【US20200054608A1】ALPHAADRENERGICAGONISTSFORTHETREA
阿尔法拉瓦尔药业线_S用户手册说明书
2. Installation .............................................................................................. 8 2.1. Clearance for dismantling ........................................................................ 8 2.2. Foundations ....................................................................................... 8 2.3. Positioning and slope ............................................................................. 8 2.3.1 Horizontal positioning ............................................................................. 8 2.3.2 Vertical positioning ................................................................................ 8 2.4 Levelling .............................................................................................. 9 2.5 Cleanliness provisions .............................................................................. 9 2.6 Connecting the heat exchanger to the piping system ........................................... 9 2.7 Fitting and piping .................................................................................... 10
阿尔法拉瓦尔纯球胶3.0系列产品介绍说明书
Press editorialApril 2013Redefining leadership in ballast water treatment: inside PureBallast 3.0April marks the official unveiling of the third generation of Alfa Laval’s chemical-free system for ballast water treatment. Less of an update than a sweeping redefinition of the system, PureBallast 3.0 re-establishes Alfa Laval as a groundbreaker in ballast water treatment.PureBallast, which was developed in cooperation with Wallenius Water, was originally launched in 2006 as the world’s very first commercially available ballast water treatment system. Since then it has matured considerably, arriving in an updated PureBallast 2.0 version with EX options in 2010. Already then there were improvements to its energy efficiency and its basic construction, but nothing to compare with the advances in PureBallast 3.0.“This time we’ve completely rewritten the book when it comes to PureBallast,” says Per Warg, the Alfa Laval Business Manager responsible for the system. “We’ve achieved space savings of 50%, energy savings of up to 60% and huge improvements in flexibility and flow capacity. But we’ve also learned a great deal that can be of impact for ballast water treatment in general.”Going back to the beginningThe development of PureBallast 3.0 began almost immediately after the release of its predecessor, with Alfa Laval returning to the drawing board in in early 2011. Jonas Alván, Product Development Manager for PureBallast, points out that this was really a new start for the system. “The original construction had been streamlined as much as was possible, which meant we were forced to think in new ways to move forward,” he says.That original construction had been decided at a time when no supplier knew what would be needed to pass the IMO tests. Not being a company to take risks with compliance, Alfa Laval had thus created PureBallast with a good margin of error in terms of biological efficiency. Now, drawing on real experience from around 100 PureBallast systems commissioned andhundreds more sold, it was possible to re-evaluate. So the development team set tough goals for the new system, especially when it came to energy efficiency.Identifying potential parametersThe key component in a UV-based system is its reactor, the chamber where UV treatment actually occurs. In standard UV treatment, organisms are eliminated directly or rendered unable to reproduce through damage to their DNA and biological structure. In PureBallast, the treatment process is enhanced by AOT (advanced oxidation technology), which creates free radicals that cause irreversible cell membrane damage. The AOT effect has a proven biological impact leading to better treatment performance and lower energy consumption.In approaching a new PureBallast system, the development team asked itself one fundamental question: What factors determine the effectiveness of a UV-based reactor to be used with seawater at a high flow rate?The latter part of that question was critical, according to Jonas Alván. “The UV treatment of seawater is a very different process from the UV treatment of drinking water on land,” he explains. “In drinking water applications, which many ballast water treatment systems are adapted from, the process is continuous and targets mainly bacteria in pre-cleaned and well-regulated water. In ballast water treatment, the process is intermittent and involves a lot of standstill with saline water in the reactor. Plus the organisms targeted are hardier and more varied.”At sea, continuous treatment is not practically feasible. Neither is increasing residence time in the reactor, since ballasting and deballasting have to occur quickly. Adding stronger UV lamps or increasing the lamp number can increase biological efficiency, but only at the expense of energy efficiency. So the team was left with two main reactor parameters that could be adjusted: flow patterns and lamp placement.Developing the new reactor“One of the things we were looking for was greater mixing, which would both increase the effect of the AOT and help to compensate for low UV transmittance,” Alván says, referring to the distance UV light travels in water. “With more fluid mixing, the chance of an organism passing close to the UV lamps – and thereby the biological efficiency – increases.”Again, the difference between land-based and marine UV treatment was important. As Alván puts it, “Finding an acceptable balance of parameters is easier in a drinking water application, where clear and consistent water provides high UV transmittance. But the varying UV transmittance of ballast water, along with the need to minimize power consumption, makes it a more complex challenge to find an ideal reactor design.”That design was finally found with the help of a unique CFD (computational fluid dynamics) model, which was developed around a well-established model for standard UV treatment. In the new model, light sources were introduced into the equation, making it possible to see the UV dose for each of 50,000 theoretical particles (organisms) passing through the reactor.