REVIEW ARTICLE
published:27March2013
doi:10.3389/?mmu.2013.00076 Natural killer cell mediated antibody-dependent cellular cytotoxicity in tumor immunotherapy with therapeutic antibodies
Ursula J.E.Seidel,Patrick Schlegel and Peter Lang*
Department of General Paediatrics,Oncology/Haematology,University Children’s Hospital Tübingen,Tübingen,Germany
Edited by:
Hermann Einsele,University Hospital Würzburg,Germany
Reviewed by:
Rupali Das,Children’s Hospital of Philadelphia,USA
Stanislaw Stepkowski,University of Toledo College of Medicine,USA
*Correspondence:
Peter Lang,Department of General Paediatrics,Oncology/Haematology, University Children’s Hospital
Tübingen,Hoppe-Seyler-Str.1,72076 Tübingen,Germany.
e-mail:https://www.doczj.com/doc/1d10541630.html,ng@
med.uni-tuebingen.de In the last decade several therapeutic antibodies have been Federal Drug Administration (FDA)and European Medicines Agency(EMEA)approved.Although their mechanisms of action in vivo is not fully elucidated,antibody-dependent cellular cytotoxicity(ADCC)medi-ated by natural killer(NK)cells is presumed to be a key effector function.A substantial role of ADCC has been demonstrated in vitro and in mouse tumor models.However,a direct in vivo effect of ADCC in tumor reactivity in humans remains to be shown.Several studies revealed a predictive value of FcγRIIIa-V158F polymorphism in monoclonal anti-body treatment,indicating a potential effect of ADCC on outcome for certain indications. Furthermore,the use of therapeutic antibodies after allogeneic hematopoietic stem cell transplantation is an interesting option.Studying the role of the FcγRIIIa-V158F polymor-phism and the in?uence of Killer-cell Immunoglobuline-like Receptor(KIR)receptor ligand incompatibility on ADCC in this approach may contribute to future transplantation strate-gies.Despite the success of approved second-generation antibodies in the treatment of several malignancies,efforts are made to further augment ADCC in vivo by antibody engi-neering.Here,we review currently used therapeutic antibodies for which ADCC has been suggested as effector function.
Keywords:natural killer cells,ADCC,tumor immunotherapy,therapeutic antibodies,allogeneic stem cell transplan-tation
INTRODUCTION
Naturally cytotoxic cells against tumor cells were?rst described in humans and mice in the1970s of the last century(Rosenberg et al., 1972;Oldham and Herberman,1973;Herberman et al.,1975a,b; Kiessling et al.,1975a,b).Initially regarded as artifacts,these cells were recognized eventually as a novel lymphocyte population and named natural killer(NK)cells after their natural occurrence and spontaneous capacity to kill lymphomas and leukemic cells in non-immunized animals(Kiessling et al.,1975a,b).Nowadays,NK cells are recognized as a subset of cytotoxic innate lymphoid cells(ILCs) which are able to directly kill virus-infected cells and tumor cells and participate in shaping the adaptive immunity by secretion of cytokines(e.g.,IFN-γ)(Vivier et al.,2011).The role of NK cells in human cancer is highlighted by a study linking low peripheral blood NK cell activity with increased cancer risk(Imai et al.,2000). Furthermore,an association of NK cell in?ltration into the tumor site with better disease prognosis has been shown for several malig-nancies(Carrega et al.,2008;Halama et al.,2011;Platonova et al., 2011;Eckl et al.,2012).
Human NK cells are de?ned by the phenotype CD3?CD56+; additionally they are CD19and CD14negative.The only marker that is speci?c for NK cells is NKp46.NK cells comprise5–15% of all circulating lymphocytes(Lanier et al.,1986;Walzer et al., 2007).They are commonly divided into two major subpopula-tions,CD56dim CD16+and CD56bright CD16?,with each of those possessing distinct effector functions.The CD56dim CD16+subset comprises90%of all peripheral blood NK cells and mediates an early response via direct cellular cytotoxicity induced by perforin and granzyme,FasL,and TRAIL interactions as well as cytokine production(De Maria et al.,2011).One major characteristic of NK cells is their constant state of readiness to respond immedi-ately.In contrast to T cells,NK cells constitutively express perforin. This facilitates the instant polarized delivery of apoptosis-inducing granzymes after formation of a lytic synapse between the NK cell and a target cell(Shresta et al.,1995).The CD56bright CD16?subset mediates a late but sustained effector function via potent pro-in?ammatory cytokine and chemokine release of mainly IFN-γ,but is poorly cytotoxic(De Maria et al.,2011).NK cell activation and cytotoxicity is controlled by a complex balance between acti-vating receptors,inhibitory receptors and co-receptors(Lanier, 2003;Leung,2011).Positive and negative downstream signals of these receptors are integrated and decisive for NK cell activa-tion(Figure1).Hence,absence of inhibitory signals on target cells together with engagement of activating receptors as NKG2D, DNAM-1,and2B4as well as the natural cytotoxicity receptors (NCRs),including NKp46,NKp44,and NKp30mediate triggering of resting NK cells(Moretta et al.,2001;Bryceson and Long,2008; Lanier,2008).Whereas for NKG2D,DNAM-1,and2B4multiple ligands are known(Bottino et al.,2005),despite their involvement in tumor cell lysis the NCR ligands have remained rather elusive (Moretta et al.,2006).Nevertheless,NKp30has been shown to recognize a tumor cell ligand of the B7family,B7-H6(Brandt et al.,2009)and NKp44is suggested to recognize proliferating cell nuclear antigen(PCNA),which surprisingly triggers inhibition of
FIGURE1|Antibody-dependent cellular cytotoxicity in therapeutic antibody treatment.(A)Without antibody therapy,NK cells are tolerant to healthy cells and tumor cells,if the strength of activating signal they receive upon encountering activating ligands on these malignant cells does not overcome the inhibitory signaling delivered by inhibitory ligands as,e.g.,MHC class I molecules.(B)Upon treatment with tumor antigen-associated(TAA) specifc antibody,the activating stimulus from FcγRIIIa induced by antibodies cross-linking NK cells with TAA-expressing healthy and malignant cells overcomes inhibitory signals.This leads to the activation of NK cells and ADCC is mediated by releasing cytotoxic granules containing perforin and granzyme.
NK cells(Rosental et al.,2011).However,several of those receptors need to be triggered by target cells for activating downstream sig-nals to prevail over inhibitory signals and NK cells to be activated and to mediate target cell lysis(Moretta et al.,2001;Bryceson et al., 2006).
ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY
Most hematopoietic cells,except most T cell subsets,express Fcγreceptors(FcγRs)(Nimmerjahn and Ravetch,2008).There are three types of FcγRs which recognize the Fc part of IgG antibody subclasses with different af?nities.The activating FcγRI(CD64) binds to human IgG1and IgG3with high af?nity,is expressed on macrophages and neutrophils,and mediates phagocytosis of target cells.The FcγRII(CD32)class comprises activating low af?nity FcγRIIa(which binds human IgG1,IgG2,and IgG3)and inhibitory FcγRIIb(which recognizes human IgG1and IgG3with low af?nity)and may attenuate signaling from activating receptors as FcγRI if engaged in phagocytes.FcγRIIIb is a protein expressed by neutrophils and may play a role in neutrophil activation.Acti-vating low af?nity FcγRIIIa(type III receptor for IgG;CD16) mediates antibody-dependent cellular cytotoxicity(ADCC)and is highly expressed on the cytotoxic CD56dim CD16+NK cell subset as well as on other hematopoietic cells.Nevertheless,NK cells are thought to be the key mediators of ADCC,since only NK cells do not co-express the inhibitory FcγRIIb.In contrast, all other FcγR-expressing cells are tightly controlled by the bal-ance between activating and inhibitory FcγRs.Ef?cient FcγRIIIa signaling depends on high avidity for speci?c binding to anti-bodies which ensures that NK cells are activated when antibodies have bound to a multimeric or multivalent cognate antigen only (Banks et al.,2002).These antibodies of the subclasses IgG1and IgG3binding to FcγRIIIa induce a potent activating signal which overcomes inhibitory signals and results in both cytotoxicity and a cytokine response(Chan et al.,2012)(Figure1).Co-engagement of other activating receptors has a synergistic effect and may enhance NK cell activation(Bryceson et al.,2006).
Several mouse model studies postulated the impact of activat-ing FcγRs on anti-tumor effects in antibody therapy indicating that ADCC has a substantial effect on tumor rejection.A study using a xenograft breast carcinoma model has shown that an antibody engineered to prevent Fc binding to FcγRIIIa and spe-ci?c to Her2/neu[Human Epidermal Growth Factor Receptor (EGFR)2,CD340]which is overexpressed in certain aggressive types of breast cancer,was,in contrary to its murine parental anti-body targeting Her2/neu,unable to arrest tumor growth in vivo (Clynes et al.,2000).Additionally,this study in mice showed in a murine lymphoma model that treatment with CD20-speci?c anti-body rituximab was capable of preventing tumor growth in FcR wild-type mice whereas FcR knock-out mice failed to mediate antibody-dependent tumor protection.Another study demon-strated ADCC in mice in vivo by showing formation of ADCC synapses in immunocompetent mice bearing a murine breast tumor treated with an antibody speci?c to Tn,a glycopeptidic antigen which is expressed by breast cancer and a variety of other epithelial tumors in mice and humans(Hubert et al.,2011). Additionally,tumor rejection was abolished in mice de?cient for FcγRs–emphasizing the potential role of ADCC(Hubert et al., 2011).
