Brain’s neural activities encompass both periodic rhythmic oscillations and aperiodic neural fluctuations. Rhythmic oscillations manifest as spectral peaks of neural signals, directly reflecting the synchronized activities of neural populations and closely tied to cognitive and behavioral states. In contrast, aperiodic fluctuations exhibit a power-law decaying spectral trend, revealing the multiscale dynamics of brain neural activity. In recent years, researchers have made notable progress in studying brain aperiodic dynamics. These studies demonstrate that aperiodic activity holds significant physiological relevance, correlating with various physiological states such as external stimuli, drug induction, sleep states, and aging. Aperiodic activity serves as a reflection of the brain’s sensory capacity, consciousness level, and cognitive ability. In clinical research, the aperiodic exponent has emerged as a significant potential biomarker, capable of reflecting the progression and trends of brain diseases while being intricately intertwined with the excitation-inhibition balance of neural system. The physiological mechanisms underlying aperiodic dynamics span multiple neural scales, with activities at the levels of individual neurons, neuronal ensembles, and neural networks collectively influencing the frequency, oscillatory patterns, and spatiotemporal characteristics of aperiodic signals. Aperiodic dynamics currently boasts broad application prospects. It not only provides a novel perspective for investigating brain neural dynamics but also holds immense potential as a neural marker in neuromodulation or brain-computer interface technologies. This paper summarizes methods for extracting characteristic parameters of aperiodic activity, analyzes its physiological relevance and potential as a biomarker in brain diseases, summarizes its physiological mechanisms, and based on these findings, elaborates on the research prospects of aperiodic dynamics.

The European Society of Cardiology (ESC) released the "2024 ESC guidelines for the management of elevated blood pressure and hypertension" on August 30, 2024. This guideline updates the 2018 "Guidelines for the management of arterial hypertension." One notable update is the introduction of the concept of "elevated blood pressure" (120-139/70-89 mm Hg). Additionally, a new systolic blood pressure target range of 120-129 mm Hg has been proposed for most patients receiving antihypertensive treatment. The guideline also includes numerous additions or revisions in areas such as non-pharmacological interventions and device-based treatments for hypertension. This article interprets the guideline's recommendations on definition and classification of elevated blood pressure and hypertension, and cardiovascular disease risk assessment, diagnosing hypertension and investigating underlying causes, preventing and treating elevated blood pressure and hypertension. We provide a comparison interpretation with the 2018 "Guidelines for the management of arterial hypertension" and the "2017 ACC/AHA guideline on the prevention, detection, evaluation, and management of high blood pressure in adults."

Alzheimer’s disease (AD) is a central neurodegenerative disease characterized by progressive cognitive decline and memory impairment in clinical. Currently, there are no effective treatments for AD. In recent years, a variety of therapeutic approaches from different perspectives have been explored to treat AD. Although the drug therapies targeted at the clearance of amyloid β-protein (Aβ) had made a breakthrough in clinical trials, there were associated with adverse events. Neuroinflammation plays a crucial role in the onset and progression of AD. Continuous neuroinflammatory was considered to be the third major pathological feature of AD, which could promote the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles. At the same time, these toxic substances could accelerate the development of neuroinflammation, form a vicious cycle, and exacerbate disease progression. Reducing neuroinflammation could break the feedback loop pattern between neuroinflammation, Aβ plaque deposition and Tau tangles, which might be an effective therapeutic strategy for treating AD. Traditional Chinese herbs such as Polygonum multiflorum and Curcuma were utilized in the treatment of AD due to their ability to mitigate neuroinflammation. Non-steroidal anti-inflammatory drugs such as ibuprofen and indomethacin had been shown to reduce the level of inflammasomes in the body, and taking these drugs was associated with a low incidence of AD. Biosynthetic nanomaterials loaded with oxytocin were demonstrated to have the capability to anti-inflammatory and penetrate the blood-brain barrier effectively, and they played an anti-inflammatory role via sustained-releasing oxytocin in the brain. Transplantation of mesenchymal stem cells could reduce neuroinflammation and inhibit the activation of microglia. The secretion of mesenchymal stem cells could not only improve neuroinflammation, but also exert a multi-target comprehensive therapeutic effect, making it potentially more suitable for the treatment of AD. Enhancing the level of TREM2 in microglial cells using gene editing technologies, or application of TREM2 antibodies such as Ab-T1, hT2AB could improve microglial cell function and reduce the level of neuroinflammation, which might be a potential treatment for AD. Probiotic therapy, fecal flora transplantation, antibiotic therapy, and dietary intervention could reshape the composition of the gut microbiota and alleviate neuroinflammation through the gut-brain axis. However, the drugs of sodium oligomannose remain controversial. Both exercise intervention and electromagnetic intervention had the potential to attenuate neuroinflammation, thereby delaying AD process. This article focuses on the role of drug therapy, gene therapy, stem cell therapy, gut microbiota therapy, exercise intervention, and brain stimulation in improving neuroinflammation in recent years, aiming to provide a novel insight for the treatment of AD by intervening neuroinflammation in the future.

