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Vascular cognitive impairment (VCI) is the second most common type of dementia after Alzheimer's disease (AD) in elderly people. Chronic cerebral hypoperfusion (CCH) is the early pathophysiological basis of VCI. β-Hydroxybutyrate (BHB) is one of the important components of ketone bodies, an intermediate product of endogenous energy metabolism, which can mitigate neuroinflammation in stroke and neurodegenerative diseases. The present study aimed to investigate whether BHB can improve cognitive impairment caused by CCH and the underlying mechanism.The CCH model was established by permanent bilateral common carotid artery occlusion (2VO). CCH rats were intraperitoneally injected with BHB (1.5 mmol/kg/d) every day for 8 consecutive weeks from 2 weeks before surgery. The hippocampal blood flow of rats was measured by using a laser Doppler velocimetry. Used the Morris water maze test (MWM) to assess spatial learning and memory of rats, and harvested brain tissues for molecular, biochemical, and pathological tests.We found that BHB intervention for 8 weeks could effectively restore hippocampal blood flow and improve spatial learning and memory in CCH rats. BHB can protect the blood-brain barrier (BBB), as manifested by reducing the ultrastructural damage and leakage of the BBB, restoring the expression of tight junction-related proteins and reducing the expression of Matrix Metalloproteinases-9 (MMP-9). Additionally, after BHB intervention, microglia activation was reduced, oligodendrocyte motility was active, and the expression levels of pro-inflammatory factors such as tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), nuclear factor-κB (NF-κB) and advanced glycation end-products (RAGE) were lower, which also indicated that BHB had a beneficial effect in mitigating neuroinflammation.BHB can improve the cognitive impairment caused by CCH. The potential mechanisms of BHB may be through reducing neuroinflammation and protecting BBB.

Chronic cerebral hypoperfusion (CCH) has been gradually regarded as a common etiologic mechanism for cognitive and psychiatric disturbances. Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) played an important role in adult hippocampal neurogenesis (AHN), neuronal circuits formation, cognition and psychiatric disorders. Enriched environment (EE) showed a beneficial effect on cognition and depression via effectively regulating AHN and glial reactivity. This study aimed to assess which strategy was feasible to improve cognition and psychiatric disturbances by comparing the TET1 hippocampal microinjection and EE in CCH models and to investigate the possible mechanisms.CCH rats were established via permanent bilateral common carotid artery occlusion (2-VO). Rats were stereotaxically injected with the human catalytic domain of TET1 (hTET1) to overexpress the hTET1 in the hippocampus 10 days before 2-VO. 3 days after 2-VO, rats were subjected to standard environment or EE with free access to food and water. Behavioral tests were used to appraise depression and cognition before sacrifice. Epigenetic molecules, adult neurogenesis, synaptic proteins expression, and glial activation were analyzed using immunofluorescent staining, qRT-PCR and western blot.In the present study, we found both EE and genetical treatment with overexpressing hTET1 were sufficient for stimulating AHN. However, promoting ANH could not deal with the cognitive dysfunction and depressive-like behaviors in CCH rats. Notably, a healthy local brain environment with elevated BDNF and astrocytes was conducive to improving cognitive dysfunction. Meanwhile, astrocytes were involved in the cognitive regulating process of neurons, presynaptic function and microglia. In general, we held that depressive disturbances were determined by BDNF levels, neuronal and presynaptic function, as well as glial activation containing astrocytes and microglia. To further support this point, we investigated severe depressive symptoms that were strongly correlated with the activation of astroglia and microglia. Importantly, causal mediation analysis showed significant mediation by the presence of reactive glial cells in the relation between neural plasticity and depressive symptoms. Finally, we showed EE performed better than hTET1 treatment for cognitive deficits and depression. EE with less glial reactivity was much more resistant to depression, while hTET1 with more glial activation was more vulnerable to depressive disorders.EE was likely to be superior to TET1 hippocampal administration for cognition and psychiatric behaviors in CCH rats. Furthermore, a healthy local brain environment with elevated BDNF and astrocytes was conducive to improving cognitive dysfunction. More glial activation, and more vulnerable to depressive disorders. These results were important for our understanding of disease mechanisms and provided valuable tools for the overall management of CCH patients.