“In our visualizations, we assigned each particle a colour according to the UV dose incurred,” Alván explains. “By optimizing the reactor design for a uniform colour among exiting paths, we could ensure the most even UV dose possible. And that gave us the reactor design with the least possible energy consumption. The end result is startling.”Taking a hard look at CIPOf course, the reactor was not the only focus of the PureBallast 3.0 development project. Another component re-evaluated was PureBallast’s CIP (Cleaning-In-Place) unit, which cleans the UV lamp sleeves between treatments by circulating a non-toxic, low-pH fluid. In this case, however, the unit was left unchanged.“A lot of suppliers leave out CIP as a way to save space and cost,” says Alván. To evaluate the consequences of doing so, the team performed its own tests, allowing PureBallast to run for many cycles without performing CIP. “As it turns out, CIP was even more important than we expected,” Alván says.The reason is the build-up of calcium chlorides and metal ions on the UV lamp sleeves, which occurs not only in PureBallast, but in all UV treatment involving seawater. This build-up degrades the sleeves’ UV transmittance, which greatly lowers the biological effect.“We saw clear value in performing CIP to retain full equipment performance after ballasting or deballasting,” Alván says. “Mechanical wipers remove calcium chlorides but not metal ions,and both wipers and manual cleaning will eventually cause performance-reducing scratches on the quartz glass. CIP is the most gentle and effective means available to keep performance at type-approved levels.”The finished system – a small wonderThe completed PureBallast 3.0 system, while based on the same treatment technology as its predecessors, is a remarkable leap forward in terms of its compactness, energy efficiency and flexibility. Most striking at a first glance is its size.Where previous PureBallast reactors handled 250 m3/h each, individual PureBallast 3.0 reactors can handle either 300 m3/h or 1000 m3/h. Using the larger reactor, which is not much bigger than the original 250 m3/h version, the footprint of a 1000 m3/h system is literally cut in half. The bigger the system, the bigger the space savings.“Needless to say, the new reactor capacities greatly reduce the footprint of larger systems,” says Per Warg. “With one reactor doing the same job that four did before, PureBallast 3.0 is competitive across the entire flow range up to 6000 m3/h.”Energy savings of 30-60%The size, however, is not the only thing that makes PureBallast 3.0 competitive. The new system is also as energy efficient as it is compact.“The new 1000 m3/h reactors consume just 100 kW at full power, which is a minimum energy savings of 30% over previous versions,” Warg says. “And when full power isn’t needed, the energy savings can be as much as 60%.”Warg is referring to the new dimming function in PureBallast 3.0, which lowers the system’s power consumption in clearer waters with good UV transmittance. In such conditions, less energy is needed to neutralize the organisms present. “PureBallast 3.0 has a dimming capacity of 50% and handles the dimming process automatically,” says Warg. “The system will operate with some level of dimming in the majority of circumstances, providing up to 60% energy savings over previous versions in fully dimmed mode.”Installation flexibility and economyFor shipyards, the most appealing aspect of PureBallast 3.0 will not be its energy-efficient operation, but rather its high degree of flexibility and ease of installation – even when it comes to the highest flow rates. With the new reactor capacities, only one reactor will be needed per 1000 m3/h, which makes designing a system considerably simpler.“When individual reactors can handle a greater amount of ballast water, there are fewer reactors and lamp drive cabinets to install,” says Warg. “That means not only less installation time, but also easier and more economical installation, since it does away with a considerable amount of pipework.”When it comes to the lamp drive cabinets, there is an additional bit of flexibility. Whereas reactors and cabinets were attached in previous versions of PureBallast, the cabinets can now be placed anywhere up to 150 m away. “The free placement of lamp drive cabinets within 150 metres simplifies the design of EX systems, since the power supply is easy to place outside the hazardous zone,” says Warg. “But it’s of benefit to everyone, since it can save space in the engine room where it’s needed most.”Leadership redefinedWarg and Alván are visibly proud of the new PureBallast 3.0, and certainly not without reason. Its capabilities and features place the new system firmly at the cutting edge of ballast water treatment.“Alfa Laval has always been at the forefront of ballast water treatment, but PureBallast 3.0 truly redefines that leadership,” says Warg. “We’re looking not just at a new generation of the system, but rather at a whole new standard that lives up to the tougher demands raised by today’s customers.” His colleague Alván agrees, concluding, “Where size, economy and energy efficiency are important, I’ve no doubt that customers will find what they’re looking for in PureBallast 3.0.”To learn more about PureBallast 3.0 and Alfa Laval’s approach to ballast water treatment, visit /pureballast3Editor’s notesAbout Alfa LavalAlfa Laval is a leading global provider of specialized products and engineering solutions based on its key technologies of heat transfer, separation and fluid handling.The company’s equipment, systems and services are dedicated to assisting customers in optimizing the performance of their processes. The solutions help them to heat, cool, separate and transport products in industries that produce food and beverages, chemicals and petrochemicals, pharmaceuticals, starch, sugar and ethanol.Alfa Laval’s products are also used in power plants, aboard ships, in the mechanical engineering industry, in the mining industry and for wastewater treatment, as well as for comfort climate and refrigeration applications.Alfa Laval’s worldwide organization works closely with customers in nearly 100 countries to help them stay ahead in the global arena.Alfa Laval is listed on Nasdaq OMX, and, in 2012, posted annual sales of about SEK 29.8 billion (approx. 3.5 billion Euros). The company has today about 16 400 employees.For further information, please contact:André SzczerbaCentral Communication ManagerMarine & Diesel EquipmentAlfa Laval Tumba AB, SwedenPhone: +46-8 530 651 17Fax: +46-8 530 345 55E-mail:****************************/marine。
国内外异种器官移植的现状及进展
