Microstructure and tribological behavior of Ti–Si eutectic alloys with Al additions

微生物代谢动力学英语Microbial Metabolic Kinetics.Microbial metabolic kinetics is the study of the rates of microbial growth and metabolism. It is a complex field that encompasses a wide range of topics, including the effects of environmental factors on microbial growth, the regulation of microbial metabolism, and the use of mathematical models to describe microbial growth and metabolism. Microbial metabolic kinetics is of great importance in a variety of fields, including biotechnology, food microbiology, and environmental microbiology.Microbial Growth.Microbial growth is the increase in the number of cells in a population. It is a complex process that is influenced by a variety of factors, including the availability of nutrients, the temperature, the pH, and the presence of inhibitors. Microbial growth can be described by a varietyof mathematical models, including the Monod model and the Gompertz model.Microbial Metabolism.Microbial metabolism is the process by which microorganisms convert nutrients into energy and new cells. It is a complex process that involves a variety of enzymatic reactions. Microbial metabolism can be divided into two main types: catabolism and anabolism. Catabolismis the breakdown of complex molecules into simpler molecules, while anabolism is the synthesis of new molecules from simpler molecules.Environmental Factors.A variety of environmental factors can affect microbial growth and metabolism. These factors include theavailability of nutrients, the temperature, the pH, and the presence of inhibitors. The optimal conditions for microbial growth and metabolism vary depending on the microorganism. Some microorganisms are able to grow in awide range of conditions, while others are more specialized and require specific conditions for growth.Regulation of Microbial Metabolism.Microbial metabolism is regulated by a variety of factors, including the availability of nutrients, the temperature, the pH, and the presence of inhibitors. The regulation of microbial metabolism is essential for the survival of the microorganism. For example, if the availability of nutrients is limited, the microorganismwill need to regulate its metabolism in order to conserve energy.Mathematical Models of Microbial Growth and Metabolism.Mathematical models of microbial growth and metabolism can be used to describe the growth and metabolism of microorganisms. These models can be used to predict the behavior of microorganisms in a variety of environments. Mathematical models of microbial growth and metabolism are often used in biotechnology, food microbiology, andenvironmental microbiology.Applications of Microbial Metabolic Kinetics.Microbial metabolic kinetics has a wide range of applications in a variety of fields, including biotechnology, food microbiology, and environmental microbiology. In biotechnology, microbial metabolickinetics is used to design and optimize fermentation processes. In food microbiology, microbial metabolic kinetics is used to predict the growth and survival of microorganisms in food products. In environmental microbiology, microbial metabolic kinetics is used to study the role of microorganisms in the environment.Conclusion.Microbial metabolic kinetics is a complex field that encompasses a wide range of topics. It is a field of great importance in a variety of fields, including biotechnology, food microbiology, and environmental microbiology.。

细胞生物学专业词中英文对照第一章细胞学——Cytology细胞生物——Cell biology细胞学说——Cell theory原生质——protoplasm原生质体——protoplast有丝分裂——mitosis福尔根反应——Feulgen reaction哺乳动物雷帕霉素靶蛋白——mammalian target of rapamycin (mTOR)支原体——mycoplast真核细胞——rucaryotic cell真核生物——procaryote原核细胞——prokaryotic cell原核生物——prokaryote类群、域——domain古核细胞——archaea古核生物——archaeon古细菌——archaebacteria真细菌——eubacteria鞭毛——flagellum鞭毛蛋白——flagellin类核——nucleoid质粒——plasmid管蛋白——tubulin蓝细菌——cyanobacteria类囊体——thylakoid异形胞——heterocyst直系同源基因——orthologous gene 盐细菌——halobacteria热源体——thermoplasma硫氧化菌——sulfolobus核小体——nucleosome核纤层——nuclear lamina核纤层蛋白——lamin核基质——nuclear matrix纳米生物学——nanobiology自我装配——self-assembly协助装配——aided-assembly直接装配——direct-assembly次生代谢产物——secondary metabolite天然产物——natural product衣壳——capsid核壳体——nucleocapsid囊膜——envelope第二章光学显微镜——light microscope分辨率——resolution相差显微镜——phase-contrast microscope微分干涉显微镜——differential-interference microscope录像增差显微镜——video-enhance microscope荧光显微镜——fluorescence microscope绿色荧光蛋白——green fluorescent protein, GFP激光扫描共焦显微镜——laser scanning confocal microscope, LSCM全内反射荧光显微术——total internal reflection fluorescence microscopy 光激活定位显微术——photoactivated localization microscopy, PALM随机光学重构显微术——stochastic optical reconstruction microscopy受激发射损耗显微术——stimulated emission depletion microscopy结构照明显微术——structured-illumination microscopy, SIM电子显微镜——electron microscope, EM电荷耦合器件——charge-coupled device, CCD超薄切片——ultrathin section负染色技术——negative staining冷冻蚀刻技术——frezze etching快速冷冻深度蚀刻技术——quick freeze deep etching低温电镜技术——cryo-electron microscopy单颗粒分析技术——single particle analysis电子断层成像技术——electron tomography背散射电子成像——back scattered electron imaging扫描电镜——scanning electron microscope, SEM光-电关联技术——correlative light microscopy and electron microscopy 扫描隧道显微镜——Scanning tunnel microscope, STM原子力显微镜——atomic force microscope, AFM免疫印记——western blotting放射免疫沉淀——radioimmuno-precipitation原位杂交——in situ hybridization流式细胞术——flow cytometry原代细胞——primary culture cell传代细胞——subculture cell单层细胞——single layer cell细胞系——cell line有限细胞系——finite cell line永生细胞系——infinite cell line连续细胞系——continuous cell line细胞株——cell strain成纤维样细胞——fibroblast like cell上皮样细胞——epithelial like cell外殖体——explant愈伤组织——callus细胞融合——cell fusion电融合技术——electrofusion methodB淋巴细胞杂交瘤技术——B-lymphocyte hybridoma technique 单克隆抗体——monoclonal antibody胞质体——cytoplast核质体——karyoplast细胞松弛素B——cytochalasin B显微操作——micromanipulation微量注射——microinjection荧光漂白恢复技术——fluorescence photobleaching recovery, FPR 荧光恢复——fluorescence recovery酵母双杂交系统——yeast two-hybrid systemDNA结合域——DNA binding domain转录激活域——activation domain荧光共振能量转移——fluorescence resonance energy transfer, FRET 放射自显影技术——autoradiography第三章细胞质膜——plasma membrane细胞内膜系统——internal membrane生物膜——biomembrane单位膜模型——unit membrane model流动镶嵌模型——fluid mosaic model菌紫红质——bacteria rhodopsin脂筏模型——lipid raft model辛德毕斯病毒——sindbis virus, SbV甘油磷脂——glycerophosphatide鞘脂——sphingolipid固醇——sterol磷脂酰胆碱——phosphatidylcholine, PC(卵磷脂)磷脂酰乙醇胺——phosphatidylethanolamine, PE磷脂酰丝氨酸——phosphatidyserine, PS磷脂酰肌醇——phosphaditylinositol, PI心磷脂——cardiolipin鞘磷脂——sphingomyelin, SM磷脂——phospholipid豆固醇——stigmasterol麦角固醇——ergosterol翻转酶——flippase脂质体——liposome微团——micelle膜蛋白——membrane protein周边膜蛋白——peripheral membrane protein外在膜蛋白——extrinsic membrane protein整合膜蛋白——integral membrane protein内在膜蛋白——intrinsic membrane protein脂锚定膜蛋白——lipid-anchored membrane protein 磷脂酶——phospholipase蛋白聚糖——proteoglycan磷脂酰肌醇糖脂——glycosylphosphaditylinositol跨膜蛋白——transmembrane protein单次跨膜蛋白——single-pass transmembrane protein 多次跨膜蛋白——multipass transmembrane protein 孔蛋白——porin卷曲结构——coiled-coil水孔蛋白——aquaporin去垢剂——detergent微团临界浓度——critical micelle concentration,CMC相变温度——phase transition temperature扩散常数——diffusion constant细胞外表面——extrocytoplasmic surface, ES外小叶——outer leaflet原生质表面——protoplasmic surface, PS内小叶——inner leaflet细胞外小叶断裂面——extrocytoplasmic face，EF原生质小叶断裂面——protoplasmic face，PF脂肪细胞——adipocyte鞭毛——flagellum纤毛——cilium微绒毛——microvillus膜相关的细胞骨架——membrane associated cytoskeleton 肌动蛋白——actin基于肌动蛋白的膜骨架——actin-based membrane skeleton 细胞皮层——cortex血影——ghost血影蛋白（或红膜肽）——spectrin锚蛋白——ankyrin血型糖蛋白——glycoprotein内收蛋白——adducin阀蛋白——flotillin膜脂微区——membrane lipid microdomain 阿尔兹海默症——Alzheimer disease。

