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Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by progressive dementia, and amnestic mild cognitive impairment (aMCI) has been defined as a transitional stage between normal aging and AD. Accumulating evidence has shown that altered functional connectivity (FC) and structural connectivity (SC) in the default mode network (DMN) is the prominent hallmarks of AD. However, the relationship between the changes in SC and FC of the DMN is not yet clear. In the present study, we derived the FC and SC matrices of the DMN with functional magnetic resonance imaging (fMRI) and diffusion-weighted imaging (DWI) data and further assessed FC and SC abnormalities within a discovery dataset of 120 participants (39 normal controls, 34 patients with aMCI and 47 patients with AD), as well as a replication dataset of 122 participants (43 normal controls, 37 patients with aMCI and 42 patients with AD). Disrupted SC and FC were found among DMN components (e.g., the posterior cingulate cortex (PCC), medial prefrontal cortex (mPFC), and hippocampus) in patients in the aMCI and AD groups in the discovery dataset; most of the disrupted connections were also identified in the replication dataset. More importantly, some SC and FC elements were significantly correlated with the cognitive ability of patients with aMCI and AD. In addition, we found structural-functional decoupling between the PCC and the right hippocampus in patients in the aMCI and AD groups. These findings of the alteration of DMN connectivity in neurodegenerative cohorts deepen our understanding of the pathophysiological mechanisms of AD.

Objective To investigate the effect of caspase-3-specific inhibitors of extracorporeal circulation (CPB) on pulmonary ischaemia-reperfusion injury in dogs.Methods Eighteen healthy mongrel dogs were divided into three groups (n = 6) by random number table method, sham-operated group (group C), ischemia-reperfusion group (group I/R) and caspase-3 specific inhibitor (group Z), and the rest of the groups were established as CPB left lung ischemia-reperfusion injury model, and group Z was given caspase-3 specific inhibitor (Z-DEVD) via femoral vein immediately after opening the left pulmonary artery. The caspase-3 specific inhibitor (Z-DEVD-fmk) 0.6mg/Kg was administered to the Z group immediately after opening the left pulmonary artery via the femoral vein. Arterial blood was collected from the femoral artery before chest opening (T1), at the time of shutdown (T2) and at the end of the experiment (T3), and arterial blood gas analysis was performed to calculate respiratory index (RI) and oxygenation index (OI). -N expression, TUNEL assay for apoptosis and HE assay for pathological changes in lung tissue at each time point.Results The expression of RI, Cleaved-caspase3, NLRP3, Clleaved-caspase-1, GSDME-N and apoptotic index in lung tissue increased in the I/R group at T2 and T3 compared with the C group, while the OI decreased (P Conclusion Caspase-3-specific inhibitors can improve lung function and reduce apoptosis in lung tissue after CPB, it also reduce oxidative stress level and inflammation level. These effects may be achieved by regulating Caspase-3/GSDME signaling pathway and inhibiting pyroptosis.

Research on the mechanism and protective measures of lung injury caused by CPB has attracted extensive attention. But the exact mechanism is still being explored. This study explored the role of autophagy in CPB lung injury by establishing the left lung ischemia-reperfusion injury model of rats and observing the relationship between CPB lung injury and autophagy. The effects of exogenous membrane tripeptide (AnxA1sp) on lung injury and autophagy in rats were investigated. Compared with the control group, the expressions of autophagy bodies and autophagy-related proteins in the lung tissue of rats after CPB were increased in the model group. With the aggravation of lung injury, autophagy was significantly increased and the degradation of autophagy was blocked. Autophagy was involved in the occurrence and development of CPB lung injury. In the rat model group of AnxA1-/-, lack of AnxA1 can cause insufficient autophagy and aggravated lung injury in CPB rats. The addition of exogenous AnxA1sp can reduce lung I/R injury in CPB rats, activate lung autophagy, promote autophagy flow, reduce the release of lung inflammatory factors, reduce lung pathological injury, and improve lung function. In conclusion, regulating the autophagy of lung tissue can produce a lung protection effect.

