Aerobic Exercise Changes Low-Frequency Functional and Effective Connectivity in Cognitive Load Task.

As is well known, cognitive performances are highly influenced by cognitive load, so it is meaningful to find some ways to effectively reduce the cognitive load. In particular, aerobic exercise is a promising way. However, the neural evidence is still lacking in understanding how aerobic exercise minimizes cognitive load. To solve the problem, this study adopted the N-back task in both the before (BE) and after (AE) aerobic exercise periods, behavioral and EEG data were recorded from 21 participants. Functional connectivity was constructed by the weighted phase lag index (WPLI), and effective connectivity was constructed by the partially directed coherent (PDC). Consequently, by comparing the connection strength and pattern of BE and AE, it is found that in low-frequency (0~8 Hz), aerobic exercise could enhance the connection strength of WPLI networks under high cognitive load, and increase the importance of the forehead region in the communication of PDC networks under low cognitive load. These results could advance our understanding of the underlying mechanisms of how aerobic exercise modulates cognitive load.

Establishment and evaluation of a three-dimensional quantitative analysis method of dental plaque based on intraoral scanner technique.

AIM: Quantitative dental plaque evaluation is necessary for clinical and scientific work. This study aimed to examine the reliability of this 3D image analysis method by digitally analysing the colour 3D images obtained from an intraoral scanner, and then detecting and quantifying the plaque information and comparing it with the clinical examination results. MATERIALS AND METHODS: A total of 140 teeth from 5 subjects with a standard dentition were enrolled in this study, and plaque examination was performed at two different stages: after 24 hours without oral hygiene (T1) and after habitual brushing (T2). At each time point, the Quigley-Hein plaque index of each tooth surface was recorded separately, followed by colour 3D images obtained using an intraoral scanner, and image analysis and calculation using Geomagic Wrap 2021. RESULTS: It was found that the percentage of plaque staining area calculated from the 3D image analysis correlated well with the plaque index recorded during the clinical examination: the Spearman correlation coefficients were 0.9136 and 0.9061 (p<0.001) for all tooth surfaces at T1 and T2, respectively. The measurements of the three investigators were in good agreement, with intraclass correlation coefficients of 0.989 and 0.992 (P<0.001) for the vestibular and lingual surfaces at T1, and 0.964 and 0.983 (P<0.001) for the vestibular and lingual surfaces at T2. CONCLUSION: In this study, we initially developed a digital 3D evaluation system of dental plaque suitable for research and clinical practice and demonstrated its reliability.

miR-497-5p induces apoptosis in K562 cells by downregulating ROCK1.

OBJECTIVE: To validate the role of miR-497-5p in apoptosis in K562 cells by targeting Rho-associated kinase isoform 1 (ROCK1). METHODS: From January, 2017 to February, 2019, 57 patients with chronic myeloid leukemia (CML) treated in our hospital were included in patient group, and 50 healthy individuals were recruited as control group. miR-497-5p level in peripheral blood was quantitated using qRT-PCR. After transfecting with miR-497-5p overexpression vector and ROCK1 inhibitor, K562 cells were monitored in terms of proliferation (CCK8 assay), migration and invasion (Transwell), and apoptosis (flow cytometry). Binding loci between miR-497-5p and ROCK1 were predicted, and the targeting relationship was confirmed (dual-luciferase reporter (DLR) assay). RESULTS: miR-497-5p was poorly expressed in CML (P < 0.05). Forced overexpression of miR-497-5p or inhibition of ROCK1 suppressed malignant processes (proliferation, proliferation, migration and invasion) in K562 cells and induced apoptosis (P < 0.05). DLR assay revealed a decreased luciferase activity after miR-497-5p binding to ROCK1 (P < 0.05). CONCLUSION: miR-497-5p induces apoptosis in K562 cells by downregulating ROCK1.

miR-506 in patients with chronic myeloid leukemia and its effect on apoptosis of K562 cells.

OBJECTIVE: To explore the expression of miR-506 in chronic myeloid leukemia (CML) and its influence on the biological function of CML cells. METHODS: Altogether 84 CML patients from February 2012 to September 2014 were obtained as the observation group (OG), and 71 healthy people were taken as the control group (CG). miR-506 was tested using RT-qPCR, and the 5-year survival of patients with high and low expression of miR-506 was compared with the median value of miR-506 as the limit. ROC curve was applied to detect the value of miR-506 in diagnosing CML and predicting the 5-year survival of patients, and K562 cell line was transfected with miR-506 inhibitor and miR-506 mimic for observing its effects on the cell proliferation and apoptosis. RESULTS: miR-506 in CML patients was evidently lower than that in healthy people, the AUC of diagnosis of miR-506 was 0.883, the total survival of patients with low miR-506 was evidently lower than those with high miR-506, and the AUC of predicted survival of patients was 0.778. The proliferation of cells transfected with miR-506 inhibitor was promoted, the apoptosis and the survival rate reduced. CONCLUSION: miR-506 is evidently reduced in CML, and may be applied as a diagnostic and predictive treatment for CML and 5-year related survival; it can also can hinder the viability of K562 cells and promote apoptosis.

Surgical treatment of carotid artery stent infection: a case report.

The most effective treatment for graft infection is still debated, and the success rate of current treatments is low. We herein report the results of surgical treatment and follow-up of a case of infection acquired during carotid stenting with the aim of exploring the most effective treatments for graft infection. We retrospectively analyzed a patient who was admitted in September 2019. This patient underwent debridement, autologous saphenous vein replacement of the common carotid to internal carotid artery, external carotid artery suturing, and continuous negative-pressure wound therapy for carotid stent infection. Ten days after carotid artery revascularization, the growth of granulation tissue in the incision was good, and we decided to suture the neck incision. Five days after removing the stitches, grade A healing was noted. Furthermore, the carotid artery and autologous vein grafts were unobstructed as shown by carotid artery computed tomography angiography reexamination. The patient was monitored for 8 months with no new neurological symptoms and good healing of the incision. Effective treatment of vascular graft infection includes debridement and removal of the infected graft, autologous vein graft revascularization, and negative-pressure wound therapy combined with antibiotic therapy.

Depletion of CPEB1 protects against oxidized LDL-induced endothelial apoptosis and inflammation though SIRT1/LOX-1 signalling pathway.

Atherosclerosis (AS) is a chronic inflammatory disease that results from Oxidized low-density lipoprotein (Ox-LDL) induced endothelial dysfunction. Cytoplasmic polyadenylation element binding protein 1 (CPEB1) is closely related to the development of epithelial cells, but the role of CPEB1 in AS remains unknown. The RNA and protein levels of CPEB1 expression are increased by Ox-LDL exposure, which is abrogated by c-Jun amino-terminal kinase (JNK) inhibitor SP600125. CPEB1 small interfering RNA (siRNA) suppressed the oxidative stress, inflammation, and apoptosis. Furthermore, CPEB1 siRNA enhanced the sirtuin 1 (SIRT1) transcription levels in Ox-LDL-treated HUVECs. Co-Immunoprecipitation (Co-IP) assay showed that CPEB1 siRNA declined the ubiquitination of SIRT1, and SIRT1 siRNA enhanced the Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), which were decreased by CPEB1 siRNA. In addition, LOX-1 and SIRT1 attenuated the protection of SIRT1 siRNA on Ox-LDL-induced oxidative stress. Therefore, our study revealed that CPEB1 depletion might play an anti-inflammatory and antiapoptotic role in Ox-LDL-induced apoptosis and inflammation though SIRT1/LOX-1 signalling pathway.