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The Norwegian delegation is proud to have participated in The 58th Nordic Technical Universities Shipbuilder Congress in Finland. Few student congresses or conferences can refer to a greater tradition then the NTHS. Since 1948, NTHS has been arranged in different Nordic countries. It's a remarkable tradition, where we establish contacts with universities from Denmark, Sweden, Finland, as well as with the "Nordic ship industry". Today's world of finance and industry struggle in worldwide playground. NTHS is a golden opportunity for different Nordic nations to get a view into a small, though remarkable, part of this world. Some of our sponsors have previously been NTHS members, and they remember their time as a very good learning experience and a lot of fun! This years congress in Finland guided us through Finish shipping industry. They are an important reminder of that large vessel construction still can be done to a competitive cost in the western world. Finish cruise deign is a world known success and we where lucky enough to be guided through this world during one very interesting week. One of the issues being discussed at the congress was the ever growing importance of international understanding and qualifications during marine studies. I also want to use this opportunity to thank all of our sponsors that made it possible for us to attend to this years congress. This congress report is chance for Norwegian shipping and marine industry to state that they are supporting marine education and research. NTHS is not just an investment for the delegates, but also for the sponsoring companies. They make sure we get a wider background when entering the job market. Last, but not least, I want to thank all my helpful delegates that helped me make it possible for us to attend the 58th NTHS. You've done a great job.
Concentrations by both the kinetic and end-point methods Table 3 ; . Our data fail to demonstrate a significant interference of bilirubin in the kinetic reaction.
Involves Chicago-based Abbott Laboratories. The maker of the extremely unique and powerful AIDS "booster" drug called Norvir. Abbott bundled Norvir with its own protease inhibitor PI ; drug, Lopinavir, which was but one of several PI's available in the marketplace. The Norvir Lopinavir combination drug is called Kaletra. Although Abbott still manufactures Norvir separately, patients who did not buy Kaletra Norvir bundled with Lopinavir ; were forced to pay a much higher price for Norvir. The result of this pricing strategy was a 400 percent increase in the price of patented Norvir to patients who did not buy Abbott's bundled drug, Kaletra.13 Abbott is capable of accomplishing this "forcing" because of the market power it has in the AIDS "booster" market, which is a direct result of it having a patent on its "booster, " Norvir. The possibilities of drug manufacturers combining two drugs in one pill are endless and, as a result, the possible economic and health consequences for the public from such arrangements should be recognized and addressed. Medically, the soundness of fixed drug combinations, as opposed to flexible combinations of separate drugs, is debatable. Marcia Angell, The Pharmaceutical Industry: To Whom is It Accountable?, 342 New Eng J. Med. 1902, 1903 2000 ; . Economically, there remains a powerful truth in the common sense observation of Justice Frankfurter that in many cases "[t]ying agreements serve hardly any purpose beyond the suppression of competition." Standard Oil Co. v. United States, 337 U.S. 293, 305-306 1949 ; . Legally, pharmaceutical companies should not be given free reign to limit competition.
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1. Call to Order The regular meeting of the WVSSAC Board of Directors was called to order Wednesday, October 25, 2006 at 1: 00 President Warren Grace in the Sam Williams Conference Room of the WVSSAC Office in Parkersburg, WV. The following members were present: Tom Kidd, Harold Erwin, Sandra Chapman, Ron Spencer, Jack Wiseman, Tom Eschbacher, Dave Rogers, Frank Aliveto, and Ray Londeree. Representing the WVSSAC administrative staff were Mike Hayden, Gary Ray, Butch Powell and Kelly Geddis. The meeting was called back to order on Thursday, October 26, 2006 with all members previously listed in attendance. 2. Interview Candidates for Executive Director's Position The Board immediately went into Executive Session to conduct interviews for the position of Executive Director. On Thursday, October 26, 2006, the meeting was called back to order by President Warren Grace. The Board voted unanimously to select Gary Ray to succeed Mike Hayden as Executive Director beginning July 1, 2007. Mr. Ray was given a one-year contract. 3. Approval of Minutes A. September Regular Meeting - On a motion by Mr. Kidd and a second by Mr. Wiseman, the minutes of the September Regular Meeting were unanimously approved with recommended editorial changes.
