Adenosine Triphosphate ; Mouth ; metabolism ; Receptors, Purinergic P2X ; metabolism

miRNA is a kind of endogenous non-coding short RNA. Mature miRNA was formed through the process of shearing and transporting after genetic transcription. miRNA exhibits many important biological functions through regulating expression and translation of target mRNAs. Different miRNAs may act as oncogenes or antioncogenes, and have tissue specificity. The progress of the tumorigenesis is usually accompanied by expression-profile changes of miRNAs. MiRNA regulates many tumor biological behaviors such as differentiation, proliferation, apoptosis, invasion, metastasis, and drug resistance of tumors. Furthermore, some miRNAs have clinical significance in predicting prognosis of tumor patients.

Objective To study on purication of stilbene glycoside and icarrin with macroporous resin of radix polygoni multiflori praeparata cum succo glycines sotae and herba epimedii of Fufang Bushenshengjing Capsule. Methods To select the best type of resin from NKA-9, AB-8, D101, X-5 and DM130, to observe the factor of the concentration of water-extraction, the volume of resin, pH of water-extraction, the concentration and volume of ethanol. Results Using AB-8 resin, the concentration of water-extraction is 0.3 g/mL, the volume of resin (mL) to the mass of medicinal materials is 2, pH of water-extraction need't change, eluant is 70% ethanol and its volume (mL) is 5 times of the mass of medicinal materials (g). Conclusion This research can provide reference for the extraction of active component from Fufang Bushenshengjing capsule in industrial production.

Best vitelliform macular dystrophy ( BVMD ) is an autosomal dominant disease mostly caused by mutations in BEST1 gene. These mutations change the normal physiological functions of BEST1-encoded bestrophin-1 protein, and finally lead to a reduction of visual acuity. This review is composed of the following aspects: the structure and functions of BEST1 gene, the characteristics of the mutations, clinical features of BVMD, genotype-phenotype correlations as well as possible gene therapy. Our contribution serves for further research on BVMD and BEST1 gene.

AlM: To investigate the clinical effect of preserved amniotic membrane transplantation in the treatment to conjunctival rupture, dehiscence and socket contracture after hydroxyapatite ( HA) orbital implantation.
METHODS: ln 16 cases of conjunctival rupture and socket contracture after HA orbital implantation, conjunctival tension was release by operation and preserved amniotic membrane was transplanted on conjunctival scleral exposure area.
RESULTS:ln all cases, conjunctiva healing, completely cover the sclera and conjunctiva socket recover ideal depth after operation in 15 cases, 1 case was fail.
CONCLUSlON: Preserved amniotic membrane transplantation is an effective method to treat conjunctival dehiscence and keeping the ideal conjunctival socket depth after orbital implantation.

Animals ; Gallbladder ; physiology ; Rabbits ; Solitary Nucleus ; drug effects ; Thyrotropin-Releasing Hormone ; pharmacology ; Vagus Nerve ; drug effects ; physiology

Objective To study the effect of infrasound on the changes of expression of NMDAR1 in hipp- ocampal cells.Methods Eighty-eight male Sprague-Dawley rats were randomized into eleven groups:control group,90 dB/1 d,7 d,14 d,21 d and 28 d infrasound exposed groups;130 dB/1 d,7 d,14 d,21 d and 28 d infra- sound exposed groups.All the animals in the test groups were put in an infrasound field with 8 Hz,90 dB or 130 dB for 2 hours daily.Immunohistochemistry methods were used to detect the changes of intracellular expression of NMDARI in hippocampal cells.Methods The expression of NMDAR1 in hippocampus after the rats were exposed to infrasound of 8 Hz,90 dB SPL showed a procedure from reducing on the 1st day to rising on the 7th and peaked on the 14th day,then to descending on 21st day and returning to the standard level on the 28th day.Exposure to infra- sound of 8 Hz,130 dB SPL induced opposite effects on the expression of NMDAR1 compared with 90 dB SPL,which showed a process of increasing,descending,reaching to the lowest,then ascending and returning to the normal.The lowest expression of NMDAR1 occurred on the 14th day in every observed hippocampal area.Conclusion 8 Hz, 90 dB/130 dB infrasound induced certain reversible reaction in the expression of NMDAR1 of hippoeampal cells in rats,which may disturb their learning and memory function.

