An automated detection of epileptic seizures EEG using CNN classifier based on feature fusion with high accuracy.

BACKGROUND: Epilepsy is a neurological disorder that is usually detected by electroencephalogram (EEG) signals. Since manual examination of epilepsy seizures is a laborious and time-consuming process, lots of automatic epilepsy detection algorithms have been proposed. However, most of the available classification algorithms for epilepsy EEG signals adopted a single feature extraction, in turn to result in low classification accuracy. Although a small account of studies have carried out feature fusion, the computational efficiency is reduced due to too many features, because there are also some poor features that interfere with the classification results. METHODS: In order to solve the above problems, an automatic recognition method of epilepsy EEG signals based on feature fusion and selection is proposed in this paper. Firstly, the Approximate Entropy (ApEn), Fuzzy Entropy (FuzzyEn), Sample Entropy (SampEn), and Standard Deviation (STD) mixed features of the subband obtained by the Discrete Wavelet Transform (DWT) decomposition of EEG signals are extracted. Secondly, the random forest algorithm is used for feature selection. Finally, the Convolutional Neural Network (CNN) is used to classify epilepsy EEG signals. RESULTS: The empirical evaluation of the presented algorithm is performed on the benchmark Bonn EEG datasets and New Delhi datasets. In the interictal and ictal classification tasks of Bonn datasets, the proposed model achieves an accuracy of 99.9%, a sensitivity of 100%, a precision of 99.81%, and a specificity of 99.8%. For the interictal-ictal case of New Delhi datasets, the proposed model achieves a classification accuracy of 100%, a sensitivity of 100%, a specificity of 100%, and a precision of 100%. CONCLUSION: The proposed model can effectively realize the high-precision automatic detection and classification of epilepsy EEG signals. This model can provide high-precision automatic detection capability for clinical epilepsy EEG detection. We hope to provide positive implications for the prediction of seizure EEG.

[Mechanism of puerarin reversing SH-SY5Y cell injury induced by Aß_(1-42) based on proteomics].

Puerarin has the anti-Alzheimer's disease (AD) activity,which can reverse nerve injury induced by Aßand inhibit neuronal apoptosis.However,its potential pharmacodynamic mechanism still needs to be further researched.The occurrence and development of AD is due to the change of multiple metabolic links in the body,which leads to the destruction of balance.Puerarin may act on multiple targets and multiple metabolic processes to achieve therapeutic purposes.Quantitative proteomic analysis provides a new choice to understand the mechanism as completely as possible.This research adopted SH-SY5Y cells induced by Aß_(1-42)to establish AD cell model,and Aßimmunofluorescence detection showed that Aßdecreased significantly after puerarin intervention.The mechanism of puerarin reversing SH-SY5Y cell injured by Aß_(1-42)was further explored by using label-free non-labeled quantitative technology and Western blot detection based on bioinformatics analysis result.The results showed that most of the differential proteins were related to biological processes such as cellular component organization or biogenesis,cellular component organization and cellular component biogenesis,and they mainly participated in the top ten pathways of P value such as pathogenic Escherichia coli infection,m TOR signaling pathway,regulation of autophagy,regulation of actin cytoskeleton,spliceosome,hepatocellular carcinoma,tight junction,non-small cell lung cancer,apoptosis and gap junction.Annexin V/PI flow cytometry and TUNEL were used to detect apoptosis,and the results showed that Aßdecreased significantly and the rate of apoptosis decreased significantly after puerarin intervention.Western blot analysis found that the protein expression level of autophagy related protein LC3Ⅱwas up-regulated after Aßinduction,and the degree of this up-regulation was further enhanced in puerarin intervention group.The trend of the ratio of LC3Ⅱ/LC3Ⅰamong groups was the same as the protein expression level of LC3Ⅱ，the protein expression level of p62 in the control group,AD model group and puerarin intervention group decreased successively.Protein interaction network analysis showed that CAP1 was correlated with TUBA1B,HSP90AB2P,DNM1L,TUBA1A and ERK1/2,and the correlation between CAP1 and ERK1/2 was the highest among them.Western blot showed that the expressions of p-ERK1/2,Bax and CAP1 were significantly down-regulated and the protein expression level of Bcl-2 was significantly up-regulated after puerarin intervention.Therefore,puerarin might improve the SH-SY5Y cells injured by Aß_(1-42)through the interaction of multiple biological processes and pathways in cells multiple locations,and CAP1 might play an important role among them.

