Stimulation of renin secretion by angiotensin II blockade is Gsalpha-dependent.

Angiotensin II converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB) presumably stimulate renin secretion by interrupting angiotensin II feedback inhibition. The increase in cytosolic calcium caused by activation of Gq-coupled AT1 receptors may mediate the renin-inhibitory effect of angiotensin II at the cellular level, implying that ACEI and ARB may work by reducing intracellular calcium. Here, we investigated whether angiotensin II blockade acts predominantly through Gs-mediated stimulation of adenylyl cyclase (AC) by testing the effect of ACEI and ARB in mice with juxtaglomerular cell-specific deficiency of the AC-stimulatory Gsalpha.

Enhanced tubuloglomerular feedback in mice with vascular overexpression of A1 adenosine receptors.

Adenosine 1 receptors (A1AR) in the kidney are expressed in the vasculature and the tubular system. Pharmacological inhibition or global genetic deletion of A1AR causes marked reductions or abolishment of tubuloglomerular feedback (TGF) responses. To assess the function of vascular A1AR in TGF, we generated transgenic mouse lines in which A1AR expression in smooth muscle was augmented by placing A1AR under the control of a 5.

[Study on collector for spores of Ganoderma spp].

Objective: To develop a convenient, practical low-cost and efficient Ganoderma spore collector.

Method: The spore collector was made from common materials such as white cardboard and oil-lustrous paper, temperature and humidity were used as indexes to study the effect of the collector on the growth environment of Ganoderma and spore collection.

Result: The spore collector developed could effectively separate Ganoderma fruit bodies from the outside to form an independent closed space and stop free flow of spores.

Overexpression of PwTUA1, a pollen-specific tubulin gene, increases pollen tube elongation by altering the distribution of alpha-tubulin and promoting vesicle transport.

Tubulin genes are intimately associated with cell division and cell elongation, which are central to plant secondary cell wall development. However, their roles in pollen tube polar growth remain elusive. Here, a TUA1 gene from Picea wilsonii, which is specifically expressed in pollen, was isolated.

Gene induction for the treatment of methylmalonic aciduria.

Background: Methylmalonic aciduria is an autosomal recessive inborn error of the propionate metabolic pathway. One form of this disorder is caused by mutations in methylmalonyl-coenzyme A mutase (MCM), resulting in reduced levels of enzyme activity. The pharmacological up-regulation of residual mutase activity is one approach to advance treatment strategies for individuals affected by this disorder.

[Mental status of surgical medical staff who treated or did not treat the victims in Wenchuan earthquake].

Objective: To compare and analyze the mental status of medical staff between Orthopedics Department who treated the victims in the earthquake and other surgical departments who did not treat the victims in the earthquake, and to provide evidence for psychological prevention and intervention in the earthquake aids.

Methods: Cross-sectional study was used to choose staff in the Orthopedics Department who treated the victims and other surgical departments who did not treat victims in the earthquake as eligible subject with convenient sampling. The research tool is Symptom Checklist-90.

Cyclophilin A mediates vascular remodeling by promoting inflammation and vascular smooth muscle cell proliferation.

Background: Oxidative stress, generated by excessive reactive oxygen species, promotes cardiovascular disease. Cyclophilin A (CyPA) is a 20-kDa chaperone protein secreted from vascular smooth muscle cells (VSMCs) in response to reactive oxygen species that stimulates VSMC proliferation and inflammatory cell migration in vitro; however, the role CyPA plays in vascular function in vivo remains unknown.

Methods And Results: We tested the hypothesis that CyPA contributes to vascular remodeling by analyzing the response to complete carotid ligation in CyPA knockout mice, wild-type mice, and mice that overexpress CyPA in VSMC (VSMC-Tg).

TrkA pathway(s) is involved in regulation of TRPM7 expression in hippocampal neurons subjected to ischemic-reperfusion and oxygen-glucose deprivation.

The transient receptor potential melastatin 7 (TRPM7) is recently revealed playing a key role in anoxic neuronal death. Meanwhile, nerve growth factor (NGF), through activating TrkA pathway, has been widely accepted as a crucial factor for neuronal survival during cerebral ischemia. In this study, middle cerebral artery occlusion (MCAO) for 1h and reperfusion for 5, 10, 20 and 30 h revealed an increasing up-regulation of TRPM7 expression in ipsilateral hippocampus after reperfusion and such a change reached a peak at 20 h, with high expression being maintained up to 30 h.

Fluid shear stress inhibits TNF-mediated JNK activation via MEK5-BMK1 in endothelial cells.

Steady laminar blood flow protects vessels from atherosclerosis. We showed that flow decreased tumor necrosis factor-alpha (TNF)-mediated VCAM1 expression in endothelial cells (EC) by inhibiting JNK. Here, we determined the relative roles of MEK1, MEK5 and their downstream kinases ERK1/2 and BMK1 (ERK5) in flow-mediated inhibition of JNK activation.

