Mutation Research 501(2002)1–12
Mini review
Cellular communication and bystander effects:a critical review
for modelling low-dose radiation action ?
Francesca Ballarini a ,d ,Marco Biaggi a ,d ,Andrea Ottolenghi b ,d ,?,Orazio Sapora c
a
Universitàdegli Studi di Milano,Dipartimento di Fisica,via Celoria 16,20133Milan,Italy b
Universitàdi Pavia,Dipartimento di Fisica Nucleare e Teorica,via U.Bassi 6,I-27100Pavia,Italy
c
Laboratorio di Tossicologia Comparata ed Ecotossicologia,Istituto Superiore di Sanità,viale Regina Elena 299,00161Rome,Italy
d INFN,sezion
e di Milano,via Celoria 16,20133Milan,Italy
Received 20July 2001;received in revised form 12December 2001;accepted 21December 2001
Abstract
Available data suggesting the occurrence of “bystander effects”(i.e.damage induction in cells not traversed by radiation)were collected and critically evaluated,in view of the development of low-dose risk models.Although the underlying mech-anisms are largely unknown,cellular communication seems to play a key role.In this context,the main features of cellular communication were summarised and a few representative studies on bystander effects were reported and discussed.Three main approaches were identi?ed:(1)conventional irradiation of cell cultures with very low doses of light ions;(2)irradiation of single cells with microbeam probes;(3)treatment with irradiated conditioned medium (ICM),i.e.feeding of unexposed cells with medium taken from irradiated cultures.Indication of different types of bystander damage (e.g.cell killing,gene mutations and modi?cations in gene expression)has been found in each of the three cases.The interpretations proposed by the investigators were discussed and possible biases introduced by speci?c experimental conditions were outlined.New arguments and experiments were suggested,with the main purpose of obtaining quantitative information to be included in models of low-dose radiation action.Implications in interpreting low-dose data and modelling low-dose effects at cellular and supra-cellular level,including cancer induction,were analysed.Possible synergism with other low-dose speci?c phenomena such as adaptive response (AR)(i.e.low-dose induced resistance to subsequent irradiation)was discussed.?2002Elsevier Science B.V .All rights reserved.
Keywords:Bystander effect;Adaptive response;Cellular communication;Low doses;Mechanistic models
1.Introduction
Estimates of the various damage types at sub-cel-lular,cellular and supra-cellular level induced by low
?Presented at Bystander Effect Workshop,Dublin,Ireland,December 2000.
?Corresponding author.Tel.:+39-02-5031-7655;fax:+39-02-5031-7630.
E-mail address:andrea.ottolenghi@mi.infn.it (A.Ottolenghi).
doses,where no experimental data are available,are generally based on linear back-extrapolations from data at higher doses.However,a large amount of data produced during the last decade seem to indicate higher damage yields than expected,possibly due to the so-called “bystander effect”(i.e.the induction of damage in cells that were not directly hit by radiation).One of the most intriguing aspects of these experi-ments relies in that bystander damage is observed even
0027-5107/02/$–see front matter ?2002Elsevier Science B.V .All rights reserved.PII:S 0027-5107(02)00010-6
2F.Ballarini et al./Mutation Research501(2002)1–12
at very low doses,down to the mGy level,and it does not signi?cantly increase with dose.No clear-cut con-clusions can be drawn on the mechanisms underlying bystander effect observations.Different pathways may be involved,depending on the speci?c conditions.In any case the various forms of cellular communication seem to play a key role,since damage in non directly hit cells may represent a response to signals coming from cells that were directly hit by radiation.If these ?ndings are con?rmed,radiobiology experiments may need to be re-interpreted and the models of low-dose radiation action may need to be revised.Furthermore, a signi?cant role of bystander effects in vivo would imply the re-evaluation of models of damage at tis-sue and organ level.A typical example is provided by low-dose cancer risk,which up to now has gener-ally been estimated by assuming a linear,no-threshold dose-response.
This scenario might be further complicated by the presence of other phenomena such as adaptive response(AR).The expression“AR”is used by dif-ferent investigators to indicate different effects also including hormesis,de?ned as a“stimulatory effect caused by low levels of toxic agents”[1],and increased radioresistance,i.e.sub-linear response at low doses.Strictly speaking,the term AR applies to protection provided by low-dose irradiation with respect to subsequent(higher-dose)irradiation[2]. Although the mechanisms underlying this effect are largely unknown,several similarities between AR and bystander effects can be found.In the framework of low-dose effect estimates,it has been inferred that AR might lead to a sub-linearity in cancer risk at low doses(e.g.[3]).If so,AR should be considered as a possible competing phenomenon with respect to bystander effects.
2.General features of cellular communication Cells possess complex systems—including recep-tors,kinases,phosphatases,GTP-binding proteins and several other molecules—that enable them to send or respond to signals to or from other cells.There exist three main forms of cell signalling:paracrine,synaptic and endocrine.Molecules secreted by a cell can be car-ried far apart to act on distant targets(synaptic and en-docrine signalling),or can act locally by affecting the cells in the close environment(paracrine signalling). By the same mechanisms,cells can send signals to other cells of the same type(autocrine signalling); it follows that they can send signals to themselves also.As can be de?ned from the currently available in vitro experiments,bystander effects are mainly a consequence of paracrine/autocrine signalling.In the literature there are several examples that can help in understanding these effects(for a review see[4]). The production and release of eicosanoids is an example of paracrine signalling.These molecules are continuously synthesised in cell membranes starting from20-carbon fatty acids with at least three dou-ble bonds.There exist four classes of eicosanoids: prostaglandines;prostacyclines;thromboxanes and leukotrienes.They mainly derive from arachidonic acid and they are involved in a wide variety of bio-logical activities,including in?ammatory responses. When cells are activated by damage induction or by chemical signalling,the rate of eicosanoid synthesis increases.The local levels of eicosanoids in?uence both the cells that produce them and their immediate neighbours.The?rst step of the synthesis is the release of the fatty acid cleaved from membrane phospho-lipids by phospholipases.This process can be triggered by low levels of oxidised poly-unsaturated fatty acids (PUFA)and can be ampli?ed by the action of phos-pholipases.The subsequent oxidation step involves the activity of cyclooxygenases and lipoxygenases. Other signalling molecules are also produced in response to oxidative stress induced by chemical and physical agents.Phospholipase C,produced in res-ponse to signals to plasma membrane growth-factor receptors,can catalyse the hydrolysis of phosphati-dylionsitol-4-5-bisphosphate(PIP2).The products of such hydrolysis,inositol(1,4,5)triphosphate(IP3)and diacylglycerol(DG),can cause a release of Ca2+ and an activation of phosphokinase C(PKC).PKC is a key enzyme representing a family of more than 11isoenzymes,dependent or not dependent on the presence of Ca2+.This family of enzymes can phos-phorylate various cellular proteins involved in cell proliferation control.
Also cyclic AMP(cAMP)can play a signi?cant role as a second messenger in cell proliferation con-trol.cAMP can also regulate PKC and the transcrip-tion of several genes.More than25years ago it has been shown that the intracellular levels of cAMP can
F.Ballarini et al./Mutation Research501(2002)1–123
be increased by treatment with prostaglandines E1, which can react with adenyl-cyclase receptors on the outer membrane leading to an increase of intracellular cAMP levels and,secondary,Ca2+levels.This treat-ment can in?uence the shape of survival curves of V79 cells irradiated with X-rays,mainly in the low-dose range[5].Finally,oxidative damage can produce a family of second messengers from membrane phos-pholipids.Oxidative products of linoleic and arachi-donic acid,such as the hydroperoxy-eicosatetraenoic acid(H-PETE),the hydroxy-2-nonenal(HNE)and the hydroxy-octadecadienoic acid(HODE),can be released by a cell and can react in neighbouring cells by activating signal cascade triggering repair pro-cesses or by activating cell death mechanisms.It has recently been reported that DNA damage induced by human mammary lipid extracts can be detected in breast epithelial cells[6].Interestingly,the authors showed that the most active lipid extracts were those obtained from donors whose cells contained the higher pre-existing DNA damage.
Intercellular communication through gap-junctions represents another way to co-ordinate the activities of neighbouring cells.These structures are specialised cell–cell junctions that can form between adjacent plasma membranes:gap-junctions directly connect the cytoplasms of neighbouring cells via narrow channels (≈2nm in diameter).Intercellular communication via gap-junctions allows the exchange of small molecules (<2000Da)such as Ca2+and cAMP,but not macro-molecules such as proteins and nucleic acids.Also compounds such as eicosanoids and lipid oxidative products can hardly diffuse trough gap-junctions,due to the high lipophylicity of these compounds and to the presence of water in gap-junction channels.
A clear general frame emerges from the available data:the different forms of cell signalling triggered by oxidative stress(ionising radiation acts mainly trough reactive oxygen species,ROS)are strictly correlated with cell proliferation and cell https://www.doczj.com/doc/a913412907.html,munication between damaged and undamaged cells has been sug-gested to lead to a general increase in genomic insta-bility.More speci?cally,it has been shown that factors secreted by UV-irradiated cells can increase muta-tion rates in unirradiated cells up to10-fold over?ve generations[7,8].Similar results have been obtained following irradiation with UV A rays in presence of psoralen,suggesting that the sensitisers may extend this response to long wavelengths.UV-irradiated skin
?broblasts can secrete at least two proteins,identi?ed
as interleukin-1and the basic?broblast growth factor
[9].Moreover,also interleukin-8and tumour necrosis
factor alpha(TNF-?)have been shown to be secreted
together with the already mentioned eicosanoids as a
consequence of in?ammation processes[10].
3.Bystander effects:experimental
approaches and indications
3.1.Treatment with irradiated conditioned
medium(ICM)
A large amount of data on bystander effects has
been obtained with the so-called“ICM treatment”
[11–14].This technique consists in replacing the
culture medium of non-irradiated cells with medium
taken from cell cultures previously exposed to radia-
tion.The main?nding of these studies relies in that
such treatment can reduce survival of unexposed cells.
This suggests that,as a result of a radiation insult,
certain cell types can release factors in the medium,
which therefore becomes potentially cytotoxic.
A detailed description of this approach can be
found in[11].The essential points will be summarised
herein.Non-irradiated human cell lines—including
normal keratinocytes,which are epithelial cells,and
normal?broblasts—seeded at cloning densities were
fed with medium taken from cultures of the same cell
type,previously irradiated as single cells with5Gy 60Co gamma-rays.Before being transferred to recip-ient?asks,the medium was?ltered to ensure that no
cells could still be present.This treatment was found to
reduce clonogenic survival of keratinocytes,whereas
no effect was observed for?broblasts.Furthermore,
medium taken from irradiated keratinocytes reduced
survival of unexposed?broblast,whereas medium
from irradiated?broblasts had no effect on unexposed
keratinocytes.Treatment with medium irradiated in
absence of cells had no effect on any of the cell lines,
indicating that a role of free radicals produced by
hydrolysis of medium components can be excluded.