Vascular cognitive impairment, no dementia (VCIND) refers to cognitive deficits associated with underlying vascular causes that are insufficient to confirm a diagnosis of dementia. The default mode network (DMN) is a large-scale brain network of interacting brain regions involved in attention, working memory and executive function. The role of DMN white matter integrity in cognitive deficits of VCIND patients is unclear. Using diffusion tensor imaging (DTI), this study was carried out to investigate white matter microstructural changes in the DMN in VCIND patients and their contributions to cognitive deficits. Thirty-one patients with subcortical VCIND and twenty-two healthy elderly subjects were recruited. All patients underwent neuropsychological assessments and DTI examination. Voxel-based analyses were performed to extract fractional anisotropy (FA) and mean diffusivity (MD) measures in the DMN. Compared with the healthy elderly subjects, patients diagnosed with subcortical VCIND presented with abnormal white matter integrity in several key hubs of the DMN. The severity of damage in the white matter microstructure in the DMN significantly correlated with cognitive dysfunction. Mediation analyses demonstrated that DTI values could account for attention, executive and language impairments, and partly mediated global cognitive dysfunction in the subcortical VCIND patients. DMN integrity is significantly impaired in subcortical VCIND patients. The disrupted DMN connectivity could explain the attention, language and executive dysfunction, which indicates that the white matter integrity of the DMN may be a neuroimaging marker for VCIND.

Introduction: Hypertension patients often suffered from insomnia problems which lowered the quality of life. Studies have shown that acupuncture is effective to treat perimenopausal and cancer-related insomnia. However, there is a lack of randomized controlled trials to support the effectiveness of acupuncture on insomnia of hypertension patients. Methods and analysis: This study is a randomized, double-blind (patients and evaluators), and placebo-controlled clinical trial to investigate the effect of acupuncture in hypertension patients’ insomnia management. We will recruit 158 hypertension patients suffering from insomnia in Bao’an People's Hospital, Shenzhen and randomly assign them into treatment group (antihypertensive drugs + acupuncture) and control group (antihypertensive drugs + sham acupuncture) in a 1:1 ratio. The patients will receive acupuncture 3 times a week for 12 weeks, and then a 6-months follow-up will be conducted after the treatment. The primary outcome is the Pittsburgh Sleep Quality Index. The secondary outcomes include sleep parameters, blood pressure dropping, sleeping pill dosage, Rating Depression Scale score, and Self-Rating Anxiety Scale score. The primary outcome will be evaluated at baseline, 4, 8, and 12 weeks, and 1, 3, and 6 months following the end of treatment. The secondary outcomes will be assessed at baseline and 12 weeks of the treatment period.

Purpose: To investigate the protective effects of dexmedetomidine (Dex) on post cardiopulmonary bypass (CPB) lung injury in rats and to explore the possibility of underlying mechanisms involving ph...

Vascular cognitive impairment, no dementia (VCIND) refers to cognitive deficits associated with underlying vascular causes that are insufficient to confirm a diagnosis of dementia. The default mode network (DMN) is a large-scale brain network of interacting brain regions involved in attention, working memory and executive function. The role of DMN white matter integrity in cognitive deficits of VCIND patients is unclear. Using diffusion tensor imaging (DTI), this study was carried out to investigate white matter microstructural changes in the DMN in VCIND patients and their contributions to cognitive deficits. Thirty-one patients with subcortical VCIND and twenty-two healthy elderly subjects were recruited. All patients underwent neuropsychological assessments and DTI examination. Voxel-based analyses were performed to extract fractional anisotropy (FA) and mean diffusivity (MD) measures in the DMN. Compared with the healthy elderly subjects, patients diagnosed with subcortical VCIND presented with abnormal white matter integrity in several key hubs of the DMN. The severity of damage in the white matter microstructure in the DMN significantly correlated with cognitive dysfunction. Mediation analyses demonstrated that DTI values could account for attention, executive and language impairments, and partly mediated global cognitive dysfunction in the subcortical VCIND patients. DMN integrity is significantly impaired in subcortical VCIND patients. The disrupted DMN connectivity could explain the attention, language and executive dysfunction, which indicates that the white matter integrity of the DMN may be a neuroimaging marker for VCIND.

