J Physiol574.1(2006)pp85–9385 T o p i c a l R e v i e w
Developing a head for energy sensing:AMP-activated protein kinase as a multifunctional metabolic sensor
in the brain
Santosh Ramamurthy1and Gabriele V.Ronnett1,2
Departments of1Neuroscience and2Neurology,The Johns Hopkins University School of Medicine,Baltimore,MD21205,USA
The5 -adenosine monophosphate-activated protein kinase(AMPK)is a metabolic and stress
sensor that has been functionally conserved throughout eukaryotic evolution.Activation of the
AMPK system by various physiological or pathological stimuli that deplete cellular energy levels
promotes activation of energy restorative processes and inhibits energy consumptive processes.
AMPK has a prominent role not only as a peripheral sensor of energy balance,but also in the
CNS as a multifunctional metabolic sensor.Recent work suggests that AMPK plays an important
role in maintaining whole body energy balance by coordinating feeding behaviour through the
hypothalamus in conjunction with peripheral energy expenditure.In addition,brain AMPK
is activated by energy-poor conditions induced by hypoxia,starvation,and ischaemic stroke.
Under these conditions,AMPK is activated as a protective response in an attempt to restore
cellular homeostasis.However in vivo,it appears that the overall consequence of activation of
AMPK is more complex than previously imagined,in that over-activation may be deleterious
rather than neuroprotective.This review discusses recent?ndings that support the role of AMPK
in brain as a multidimensional energy sensor and the consequences of its activation or inhibition
under physiological and pathological states.
(Received21March2006;accepted after revision11May2006;?rst published online11May2006)
Correspondingauthor G.V.Ronnett:1006B Preclinical Teaching Building,Johns Hopkins University School of Medicine,
725North Wolfe Street,Baltimore,MD21205,USA.Email:gronnett@https://www.doczj.com/doc/d714276578.html,
Introduction
It is well established that a fundamental necessity for survival is the maintenance of energy homeostasis. This requires the presence of appropriate energy sensors that can detect and initiate adaptive changes in response to variations in energy balance.The adenosine monophosphate-activated protein kinase(AMPK) signalling complex is one such sensor.Although previous studies focused on the role of AMPK as cellular metabolic sensor,it is becoming evident that AMPK also plays more complex roles as an organismal metabolic sensor(Carling, 2004).
Functions described for AMPK have included the coordination of anabolic and catabolic metabolic processes in various tissues,including cardiac and skeletal muscle,adipose tissue,pancreas and liver(Kahn et al. 2005).In these tissues,AMPK responds to diverse hormonal,physiological and pathological stimuli,and in turn inhibits ATP-consuming(anabolic)processes and stimulates ATP-generating(catabolic)processes.Thus,the consequences of AMPK activation encompass acute modulation of energy metabolism and chronic changes in gene expression.This is accomplished by phosphorylation and modi?cation of numerous target proteins including biosynthetic enzymes,transporters,transcription factors, ion channels and cell-cycle/signalling proteins(Leff,2003; Hardie,2004a,2005;Hallows,2005).
It is only within the past several years that the complex physiological role of AMPK in the brain has become evident.In the CNS,it appears that AMPK has a dual function,not only as a cell-autonomous energy sensor, but also as an integrative metabolic sensor.In this regard, AMPK may play a role in the neuronal survival response to energy depletion and as well in hypothalamic control food intake and peripheral energy utilization.
Another emerging concept is that the result of AMPK activation is context speci?c,i.e.AMPK activation can be either bene?cial or deleterious,depending on the tissue, degree of stimulation,or conditions of activation.The differential regulation of AMPK activation is therefore another active area of investigation.Thus,the AMPK
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86S.Ramamurthy and G.V.Ronnett J Physiol574.1
pathway and modulation of energy balance through the
AMPK system presents an attractive therapeutic target
for intervention in many conditions of disordered energy
balance,including obesity,type-2diabetes,and stroke.The
scope of this review will be limited to new developments
related to AMPK as a metabolic sensor in the brain.Several
recent reviews provide further information on the role of
the AMPK signalling pathway in the cellular physiology of
other systems(Kemp et al.2003;Hardie,2004b;Kahn et al.
2005;Luo et al.2005;Young et al.2005).
Regulation of AMPK
Functional AMPK is a heterotrimeric kinase complex
composed of a catalyticαsubunit and regulatoryβandγ
subunits.In mammals,several alternative genes have been
identi?ed for each of the subunits,e.g.α1,α2,β1,β2,γ1,γ2,γ3.Therefore,depending on the tissue or cell type examined,varying combinations ofαβγheterotrimers are
possible(Stapleton et al.1996).The subunit composition
in a speci?c tissue or cell type may be important to the
role that AMPK plays in regard to energy sensing in that
particular tissue.Several studies have examined AMPK
subunit expression in the brain and are discussed in further
detail below(Turnley et al.1999;Culmsee et al.2001).
AMPK catalytic activity is enhanced not only by AMP
binding,but also byαsubunit phosphorylation by an
upstream kinase(Davies et al.1995;Hawley et al.1996;
Stein et al.2000).The search for the identity of the
upstream kinases that phosphorylate and activate AMPK
has been a long one(Witters et al.2006).However,
the identi?cation of these kinases may provide further
insight into the tissue-speci?c as well as brain-speci?c
regulation of AMPK.Initially it was shown that the
Peutz–Jeghers syndrome tumour suppressor gene,LKB1,
is an AMPK kinase(Hawley et al.2003;Woods et al.2003).
Subsequently,studies in various cell-lines,tissues and in
vivo models demonstrated the physiological importance of
activation of the LKB1-AMPK signalling pathway(Shaw
et al.2004,2005;Jones et al.2005;Sakamoto et al.2005).
However,despite the fact that LKB1has been reported to be
widely expressed in various tissues,its role in brain AMPK
regulation has not yet been elucidated(Rowan et al.2000).
Most recently,three groups independently reported
that calcium/calmodulin-dependent protein kinaseβ
(CaMKKβ)is an additional upstream kinase of AMPK
(Hawley et al.2005;Hurley et al.2005;Woods et al.
2005).Although the precise physiological relevance of
this activation is unclear,several possibilities exist.Since
CaMKKβis a Ca2+-activated kinase,it is possible
that stimuli that elevate intracellular calcium levels
(e.g.extracellular ligands,hormones)are capable of
eliciting AMPK activation.This may be a predominant
upstream pathway of AMPK activation in tissues with
high CaMKKβexpression,such as the brain(Anderson et al.1998;Sakagami et al.1998).Another intriguing possibility is that in tissues where both CaMKKβand LKB1are expressed,different stimuli(e.g.hormonal versus metabolic)may elicit AMPK activation through divergent upstream kinases and mediate different physio-logical responses.Together,these new?ndings open many avenues of research into mechanisms of AMPK regulation in the brain and further experimentation is needed to test these possibilities.
AMPK expression in the brain
Neurons.While early studies demonstrated expression of AMPK in numerous tissues,only recently has brain-speci?c AMPK been examined in detail(Gao et al.1995; Stapleton et al.1996).Initially,immunohistochemical and Northern Blot analysis demonstrated the expression of AMPK subunits in the embryonic and postnatal mouse brain(Turnley et al.1999).The authors found that AMPK subunits exhibited a predominant neuronal localization with some expression in activated astrocytes and oligodendrocytes.Notably,theα2isoform was expressed at higher levels than theα1isoform,and localized to the nucleus of neurons in many brain regions.Theβ1subunit also showed a preferential nuclear localization,whereas theβ2was mainly cytosolic. Theγ1subunit displayed differential region-speci?c nuclear expression,while theγ2subunit was primarily cytosolic.Additionally,the authors observed that AMPK expression was especially high in cerebellar Purkinje neurons and hippocampal pyramidal neurons,regions that had previously been shown to exhibit high metabolic rate and glucose utilization(Pertsch et al.1988).A subsequent immunohistochemical study of rat embryonic and adult cortex and hippocampus as well as dissociated rat hippocampal neurons detected substantialα1subunit expression in addition toα2,β1,β2andγ1subunits (Culmsee et al.2001).Lastly,work from our laboratory has demonstrated that AMPK catalytic subunits are present in the hypothalamic arcuate nucleus(ARC), colocalize with neuropeptide Y(NPY)expressing neurons, and play a role in feeding control(see below)(Kim et al. 2004a).Collectively these studies provide evidence that AMPK catalytic and regulatory subunits are differentially expressed in various brain and subcellular regions.It would be of great interest to determine whether AMPK has different roles in different brain regions and whether region-speci?c AMPK subunit expression contributes to potentially different physiological functions.These are interesting ideas that have not yet been tested experimentally.
Glial cells.Previously,several groups have also reported the expression of AMPK in oligodendrocytes and astrocytes in culture(Moore&Brophy,1994;Cox et al.
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1997).Separate studies showed that AMPK in astrocytes plays a role in ketogenesis and in the prevention of apoptosis(Blazquez et al.1999;Blazquez et al.2001). However,in our recent work,AMPK expression was con?ned to neurons and was undetectable in glial cell types both in culture and in vivo(Landree et al.2004; McCullough et al.2005).This discrepancy may derive not only from differences in culture conditions,but also from differences between in vitro culture and in vivo conditions.Interestingly,it was found in vivo that AMPK is up-regulated in activated astrocytes during reactive gliosis(Turnley et al.1999).The fact that astrocytes in long-term cell culture exhibit similarities to reactive astrocytes supports the earlier in vitro?ndings of astrocyte AMPK expression(Cox et al.1997).Thus,it is likely the astrocytic AMPK may play an important role under pathophysiological conditions.Clearly,additional studies are required to investigate the mechanisms of this cell-speci?c regulation of AMPK expression under normal and pathological conditions.
