關(guān)于排氣道、通風(fēng)道高度的規(guī)范要求

1、關(guān)于排氣道、通風(fēng)道高度的規(guī)范要求來源：    發(fā)布時間：2011-4-19:42:12    點擊次數(shù)：157 關(guān)于排氣道、通風(fēng)道高度的規(guī)范要求我站在日常工程質(zhì)量監(jiān)督中，特別是住宅工程監(jiān)督過程中，發(fā)現(xiàn)相當(dāng)多工程屋面排氣道、煙道等設(shè)置位置及出屋面高度錯誤，現(xiàn)場了解發(fā)現(xiàn)相當(dāng)多參建單位對此方面規(guī)范要求模糊，概念不清，而查閱有關(guān)圖紙也是標(biāo)注不詳。2010版江蘇住宅工程質(zhì)量分戶驗收規(guī)程DGJ32/J103-2010中對排水通氣管出屋面高度有明確要求，但煙道出屋面高度未做明確?，F(xiàn)將有關(guān)規(guī)范要求整理，供參建單位工程技術(shù)

2、人員參考。1、各圖審機(jī)構(gòu)審查時參照的全國民用建筑工程設(shè)計技術(shù)措施09版：第條規(guī)定了出屋面高度“當(dāng)住宅有退臺或上人屋面時，排氣道和通風(fēng)道應(yīng)高出屋面2m，并避開同層所開啟的門窗，以免煙氣回竄入室”；2、另外，措施條，對坡屋面的排氣管及通風(fēng)道的高度也做了非常具體的規(guī)定。，高出屋脊，且伸出屋面高度不小于大于3.0米，管道頂部同屋脊連線與水平線夾角不大于10度，且伸出屋面高度不小于0.6米。此外，民用設(shè)計通則>GB50352-2005第6.14條也有類似規(guī)定：  上述要求應(yīng)適用于各類民用建筑，包括住宅工程。3、蘇J19-2009 住宅煙氣集中排放系統(tǒng)規(guī)定了“對于平屋面采用蓋板時。風(fēng)帽的底

3、部隔板下端距屋面高度不應(yīng)小于600并應(yīng)高出女兒墻300”（見下圖示標(biāo)注尺寸）。4、關(guān)于排水通氣管出屋面高度，江蘇的住宅工程質(zhì)量分戶驗收規(guī)程DGJ32/J103-2010第條第7款規(guī)定：1）通氣管應(yīng)高出屋面300mm；2）在通氣管出口4米范圍內(nèi)有門、窗時，通氣管高度應(yīng)高出門、窗頂600mm或引向沒有門、窗一側(cè)；3）上人屋面通氣管高度應(yīng)高出屋面2米。該項要求應(yīng)在住宅工程質(zhì)量控制中嚴(yán)格落實。昆山經(jīng)濟(jì)技術(shù)開發(fā)區(qū)建設(shè)工程質(zhì)量安全監(jiān)督站二0一一年四月一日AcknowledgmentsThe authors would like to thank Johns Hopkins University for t

4、he TC-1 cells. This work was supportedby a National Health Research Institutes intramural grant (IV-103-PP-22) and grants from the NationalScience Council, which were awarded to Y.C. Song (NSC 99-2321-B-400-004-MY3) and S.J. Liu (NSC103-2321-B-400-008).Author ContributionsY.C.S. and S.J.L. designed

5、the studies. Y.C.S. performed the research and analyzed the data. Y.C.S. andS.J.L. wrote the manuscript.Additional InformationC57BL/6 mice were immunized subcutaneously (s.c.)once with 1 g of peptide mixed with or without 10 g of CpG adjuvant. After one week, splenocytes wereharvested, and the respo

6、nse of IFN- -secreting cells was determined by ELISPOT after 48 h of peptidestimulation. Briefly, 2 × 105 splenocytes were incubated with 1 g/ml irrelevant peptide or RAH peptidein an anti-IFN- -coated polyvinylidene fluoride (PVDF) plate for 48 h. After incubation, the cells wereremoved, and a

7、 biotinylated anti-IFN- Ab (eBioscience, San Diego, CA, USA) was added to each well.The plates were incubated at 37 °C for 2 h. Following the addition of the avidin-HRP reagent (eBioscience,CA, USA), the assay was developed using a 3-amine-9-ethyl carbazole (AEC; Sigma-Aldrich, MO,USA) staining

8、 solution. The reaction was stopped after 46 min by placing the plate under tap water.The spots were counted using an ELISPOT reader (Cellular Technology Ltd., Shaker Heights, OH, USA).For RAH-specific T cell staining, spleens were harvested seven days after the immunizations, andRAH-specific CD8+ T

