0.1),and there were significant differences in the other groups[F(H)=33.57,F(I)=133.6,F(HI)=69.75 Pa

Objective To explore the significance of nuclear factor-?B(NF-?B)activation in peripheral blood mononuclear cells(PBMC)during acute Kawasaki disease(KD).Methods Peripheral blood was collected from children with acute KD(n=30)and healthy age-matched children(n=20).PBMC were cultured in vitro and divided into 3 groups:naturally cultured blank control group,protein kinase C(PKC)activator stimulated phorbol 12-myristate 13-acetate(PMA)group and PMA plus NF-?B inhibitor treated PMA plus pyrrolidine dithiocarbamate(PDTC)group.Percentages of NF-?B activation were detected by immunohistochemistry.Results Under natural culturing,the percentage of cells with activated NF-?B was significantly higher in acute KD blank control group than that in healthy blank control group.The percentage of cells with activated NF-?B was significantly higher in acute KD PMA group than that in acute KD blank group and that in normal control PMA group,respectively(Pa0.05).Conclusions NF-?B activation in PBMC during acute KD is markedly increased,which suggests that NF-?B activation plays an important role in the formation of vasulitis and CAL in this disease.NF-?B activation in PBMCs in children with KD is regulated by the PKC signaling pathway and PDTC obviously inhibits the activation of NF-?B.J Appl Clin Pediatr,2009,24(1):35-37

Objective To investigate the clinical features and electron transfer flavoprotein dehydrogenase (ETFDH) gene mutations in 35 Chinese patients with lipid storage myopathy. Methods The clinical data of 35 cases with lipid storage myopathy confirmed by muscle biopsy were collected. The sequences of all 13 exons of ETFDH were analyzed. Results All 35 patients showed proximal weakness. Ten of them demonstrated masseter weakness and 28 of them showed weakness in neck flexion. Twenty-nine of 32 patients who were followed up showed improvement after treatment with VitB2 and CoQ10. Mutations of ETFDH were found in 30 of 35 patients,which included 8 homozygosises,20 compound heterozygosises and 2 single heterozygosises. Fourteen novel mutations were found, including 9 missense mutations ( c. 3G > C, c. 152G>A, c. 191G > A, c.349G>C, c.433G>C, c. 949C > A, c. 1454C > G, c. 1744A >T and c. 1763A>G), 1 nonsense mutation(c. 172G>T), 2 deletions(c. 1282_1283del and 1773_1774del) and 2 splice mutations (c. 405 + 1G > T and c. 1691 -3C > G). Nine of them showed c. 250G > A mutation and 6 of them showed c. 770A > G mutation. Conclusions Lipid storage myopathy is presented as proximal weakness. Multiple acyl-CoA dehydrogenase deficiency caused by mutations of ETFDH is the major cause of lipid storage disease in this group. ETFDH c. 250G > A and c. 770A > G mutations show a high frequency.

Current study was carried out to optimize the priming condition of Oldenlandia diffusa seeds, and improve germination rate and seed vigor of 0. diffusa seeds under drought conditions. Uniform design was used to optimize the concentration and priming time of three priming materials (PEG, KNO3, GA3). Different concentrations of polyethylene glycol (PEG) was used to simulate drought stress. The seedling was cultured in 1/4 Hoagland medium for 30 d. The results showed that seed priming treatment with 366 mg x kg(-1) GA3 for 1h resulted in significant increase in germination rate, germination index, vigor, root length, plant height and biomass of O. diffusa seeds under drought stress (15% PEG), while seed priming with 3.0% KNO3 for 1 h showed little effect on germination and growth of O. diffusa seeds under drought stress. Seed priming treatment with appropriate GA3 concentration and priming time could enhance seed germination and drought resistance of O. diffusa in seedling stage.
Droughts ; Germination ; Oldenlandia ; growth & development ; physiology ; Seedlings ; growth & development ; physiology ; Seeds ; growth & development ; physiology ; Stress, Physiological

Alleles ; Amelogenin/genetics* ; Chromosomes, Human, Y ; Humans ; Male ; Sex Determination Analysis

OBJECTIVEto investigate the changes of γ-aminobutyric acid (GABA) and glutamate (Glu) in the cerebral cortex following acute bromoxynil intoxication in mice and the protective effect of sodium dimercaptopropane sulfonate (Na-DMPS).

METHODS30 ICR mice were randomly divided into blank control group (10), exposure group (10) and Na-DMPS protection group (10). The levels of GABA and Glu in the cerebral cortex were measured by RP-HPLC. The glutamine (Gln) level and the glutamine synthetase (GS), glutamate decarboxylation enzyme (GAD), γ-aminobutyric acid transaminase (GABA-T) activity in the cerebral cortex were determined by UV colorimetric.

