OBJECTIVETo observe therapeutic effect of tongue acupuncture on stroke.

METHODSOne hundred and ninety cases were randomly divided into an observation group and a control group, 95 cases in each group. The patients in the observation group were treated by tongue acupuncture combined with body acupuncture, and the control group by simple body acupuncture.

RESULTSThe total effective rate was 95.8% in the observation group and 80.0% in the control group, the observation group being significantly better than the control group.

CONCLUSIONTongue acupuncture has a better therapeutic effect on stroke.

Acupuncture Therapy ; Humans ; Stroke ; therapy

Antioxidant activity of bronchial epithelial cells (BECs) plays an essential role in preventing the airway epithelium integrity from damage in structure and function. Integrin expressed by BECs is the receptor of extracellular matrix such as fibronectin (Fn), and it is involved in modulation of proliferation, differentiation and metabolism of the cells. In order to test the hypothesis that integrin-ligand binding reaction supports the ability of cells to withstand oxidant attack, the present study evaluated the antioxidant activity of primary cultured rabbit BECs treated with fibronectin or its sequence Arg-Gly-Asp (RGD peptide), by determining changes in the activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) and in the level of glutathione (GSH). The results are as follows: (1) Fn (10 μg/ml) increased significantly the activity unit of GSH-Px (P<0.05, n=5), which was inhibited by calmodulin-inhibitor W7 　(10－5 mol/L) (P<0.05). Both Fn (5～20 μg/ml) and RGD (15～60 μg/ml) showed a dose-dependent upregulatory effect (respectively r=0.93 and r=0.73). (2) Treatment with Fn increased SOD activity (P<0.01,　n=7), which was abolished by W7 　(P<0.01). (3) Catalase activity was also stimulated by Fn (P<0.05, n=6) and reversed by W7 　(P<0.01). (4) A dose-dependent increase of GSH level was observed in both Fn (r=0.82) and RGD treatment (r=0.84). The data suggest that the binding of integrin with extracellular matrix can upregulate activity of antioxidant enzymes, and increase the content of GSH and improve the ability of BECs to resist oxidant injury.

To investigate the function of ALK3 gene, the gene regulation and the signaling pathway related to ventricular septum defect during heart development. The model mice with ALK3 gene knock-out via alpha-MHC-Cre/lox P system were bred. The mRNA expression level of control group was compared with that of experiment group and ALK3 downstream genes were screened using PCR-select cDNA subtraction microarray. The mRNA of control group was extracted from E11.5 normal mouse hearts, and that of experiment group, from E11.5 hearts of mice with alpha-MHC Cre(+/-) ALK3(F/+) genotype. It was found that the mice with ALK3 gene knock-out produced heart defects involving the interventricular septum. The platelet-activating factors acetylhydrolase and the transcription factor Pax-8 and so on, were down-regulated. However, the Protein Tyrosine Kinase (PTK) of Focal Adhesion Kinase (FAK) subfamily and beta subtype protein 14-3-3 were up-regulated in the alpha-MHC Cre(+/-) ALK3(F/-) mice. These data provide support that ALK3 gene played an important role during heart development. The platelet-activating factors acetylhydrolase and Pax-8 genes could be important ALK3 downstream genes in the BMP signaling pathway during interventricular septum development. PTK and beta subtype protein 14-3-3 might be regulatory factors in this pathway.
1-Alkyl-2-acetylglycerophosphocholine Esterase ; genetics ; metabolism ; 14-3-3 Proteins ; genetics ; metabolism ; Animals ; Bone Morphogenetic Protein Receptors, Type I ; genetics ; metabolism ; Genotype ; Heart Septal Defects, Ventricular ; genetics ; Mice ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; PAX8 Transcription Factor ; Paired Box Transcription Factors ; genetics ; metabolism ; Protein-Tyrosine Kinases ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; genetics ; physiology

OBJECTIVETo investigate stress distribution of different material restored post-cores in dentine and provide a theoretical guidance for clinical use.

METHODSA three-dimensional finite element model of maxillary central incisor restored with post-core and PFM crown was constructed by SCT scan technology. Based on this model, stress distribution in dentine was analyzed before and after post-core restorations with 6 different materials, including cast Ni-Cr alloy, cast titanium alloy, cast gold alloy, glass fiber reinforced composite, polythene fiber reinforced composite, and common composite resin.

