Atypical characteristic changes of surface morphology and structural covariance network in developmental dyslexia.

BACKGROUND: Developmental dyslexia (DD) is a neurodevelopmental disorder that is characterized by difficulties with all aspects of information acquisition in the written word, including slow and inaccurate word recognition. The neural basis behind DD has not been fully elucidated. METHOD: The study included 22 typically developing (TD) children, 16 children with isolated spelling disorder (SpD), and 20 children with DD. The cortical thickness, folding index, and mean curvature of Broca's area, including the triangular part of the left inferior frontal gyrus (IFGtriang) and the opercular part of the left inferior frontal gyrus, were assessed to explore the differences of surface morphology among the TD, SpD, and DD groups. Furthermore, the structural covariance network (SCN) of the triangular part of the left inferior frontal gyrus was analyzed to explore the changes of structural connectivity in the SpD and DD groups. RESULTS: The DD group showed higher curvature and cortical folding of the left IFGtriang than the TD group and SpD group. In addition, compared with the TD group and the SpD group, the structural connectivity between the left IFGtriang and the left middle-frontal gyrus and the right mid-orbital frontal gyrus was increased in the DD group, and the structural connectivity between the left IFGtriang and the right precuneus and anterior cingulate was decreased in the DD group. CONCLUSION: DD had atypical structural connectivity in brain regions related to visual attention, memory and which might impact the information input and integration needed for reading and spelling.

Establishment and study of a rat internal haemorrhoid model.

To establish a relatively stable internal haemorrhoid model in rats. A total of 48 SPF SD rats were selected and randomly divided into a blank group of 16 and a model group of 32. The model was created by croton oil-mixed liquid stimulation combined with standing and swimming experiments, and the modelling times were 1 week and 2 weeks, respectively. By observing the symptoms and signs of rats, pathological morphology and immunohistochemical staining of anorectal tissue, anorectal laser speckle blood-flow imaging and defecation contrast, etc., the effect of different modelling times was evaluated. The stability of the model was evaluated after feeding for 2 weeks. Both model-formation times caused rats to produce local symptoms of tissue bulging in the haemorrhoid area. Microscopy showed that the rectal submucosal interstitial blood vessels were dilated, and inflammatory cell infiltration and other manifestations were observed. Laser speckle blood-flow imaging revealed increased anorectal blood perfusion and capillary dilatation, and defecography showed a longitudinal and continuous rectal mucosa. After 2 weeks of normal feeding, lifting of the haemorrhoidal tissue was still present. The effect of modelling for 1 week was most in line with the clinical manifestations of internal haemorrhoids. The 1-week modelling scheme in this study can effectively establish a rat internal haemorrhoid model that closely approximates clinical internal haemorrhoid symptoms and pathological manifestations. The operation is simple, the success rate is high, and the model has certain stability. This model can be used as an important basis for studying various treatment methods for internal haemorrhoids.

Automatic brain extraction for rat magnetic resonance imaging data using U2-Net.

Objective.Skull stripping is a key step in the pre-processing of rodent brain magnetic resonance images (MRI). This study aimed to develop a new skull stripping method via U2-Net, a neural network model based on deep learning method, for rat brain MRI.Approach.In this study, 599 rats were enrolled and U2-Net was applied to segment MRI images of rat brain. The intercranial tissue of each rat was manually labeled. 476 rats (approximate 80%) were used for training set while 123 rats (approximate 20%) were used to test the performance of the trained U2-Net model. For evaluation, the segmentation result by the U2-Net model is compared with the manual label, and traditional segment methods. Quantitative evaluation, including Dice coefficient, Jaccard coefficient, Sensitivity, Specificity, Pixel accuracy, Hausdorff coefficient, True positive rate, False positive rate and the volumes of whole brain, were calculated to compare the segmentation results among different models.Main results.The U2-Net model was performed better than the software of RATS and BrainSuite, in which the quantitative values of training U2-Net model were 0.9907 ± 0.0016 (Dice coefficient), 0.9816 ± 0.0032 (Jaccard coefficient), 0.9912 ± 0.0020 (Sensitivity), 0.9989 ± 0.0002 (Specificity), 0.9982 ± 0.0003 (Pixel accuracy), 5.2390 ± 2.5334 (Hausdorff coefficient), 0.9902 ± 0.0025 (True positive rate), 0.0009 ± 0.0002(False positive rate) respectively.Significance.This study provides a new method that achieves reliable performance in rat brain skull stripping of MRI images, which could contribute to the processing of rat brain MRI.

