玻璃钢化粪池技术要求0123

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1、CJ中华人民共和国城镇建设行业标准CJ/T 玻璃钢化粪池技术要求发布 实施中华人民共和国住房和城乡建设部 发布 前 言 本标准由住房和城乡建设部标准定额研究所提出。 本标准由住房和城乡建设部给水排水产品标准化技术委员会归口。本标准为首次发布。本标准现只为征求意见稿。玻璃钢化粪池技术要求1 主题内容与适用范围本标准规定了玻璃钢化粪池的规格型号、技术要求、试验方法、检验规则、标志、运输与贮存及其它。本标准适用于以玻璃纤维和不饱和聚酯树脂为主要原材料制作成型的玻璃钢化粪池。2 引用标准下列文件中的条款通过本标准的引用而成为本标准的条款。凡是注日期的引用文件，其随后所有的修改单（不包括勘误的内容）或修

2、订版均不适用于本标准，然而，鼓励根据本标准达成协议的各方研究是否可使用这些文件的最新版本。凡是不注日期的引用文件，其最新版本适用于本标准。GB/T 1446 纤维增强塑料性能试验方法总则GB/T 1447 玻璃纤维增强塑料拉伸性能试验方法GB/T 1449 玻璃纤维增强塑料弯曲性能试验方法GB/T 2576 玻璃纤维增强塑料树脂不可溶分含量试验方法GB/T 2577 玻璃纤维增强塑料树脂含量试验方法GB/T 3854 纤维增强巴氏（马柯尔）硬度试验方法GB/T 8237-2005 玻璃纤维增强塑料（玻璃钢）用液体不饱和聚酯树脂GB/T 18370-2001 中碱玻璃纤维无捻粗纱布GB/T 38

3、57 玻璃纤维增强热固性塑料耐化学介质性能试验方法GB/T 1462 纤维增强塑料吸水性试验方法GB 2575 玻璃纤维增强塑料耐水性试验方法3 规格型号3.1型号 H FRP 型号；玻璃钢代号；污水处理装置。 3.2规格尺寸见表1，外型结构见图1。表1 尺寸号型号L(mm)(mm)H(mm)h1(mm)h2(mm)有效V(m3)12200120014001100105022270015001700140013004337001500170014001300643700180020001700160095500018002000170016001264000230025002200210016

4、7510023002500220021002086200230025002200210025963002500270024002300308000230025002200210030107000280030002700260040118600280030002700260050图14 技术要求 4.1原材料 4.1.1基体树脂：采用不饱和聚酯树脂，其技术要求应符合GB/T 8237-2005相应规定。 4.1.2增强材料：采用无捻玻璃纤维粗纱布，玻璃纤维原丝不得采用石腊型浸润剂，其技术标准应符合GB 18370-2001相应规范。 4.1.3辅助材料：所用的引发剂、促进剂和颜料等的选用应参照树

5、脂生产厂的规定执行。4.2尺寸极限偏差尺寸偏差应符合表2要求表2项目指标长度 100mm直径20mm高度 20mm壁厚 1mm，且罐体均匀分布取10个点，平均值误差为正偏差。进出口水管高度 20mm4.3外观4.3.1罐体外表面应有均匀胶衣层，表面光滑、无裂纹，不允许有明显伤痕，色泽均匀，外表面缺陷允许修补，但修补后的颜色保持一致。4.3.2罐体内表面为富树脂层，表面应光滑平整，不允许纤维裸露，无目测可见裂纹、划痕、疵点及白化分层等缺陷，在任取300mm300mm面积内最大直径为4mm的气泡不得超过5个。4.3.3罐体清掏孔边缘应整齐、厚度均匀、无分层，加工断面应加封树脂。4.4化粪池罐体理化

6、性能4.4.1拉伸强度表3罐体厚度mm拉伸强度Mpa（kgf/cm2）3.2.060（632）5.06.583（847）6.510.093（949）大于10.0108（1102）注：该参数仅用于检验制品材料的力学性能和工艺质量，不作为设计依据。4.4.2弯曲强度表4 罐体厚度mm弯曲强度Mpa（kgf/cm2）3.2.0109（1112）5.06.5127（1295）6.510.0137（1400）大于10.0147（1500）注：该参数仅用于检验制品材料的力学性能和工艺质量，不作为设计依据。4.4.3树脂固化度80%4.4.4树脂含量：富树脂层树脂含量70%；强度层树脂含量4555%。 4.