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Of data collection and audit that is required. The larger the scope of data collected and the greater the need for representation from a wide variety of patient characteristics, the larger is the expense. In addition, the method of data collection will contribute to expense, with electronic collection being more expensive to implement but generally less expensive to maintain compared with fax and scan or mailed forms.44 Funding will be affected by whether other relevant data sources and or infrastructures exist that capture some of the information of interest, whether the registry adapts to new issues over time, and whether multiple funding sources participate. Funding needs also should be examined in terms of the projected life of the registry and or its long-term sustainability. If de-identified data will be accessible to either internal or external groups after the registry closes, it is important to clarify how that activity will be managed and supported. There are many potential funding sources for registries. Funding sources are likely to want to share in planning and provide input for the many choices that will need to be made in the implementation plans. Funding sources may negotiate to receive access to de-identified data as a requirement for their participation. For a variety of reasons, some funding sources as is also the case in clinical trials ; may require that such access be restricted or exclusive outside of addressing the scientific questions in the registry protocol. Funding models for registries may vary significantly, and a preferred approach does not exist. Rather, the funding model for a registry should be dictated by the needs of the registry. Potential sources of funding include: Government: The branches of the government, such as NIH, CDC, and State agencies, may be interested in a registry to determine long-term outcomes of agents, devices, or groups of drugs. While the pharmaceutical industry or device manufacturers collect most long-term data on drug and device safety, many research questions arise that could potentially be suitable for government funding in the context of sponsored Phase IV safety studies mandated by FDA. To and kaon.
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B.1 Scientific and technological objectives of the project and state of the art Aim Science as a whole can be viewed as a very complex, multilayered network, formed by the researchers, the concepts they use and the publications they produce. All these "nodes" of the network are directly or indirectly linked, by relations such as citation, collaboration or information exchange. This complex system is intrinsically self-organizing [Heylighen, 2002; Gershenson & Heylighen, 2003] names in bold refer to members of one of the participating teams ; : no individual or organization is in charge, or can decide in which direction science should develop. Novel, globally available knowledge emerges out of the spontaneous, local interactions between the individual agents. Yet, there are a number of institutional structures, such as universities, departments, associations and journals, that try to canalize the often chaotic flow of information along this network. These structures typically are grouped into disciplines, specializations or subject domains, so that most information is exchanged between scientists within the same subject domain, while relatively little information is exchanged across domains. Yet, we know that the most innovative research typically takes place in between established disciplines or domains, eventually resulting in the emergence of a new research community with its own paradigm. Therefore, an approach based on a mere subdivision of science into discrete, static domains will fail to capture the essential dynamics of innovation. To understand scientific development, we need a different approach that focuses on the interconnections and the complex dynamics these engender. In the present project, we wish to investigate how science self-organizes, using concepts and methods from the domain of complexity [Gershenson & Heylighen, 2005]. Thus, we hope to better understand its natural development, rather than the development that institutions, such as departmental structures, science policy, or funding agencies, try to impose. A deeper understanding of such science dynamics should help us to promote innovation, by devising more effective institutions, management methods and technologies to support research. It should in particular help us to stimulate and guide interdisciplinary cross-fertilization, while helping researchers to cope with the information explosion caused by ever faster generation and transmission of data and knowledge. Moreover, it may.