The chemical constituents in dried roots of Atractylodes macrocephala were investigated in this study. Through utilizing normal-phase silica gel and ODS column chromatography, TLC, and semi-preparative HPLC, 4 new sesquiterpenoids were purified from the ethyl acetate extract of A. macrocephala. By various spectroscopic techniques, such as 1D and 2D NMR, HR-ESI-MS, IR, UV, and CD, their structures were identified as atractylmacron A (1), 9β-hydroxyasterolide (2), atractylenolide H (3), atractylenolide J (4). Compound 1 possesses a rare 6/7 bicyclic skeleton.

Objective To investigate the activation of microglia and astrocytes, the secretion of pro-inflammatory factors, and the survival of neurons in the hippocampus of mice with acute seizures induced by pentylenetetrazol (PTZ) 24 hours after the onset of seizures. Methods Adult male C57BL/6 mice were randomly assigned to the control group and the PTZ-induced acute epileptic seizure group using random numbers, with 28 mice in each group. The activation status of microglia and astrocytes in the CA1 region of the hippocampus was evaluated by immunofluorescence 24 hours after the onset of seizures. RNA was extracted from the hippocampal tissue to detect the expression level of inflammatory factor mRNA, and HE staining was used to assess the survival of neurons in the hippocampus. Results Twenty-four hours after PTZ-induced acute seizures in mice, the numbers of activated Iba1⁺ microglia (55.72±4.29 vs 35.71±9.66, P＜0.001) and GFAP⁺ astrocytes (51.61±8.21 vs 37.64±5.27, P＜0.01) in the CA1 region were significantly increased compared with the control group; the proportion of M1 microglia was significantly increased (0.58±0.02 vs 0.35±0.08, P＜0.0001), while the proportion of M2 microglia was significantly decreased (0.25±0.08 vs 0.44±0.09，P＜0.01); the mRNA level of pro-inflammatory factor IL-1β in the hippocampus was significantly higher than that in the control group (2.49±1.61 vs 1.02±0.68, P＜0.05); the numbers of neurons in the CA1 (284.91±73.32 vs 498.88±176.79, P＜0.05) and CA3 (247.42±50.20 vs 457.78±150.08, P＜0.05) regions during the acute phase was significantly reduced compared with the control group. Conclusions Twenty-four hours after PTZ-induced acute epileptic seizures in mice, microglia and astrocytes in the CA1 region of the hippocampus are activated, with microglia mainly presenting the M1 phenotype to exert pro-inflammatory effects, secretions of pro-inflammatory factors increasing, and surviving hippocampal neurons decreasing.

Objective To evaluate the clinical characteristics of human immunodeficiency virus (HIV) infected patients with peripheral lung masses (PLMs), and to assess the diagnostic utility of contrast-enhanced ultrasound (CEUS) in differentiating benign and malignant PLMs. Methods A retrospective analysis was performed on the clinical data of 69 patients with PLM treated in Shanghai Public Health Clinical Center from January 2020 to December 2023. All patients underwent percutaneous biopsy, and were categorized into benign group (n＝36) and malignant group (n＝33). 25 patients were HIV-positive and 44 patients were HIV-negative. The clinical features and CEUS parameters in patients were compared across these groups. Results Patients with malignant masses were significantly older than those with benign masses (P＜0.05). In the malignant group, HIV-negative patients exhibited significantly larger tumor diameters compared to HIV-positive patients (P＜0.05); in the HIV-positive patients, no significant difference in tumor size was observed between benign and malignant masses. 19 patients underwent CEUS. 10 malignant masses, irrespective of HIV status (10 positive and 9 negative), commonly presented with indistinct margins, delayed enhancement, heterogeneous perfusion, and delayed peak enhancement on CEUS. 9 benign masses showed earlier peak enhancement compared to 10 malignant masses (P＜0.05); no significant differences were observed in the initiation and washout time of enhancement between benign and malignant masses. In HIV-positive patients, 5 benign masses frequently demonstrated discrepancies between CEUS findings and pathological results. Conclusions The clinical and CEUS characteristics were different between benign and malignant PLMs. However, CEUS shows limited accuracy in distinguishing benign and malignant PLMs, underscoring the need for pathological confirmation.