RESULTSWhen the tooth was restored with cast Ni-Cr alloy post and PFM crown, the maximum tensile stress and Von Mises stress in dentin at post apex increased 152% and 162% respectively, compared with a tooth restored only with PFM crown. If polythene fiber reinforced composite was used as post material, the stress distribution did not significantly change. When the other materials were used for the post, the stress distribution changed greatly. The elastic modulus of post-core materials affected the stress distribution pattern in dentine.

CONCLUSIONThe materials with elastic modulus similar to that of dentin, such as polythene fiber reinforced composite, may be suitable for post restoration.

Chromium Alloys ; Dental Materials ; Dental Restoration, Permanent ; Dental Stress Analysis ; methods ; Dentin ; Finite Element Analysis ; Humans ; Incisor ; physiology ; Materials Testing ; Post and Core Technique ; Tensile Strength

OBJECTIVETo evaluate the efficacy and safety of using Jiangzhi Tongluo Soft Capsule (JTSC) combined with Atorvastatin Calcium Tablet (ACT) or ACT alone in treatment of combined hyperlipidemia.

METHODSA randomized, double blinded, parallel control, and multi-center clinical research design was adopted. Totally 138 combined hyperlipidemia patients were randomly assigned to the combined treatment group (A) and the atorvastatin treatment group (B) by random digit table, 69 in each group. All patients took ACT 20 mg per day. Patients in the A group took JTSC 100 mg each time, 3 times per day. Those in the B group took JTSC simulated agent, 100 mg each time, 3 times per day. The treatment period for all was 8 weeks. Serum levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C) were observed before treatment, at week 4 and 8 after treatment; and safety was assessed as well.

RESULTSAt week 4 and 8 after treatment serum TG decreased by 26.69% and 33.29% respectively in the A group (both P < 0.01), while it was decreased by 25.7% and 22.98% respectively in the B group (both P < 0.01). At week 8 decreased serum TG was obviously higher in the A group than in the B group (P < 0.05). Compared with before treatment, serum levels of LDL-C and TC levels decreased significantly in the two groups (all P < 0.01). There was no statistical difference in the drop-out value and the drop-out rate of serum LDL-C and TC levels (P > 0.05). At week 8 the serum HDL-C level showed an increasing tendency in the two groups. No obvious increase in peptase or creatase occurred in the two groups after treatment.

CONCLUSIONJTSC combined with ACT could lower the serum TG level of combined hyperlipidemia patients with safety.

Adult ; Atorvastatin Calcium ; Double-Blind Method ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Heptanoic Acids ; therapeutic use ; Humans ; Hyperlipidemias ; drug therapy ; Male ; Middle Aged ; Pyrroles ; therapeutic use ; Treatment Outcome ; Triglycerides ; blood

To explore the roles of regulatory peptides in the process of various anaphylactic inflammation of the airway, we observed the influence of four peptides, i.e., vasoactive intestinal peptide (VIP), epidermal growth factor (EGF), endothelin-1 (ET-1), and calcitonin gene-related peptide (CGRP), on the adhesion of eosinophil (EOS) to unstimulated and O(3)-stressed bronchial epithelial cells (BEC). From the experiments we observed that VIP and EGF decreased EOS adherence to O(3)-stressed BEC and downregulated airway inflammation; ET-1 and CGRP increased the adhesion of EOS to BEC in the inflammatory process; and CGRP aggravated O(3)-stressed reactions. The effects of ET-1 and CGRP were inhibited by W(7)and H(7). Anti-ICAM-1 antibody inhibited the adhesion of EOS to BEC, which brings to light that EOS adherence to BEC may be related to the expression of ICAM-1 of BEC.
Animals ; Antibodies ; pharmacology ; Bronchi ; cytology ; Cell Adhesion ; drug effects ; physiology ; Cells, Cultured ; Endothelin-1 ; pharmacology ; Eosinophils ; physiology ; Epidermal Growth Factor ; pharmacology ; Epithelial Cells ; physiology ; Female ; Intercellular Adhesion Molecule-1 ; immunology ; physiology ; Male ; Rabbits ; Vasoactive Intestinal Peptide ; pharmacology

