lentivirus-transfection of α7nAChR-shRNA, the change of ACh effect was observed. The results showed that LPS induced microglial activation, up-regulated inducible nitric oxide synthase (iNOS) protein expression, increased the expressions and release of IL-1ß and TNF-α, and decreased the expression and release of the neurotrophic factor, IGF-1. ACh could reverse these effects of LPS. Meanwhile, LPS reduced the protein expression of α7nAChR on the microglial cells, whereas ACh could reverse the effect. Silencing of α7nAChR gene in microglia abolished the ability of ACh to inhibit LPS-induced inflammatory responses. These results suggest that ACh exerts its protection against LPS-induced microglial inflammation via acting on α7nAChR on microglia, which may provide a novel target for the treatment of neuro-inflammatory diseases.

Cardioprotective Effect of Electroacupuncture Pretreatment on Myocardial Ischemia/Reperfusion Injury via Antiapoptotic Signaling.

Objectives. Our previous study has used RNA-seq technology to show that apoptotic molecules were involved in the myocardial protection of electroacupuncture pretreatment (EAP) on the ischemia/reperfusion (I/R) animal model. Therefore, this study was designed to investigate how EAP protects myocardium against myocardial I/R injury through antiapoptotic mechanism. Methods. By using rats with myocardial I/R, we ligated the left anterior descending artery (LAD) for 30 minutes followed by 4 hr of reperfusion after EAP at the Neiguan (PC6) acupoint for 12 days; we employed arrhythmia scores, serum myocardial enzymes, and cardiac troponin T (cTnT) to evaluate the cardioprotective effect. Heart tissues were harvested for western blot analyses for the expressions of pro- and antiapoptotic signaling molecules. Results. Our preliminary findings showed that EAP increased the survival of the animals along with declined arrhythmia scores and decreased CK, LDH, CK-Mb, and cTnT levels. Further analyses with the heart tissues detected reduced myocardial fiber damage, decreased number of apoptotic cells and the protein expressions of Cyt c and cleaved caspase 3, and the elevated level of Endo G and AIF after EAP intervention. At the same time, the protein expressions of antiapoptotic molecules, including Xiap, BclxL, and Bcl2, were obviously increased. Conclusions. The present study suggested that EAP protected the myocardium from I/R injury at least partially through the activation of endogenous antiapoptotic signaling.

Effects and mechanisms of auricular vagus nerve stimulation on high-fat-diet--induced obese rats.

OBJECTIVE: Obesity is a major public health problem. Regulating food intake and promoting metabolism of fat are two important options for treating obesity. Auricular vagus nerve stimulation (AVNS) is considered as an alternative approach to vagal nerve stimulation. The aim of this study was to investigate the effects of AVNS and its mechanisms on obesity in obese rats. METHODS: Male Sprague-Dawley rats were fed either a high-fat diet (HFD) or a normal diet for 8 wk. Qualified HFD rats were randomly divided into three groups: the HFD group, the AVNS group, and the sham group for 6 wk treatment. Body weight and daily energy intake were recorded weekly. The rats were sacrificed for measurement of weight of bilateral perirenal, epididymal white adipose tissue (WAT), dorsal brown adipose tissue (BAT), and gastric emptying. Serum cholecystokinin (CCK), peptide YY3 to 36 (PYY3-36) and norepinephrine (NE) were assayed by enzyme-linked immunosorbent assay. Real-time quantitative polymerase chain reaction was used to assess the mRNA expressions of CCK subtype receptor a (CCKa) in the antrum, PYY3-36 receptor in the distal ileum, ß3-adrenoceptor, and uncoupling protein gene 1 (UCP1) in the BAT. RESULTS: Compared with HFD group, AVNS significantly reduced body weight and epididymal WAT and increased BAT weight, serum NE, mRNA expressions of ß3-adrenoceptors, and UCP1 of the BAT, but had no effect on daily energy intake, perirenal WAT weight, gastric emptying, serum levels of CCK and PYY, or mRNA expressions of CCKa receptor and PYY3-36 receptor in the relevant tissues. The sham group, as a comparison group for AVNS, saw less effect in any of the indexes compared with the HFD group. AVNS had more effect on weight loss, reduction of perirenal WAT, and increase of NE, ß3-adrenoceptor, and UCP1 than sham. CONCLUSIONS: AVNS was more effective in reducing body weight and causing visceral fat loss. Biochemical tests found more NE released in the serum and more ß3-adrenoceptor and UCP1 expression in the BAT. All of these features suggested that energy expenditure might play an important role in obesity management by AVNS.

