Development of a dynamic gas lock inhibited model for EUV-induced carbon deposition.

The optical surface of extreme ultraviolet (EUV) lithography machines is highly vulnerable to contamination by hydrocarbons, resulting in the formation of carbon deposits that significantly degrade the quality and efficiency of lithography. The dynamic gas lock (DGL) has been proven as an effective approach to alleviate carbon deposition. However, the majority of existing studies on carbon deposition neglect the influence of the DGL. This paper is dedicated to investigating the phenomena of hydrocarbon adsorption, desorption, and cleavage with considering the effects of the DGL. A comprehensive mathematical model of the carbon deposition process is established, and the impact of radiation intensity, temperature, and hydrocarbon types on the depositing rate is considered. The results suggest that the primary cause of carbon deposition is the direct cracking of hydrocarbons induced by photons with a wavelength range between 12.5 and 14.5 nm. Additionally, it has been observed that the carbon deposition rate decreases exponentially as clean gas flow increases when EUV radiation intensity exceeds 50 mW/mm2. Conversely, at low EUV radiation intensity, clean gas flow has little effect on the carbon deposition rate. An effective approach to mitigate carbon deposition is to elevate the temperature of the optical surface and employ light hydrocarbon materials in the EUV process.

Carboxypeptidase E Regulates Activity-Dependent TrkB Neuronal Surface Insertion and Hippocampal Memory.

Activity-dependent insertion of the tropomyosin-related kinase B (TrkB) receptor into the plasma membrane can explain, in part, the preferential effect of brain-derived neurotrophic factor (BDNF) on active neurons and synapses; however, the underlying molecular mechanisms remain obscure. Here, we report a novel function for carboxypeptidase E (CPE) in controlling chemical long-term potentiation stimuli-induced TrkB surface delivery in hippocampal neurons. Total internal reflection fluorescence assays and line plot assays showed that CPE facilitates TrkB transport from dendritic shafts to the plasma membrane. The Box2 domain in the juxtamembrane region of TrkB and the C terminus of CPE are critical for the activity-dependent plasma membrane insertion of TrkB. Moreover, the transactivator of transcription TAT-CPE452-466, which could block the association between CPE and TrkB, significantly inhibited neuronal activity-enhanced BDNF signaling and dendritic spine morphologic plasticity in cultured hippocampal neurons. Microinfusion of TAT-CPE452-466 into the dorsal hippocampus of male C57BL/6 mice inhibited the endogenous interaction between TrkB and CPE and diminished fear-conditioning-induced TrkB phosphorylation, which might lead to an impairment in hippocampal memory acquisition and consolidation but not retrieval. These results suggest that CPE modulates activity-induced TrkB surface insertion and hippocampal-dependent memory and sheds light on our understanding of the role of CPE in TrkB-dependent synaptic plasticity and memory modulation.SIGNIFICANCE STATEMENT It is well known that BDNF acts preferentially on active neurons; however, the underlying molecular mechanism is not fully understood. In this study, we found that the cytoplasmic tail of CPE could interact with TrkB and facilitate the neuronal activity-dependent movement of TrkB vesicles to the plasma membrane. Blocking the association between CPE and TrkB decreased fear-conditioning-induced TrkB phosphorylation and led to hippocampal memory deficits. These findings provide novel insights into the role of CPE in TrkB intracellular trafficking as well as in mediating BDNF/TrkB function in synaptic plasticity and hippocampal memory.

The relationship between post-traumatic stress and negative emotions in patients with breast cancer: the mediating role of emotion regulation.

Purpose:Negative emotions can adversely affect the treatment and recovery of breast cancer patients. Post-traumatic stress caused by cancer can increase the negative emotions of patients. This study assessed the relationship between post-traumatic stress and emotional regulation strategies, and the role of emotional regulation in the relationship between post-traumatic stress and negative emotions in breast cancer patients.Design:Cross-sectional questionnaire with sample of 214 Chinese women with breast cancerMethods:Participants completed the Impact of Event Scale-Revised, Hospital Anxiety and Depression Scale, and Emotion Regulation Questionnaire. Correlation and mediation analyses were conducted to assess associations among the scores of these scales.Findings:Patients with low post-traumatic stress chose cognitive reappraisal strategies, while those with high post-traumatic stress chose expressive suppression strategies. Cognitive reappraisal had a significant negative predictive effect on negative emotions, while expressive suppression had a significant positive predictive effect on patient's negative emotions.Conclusions:Cognitive reappraisal may reduce the impact of post-traumatic stress on negative emotions experienced by breast cancer patients. Implications for psychosocial providers or policy: Psychosocial workers in China should conduct cognitive reappraisal training for breast cancer patients with high negative emotions and severe post-traumatic stress. For Chinese breast cancer patients living in other regions, the local oncology social workers should take into account their cultural background and lack of expression, and encourage them to choose cognitive reappraisal strategies.

