Blue laser imaging (BLI) is a new endoscopic system equipped with the laser beam emitting two different wavelengths.It produces bright and high resolution images for observation of microvascular and microsurface patterns of esophageal and gastric mucosa, helping the diagnosis of early upper gastrointestinal cancer.Compared with the existed endoscopic techniques, BLI shows its unique advantages.In this article, advances in application of BLI in diagnosis of early upper gastrointestinal cancer were reviewed.

OBJECTIVETo analyze the status and characteristics of dental manpower in the center for disease controls (CDC) in Sichuan Province and to provide more evidence for strengthening the oral healthcare workforce in the CDC system.

METHODSA mass survey on dental manpower was made in CDCs in Sichuan Province through questionnaire investigation. Data were collected and entered with the Epidemiological Dynamic Data Collection (EDDC) platform and analyzed with SPSS 13.0 software.

RESULTSSichuan Province had 0.15 hospitals providing oral health services and 0.38 dentists on average per 10,000 people. About 65.53% (135/206) of the CDCs had one department responsible for the oral health service. However, oral health care personnel comprised only 2.23% (237/10,624) of the personnel of the whole CDC system. About 64.67% (119/184) of county CDCs and 47.62% (10/21) of city CDCs knew well the dental health status of local residents. Less than 5% of the CDCs used the data and assisted in the policy making of public health administrators.

CONCLUSIONThe dental care personal deficit exists in the CDC system in Sichuan Province. The distribution and composition of dental manpower are not reasonable. The oral health service ability of CDCs in Sichuan Province should be strengthened and improved.

China ; Dental Care ; statistics & numerical data ; Dentists ; Humans ; Oral Health ; Surveys and Questionnaires

AIM To investigate the neuroprotective effects and possible mechanisms of saponins from Anemarrhena asphodeloides Bge. (SAaB) on neuronal damage induced by amyloid β-protein fragments 25-35 (Aβ25-35). METHODS Cultured mouse peritoneal macrophages were stimulated with Aβ25-35 (20 μmol·L-1) for 0.5, 1, 2 and 6 h or preincubated with SAaB (10, 30 and 100 μmol·L-1)for 10 min or mitogen-activated protein kinase (MAPK) specific inhibitors (p38 MAPK inhibitor SB 203580 and MEK specific inhibitor PD98059) for 30 min prior to the addition of Aβ25-35(20 μmol·L-1). After stimulation with Aβ25-35 for the indicated times, total cellular extracts were prepared for Western blotting of extracellular signal-regulated kinase (ERK) and p38 MAPK. After stimulation with Aβ25-35 for 48 h, the supernatants of cultured macrophages were collected for quantification of tumor necrosis factor-α (TNF-α) and nitric oxide (NO) and protein expression of inducible nitric oxide synthase (iNOS) in macrophages was determined by immunocytochemical staining. To determine whether SAaB has protective effect against neuronal apoptosis mediated by Aβ25-35-induced macrophages activation, macrophages were stimulated with Aβ25-35 in the presence or absence of SAaB (10, 30 and 100 μmol·L-1) for 48 h and then the cell-free supernatant of Aβ25-35-stimulated macrophages was transferred to the culture of cerebellar granule neurons for 72 h. Neuronal apoptosis was quantitated by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. RESULTS Aβ25-35(20 μmol·L-1) significantly induced increase in phospho-ERK1/2 and phospho-p38 MAPK protein expression without affecting total protein levels and in the production of TNF-α and NO in cultured macrophages. Aβ25-35-induced increase of TNF-α production in macrophages involved activation of ERK1/2 signal pathway. Importantly, TNF-α and NO generated by cultured macrophages after Aβ25-35 stimulation may be responsible for the majority of the neuronal apoptosis. SAaB (30 and 100 μmol·L-1) significantly suppressed Aβ25-35-induced increase in phospho-ERK1/2 and phospho-p38 MAPK protein. In addition, SAaB (10, 30 and 100 μmol·L-1) also decreased the level of TNF-α and NO in supernatants of cultured macrophage and inhibited Aβ25-35-induced increase in iNOS protein expression of macrophages. Neuronal apoptosis mediated by Aβ25-35-induced macrophage activation was also significantly attenuated by treatment with SAaB (10, 30 and 100 μmol·L-1). CONCLUSION SAaB protects neurons against the neuronal cell death induced by Aβ25-35. The beneficial effects of SAaB may be related to the reduction of TNF-α and NO from activated macrophage induced by Aβ25-35.