Interleukin-6 reduces NMDAR-mediated cytosolic Ca²âº overload and neuronal death via JAK/CaN signaling.

Cytosolic Ca(2+) overload induced by N-methyl-D-aspartate (NMDA) is one of the major causes for neuronal cell death during cerebral ischemic insult and neurodegenerative disorders. Previously, we have reported that the cytokine interleukin-6 (IL-6) reduces NMDA-induced cytosolic Ca(2+) overload by inhibiting both L-type voltage-gated calcium channel (L-VGCC) activity and intracellular Ca(2+) store release in cultured cerebellar granule neurons (CGNs). Here we aimed to show that NMDA-gated receptor channels (i.e., NMDA receptors, NMDARs) are an inhibitory target of IL-6 via a mediation of calcineurin (CaN) signaling. As expected, IL-6 decreased NMDAR-mediated cytosolic Ca(2+) overload and inward current in cultured CGNs. The NMDAR subunits, NR1, NR2A, NR2B and NR2C, were expressed in CGNs. Blocking either of NR2A, NR2B and NR2C with respective antagonist reduced NMDA-induced extracellular Ca(2+) influx and neuronal death. Importantly, the reduced percentages in extracellular Ca(2+) influx and neuronal death by either NR2B or NR2C antagonist were weaker in the presence of IL-6 than in the absence of IL-6, while the reduced percentage by NR2A antagonist was not significantly different between the presence and the absence of IL-6. AG490, an inhibitor of Janus kinase (JAK), abolished IL-6 protection against extracellular Ca(2+) influx, mitochondrial membrane depolarization, neuronal death, and CaN activity impairment induced by NMDA. The CaN inhibitor FK506 reduced these IL-6 neuroprotective properties. Collectively, these results suggest that IL-6 exerts neuroprotection by inhibiting activities of the NMDAR subunits NR2B and NR2C (but not NR2A) via the intermediation of JAK/CaN signaling.

[Relevance of cancer toxin pathogenesis theory with transformation of inflammation to carcinoma].

The "Cancer Toxin" pathogenesis theory is an innovate theoretical system for cancer pathogenesis of Chinese Medicine, which was built on the basis of "Cancer Toxin" concept initially raised by Professor ZHOU Zhong-ying. The mechanism of the transformation from inflammation to carcinoma has become one of hot-points in the field of cancer research at home and abroad in recent years. We focused on discussing the relevance of the "Cancer Toxin" pathogenesis theory with the transformation mechanism from inflammation to cancer, provided evidence for using "Cancer Toxin" pathogenesis theory in intervening transformation from inflammation to cancer, hoping to guide for Chinese medical prevention and treatment of tumor.

Longikaurin E induces apoptosis of pancreatic cancer cells via modulation of the p38 and PI3K/AKT pathways by ROS.

Pancreatic cancer is a devastating disease with a poor prognosis. It ranks as the fourth or fifth most common cancer in men and women and has the lowest 5-year survival rate. Therefore, there is an urgent need to develop novel therapeutic agents for pancreatic cancer. Longikaurin E (LE), which is derived from the traditional herbal medicine Rabdosia longituba, had been reported to have anti-proliferative and pro-apoptotic properties in several types of cancers. In this study, we investigated the cytotoxic properties of LE against pancreatic cancer cells and explored the mechanism behind the observed apoptosis. Pancreatic cancer cell lines cultured in the presence of LE exhibited dose- and time-dependent growth suppression by clone formation, methylthiazoltetrazolium assay, lactate dehydrogenase cytotoxicity assay, and fluorescence-activated cell sorting analysis, respectively. In addition, these culture conditions also induced the generation of cellular reactive oxygen species (ROS). In order to determine the mechanisms underlying LE-induced cytotoxicity, we used reverse transcription polymerase chain reaction and Western blot analysis in the pancreatic cancer cell line PANC1. The results showed that the expression of Bax was noticeably upregulated and the expression levels of Bcl-2, Bcl-XL, survivin, and c-Myc were significantly downregulated. We also observed increased p38 phosphorylation and decreased phosphorylation of the PI3K/AKT pathway. Interestingly, we also found that LE activated caspase-3. However, N-acetyl-L-cysteine, a kind of antioxidant, reversed all of these cellular activities. In conclusion, this study suggested that LE induced apoptosis of pancreatic cancer cells via ROS generation to modulate the p38 and PI3K/AKT pathways and could be a promising anti-pancreatic agent.