HMGB1 impairs endothelium-dependent relaxation in diabetes through TLR4/eNOS pathway.

Endothelium-dependent relaxation (EDR) is an initial key step leading to various vascular complications in patients with diabetes. However, the underlying mechanism of EDR impairment in diabetes is not fully understood. Present study defined the role of high-mobility group protein (HMGB1) in EDR related to diabetes. Serum level of HMGB1 was increased in diabetic patients and in db/db mice. Serum HMGB1 level was also positively correlated with HbA1c and negatively correlated with nitric oxide (NO) in diabetic patients. Results from wire myograph showed that recombinant HMGB1 (rHMGB1) was capable of impairing EDR of aortas from wild-type (WT) mice by an eNOS-dependent mechanism. Consistently, HMGB1 inhibitor glycyrrhizin acid (GA) decreased the serum level of HMGB1 and rescued EDR impairment partly in db/db mice. Furthermore, rHMGB1 mediated EDR impairment was abolished in aortas of TLR4-/- mice. In addition, high-glucose-induced HMGB1 upregulation and secretion in endothelial cells. In conclusion, HMGB1 contributes to the EDR impairment through TLR4/eNOS pathway in the setting of diabetes. GA as the HMGB1 inhibitor could attenuate EDR impairment in an animal model of diabetes.

Attentional bias of subliminal emotional faces in adolescents with obsessive-compulsive disorder.

Attentional bias to threatening information may play a vital role in the onset and maintenance of obsessive-compulsive disorder (OCD). This study aimed to explore whether adolescents with OCD exhibited attentional bias toward faces that express disgust or fear. Participants were 27 adolescents with a first-time primary diagnosis of OCD and 27 healthy controls. To assess OCD, depression, and anxiety symptoms, all participants completed the Yale-Brown Obsessive Compulsive Scale, the Hamilton Depression Scale, and the Hamilton Anxiety Scale, respectively, followed by the modified dot probe task. Repeated measures ANOVA revealed a main effect of validity type and a significant group × validity type interaction effect. The results of one sample t-tests showed that participants in the OCD group had an attentional bias toward both disgusted and fearful faces. Further analysis indicated that adolescents in the OCD group showed facilitated attention toward the fearful faces and difficulty disengaging from disgusted faces. Adolescents with OCD exhibited facilitated attention toward threat stimuli, and when they allocated attention to threat, they experienced difficulty disengaging from it. Treatment procedures to modify the attentional bias may be effective.

Multi-Sensor and Decision-Level Fusion-Based Structural Damage Detection Using a One-Dimensional Convolutional Neural Network.

This paper presents a novel approach to substantially improve the detection accuracy of structural damage via a one-dimensional convolutional neural network (1-D CNN) and a decision-level fusion strategy. As structural damage usually induces changes in the dynamic responses of a structure, a CNN can effectively extract structural damage information from the vibration signals and classify them into the corresponding damage categories. However, it is difficult to build a large-scale sensor system in practical engineering; the collected vibration signals are usually non-synchronous and contain incomplete structure information, resulting in some evident errors in the decision stage of the CNN. In this study, the acceleration signals of multiple acquisition points were obtained, and the signals of each acquisition point were used to train a 1-D CNN, and their performances were evaluated by using the corresponding testing samples. Subsequently, the prediction results of all CNNs were fused (decision-level fusion) to obtain the integrated detection results. This method was validated using both numerical and experimental models and compared with a control experiment (data-level fusion) in which all the acceleration signals were used to train a CNN. The results confirmed that: by fusing the prediction results of multiple CNN models, the detection accuracy was significantly improved; for the numerical and experimental models, the detection accuracy was 10% and 16-30%, respectively, higher than that of the control experiment. It was demonstrated that: training a CNN using the acceleration signals of each acquisition point and making its own decision (the CNN output) and then fusing these decisions could effectively improve the accuracy of damage detection of the CNN.