RESULTScompared with the control group [GABA: (3.41 ± 0.12) micromol/g, Glu (14.00 ± 0.16) micromol/g, Gln (1.25 ± 0.19) micromol/g, GAD (13.50 ± 0.25) micromol × g(-1) × h(-1), GABA-T (25.51 ± 0.21) micromol × g(-1) × h(-1), GS(142.19 ± 1.31) U/mg pro], the level of GABA [(3.14 ± 0.14) micromol/g] was decreased (P < 0.05), whereas the level of Glu [(17.54 ± 0.40) micromol/g] and Gln [(3.35 ± 0.27) micromol/g] were increased (P < 0.05), the activity of GAD [(11.93 ± 0.15 micromol × g(-1) × h(-1)], GABA-T [(24.15 ± 0.22) micromol × g(-1) × h(-1)], GS [(140.75 ± 1.01) U/mg pro] was decreased (P < 0.05) in acute intoxication group; Compared with the acute intoxication group, the level of GABA [(3.52 ± 0.30) micromol/g] was increased (P < 0.05), whereas the level of Glu [(14.20 ± 0.32) micromol/g] and Gln [(1.32 ± 0.17) micromol/g] were decreased (P < 0.05), the activity of GAD [(13.01 ± 0.45 micromol × g(-1) × h(-1)], GABA-T [(25.19 ± 0.26) micromol × g(-1) × h(-1), GS [(142.35 ± 1.20) U/mg pro] was increased (P < 0.05); In contrast, the levels of GABA, Glu, Gln and the activity of GAD, GABA-T, and GS in Na-DMPS protection group were not significantly different in comparison with control group (P > 0.05).

CONCLUSIONthe central toxic effects of mice with acute bromoxynil intoxication may be related to the changes of GABA and Glu content in the cerebral cortex;Na-DMPS can protect mice from bromoxynil-induced central toxic effects and GABA and Glu abnormal change in the cerebral cortex.

Animals ; Cerebral Cortex ; drug effects ; metabolism ; Female ; Glutamic Acid ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Nitriles ; poisoning ; Toxicity Tests, Acute ; Unithiol ; pharmacology ; gamma-Aminobutyric Acid ; metabolism

OBJECTIVETo observe the clinical efficacy of transcutaneous acupoint electrical stimulation (TAES) combined intravenous injection and/or Neiguan (P6) injection with droperidol in preventing and treating post-operative nausea and vomiting (PONV) after thyroid tumor surgery.

METHODSRecruited were 120 female patients who underwent selective thyroid tumor surgery were randomly assigned to the control group, the TAES group, the IV group (intravenous injection of droperidol), and the P6 group [Neiguan point (P6) injection of droperidol], respectively, 30 cases in each group. Thirty min before anesthesia induction, 2 mL 0.9% normal saline injection was intravenously injected to those in the control group. Patients in the TAES group received TEAS at bilateral P6 points. 2.5 mg (1 mL) droperidol added in 1 mL 0.9 normal saline was intravenously injected to those in the IV group and injected at bilateral P6 points of those in the P6 group. The occurrence and severity of PONV were observed within 0 - 6 h and within 6 - 24 h after operation in each group.

RESULTSCompared with the control group, the incidence and the severity of PONV within 0 - 6 h and within 6 - 24 h after thyroid surgery were significantly reduced in the three treatment groups (P < 0.05). There was no statistical difference in the incidence or the severity of PONV among the TAES, IV and P6 groups (P > 0.05).

CONCLUSIONSTEAS at P6 could dramatically reduce the occurrence and the severity of PONV after thyroid tumor surgery. Besides, it got equivalent effect to that by intravenous injecting droperidol or by injecting droperidol at P6.

Acupuncture Points ; Adult ; Female ; Humans ; Middle Aged ; Postoperative Nausea and Vomiting ; prevention & control ; Prospective Studies ; Single-Blind Method ; Thyroid Neoplasms ; surgery ; Transcutaneous Electric Nerve Stimulation

OBJECTIVETo investigate the effects of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) preconditioning and postconditioning on Ca(2+)-handling proteins in myocardial ischemia/reperfusion (IR) injury in rats and reveal the effects and mechanism of 11, 12-EET on cardioprotection. METHODS The IR injury model was built by stopping perfusion for 40 minutes followed by reperfusion for 30 minutes. The isolated Langendorff-perfused rat hearts were divided into 4 groups: control group, IR group, EET preconditioning (Pre-EET) group and EET postconditioning (Post-EET) group. The computer-based electrophysiological recorder system was used to measure the changes of the maximal rate of pressure increased in the contraction phase (+dp/dt(max)), the maximal rate of pressure decreased in the diastole phase (-dp/dt(max)), the left ventricular end diastolic pressure (LVEDP) and the difference of left ventricular pressure (delta LVP). The activity of Ca(2+)-ATPase in sarcoplasmic reticulum was measured with colorimetric method. Reverse transcription-polymerase chain reaction was used to assess the gene expression of C(a2+)-handling protein [sarcoplasic reticulum Ca(2+)-ATPase (SERCA), phospholamban (PLB), ryanodine receptor type 2 (RyR,), and 1, 4, 5-trisphosphate inositol receptor type 2 (IP3 R2) ] mRNAs level.