微生物在药用中的作用300字作文英文回答：Microorganisms play a crucial role in medicine. They have both positive and negative effects on human health. Let's focus on their positive contributions.Firstly, microorganisms are used in the production of antibiotics. Antibiotics are essential in treatingbacterial infections. They work by killing or inhibiting the growth of bacteria. Many antibiotics, such aspenicillin and erythromycin, are derived from microorganisms like fungi and bacteria. These medications have saved countless lives and continue to be a cornerstone of modern medicine.Secondly, microorganisms are involved in the production of vaccines. Vaccines are crucial in preventing the spread of infectious diseases. They contain weakened or killed microorganisms that stimulate the immune system to produceantibodies. These antibodies provide immunity againstfuture infections. Vaccines have eradicated orsignificantly reduced the incidence of diseases like polio, measles, and smallpox.Furthermore, microorganisms are used in the productionof various biologics, such as insulin and growth hormones. These biologics are used to treat conditions like diabetes and growth disorders. Microorganisms are genetically engineered to produce these substances in large quantities, making them more accessible and affordable for patients.In addition to their direct medical applications, microorganisms also play a role in research and development. They are used in studying diseases, testing the efficacy of drugs, and understanding the mechanisms of variousbiological processes. Microorganisms, especially bacteria, are also used as model organisms in genetic studies.In conclusion, microorganisms have a significant impact on medicine. They are essential in the production of antibiotics, vaccines, and other biologics. They alsocontribute to research and development in the field of medicine. Without microorganisms, many medical advancements and treatments would not be possible.中文回答：微生物在药用中扮演着至关重要的角色。

The Gut MicrobiotaREVIEWInteractions Between the Microbiota and the Immune SystemLora V.Hooper,1*Dan R.Littman,2Andrew J.Macpherson 3The large numbers of microorganisms that inhabit mammalian body surfaces have a highly coevolved relationship with the immune system.Although many of these microbes carry out functions that are critical for host physiology,they nevertheless pose the threat of breach with ensuing pathologies.The mammalian immune system plays an essential role in maintaining homeostasis with resident microbial communities,thus ensuring that the mutualistic nature of the host-microbial relationship is maintained.At the same time,resident bacteria profoundly shape mammalian immunity.Here,we review advances in our understanding of the interactions between resident microbes and the immune system and the implications of these findings for human health.Complex communities of microorganisms,termed the “microbiota,”inhabit the body surfaces of virtually all vertebrates.In the lower intestine,these organisms reach extraordi-nary densities and have evolved to degrade a variety of plant polysaccharides and other dietary substances (1).This simultaneously enhances host digestive efficiency and ensures a steady nutrient supply for the microbes.Metabolic efficiency was likely a potent selective force that shaped the evolution of both sides of the host-microbiota lions of years of coevolution,however,have forged pervasive interconnections between the physiologies of microbial commu-nities and their hosts that extend beyond metabolic functions.These interconnections are particularly apparent in the relationship between the microbiota and the immune system.Despite the symbiotic nature of the intestinal host-microbial relationship,the close association of an abundant bacterial community with intesti-nal tissues poses immense health challenges.The dense communities of bacteria in the lower intes-tine (≥1012/cm 3intestinal contents)are separated from body tissues by the epithelial layer (10m m)over a large intestinal surface area (~200m 2in humans).Opportunistic invasion of host tissue by resident bacteria has serious health consequences,including inflammation and sepsis.The immune system has thus evolved adaptations that work to-gether to contain the microbiota and preserve the symbiotic relationship between host and microbiota.The evolution of the vertebrate immune system has therefore been driven by the need to protect thehost from pathogens and to foster complex micro-bial communities for their metabolic benefits (2).In this Review,we survey the state of our understanding of microbiota-immune system in-teractions.We also highlight key experimental challenges that must be confronted to advance our understanding in this area and consider how our knowledge of these interactions might be harnessed to improve public health.Tools for Analyzing the Microbiota –Immune System RelationshipMuch of our current understanding of microbiota –immune system interactions has been acquired from studies of germ-free animals.Such animals are reared in sterile isolators to control their exposure to microorganisms,including viruses,bacteria,and eukaryotic parasites.Germ-free animals can be studied in their microbiologically sterile state or can serve as living test tubes for the establishment of simplified microbial ecosystems composed of a single microbial species or defined species mixtures.The technology has thus come to be known as “gnotobiotics,”a term derived from Greek meaning “known life.”Gnotobiotic ani-mals,particularly rodents,have become critical experimental tools for determining which host immune functions are genetically encoded and which require interactions with microbes.The current impetus for gnotobiotic exper-imentation has been driven by several impor-tant technical advances.First,because any mouse strain can be derived to germ-free status (3),large numbers of genetically targeted and wild-type inbred isogenic mouse strains have become avail-able in the germ-free state.The contribution of different immune system constituents to host-microbial mutualism can thus be determined by comparing the effects of microbial colonization in genetically altered and wild-type mice (4,5).Second,next-generation sequencing tech-nologies have opened the black box of micro-biota complexity.Although advances in ex vivo culturability are still needed,the composition ofhuman and animal microbiotas can be opera-tionally defined from polymorphisms of bacterial genes,especially those encoding the 16S ribo-somal RNA sequences.Such analyses have made possible the construction of defined microbiotas,whose distinct effects on host immunity can now be examined (6).Moreover,these advances allow the study of experimental animals that are both isobiotic and,in a defined inbred host,isogenic.A dominant goal of these efforts is to benefit hu-man health [see Blumberg and Powie (7)].With the developing technology,the species differ-ences can be closed using mice with a defined humanized microbiota (8).On the horizon,there is even the prospect of humanized isobiotic mice that also have a humanized immune system (9).A third advance has been the development of experimental systems that allow the uncoupling of commensal effects on the immune system from microbial colonization.This cannot be achieved by antibiotic treatment alone because a small pro-portion of the targeted microbes will persist.Deletion strains of bacteria lacking the ability to synthesize prokaryotic-specific amino acids have been developed that can be grown in culture but do not persist in vivo,so the animals become germ-free again.This allows issues of mucosal immune induction,memory,and functional protection to be explored without permanent colonization (10).Finally,important insights about the impact of resident microbial communities on mammalian host biology have been acquired by using high-throughput transcriptomic and metabolomic tools to compare germ-free and colonized mice (11,12).These tools include DNA microarrays,which have led to a detailed understanding of how