Metal-organic frameworks (MOFs) derivatives have been widely explored as highly efficient electromagnetic absorbing materials. Due to their diverse coordination arrangements, morphologies, and unique structures, MOFs provide promising avenues for synthesizing materials with customized properties. However, strategies for tailoring properties of low-dimensional MOFs-derived absorbers with hollow structures remain a considerable challenge. Herein, a well-defined Co@N-doped porous carbon composite (Co/N PC) with double-shell hollow structures has been successfully developed through self-templating-polymerization and subsequent pyrolysis. The proposed strategy for the synthesis of hollow architecture involves three simple steps (i) coordination, (ii) dissociation, and (iii) dopamine (DA) polymerization. The synthetic approach is realized at room temperature without a need for solvent etching. By effectively optimizing parameters including void thickness, surface structures, and graphitization levels, the as-designed Co/N PC composites feature wide absorption bandwidth of 5.93 GHz at a thickness of 2.4 mm with a filler loading of 15 wt%. The exceptional performance of microwave absorption (MA) is primarily achieved through excellent dielectric loss, and enhanced impedance matching, due to increased conductive loss through porous hollow structures and dipolar/interfacial polarization. This work provides an eco-friendly and facile route to designing hollow MOFs derivatives, offering substantial parameter space for optimized future lightweight and efficient absorbing materials.

The engineering of core-shell nanostructures provides a great potential to induce interfacial polarization relaxation and optimize impedance matching. Herein, core-shell-structured MHCS@MoS2 nanospheres are developed using hollow carbon (MHCS) and stacked MoS2 nanosheets. Heterostructures between cores and shells significantly boost the interface polarization effect and effectively reduce the electromagnetic wave (EMW) reflection caused by highly conductive MHCS. Thereby, efficient and broadband electromagnetic microwave absorption (EMA) performance can be achieved. Through controlling the thickness of MoS2 shells and the graphitization of MHCS cores, the effective absorption bandwidth (fE) of MHCS@MoS2 can reach 6.21 GHz at the thickness of only 2.1 mm. The nanodesigned core-shell-shaped MHCS@MoS2 nanospheres are demonstrated as a promising high-performance EMA material.

As a typical fascinating microstructure, the core-shell structure provides abundant possibility for material design in various fields including nano-engineering. In addition, the popular MOF derivatives have been widely explored and recognized as the most potential candidates for functional materials, especially in the field of microwave absorption (MA). Combined with the advantages of their structure and function, it is expected to maximize the synergistic effect and achieve amazing MA performance. In this paper, a series of core-shell CF@C/Co composites were assembled by using lightweight and conductive CF as the core and cubic ZIF-67-derived C/Co with controllable structure and adjustable graphitization as the shell. The intrinsic relationships between shell structure, component content, graphitization degree, electromagnetic parameters and various microwave loss behaviors are analyzed. After properly adjusting the degree of graphitization on the basis of derivation of various C/Co shells, A3-600 with obvious multi-polarization effect were obtained. A3-600 achieves an effective absorption bandwidth of 6.25 GHz at 1.71 mm and the best reflection loss of −71.95 dB at 1.78 mm. This dual strategy of shell evolution design and graphitization control has been proved to be an effective method to coordinate electromagnetic matching and construct multi-polarization effect to enhance the performance of MA.

The combination of Ag nanomaterials and special nanostructures can significantly amplify the conversion of electromagnetic energy, especially in microwave absorption applications. Herein, a kind of...