Apoptotic?gures were also scored in ICM-treated ker-
atinocytes.No signi?cant dose-dependence was obser-
ved in the range0.5–10Gy.A signi?cant increase of
cell killing with the number of irradiated cells was
4F.Ballarini et al./Mutation Research501(2002)1–12
observed:medium taken from cultures of300,000 keratinocytes induced a response close to that of cells directly irradiated with5Gy.By transferring the medium at different post-irradiation times,the ICM toxicity was found to increase rapidly in the?rst few hours post-irradiation.Only a slow increase was ob-served in the range from3to60h.The time-response and the fact that an increased number of irradiated cells led to an increase in the medium toxicity were inter-preted as an indication that irradiated cells can release into the medium a factor able to in?uence survival of unexposed cells.In a subsequent work the authors hypothesised the secretion of a signalling molecule, rather than a factor toxic per se.Indeed the latter might be expected to provide a linear dose-response rather than a saturation-type effect[12].Furthermore, on the basis of heating/freezing tests,this signal was supposed to be protein-like:interleukin-8was consid-ered an“attractive candidate”.This protein,which is involved in in?ammatory responses(see Section2), has also been shown to be involved in a bystander in-crease of sister chromatid exchanges(SCEs)observed after conventional irradiation of human?broblasts with very low doses of alpha particles[15,16].
A possible role of the degree of cell-to-cell contact during irradiation was investigated[12]:medium was taken from normal human keratinocytes irradiated either as single cells,or microcolonies of three/four cells or con?uent monolayers.No signi?cant dif-ference was found between single cells and micro-colonies,whereas an increase in the medium toxicity was observed in the case of con?uent cultures.The authors concluded that the degree of cell–cell con-tact during irradiation was not signi?cant,whereas the number of irradiated cells is the only relevant parameter.Inhibition of gap-junction intercellular communication(GJIC)with the tumour promoter phorbol myristate acid(PMA)in con?uent cells led to a further increase in cell killing.The investigators provided no explanation for this phenomenon.On this subject,it is worthy remarking that the test for a possible role of GJIC is not consistent with the hy-pothesis of a protein-like signal,since the dimensions of gap-junction channels do not allow diffusion of proteins(see also Section2).By contrast,if smaller molecules were involved,the enhanced cell killing observed after GJIC inhibition might be explained as follows.If the signalling molecule is small enough to diffuse through gap-junction channels,it is likely that a fraction of the signal will be delivered to neigh-bouring cells rather than to the medium.Therefore, GJIC inhibition would lead to lower signal levels in neighbouring cells and thus higher signal levels in the medium,which would become more cytotoxic, consistent with the observed increase of cell killing. In a subsequent work the relative contributions of bystander and targeted cell killing were calculated after irradiation of human keratinocytes with60Co in the dose range between1and5Gy[14].Clonogenic survival was assumed to be a mixture of direct cell killing and bystander death.Direct cell death was calculated as the difference between total cell death (reduction in cloning ef?ciency of conventionally irradiated cells)and bystander cell death(reduction in cloning ef?ciency of unexposed cells treated with ICM).The data showed that below0.5Gy clonogenic cell death was due to bystander effects only,whereas after doses of0.5Gy and higher the curves were a combination between a dose-independent bystander effect and a non-bystander effect increasing with dose. Interestingly,a similar study on delayed cell death showed no signi?cant evidence for a non-bystander contribution below5Gy.
3.2.Conventional irradiation with low doses
of light ions
Evidence for some forms of bystander effect has been suggested also by conventional irradiation with low doses.One of the?rst studies in this?eld has showed a signi?cant,unexpected increase in the fre-quency of SCEs after exposure of Chinese hamster ovary(CHO)cells to very low doses of alpha particles, from0.03to0.25cGy[17].While about1%or less of the cells were actually traversed by a particle track, 30–45%of the individual cells showed increased levels of SCE.This suggests that genetic damage following exposure to very low doses of light ions may occur also in non directly-irradiated bystander cells.These?ndings,which have been ascribed to the generation of ROS outside of the nucleus,have been con?rmed by other research groups in the case of con?uent human?broblasts[15].The lowest dose delivered in the CHO cell experiment is almost10-fold lower than the annual exposure limit for the public indicated by the International Commission of Radi-
F.Ballarini et al./Mutation Research501(2002)1–125
ation Protection[18].This makes this study of great interest for its possible implications in the evaluation of the radiation action at very low doses.However, these results are of dif?cult interpretation in terms of health risks,since it is still not clear how SCE can be related to endpoints such as cell conversion to malignancy.
A few years later,the same group of authors has investigated a possible bystander modulation of the expression of speci?c genes following alpha particle irradiation[19].Normal human?broblasts synchro-nised in G0/G1phase were exposed to238Pu alpha particles in the dose range0.66–75cGy.The cells were then harvested for Western analysis of the expression of different genes including p53and p21, which are tumour suppressors involved in apoptosis and cell-cycle control.The fraction of cell nuclei tra-versed by an alpha particle was calculated by assum-ing that the average nuclear cross-section of a normal human?broblast is140?m2.This may represent a weak point for this study:a measurement of the actual dimensions of the cell nuclei would make the calcula-tion more accurate and reliable.Indeed the calculation of the fraction of actually traversed cells(generally based on the average number of particles and cells in a certain surface and on the average minimum energy deposited by each traversal)is one of the most critical points in bystander effect observations with low dose, charged-particle broad beams.Moreover,the role of intercellular communication might be overestimated, since a fraction of the effects ascribed to bystander mechanisms might be due to cytoplasmic irradiation. In any case,only a?ve-fold relative increase in the expression of p21was observed in correspondence to a16-fold increase in the fraction of traversed nuclei. This suggests that at0.66cGy a larger number of cells than those whose nuclei were actually traversed may contribute to the increase of p21levels[19].The extent of p53and p21modulation was signi?cantly reduced when cells were treated with lindane,which inhibits gap-junction intercellular communication via inhibition of connexin43,a major component of gap-junctions in skin?broblasts.The authors there-fore concluded that gap-junction-mediated communi-cation might be involved in the observed modulation of p53/p21expression in bystander cells.Seymour and Mothersill[13]commented that the role of gap-junctions suggested by Little and co-workers [19]disagrees with their results with ICM treatment. Indeed,by treating human keratinocytes with ICM [12],they found an increase(rather than the decrease that they expected)in the medium cytotoxicity after inhibiting gap-junctions with PMA.
However,it has to be taken into account that these two studies are completely different.In the experi-ment of Mothersill and Seymour(see also Section 3.1)each cell in the population would be exposed to photons and the endpoint of interest(i.e.cell death) was observed in non-exposed cells fed with medium taken from exposed cultures.By contrast,Little and co-workers directly irradiated a population of con-?uent cells(normal human?broblasts)with alpha particles.The doses were so low that only a small fraction of the cells were actually traversed by a parti-cle track.Therefore,the?ndings of these two studies can hardly be compared:different treatments(ICM treatment or direct radiation exposure),different doses (a few Gy or a few cGy)and also different,although probably correlated,endpoints(cell death or p53/p21 modulation).Indeed,when Mothersill and Seymour observed survival of human keratinocytes directly ir-radiated with60Co as single cells or microcolonies of different sizes(up to50cells),they did?nd a role of GJIC!In fact cell death was found to increase with the microcolony size.Moreover,GJIC inhibition dur-ing microcolony irradiation led to lower inactivation levels,similar to those observed with single cells[20]. Also a possible bystander induction of gene mu-tations,which are thought to have a major role in the initiation of radiation carcinogenesis,has been investigated with low-dose conventional irradiation [21].An unexpected increase of hprt gene mutations was observed in con?uent CHO cells exposed to very low?uences of238Pu alpha particles during the G1 phase of the cell cycle.The usual linear response was found over the range between5and1.2Gy.How-ever,mutation yields higher than those predicted by a linear back-extrapolation of higher dose data were measured below5cGy,where the mean number of traversals per nucleus was calculated to be in the range 0.05–0.3.This suggests the occurrence of mutations in non-irradiated bystander cells.On the basis of mi-crobeam experiments described in the literature[22], a role of cytoplasm irradiation was judged unlikely by the authors:indeed such experiments indicated that cytoplasm irradiation is much less effective than
6F.Ballarini et al./Mutation Research501(2002)1–12
nucleus irradiation in mutation induction.Further-more,it has to be taken into account that the volume occupied by the nucleus of CHO cells is very large with respect to the cytoplasmic volume.
The results reported by Nagasawa and Little might be of great interest for the estimate of health risks fol-lowing very low doses of alpha particles.It is worthy reminding that the estimation that as much as15%of lung cancers may be due to residential radon expo-sure[23]has been derived from linear,no-threshold back-extrapolations of data from underground miners exposed to higher doses.If the non-linearity found by Nagasawa and Little at low doses is con?rmed by further studies,also for in vivo exposure,data on cancer incidence may need to be re-interpreted and carcinogenesis models may need to be revised,at least at low doses.In this context it has to be taken into account a comment of Chadwick and Leenhouts[24], who re-examined the work described above by?tting a straight line to the complete set of mutation data, except the background point.The value of the back-ground mutation frequency resulting from this anal-ysis(0.41×10?5)was signi?cantly higher than the mutation yield measured in control cells by Nagasawa and Little(0.14×10?5).Chadwick and Leenhouts therefore concluded that this experiment provides no evidence for a bystander effect.However,Little and Nagasawa[25]responded that the measurement of the spontaneous mutation frequency was performed very carefully,and that there is no reason why the background value should be three-fold higher than the value that they actually measured.To support their interpretation,Little and Nagasawa outlined that their ?ndings are consistent with a published microbeam experiment,which showed mutation yields higher than expected after irradiation of mammalian cells with an alpha particle microbeam able to target indi-vidual cells[26].In any case it has to be pointed out that spontaneous mutation frequencies should be mea-sured in parallel to each dose value and then subtracted (taking also into account the propagation of errors), to minimise the risk of possible biases introduced by statistical?uctuations and biological variability.
