Neurological diseases have high morbidity and disability rates， posing a severe threat to human health. Cli nical manifestations include motor， sensory， cognitive and conscious disorders. Chaihu jia longgu muli decoction is derived from Treatise on Febrile Diseases ， with the effects of harmonizing Shaoyang， activating Yang and clearing heat， and tranquilizing the mind. This paper systematically reviews the research progress in clinical application and mechanism of Chaihu jia longgu muli decoction in the field of neurological diseases. It has been found that the decoction shows favorable efficacy in various neurological diseases such as insomnia， depression， epilepsy， vertigo， migraine and vascular dementia. The specific mechanisms are related to regulating neurotransmitter levels， repairing neuronal function， alleviating neuroinflammation， improving mitochondrial dysfunction and regulating intestinal flora. In the future， standardized prospective follow-up cohorts should be established， and core outcome indicators should be clearly defined to strengthen the evidence base. Furthermore， multidisciplinary research should be leveraged to expand the therapeutic value of Chaihu jia longgu muli decoction in the management of neurological diseases.

Objective To explore the feasibility and image quality of respiratory-gated total-body ¹⁸F-FDG PET/CT imaging with a 4-minute acquisition in patients with malignant tumors. Methods Sixty-two patients with pathologically confirmed malignant tumors (118 lesions measured) who underwent total-body ¹⁸F-FDG PET/CT examination were consecutively enrolled at the Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, from September 23, 2021 to November 23, 2021, and their clinical and imaging data were retrospectively collected. PET data was acquired over 12 minutes with simultaneous respiratory waveform recorded. The data were reconstructed into four image sets: gated-12 group and gated-4 group (using all counts and the first 4-minute counts, respectively) and ungated-12 group and ungated-6 group (using all counts and the first 6-minute counts, respectively) reconstructed with respiratory gating that retained counts corresponding to the half respiratory window near end-expiration. Image quality assessment and quantitative analysis of lesions were performed and compared among the four image sets, and subgroup analyses were performed according to lesion location, size, and metabolic activity. Results The effective counts of 4 sets of PET images were highest in ungated-12 group, followed by ungated-6 group and gated-12 group, and lowest in gated-4 group (P＜0.001). Regardless of the metabolic level and size of the lesions, compared with the ungated-12 group and the ungated-6 group, the lesions in the gated-12 group showed higher maximum, average, and peak standardized uptake values (SUV_max, SUV_mean, and SUV_peak), tumor liver uptake ratio, tumor blood pool uptake ratio, and smaller metabolic volume (P＜0.05); There was no statistically significant difference in the above indicators between the gate-12 group and the gate-4 group. The background noise of gate-4 group images is slightly higher than that of gate-12 group images (Liver SUV_SD: [0.17＋0.05] vs [0.14＋0.04]); Blood pool SUV_SD: (0.08 ± 0.03) vs (0.06 ± 0.03). There was a statistically significant difference in subjective scores of PET image quality among the four groups (P＜0.001). The subjective scores of image quality in the gated-12 group (4.79 ± 0.41) were not significantly different from those in the non gated-12 group (4.97 ± 0.17) and non gated-6 group (4.79 ± 0.45), but were higher than those in the gated-4 group ([4.17 ± 0.45], P＜0.001)， And the scores have good consistency (Kappa＞0.75). Conclusion In total-body PET/CT imaging for malignant tumors, 4-minute respiratory-gated acquisition can achieve comparable quantitative performance to longer respiratory gating imaging while significantly shortening acquisition time. This approach demonstrates promising potential for clinical application.