Objective To investigate the mechanism of dasatinib,tyrosine kinase inhibitor,inhibiting androgen receptor (AR) phosphorylation in prostate cancer cells.Methods HEK-293T and COS7 cell lines were cotransfected by wild-type (WT)-AR,ARY267F or ARY534F with Ack1 or Src,respectively,and Western blot was used to detect the AR phosphorylation sites.LNCaP cells were treated by EGF or heregulin without androgen,then Western blot was used to detect AR phosphorylation.After these LNCaP cells were treated by dasatinib or transfection with siRNA to silence Ack1 or Src gene,Western blot was used to observe the effect on AR phosphorylation,and quantitative real-time reverse transcription polymerase chain (RT-PCR)was applied to detect PSA mRNA and hk2 mRNA.Results After transfection,Ack1 kinase mediated the phosphorylation of AR Tyr267 in HEK-293T cells,and Src mediated AR Tyr534 phosphorylation in COS7cells.When LNCaP cells were treated by heregulin,AR Tyr267 was phosphorylated,but its phosphorylation was inhibited after these cells were treated by dasatinib or ack1 gene was silenced.When LNCaP cells were treated by EGF,AR Tyr534 was phosphorylated,but its phosphorylation was inhibited after these cells were treated by dasatinib or Src gene was silenced.EGF or heregulin raised endogenous AR target gene,PSA and hK2,mRNA levels in LNCaP cells (P ＜ 0.05).However,after these cells were treated by dasatinib,PSA and hK2 mRNA levels induced by heregulin were decreased (P ＜ 0.05),but those induced by EGF PSA were no significant changes (P ＞ 0.05).Conclusion Dasatinib can inhibit AR Tyr267 and AR Tyr 534phosphorylation,and it may play a significant role in anti-prostate cancer cells by inhibiting Ack1-mediated AR Tyr-267 phosphorylation and the expression of PSA mRNA and hk2 mRNA induced by heregulin.

BACKGROUND: Serious scalding leads to dysfunction of each aspect in immune system, and activated macrophage can secret many bioactive transmitters. The relationship between macrophage dysfunction and signal conduction after scalding is unclear at present.OBJECTIVE: To observe the alternation of tumor necrosis factor- alpha(TNF-α) at different time points after scalding and the activity of nuclear factor κB(NF-κB) and alternation of protein kinase C (PKC) after the application of specific modulator H-7 to explore whether PKC participates in the modulation of TNF-α in macrophage on signal conduction level for the clarification of some mechanisms of macrophage dysfunction.DESIGN: A randomized controlled experimental study by employing experimental animals as subjectsSETTING: An institute of burn research of a military medical university MATERIALS: The study was conducted in the Laboratory (state) of the Institute of Burn Research, Third Military Medical University of Chinese PLA between January and December 1999. Experimental animals were 32 healthy clean inbreeding Kunming white mice.METHODS: 15% Ⅲ scalding was created in mice for the establishment of routine scalding model. Mice were randomly divided into 6 groups according to different time points before or after scalding, I.e. 0(normal control group), 2, 6, 12, 24, or 48 hours group. Celiac macrophages were collected for the detection of TNF-α content by radioimmunoassay, NF-κB activity by electrophoretic mobility shift analysis (EMSA), and membrane or plasma PKC activity by isotope analysis.MAIN OUTCOME MEASURES: ① TNF-α content; ② NF-κB activity; ③Membrane or plasma PKC activity RESULTS: After scalding, macrophage excessively secreted TNF-α and reached its peak of (1 085.65 ± 122.99) ng/L at 12 hours, which was significantly higher than that of control group( t = 14.92, P ＜ 0.01 ).Compared with control group, membrane PKC activity increased after scalding, which significantly heightened to(231.80 ± 31.66) nmol/min · g at 2hours( t = 7. 930, P ＜ 0.01 ), slightly decreased to close to normal level of (174.29±16.80) nmol/min· gat 6hours(t=2.531, P ＜0.05), and rapidly elevated at 12 hours [512. 10 ±33.42) nmol/min · g] and 24 hours [ (454.70 ± 21.06) nmol/min · g] to reach its peak of(530.49 ± 28.54)nmol/min. G at 48 hours( t = 29.42, 28.03, 30. 19, P ＜ 0. 01 ). Correlation analysis of the alternation between TNF-α and membrane PKC indicated a significant positive correlation( r = 0. 796 4, P ＜ 0. 05) . As indicated by EMSA image, NF-κB activity significantly elevated after scalding. Twelve hours after scalding was set as modulation point, NF-κB activity was significantly inhibited by the application of H-7.CONCLUSION: The secretion of TNF-α and the activities of PKC and NF-κB are significantly activated in celiac macrophage after scalding, and PKC-NF-κB signal pathway participates in the modulation of TNF-α expression, which provide experimental data for the modulation of immune function and rehabilitative intervention during scalding.serious scalding.