Another study investigated the relative contributions of complement-dependent cytotoxicity(CDC)and ADCC in a murine GD2-expressing metastatic lymphoma model treated with an antibody speci?c to the disialoganglioside GD2utilizing wild-type,complement-de?cient,complement-receptor-de?cient,and FcγRI/III-de?cient mice.Outcome after treatment with the ADCC and CDC mediating GD2antibody was unaffected in mice inca-pable for CDC but was almost completely abrogated in FcγRI/III-de?cient mice that were disquali?ed for ADCC(Imai et al.,2005). These results further highlight the key role of ADCC in anti-tumor effects in mice in vivo.In men it has been shown,that breast can-cer patients who responded with partial or complete remission to Her2/neu-speci?c antibody trastuzumab have a higher capacity to mediate ADCC in vitro than patients which failed to respond to antibody therapy(Musolino et al.,2008).
These studies indicate that,at least in murine models,ADCC is a considerable component of the in vivo activity of therapeu-tic antibodies against tumors.However,studies with therapeutic antibodies in humans which demonstrate the direct in?uence of ADCC,as,e.g.,ADCC as the single effector mechanism,remain to be conducted.Therefore,the direct in vivo effect of ADCC in tumor reactivity in humans remains to be shown. INFLUENCE OF FcγRIIIa POLYMORPHISM AND KILLER-CELL IMMUNOGLOBULINE-LIKE RECEPTOR(KIR)RECEPTOR LIGAND INCOMPATIBILITY ON ADCC IN PATIENTS
In the past15years,12therapeutic antibodies have reached FDA approval for hematological malignancies as well as solid tumors (Scott et al.,2012).Their mechanisms of action include direct anti-tumor effects as induction of apoptosis,blocking receptor signaling or acting as an agonist,delivery of a cytotoxic agent, immune-mediated effects as CDC and ADCC as well as effects on the tumor microenvironment.At least?ve of these antibod-ies mediate ef?cient ADCC and a large number of new con-structs are currently under investigation in early and late phase clinical trials(Table1).In this review we will use anti-CD20-speci?c monoclonal antibody(mAb)rituximab,CD52-speci?c mAb alemtuzumab,Her2/neu-speci?c mAb trastuzumab,EGFR-speci?c mAb cetuximab,and anti-GD2antibodies to discuss the in?uence of ADCC in treatment with therapeutic antibodies.
The CD16encoding gene FCGR3A bears a single nucleotide polymorphism(SNP)at nucleotide526[thymidine (T)→guanine(G)]resulting in an amino acid(aa)exchange at aa position158of phenylalanine(F)to valine(V).It has been demonstrated that human IgG1binds more ef?ciently to NK cells expressing the FcγRIIIa-158V allotype than to the FcγRIIIa-158F allotype(Koene et al.,1997;Wu et al.,1997).In vitro studies have shown that the increased binding is caused by a signi?cantly higher af?nity of IgG antibodies to FcγRIIIa-158V receptors,whereas expression levels of FcγRIIIa on NK cells are not in?uenced by the FcγRIIIa polymorphism(Dall’Ozzo et al.,2004;Congy-Jolivet et al.,2008).Furthermore,the adequate rituximab concentration exciting50%lysis of a CD20+tumor cell line has been shown to be signi?cantly lower in FcγRIIIa-158V/V donors compared to FcγRIIIa-158F/F donors(Dall’Ozzo et al.,2004).
Several clinical studies investigating antibodies which utilize an ADCC-mediating therapeutic antibody suggest that patients with the FcγRIIIa-158V allotype have a better clinical outcome. However,con?icting data have been published.First,we will dis-cuss the chimeric IgG1CD20-speci?c antibody rituximab which is approved for treatment of CD20+B-cell non-Hodgkin’s lym-phoma(NHL),CD20+follicular NHL,and chronic lymphocytic leukemia(CLL).Rituximab is the most extensively studied anti-body mediating ADCC as its key effector mechanism(Cheson and Leonard,2008;Alduaij and Illidge,2011).The?rst study by Cartron et al.(2002)suggested that the homozygous FcγRIIIa-158V/V genotype is bene?cial in patients with follicular NHL regarding clinical and molecular responses to single agent ritux-imab.These results were con?rmed in a larger follicular lymphoma patient cohort treated with rituximab as monotherapy and an association of the FcγRIIIa-158V/V genotype with progression-free survival could be shown(Weng and Levy,2003).Another study analyzing the effect of the FcγRIIIa genotype on the outcome of patients to single agent rituximab promoted some of the above mentioned reports by suggesting a signi?cant improvement in event-free survival in FcγRIIIa-158V/V patients(Ghielmini et al., 2005).Furthermore,it has been postulated that NK cells from lymphoma patients with the FcγRIIIa-158V allotype but not from patients that are homozygous for FcγRIIIa-158F/F were activated after rituximab application(Veeramani et al.,2011).
On the contrary,no in?uence of the FcγRIIIa-F158V polymor-phism on the outcome of follicular lymphoma patients treated with risk-adapted chemotherapy and rituximab has been shown (Prochazka et al.,2011).Similarly,in relapsed or refractory CLL
T able1|ADCC-mediating therapeutic antibodies currently FDA approved for cancer therapy.
Antibody Antigen Cancer indication Mechanisms of action
Rituximab CD20CD20+B cell NHL,CD20+follicular NHL,CLL ADCC,CDC,direct induction of apoptosis Ofatumumab CD20CLL ADCC,CDC
Trastuzumab Her2/neu Breast cancer ADCC,abrogation of tumor cell signaling Cetuximab EGFR colorectal cancer,SCCHN ADCC,abrogation of tumor cell signaling Alemtuzumab*CD52CLL ADCC,CDC,direct induction of apoptosis
NHL,non-Hodgkin’s lymphoma;CLL,chronic lymphocytic leukemia;ADCC,antibody-dependent cellular cytotoxicity;CDC,complement-dependent cytotoxicity; SCCHN,squamous cell carcinoma of the head and neck.
*Withdrawn from the market in August,2012.
patients treated with chemotherapy and rituximab,no signi?cant in?uence of the FcγRIIIa-F158V polymorphism was demon-strated(Dornan et al.,2010).Another study evaluated the impact of the FcγRIIIa-F158V polymorphism on the response to rit-uximab in combination with a chemotherapy regimen(ritux-imab with cyclophosphamide,hydroxydaunorubicin,oncovin, and predniso(lo)ne,R-CHOP)in diffuse large B cell lymphoma (DLBCL)patients.The FcγRIIIa-158V allotype was shown to be signi?cantly correlated with a higher complete response rate com-pared with the FcγRIIIa-158F allotype(Kim et al.,2006).However, overall survival did not correlate with the FcγRIIIa-158V/V geno-type and several other studies investigating the impact of the FcγRIIIa-F158V polymorphism in DLBCL found no association with the response to R-CHOP(Carlotti et al.,2007;Mitrovic et al., 2007;Varoczy et al.,2012).Interestingly,all studies conducted with rituximab as monotherapy show an impact of the FcγRIIIa-F158V polymorphism and therefore indicate an important in?uence of ADCC on clinical outcome.However,the picture is less clear when rituximab is combined with chemotherapy.Since combined chemotherapy may hamper ADCC due to impaired NK cell func-tion the combination of rituximab with chemotherapy might mask the in?uence of the FcγRIIIa genotype and ADCC.Nevertheless,a combination of rituximab with chemotherapy generally improves clinical results.
The humanized IgG1mAb alemtuzumab was approved for treatment of B-CLL and is directed against the glycoprotein CD52 (Hillmen et al.,2007).The therapeutic antibody was withdrawn from the market in2012in order to optimize the pending launch of the agent as a treatment for multiple sclerosis.The predomi-nant mechanism of action of alemtuzumab in vivo has not been clearly de?ned but involvement of ADCC mediated by NK cells and neutrophils has been suggested by studies employing a human CD52transgenic mouse model and a xenograft model(Hu et al., 2009;Siders et al.,2010).In addition,CDC and direct induction of apoptosis have been identi?ed as other potential mechanisms of action in in vitro studies(Table1)(Crowe et al.,1992;Mone et al.,2006).A study exploiting the predictive value of FcγRIIIa polymorphism in a small CLL patient cohort(n=33)treated with alemtuzumab found no association of responsiveness to the mAb with a FcγRIIIa-F158V allotype(Lin et al.,2005).However,further studies with larger patient cohorts are required in order to deter-mine the potential in?uence of FcγRIIIa-F158V polymorphism and ADCC in treatment with alemtuzumab.
The humanized IgG1mAb trastuzumab is applicable in HER2/neu-positive breast cancer patients and mediates abroga-tion of tumor cell signaling and ADCC(Table1)(Hudis,2007).A study investigating breast cancer patients treated with trastuzumab and a chemotherapeutic agent postulated a higher response rate and longer progression-free survival in homozygous FcγRIIIa-158V/V patients compared to patients with the FcγRIIIa-158F allotype(Musolino et al.,2008).In contrast,another study sug-gested a correlation of the FcγRIIa-131H/H genotype with objec-tive response and progression-free survival in HER2/neu-positive non-metastatic and metastatic breast cancer patients treated with chemotherapy and trastuzumab but no signi?cant correlation was observed for the FcγRIIIa-F158V/V genotype(Tamura et al., 2011).Furthermore,another recent study postulated a lack of correlation between FcγRIIIa genotypes and trastuzumab ef?cacy in HER2/neu-positive non-metastatic breast cancer patients treated with a combined trastuzumab-chemotherapy(Hurvitz et al.,2012).Since no studies with trastuzumab as single agent have been published and besides ADCC abrogation of tumor cell signaling being a major effector mechanism of trastuzumab the in?uence of FcγRIIIa-F158V polymorphism and ADCC on clinical outcome is hard to substantiate.