RESULTSCompared with IR group, the myocardial functions, the value of Ca(2+)-ATPase, and the expressions of IP3 R2 mRNA were significantly increased and the expression of PLB mRNA was significantly decreased in both Pre-EET group and Post-EET group (P < 0.05, P < 0.01). And the expression of SERCA mRNA was significantly increased in Pre-EET group (P < 0. 05). However, no significant differences were detected between Pre-EET and Post-EET groups. Moreover, the expression of RyR2 mRNA was not significantly different among all groups.

CONCLUSIONS11, 12-EET preconditioning and post-conditioning can protect myocardium from IR injury by elevating the activity of Ca(2+)-ATPase in sarcoplasmic reticulum, up-regulating the expression of IP3 R2 mRNA, and down-regulating the expression of PLB mRNA. Moreover, up-regulating the expression of SERCA mRNA maybe one of mechanisms of 11, 12-EET preconditioning on cardio protection against IR injury.

8,11,14-Eicosatrienoic Acid ; analogs & derivatives ; pharmacology ; Animals ; Calcium-Binding Proteins ; drug effects ; metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; drug effects ; metabolism ; Ischemic Preconditioning, Myocardial ; methods ; Myocardial Reperfusion Injury ; metabolism ; prevention & control ; Rats ; Ryanodine Receptor Calcium Release Channel ; metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; drug effects ; metabolism

OBJECTIVETo investigate the influence of dermal template on the expressions of signal transduction protein Smad 3 and transforming growth factor beta1 and its receptor during wound healing process in patients with deep burns.

METHODSTwenty burn patients with excision of full thickness burn in the extremities were enrolled in the study and divided into two groups, i.e. template interfering group (E, n = 20, grafting of dermal template [allogeneic acellular dermal matrix] with razor thin autoskin) and control group (C, n = 20, grafting of razor thin autoskin only). The contralateral side served as the self-control. Tissue samples from the burn wounds were harvested at 1, 2, 3 and 4 post-operative weeks (POW) for immunohistochemistry staining. The positive expression rates of TGF-beta1, TbetaRI, TbetaRII and Smad3 proteins were determined by image analysis system.

RESULTSThe positive expressions of TGFbeta1, TbetaRI, TbetaRII and signal transduction protein Smad 3 in the tissue samples in both groups could be identified during 1 approximately 4 POW, and they diminished thereafter with the process of wound healing. The expression rate of TGF-beta1 in E group was (13.08 +/- 4.65)% at 1 POW and (9.03 +/- 1.89)% at 4 POW. The positive expression rate of above indices in E group was obviously lower than that in C group in corresponding time points (P < 0.05).

CONCLUSIONThe expression levels of TGFbeta1, TbetaRI, TbetaRII and Smad 3 protein in deep burn wounds could be lowered by mixed grafting of dermal template with razor thin autoskin, which might be beneficial in ameliorating of scar hyperplasia in the burn wound.

Adolescent ; Adult ; Burns ; metabolism ; surgery ; Dermis ; transplantation ; Humans ; Middle Aged ; Receptors, Transforming Growth Factor beta ; biosynthesis ; Signal Transduction ; Skin Transplantation ; Smad3 Protein ; biosynthesis ; Transforming Growth Factor beta1 ; biosynthesis ; Transplantation, Heterologous ; Wound Healing

OBJECTIVETo investigate the role of 83 site in interaction of GluR2 C-terminal and PICK1 PDZ domain.

METHODSDocking structure of PICK1 PDZ domain with GluR2 C terminal PDZ binding motif was built with computer software. After K83 site was substituted by other amino acid, the structure and binding energy were recalculated; meanwhile, site specific mutants were constructed using wild type full length cDNA as template. Mutants were co-transfected with GluR2 into HEK293T cells. After staining, the distribution of PICK1 and GluR2 were observed under confocal microscope.

RESULTSWild type PICK1 and GluR2 formed many co-clusters in HEK293T cells as reported by other research groups; but different K83 mutant had different distribution in HEK293T cells.

CONCLUSIONThe K83 site in PDZ domain of PICK1 is important for the interaction between PICK1 and GluR2. Altering lysine will probably change the hydrophobic interactions, the hydrogen bonds or the electrostatic interactions formed between PICK1 PDZ domain and GluR2 C terminal; accordingly, that will change the binding capacity between PICK1 and GluR2 in varying degrees.

Binding Sites ; Carrier Proteins ; chemistry ; metabolism ; Computer Simulation ; HEK293 Cells ; Humans ; Nuclear Proteins ; chemistry ; metabolism ; PDZ Domains ; Protein Binding ; Receptors, AMPA ; metabolism