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Trifluoride diethyl etherate BF3.OEt2 ; were distilled from calcium hydride. Chloromethyl methyl ether MOM-Cl ; was prepared according to the literature procedure4 and stored in the freezer. The palladium catalysts [Pd PPh3 ; 2Cl2, Pd PPh3 ; 4, Pd2 dba ; 3, Pd AsPh3 ; 2Cl2 and Pd MeCN ; 2Cl2], 5, 6 CuBr.SMe26 and Mo tert-BuNC ; 3 CO ; 37 were prepared according to literature procedure. Copper thiophene carboxylate CuTC ; was prepared via the method of Liebeskind et al.8 2, 2'-Azobisisobutyronitrile AIBN ; was prepared according to literature methods and stored in the freezer.9 The Dess-Martin periodinane DMP ; was prepared by the modified methods of Ireland and Liu.10 Diethylzinc Et2Zn ; was prepared as detailed by Foster and Cole-Hamilton11 on a 0.2 mol scale to yield pure diethylzinc 20.77 g, 0.168 mol, 84% ; which was dissolved in distilled toluene to give a ~1.2 M stock solution and stored at -8C under Ar. 1, 1-Diethoxy-2-bromoethane and 1, 1-diethoxy-2-iodoethane were prepared via literature methods.12, 13 The MOM, THP and benzyl protected acetaldehydes 3.79a-3.79c were prepared via ozonolysis of their respective bis-protected-1, 4-but-2-ene precursors.14 Grubbs 2nd generation catalyst, 4.25 was purchased from Strem or Aldrich and stored under an argon atmosphere at 0C. Allyl chloro ; dimethylsilane was prepared via the method of Chihi and Weber.15 Unless otherwise stated, all reactions were performed in oven- or flame-dried glassware under an atmosphere of argon or nitrogen with the reaction temperature referring to the external bath temperature. All organic extracts were washed with brine and dried over anhydrous sodium sulfate. After filtration of the solutions to remove solids, the solvents were evaporated under reduced pressure on a Bchi rotary evaporator ~12 mmHg ; . When necessary, a high-vacuum pump ~0.1 mmHg ; was used to remove the last traces of solvent from purified compounds. Evaporation under an inert atmosphere was achieved using a three way tap connected to a vacuum source and an inert atmosphere and kava.
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May coexist with or precede the onset of asthma. Risk Factors The exact cause of asthma is not known. It could be partly genetic and partly environmental in origin1. Some of the factors which are important either to cause or to produce its clinical manifestations or both ; are listed as under: Host Factors 1. Family history of asthma or atopy3, 6, 7, 11, Atopy 3, 11 3. Airway hyper-responsiveness Environmental Factors 1. Indoor allergens House dust mites3 Insect allergens Fungi, molds, yeasts Pet animal allergens Pollens Fungi, molds, yeasts Exposures to tobacco smoke lead to increase in severity of asthma, decreased response to treatment and accelerated decline in lung functions 1. The different ways in which tobacco smoke affects.
Efavirenz is currently used by 75, 000 patients in brazil, and costs the brazilian government million a year abbott on the eve of the agm in a desperate bid to improve its tarnished public image, abbott announced its plans to reduce the cost of kaletra in thailand and more than 40 low- and low-middle-income countries by more than half and kenalog.
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The strongly recommended medications follow: choose one from column a and one pair from column b sustiva efavirenz ; crixivan indinavir ; viracept nelfinavir ; norvir + crixivan ritonavir + indinavir ; kaletra lopinavir ritonavir ; norvir + invirase or fortovase ritonavir + saquinavir ; zerit + videx stavudine, d4t ; + didanosine, ddi ; zerit + epivir stavudine, d4t ; + lamivudine, 3tc ; retrovir + videx zidovudine, azt ; + didanosine, ddi ; retrovir + epivir zidovudine, azt ; + lamivudine, 3tc ; ziagen abacavir ; agenerase amprenavir ; rescriptor delavirdine ; viracept + fortovase nelfinavir + saquinavir ; viramune nevirapine ; norvir ritonavir ; fortovase saquinavir ; videx + epivir didanosine, ddi ; + lamivudine, 3tc ; retrovir + hivid zidovudine, azt ; + ddc, zalcitabine ; comparing pis a quick glance at the guidelines reveals that most of the drugs in column a are pis.