microbiota shape many aspects of host physiology,includ-ing immunity (13,14)and development (15),as well as mass spectrometry and nuclear magnetic resonance spectroscopy,which have provided im-portant insights into how microbiota influence metabolic signaling in mammalian hosts (12).The application of these new approaches to the older technology of gnotobiotics has revolutionized the study of interactions between the microbiota and the immune system.Looking Inside-Out:Immune System Control of the MicrobiotaA major driving force in the evolution of the mammalian immune system has been the need to maintain homeostatic relationships with the microbiota.This encompasses control of micro-bial interactions with host tissues as well as the composition of microbial consortia.Here,we dis-cuss recent insights into how the immune system exerts “inside-out ”control over microbiota local-ization and community composition (see Fig.1).Stratification and compartmentalization of the microbiota.The intestinal immune system faces unique challenges relative to other organs,as it must continuously confront an enormous micro-bial load.At the same time,it is necessary to avoid1The Howard Hughes Medical Institute and Department of Im-munology,The University of Texas Southwestern Medical Center at Dallas,Dallas,TX 75390,USA.2Howard Hughes Medical Institute and Molecular Pathogenesis Program,The Kimmel Center for Biology and Medicine of the Skirball Institute,New York University School of Medicine,New York,NY 10016,USA.3Maurice Müller Laboratories,University Clinic for Visceral Sur-gery and Medicine,University of Bern,Bern,Switzerland.*To whom correspondence should be addressed.E-mail:lora.hooper@8JUNE 2012VOL 336SCIENCE1268 o n M a y 20, 2015w w w .s c i e n c e m a g .o r g D o w n l o a d e d f r o mpathologies arising from innate immune signaling or from microbiota alterations that disturb essential metabolic functions.An important function of the intestinal immune system is to control the expo-sure of bacteria to host tissues,thereby lessening the potential for pathologic outcomes.This oc-curs at two distinct levels:first,by minimizing direct contact between intestinal bacteria and the epithelial cell surface(stratification)and,second, by confining penetrant bacteria to intestinal sites and limiting their exposure to the systemic im-mune compartment(compartmentalization).Several immune effectors function together to stratify luminal microbes and to minimize bacterial-epithelial contact.Intestinal goblet cells secrete mucin glycoproteins that assemble into a~150-m m-thick viscous coating at the intestinal epithelial cell surface.In the colon,there are two structurally distinct mucus layers.Although the outer mucus layer contains large numbers of bacteria,the inner mucus layer is resistant to bacterial penetration (16).In contrast,the small intestine lacks clearly distinct inner and outer mucus layers(17).Here, compartmentalization depends in part on antibac-terial proteins that are secreted by the intestinal epithelium.RegIII g is an antibacterial lectin that is expressed in epithelial cells under the control of Toll-like receptors(TLRs)(18–20).RegIII g limits bacterial penetration of the small intestinal mucus layer,thus restricting the number of bacteria that contact the epithelial surface(5).Stratification of intestinal bacteria on the luminal side of the epithelial barrier also depends on secreted immunoglobulin A(IgA).IgA spe-cific for intestinal bacteria is produced with the help of intestinal dendritic cells that sample the small numbers of bacteria that penetrate the over-lying epithelium.These bacteria-laden dendritic cells interact with B and T cells in the Peyer’s patches,inducing B cells to produce IgA directed against intestinal bacteria(21).IgA+B cells home to the intestinal lamina propria and secrete IgA that is transcytosed across the epithelium and deposited on the apical surface.The transcytosed IgAs bind to luminal bacteria,preventing micro-bial translocation across the epithelial barrier(22).Mucosal compartmentalization functions to minimize exposure of resident bacteria to the sys-temic immune system(Fig.1B).Although bacteria are largely confined to the luminal side of the epithelial barrier,the sheer number of intestinal bacteria makes an occasional breach inevita-ble.Typically,commensal microorganisms that penetrate the intestinal epithelial cell barrier are phagocytosed and eliminated by lamina propria macrophages(23).However,the intestinal im-mune system samples some of the penetrant bac-teria,engendering specific immune responses that are distributed along the length of the intes-tine(21).Bacteria that penetrate the intestinal barrier are engulfed by dendritic cells(DCs)re-siding in the lamina propria and are carried alive to the mesenteric lymph nodes.However,these bacteria do not penetrate to systemic secondarylymphoid tissues.Rather,the commensal-bearingDCs induce protective secretory IgAs(21),whichare distributed throughout all mucosal surfacesby recirculation of activated B and T cells.Thus,distinctive anatomical adaptations in the mucosalimmune system allow immune responses directedagainst commensals to be distributed widely whilestill being confined to mucosal tissues.Other immune cell populations also promotethe containment of commensal bacteria to in-testinal sites.Innate lymphoid cells reside in thelamina propria and have effector cytokine pro-files resembling those of T helper(T H)cells(24).Innate lymphoid cells that produce interleukin(IL)–22are essential for containment of lymphoid-resident bacteria to the intestine,thus preventingtheir spread to systemic sites(25).The compartmentalization of mucosal andsystemic immune priming can be severely per-turbed in immune-deficient mice.For example,mice engineered to lack IgA show priming ofserum IgG responses against commensals,indi-cating that these bacteria have been exposed tothe systemic immune system(22).A similar out-come is observed when innate immune sensingisFig.1.Looking inside-out:immune system control of the microbiota.Several immune effectors function together to stratify luminal microbes and to minimize bacterial-epithelial contact.This includes the mucus layer,epithelial antibacterial proteins,and IgA secreted by lamina propria plasma partmen-talization is accomplished by unique anatomic adaptations that limit commensal bacterial exposure to the immune system.Some microbes are sampled by intestinal DCs.The loaded DCs traffic to the mesenteric lymph nodes through the intestinal lymphatics but do not penetrate further into the body.This compartmentalizes live bacteria and induction of immune responses to the mucosal immune system. There is recirculation of induced B cells and some T cell subsets through the lymphatics and the bloodstream to home back to mucosal sites,where B cells differentiate into IgA-secreting plasma cells. SCIENCE VOL3368JUNE20121269SPECIAL SECTIONThe Gut Microbiotadefective.Mice lacking MyD88or TRIF signal-ing adaptors for TLR-mediated sensing of bacteria also produce serum IgG responses against com-mensals(26).This probably results from the fact that in these settings,large numbers of commensals cross the epithelial barrier and phagocytic cells are less able to eliminate the penetrant organisms.Immune system control of microbiota com-position.The development of high-throughput sequencing technologies for microbiota analysis has provided insight into the many factors that determine microbiota composition.For example nutrients,whether derived from the host diet (27)or from endogenous host sources(28),are critically important in shaping the structure of host-associated microbial communities.Recent evidence suggests that the immune system is also likely to be an important contributor to“inside-out”host control