3.3.Irradiation with microbeams
The studies discussed above strongly suggest a role of extranuclear-and possibly extracellular-targets in the propagation of certain damage types after irradia-tion with very low doses of light ions or treatment with ICM.Experiments allowing the identi?cation of spe-ci?c targets for such phenomena can be of great help to better understand the underlying mechanisms and to quantify the relative contributions of different targets. This kind of studies is now possible due to the increas-ing number of microbeam facilities(e.g.[27–37]).A few representative works will be discussed herein. At the Gray Laboratory(UK)human?broblasts in plateau phase were seeded into special dishes.Each dish was divided into four regions of5mm×5mm containing100–200cells and four targeted cells per dish(one per region)received?ve3MeV3He2+ particles through the centre of the nucleus[38]. Although only four cells had been directly traversed by radiation,80micronucleated and33apoptotic cells were observed over a total of3256scored cells.As a comparison,30micronucleated cells and no apoptotic cells were observed in a sham-irradiated control dish in which3076cells were scored.No signi?cant dif-ference was found by delivering to each targeted cell a higher number of particles(10or15).The authors explicitly stated that their data provide direct evidence for a cell-to-cell transmissible effect.Although they did not provide detailed suggestions for the underlying mechanisms,they judged more likely a medium-born effect with respect to gap-junction intercellular com-munication,since the targeted cells were irradiated as single units.Furthermore,on the basis of similarities with the instability phenotype observed by many in-vestigators(see,e.g.[39]),the authors suggested that the subcellular location of radiation may be a small component of the initial acute response,but may be-come more important in subsequent cell generations. The experiment described above has been re?ned later [40],when1–153He2+particles of105keV/?m were delivered through the centre of a human?broblast nu-cleus selected within600–800cells.A two–three-fold increase in the background frequency of micronucle-ated/apoptotic cells was found with respect to control dishes,where the same number of particles were deli-vered to a location outside a cell.The effect was observed also after a single particle traversal and no increase in the effect was observed by increasing the number of delivered particles.Since cell–cell contact was minimal and damaged cells appeared randomly distributed over the dish,the authors concluded that
F.Ballarini et al./Mutation Research501(2002)1–127
an extracellular factor was likely to be involved, although a possible role of gap-junctions could not be ruled out if cells were irradiated in close contact. In a subsequent work the3He2+microbeam has been used to irradiate a human epithelial tissue under in vivo-like conditions,where dividing and differen-tiated cells were present[41].Although the nuclei of only10cells from a primary uroepithelial explant were irradiated(with10particles),several thousand apoptotic and micronucleated cells were scored3days after irradiation.The higher effect observed with re-spect to the case of the?broblast experiment[38,40] was ascribed to the higher degree of cell-to-cell con-tact.Furthermore,irradiation of cells on the actively proliferating edge of the explant resulted in damaged cells mainly concentrated at the explant periphery. These?ndings are consistent with similar works available in the literature[42,43],in which an unusual response of human uroepithelium primary explants to low doses of60Co gamma-rays has been observed.To investigate whether similar bystander effects can oc-cur also after photon irradiation,a focused low-energy X-ray microprobe has recently been developed at the Gray Laboratory.This microbeam has a0.5?m diam-eter and is able to target speci?c regions of individual cells and to revisit both the irradiated and the unirra-diated cells—and their progeny—for scoring of dif-ferent damage types[44].This project is of particular interest because the irradiation of speci?c non-nuclear targets(such as mitochondria,which play a key role in modulating oxidative activity and apoptosis)can be of great help in elucidating the mechanisms underlying the various types of observable bystander effects.
A possible bystander induction of mutations has also been investigated with a microbeam[26].A randomly selected fraction(20%)of human–hamster hybrid cells in close contact was irradiated with20 alpha particles delivered by a microbeam targeting the cell nuclei.The cells were scored for mutations at the CD59locus of the human chromosome11and the ob-served mutant fraction was three-fold higher than the fraction predicted by assuming no bystander effect.No signi?cant difference was found by reducing the frac-tion of irradiated cells to10%.Pre-treatment of cells with the?OH scavenger DMSO had no signi?cant effect on mutation induction,whereas pre-treatment with lindane,which inhibits gap-junction intercellu-lar communication,led to a signi?cant decrease in the yield of mutants.This suggests a major role of cell-to-cell communication via gap-junctions with re-spect to free radicals.A signi?cant role of the culture medium was judged unlikely,since less than3?l of medium per dish were present at irradiation time.
In a previous work of the same group[22],the same endpoint has been investigated after targeted cytoplasmic irradiation.The treatment was found to be mutagenic at the CD59locus,but the toxicity was minimal.Moreover,most of the induced mutations were similar to spontaneous mutations and entirely different from mutations arising from irradiation of the cell nucleus.Experiments with radical scavengers suggested that the mutagenicity of cytoplasmic irra-diation might be mediated by the production of ROS.
4.Radiation-induced AR
Radiation-induced AR has been originally des-cribed more than15years ago in studies on chro-mosome aberration induction in human lymphocytes [45].Several experimental data have provided support for the occurrence of ARs in different cell systems.
A review can be found in[46,47].So far,this phe-nomenon has been observed both in vitro(human and animal,normal and tumour cell lines)and in vivo (mice)[48,49].AR can be expressed in different bio-logical endpoints including chromosome aberrations, gene mutations and cell survival[2].Adapting doses, i.e.doses that are effective at inducing AR,were found to be in the range5–20cGy for a single expo-sure to low LET radiation.ARs have been observed to decline with doses above20cGy and disappear with doses exceeding0.5Gy[50].
The biochemical and biological pathways involved in AR have not been clari?ed yet.The main hypothe-ses propose that low radiation doses can enhance DNA repair ability and antioxidant activity.Further-more,speci?c protective proteins might be produced ad hoc to compete with indirect damage induced by subsequent irradiation[51].An increase in apop-totic cell death has also been taken into account as a possible mechanism underlying AR[52].The most mentioned upside of AR is possible protection against radiation-induced tumours.However,it has to be taken into account that long-term AR might protect tumour masses against eradication by radiotherapy
8F.Ballarini et al./Mutation Research501(2002)1–12
[53].To what extent AR can decrease cancer risk and whether AR should affect current risk assessments is still an open question:opinion is split on this latter point.Some investigators have explicitly stated that the role of AR effects is so important that the lin-ear,no-threshold model has to be reconsidered(e.g. [2,3]).By contrast,others think that the current policy should not be changed until the mechanisms under-lying this phenomena are more clearly understood [54–56]:“(We)do not know enough about AR(or hormesis)to modify the entire set of guidelines”[56].
5.Possible implications for the estimate of
low-dose radiation action and the understanding of radiation carcinogenesis
“The understanding of the cellular basis of can-cer means being able to describe the biochemical of the regulated pathways between the cell surface and the nucleus that control cell growth”[57].This sen-tence summarises well what James Trosko named the “reductionalistic”view of carcinogenesis[58].On the other side,the“holistic”view of the problem is well represented by the approach of Potter[59],who has stated that“the cancer problem is not merely a cell problem,it is a problem of cell interaction,not only within tissues,but with distant cells in other tissues”. More generally,cancer can be viewed as a disease of homeostasis,i.e.the orchestration of speci?c cell/tissue/organ and organism functions such as cell proliferation,differentiation and ability to undergo apoptosis or adaptively respond.Indeed,a synthesis of these apparently con?icting approaches can be found only on the basis of deep mechanistic studies of the possible occurring events,taking into account possi-ble stochastic phenomena.In this context it has been hypothesised that the disruption of GJIC plays a major role in tumour promotion,starting from the working assumption that the“dysfunctional GJIC theory”can integrate all of the other carcinogenesis theories,since each of them is related to GJIC[58].The integration of the“initiation/promotion/progression theory”is worthy being reported as a paradigm of this approach, which led to a re-interpretation of the three classical steps(initiation,promotion and progression)of one of the most diffused carcinogenesis theory in terms of cell-to-cell communication.The?rst step was identi?ed with a stable alteration of a gene controlling terminal differentiation but not altering proliferation, leading to a certain number of non-terminally differ-entiated cells.Inhibition of GJIC in these“initiated”cells by endogenous factors or exogenous chemicals would then lead to clonal expansion,i.e.the forma-tion of a monoclonally-derived focus of benign cells (promotion).Finally,genomic inhibition of GJIC would lead to progression,i.e.the autonomous growth of the tumour mass.The thesis of a major role of gap-junctions in tumour promotion is supported by a series of experimental evidences:(a)GJIC is reduced in most neoplastic cells,which have fewer and smaller gap-junctions;(b)GJIC can be inhibited by growth stimuli such as carcinogens and oncogenes;(c)GJIC is stimulated by growth inhibitors such as retinoids and(d)growth of neoplastic cells can be inhibited by co-culture with normal cells,which possibly secrete growth inhibitors in the medium.It is worthy remind-ing that modulation of intercellular communication is the basis of gene therapy,which consists in intro-ducing active connexin genes in tumour cells.This treatment leads to an increase of gap-junction activity, which can help in increasing drug penetration in the tumour mass.Gene therapy itself can be viewed as a bystander effect,since many cells are killed although only a few cells are injected.
A non-linear response at low doses is one of the most interesting characteristics of bystander effect observations.If this feature is con?rmed also in vivo,cancer risk models at low doses,which are of interest for occupational exposures and also public exposures(e.g.inhalation of residential radon),may need to be re-evaluated.Low-dose cancer risk is gen-erally estimated on the basis of linear,no-threshold back-extrapolations of higher dose data from epi-demiological studies,such as the analyses on the atom-bomb survivors of Hiroshima and Nagasaki. However,a low-dose supra-linear response for end-points such as gene mutations,possibly due to by-stander effects,would lead to an increase in the number of“initiated”cells,and thus an increase of low-dose cancer risk.On the other side,bystander effects can enhance cell killing and this might act as a protective mechanism competing with the increase of non-lethal,potentially carcinogenic damage(e.g. mutations).Thus,the overall effect of bystander path-ways on low-dose radiation risk would be determined
F.Ballarini et al./Mutation Research501(2002)1–129
by the balance between these two contributions(cell
killing versus damage types such as mutations,which
generally do not affect cell proliferation but can initi-
ate carcinogenesis).A quantitative estimation of these
two contributions is therefore one of the main goals
in this?eld.Some experimental studies seem to sug-
gest that the contribution of bystander effects to cell
killing is signi?cantly higher than the contribution to
mutations.For instance33apoptotic cells were ob-
served after microbeam irradiation of four cells[38],
whereas only a?ve-fold increase of hprt mutations
in CHO cells was found[21].However,the scenario
might be much more complicated due to a possible
role of bystander-induced delayed effects,i.e.bio-
logical effects that appear only in the cell progenie.
Dose-response curves found in studies on bystander
effects are very similar to those found for genomic
instability,which includes both delayed cell death
and delayed non-lethal damage.Thus,it is likely that
at low doses genomic instability also can be induced
in non-irradiated bystander cells.This hypothesis is
supported by a work suggesting a role of GJIC in de-
layed death of human epithelial cells irradiated with 60Co[20].Interestingly,for initial clonogenic cell death a dose-dependent contribution of direct irradi-
ation appeared above0.5Gy,whereas no signi?cant
contribution of direct irradiation to delayed death
was observed in the dose range0–5Gy.This would
imply that the relative contributions of bystander ef-
fects to initial cell death and non-lethal damage may
not be suf?cient to re-evaluate low-dose cancer risk:
also the contributions of genomic instability should
be taken into account.Further complications would
arise by taking into account also a possible synergism
between bystander effects and AR,whose implica-
tions for low-dose risk have been discussed above.