7、4.5巴氏硬度34 4.4.6吸水率,%1 4.4.7耐酸性：用10%H2SO4溶液常温浸泡100h，应无异状，强度保留85%以上。 4.4.8耐碱性：用10%NaOH溶液常温浸泡100h，应无异状，强度保留85%以上。 4.4.9耐水性：耐水试验30d，应无异状，强度保留85%以上。4.4.10冲击强度：方法按5.12，结果要求表面无裂纹、损伤。 4.4.11渗漏试验：方法按5.13，应无渗漏现象、无冒汗、无明显变形为合格。 4.4.12外压荷载：方法按5.14 ，玻璃钢化粪池普通型承受外压荷载能力不小于200KN，加强型承受外压荷载能力不小于400KN。5 试验方法 5.1外观目测法。5.

8、2尺寸及偏差长度用卷尺进行测量，壁厚用游标卡尺进行测量。结果应符合4.2。 5.3拉伸强度拉伸强度按GB/T 1447测定。结果应符合4.4.1。 5.4弯曲强度弯曲强度按GB/T 1449测定。结果应符合4.4.2。 5.5固化度固化度按GB/T 2576测定。结果应符合4.4.3。 5.6树脂含量树脂含量按GB/T 2577。结果应符合4.4.4。 5.7巴氏硬度巴氏硬度按GB/T 3854。结果应符合4.4.5。 5.8吸水率吸水率按GB/T 1462。结果应符合4.4.6。 5.9耐酸性耐酸性按GB/T 3857。结果应符合4.4.7。 5.10耐碱性耐碱性按GB/T 3857。结果应

9、符合4.4.8。 5.11耐水性耐水性按GB/T 2575。结果应符合4.4.9。 5.12冲击强度：在置于罐体的中央部位的上方，用一个质量2000g重的钢球，从2m高度自由落下，在钢球冲击处，进行测定。结果应符合4.4.10。 5.13渗漏试验：将玻璃钢化粪池进出口封闭后注满水，放置48小时观察，其最大应变不大于0.1%。结果应符合4.4.11。 5.14外压荷载：将产品置于地面以下，上面覆土500mm，回填密实后分别用重车进行碾压。结果应符合4.4.12。6 检验规则 6.1出厂检验6.1.1检验项目：每台玻璃钢化粪池出厂前，应进行：4.2、4.3、4.4.10项目检验。6.1.2判定规则

10、出厂检验各项均符合要求，判产品合格。如有不符合要求的，允许修补，修补后仍不合格则判为不合格品。 6.2型式检验型式检验为全项检验，有下列情况之一时，应进行型式检验：a）产品定型投产时；b）工艺原材料、配方有重大改变，可能影响产品性能时；c）正常生产每五年进行一次；d）停产半年以上再恢复生产时；e）国家质量监督部门提出要求时。 6.3抽样从出厂检验合格产品中进行抽样。 6.4判定产品经检验后，若有一项不合格，允许加倍抽样进行复检。如仍有一项不合格，则判该批产品不合格。7 标志、包装、运输与贮存及其它7.1标志产品经检验合格应印有如下标志：a）商标b）编号c）产品名称d）规格、型号e）进、出水管方

11、向标志f）制造厂名g）联系电话 7.2包装玻璃钢化粪池一般不包装，但各部位的孔应包好，防止污染；产品出厂应有合格证、产品说明书。 7.3运输与贮存 7.3.1在装卸、运输过程中要平稳，在磨擦处应放置软质垫，并用绳子或铁丝扎紧，防止与车厢碰撞。超高应加红色标志，路面情况恶劣，小心慢行，以防止颠簸损坏玻璃钢化粪池。 7.3.2产品在搬运、安装时禁止钢丝绳直接与玻璃钢化粪池接触，禁止捆缚检查孔与进出水管等附件提吊，严禁加载吊装。 7.3.3产品在运输过程中必须有专用支座固定，不得有滚动和碰伤。 7.3.4两台玻璃钢化粪池同时装运时应用软垫隔开，不得直接接触和碰撞。7.3.5产品不得在地面上滚、拖。