TGF-ß1 protection against Aß1-42-induced neuroinflammation and neurodegeneration in rats.

Transforming growth factor (TGF)-ß1, a cytokine that can be expressed in the brain, is a key regulator of the brain's responses to injury and inflammation. Alzheimer's disease (AD), the most common neurodegenerative disorder, involves inflammatory processes in the brain in addition to the hallmarks, amyloid-ß (Aß) plaques and neurofibrillary tangles. Recently, we have shown that T-helper (Th) 17 cells, a subpopulation of CD4+ T-cells with high proinflammation, also participate in the brain inflammatory process of AD. However, it is poorly known whether TGF-ß1 ameliorates the lymphocyte-mediated neuroinflammation and, thereby, alleviates neurodegeneration in AD. Herein, we administered TGF-ß1 via the intracerebroventricle (ICV) in AD model rats, by Aß1-42 injection in both sides of the hippocampus, to show the neuroprotection of TGF-ß1. The TGF-ß1 administration after the Aß1-42 injection ameliorated cognitive deficit and neuronal loss and apoptosis, reduced amyloid precursor protein (APP) expression, elevated protein phosphatase (PP)2A expression, attenuated glial activation and alleviated the imbalance of the pro-inflammatory/anti-inflammatory responses of T-lymphocytes, compared to the Aß1-42 injection alone. These findings demonstrate that TGF-ß1 provides protection against AD neurodegeneration and suggest that the TGF-ß1 neuroprotection is implemented by the alleviation of glial and T-cell-mediated neuroinflammation.

Electro-acupuncture at Neiguan pretreatment alters genome-wide gene expressions and protects rat myocardium against ischemia-reperfusion.

This study investigated genome-wide gene expressions and the cardioprotective effects of electro-acupuncture pretreatment at the PC6 Neiguan acupoint on myocardial ischemia reperfusion (I/R) injury. Male SD rats were randomly divided into four groups: sham operation (SO), I/R, electro-acupuncture at the PC6 Neiguan acupoint pretreatment (EA) and electro-acupuncture at non-acupoint pretreatment (NA). Compared with the I/R group, the survival rate of the EA group was significantly increased, the arrhythmia score, infarction area, serum concentrations of CK, LDH and CK-Mb and plasma level of cTnT were significantly decreased. RNA-seq results showed that 725 genes were up-regulated and 861 genes were down-regulated under I/R conditions compared to the SO group; both EA and NA reversed some of these gene expression levels (592 in EA and 238 in NA group). KEGG pathway analysis indicated that these genes were involved in multiple pathways, including ECM, MAPK signaling, apoptosis, cytokine and leukocyte pathways. In addition, some pathways were uniquely regulated by EA, but not NA pretreatment, such as oxidative stress, cardiac muscle contraction, gap junction, vascular smooth muscle contraction, hypertrophic, NOD-like receptor, and P53 and B-cell receptor pathways. This study was first to reveal the gene expression signatures of acute myocardial I/R injury and electro-acupuncture pretreatment in rats.

Acupuncture promotes angiogenesis after myocardial ischemia through H3K9 acetylation regulation at VEGF gene.