· 综述·国内外异种器官移植的现状及进展张小燕 王国辉 韩士超 戚若晨 刘克普 魏迪 杨晓剑 马帅军 窦科峰 秦卫军【摘要】 器官短缺已成为阻碍器官移植发展的主要难题，异种移植是解决全球器官匮乏最有价值的方法之一。
近年来，基因工程技术的发展和新型免疫抑制药的研发为异种移植提供了新的理论基础。
国外陆续开展基因修饰猪-非人灵长类动物或脑死亡受者的相关异种移植研究，并取得一些实质性的进展，但大部分的研究仍处于临床前阶段，距离投入临床跨越巨大。
因此，本文结合目前国内外最新的临床前实验研究进展，对异种移植的历史、基因修饰技术发展、异种移植排斥反应及免疫抑制方案等问题进行综述，以期为异种移植的进一步研究提供参考，促进异种移植临床应用，造福更多终末期疾病患者。
【关键词】 异种移植；基因修饰猪；免疫抑制药；非人灵长类动物；排斥反应；炎症反应；凝血功能障碍；感染【中图分类号】 R617,Q78 【文献标志码】 A 【文章编号】 1674-7445（2024）02-0017-06Present situation and progress of xenotransplantation at home and abroad Zhang Xiaoyan, Wang Guohui, Han Shichao,Qi Ruochen, Liu Kepu, Wei Di, Yang Xiaojian, Ma Shuaijun, Dou Kefeng, Qin Weijun. Department of Urology , Xijing Hospital of Air Force Medical University , Xi’an 710032, ChinaCorresponding authors: Dou Kefeng, Email: ***************.cnQin Weijun, Email: **************.cn【Abstract 】 Organ shortage has become one of the major challenges hindering the development of organ transplantation. Xenotransplantation is one of the most valuable methods to resolve global organ shortage. In recent years,the development of genetic engineering technique and research and development of new immunosuppressant have provided novel theoretical basis for xenotransplantation. International scholars have successively carried out researches on xenotransplantation in genetically modified pigs to non-human primates or brain death recipients, making certain substantial progresses. However, most of the researches are still in the preclinical stage, far from clinical application.Therefore, according to the latest preclinical experimental research progress at home and abroad, the history of xenotransplantation, the development of gene modification technology, xenotransplantation rejection and immunosuppression regimens were reviewed, aiming to provide reference for subsequent research of xenotransplantation,promote clinical application of xenotransplantation and bring benefits to more patients with end-stage diseases.【Key words 】 Xenotransplantation; Genetically modified pig; Immunosuppressant; Non-human primate; Rejection;Inflammation; Coagulation disorder; InfectionDOI: 10.3969/j.issn.1674-7445.2023193基金项目：国家自然科学基金（82101322、82200845）作者单位： 710032 西安，空军军医大学西京医院泌尿外科作者简介：张小燕（ORCID 0000-0002-1199-988X ），硕士，住院医师，研究方向为肾移植与肾纤维化，Email ：156****6095@通信作者：窦科峰（ORCID 0000-0003-1708-8048），主任医师，中国科学院院士，研究方向为异种移植与肝胆疾病，Email:***************.cn ；秦卫军（ORCID 0000-0001-5202-642X ），博士，主任医师，研究方向为肾移植与泌尿系肿瘤，Email:**************.cn第 15 卷 第 2 期器官移植Vol. 15 No.2 2024 年 3 月Organ Transplantation Mar. 2024 我国慢性肾病的发病率高达10.8%[1]。
爱利亚（阿培布塞普）商品说明书
Eylea® (aflibercept)Document Number: IC-0026 Last Review Date: 04/26/2016Date of Origin: 02/07/2013Dates Reviewed: 03/07/2013, 06/2013, 09/2013, 12/2013, 03/2014, 06/2014, 09/2014, 12/2014, 03/2015,4/2015, 6/2015, 9/2015, 3/2016, 4/2016I.Length of AuthorizationCoverage will be provided for six months and may be renewed.II.Dosing LimitsA.Quantity Limit (max daily dose) [Pharmacy Benefit]:− 2 mg injection - 1 vial every 28 daysB.Max Units (per dose and over time) [Medical Benefit]:AMD:Loading dose:Male 2 units every 28 days per eye x 3 doses*Female 2 units every 28 days per eye x 3 doses*Maintenance:Male 2 units every 56 days per eye*Female 2 units every 56 days per eye*Macular Edema following RVOMale 2 units every 28 days per eye*Female 2 units every 28 days per eye*Diabetic Macular EdemaLoading dose:Male 2 units every 28 days per eye x 5 doses*Female 2 units every 28 days per eye x 5 doses*Maintenance:Male 2 units every 56 days per eye*Female 2 units every 56 days per eye**Max units are doubled (4 billable units) when the claim is submitted with bilateral ICD 10 codesIII.Initial Approval CriteriaCoverage is provided in the following conditions:•Patient is free of ocular and/or peri-ocular infections: AND•Baseline visual acuity test (required for renewal); AND one of the following:o Neovascular age-related macular degeneration (AMD) †o Macular edema following retinal vein occlusion (RVO) †o Diabetic Macular Edema (DME) †o Diabetic retinopathy (DR) associated with diabetic macular edema (DME) † † FDA Approved Indication(s)IV.Renewal CriteriaCoverage can be renewed based upon the following criteria:•Patient continues to meet criteria identified in section III; AND•Disease response as indicated by stabilization of visual acuity or improvement in BCVA score when compared to baseline; AND•Absence of unacceptable toxicity from the drug. Examples of unacceptable toxicity include the following: Endophthalmitis and retinal detachments; increase in intraocularpressure; arterial thromboembolic events.V.Dosage/AdministrationVI.Billing Code/Availability InformationJcode:J0178– Eylea (Regeneron) 2 mg Injection: 1 billable unit = 1 mgNDC:Eylea 2 mg Injection – 61755-0005-xx (Regeneron)VII.References1.Eylea [package insert]. Tarrytown, NY; Regeneron Pharmaceuticals, Inc.; July 2015.Accessed February 2016.2.Wisconsin Physicians Service Insurance Corporation. Local Coverage Determination (LCD):Drugs and Biologics (Non-chemotherapy) (L4741). Centers for Medicare & MedicaidServices, Inc. Updated on 01/01/2016 with effective date 01/01/2016. Accessed February2016.3.National Government Services, Inc. Local Coverage Article for Ranibizumab (e.g.,Lucentis™) and Aflibercept (e.g., Eylea™) – Related to LCD L33394 (A52451). Centers forMedicare & Medicaid Services, Inc. Updated on 09/13/2015 with effective date of10/01/2015. Accessed February 2016.Appendix 1 – Covered Diagnosis Codes (*Max Units for bilateral indications are doubled)E08.311 Diabetes mellitus due to underlying condition with unspecified diabetic retinopathy with macular edemaE08.321 Diabetes mellitus due to underlying condition with mild nonproliferative diabetic retinopathy with macular edemaE08.331 Diabetes mellitus due to underlying condition with moderate nonproliferative diabetic retinopathy with macular edemaE08.341 Diabetes mellitus due to underlying condition with severe nonproliferative diabetic retinopathy with macular edemaE08.351 Diabetes mellitus due to underlying condition with proliferative diabetic retinopathy with macular edemaE09.311 Drug or chemical induced diabetes mellitus with unspecified diabetic retinopathy with macular edemaE09.321 Drug or chemical induced diabetes mellitus with mild nonproliferative diabetic retinopathy with macular edemaE09.331 Drug or chemical induced diabetes mellitus with moderate nonproliferative diabetic retinopathy with macular edemaE09.341 Drug or chemical induced diabetes mellitus with severe