Development and characterization of 16 novel microsatellite markers by Transcriptome sequencing for Angelica dahurica and test for cross-species amplification.

BACKGROUND: Angelica dahurica (Apiaceae) is an important herb in traditional Chinese medicine. Because of its important medicinal and economic values, its wild resources were over-exploited and increasingly reduced. Meanwhile, the diversity of cultivars of A. dahurica has decreased as a result of long-term artificial cultivation. However, there are no population genetics studies of natural A. dahurica reported yet, especially for using microsatellite markers (SSRs) to investigate population genetics of the species. RESULTS: Sixteen polymorphic EST-SSR loci were isolated from A. dahurica with transcriptome sequencing technology (RNA-Seq). The number of alleles varied from 2 to 15 per polymorphic locus over populations with the observed and expected heterozygosities ranging from 0.000 to 1.000 and from 0.000 to 0.829, respectively. Significant deviations from Hardy-Weinberg equilibrium were observed at 8 loci. Tests of linkage disequilibrium showed 11 informative locus pairs were significant across all populations. Cross-species amplification showed that 14 out of 16 SSR loci have the transferability in cultivar-A. dahurica cv. 'Hangbaizhi' and A. decursiva. CONCLUSIONS: The 16 newly developed loci microsatellite primers with RNA-Seq will be useful for further investigating population genetics of A. dahurica, cultivars and other members of this genus.

miR-378a Modulates Macrophage Phagocytosis and Differentiation through Targeting CD47-SIRPα Axis in Atherosclerosis.

BACKGROUND: Signal regulatory protein alpha (SIRPa) is an essential signalling molecule that modulates inflammatory responses in macrophages. However, the regulation of SIRPs and its dynamic changes in macrophages under inflammatory stimulation in atherosclerosis remain uncertain. OBJECTIVE: The study aimed to identify the miRNAs that regulate SIRPa transcription and their roles in modulating phagocytosis, differentiation and cholesterol efflux in macrophages. METHODS: ApoE knockout mice were fed with a high-fat diet for 12 weeks. Intimal lesion areas and lipid accumulation were assessed by haematoxylin and eosin (HE) and oil red O staining. The expression of mRNAs/miRNAs was assessed by RNA-seq (RNA sequencing) and RT-qPCR (real-time quantitative polymerase chain reaction). The identification of miR-378a associated with SIRPa regulation in macrophages induced by ox-LDL was confirmed by RT-qPCR and Western blot. The phagocytosis and differentiation of macrophages were detected to figure out the role of miR-378a and SIRPa. RESULTS: SIRPa was proved to be a target of miR-378a. Reduced miR-378a can promote the expression of SIRPa. RNA-seq data showed that the levels of mRNA associated with macrophage phenotypes and SIRPa-CD47 axis were increasing significantly with a decreasing phagocytic phenotype in ApoE-/- mice vs wild-type (WT) mice (P < 0.01). The level of miR-378a was reduced in the aorta of ApoE-/- mice vs WT mice. The experiment in vitro showed that overexpression of miR-378a in macrophages decreased the level of Sirpa mRNA obviously vs control (P < 0.01). The phagocytic activity of miR-378a-transfected macrophages was promoted vs control (P < 0.05). miR-378a significantly depleted Sirpa levels in oxidized low-density lipoprotein (ox-LDL)-stimulated macrophages (P < 0.05), and depletion of miR-378a reversed Sirpa reduction obviously (P < 0.05). miR-378a promoted the secretion of TNF-a and IL-6 indirectly. CONCLUSION: It has been demonstrated that miR-378a regulates SIRPa-mediated phagocytosis and polarization of macrophages by a direct or indirect way. This research may provide a new path to promote reverse cholesterol transport of macrophages and hinder the progress of atherosclerosis.

