OBJECTIVE: To observe the therapeutic effect of electroacupuncture (EA) in improving early enteral nutrition tolerance in patients with acute pancreatitis (AP) under the concept of accelerated rehabilitation, and to explore the related mechanism based on the changes in autonomic nerve characteristics. METHODS: A total of 42 patients with AP were randomized into an observation group (21 cases, 1 case dropped out) and a control group (21 cases, 1 case dropped out). The control group received standard basic treatment for AP. On the basis of the treatment in the control group, EA was applied in the observation group, bilateral Zusanli (ST36), Yixian point (Extra), Tianshu (ST25), Neiguan (PC6) and Zhongwan (CV12) were selected as the main points, and the supplementary points were selected according to syndrome differentiation. Ipsilateral Zusanli (ST36) and Yixian point (Extra) were connected to EA, using discontinuous wave, in frequency of 2 Hz, 30 min a time, once a day for 6 continuous days. The enteral nutrition tolerance score was observed before treatment and after 3 and 5 days of treatment; the visual analogue scale (VAS) score for abdominal pain was observed before treatment and after 3 days of treatment; the time of reaching the feeding goal and hospital stay was recorded; the levels of C-reactive protein (CRP) and amylase were measured before treatment and after 5 days of treatment; the heart rate variability (HRV) indexes (standard deviation of NN intervals [SDNN], average standard deviation of NN intervals [SDANN], root mean square of successive NN interval differences [rMSSD], low frequency [LF] and high frequency [HF], ratio of low frequency to high frequency [LF/HF]) were monitored in the two groups. RESULTS: After 3 and 5 days of treatment, the enteral nutrition tolerance scores were decreased compared with those before treatment in both groups (P<0.01), the reductions in the observation group were larger than those in the control group (P<0.01). After 3 days of treatment, the VAS scores for abdominal pain were decreased compared with those before treatment in both groups (P<0.01), the reduction in the observation group was larger than that in the control group (P<0.01). The time of reaching the feeding goal and hospital stay in the observation group was shorter than that in the control group (P<0.05). After 5 days of treatment, the CRP and amylase levels were decreased compared with those before treatment in both groups (P<0.01), the reduction of CRP level in the observation group was larger than that in the control group (P<0.01). In the observation group, SDNN, SDANN and LF/HF were lower than those in the control group (P<0.05, P<0.01), while rMSSD was higher than that in the control group (P<0.01). SDNN, SDANN and LF/HF were positively correlated with the enteral nutrition tolerance scores after 3 and 5 days of treatment (P<0.05), while rMSSD was negatively correlated with the enteral nutrition tolerance scores after 3 and 5 days of treatment (P<0.01). CONCLUSION Electroacupuncture can improve enteral nutrition tolerance in patients with AP by regulating autonomic nervous function, alleviating the inflammation, promoting accelerated recovery, and reducing the length of hospital stay.
Humans ; Electroacupuncture ; Male ; Female ; Enteral Nutrition ; Middle Aged ; Adult ; Pancreatitis/physiopathology* ; Aged ; Acupuncture Points ; Young Adult ; Acute Disease/therapy* ; Autonomic Pathways/physiopathology*

