Objective To evaluate the effects of calcitonin and 1, 25 vitamin D on the bone loss in experimental periodontitis in rats. Methods A total of 125 male Wistar rats were randomly allocated to five groups according to the treatments during 8 weeks: normal control (group A, n=25), periodontitis(group B, n=25), calcitonin (group C, prepared in sterile saline at 2 mg/L, and 2μg/kg was administered daily, s.c. , n=25), 1,25 vitamin D (group D, prepared in corn oil daily at a concentration of 2 mg/L, and 2μg/kg was administered daily, p.o. , n=25), 1,25 vitamin D plus calcitonin (group E, n=25). The experimental model of periodontitis was induced by ligating floss around mandibular first molars with orthodontic wires in B,C,D and E groups. Five rats from each group were sacrificed, and the specimens were prepared at 2, 4, 6 and 8-week. The probing depth (PD) and alveolar bone level were observed. The serum bone-specific alkaline phosphatase (BALP) and osteocalcin (OC) were measured by enzyme-linked immunosorbent assay (ELISA) at 8-week in each group. Results The values of PD were significantly lower after 4, 6 and 8 weeks in E group than those of B, C and D groups (P＜0.05). The alveolar bone loss was significantly lower after 6 and 8 weeks in group E compared with that of B, C and D groups (P＜0.05). The serum levels of BALP and OC were significantly higher after 8 weeks in E group than those of B, C and D groups (P＜0.05). Conclusion The present study suggests that 1, 25 vitamin D and calcitonin can partially inhibit the alveolar bone loss induced by periodontitis. Especially, the application of both is more effective than either drug treatment alone.

Objective To evaluate the effects of root canal cleanliness on the fracture resistance of roots filled with AH-Plus. Methods Eighty single canal premolars were instrumented using step-back technique, then were randomly di-vided into four groups (n=20 for each group). Group A was washed with distilled water for 10 min, group B1 was washed with 5%EDTA for 1 min, group B2 was washed with 5%EDTA for 5 min and group B3 was washed with 5%EDTA for 10 min. Ten samples of each group were observed by scanning electron microscope at the coronal, middle and apical thirds to exam-ine smear layer removal. The remaining samples of each group were fixed into a electronic universal testing machine and ver-tically loaded until fracture. Results The difference of coronal and middle thirds was significant between group B3 and group B2 (P<0.05). At the middle third, there was significantly improved efficiency in smear layer removal in group B2 than that of group B1(P<0.05). The mean fracture resistance was significantly higher in group B3 (391.91±12.82)N than that of group B2 (335.54±16.14)N, group B1(296.47±17.82) N and group A (264.77±16.64)N (P<0.05). Group B2 showed a signifi-cantly better fracture resistance than that of group B1 and group A (P<0.05). Conclusion The complete removal of root ca-nal smear layer can significantly improve the fracture resistances of roots filled with AH-Plus.

OBJECTIVETo study the effect and mechanism of arsenic trioxide (As2O3) on apoptosis of pulmonary eosinophiles (PE) in asthmatic guinea-pigs.

METHODSThirty guinea-pigs were divided into 3 groups at random, the control group, the asthmatic group and the As2O3 group. The dosage of As2O3 used was 2 mg/kg. The apoptotic PE were labelled by TdT-mediated dUTP nick end labelling technique, and the PE infiltration and apoptosis were detected quantitatively using computerized image analysis technique.

RESULTSIn the control group, the amount of infiltrating PE was 4.4 +/- 2.5 cells/HP and the PE apoptotic index (AI) was 0.42 +/- 0.08%. In the asthmatic group, the amount increased (P < 0.01) and AI decreased significantly (P < 0.01). After the asthmatic animals had been treated with As2O3, the two parameters changed reversedly significantly (P < 0.01), and there was a significantly negative correlation between them (r = -0.949, P < 0.01).

CONCLUSIONThe PE apoptosis abnormality is one of the important mechanisms that cause bronchial asthma, As2O3 could alleviate the airway inflammation through promoting PE apoptosis and lower PE infiltration. Low dose of As2O3 is proved to be effective with relative safety, it also has potential value in treating asthma.