Apoptosis is a cellular mechanism contributing to cardiac surgery using cardiopulmonary bypass (CPB)-induced lung injury. The ubiquitous PI3K/Akt pathway regulates proliferation, apoptosis and differentiation by controlling a broad range of target proteins including NF-κB and GSK-3β. The roles of the PI3K/Akt/NF-κB and PI3K/Akt/GSK-3β pathways in CPB-related lung injury are unclear.Seventy-two male Sprague-Dawley rats were assigned into sham, CPB, Wortmannin (Wtn) and insulin-like growth factor-I (IGF-I) groups (n = 18, each). Six subjects per group were evaluated at each of three time points: Prior to CPB (T1); opening of the left hilus pulmonis (T2); and 90 min after CPB (T3). Arterial blood specimens were obtained at each time point to test respiratory and oxygenation indices. Left lung tissues were processed for HE and TUNEL staining. Western blot was employed to evaluate protein levels and activities of Akt, phospho-Akt (p-Akt), GSK-3β, phospho-GSK-3β (p-GSK-3β) and nuclear NF-κB.Lung ischemia/reperfusion and CPB caused notable lung injury, as evidenced by lung functional decline and pathological deterioration, accompanied by increases in apoptosis and expression levels of p-Akt, p-GSK-3β and nuclear NF-κB in lungs (all P0.05 vs. Sham). At T3, Wtn-treated CPB subjects showed worsened lung function and pathological lung structures, as well as apoptosis in lungs (all P0.05 vs. CPB); additionally, Wtn inhibited Akt phosphorylation and slightly, but significantly increased expression of nuclear NF-κB (both P0.001 vs. CPB). Conversely, treatment of subjects with IGF-I increased Akt phosphorylation (P0.001 vs. CPB), inhibited expression of nuclear NF-κB (P = 0.008 vs. CPB), improved lung function and tissue morphology (both P0.05 vs. CPB), and reduced apoptosis in lungs (P0.001 vs. CPB). Neither Wtn nor IGF-I did alter GSK-3β phosphorylation levels (P = 0.836 and P = 0.669 vs. CPB, respectively).The PI3K/Akt/NF-κB pathway played a role in CPB-related lung injury, possibly through mediating apoptosis in lungs. GSK-3β, a signaling effector that also participated in CPB-induced apoptosis in lungs, but was not regulated by the PI3K/Akt pathway in this context.

Findings on the effect of social status on corruption perception are mixed. To make sense of the mixed results, three studies were conducted to examine whether meritocracy moderates this effect. In Study 1, we measured all variables using a questionnaire-based correlational design. In the preregistered Study 2, we adopted an experimental design in which we manipulated social status using a false feedback paradigm and measured corruption perception and meritocracy. In Study 3, we manipulated meritocracy using a scrambled sentence task and measured its effect on the relationship between social status and corruption perception. The results consistently demonstrated that meritocracy could moderate the influence of social status on corruption perception. Specifically, social status was negatively associated with corruption perception when meritocracy was weak, whereas the association was not significant when meritocracy was strong. Our results suggest that meritocracy critically affects acknowledgment of the pervasiveness of social injustice and even deters the disadvantaged from fighting against corruption.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive dementia. Diffusion tensor imaging (DTI) has been used widely to delineate the white matter integrity/degeneration in AD. Automated fiber quantification (AFQ) method is a fully automated method, which can identify the major white matter fiber tracts and then evaluate the white matter properties. The main purpose of this study is to assess the white matter integrity and abnormities in a cohort of amnestic Mild Cognitive Impairment (aMCI) and AD patients as well as normal controls (NCs). We tested the utility of diffusion tensor imaging measures along white matter tracts as features to classify the AD from NCs using support vector machine. The results showed that we have detected credible and robust potential early biomarker that may be useful for clinical application in AD.