nonproliferative diabetic retinopathy with macular edemaE09.351 Drug or chemical induced diabetes mellitus with proliferative diabetic retinopathy with macular edemaE10.311 Type 1 diabetes mellitus with unspecified diabetic retinopathy with macular edemaE10.321 Type 1 diabetes mellitus with mild nonproliferative diabetic retinopathy with macular edema E10.331 Type 1 diabetes mellitus with moderate nonproliferative diabetic retinopathy with macular edemaE10.341 Type 1 diabetes mellitus with severe nonproliferative diabetic retinopathy with macular edema E10.351 Type 1 diabetes mellitus with proliferative diabetic retinopathy with macular edemaE11.311 Type 2 diabetes mellitus with unspecified diabetic retinopathy with macular edemaE11.321 Type 2 diabetes mellitus with mild nonproliferative diabetic retinopathy with macular edema E11.331 Type 2 diabetes mellitus with moderate nonproliferative diabetic retinopathy with macular edemaE11.341 Type 2 diabetes mellitus with severe nonproliferative diabetic retinopathy with macular edema E11.351 Type 2 diabetes mellitus with proliferative diabetic retinopathy with macular edemaE13.311 Other specified diabetes mellitus with unspecified diabetic retinopathy with macular edemaE13.321 Other specified diabetes mellitus with mild nonproliferative diabetic retinopathy with macular edemaE13.331 Other specified diabetes mellitus with moderate nonproliferative diabetic retinopathy with macular edemaE13.341 Other specified diabetes mellitus with severe nonproliferative diabetic retinopathy with macular edemaE13.351 Other specified diabetes mellitus with proliferative diabetic retinopathy with macular edemaH34.811 Central retinal vein occlusion, right eyeH34.812 Central retinal vein occlusion, left eyeH34.813 Central retinal vein occlusion, bilateral*H34.819 Central retinal vein occlusion, unspecified eyeH34.831 Tributary (branch) retinal vein occlusion, right eyeH34.832 Tributary (branch) retinal vein occlusion, left eyeH34.833 Tributary (branch) retinal vein occlusion, bilateral*H34.839 Tributary (branch) retinal vein occlusion, unspecified eyeH35.32 Exudative age-related macular degenerationH35.81 Retinal edemaAppendix 2 – Centers for Medicare and Medicaid Services (CMS)Medicare coverage for outpatient (Part B) drugs is outlined in the Medicare Benefit Policy Manual (Pub. 100-2), Chapter 15, §50 Drugs and Biologicals. In addition, National Coverage Determination (NCD) and Local Coverage Determinations (LCDs) may exist and compliance with these policies is required where applicable. They can be found at: /medicare-coverage-database/search/advanced-search.aspx. Additional indications may be covered at the discretion of the health plan.Medicare Part B Covered Diagnosis Codes (applicable to existing NCD/LCD):Jurisdiction(s): 5, 8NCD/LCD Document (s): L34741https:///medicare-coverage-database/details/lcd-details.aspx?LCDId=34741&ver=22&Date=02%2f02%2f2016&DocID=L34741&bc=iAAAAAgAA AAAAA%3d%3d&Jurisdiction(s): 6, J-K NCD/LCD Document (s): A52451https:///medicare-coverage-database/details/article-details.aspx?articleId=52451&ver=9&Date=02%2f02%2f2016&DocID=A52451&SearchType=Ad vanced&bc=JAAAAAgAAAAAAA%3d%3d&Jurisdiction Applicable State/US Territory ContractorE CA,HI, NV, AS, GU, CNMI Noridian Administrative Services (NAS)Noridian Administrative Services (NAS)F AK, WA, OR, ID, ND, SD, MT, WY,UT, AZ5 KS, NE, IA, MO Wisconsin Physicians Service (WPS)6 MN, WI, IL National Government Services (NGS)H LA, AR, MS, TX, OK, CO, NM Novitas Solutions8 MI, IN Wisconsin Physicians Service (WPS)9 (N) FL, PR, VI First Coast Service Options10 (J) TN, GA, AL Cahaba Government Benefit Administrators11 (M) NC, SC, VA, WV Palmetto GBA12 (L) DE, MD, PA, NJ, DC Novitas SolutionsK NY, CT, MA, RI, VT, ME, NH National Government Services (NGS)15 KY, OH CGS Administrators, LLC。
食管鳞癌组织中VEGFR-2基因扩增情况观察及与患者预后关系分析
食管鳞癌组织中VEGFR -2基因扩增情况观察及与患者预后关系分析吐尔洪·托合提1，阿丽米热·库尔班2，卡吾力·居买1，居来提·艾尼瓦尔1，张海平1，伊地力斯·阿吾提11 新疆医科大学第一附属医院，乌鲁木齐830054；2 新疆医科大学基础医学院摘要：目的 观察食管鳞癌组织中血管内皮生长因子受体-2（VEGFR -2）基因扩增情况，并分析VEGFR -2基因扩增与食管鳞癌患者预后的关系。
方法 食管鳞癌患者120例，术中留取食管癌组织，采用荧光原位杂交（FISH ）法观察食管鳞癌组织中VEGFR -2基因扩增情况，并分析VEGFR -2基因扩增与食管鳞癌患者临床病理参数的关系。
根据有无VEGFR -2基因扩增，将120例食管鳞癌患者分为阳性组（VEGFR -2基因扩增阳性）和阴性组（VEGFR -2基因扩增阴性），采用Kaplan -Meier 生存分析法及多因素COX 回归模型分析VEGFR -2基因扩增与食管鳞癌患者预后的关系。
结果 120例食管鳞癌患者中，49例患者存在VEGFR -2基因扩增，VEGFR -2基因扩增率为40.8%。
VEGFR -2基因扩增与食管鳞癌患者肿瘤分化程度、有无淋巴结转移、有无脉管浸润有关（P 均<0.05）。
阴性组的食管鳞癌患者生存时间为16（11.15～20.84）个月，阳性组为13（8.27～17.72）个月，两组相比，P <0.05。
多因素COX 回归分析结果显示，VEGFR -2基因扩增是食管鳞癌患者不良预后的独立危险因素（HR=0.562，95%CI ：0.374～0.844，P =0.006）。
结论 部分食管鳞癌患者存在VEGFR -2基因扩增。
VEGFR -2基因扩增与食管鳞癌肿瘤分化程度、有无淋巴结转移、有无脉管浸润有关，是食管鳞癌患者不良预后的独立危险因素。
关键词：血管内皮生长因子受体-2基因；基因扩增；食管癌；食管鳞状细胞癌doi ：10.3969/j.issn.1002-266X.2023.09.008中图分类号：R 文献标志码：A 文章编号：1002-266X （2023）09-0031-05VEGFR -2 gene amplification in esophageal squamous cell carcinoma and its relationship with prognosis Turgon Tohti 1， Alimire Kurban ， Kawul Juma ， Jurat Anwar ， ZHANG Haiping ， Edris Awut 1 The First Affiliated Hospital of Xinjiang Medical University ， Urumqi 830054， ChinaAbstract ： Objective To observe the amplification of vascular endothelial growth factor receptor -2 （VEGFR -2）gene in esophageal squamous cell carcinoma ， and to analyze the relationship between the amplification of VEGFR -2 gene and the prognosis of esophageal squamous cell carcinoma patients. Methods In 120 patients with esophageal squamous cell carcinoma ， esophageal cancer tissues were taken during operation. The amplification of VEGFR -2 gene in esophageal squamous cell carcinoma tissue was observed by fluorescence in situ hybridization （FISH ）， and the relationships between the amplification of VEGFR -2 gene and the clinicopathologic parameters of esophageal squamous cell carcinoma patients were analyzed. According to the presence or absence of VEGFR -2 gene amplification ， 120 patients with esophageal squa‐mous cell carcinoma were divided into the positive group （VEGFR -2 gene amplification positive ） and negative group（VEGFR -2 gene amplification negative ）. The relationship between VEGFR -2 gene amplification and prognosis of patients with esophageal squamous cell carcinoma was analyzed by Kaplan -Meier survival analysis and multivariate COX regres‐sion model. Results Among 120 patients with esophageal squamous cell carcinoma ， 49 patients had VEGFR -2 gene am‐plification ， and the amplification rate of VEGFR -2 gene was 40.8%. The amplification of VEGFR -2 gene was related to the degree of tumor differentiation ， lymph node metastasis and vascular invasion in patients with esophageal squamous cell carcinoma （all P<0.05）. The survival time of esophageal squamous cell carcinoma patients in the negative group was 16 （11.15–20.84） months ， and that in the positive group was 13 （8.27–17.72） months ， with statistically significant dif‐ference （P<0.05）. Multivariate COX regression analysis showed that VEGFR -2 gene amplification was an independent基金项目：国家自然科学基金资助项目（81960498）。