Cephalic electroacupuncture restores learning and memory in rats with induced ischemic stroke via inhibition of NF-κB nuclear translocation.

Inflammatory responses in the brain contribute to cognitive deficits. Nuclear factor-κB (NF-κB), a critical transcription factor in inflammatory responses, is activated in post-stroke cognitive deficit. Baihui (DU20) and Shenting (DU24) acupoints, the main acupoints of Du Meridian, are widely used to improve cognitive deficits in Chinese patients with stroke. It has been reported that post-stroke cognitive deficits can be treated by electroacupuncture (EA) but the underlying mechanisms of these effects are unclear. Using the rat middle cerebral artery occlusion cerebral ischemia-reperfusion injury model, we found that EA at these 2 acupoints improved neurological function, decreased cerebral infarct lesion volumes, and ameliorated the inflammatory response in the hippocampal CA1 region. The treatment also ameliorated memory and learning deficits by inhibiting the NF-κB signaling pathway in the ischemic hippocampal CA 1 region. This coincided with downregulation of interleukin-1ß, interleukin-6, CD45, and tumor necrosis factor-α. We conclude that EA at these 2 acupoints ameliorates memory and learning deficits following experimental cerebral infarction by inhibiting NF-κB-mediated inflammatory injury in the hippocampal CA1 region.

The current status and trend of the functional magnetic resonance combined with stimulation in animals.

As a non-radiative, non-invasive imaging technique, functional magnetic resonance imaging (fMRI) has excellent effects on studying the activation of blood oxygen levels and functional connectivity of the brain in human and animal models. Compared with resting-state fMRI, fMRI combined with stimulation could be used to assess the activation of specific brain regions and the connectivity of specific pathways and achieve better signal capture with a clear purpose and more significant results. Various fMRI methods and specific stimulation paradigms have been proposed to investigate brain activation in a specific state, such as electrical, mechanical, visual, olfactory, and direct brain stimulation. In this review, the studies on animal brain activation using fMRI combined with different stimulation methods were retrieved. The instruments, experimental parameters, anesthesia, and animal models in different stimulation conditions were summarized. The findings would provide a reference for studies on estimating specific brain activation using fMRI combined with stimulation.

Aberrant pattern of regional cerebral blood flow in mild cognitive impairment: A meta-analysis of arterial spin labeling magnetic resonance imaging.

In mild cognitive impairment (MCI), cognitive decline is associated with abnormal changes of cerebral blood flow (CBF). Arterial spin labeling magnetic resonance imaging (ASL-MRI) is an effective method for assessing regional cerebral blood flow (rCBF). However, the CBF estimated via ASL-MRI in MCI often differs between studies, and the consistency of CBF changes in MCI is unclear. In this study, 13 ASL-MRI studies with 495 MCI patients and 441 health controls were screened out from PubMed, Embase, Cochrane, Web of Science, Wanfang, and CNKI. An activation likelihood estimation (ALE) meta-analysis was performed to explore the brain regions with abnormal CBF in MCI. It showed that the decreased CBF in MCI was identified in the precuneus, inferior parietal lobule (IPL), superior occipital gyrus (SOG), middle temporal gyrus (MTG), and middle occipital gyrus (MOG), while the increased CBF in MCI was identified in the lentiform nucleus (LN) compared with healthy controls. The study characterized the abnormal pattern of regional CBF in MCI, which would promote our knowledge of MCI and might be used as a biomarker in clinic. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=259633.

Corrigendum: Swimming attenuates muscle wasting and mediates multiple signaling pathways and metabolites in CT-26 bearing mice.

[This corrects the article DOI: 10.3389/fmolb.2021.812681.].