To summarize the effectiveness of Ilizarov technique in the correction of flexion contracture deformity of the knee after burn.Between April 2012 and July 2017, Ilizarov technique was used to treat 14 cases (17 knees) of knee flexion contracture patients. There were 11 males (13 knees) and 3 females (4 knees), with an age of 20-48 years (mean, 37 years). The duration of scar formation was 8 months to 24 years (mean, 5 years). The scar ranged from the upper part of the thigh, down to the middle part of the leg, from both sides to the inside and outside of the popliteal fossa, without ulceration. The area after scar contracture was 12 cm×10 cm to 30 cm×22 cm. Preoperative total activity of motion (TAM) was 30-115° (mean, 69°). There were 4 cases in wheelchair, 5 cases walking with double crutches, 3 cases with limp, and 2 cases with half squat walking. According to the knee function evaluation criteria by QIN Sihe, the preoperative knee function was fair in 3 knees, poor in 5 knees, and very poor in 9 knees.All patients were followed up 6 months to 5 years (mean, 2 years). No local skin necrosis, needle tract infection, limb numbness, and other complications occurred. Knee flexion deformities were all corrected. The postoperative TAM was 70-145° (mean, 125°). All patients were able to walk with plantar weight-bearing, and their gait improved when compared with that before operation. Five cases could walk without a crutch and only slightly claudication after operation. At last follow-up, according to the knee function evaluation criteria, the results were excellent in 9 knees, good in 5 knees, and fair in 3 knees, all were significantly improved when compared with that before operation (Ilizarov technique has the advantages of minimally invasive, safe, and easy to operate for the treatment of flexion contracture deformity of the knee after burn.总结应用 Ilizarov 技术矫正烧伤后膝关节屈曲挛缩畸形的疗效。.2012 年 4 月—2017 年 7 月，应用 Ilizarov 技术治疗 14 例（17 膝）烧伤后膝关节屈曲挛缩畸形患者。男 11 例（13 膝），女 3 例（4 膝）；年龄 20～48 岁，平均 37 岁。瘢痕形成 8 个月～24 年，平均 5 年。瘢痕范围上至大腿上段，下至小腿中段，两侧至腘窝内、外侧，均无破溃。瘢痕挛缩后范围为 12 cm×10 cm～30 cm×22 cm。术前膝关节活动度（total activity of motion，TAM）为 30～115°，平均 69°。患者坐轮椅 4 例，扶双拐行走 5 例，跛行 3 例，半蹲行走 2 例。根据膝关节功能评价标准，术前患者膝关节功能可 3 膝，差 5 膝，很差 9 膝。.患者均获随访，随访时间 6 个月～5 年，平均 2 年。无局部皮肤坏死、针道感染、肢端感觉麻木等并发症发生。膝关节屈曲畸形均获得矫正；TAM 为 70～145°，平均 125°。可足底负重行走，患者步态较术前均有所改善。5 例术后可不扶拐行走，仅轻度跛行；2 例坐轮椅患者术后可扶拐行走。末次随访时根据秦泗河膝关节功能评价标准，优 9 膝、良 5 膝、可 3 膝，较术前显著改善（应用 Ilizarov 技术治疗烧伤后膝关节屈曲挛缩畸形具有微创、安全、操作简便的优点，可获得较好疗效。.

Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by progressive dementia. Diffusion tensor imaging (DTI) has been widely used to show structural integrity and delineate white matter (WM) degeneration in AD. The automated fiber quantification (AFQ) method is a fully automated method that can rapidly and reliably identify major WM fiber tracts and evaluate white matter properties. The main aim of this study was to assess WM integrity and abnormities in a cohort of patients with amnestic mild cognitive impairment (aMCI) and AD as well as normal controls (NCs). For this purpose, we first used AFQ to identify 20 major WM tracts and assessed WM integrity and abnormities in a cohort of patients with 120 participants (39 NCs, 34 aMCI and 47 AD) in the discovery dataset, as well as 122 participants (43 NCs, 37aMCI and 42 AD) in the replicated dataset. Pointwise differences along the WM tracts were identified in the discovery dataset and simultaneously confirmed by the replicated dataset. Next, we investigated the utility of DTI measures along WM tracts as features to classify patients with AD from NCs with multilevel cross validations using a support vector machine. The correlation analysis revealed that the identified impaired microstructural WM alterations and classification output were highly associated with cognitive ability in the patient groups, indicating that this credible, robust potential early biomarker may be useful for clinical application in AD. This systematic study provides a pipeline to examine WM integrity and its potential clinical application in AD and may be useful in studying other neurological and psychiatric disorders. Funding: This work was partially supported by the National Key Research and Development Program of China (No. 2016YFC1305904), the National Natural Science Foundation of China (Grant Nos. 81871438, 81571062, 81471120), and the Strategic Priority Research Program of the Chinese Academy of Sciences (Grant No. XDB32020200). Declaration of Interest: The authors declare no conflicts of interest. Ethical Approval: This study was approved by the Medical Ethics Committee of the Chinese PLA General Hospital.

In the context of rapid social change, the perception of social stratification has far-reaching and complex influences on human psychology and behavior, including citizen participation. The current research explored the interactive influence of social status and subjective social mobility on citizen participation. Two studies used experimental methods to manipulate subjective social mobility and social status, respectively, to examine the interactive effect. Taken together, the results of both studies revealed that the interaction between social status and subjective social mobility had a significant influence on citizen participation: whereas citizen participation with high social status was not affected by subjective social mobility, citizen participation with low social status decreased with increases in subjective social mobility. This research established a combined dynamic and static analysis framework of social stratification structure, elucidating the current status of citizen participation under the influence of the interaction between social status and subjective social mobility, and providing a countermeasure reference for effectively promoting citizen participation.

Convergent evidence has been collected to support that Alzheimer’s disease (AD) is associated with reduction in hippocampal volume based on anatomical magnetic resonance imaging (MRI) and impaired functional connectivity based on functional MRI. Radiomics texture analysis has been previously successfully used to identify MRI biomarkers of several diseases, including AD, mild cognitive impairment and multiple sclerosis. In this study, our goal was to determine if MRI hippocampal textures, including the intensity, shape, texture and wavelet features, could be served as an MRI biomarker of AD. For this purpose, the texture marker was trained and evaluated from MRI data of 48 AD and 39 normal samples. The result highlights the presence of hippocampal texture abnormalities in AD, and the possibility that texture may serve as a neuroimaging biomarker for AD.

Aims Sevoflurane, a widely used inhaled anesthetic, showed valid protective effect against ischemia reperfusion injury in lung, however, the underlying molecular mechanisms has yet to be explained. Materials and methods Dogs were divided into four groups: control group, cardiopulmonary bypass (CPB) group, sevoflurane postconditioning group and wortmannin group. Arterial blood was obtained from each group to test the respiratory index and oxygenation index and pulmonary tissues were sampled for apoptotic TUNEL stain. Western Blot was performed to check the level of Akt, p-Akt and nuclear factor kappa B (NF-κB), while ELISA was performed to determine the protein concentrations of tumor necrosis factor α (TNF-α). Key findings Pharmacological postconditioning with sevoflurane protected dog lung from I/R injury with CPB, improved pulmonary dysfunction, and decreased pneumonocyte apoptosis. Application of wortmannin, a specific inhibitor of PI3K, abolished the protective effects and anti-apoptotic effects of sevoflurane-postcondition. Wortmannin also inhibited the sevoflurane-postcondition-induced phosphorylation of AKT and up-regulated the level of NF-κB and TNF-α. Significance Accordingly, present study demonstrated that PI3K/AKT/NF-κB pathway plays an important role in the protective effect of sevoflurane postconditioning against CPB induced lung injury.