Impact of community public health care on treatment effect,health cognition,and self-management in patients with type 2 diabetes

BACKGROUND At present,China has become the country with the largest number of individuals with diabetes mellitus(DM)in the world,with a total of approximately 140 million patients,the majority of whom have type 2 DM(T2DM).Based on conven-tional nursing methods,community home care has important clinical significance in controlling blood sugar and disease progression.AIM To explore the impact of community public health nursing on treatment effect,health cognition,and self-management in patients with T2DM.METHODS One hundred patients with T2DM were selected as the research subjects.The patients were divided into either a conventional nursing group or community nursing(CN)group using the random number table method.The conventional nursing group(50 cases)received routine care,while the CN group(50 cases)received community public health care in addition to routine care as that for the conventional nursing group.The rate of excellent and good blood glucose control,fasting blood glucose before and after care,2-h postprandial blood glucose,health cognition,and self-management ability,and patient satisfaction were compared between the two groups.RESULTS The CN group had a higher rate of excellent blood sugar control than the conventional nursing group(88%vs 70%,P<0.05).Before care,there was no significant difference in fasting blood glucose or 2-h postprandial blood glucose between the two groups of patients(P>0.05).After nursing,fasting blood glucose and 2-h postprandial blood glucose were reduced to varying degrees in both groups,and both blood glucose levels in the CN group were lower than those of the conventional nursing group(P<0.05).Compared with the scores before care,the cognitive level score for diabetes and self-management ability score improved after care in both groups.The cognitive level and self-management ability of patients in the CN group were higher than those of the conventional nursing group(P<0.05).The overall satisfaction of the CN group was better than that of the conventional nursing group(98%vs 86%,P<0.05).CONCLUSION Community public health care based on conventional care of T2DM can achieve better blood sugar control,and improve patients’health cognitive level and self-management ability.

Gamma-glutamyl transferase 5 overexpression in cerebrovascular endothelial cells improves brain pathology,cognition,and behavior in APP/PS1 mice

In patients with Alzheimer’s disease,gamma-glutamyl transferase 5(GGT5)expression has been observed to be downregulated in cerebrovascular endothelial cells.However,the functional role of GGT5 in the development of Alzheimer’s disease remains unclear.This study aimed to explore the effect of GGT5 on cognitive function and brain pathology in an APP/PS1 mouse model of Alzheimer’s disease,as well as the underlying mechanism.We observed a significant reduction in GGT5 expression in two in vitro models of Alzheimer’s disease(Aβ_(1-42)-treated hCMEC/D3 and bEnd.3 cells),as well as in the APP/PS1 mouse model.Additionally,injection of APP/PS1 mice with an adeno-associated virus encoding GGT5 enhanced hippocampal synaptic plasticity and mitigated cognitive deficits.Interestingly,increasing GGT5 expression in cerebrovascular endothelial cells reduced levels of both soluble and insoluble amyloid-βin the brains of APP/PS1 mice.This effect may be attributable to inhibition of the expression ofβ-site APP cleaving enzyme 1,which is mediated by nuclear factor-kappa B.Our findings demonstrate that GGT5 expression in cerebrovascular endothelial cells is inversely associated with Alzheimer’s disease pathogenesis,and that GGT5 upregulation mitigates cognitive deficits in APP/PS1 mice.These findings suggest that GGT5 expression in cerebrovascular endothelial cells is a potential therapeutic target and biomarker for Alzheimer’s disease.