Effect of Physical Activity on Cognitive Impairment in Patients With Cerebrovascular Diseases: A Systematic Review and Meta-Analysis.

Background and Purpose: This study investigates the effect of physical activity (PA) on cognition in patients with cerebrovascular disease and explored the maximum benefit of different PA characteristics. Methods: Databases, such as Pubmed, Web of Science, Embase, and Cochrane Library, were searched from their inception to May 31, 2021. Standardized mean difference (SMD) and 95% confidence intervals (CIs) were calculated to generate a forest plot. In addition, subgroup analysis, moderation analysis, and regression analysis were performed to explore the possible adjustment factors. Results: In total, 22 studies that met the criteria were included, demonstrating data from 1,601 participants. The results indicated that PA produced a positive effect on the global cognition for patients with cerebrovascular disease (SMD: 0.20 [95% CI: 0.12-0.27]), at the same time, PA training prominently improved executive function (SMD: 0.09 [95% CI: 0.00-0.17]) and working memory (SMD: 0.25 [95% CI: 0.10-0.40]). Furthermore, patients with baseline cognitive impairment received the greater benefit of PA on cognition (SMD: 0.24 [95% CI: 0.14-0.34]) than those without cognitive impairment before intervention (SMD: 0.15 [95% CI: 0.04-0.26]). For patients in the acute stage (≤ 3 months), PA did not rescue impairment dysfunction significantly (SMD: 0.08 [95% CI: -0.04-0.21]) and remarkable cognitive gains were detected in the chronic stage of participants (>3 months) (SMD: 0.25 [95% CI: 0.16-0.35]). Moderate intensity PA showed a larger pooled effect size (SMD: 0.23 [95% CI: 0.11-0.36]) than low intensity (SMD: -0.01 [95% CI: -0.44-0.43]) and high intensity (SMD: 0.16 [95% CI: 0.03-0.29]). However, the different types, duration, and frequency of PA resulted in no differences in the improvement of cognitive function. Further regression analysis demonstrated that the beneficial effects of PA on cognition are negatively correlated with age (p < 0.05). Conclusions: This study revealed that PA can prominently improve the cognitive ability in patients with cerebrovascular diseases and strengthened the evidence that PA held promise as a widely accessible and effective non-drug therapy for vascular cognitive impairment (VCI).

Swimming attenuates tumor growth in CT-26 tumor-bearing mice and suppresses angiogenesis by mediating the HIF-1α/VEGFA pathway.

Low physical activity correlates with increased cancer risk in various cancer types, including colorectal cancer (CRC). However, the ways in which swimming can benefit CRC remain largely unknown. In this study, mice bearing tumors derived from CT-26 cells were randomly divided into the control and swimming groups. Mice in the swimming group were subjected to physical training (swimming) for 3 weeks. Compared with the control group, swimming clearly attenuated tumor volume and tumor weight in CT-26 tumor-bearing mice. RNA sequencing (RNA-seq) identified 715 upregulated and 629 downregulated transcripts (including VEGFA) in tumor tissues of mice in the swimming group. KEGG pathway analysis based on differentially expressed transcripts identified multiple enriched signaling pathways, including angiogenesis, hypoxia, and vascular endothelial growth factor (VEGF) pathways. Consistently, IHC analysis revealed that swimming significantly downregulated CD31, HIF-1α, VEGFA, and VEGFR2 protein expression in tumor tissues. In conclusion, swimming significantly attenuates tumor growth in CT-26 tumor-bearing mice by inhibiting tumor angiogenesis via the suppression of the HIF-1α/VEGFA pathway.

Electroacupuncture Ameliorates Cognitive Impairment Through the Inhibition of NLRP3 Inflammasome Activation by Regulating Melatonin-Mediated Mitophagy in Stroke Rats.