ObjectiveTo investigate the mechanism of Huazhuo Jiedu prescription in treating ulcerative colitis （UC） by regulating mitophagy. MethodsThe genes related to mitophagy and UC were retrieved from GeneCards， and then the common genes of mitophagy and UC were analyzed by metascape to identify the genes related to mitophagy in UC. Animal experiments were carried out to decipher the mechanism by which Huazhuo Jiedu prescription treated UC by regulating mitophagy. Sixty C57BL/6 male mice were randomized into normal， model， high-， medium-， and low-dose （50， 25， 12.5 g·kg^-1， respectively） Huazhuo Jiedu prescription， and mesalazine （0.52 g·kg^-1·d^-1） groups， with 10 mice in each group. After successful modeling by the dextran sulfate sodium-free drinking method， the colonic mucosal damage was observed by hematoxylin-eosin staining， and the ultracellular structure of colon mucosa was observed by transmission electron microscopy. The expression levels of mitophagy-related proteins PTEN-induced putative kinase 1 （PINK1） and Parkin protein were determined by Western blot. The expression of prohibitin 2 （PHB2）， ubiquitin-specific protease 15 （USP15）， ubiquitin-specific protease 30 （USP30） in the colon tissue was detected by immunofluorescence （IF）. ResultsAll the drug intervention groups showed ameliorated pathological manifestations of the colonic mucosa and improved mitochondrial structures in UC mice. Compared with the normal group， the model group demonstrated up-regulated protein levels of PINK1 and Parkin （P<0.05）， enhanced average fluorescence intensity of PHB2 （P<0.05）， and weakened average fluorescence intensity of USP15 and USP30 （P<0.05）. Compared with the model group， the mesalazine group and the high- and medium-dose Huazhuo Jiedu prescription groups showcased down-regulated protein levels of PINK1 and Parkin （P<0.05）， decreased average fluorescence intensity of PHB2 （P<0.05）， and enhanced average fluorescence intensity of USP15 and USP30 （P<0.05）. The low-dose Huazhuo Jiedu prescription group showed down-regulated protein levels of PINK1 and Parkin （P<0.05）， weakened average fluorescence intensity of PHB2 （P<0.05）， and enhanced average fluorescence intensity of USP15 and USP30 （P<0.05）. ConclusionHuazhuo Jiedu prescription can attenuate the intestinal mucosal injury and improve the mitochondrial cell ultrastructure in UC mice by regulating the expression of PINK1-Parkin pathway and inhibiting excessive mitophagy.

ObjectiveTo investigate the mechanism of Huazhuo Jiedu prescription in treating ulcerative colitis （UC） by regulating mitophagy. MethodsThe genes related to mitophagy and UC were retrieved from GeneCards， and then the common genes of mitophagy and UC were analyzed by metascape to identify the genes related to mitophagy in UC. Animal experiments were carried out to decipher the mechanism by which Huazhuo Jiedu prescription treated UC by regulating mitophagy. Sixty C57BL/6 male mice were randomized into normal， model， high-， medium-， and low-dose （50， 25， 12.5 g·kg^-1， respectively） Huazhuo Jiedu prescription， and mesalazine （0.52 g·kg^-1·d^-1） groups， with 10 mice in each group. After successful modeling by the dextran sulfate sodium-free drinking method， the colonic mucosal damage was observed by hematoxylin-eosin staining， and the ultracellular structure of colon mucosa was observed by transmission electron microscopy. The expression levels of mitophagy-related proteins PTEN-induced putative kinase 1 （PINK1） and Parkin protein were determined by Western blot. The expression of prohibitin 2 （PHB2）， ubiquitin-specific protease 15 （USP15）， ubiquitin-specific protease 30 （USP30） in the colon tissue was detected by immunofluorescence （IF）. ResultsAll the drug intervention groups showed ameliorated pathological manifestations of the colonic mucosa and improved mitochondrial structures in UC mice. Compared with the normal group， the model group demonstrated up-regulated protein levels of PINK1 and Parkin （P<0.05）， enhanced average fluorescence intensity of PHB2 （P<0.05）， and weakened average fluorescence intensity of USP15 and USP30 （P<0.05）. Compared with the model group， the mesalazine group and the high- and medium-dose Huazhuo Jiedu prescription groups showcased down-regulated protein levels of PINK1 and Parkin （P<0.05）， decreased average fluorescence intensity of PHB2 （P<0.05）， and enhanced average fluorescence intensity of USP15 and USP30 （P<0.05）. The low-dose Huazhuo Jiedu prescription group showed down-regulated protein levels of PINK1 and Parkin （P<0.05）， weakened average fluorescence intensity of PHB2 （P<0.05）， and enhanced average fluorescence intensity of USP15 and USP30 （P<0.05）. ConclusionHuazhuo Jiedu prescription can attenuate the intestinal mucosal injury and improve the mitochondrial cell ultrastructure in UC mice by regulating the expression of PINK1-Parkin pathway and inhibiting excessive mitophagy.