Incidentally,some low-dose supra-linearity in cancer
incidence has been inferred by a re-evaluation of the
data provided by Japanese survivors[60].It is not
easy to assess the reliability of this analysis.However,
the following comment is worthy being reported:
“The linear non-threshold dose-response hypothe-
sis may be used as a simple,convenient method to
calculate numbers in radiation protection planning
but should not be mistaken as a stringent scienti?c
conclusion directly derived from the present state
of knowledge of the processes involved in radiation
carcinogenesis”[61].6.Discussion and conclusions
A few representative,and therefore non-exhaustive, experimental studies suggesting evidence for different radiation-induced bystander effects(e.g.cell killing and gene mutations)were discussed.Some general features were identi?ed:bystander effects are ob-served at very low doses(down to the order of the mGy),do not increase signi?cantly with dose and do not contribute signi?cantly to total damage at higher doses.The features of such phenomena seem to be strongly dependent on different factors,such as:(a) the way in which the radiation insult is delivered (conventional irradiation with low doses,irradiation with microbeams or treatment with ICM);(b)the cell type(normal or cancerous,human or animal,epithe-lial or?broblastic,etc.)and the cell-cycle stage;(c)in the case of direct irradiation,the degree of cell-to-cell contact;(d)in the case of ICM treatment,the number of irradiated cells and possibly the medium con-stituents and(e)the particular endpoint in study. Bystander effects have many aspects in common with AR,which might represent a competing phenomenon with respect to the determination of low-dose effects. Several models of the induction of different damage types following direct irradiation have been devel-oped(see, e.g.[62]for cell inactivation,[63]for chromosome aberrations,[64]for hprt mutations and [65]for free radical production).However,modelling bystander effects and/or AR would require a quanti?-cation of the role played by the factors outlined above. In the case of ICM treatment,killing of unex-posed cells has been ascribed to the secretion of a protein-like signal able to initiate apoptosis in cells fed with ICM.Interleukin-8has been proposed as a possible candidate.An alternative,equally attractive candidate is the TNF-?mentioned in Section2.This protein belongs to the cytokine family and can trigger apoptosis of keratinocytes via the receptor TNF-Rp55 (see[66]for a review on UV-induced apoptosis in keratinocytes).In fact while TNF-?can be produced by keratinocytes,TNF-Rp55,which is ubiquitously expressed and is thought to be involved in mediat-ing cytotoxicity and?broblast proliferation,has been shown to be implicated as the main mediator of apop-tosis in non-lymphoid cells.This is consistent with the observation that medium from irradiated keratinocytes can induce cell killing in unexposed?broblasts.The
10F.Ballarini et al./Mutation Research501(2002)1–12
fact that medium from irradiated keratinocytes is toxic to unexposed?broblasts is extremely intriguing, since it can be viewed as an in vitro reproduction of tissue-speci?c responses that can be observed in vivo:the skin response to UV irradiation is a typical example.A product of lipid oxydation may represent another candidate.To what extent the particular con-ditions of ICM treatments can reproduce the in vivo cellular environment,and thus to what extent these ?ndings can be applied to radiation carcinogenesis studies,has still to be clari?ed.
By contrast,in the case of direct exposure of cell cultures to radiation the degree of cell-to-cell contact seems to be a key parameter.If cells are in close contact,gap-junctions seem to have a major role, whereas if the degree of contact is poor,the culture medium also seems to be important.In fact inhibition of gap-junction activity in cells irradiated in close contact resulted in decreased levels of cell death[20], p53/p21induction[19]and gene mutations[26].On the other side,a microbeam experiment performed with minimal cell-to-cell contact resulted in a random distribution of damaged cells over the entire surface of the culture dish[40],suggesting a major role of an extracellular factor released in the medium,rather than gap-junctions.With respect to low-dose conven-tional irradiation,for which the fraction of traversed cells is estimated on the basis of the cell dimensions, microbeam techniques have the great advantage to allow targeting and monitoring of speci?c regions of individual cells.However,it cannot be neglected that some procedures of cell staining(for example UV ill-umination)might modify the experimental conditions and introduce a bias in these experiments. Microbeam irradiation of human cells harvested for both initial and delayed cell death and hprt muta-tions can be crucial experiments to better understand the mechanisms underlying bystander effects.From one side microbeam techniques would allow one to target and“follow up”individual cell nuclei,whereas on the other side radiation-induced hprt mutations are one of the most well known endpoints in radiobi-ology.As for concerns the identi?cation of possible signalling molecules,the hypothesis of a major role of TNF-?in cell-killing induction after ICM treat-ment of human keratinocytes(see Section4)might be tested by a treatment with an anti-TNF-?anti-body,which has been found to signi?cantly reduce UVB-induced apoptosis in keratinocytes.If this test is not successful,speci?c molecules might be identi?ed by comparison of gel electrophoresis bands obtained before and after irradiation:when a band of increased intensity appears,that band might be isolated and sequenced.More generally,a progressive separation of the different medium components might be of some help as a?rst approximation.Animal studies, together with microbeam irradiation of tissue cultures obtained with the primary explant growth technique, can be of great help in clarifying to what extent in vitro?ndings can be applied to the in vivo case. Acknowledgements
We are extremely grateful to Dr.Mario Faretta of the European Institute of Oncology(Milan,Italy)and Dr.Roberto Cherubini of the National Laboratories of Legnaro(Italy)for useful discussions and sug-gestions.This work was partially funded by the EC (contract no.FIGH-CT1999-00005,“Low dose risk models”)and the Italian Space Agency(ASI,contract no.I/R/090/00).
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两学一做当先锋改革强军显作为演讲 稿 我，是一名入警大学生，11年大学毕业时，我毅然决然的选择了携笔从戎，成为了光荣的边防部队中的一员。XX 年1月，刚刚结束集训的我，被分配到了丽江边防检查站。每当我向朋友说起我在丽江工作时，他们总是不解的问我：丽江边防？丽江又不在边境线，哪来的边防？也许，这也是在座的许多人对我们这支部队的疑惑，可大家却忘了，我们美丽的丽江，为了更好的迎接海外游客，开通了多达五条的国际航线，我们丽江边防检查站，正是驻守在丽江机场这个国门一线的哨兵，担负着服务广大出入境旅客的职责任务。4年多来，我们顺利查验了近XX架次的出入境航班，验放了多达18万名的中外游客。而在这些数字的背后，却有着一个关于梦想的故事。 我刚到丽江站的时候，丽江站才刚刚组建，大门上连块门牌都没有，全站加起来，只有17个人，整个营区空旷得出奇，连说话稍微大声一些，都感觉带着回音。 入夜，一月的丽江出奇的寒冷，宿舍里除了两张床，再无一物，我几乎是把所有的军装盖在被子上才觉得温暖，睡不着的时候，我在想，这样的一个单位，日子怎么过呀！ 之后的日子里，我们第一批丽江边检人拿着清扫工具，打扫着空空荡荡的营区与办公楼；我们在仅有的一间会议室
里开着武警大会，因为椅子不够，很多人得站着；我们去山上挖树苗回单位栽种来美化营区；因为缺少桌椅电脑，综合办公室的战友必须排队使用电脑办公；因为兵员紧张，所有干部白天要上班，夜里还要负责岗哨；我们自己动手画篮球场的标线，自己动手搭篮球架；12年3月15日，丽江站正式挂牌成立、5月31日，第一架飞往香港的航班我们顺利验放……这一件件、一桩桩的小事，成了我最珍贵的回忆。 如今的丽江站，有了一流的信息化硬件设施，有了崭新的官兵宿舍，有了宽敞的食堂，有了丰富的文体活动场所。可我不会忘记我们曾经度过的那段艰难的日子。 这段日子，记录的不仅仅是丽江站从无到有的岁月，更是一群丽江边检人带着"敢想、敢试、敢干"精神顽强拼搏的见证。我们缺少物质上的支持，可我们有一个信仰：党和国家选择在丽江设立机场口岸，就是需要我们为口岸的顺畅运行保驾护航，我们不可以辜负这一期望。为了这一个信仰，丽江边检人已经在这片热土上度过了四个春夏秋冬！ 工作之余，会有战友聊天时说起老单位的情况，对比丽江站，觉得丽江站很艰苦。我很羡慕的听着他们聊老单位的一切，觉得他们的军旅生涯真是丰富多彩，可对我而言，丽江站是我军旅生涯的第一站，可就这第一站在一步步变得更加美好时，军改的消息如雷鸣般轰入我们每一名官兵的脑海里。一时间，众说纷纭、谣言四起。我忽然觉得，我的第
关于心态的演讲稿积极心态的励志演讲稿一个人是否是真正的成功,关键在于心态.良好的心态帮助你理智地迎接人生道路上的各种,帮助你成为一个智者,成为最大的赢家.下面我们一起来看看积极心态的励志演讲稿,希望大家喜欢. 乐观心态看人生 亲爱的老师,同学们: 大家好! 往事随风飘,沧海博一笑. 假如上帝给你一双黑色的眼睛,那你就用黑色的眼睛寻找光明;假如上帝给你一具残损的肢体,那么就用残损的肢体来选完美的人生,因为人生就是不完美的.黑暗中往往蕴藏着希望,相反,如果你用躲避来面对黑暗,那么黑暗会永远跟随你,这就告诉我们要用乐观的心态来看待事物. 爱迪生为发明一只小小的灯泡而失败了千万次.当时有点人不解,认为他这么做无非是浪费大量时间与生命在一个很不起眼的东西上罢了.但爱迪生却轻松的说:“我证明出了一千多种不能制造灯泡的方
法,这难道不是巨大的财富吗?乐观向上的心态鼓舞着爱迪生一次又一次地为人类做贡献,为人类的历史翻开了新的一页. 著名表演艺术家英子面对媒体对她的各种绯闻,不但没有生气,反而风趣地说:“这只能说明大家都在乎我,挂念我.她也因此获得中国演员特别奖. 面朝大海,春暖花开.海子虽然走了,但他的诗却一直是诗坛上一道亮丽的风景线.在他的那个时代,国家是贫穷的,生活是潦倒的,民众是麻木的,而他心中的世界却是那么和谐,“从明天起,做一个幸福的人,喂马、劈材、周游世界.”能写出这么美的诗,也不愧为中国诗坛的奠基人.但他却匆匆地走了,留给了后人一片空白,他认为这世界太无能,根本无需留恋.是的,恰恰是他那颗悲观的心置他于死地,铸成了诗坛一大损失. 把心态调整好.生活就像是由一些叫烦恼、失败、痛苦的珠子串在一起的,不管有多困难,微笑着面对它,用客观的心态看人生. 我的演讲完毕. 谢谢大家!