MOFs with high tunability are considered ideal candidates as microwave-absorbing materials. Strict experimental conditions can ensure the repeatability and maximize the potential of such materials. In this study, cubic ZIF-67 carbides synthesized at different solution temperatures showed an adjustable average size, and then by adjusting the calcination temperature we could control the degree of graphitization, so as to explore the synergistic effect of these two aspects to achieve an in-depth understanding of the electromagnetic properties and microwave absorption properties. The results showed that sample 30-600 (with the former number referring to the synthesis temperature and the latter to the calcination temperature) showed the widest effective absorption bandwidth (5.75 GHz, 1.8 mm) and the optimal reflection loss (-56.92 dB, 2.1 mm). The best matching electromagnetic parameters were obtained under the synergistic action of a smaller particle size and appropriate degree of graphitization, so as to achieve strong attenuation characteristics under low electromagnetic wave reflection. The microwave loss mechanism of the sample mainly involved dielectric losses, such as from conductance loss, dipole polarization, and interface polarization. Starting from the experimental details, this work proposes a dual control strategy for developing microwave-absorbing materials with both simplicity and practicability, which provides a useful reference for other microwave absorbents synthesized at room temperature.

Background Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism in neurodegenerative diseases, such as Alzheimer’s disease and vascular dementia. The orphan nuclear receptor TLX plays an important role in neural development, adult neurogenesis and cognition. The aim of this study was to investigate the neuroprotective effects of TLX on cognitive dysfunction, hippocampal neurogenesis and neuroinflammation in a rat model of CCH and to assess the possible mechanisms. Methods Permanent bilateral common carotid artery occlusion (2-VO) was used to establish a model of CCH. Stereotaxic injection of an adeno-associated virus vector expressing TLX was used to overexpress TLX in the hippocampus. Cognitive function was evaluated by the Morris Water Maze test. Immunofluorescent staining was used to assess hippocampal neurogenesis. The effects of overexpression of TLX on SIRT1 and inflammatory cytokines were analyzed with qRT-PCR and western blot. Result After 2-VO, CCH rats exhibited cognitive impairment and reduction of hippocampal TLX levels. Overexpression of TLX ameliorated cognitive impairments with increasing number of BrdU + cells and BrdU + NeuN + cells in DG. Furthermore, TLX rescued the reduced SIRT1 usually induced by CCH. Additionally, TLX also inhibited the expression of inflammatory cytokines such as NF-κB and IL-1β. Conclusions The present findings suggested that TLX exerted protective effects against cognitive deficits induced by CCH. The possible mechanisms of TLX may be through regulating the SIRT1/NF-κB pathway, promoting hippocampal neurogenesis and inhibiting the neuroinflammatory response.

Purpose The purpose of this study was to clarify the association between the NLRC4 gene and the susceptibility and clinical characteristics of type 1 diabetes (T1D) in a Chinese Han population. Patients and methods A case-control study was performed in a Chinese Han population including 510 classical T1D patients and 531 healthy controls. rs212704 and rs385076 of the NLRC4 gene were genotyped by MassARRAY. The frequency distributions of alleles and genotypes of polymorphisms in the NLRC4 gene were compared by logistic regression and the chi-square test. The relationships between the polymorphisms of the NLRC4 gene and various clinical characteristics were analyzed by Kruskal-Wallis one-way ANOVA. The statistical power was calculated by Quanto software. Results 1) rs385076 of the NLRC4 gene was significantly correlated with the onset age of T1D patients and the positive rate of GADA. The relationship between rs212704 and 2-h postprandial C-peptide was statistically significant. 2) There was no significant difference in the frequency distributions of the genotypes and alleles of rs212704 and rs385076 between T1D patients and controls. 3) rs212704 and rs385076 were not correlated with T1D susceptibility under different genetic models. Conclusion rs212704 was associated with 2-h postprandial C-peptide, while rs385076 of the NLRC4 gene was associated with the onset age and positive rate of GADA in patients with T1D.