ObjectiveTo find out if the immune system derived thyroid stimulating hormone(TSH) β splice variant(TSHβ-Ⅴ) would be regulated by circulating thyroid hormone levels to get a further understanding of the function and mechanism of this TSHβ-Ⅴ in thyroid homeostasis.MethodsA total of 20 weaning Balb/c mice (half male and half female) were selected and randomly divided into two groups according to their body mass and gender(n =10).Mice of control group were fed with common diet and deionized water.Mice of the low-iodine(LI) group were fed with low-iodine diet(containing iodine 20 - 40 μg/kg,iodine-intake about 0.25 μg/d) and deionized water.The experimental period was 3 months.At the end of the experiment,mice were executed and the blood was collected to observe the levels of TSH and thyroid hormone by chemiluminescence immunoassay (CIA) ; bone marrow (BM),peripheral blood(PBL),thyroid gland and pituitary were collected to assay the TSHβ-Ⅴ mRNA expression by real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR).ResultsThe serum free thyroxine(FT4) and total thyroxine(TT4) levels in LI group of mice[(0.47 ± 0.70)nmol/L,(2.41 ± 0.28)pmol/L] were significantly lower than that of the control group of mice [(55.2 ± 3.68) nmol/L, (32.72 ± 1.02) pmol/L,t =43.81,86.04 、all P ＜ 0.01 ] and the serum total triiodothyronine(TT3) and free triiodothyronine(FT3) reduction in LI group of mice[ (0.76 ± 0.08)nmol/L,(4.01 ± 0.40)pmol/L] were significantly lower than that of the control group of mice [ (1.10 ± 0.06)nmol/L,(5.40 ± 0.38)pmol/L,t =9.81,7.5 1,P ＜ 0.01 ].Iodine insufficiency strongly elevated the serum TSH in LI group of mice[ (35.67 ± 17.39)mU/L] than that in control group of mice[ (0.24 ± 0.10)mU/L,t =- 6.11,P ＜ 0.01 ].The mRNA levels of TSH β-Ⅴ in BM (9.62 ± 0.60) and in PBL( 9.25 ± 0.83 ) of LI group of mice were lower than those in control group of mice (7.69 ± 0.36,7.11 ± 0.41,t =6.77,5.64,P ＜ 0.01),while the mRNA level of TSH β-Ⅴ in pituitary of LI group of mice (1.99 ± 0.61) was increased compared with that in control group of mice (5.75 ± 0.98,t =- 8.02,P＜ 0.01).Compared with control group of mice(9.12 ± 0.62),the level of thyroid TSH β-Ⅴ mRNA in LI group of mice (9.32 ± 0.91 ) was not significantly changed (t =0.45,P ＞ 0.05).There was no detectable native TSHβ in BM,PBL and thyroid.The mRNA level of native TSHβ in pituitary in LI group of mice( - 7.17 ± 1.78) was dramatically elevated compared to that in control group of mice( - 1.43 ± 0.51,t =- 7.60,P ＜ 0.01 ).ConclusionsThe mRNA levels of TSHβ-Ⅴ are suppressed in BM and PBL in low iodinediet induced hypothyroidism mice,which suggest that immune system derived TSHβ-Ⅴ may be more important thannative TSHβ in immune-thyroid regulation.

Objective To determine potential gene-gene interactions of TNF-? and VDR loci with outcomes of hepatitis B virus(HBV) infection.Methods A total of 391 chronic hepatitis B(HB) patients as a case group and 212 HBV self-limited infected subjects as a control group were recruited to conduct a case-control study.TNF-?-238G/A,-857C/T,-863C/A,VDR-TaqⅠT/C and FokⅠC/T gene polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).The interactions between TNF-? and VDR genes were analyzed by multiple model.Results There were positive gene-gene interactions between TNF-?-238 GA and FokⅠ CT/CC(ORint=4.04),between-863 CC and-857 CC(ORint=1.26) and between-857 CC and FokⅠ CT/CC(ORint=1.37),respectively,which increase the risk of chronic hepatitis B.There were negative gene-gene interactions between TNF-?-238 GA and-857 CC(ORint=0.92)and between FokⅠ CT/CC and TNF-?-863 CC(ORint=0.95),which decrease the risk of chronic hepatitis B.Conclusion Interaction between TNF-? loci and VDR loci potentially increase the risk of chronic hepatitis B after HBV infection.

WNT signaling plays an important role in cardiac development, but abnormal activity is often associated with cardiac hypertrophy, myocardial infarction, remodeling, and heart failure. The effect of WNT signaling on regulation of atrial natriuretic peptide (ANP) secretion is unclear. Therefore, the purpose of this study was to investigate the effect of Wnt agonist 1 (Wnta1) on ANP secretion and mechanical dynamics in beating rat atria. Wnta1 treatment significantly increased atrial ANP secretion and pulse pressure; these effects were blocked by U73122, an antagonist of phospholipase C. U73122 also abolished the effects of Wnta1-mediated upregulation of protein kinase C (PKC) β and γ expression, and the PKC antagonist Go 6983 eliminated Wnta1-induced secretion of ANP. In addition, Wnta1 upregulated levels of phospho-transforming growth factor-β activated kinase 1 (p-TAK1), TAK1 banding 1 (TAB1) and phospho-activating transcription factor 2 (p-ATF2); these effects were blocked by both U73122 and Go 6983. Wnta1-induced ATF2 was abrogated by inhibition of TAK1. Furthermore, Wnta1 upregulated the expression of T cell factor (TCF) 3, TCF4, and lymphoid enhancer factor 1 (LEF1), and these effects were blocked by U73122 and Go 6983. Tak1 inhibition abolished the Wnta1-induced expression of TCF3, TCF4, and LEF1 and Wnta1-mediated ANP secretion and changes in mechanical dynamics. These results suggest that Wnta1 increased the secretion of ANP and mechanical dynamics in beating rat atria by activation of PKC–TAK1–ATF2–TCF3/LEF1 and TCF4/LEF1 signaling mainly via the WNT/Ca2+ pathway. It is also suggested that WNT–ANP signaling is implicated in cardiac physiology and pathophysiology.