2-adrenergic antagonists
Alpha adrenergic receptor antagonists -phentolamine Effects on cardiovascular system a. Vasodilation: decrease peripheral resistance b. Cardiac stimulation: increase cardiac output. reflex sympathetic nerve stimulation
掩盖低血糖而出现严重后果。
禁忌证：禁用于严重左室心功能不全、窦性心动过缓、重度房室传导阻 滞和支气管哮喘的病人。心肌梗死病人及肝功能不良者应慎用。
β肾上腺素受体阻断药
普萘洛尔（propranolol，心得安）
是β受体阻断药的代表药 【体内过程】
1.口服吸收率大于90％ 2. 主要在肝脏代谢，其代谢产物为4-羟普萘洛尔，仍 具有β受体阻断药的活性 3. 首关消除率60％～70％，生物利用度仅为30％ 4. 易于通过血脑屏障和胎盘屏障，也可分泌于乳汁中
• Irreversibly block 1 and 2 receptors. Longterm blocker. 【pharmacological properties】 • attenuates catecholamine-induced vasoconstriction 【therapeutic uses】 • pheochromocytoma • peripheral vascular disease: • Septic shock
【Pharmacological effects】 A. Blockade of β receptors a. b. c. d. Effects on the cardiovascular system Effects on the respiratory tract Metabolic and endocrine effects Renin release
α-Hederin_Hed_alpha-hederin_CAS号27013-91-8_M3967说明书_AbMole中国
分子量750.96溶解性（25°C）DMSO分子式C H O WaterCAS号27013-91-8Ethanol储存条件3年 -20°C 粉末状生物活性α-Hederin stimulates NO release and is able to upregulate iNOS expression through NF-kappa B transactivation, which may be a mechanism, whereby α-Hederin elicits its biological effects.α-Hederin enhanced some nonenzymatic antioxidant components in liver, which play a partial role in Hed protection against hepatotoxicity produced by some chemicals.treatment of mice with α-Hederin decreases the levels and activities of several P450 enzymes.The suppression ofP450 appears to be one of mechanisms by which alpha-hederin protects mice from the hepatotoxicity of some chemicals.It is possible to optimize colorectal cancer cell sensitivity to 5-FU with α-Hederin.不同实验动物依据体表面积的等效剂量转换表（数据来源于FDA指南）小鼠大鼠兔豚鼠仓鼠狗重量 (kg)0.020.15 1.80.40.0810体表面积 (m)0.0070.0250.150.050.020.5K系数36128520动物 A (mg/kg) = 动物 B (mg/kg) ×动物 B的K系数动物 A的K系数例如，依据体表面积折算法，将白藜芦醇用于小鼠的剂量22.4 mg/kg 换算成大鼠的剂量，需要将22.4 mg/kg 乘以小鼠的K系数（3），再除以大鼠的K系数（6），得到白藜芦醇用于大鼠的等效剂量为11.2 mg/kg。
leptospira interrogans ss. icterohaemorrhagiae-感染的
LEPTOSPIRA INTERROGANS SSP.Aetiology Epidemiology Diagnosis Prevention and ControlPotential Impacts of Disease Agent Beyond Clinical Illness References AETIOLOGYClassification of the causative agentLeptospira interrogans, the causative agent of leptospirosis, consists of numerable serotypes capable of causing a variety of disease manifestations in a wide range of hosts. This motile and flagellated spirochete bacterium is recognizable via microscopy and earned its name from a characteristic hooked appearance that resembles a question mark. The taxonomic classifications within the Leptospira genus have been reorganized many times in accordance with new antigenic, genomic, and pathologic data. What was once over 250 serovars grouped into two Leptospira species is now 21 genomospecies of Leptospira with reclassified serovars. While the new taxonomic names are typically used in the scientific literature, historical names still circulate on product labels and in common use.Not all serovars of Leptospira are pathogenic, and many are associated with a reservoir species in which little disease is apparent. Many serovars are highly prevalent within maintenance host populations and persist in the kidneys or genital tract. Small antibody responses and low tissue burdens are typical in these animals. Incidental hosts, however, typically develop serious disease with high tissue burdens and robust antibody responses. These classifications are not always entirely distinct and some overlap between presentations can exist.Leptospirosis is a zoonotic disease but is typically associated with at-risk occupations (veterinarian, livestock owners, dairy workers, etc.) and exposure to contaminated water.Resistance to physical and chemical actionTemperature: Generally fails to persist at <10°C or >34°C;pasteurization and moist heat at 121°C/15 minutes are effective methodsof killing leptospirespH: Prefers neutral to slightly alkaline conditionsChemicals/Disinfectants: Inactivated by 1% sodium hypochlorite, 70%ethanol, formaldehyde, detergents, quaternary ammonium compounds,iodine based compounds, glutaraldehyde, and hydrogen peroxideSurvival: Warm, moist conditions greatly enhance survival; maypersist up to 6 weeks under favorable conditions; freezing, dehydration,and UV radiation inactivate leptospiresEPIDEMIOLOGYHosts●Virtually all mammals are vulnerable to pathogenic Leptospira serovars to varying degrees○Many serovars have specific maintenance hosts while others are more promiscuous●Leptospira serovars known to cause disease in mammals have been isolated from amphibians○Some serovars have also been isolated from invertebrates, reptiles, and birdsProminent host-serovar associations●Armadillos (Dasypus novemcinctus, Euphractus sexcinctus) - Autumnalis, Cynopteri, Hebdomadis,Pomona●Bandicoots (Isoodon macrourus, Perameles spp.) - numerous serovars have been associated withthese species●Brazilian tapir (Tapirus terrestris) - Pomona●Canids (Canis latrans, C. familiaris, C. lupus) - Bratislava, Canicola, Grippotyphosa, Hardjo,Icterohaemorrhagiae, Pomona●Cattle (Bos taurus, Syncerus caffer) - Hardjo and others●Cervids - Bratislava, Canicola, Grippotyphosa, Hardjo, Icterohaemorrhagiae, Pomona●European hedgehog (Erinaceus europaeus)●Felids (Felis silvestris silvestris, F. silvestris catus, Lynx spp.)