防火墙设备技术要求 一、防火墙参数要求： 1.性能方面： 1.1网络吞吐量>10Gbps，应用层吞吐率>2Gbps，最大并发连接数>400万（性能要求真实可靠，必须在设备界面显示最大并发连接数不少于400万），每秒新建连接＞15万。 1.2万兆级防火墙，网络接口数量不少于12个接口，其中千兆光口不少于4个、千兆电口不少于6个、万兆光接口不少于2个，另外具有不少于2个通用扩展插槽。 1.3冗余双电源，支持HA、冗余或热备特性。 1.4具备外挂日志存储系统，用于存储防火墙日志文件等相关信息，另外支持不同品牌网络设备、服务器等符合标准协议的日志格式，日志存储数量无限制。 1.5内置硬盘，不小于600G，用于日志存储。 2.功能方面（包含并不仅限于以下功能）： 2.1具有静态路由功能，包括基于接口、网关、下一跳IP地址的静态路由功能。 2.2具有OSPF动态路由功能，符合行业通用的OSPF协议标准。 2.3具有网络地址转换功能，支持一对一、多对一、多对多的网络地址转换功能。
2.4具有OSI网络模型三层至七层访问控制功能，可基于IP、端口号、应用特征、数据包大小、URL、文件格式、内容、时间段等进行安全访问控制和过滤。 2.5具有基于资源和对象的流量分配功能，包括基于单个IP、网段、IP组、访问源地址及目标地址、应用等的流量管理、分配。 2.6完善的日志及审计系统，防火墙内所有功能均具备相应的日志可供查看和审计。 2.7具有内置或第三方CA证书生成、下发及管理功能。 2.8具有身份认证、身份审计功能，支持用户ID与用户IP 地址、MAC地址的绑定，支持基于CA证书、AD域、短信、微信等多种身份认证方式。 2.9具有入侵检测模块，支持入侵防护、DoS/DDoS防护,包含5年特征库升级服务。 2.10具有上网行为管理模块，支持上网行为检测、内容过滤等功能，包含5年应用特征库升级服务。 2.11具有病毒防护模块，可包含5年病毒库升级服务。 2.12具备基于WEB页面的管理、配置功能，可通过WEB 页面实现所有功能的配置、管理和实时状态查看。 2.13具有SSL VPN模块，含不低于50人的并发在线数。针对手机和电脑，有专门的SSL VPN客户端。 3.质保和服务
逐梦军旅演讲稿 逐梦军旅演讲稿篇一 尊敬的各位领导、各位老师，亲爱的同学们：大家下午好!我是来自高20xx级2班的一名学生，今天很荣幸能够代表本届高三学子在这里发表演讲。高考在即，我们每一个人都承载着自己的责任在努力复习备战高考。闲暇之余，也曾畅谈理想，规划自己的未来。有人想学医悬壶济世，有人想研究科学探索自然奥秘，有人想手持朱笔诲人不倦，有人想游走商界叱咤风云。这些都是很美好的憧憬，那，你们有没有和我一样想到过另一种选择，那，1就是逐梦军旅，献身国防。从小时候起，我们便学习中国的近代史，知道百年前积弱的旧中国是如何被无情的帝国主义践踏，在那样几近灭国的危亡中，使我们伟大的中国共产党带领着顽强英勇的人民解放军赶跑了帝国主义，同所有中国人民一起建立了一个全新的中国。而如今我们的幸福生活不仅有革命先辈们打下的基础，更有此时此刻正坚守在岗位的解放军战士们的功劳。有了他们的不懈努力，有了他们活跃在祖国母亲的血脉中，祖国才能在而今国际形势瞬息万变，风起云涌的时事政变中泰然自若，敢对他国挑衅予以还击，能在世界大局中引导潮流，参与到世界维和的任务中去。所以，能成为一名铁骨铮铮、保家卫国的解放军战士是多么庄严而又光荣的事!我知道，我们当中有很多人其实是很向往军旅生活的，只是想到军旅生活的艰苦便退缩了。但，我们不能退缩。古人曾
说：天将降大任于是人也，必先苦其心志，劳其筋骨，饿其体肤，空乏其身，行拂乱其所为，所以动心忍性，曾益其所不能。只有当我们融入到解放军艰苦紧张的军营生活锤炼出坚强的品格，学习政治、军事、科学技术掌握过硬的本领;通过正规的教育训练培养出过硬的军政素质、严格的组织纪律和良好的作风，我们才会成长，从思想上成长为有道德、有担当、有毅力的青年，从能力上成长为生活自强、专业技术精通，能打硬仗的战士，磨砺出自己的锋芒，成为国家现代化建设的优秀人才，为祖国更美好的未来添砖加瓦，贡献力量。我们是新时代的青年，是祖国未来的希望，更是祖国国防发展的主力军。哪一只雄鹰不曾在疾风中振翅，越飞越高?哪一柄利剑不是在熔炉里冶炼，越炼越强?携笔从戎，献身国防，我们要证明我们并非软弱畏难的一代青年，我们有气节与志向，有磊落与坦荡，我们愿意响应国家号召，满怀理想、壮志与激情，选择军营，选择戎马山河，用自己的血与火，汗与泪，为国防建设燃烧自己青春的热血。携笔从戎，献身国防，只要我们干一行，爱一行，专一行，把全心全意为人民服务的崇高思想，化为实际行动，踏踏实实，坚持不懈的做好本职工作，我相信我们一定会在从军的道路上走得越来越远，为我国国防事业添砖加瓦，在我国新军事变革的征程中留下浓重的一笔!犹记得戊戌变法运动领袖之一的梁启超先生曾对我们殷切寄语：故今日之责任，不在他人，而全在我少年。少年智则国智，少年富则国富，少年强则国强，少年独立则国独立。看到部队的战士们齐步列队走在军营的
文明守纪演讲稿Document of civilized speech 编订：JinTai College
文明守纪演讲稿 小泰温馨提示：演讲稿是在较为隆重的仪式上和某些公众场合发表的讲话文稿。演讲稿是进行演讲的依据，对演讲内容和形式的规范和提示，体现着演讲的目的和手段，用来交流思想、感情，表达主张、见解；也可以用来介绍自己的学习、工作情况和经验等等；同时具有宣传、鼓动、教育和欣赏等作用，可以把演讲者的观点、主张与思想感情传达给听众以及读者，使他们信服并在思想感情上产生共鸣。本文档根据演讲稿内容要求展开说明，具有实践指导意义，便于学习和使用，本文下载后内容可随意修改调整及打印。 尊敬的老师，亲爱的同学们： 大家好！今天我演讲的题目是《做一个文明守纪的中学生》 我曾经在书上看到这样一则故事：一头牛饿了，它会在本能驱使下寻找食物：遇上青草就大嚼一通，即使是人家的庄稼，甚至名贵的花草，只要可口，都会照吃不误。而人就不同了。我们饥肠辘辘时，尽管看到商店橱窗里的美味近在咫尺，但如果囊中羞涩，也不敢有非分之想。甚至，当你已经坐在餐桌前面对香喷喷的菜肴时，如果主宾还未到来，也许就需要忍饥等待。为什么呢？道德规范的约束！在我们日常生活中的道
德观念时时提醒我们做一个文明的人，做一个遵守社会规范的人。 刘备临终前告诫儿子刘禅“勿以恶小而为之，勿以善小 而不为”。但我们生活中的不良行为却比比皆是： 1.乱丢垃圾。在校园公共区域和教室内，吐出的痰迹、 空饮料瓶、废纸片和食品包装袋等经常可以见到。 2.损害公物。最典型的是在书桌、椅子上用刀、用笔刻 划“留言”，用涂改液等在上面乱写乱画，在教室的墙壁上涂抹。上面写出的内容大都是消极颓废、甚至是思想不健康的语言垃圾。这不但破坏了公物，也污染了我们学生的视觉及心灵。 3.语言不美。少数同学说话便带出脏字，而且自己并没 有意识到。他们自己也说：“不是故意的，只是习惯而已。”一些同学当别人意见与自己不同时，尤其是当自己的不文明行为受到制止时，往往恶语伤人，庸俗不堪。 4.言行不雅。个别同学在教学楼道甚至在教室内大声喧哗，破坏了教学环境应有的宁静与和谐；少数同学身着比较新潮的衣服，或是自己“创造”的衣服，把自己打扮得象一个模特；有些同学的头发太长，让人以为是“问题少年”。
阳光心态演讲稿 尊敬的各位领导，亲爱的同事们、大家好! 非常感谢领导及同志们给我这次锻炼自己的机会。我演讲的题目是《心态决定成败，我的阳光心态》 我先给大家讲个故事，说从前有个秀才进京赶考去了，考试前一晚上却做了两个梦。第一个梦是梦见自己在高墙上面种白菜，第二个梦见自己在下雨天里戴著斗笠而且还打著伞。醒来后他觉得这两个梦都暗藏著含义，于是便找了个算命先生解梦。秀才把梦的经过和算命先生说了一番后，算命先生摇了摇头说：妳还是回家去吧。妳想：高墙上面种白菜不就意味著白忙活吗?下雨天带斗笠又打伞不是明摆著多此一举吗?秀才听后心灰意冷，于是回店里收拾衣服准备回家。店老板看见觉得奇怪，于是便问：妳回家难道不准备考试了?秀才便把做的梦和算命先生解梦的经过和店老板如实说了一下。店老板一听乐了，说：我也会解梦。我倒觉得妳非留下来参加考试。妳想啊，高墙上面种白菜不是指高中吗?下雨天带斗笠又打伞不是说明妳准备充分，有备无患吗?秀才一听觉得更有道理，于是便留下来参加了考试，结果高中了。 这个故事启示大家任何事情都有两面性，关键是看当事者以怎样的心态对待它，积极的心态创造人生，消极的心态消耗人生。积极的心态像太阳，照到哪里哪里亮，消极的心像月亮，初一十五不一样，这就是阳光心态!心态决定成败。 当今社会，是个渴望成功的时代，每个人都希望自己能够成为成功者，但并不是每个人都能取得成功，成功者之所以能够成功，不仅因为他们具有超越常人的才华，更重要的是因为他们具备成为成功者的心态。积极的心态有助于人们克服困难，即使遇到挫折与坎坷，依然能保持乐观的情绪，保持必胜的斗志。身处这个多变的时代，我们唯一能控制的就是自己的心态。