Previous studies found that electroacupuncture (EA) at the Shenting (DU24) and Baihui (DU20) acupoints alleviates cognitive impairment in cerebral ischemia-reperfusion (I/R) injury rats. Nonetheless, the mechanisms of the anti-inflammatory effects of EA are unclear. Cerebral I/R injury was induced in rats by middle cerebral artery occlusion (MCAO). Following I/R injury, the rats underwent EA therapy at the Shenting (DU24) and Baihui (DU20) acupoints for seven successive days. The Morris water maze test, magnetic resonance imaging (MRI) and molecular biology assays were utilized to assess the establishment of the rat stroke model with cognitive impairment and the therapeutic effect of EA. EA treatment of rats subjected to MCAO showed a significant reduction in infarct volumes accompanied by cognitive recovery, as observed in Morris water maze test outcomes. The possible mechanisms by which EA treatment attenuates cognitive impairment are by regulating endogenous melatonin secretion through aralkylamine N-acetyltransferase gene (AANAT, a rate-limiting enzyme of melatonin) synthesis in the pineal gland in stroke rats. Simultaneously, through melatonin regulation, EA exerts neuroprotective effects by upregulating mitophagy-associated proteins and suppressing reactive oxygen species (ROS)-induced NLRP3 inflammasome activation after I/R injury. However, melatonin receptor inhibitor (luzindole) treatment reversed these changes. The findings from this research suggested that EA ameliorates cognitive impairment through the inhibition of NLRP3 inflammasome activation by regulating melatonin-mediated mitophagy in stroke rats.

Taurine supplementation improves hippocampal metabolism in immature rats with intrauterine growth restriction (IUGR) through protecting neurons and reducing gliosis.

Taurine as an essential amino acid in the brain could play an important role in protecting the fetal brain of intrauterine growth restriction (IUGR). The hippocampus with IUGR showed neural metabolic disorder and structure changed that affected memory and learning ability. This study was aimed to identify the effect of taurine supplementation on the metabolism alterations and cellular composition changes of the hippocampus in IUGR immature rats. Metabolite concentrations were determined by magnetic resonance spectroscopy (MRS) in the hippocampus of juvenile rats with IUGR following taurine supplementation with antenatal or postnatal supply. The composition of neural cells in the hippocampus was observed by immunohistochemical staining (IHC) and western blotting (WB). Antenatal taurine supplementation increased the ratios of N-acetylaspartate (NAA) /creatine (Cr) and glutamate (Glu) /Cr of the hippocampus in the IUGR immature rats, but reduced the ratios of choline (Cho) /Cr and myoinositol (mI) /Cr. At the same time, the protein expression of NeuN in the IUGR rats was increased through intrauterine taurine supplementation, and the GFAP expression was reduced. Especially the effect of antenatal taurine was better than postpartum. Furthermore, there existed a positive correlation between the NAA/Cr ratio and the NeuN protein expression (R = 0.496 p < 0.001 IHC; R = 0.568 p < 0.001 WB), the same results existed in the relationship between the mI/Cr ratio and the GFAP protein expression (R = 0.338 p = 0.019 IHC; R = 0.440 p = 0.002 WB). Prenatal taurine supplementation can better improve hippocampal neuronal metabolism by increasing NAA / Cr ratio related to the number of neurons and reducing Cho / Cr ratio related to the number of glial cells.

Meta-Analysis of Neurochemical Changes Estimated via Magnetic Resonance Spectroscopy in Mild Cognitive Impairment and Alzheimer's Disease.

The changes of neurochemicals in mild cognitive impairment (MCI) and Alzheimer's disease (AD) patients has been observed via magnetic resonance spectroscopy in several studies. However, whether it exists the consistent pattern of changes of neurochemicals in the encephalic region during the progression of MCI to AD were still not clear. The study performed meta-analysis to investigate the patterns of neurochemical changes in the encephalic region in the progress of AD. We searched the PubMed, Embase, Cochrane Library, and Web of Science databases, and finally included 63 studies comprising 1,086 MCI patients, 1,256 AD patients, and 1,907 healthy controls. It showed that during the progression from MCI to AD, N-acetyl aspartate (NAA) decreased continuously in the posterior cingulate (PC) (SMD: -0.42 [95% CI: -0.62 to -0.21], z = -3.89, P < 0.05), NAA/Cr (creatine) was consistently reduced in PC (SMD: -0.58 [95% CI: -0.86 to -0.30], z = -4.06, P < 0.05) and hippocampus (SMD: -0.65 [95% CI: -1.11 to -0.12], z = -2.44, P < 0.05), while myo-inositol (mI) (SMD: 0.44 [95% CI: 0.26-0.61], z = 4.97, P < 0.05) and mI/Cr (SMD: 0.43 [95% CI: 0.17-0.68], z = 3.30, P < 0.05) were raised in PC. Furthermore, these results were further verified by a sustained decrease in the NAA/mI of PC (SMD: -0.94 [95% CI: -1.24 to -0.65], z = -6.26, P < 0.05). Therefore, the levels of NAA and mI were associated with the cognitive decline and might be used as potentially biomarkers to predict the possible progression from MCI to AD. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42020200308.