Immune-checkpoint proteins VISTA and PD-1 nonredundantly regulate murine T-cell responses.

V-domain immunoglobulin suppressor of T-cell activation (VISTA) is a negative immune-checkpoint protein that suppresses T-cell responses. To determine whether VISTA synergizes with another immune-checkpoint, programmed death 1 (PD-1), this study characterizes the immune responses in VISTA-deficient, PD-1-deficient (KO) mice and VISTA/PD-1 double KO mice. Chronic inflammation and spontaneous activation of T cells were observed in both single KO mice, demonstrating their nonredundancy. However, the VISTA/PD-1 double KO mice exhibited significantly higher levels of these phenotypes than the single KO mice. When bred onto the 2D2 T-cell receptor transgenic mice, which are predisposed to development of inflammatory autoimmune disease in the CNS, the level of disease penetrance was significantly enhanced in the double KO mice compared with in the single KO mice. Consistently, the magnitude of T-cell response toward foreign antigens was synergistically higher in the VISTA/PD-1 double KO mice. A combinatorial blockade using monoclonal antibodies specific for VISTA and PD-L1 achieved optimal tumor-clearing therapeutic efficacy. In conclusion, our study demonstrates the nonredundant role of VISTA that is distinct from the PD-1/PD-L1 pathway in controlling T-cell activation. These findings provide the rationale to concurrently target VISTA and PD-1 pathways for treating T-cell-regulated diseases such as cancer.

6-Hydroxydopamine induces brain vascular endothelial inflammation.

Disruption of the blood-brain barrier associated with endothelial dysfunction is an important hallmark of Parkinson's disease (PD). 6-Hydroxydopamine (6-OHDA) is a synthetic dopamine derivate often used to model PD as it results in retrograde degeneration of striatal dopaminergic (DA) terminals. Presently, the effects of 6-OHDA on endothelial dysfunction remain unknown. Using a 6-OHDA rodent model of PD, we found that administration of 6-OHDA could increase the expression of endothelial adhesion molecules, such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin. An in vitro study displayed that treatment with 6-OHDA increased the release of these molecules in human brain microvascular endothelial cells in a dose-dependent manner. Correspondingly, 6-OHDA significantly increased attachment of THP-1 monocytes to brain endothelial cells. In addition, real-time polymerase chain reaction and enzyme-linked immunosorbent assay results indicated that 6-OHDA elevated the production of proinflammatory cytokines, such as interleukin-1ß, interleukin-6, and tumor necrosis factor-α. Furthermore, 6-OHDA treatment increased the expression of cyclooxygenase-2 and inducible nitric oxide synthase, as well as the production of prostaglandin E2 and nitric oxide. Importantly, 6-OHDA elevated the transcriptional activity of NF-кB by increasing the phosphorylation, degradation, and subsequent nuclear translocation of p65. Mechanistically, the angiotensin II type 1 receptor was found to mediate 6-OHDA-induced endothelial dysfunction. Our findings suggest that 6-OHDA-induced endothelial inflammation may play an important role in the pathogenesis of PD. © 2017 IUBMB Life, 69(11):887-895, 2017.

Disruption of the immune-checkpoint VISTA gene imparts a proinflammatory phenotype with predisposition to the development of autoimmunity.

V domain-containing Ig suppressor of T-cell activation (VISTA) is a negative checkpoint regulator that suppresses T cell-mediated immune responses. Previous studies using a VISTA-neutralizing monoclonal antibody show that VISTA blockade enhances T-cell activation. The current study describes a comprehensive characterization of mice in which the gene for VISTA has been deleted. Despite the apparent normal hematopoietic development in young mice, VISTA genetic deficiency leads to a gradual accumulation of spontaneously activated T cells, accompanied by the production of a spectrum of inflammatory cytokines and chemokines. Enhanced T-cell responsiveness was also observed upon immunization with neoantigen. Despite the presence of multiorgan chronic inflammation, aged VISTA-deficient mice did not develop systemic or organ-specific autoimmune disease. Interbreeding of the VISTA-deficient mice with 2D2 T-cell receptor transgenic mice, which are predisposed to the development of experimental autoimmune encephalomyelitis, drastically enhanced disease incidence and intensity. Disease development is correlated with the increase in the activation of encephalitogenic T cells in the periphery and enhanced infiltration into the CNS. Taken together, our data suggest that VISTA is a negative checkpoint regulator whose loss of function lowers the threshold for T-cell activation, allowing for an enhanced proinflammatory phenotype and an increase in the frequency and intensity of autoimmunity under susceptible conditions.