The chimeric IgG1therapeutic antibody cetuximab targets EGFR in colorectal cancer(CRC)and has like trastuzumab ADCC and abrogation of tumor cell signaling as the modes of action (Table1)(Van Cutsem et al.,2009).A study suggested a signi?-cantly higher clinical bene?t after treatment with cetuximab and chemotherapy in homozygous FcγRIIIa-158V/V and or FcγRIIa-131H/H patients.These results were independent from the GTPase KRas(KRAS)mutation status in metastatic CRC(mCRC)(Bibeau et al.,2009).Furthermore,a higher disease control rate in KRAS-mutated mCRC patients harboring the FcγRIIa-131H/H genotype and treated with combined cetuximab-chemotherapy has been shown(Rodriguez et al.,2012).It has been suggested that the pre-dictive value of FcγRIIa-H131R polymorphism may result from linkage disequilibrium between FcγRIIIa-V158F and FcγRIIa-H131R and therefore nevertheless indicates an effect of ADCC (Lejeune et al.,2008).Similarly,the association of the FcγRIIIa-F158V polymorphism with progression-free survival has been sug-gested for single agent cetuximab treated mCRC patients(Zhang et al.,2007).However,in this study and in another study from Dahan et al.investigating combined cetuximab-chemotherapy treatment,the FcγRIIIa-158F allele rather than the FcγRIIIa-158V allele had a favorable in?uence on overall and progression-free sur-vival(Zhang et al.,2007;Dahan et al.,2011).Beyond that,a recent study found no association of clinical outcome in a patient cohort of107mCRC patients treated with cetuximab and chemother-apy and FcγRIIIa-F158V and FcγRIIa-H131R polymorphisms (Park et al.,2012).These discrepancies related to the predictive value of the FcγRIIIa-F158V polymorphism on cetuximab treat-ment are dif?cult to explain and indicate a demand for further elaborated investigations in larger patient cohorts.Interestingly, mutated KRAS induces a ligand-independent activation of EGFR downstream signaling pathways.Hence,the key effector mecha-nism of cetuximab besides ADCC,namely abrogation of tumor signaling,is invalidated by KRAS mutations.Clinical bene?t of cetuximab yet seen in these patients and the predictive value of FcγRIIIa-V158F genotype emphasizes the impact of ADCC.
Disialoganglioside GD2is a sialic acid containing glycosphin-golipid which is uniformly expressed in neuroblastoma and most melanomas but also to a variable degree in some other tumors (Navid et al.,2010).Due to its tumor-associated expression,several anti-GD2antibodies such as the chimeric IgG1antibody ch14.18 and its humanized counterpart hu14.18as well as3F8have been developed and deployed in the clinic.The mechanisms of actions of these antibodies are ADCC and CDC.Several years ago,a phase I study with pediatric neuroblastoma patients treated with anti-GD2antibody ch14.18was conducted at our institute and elicited some complete and partial tumor responses in neuroblastoma patients(Handgretinger et al.,1995).Currently,we are conducting an ongoing phase I/II-trial for relapsed metastatic neuroblastoma
with subsequent immunotherapy with ch14.18/Chinese hamster ovary(CHO)after HLA mismatched,haploidentical stem cell transplantation(SCT)at our institution.Preliminary results show effective ADCC and complement-mediated anti-tumor effects against neuroblastoma cells with donor-derived NK cells in vitro as well as signi?cant anti-tumor effects in vivo(unpublished data). Due to yet small patient cohorts,the role of FcγRIIIa-F158V poly-morphism in treatment with GD2antibodies has not been studied up to now.However,there are a variety of further studies ongoing which investigate the in vivo ef?cacy of GD2antibodies(Navid et al.,2010;Shusterman et al.,2010;Yu et al.,2010;Alderson and Sondel,2011;Simon et al.,2011).Yu et al.demonstrated in a ran-domized trial a signi?cantly better event-free survival for patients who received a combination of ch14.18,GM-CSF,and interleukin 2than patients without ch14.18.Additionally,the third-generation antibody hu14.18K322A,which bears an aa substitution in the CH2part,has been suggested to induce increased dose-dependent ADCC compared to ch14.18and hu14.18,whereas dose-limiting CDC is intercepted by the Fc modi?cation(Navid et al.,2010). In fact,results from studies conducted with this antibody in vivo will be interesting regarding anti-tumor effects caused by ADCC as single mode of action without involvement of any other effector mechanisms.
In adult acute myeloid leukemia(AML)and pediatric acute lymphoblastic leukemia(ALL)donor versus recipient NK cell alloreactivity is a key mechanism after HLA mismatched,hap-loidentical SCT,and has been reviewed elsewhere(Velardi et al., 2012).These“unlicensed”NK cells are characterized in the autol-ogous setting by lacking self-KIRs and are thought to be bene?cial in patients with neuroblastoma as well(Venstrom et al.,2009; Delgado et al.,2010).Interestingly,a recent study investigating the differential potential for ADCC of“licensed”and“unlicensed”NK cells in neuroblastoma,showed that“unlicensed”NK cells mediate ADCC most effectively against neuroblastoma cell lines under in?ammatory conditions(Tarek et al.,2012).Based on these studies and our ongoing trial with HLA mismatched,haploiden-tical stem cell transplanted neuroblastoma patients treated with ch14.18/CHO we suggest that in the allogeneic,HLA mismatched SCT setting,KIR receptor ligand incompatibility may have syn-ergistic effects with subsequent antibody therapy and propose further exploration of this hypothesis in larger clinical trials. ENHANCED ADCC BY THIRD-GENERATION MONOCLONAL ANTIBODIES
Presuming that ADCC is a key mediator of anti-tumor effects in vivo,enhancing ADCC by engineering mAbs is expected to markedly improve clinical ef?cacy of therapeutic antibodies.Two main approaches of optimizing FcγRIIIa binding by enhancing the af?nity of mAbs have been suggested and shown to induce 5-to100-fold increased ADCC in vitro in recent years:molecular modi?cations in the Fc portion leading to aa substitutions(Shields et al.,2001;Lazar et al.,2006;Stavenhagen et al.,2007)and mod-ifying Fc-linked glycosylation(Umana et al.,1999;Davies et al., 2001;Shinkawa et al.,2003).
The approach of optimizing the Fc portion of a therapeutic antibody via aa substitutions predominantly intends to enhance ADCC by increasing the af?nity to activating FcγRIIIa and reducing the af?nity to inhibitory FcγRIIb.A considerable number of these third-generation monoclonal antibodies are currently under early clinical investigation.These therapeutic antibodies target among others CD19,CD20,CD30,CD40,and FLT3in hematological malignancies and all of them aim at achieving highly augmented ADCC in vivo(Awan et al.,2010;Foyil and Bartlett,2010;Horton et al.,2010;Le Garff-Tavernier et al.,2011; Hofmann et al.,2012;Kellner et al.,2013).Furthermore,a CD19-speci?c Fc-optimized therapeutic antibody is currently evaluated in pediatric patients with refractory acute B-lineage leukemia after allogeneic SCT within the scope of a compassionate use program at our institution.In four out of six patients at very high risk of relapse,minimal residual disease could be signi?cantly reduced or completely eradicated with a longest follow up of15months (unpublished data).Other attempts aim at reduction of CDC related toxicity as applied in GD2targeting hu14.18K322A in neu-roblastoma(Lazar et al.,2006;Sorkin et al.,2010)or enhancing af?nity to low af?nity allele FcγRIIIa-158F(Bowles et al.,2006; Nordstrom et al.,2011).Recently,a phase I trial investigating a Fc-engineered antibody targeting CD20in follicular lymphoma patients has suggested encouraging results even in patients with the less favorable FcγRIIIa-F allotype(Forero-Torres et al.,2012).
Glyco-engineered therapeutic antibodies either bear oligosac-charides modi?ed by bisecting GlcNAc,aβ1,4-GlcnAc residue attached to a coreβ-mannose residue,or lack the core fucose of the Fc oligosaccharides and have been found to exhibit signi?cantly higher ADCC than their unmodi?ed counterparts(Lifely et al., 1995;Shinkawa et al.,2003).These modi?cations of oligosaccha-rides are mainly obtained by either transfecting CHO cell line with N-acetylglucosaminyltransferase III(GnTIII)or eliminat-ing its intrinsicα-1,6-fucosyltransferase(FUT8)activity.Alter-native expression systems such as Sf21insect cells,resulting in fucosylated paucimannosidic N-linked glycosylation,have been suggested to elicit an enhanced ADCC and have been investigated with a chimeric CD19antibody at our institution(Lang et al., 2004;Barbin et al.,2006).Several other glyco-engineered antibod-ies targeting a variety of different tumor associated antigens like CD19,CD20,EGFR,and GD2are currently investigated in early clinical studies(Robak,2009;Navid et al.,2010;Paz-Ares et al., 2011;Ward et al.,2011).All glyco-engineered antibodies in clini-cal trials have been reviewed in more detail elsewhere(Beck and Reichert,2012).Recently,the C–C chemokine receptor4(CCR4) targeting glyco-engineered antibody mogamulizumab has been approved in Japan for use in patients with relapsed and refrac-tory CCR4-positive adult T cell leukemia/lymphoma(ATL)(Beck and Reichert,2012).Clinical superiority of these third-generation mAbs over clinically established therapeutic antibodies remains to be shown and may further portend the key role of ADCC for clinical use.
CONCLUSION
The studies discussed here clearly demonstrate a substantial role of ADCC in vitro and in mouse tumor models.However,the direct in vivo effect of ADCC in tumor reactivity in humans remains to be shown since no therapeutic antibody with ADCC as single mechanism of action has been investigated in clini-cal trials to date.Con?icting results have been obtained about the role of FcγRIIIa-V158F polymorphism in mAb treatment. Several studies have shown a predictive value,which underlines
the in?uence of ADCC in vivo and suggests that ADCC is one of the key mechanisms for clinical ef?cacy of therapeutic anti-bodies.On the other hand,some studies could not con?rm these results.Further studies investigating the clinical relevance of FcγRIIIa-V158F polymorphism may be required for each therapeutic antibody and its indications.Although additional chemotherapy can mask the in?uence of the FcγRIIIa genotype and may hamper ADCC due to impaired NK cell function,a combination of both is able to improve clinical results.In partic-ular,the use of therapeutic antibodies after hematopoietic SCT is an interesting treatment option,as the new donor-derived immune system usually faces minimal tumor burden.Further exploration of the role of the FcγRIIIa-V158F polymorphism and the in?uence of KIR-receptor-ligand incompatibility on ADCC in allogeneic hematopoietic SCT may contribute to future transplan-tation strategies in this setting.Furthermore,clinical superiority of ADCC improved third-generation mAbs over clinically estab-lished second-generation antibodies remains to be shown and may further portend the key role of ADCC in cancer therapy with monoclonal antibodies.