Objective To discuss the application of ultrasound multimodal diagnostic mode combined with ultrasonic precision interventional technology in differentiating the benign from malignant solid breast masses.Methods A total of 396 patients who underwent breast surgery at the Wuwei Cancer Hospital of China from May 2021 to July 2023 were enrolled in this study.Within 2 weeks before surgery,multimodal ultrasound examination(including two-dimensional ultrasound,color Doppler ultrasound,elastic ultrasound,breast three-dimensional ultrasound,and contrast-enhanced ultrasound)and ultrasound-guided needle biopsy were performed in all patients.The consistency between the results of multimodal ultrasound examination,ultrasound-guided needle biopsy,combination diagnosis and the postoperative pathological diagnoses was analyzed.Results Of the 396 patients with solid breast mass,malignant lesion was seen in 237(59.85％)and benign lesion was seen in 159(40.15％).The sensitivity of multimodal ultrasound in diagnosing benign and malignant solid breast masses was 77.64％(184/237),the specificity was 90.57％(144/159),the positive predictive value was 92.46％(184/199),the negative predictive value was 73.10％(144/197),the accuracy was 82.83％(328/396),and the consistency with the postoperative pathological diagnosis was 0.656.The sensitivity of ultrasound-guided needle puncture in diagnosing benign and malignant solid breast masses was 94.51％(224/237),the specificity was 100.00％(159/159),the positive predictive value was 100.00％(224/224),the negative predictive value was 92.44％(159/172),the accuracy was 96.72％(383/396),and the consistency with the postoperative pathological diagnosis was 0.933.The sensitivity of multimodal ultrasound combined with ultrasound-guided needle puncture in diagnosing benign and malignant solid breast masses was 100.00％(228/228),the specificity was 94.64％(159/168),the positive predictive value was 96.20％(228/237),the negative predictive value was 100.00％(159/159),the accuracy was 97.73％(387/396),and the consistency with the postoperative pathological diagnosis was 0.937.Conclusion The ultrasound multimodal diagnostic mode and ultrasonic precision interventional technology can be used in differentiating the benign from malignant solid breast masses with high diagnostic accuracy.

Ankylosing spondylitis is a chronic immunoinflammatory disease that mainly affects the spine and the sacroiliac joint,the mechanism of which is closely related to signaling pathways,such as osteoprotegerin(OPG)/receptor activator of nuclear factor-κB(RANK)/RANK ligand,mitogen-activated protein kinase(MAPK),Wnt/β-catenin(β-catenin),phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR).Traditional Chinese medicine has the characteristics of multiple components and targets,and is widely used for the treatment of autoimmune diseases due to its low toxicity,strong specificity,and high efficacy.This review found that monomers and compounds of traditional Chinese medicine can exert anti ankylosing spondylitis effects by intervening in the aforementioned signaling pathways,regulating immune inflammatory responses,and inhibiting biological processes such as bone destruction,ectopic osteogenic differentiation,cell apoptosis,and autophagy.

Interferon regulatory factor 1(IRF-1)is a member of the IRF family.It is the first transcription factor to be identified that could bind to the interferon-stimulated response element(ISRE)on the target gene and displays crucial roles in the interferon-induced signals and pathways.IRF-1,as an important medium,has all of the advantages of full cell cycle regulation,cell death signaling transduction,and reinforcing immune surveillance,which are well documented.Current studies indicate that IRF-1 is of vital importance to the occurrence and evolution of multifarious liver diseases,including but not limited to inhibiting the replication of the hepatitis virus(A/B/C/E),alleviating the progression of liver fibrosis,and aggravating hepatic ischemia-reperfusion injury(HIRI).The tumor suppression of IRF-1 is related to the clinical characteristics of liver cancer patients,which makes it a potential indicator for predicting the prognosis and recurrence of liver cancer;additionally,the latest studies have revealed other effects of IRF-1 such as protection against alcoholic/non-alcoholic fatty liver disease(AFLD/NAFLD),cholangiocarcinoma suppression,and uncommon traits in other liver diseases that had previously received little attention.Intriguingly,several compounds and drugs have featured a protective function in specific liver disease models in which there is significant involvement of the IRF-1 signal.In this paper,we hope to propose a prospective research basis upon which to help decipher translational medicine applications of IRF-1 in liver disease treatment.