over microbiota composition.Certain secreted antibacterial proteins produced by epithelial cells can shape the composition of in-testinal microbial communities.a-defensins are small(2to3kD)antibacterial peptides secreted by Paneth cells of the small intestinal epithelium.Anal-ysis of the microbiota in mice that were either de-ficient in functional a-defensins or that overexpressed human a-defensin-5showed that although there was no impact on total numbers of colonizing bacte-ria,there were substantial a-defensin–dependent changes in community composition,with reciprocal differences observed in the two mouse strains(29).An interesting question is how far secreted in-nate immune effectors“reach”into the luminal microbial consortia.For example,the impact of hu-man a-defensin-5on luminal community composi-tion contrasts with the antibacterial lectin RegIII g, which limits penetration of bacteria to the epithelial surface but does not alter luminal communities(5). This suggests that some antimicrobial proteins,such as a-defensins,reach into the lumen to shape overall community composition,whereas others,such as RegIII g,have restricted effects on surface-associated bacteria and thus control microbiota location relative to host surface tissues.Questions remain as to ex-actly how a-defensin-5controls luminal community composition,however.In one scenario,these small antimicrobial peptides diffuse through the mucus layer and directly act on bacteria that inhabit the lu-men.Another possibility is that a-defensin-5exerts its antibacterial activity on bacteria that are trapped in the outer reaches of the mucus layer,with those bac-teria acting as reservoirs that seed luminal commu-nities and thus dictate their composition.Answering these questions will require improved tools for fine-mapping microbiota composition and consortia from the surface of the intestine to the interior of the lumen.The impact of the immune system on micro-biota composition is also suggested by several im-mune deficiencies that alter microbial communities in ways that predispose to disease.For example, Garrett et al.studied mice that lack the transcription factor T-bet(encoded by Tbx21),which governs inflammatory responses in cells of both the innate and the adaptive immune system(30).WhenTbx21–/–mice were crossed onto Rag2–/–mice,which lack adaptive immunity,the Tbx21–/–/Rag2–/–progeny developed ulcerative colitis in a microbiota-dependent manner(30).Remarkably,this colitisphenotype was transmissible to wild-type mice byadoptive transfer of the Tbx21–/–/Rag2–/–micro-biota.This demonstrated that altered microbiotawere sufficient to induce disease and could thus beconsidered“dysbiotic.”Similarly,mice lacking thebacterial flagellin receptor TLR5exhibit a syn-drome encompassing insulin resistance,hyper-lipidemia,and increased fat deposition associatedwith alterations in microbiota composition(31).These metabolic changes are transferable to wild-type mice that acquire the Tlr5–/–gut microbiota.A third example of immune-driven dysbiosis isseen in mice deficient for epithelial cell expres-sion of the inflammasome component NLRP6.These mice develop an altered microbiota withincreased abundance of members of the Bacte-roidetes phylum associated with increased intes-tinal inflammatory cell recruitment and susceptibilityto chemically induced colitis.Again,there is evi-dence that dysbiosis alone is sufficient to drive theintestinal inflammation,because conventionallyraised wild-type mice that acquire the dysbioticmicrobiota show similar immunopathology(32).Together,these findings suggest that the im-mune system affords mammalian hosts some con-trol over the composition of their resident microbialcommunities.It is also clear that these commu-nities can be perturbed by defects in the host im-mune system.This leads to the idea of the immunesystem as a form of ecosystem management thatexerts critical control over microbiota compo-sition,diversity,and location[see Costello et al.(33)].However,a number of questions remain.First,although it is apparent that the immune sys-tem shapes community composition at the specieslevel,it is not yet clear whether the immune sys-tem shapes the genetics and physiology of indi-vidual microbial species.Second,how much doesthe immune system combine with gastric acid andintestinal motility to control the longitudinal dis-tribution of microbial species in the gastrointes-tinal tract?Finally,it will be important to determinethe extent to which the immune system also con-trols microbial community composition and loca-tion in other organ systems,such as the respiratorytract,urogenital tract,and skin.Looking Outside-In:How MicrobiotaShape ImmunityThe earliest comparisons of germ-free and colonizedmice revealed a profound effect of microbial colo-nization on the formation of lymphoid tissues andsubsequent immune system development.It wasthus quickly apparent that the microbiota influ-ence the immune system from“outside-in.”Recentstudies have greatly amplified this understandingand have revealed some of the cellular and mo-lecular mediators of these interactions(see Fig.2).The impact of the microbiota on lymphoidstructure development and epithelial function.The tissues of the gastrointestinal tract are rich inmyeloid and lymphoid cells,many of whichreside in organized lymphoid tissues.It has longbeen appreciated that the gut microbiota have acritical role in the development of organized lym-phoid structures and in the function of immunesystem cells.For example,isolated lymphoid fol-licles in the small intestine do not develop ingerm-free mice,and such mice are also deficientin secretory IgA and CD8ab intraepithelial lym-phocytes.The specific microbial molecules en-dowed with this inductive function have not yetbeen described,however.Sensing of commensal microbiota through theTLR-MyD88signaling pathway triggers severalresponses that are critical for maintaining host-microbial homeostasis.The microbiota inducerepair of damaged intestinal epithelium through aMyD88-dependent process that can be rescued inmicrobe-depleted animals by gavage with bacteriallipopolysaccharide(LPS).The innate signals,con-veyed largely through myeloid cells,are required toenhance epithelial cell proliferation(34,35).Asdiscussed above,MyD88-dependent bacterial sig-nals are also required for the induction of epithelialantimicrobial proteins such as RegIII g(5,19).Thisexpression can be induced by LPS(19,20)or flagel-lin(36).The flagellin signals are relayed throughTLR5expressed by CD103+CD11b+dendritic cellsin the lamina propria,stimulating production of IL-23that,in turn,promotes the expression of IL-22by innate lymphoid cells(37).IL-22then stimu-lates production of RegIII g,which is also secretedupon direct activation of MyD88in epithelialcells(5,20).This is one clear example of theimportance of commensals in the induction of hostinnate responses,but it likely represents a tinyfraction of the multitude of effects of microbiota onthe host immune system.Microbiota shaping of T cell subsets.It hasrecently become evident that individual commensalspecies influence the makeup of lamina propria Tlymphocyte subsets that have distinct effector func-tions.Homeostasis in the gut mucosa is maintainedby a system of checks and balances between poten-tially proinflammatory cells,which include T H1cellsthat produce interferon-g;T H17cells that produceIL-17a,IL-17f,and IL-22;diverse innate lymphoidcells with cytokine effector features resemblingT H2and T H17cells;and anti-inflammatory Foxp3+regulatory T cells(T regs).Colonization of mice withsegmented filamentous bacteria(SFB)results inaccumulation of T H17cells and,to a lesser extent,inan increase in T H1cells(38,39).SFB appear able topenetrate the mucus layer overlying the intestinalepithelial cells in the terminal