BACKGROUND:The extracellular-regulated protein kinase 5(ERK5)signaling protein is essential for the survival of organisms,and resveratrol can promote osteoblast proliferation through various pathways.However,whether resveratrol can regulate osteoblast function through the ERK5 signaling protein needs further verification. OBJECTIVE:To explore the regulatory effect of ERK5 on the proliferation of MC3T3-E1 cells and related secreted proteins,and to further verify whether resveratrol can complete the above process by activating ERK5. METHODS:Mouse MC3T3-E1 preosteoblasts were treated with complete culture medium,XMD8-92(an ERK5 inhibitor),epidermal growth factor(an ERK5 activator),resveratrol alone,XMD8-92+EGF,and resveratrol+XMD8-92,respectively.Western blot assay was used to detect the expression of ERK5 and p-ERK5 proteins,proliferation-related proteins Cyclin D1,CDK4 and PCNA,and osteoblast-secreted proteins osteoprotegerin and receptor activator of nuclear factor-κB ligand in MC3T3-E1 cells of each group.The fluorescence intensity of ERK5,osteoprotegerin and receptor activator of nuclear factor-κB ligand in each group was detected by cell immunofluorescence staining,and cell proliferation was detected by EdU staining,respectively.The appropriate concentration and time of resveratrol intervention in MC3T3-E1 cells were determined by cell morphology observation and cell counting kit-8 assay. RESULTS AND CONCLUSION:The activation of ERK5 signaling protein could effectively promote the proliferation of MC3T3-E1 cells,up-regulate the osteoprotegerin/receptor activator of nuclear factor-κB ligand ratio.The appropriate concentration and time for resveratrol intervention in MC3T3-E1 cells was 5 μmol/L and 24 hours,respectively.Resveratrol could activate ERK5 signaling protein,thereby promoting osteoblast proliferation and up-regulating the osteoprotegerin/RANKL ratio.All these results indicate that resveratrol can promote the proliferation of MC3T3-E1 cells and up-regulate the osteoprotegerin/RANKL ratio by activating the ERK5 signaling protein.

BACKGROUND:The combination of platelet-rich fibrin and autogenous bone has achieved good results in the treatment of periodontal bone defects,but the study of the combination of the two in the treatment of severe alveolar bone defects is scarce. OBJECTIVE:To observe the effect of autologous bone transplantation plus platelet-rich fibrin on the repair of severe alveolar bone defects. METHODS:A total of 102 patients with severe alveolar bone defects in Hengshui People's Hospital from April 2022 to February 2023 were selected and divided into control and observation groups(n=51 per group)by random number table method.Guided tissue regeneration was performed in both groups.The bone defect was filled with autogenous bone in the control group,and the observation group underwent platelet-rich fibrin+autogenous bone filling for bone defects during the operation.The clinical efficacy,changes in tooth mobility,periodontal microecological environment(probing depth,clinical attachment loss,and bleeding index),height and density of alveolar bone,gingival crevicular fluid indicators(transforming growth factor-β,serine protease inhibitor,and matrix metalloproteinase-3)before and after surgery,as well as adverse reactions were observed between the two groups. RESULTS AND CONCLUSION:Six months after operation,there was no significant difference in treatment efficacy rate between the two groups(P>0.05).At 3 and 6 months after surgery,the levels of tooth mobility,probing depth,clinical attachment loss,and bleeding index in the observation group were lower than those in the control group(P<0.05).At 6 months after surgery,the height of alveolar bone in the observation group was higher than that in the control group(P<0.05).At 3 and 6 months after surgery,the levels of transforming growth factor-β in gingival crevicular fluid in the observation group were higher than those in the control group(P<0.05).At 3 and 6 months after surgery,the levels of serine protease inhibitor and matrix metalloproteinase-3 in the observation group were lower than those in the control group(P<0.05).The results suggest that using platelet-rich fibrin+autogenous bone filling in guided tissue regeneration treatment of patients with severe alveolar bone defects can improve the periodontal microenvironment,reduce gingival tissue inflammation,promote alveolar bone tissue regeneration and repair,and reduce tooth mobility.