9、 cells were detected by tetramer staining using a PE-labeled RAH tetramer(Beckman Coulter, CA, USA) and a FITC-labeled anti-CD8 monoclonal antibody (mAb) (eBioscience,CA, USA). The stained RAH-specific CD8+ T cells were analyzed by flow cytometry.Supplementary informationCompeting financial interest

10、s: The authors declare no competing financial interests.How to cite this article: Song, Y.-C. and Liu, S.-J. A TLR9 agonist enhances the anti-tumor immunitysrep12578 (2015).This work is licensed under a Creative Commons Attribution 4.0 International License.The images or other third party material i

11、n this article are included in the articles CreativeCommons license, unless indicated otherwise in the credit line; if the material is not included underthe Creative Commons license, users will need to obtain permission from the license holder toreproduce the material. To view a copy of this license

12、, visit expression of anti-apoptotic molecules such as the BCL-2 familymembers BCL-XL and CASP8 and FADD-like apoptosis regulator(CFLAR, best known as cFLIP), thereby allowing CTLs to surviveand reach neoplastic of various TLR agonists promotes the immunogenicity of DC/malignant cell fusions through

13、 the upregulation of IL-12.14,18In this setting, we used a de from Coriolus versicolor (PSK, which operates as a TLR2 agonist)and lyophilized preparations of a low-virulence strain (Su) ofStreptococcus pyogenes (OK-432, which acts as a TLR4 agonist),both of which can be produced as good manufacturin

14、g practice(GMP)-grade agents and have been previously used in the clinic asbiological response modifiers.18,19 Of note, DC/cancer cell fusionsactivated in the presence of both TLR2 and TLR4 agonists,but not DC/malignant cell fusions that were left unstimulatedor were exposed to either TLR agonist al

15、one, overcame theimmunosuppressive activity of tumor-derived molecules suchas transforming growth factor 1 (TGF1). In particular,TLR2/4-activated DCs (or the corresponding fusions): (1) exhibitincreased expression levels of MHC class II molecules and CD86on the cell surface; (2) manifest an improved

16、 fusion efficacy;(3) produce elevated levels of IL-12; (4) simultaneously activateCD4+ and CD8+ T cells, which secrete high levels of interferon (IFN); (5) potently induce antigen-specific CTL activity;and (6) manifest a superior efficacy in inhibiting the generationof CD4+CD25+FOXP3+ Tregs.20 Nonet

17、heless, when DC/cancercell fusions are generated with neoplastic cells producing extremelyhigh levels of TGF1, they inhibit the activity of CTLs in vitro.Therefore, incorporating the simultaneous activation of multipleTLRs and the blockade of immunosuppressive that are intrinsicallyproduced by DC/ne

18、oplastic cell fusions may significantly enhancethe therapeutic potential of this approach.Improving the Immunogenicity of Malignant CellsMost, if not all, malignant cells secrete multipleimmunosuppressive mediators such as TGFmolecules normally inhibit the initiation of efficient CTLresponses,21 the

19、 microenvironment of malignant cells used forthe generation of DC/cancer cell fusions immunostimulatory. Several strategies to inhibit the production ofimmunosuppressive factors by cancer cells have been developed,including the administration of neutralizing antibodies22 and smallchemical inhibitors

20、,23 as well as the transfection of specific smallinterferingRNAs (siRNAs)24 or constructs coding for a solublevariant of the TGF receptor.25 Also heat-shock proteins (HSPs),which have recently been implicated in the immunogenicity ofapoptotic and necrotic cells, might constitute effective adjuvantfo

21、r boosting the efficacy of DC/neoplastic cell fusions.26,27 HSPsgenerally operate as chaperons for a wide panel of peptides,including antigenic peptides, and HSP/peptide complexes notonly can be efficiently taken up by DCs through specific receptors,but also can be presented in molecules the DC surf

22、ace.28 We have previously reported thatTLR2-stimulated DCs fused with heat-treated cancer cells areimmunogenic, as demonstrated by: (1) the upregulation of multipleHSPs, MHC class I and II molecules, TAAs, CD80, CD86, CD83,and IL-12; (2) their ability producing high levels of IFN; and (3) the capaci

23、ty to efficientlyelicited antigen-specific CTL activity.26 More recently, we havedemonstrated that the secretion of TGF1, IL-10 and VEGRfrom whole cancer cells is significantly limited upon exposure toMoreover, ethanol, employed at concentrations that affect tumorgrowth, promoted the upregulation of HSPs. HSPs exposed byOf note, malignant cells that undergo immunogenic apoptosisectopically expos