Tanshinone IIA affects the HDL subfractions distribution not serum lipid levels: Involving in intake and efflux of cholesterol.

AIM OF STUDY: Tanshinone IIA is an active component of the traditional Chinese medicine. This study aimed at investigating the mechanism of tanshinone IIA on anti-atherosclerosis, which may be because of that Tanshinone IIA can affect the HDL subfractions distribution and then regulate reverse cholesterol transport. MATERIALS AND METHODS: A model of hyperlipidaemia in rats was used. Tanshinone IIA was given daily after hyperlipidaemia. In vivo, lipid deposition and morphological changes in liver were analyzed; HDL subfractions and lipid level in serum as well as in liver were measured; the expression of genes related to cholesterol intake in liver and peritoneal macrophage cholesterol efflux were evaluated. In vitro, HepG2 cells and THP-1 cells were pretreated with tanshinone IIA and subsequently with ox-LDL to evaluate the total cholesterol and the expression of related genes. RESULTS: Tanshinone IIA reduced the lipid deposition in liver. Moreover, it did not affect the serum lipid levels but reduced the levels of HDL middle subfractions and increased the levels of HDL large subfractions. Furthermore, tanshinone IIA could regulate the expressions of CYP7A1, LDL-R, SREBP2 and LCAT in the liver as well as the ABCA1 and CD36 in macrophage cells which is involving in the cholesterol intake and efflux respectively. It could reduce lipid accumulation caused by ox-LDL induction, and that also regulate the expressions of LDL-R, HMGCR and SREBP2 in HepG2 and ABCA1, CD36 in THP-1 cells. CONCLUSION: A novel finding that tanshinone IIA was not reduce the serum lipid level but affects the HDL subfractions distribution and thereby regulating the intake and efflux of cholesterol.

The bitter side of sweet: the role of Galectin-9 in immunopathogenesis of viral infections.

In recent years, a critical role for ß-galactoside-binding protein, Galectin-9 (Gal-9) has emerged in infectious disease, autoimmunity, and cancer. It is a ligand for T cell immunoglobulin mucin domain 3 (Tim-3), a type-I glycoprotein that is persistently expressed on dysfunctional T cells during chronic viral infections. Gal-9 exerts its pivotal immunomodulatory effects by inducing apoptosis or suppressing effector functions via engagement with its receptor, Tim-3. Recent studies report elevation of circulating Gal-9 in humans infected with different viral infections. Interaction of soluble Gal-9 with Tim-3 expressed on the surface of activated CD4+ T cells renders them less susceptible to HIV-1 infection, while enhanced HIV infection occurs when Gal-9 interacts with a different receptor than Tim-3. This indicates the versatile role of Gal-9 in viral pathogenesis. For instance, higher expression of Tim-3 during chronic viral infection and elevation of plasma Gal-9 may have evolved to limit persistent immune activation and pathogenic T cells activity. In contrast, Gal-9 can suppress the effectiveness of immunity against viral infections. In agreement, Gal-9 knockout mice mount a more robust and vigorous virus-specific immune response in acute and chronic viral infections resulting in rapid viral clearance. In line with this observation, blocking Gal-9 signals to Tim-3-expressing T cells result in improved immune responses. Here we review the biological and immunological properties of Gal-9 in viral infections (HIV, HCV, HBV, HSV, CMV, influenza, and dengue virus). Manipulating Gal-9 signals may have immunotherapeutic potential and could represent an alternative approach for improving immune responses to viral infections/vaccines.