AMPK and energy balance:role in feeding Although studies had reported expression of AMPK in the brain,its physiological function remained unclear until recently.In peripheral tissues,AMPK was hypothesized to function as a‘cellular fuel gauge’(Hardie&Carling,1997). Several groups demonstrated that a physiological stimulus such as exercise(skeletal muscle contraction)induces AMPK activation and promotes glucose uptake and fatty acid oxidation(Winder&Hardie,1996;Merrill et al.1997; Vavvas et al.1997;Hayashi et al.1998;Mu et al.2001). Additionally,adipocyte-derived hormones(adipokines) such leptin and adiponectin increased AMPK activity in muscle and liver to promote fatty acid oxidation and/or glucose utilization(Minokoshi et al.2002;Yamauchi et al. 2002).Thus,it became apparent that AMPK could be activated not only by physiological stimuli but also by hormonal cues to restore bodily energy homeostasis. Therefore,due to this role as a peripheral energy status sensor,it was postulated that AMPK might have a more global role in the hypothalamus as a central integrator of energy status and master controller of feeding behaviour (Ruderman et al.2003).In this regard,several independent studies(discussed below)have demonstrated that hypo-thalamic AMPK is responsive to circulating hormones (orexigenic and anorexigenic),alterations in cellular energy levels,as well as nutrient cues.In turn,modulation of AMPK activity initiates a series of events leading to alterations in feeding behaviour(Fig.1).Although many of these studies have utilized pharmacological or genetic approaches to alter AMPK activity,collectively they provide insight into the physiological relevance of this pathway.Thus,the fact that AMPK has the capability to respond to multiple cues makes it a likely candidate to act as a physiologically relevant‘signal integrator’and output controller under normal as well as pathological conditions.
Anorexigenic and orexigenic hormones.An initial report in rats demonstrated that intraperitoneal(i.p.)injection of the anorexigenic hormone leptin reduced hypothalamic AMPK activity(Andersson et al.2004).Consistent with these?ndings,a separate study showed that injection of mice with leptin produced a decrease in AMPK α2activity in paraventricular and arcuate hypothalamic feeding centres(Minokoshi et al.2004).A similar response was found with intracerebroventricular(i.c.v.)injection of other anorexigenic stimuli,such as insulin,glucose,the melanocortin receptor agonist,MT-II,or re-feeding after overnight fasting.To provide a link between hormonal regulation of hypothalamic AMPK and feeding behaviour, the authors of this latter study used a genetic approach, expressing constitutively active or dominant negative AMPKα2constructs in hypothalamic feeding nuclei.In these experiments it was found that a reduction in AMPK activity was required for the central anorexigenic effects of leptin and that a reduction in hypothalamic AMPK activity is suf?cient to reduce body weight and food intake (Minokoshi et al.2004).
In contrast,it has also been observed that elevation of AMPK activity is involved in the feeding response to orexigenic stimuli.Thus,either direct hypothalamic injection of the pharmacological AMPK activator 5-amino-4-imidazole carboxamide riboside(AICAR), or expression of a constitutively active AMPK is suf?cient to cause an increase in food intake and body weight(Andersson et al.2004;Minokoshi et al. 2004).Similarly,injection of orexigenic hormones such as ghrelin and cannabinoids leads to an elevation of hypothalamic AMPK activity,suggesting that this may be a mechanism to mediate increased feeding (Andersson et al.2004;Kirkham,2005;Kola et al. 2005).Lastly,expression of a constitutively active AMPK increased fasting-induced expression of the orexigenic hormones neuropeptide Y(NPY)and agouti-related peptide,whereas a dominant-negative AMPK suppressed expression of these hormones under ad libitum fed conditions(Minokoshi et al.2004).Thus,hypothalamic AMPK activation can be reciprocally regulated by orexigenic and anorexigenic stimuli and coordinate the feeding response.This is mostly likely due to direct action upon hypothalamic targets as receptors for these hormones were shown to localize to speci?c neuronal populations(Williams et al.2001).However,the mechanism by which hormones modulate hypothalamic AMPK activity and elicit changes in feeding behaviour is not yet known.This may involve changes in hypothalamic gene expression as well as alterations in neuronal activity and signalling.
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88S.Ramamurthy and G.V.Ronnett J Physiol574.1 Cellular energy status.Independently,work from our
group demonstrated a role for hypothalamic AMPK in the
control of food intake by pharmacological manipulation
of cellular energy pathways.While developing agents
to modulate fatty acid metabolism,we found that
mice treated with C75,a synthetic fatty acid synthase
(FAS)inhibitor/carnitine palmitoyltransferase(CPT-1)
stimulator,exhibited a dramatic reduction in food intake
Cell Survival
Cell Death
Figure1.Mechanisms of AMPK regulation in the brain
In the hypothalamus,positive energy balance signals inhibit AMPK phosphorylation,whereas negative energy
balance signals stimulate AMPK phosphorylation and activation.These signals are integrated and proceed through
alterations in either the LKB1or CaMKKβpathways.A series of metabolic and gene transcription events is
initiated,ultimately leading to an inhibition or stimulation of the feeding response.In the cortex or hippocampus,
physiological or pathological stimuli either inhibit or activate AMPK.Low levels of AMPK activation may elicit compensatory metabolic and survival pathways.Pathological stimuli such as ischaemic stroke may overactivate
AMPK and compensatory pathways ultimately leading to metabolic failure and cell death.
and body weight(Loftus et al.2000).Subsequently it
was determined using dissociated rat cortical neurons
in vitro that C75treatment causes an increase in both
fatty acid and glucose oxidation and intracellular ATP
levels.This was accompanied by a transient rise and a
prolonged inhibition of AMPK activity,resulting in the
production of an‘energy-rich’state(Landree et al.2004).
Thus,through modulation of FAS and CPT-1activities,
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J Physiol574.1AMP-activated kinase in the brain89
neuronal energy levels were altered to affect AMPK activity,
probably through a change in the perception of neuronal
energy balance.On the basis of these data,in vivo studies
were performed to investigate the connection between
alterations of hypothalamic AMPK activity/energy balance
and C75-induced anorexia and weight loss.It was found
that either i.p.or i.c.v.injection of C75in mice induced
a rapid reduction in hypothalamic phospho-AMPK levels
(Kim et al.2004a).Treatment with C75also produced an
increase in ATP levels in hypothalamic neuronal cultures.
Additionally,i.c.v.injection of AICAR increased food
intake(consistent with Andersson et al.2004),whereas
i.c.v.administration of the AMPK inhibitor,compound C,substantially reduced food intake in mice.Furthermore,
administration of AICAR with C75reversed not only
the C75-mediated inhibition of AMPK phosphorylation,
but also the anorexigenic effects of C75.These studies
also showed that C75treatment was associated with
decreased hypothalamic cyclic AMP response element
binding protein(CREB)phosphorylation and reduced
orexigenic NPY gene transcription in the arcuate nucleus,
whereas the opposite was observed with AICAR treatment.
Based on these data,it was suggested that changes in
hypothalamic energy?ux,e.g.by changes in ATP/AMP
levels induced by long-term fasting or modulation of
fatty acid metabolism,could be monitored by AMPK
and transduced to changes in gene expression to control
whole organism energy balance,i.e.by altering feeding
behaviour.It remains to be resolved whether AMPK kinase
can respond to transient physiological?uctuations,or
whether it indeed serves as a master sensor that is only
activated with more extreme changes in energy levels. Fatty acids and glucose.Several groups have also investigated the effects of circulating nutrients such as
fatty acids and glucose on AMPK activation and feeding.
Initially,the effect of the naturally occurring fatty acid α-lipoic acid,a cofactor of mitochondrial respiratory enzymes,on obesity and feeding was studied(Kim
et al.2004b).It was found in rats,that injection of α-lipoic acid or administration of a diet containing α-lipoic acid,produced a signi?cant reduction in body weight and food intake.It was determined that these
anorexigenic effects were mediated by a reduction in
hypothalamic AMPK activity.Interestingly,it was
found thatα-lipoic acid did not affect hypothalamic
neuropeptide expression.Therefore,it would be of
considerable interest to determine howα-lipoic acid
elicits its anorexigenic effects through AMPK activation,
perhaps though a central gene transcription-independent
mechanism.However,the authors did observe an increase
in peripheral energy expenditure,an effect that was
associated with increased expression of uncoupling
protein-1(UCP-1)in adipose tissue.Although it is likely
that activation of peripheral AMPK and subsequent stimulation of energy expenditure is involved in this effect, a de?nitive molecular mechanism remains to be further elucidated.
AMPK has also been suggested to be a glucose sensor. In this regard,it was shown in cell lines and ex vivo hypothalamic tissue that AMPK activity is stimulated by low glucose levels and that direct AMPK activation up-regulates orexigenic agouti-related peptide expression (Lee et al.2005).This study also demonstrated that small changes in hypothalamic glucose levels in the physiological range of1–5m m altered cellular ATP levels suf?ciently to induce AMPK activation and gene expression.Another recent study suggested a potential role for ventromedial hypothalamic AMPK in the counteregulatory response to insulin-induced hypoglycaemia in vivo(McCrimmon et al.2004).In this study it was found that injection of AICAR reduced the amount of infused glucose required for hyperinsulinaemic–hypoglycaemic clamp conditions. The authors attributed this effect to stimulation of hepatic glucose production via a non-hormonal signalling mechanism.Together these studies raise the possibility that‘glucose-sensing neurons’in various hypothalamic regions,which have been shown to respond to small alterations in glucose levels and change their?ring rate, may utilize the AMPK system in their signalling pathway (Levin,2001;Levin et al.2004).These hypothalamic neurons have also been shown to respond to circulating hormones as well as glucose(Spanswick et al.1997,2000; Wang et al.2004).However,a de?nite role for AMPK in the regulation of hypothalamic neuronal excitability and?ring rate has not yet been shown in response to any stimulus.It is also unclear whether glucose-sensing is directly related to alterations in food intake,or more likely whether it is one of many signals that are integrated by hypothalamic feeding centres(Levin et al.2004).However,a recent study showed that abnormal elevation of hypothalamic AMPK contributes to hyperphagia in a diabetic rat model (Namkoong et al.2005).Further studies are required both in vivo and in vitro,to investigate the physiological role of AMPK and the connection between glucose-sensing and feeding behaviour.