BACKGROUND: Acupuncture exerts cardioprotective effects on several types of cardiac injuries, especially myocardial ischemia (MI), but the mechanisms have not yet been well elucidated. Angiogenesis mediated by VEGF gene expression and its modification through histone acetylation has been considered a target in treating myocardial ischemia. This study aims to exam whether modulation of angiogenesis through H3K9 acetylation regulation at VEGF gene is one possible cardioprotective mechanism of acupuncture. RESULTS: We generated rat MI models by ligating the left anterior descending coronary artery and applied electroacupuncture (EA) treatment at the Neiguan (PC6) acupoint. Our results showed that acupuncture reversed the S-T segment change, reduced Q-wave area, decreased CK, CK-MB, LDH levels, mitigated myocardial remodeling, and promoted microvessel formation in the MI heart. RNA-seq analysis showed that VEGF-induced angiogenesis signaling was involved in the modulation of EA. Western blot results verified that the protein expressions of VEGF, Ras, phospho-p44/42 MAPK, phospho-p38 MAPK, phospho-SAPK/JNK and Akt, were all elevated significantly by EA treatment in the MI heart. Furthermore, increased H3K9 acetylation was also observed according with the VEGF. ChIP assay confirmed that EA treatment could notably stimulate the recruitment of H3K9ace at the VEGF promoter. CONCLUSIONS: Our study demonstrates for the first time that acupuncture can effectively up-regulate VEGF expression through H3K9 acetylation modification directly at the VEGF promoter and hence activate VEGF-induced angiogenesis in rat MI models. We employed high throughput sequencing in this study and, for the first time, generated genome-wide gene expression profiles both in the rat MI model and in acupuncture treatment.

[Experimental study of recording and analysing electrophysiological signals from corticospinal tract in rats].

OBJECTIVE: To explore the recording method of the electrophysiological signals in corticospinal tract (CST) of adult rats by plugging microelectrodes and analyze the characteristics of these signals. These could provide some valuable and basic neural electrophysiological information for further research of recovering and refunctioning after spinal cord injury. METHODS: The microelectrodes were plugged into the corticospinal tract at the T8 spinal section of Sprague-Dawley rats and the neuro-electrical signals were identified and recorded from CST by means of the Cerebus System. The characteristics of the recorded signals were described with the help of the Offline sorter and Neuroexplorer softwares, including the wavelength, amplitude, discharging frequency, the synchrony among the multi-discharging units from the same electrode and two different electrodes, analysis of interspike interval (ISI), etc. RESULTS: The continuous and steady spontaneous electrophysiological signals were recorded from CST. Three or four types of discharging signals originated from different discharging units were collected with each electrode. The waveform of the signals appeared bidirectional. The wavelengths were 0.6 - 1.3 ms with wave amplitudes at a grade of hundred microvoltage and high signal-noise ratios. The LFB staining proved that the electrodes were accurately plugged into the corticospinal tract. CONCLUSION: The neuro-electrical signals at a grade of hundred microvoltage could be recorded stably from the corticospinal tract of rats by the Cerebus System with the microelectrodes, which provided valuable and basic neural electrophysiological information for further research on recovering and refunctioning after spinal cord injury (SCI) by analyzing the characteristics of electrophysiological signals.

Requirement of hydrogen peroxide and Sp1 in the stimulation of Na,K-ATPase by low potassium in MDCK epithelial cells.

We have previously implicated reactive oxygen species oxygen (ROS) as a critical signal transducer in the upregulation of Na,K-ATPase by low K+ in MDCK cells, but how ROS mediate this process has not been well defined. We reported here that both of hydrogen peroxide (H2O2) and superoxide anion (O2*(-)) were rapidly produced at the early stage of low K+-treated MDCK cells. Further analysis revealed that NADP/NADPH oxidase-derived H2O2 was specifically involved in low K+-induced Na,K-ATPase alpha1 gene transcription as well as alpha1 and beta1 subunits expressions. Exogenous H2O2 even mimicked the stimulatory effect of low K+ on Na,K-ATPase alpha1 gene transcription. Low K+ triggered a H2O2-dependent ERK1/2 phosphorylation in MDCK cells, nonetheless, this ERK1/2 activation did not finally lead to the upregulation of Na,K-ATPase. Similar to previous findings that Na,K-ATPase beta1 gene transcription was mediated by Sp1, Na,K-ATPase alpha1 gene transcription in low K+-treated MDCK cells was also closely relevant to Sp1 participation, as confirmed by siRNA as well as PCR mutagenesis technologies. Furthermore, Sp1 activation was dependent on H2O2 generation triggered by low K+. Taken together, the data described in this study outlines an essential role of H2O2 and Sp1 in mediating the upregulation of Na,K-ATPase in MDCK cells by low external K+.