Objective:To evaluate the preservation efficacy of 7 non-inactivating virus preservation solutions.Methods:Equal amounts of H1N1 virus were added to 7 commercially available non-inactivating virus preservation solutions, and the samples were stored at -20 ℃, 4 ℃, 25 ℃ and 37 ℃ for 1 hour, 6 hours, 1 day, 3 days, and 5 days. The viral nucleic acid in each simulated sample under different storage conditions was measured using real-time quantitative PCR. The hemagglutination (HA) titer was determined through viral isolation culture and hemagglutination assay, comparing the differences in viral growth activity across different storage solutions and conditions.Results:Except for solution E, the other solutions effectively protected viral nucleic acid at the 4 storage temperatures. In terms of viral activity, solutions A, B, C, and D effectively maintained viral viability. A and B showing the best performance, E and F showed poorer performance, and G performed the worst.Conclusions:Most non-inactivating virus preservation solutions effectively protect viral nucleic acid, but there are significant differences in their ability to maintain viral viability. To ensure optimal virus preservation, it is recommended that medical institutions evaluate the effectiveness of preservation solutions before use.

Objective To investigate the impact of sleep modes on the risk for diseases of the body systems.Methods Based on a subset of UK Biobank dataset comprising 87 617 participants,3 sleep dimensions including 6 sleep indicators were obtained through a wrist-worn accelerometer,that is sleep duration and onset,sleep rhythm(relative amplitude and stability),and sleep quality(sleep efficiency and number of awakenings).Latent profile analysis(LPA)was applied to identify and classify distinct sleep modes.Then their longitudinal medical records were the association between different sleep modes and the risk for 467 diseases.Results LPA identified 5 subgroups of unique sleep modes in the participants.Among the 5 subgroups,the subgroup 4 had relatively optimal levels in above sleep indicators.Compared to the subgroup 4,the other 4 subgroups exhibited variations in different sleep dimensions,with at least one indicator demonstrating an unfavorable trend.These subgroups also revealed differences in racial composition,shift work and social deprivation index.Moreover,there were notable differences in the risk of various system diseases among the subgroups(P<0.05).When compared to the subgroup 4,the other 4 subgroups exhibited an elevated risk for certain diseases(comprising a total of 126 diseases),with the diseases of the circulatory system,digestive system and musculoskeletal system most common.Among the 5 subgroups,the subgroup 2(shorter sleep duration and later sleep onset)and the subgroup 5(rhythm disorder)had the highest counts of associated risks,amounting to 85 and 91 types,respectively,but there was certain difference in their systematic composition.Conclusion There are different sleep modes within the participants,and the modes are potentially associated with an increased risk for diseases of body systems.Comprehensive interventions targeting overall sleep modes rather than single sleep indicator may yield obvious health benefits.

This literature review investigates the mechanisms of resistance to human epidermal growth factor receptor 2 (HER2)-targeted therapies in HER2⁺ breast cancer, a subtype that accounts for approximately 20% of breast cancer cases. Despite the effectiveness of treatments such as trastuzumab and lapatinib, many patients experience either primary or acquired resistance, leading to treatment failure. The review systematically categorizes various resistance mechanisms, including the role of receptor activator of nuclear factor kappaΒ (RANK) expression, which has been shown to activate the nuclear factor kappaB (NF-κB) pathway, promoting cell survival and contributing to resistance. Other mechanisms include the activation of alternative signaling pathways, such as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway, and the involvement of tumor-associated fibroblasts, which can drive resistance through receptor tyrosine kinase (RTK) activation. Additionally, the review highlights the importance of understanding these mechanisms to inform the development of novel therapeutic strategies. By identifying potential biomarkers and therapeutic targets, the review suggests that combining HER2 inhibitors with agents that target resistance pathways may enhance treatment efficacy and improve patient outcomes. Overall, this review underscores the complexity of HER2⁺ breast cancer treatment and the need for continued research to overcome resistance challenges.

Objective:To evaluate the preservation efficacy of 7 non-inactivating virus preservation solutions.Methods:Equal amounts of H1N1 virus were added to 7 commercially available non-inactivating virus preservation solutions, and the samples were stored at -20 ℃, 4 ℃, 25 ℃ and 37 ℃ for 1 hour, 6 hours, 1 day, 3 days, and 5 days. The viral nucleic acid in each simulated sample under different storage conditions was measured using real-time quantitative PCR. The hemagglutination (HA) titer was determined through viral isolation culture and hemagglutination assay, comparing the differences in viral growth activity across different storage solutions and conditions.Results:Except for solution E, the other solutions effectively protected viral nucleic acid at the 4 storage temperatures. In terms of viral activity, solutions A, B, C, and D effectively maintained viral viability. A and B showing the best performance, E and F showed poorer performance, and G performed the worst.Conclusions:Most non-inactivating virus preservation solutions effectively protect viral nucleic acid, but there are significant differences in their ability to maintain viral viability. To ensure optimal virus preservation, it is recommended that medical institutions evaluate the effectiveness of preservation solutions before use.