[Effects of electroacupuncture on the expression of epidermal growth factor receptor and glial fibrillary acidic protein after spinal cord injury in rats].

Objective: To study the molecular mechanism of electroacupuncture (EA) in the treatment of spinal cord injury (SCI) in rats.

Methods: Forty-five male SD rats were randomized into control, model and EA groups with 15 cases in each group which was further divided into 3 subgroups (3 d, 7 d and 14 d) at average. SCI (T10) model was duplicated by using modified Allen's method.

Electroacupuncture regulates TRPM7 expression through the trkA/PI3K pathway after cerebral ischemia-reperfusion in rats.

Recently, it was demonstrated that TRPM7 is an essential mediator of anoxia-induced neuronal death. Meanwhile, nerve growth factor (NGF) is known to have survival and neuroprotective effects by interacting with the high affinity neurotrophin receptor, tropomyosin-related kinase A (trkA). In the present study, we found that electroacupuncture (EA) treatment could up-regulate trkA expression after focal cerebral ischemia in rats.

NGF-induced reduction of an outward-rectifying TRPM7-like current in rat CA1 hippocampal neurons.

Transient receptor potential melastatin 7 (TRPM7) channels are widely expressed in the nervous system; however, their function and regulation are largely unknown. This study aimed to explore whether the current mediated by TRPM7-like channels in rat CA1 hippocampal neurons could be modulated by nerve growth factor (NGF). Using whole-cell patch clamp techniques, we identified an outward-rectifying TRPM7-like current in hippocampal neurons freshly isolated from postnatal (10-day-old) rats.

Growth factor regulation of hyaluronan synthesis and degradation in human dermal fibroblasts: importance of hyaluronan for the mitogenic response of PDGF-BB.

The glycosaminoglycan hyaluronan is important in many tissuerepair processes. We have investigated the synthesis of hyaluronan in a panel of cell lines of fibroblastic and epithelial origin in response to PDGF (platelet-derived growth factor)-BB and other growth factors. Human dermal fibroblasts exhibited the highest hyaluronan-synthesizing activity in response to PDGF-BB.

Silencing of hyaluronan synthase 2 suppresses the malignant phenotype of invasive breast cancer cells.

Accumulation of hyaluronan has been demonstrated in the peritumoral breast cancer stroma and nests of tumor cells. In this study, we have quantified the production of hyaluronan and the expression of mRNAs encoding hyaluronan synthesizing (HAS) and hyaluronan degrading (HYAL) enzymes in a panel of breast cancer cell lines. The analysis revealed that highly invasive breast cancer cells produce high amounts of hyaluronan and express preferentially HAS2 mRNA, whereas less invasive breast cancer cells produce low amount of hyaluronan and express HAS1 and HYAL1 mRNAs.

Effects of overexpression of Sim2 on spatial memory and expression of synapsin I in rat hippocampus.

The single-minded 2 gene (Sim2) plays a crucial role in the mental retardation of Down Syndrome (DS). To explore how Sim2 influences spatial memory, a DNA plasmid-encoding mouse Sim2 (mSim2) wrapped with liposome was bilaterally injected into the hippocampus of rats. The effect of overexpressing mSim2 on spatial learning was determined by a Morris water maze task.

[Effects of electroacupuncture on GDNF positive cell immunoreactivity in local dermal tissue of the inflammatory pain focus in the rat of adjuvant arthritis].

Objective: To study on the analgesic mechanism of electroacupuncture (EA) in the rat of adjuvant arthritis (AA).

Methods: Forty-eight SD rats were randomly divided into a blank control group (n = 8), an inflammatory group (n = 10), an acupoint EA group (n = 10), a non-acupoint EA group (n = 10) and a contralateral acupoint EA group (n = 10). Complete Freund's adjuvant (CFA) 50 microL were injected into the left malleolus' articular cavity in the rats except the blank control group for preparing single local adjuvant arthritis (AA) model.

Inhibition of platelet-derived growth factor-BB-induced receptor activation and fibroblast migration by hyaluronan activation of CD44.

The extracellular matrix molecule hyaluronan was found to suppress platelet-derived growth factor (PDGF) beta-receptor activation and PDGF-BB-induced migration of primary human dermal fibroblasts. The suppressive effect of hyaluronan was neutralized by a monoclonal antibody that specifically inhibits hyaluronan binding to its receptor CD44. Moreover, co-immunoprecipitation experiments showed that the PDGF beta-receptor and CD44 can form a complex.

Introduction of in vitro transcribed ENO1 mRNA into neuroblastoma cells induces cell death.

Background: Neuroblastoma is a solid tumour of childhood often with an unfavourable outcome. One common genetic feature in aggressive tumours is 1p-deletion. The alpha-enolase (ENO1) gene is located in chromosome region 1p36.