Impact of propofol and sevoflurane anesthesia on cognition and emotion in gastric cancer patients undergoing radical resection

BACKGROUND Propofol and sevoflurane are commonly used anesthetic agents for maintenance anesthesia during radical resection of gastric cancer.However,there is a debate concerning their differential effects on cognitive function,anxiety,and depression in patients undergoing this procedure.AIM To compare the effects of propofol and sevoflurane anesthesia on postoperative cognitive function,anxiety,depression,and organ function in patients undergoing radical resection of gastric cancer.METHODS A total of 80 patients were involved in this research.The subjects were divided into two groups:Propofol group and sevoflurane group.The evaluation scale for cognitive function was the Loewenstein occupational therapy cognitive assessment(LOTCA),and anxiety and depression were assessed with the aid of the self-rating anxiety scale(SAS)and self-rating depression scale(SDS).Hemodynamic indicators,oxidative stress levels,and pulmonary function were also measured.RESULTS The LOTCA score at 1 d after surgery was significantly lower in the propofol group than in the sevoflurane group.Additionally,the SAS and SDS scores of the sevoflurane group were significantly lower than those of the propofol group.The sevoflurane group showed greater stability in heart rate as well as the mean arterial pressure compared to the propofol group.Moreover,the sevoflurane group displayed better pulmonary function and less lung injury than the propofol group.CONCLUSION Both propofol and sevoflurane could be utilized as maintenance anesthesia during radical resection of gastric cancer.Propofol anesthesia has a minimal effect on patients'pulmonary function,consequently enhancing their postoperative recovery.Sevoflurane anesthesia causes less impairment on patients'cognitive function and mitigates negative emotions,leading to an improved postoperative mental state.Therefore,the selection of anesthetic agents should be based on the individual patient's specific circumstances.

Treadmill exercise in combination with acousto-optic and olfactory stimulation improves cognitive function in APP/PS1 mice through the brain-derived neurotrophic factor-and Cygb-associated signaling pathways

A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigating disease symptoms and progression.Nonetheless,nonpharmacological interventions aimed at inducing adult neurogenesis are currently limited.Although individual non-pharmacological interventions,such as aerobic exercise,acousto-optic stimulation,and olfactory stimulation,have shown limited capacity to improve neurogenesis and cognitive function in patients with Alzheimer's disease,the therapeutic effect of a strategy that combines these interventions has not been fully explored.In this study,we observed an age-dependent decrease in adult neurogenesis and a concurrent increase in amyloid-beta accumulation in the hippocampus of amyloid precursor protein/presenilin 1 mice aged 2-8 months.Amyloid deposition became evident at 4 months,while neurogenesis declined by 6 months,further deteriorating as the disease progressed.However,following a 4-week multifactor stimulation protocol,which encompassed treadmill running(46 min/d,10 m/min,6 days per week),40 Hz acousto-optic stimulation(1 hour/day,6 days/week),and olfactory stimulation(1 hour/day,6 days/week),we found a significant increase in the number of newborn cells(5'-bromo-2'-deoxyuridine-positive cells),immature neurons(doublecortin-positive cells),newborn immature neurons(5'-bromo-2'-deoxyuridine-positive/doublecortin-positive cells),and newborn astrocytes(5'-bromo-2'-deoxyuridine-positive/glial fibrillary acidic protein-positive cells).Additionally,the amyloid-beta load in the hippocampus decreased.These findings suggest that multifactor stimulation can enhance adult hippocampal neurogenesis and mitigate amyloid-beta neuropathology in amyloid precursor protein/presenilin 1 mice.Furthermore,cognitive abilities were improved,and depressive symptoms were alleviated in amyloid precursor protein/presenilin 1 mice following multifactor stimulation,as evidenced by Morris water maze,novel object recognition,forced swimming test,and tail suspension test results.Notably,the efficacy of multifactor stimulation in consolidating immature neurons persisted for at least 2weeks after treatment cessation.At the molecular level,multifactor stimulation upregulated the expression of neuron-related proteins(NeuN,doublecortin,postsynaptic density protein-95,and synaptophysin),anti-apoptosis-related proteins(Bcl-2 and PARP),and an autophagyassociated protein(LC3B),while decreasing the expression of apoptosis-related proteins(BAX and caspase-9),in the hippocampus of amyloid precursor protein/presenilin 1 mice.These observations might be attributable to both the brain-derived neurotrophic factor-mediated signaling pathway and antioxidant pathways.Furthermore,serum metabolomics analysis indicated that multifactor stimulation regulated differentially expressed metabolites associated with cell apoptosis,oxidative damage,and cognition.Collectively,these findings suggest that multifactor stimulation is a novel non-invasive approach for the prevention and treatment of Alzheimer's disease.

Promotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents

Memory deficit,which is often associated with aging and many psychiatric,neurological,and neurodegenerative diseases,has been a challenging issue for treatment.Up till now,all potential drug candidates have failed to produce satisfa ctory effects.Therefore,in the search for a solution,we found that a treatment with the gene corresponding to the RGS14414protein in visual area V2,a brain area connected with brain circuits of the ventral stream and the medial temporal lobe,which is crucial for object recognition memory(ORM),can induce enhancement of ORM.In this study,we demonstrated that the same treatment with RGS14414in visual area V2,which is relatively unaffected in neurodegenerative diseases such as Alzheimer s disease,produced longlasting enhancement of ORM in young animals and prevent ORM deficits in rodent models of aging and Alzheimer’s disease.Furthermore,we found that the prevention of memory deficits was mediated through the upregulation of neuronal arbo rization and spine density,as well as an increase in brain-derived neurotrophic factor(BDNF).A knockdown of BDNF gene in RGS14414-treated aging rats and Alzheimer s disease model mice caused complete loss in the upregulation of neuronal structural plasticity and in the prevention of ORM deficits.These findings suggest that BDNF-mediated neuronal structural plasticity in area V2 is crucial in the prevention of memory deficits in RGS14414-treated rodent models of aging and Alzheimer’s disease.Therefore,our findings of RGS14414gene-mediated activation of neuronal circuits in visual area V2 have therapeutic relevance in the treatment of memory deficits.

Design of a Landscape Device for Children from the Perspective of Embodied Cognition in the New Era

In recent years,embodied cognition has ushered in a new research upsurge in the academic field,and has become a hot topic in the field of cognitive psychology.In this paper,from the perspective of embodied cognition,the interaction ways of a landscape device for children were discussed to achieve a more real and harmonious interaction between children and scenes.The research data of embodied cognition used by children was analyzed,and the drawbacks and breakthrough points of current landscape devices for children were discussed.The core characteristics of children’s growth period were extracted to establish children’s interaction model and summarize the interactive design methods of landscape devices for children.Embodied cognition has become the most intuitive way for children to know and understand the environment,and plays a pivotal role in children’s growth.Based on embodied cognition principle and interactive behavior mode,the interactive design of a landscape device for children was studied,and three interactive design modes,including simple and convenient interaction mode,multi-sensory interaction mode and game natural interaction mode were summarized.On the basis of this research,relevant design practice and research were carried out to bring a new vision to the design of children’s landscape.

Impaired Cognition and Stroke Rehabilitation Outcomes: Are They Related?

Background: Stroke survivors who exhibit impaired cognition at admission to inpatient rehabilitation may experience participation challenges and poorer functional outcomes than those without impaired cognition. Differences in functional outcomes between stroke survivors with and without impaired cognition may be attributed to age, level of cognitive impairment, and severity of stroke. Materials and Methods: A retrospective secondary data analysis was conducted using health-related administrative data acquired from a Southwestern Ontario hospital’s stroke rehabilitation database. The aim was to explore potential linkages between post-stroke impaired cognition and functional gains, rehabilitation stays, and living settings after discharge from rehabilitation. Results: An aggregate sample of 393 males and 314 females subclassified as experiencing mild, moderate, and severe stroke was analyzed. At inpatient rehabilitation admission, 21.5% (n = 152) of these patients had no impaired cognition, 33.7% (n = 238) had mild impaired cognition, 22.2% (n = 157) had moderate impaired cognition, and 22.6% (n = 160) had severe impaired cognition. Cognitively impaired stroke patients were significantly (p 0.001) older, had (mostly) moderate to severe stroke with significantly (p = 0.012) more moderate cognitive impairment, had significantly (p 0.001) longer rehabilitation stays, and a high propensity for being discharged to longer-term care facilities compared to non-cognitively impaired patients. Conclusion: Presence of significant dissimilarity in rehabilitation stays and post-discharge destinations among stroke survivors with and without cognitive impairment is attributed to the age of the patient, level of cognitive impairment, and rigorous rehabilitation interventions.