Background: Diabetes-induced cardiac fibrosis is one of the main mechanisms of diabetic cardiomyopathy. As a common histone methyltransferase, enhancer of zeste homolog 2 (EZH2) has been implicated in fibrosis progression in multiple organs. However, the mechanism of EZH2 in diabetic myocardial fibrosis has not been clarified. Methods: In the current study, rat and mouse diabetic model were established, the left ventricular function of rat and mouse were evaluated by echocardiography and the fibrosis of rat ventricle was evaluated by Masson staining. Primary rat ventricular fibroblasts were cultured and stimulated with high glucose (HG) in vitro. The expression of histone H3 lysine 27 (H3K27) trimethylation, EZH2, and myocardial fibrosis proteins were assayed. Results: In STZ-induced diabetic ventricular tissues and HG-induced primary ventricular fibroblasts in vitro, H3K27 trimethylation was increased and the phosphorylation of EZH2 was reduced. Inhibition of EZH2 with GSK126 suppressed the activation, differentiation, and migration of cardiac fibroblasts as well as the overexpression of the fibrotic proteins induced by HG. Mechanical study demonstrated that HG reduced phosphorylation of EZH2 on Thr311 by inactivating AMP-activated protein kinase (AMPK), which transcriptionally inhibited peroxisome proliferator-activated receptor γ (PPAR-γ) expression to promote the fibroblasts activation and differentiation. Conclusion Our data revealed an AMPK/EZH2/PPAR-γ signal pathway is involved in HG-induced cardiac fibrosis.

Changes in the enteric nervous system(ENS)play a critical role in the generation and development of constipation.Chronic constipation is thought to be largely caused by the lack or deterioration of enteric nerve cells.At present,most domestic and foreign medical institutions still rely on paraffin pathological sections for the identification and detection of ENS in patients with constipation.However,even major ENS defects are difficult to precisely identify in pathological sections of the human gut.Therefore,studying new technologies that can better visualize ENS is a crucial link in exploring the relevant development mechanisms of constipation.This review reviews the development venation of quantitative studies on ENS in the past two decades,and discusses the relationship between quantitative data on ENS and various types of constipation.This article reviewed the methods of recognition and detection of the ENS,hoping to provide more stable observation criteria,and then help explore the mechanism of the generation and development of constipation.

Changes in the enteric nervous system(ENS)play a critical role in the generation and development of constipation.Chronic constipation is thought to be largely caused by the lack or deterioration of enteric nerve cells.At present,most domestic and foreign medical institutions still rely on paraffin pathological sections for the identification and detection of ENS in patients with constipation.However,even major ENS defects are difficult to precisely identify in pathological sections of the human gut.Therefore,studying new technologies that can better visualize ENS is a crucial link in exploring the relevant development mechanisms of constipation.This review reviews the development venation of quantitative studies on ENS in the past two decades,and discusses the relationship between quantitative data on ENS and various types of constipation.This article reviewed the methods of recognition and detection of the ENS,hoping to provide more stable observation criteria,and then help explore the mechanism of the generation and development of constipation.

Objective To investigate the mechanism and the effect of miR-524-5p regulating HEG1 expression on the proliferation and epithelial-mesenchymal transition of esophageal cancer cells. Methods The expression levels of miR-524-5p and HEG1 mRNA in esophageal cancer cells and normal esophageal epithelial cells were detected by qRT-PCR. KYSE30 cells were divided into miR-524-5p mimic group, miR-524-5p NC group, miR-524-5p mimic+pcDNA3.1 group, and miR-524-5p mimic+pcDNA3.1-HEG1 group. Non-transfected cells were set as the normal control group (group Control). CCK-8 method was applied to detect the proliferation ability of KYSE30 cells. Western blot analysis was conducted to detect the expression of proteins related to EMT, invasion, and migration and the HEG1 protein. Scratch and Transwell assays were applied to detect the migration and invasion abilities of KYSE30 cells. A dual-luciferase reporter gene was used to examine the targeting relationship between miR-524-5p and HEG1. Results miR-524-5p was lowly expressed in four esophageal cancer cell lines, namely, TE-1, KYSE30, KYSE150, and NEC (P < 0.05). KYSE30 cells with the lowest expression level were selected for subsequent experiments. HEG1 mRNA was highly expressed in four esophageal cancer cell lines (P < 0.05). The GEPIA database showed that HEG1 was highly expressed in esophageal cancer tumor tissues (P < 0.05). KYSE30 cells in the miR-524-5p mimic group had lower proliferation ability, colony formation number, mesenchymal marker protein expression, and migration and invasion abilities and upregulated epithelial marker protein E-cadherin level than cells in the miR-524-5p NC group (P < 0.05). The miR-524-5p mimic+pcDNA3.1-HEG1 group significantly reversed the inhibitory effect of overexpression of miR-524-5p on the proliferation, epithelial–mesenchymal transformation, invasion, and metastasis of KYSE30 cells (P < 0.05). The luciferase activity of cells in the miR-524-5p mimic and WT-HEG1 co-transfection groups was lower than that in the miR-524-5p NC and WT-HEG1 co-transfection groups (P < 0.05). Conclusion miR-524-5p is lowly expressed in EC cells and tissues. The overexpression of miR-524-5p can negatively regulate the expression of HEG1 in esophageal cancer cell line (KYSE30 cells) and reduce the proliferation, EMT process, and invasion and migration abilities of KYSE30 cells.