Lopinavir 10x, 10-40x a 40x. U 91% 21 23 ; , 71% 15 21 ; a 33% 2 6 ; pacient byla pozorovna virologick odpov s mutacemi v poctu 0-5, 6-7 a 8-10 z vse uvedench mutac HIV protezy, kter mly vztah ke snzen citlivosti na lopinavir in vitro. Protoze tito pacienti nebyli pedtm vystaveni ani Kalete ani efavirenzu, cst tto odpovdi mze bt pictena antivirov cinnosti efavirenzu, a to zejmna u pacient, u kterch se vyskytuje virus vysoce rezistentn na lopinavir. Studie neobsahovala kontroln vtev pacient, kte neuzvali Kaletru. Zkzen rezistence: psoben jinch protezovch inhibitor vci izoltm, dky nmuz se u pacient se zkusenost s lcbou protezovmi inhibitory po lcb ppravkem Kaletra vyvinula vzrstajc rezistence na lopinavir: Ptomnost zkzen rezistence na jin protezov inhibitory byla zkoumna u 18 izolt, zskanch po optovnm pomnozen viru, kter vykazovaly vvin rezistence na lopinavir v prbhu 3 studi fze II a jedn studie fze III s ppravkem Kaletra u pacient se zkusenost s lcbou protezovm inhibitorem. Prmrn zvsen IC50 lopinaviru bylo u tchto 18 vchozch izolt 6, 9-nsobn a u izolt, zskanch po optovnm pomnozen viru 63-nsobn, v porovnn s divokm typem viru. Obecn lze ci, ze izolty, zskan po optovnm pomnozen viru bu zstvaly beze zmn byly-li zkzen rezistentn ve vchozm stavu ; nebo se u nich vyvinula vznamn zkzen rezistence na indinavir, sakvinavir a atazanavir. Byl zaznamenn mrn pokles v aktivit amprenaviru s prmrnm vzestupem IC50 od 3, 7-nsobnho vzestupu u vchozch izolt do 8-nsobnho vzestupu u izolt, zskanch po pomnozen viru. Izolty s nezmnnou citlivost na tipranavir vykazovaly v prmru 1, 9-nsobn zvsen IC50 u vchozch izolt a 1, 8-nsobn zvsen IC50 u izolt, zskanch po optovnm pomnozen viru, ve srovnn s divokm typem viru. Pro dals informace ohledn uzvn tipranaviru, vcetn genotypickch znmek odpovdi na lcbu na lopinavir rezistentn infekce HIV-1 odkazujeme na souhrn daj o ppravku Aptivis. Klinick farmakodynamick daje V kontrolovan studii s Kaletrou trvajc 48 tdn a v dalsch studich trvajcch 360 tdn byly sledovny cinky Kaletry v kombinaci s dalsmi antiretrovirotiky ; na biologick markery plazmatick hladiny HIV RNA a pocet CD4 ; . Uzit u dosplch osob Pacienti, kte dosud nebyli lceni antiretrovirotiky Studie M98-863 je randomizovan, dvojit zaslepen studie s 653 pacienty, dosud nelcenmi antiretrovirotiky, ve kter se hodnotila lcba Kaletrou 400 100 mg dvakrt denn ; ve srovnn s nelfinavirem 750 mg tikrt denn ; a nukleosidovmi inhibitory reverzn transkriptzy. Pi analze spsnosti lcby vsech pacient, kte byli zaazeni do studie intent-to-treat analza ; , cinil po 48 tdnech podl pacient s nloz HIV RNA 400 kopi ml ve skupin pacient lcench Kaletrou 75% a ve skupin pacient lcench nelfinavirem 63%, pi cemz pacienti s chybjcmi hodnotami v analze spsnosti lcby byli povazovni za pacienty, u kterch doslo k virologickmu selhn. Prmrn vchoz pocet CD4 bunk byl 259 bunk mm3 rozptyl: 2 - 949 bunk mm3 ; a prmrn vchoz plazmatick nloz HIV-1 RNA byla 4, 9 log10 kopi ml rozptyl: 2, 6 - 6, 8 log10 kopi ml ; . Bhem 48 tdn lcby cinil podl pacient ve skupin pacient lcench Kaletrou s plazmatickou RNA 50 kopi ml 67% a 52% ve skupin pacient lcench nelfinavirem. Prmrn vzestup oproti vchozmu poctu bunk CD4 byl 207 bunk mm3 ve skupin pacient lcench Kaletrou a 195 bunk mm3 ve skupin pacient lcench nelfinavirem. Bhem 48 tdn lcby statisticky vznamn vts podl pacient ve skupin pacient lcench Kaletrou ml HIV RNA 50 kopi ml ve srovnn se skupinou pacient lcench nelfinavirem. Petrvvajc virologick odpov na lcbu Kaletrou v kombinaci s nukleosidovmi nukleotidovmi inhibitory reverzn transkriptzy ; byla rovnz pozorovna v mal studii fze II M97-720 ; bhem 360 tdn lcby. V tto studii bylo pvodn lceno 100 pacient ppravkem Kaletra vcetn 51 pacient, jez uzvali dvku 400 100 mg dvakrt denn a 49 pacient na dvce 200 100 mg dvakrt denn nebo 400 200 mg dvakrt denn ; . Vsichni pacienti byli v obdob mezi 48. a 72. tdnem and ketek.