Electroacupuncture regulates NMDA receptor NR1 subunit expression via PI3-K pathway in a rat model of cerebral ischemia-reperfusion.

Cell survival is regulated by the balance between death and survival signals. Previous studies have shown that the N-methyl-d-aspartate receptors (NMDARs) are responsible for the glutamate-induced excitotoxicity in the postischemic brain. Meanwhile, nerve growth factor (NGF) is critically involved in cell survival and neuroprotective effects via the extracellular signal-related kinase (ERK) pathway or the phosphatidylinositol 3-kinase (PI3-K) pathway mediated by the high affinity NGF receptor, tropomyosin-related kinase A (TrkA).

Effect of electroacupuncture on TRPM7 mRNA expression after cerebral ischemia/reperfusion in rats via TrkA pathway.

The effect of electroacupuncture (EA) on TRPM7 mRNA expression of focal cerebral ischemia in rats and further the role of EA in the relationship between TRPM7 and trkA pathway was investigated. Thirty SD rats were randomly divided into 5 groups : normal group, ischemia/reperfusion group, EA treated group (ischemic rats with EA treatment), TE infusion group (ischemic rats with EA treatment and TE buffer infusion), AS-ODN group (ischemic rats with EA treatment and antisense trkA oligonucleotide infusion). The stroke animal model was established by the modified method of middle cerebral artery occlusion.

Evaluation of an FRDA-EGFP genomic reporter assay in transgenic mice.

Friedreich ataxia is an autosomal recessive neurodegenerative disorder caused by a GAA trinucleotide expansion in the first intron of the Friedreich ataxia gene (FRDA) that causes reduced synthesis of frataxin, a mitochondrial protein likely to be involved in biosynthesis of iron-sulfur clusters. This leads to increased oxidative stress, progressive loss of large sensory neurons, and hypertrophic cardiomyopathy. To elucidate the mechanisms regulating FRDA expression and to develop an in vivo assay for agents that might upregulate FRDA expression in a therapeutically relevant manner, we have generated transgenic mice with a BAC genomic reporter construct consisting of an in-frame fusion between FRDA and the gene coding for enhanced green fluorescent protein (EGFP).

Phase I and pharmacokinetic evaluation of intravenous hyaluronic acid in combination with doxorubicin or 5-fluorouracil.

Background: Pre-clinically, hyaluronan (HA) has been demonstrated to systemically target chemotherapeutic drugs to tumours while ameliorating treatment toxicities. This study is a preliminary clinical investigation to determine if HA could be safely used in combination with 5-fluorouracil (5-FU) and doxorubicin (DOX).

Methods: Thirty patients with metastatic cancer were intravenously administered 500 mg/m2 HA in combination with escalating doses of DOX (30-60 mg/m2) or 5-FU (cumulative dose of 1,350-2,250 mg/m2 per cycle).

Hyaluronan fragments induce endothelial cell differentiation in a CD44- and CXCL1/GRO1-dependent manner.

Hyaluronan is a glycosaminoglycan of the extracellular matrix. In tumors and during chronic inflammatory diseases, hyaluronan is degraded to smaller fragments, which are known to stimulate endothelial cell differentiation. In this study, we have compared the molecular mechanisms through which hyaluronan dodecasaccharides (HA12), and the known angiogenic factor, fibroblast growth factor 2 (FGF-2), induce capillary endothelial cell sprouting in a three-dimensional collagen gel.

Effects of complete Freund's adjuvant on immunohistochemical distribution of IL-1beta and IL-1R I in neurons and glia cells of dorsal root ganglion.

Aim: To investigate the effects of complete Freund adjuvant (CFA) on inflammatory hyperalgesia and morphological change of the coexistence of interleukin-1 beta (IL-1beta) and type I IL-1 receptor (IL-1RI) in neurons and glia cells of rat dorsal root ganglion (DRG).

Methods: The pain-related parameters and the expression of IL-1RI and IL-1beta positive neurons and glia cells of DRG in normal saline (NS) and adjuvant-induced arthritic (AA) group were examined with pain behavior assessment methods and immunohistochemical assay, respectively.

Results: Five hours, 1 d, and 2 d after intra-articular injection of 50 microL CFA, tactile hyperalgesia induced by CFA was observed in the foot flexion and extension scores of the ipsilateral hindpaw of AA group.

Human BAC-mediated rescue of the Friedreich ataxia knockout mutation in transgenic mice.

Three independent transgenic mouse lines were generated with the human Friedreich ataxia gene, FRDA, in an 188-kb bacterial artificial chromosome (BAC) genomic sequence. Three copies of the transgene per diploid mouse genome were integrated in a single site in each mouse line. Transgenic mice were mated with mice heterozygous for a knockout mutation of the murine Frda gene, to generate mice homozygous for the Frda knockout mutation and hemizygous or homozygous for the human transgene.