ACKNOWLEDGMENTS
We acknowledge support by Deutsche Forschungsgemeinschaft (DFG),CRC685Immunotherapy,Open Access Publishing Fund of Tübingen University,Bundesministerium für Bildung und Forschung(BMBF iVac ALL and Reinhold Beitlich Stiftung.The authors thank David Martin and Christina Kyzirakos for help with editing this manuscript.
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植物的光合作用、蒸腾作用和呼吸作用中考试卷汇编 1．（2010·深圳市）2010上海世博会主题馆拥有世界最大的5000平方M生态绿墙，栽种上海本地的绿色植物，成为世博园里“绿色的明珠”。生态绿墙不仅能够美化环境，还能够帮助吸收园区内二氧化碳，降低夏季温度，这一功能是由植物的哪些生命活动来实现的 A．光合作用和呼吸作用 B．光合作用和蒸腾作用 C．呼吸作用和蒸腾作用 D．气体扩散和蒸腾作用 2．（2010·深圳市）在观察了叶片的结构后，晓东将刚摘下的叶片放人70度的热水中，很快发 现叶片表面产生许多的小气泡，并且下表皮的气泡比上表皮的气泡多，这种现 象说明 ．叶片上表面含叶 B A．叶片下表面的光照弱 绿体比下表面的多 ．叶片下表面的气孔多 D C．叶片下表面产生的氧气多 ·景德镇）我们行进在公园里时，经常发现草坪上有爱心提示牌：“请勿践20103．（踏，爱护我”。这是因为经常践踏草坪会造成土壤板结，从而影响草的生长。其中的科学道理是 ．植物缺少水，影响光合作用 BA．植物缺少无机盐，影响生长 D．气孔关闭，影响蒸腾作用．土壤缺少氧气，影响根的呼吸C 表示一昼夜中二氧化碳、氧进出植物叶片的情况，你认为哪·承德市）图44．（2010幅图所示的现象发生在夜间 ·宿州）绿色植物在生物圈水循环中有重要作用，主要是因为它的．（ 52010 ．吸收作用．蒸腾作用 D C B A．光合作用．呼吸作用 201．（60·内江市）当踏入山林时，会感到空气特别地清新和湿润，这主要是由于 1 / 11
．植物的分泌物有杀菌作用 B．植物的光合作用和呼吸作用 A C．植物的光合作用和蒸滕作用 D．茂盛的林木遮住了大部分太阳光 7．（2010·威海市）绿色植物蒸腾作用的意义不包括 A．降低叶片的温度 B．促进植物对水分的吸收 C．增加空气湿度，增加降水量 D．有利于植物进行呼吸作用 8．（2010·威海市）呼吸作用是生物的共同特征，其根本原因在于 A．生命活动每时每刻都需要氧 B．生命活动都需要能量作为动力 C．呼吸作用产生的水是生命活动所必需的 D．呼吸作用产生的二氧化碳必须及时排出9．（2010·乐山市）下列有关光合作用的叙述中，不正确的是 A．光合作用的条件之一是必须要有光照 B．光合作用是一切生物生存的根本保障 C．光合作用的场所是叶绿体 D．绿色植物所有的器官都能进行光合作10．（2010·乐山市）为了提高温室中的蔬菜产量，应将温度控制为 A．白天比晚上高 B．晚上比白天高 C．晚上和白天都高 D．晚上和白天都低11．（2010·乐山市）绿色植物在光下能进行的生命活动是 ①光合作用②呼吸作用③蒸腾作用④吸收水和无机盐 A．① B．①② C．①②③ D．①②③④ 12．（2010·苏州市）一株生理功能正常的绿色植物，在下图所示的五种不同条件下都能持续进行的生理活动是 2 / 11 吸根毛 C．．呼吸作用台 A．光作用 B D．蒸腾作用水
地铁车站施工变更影响因素及其作用路径研究 发表时间：2017-09-28T10:42:41.887Z 来源：《基层建设》2017年第14期作者：张博施海英 [导读] 摘要：近年来随着我国经济科技的快速发展，人口的增多，交通面临越来越大的压力。 中交一公局厦门工程有限公司福建省福州市 350108 摘要：近年来随着我国经济科技的快速发展，人口的增多，交通面临越来越大的压力。人们的生活和经济的发展都对交通的需求提出了更多的要求。为了满足人们生活的需求，同时也为了为经济的发展进一步增加活力，各地都在加大对城市轨道交通的建设。地铁这一出行方式在交通运输中扮演着不可或缺的重要角色。但是地铁作为一个浩大的工程，在建设当中会面临着各种各样的问题和困难，比如地铁的建设时间长，建设成本高，地铁的建设容易受自然因素和社会因素等不确定因素的影响，地铁的建设需要专业的技能和人才等等。这些问题迫切地需要我们去探索，去解决。本文针对地铁在施工建设中可能遇到的问题以及对这些问题的解决方法和预防措施做了分析和探讨。对引起地铁施工变更影响的因素逐一的进行讨论。希望我国的地铁建设能够发挥最大的作用，更好的为社会和人民生活带来便利。关键词：地铁施工变更影响因素作用路径 引言 地铁有其自身的特点和作用，它节省了我们交通运输的时间。它的使用区别于其他交通工具受路面交通状况和天气的影响。在环境污染方面，能够减少废气的排放，有利于环境净化。在地铁车站施工变更影响因素方面。很多的交通运输业的工作者和一些专家学者也都进行过分析和研究。本文的目的在于讲这些分析系统的整理，从一个全面宏观的角度分析这些因素，将各个因素用联系的方式让它们形成一个思路清晰的系统，以此来推进我国地铁建设技术的发展。减少在施工中的变更带来的经济损失和资源浪费。 一、地铁站施工变更所受到影响的因素分析 （1）受地理环境社会因素的影响 地铁作为一种高投入的工程，它的建设离不开国家的经济的发展，离不开政府的财政支持。政府一项旧政策的废除，一项新政策的发布，都与地铁的建设息息相关。地铁建设工程的顺利进行需要紧跟国家政策的发展和变化。因此，政策成了硬性地铁车站施工变更影响的因素。其次，从宏观的角度上来说，不只是政府政策，市场也是影响变更的宏观因素之一。众所周知，地铁的建设需要有大量的原材料作为基础，建筑市场的变动，会导致材料价格的浮动，使地铁在建造时的成本和预算有着较大的差距，不得不对地铁的施工计划进行变更。从微观的角度来看，地铁的建设主要是沟通不同地区之间的联系，但是不同的地区的地质地貌在实际建设时会和最初的预设有差距，地理环境也成了影响施工变工影响的因素。其次，地铁的建设还可以拉动地区经济的增长，在建设时需要考虑建设地区周边的交通状况，和经济社会的发展形势，容易受不可预见因素的影响。 （2）受勘测技术的客观环境的影响 地铁的建设是一个庞大的工程，这个庞大工的顺利完成需要不同的部门共同参与，共同设计。因此，在工程建设前的勘测对整个工程来说异常重要。当前我国地铁建设在前期的调研活动时期准备不充分，不具体，可操作性的难度大。前期的勘测直接影响到后期的建设环节，由于我国目前的地铁建造技术还有很大的进步空间，在建造时，大多数都是对最初的设计进行一个扩大式的建造。不能提供一个深度的设计方案，以至于在最后的建造时出现的诸多问题不能得到准确数据的支持，也没有应急转化方案的帮助，不能够灵活快速的适应实际的工程操作。为了地铁建设工程的顺利进行，出现这种由于勘测技术客观环境影响的情况时，一般都会采用对施工变更的方法。前期的勘测技术和深度计划的设计是否合理和科学，是否灵活和准确，是影响地铁建设是否变更的根本原因。总而言之，这些因素是影响是否变更的直接因素。 （3）受施工环境的间接影响 众所周知，一项工程的进行，过程都不是完全一帆风顺的。地铁的建设更是如此。在进行了前期计划准备和勘测准备之后，地铁的建设算是正式开始。但是，在具体的施工中会遇到各种不可预料的因素。地铁的建设首先必要要保证它的安全性能，如果在建设中，安全这一关出现了问题，就必须立刻对该工程进行调整和变更。为了保障人们能在短时间内享受到地铁带来的便利，对施工的过程就有着极其高的标准，既要保证工程的安全，又要注重工期的长短，既要考虑地铁建设对周边人文环境的影响，又要兼顾地理环境的因素。 由此看来，地铁的施工环境其实是处在一种高度紧张高度认真的环境之中。在这种施工环境中如果出现了其中一个环节的矛盾，需要相关人员和部门在最快的时间内解决，直接快速有效的解决矛盾。当有关部门和有关人员无法解决出现的矛盾和问题，找不到最佳解决问题和协商问题的方法，这时，这种高度紧张高效的施工环境就会间接要求人们对地铁的施工及时的做出变更，以此来保证工程的顺利进行。由以上可看出。施工的变更还会在施工过程的环境中产生。 二、研究地铁车站施工变更作用路径的方法 （1）搜集丰富具有权威性的资料 真实的案列及其它的解决方法有助我们在解决新问题时的举一反三，推陈出新。