The eukaryotic genome is folded into higher-order conformation accompanied with constrained dynamics for coordinated genome functions. However, the molecular machinery underlying these hierarchically organized three-dimensional (3D) chromatin architecture and dynamics remains poorly understood. Here by combining imaging and sequencing, we studied the role of lamin B1 in chromatin architecture and dynamics. We found that lamin B1 depletion leads to detachment of lamina-associated domains (LADs) from the nuclear periphery accompanied with global chromatin redistribution and decompaction. Consequently, the inter-chromosomal as well as inter-compartment interactions are increased, but the structure of topologically associating domains (TADs) is not affected. Using live-cell genomic loci tracking, we further proved that depletion of lamin B1 leads to increased chromatin dynamics, owing to chromatin decompaction and redistribution toward nucleoplasm. Taken together, our data suggest that lamin B1 and chromatin interactions at the nuclear periphery promote LAD maintenance, chromatin compaction, genomic compartmentalization into chromosome territories and A/B compartments and confine chromatin dynamics, supporting their crucial roles in chromatin higher-order structure and chromatin dynamics.
Chromatin ; Chromosomes ; Genome ; Humans ; Lamin Type B/genetics*

Targeted gene therapy has become a promising approach for lung cancer treatment. In our previous work, we reported that the targeted expression of microRNA-7 (miR-7) operated by thyroid transcription factor-1 (TTF-1) promoter inhibited the growth of human lung cancer cells in vitro and in vivo; however, the intervention efficiency needed to be further improved. In this study, we identified the core promoter of TTF-1 (from -1299 bp to -871 bp) by 5' deletion assay and screened out the putative transcription factors nuclear factor-1 (NF-1) and activator protein-1 (AP-1). Further analysis revealed that the expression level of NF-1, but not AP-1, was positively connected with the activation of TTF-1 core promoter in human non-small-cell lung cancer (NSCLC) cells. Moreover, the silencing of NF-1 could reduce the expression level of miR-7 operated by TTF-1 core promoter. Of note, we optimized four distinct sequences to form additional NF-1-binding sites (TGGCA) in the sequence of TTF-1 core promoter (termed as ^optTTF-1 promoter), and verified the binding efficiency of NF-1 on the ^optTTF-1 promoter by electrophoretic mobility shift assay (EMSA). As expected, the ^optTTF-1 promoter could more effectively drive miR-7 expression and inhibit the growth of human NSCLC cells in vitro, accompanied by a reduced transduction of NADH dehydrogenase (ubiquinone) 1α subcomplex 4 (NDUFA4)/protein kinase B (Akt) pathway. Consistently, ^optTTF-1 promoter-driven miR-7 expression could also effectively abrogate the growth and metastasis of tumor cells in a murine xenograft model of human NSCLC. Finally, no significant changes were detected in the biological indicators or the histology of some important tissues and organs, including heart, liver, and spleen. On the whole, our study revealed that the optimized TTF-1 promoter could more effectively operate miR-7 to influence the growth of human NSCLC cells, providing a new basis for the development of microRNA-based targeting gene therapy against clinical lung cancer.
Animals ; Humans ; Mice ; Carcinoma, Non-Small-Cell Lung/therapy* ; Lung Neoplasms/metabolism* ; MicroRNAs/metabolism* ; Nuclear Proteins/metabolism* ; Thyroid Gland/pathology* ; Thyroid Nuclear Factor 1/genetics* ; Transcription Factors/metabolism*