Exploration and Practice of Life Education Curriculum Based on Embodied Cognition Theory

In recent years,the suicide rate of adolescents has been increasing year by year,and life and health problems have become the most important in education.It is urgent to promote the construction of the curriculum of life education effectively.In view of the“vacuity”and“fragmented”state of traditional life education,this paper combs the teaching objectives,teaching contents,teaching methods,and teaching evaluation of life education from the perspective of embodied cognition theory,to explore the construction of positive experience of life education curriculum.

The compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one alleviates neuroinflammation and cognitive impairment in a mouse model of Alzheimer's disease

Previous studies have shown that the compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one(D30),a pyromeconic acid derivative,possesses antioxidant and anti-inflammatory properties,inhibits amyloid-β aggregation,and alleviates scopolamine-induced cognitive impairment,similar to the phase Ⅲ clinical drug resveratrol.In this study,we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced neuropathology.Our results showed that D30 alleviated fibrillar amyloid-β-induced cognitive impairment,promoted fibrillar amyloid-β clearance from the hippocampus and cortex,suppressed oxidative stress,and inhibited activation of microglia and astrocytes.D30 also reversed the fibrillar amyloid-β-induced loss of dendritic spines and synaptic protein expression.Notably,we demonstrated that exogenous fibrillar amyloid-βintroduced by intracerebroventricular injection greatly increased galectin-3 expression levels in the brain,and this increase was blocked by D30.Considering the role of D30 in clearing amyloid-β,inhibiting neuroinflammation,protecting synapses,and improving cognition,this study highlights the potential of galectin-3 as a promising treatment target for patients with Alzheimer's disease.

Small heat shock protein B8:from cell functions to its involvement in diseases and potential therapeutic applications

Heat shock protein family B(small)member 8(HSPB8)is a 22 kDa ubiquitously expressed protein belonging to the family of small heat shock proteins.HSPB8 is involved in various cellular mechanisms mainly related to proteotoxic stress response and in other processes such as inflammation,cell division,and migration.HSPB8 binds misfolded clients to prevent their aggregation by assisting protein refolding or degradation through chaperone-assisted selective autophagy.In line with this function,the pro-degradative activity of HSPB8 has been found protective in several neurodegenerative and neuromuscular diseases characterized by protein misfolding and aggregation.In cancer,HSPB8 has a dual role being capable of exerting either a pro-or an anti-tumoral activity depending on the pathways and factors expressed by the model of cancer under investigation.Moreover,HSPB8 exerts a protective function in different diseases by modulating the inflammatory response,which characterizes not only neurodegenerative diseases,but also other chronic or acute conditions affecting the nervous system,such as multiple sclerosis and intracerebellar hemorrhage.Of note,HSPB8 modulation may represent a therapeutic approach in other neurological conditions that develop as a secondary consequence of other diseases.This is the case of cognitive impairment related to diabetes mellitus,in which HSPB8 exerts a protective activity by assuring mitochondrial homeostasis.This review aims to summarize the diverse and multiple functions of HSPB8 in different pathological conditions,focusing on the beneficial effects of its modulation.Drug-based and alternative therapeutic approaches targeting HSPB8 and its regulated pathways will be discussed,emphasizing how new strategies for cell and tissue-specific delivery represent an avenue to advance in disease treatments.