Psychometric properties of the Mandarin Chinese version of the KIDSCREEN-52 health-related quality of life questionnaire in adolescents: a cross-sectional study.

PURPOSE: To evaluate the psychometric properties of the Mandarin Chinese version of KIDSCREEN-52 health-related quality of life (HRQOL) questionnaire. METHODS: We conducted a cross-sectional study with two cohorts of school-based data in the urban areas of Weifang, China. 4385 and 841 representative adolescents aged 11-17 years have recruited into the baseline and test-retest group, respectively. Psychometric analyses included feasibility, item and dimension properties, reliability, construct validity, measurement invariance, convergent and discriminant validity, and known-group validity. RESULTS: The response rates of both baseline and test-retest surveys were more than 90%. Low missing values were found (0.02-1.92%) across ten dimensions. The measurement properties of items were satisfactory. Noteworthy ceiling effects were observed for ten dimensions (6.75-31.84%), while the observed floor effects were negligible (0.02-1.37%). Internal consistency was robust with Cronbach's alpha (0.819-0.959), while the test-retest reliability was acceptable with the ICCs (0.724-0.849). Confirmatory factor analysis confirmed the ten-dimensional structure and supported the configural and metric invariance across gender and age groups. The Pearson correlation coefficients between the KIDSCREEN-52 and the PedsQL™ 4.0 were stronger in comparable dimensions than those in less comparable dimensions, demonstrating the convergent and discriminant validity. In most dimensions, statistically significant and medium or large effect size differences were found across socioeconomic and mental health status, supporting the known-group validity. CONCLUSION: These findings demonstrate that the Mandarin Chinese version of KIDSCREEN-52 seems to work well in a Chinese context, and is a psychometrically valid and reliable HRQOL instrument.

Inflachromene inhibits intimal hyperplasia through the HMGB1/2- regulated TLR4-NF-κB pathway.

The contractile-syntheticphenotypicconversion of vascular smooth muscle cells (VSMCs) plays a key role in atherosclerosis, vascular restenosis, and hypertension. Our previous study explored the correlation between high mobility group box protein (HMGB) 1 and HMGB2 and neointimal hyperplasia after vascular injury. In the present study, we explore whether inflachromene (ICM), a novel inhibitor of the expression of both HMGB1 and HMGB2, modulates phenotypic changes in VSMCs and the mechanisms involved. Mice treated with ICM after carotid artery wire injury showed a decrease in excessive neointimal hyperplasia compared with that in the vehicle groups. In cultured VSMCs, pretreatment with ICM suppressed the angiotensin II (Ang II)-induced phenotypic conversion, proliferation, and migration. We discovered that ICM reduced the Ang II-induced upregulation of the expression of HMGB1 and HMGB2 and inhibited their shuttling between the nucleus and the cytosol. Mechanistically, Ang II-treated VSMCs exhibited higher levels of Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) phosphorylation, which were attenuated by ICM. In addition, the NF-κB inhibitor Bay-117082 abolished the recombinant HMGB1-mediated VSMC phenotypic conversion, proliferation, and migration. Furthermore, ICM ameliorated the Ang II-induced increases in NAD[P]H oxidase expression, thereby attenuating the Ang II-induced proliferation and migration. These results reveal that ICM pretreatment attenuates Ang II-induced VSMC dedifferentiation, proliferation, and migration may by regulating the TLR4-NF-kB pathway. Thus, ICM is a potential therapy and preventive treatment for vascular proliferative diseases.

A novel glycyrrhizin acid-coated stent reduces neointimal formation in a rabbit iliac artery model.