案列研究这一方法近几年来发展迅速，被很多人采用，随着时代的发展，现在已经成了理论研究的基础方法。 通过真实的案列，能让我们迅速的了解各个要素之间存在的联系以及他们的相互作用。能够在宏观的角度系统的认识到地铁工程在建造时如何减少变更带来的损耗。其次，要注意搜集大量的资料和材料，这些资料可以是自己实地的勘测，测量，可以是以往工程建设留下来的资料和数据，可以是企业的档案，也可以是在地铁建造方面有着研究的专家学者的书籍和报刊等等。 不同的资料之间可以进行补充说明，也可以让读者有更多的选择途径，多方面的考虑和思考地铁车站施工变更问题的解决办法。本文提出了研究的方法，现在用这些方法来分析某地铁车站变更建设的案例，让我们更深沉的学会并理解这些方法，能把理论真正的应用到地铁车站施工变更因素的研究当中。 （2）具体的地铁车站施工影响因素案例分析 在某地地铁车站的建设当中。原方案是用主体机构采用明暗挖结合施工，但是正如我们本文中提到的地铁车站的变更，最终在实际的建造中采取的却是浅埋暗挖法。探究其中的原因，外部环境在于该地铁线的位置周围有着大量的文物，古建筑较多，地铁的建造不应以破坏文化遗址为代价。该地的经济收入主要是旅游业，且地铁站周围有较多旅游景点，因此，不得不改变施工方案。 从内部条件来看，前期的勘测准备工作不充分，在后期建造过程中，发现存在着安全隐患问题，不确定的危险源会使该地铁站的安全
影响人的发展的主要因素 影响个体身心发展的因素非常多，但最主要的是遗传、环境、教育和个体的主观能动性等方面，这几个因素是相互联系、相互影响的。 1.遗传 遗传素质在个体身心发展中具有重要的意义。遗传素质是指个体从上代继承下来的一些天赋特点，包括一些与生俱来的解剖生理特征，如机体的特点、感官和神经系统的特征等。首先，遗传素质为人的身心发展提供了可能性，它是人的身心发展的生理前提。如果没有这些生理条件，人的身心发展就无从实现。其次，遗传素质的生理成熟程度影响着人的身心发展的年龄特征。心理学家格塞尔的同卵双生子的爬梯试验证明，遗传素质的成熟程度制约着人的身心发展水平及阶段。再次，人的遗传素质是有差异的，遗传素质的差异性对人的身心发展有一定的影响作用。这种差异主要表现在人的体态、感官和神经活动的类型上。最后，遗传素质又具有可塑性。人的遗传素质会随着外界环境、教育和实践活动的介入而发生变化。 2.环境 环境是直接或间接地影响个体身心发展的全部外在因素的总和，所有不以培养人为目标的外界对个体发展的影响，例如社会经济生活、文化生活、亲戚、朋友的交往都可以看做是环境的影响。个体身心的发展离不开外界环境的影响。首先，外部社会环境是个体身心发展、成熟的客观条件，对人一生的发展都具有一定的制约作用。如果说遗传素质为人的发展提供了可能性，那么社会环境的影响则能把这种可能性转化为现实。我国古代的荀子就很重视环境对人的潜移默化的影响，他提出：“蓬生麻中，不扶自直；白沙在涅，与之俱黑。”其次，环境对人的作用离不开社会实践，社会实践对于人的发展具有决定性的作用。 3.教育 学校是专门培养人的场所，教育对人的身心发展具有非常重要的意义。首先，教育是人的发展的最重要的外因，教育决定了人的发展方向和发展水平。教育是一种有目的地培养人的活动，能够排除一些外在不良因素的影响，使年轻一代朝着健康、正面的方向发展。学校教育在人的身心发展中具有主导作用，其目的性、系统性、专门性和基础性对青少年的发展具有举足轻重的作用。尤其是学校教育的选择性，对于培养目标的选择、教育内容的选择、教育方式、方法和手段的选择都为青少年、儿童的发展创造了优越的条件和更多的发展可能性。但是，我们也应该看到学校教育对于个体身心发展的主导作用不是无限的，必须要以遗传素质为基础，以外界环境为条件。因此，我们不能夸大教育的作用，而是应该实事求是地看待学校教育在个体身心发展中的作用。
第23课时 光合作用的影响因素和原理的应用 [目标导读] 1.通过探究光照强弱对光合作用强度的影响实验，学会研究光合作用影响因素的方法。2.联系日常生活实际，思考影响光合作用的环境因素以及光合作用原理的实践应用。 3.阅读教材，了解化能合成作用。 [重难点击] 影响光合作用的环境因素以及光合作用原理的实践应用。 一 探究光照强弱对光合作用强度的影响 多种环境因素对光合作用有着重要的影响，其中光照的影响最为重要。 1.光合作用强度的表示方法 ????? 单位时间内光合作用产生的有机物的量单位时间内光合作用吸收CO 2的量单位时间内光合作用放出O 2的量 2.探究光照强弱对光合作用强度的影响 (1)实验原理：抽去小圆形叶片中的气体后，叶片在水中下沉，光照下叶片进行光合作用产生氧气，充满细胞间隙，叶片又会上浮。光合作用越强，单位时间内小圆形叶片上浮的数量越多。 (2)实验流程 打出小圆形叶片(30片)：用打孔器在生长旺盛的绿叶上打出(直径＝1cm) ↓ 抽出叶片内气体：用注射器(内有清水、小圆形叶片)抽出叶片内气体(O 2)等 ↓ 小圆形叶片沉水底：将抽出内部气体的小圆形叶片放入黑暗处盛有清水 ↓的烧杯中，小圆形叶片全部沉到水底 强、中、弱三种光照处理：取3只小烧杯，分别倒入20mL 富含CO 2的清水，各放入 10片小圆形叶片，用强、中、弱三种光照分别照射 ↓ 观察并记录同一时间段内各实验装置中小圆形叶片浮起的数量 (3)实验现象与结果分析：光照越强，烧杯内小圆形叶片浮起的数量越多，说明在一定范围内，随着光照强度的不断增强，光合作用强度不断增强。 3.结合细胞呼吸，人们用下面的曲线来表示光照强度和光合作用强度之间的关系，请分析：
教学目标:1、了解蒸腾作用的基本含义及其意义 2、知道气孔的分布状况 3、知道保卫细胞和气孔的结构 4、完整地描述水、无机盐的运输路径 重点难点:叶的结构水和无机盐的运输 教学过程: *************************************** 第一课时 课堂引入:我们都知道“水从低处留”,可在植物体内,是什么促使水从根部向茎、叶运输呢? 一、蒸腾作用 1、实验观察:选取一盆正处于生长旺盛期的植物,用一透明的塑料袋将邻近的叶片包扎起来,对该植物浇水后,置于阳光下照射。观察塑料袋上有无水珠生成,这说明____________________________。 2、水分以气体状态从体内散发到体外的过程,叫做蒸腾作用,蒸腾作用主要在叶片进行。 3、土壤中的水分由根毛进入根后,然后通过根、茎、叶的导管输送到叶肉细胞。这些水分,除了很小一部分参加植物体内各项生命活动外,99%通过蒸腾作用从叶中散发出去,蒸腾作用可以在温度偏高的情况下有效地降低叶片的温度,同时也是根吸水的主要动力,利于植物对水的吸收和运输,也利于溶解在水中的无机盐在植物体内的运输。由此可见,蒸腾作用不是在浪费水分,而是对植物的生活具有重要的意义。 4、学生讨论:①在春天的阳光下,水银柱将会有什么变化?为什么? ②如果把这一装置放在夏天的烈日下,水银柱会有什么变化?为什么? ③如果把这一装置放在阴暗潮湿的环境中,水银柱将会有什么变化?为什么? ④如果在实验室里,用电吹风吹叶片,水银柱将会有什么变化? ⑤请设计一个实验:证明蒸腾作用的强弱与光照条件有关。 5、课堂练习: ①在阴天或傍晚进行移植,并去掉部分枝叶,是为了降低: ( ) A.降低光合作用 B.减小呼吸作用 C.减少水分蒸腾作用 D.移栽方便 ②仙人掌在强烈的阳光下,不会被太阳光灼伤的原因是( ) A、吸水力大 B、储水多 C、蒸腾作用强 D、叶变成刺 ③关于植物体水分散失的意义,下列哪项是不正确的?( ) A、促进植物体对水分的吸收 B、促进矿质元素在植物体内的运输 C、促进溶于水的矿质元素的吸收 D、降低植物体特别是叶片的温度 ④北方果树由根系吸收的水分主要用于( ) A、光合作用 B、蒸腾作用 C、植物的生长 D、果实的形成 6、作业:作业本 第二课时 二、叶的结构: 1、实验观察1:①选取一张生长旺盛的蚕豆叶,用滤纸把它上、下表皮的水分吸干。 ②将两张浸有氯化钴溶液的蓝色滤纸,相对应地贴在叶片上、下表皮的表面,并用回形针将其固定。 ③观察贴在叶片上、下表皮上的滤纸的颜色变化。哪一张纸先变色?哪一张纸的颜色
植物的蒸腾作用、呼吸作用和光合作用 [复习目标] 1、举例说明植物的生活离不开水的原因以及水对植物分布的影响。 2、列举根毛对植物吸水的意义，概述水分在植物体内的运输途径，识别茎的结构和各部分 的作用。 3、掌握绿色植物叶片的结构和功能，描述气孔控制水蒸气和二氧化碳进出叶片的机制。 4、描述蒸腾作用、光合作用、呼吸作用过程及意义。 5、认同绿色植物在生物圈水循环中的作用以及在维持碳—氧平衡方面的重要作用。 [考点提示] 1、植物的生活为什么需要水。 2、导管和筛管的结构及作用，水分进入植物体内的途径。 3、叶片的结构和功能。 4、蒸腾作用的概念及意义。 5、光合作用、呼吸作用的概念、公式、实质、意义及有关实验。 6、光合作用与呼吸作用的关系。