Other feeding mechanisms.In addition to AMPK, other central mechanisms of food intake regulation have been suggested(Ruderman et al.1999,2003).In this regard,it has been proposed that inhibition of the enzyme carnitine palmitoyltransferase-1(CPT-1)by accumulation of either long-chain(oleic acid)or short-chain fatty acids/malonyl-CoA in the hypothalamus causes a reduction in food intake(Obici et al.2003;Lane et al.2005).CPT-1is the enzyme that controls the entry of long chain-fatty acyl-CoAs into the mitochondria to undergoβ-oxidation.This hypothesis(originally derived from studies of muscle),suggests that an increase in hypothalamic fatty acids signals that energy stores are
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suf?cient and subsequently inhibits the feeding response.
Interestingly,it was found that the anorexigenic compound
C75,also stimulates CPT-1activity and fatty acid oxidation
in addition to inhibiting fatty acid synthesis(Thupari
et al.2002;Landree et al.2004).Thus,the interplay
between malonyl-CoA,CPT-1and feeding behaviour is
complicated.Because the precise mechanism of these
effects is not yet identi?ed,further study is needed into
the role of CPT-1activity,as well as its possible regulation
by AMPK in hypothalamic energy perception.
AMPK and energy balance:role in neuroprotection
In addition to being regulated by hormones and?uxes in
cellular ATP/AMP levels,AMPK is also activated by cellular
stresses such hypoxia,ischaemia,oxidative and nitrosative
stresses,as well as and metabolic poisons(Hardie,2004a).
Furthermore,given the high metabolic demands of the
brain and its relative intolerance of ischaemia,hypoxia,
as well as energy depletion,it is very likely that AMPK
activity plays an important role in brain energy homeo-
stasis.Despite this fact,the function of AMPK in neuronal
energy metabolism,either under normal or pathological
conditions,has not been extensively studied.However,
some clues regarding the role of AMPK in neuroprotection
are emerging(Fig.1).
Culmsee et al.(2001)initially reported,using isolated
hippocampal neurons,that AMPK activation with AICAR
provided cytoprotection following glucose deprivation,
glutamate excitotoxicity,Aβpeptide exposure(an
oxidative stress),or sodium cyanide treatment(a
mitochondrial toxin).Additionally,depletion of AMPK αsubunits using antisense RNAs abrogated the protective effect of AICAR stimulation.Therefore,according these
treatment protocols,it was shown that AMPK activation
promotes neuronal survival at least under in vitro
conditions.It is unclear whether these neuronal insults
activated AMPK by themselves or what the effectors of
AMPK-mediated neuroprotection are.Other work has
shown that AMPK activation can have either pro-survival
or pro-apoptotic effects in various brain cell-lines/types
under different experimental conditions(Blazquez et al.
2001;Garcia-Gil et al.2003;Jung et al.2004).It is possible
that differential AMPK subunit expression,activation,
or effectors,may explain these discrepancies.Therefore,
additional studies are required to elucidate the molecular
mechanisms and consequences of AMPK activation or
inhibition in the setting of these varied conditions and
injury models as well their relevance to in vivo physiology.
Further insight into the function of AMPK under one
CNS injury model,i.e.cerebral ischaemia,was provided
by our most recent work(McCullough et al.2005).
In these studies,using an in vivo mid-cerebral artery
occlusion(MCAO)and reperfusion system,it was found that AMPK was phosphorylated in cortical tissue within 90min of vessel occlusion.Similar results were observed in hippocampal slice cultures subjected to2h of oxygen glucose deprivation(OGD),an in vitro stroke model.A global activation of AMPK was seen following these insults, suggesting that this was a compensatory response to facilitate the restoration of falling ATP levels.Surprisingly, administration of AICAR exacerbated stroke damage, whereas the AMPK inhibitor,compound C,provided neuroprotection.Additionally,the FAS inhibitor/CPT-1 stimulator C75,a compound known to increase neuronal ATP levels and inhibit AMPK,was also neuroprotective in this stroke model.It was also noted that mice de?cient in neuronal nitric oxide synthase(nNOS)had smaller infarcts and lower AMPK phosphorylation levels than their wild-type counterparts,suggesting that excessive nitric oxide(NO)or peroxynitrate(ONOO)production may contribute to AMPK activation in stroke.Collectively, these data suggest that in the setting of ischaemia and reperfusion injury,AMPK activation is detrimental to neuronal survival,and that prevention of AMPK activity may be neuroprotective.
This?nding illustrates that the consequences of AMPK activation under stress may be more complex than previously imagined,and the outcome of AMPK activation may be cell or tissue speci?c.Several recent studies have suggested that AMPK activation in the heart following ischaemia and reperfusion is cardioprotective(Marsin et al.2000;Russell et al.2004).These groups found that following injury,AMPK activation promotes glucose uptake and glycolysis,and limits apoptosis and cell damage.Whereas in peripheral tissues,activation of AMPK may inhibit energy-consumptive processes and promote energy-generating and survival pathways in an attempt to restore homeostasis,similar mechanisms may not exist or fail to operate in the brain.For example, following ischaemic stroke,a series of detrimental events is initiated,including a decrease in protein synthesis,disruption of membrane integrity and excessive intracellular Ca2+in?ux(excitotoxicity)(Johnston,2005). Although it is not known how AMPK is activated under these conditions,it is possible that Ca2+in?ux and subsequent activation of CaMKKβis a major pathway. Despite the fact that this kinase has not been implicated in ischaemic neuronal death,further experiments are required to test this notion.
Another hallmark of ischaemic injury is NO/ONOO/ superoxide overproduction and oxidative stress(Lewen et al.2000).In this regard,it has been demonstrated that astrocytes and neurons may respond differently to these insults,in particular to NO exposure(either derived from eNOS or nNOS)(Almeida et al.2001, 2004).Whereas NO induces inhibition of mitochondrial respiration,induction of AMPK activity,and restoration of glycolysis and improved survival in astrocytes,a
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similar response is not observed in neurons due to their low expression of6-phosphofructo-2-kinase(PFK2),a target of AMPK phosphorylation(Almeida et al.2004). As a consequence,numerous compensatory energy-consuming neuronal pathways are activated which may further exacerbate cellular dysfunction.Thus,it is plausible that excessive neuronal AMPK activation when oxygen and glucose substrates are lacking may induce a detrimental ‘metabolic failure-like’state.Under these conditions, pharmacological AMPK inhibition would be bene?cial to neuronal survival.Therefore,much further work is necessary to investigate the mechanisms of AMPK activation in ischaemic injury in vivo and the effect of alterations in neuronal energy status under these conditions.