Design, Synthesis and Antibacterial Evaluation of Some New 2-Phenyl-quinoline-4-carboxylic Acid Derivatives.

A series of new 2-phenyl-quinoline-4-carboxylic acid derivatives was synthesized starting from aniline, 2-nitrobenzaldehyde, pyruvic acid followed by Doebner reaction, amidation, reduction, acylation and amination. All of the newly-synthesized compounds were characterized by ¹H-NMR, (13)C-NMR and HRMS. The antibacterial activities of these compounds against Gram-negative (Escherichia coli, Pseudomonas aeruginosa) and Gram-positive bacteria (Staphylococcus aureus, Bacillus subtilis), as well as one strain of methicillin-resistant Staphylococcus aureus (MRSA) bacteria were evaluated by the agar diffusion method (zone of inhibition) and a broth dilution method (minimum inhibitory concentration (MIC)), and their structure-activity relationships were obtained and discussed. The results revealed that some compounds displayed good antibacterial activity against Staphylococcus aureus, and Compounds 5a4 and 5a7 showed the best inhibition with an MIC value of 64 µg/mL against Staphylococcus aureus and with an MIC value of 128 µg/mL against Escherichia coli, respectively. The results of the MTT assay illustrated the low cytotoxicity of Compound 5a4.

[Correlation between autophagy and polarization of macrophages in atherosclerosis plaque in arteriosclerosis obliterans amputees].

This study was designed to investigate the correlation between autophagy and polarization of macrophages in atherosclerosis (AS) plaque in arteriosclerosis obliterans amputees. Femoral artery specimens from arteriosclerosis obliterans amputees were performed hematoxylin and eosin (HE) staining, oil red O and immunofluorescence staining to observe the morphology of atherosclerotic plaque, phenotype of macrophages and autophagy in plaque; using real-time quantitative RT-PCR technology to detect the mRNA level of M1 and M2 type markers in arterial tissue; to analyze polarized signal pathway and autophagy protein levels in macrophages by Western blotting. Arterial specimens staining showed obvious lipid deposition and obvious infiltration of amount of foam cells and inflammatory cells. Macrophages were mainly expression M1 type in percentage in fibrous plaque. Although both M1 and M2 macrophages were upregulated in atheromatous plaque, the increase was dominant in M2 type in percentage. The level of autophagy was significantly higher in the atheromatous plaque than that of fibrous plaque. The expression of tumor necrosis factor- α (TNF-α), monocyte chemotactic protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and interleukin-12 (IL-12) mRNA was significantly higher in fibrous plaque than that of atheromatous plaque (P < 0.01 or 0.05), and arginase-1 (Arg-1), transforming growth factor-ß (TGF-ß), CD163 and interleukin-10 (IL-10) mRNA was significantly lower than that in atheromatous plaque (P < 0.01). The levels of p-STAT1 and NF-κB were significantly increased in fibrous plaque (P < 0.01), while p-STAT6 expression was significantly increased in atheromatous plaque (P < 0.01). The level of LC3-II was significantly higher in atheromatous plaque than that in fibrous plaque (P < 0.01). Macrophages in early atherosclerotic plaque were induced to M1 type through p-STAT1/NF-κB pathway and expressed moderate levels of autophagy; while macrophages in advanced plaques were induced to polarization of M2 type through p-STAT6 pathway. M2 macrophages expressed a higher level of autophagy than M1 macrophages.

Comparison of Beneficial Effects of Acupuncture at PC6, LU7 & Non- acupuncture Points on Cardiac Cell Function in Myocardial Ischemia (MI) Rats by Testing Protein Expression of L-type Calcium Channel Protein and its Related Protein.