ileum,and they in-teract closely with the epithelial cells,inducing hostcell actin polymerization at the site of interactionand,presumably,signaling events that result in aT H17polarizing environment within the laminapropria.There is little known about host cell8JUNE2012VOL336SCIENCE 1270signaling pathways initiated by SFB.It is possible that SFB influence epithelial gene expression,re-sulting,for example,in expression of antimicro-bial proteins such as RegIII g and of molecules that participate in T H 17cell polarization.SFB may also act directly on cells of the immune sys-tem,either through interactions with myeloid cells that extend processes through the epithelium to the mucus layer or by production of metabolites that act on various receptors expressed by host cells.Other bacteria have been shown to enhance the anti-inflammatory branches of the adaptive immune system by directing the differentiation of T regs or by inducing IL-10expression.For example,coloniza-tion of gnotobiotic mice with a complex cocktail of 46mouse Clostridial strains,originally isolated from mouse feces and belonging mainly to cluster IVand XIV a of the Clostridium genus,results in the expansion of lamina propria and systemic T regs .These have a phenotype characteristic of T regs in-duced in the periphery in response to transforming growth factor (TGF)–b and retinoic acid [in contrast to thymic-derived natural (n)T regs (40)],and manyof these inducible T regs (iT regs )express IL-10.The exact Clostridial strains within the complex exper-imental mixture that drive this regulatory response remain to be defined.Furthermore,polysaccharide A (PSA)of Bacteroides fragilis induces an IL-10response in intestinal T cells,which prevents the expansion of T H 17cells and potential damage to the mucosal barrier (41).In contrast,mutant B.fragilis lacking PSA has a proinflammatory profile and fails to induce IL-10.Production of PSA by B.fragilis has been proposed to be instrumental for the bac-terium ’s success as a commensal.Within the intestine,the balance of effector lym-phoid cells and T reg cells can have a profound in-fluence on how the mucosa responds to stresses that elicit damage.The relative roles of commensal-regulated Tcells differ according to the models used to study inflammation.For example,in mice sub-jected to chemical or pathogen-induced damage to the mucosa,T H 17cells have a beneficial effect that promotes healing.In contrast,T H 1and T H 17cells,as well as IL-23–dependent innate lymphoid cells,promote colitis in models in which T reg cells aredepleted.It is likely that inflammatory bowel dis-eases in humans can be similarly triggered by commensal-influenced imbalance of lymphoid cell subsets.This is supported by numerous observations,including the strong linkage of IL23R polymor-phisms with Crohn ’s disease,a serious condition with relapsing intestinal inflammation and a risk of malignancy,and the severe enterocolitis associated with IL10and IL10R mutations (42,43).Microbiota effects on systemic immunity.The influence of commensal bacteria on the balance of T cell subsets is now known to extend well beyond the intestinal lamina propria.Homeostatic T cell proliferation itself is driven by the microbiota or their penetrant molecules (44).Systemic auto-immune diseases have long been suggested to have links to infections,but firm evidence for causality has been lacking.Recent studies in animal models,however,have reinforced the notion that commen-sal microbiota contribute to systemic autoimmune and allergic diseases at sites distal to the intestinal mucosa.Several mouse models for autoimmunity are dependent on colonization status.Thus,germ-free mice have marked attenuation of disease in models of arthritis and experimental autoimmune encephalomyelitis (EAE),as well as in various colitis models.In models of T H 17cell –dependent arthritis and EAE,monoassociation with SFB is sufficient to induce disease (42,45,46).In all of these models,induction of T H 17cells in the in-testine has a profound influence on systemic dis-ease.Exacerbation of arthritis and EAE is likely the consequence of an increase in the number of arthritogenic or encephalitogenic T H 17cells that traffic out of the lamina propria.The antigen spec-ificity of such cells remains to be examined.Induction of iT regs by the cluster IV and XIV a Clostridia also has a systemic effect on inflamma-tory processes.Colonization of germ-free mice with these bacteria not only results in attenuated disease after chemical damage of the gut epithelium but also reduces the serum IgE response after immuni-zation with antigen under conditions that favor a T H 2response (40).As with pathogenic T H 17cells,the antigen specificity of the commensal-induced iT regs that execute systemic anti-inflammatory func-tions is not yet known,although at least some of the T regs in the gut have Tcell receptors with specificity for distinct commensal bacteria (47).Finally,B.fragilis PSA affects the develop-ment of systemic T cell responses.Colonization of germ-free mice with PSA-producing B.fragilis results in higher numbers of circulating CD4+T cells compared to mice colonized with B.fragilis lacking PSA.PSA-producing B.fragilis also elicits higher T H 1cell frequencies in the circulation (48).Together,these findings show that commen-sal bacteria have a general impact on immunity that reaches well beyond mucosal tissues.Microbiota influences on invariant Tcells and innate lymphoid cells.A recent study extends the role of microbiota to the control of the function invariant natural killer T cells (iNKT cells),whichFig.2.Looking outside-in:how microbiota shape host immunity.Some of the many ways that intestinal microbiota shape host immunity are depicted.These include microbiota effects on mucosal as well as systemic immunity.ILFs,isolated lymphoid follicles.SCIENCEVOL 3368JUNE 20121271SPECIAL SECTION。

微生物组学英语Microbiome: The Unseen World Within UsThe human body is a complex and intricate ecosystem, teeming with trillions of microorganisms that play a vital role in our overall health and well-being. This vast and diverse community of microbes, collectively known as the microbiome, has been the subject of extensive research in recent years, as scientists strive to unravel the mysteries of this unseen world within us.The microbiome is a term that encompasses the entirety of the microbial communities that reside in various parts of the human body, including the gut, skin, oral cavity, and even the respiratory system. These microorganisms, which include bacteria, viruses, fungi, and archaea, have evolved alongside humans over millions of years, forming a symbiotic relationship that is essential for our survival.One of the most well-studied aspects of the microbiome is its role in the gut. The human gut is home to a vast and diverse array of microbes, with an estimated 100 trillion bacteria residing in thedigestive tract. These gut microbes play a crucial role in digesting and metabolizing the food we consume, extracting essential nutrients and energy that our bodies can then utilize.Beyond their role in digestion, gut microbes also have a profound impact on our immune system. They help to train and regulate the immune cells, ensuring that they are able to effectively fight off harmful pathogens while also maintaining a delicate balance that prevents autoimmune disorders. This intricate relationship between the gut microbiome and the immune system has been the focus of numerous studies, with researchers exploring the potential of probiotics and other microbial-based therapies to treat a wide range of health conditions.The skin microbiome is another area of intense research. The skin is the largest organ in the human body and is home to a diverse array of microbes, including bacteria, fungi, and