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Kaletra should not be taken by patients who have had an allergic reaction to lopinavir ritonavir or any of its ingredients, including lopinavir or ritonavir and kaletra.
Abbott has had a long-standing commitment to develop HIV medicines appropriate for pediatric use. Kaletra is indicated as the recommended second-line therapy in the World Health Organization WHO ; guidelines for the treatment of children living with HIV in the developing world. Kaletra oral solution is the only co-formulated protease inhibitor that is approved for the treatment of children with HIV. Building on this commitment, Abbott has used its proprietary Meltrex technology to develop a lower-strength formulation of the LPV r tablet. Global filings for this new product will begin by mid-2007. This will be of significant importance to children living with HIV, because this tablet, too, can be taken with or without food and does not require refrigeration. Abbott will continue the development of a heat-stable ritonavir tablet. At the recent Conference on Retroviruses and Opportunistic Infections CROI ; , we presented encouraging human bioavailability data on a variety of potential tablet formulations. While these data are promising, significant work is required to finalize this complex formulation and ketoprofen.
Anti-Virals: Nucleoside Reverse Transcriptase Inhibitors NRTIs ; Abacavir Ziagen ; Stavudine d4T, Zerit ; Abacavir Lamivudine Zidovudine Trizivir ; Tenofovir DF Viread ; Didanosine ddI, Videx ; Zalcitabine ddC, Hivid ; Lamivudine 3TC, Epivir ; Zidovudine AZT, Retrovir ; Lamivudine Zidovudine Combivir ; Anti-Virals: Protease Inhibitors PIs ; Amprenavir Agenerase ; Ritonavir Norvir ; Indinavir Crixivan ; Saquinavir Fortovase ; Lopinavir Ritonavir Kaletra ; Saquinavir mesylate Invirase ; Nelfinavir Viracept ; Anti-Virals: Non-nucleoside Reverse Transcriptase Inhibitors NNRTIs ; Delavirdine Rescriptor ; Nevirapine Viramune ; Efavirenz Sustiva ; Anti-Virals: Herpes treatments CMV Disease Acyclovir Zovirax ; Ganciclovir Cytovene ; Cidofovir Vistide ; Valacyclovir Valtrex ; Famciclovir Famvir ; Valganciclovir Valcyte ; Foscarnet Foscavir ; Anti-Virals: Hepatitis C Treatments PEG-Interferon alfa-2b PEG-Intron ; Ribavirin Rebetol ; Antibiotics Amoxicillin Doxycycline hyclate Amoxicillin Clavulanate pot. Augmentin ; Gentamicin Ampicillin Minocycline HCL Dynacin ; Azithromycin Zithromax ; Nitrofurantoin Monohydrate Macrobid ; Cefuroxime Ofloxacin Floxin ; Cephalexin Keflex ; Paromomycin Humatin ; Ciprofloxacin Cipro ; Penicillin G Benzathine Bicillin ; Clarithromycin Biaxin ; Penicillin V Potassium Veetids ; Clindamycin Cleocin ; Rifabutin Mycobutin ; Dicloxacillin Vancomycin Anti-fungal Agents Amphotericin B Fungizone B ; Ketoconazole Nizoral ; Clotrimazole Mycelex, Lotrimin ; Nystatin Fluconazole Diflucan ; Terconazole Terazol 3 & 7 ; Itraconazole Sporanox ; Other Anti-infective Agents Dapsone Primaquine Ethambutol Myambutol ; Pyrimethamine Mepron Sulfadiazine Metronidazole Flagyl ; Trimethoprim-sulfamethoxazole, TMP-SMZ Pentamidine Pentam 300, NebuPent ; Trimethoprim Proloprim ; Antihyperlipidemic Agents Atorvastatin Lipitor ; Fenofibrate Tricor ; Gemfibrozil Lopid ; Cholestyramine Questran ; Pravastatin Pravachol ; Clofibrate Atromid-S ; Analgesic Agents Acetaminophen with codeine Oxycodone HCL controlled release Oxycontin ; Fentanyl transdermal system Duragesic ; Anti-inflammatory Agents NSAID ; Celecoxib Celebrex ; Naproxen Naprosyn ; Ibuprofen Motrin ; Rofecoxib Vioxx ; Ketoprofen Orudis.