[精题解析] [例一]（2005湖南益阳）一些老人特别喜欢早晨到树林里锻炼身体，感到空气清新，主要原因是（） A、空气中氧含量高 B、空气中二氧化碳含量高 C、空气中水蒸气多 D、空气中有毒气体、灰尘减少 {解析}早晨的树林中氧气含量较低，而二氧化碳含量教高，因为晚上树木不进行光合作用，只进行呼吸作用，吸入氧，呼出二氧化碳。人们之所以感到空气清新，只是空气中的有毒气体和灰尘减少了的缘故。 {答案} D {例二}（2006 莱芜）为探究绿色植物进行光合作用的条件，某同学选择一盆栽的斑叶植物作为实验材料，该植物叶片的绿色部分和非绿色部分界限清晰。他的实验装置如图所示， 请分析回答： （1）在透明塑料袋中放置固体氢氧化钠的用途是。 （2）请你设计一个简单方案，以排除叶片中原有的淀粉对实验结果的影响？ （3）将实验装置放在阳光下4小时后，同时摘下叶片A、B利用进行脱色处理，然后滴加碘液，观察实验结果。 （4）叶片A绿色部分和非绿色部分的结果比较，表明；叶片A绿色部分和叶片B绿色部分的结果比较，表明。 [解析] 本题是考查有关光合作用的知识内容，氢氧化钠能吸收空气中的二氧化碳，因此是用固体氢氧化钠来除去塑料袋内二氧化碳的。要想排除叶内原有淀粉，采用的方法是将其放在黑暗环境中一昼夜，使其只进行呼吸作用，这样叶内原有的淀粉就能运走或耗尽。脱去叶片中的叶绿素用酒精这种有机溶剂，叶片A绿色部分有叶绿体能进行光合作用，制造淀粉，叶片A中非绿色部分则没有叶绿体，不能进行光合作用，说明光合作用的场所是叶绿体。叶片A、B两片绿色部分的区别是A叶有二氧化碳，因此能进行光合作用；B叶片没有二氧化碳，不进行光合作用，说明光合作用的原料之一是二氧化碳。
影响组织承诺的因素及作用机制摘要：组织承诺是近年来组织行为学领域研究的热点内容之一。有关研究人员对其内涵、影响因素、作用机理、作用环境等等方面做了很多研究，研究表明，不同的工作环境、工作人群对组织承诺作用的影响都不尽相同。本文根据近十年来研究组织承诺的论文对其影响因素和作用机制进行简单的梳理和总结。 关键词：组织行为组织承诺影响因素 二十一世纪的管理所依照的思想基础应当是以人为本。换言之，处理好员工需求与企业发展的关系、提高组织承诺是企业管理的重要内容，是人力资源管理的从业人员进行实际管理工作时要考虑的核心问题之一。本文就近十年之内有关组织承诺的文献对组织承诺的影响因素及作用机制进行简单的阐述。 一、什么是组织承诺及其构成 组织承诺这一概念最早于1960年由贝克提出。他将承诺定义为由单方投产生的维持“活动一致性”的倾向。他认为组织承诺的产生是由于员工单方面投入过多而产生的，员工对工作倾注的心血越多，对工作的热情就越高。到了80年代，Porter等人对于组织承诺又进行了新的解读，他们认为，组织承诺是员工对于工作的卷入程度和认可程度。国外有关组织承诺的各类研究也激发了我国学者研究的热情，方俐落、凌文辁和张治灿在千禧年的研究发现，组织承诺是员工对现有组织在情感上的认可，以及乐于承担身为组织中的一员所要承担的责任和义务。 根据各种研究我们可以看出，我们对组织承诺这一概念和现象的认识随时间推移不断深化。目前对于组织承诺并无统一的标准定义，但综合各时期各研究我们可以看出，组织承诺包含态度和行为两方面内容。态度主要指员工对工作的忠诚、依赖和热情；行为主要指员工的外在行为，表现为对工作稳定的、相应的反应。 组织承诺的结构并不是单一的。梅尔和艾伦将组织承诺分解为三维结构：感情承诺、持续承诺与规范承诺。情感承诺是指组织成员被卷入组织的程度，包括参与组织建设运行的程度、参与组织社会交往程度等方面，它是个体对组织的情感，是一种肯定的心理倾向。持续承诺是指员工为了保有多年来在组织当中通过
蒸腾作用 一、水分的吸收与运输 1.植物主要通过哪个器官吸收水分——根 根吸收水分的主要部位——根尖成熟区 原因：成熟区有大量根毛，增大了吸收水和无机盐的表面积 2.导管与筛管的比较 3.无机盐只有溶解在水中，才能被植物体吸收并运输到植物体的各个器官。 二、蒸腾作用 （一）定义：水分从活的植物体表面以水蒸气状态散失到大气中的过程。 （二）形式：水蒸气 （三）主要部位：叶片 （四）散失门户：气孔 （五）途径：根尖成熟区 茎中导管叶脉 气孔 大气 （六）意义： ①蒸腾作用能降低叶片表面的温度
水分的吸收 的运输 ①蒸腾作用能够提高大气湿度，增加降水，参与了生物圈的水循环 ②植物的茎叶承接着雨水，能够大大减缓雨水对地面的冲刷 ③落叶能够吸纳大量的雨水，也使大量雨水渗入地下，补充地下水 （七）影响蒸腾作用的因素（一定范围之内）（类比晒衣服的过程） 1.光照：光照越强，蒸腾作用越强（注意：夏日正午十二点，蒸腾作用会减弱，原因是保卫细胞失水，大多数气孔关闭，防止水分过度散失） 2.温度：温度越高，蒸腾作用越强 3.湿度：湿度越低，蒸腾作用越强 4.空气流速：空气流速越快，蒸腾作用越强 三、叶片的结构 1.叶片由表皮（包括【1】上表皮和【3】下表皮）、【2】叶肉、 【5】叶脉三部分组成。 2.表皮属于保护组织，由一层细胞组成，分布有【6】气孔， 该结构是由两个半月形的【4】保卫细胞组成的，对于大多数 陆生植物来说，气孔在【3】下表皮分布较多； 【5】叶脉中有导管和筛管，属于输导组织；【2】叶肉属于营 养组织，这一部分的细胞中含有可进行光合作用的叶绿体。 3.气孔是植物蒸腾作用的门户，也是气体交换的窗口。 4. 白天，气孔张开（保卫细胞吸水膨胀），空气进入，为光合作用提供二氧化碳，同时水分散失，即蒸腾作用强。 夜晚，光合作用停止，大多数气孔缩小或闭合（保卫细胞失水收缩），蒸腾作用减弱。 四、移栽问题 1.保护根毛和幼根，保证植物正常吸收水和无机盐——具体做法：带一个土坨 ①剪掉部分枝叶 2.降低蒸腾作用，减少植物体内水分的散失——具体做法②傍晚、阴天时移栽 ③适当遮阴
世界工厂网企业线上生态学院课程目录 一、企业线上生态分析 二、团队建设与管理 1.团队建设 2.团队管理 3.法务安全 三、企业线上总部建设 四、国内外贸易 1.B2B平台推广 2.SEO推广 a.产品发布优化技巧 b.影响关键词排名的五个因素 c.SEO推广计划表 d.关键词挖掘信息表 3.竞价推广 4.SNS推广 五、品牌互动营销 六、企业线上线下融合
影响关键词排名的五个因素 SEO从业人员其实每天都是相当忙碌的，不断地更新着网站内容，寻求着更好的外链，想着怎么截流，怎么争取更好的排名。但是很多站长都遇到过这个问题，自己辛辛苦苦做了好几个月，排名就是上不去，一直在几十名开外甚至上百名开外徘徊，不知道下一步应该怎么走了。 其实，当局者迷，旁观者清，从工作中跳出来，我们就会发现很多问题，那么导致关键词没有排名的原因到底有哪些呢？ 一、外链的量 1、质量是不是低了 很多朋友每天需要抽出大把的时间来放到外链的建设上面，不管其网站和论坛怎么样，先发了链接再说，久而久之你的外链是很脆弱的，很多轻易接受外链的网站或论坛根本没有被搜索引擎收录的资本，甚至很多的网站和论坛都无人更新无人管理，你在上面发布再多外链也是无济于事，所以外链质量很重要，好的外链不仅可以给你的网站带来好的排名更可以带来流量，所以各位朋友在外链的建设方面要更多的关注质量是否够高，有没有价值。 2、数量是不是多了或者少了 一些SEO从业人员在给新站做排名的时候本着“内容为王，外链为皇”的江湖秘籍，一股脑的在X宝或者一些链接交易网站给自己的网站买几百几千个外链，这样做是毫无意义甚至很危险的，搜索引擎看到你是一个新站并且一夜之间冒出来成百上千的外链，就会判断你为作弊，有被K的风险。 当然外链太少跟不上节奏也没有效果，也有些朋友的外链建设就是三天打渔两天晒网，没有一个规律也不成方圆。建议各位朋友坚持每天给自己站做三到五条质量高的外链，长久下来你网站的外链数量和质量也是很可观的，排名当然也会上去了。 二、内链是否合理 内链是优化网站体验很好的方式，目的就是满足用户的次级需求，就像超市的电梯扶手旁为什么要放一堆零食，目的就是刺激消费。 内链建设一定要有理有据，不可太多也不能太少，要充分的从用户体验的角度出发，哪些关键词可以做，哪个位置最适合做内链，是不是图文形式比单纯的文字更有吸引力。都需要各位SEO从业者认真的从用户角度出发来建设自己网站的内链。分析内链是否合格就可以从跳出率入手，如果你的内链跳出率很高，那么就该想想内链是否有问题了。 三、关键词有无堆砌 很多站长为了让自己网站能快速的有排名，就在网站里到处散布网站关键词，这样也是导致关键词没有排名的重要杀手。关键词的堆砌第一是对网站的内容来说会有一定的影响，第二就是搜索引擎同样会认为你是在作弊，有时候不仅不给你排名，更会用K站来警示你！