Electroacupuncture Attenuates Ischemic Brain Injury and Cellular Apoptosis via Mitochondrial Translocation of Cofilin.

OBJECTIVE: To investigate the potential mechanisms of electroacupuncture (EA) to prevent ischemic stroke. METHODS: The method of middle cerebral artery occlusion (MCAO) was employed to establish a rat model of ischemic stroke. Seventy-eight Sprague-Dawley rats were divided into the sham group, MCAO + EA control (EC) group, and MCAO + EA (EA) group according to a random number table (n=26 per group). EA was applied to the acupoints of Baihui (DU 20) and Shenting (DU 24) 5 min and 6 h, respectively after the onset of MCAO. Rats in the sham and EC groups received only light isoflurane anesthesia for 30 min after MCAO. The neuroprotective effects of EA were evaluated by rota-rod test, neurological deficit scores and infarct volumes. Additionally, Nissl staining and immunostaining were performed to examine brain damage, rod formation, cellular apoptosis, and neuronal loss induced by ischemia. The activities of caspase-3, and expression levels of cofilin and p-cofilin in mitochondria and cytoplasm after ischemic injury were determined by Western blot. RESULTS: Compared with the EC group, EA significantly improved neuromotor function and cognitive ability after ischemic stroke (P<0.05 or P<0.01). Therapeutic use of EA also resulted in a significant decrease of cofilin rod formation and microtubule-associated protein-2 (MAP2) degradation in the cortical penumbra area compared with the EC rats (P<0.01). Furthermore, Western blot analysis showed that EA stimulation significantly inhibited mitochondrial translocation of cofilin and caspase-3 cleavage (P<0.05 or P<0.01). Additionally, brain damage (infarct volume and neuropathy), cellular apoptosis and neuronal loss induced by ischemia were remarkably suppressed by EA in the cortical penumbra of rats (P<0.05 or P<0.01). CONCLUSION: EA treatment after ischemic stroke may attenuate ischemic brain injury and cellular apoptosis through the regulation of mitochondrial translocation of cofilin, a novel mechanism of EA therapy.

Swimming Attenuates Muscle Wasting and Mediates Multiple Signaling Pathways and Metabolites in CT-26 Bearing Mice.

Objectives: To investigate the effects of swimming on cancer induced muscle wasting and explore its underlying mechanism in CT-26 bearing mice. Methods: BALB/c mice (n = 16) injected with CT-26 cells were divided into two groups, including Tumor group (n = 8) and Swimming group (n = 8). Another 8 un-injected mice were set as Control group. Mice in Swimming group were subjected to physical training for swimming twice per day for 30 min intervals and 6 days per week for a total of 4 weeks. The tumor volume was monitored every 3 days and tumor weight was measured at the end of experiment. The changes of muscle function, pathological and cell apoptosis of quadriceps muscles were further assessed, and its underlying mechanisms were further explored using multiple biological technologies. Results: Swimming obviously alleviated tumor volume and weight in CT-26 bearing mice. Moreover, swimming attenuated the decrease of muscle tension, autonomic activities, and increase of muscle atrophy, pathological ultrastructure, as well as cell apoptosis of quadriceps muscles in CT-26 bearing mice. Furthermore, swimming significantly down-regulated the protein expression of NF-κB, p-NF-κB, TNF-α, IL-1ß, IL-6 and Bax, while up-regulated the expression of Bcl-2. Further differential expressed metabolites (DEMs) analysis identified a total of 76 (in anion mode) and 330 (in cationic mode) DEMs in quadriceps muscles of CT-26 bearing mice after swimming, including taurochenodeoxycholic acid, taurocholic acid, ascorbic acid and eicosapentaenoic acid. Conclusion: Swimming attenuates tumor growth and muscle wasting, and by suppressing the activation of NF-κB signaling pathway mediated inflammation, reducing the level of Bax medicated cell apoptosis, as well as modulating multiple metabolites might be the importantly underlying mechanisms.