OBJECTIVETo examine the effect of ginsenoside Rb1 (GRb1) on the immune maturation of monocyte-derived dendritic cells (DCs) induced by oxidized low-density lipoprotein (OX-LDL).

METHODSHuman monocytes purified by CD14+ immuno-magnetic beads were differentiated and induced into immature DCs, which were randomly divided into 6 groups, Group A treated with PBS, Group B treated with OX-LDL, Group C and D treated respectively with GRb1 and ciglitazone, Group E and F were pretreated with the two testing drugs respectively followed by OX-LDL. The immuno-phenotypic expression (CD40, CD1a, and HLA-DR) and endocytosis function of DCs were examined using flow cytometry, the concentration of interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-alpha) in the culture supernatants were measured with ELISA.

RESULTSCompared with Group B, Group E showed significantly lowered immuno-phenotypic expression of DCs in terms of CD40 (67.4 +/- 1.62 vs. 145.69 +/- 14.86), CD1a (79.64 +/- 3.04 vs. 159.89 +/- 6.09), and HLA-DR (46.43 +/- 2.85 vs. 99.33 +/- 17.11), as well as higher endocytosis level (88.13% +/- 1.06% vs. 25.90% +/- 5.77%, all P < 0.01). Meantime, the serum levels of IL-12 (88.65 +/- 5.59 ng/L vs. 716.69 +/- 36.35 ng/L) and TNF-alpha (133.27 +/- 11.98 ng/L vs. 968.10 +/- 36.42 ng/L) obviously decreased (P < 0.01). The surface molecular expression of DCs and the secretion of inflammatory factors in Group F also obviously decreased, showing insignificant difference from Group E (P > 0.05).

CONCLUSIONGRb1 could obviously inhibit the OX-LDL-induced maturation of DCs, showing similar effects to ciglitazone.

Cell Differentiation ; drug effects ; Cells, Cultured ; Dendritic Cells ; cytology ; drug effects ; immunology ; Flow Cytometry ; Ginsenosides ; pharmacology ; Humans ; Lipoproteins, LDL ; Monocytes ; cytology ; drug effects ; immunology

Objective To evaluate the storage performance of storage bags for apheresis platelets produced by Shandong Weigao Group Medical Polymer Co .,Ltd ( experimental bags ) with Trima set platelet storage bags produced by the U .S. Gambro BCT as the control .Method One unit of apheresis platelets was divided into two equal parts , added to control blood bags and experimental blood bags respectively .All samples were stored at ( 22 ±2 )℃ with consecutive oscillation . The platelets′count, mean volume, aggregate activity (ADP, THR), pH, glucose, lactate concentration, lactate dehydro-genase concentration , hypotonic shock reaction , expression of CD62P and phosphatidyl serine on surface of cell membrane were detected at 0,3,5 and 7 d respectively.Results There was no significant difference in platelet quality after five days of storage between the experimental group and the control group (t-test, P>0.05).Conclusion Two types of platelet stor-age blood bags have similar storage performance for apheresis platelets .

AIM: Accommodation is one of the most important functions of human eye, while its mechanism is still under discussion. This paper aimed to study accommodation mechanism with numerical simulation.METHODS: A simulation model was constructed to study the mechanism of accommodation based on the experimental data derived from published resources. The displacement and pressure are applied on the model to study the deformation of lens during accommodating.RESULTS: The simulation showed that, as the eye was accommodating, the thickness of the lens increased linearly,and the lens diameter decreased linearly. The optical power of the lens increased as the accommodation increased. This result was accord with the public facts in accommodation.Furthermore, the pressure was found to have a great influence on the shape of the lens and the optical power. The lens became thinner and flatter as the pressure increased and the pressure caused a remarkable increase of lens' optical power.CONCLUSION: The outcome of this paper is consistent with the Helmholtz's hypothesis on accommodation to some extent. The analytical model presented in this paper can be used in the theoretical study of the accommodation mechanism of the human lens.

Objective To investigate the neutralized antibody level of poliomyelitis among healthy children before and after implementation of the new immunization strategy in Shanghai. Methods The poliomyelitis levels of healthy children were detected by neutralization test of the micro cells. Results The neutralizing antibody positive rates were 100% for polioⅠand polioⅢ before and after implementation of the new immunization strategy.GMTs (geometric mean titers) for polioⅠwere 1:1 047.46 before it, and 1:254.70 after it; those for polio Ⅲ were 1:513.52 before it and 1:185.49 after it. Conclusion The neutralized antibody levels of the poliomyelitis among healthy infants maintain a high level before and after implementing the new immunization strategy in Shanghai.