Background Chronic unpredictable mild stress (CUMS) is an important risk factor for depression and cognitive deficits in humans. Enriched environment (EE) showed a beneficial effect on depression and cognition by enhancing brain derived neurotrophic factor (BDNF) expression and synaptic plasticity. However, it is still not clearly understood whether an epigenetic mechanism is involved in the BDNF modulation and synaptic plasticity that occurs after EE treatment for the depressive-like behaviors and cognitive deficits elicited by CUMS. In this study, we investigated the possible mechanism of the neuroprotective effect of EE. Methods All rats were exposed to the 5-week CUMS procedure except the control group. After CUMS procedure, some rats were stereotaxically injected with SIRT1 pharmacologic inhibitor EX527 or SIRT1 knocking down lentivirus (sh-SIRT1) in the hippocampus followed by EE treatment for 3 weeks. Other rats were directly subjected to EE treatment without stereotaxic injection. Behavioral tests were used to appraise depression and cognition after EE treatment. Then epigenetic molecules, synaptic proteins, dendritic spine density and branches, and synaptic morphology of the dorsal hippocampus were determined. Results We found that CUMS induced depressive-like behaviors including decreased sucrose preference ratio, prolonged immobility and reduced locomotor and exploratory activity; cognitive deficits including spatial learning and memory impairment; reduced dendritic spine density and number of branches; thinned postsynaptic density; downregulated SIRT1/microRNA-134 pathway, decreased BDNF and synaptic proteins including synaptophysin (SYN) and postsynaptic density protein 95 (PSD95) expression in the hippocampus. However, the CUMS-induced depressive-like behaviors, cognitive deficits, dendritic spine density and branch number reduction, postsynaptic density thinning, SIRT1/microRNA-134 pathway downregulation, BDNF and synaptic proteins reduction, including synaptophysin (SYN) and postsynaptic density protein 95 (PSD95), were reversed by EE treatment. However, depressive-like behaviors and cognitive deficits were observed again in rats subjected to stereotaxic injection with EX527 or sh-SIRT1. Furthermore, this study also found that SIRT1/microRNA-134 regulates the downstream molecules BDNF, and the synaptic proteins SYN and PSD95 in primary cultured hippocampal neurons. Conclusions This study provides evidence for the neuroprotective role of EE on depression and cognitive deficits by activating the SIRT1/microRNA-134 pathway, which accounts for the regulation of synaptic proteins, including BDNF, PSD95 and SYN, dendritic remodeling and ultrastructure changes of synapses in the hippocampus.

Due to the extensive use and incomplete removal, pharmaceutical and personal care products (PPCPs) are introduced into the water continuously. It has been proved that the unique properties of PPCPs are influential to organisms and the environment, and gradually affect human health. In this paper, the toxicological effects of typical PPCPs, and the environmental behavior of PPCPs in aquatic are reviewed. The risk assessments of PPCPs in the water are summarized. The research directions of environmental toxicology research of PPCPs in the future are proposed. Many PPCPs were found to be toxic or even highly toxic toward aquatic organisms, and have the potential for bioaccumulation. It is essential to study the acute and long-term toxicity of PPCPs and their metabolites, evaluate the environmental behaviors and make a reasonable assessment of ecotoxicology and human health risks of PPCPs.

Biosensors are essential components for effective healthcare management. Since biological processes occur on molecular scales, nanomaterials and nanosensors intrinsically provide the most appropriate landscapes for developing biosensors. Low-dimensional materials have the advantage of offering high surface areas, increased reactivity and unique physicochemical properties for efficient and selective biosensing. So far, nanomaterials and nanodevices have offered significant prospects for glucose sensing. Targeted glucose biosensing using such low-dimensional materials enables much more effective monitoring of blood glucose levels, thus providing significantly better predictive diabetes diagnostics and management. In this review, recent advances in using low dimensional materials for sensing glucose are summarized. Sensing fundamentals are discussed, as well as invasive, minimally-invasive and non-invasive sensing methods. The effects of morphological characteristics and size-dependent properties of low dimensional materials are explored for glucose sensing, and the key performance parameters such as selectivity, stability and sensitivity are also discussed. Finally, the challenges and future opportunities that low dimensional materials can offer for glucose sensing are outlined.