Animals ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Asthma ; chemically induced ; pathology ; Eosinophils ; pathology ; Guinea Pigs ; Image Processing, Computer-Assisted ; Lung ; pathology ; Male ; Ovalbumin ; Oxides ; pharmacology ; Random Allocation

BACKGROUND: Triggering receptor expressed on myeloid cells-1 (TREM-1) in the intestine was upregulated and correlated with disease activity in inflammatory bowel diseases. Membrane-bound TREM-1 protein is increased in the pancreas, liver and kidneys of patients with severe acute pancreatitis (SAP), suggesting that TREM-1 may act as an important mediator of inflammation and subsequent extra-pancreatic organ injury. This study aimed to investigate the relationship between the expression of TREM-1 in intestinal tissue and intestinal barrier dysfunction in SAP. METHODS: Sixty-four male Wistar rats were randomly divided into a sham operation group (SO group, n=32) and a SAP group (n=32). A SAP model was established by retrograde injection of 5％sodium deoxycholate into the bile-pancreatic duct. Specimens were taken from blood and intestinal tissue 2, 6, 12, and 48 hours after operation respectively. The levels of D-lactate, diamine oxidase (DAO) and endotoxin in serum were measured using an improved spectro-photometric method. The expression levels of TREM-1, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) mRNA in terminal ileum were detected by real-time reverse transcription-polymerase chain reaction (RT-PCR). Specimens of the distal ileum were taken to determine pathological changes by a validated histology score. RESULTS: The serum levels of D-lactate, DAO and endotoxin were significantly increased in each subgroup of SAP compared with the SO group (P<0.01, P<0.05). The expression levels of TREM-1, IL-1β and TNF-α mRNA in the terminal ileum in each subgroup of SAP were significantly higher than those in the SO group (P<0.01, P<0.05). The expression level of TREM-1mRNA was positively correlated with IL-1β and TNF-α mRNA (r=0.956, P=0.044; r=0.986, P=0.015), but the correlation was not found between IL-1β mRNA and TNF-α mRNA (P=0.133). Compared to the SO group, the pathological changes were aggravated significantly in the SAP group. CONCLUSIONS: The expression level of TREM-1 in intestinal tissue of rats with SAP was elevated, leading to the release of inflammatory mediators and intestinal mucosal injury. This finding indicates that TREM-l might play an important role in the development of intestinal barrier dysfunction in rats with SAP.

0.05), but the level of albumin dropped significantly(P

Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation ; physiology ; Asthma ; etiology ; Humans ; Immune Tolerance ; Immunity, Innate ; Membrane Glycoproteins ; physiology ; Myeloid Differentiation Factor 88 ; Proteins ; physiology ; Receptors, Cell Surface ; physiology ; Receptors, Immunologic ; physiology ; Signal Transduction ; Toll-Like Receptors

AIMTo study the effects of sodium salicylate on the expression of GABAalpha NR1 and hearing response properties of inferior colliculus neurons in mice.

METHODSThirty-six kunming mice were divided into three groups (A, B, C,). The expression of GABAalpha NR1 were measured by using RT-PCR. The intensity-rates functions, intensity-latency functions and frequency-turning curves were recorded by extracellular electrophysiological recording techniques.

RESULTS(1) The expression of GABAalpha mRNA of B group was decreased remarkably than the control group (A group, P < 0.05), there weren't noticeable differences between A group and C group (P > 0.05). The expression of NR1 mRNA of B group was increased remarkably than the control group (A group, P < 0.01), there were noticeable differences between A group and C group P < 0.05). (2) The intensity-rates functions, intensity-latency functions were monotonic while the frequency-turning curves were more broad when sodium salicylate was given. (3) The intensity-rates functions, intensity-latency functions were non-monotonic while the frequency-turning curves were sharpened after lidocaine was given.

CONCLUSIONS(1) The results suggested that administration of sodium salicylate decreased the expression of GABAalpha while increased the expression of NR1mRNA. (2) The intensity-rates functions, intensity-latency functions were monotonic, the frequency-turning curves were more broad when salicylate was given and the changes above could be reversed by given lidocaine.

Acoustic Stimulation ; Animals ; Inferior Colliculi ; drug effects ; metabolism ; physiology ; Mice ; Mice, Inbred Strains ; Neurons ; drug effects ; metabolism ; physiology ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Sodium Salicylate ; pharmacology ; gamma-Aminobutyric Acid ; metabolism

OBJECTIVETo investigate the outcomes after 2 methods of laparoscopic gastric bypass surgery for patients with type 2 diabetes mellitus(T2DM).

METHODSFrom December 2009 to June 2011, 21 patients with T2DM underwent laparoscopic gastric bypass surgery, including laparoscopic Roux-en-Y gastric bypass (LRYGB, n=11), and laparoscopic mini-gastric bypass (LMGB, n=10). Clinical data were analyzed retrospectively.