●Flying foxes (Pteropus spp.) - a multitude of Leptospira serovars have been identified in variousspecies of bat●Foxes (Vulpes lagopus, V. vulpes, Urocyon cinereoargenteus, Lycalopex griseus) - Bratislava,Canicola, Grippotyphosa●Giant anteater (Myrmecophaga tridactyla) - Djasiman●Horses (Equus ferus) - Bratislava●Lagomorphs (Lepus europaeus, L. timidus, Oryctolagus cuniculus) - Grippotyphosa●Marine mammals (Eubalaena australis,Trichechus manatus ) - Australis, Manaua○Sea lions (Zalophus californianus, Z. wollebaeki) and seals (Callorhinus ursinus, Phoca vitulina, Mirounga angustirostris, Arctocephalus forsteri) - Canicola, Hardjo, Pomona ○There have been multiple mass-mortality events attributed to leptospirosis in California sea lions●Marsupials - Australis, Autumnalis, Ballum, Bataviae, Celledoni, Cynopteri, Djasiman,Grippotyphosa, Hardjo, Hebdomadis, Icterohaemorrhagiae, Javanica, Mini, Panama, Pomona, Pyrogenes, Sejroe, Tarassov, Topaz●Mongooses (Herpestes auropunctatus, Mungos mungo, Paracynictis selousi) - Bratislava, Hardjo●Mustelids (Meles meles, Martes fiona, M. martes, Mustela putorius, M. nivalis, M. ermine, Lutra lutra)●Platypus (Ornithorhynchus anatinus) - Autumnalis, Hardjo, Grippotyphosa●Raccoons (Procyon itor) and skunks (Mephitis mephitis) - Bratislava, Canicola, Grippotyphosa,Hardjo, Icterohaemorrhagiae, Pomona●Rodents and insectivores - Arborea, Australis, Ballum, Bindjei, Broomi, Canicola, Celledoni,Gryppotyphosa, Icterohaemorrhagiae, Javanica, Mini, Pomona, Pyrogenes, Sejroe, Tarrasovi, Zanoni○Rats are well-appreciated hosts for serotype Icterohaemorrhagiae●Swine (Sus scrofa and other spp.) - Bratislava, Hardjo, Pomona●Vervet monkey (Cercopithecus aethiops sabaeus) - Australis, Grippotyphosa, Javanica●Multiple snake, turtle, toad, and frog species have also been identified as PCR and/or serologicallypositiveTransmission●Ingestion●Contact with mucous membranes or wet, abraded skin●Some serovars can be transmitted venerally or transplacentallySources●Urine●Contaminated soil and water●Placental fluids●Genital secretions●Milk●BloodOccurrenceMany wildlife species are reservoirs for Leptospira and subsequently maintain host-bacterium interactions that do not negatively impact the animal. Over time, selection pressures on the leptospires many change and drive reservoir species relationships to shift accordingly. Therefore, it is important to assess the epidemiology of leptospirosis on a more local level to understand transmission risks and disease impacts.Leptospira is globally enzootic, but disease is more frequently seen in warm and moist environments. This may be seasonal (temperate zones) or more constant (tropical regions). Rainfall encourages persistence of the organism in the environment. Additionally, some serotypes are much more geographically dispersed and others are found in more limited regions.For more recent, detailed information on the occurrence of this disease worldwide, see the OIE World Animal Health Information System - Wild (WAHIS-Wild) Interface [http://www.oie.int/wahis_2/public/wahidwild.php/Index].DIAGNOSISAfter invasion of mucous membranes or damaged skin, there is a 4-20 day incubation period followed by a 7-10 day period of circulation in the bloodstream. Clinical signs of acute leptospirosis depend on the tissues colonized during this period of bacteraemia, the host species, and infecting serovar. A robust antibody response follows and is associated with a declining bacteraemia. Tissues may recover slowly or not at all depending on the degree of damage. Death is possible in severe cases.Incidental hosts maintain the bacterium in renal tubules for days to weeks and shed the organism in urine. Maintenance hosts, however, maintain the bacterium in the renal tubules, genital tract, and/or eyes and shed it in urine or genital secretions for months to years after infection.Clinical diagnosisLeptospirosis is a highly variable, systemic infection and the presentation depends on the infecting serovar, the host species, and the host’s general health and immune status. Maintenance hosts typically do not develop significant clinical disease. Incidental hosts typically experience severe, acute disease secondary to bacterial toxins and inflammatory responses generated by the immune system. Initially, animals may be febrile and anorectic. They may quickly develop signs of haemorrhage and haemolytic anaemia secondary to endothelial damage such as mucosal petechiation, icterus, haemoglobinuria/haematuria, dehydration, vomiting, and colic. Acute renal injury develops rapidly and is a significant contributor to mortality. Pneumonia, meningitis, uveitis, corneal opacification, photosensitization, myalgia, and pancreatitis are also possible.Reproductive disease is often characterised by abortion/stillbirth, mummified fetuses, infertility, blood in milk, or a cessation of milk production. If not aborted, neonates infected transplacentally are typically weak. Maintenance hosts do not develop reproductive disease acutely like incidental hosts, but instead remain subclinical for weeks to months.Lesions●Renal tubular necrosis and suppurative nephritis○Pale, oedematous parenchyma +/- pitting of the serosal surface and capsular adhesions○Subcapsular haemorrhage○Inflammation initially characterised by neutrophils but becomes lymphoplasmacytic○Mixed inflammatory processes are associated with higher mortality rates●Hepatomegaly +/- necrotizing hepatitis○The liver is often friable and discolored in a lobular pattern●Pulmonary haemorrhage●Petechiae and ecchymoses on mucous membranes and internal organs●Horses may develop uveitis with conjunctivitis, corneal oedema, synechia, or cataractsDifferential diagnoses●Ocular disease○Equine recurrent uveitis○Traumatic uveitis/reflex uveitis○Infectious conjunctivitis●Kidney disease○Toxin exposure (e.g., ethylene glycol)○Infectious nephritis, pyelonephritis, glomerulonephritis○Renal tubular acidosis○Nematodes (Stephanurus dentatus, Dioctophyma renale)●Reproductive failure or compromise○Brucellosis○Bovine viral diarrhea virus (BVDV)○Porcine reproductive and respiratory syndrome (PRRS)○Q-Fever (Coxiella burnetii)○Neospora spp.