华为USG6000系列下一代防火墙详细性能参数表
能，与Agile Controller配合可以实现微信认证。 应用安全●6000+应用协议识别、识别粒度细化到具体动作，自定义协议类型，可与阻断、限流、审计、统计等多种手段自由结合在线协议库升 级。注：USG6320可识别1600+应用。 ●应用识别与病毒扫描结合，发现隐藏于应用中的病毒，木马和恶意软件，可检出超过500多万种病毒。 ●应用识别与内容检测结合，发现应用中的文件类型和敏感信息，防范敏感信息泄露。 入侵防御●基于特征检测，支持超过3500漏洞特征的攻击检测和防御。 ●基于协议检测，支持协议自识别，基于协议异常检测。 ●支持自定义IPS签名。 APT防御与沙箱联动，对恶意文件进行检测和阻断。 Web安全●基于云的URL分类过滤，支持8500万URL库，80+分类。 ●提供专业的安全URL分类，包括钓鱼网站库分类和恶意URL库分类。 ●基于Web的防攻击支持，如跨站脚本攻击、SQL注入攻击。 ●提供URL关键字过滤，和URL黑白名单。 邮件安全●实时反垃圾邮件功能，在线检测，防范钓鱼邮件。 ●本地黑、白名单，远程实时黑名单、内容过滤、关键字过滤、附件类型、大小、数量。 ●支持对邮件附件进行病毒检查和安全性提醒。 数据安全●基于内容感知数据防泄露，对邮件，HTTP，FTP，IM、SNS等传输的文件和文本内容进行识别过滤。 ●20+文件还原和内容过滤，如Word、Excel、PPT、PDF等），60+文件类型过滤。 安全虚拟化安全全特性虚拟化，转发虚拟化、用户虚拟化、管理虚拟化、视图虚拟化、资源虚拟化（带宽、会话等）。 网络安全●DDoS攻击防护，防范多种类型DDoS攻击，如SYN flood、UDP flood、ICMP flood、HTTP flood、DNS flood、ARP flood和ARP 欺骗等。 ●丰富的VPN特性，IPSec VPN、SSL VPN、L2TP VPN、MPLS VPN、GRE等。 路由特性●IPv4：静态路由、RIP、OSPF、BGP、IS-IS。 ●IPv6：RIPng、OSPFv3、BGP4+、IPv6 IS-IS、IPv6RD、ACL6。 部署及可靠性透明、路由、混合部署模式，支持主/主、主/备HA特性。 智能管理●支持根据应用场景模板生成安全策略，智能对安全策略进行优化，自动发现冗余和长期不使用的策略。 ●全局配置视图和一体化策略管理，配置可在一个页面中完成。 ●可视化多维度报表呈现，支持用户、应用、内容、时间、流量、威胁、URL等多维度呈现报表。 标准服务●USG6300-AC：SSL VPN 100用户。 ●USG6300-BDL-AC：IPS-AV-URL功能集升级服务时间12个月，SSL VPN 100用户。 可选服务●IPS升级服务：12个月/36个月 ●URL过滤升级服务：12个月/36个月●反病毒升级服务：12个月/36个月 ●IPS-AV-URL功能集：12个月/36个月 注：√表示为支持此项功能，—表示为不支持此项功能。
中国梦强军梦我的梦 五千年的斗转星移，五千年的潮起潮落 五千年的沧桑巨变，五千年 孕育着一个伟大民族的复兴之梦 习主席深情阐述：“中国梦是强国梦，更是强军梦”。他引用了三句诗：“雄关漫道真如铁，人间正道是沧桑，长风破浪会有时”将中华民族的昨天、今天和明天，熔铸于百余年中国沧桑巨变的历史图景中，展现了几代人为民族复兴奋斗的艰辛历程，令人感慨，催人奋进。 国无军不强，民无军不安，没有强大的人民军队中国梦的实现不过是纸上谈兵的笑谈，没有强大的人民军队就不会有安宁和平的发展环境。 历史往往经过时间的沉淀后会变得更加明晰，追根溯源，伟大的中华民族有着悠久灿烂的文明，长久居于世界文明发展的前列。然而中华民族却有那么一段屈辱的历程，使得近代中国满目疮痍。 1840年鸦片战争，英国用“坚船利炮”击碎了清王朝以“天朝上国”自居的美梦，1900年，八国联军拼凑起来的兵力不足两万而京城一带纵有十几万清军、几十万义和团之众。仍无法阻止京师沦陷和赔白银四亿余万两。1840年到1919年，80年间，旧中国与列强签订了900多个丧权辱国的不平等条约，平均每月一个，合约越签越多，而和平、安全和主权却越来越少。 百年屈辱、百年渴望，当中华民族面对“千年未有之巨变，千年未有之强敌”。我中华儿女便萌生了一个执着的梦，民族复兴的梦。 新中国成立以来，无数科研工作者为富国强军孜孜贡献。1964年第一课原子弹试爆成功，让所有中国人挺立了腰杆，让世界惊叹那一朵“蘑菇云” 2003年神州五号顺利升空，证明中国千年来的登天梦实现了，2012年中国首艘航母---辽宁舰下水，结束了五大国中唯一没有航母的历史。这些都是我们军队强盛的证明，更是强军梦逐步实现的脚印。 习主席在五四讲话中指出：“历史和现实都告诉我们青年一代有理想有担当，国家就有前途，民族就有希望。实现我们的发展目标就有源源不断的力量。” 入伍前，我是一名大学生。校园的欢声笑语无忧无虑，自由安逸，似乎让我忘却了什么是梦想，甚至中国梦在我记忆深处埋没。“进来是铁，出去是刚”。昨天的我就是今天的你，今天的我就是明天的你。人生因梦想而精彩，青春因奋斗而美丽。一位退伍大学生老兵点醒了我。位卑未敢忘忧国，天下兴亡匹夫有责等箴言在我脑中萦绕，投笔从戎，参军报国，让青春无悔，让我再一次舞动起青春的乐章。 路漫漫其修远兮，吾将上下而求索。人的生命犹如一条奔腾的江河，不经历海岛和暗礁难以激起生命的浪花。严格要求，苦练杀敌本领，一千次跌倒将会在一千零一次中爬起，拍打灰尘、挺起胸脯、毅然前进。站军姿、叠被子、练擒敌、爬战术，平凡但不平庸，一个胸怀抱负的士兵，注定要在平凡的岗位上刻下浓浓一笔，一个勇于担当的士兵，注定让精彩的梦想充满军旅生涯。 做为新世纪和平年代可爱的武警战士，自觉发扬爱国主义优良传统，把警营当做爱国报国建功立业的最好平台。立足本职岗位，脚踏实地工作，用实实在在的行动展示新一代革命军人的时代风采。 我相信只要坚持不懈、努力拼搏，梦一定能成真。我的梦，我们的梦，铸就了实现国富民强的强军梦。强军梦要靠我们的梦来实现，我们要为实现强军梦而奋斗。
文明守纪中学生演讲稿3篇 Speech document of civilized and discipline abiding mid dle school students 编订：JinTai College
文明守纪中学生演讲稿3篇 小泰温馨提示：讲话稿是为了在会议或重要活动上表达自己意见、看法或汇报思想工作情况而事先准备好的文稿，用来交流思想、感情，表达主张、见解，是演讲上一个重要的准备工作。本文档根据讲话稿内容要求和特点展开说明，具有实践指导意义，便于学习和使用，本文下载后内容可随意修改调整及打印。 本文简要目录如下：【下载该文档后使用Word打开，按住键盘Ctrl键且鼠标单击目录内容即可跳转到对应篇章】 1、篇章1：文明守纪中学生演讲稿 2、篇章2：文明守纪中学生演讲稿 3、篇章3：文明守纪中学生演讲稿 文明是什么呢?文明是路上相遇时的微笑，是同学有难时的热情帮助，是不小心撞到对方时的一声“对不起”，是自觉将垃圾放入垃圾箱的举动，是不讲脏话、粗话，是在安静无声的自修课上自觉遵守纪律……文明是一种品质，文明是一种修养，一种受人尊敬并被大家广泛推崇的行为。本文是小泰为大家整理的文明守纪的中学生演讲稿，仅供参考。 篇章1:文明守纪中学生演讲稿
尊敬的各位老师、亲爱的同学们： 今天我演讲的题目是《文明之手编织和谐校园》 众所周知，我国是世界四大文明古国之一，也是传统的 礼仪之邦。作为新时代的少先队员，我们更应当注重自己在 日常的学习和生活中，从自己言谈举止的每一个细节入手，自觉履行我们应当遵守的文明礼仪。 当你踏着光洁的地板走进教学楼的时候，你是否会想起 那位经常手拿扫把，埋头辛苦扫地同学;当你在操场上与朋友 尽情嬉戏的时候，你是否看见学校老师栽培草坪的背影;当你 在干净、整洁的校园里漫步徜徉的时候，你是否感觉到那位拖垃圾车的老爷爷的艰辛。 在生活中，在我们的身边，不乏有这样的现象： 校园里，见到老师，不知道问好;生活中没有秩序，不懂 得谦让;大庭广众之下，公开骂一些不堪入耳的脏话!这难道是礼貌吗?不，这是无礼!干净的教室转瞬间成为了垃圾的天堂! 崭新的门板霎时被破坏得惨不忍睹!这难道是文明吗?不!这是 无耻!平日里，披头散发，不修边幅，长长的指甲中藏污纳垢。这难道是潇洒吗?不!这是邋遢à !