Introduction: Most drug-eluting stents (DESs) inhibit intimal hyperplasia but impair re-endothelialization. This study aimed to evaluate in vivo strut coverage and neointimal growth in a new glycyrrhizin acid (GA)-eluting stent. Methods: New Zealand White rabbits (n = 20) with atherosclerotic plaques were randomly divided into three groups based on implanted iliac artery stents: bare-metal stents (BMSs), rapamycin-eluting stents, and GA-eluting stents. After the in vivo intravascular ultrasound (IVUS) assessment at 28 days, the vessels were harvested for scanning electron microscopy (SEM) and histology. After 4 weeks of follow-up, the stent and external elastic lamina (EEL) areas were compared among the groups. Results: The rapamycin- or GA-eluting stents significantly reduced the neointimal area compared with BMSs, though GA-eluting stents had the lowest reduction. There were more uncovered struts for rapamycin-eluting stents than those for GA-eluting stents and bare-metal stents. The endothelial nitric oxide synthase (eNOS) expression in GA-eluting stents was much higher than that in BMSs and rapamycin-eluting stents, even though the endothelial coverage between struts was equivalent between BMSs and GA-eluting stents. Moreover, GA-eluting stents markedly promoted re-endothelialization and improved arterial healing compared to rapamycin-eluting stents in a rabbit atherosclerotic model. Conclusion: In conclusion, the novel GA-coated stent used in this study inhibited intimal hyperplasia and promoted re-endothelialization.

Changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease: proteomics in human left atrial appendage tissue.

Background: Correlations between posttranslational modifications and atrial fibrillation (AF) have been demonstrated in recent studies. However, it is still unclear whether and how ubiquitylated proteins relate to AF in the left atrial appendage of patients with AF and valvular heart disease. Methods: Through LC-MS/MS analyses, we performed a study on tissues from eighteen subjects (9 with sinus rhythm and 9 with AF) who underwent cardiac valvular surgery. Specifically, we explored the ubiquitination profiles of left atrial appendage samples. Results: In summary, after the quantification ratios for the upregulated and downregulated ubiquitination cutoff values were set at >1.5 and <1:1.5, respectively, a total of 271 sites in 162 proteins exhibiting upregulated ubiquitination and 467 sites in 156 proteins exhibiting downregulated ubiquitination were identified. The ubiquitylated proteins in the AF samples were enriched in proteins associated with ribosomes, hypertrophic cardiomyopathy (HCM), glycolysis, and endocytosis. Conclusions: Our findings can be used to clarify differences in the ubiquitination levels of ribosome-related and HCM-related proteins, especially titin (TTN) and myosin heavy chain 6 (MYH6), in patients with AF, and therefore, regulating ubiquitination may be a feasible strategy for AF.

Altered fear engram encoding underlying conditioned versus unconditioned stimulus-initiated memory updating.

It is known that post-retrieval extinction but not extinction alone could erase fear memory. However, whether the coding pattern of original fear engrams is remodeled or inhibited remains largely unclear. We found increased reactivation of engram cells in the prelimbic cortex and basolateral amygdala during memory updating. Moreover, conditioned stimulus- and unconditioned stimulus-initiated memory updating depends on the engram cell reactivation in the prelimbic cortex and basolateral amygdala, respectively. Last, we found that memory updating causes increased overlapping between fear and extinction cells, and the original fear engram encoding was altered during memory updating. Our data provide the first evidence to show the overlapping ensembles between fear and extinction cells and the functional reorganization of original engrams underlying conditioned stimulus- and unconditioned stimulus-initiated memory updating.

Research on the Adhesive Performance of a Biomimetic Goat Hoof Track Shoe Pattern.

In this paper, reverse engineering technique was employed to extract the ridges of the hoof ball contour, and hoof ball tissue structure was analyzed based on the bionic prototype of goat hooves. The quantified geometric features were used to design the bionic track shoe pattern, which can enhance its adhesive performance and solve the problem that agricultural tracked vehicles in hilly and mountainous areas are prone to slip due to poor adhesive performance. The monolithic structure of the biomimetic goat hoof track shoe pattern and the ordinary one-line track pattern were arranged and combined; they included six kinds of track shoe models and the adhesive performance was compared. A discrete element system was established based on soil parameter determination to compare the maximum adhesion of different track shoe models. The bionic track shoe samples were prepared for soil bin tests to verify the reliability of the discrete element analysis results. Compared with the ordinary track shoe, the adhesion of the optimal bionic track shoe was improved by 9.1%.

Design and Test of Tread-Pattern Structure of Biomimetic Goat-Sole Tires.

To solve the technical problem that wheeled vehicles are prone to skidding on complex ground, due to poor adhesion performance, a tire-tread-structure design method based on the bionic principle is proposed in this paper. The 3D model of a goat's foot was obtained using reverse engineering technology, and the curve equation was fitted by extracting the contour data of its outer-hoof flap edge, which was applied to the tire-tread-structure design. The bionic and herringbone-pattern rubber samples were manufactured, and a soil-tank test was carried out using an electronic universal tensile-testing machine, in order to verify the simulation results. The results showed that the overall adhesion of the bionic tread-pattern was greater than that of the normal tread-pattern with the same load applied and the same height and angle of the tread-pattern structure, and the maximum adhesion was increased by 14.23%. This research will provide a reference for optimizing the pattern structure and thus improving the passing performance of wheeled vehicles.