Disruption of the blood–brain barrier (BBB) can lead to cognitive impairment. Major facilitator superfamily domain-containing protein 2a (Mfsd2a) is a newly discovered protein that is essential for maintaining BBB integrity. However, the role of Mfsd2a in vascular cognitive impairment has not been explored yet. In this study, a rat model of chronic cerebral hypoperfusion (CCH) was established by producing permanent bilateral common carotid artery occlusion (2VO) in rats. We found that after the 2VO procedure, the rats exhibited cognitive impairment, showed increased BBB leakage within the hippocampus, and had reduced expression of the Mfsd2a protein. The overexpression of Mfsd2a in the rat hippocampus reversed these changes. Further investigations using transmission electron microscopy revealed a significantly increased rate of vesicular transcytosis in the BBB of the hippocampus of the CCH rats; the rate reduced after overexpression of Mfsd2a. Moreover, Mfsd2a overexpression did not cause changes in the expression of tight junction-associated proteins and in the ultrastructures of the tight junctions. In conclusion, Mfsd2a attenuated BBB damage and ameliorated cognitive impairment in CCH rats, and its protective effect on the BBB was achieved via inhibition of vesicular transcytosis.

Purpose The purpose of this study was to clarify the association between the NLRC4 gene and the susceptibility and clinical characteristics of type 1 diabetes (T1D) in a Chinese Han population. Patients and Methods A case-control study was performed in a Chinese Han population including 510 classical T1D patients and 531 healthy controls. rs212704 and rs385076 of the NLRC4 gene were genotyped by MassARRAY. The frequency distributions of alleles and genotypes of polymorphisms in the NLRC4 gene were compared by logistic regression and the chi-square test. The relationships between the polymorphisms of the NLRC4 gene and various clinical characteristics were analyzed by Kruskal–Wallis one-way ANOVA. The statistical power was calculated by Quanto software. Results 1) rs385076 of the NLRC4 gene was significantly correlated with the onset age of T1D patients and the positive rate of GADA. The relationship between rs212704 and 2-h postprandial C-peptide was statistically significant. 2) There was no significant difference in the frequency distributions of the genotypes and alleles of rs212704 and rs385076 between T1D patients and controls. 3) rs212704 and rs385076 were not correlated with T1D susceptibility under different genetic models. Conclusion rs212704 was associated with 2-h postprandial C-peptide, while rs385076 of the NLRC4 gene was associated with the onset age and positive rate of GADA in patients with T1D.

Due to the excessively high electrical conductivity and single dielectric properties of the graphene material, when used as a wave absorbing material, the imbalance of impedance matching causes strong reflection effects, resulting in poor wave absorbing performance. In this research, we partially reduced graphene oxide (GO) and loaded magnetic quantum dots (MQDs) through a one-step pyrolysis method, and a novel composite material of three MQDs (Fe, Fe3O4, Fe3C) embedded partially reduced graphene oxide (P-rGO) was prepared and the influence of pyrolysis temperature on its electromagnetic performance was systematically studied. The research found that ethylene glycol selectively reduced the C O functional group of the GO component and enhanced its dielectric properties; the loading of MQDs for a single carbon material increased the magnetic loss mechanism and improved the impedance matching and attenuation capabilities. In addition, the flaky structure of GO and the ultra-small nanostructure of MQDs suppress the eddy current effect and promote the occurrence of exchange resonance between magnetic particles. The prepared four sets of samples exhibit excellent absorbing properties in the 2–18 GHz frequency band. Among them, the samples prepared by pyrolysis at 800 °C can obtain 5.59 GHz broadband electromagnetic wave absorption at an ultra-thin thickness of 1.7 mm. The special quantum size effect and enhanced electromagnetic wave attenuation capabilities are the main reasons for the high-efficiency microwave absorption of MQDs/P-rGO composite materials.