Electroacupuncture promotes motor function and functional connectivity in rats with ischemic stroke: an animal resting-state functional magnetic resonance imaging study.

BACKGROUND: To evaluate whether electroacupuncture (EA) treatment at LI11 and ST36 could reduce motor impairments and enhance brain functional recovery in a rat model of ischemic stroke. METHODS: A rat model of middle cerebral artery occlusion (MCAO) was established. EA at LI11 and ST36 was started at 24 h (MCAO + EA group) after ischemic stroke modeling. Untreated model (MCAO) and sham-operated (Sham) groups were included as controls. The neurological deficits of all groups were assessed using modified neurologic severity scores (mNSS) at 24 h and 14 days after MCAO. To further investigate the effect of EA on infarct volume and brain function, functional magnetic resonance imaging was used to estimate the size of the brain lesions and neural activities of each group at 14 days after ischemic stroke. RESULTS: EA treatment of MCAO rats led to a significant reduction in the infarct volumes accompanied by functional recovery, reflected in improved mNSS outcomes and motor functional performances. Furthermore, functional connectivity between the left motor cortex and left cerebellum posterior lobe, right motor cortex, left striatum and bilateral sensory cortex were decreased in MCAO group but increased after EA treatment. CONCLUSION: EA at LI11 and ST36 could enhance the functional connectivity between the left motor cortex and the motor function-related brain regions, including the motor cortex, sensory cortex and striatum, in rats. EA exhibits potential as a treatment for ischemic stroke.

Tougu Xiaotong capsule exerts a therapeutic effect by improving knee meniscus in the early osteoarthritis rat model.

The aim of the study was to observe the effects of Tougu Xiaotong capsule (TGXTC) on the microstructure and ultrastructure of meniscus in rats with early knee osteoarthritis (KOA). A total of 27 Sprague Dawley rats were randomly divided into three groups: The normal group (non-papain-induced KOA; received saline only), the model group (papain-induced KOA; received saline only) and the TGXTC group [papain-induced KOA; received TGXTC (0.31g·kg-1·d-1)]. After 4 weeks treatment, the animals were anesthetized and the sagittal plane of the intact knees (n=6 per group) was obtained and prepared in paraffin section. Following hematoxylin and eosin staining, the degeneration of cartilage structure was evaluated via Mankin score, the microstructure of meniscus was observed and the area of calcification in meniscus was analyzed. Following toluidine blue staining, the content of proteoglycan in meniscus was analyzed. Three samples in each group were obtained and the ultrathin sections of meniscus were observed through a transmission electron microscope. The results showed that compared with the normal group, in the model group the joint space became narrow and the cartilage layer was slightly damaged and the Mankin score was 4.17±0.76, suggesting that the early KOA model was successfully established. After TGXTC treatment, the joint space stenosis and cartilage damage were improved as the Mankin score significantly decreased. Compared with the normal group, in the model group the surface of meniscal cartilage was much more uneven, the area of calcification was significantly increased and the content of proteoglycan of cartilage matrix was significantly decreased. However, following TGXTC treatment, the surface of the meniscal cartilage was much more smooth and flat, and the damage of tissue structure and the calcified area were significantly reduced, and the proteoglycan of cartilage matrix content was significantly increased. Compared with the normal group, the number of cellular processes and organelles, including the rough endoplasmic reticulum, mitochondria and Golgi apparatus of meniscal cartilage were reduced and swollen in the model group. In addition, the nuclei were deformed and heterochromatin agglutinated. The extracellular collagen fibrils became slender, disordered and sparse. Compared with the model group, the TGXTC group had more cell processes and organelles, alleviated swelling and heterochromatin agglutinating. Additionally, the collagen fibrils around the cells were thicker, larger and arranged in an orderly manner. In conclusion, TGXTC exerted its therapeutic effects on the development of KOA via reducing the destruction of the cartilage structure of the meniscus and improving the composition and function of the meniscus cartilage matrix.