Decoding molecular mechanisms:brain aging and Alzheimer's disease

The complex morphological,anatomical,physiological,and chemical mechanisms within the aging brain have been the hot topic of research for centuries.The aging process alters the brain structure that affects functions and cognitions,but the worsening of such processes contributes to the pathogenesis of neurodegenerative disorders,such as Alzheimer's disease.Beyond these observable,mild morphological shifts,significant functional modifications in neurotransmission and neuronal activity critically influence the aging brain.Understanding these changes is important for maintaining cognitive health,especially given the increasing prevalence of age-related conditions that affect cognition.This review aims to explore the age-induced changes in brain plasticity and molecular processes,differentiating normal aging from the pathogenesis of Alzheimer's disease,thereby providing insights into predicting the risk of dementia,particularly Alzheimer's disease.

Acute and chronic excitotoxicity in ischemic stroke and late-onset Alzheimer's disease

Stroke and Alzheimer's disease are common neurological disorders and often occur in the same individuals.The comorbidity of the two neurological disorders represents a grave health threat to older populations.This review presents a brief background of the development of novel concepts and their clinical potentials.The activity of glutamatergic N-methyl-D-aspartate receptors and N-methyl-D-aspartate receptor-mediated Ca^(2+)influx is critical for neuronal function.An ischemic insult induces prompt and excessive glutamate release and drastic increases of intracellular Ca^(2+)mainly via N-methyl-D-aspartate receptors,particularly of those at the extrasynaptic site.This Ca^(2+)-evoked neuronal cell death in the ischemic core is dominated by necrosis within a few hours and days known as acute excitotoxicity.Furthermore,mild but sustained Ca^(2+)increases under neurodegenerative conditions such as in the distant penumbra of the ischemic brain and early stages of Alzheimer's disease are not immediately toxic,but gradually set off deteriorating Ca^(2+)-dependent signals and neuronal cell loss mostly because of activation of programmed cell death pathways.Based on the Ca^(2+)hypothesis of Alzheimer's disease and recent advances,this Ca^(2+)-activated“silent”degenerative excitotoxicity evolves from years to decades and is recognized as a unique slow and chronic neuropathogenesis.The N-methyl-D-aspartate receptor subunit GluN3A,primarily at the extrasynaptic site,serves as a gatekeeper for the N-methyl-D-aspartate receptor activity and is neuroprotective against both acute and chronic excitotoxicity.Ischemic stroke and Alzheimer's disease,therefore,share an N-methyl-D-aspartate receptor-and Ca^(2+)-mediated mechanism,although with much different time courses.It is thus proposed that early interventions to control Ca^(2+)homeostasis at the preclinical stage are pivotal for individuals who are susceptible to sporadic late-onset Alzheimer's disease and Alzheimer's disease-related dementia.This early treatment simultaneously serves as a preconditioning therapy against ischemic stroke that often attacks the same individuals during abnormal aging.

Enhanced autophagic clearance of amyloid-βvia histone deacetylase 6-mediated V-ATPase assembly and lysosomal acidification protects against Alzheimer's disease in vitro and in vivo

Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.

Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice

Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.

Brain-derived neurotrophic factor alterations and cognitive decline in schizophrenia:Implications for early intervention

This manuscript explores the recent study by Cui et al which assessed the interplay between inflammatory cytokines and brain-derived neurotrophic factor(BDNF)levels in first-episode schizophrenia patients.The study revealed that higher levels of interleukin-6 and tumor necrosis factor-αcorrelated with reduced BDNF levels and poorer cognitive performance.Schizophrenia is a severe psy-chiatric disorder impacting approximately 1%of the global population,charac-terized by positive symptoms(hallucinations and delusions),negative symptoms(diminished motivation and cognitive impairments)and disorganized thoughts and behaviors.Emerging research highlights the role of BDNF as a potential biomarker for early diagnosis and therapeutic targeting.The findings from Cui et al’s study suggest that targeting neuroinflammation and enhancing BDNF levels may improve cognitive outcomes.Effective treatment approaches involve a com-bination of pharmacological and non-pharmacological interventions tailored to individual patient needs.Hence,monitoring cognitive and neuroinflammatory markers is essential for improving patient outcomes and quality of life.Conse-quently,this manuscript highlights the need for an integrated approach to schizo-phrenia management,considering both clinical symptoms and underlying neuro-biological changes.