Objective To investigate the distribution and evolutionary patterns of traditional Chinese medicine(TCM)syndromes and syndrome elements during the malignant transformation from chronic pancreatitis(CP)to pancreatic intraepithelial neoplasia(Pan IN)and pancreatic ductal adenocarcinoma(PDAC).Methods A retrospective analysis was conducted on 710 patients(330 of CP,104 of Pan IN,276 of PDAC)diagnosed pathologically or clinically at Shanxi Institute of Traditional Chinese Medicine from January 2021 to June 2024.Data including demographics,laboratory results,and TCM diagnostic information were recorded using EpiData 3.1.Syndrome and syndrome-element patterns were determined via factor analysis and K-means clustering using SPSS 27.0.Results The study identifies seven TCM syndrome types in CP,Pan IN,and PDAC.Among CP patients,the syndrome distribution was primarily liver-gallbladder damp-heat syndrome(22.42％)and gastrointestinal excess-heat syndrome(20.91％),with excess syndromes accounting for a higher proportion(43.33％);the syndrome elements were mainly heat(51.52％)and dampness(35.15％),with the disease location in the pancreas,related to the liver,spleen,and stomach.In Pan IN patients,the syndrome distribution was mainly spleen deficiency with dampness obstruction(23.08％)and liver-gallbladder damp-heat syndrome(17.31％),with mixed deficiency-excess syndrome accounting for a higher proportion(30.00％);the syndrome elements were mainly heat(41.35％),dampness(40.38％),and qi deficiency(37.50％),with the disease location in the pancreas,related to the spleen and liver.In PDAC patients,the syndrome distribution was mainly spleen deficiency with dampness obstruction(29.71％)and qi-blood deficiency syndrome(20.29％),with deficiency syndromes accounting for a higher proportion(49.82％);the syndrome elements were mainly qi deficiency(50.00％)and dampness(36.23％),with the disease location in the pancreas,related to the spleen,kidney,and liver.Chi-square tests revealed significant differences in syndrome types(TCM syndromes:x2=100.419,P＜0.001;deficiency-excess syndromes:x2=73.722,P＜0.001),syndrome elements(x2=117.384,P＜0.001),and disease locations(x2=127.191,P＜0.001)across different stages of CP malignant transformation.During CP malignant progression,the proportion of excess syndromes gradually decreased(43.33％→12.32％),while deficiency syndromes increased(26.67％→49.82％).Excess syndrome elements(fire,heat,qi stagnation,blood stasis)decreased(53.48％→25.36％),whereas deficiency syndrome elements(qi deficiency,yin deficiency,yang deficiency,blood deficiency)increased(25.15％→49.64％).The disease location shifted from primarily the liver,spleen,and stomach in the inflammatory stage to the spleen and kidney in the cancerous stage.Conclusion The malignant transformation of CP basically involves the pancreas,is correlated early with liver and spleen-stomach and later with kidney,and exhibits a progression from excess to deficiency in the pattern of"deficiency interweaved with excess syndrome,transition from excess to deficiency,and progressive spleen deficiency".