植物的光合作用、蒸腾作用和呼吸作用中考试题汇编 1．（2010·深圳市）2010上海世博会主题馆拥有世界最大的5000平方米生态绿墙，栽种上海本地的绿色植物，成为世博园里“绿色的明珠”。生态绿墙不仅能够美化环境，还能够帮助吸收园区内二氧化碳，降低夏季温度，这一功能是由植物的哪些生命活动来实现的 A．光合作用和呼吸作用 B．光合作用和蒸腾作用 C．呼吸作用和蒸腾作用 D．气体扩散和蒸腾作用 2．（2010·深圳市）在观察了叶片的结构后，晓东将刚摘下的叶片放人70度的热水中，很快发现叶片表面产生许多的小气泡，并且下表皮的气泡比上表皮的气泡多，这种现象说明 A．叶片下表面的光照弱 B．叶片上表面含叶 绿体比下表面的多 C．叶片下表面产生的氧气多 D．叶片下表面的气孔多 3．（2010·景德镇）我们行进在公园里时，经常发现草坪上有爱心提示牌：“请勿践踏，爱护我”。这是因为经常践踏草坪会造成土壤板结，从而影响草的生长。其中的科学道理是 A．植物缺少无机盐，影响生长 B．植物缺少水，影响光合作用 C．土壤缺少氧气，影响根的呼吸 D．气孔关闭，影响蒸腾作用 4．（2010·承德市）图4表示一昼夜中二氧化碳、氧进出植物叶片的情况，你认为哪幅图所示的现象发生在夜间 5．（2010·宿州）绿色植物在生物圈水循环中有重要作用，主要是因为它的 A．光合作用 B．呼吸作用 C．蒸腾作用 D．吸收作用 6．（2010·内江市）当踏入山林时，会感到空气特别地清新和湿润，这主要是由于
A．植物的光合作用和呼吸作用 B．植物的分泌物有杀菌作用 C．植物的光合作用和蒸滕作用 D．茂盛的林木遮住了大部分太阳光 7．（2010·威海市）绿色植物蒸腾作用的意义不包括 A．降低叶片的温度 B．促进植物对水分的吸收 C．增加空气湿度，增加降水量 D．有利于植物进行呼吸作用 8．（2010·威海市）呼吸作用是生物的共同特征，其根本原因在于 A．生命活动每时每刻都需要氧 B．生命活动都需要能量作为动力 C．呼吸作用产生的水是生命活动所必需的 D．呼吸作用产生的二氧化碳必须及时排出 9．（2010·乐山市）下列有关光合作用的叙述中，不正确的是 A．光合作用的条件之一是必须要有光照 B．光合作用是一切生物生存的根本保障 C．光合作用的场所是叶绿体 D．绿色植物所有的器官都能进行光合作 10．（2010·乐山市）为了提高温室中的蔬菜产量，应将温度控制为 A．白天比晚上高 B．晚上比白天高 C．晚上和白天都高 D．晚上和白天都低 11．（2010·乐山市）绿色植物在光下能进行的生命活动是 ①光合作用②呼吸作用③蒸腾作用④吸收水和无机盐 A．① B．①② C．①②③ D．①②③④ 12．（2010·苏州市）一株生理功能正常的绿色植物，在下图所示的五种不同条件下都能持续进行的生理活动是
影响药物作用的因素的研究 孟刚，时晓丽 （南京农业大学动物医学院，南京210095） 摘要：药物的作用是药物与机体互相作用过程的综合表现，许多因素都可能影响或干扰这个过程，使药物的效应发生改变。本文主要探讨给药途径、动物年龄和药物的理化性质对药效的影响，以指导临床用药。关键词：药物作用；给药途径；动物年龄；理化性质 药物的作用是药物与机体互相作用过程的综合表现，许多因素都可能影响或干扰这个过程，使药物的效应发生改变。在兽医临床上，我们可以把这些因素归纳为药物方面、动物方面和环境生态方面的因素。本文将主要探讨不同的给药途径、动物年龄和药物的理化性质对药物作用的影响及其机制。 1 不同给药途径对药物作用的影响 1.1 实验用品 （1）仪器：普通天平、注射器、注射针头、灌胃针头、鼠笼;（2）药品：4%硫酸镁注射液；（3）动物：小鼠两只（体重20 克左右） 1.2 实验方法 取体重相似的两只小鼠，称好体重，一只以4%硫酸镁0.25ml/10g腹腔注射，另一只以同样剂量灌胃，观察两鼠的反应有何不同。 1.3 实验结果 表1 应用硫酸镁后小鼠的变化 鼠号体重（克）药物剂量（毫升）给药途径反应情况 甲21.61 0.54 腹腔注射四分钟后出现爬行异常，大约十分钟后开 始瘫痪 乙20.63 0.52 灌胃无异常 1.4 小结 不同的给药途径可引起不同的药物作用效果。硫酸镁注射给药主要发挥镁离子的作用。当血浆中镁离子浓度过低时，出现神经和肌肉组织过度兴奋，可致激动。当镁离子浓度升高时，可引起中枢神经系统抑制，产生镇静和抗惊厥作用。同时镁离子又引起神经肌肉传导阻断，使骨骼肌松弛，原因主要是运动神经末梢乙酰胆碱释放量减少，其次是乙酰胆碱在终板去极化减弱及肌纤维的兴奋性下降。所以，不难解释，甲鼠出现爬行异常和瘫痪的现象。另外，硫酸镁口服，由于肠道内镁离子浓度的升高，形成高渗液体能吸收大量水分，阻止肠道水分的吸收，同时水分增加可以软化粪便，而且肠容积变大，对肠粘膜产生机械性的刺激作用，解离出的镁离子及溶液的渗透压对肠粘膜也有一定的刺激作用，促进蠕动，引起排便。本实验中，硫酸镁灌胃量比较少，故没有出现下泻的现象。所以，我们必须注意根据用药目的，选择正确的给药途径。 2 动物年龄对药物的影响 2.1实验用品 （1）仪器：注射器、注射针头、鼠笼、天平；(2)药品：0.5%巴比妥溶液；（3）动物：小鼠（成年及未断奶各一只）
一、茎的结构 A、木质部：导管：输导水分和无机盐。 B、韧皮部：筛管：输导有机物。 二、水分、无机盐的运输 实验结论：水份和无机盐在茎中央的导管中能自下而上地向枝端运输。 三、有机物的运输 实验结论：有机物在茎的筛管中是自上而下地运输。 习题：右图是一段枝条，上面长有两个大小相同的果实。如果将枝条两A、B两个部位间的 树皮进行环剥，⑴伤口的＿＿＿（填“上方”或“下方”）的树皮会形成瘤状物。 ⑵这两个果实会发生什么变化？ 处的果实在一段时间内能继续长大，处的果实得不到营养物质，将逐渐萎缩、变小。 练习： 1、茎具有运输功能，能够运输（） A、水、无机盐、二氧化碳 B、水、有机物、氧气 C、水、无机盐、有机物 D、水、有机 物、二氧化碳 2、根从土壤里吸水，土壤里的水通过根向上输送到茎的途径是（） A、土壤水分→导管→根毛→根毛区表皮细胞以内的各层细胞→茎 B、导管→土壤水分→根毛→根毛区表皮细胞以内的各层细胞→导管→茎 C、根毛→土壤水分→根毛区表皮细胞以内的各层细胞→导管→茎 D、土壤水分→根毛→根毛区表皮细胞以内的各层细胞→导管→茎 4、根吸收的水分和无机盐是通过茎里的＿＿＿向上运输的；叶制造的有机物是通过茎里的＿＿＿向下运输的。 四、蒸腾作用： 1、水分以气体状态从体内散发到体外的过程，叫做，蒸腾作用主要在进行。 2、蒸腾作用的意义： ⑴有效降低温度⑵是根部吸水的主要，利于植物对的吸收和运输，也利于溶解在水中的在植物体内的的运输（3）促进根对水分的吸收 3.蒸腾作用的影响因素:光照；湿度；温度；空气流动快慢。 练习： 1在阴天或傍晚进行移植，并去掉部分枝叶，是为了降低：（） A.降低光合作用 B.减小呼吸作用 C.减少水分蒸腾作用 D.移栽方便 2仙人掌在强烈的阳光下，不会被太阳光灼伤的原因是（） A、吸水力大 B、储水多 C、蒸腾作用强 D、叶变成刺 3关于植物体水分散失的意义，下列哪项是不正确的？（） A、促进植物体对水分的吸收 B、促进矿质元素在植物体内的运输 C、促进溶于水的矿质元素的吸收 D、降低植物体特别是叶片的温度 4北方果树由根系吸收的水分主要用于（） A、光合作用 B、蒸腾作用 C、植物的生长 D、果实的形成 5、下列关于蒸腾作用的说法中，错误的是（） A 植物蒸腾作用的主要器官是叶 B 水分是以气态的形式通过植物体而蒸发散失 C 蒸腾作用只有在白天进行 D 蒸腾作用有利于降低叶片的温度 6、请将植物体内水分和无机盐的吸收和运输的路径进行排序： A、根尖吸收水分和无机盐 B、叶脉中导管运输 C、根中导管运输 D、叶肉细胞利用或经气孔散失 E、茎木质部中导管运输 7、移栽植物后，往往剪掉一些枝叶，这是为了（） A．减少呼吸作用B．减少水分的散失C．加强蒸腾作用D．减弱光合作用 8、根吸收水分向上运输的主要动力是（） A．光合作用B．蒸腾作用C．呼吸作用D．根压 9、在夏季中午的烈日下，草地上放有木板、钢管和石块，其中温度最低的是（） A、地上的草 B、木板 C、钢管 D、石块 10、大树底下好乘凉，这与植物的哪个功能有关（） A、光合作用 B、呼吸作用 C、蒸腾作用 D、扩散作用