viruses. These skin-dwelling microbes play a crucial role in maintaining the skin's barrier function, protecting us from harmful environmental factors and pathogens. They also contribute to the skin's overall health, helping to regulate inflammation, prevent the overgrowth of harmful microbes, and even influence the appearance of the skin.The oral microbiome is another important aspect of the human microbiome. The mouth is a complex ecosystem, with a diverse arrayof microbes that play a critical role in maintaining oral health. These microbes help to break down food, regulate pH levels, and prevent the overgrowth of harmful bacteria that can lead to dental problems such as cavities and gum disease.In addition to these well-known aspects of the microbiome, there is growing evidence that the microbial communities in other parts of the body, such as the respiratory system and the urogenital tract, also play important roles in human health and disease.One of the most exciting areas of microbiome research is the potential for microbiome-based therapies to treat a wide range of health conditions. By understanding the composition and function of the microbiome, researchers are exploring ways to manipulate it to improve human health. This includes the use of probiotics, which are live microorganisms that can be consumed to help restore the balance of the microbiome, as well as the development of personalized therapies that target specific microbial imbalances.Another promising area of research is the role of the microbiome in mental health. Emerging evidence suggests that the gut microbiome may play a significant role in the development and maintenance of mental health disorders, such as depression and anxiety. This has led to the concept of the "gut-brain axis," which posits that the bidirectional communication between the gut and the brain can havea profound impact on our emotional and cognitive well-being.As our understanding of the microbiome continues to grow, it is clear that this unseen world within us is a critical component of human health and well-being. By unraveling the complexities of the microbiome, researchers and clinicians are paving the way for new and innovative approaches to disease prevention and treatment. From improving gut health to enhancing mental well-being, the potential of the microbiome is limitless, and the future of personalized, microbiome-based medicine is rapidly taking shape.。

闫新璐，刘倩倩，侯庆安，等. 微藻的功能特性及其在食品中的应用研究进展[J]. 食品工业科技，2024，45（2）：392−400. doi:10.13386/j.issn1002-0306.2023030254YAN Xinlu, LIU Qianqian, HOU Qing'an, et al. Research Progress on the Functional Characteristics of Microalgae and Their Application in Food[J]. Science and Technology of Food Industry, 2024, 45(2): 392−400. (in Chinese with English abstract). doi:10.13386/j.issn1002-0306.2023030254· 专题综述 ·微藻的功能特性及其在食品中的应用研究进展闫新璐，刘倩倩，侯庆安，孙承锋，喻倩倩*，温荣欣*（烟台大学生命科学学院，山东烟台 264005）摘　要：随着全球人口的增长，粮食生产逐渐呈现供不应求的局面，与此同时，日趋下降的环境质量也在迫使传统的食品供应体系发生改变。

微藻中含有丰富的宏量营养素和生物活性物质，不仅可以为人体提供营养，而且具有抗氧化、抗菌、免疫调节等功能，作为潜在的食品原料新来源，受到越来越多的关注。

本文综述了微藻的特征及可食用种类，详细介绍了微藻蛋白、多不饱和脂肪酸、多糖和其它生物活性物质的生理活性功能，深入讨论了其在替代肉类蛋白、补偿减盐食品风味、抑菌防腐和功能性食品开发方面的应用潜力及前景，总结了其在食品应用中现存的问题与挑战，展望未来的发展方向，旨在为微藻类食品的开发和食品新资源的探索提供理论参考。

关键词：微藻，营养成分，生物活性，功能特性，未来食品本文网刊:中图分类号：TS202.1 文献标识码：A 文章编号：1002−0306（2024）02−0392−09DOI: 10.13386/j.issn1002-0306.2023030254Research Progress on the Functional Characteristics of Microalgaeand Their Application in FoodYAN Xinlu ，LIU Qianqian ，HOU Qing'an ，SUN Chengfeng ，YU Qianqian *，WEN Rongxin *（College of Life Science, Yantai University, Yantai 264005, China ）Abstract ：As the global population grows, food production is falling short of demand, while environmental degradation is forcing changes in traditional food supply systems. Microalgae are rich in macronutrients and bioactive substances, which can provide nutrients for the human body and have antioxidant, antibacterial, immune regulation, and other functions. As a potential new food source, microalgae are gaining increasing interest. This paper reviews the characteristics and extant edible microalgal species, as well as the physiological functions of microalgal proteins, polyunsaturated fatty acids,polysaccharides, and bioactive substances. The application potential and prospect of microalgae in replacing meat proteins,compensating for salt reduction food flavor, bacteriostasis and preservatives, and the development of functional foods are discussed in detail, as are the existing challenges in their application as food. The objective is to provide theoretical references for the development of microalgae food and the exploration of new food resources.Key words ：microalgae ；nutritional ingredient ；biological activity ；functional properties ；future food微藻是一类形态微小、结构简单的水生生物，在地球生存35亿年之久。

Microwave specific effects in organic synthesis:A proposed model fromthe solvent-free synthesis of monoglycerylcetyldimethylammonium chlorideSatoshi Horikoshi a,*,Motoki Fukui b ,Koji Tsuchiya c ,Masahiko Abe b ,Nick Serpone d,**aResearch Institute for Science and Technology,Tokyo University of Science,2641Yamazaki,Noda,Chiba 278-8510,JapanbDepartment of Pure and Applied Chemistry,Faculty of Science and Technology,Tokyo University of Science,2641Yamazaki,Noda,Chiba 278-8510,Japan cDepartment of Applied Chemistry,Faculty of Science Division I,Tokyo University of Science,1–3Kagurazaka,Shinjuku-ku,Tokyo 162-8601,Japan dGruppo Fotochimico,Dipartimento di Chimica Organica,Universita di Pavia,Via Taramelli 10,Pavia 27100,Italya r t i c l e i n f o Article history:Received 17March 2010In final form 6April 2010Available online 9April 2010a b s t r a c tMonoglycerylcetyldimethylammonium chloride was synthesized from 3-chloro-1,2-propanediol (CP)and N ,N -dimethylhexadecylamine (DMHA)in 2-propanol in solvent-free conditions to exam-ine microwave specific effects.None were evident in homogeneous 2-propanol media under temperature conditions identical to conventional heating.In contrast,heterogeneous solvent-free conditions brought out specific microwave effects as evidenced by variant product yields (130°C;30min):62%by micro-wave and 47%by conventional heating.This variance is attributed to thermal conduction and localized hot spots formed under microwave irradiation.The model proposed for the solvent-free synthesis consid-ers hydrophilic 3-chloro-1,2-propanediol molecules form H-bonded domains (size,2–20l m)preferen-tially heated by the microwaves and dispersed in a sea of hydrophobic N ,N -dimethylhexadecylamine molecules.Ó2010Elsevier B.V.All rights reserved.1.IntroductionMicrowave heating has become a widely employed tool in or-ganic synthesis since it improves product yields and enhances the rate of reactions,as well as being a safe and convenient method for heating reaction mixtures to elevated temperatures [1].In this context,various discussions continue to appear in the literature about the elusive specific microwave (non-caloric)effect(s)in or-ganic synthesis besides the utilization of microwaves as a simple heat source [2,3].In many examples,the specific microwave effect claimed in the past could easily be attributed to thermal (caloric)effects.Microwave heating can be very rapid,producing heat pro-files that are not easily accessible by other heating techniques such as oil-bath heating.This notwithstanding,however,the non-caloric effect of the microwaves may have some exceptional impact on syntheses.In an earlier report of organic syntheses that involved reactions of radicals [4,5],the reactants were activated by micro-wave irradiation while maintaining the temperature at ambient conditions.This led to relatively high product yields and to a signif-icant minimization of generated side products (impurities),an important attractive feature of this methodology.In those experi-ments,whether the effect was a non-thermal