Visualization of cortical cerebral blood flow dynamics during craniotomy in acute subdural hematoma using laser speckle imaging in a rat model.

Mass evacuation with decompressive craniotomy is considered a standard intervention for acute subdural hematoma (ASDH). However, hemispheric swelling complicates the intraoperative and postoperative management of ASDH patients, and previous studies have revealed that this approach can damage ischemic/reperfusion (I/R) injury. Few studies have focused on the cerebrovascular response following traumatic brain injury (TBI). To characterize the relative cerebral blood flow (rCBF) before and after removal of the hematoma, rats were injured by a subdural infusion of 400 µL of venous blood or paraffin oil. MRI scans were performed. Then, we monitored cortical rCBF during hematoma removal in real time using laser speckle imaging (LSCI) in ASDH rats. The CBF of arteriovenous and capillary regions were quantified and normalized to their own baseline values via a custom algorithm. In the sham group, the cortical CBF was higher post-craniotomy than pre-craniotomy. However, in the hematoma injection group, the CBF of arteries and capillaries was higher while the venous CBF was lower post-craniotomy than pre-craniotomy. The difference in the changes in vein CBF that occurred between the two groups was statistically significant. The three components of the vascular system showed heterogeneous responses to craniotomy, which may be the basis for secondary brain injury.

[Retracted] Differential miRNAomics of the synovial membrane in knee osteoarthritis induced by bilateral anterior cruciate ligament transection in rats.

Following the publication of the above article, a number of errors were identified in the paper, and after having consulted with the editor of Molecular Medicine Reports, a corrigendum was published last year ("[Corrigendum] Differential miRNAomics of the synovial membrane in knee osteoarthritis induced by bilateral anterior cruciate ligament transection in rats." Zhou J, Zhao Y, Wu G, Lin B, Li Z and Liu X. Mol Med Rep 20: 5363, 2019). However, following publication of the above corrigendum, the paper was re­examined by the authors, and additional errors were identified; therefore, the authors are going to retract this paper from the publication. All the authors agree to this retraction, and apologize to the Editor of Molecular Medicine Reports and to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 18: 4051­4057, 2018; DOI: 10.3892/mmr.2018.9385].

Electroacupuncture ameliorates learning and memory deficits via hippocampal 5-HT1A receptors and the PKA signaling pathway in rats with ischemic stroke.

Hippocampal 5-HT1A receptors and the PKA signaling pathway have been implicated in learning and memory. This study aimed to investigate whether PKA signaling mediated by 5-HT1A receptors was involved in the electroacupuncture (EA)-mediated learning and memory in a rat model of middle cerebral artery occlusion-induced cognitive deficit (MICD). Compared to no treatment or non-acupoint EA treatment, EA at DU20 and DU24 acupoints improved the neurological deficit of scores, shortened escape latency and increased the frequency of crossing the platform in the Morris water maze test. T2-weighted imaging demonstrated that the MICD rat brain lesions were mainly located in the cortex and hippocampus, and injured volumes were reduced after EA. Furthermore, we found that these behavioral changes were concomitant with the deficit of the 5HT1A and PKA signaling pathways in the hippocampus, as the activation of the 5-HT1A receptor, the reduction of PKA kinase activity, and AMPA and NMDA receptor phosphorylation occurred in the injured hippocampus at Day 14 after MICD. Additionally, EA dramatically elevated the activation of PKA. Moreover, EA significantly increased intracellular calcium concentrations regulated by the activation of NMDA receptors. Therefore, PKA kinase and NMDA receptors mediated by 5-HT1A receptors in the hippocampus might contribute to improving learning and memory during the recovery process following ischemic stroke with an EA intervention.