Conclusions
Recent years have witnessed an expanded interest in the roles of AMPK in numerous physiological systems. Additional methods of AMPK regulation have been discovered.Whereas,once it was thought to be regulated primarily by cellular AMP/ATP and nutrient levels,it is now clear that additional pathways for activation of AMPK are possible.These various stimuli include hormones,physiological state,as well as pathological events.This complexity of function is evident in the brain where AMPK is a coordinator of whole body metabolism through feeding behaviour as well as local regulator of neuronal homeostasis.In hypothalamus,the role of hormonal control of AMPK activation is an exciting area of research with many unanswered questions.What are the precise signalling mechanisms that mediate orexigenic and anorexigenic hormone action in the hypothalamus to coordinate the feeding response?Additionally,the molecular basis for divergent AMPK regulation in the brain and periphery,tissue/cell-speci?c AMPK regulation, and physiological/pathological AMPK activation remains to be elucidated.It would be intriguing to study the relative importance of the LKB1or the CaMKKβpathways in these varied conditions in the brain.Additional AMPK kinases may remain to be discovered,which will provide clues to additional AMPK functions.Determination of the signi?cance of differential tissue-speci?c or sub-cellular(cytosolic versus nuclear)localization of AMPK subunits may also provide insight into AMPK regulation. Whereas nuclear AMPK activation may elicit long-term gene expression changes,cytosolic AMPK may be involved in the modulation of more immediate metabolic and homeostatic responses.Together,additional insight into AMPK physiology in the brain as well as the consequences of its modi?cation may suggest novel therapeutic targets for obesity,type-2diabetes,stroke and neurodegeneration.References
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一生励志的正能量短句子大全 一生励志的正能量短句子摘抄 1. 不经历风雨，长不成大树，不受百炼，难以成钢。 2. 耐心和恒心总会得到报酬的。 3. 宝剑锋从磨砺出，梅花香自苦寒来。 4. 表示惊讶，只需一分钟;要做出惊人的事业，却要许多年。 5. 不放弃!决不放弃!永不放弃! ——邱吉尔 6. 不积跬步，无以至千里;不积小流，无以成江海。——荀子 7. 苟有恒，何必三更起五更眠;最无益，只怕一日曝十日寒。——毛泽东 8. 成功最终属于耐心等待得人。 9. 凡是新的事情在起头总是这样一来的，起初热心的人很多，而不久就冷淡下去，撒手不做了，因为他已经明白，不经过一番苦工是做不成的，而只有想做的人，才忍得过这番痛苦。——陀思妥耶夫斯基 10. 放弃时间的人，时间也会放弃他。——莎士比亚 11. 斧头虽小，但经历多次劈砍，终能将一棵最坚硬的
橡树砍刀。 12. 告诉你使我达到目标的奥秘吧，我惟一的力量就是我的坚持精神——巴斯德 13. 一个人最痛苦的时候不是吃不上饭的时候，而是想努力奋斗没有机会。 14. 与其做一个有价钱的人，不如做一个有价值的人;与其做一个忙碌的人，不如做一个有效率的人。 15. 没有目标的人，永远为有目标的人打工。 16. 智者创造机会，强者把握机会，弱者坐等机会。 17. 说出的苦不叫苦，说不出的苦才叫苦。 18. 人若把自己框在一定的范围内，就容易限制了自己的思维和格局。 19. 人往往年轻时用健康换财富，老时再用财富换健康。发达国家的人们是透支金钱，储存健康;我们国家的人是透支健康，储存金钱。 20. 人因为有理想、梦想而变得伟大，而真正伟大就是不断努力实现理想、梦想。 一生励志的正能量短句子精选 1. 一件事被所有人都认为是机会的时候，其实它已不是机会了。 2. 天上最美的是星星，人间最美的是真情。 3. 活鱼会逆流而上，死鱼才随波逐流。 4. 怕苦的人苦一辈子，不怕苦的人苦一阵子。
能量的转化和转移（北京习题集）（教师版） 一．选择题（共5小题） 1．（2016秋?昌平区期末）下列说法中不正确的是 A ．发电机工作时，将机械能转化为电能 B ．电风扇工作时，扇叶的机械能是由电能转化的 C ．在被阳光照射时，太阳能电池将太阳能转化为电能 D ．干电池给小灯泡供电时，干电池将电能转化为化学能 2．（2016秋?西城区校级期中）下列生活实例中，只有能量的转化而没有能量的转移的是 A ．利用煤气灶将冷水烧热 B ．汽车行驶一段路程后，轮胎会发热 C ．太阳能水箱中的水被晒热了 D ．把冰块放在果汁里，饮用时感觉很凉快 3．（2015秋?东城区校级期中）在能的转化过程中，下列叙述不正确的是 A ．木柴燃烧过程中是化学能转化为内能 B ．发电机工作时是机械能转化为电能 C ．电源是将其它形式的能转化为电能的装置 D ．干电池使用时，是把电能转化为化学能 4．（2014秋?北京校级月考）下列现象中，只有能的转移而不发生能的转化的过程是 A ．水蒸气会把壶盖顶起来 B ．洗衣机工作 C ．用锤子打铁件，铁件发热 D ．冬天用手摸户外的东西时感到冷 5．（2011秋?西城区校级月考）下列过程中，机械能转化为内能的是 A ．锯木头，经过一段时间后，锯条和木头都发热 B ．锅里的水沸腾时，水蒸气把锅盖顶起 C ．神州号飞船点火后，腾空而起 D ．礼花弹在节日的夜空中绽开 二．多选题（共1小题） 6．（2008?宣武区二模）在以下事例中，机械能转化为内能的是 ()()()() ()()
A ．流星与空气摩擦，生热发光 B ．水壶中的水沸腾后，壶盖被水蒸气顶起 C ．反复弯折铁丝，铁丝弯折处温度升高 D ．金属汤勺放在热汤中，其温度升高 三．填空题（共3小题） 7．（2016秋?西城区校级期中）如果你去参观中国科技馆四层“挑战与未来” 厅 “新型材料”展区，你就可以看到这种能发电的神奇布料。会发电的衣服是用一种可以利用运动产生电力的新型纤维织造的，当人穿上这种纤维织成的衣物后，在身体运动过程中会产生一些压折，或者遇上一阵微风，就能够形成源源不断的电流，这种发电方式是将人体的 能转化为电能、并加以应用的最简单也最经济的方式。发电纤维与压电陶瓷都是通过压力来产生电力，而使小灯泡发光的。 8．（2013?西城区一模）如图所示是北京郊区官厅风力发电场的巨大的风车。这种装置可以利用风能带动扇叶转动，并把风车的机械能转化为 能。 9．（2012秋?宣武区校级月考）某人使用手机通话时，锂电池此时的能量转化是 。 四．实验探究题（共1小题） 10．（2016秋?海淀区期中）阅读《压电陶瓷》回答问题。 压电陶瓷 打火机是日常生活中常用的物品，最初的打火机是靠拨动齿轮与火石摩擦起火的，而今人们常用的是压电式打火机。这种打火机中装有一块压电陶瓷。使用时只需按压点火开关，利用压电陶瓷的压电效应，在两点火极之间产生 的电压而引起火花，引燃丁烷气（如图甲所示）。 某些物质在沿一定方向上受到外力的作用而变形时，就会在它的两个相对表面上形成一定的电压。当外力去掉后，它又会恢复到不带电的状态，这种现象称为压电效应。这种压电效应不仅仅用于打火机，还应用于煤气灶打火开关、炮弹触发引线、压电地震仪等许多场合。 某种压电陶瓷片外形如图乙所示。它是把圆形压电陶瓷片与金属振动片粘合在一起。当在压电陶瓷片上施加一个压力时，在陶瓷片与金属振动片之间就会产生电压。可用如图丙的方法来观察压电现象并检查压电陶瓷片的质量好坏，即用导线把金属振动片和压电陶瓷片分别与电压表的、接线柱连接，当用拇指与食指挤压压电陶瓷片和金属振动片的两面时，电压表的指针就会偏转，这说明在压电陶瓷片与金属振动片之间产生了电压。 在压力相同的情况下，电压表指针摆幅越大，说明压电陶瓷片的灵敏度越高 。 A --10~20kV +-
工作励志正能量句子 1)对于攀登者来说，失掉往昔的足迹并不可惜，迷失了继续前时的方向却很危险。 2)奋斗者在汗水汇集的江河里，将事业之舟驶到了理想的彼岸。 3)含泪播种的人一定能含笑收获。 4)很多失败不是因为能力有限，而是因为没有坚持到底。 5)机会不会主动找到你，必须亮出你自己。 6)驾驭命运的舵是奋斗。不抱有一丝幻想，不放弃一点机会，不停止一日努力。 7)困难和挫折都不可怕，可怕的是丧失做人的志气和勇气。 8)漫漫长路，你愿一人独撑，忍受着孤独与寂寞，承受着体力与精神的压迫，只任汗水溶于泪水，可脚步却从不停歇。好样的，纵然得不了桂冠，可坚持的你，定会赢得最后的掌声。 9)莫找借口失败，只找理由成功。 10)世上没有绝望的处境，只有对处境绝望的人。 11)每一发奋努力的背后，必有加倍的赏赐。 12)赚钱之道很多，但是找不到赚钱的种子，便成不了事业家。 13)大多数人想要改造这个世界，但却罕有人想改造自己。 14)当一个人先从自己的内心开始奋斗，他就是个有价值的人。 15)即使爬到最高的山上，一次也只能脚踏实地地迈一步。 16)穷人缺的是钱而不是时间，富人缺的是时间而不是钱。