BACKGROUND: Severe scald injury leads to a variety of disorders in the immune system. Activated macrophages are known to secrete many kinds of biologically active transmitter, but the relation between the functional disorder of the macrophages and signal transduction after burn injury has not been fully understood.OBJECTIVE: To observe the changes in nuclear factor(NF) -κκB activity and expressions of IκκB-α and tumor necrosis factor(TNF) -α in peritoneal macrophage of mice at different time points after severe scald injury and after the application of specific NF-κκB inhibitor pyrrolidine dithiocarbamate (PDTC), thereby to explore the mechanism of macrophage dysfunction in light of signal transduction.DESIGN: A randomized controlled experimental research.SETTING: State Key Laboratory of Trauma, Burn and Combined Injury.MATERIALS: The experiment was carried out in the State Key Laboratory of Institute of Burn Research, Third Military Medical University during the period from January to June, 1999, using 30 healthy clean-grade Kunming mice of inbred strain.INTERVENTIONS: Common scald injury models(with third degree burn of 15% total body surface area) were established in the mice, which were randomized into 6 groups according to different time points after the injury for observation, namely 0 hour(normal control group) and postburn 2, 6, 12,24 and 48 hours. Peritoneal macrophages were collected at these time points for examining TNF-α content using radio-immunoassay and NF-κκB activity by means of electrophoretic mobility shift assay(EMSA). The expressions of IκκB-α and TNF-α mRNA were determined by immunoblotting method and reverse transcription-PCR, respectively.MAIN OUTCOME MEASURES:Examinations of ① the content of TNF-α, ② NF-κκB activity,③ expression of IκB-α, and ④ expression of TNF-α mRNA.RESULTS: Macrophage secretion of TNF-α was enhanced postburn, reaching the peak level at 12 hours[(1085.65 ± 122.99) ng/L], which was significantly higher than that in the normal control group( t = 14.92, P ＜ 0.01) .Postburn NF-κκB activity significantly increased after the injury, peaking at 2 hours[ (56. 8 ± 7.3)RDU], which occurred much earlier than the peak of TNF-α secretion( t=13. 31, P ＜ 0.01 ). Compared with that in the normal control group, IκB-α expression decreased significantly 2 hours postburn ( t =4. 23, P ＜ 0. 01) to 0. 632 ±0. 086, followed by gradual increase to the peak level to 1. 161 ± 0. 097 24 hours after the burn injury( t = 7.06, P＜ 0. 01) and then by slight decrease to 1. 149 ±0. 167 till 48 hours(t = 4. 82, P ＜ 0.01) . Twelve hours after injury was the time point for intervention with PDTC application, when NF-κκB activity and TNF-α mRNA expression both decreased significantly( P ＜ 0.01 ).CONCLUSION: NF-κB activity and TNF-αmRNA expression decrease significantly after severe scald. At high levels, IκB-α and NF-κκB maintain an interaction for their restriction. After burn injury, NF-κκB signal transduction pathway is involved in the modulation of TNF-α expression in mouse peritoneal macrophage.