The mechanism of why electro-acupuncture (EA) at PC6 improves the heart function was investigated by studying how the L-type cardiac voltage-dependent calcium channel in myocardial ischemia (MI) is regulated. Cava,., Cavo and Cava2-61 are main component proteins of L-type calcium channel; CaM and Calmodulin kinase II (CaMKII) are Ca2+ channel associated proteins. In this experiment, MI was induced by injection of isoproterenol (ISO) in rats and electrocardiograms (ECGs) were recorded before and after every injection, and protein expressions of Cava,c, Cavp, Cava2_61, CaM and CaMKII were higher [The protein expression increased 43.39%, 54.85%, 47.08%, 48.29% and 50.36% respectively] than the control rats significantly (p<0.05). After MI induction, the MI rats were divided into three groups, including PC6 (Neiguan-point), LU7 (Lieque-point) and Non-acupuncture-point group, which were acupunctured once a day for 7 days respectively. After EA at PC6, the protein expressions showed obvious decrease [EA at PC6: the protein expressions of Cava1c, CavP, Cava2-81, CaM and CaMKII decreased 26.36%, 27.58%, 25.21%, 27.21% and 26.61% respectively.] and they are all lower than MI rats significantly (p<0.05). After EA at LU7 and Non-acupuncture-point, the protein expressions showed no significant changes. The effect of EA at PC6 was significantly better than LU7 and Non- acupuncture-point (p<0.05). PC6 is an acupoint of the pericardium meridian, and the pericardium meridian, which corresponds to opioid system according to Li P's research, can affect the cardio-vascular function directly. LU7 is located on the lung meridian; it cannot affect the heart function directly although the lung is related to the heart in blood circulation function so PC6 showed the target treating effect of meridian specificity on regulating the L-type calcium channel in MI.

Can we predict the outcome of 595-nm wavelength pulsed dye laser therapy on capillary vascular malformations from the first beginning: a pilot study of efficacy co-related factors in 686 Chinese patients.

Currently, there are no standardized, objective, and clinically applicable methods to predict the outcome of pulsed dye laser (PDL) therapy on capillary vascular malformation (CVM) patients. The introduction of a method that can predict the outcome prior to treatment will be valuable for both the patients and the doctors. In this study, the authors treated CVM with 595-nm wavelength PDL in Chinese patients (n = 686) and analyzed the efficacy of treatment and complications retrospectively in a 5-year period. Nearly 18 % of patients (n = 122) had 76 % or more clearing of lesions; over 52 % of patients (n = 360) had more than 50 % of clearing. The lesions in head and neck region had the best effective rate (58.3 %), followed by trunk (42.9 %) and extremities (35.6 %). The efficacy of PDL therapy is related to age, type, and location of lesions. Fifty-seven patients (8.3 %) had complications, including 2.0 % blistering (n = 14), 4.5 % hyperpigmentation (n = 31), 1.3 % hypopigmentation (n = 9), and 0.4 % hypertrophic scarring (n = 3). Based on these preliminary data, the authors established a standardized, objective, and clinically applicable equation that may be applied to predict the efficacy of 595 nm PDL therapy on a newly diagnosed Chinese CVM patients based on the age, type, and location of lesions.

Effect of acupuncture at Neiguan (PC 6) on cardiac function using echocardiography in myocardial ischemia rats induced by isoproterenol.

OBJECTIVE: To investigate the effect of acupuncture at Neiguan (PC 6) on cardiac function using echocardiography in rat models of myocardial ischemia (MI) induced by isoproterenol (ISO). METHODS: Twenty-seven Sprague-Dawley rats were randomly assigned to normal, model, and acupuncture groups. The model and acupuncture groups were given injections of ISO (85 mg/kg) to establish the MI model. After model establishment, the acupuncture group was treated with acupuncture at Neiguan (PC 6) for 30 min. Echocardiography was used to monitor diastolic and systolic function for 30 min starting from the time after the acupuncture needles were removed. Changes in the length of left ventricular internal diameter at end-diastole (LVIDd), length of left ventricular internal diameter at end-systole (LVIDs), the ratio of mitral peak velocity at early diastole and atrial contraction (E/A), ejection fraction (EF), fractional shortening (FS), and stroke volume (SV) were measured. RESULTS: Compared with the model group at 0 and 15 min after needles were removed, the means of LVIDd and LVIDs were significantly lower (P < 0.01) and E/A, EF, FS, and SV significantly higher (P < 0.01) in the acupuncture group. In the acupuncture group, the means of LVIDd and LVIDs 15 min after the needles were removed were significantly higher (P < 0.01) than those at 0 min. The means of E/A, EF, FS, and SV significantly decreased (P < 0.01) from 0 to 15 min in the acupuncture group. CONCLUSION: These findings indicate that acupuncture at Neiguan (PC 6) can affect cardiac function by increasing left ventricular diastolic and systolic function in MI rat models, but the effect only lasts for 15 min.