To explore the role of regulatory peptides in the secretion of bronchial epithelial cells (BECs), we observed the effects of four peptides, i.e.vasoactive intestinal peptide (VIP), epidermal growth factor (EGF), endothelin-1 (ET-1), and calcitonin gene-related peptide (CGRP), on the secretion of ILs from unstimulated or O3-stressed BECs. The results of the experiments showed that VIP exerted an inhibitory effect on the secretion of IL-1 and IL-8 from unstimulated and O3-stressed BECs, VIP also decreased the secretion of IL-5 from O3-stressed BECs; EGF promoted secretion of IL-1 and IL-8 from unstimulated BECs, but decreased the secretion of ILs from O3-stressed BECs; ET-1 and CGRP enhanced the secretion of IL-1, IL-5, and IL-8 from unstimlated BECs, CGRP also increased the secretion of ILs from O3-stressed BECs. The results obtained demonstrate that intrapulmonary regulatory peptides modulate the secretion of ILs from BECs, and may play an important part in transduction of inflammatory signals.
Animals ; Bronchi ; cytology ; Calcitonin Gene-Related Peptide ; pharmacology ; Cells, Cultured ; Endothelin-1 ; pharmacology ; Epidermal Growth Factor ; pharmacology ; Epithelial Cells ; drug effects ; secretion ; Female ; Interleukins ; secretion ; Male ; Rabbits ; Vasoactive Intestinal Peptide ; pharmacology

AIMTo investigate the influence and mechanisms of 17beta-estradiol on the CTP: phosphorylcholine cytidylyltransferase (CCT) activity from cultured lung explants without serum.

METHODSWe detected the amount of [M-14C] choline incorporation into phosphatidylcholine so as to reflect CCT activity by liquid scintillation.

RESULTS(1) 17beta-estradiol increased the CCT activity in dose-dependence and time-dependence. (2) Both the protein kinase C inhibitor H-7 and calmodulin antagonist W-7 abolished the stimulatory effect of 17beta-estradiol (3 x 10(-6) mol/L) on the CCT activity.

CONCLUSION17beta-estradiol can increase CCT activity in cultured lung explants, its mechanism is related to protein kinase C and calmodulin.

Animals ; Calmodulin ; metabolism ; Choline-Phosphate Cytidylyltransferase ; metabolism ; Culture Media, Serum-Free ; Estradiol ; pharmacology ; In Vitro Techniques ; Lung ; drug effects ; enzymology ; Male ; Protein Kinase C ; metabolism ; Rats ; Rats, Wistar

OBJECTIVE: To explore the role of vasoactive intestinal peptide (VIP) on LPS-induced MMP-9 expression by alveolar macrophages (AM) in rats. METHODS: LPS-induced cultured Wistar rats AMs were treated with different concentrations of VIP (10(-10) to approximately 10(-6) mol/L) for 24 h. AMs and the supernatant were collected to measure the MMP-9 expression and activity by RT-PCR and gelatin zymography, respectively. Results The MMP-9 activity and expression of LPS-induced AMs were significantly higher than those in the control group (P < 0.01). VIP (10(-9) to approximately 10(-6) mol/L) down-regulated LPS-induced MMP-9 activity and its expression. The effects were diminished by H-7 and W-7, an antagonist of protein kinase C (PKC) and calmodulin (CaM) (P < 0.01). CONCLUSION VIP can decrease LPS-induced MMP-9 activity and its expression, which may be related to protein kinase C and calmodulin pathway. VIP may have protective roles in the lung injury.
Animals ; Calmodulin ; metabolism ; Cells, Cultured ; Down-Regulation ; Female ; Lipopolysaccharides ; Macrophages, Alveolar ; cytology ; metabolism ; Male ; Matrix Metalloproteinase 9 ; biosynthesis ; genetics ; Protein Kinase C ; metabolism ; Rats ; Rats, Wistar ; Vasoactive Intestinal Peptide ; pharmacology

Objective To study the derect action and part possible mechanism of sitagliptin ( SIT ) on the delay or stop of the progress of type 2 diabetic nephropathy (DN).Methods The rats were randomly divided into normal group ( NC group ) , diabetic nephropathy group ( DN group) and sitagliptin treatment group (SIT group).The type 2 diabetes mellitus rats were induced by a high fat diet and repeated low dose strep-tozocin injections.At the end of the 12th week in treatment, Masson stai-ning was used to observe the renal fibrosis .RT-PCR was used to detect the mRNA levels of Toll-like-receptor 2 (TLR2), TLR4, nuclear fac-tor-κB ( NF-κB ) .Immunohistochemical method was used to detect the content of TLR2 and TLR4.Western blotting was used to detect the content of NF-κB.Results Compared with NC group , the degree of renal fibrosis, and the expressions of TLR2, TLR4, NF -κB of DN group significantly increased ( P<0.01 ) .However , compared with DN group, the degree of renal fibrosis , and the expressions of TLR2, TLR4, NF-κB of SIT -treated rats significantly decreased ( P <0.05 ) . Conclusion SIT can prevent the renal fibrosis by down -regulating the expression of TLR2, TLR4/NF-κB pathway.