我国就业的主要影响因素分析 影响我国就业形势的因素纷繁复杂，既有来自国内经济增长速度和产业结构的变化、人口年龄结构和生育政策的变化等，也有来自国际经济环境变化等因素。这些因素当中既有积极有利的方面，也有消极不利的方面，因此需要在仔细分析这些因素影响的基础上预测未来我国的就业趋势变化。 （一）国际政治经济形势将愈发复杂多变 国际政治经济环境的变化会通过各种渠道传导到国内，从而对国内的经济和就业产生影响。在经济方面，美国经济的逐渐复苏和欧洲债务危机的逐渐化解都将增强世界经济发展的动力，有利于我国扩大对外贸易和出口，从而带来就业的增长；而印度、巴西、俄罗斯和南非等金砖国家和新兴经济体的增长乏力又会减弱对我国出口产品的需求，从而直接或间接影响到我国的经济增长和就业。在地缘政治方面，乌克兰危机对俄罗斯乃至全球经济增长带来较大挑战；与日本、菲律宾等国在领土上的争端和政治上的分歧会使我国双边经贸关系受到一定影响，从而波及我国相关出口企业的就业状况。 （二）我国经济下行压力进一步加大 与就业增长最为密切相关的因素就是经济增长率。我国改革开放30多年来经济长期保持了高速增长的水平，1978-2013年经济增长的平均增速达到了9.8%。然而，我国宏观经济面临三期叠加，潜在增长率将明显下降，2012和2013年的经济增长率均在7.7%左右，预计2014年我国经济增速将回落至7.3%左右。我国经济增速回落属于向新常态的过渡，将逐步由高速回调至中高速增长平台，这种增速的放缓必然会给就业增长带来一定的压力。 （三）人口老龄化的趋势将更加明显 上世纪80年代以来的较长时间内，我国实行了独生子女政策，当时是为了应对人口的高生育率和高增长率而采取的强制措施。这一措施在一段时间内确实起到了有效控制人口增长、提高人口素质的作用。然而，进入新世纪以来我国进入了快速老龄化社会，2002年我国65岁及以上的人口占总人口的比例为7.3%，到2013年这一数值已上升至9.7%。与此同时，我国适龄劳动人口的比重也从2011年开始逐渐下降。为了适应未来人口老龄化的严峻局面，国家人口政策开始调整，从严格的独生子女政策转变为放开“双独”家庭二胎限制再到允许“单独”家庭生养第二个子女。人口生育政策的这种调整将会减少近期育龄妇女的劳动参与率，但将有利于远期劳动力的供给。
2016年中考生物-专题训练《植物的光合作用、呼吸作用和蒸腾作用》
2016中考生物专题训练《植物的光合作用、呼吸作用和蒸腾作用》一．选择题（共20小题） 1．（2015?孝感）玉兰、海棠等植物在早春时节，当叶片还没有完全长出时，却可以开出满树娇艳的花朵．推测这些花瓣中有机物的主要来源，正确的是（） A．它们是根从土壤中吸收并运输到花瓣的B．它们是花瓣在光照条件下进行光合作用合成的 C．它们是树皮将二氧化碳和水转变成有机物再运输到花瓣的 D．它们是叶在上一年通过光合作用制造并储存于树干，在开花时通过筛管转运到花瓣的2．（2015?临沂）关于绿色植物在生物圈中的作用，说法错误的是（） A．绿色植物制造的有机物养育了生物圈中的其他生物 B．绿色植物能维持生物圈中的碳﹣氧平衡C．植物的蒸腾作用能够提高大气湿度，减少降水 D．绿色植物在保持水土、防风固沙、调节气候等方面起重要作用
A．①③B．②④C．①④D．②③5．（2015?茂名）下面是实验“绿叶在光下制造有机物”的方法步骤，其中有操作错误的是（） ①把盆栽的天竺葵放到黑暗处一昼夜 ②用黑纸片把叶片一部分从上下两面遮盖 ③把天竺葵放在阳光下照射 ④一段时间后摘下叶片并去掉纸片 ⑤将叶片放入盛有酒精的小烧杯中，用酒精灯加热小烧杯 ⑥用清水漂洗叶片厚滴加碘液，观察叶色变化．A．①B．②C．④D．⑤ 6．（2015?龙沙区模拟）当你和同学们漫步绿树成荫、遍地青草的林间小路上，你会感觉到空气特别地清新和湿润，此时你会想到这是绿色植物的什么作用改善了空气的质量？（） A．光合作用和呼吸作用B．呼吸作用和运输作用 C．光合作用和蒸腾作用D．蒸腾作用和输导作用 7．（2012?济宁）俄国著名植物生理学家季米里亚捷夫说：它（绿色植物）是窃取天火的普罗米
1.1影响因素作用原因研究 研究表明，随着有机质含量和有效土层厚度的增加，灌溉和排水条件的改善，耕地质量也随之提高；伴随着地形坡度的增加变剖面构形的复杂化和土壤盐碱化程度的加深，耕地质量明显降低。农业机械化程度和生产投入的增加促使农作物产量的提高，同时改善项目区耕地质量状况。 土地整治与耕地质量存在正相关关系。对项目区耕地质量变化影响较大的因素主要有有机质含量、土壤pH 值、排水条件、灌溉保证率。土地整治项目工程对耕地的基础建设条件改善比较明显。通过相关性分析和多元回归分析得出土壤pH值是制约项目区耕地质量发展的主要因素。减少酸性化肥施用量，增加有机肥料即可提高土壤有机质含量，又能改善土壤盐碱度。 。 通过单因素和多因素分析得出土壤pH值是制约耕地质量发展的因素之一。减少化肥施用量，增加有机肥料提高土壤有机质含量，改善土壤盐碱度。推广测土配方施肥，形成合理的肥料施用结构，以充分发挥综合肥效，平衡土壤pH值和养分供给。 本研究通过耕地质量等别的变化及影响因素分析来研究土地整治项目对耕地质量的影响。通过判别构成耕地自然质量的稳定因素和变化因素，对变化因素进行更新，增加土地利用修正，结合项目工程实际情况选取路网密度、田块规整度、有效灌溉面积指数、旱涝分布情况为土地利用修正因素，根据农用地分等方法、思路来确定整治前后耕地质量等别。 上高县土地整治项目使耕地自然等别评价提升0.25 等，利用等别评价提升1.35 等，对耕地质量变化影响较大的因素主要有有机质含量、土壤pH 值、排水条件、灌溉保证率、田块规整度、路网密度。土地整治项目工程对耕地的基础建设条件改善比较明显，在今后的耕地利用与管理保护中要通过增施有机肥、减少偏酸化肥的使用等措施改善耕地土壤的酸碱环境。评价结果符合耕地质量真实情况，可作为衡量土地整治项目绩效评价的依据之一。 土地整治与耕地质量存在一定正相关关系 因此，土地整治通过土地整理，土地开发，土地复垦三类项目，可以有效地推动田、水、路、林、村综合整治，改善农村生产条件和生态环境，能有效提高耕地质量，增加农业基础设施。土地整治中各指标对耕地质量影响的影响方向，作用程度及显著性水平存在差异。其中，土地整理项目中耕地质量主要受 此，土地整治对耕地质量影响应区分不同土地整治项目类型。应把高标准农田建设、土地复垦作为未来土地整治的重点类型，强化培肥和地力建设提升措施。 在农用地分等定级的基础上对阿勒泰市耕地质量影响因素进行研究，得出制约耕地质量发展影响因素，同时提出改善耕地质量的措施。 通过耕地质量与影响因素相关性分析，得出土地利用系数、有效土层厚度、表层土壤质地、
叶的蒸腾作用和结构 教学目标:1、了解蒸腾作用的基本含义及其意义 2、知道气孔的分布状况 3、知道保卫细胞和气孔的结构 4、完整地描述水、无机盐的运输路径 重点难点:叶的结构水和无机盐的运输 教学过程: *************************************** 第一课时 课堂引入:我们都知道“水从低处留”,可在植物体内,是什么促使水从根部向茎、叶运输呢? 一、蒸腾作用 1、实验观察:选取一盆正处于生长旺盛期的植物,用一透明的塑料袋将邻近的叶片包扎起来,对该植物浇水后,置于阳光下照射。观察塑料袋上有无水珠生成,这说明____________________________。 2、水分以气体状态从体内散发到体外的过程,叫做蒸腾作用,蒸腾作用主要在叶片进行。 3、土壤中的水分由根毛进入根后,然后通过根、茎、叶的导管输送到叶肉细胞。这些水分,除了很小一部分参加植物体内各项生命活动外,99%通过蒸腾作用从叶中散发出去,蒸腾作用可以在温度偏高的情况下有效地降低叶片的温度,同时也是根吸水的主要动力,利于植物对水的吸收和运输,也利于溶解在水中的无机盐在植物体内的运输。由此可见,蒸腾作用不是在浪费水分,而是对植物的生活具有重要的意义。 4、学生讨论:①在春天的阳光下,水银柱将会有什么变化?为什么? ②如果把这一装置放在夏天的烈日下,水银柱会有什么变化?为什么? ③如果把这一装置放在阴暗潮湿的环境中,水银柱将会有什么变化?为什么? ④如果在实验室里,用电吹风吹叶片,水银柱将会有什么变化? ⑤请设计一个实验:证明蒸腾作用的强弱与光照条件有关。 5、课堂练习: ①在阴天或傍晚进行移植,并去掉部分枝叶,是为了降低: ( ) A.降低光合作用 B.减小呼吸作用 C.减少水分蒸腾作用 D.移栽方便 ②仙人掌在强烈的阳光下,不会被太阳光灼伤的原因是( ) A、吸水力大 B、储水多 C、蒸腾作用强 D、叶变成刺 ③关于植物体水分散失的意义,下列哪项是不正确的?( ) A、促进植物体对水分的吸收 B、促进矿质元素在植物体内的运输 C、促进溶于水的矿质元素的吸收 D、降低植物体特别是叶片的温度 ④北方果树由根系吸收的水分主要用于( ) A、光合作用 B、蒸腾作用 C、植物的生长 D、果实的形成 6、作业:作业本 第二课时 二、叶的结构: 1、实验观察1:①选取一张生长旺盛的蚕豆叶,用滤纸把它上、下表皮的水分吸干。 ②将两张浸有氯化钴溶液的蓝色滤纸,相对应地贴在叶片上、下表皮的表面,并用回