effect of the micro-waves or a thermal effect at the microscopic level was not discussed.To date,evidence of a mechanism of the non-thermal ef-fect(s)often eludes experimentation as it requires precise temper-ature measurements whenever microwave dielectric heating is compared to conventional heating [6,7].In this regard,Stuerga and Gaillard [8,9]have used a thermodynamic model to describe the specific behavior of the microwaves’electromagnetic energy in chemical reactions.In microwave-assisted reactions,both the heating and the thermal conduction mechanisms are different from those of conventional heating as described earlier in our syn-thesis of an ionic liquid [10].This short Letter reports an examination of the microwave spe-cific effect and proposes a model based on thermal conduction occurring at the microscopic level in the synthesis of the monog-lycerylcetyldimethylammonium chloride surfactant in homoge-neous 2-propanol media and under solvent-free heterogeneous conditions.2.Experimental setupMonoglycerylcetyldimethylammonium chloride (MGCA)was synthesized under reflux conditions with Tokyo Chemical Industry,Co.,Ltd.reagents 3-chloro-1,2-propanediol (CP;5.9g;0.053mol)and N ,N -dimethylhexadecylamine (DMHA;12.6g;0047mol)in 2-propanol (7.7mL)by microwave irradiation and by conventional heating at ca.95°C (reaction (1))in a reactor setup described ear-lier [11].0009-2614/$-see front matter Ó2010Elsevier B.V.All rights reserved.doi:10.1016/j.cplett.2010.04.011*Corresponding author.**Corresponding author.E-mail addresses:horikosi@rs.noda.tus.ac.jp (S.Horikoshi),nick.serpone@unipv.it (N.Serpone).Chemical Physics Letters 491(2010)244–247Contents lists available at ScienceDirectChemical Physics Lettersj o u r n a l h o m e p a g e :w w w.e l s e v i e r.c o m /l o c a t e /c p l e ttCl OHOHN C16H (CP)(DMHA)NHOOHC16H33Cl+(MGCA)OBð1ÞIn the former case,the three-neckflask(75mL)containing the sam-ple solution was positioned at the maximum of the microwaves’electricfield in the microwave waveguide(2.45GHz;WRJ-2)with the position adjusted with a three stub tuner and a short plunger; continuous microwave irradiation was provided by an Arios Inc.2.45GHz microwave generator(maximal power,200W).In con-ventional heating,an oil bath was used to carry out the synthesis for comparison with microwave heating under otherwise identical temperature conditions.The2-propanol solvent was subsequently removed by evaporation,followed by addition of n-butanol to theresidue.The resulting butanolic solution was poured into water sat-urated with NaCl in a separating funnel.After vigorous agitation the lower aqueous phase was separated from the upper organic phase, following which the n-butanol solvent was removed by distillation. No glycerin was detected in the upper phase by TLC techniques.The residue obtained after distillation was recrystallized3times from acetone–ethanol mixtures to give a white powder of high purity [12]as evidenced by300-MHz1H NMR spectrometry(CDCl3):d (ppm)=0.86(3H,t,C H3–(CH2)14–),1.25(28H,m,–(C H2)14–),1.78 (2H,d,–(CH2)14–C H2–N+),3.33(6H,t,–N+(C H3)2–CH2–),3.44–3.82 (4H,m,–C H2–CH(OH)–C H2–), 4.42(1H,b,–CH2–C H(OH)–CH2–), 4.83(1H,d,–CH2–CH(O H)–CH2–),5.78(1H,t,–CH2–O H).FAB-mass spectra showed m/z=344.35.Elemental analysis of the product gave results within experimental error(<0.4%)of theoretical expec-tations[12].The rate of increase of temperature in the oil-bath heating method was maintained at levels identical to those used for the microwave heating method,so as to avoid differences in synthetic yield that may be caused by differences in temperature between microwave and oil-bath heating.Temperatures were measured precisely using a K-type thermocouple prior to which we verified with an opticalfiber thermometer that the thermocouple was not affected by the microwaves.In another exploratory experi-ment,continuous15-W(applied power)microwave irradiation of the reactants showed a rate of temperature rise of0.15°C sÀ1for the solution,whereas for the oil-bath heating method the rate was0.08°C sÀ1for a power consumption of400W.In this manner, the oil-bath heating rate could not be matched to the microwave heating rate.To overcome this mismatch,the reactor wasfirst soaked in the pre-heated oil bath and the time profile of the rate of temperature rise determined,following which the time profile of the rate of temperature rise of the reactants under microwave irradiation was matched to that of the oil-bath heating by adjust-ing the applied power of the microwaves.3.Results and discussion3.1.Synthesis of the MGCA surfactant in2-propanol mediaThe time profiles of the yields of MGCA obtained in2-propanol media using microwave heating(MW method)and oil-bath heat-ing(OB method)are displayed in Fig.1.Microwave heating in or-ganic synthesis is known to produce products in high yields. Differences in the time profiles of product yields in the synthesis of MGCA under matched temperature conditions were negligible within experimental error.That is,the microwave thermal(caloric) effect(s)followed closely conventional heating to yield nearly80% product after ca.200min.Thus,in this instance,microwaves were a mere source of heat[13],and no microwave specific(non-caloric) effect(s)was evident in the MGCA synthesis taking place in the homogeneous solvent media.Related to this,special(non-caloric) effects of the microwaves in several organic syntheses reported earlier were mostly due to inconsistencies in the temperature mea-surements–see the many examples reported by Stuerga and Gail-lard[8].Accordingly,in the present instance we chose to examine the mechanistic difference(s)between microwave and oil-bath heating from the variance of dielectric factors of the substrates since the heating efficiency of the reaction is controlled by the dielectric factors of the materials contained in the reactor.In the oil-bath heating method,the oil heated the sample initially by thermal conduction through the reactor walls,after which the heat on the inner walls radiated throughout the solution by convection and vigorous mechanical agitation.By contrast,microwave radia-tion penetrated the reactor walls and heated the dielectric substances directly by the dielectric heating mechanism[14,15]. The dielectric constants(e0)and the dielectric loss factors(e00)for pure CP,DMHA,and2-propanol solution were analyzed at the 2.45GHz microwave frequency using an Agilent Technologies HP-85070B Network Analyzer;they are summarized in Table1. The penetration depths of the microwaves into each solution were estimated as suggested by Bogdal[16].The dielectric loss data infer that the CP substrate in the react-ing solution is heated selectively because it displays the highest dielectric loss factor with2-propanol being heated next by dielec-tric heating and by thermal conduction from the heated CP stly,DMHA is heated by thermal conduction by the heat radiated by CP and the2-propanol solvent medium.Note that DMHA occupies a larger volume than CP in the reacting solution. Notwithstanding the differences in the dielectric factors of Table 1,no differences were seen in the product yields(see Fig.1) whether by microwave dielectric heating or by oil-bath heating. Evidently,the characteristics of the microwaves for each molecule did not impact on the reaction since the CP and DMHA substrates dissolved completely in the2-propanol solvent.Sato and Tanaka[17]reported recently that conventional heat-ing of a solid is uneven at the macroscopic level,but is uniform when seen at the microscopic level.By contrast,microwave heat-ing of a solid is uniform at the macroscopic level and uneven atTable1Dielectric constants(e0)and dielectric loss factors(e00)of3-chloro-1,2-propanediol (CP),N,N-dimethylhexadecylamine(DMHA)and2-propanol at a microwave fre-quency