17)好心不一定会换来感恩，但千万不要因此而灰心。 18)若不给自己设限，则人生中就没有限制你发挥的藩篱。 19)最有效的资本是我们的信誉，它小时不停为我们工作。 20)人生不是一种享乐，而是一桩十分沉重的工作。 1)忙于采集的蜜蜂，无暇在人前高谈阔论。 2)你追我赶拼搏争先，流血流汗不留遗憾。 3)懦弱的人只会裹足不前，莽撞的人只能引为烧身，只有真正勇敢的人才能所向披靡。 4)勤奋是你生命的密码，能译出你一部壮丽的史诗。 5)人生伟业的建立，不在能知，乃在能行。 6)你的上司越忙，你的饭碗越危险。 7)如果你最近的工作很闲，注意了，这可能是危机的先兆。 8)到处都是有才华的穷人，千万别觉得自己无可替代。 9)每一个成功者都有一个开始。勇于开始，才能找到成功的路。 10)当一个人用工作去迎接光明，光明很快就会来照耀着他。 11)如果我们想要更多的玫瑰花，就必须种植更多的玫瑰树。 12)漂亮的脸孔是给别人看的，而有智慧的头脑才是给自己利用的。 13)人只有在布满陡峭的路上，才能使自己的脚跟变的更稳;人只有在布满荆棘的路上，才能使自己的身体变的不怕伤痕;人只有在布满危险的路上，才能使自己的战斗力变的无比之强! 14)选择自信，就是选择豁达坦然，就是选择在名利面前岿然不动，就是选择在势力面前昂首挺胸，撑开自信的帆破流向前，展示搏击的风采。
正能量励志短句子(精选300句) 2021-02-28 正能量励志短句子(精选300句) 1、当你尽了自我的最大努力时，失败也是伟大的。 2、生命力的意义在于拼搏，因为世界本身就是一个竞技场。 3、荆棘的存在是为了野草不轻易地任人践踏。 4、少一点预设的期盼，那份对人的关怀会更自在。 5、当你能梦的时候就不好放下梦。 6、以往拥有的，不要忘记；已经得到的，更要珍惜；属于自我的，不要放下；已经失去的，留着回忆；想要得到的，必须努力；但最重要的，是好好爱惜自我。 7、留心记下自我平常所说的话，看看其中有多少是陈述性的，有多少是询问性的。假如你总是向别人发问，你就是在寻求赞许。 8、学习是苦根上长出来的甜果。 9、我们一向以为最艰难的总是当下，却发现人生从来不曾有最艰难，只会有更艰难。唯一还值得庆幸的是，所有打不倒你的都将使你变得更强大，所有打倒了你的也并没将你彻底击垮。风是无常的，人，也是无常的，我的忙碌，也是无常，世事无常。 10、生活中若没有兄弟姐妹，就像生活中没有阳光一样。 11、不要因为没有掌声而放下你的梦想。 12、人生就是一般此刻时和此刻进行时，没有一般过去时。 13、拒绝严峻的冶炼，矿石并不比被发掘前更有价值。 14、人生的路经历过，才知道有短有长；岁月，在无憾中微笑，才美丽；回过头，想着明天抱一抱。那些年最初的梦想在我们心中依旧完美，我们只需要记住那些完美。把握此刻，活在当下才是真理。 15、此岸，彼岸，终究是尘归尘，土归土。一季绯红也只是一季花凉，几许艳丽，几许妩媚，几经风雨，尘埃落地。活着，就要慢慢老去，途径坎坷，感受
悲喜，生命最终是寂灭。缘有长短，人有来去，再深的情也会淡泊，再浓的意也会无痕，初见永远不会再见。 16、命是弱者的借口，运是强者的谦词。 17、要假设你融不到一分钱的情景去做事业。 18、人生如逆旅，我亦是行人。 19、就算全世界都说我漂亮，但你却说我不漂亮，那么我就是不漂亮。 20、如果我们能够改变情绪，我们就能够改变未来。 21、拥有的，要珍惜，要知足；做人必须要有一颗平常心，肤浅的羡慕，无聊的攀比，笨拙的效仿，只会让自我整天活在他人的影子里面。我们应当认清自我，找到属于自我的位置，走自我的道路，过自我的生活。 22、一些伤口之所以总会痛，那是因为你总是去摸。 23、一个人变强大的最好方式，就是拥有一个想要保护的人。 24、欲望得不到满足痛苦；欲望一旦满足就无聊，生命就是在痛苦和无聊之间摇摆。 25、萤火虫的光点虽然微弱，但亮着便是向黑暗挑战。 26、人格的完善是本，财富的确立是末。 27、若不尝试着做些本事之外的事，你就永远不会成长。 28、名利都是虚幻的，自我的心才是最实在的。[由https://www.doczj.com/doc/d714276578.html,整理] 29、要诚恳，要坦然，要慷慨，要宽容，要有平常心。 30、做一名自信者，牢牢把住自我生命的罗盘，让生命充畅。做一名自谦者，慢慢拓展自我生命的容量，让生命充实。做一名自爱者，深深领会自我生命的价值，让生命充美。做一名自安者，悄悄抚平自我生命的伤痕，让生命充悦。做一名自洁者，时时清除自我生命的淤积，让生命充盈。 31、经过云端的道路，只亲吻攀登者的足迹。 32、单纯是我追求的一种生活方式，也是我持续的一种创作心态，但追求单纯需付出许多代价，你必须要有勇气承担因为单纯而带来的被他人利用欺瞒及孤立。但我觉得人生本来就该尽可能坚持一种单纯的状态，因这种状态是最接近自我的内心，一个纯静的内心会把许多事情导入正向，让你拥有一个物质之外的丰富人生。
《能量的转化和守恒》教案 一、教学目标： 1、知道各种形式的能是可以相互转化的。 2、知道在转化的过程中，能量的总量是保持不变的。 3、列举出日常生活中能量守恒的实例。 4、有用能量守恒的观点分析物理现象的意识。 教学重点：能的转化和守恒定律，强调能的转化和守恒定律是自然科学中最基本定律。 教学难点：运用能的转化和守恒原理计算一些物理习题；运用能的转化和守恒定律对具体的自然现象进行分析，说明能是怎样转化的。 二、资料准备：教材分析： 教材从能量的转化与守恒中，列举出生活中的能量守恒实例来加强教学。 三、教学过程： 环节一：引入新课 我们知道物体的动能和热能，是由物体的机械能运动情况决定的能量，内能跟物体内部分子的热运动和分子间的相互作用情况有关。物体内部分子的热运动，物体的机械运动都是物质运动的形式，由于运动形式不同，与之相联系的能量也不相同。 环节二：进行新课 的事例，说明各种形式的能的转化和转移）。在热传递过程中，高温物体的内能转移到低温物体。运动的甲钢球碰击静止的乙钢球，甲球的机械能转移到乙球。在这种转移的过程中能量形式没有变。 在自然界中能量的转化也是普遍存在的。小朋友滑滑梯，由于摩擦而使机械能转化为内能；在气体膨胀做功的现象中，内能转化为机械能；在水力发电中，水的机械能转化为电能；在火力发电厂，燃料燃烧释放的化学能，转化成电能；在核电站，核能转化为电能；电流通过电热器时，电能转化为内能；电流通过电动机，电能转化为机械能。有关能量转化的事例同学们一定能举出许多，课本图2-17中画出了一些农常用的生活、生产设备。请同学分析在使用图中设备时能量的转化。 (3)在能量转化和转移的过程中，能的总量保持不变。大量事实证明，在普遍存在的能量的转化和转移过程中，消耗多少某种形式的能量，就得到多少其他形式的能量。如在热传递过程中，高温物体放出多少热量（减少多少内能），低温物体就吸收多少热量（增加多少内能）；克服摩擦力做了多少功，就有多少机械能转化为能量，但能量的总量不变。就是说某物体损失的能量等于几个物体得到几个物体得到的能量的总和。例如，把烧热的金属块，投到冷水中，冷水，盛水的容器以及周围的空气等，都要吸收热量，它们所吸收的热量总和跟金属块放出的热量相等。再如水电站里，水从高处流下，损失了机械能，一方面由于推动发电机转动而转化为电能，一方面水跟水轮机、管道摩擦而转化为内能。那么水的机械能的损失等于产生的电能和内能的总和。 以上规律是人类经过长期的实践探索，直到19世纪，才确立了这个自然界最普遍的定律棗能量的转化守恒定律。通常把它表述为： 能量既不会消灭，也不会创生，它只会从一种形式转化为其他形式，或者从一个物体转移
50条超励志的正能量经典句子 1、当你觉得自已充满斗志，充满信心，别人就会觉得你就是值得相信的你。 2、当你觉得没有人来爱你，别人看见的就是可怜兮兮，毫无魅力的你。 3、当你觉得自己满怀希望，对未来充满信心，别人看到的就是有魅力，风华绝代的你。 4、人生与其说你有不幸的事实存在，倒不如说是你的悲观的观念所带来的。 5、有一则谚语说，绵羊每"咩咩"叫上一次，它就会失掉一口干草，如果你的心态是沉重的，总是抱怨你的苦恼，那么每说一次你便失掉一个快乐的机会。 6、相信自已。 不要妄加评判自已，也不会把自已交给别人评判，更不会贬低自已。 7、你想要别人是你的朋友，你必须是别人的朋友，心要靠心来交换，感情只有用感情来博取。 8、人生的游戏不在于拿了一副好牌，而在于怎样去打好坏牌，世上没有常胜将军，勇于超越自我者才能得到最后的奖杯。 9、既然时间是最宝贵的财富，那么珍惜时间，合理地运用时间就很重要，如何合理地花费时间，就如同花钱的规划一样重要，钱花
完了可再挣，时间花完了就不能再生，因此，更要利用好你的时间。 10、解铃还需系铃人，躲避责任会解决不了任何问题，它只导致一个失败的人生。 11、人不怕走在黑夜里，就怕心中没有阳光。 12、逃避不一定躲得过，面对不一定难受.转身不一定最软 弱.13、话多不如话少，话少不如话好。 14、曾经拥有的不要忘记，已经得到的要珍惜，属于自已的不要放弃。 15、永远都不要停止微笑，即使是在你难过的时候，说不定哪一天有人会因为你的笑容面爱上你。 16、因为某人不如你所愿爱你，并不意味着你不被别人所爱。 17、一个真正的朋友会握着你的手，触动你的心。 18、也许上帝让遇见那个适合你的人之前，会遇见很多错误的人，所以当一切发生的时候，你应该心存感激。 19、勇敢的面对不一定成功，但你不面对就一定不成功。 20、黑夜的转弯是白天，愤怒的转弯是快乐，所以有的时候让心情转个弯就好了。 21、一天要做三件事，第一要笑，第二要微笑，第三要哈哈大笑。 22、小树会大，大树会老，老树会凋零。 23、如果你不想做，你可以找一个理由，如果你肯做，你也可以
激励自己奋斗的正能量励志句子 励志句子 1、在别人肆意说你的时候，问问自己，到底怕不怕，输不输的起。不必害怕，不要后退，不须犹豫，难过的时候就一个人去看看这世界。多问问自己，你是不是已经为了梦想而竭尽全力了? 2、人生从来没有真正的绝境。无论遭受多少艰辛，无论经历多少苦难，只要一个人的心中还怀着一粒信念的种子，那么总有一天，他就能走出困境，让生命重新开花结果。 3、幻想一步成功者突遭失败，会觉得浪费了时间，付出了精力，却认为没有任何收获;在失败面前，懦弱者痛苦迷茫，彷徨畏缩;而强者却坚持不懈，紧追不舍。 4、进步和成长的过程总是有许多的困难与坎坷的。有时我们是由于志向不明，没有明确的目的而碌碌无为。但是还有另外一种情况，是由于我们自己的退缩，与自己亲密的妥协没有坚持到底的意志，才使得机会逝去，颗粒无收。 5、决不能习惯失败，因为你要知道，身体的疲惫，不是真正的疲惫;精神上的疲惫，才是真的劳累。 6、理想是什么?它不是口上说的计划，也不是敷衍的借口，它是自己的心，理想的最终汇集地，是幸福，为了自己有了理想，为了恋人有了理想，为了家人有了理想，有了理想才有梦，梦想与理想，一字之差千里之遥。
7、路是自己选的，后悔的话，也只能往自己的肚子里咽。 8、没有钱、没有经验、没有阅历、没有社会关系，这些都不可怕。没有钱，可以通过辛勤劳动去赚;没有经验，可以通过实践操作去总结;没有阅历，可以一步一步去积累;没有社会关系，可以一点一点去编织。但是，没有梦想、没有思路才是最可怕的，才让人感到恐惧，很想逃避! 9、每颗珍珠原本都是一粒沙子，但并不是每一粒沙子都能成为一颗珍珠。想要卓尔不群，就要有鹤立鸡群的资本。忍受不了打击和挫折，承受不住忽视和平淡，就很难达到辉煌。年轻人要想让自己得到重用，取得成功，就必须把自己从一粒沙子变成一颗价值连城的珍珠。 10、每一个人的成功之路或许都不尽相同，但我相信，成功都需要每一位想成功的人去努力、去奋斗，而每一条成功之路，都是充满坎坷的，只有那些坚信自己目标，不断努力、不断奋斗的人，才能取得最终的成功。但有一点我始终坚信，那就是，当你能把自己感动得哭了的时候，你就成功了!