Tanshinone IIA inhibits lipopolysaccharide­induced inflammatory responses through the TLR4/TAK1/NF­κB signaling pathway in vascular smooth muscle cells.

To aim of the present study was to determine whether Tanshinone IIA (Tan IIA) inhibits lipopolysaccharide (LPS)­induced inflammation in vascular smooth muscle cells (VSMCs) from rats and elucidate the underlying molecular mechanism. VSMCs were primarily cultured and then treated with LPS (1 µg/l) and Tan IIA (25, 50 and 100 µmol/l) for 24 h. Monocyte chemoattractant protein (MCP)­1, interleukin (IL)­6 and tumor necrosis factor (TNF)­α levels were detected by ELISA and reverse transcription­quantitative polymerase chain reaction. Nitric oxide (NO) production was measured using the Griess reaction. The expression of Toll­like receptor 4 (TLR4), nuclear factor (NF)­κB (p65), and inducible NO synthase (iNOS), and the phosphorylation of transforming growth factor­ß­activated kinase 1 (TAK1) were detected by western blot analysis. Tan IIA inhibited the LPS­induced expression of MCP­1, IL­6, and TNF­α in a concentration­dependent manner and inhibited iNOS­mediated NO production. In addition, Tan IIA suppressed the expression of TLR4, the phosphorylation of TAK1, and the nuclear translocation of NF­κB (p65). The anti­TLR4 antibody and TAK1 inhibitor 5Z­7­oxozeaenol partially attenuated the LPS­induced expression of proinflammatory cytokines. In conclusion, Tan IIA inhibits LPS­induced inflammatory responses in VSMCs in vitro through the partial suppression of the TLR4/TAK1/NF­κB signaling pathway.

Asiatic acid inhibits cardiac fibrosis throughNrf2/HO-1 and TGF-ß1/Smads signaling pathways in spontaneous hypertension rats.

OBJECTIVE: Asiatic acid (AA) has been suggested to inhibit pulmonary and hepatic fibrosis, while its influence on cardiac fibrosis remains unclear. We aimed to investigate whether AA could inhibit overpressure-induced cardiac fibrosis in spontaneous hypertension rats (SHRs). METHOD: SHRs were treated with AA (20 mg kg-1 day-1) for 12 weeks and cultured cardiac fibroblasts (CFs) were treated with Ang II (10-7 mol/L) in vitro. Markers of oxidative stress were measured and extent of cardiac fibrosis was evaluated with Sirius Red staining. Levels of Superoxide Dismutase (SOD), Malondialdehyde (MDA), reactive oxygen spices (ROS) and Glutathione (GSH) were measured by using commercial assay kits. Collagen deposition was detected. The expression of relative protein and mRNA was measured by Western blot and real-time PCR, respectively. RESULTS: AA reduced systolic blood pressure, attenuated myocardial hypertrophy, reduced college deposition and the expression of collagen I and III, connective tissue growth factor, and plasminogen activator inhibitor-1, in mRNA and protein levels, with inhibition of TGF-ß1 expression, phosphorylation of Smad2/3, and increase of Smad7 expression. AA reduced malondialdehyde and reactive oxygen spices, while increased the activities of superoxide dismutase and glutathione, accompanied with elevation of nuclear translocation of nuclear-factor erythroid 2-related factor 2 (Nrf2) and expression of heme oxygenase (HO-1) and NAD(P)H dehydrogenase [quinone] 1 (NQO-1) in vivo and in vitro. Moreover, pretreating CFs with siRNA for Smad7 or Nrf2 both partially reversed the inhibition of AA on Ang II-induced cardiac fibrosis. CONCLUSION: AA attenuates pressure overload-induced cardiac fibrosis via enhancing of Nrf2/HO-1 and suppressing TGF-ß1/Smads phosphorylation.

Sitagliptin protects the cognition function of the Alzheimer's disease mice through activating glucagon-like peptide-1 and BDNF-TrkB signalings.