付出的心态感悟演讲稿6篇 演讲稿应该富有说服力和感染力,那么怎样对付出的心态感悟演讲才富有说服力和感染力?下面小编整理了付出的心态演讲稿,供你参考。 付出的心态感悟演讲稿篇1 提起付出心态,我立刻想起了“受得苦中苦,方为人上人”,这名格言,这句格言虽然是激励人艰苦奋斗,奋发向上的诗意,之间也包含了付出的意思,“受得苦中苦”实际就是一种不平凡的付出, 你看那位古代练武的,为了练一身好武艺,冬练三九,夏练三伏,练的一身伤痕,两手老茧,吃尽了苦头, 才有了成就,再看古代习文的书生,... 一个学生问智者:什么是地狱?什么是天堂? 智者回答:地狱就好像一群
人围坐在一口锅周围,每个人手里都有一双很长的筷子,都想把肉夹到自己嘴里,结果谁也无法办到,最后大家都骨瘦如柴,彼此诅咒谩骂。那么天堂呢? 天堂也是同样的锅与筷子,不同的是大家夹起肉彼此喂食,所有人都可以吃饱,最后大家都满面红光,谈笑风生。 随时随地的愿意为别人付出,任何地方都会是幸福的天堂。在我们生活的周围,形形色色的人都有,自私心胸狭隘的人往往对别人心存嫉妒,任何利益都想沾边, 而从来不愿意帮助别人一点点忙, 那么当他遇到困难的时候也很少有人愿意帮他_就好像地狱里的食客拼命往嘴里夹肉,最后却一无所得。而另外一些人对别人的点滴帮助都铭记在心, 在对待别人的时候也总是愿意多付出一点, 在碰到困难的时候也会获得更多的帮助_像天堂里的食客, 总是有更多的人愿意把食物夹到他的嘴里。付出汗水,才能收获麦穗;付出真诚,才能收获友谊;付出微笑,才能得到友善! 我们知道行业给我
们策划了一个美好的未来,可以让我们在实现自己的梦想。但罗马不是一天建成的,我们不可能一步登天,这个世界上没有白吃的午餐。不经历风雨,怎会见彩虹?人生不去经历,不去拼搏,不去奋斗,再美好的事业都不可能实现!没有从天而降的幸福,也没有不劳而获的收获! 斤斤计较的人一生只能得到两斤。我们付出的理由是荣耀和财富, 但更多的是对美好人生的追求,对幸福生活的向往,促使我们不断付出努力。一个“以人为本,人人互助”的行业, 主动去帮助别人其实也就没是帮助了自己,因为“人”字的结构就是相互的支撑,而“众”人的事业需要每个人的参与和付出。 没有哪一个人富得可以不需要别人的帮助, 也没有人穷得不能在某方面帮助别人,其关键就在于自身,在心理上的拒绝就表现了行动上的自私自利,我们可以没有金钱没有权势,但是不能没有互相帮助互相关怀的爱心。独在异乡结识了许许多多的朋友,感谢他们的热情、微
改性沥青防水卷材执行标准 SBS弹性体改性沥青防水卷材是以SBS（苯乙烯-丁二烯-苯乙烯）热塑性弹性体改性沥青为浸涂材料，以优质聚酯毡、玻璃纤毡、玻璃增强聚酯毡为胎基，以细砂、矿物粒料、PE膜、铝膜等为覆面材料，采用专用机械搅拌、研磨而成的弹性体改性沥青防水卷材。 APP塑性体改性沥青防水卷材是以APP（无规聚丙烯）或APAO、APO（聚烯烃类聚合物）改性沥青为浸涂材料，以优质聚酯毡、玻纤毡为胎基，以细砂、矿物粒（片）料、PE膜为覆面材料，采用先进工艺精制而成的塑性体改性沥青防水卷材。 凯鑫防水改性沥青防水卷材性能指标： SBS执行标准GB18242-2008 序号项目 ⅠⅡ PY G PY G PYG 1 可溶物含量 （g/㎡）≥ 3mm 2100 * 4mm 2900 * 5mm 3500 试验现象* 胎基不燃* 胎基不燃* 2 耐热性 ℃90 105 ≤mm 2 试验现象无流淌、滴落 3 低温柔度℃-20 -25 无裂纹 4 不透水性30min 0.3Mpa 0.2Mpa 0.3Mpa 5 拉力最大峰拉力 （N/50mm） ≥ 500 350 800 500 900 次高峰拉力 （N/50mm） ≥ * * * * 800 试验现象 拉伸过程中，试件中部无沥青涂盖层开裂或 与胎基分离现象 6 延伸率最大峰时延 伸率%≥ 30 * 40 * * 第二峰时延* * 15
伸率%≥ 7 渗油性张数≤ 2 APP执行标准GB18243-2008 序号项目 ⅠⅡ PY G PY G PYG 1 可溶物含量 （g/㎡）≥ 3mm 2100 * 4mm 2900 * 5mm 3500 试验现象* 胎基不燃* 胎基不燃* 2 耐热性 ℃110 130 ≤mm 2 试验现象无流淌、滴落 3 低温柔度℃ -7 -15 无裂纹 4 不透水性30min 0.3Mpa 0.2Mpa 0.3Mpa 5 拉力最大峰拉力 （N/50mm） ≥ 500 350 800 500 900 次高峰拉力 （N/50mm） ≥ * * * * 800 试验现象 拉伸过程中，试件中部无沥青涂盖层开裂或 与胎基分离现象 6 延伸率最大峰时延 伸率%≥ 30 * 40 * * 第二峰时延 伸率%≥ * * 15
遵规守纪做文明中学生演讲稿 遵规守纪做文明中学生演讲稿（一） 各位领导、老师、同学们： 大家早上好！ 冬天的早晨是寒冷的，但是每周一早晨同学们都会排着整齐的队伍，喊着响亮的口号站在国旗下举行庄严的升国旗仪式。为什么？答难只有两个字---纪律。俗话说；没有纪律不成方圆。一个社会，一个团体，只有在良好的纪律维持下，才会逐渐的走向成熟。今天我要和同学们说遵守纪律做文明xx人。《中小学生守则》和《中学生日常行为规范》已经给了我们明确的目标：自尊自爱，注重仪表，真诚友爱，礼貌待人，遵规守纪，勤奋学习，勤劳俭朴，孝敬父母。我们xx实验学校的各项校规、校纪和这些守则规范是完全一致的。比如说，学校有明确要求：穿着得体大方，待人谦虚礼貌、言行文明适度等等。这些说起来简单，但做起来可就不那么容易了。有些同学总是怀着侥幸心理，认为偶尔违反一两条纪律没什么关系。偶尔犯一两次错误本来是可以原谅的，但如果总是怀有这些侥幸心理的话，天长日久养成了不良习惯，再改可就非常难了。要知道，我们学校的各种规章制并不是为了限制同学们的自由，而是为了让同学们拥有一个更加有序的环境，获得更大意义上的自由；使同学们能够更好的学习、工作，这才是学校制定各种纪律、规范的真正目的。 同学们，作为xx的一名学生，我们应当感谢学校对我们的重视，
从现在做起，从我做起，从身边做起，不但自觉遵守各项校规校纪、法规法纪，养成良好的习惯，而且，积极主动作好宣传。这样做不仅为了使学校环境更加美好，更为了使我们能够健康的成长，有效的学习，使我们每一个人都拥有一个更加美好的前程，成为对社会有用的人。 让我们积极行动起来，从身边的小事做起，规范自己，监督自己，使自己率先成为守纪.护法的文明xx人！ 遵规守纪做文明中学生演讲稿（二） 老师们、同学们： 大家好！ 我今天演讲的主题是：遵规守纪，做文明中学生 中国是一个有着五千年历史的文明古国，中华民族素来是一个谦恭礼让的文明礼仪之邦。华夏儿女的举手投足，无不体现一个人的气质与素养。荀子云：“不学礼无以立，人无礼则不生，事无礼则不成，国无礼则不宁。”文明礼仪是我们学习、生活的根基，是我们健康成长的臂膀。 然而在我们美丽的校园里，在少数学生中仍然存在着言不美、行不端等违纪违规、不讲文明的现象：比如校园里随处可见的垃圾，集会时交头接耳，文艺汇演时站立起来影响其他学生观看，在楼道里追逐打闹，课上不认真听讲……虽然这是个别学生的行为，但我们也对此深表遗憾！因为孩子是家长的缩影。在你不文明的行为背后不免让人猜测是什么样的家庭，什么样的家长培养了不讲文明的学生。同学
付出心态素质稿4篇 付出心态素质稿（一）： 付出就是舍得中的;舍;，先舍再求得，要想在事业中获得成功，必须先付出。仅有我们每个人都真心付出，全力去帮忙别人，才会得到同样的回报。你付出多少你就会得到多少，你付出的越多你得到的就越多，条件是你必须先付出。 付出的心态，是一种因果关系。舍就是付出，付出的心态是老板心态。是为自我做事的心态，要懂得舍得的关系。舍的本身就是得，小舍小得，大舍大得，不舍不得。不愿付出的人，总是省钱，省力，省事，最终把成功也省了。世界上没有免费的午餐，想想从古至今哪一位成功人士的里程碑能缺少艰辛的付出。俗话说的好，要想人前显贵，就得人后受罪，付出和获得是辩证统一的。 种瓜得瓜，种豆得豆这是我们老百姓都常念叨的一句话，当我们想要得到某些东西的时候，我们就必须要舍得去做我们都不喜欢做的事情，为此好
好的努力，付出我们的汗水和时间，当然仅仅靠这两样是不够的，重要的还是要付出智慧!有一个付出心态。 当今此刻的社会，很多人都觉得要对自我有利益的事情才会去做，都是自私的想着自我的一亩三分地，而往往这样的去付出，我想也不会有太大的收获。 有句古话说的很好，赠人玫瑰，手留余香!当你在帮忙别人的时候，你同时也能获到很多。 很小的时候就听过这么一个故事，以前有一个盲人，每一天都工作到很晚才回家，并且每次手上都会提个灯笼，很多人都很不解，有一天有个年轻人就问他说，大爷，您不是看不见么，怎样还要提灯笼呀，不是多此一举呀，只听那位大爷回答说我提着灯笼别人能够看清楚回家的路，同时不让别人撞到我!照亮了别人回家的路，还能照顾到自我这确实是利人利已的事。 付出总会回报，当然也要看你付出了多少，付出的多收获的自然也多，