How Product Importance Perception, Need for Cognition and Enduring Involvement Influence Investors＇ Knowledge of Investment Products？

The lack of proper knowledge about investment products can have a large negative influence on the financial well being of investors. Inspire of that, there is a dearth of studies conducted, specifically to investigate the factors influencing the knowledge of investors about investment products. This paper propose a model and investigates the direct and indirect （mediated through investor＇s enduring involvement with product） influence of investor＇s product importance perception （PIP） and need for cognition （NFC） on investor＇s knowledge of investment products. The hypothesized relationship is empirically validated in the context of mutual fund schemes （MFs）. Survey conducted on the sample of 268 MF investors suggests that there is an insignificant direct influence of investor＇s PIP and NFC on investor＇s knowledge of investment product （KIP）. However, when mediated through enduring involvement with product （EIP）, the influence was found to be significant. The results suggest that EIP perfectly mediates the influence of PIP and NFC on investor＇s KIP. The relevance of the results to the policy makers is also discussed.

On English teaching from psychology and cognition

In English teaching, it is necessary to pay attention to students＇ psychology and cognition in order to make them harmonious and effective. Therefore, English teacher would change their teaching opinions, realizing teaching object, guiding student＇s minds and ideas to study by some measures, such as accordant teaching and study, making students as a base in study, and students＇ self-study. In other words, making student study actively rather than passively is much better for their English abilities.

象似性研究新进展——Language and Cognition杂志2019—2020专刊述评

基于剑桥大学出版社出版的认知语言学权威期刊Language and Cognition所刊发的10篇象似性论文,本文深度描写、分析并展望象似性研究的国际前沿现状,并对该辑专刊进行述评。结果发现,近年来国外象似性研究主要集中于象似性理论的跨学科研究、手语语言学及其应用与实践等领域。上述发现不但有助于揭示语言与认知的关系,而且对于国内学者把握国际象似性研究的最新进展具有一定的参考意义。

Situated Cognition Theory and English Teaching under the Background of New Curriculum

Contextual Cognitive Theory （CCT） is the latest teaching and learning theory in west countries, which reveals the nature of knowledge in a new perspective as well as the conditions of meaningful learning. The concept based on CCT corresponds to the principles proposed by the new curriculum standard for English. Therefore, it has great implications for the reform of English teaching in the classroom. In this paper, the author gives a brief account of the main points of CCT, and then, she discusses its pedagogical implications for the construction of new teaching strategies in the classroom through designing and analyzing teaching cases.

The Impact of the Cognition of Landscape Experience on Tourist Environmental Conservation Behaviors

This article explores the relationship between the tourist's cognition of the landscape experience and the environmental conservation efforts at three distinct tourist sites in mountains of southwestern China. A total of 1500 on-site questionnaire surveys were distributed and 1142 valid questionnaires were used for statistical analysis. Results from multi-group path analysis showed that both cognition of the cultural landscape experience and cognition of the natural landscape experience had positive impacts on environmental conservation behaviors and behavior intentions of tourists. Results from comparative analysis among the three tourist sites indicated that cognition of the cultural landscape experience had a stronger power to predict senior environmental conservation behaviors and behavior intentions than cognition of the natural landscape experience, whereas cognition of the natural landscape experience had more power to predict general environmental conservation behaviors and behavior intentions than cognition of the cultural landscape experience. Furthermore, our findings benefit environmental management and sustainabilityat tourist sites.