BACKGROUND: Sitagliptin is an anti-diabetic drug and its effects on Alzheimer's disease (AD) remain controversial. This study aimed to investigate the protective effect of sitagliptin on the cognition in AD and its underlying molecular mechanism. METHODS: The APP/PS1 (a model of AD) mice received daily gastric gavage administration of sitagliptin (20 mg/kg) for 8 weeks. Then animals were subjected to behavioral experiment or sacrificed to histological staining and protein level analysis. RESULTS: The MWM test showed that sitagliptin treatment significantly reduced the escape latency times in APP/PS1 mice in the learning phase (day 3-5) and elongated the time spent in the target quadrant in the probe test. Sitagliptin significantly reduced amyloid plaque deposition and elevated the spine density and the protein levels of synaptoneurosome GluA1- and GluA2-containing AMPA receptor (GluA1R and GluA2R) in the brain of the APP/PS1 mice. Sitagliptin treatment significantly up-regulated the brain BNDF protein and phosphorylation of tyrosine receptor kinase B (TrkB). Furthermore, exendin-(9-39) (a glucagon-like peptide-1 [GLP-1] receptor antagonist) and K252a (a Trk tyrosine kinase inhibitor) treatment significantly abolished the cognitive protective effect of sitagliptin in the MWM test. CONCLUSION: Sitagliptin treatment effectively protected the cognition function of the AD mice by regulating synaptic plasticity, at least partially, through activating GLP-1 and BDNF-TrkB signalings.

Uhrf2 deletion impairs the formation of hippocampus-dependent memory by changing the structure of the dentate gyrus.

Ubiquitin-like with PHD and ring finger domains 2 (Uhrf2) is distributed in many brain regions, including the cortex and hippocampus. Decreased Uhrf2 expression is involved in neurodegenerative disease. A recent study showed Uhrf2 deletion impaired spatial memory; however, the mechanism remains elusive. In our study, we determined that Uhrf2+/- and Uhrf2-/- mice had significant learning and memory deficiencies in contextual fear conditioning (CFC) and the novel place recognition test but not in the novel object recognition test. Interestingly, there were no changes in the Uhrf2 protein levels in the hippocampus of C57BL6 mice after CFC training, which suggests Uhrf2 in adult mice may not be related to the formation of CFC long-term memory. Based on Nissl staining, Uhrf2 deletion caused neuropathological changes specifically in the crest of the dentate gyrus (DG), such as cell swelling, a vague outline and confused boundary; however, no changes were identified in the medial prefrontal cortex (mPFC). Transmission electron microscope assay further indicated a series of abnormal ultrastructure changes in neurons and glia in the DG crest. These results suggested that Uhrf2 deletion selectively blocked the development of the DG crest and impaired hippocampus-dependent learning and memory. Our study will facilitate a better understanding of the role of Uhrf2 protein in the central nervous system.

Direct Neuronal Glucose Uptake Is Required for Contextual Fear Acquisition in the Dorsal Hippocampus.

The metabolism of glucose is a nearly exclusive source of energy for maintaining neuronal survival, synaptic transmission and information processing in the brain. Two glucose metabolism pathways have been reported, direct neuronal glucose uptake and the astrocyte-neuron lactate shuttle (ANLS), which can be involved in these functions simultaneously or separately. Although ANLS in the dorsal hippocampus (DH) has been proved to be required for memory consolidation, the specific metabolic pathway involved during memory acquisition remains unclear. The DH and amygdala are two key brain regions for acquisition of contextual fear conditioning (CFC). In 2-NBDG experiments, we observed that 2-NBDG-positive neurons were significantly increased during the acquisition of CFC in the DH. However, in the amygdala and cerebellum, 2-NBDG-positive neurons were not changed during CFC training. Strikingly, microinjection of a glucose transporter (GLUT) inhibitor into the DH decreased freezing values during CFC training and 1 h later, while injection of a monocarboxylate transporter (MCT) inhibitor into the amygdala also reduced freezing values. Therefore, we demonstrated that direct neuronal glucose uptake was the primary means of energy supply in the DH, while ANLS might supply energy in the amygdala during acquisition. Furthermore, knockdown of GLUT3 by a lentivirus in the DH impaired the acquisition of CFC. Taken together, the results indicated that there were two different glucose metabolism pathways in the DH and amygdala during acquisition of contextual fear memory and that direct neuronal glucose uptake in the DH may be regulated by GLUT3.