正能量励志的句子经典短句50个 1、经历，只是让我们在下一次面对困难时更加淡定和从容！ 2、十年前，你周围的人会根据你父母的收入对待你。十年后，你周围的人会根据你的收入对待你的父母和你的孩子！这就是人性和人生，除了努力别无选择。记住：没有伞的孩子，必须努力奔跑！ 3、成功没有快车道，幸福没有高速路，一份耕耘一份收获，所有的成功都来自不倦的努力和奔跑，所有幸福都来自平凡的奋斗和坚持。 4、立志越高，所需要的能力越强，相应的，逼迫自己所学的，也就越多。 5、人活着不是要用眼泪博得同情，而是用汗水赢得掌声。 6、认定了的路，再痛也不要皱一下眉头，再怎么难走都是你自己选的，你没有资格喊疼。 7、该来的自然来，会走的留不住。不违心，不刻意，不必太在乎，放开执念，随缘是最好的生活。 8、有句话说的好，不打没有准备的仗，做事之前要修炼自己，有能力才会有魄力，有魄力才会有勇气，有这样的胆色才能把能力发挥到极致，那么你就成功了！ 9、人生是一种承受，我们要学会支撑自己。人的成长，在于学习，也在于经历。人的修养，在于领悟，也在于静修。人的幸福，在于得到，也在于放下。人生秘诀，在于别人，也在于自己。
10、世界那么大，你的野心再大，它也一定装得下。 11、走过的路成为背后的风景，不能回头不能停留，若此刻停留，将会错过更好的风景，保持一份平和，保持一份清醒。 12、多和优秀的人在一起，他们就像一团光芒，呆久了，就再也不想走回黑暗了。 13、每天提升正能量，心中充满小太阳。 14、没有太晚的开始，不如就从今天行动。总有一天，那个一点一点可见的未来，会在你心里，也在你的脚下慢慢清透。生活，从不亏待每一个努力向上的人。 15、如果你真的想做一件事情，那么就算障碍重重，你也会想尽一切办法去办到它。但若是你不是真心的想要去完成一件事情，那么纵使前方道路平坦，你也会想尽一切理由阻止自己向前。 16、过去的事，交给岁月去处理；将来的事，留给时间去证明。我们真正要做的，就是牢牢地抓住今天，让今天的自己胜过昨天的自己。 17、做事不需要人人都理解，但你要尽心尽力；做人不需要人人都喜欢，但你要坦坦荡荡。梦想的坚持注定有孤独彷徨，因为少不了他人的质疑和嘲笑，但那又怎样，哪怕遍体鳞伤，也要活得漂亮！ 18、人的一生不长，今天的辛酸经历，就是明天最美好的回忆，今天的努力将成为明天更多的收获！错过的就让它永远的错过。要珍惜眼前的生活，活出自己的人生，为自己的人生加油！ 19、你走过的每一条弯路，其实都是必经之路，你要记住的是，
四、能量转化的基本规律 学习要求 1．知道能量守恒定律。能举出日常生活中能量守恒的实例。有用能量转化与守恒的分析物理现象的意识。 2.初步了解在现实生活中能量的转化与转移有一定的方向性。 3.讨论和分析两个具体的永动机设计方案，说明永动机是不可能的。 学习指导 1．能量守恒定律：能量既不会凭空消灭，也不会凭空产生，它只会从一种形式转化为另一种形式，或者从一个物体转移到另一个物体，而在转化或转移的过程中，其总量保持不变。能量守恒定律是自然界最普遍、最重要的基本定律之一。一切有能量转化或转移的场合，大到宇宙、小到原子核内部，也不论是生物、化学还是物理、地质现象，都遵守能量守恒定律。自然界中能的总量保持不变，但是对于某一物体可能改变。 2．能量转化和转移的方向性：热量只能从高温物体转移到低温物体，不能相反，具有方向性，否则就要消耗其他的能。不是什么能源都可以利用，能源的利用是有条件的，也是有代价的，有的东西能成为能源，有的则不能。虽然能量在转化和转移的过程中是守恒的，但具有方向性，因此我们一定要节约能源。 典型范例 例题市场经济的今天，一些厂商一改过去“酒香不怕巷子深”的做法，纷纷对产品进行广告宣传。可是有些厂商在广告上弄虚作假，夸大其词，欺骗消费者。如某品牌电热水器这样写道：“我厂电热水器功率只有55W，烧开一瓶水只需5min，节钱省电，最适合普通家庭使用。”这则广告可信吗？ 精析：电热水器烧开水，是电能转化为热能被水吸收的过程。方法一：根据题意求出电热水器所产生的热能，再利用热量公式，算出这些热量能够烧开多少质量的水，与事实进行比较，判断信息是否可信；方法二：先求出电热电热水器所产生的热能，再估算出烧开一瓶水所需要的热量，两者进行比较，判断信息是否可信，判断的依据是能量守恒定律。 全解：方法一：电热水器产生的热能为W=Pt=55W×5×60s=1.65×104J。 假设一般情况下烧开水是把水从20℃加热到100℃，则这些热量可以烧开的水的质量m＝ Q c△t ＝ W c△t ＝ 1.65×104J 4.2×103J/（kg·℃×（100℃-20℃）） ＝0.049kg。
关于唯美励志充满正能量的句子和图片 在路上，我们生命得到了肯定，一路上，我们有失败也有成功，有泪水也有感动，有曲折也有坦途，有机遇也有梦想。下面是我精心整理的唯美励志充满正能量的句子和图片，希望能给大家带来帮助! 1.你不喜欢我，我一点都不介意。因为我活下来，不是为了取悦你! 2.要成功，就要长期等待而不焦躁，态度从容却保持敏锐，不怕挫折且充满希望。 3.行走红尘，别被欲望左右迷失了方向，别被物质打败做了生活的奴隶，给心灵腾出一方空间，让那些够得着的幸福安全抵达，攥在自己手里的，才是实实在在的幸福。 4.所谓成长，就是逼着你一个人，踉踉跄跄的受伤，跌跌撞撞的坚强。 5.如有谁让你难过，一定不要难过太久，因为太多时候，都是被自己编织故事困扰，只是从自己的角度看了事实的一角，只是需求没有满足的夸大，只是习惯于按自己的模式判断，远离事实真相的结果。真相往往没有你想像的悲壮和恶劣，真相中，多有你的误解，和自以为是的受伤，而真心伤人的人真不多见。 6.有时候不是不懂，只是不想懂;有时候不是不知道，只是不想说出来;有时候不是不明白，而是明白了也不知道该怎么做，于是就保持了沉默。 7.人生的每一场相遇，都是缘分，没有对错。人生的每一个清晨，
都该努力，不能拖延。 8.有些人、有些话、说不说、理不理都无所谓。因为看清了，也就看轻了。 9.爱上一个人，会从高傲变成卑微。一举一动，一句话，都会小心翼翼如履薄冰。但对方若爱你，肯定会将这卑微慢慢扳平，变成毫无拘束的相处。如果一段感情让你只能处在下风才能进行，那一定不是真正相互深爱的感情。 10.不管脚步有多慢都不要紧，只要你在走，总会看到进步。 11.如果我在意的人对我忽冷忽热，而我又为此感到了患得患失，那么我便会选择不辞而别，因为我没那么多耐心去品尝患得患失的感觉。 .一辈子不长，只有珍惜了，才不至于后悔。 13.人生是坎坷的，人生是崎岖的。我坚信：在人生中只有曲线前进的快乐，没有直线上升的成功。只有珍惜今天，才会有美好的明天;只有把握住今天，才会有更辉煌的明天!人生啊，朋友啊!还等什么?奋斗吧! 14.没有伞的孩子，必须努力奔跑! 15.当我觉得我倒霉了，我就会想：这是在挥洒我的霉运，挥洒之后，剩下的就全都是幸运了! 16.如果你的面前有阴影，那是因为你的背后有阳光。 17.心情的颜色是活泼热烈的红色，是生机盎然的绿色，是尊贵华丽的黄色，好好地，用这种种颜色做心情，来书写生活，不要让它变得灰暗...... 18.你向我张开手臂，我会小跑几步;你向我微笑，我会驻足聆听;
关于拼搏正能量励志句子大全100句 关于拼搏正能量励志句子大全100句 1、没有人陪你走一辈子，所以你要适应孤独，没有人会帮你一辈子，所以你要一直奋斗。 2、我们自己选择的路，即使跪着也要走完;因为一旦开始，便不能终止。这才叫做真正的坚持。 3、不如意的时候不要尽往悲伤里钻，想想有笑声的日子吧。 4、把困难举在头上，它就是灭顶石;把困难踩在脚下，它 就是垫脚石。 5、思路决定出路，气度决定高度，细节决定成败，性格决定命运。 6、后悔是一种耗费精神的情绪，后悔是比损失更大的损失，比错误更大的错误，所以不要后悔。
7、我们比较容易承认行为上的错误、过失和缺点，而对于思想上的错误、过失和缺点则不然。 8、相信朋友的忠诚。相信自己的勇气。相信敌人的愚蠢。 9、每一枝玫瑰都有刺正如每个人的性格里都有你不能容忍的部分。 10、为自己选择的跑道去冲刺，即使很漫长，即使有阻碍，即使会跌倒;但是，坚定的信念会一直陪伴着我欢笑的、努力地、飞快地奔跑。即使非常非常的辛苦，只要有坚持下去的勇气，再大的山、再阔的海都可以跨越，努力的奔跑，天空的那一边就不再遥远! 11、在人生的道路上，谁都会遇到困难和挫折，就看你能 不能战胜它。战胜了，你就是英雄，就是生活的强者。 12、顺境的美德是节制，逆境的美德是坚韧，这后一种是 较为伟大的德性。 13、一个社团的基本努力或许就是设法使其成员平等，但 其成员个人的自尊心却总是希望自己出人头地，在某处形成某种对自己有利的不平等。