○Tritrichomonas foetus○Mastitis, metritis●Liver disease, icterus, and haemolytic anaemia○Viral hepatitis○Toxin exposure (e.g., heavy metals, anticoagulant rodenticides)○Rickettsial infection○Clostridium haemolyticum, C. perfringens A○Neonatal isoerythrolysis●Bacterial septicaemiaLaboratory diagnosisSamplesFor isolation of agent●Kidney●Blood●Urine●Other grossly affected tissue such as liverSerological tests●Serum●Whole bloodProceduresIdentification of the agent●Silver-stained histopathology slides allow for direct visualization of the organism in renal tubules●Immunohistochemistry (IHC)●Bacterial culture○Because the organism is low-growing, this may take 12-26 weeks○Best available method to determine infecting serovar●Polymerase chain reaction (PCR)○Widely variable protocols○Does not provide serovar-specific resultsSerological tests●Microscopic agglutination test (MAT)○Uses live, regionally common serovars of Leptospira○Requires diagnostic laboratory to maintain live cultures of serovars○Provides quantitative titre level●Antibody capture enzyme-linked immunosorbent assay (ELISA)○Currently used for domestic canines; detects antibodies to LipL32 protein○Results are qualitative (positive/negative) and may yield false positives in the event of prior vaccination●Immunofluorescence assay (IFA)●There is not yet a consensus on what a diagnostic titre for Leptospira should be, therefore pairedacute and convalescent sera are recommended for testing●Caution should be taken when interpreting serology data; antibody titre does not always correspondwith disease stateFor more detailed information regarding laboratory diagnostic methodologies, please refer to Chapter 3.1.12 Leptospirosis in the latest edition of the OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals.PREVENTION AND CONTROLSanitary prophylaxis●Extra precautions should be taken when cleaning areas frequented by potential Leptospira hosts.Wear gowns, shoe covers, and gloves to prevent contamination of personal clothing. Face shields are recommended to protect mucous membranes from aerosols.Medical prophylaxis●There are a variety of Leptospira vaccines available for domestic animals, including livestock○Vaccine intent may vary from prevention of infection to reduction of renal colonization and urine shedding○Read vaccine labels to determine which serovars are targeted, as immunity is believed to be serovar-specificPOTENTIAL IMPACTS OF DISEASE AGENT BEYOND CLINICAL ILLNESS Risks to public health●Leptospirosis is a zoonotic disease. Because clinical signs can be vague and maintenance hostscan be asymptomatic carriers, basic protective measures are suggested for at-risk populations (veterinarians, livestock owners, dairy workers, etc.): protect eyes with safety glasses, wear gloves especially if there are openings in the skin, thoroughly wash hands after interacting with animals of unknown status and before consuming food or water, etc.○Pregnant individuals within at-risk populations are particularly advised to utilise protective measures.●Many domestic animal species, including dogs, horses, and livestock, are susceptible to leptospirosisand could potentially transmit it to humans. Individuals should speak with local veterinarians to determine risk and appropriate prevention strategies, including animal vaccines.Risks to agriculture●If livestock or working animals (horses, dogs) develop clinical disease due to Leptospira, decreasedthrift and reproductive compromise can significantly impact production. Working animals may not beable to do their jobs as efficiently, and livestock may demand increased resources for treatment while producing less.REFERENCES AND OTHER INFORMATION●Atherstone, C., Picozzi, K., & Kalema-Zikusoka, G. (2014). Seroprevalence of Leptospira hardjo incattle and African buffalos in southwestern Uganda. The American Journal of Tropical Medicine and Hygiene, 90(2), 288–290.●Ayral, F., Djelouadji, Z., Raton, V., Zilber, A. L., Gasqui, P., et al. (2016). Hedgehogs and mustelidspecies: major carriers of pathogenic Leptospira, a survey in 28 animal species in France (20122015). PloS One, 11(9), e0162549.●Biscola, N. P., Fornazari, F., Saad, E., Richini-Pereira, V. B., Campagner, M. V., et al. (2011).Serological investigation and PCR in detection of pathogenic leptospires in snakes. Pesquisa Veterinária Brasileira, 31(9), 806-811.●Buhnerkempe, M. G., Pragger, K. C., Strelloff, C. C., Greig, D. J., Laake, J. L., et al. (2017). Detectingsignals of chronic shedding to explain pathogen persistence: Leptospira interrogans in California sea lions. Journal of Animal Ecology, 86(3), 460-472.●Denkinger, J., Guevara, N., Ayala, S., Murillo, J. C., Hirschfeld, M., et al. (2017). Pup mortality andevidence for pathogen exposure in Galapagos sea lions (Zalophus wollebaeki) on San Cristobal Island, Galapagos, Ecuador. Journal of Wildlife Disease, 53(3), 491-498.●Gravekamp, C., Korver, H., Montgomery, J., Everard, C. O. R., Carrington, D., et al. (1991).Leptospires isolated from toads and frogs on the island of Barbados. Zentralblatt für Bakteriologie, 275(3), 403-411.●Jobbins, S. E., Sanderson, S. E., & Alexander, K. A. (2014). Leptospira interrogans at the human-wildlife interface in northern Botswana: a newly identified public health threat. Zoonoses and Public Health, 61, 113-123.●Karesh, W. B., Hart, J. A., Hart, T. B., House, C., Torres, A., et al. (1995). Health evaluation of fivesympatric duiker species (Cephalophus spp). Journal of Zoo and Wildlife Medicine, 26(4), 485-502.●Leighton, F. A. & Kuiken, T. (2001). Leptospirosis. In E. S. Williams and I. K. Barker (Eds.), InfectiousDiseases of Wild Mammals (3rd ed., pp. 498-502). Iowa State Press.●Loffler, G. S., Rago, V., Martinez, M., Uhart, M., Florin-Christensen, M., et al. (2015). Isolation of aseawater tolerant Leptospira spp. from a southern right whale (Eubalaena australis). PLoS One, 10(12), e0144974.●Lunn, K. F. (2018). Overview of leptospirosis. Merck Veterinary Manual.Accessed 2020:https:///generalized-conditions/leptospirosis/overview-of-leptospirosis?query=leptospira●Pedersen, K., Anderson, T. D., Maison, R. M., Wiscomb, G. W., Pipas, M. J., et al. (2018). Leptospiraantibodies detected in wildlife in the USA and the US Virgin Islands. Journal of Wildlife Diseases, 54(3), 450-459.●Spickler, A. R. & Leedom, L. K. R. (2013). Leptospirosis. Accessed 2020:/Factsheets/pdfs/leptospirosis.pdf●The World Organisation for Animal Health (2018). Leptospirosis. Accessed 2020:https://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/3.01.12_LEPTO.pdf●Vieira, A. S., Pinto, P. S, & Lillenbaum, W. (2018). A systematic review of leptospirosis on wildanimals in Latin America. Tropical Animal Health and Production, 50(2), 229-238.●Wildlife Health Australia (2018). Leptospira infection in Australian mammals. Accessed 2020:https://.au/FactSheets.aspx●Wildlife Health Australia (2011). Leptospira infection in Australian seals. Accessed 2020:https://.au/FactSheets.aspx** *。
阿尔法拉瓦尔Alpacon Descalant II 商品说明说明书