[Effect of ASO Blood Stasis Syndrome Serum on Vascular Endothelial Cell Injury and Regulation of Taohong Siwu Decoction on it].

OBJECTIVE: To explore the effect of arteriosclerosis obliterans (ASO) blood stasis syndrome (BSS) serum on vascular endothelial cell injury and to study the regulation of Taohong Siwu Decoction (TSD) on it. METHODS: Umbilical vein endothelial cell culture system was established. The serum endothelial cell injury model with ASO BSS was prepared. Low, medium, and high concentrations TSD containing serums were respectively added. The endothelial cell proliferation activity was observed by MTT method. Ultrastructures of endothelial cells were observed under transmission electron microscope. Changes of intracellular calcium ion concentration and the cytoskeleton were observed under laser confocal microscope. Contents of ET, NO, and transforming growth factor beta1 (TGF-beta1) in endothelial cell culture supernatant were detected by ELISA. RESULTS: In ASO BSS serum group endothelial cell proliferation activities decreased, the cell structure was obviously destroyed, calcium ion concentration increased, contents of ET, NO and TGF-beta1 increased significantly (P < 0.01), and ET/NO ratio was imbalanced. After incubating with TSD drug containing serum, endothelial cell proliferation activities and injured cell structures were obviously improved; ET, NO and TGF-beta1 levels decreased (P < 0.05, P < 0.01), ET/NO ratios approximated to the normal level. CONCLUSION: The main mechanism of TSD for treating ASO ASS lied in improving injured vascular endothelial cells and endocrine disorder.

[Taohong Siwu Decoction regulated functions of endothelial cells and treated arteriosclerosis obliterans: an experimental study].

OBJECTIVE: To discuss the effect of Taohong Siwu Decoction (TSD) in regulating functions of endothelial cells and treating arteriosclerosis obliterans (ASO). METHODS: The ASO model was prepared by using high-fat diet plus intimal injury. They were randomly divided into the model group (n = 10), the normal control group (n = 9), the low dose TSD group (group A, n = 12), the middle dose TSD group (group B, n = 10), and the high dose TSD group (group C, n = 9). Eight weeks after modeling, the limb blood perfusion was observed using laser Doppler flowmetry. The arterial morphology was observed using light microscope and transmission electron microscope. The number of circulating endothelial cells (CECs) was determined using Percoll density gradient centrifugation method. Serum levels of TNF-alpha, IL-1, ET-1, and NO were detected using double antibody sandwich assay of enzyme linked immunosorbent assay (ELISA). RESULTS: The ASO rat model was successfully established. Blood lipids levels significantly increased, the blood perfusion of left hind limbs significantly decreased, the number of CECs in the peripheral blood significantly increased, the arterial lumen was irregularly narrowed, the ultra-structure of vessel walls was damaged, serum levels of TNF-alpha, IL-1, and ET-1 significantly increased, and the serum level of NO significantly decreased in the model group, showing statistical difference when compared with the normal control group (P < 0.01). Compared with the model group, significant improvement in the aforesaid indices was shown in group B and C (P < 0.05, P < 0.01). CONCLUSIONS: The injury and abnormal functions of endothelial cells is an important pathological process of ASO. As an effective recipe for treating ASO, TSD could protect vascular endothelial cells and improve the secretion function of vascular endothelial cells.

A robust approach for multi-type classification of brain tumor using deep feature fusion.