14、在青春的世界里，沙粒要变成珍珠，石头要化作黄金，青春的魅力，应当叫枯枝长出鲜果，沙漠布满森林，这才是青春的美，青春的快乐，青春的本分! 15、穷人缺什么：表面缺资金，本质缺野心，脑子缺观念，机会缺了解，骨子缺勇气，改变缺行动，事业缺毅力。 16、人终归是要生活着的，“不要以为你的努力徒劳无功，权当做磨练你的意志”，只要努力去做事了，多多少少会有收获，一直坚持做下去，就会走向成功! 17、成功不是将来才有的，而是从决定去做的那一刻起， 持续累积而成。 18、只有感受饥饿，才能知道温饱幸福;只有经历风雨，才能见到七彩虹;只有历尽崎岖，才能全力奋起拼搏。在以后的 生活中，我不知道我会遇到多少坎坷但是我相信，我会用全力征服挫折。 19、在世界的前进中起作用的不是我们的才能，而是我们 如何运用才能。 20、人世间，比青春再可宝贵的东西实在没有，然而青春
正能量工作励志短句子 1.我走得很慢，但我从不后退! 2.微笑拥抱每一天，做像向日葵般温暖的女子。 3.待人对事不好太计较，如果太计较就会有悔恨! 4.仅仅活着是不够的，还需要有阳光自由，和一点花的芬芳。 5.世上没有绝望的处境，只有对处境绝望的人。 6.有人问我，如果看不到确定的未来，还要不好付出。我只能说，并不是每一种付出都是在追寻结果。有时在付出的路上，能够收获的，是清楚地看到了自我想要的，或者不想要的，这又何尝不是一 种宝贵的结果。命运会厚待温柔多情的人，好过冷漠的一颗心。 7.没有伞的孩子务必发奋奔跑! 8.失败是什么?没有什么，只是更走近成功一步;成功是什么?就 是走过了所有通向失败的路，只剩下条路，那就是成功的路。 9.坚信梦想是价值的源泉，坚信眼光决定未来的一切，坚信成功的信念比成功本身更重要，坚信人生有挫折没有失败，坚信生命的 质量来自决不妥协的信念。 10.人的生命要疯狂一次，无论是为一个人，一段情，一段旅途，或一个梦想。 11.只有十分十分年轻时，人们才能那么用力地，去喝酒交朋友 打人耳光，往人脸上泼酒，才能如此猛烈地摧残自我。青春期的人，动作总是变形的，每一样感情的流露都放大了一百倍，爱和恨，孤 独与喜悦，都是。 12.天再高又怎样，踮起脚尖就更接近阳光。
13.自我选取的路跪着也要把它走完。 14.不乱于心，不困于情，不畏将来，不念过往。如此，安好。 15.不好去追一匹马，用追马的时刻种草，待到来年春暖花开之时，就会有一批骏马任你选取。 1.只有经历过地狱般的折磨，才有征服天堂的力量。只有流过血的手指才能弹出世间的绝唱。 2.世界愈悲伤，我要愈快乐。当人心愈险恶，我要愈善良。当挫折来了，我要挺身应对。我要做一个乐观向上，不退缩不屈不饶不 怨天尤人的人，勇敢去理解人生所有挑战的人。 3.人生没有彩排，每一天都是现场直播。 4.每个人的性格中，都有某些无法让人理解的部分，再完美的人也一样。因此不好苛求别人，不好埋怨自我。玫瑰有刺，正因是玫瑰。 5.前有阻碍，奋力把它冲开，运用炙热的激情，转动心中的期盼，血在澎湃，吃苦流汗算什么。 6.人生太短，岁月太长。生活是公平的，要活出精彩，需要一颗奋进的心。以勤为本，以韧为基，尽自己的全力，求最好的结果， 行动成就梦想，奋斗成就人生。人生苦短，财富地位都是附加的， 生不带来死不带去，简单的生活就是快乐的生活。 7.“我羡慕你，但我还是做我自我!”——成熟的人生态度。 8.必须要有你所向往的生活，那将会是你最终得到的生活。 9.沉默不是冷漠，只是不想再让那些无关痛痒的人看到真实的自我。热闹的日子看不清未来，一个人也能独自盛开。 10.沉默不是冷漠，只是不想再让那些无关痛痒的人看到真实的 自我。热闹的日子看不清未来，一个人也能独自盛开。 11.没有一种不透过蔑视忍受和奋斗就能够征服的命运。
能量（能量的转移和转化） 【复习要点】： 要点（40）：了解能量及其存在的不同形式，描述各种能量和生产生活的联系； 例题1：关于信息和能源，下列说法正确的是（） A．电风扇工作时，电能主要转化为内能 B．目前的核电站是利用核裂变释放的核能工作的 C．煤、石油、风能、天然气等都是不可再生能源 D．能量在转移、转化过程中总是守恒的，我们无需节约能源 要点（41）：通过实验，认识能量可以从一个物体转移到另一个物体，不同形式的能量可以互相转化； 例题2：随着智能手机的普及，人们的聊天方式也不断推陈出新，由于智能手机的待机时间很短，因此需要经常充电，当给电池充电时是将能转化成能．当手机正常使用时是将能转化成。将微风扇通电时它可以转动，这是将能转化成能，如果转动微风扇的风叶，还可以使与风扇插头相连的二极管发光，这是将 能转化成能。 要点（42）：结合实例，认识功的概念。知道做功的过程就是能量转化或转 移的过程； 例题3：如图，在空气压缩引火仪玻璃筒的底部放一小撮干燥的棉絮，用力 将活塞迅速向下压，棉絮燃烧起来。此实验得到的结论是：对（选 填“棉絮”或“筒内气体”）做功，它的内能会增加，其能量转化情况与 单缸四冲程汽油机的冲程相同，若汽油机的转速是2400r/min，则此汽油机每秒对外做功次。
要点（43）：知道动能、势能和机械能。通过实验，了解动能和势能的相互转化。举例说明机械能和其它形式能量的相互转化。 例题4：如图所示是演示点火爆炸的实验装置．按动电火花发生器的按钮，点燃盒内酒精，盒盖被打出去．在汽油机工作的四个冲程中，与此能量转化相同的冲程示意图是（） 【反馈练习】： 1．以下说法正确的是（） A．太阳能和核能都属于可再生能源 B．发光二极管主要使用的材料是超导体 C．热量不能自发地从低温物体传递给高温物体，说明能量转移具有方向性， D．飞 机的 机翼 做成 上面 凸起，下面平直．是因为流过机翼上方的空气流速大，压强大。 2．周末小明骑自行车去傅家边游玩．自行车下坡的过程中，为了减小车速，他捏紧车闸，这是通过的方法增大摩擦，此时刹车皮会发热，这是通过
正能量的励志句子100条 1.踩着垃圾到达的高度和踩着金子到达的高度是一样的。 2.每天告诉自己一次：我真的很不错。 3.人生最大的挑战没过于战胜自己！ 4.愚痴的人，一直想要别人了解他。有智慧的人，却努力的了解自己。 5.生命的道路上永远没有捷径可言，只有脚踏实地走下去。 6.只要还有明天，今天就永远是起跑线。 7.火把倒下，火焰依然向上。 8.认真可以把事情做对，而用心却可以做到完美。 9.宁可自己去原谅别人，莫等别人来原谅自己。 10.如果我们一直告诫自己要开心过每一天，就是说我们并不开心。 11.天气影响身体，身体决定思想，思想左右心情。 12.不论你在什么时候结束，重要的是结束之后就不要悔恨。 13.你把思考交给了电视，把联系交给了手机，把双腿交给了汽车，把健康交给了药丸。 14.不是某人使你烦恼，而是你拿某人的言行来烦恼自己。 15.人生要用简单的心境，对待复杂的人生，最无情的不是人，是时间；最珍贵的不是金钱，是情感；最可怕的不是失恋，是心身不
全；最舒适的不是酒店，是家里；最难听的不是脏话，是无言；最美好的不是未来，是今天。 16.在一切变好之前，我们总要经历一些不开心的日子，这段日子也许很长，也许只是一觉醒来。有时候，选择快乐，更需要勇气。 17.不要因为众生的愚疑，而带来了自己的烦恼。不要因为众生的无知，而痛苦了你自己。 18.如果你的生活已处于低谷，那就，大胆走，因为你怎样走都是在向上。 19.你可以哭但不能输，你可以难过但不可以落魄，你不努力怎么会知道自己可以赢得多少掌声?如果你能每天呐喊遍“我用不着为这一点小事而烦恼”，你会发现，你心里有一种不可思议的力量，试试看，很管用的。 20.我不敢休息，因为我没有存款。我不敢说累，因为我没有成就。我不敢偷懒，因为我还要生活。我能放弃选择，但是我不能选择放弃。坚强、拼搏是我唯一的选择。 21.生活不是用来妥协的，你退缩得越多，能让你喘息的空间就越有限。日子不是用来将就的，你表现得越卑微，一些幸福的东西就会离你越远。 22.过去的事，就让它过去吧，我们错过了昨日的日落，再也不能错过今日的日出，保持平衡的心态，以最美好的心情来对待每一天，每一天都会充满阳光，洋溢着希望。 23.一粒尘埃，在空气中凝结，最后生成磅礴的风雨；一粒沙石，