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Vitro immune complex kinase assay to measure the activity of p38 MAPK Fig. 4, A and B ; . The magnitude of the response to tBHQ and BNF amounted to 9 and 20%, respectively, in THP-1, and 45 and 31%, respectively, in RAW264.7 cells Fig. 4, A and B ; . While details about the pathway by which these chemicals engage the p38 MAPK cascade are unknown, p38 MAPK itself is activated by a dual specificity MAPK kinase, MKK6 65 ; . MKK6 activates p38 MAPK by phosphorylating threonine and tyrosine residues in the TGY allosteric effector site of the latter kinase 58, 65 ; . The phosphorylation of p38 MAPK can be studied by antiphosphopeptide Abs that recognize the phosphorylated but not the native species. Overlay of whole cell lysates with antiphosphopeptide antiserum showed increased p38 phosphorylation in THP-1 cells resulting from treatment with LPS, BNF, tBHQ, and PMA Fig. 5A ; . We examined the role of oxidative stress in p38 MAPK activation, and found that prior exposure of and kaon!
Presence of FSH or EGF as seen in mice; however, this factor is not essential for the expansion of porcine and bovine cumulus cells. In this study, we investigated the expressions of the HA synthase family and CD44 mRNAs in COCs, OXCs, and oocytes during cumulus expansion stimulated in vitro. The results demonstrated that HA synthase mRNAs are expressed not only in cumulus cells has2 ; but also in oocytes has3 ; , suggesting that oocytes, in addition to cumulus cells, synthesize HA Fig. 4 ; . The expression of has2 mRNA was induced by eCG and pFF, which brought about cumulus expansion Fig. 3 ; . Fulop et al. [36] reported that mouse Has2 is expressed during COC matrix expansion induced by hCG injection and that the pattern of increased Has2 mRNA levels is similar to that observed in HA synthesis in vivo. This evidence of Has2 transcription suggests a role for HAS2 in HA synthesis accompanied by cumulus expansion. In our experiments, the level of has2 mRNA in COCs and OXCs did not always conform to the degree of cumulus expansion simultaneously. This evidence suggests that the cumulus expansion consists of both the synthesis of HA and other matrix components and their deposition around the cumulus cells. In COCs after 24 h of culture, the expression of has3 mRNA remarkably increased in the medium-alone group compared with the eCG-alone, pFF-alone, and combined eCG and pFF groups. The pattern of has3 mRNA expression was different from that of has2 mRNA Fig. 3 ; . We also confirmed has3 mRNA expression in oocytes removed from cumulus cells at 0, 24, and 48 h after culture in oocytes incubated in the medium alone or in medium supplemented with eCG and pFF data not shown ; . We did not find any apparent difference of has3 transcription level between conditions or culture periods. Therefore, it seems that the regulation of has3 mRNA expression is distinct from that of has2 mRNA expression. It is not clear what part of the has3-derived HA the oocyte takes in. Several studies have demonstrated that the addition of HA to culture media effectively prevents fragmentation or segmentation of oocytes and supports the development of in vitro-matured, -fertilized, and -cultured oocytes to the blastocyst stage [32, 37]. Sato et al. [38] showed that specific GAGs purified from pFF, the fraction with a retention time nearly coincident with that of HA, promotes viability of oocytes. Hess et al. [3] demonstrated that disruption of cumulus expansion by excess HA affects the early development of embryos derived from COCs stored within the oviduct. These results indicate that HA positively participates in the development of oocytes and embryos, and thus, it is tempting to speculate that oocytes themselves produce HA to maintain development and viability [9]. Spicer et al. [29] suggested that potential differences in the function of each HAS protein HAS1, HAS2, and HAS3 ; could be related to the length of the HA chain synthesized, the rate of HA synthesis, the ability to interact with cell type-specific accessory proteins, and whether or not the HA is preferentially secreted by the cell or alternatively retained by the cell in the form of a pericellular coat. Recently, enzymatic properties of three HAS proteins have been reported by Itano et al. [39]. Kinetic studies of these enzymes in the membrane fraction isolated from HAS transfectants the host cells were COS-1 cells or rat 3Y1 fibroblasts ; demonstrated that each HAS protein is distinct in enzyme stability, elongation rate of HA, and apparent K m ; values for two substrates, i.e., UDP-GlcNAc and and klonopin.
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