Brain tumors can be classified into many different types based on their shape, texture, and location. Accurate diagnosis of brain tumor types can help doctors to develop appropriate treatment plans to save patients' lives. Therefore, it is very crucial to improve the accuracy of this classification system for brain tumors to assist doctors in their treatment. We propose a deep feature fusion method based on convolutional neural networks to enhance the accuracy and robustness of brain tumor classification while mitigating the risk of over-fitting. Firstly, the extracted features of three pre-trained models including ResNet101, DenseNet121, and EfficientNetB0 are adjusted to ensure that the shape of extracted features for the three models is the same. Secondly, the three models are fine-tuned to extract features from brain tumor images. Thirdly, pairwise summation of the extracted features is carried out to achieve feature fusion. Finally, classification of brain tumors based on fused features is performed. The public datasets including Figshare (Dataset 1) and Kaggle (Dataset 2) are used to verify the reliability of the proposed method. Experimental results demonstrate that the fusion method of ResNet101 and DenseNet121 features achieves the best performance, which achieves classification accuracy of 99.18 and 97.24% in Figshare dataset and Kaggle dataset, respectively.

Early stage alopecia areata is associated with inflammation in the upper dermis and damage to the hair follicle infundibulum.

BACKGROUND/OBJECTIVES: Alopecia areata (AA) is a non-scarring inflammatory hair loss disease. We investigated the early pathological changes of AA to identify possible factors participating in its pathogenesis. METHODS: Clinical, laboratory and pathological features of 87 AA patients were investigated. RESULTS: Anti-nuclear antibody was found in 11 of 85 patients tested (13%), with a higher percentage in women (21%) than men (5%) (P = 0.026). In early AA lesions, inflammatory infiltration in the upper dermis and epithelial cell damage of the hair follicle infundibulum, just above the sebaceous gland, was observed. Liquefaction and disarrangement of peripheral infundibular epithelial cells coexisted with T-lymphocytic invasion and regression of the lower follicle. The latter findings positively correlated with the presence of eosinophils and perivascular mononuclear cell infiltration in the upper dermis. Eosinophilic infiltration was found in 35 patients (40%) and was positively correlated to elevated serum IgE levels (r = 0.21, P = 0.044), a more severe perivascular lymphocytic inflammation in the upper dermis (r = 0.24, P = 0.026), as well as a prominent swarm of bees-like peri-follicular infiltration (r = 0.41, P < 0.001). Mast cells were abundant in the upper dermis, especially around blood vessels, and positively correlated with eosinophil presence (r = 0.30, P = 0.027). CONCLUSION: Damage to the hair follicle infundibulum in the upper dermis might be an important component of early changes in AA lesions, possibly caused by lymphocyte cell infiltration in the same area. AA may involve damage of the upper hair follicle as well as the bulb, possibly involving hypersensitivity and autoimmunity.

EFF_D_SVM: a robust multi-type brain tumor classification system.

Brain tumors are one of the most threatening diseases to human health. Accurate identification of the type of brain tumor is essential for patients and doctors. An automated brain tumor diagnosis system based on Magnetic Resonance Imaging (MRI) can help doctors to identify the type of tumor and reduce their workload, so it is vital to improve the performance of such systems. Due to the challenge of collecting sufficient data on brain tumors, utilizing pre-trained Convolutional Neural Network (CNN) models for brain tumors classification is a feasible approach. The study proposes a novel brain tumor classification system, called EFF_D_SVM, which is developed on the basic of pre-trained EfficientNetB0 model. Firstly, a new feature extraction module EFF_D was proposed, in which the classification layer of EfficientNetB0 was replaced with two dropout layers and two dense layers. Secondly, the EFF_D model was fine-tuned using Softmax, and then features of brain tumor images were extracted using the fine-tuned EFF_D. Finally, the features were classified using Support Vector Machine (SVM). In order to verify the effectiveness of the proposed brain tumor classification system, a series of comparative experiments were carried out. Moreover, to understand the extracted features of the brain tumor images, Grad-CAM technology was used to visualize the proposed model. Furthermore, cross-validation was conducted to verify the robustness of the proposed model. The evaluation metrics including accuracy, F1-score, recall, and precision were used to evaluate proposed system performance. The experimental results indicate that the proposed model is superior to other state-of-the-art models.