滨州市邹平县初中物理九年级全册14.3能量的转化和守恒练习题 姓名:________ 班级:________ 成绩:________ 一、练习题 (共12题；共25分) 1. （2分）某品牌手机充电宝，上面标有电压为5V，容量为12000mA?h，它充满电后，可以储存的电能是________J，在充电过程中，将电能转化为________能储存． 2. （2分）大量事实证明“永动机”是不可能存在的，因为它违背了________定律。热机的效率总是会________1．（填“大于”“小于”或“等于”） 3. （2分）木材燃烧是将化学能转化为________能，这一过程能量的总量将________（填变大、变小或不变）． 4. （3分） 2017年1月5日19时45分，西昌卫星发射中心用长征三号运载火箭，成功发射两颗北斗三号全球组网卫星。预计到22018年底，将有18颗北斗卫星发射升空，服务区覆盖“一带一路”沿线国家及周边国家，长征三号乙运载火箭起飞过程中燃料燃烧释放的内能将转化为火箭的________能，加速上升过程中受到________（选填“平衡力”或“非平衡力”）作用，北斗卫星与地面之间通过________传递信息。 5. （2分）(2020·绵阳模拟) 如图甲所示，小明在吹气球时，被吹大了的气球没能用手握住，呼啸着飞了出去，若他及时捡拾起气球，将会感觉到它喷气的嘴部温度和原来相比________（选填“变高”、“变低”或“没有变化”），发生的能量转化与汽油机的________冲程的能量转化是一致的。 6. （2分）关于热机中的能量转化关系，下列说法中正确的是（） A . 热机是将机械能转化为内能的机器 B . 热机是将内能转化为机械能的机器 C . 热机是将燃料的化学能转化为机械能的机器 D . 热机是利用化学能来做功，它是将化学能转化为内能 7. （2分） (2017九上·广州月考) 如图所示，在一个配有活塞的厚壁玻璃筒里放一小团硒化棉布，用力把活塞迅速下压，棉花就会立即燃烧．根据该实验现象，下列结论正确的是（）
关于拼搏的人生的正能量励志句子合集 大家要始终相信一句话：只要更好，不求最好!奋斗是成功之父! 1.人生有几件绝对不能失去的东西：自制的力量，冷静的头脑，希望和信心。 2.买得起自己喜欢的东西，去得了自己想去的地方，不会因为身边人的来或走损失生活的质量，反而会因为花自己的钱，来得更有底气一些，这就是应该更努力的原因。 3.最珍贵的不是你现在有多好，而是经过努力，每一天的自己都比之前更好。 4.你是老师的百分之一，是父母的百分之五十，但却是你自己的百分之百，所以要非常非常努力，去追求自己想要的一切。 5.不要去拒绝忙碌，因为它是一种充实;不要去抱怨挫折，因为它是一种坚强;不要去拒绝微笑，因为爱笑的女孩最美。你的优秀，不需要任何人来证明。 6.人有两条路要走，一条是必须走的，一条是想走的，你必须把必须走的路走漂亮，才可以走想走的路。 7.愿你沉稳又执着，对热爱的事情都全力以赴，又满载而归。 8.一件事如果想做，就早点下定决心。拖一天就纠结一天，早一天就多赚一天。 9.自己喜欢的日子，就是最美的日子;适合自己的生活，是最好的活法。
10.安全感不是别人给的，它取决于你有多爱自己，吃饱穿暖，手机有电，钱包永远不扁。 11.成功的人懂得熬，失败的人懂得逃，卓越的人懂得迎风前行并思考!其实放弃和坚持就在一瞬间，扛住了，世界就是你的。 12.做人要抬头有勇气，面对现实。低头有底气，面对自己。做事要有骨气，据理力争。做人要有志气，铮铮铁骨。凡事要争气。 13.在哪里跌倒，就在哪里站起来，所有不能打败你的，都会促成你的成长。 14.不要用自己的时间去见证别人的成功，愿你走过的所有弯路，最后都成为美丽彩虹! 15.没有谁的幸运，凭空而来。只有当你足够努力，你才会足够幸运，这世界不会辜负每一份努力和坚持。 16.有能力的人影响别人，没能力的人受人影响;不是某人使自己烦恼不安，而是自己拿某人的言行来烦恼自己;树一个目标，一步步前行，做好自己就好。 17.雄鹰，不需鼓掌，也在飞翔;小草，没人心疼，也在成长;野花，没人欣赏，也在芬芳;做事不需人人都理解，只需尽心尽力;做人不需人人都喜欢，只需坦坦荡荡。 18.努力到无能为力，拼搏到感动自己;吃过的苦，受过的累，会照亮未来的路;没有年少轻狂，只有胜者为王。 19.真正成功的人生，不在于成就的大小，而在于你是否努力地去实现自我，喊出自己的声音，走出属于自己的道路。 20.选一个方向，定一个时间;剩下的只管努力与坚持，时间
正能量激励人奋斗上进的好句子也许你想成为太阳，可你却只是一颗星辰;也许你想成为大树，可你却是一棵小草。于是，你有些自卑。其实，你和别人一样，也是一片风景：做不了太阳，就做星辰，在自己的星座发光发热;做不了大树，就做小草，以自己的绿色装点希望…… 行走红尘，别被欲望左右迷失了方向，别被物质打败做了生活的奴隶，给心灵腾出一方空间，让那些够得着的幸福安全抵达，攥在自己手里的，才是实实在在的幸福。 如果寒暄只是打个招呼就了事的话，那与猴子的呼叫声有什么不一样呢?事实上，正确的寒暄务必在短短一句话中明显地表露出你对他的关怀。 人活着，要有所追求，有所梦想，要生活得开心，快乐，这才是理想的人生。上天给我们机会，让我们来到世间走一遭，我们要珍惜，因为生命是如此的短暂，如果我们不知道珍惜，它将很快的逝去，到头来我们将一事无成。 要成功，就要时时怀着得意淡然失意坦然的乐观态度，笑对自己的挫折和苦难，去做，去努力，去争取成功!
人生是坎坷的，人生是崎岖的。我坚信：在人生中只有曲线前进的快乐，没有直线上升的成功。只有珍惜今天，才会有美好的明天;只有把握住今天，才会有更辉煌的明天!人生啊，朋友啊!还等什么?奋斗吧! 认定了的路，再痛也不要皱一下眉头，你要知道，再怎么难走都是你自己选的，你没有资格喊疼。到最后，你总会明白，谁是虚心假意，谁是真心实意，谁为了你不顾一切。不去期望，失去了不会伤心，得到了便是惊喜。对于过去，不可忘记，但要放下。因为有明天，今天永远只是起跑线。 敏感之人，遭遇一点风声也会千疮百孔。命运给每个人同等的安排，而选择如何经营自己的生活，酿造自己的情感，则在于自己的心性。人生应该活得舒心。人生，就是不断的面对，人生很残酷，错过的，不要奢望还会重来，放下了，才知道它的沉重，今天不做的事，往后可能永远没有机会。 恐惧自我受苦的人，已经正因自我的恐惧在受苦。 夫妇一条心，泥土变黄金。 用心的人在每一次忧患中都看到一个机会，而消极的人则在每个机会都看到某种忧患。
激励励志正能量句子50个 导读：1、哪有什么错过的人，会离开的都是路人。愿你脚踏实地，也愿你仰望星空，往事不回头，未来不将就！ 2、小黄人没有肩膀照样穿背带裤，没耳朵照样戴眼镜啊，别老埋怨你的世界缺点什么。 3、环境永远不会十全十美，消极的人受环境控制，积极的人却控制环境。 4、我不怕别人在背后捅我一刀，我怕回头后看到背后捅我的人，是我用心对待的人；我不怕把心里话告诉最好的朋友，我怕回过头他把它当成笑话告诉别人。 5、走不下去到时候停下来想想，总会找到坚持下去的理由。 6、这世界上最强大的人，就是那些能一个人孤单生活的人。 7、人与人之间的距离，要保持好，太近了会扎人，太远了会伤人。 8、别总是抱怨生活不够幸运，是你欠了生活一份努力，每一个你讨厌的现在，都有一个不够努力的曾经，未来美不美，取决于你现在拼不拼。 9、高一步立身，退一步处世。 10、人生没有如果，只有后果和结果。少问别人为什么，多问自己凭什么。现在不玩命，将来命玩你，现在不努力，未来不给力。现在不努力，将来拿什么向曾经抛弃你的人证明它有多瞎！
11、不管失败多少次，都要面对生活，充满希望。竹根即使被埋在地下无人得见，也决然不会停止探索而力争冒出新笋。希望，只有和勤奋作伴，才能如虎添翼。 12、世上没有白费的努力，也没有碰巧的成功，一切无心插柳，其实都是水到渠成。人生没有白走的路，也没有白吃的苦，跨出去的每一步，都是未来的基石与铺垫。 13、其实，没有过不去的事情，只有过不去的心情。很多事情，我们之所以过不去，是因为我们心里放不下。比如被欺骗了，报复放不下，被讽刺了，怨恨放不下，被批评了，面子放不下。 14、做个内心向阳的人。不忧伤，不心急。坚强、向上，靠近阳光。 15、成功不是将来才有的，而是从决定去做的那一刻起，持续累积而成。 16、梦想不会让一个人瞬间伟大，而是让生活拥有色彩和希望。只要你愿意努力，只要你相信，总有一天你会同样熠熠发光。 17、每个人的背后都会有心酸，都会有无法言说的艰难。每个人都会有自己的泪要擦，都会有自己的路要走。 18、人生的路漫长而多彩，在阳光中我学会欢笑，在阴云中我学会坚强;在狂风中我抓紧希望，当我站在终点回望，我走出了一条属于我的人生之路。 19、坚持不一定成功，但不坚持一定不会成功，并不是井里没水，