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal hematologic disorder. Historically, most PNH patients mainly received supportive treatment, which led to poor quality of life and high mortality rates. The advent of downstream complement C5 inhibitors has dramatically changed the natural course of PNH. These inhibitors alleviate clinical symptoms, significantly reduce severe complications, and improve survival rates. Despite their ability to control intravascular hemolysis and enhance hemoglobin levels, approximately half of the treated patients still require blood transfusions due to extravascular hemolysis (EVH) mediated by upstream complement component C3. Upstream complement inhibitors not only control IVH but also reduce the deposition of C3 fragments, thereby solving the problem of EVH and further improving the clinical outcomes of PNH patients. However, due to the cascade of complement activation and the increased accumulation of PNH red blood cells after treatment with upstream complement inhibitors, there may be an increased risk of more severe breakthrough hemolysis events. Additionally, the potential risk of infections associated with complement inhibitors is another issue that needs to be addressed.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal hematologic disorder. Historically, most PNH patients mainly received supportive treatment, which led to poor quality of life and high mortality rates. The advent of downstream complement C5 inhibitors has dramatically changed the natural course of PNH. These inhibitors alleviate clinical symptoms, significantly reduce severe complications, and improve survival rates. Despite their ability to control intravascular hemolysis and enhance hemoglobin levels, approximately half of the treated patients still require blood transfusions due to extravascular hemolysis (EVH) mediated by upstream complement component C3. Upstream complement inhibitors not only control IVH but also reduce the deposition of C3 fragments, thereby solving the problem of EVH and further improving the clinical outcomes of PNH patients. However, due to the cascade of complement activation and the increased accumulation of PNH red blood cells after treatment with upstream complement inhibitors, there may be an increased risk of more severe breakthrough hemolysis events. Additionally, the potential risk of infections associated with complement inhibitors is another issue that needs to be addressed.

BACKGROUND:Whether activating transcription factor 7 interacting protein(Atf7ip)is involved in the regulation in osteogenic differentiation is still controversial,and studying its impact on osteogenic differentiation and its specific mechanisms is of great significance. OBJECTIVE:To investigate the effect of Atf7ip on bone morphogenetic protein 2 promoting osteogenic differentiation of mouse embryonic osteoblast precursor cells(MC3T3-E1). METHODS:MC3T3-E1 cells cultured in vitro were divided into three groups:normal group,interference group(NC-siRNA group,Atf7ip-siRNA group),and high expression group(CMV-VC group and CMV-Atf7ip group),and were transfected for 24 hours,and then treated with 200 ng/mL bone morphogenetic protein 2 for 0,12,24,and 48 hours,respectively.qRT-PCR was used to detect the mRNA expression levels of Atf7ip,alkaline phosphatase,osteocalcin,type I collagen α1 in the cells of each group.Western blot assay was used to detect the protein expression of osteogenic differentiation markers Sp7 and Runx2,and the expression of Atf7ip binding molecule SETDB1,histone H3 and H3K9me3.Alkaline phosphatase activity was detected by alkaline phosphatase staining. RESULTS AND CONCLUSION:(1)With the increase of bone morphogenetic protein 2 treatment time,the protein and mRNA expression of Atf7ip decreased,while the protein expression of Sp7,Runx2 and the mRNA expression of osteocalcin and alkaline phosphatase increased significantly(P<0.05).There was no significant change in the protein expression of Atf7ip binding molecule SETDB1.(2)Compared with the NC-siRNA group,the protein expression of Sp7,Runx2 and the mRNA expression of osteocalcin and type I collagen α1 were significantly up-regulated(P<0.05),and alkaline phosphatase activity was significantly enhanced;and H3K9 methylation significantly decreased in the Atf7ip-siRNA group(P<0.05).(3)Compared with the CMV-VC group,the protein expression of Sp7 and Runx,as well as mRNA expression of osteocalcin,alkaline phosphatase,and type I collagen α1 was significantly downregulated(P<0.05),and the alkaline phosphatase activity was significantly reduced in the CMV-Atf7ip group,while the H3K9 methylation protein in the CMV-Atf7ip group was significantly upregulated compared to the control group(P<0.05).(4)In conclusion,Atf7ip expression was decreased during bone morphogenetic protein 2-induced osteogenic differentiation of MC3T3-E1,and osteogenic differentiation was significantly increased after knockdown of Atf7ip.Overexpression of Atf7ip significantly weakened osteogenic differentiation,indicating that Atf7ip is a negative regulatory factor of bone morphogenetic protein 2 promoting osteogenic differentiation of MC3T3-E1 cells.