RESULTSThe clinical complete remission rate of T2DM was 64%(7/11) in LRYGB group, and 60%(6/10) in LMGB group. The clinical partial remission rate of T2DM was 36%(4/11) in LRYGB group, and 40%(4/10) in the LMGB group. There was no significant difference between the two groups(both P>0.05). The levels of BMI, waist circumference, HOMA-IR and HbA1c within the postoperative 6 months were improved in each group (all P<0.05), but there was no significant difference between the two groups(all P>0.05). There were no conversion or perioperative deaths in both groups. Compared to LMGB, the LRYGB group had longer operative time[(147.0±35.9) min vs. (110.5±39.7) min, P=0.038] and postoperative hospital stay [(8.9±2.3) d vs. (7.1±1.4) d, P=0.046). One patient suffered from ileus in LRYGB group, one patient suffered from reflux esophagitis and one suffered chronic diarrhea in LMGB group. The incidence of postoperative complication was similar between the two groups(P>0.05).

CONCLUSIONLRYGB and LMGB may result in satisfactory and safe effects for the treatment of T2DM, while the LMGB is simpler and associates with quicker recovery.

Adult ; Diabetes Mellitus, Type 2 ; surgery ; Female ; Gastric Bypass ; methods ; Humans ; Laparoscopy ; Male ; Middle Aged ; Retrospective Studies ; Treatment Outcome

BACKGROUNDTyrosine kinase signaling cascades play a critical role in the pathogenesis of allergic airway inflammation. Sunitinib, a multitargeted receptor tyrosine kinase inhibitor, has been reported to exert potent immunoregulatory, anti-inflammatory and anti-fibrosis effects. We investigated whether sunitinib could suppress the progression of airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling in a murine model of chronic asthma.

METHODSOvalbumin (OVA)-sensitized mice were chronically challenged with aerosolized OVA for 8 weeks. Some mice were intragastrically administered with sunitinib (40 mg/kg) daily during the period of OVA challenge. Twelve hours after the last OVA challenge, mice were evaluated for the development of airway inflammation, AHR and airway remodeling. The levels of total serum immunoglobulin E (IgE) and Th2 cytokines (interleukin (IL)-4 and IL-13) in bronchoalveolar lavage fluid (BALF) were measured by ELISA. The expression of phosphorylated c-kit protein in the lungs was detected by immunoprecipitation/Western blotting (IP/WB) analysis.

RESULTSSunitinib significantly inhibited eosinophilic airway inflammation, persistent AHR and airway remodeling in chronic experimental asthma. It reduced levels of total serum IgE and BALF Th2 cytokines and also lowered the expression of phosphorylated c-kit protein in remodelled airways.

CONCLUSIONSSunitinib may inhibit the development of airway inflammation, AHR and airway remodeling. It is potentially beneficial to the prevention or treatment of asthma.

Angiogenesis Inhibitors ; pharmacology ; Animals ; Asthma ; chemically induced ; drug therapy ; immunology ; Blotting, Western ; Bronchial Hyperreactivity ; chemically induced ; immunology ; Bronchoalveolar Lavage Fluid ; chemistry ; Female ; Immunoglobulin E ; blood ; Immunohistochemistry ; Immunoprecipitation ; In Vitro Techniques ; Indoles ; pharmacology ; Inflammation ; chemically induced ; immunology ; Interleukin-13 ; metabolism ; Interleukin-4 ; metabolism ; Lung ; drug effects ; immunology ; metabolism ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; pharmacology ; Proto-Oncogene Proteins c-kit ; metabolism ; Pyrroles ; pharmacology

BACKGROUNDInterleukin-13 (IL-13) is recognized to be a key modulator in the pathogenesis of Th2-induced allergic inflammation. Transcription factors GATA3 and NFAT1 have been both implicated in the regulation of Th2 cytokines. We previously demonstrated the GATA3-NFAT1 association during human T cell activation. However, the function of the GATA3-NFAT1 complex in Th2 cytokines regulation is still unknown. Small interference RNA (siRNA) was constructed to knock down GATA3 expression in Hut-78 cells to investigate the possible role of GATA3-NFAT1 complex in IL-13 transcription.

METHODSCells were stimulated with anti-CD3 plus anti-CD28 antibodies to mimic in vivo antigen-mediated co-stimulation; the expression of IL-13 mRNA was determined by real-time PCR; chromation immunoprecipitation (CHIP) assay was employed to investigate the NFAT1 binding to IL-13 promoter.

RESULTSGATA3 siRNA suppressed the expression of GATA3 both in mRNA and protein levels in Hut-78 cells. The binding of NFAT1 to IL-13 promoter was inhibited by GATA3 siRNA in activated T cells, which was followed by the reduction of IL-13 transcription.

CONCLUSIONGATA3-NFAT1 complex may play an important role in the regulation of IL-13 transcription in human T cells.

Cells, Cultured ; GATA3 Transcription Factor ; antagonists & inhibitors ; genetics ; Humans ; Interleukin-13 ; genetics ; NFATC Transcription Factors ; metabolism ; Promoter Regions, Genetic ; RNA, Small Interfering ; genetics ; T-Lymphocytes ; metabolism ; Transfection