Background Chronic cerebral hypoperfusion (CCH) is a common pathophysiological basis for Alzheimer’s Disease and vascular dementia in the early stages. It has been confirmed that blood-brain barrier (BBB) destruction is a key factor in CCH-related cognitive impairment. Here we explored the effects of an enriched environment (EE) intervention on CCH-induced BBB destruction and cognitive impairment, and the underlying mechanism. Methods Rats in the EE group were exposed to an EE, while the standard environment (SE) group was maintained in a standard cage with bedding but no other objects. On day 14, CCH was induced via permanent bilateral common carotid artery occlusion (2VO). Next, Evans blue (EB) leakage in the hippocampus was measured by chemical colorimetry to dynamically evaluate BBB permeability. On day 28, the BBB ultrastructure was observed using transmission electron microscopy. The expression levels of BBB integrity-related proteins, matrix metalloproteinases-2/-9 (MMP-2/-9), and the classical Wnt/β-catenin signaling pathway-related proteins were detected using western-blotting techniques. On day 43, cognitive function was assessed using the Morris water maze. Results After 2VO, CCH rats exposed to the SE developed obvious cognitive impairment and BBB destruction. BBB damage was manifested through increased EB leakage, ultrastructural destruction, degradation of BBB integrity-related proteins, and up-regulation of MMP-2/-9. These changes were significantly alleviated after the EE intervention. In addition, EEs activated the Wnt/β-catenin signaling pathway in the hippocampus of rats. Conclusions These results suggest that protection of the BBB may be a novel mechanism by which EEs ameliorate CCH-induced cognitive impairment, and this effect may be related to the activation of the Wnt/β-catenin pathway.

Vascular cognitive impairment (VCI) is the second most common cause of dementia after Alzheimer's disease, and the cognitive impairment is one of the common effects of VCI. Unfortunately, it lacks effective therapeutic treatments at present. In our previous study, environmental enrichment (EE), as an early intervention for lifestyle modification, can ameliorate cognitive impairment by attenuating hippocampal blood-brain barrier (BBB) injury in chronic cerebral hypoperfusion (CCH) rats. However, the underlying mechanism remains unclear. Here, we found CCH rats in the standard environment (SE) developed cognitive impairment and BBB damage, which were significantly alleviated with the EE intervention. Meantime, EE improved the autophagy dysfunction caused by CCH in the hippocampus of rats, suggesting that the effect of EE on cognitive function and BBB may be related to the improvement of autophagy pathway.

Chronic unpredictable mild stress (CUMS) leads to neuropsychiatric disorders, such as depression, anxiety and cognitive impairment. Resveratrol is a natural polyphenol existed in polygonum cuspidatum and has been demonstrated to be a potent activator of Sirtuin 1 (Sirt1). Previous studies reported that resveratrol treatment ameliorated CUMS-induced depressive-like behavior and cognitive deficits through upregulating cAMP response element-binding protein (CREB) and brain derived neurotrophic factor (BDNF) expression. However, the upstream signalling pathway mediating CREB/BDNF expression and then exerting a protective role on cognitive function remains unclear. The present study aims to investigate the possible mechanism of resveratrol on CUMS-induced cognitive deficits. Male Sprague Dawley rats were adminstrated resveratrol (40 and 80 mg/kg) every day for 4 consecutive weeks before exposure to CUMS procedure. Morris Water Maze test was used to appraise spatial learing and memory of rats. Sirt1/miR-134 signalling pathway and CREB/BDNF expression in hippocampus of rats were measured. We also explored Sirt1/miR-134 signalling pathway and CREB/BDNF expression in primary cultured hippocampus neurons with resveratrol (25, 50 and 100 μmol/L) treatment. We found that resveratrol treatment prevented spatial learing and memory impairment induced by CUMS. Meanwhile the potential mechanism of resveratrol was associated with increased levels of Sirt1, CREB phosphorylation (p-CREB), CREB, BDNF and decreased levels of miR-134 in vivo and in vitro. In conclusion, our study showed that the neuroprotective effect of resveratrol on CUMS-induced cognitive impairment may rely on activating Sirt1/miR-134 pathway and then upregulating its downstream CREB/BDNF expression in hippocampus.