关于改革强军的演讲稿(范文一) 铸牢军魂，梦融强军 “赳赳老秦，复我河山，血不流干，死不休战。”在老秦人的呼啸声中，秦国的方阵铁骑，视战国六雄为草芥，攻城夺地，势如破竹，实现了华夏大一统;唐夏虎牢之战，李世民率领数千名玄甲军大败王世充数万之众，一役定乾坤，成就李唐王朝;嘉靖年间，戚家军抗倭，台州之役，九战九捷，为明朝海防的稳定做出了巨大贡献。历史证明，一个民族国家崛起和复兴的背后，势必有着一支强有力的军队为其披荆斩棘，开疆拓土。由此也可以看出，当前新形势下习总书记提出强军目标的重要性，要实现中华民族的伟大复兴，必定要有一支听党指挥，能打胜仗，作风优良的人民军队为坚强后盾。 一、溯游历史长河，坚定强军信仰 学习践行强军目标心得体会心得体会，学习心得二战中的德国，席卷波兰于一夜之间，甚至将德意志的军旗插至目及克里姆林宫的河畔，这样一个国土面积只有35万平方公里国家的军队创造出的战绩却不得不令世界震撼。虽然指挥这场战争的是纳粹党，但我们不得不从中看出一些东西;反观苏共，自戈尔巴乔夫推行改革以来，军队国家化的思潮逐渐开始泛滥，军队的对党忠诚开始动摇，最终导致了苏联的解体。这样一个在战争中成长起来的国家，却在和平时期的一场改革中断送了自己的前途，这不得不让人扼腕。于此可见，党对军队的绝对领导是十分必要的，听党指挥是军之魂，任何时期都要坚守住党对人民军队的绝对领导这个高地，做到招之能来，来之能战。作风优良是保证。治军之道，得之于严，失之于宽。古有诸葛亮挥泪斩马谡，曹操”割发代首”等。通过这些，我们可以看出，精兵劲旅皆出于严;相反，奢靡散懒皆是法纪不振而至：北洋水师松于法纪，惰于练兵，船坚炮利的外壳下却早已是被腐蚀的锈迹斑斑，不堪一击，难支大清帝国大厦。在近代，蒋介石赦一张灵甫，毒瘤暗生，法乱而后功溃;毛泽东毙一黄克功，三军整肃，法定而后功成。由此可见，令严方可肃军威，命重始于整纲纪。悠悠岁月，时光像纷飞的雪花尘封了红军曾经的金戈铁马，带走了浴血奋战的峥嵘画面，却如大浪淘沙般沉淀下金石般的优良传统，熠熠生辉。秉承前辈的优良传统，将红色基因薪火相传。铁打的营盘流水的兵，人民军队就这样代代相传，直至今日，老兵永远不死，只是会慢慢消亡。而今，身为国防生的我们，
小学生文明守纪演讲稿 篇一：文明守纪,从我做起学生发言稿 “文明守纪、从我做起”获奖学生发言稿 尊敬的老师，亲爱的同学们： 你们好！ 从我一进学校读书，站在庄严的五星红旗下，看着鲜艳的红旗冉冉升起的那一刻，我心中就涌起一股暖流，要严格遵守各项校规校纪，争做遵规守纪的文明学生。 遵规守纪说起来容易，可做起来，的确很难。我是一个谨慎的学生，时时刻刻处处都会提醒着自己，勤早上学，不可迟到，尊重他人，团结友爱，讲文明话，做文明人，爱护花草，爱清洁，走路轻声慢步等。因此，校园里里外外，都留下我灿烂文明的足迹。 青少年时代是最美丽的，同学们，我们大多处在天真烂漫的孩提时代，有的已步入人生最美的“花季”，青春的花朵就要在我们的生命之树上绽开，阳光是我们的，希望是我们的，世界是我们的! 歌德说过，要成就一番伟大的事业，就要从青春时代做起。那么，我们应该怎样做才能迈出正确的步子，让青春无憾无悔，走向美好的明天呢 首先，作为新时代的学生，就要遵守纪律，做现代文明的学生。
俗话说，“没有规矩，不成方圆”，我们知道，良好的纪律是学好科学文化知识的保障。作为一名学生，就要严格遵守 《学生守则》、《学生日常行为规范》：严格遵守学校各项规章制度，切实做到：尊师爱友，自律自强；诚实守法，文明礼貌；遵守公德，爱护公物。 其次，作为新时代的学生，还要学会守法。 每个公民都必须具有法制观念，不仅要学法，而且还要守法。缺乏法制观念是非常危险的。 第三、要遵守社会公德。 讲究公共卫生、爱护公共财物、维持公共秩序等，这些都是社会公德。遵守社会公德是衡量社会文明程度的标志之一。 讲究公共卫生，就是要保持优美整洁的公共环境。比如：在教室里，在马路上，不随地吐痰，不随手扔果皮、纸屑。还有一点，则是不能大喊大叫。妨碍其他人学习、工作或休息；不能在建筑物上或课桌椅上乱刻乱画。 我们身边的公共财物有很多。如学校的门窗、桌椅、教学设备等，公园里的花草、树木，马路边的路灯、路牌、公用电话等，我们不仅要做到自己爱护，而且还应当劝阻、制止有些人破坏公共财物的不文明行为。争做一个讲文明、懂礼仪的好学生。遇到师长、来宾，主动敬礼问好；上下楼梯，
平常心态的演讲稿 导语：一个健全的心态，比一百种智慧都更有力量。 一位哲人说：“你的心态就是你真正的主人。”一位伟人:说：“要么是你驾驭生命，要么是生命驾驭你。你的心态决定谁是坐骑，谁是骑师。” 无论我们做什么事情，心态都是很重要的。对每一个干一番事业来说，首先要树立一个坚定不移的的心态，无论面对什么样的困难，谁都希望自己的能回得成功，但是要做到这一点，良好的心态是不可或缺的，因为什么样的心态决定了什么样的成就，什么样的心态决定了什么样的人生。有了成功的心态就会达到成就的道路：如果一个人没有强烈一定要成功的欲望~那他是不会采取任何行动来达到成就的目标。 成功对于我们每个人来说都是一件不易之事，每一项成就都需要我们艰辛的付出，今天我们推销的是自己的职业与道德，是一个网络理念，它是一种新生勇敢的事物。当我们向别人推销慨念或是介绍这个职业时，我们面对的不仅仅是别人，也是自己，当我们在推销过程中遭到拒绝后，往往会产生一种心理障碍，害怕再去面对别人，再面向别人介绍这种理念。事实上，有些人遇到困难便失去了勇气，可是在成功者的眼里即使失败也不能是最后的决局，还会继续奋斗，路不是一帆风顺的好走，一生有成就的人，开始出发总是不顺利，而且在“抵达目标前”也终会经历许多心碎的挣扎，
看看那些成功者，其人生转折点通常会与某个危机同时出现，透过那些危机我们认识了另一个“自我”，有了成就。 我们常说富人爱创业，穷人爱打工，富人做事有永不服输的精神，但穷人遇到挫败就放弃，但有很多人还没有做事就开始放弃。成功的道路是坎坷和曲折的，有些人把困难和不幸作为借口，也有人在不幸和困难中寻找前途，只有勇敢面向困难永保活力用理智战胜一切才能成为命运的主宰者。 要坚持提升自己。剩者为王。我曾在一个经济市场上评打多年，我说在在这个80%以上的人不能成功的，因为80%的人不能坚持。坚持的心态是在遇到坎坷的时候反映出来的心态，而不是顺利的坚持。遇到瓶颈的时候还要坚持，直到突破瓶颈达到新的高峰.要坚持到底，不能输给自己。时间总是耐心等待那些坚持成功的人. 二：积极主动心态 首先我们需要具备积极主动的心态。积极心态就是向好的，正确的方面扩张开来，同时第一时间投入进去。多好的方面，也有些不够好的地方，我们就需要用积极的心态去对待。命运不是上天安排的，是我们主动去争取的。在行业里，有很多的事情也许没有人安排你去做，如果我们去主动的行动起来，你不但锻炼了自己，同时也为自己日后的工作积蓄了力量和经验。我们目前现状却不是“事不关己、高高挂起，明哲保身、少说为佳”;“座其位不谋其职，三天打鱼、两
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SBS改性沥青防水卷材、APP改性沥青防水卷材: 同一厂家、规格不大于10000㎡为一批，外观合格卷材中，每批随机取 1卷。 聚氯乙烯（PVC）防水卷材、氯化聚乙烯防水卷材：同一厂家、规格不大于5000㎡为一批，任取 1卷，在距端部300mm处截取约3m作为试样。 三元乙丙卷材、橡胶防水卷材：同一厂家、规格不大于5000m2为一批，每批抽取 2m。 防水早已不再是一个新鲜的话题，不论是隧道、桥梁、堤坝、道路、建筑还是我们日常居住的房屋，防水都不容忽视，同时，我们日常生活中所使用的电器产品也存在必须直面的防水防潮问题。 用于防水工程的防水材料，其技术性能指标应符合相应的技术规范要求，如地下工程使用的SBS卷材应选用Ⅱ型，抽样检查的项目及技术指标应符合规范要求。这是工程对材料的要求。 防水材料标准的作用，针对生产厂家，提供相应材料的技术指标要求及检测判断方法，针对施工现场材料检验，提供检测及判断方法。 从严格意义来说，技术指标要求应符合规范规定，检测方法及判定按材料标准进行。 三、取样要求 1、石油沥青纸胎油毡 批量：以同一品种、标号、等级的产品每1500卷为一批，不足1500卷者亦按一批计。 抽样：在每批产品中抽取10卷进行卷重检验，全部达到规定时即为合格。在重量检查合格的10卷中取重最轻的，外观面积合格的无接头的一卷作为物理性能试样，若最轻的一卷不符合抽样条件时，可取次轻的一卷，切除距外层卷头2.5m后，顺纵向截取0.5m长的全幅卷材两块，一块作物理力学性能用，另一块备用。 2、弹性体沥青防水卷材 批量：以同一类型、同一规格10000m2为一批，不足10000m2时亦可作为一批。 抽样：在每批产品中随机抽取5卷进行卷重、面积、厚度与外观检查，在上述检查合格的卷材中随机抽取1卷，切除距外层卷头2.5m后。顺纵向切取长度为0.8m的全幅卷材两块，一块用物理力学性能检测用，另一块备用。
关于改革强军的演讲稿关于改革强军的演讲稿(范文一) 历史证明,一个民族国家崛起和复兴的背后,势必有着一支强有力的军队为其披荆斩棘,开疆拓土.由此也可以看出,当前新形势下习总书记提出强军目标的重要性,要实现中华民族的伟大复兴,必定要有一支听党指挥,能打胜仗,作风优良的人民军队为坚强后盾. 一溯游历史长河,坚定强军信仰学习践行强. 军目标心得体会心得体会,学习心得二战中的德国,席卷波兰于一夜之间,甚至将德意志的军旗插至目及克里姆林宫的河畔,这样一个国土面积只有35万平方公里国家的军队创造出的战绩却不得不令世界震撼.虽然指挥这场战争的是纳粹党,但我们不得不从中看出一些东西;反观苏共,自戈尔巴乔夫推行改革以来,军队国家化的思潮逐渐开始泛滥,军队的对党忠诚开始动摇,最终导致了苏联的解体. 这样一个在战争中成长起来的国家,却在和平时期的一场改革中断送了自己的前途,这不得不让人扼腕.于此可见,党对军队的绝对领导是十分必要的,听党指挥是军之魂,任何时期都要坚守住党对人民军队的绝对领导这个高地,做到招之能来,来之能战. 作风优良是保证.治军之道,得之于严,失之于宽. 古有诸葛亮挥泪斩马谡,曹操割发代首等.通过这些,我们可以看出,精兵劲旅皆出于严;相反,奢靡散懒皆是法纪不振而至：北洋水师松于法纪,惰于练兵,船坚炮利的外壳下却早已是被腐蚀的锈迹斑斑,不堪一击,难支大清帝国大厦. 在近代,蒋介石赦一张灵甫,毒瘤暗生,法乱而后功溃;毙一黄克功,三军整肃,法定而后功成.由此可见,令严方可肃军威,命重始于整纲纪. 悠悠岁月,时光像纷飞的雪花尘封了红军曾经的金戈铁马,带走了浴血奋战的峥嵘画面,却如大浪淘沙般沉淀下金石般的优良传统,熠熠生辉.秉承前辈的优良传统,将红色基因薪火相传. 铁打的营盘流水的兵,人民军队就这样代代相传,直至今日,老兵永远不死,只是会慢慢消亡.而今,身为国防生的我们,要努力学习科学文化知识,用先进理论武装我们的大脑,坚定自身信仰,崇尚荣誉,献身使命. 二、树立打赢思想,炼就过硬本领不论是外邦战例还是民族亲历,思想上的马