of2.45GHz.Dielectricconstant(e0)Dielectric lossfactor(e00)Dielectric losstangent(tan d)Penetrationdepth(cm) CP 6.469 3.6610.566 1.35DMHA 2.4670.1800.07316.92-Propanol 4.586 3.2720.713 1.27S.Horikoshi et al./Chemical Physics Letters491(2010)244–247245the microscopic level.Similar behaviors of heating substrates are expected in solution.In this regard,microwave heating can,in principle,induce localized hot spots that can lead to localized reac-tion rate enhancements[18],and thus to uneven heating at the microscopic level as predicted from the dielectric factors.However, no microwave specific effect(s)was apparent even though the reaction solution contained substrates of different dielectric char-acteristics when heated in homogeneous2-propanol solvent by microwave dielectric heating.It is likely that the2-propanol sol-vent masked whatever specific effect(s)of the microwaves may have been operating.3.2.Synthesis of MGCA under solvent-free conditionsNext we synthesized the MGCA surfactant in a solvent-free het-erogeneous system using the CP and DMHA substrates without2-propanol solvent to avoid its influence in reaction(1).The solution of CP and DMHA was physically mixed by magnetic agitation and appeared as a homogeneous phase when viewed macroscopically. The product yields of MGCA under different conditions,listed in Table2,were otherwise identical at reaction temperatures below 100°C whether by microwave or oil-bath heating methods(reac-tion temperatures,94–96°C;see entries1and2).The boiling points of CP and DMHA are126°C and148°C,respectively[19]. To the extent that the3-chloro-1,2-propanediol(CP)is highly hydrophilic compared to hydrophobic dimethylhexadecylamine (DMHA)it forms self H-bonded aggregates(domains)dispersed in a hydrophobic sea of DMHA molecules,which is reminiscent of an oil-in-water structured emulsion,at least microscopically.A microscopic analysis showed a size distribution of CP domains in the2–20l m range(average size ca.15l m).Viscosity measure-ments showed the CP is16-fold more viscous(0.16Pa s;160cP)than DMHA(0.010Pa s;10cP)at ambient temperature.The viscos-ity of the CP/DMHA mixture decreased with rise in temperature, particularly above100°C.As such,at130°C the yields of MGCA were62%(microwave heating)and47%(oil-bath heating;see en-tries3and4)for the less viscous and uniformly mixed solution after a30-min heating period.The dielectrically heated molecular CP collectives are important in delineating microwave effects.In this regard,note the dramatic shortening of the reaction time(to 6min)displayed by microwave superheating the solution to 185°C yielding48%of the MGCA surfactant(see entry5of Table 2).By contrast,it was not possible to synthesize the surfactant by the oil-bath heating method at the latter temperature.The thermal conduction model portraying the initial stage of the synthesis of the MGCA surfactant at130°C in the absence of the2-propanol solvent is illustrated in Scheme1a for microwave heating and in Scheme1b for oil-bath heating.Macroscopically, the CP and DMHA mixed substrates formed a homogeneous solu-tion upon vigorous magnetic stirring.At the microscopic level, however,it is relevant to emphasize that the solution is heteroge-neous with CP domains(oil drop analogs)dispersed in the DMHA sea.The penetration depths of the microwaves into the CP domains is12.5-fold greater than in DMHA(see Table1),and the dielectric loss factors indicate that the CP aggregates are preferentially heated by the microwaves.Thus,the temperature of the CP do-mains is expected to be greater than the temperature of the DMHA sea.The heat radiated by the CP domains subsequently permeates to the DMHA as a result of thermal gradients established by micro-wave dielectric heating in accordance with the second law of ther-modynamics.After microwave irradiation the distribution of the CP domains in the sea of DMHA molecules tends to become smaller with rise in temperature.The synthesis of the surfactant takes place at the interfaces (reaction sites)between the different CP domains and the DMHA. These interfacial sites are also the sites of heat exchange.A greater number of reaction sites is anticipated under microwave heating (Scheme1a)than is the case in the oil-bath heating model(Scheme 1b)where the molecules are heated non-selectively by the inner reactor walls.In the latter case,thermal conduction throughout the reaction solution depends not so much on the thermal gradi-ents as it does from the vigorous stirring of the solution.The peculiarity of microwave heating,which depends on the dielectric loss tangent,tan d,of each reacting substrate(Table1), can lead to product distributions different from those obtained un-der conventional oil-bath heating(the tan d of CP is7.8-fold greater than that of DMHA).This effect can have a decisive role in hetero-Table2Product yields in the synthesis of monoglycerylcetyldimethylammonium chloride (MGCA)under solvent-free conditions with microwave dielectric heating(MW)and oil-bath heating(OB).Entry Heatingmethod Temperature(°C)Reaction time(min)Product yield(%)1MW9630312OB9430303MW13030624OB13030475MW185648246S.Horikoshi et al./Chemical Physics Letters491(2010)244–247geneous reactions if the domain sizes accorded.Based on the above discussion,the microwave specific effect(s)in a uniformly mixed, albeit heterogeneous system of substrates having greatly different dielectric factors may be operating owing to(i)microscopic tem-perature hot spots produced by penetration of microwaves into the various CP domains,and(ii)to the reaction occurring at the interfacial sites along with heat exchange at these same sites from the high-temperature CP domains to the lower temperature DMHA sea.We saw earlier that the advantage of microwave dielectric heating disappeared when the reaction took place in the2-propa-nol solvent media because the distributions of CP and DMHA do-mains were ill-defined at the molecular level and the reaction was no longer microscopically heterogeneous.Specific effects in organic chemistry have often been discussed on the basis of dielectric factors at the molecular level.The matched size domains may be necessary to make the microwave specific effect(s)obser-vable.Indeed,there may be cases where the influence of micro-waves on molecular domains can bring out specific microwave effects.Other factors can impart specific effects in microwave-assisted reactions.For instance,the wavelength of the2.45-GHz microwaves(k o=12.24cm)can change when the microwaves penetrate a material.It is given by the product of this wavelength (k o)and the velocity of propagation of the microwaves’electric and magneticfields(v)as given by Maxwell’s expression(Eq.(2)) [20]v¼1ffiffiffiffiffiffiffiffiffiffi’l opð2Þwhere e0is the dielectric constant(Table1)and l o is the magnetic permeability(l o%1).For the CP and DMHA substrates the wavelengths of the microwaves decrease to 4.8cm and7.8cm, respectively.This difference in the wavelengths of microwave prop-agation in materials can also lead to microwave specific effects.An examination of the optimal domain size in which the microwave specific effect(s)can be distinguished from thermal effects,perhaps unequivocally,is currently under experimentation.AcknowledgmentsFinancial support to S.H.from the Japan Society for the Promo-tion of Science(JSPS)through a Grant-in-aid for young scientists (No.B-21750210)is gratefully appreciated.One of us(N.S.)thanks Prof.Albini and his group at the Universita di Pavia,Italy,for their continued kind hospitality during the many semesters spent in their laboratory since2002.We are also grateful to the personnel of Hitachi Kyowa Engineering Co.Ltd.and Arios Inc.for technical assistance.References[1]A.Loupy(Ed.),Microwaves in Organic Synthesis,Wiley-VCH 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