Chronic unpredictable mild stress (CUMS) is an important contributing factor for depression with inflammatory response alteration, neuron apoptosis, and decreased neurogenesis. Previous study reported that the administration of resveratrol alleviated depression by normalizing the increased proinflammatory cytokine levels and inhibiting apoptosis in the hippocampus. However, the upstream signaling pathway that regulates cytokines and apoptosis in the antidepressant effect of resveratrol remains unclear. The objective of this study is to investigate the possible mechanism of the effect of resveratrol on depression. Male Sprague Dawley rats were exposed to CUMS for four consecutive weeks to elicit depressive-like behavior. The rats in the drug treatment groups were injected with resveratrol (40 or 80 mg/kg/day) and fluoxetine (10 mg/kg/day) intraperitoneally for 4 weeks. Rats in two additional groups were administered LY294002 by bilateral stereotaxic microinjection into the lateral ventricle before resveratrol administration. Behavioral tests, including sucrose preference test, forced swim test, and open field test, were used after 4 weeks of a CUMS procedure to appraise depressive-like behavior. Then, the proinflammatory cytokines (TNF-α, IL-6, and IL-1β) in the hippocampus and prefrontal cortex (PFC) tissues of rats were measured. Apoptosis-related molecules such as Bax and Bcl-2 mRNA levels in the hippocampus were analyzed. Furthermore, p-Akt/Akt and p-GSK3β/GSK3β protein expression in the hippocampus were also measured. The results show that rats were subjected to CUMS procedure exhibited depressive-like behavior, increased TNF-α, IL-6, and IL-1β levels in hippocampus and PFC, alteration of Bax and Bcl-2 mRNA levels in hippocampus, decreased p-Akt/Akt and p-GSK3β/GSK3β protein expression in hippocampus, and an increased apoptotic cell percentage in the hippocampal CA1 region. However, resveratrol (40 or 80 mg/kg) treatment reversed these behavioral and molecular changes in CUMS rats. The positive control drug fluoxetine showed a similar effect as the resveratrol treatment. When rats were injected with LY294002 before resveratrol treatment, the antidepressant effect of resveratrol was significantly attenuated, TNF-α, IL-6 and IL-1β levels in hippocampus and PFC increased again, Bax mRNA levels increased and Bcl-2 mRNA levels decreased in hippocampus, and Akt/GSK3β protein expression in hippocampus decreased. The findings in the present study suggest that the antidepressant effect of resveratrol treatment may act through activation of the Akt/GSK3β signaling pathway and then regulation of proinflammatory cytokine expression and alteration of apoptosis.

The rules of acupoints combination of ancient acupuncture for Xiaoke are mainly explored. By retrieval on ancient literature, the database of acupuncture and moxibustion for Xiaoke is established; based on the database, association analysis between acupoints and symptoms is performed. According to the association analysis in 5 databases of Xiaoke database, Xiaoke database of kidney deficiency, Xiaoke-database of dry mnouth and thirst, Xiaoke database of difficult urination, Xiaoke database of drinking addiction, the results are mainly characterized with symptom differentiation combination, distal-local combination, local combination and front-back combination, which can nourish yin and clear heat. It is believed that establishment of TCM ancient literature database and exploration of data mining technology is a potential research orientation.

To explore the status of acupuncture and moxibustion for prevention and treatment of lung cancer in current years; literature regarding acupuncture and moxibustion for prevention and treatment of lung cancer between 2003 and 2013 from SCI journals was retrieved and analyzed. As a result, 20 papers were included, which were published in 17 journals including Journal of Clinical Oncology, Chest, Respirology and Lung Cancer, etc. Of them, 3 papers discussed the effects of acupuncture on progressing of lung cancer; 4 articles confirmed that acupuncture could reduce myelosuppression and digestive tract reactions induced by radiotherapy and chemotherapy; 6 papers showed that acupuncture could relieve pain or fatigue of lung cancer; 3 papers indicated that acupuncture could palliate dyspnea in lung cancer patients. It is concluded by domestic and overseas researches that acupuncture and moxibustion are effective and safe for symptoms of lung cancer, which is worthy of further study.