Due to its highly concentrated formula, Alpacon Descalant II f urther reduces transport costs. In addition, it has notransport restrictions for all modes of transport and has been certified by major international organizations (see Certifications, overleaf).• Minimal environmental impactBased on a common biological material, this highly bio-degradable formulation has minimal environmental impact. For use in the offshore and gas industry, the Alfa Laval Alpacon Descalant Offshore, a Harmonised Offshore Chemical Notification Format (HOCNF)-approved cleaning agent, is recommended.• Global support from a leading supplierA global supplier and an experienced partner in the removal of soil from process equipment, Alfa Laval offers a com-plete range of solutions to optimize operations whetheron ships, at offshore facilities or land-based plants. Our global service network provides fast access to spare parts and equipment, expert service and technical support. Companies of all types, whether based on land or at sea, rely on us for technical support, harbour support in most major ports, onsite service and genuine spare parts – all available at short notice.Operational dataIt is important to follow these instructions when using Alpacon Descalant II.Technical data AppearanceSlightly cloudy liquidpH value at 20°C (68°F) 1Relative density 1.11 g/cm 3 at 20°C (68°F)Solubility in waterFully miscible in waterArticle number 189990018 (25L)CertificationsThe Alfa Laval Alpacon Descalant II cleaning agent has been certified by the following agencies for safe transport: European Agreements Concerning the International Carriage of Dangerous Goods by Rail (RID) and by Road (ADR),International Maritime Dangerous Goods Code (IMDG), and the ICAO (International Civil Aviation Organisation) and the IATA (International Air Transport Association).M D D 00341E N 1602Alfa Laval reserves the right to change specifications without prior notification.How to contact Alfa Laval Up-to-date Alfa Laval contact details for all countries arealways available on our website at A l f a L a v a l i s a t r a d e m a r k r e g i s t e r e d a n d o w n e d b y A l f a L a v a l C o r p o r a t e AB .w w w .f o t o s k r i f t .s e。
阿尔法拉瓦尔纯球胶3豪华版说明书
Compliance made simple Alfa Laval PureBallast 3 Yacht EditionPeace of mind is pricelessOf course, owning a superyacht is all about freedom. PureBallast 3 Yacht Edition lets owners sail at their leisure, confident of complying in the widest range of waters worldwide.Type approved by IMO and the U.S. Coast Guard, PureBallast 3 Yacht Edition excels at any water salinity and in any water temper-ature. Likewise, it handles UV transmittance (UVT) values as low as 42%, providing access to challenging ports with low water clarity. For owners, it’s value that can hardly be bought: the world at their fingertips.Service beyond the expectedWherever they choose to sail, yacht owners can trust Alfa Laval to be there. Our 100 years of experience, global service network and 24/7 support are always on their side.With our delivery capabilities, strong project management and retrofit insights, you’ll find that we’re also on yours.Simplicity at a glance•Minimal system footprint•Easy installation asa plug-and-play skid•Superior performance inall water salinities: fresh,brackish, marine•Excellent performancein low-clarity waters•Effective power managementElectrical cabinet 954 x 520 x 1466160Power supply400–440 VAC, 50/60 Hz Power consumptionOptimal 11 kW (20 kW at full ramp-up*)Working pressureMax 6 bar (up to 10 bar optional)Reactor, filter and plastic components Unpainted (filter painted on request)Piping materialSMO Winch material Stainless steel DimensionsTechnical dataColour and materials* Power consumption can be increased to handle low-clarity water with low UV transmittance.PureBallast 3 Yacht EditionOptions•Backflush pump (painted)•Drip tray (stainless steel, screw-in)。
α-galcer蛋白序列
α-Galcer（α-半乳糖神经酰胺，也称为α-Galactosylceramide）是一种合成的糖脂，具有抗肿瘤和免疫刺激作用。
它是一种高效的NKT细胞激动剂，能与CD1d有效结合，进而与NKT细胞的T细胞抗原受体结合。
α-Galcer通过刺激NKT细胞，促进淋巴细胞增殖并增强抗体产生，显示出抗血管生成、抗肿瘤和免疫调节的活性。
然而，α-Galcer并非一种蛋白质，因此并没有蛋白序列。
α-Galcer的化学结构包含一个亲水性的碳酸化物部分和一个疏水性的酰基鞘氨醇部分，通过α连接形成糖脂。
在这个分子中，半乳糖和鞘氨醇上的羟基是NKT细胞上TCR（T细胞抗原受体）的特异性识别部位。
PEX1PCI1 PCI Express转PCI转换器说明书
PEX1PCI1Conversor PCI Express a PCI Guía de instalaciónSoporte, Garantía y Declaración de conformidad con las normativas FCCSi alguna vez necesita ayuda con su producto, póngase en contacto con el 1-800-265 -1844 (En los Estados Unidos), 00 800 7827 8324 (Reino Unido) o visite nuestro sitio /support y acceda a nuestra selección completa de herramientas en línea, documentación y descargas. Este producto tiene una garantía de un año. garantiza que sus productos están libres de defectos de materiales y de mano de obra durante el período establecido a partir de la fecha de compra. Durante este período, los productos podrán ser devueltos para reparación o sustitución por productos equivalentes, según nuestro criterio. La garantía cubre piezas y mano de obra solamente. no garantiza sus productos por defectos o daños derivados del mal uso, abuso, alteración o uso y desgaste normal.Limitación de ResponsabilidadBajo ninguna circunstancia Ltd. y USA LLP (o sus funcionarios, directivos, empleados o agentes) serán responsables de ningún daño (ya sea directo o indirecto, especial, punitivo, incidental, consecuente, o de alguna otra forma), lucro cesante, pérdida de oportunidades comerciales, o cualquier pérdida pecuniaria, o de otro tipo que resulte del uso del producto y que exceda el precio real pagado por el mismo. Algunos estados no permiten la exclusión o limitación de daños incidentales o consecuentes. En cuyo caso, las limitaciones o exclusiones indicadas previamente no son aplicables.Contenido de la Caja• 1 x tarjeta adaptadora PEX1PCI1• 1 x bracket standard PCIe de repuesto • 1 x guía de instalaciónRequisitos del Sistema• Ordenador con zócalo para tarjeta PCI Express • Microsoft® Windows® 2000 o superiorInstalaciónNota: Si se utiliza el bracket de repuesto PCIe, debe retirarse primeramente el bracket de la tarjeta PCI. Las tarjetas PCI standard pueden no ser adecuadas para el sistema.1. I nserte la tarjeta PCI de perfil bajo en la ranura PCI blanca ubicada en la parte superior de la tarjeta adaptadora.2. I nstale la tarjeta adaptadora en el slot PCIe de la placa madre. (Nota: las ranuras PCI son compatibles con las tarjetas más pequeñas PCIe, de manera que puede usarse una ranura x4 o superior)3. C onecte el conector de 4 pin a la fuente de alimentación del ordenador4. E ncienda el ordenador y cargue el sistema operativoNota: No se requiere ningún driver para instalar la tarjeta adaptadora PCI. Sólo actúa como un adaptador a la tarjeta PCIcard. It only acts as a bridge adapter for the PCI card.Revisión del manual: 12/12/2018Para la información más reciente, por favor visite .。