12、7.3.6产品贮存时应注意防火。 7.4其他 产品制造厂应向用户提供产品说明书、合格证、水质、产品检验报告。 AcknowledgmentsThe authors would like to thank Johns Hopkins University for the 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 a

13、warded 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 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

14、 (s.c.)once with 1 g of peptide mixed with or without 10 g of CpG adjuvant. After one week, splenocytes wereharvested, and the response 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

15、 peptidein an anti-IFN- -coated polyvinylidene fluoride (PVDF) plate for 48 h. After incubation, the cells wereremoved, and a 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

16、 (eBioscience,CA, USA), the assay was developed using a 3-amine-9-ethyl carbazole (AEC; Sigma-Aldrich, MO,USA) staining 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, U

17、SA).For RAH-specific T cell staining, spleens were harvested seven days after the immunizations, andRAH-specific CD8+ T 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

18、stained RAH-specific CD8+ T cells were analyzed by flow cytometry.Supplementary information accompanies this paper at Competing financial interests: 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 immuni

19、tyof peptide and lipopeptide vaccines via different mechanisms. Sci. Rep. 5, 12578; doi: 10.1038/srep12578 (2015).This work is licensed under a Creative Commons Attribution 4.0 International License.The images or other third party material in this article are included in the articles CreativeCommons

20、 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, visit expression of anti-apoptotic molecules such as the

21、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 the upregulation of IL-12.14,18In this setting, we used a

22、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 manufacturing practice(GMP)-grade agents and have been previously used

23、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 alone, overcame theimmunosuppressive activity of tumor-derive

24、d 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 fusion efficacy;(3) produce elevated levels of IL-12; (4)

25、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 Nonetheless, when DC/cancercell fusions are generated with neopl

26、astic 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/neoplastic cell fusions may significantly enhancethe therapeu

27、tic 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 microenvironment of malignant cells used forthe generation

28、 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,23 as well as the transfection of specific smallinterferin

29、gRNAs (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 adjuvantfor boosting the efficacy of DC/neoplastic cell fusions.26,27

30、 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 surface.28 We have previously reported thatTLR2-stimulated DCs

31、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 capacity to efficientlyelicited antigen-specific CTL activity.26

32、More recently, we havedemonstrated that the secretion of TGF1, IL-10 and VEGRfrom whole cancer cells is significantly limited upon exposure topharmaceutical grade ethanol, a maneuver that does not reduce theevels of MHC class I molecules and TAAs on the cell surface.27Moreover, ethanol, employed at

33、concentrations that affect tumorgrowth, promoted the upregulation of HSPs. HSPs exposed bycancer cells can be recognized by DCs via TLR4, facilitating theiractivation and promoting antigen processing and presentation.29Of note, malignant cells that undergo immunogenic apoptosisectopically expose the

34、 Ca2+-binding chaperone calreticulin (CRT)on the cell surface, allowing TAAs to efficiently traffic to theDC antigen-presenting compartment.30 Moreover, high-mobilitygroup box 1 (HMGB1) passively released from dying neoplasticcells can stimulate antigen processing and presentation in DCs viaa TLR4-d

35、ependent signaling pathway.31,32 Therefore, the exposureof CRT and the release of HMGB1 by ethanol-treated malignantcells enhance the immunogenicity of DC/cancer cell fusions.27Importantly, fusions involving DCs and ethanol-treated cancercells activate T cells to produce high levels of IFN, boosting theelicitation of antigen-specific CTL response in vitro.27 In addition,HSP70-peptide complexes derived from DC/cancer cell fusionsappear to possess superior immunogenic properties as comparedwith similar complexes obtain from neoplastic cells.33Synergistic Effects of Fusions Generated