ObjectiveTo explore the mechanism by which Xiaoyaosan regulates HPT axis dysfunction in the rat model with the syndrome of liver depression and spleen deficiency by observing its effect on the glycoprotein hormone α-subunit （CGA）/glutathione peroxidase 2 （GPX2）/thyroid-stimulating hormone β-subunit （TSHβ） pathway for thyroid hormone synthesis. MethodsSeventy-two male SD rats were randomized into six groups： normal， model， high-dose （16.7 g·kg^-1）， medium-dose （8.35 g·kg^-1）， and low-dose （4.175 g·kg^-1） Xiaoyaosan， and fluoxetine （0.001 8 g·kg^-1） groups， with 12 rats in each group. The rat model of liver depression and spleen deficiency was induced by chronic restraint stress for 21 days. The intervention groups were treated with Xiaoyaosan decoctions or fluoxetine suspension， respectively. After modeling， hematoxylin-eosin staining was employed to observe morphological changes in the thyroid and pituitary tissue of the rats. Serum levels of triiodothyronine （T3）， tetraiodothyronine （T4）， and thyroid-stimulating hormone （TSH） were measured by enzyme-linked immunosorbent assay （ELISA）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were employed to determine the mRNA and protein levels， respectively， of TSH receptor （TSHR） in the thyroid tissue， thyrotropin-releasing hormone receptor （TRHR） and TSHβ in the pituitary tissue， and thyrotropin-releasing hormone （TRH）， CGA， GPX2， and TSHβ in the hypothalamic tissue. ResultsCompared with the normal group， the model group showed significant atrophy and irregularity of thyroid follicles， a marked reduction in colloid secretion， extensive vacuolar degeneration of adenocytes in the anterior pituitary， lowered serum levels of T3， T4， and TSH （P<0.01）， and down-regulated mRNA and protein levels of TSHR in the thyroid tissue， TRHR and TSHβ in the pituitary tissue， and TRH， CGA， GPX2， and TSHβ in the hypothalamic tissue （P<0.01）. Compared with the model group， high- and medium-dose Xiaoyaosan and fluoxetine alleviated the pathological changes in the thyroid and pituitary tissue， outperforming the low-dose Xiaoyaosan group. Moreover， they elevated the serum levels of T3， T4， and TSH （P<0.05， P<0.01）. The serum TSH level was also elevated in the low-dose Xiaoyaosan group （P<0.05）. The mRNA and protein levels of TSHR in the thyroid， TRHR and TSHβ in the pituitary， and TRH， CGA， GPX2， and TSHβ in the hypothalamus were up-regulated in the high- and medium-dose Xiaoyaosan groups （P<0.05， P<0.01）. Additionally， the mRNA and protein levels of TSHβ in the hypothalamus were up-regulated in the low-dose Xiaoyaosan group （P<0.01）. In the fluoxetine group， the mRNA and protein levels of TSHR in the thyroid， TRHR in the pituitary， and TRH， CGA， and GPX2 in the hypothalamus were up-regulated （P<0.05， P<0.01）. ConclusionThe downregulation of CGA/GPX2/TSHβ pathway may be one of the biological mechanisms underlying HPT axis dysfunction in the rat model with the syndrome of liver depression and spleen deficiency. Xiaoyaosan may regulate the HPT axis dysfunction by up-regulating the CGA/GPX2/TSHβ pathway.

Objective To analyze the application value of assisted compressed sensing(ACS)combined with deep reconstruction(DR)(ACS+DR)algorithm in MR abdominal T2WI.Methods A total of 60 patients were prospectively selected to undergo three types of respiratory-triggered transverse T2 sequence scans:fast spin echo(FSE),propeller scanning(ARMS),and ACS+DR.Two radiologists independently evaluated the images for respiratory motion artifacts,gastrointestinal peristalsis artifacts,sharpness of intrahepatic vessel and bile duct,lesion clarity,and overall image quality.Additionally,the signal-to-noise ratio(SNR),contrast-to-noise ratio(CNR),and contrast ratio(CR)between lesions and liver parenchyma signal intensity were calculated.Wilcoxon and independent sample Mann-Whitney U tests were used to compare objective scores and subjective evaluations among different groups.Results The scan time for the ACS+DR sequence was 35 s,for the ARMS sequence 180 s,and for the FSE sequence 210 s.The ACS+DR sequence showed superior performance over the other sequences in terms of scan time,respiratory motion artifacts,intrahepatic vessel and bile duct sharpness,lesion clarity,and overall image quality(P＜0.05).Compared with FSE sequence,the ARMS and ACS+DR sequences exhibited higher SNR,CNR,and CR(P＜0.05).The ACS+DR sequence showed better SNR and CNR than the ARMS sequence(P＜0.05);however,there was no significant difference between the two sequences in CR(P＞0.05).No significant difference was found among the three sequences in the number of detected lesions(P＞0.05).Conclusion The ACS+DR reconstruction algorithm for upper abdominal imaging not only ensures high image quality but also significantly improves scan speed,making it valuable for clinical application.

Sepsis is a life-threatening organ dysfunction caused by the host's dysregulated response to infection, with a complex pathogenesis and high mortality rate. Currently, there are no clear and effective treatment drugs available. Epigenetic modification serves as a major mechanism regulating gene expression under pathological and physiological conditions, and it has been shown to play a critical role in regulating the occurrence and development of sepsis. Histone acetylation modification, as a sophisticated epigenetic modification mechanism, plays a crucial regulatory role in many aspects of life. It can jointly regulate the acetylation status of histones through histone acetyltransferase (HAT) and histone deacetylase (HDAC), thereby changing DNA expression and dynamically regulating sepsis related gene expression at the epigenetic level. Previous studies have shown that histone acetylation can participate in the progression of sepsis by regulating inflammatory mediators, nuclear factor-ΚB (NF-ΚB) signaling pathway, autophagy, efferocytosis, ferroptosis, pyroptosis. These mechanisms are promising targets for novel sepsis treatments. In addition, with the deepening of research, it has been found that various selective/non selective histone deacetylase inhibitors (HDACI) can regulate histone acetylation status by acting on different HDAC targets, which has been shown to alleviate organ damage caused by sepsis and improve prognosis in septic animal models. This article further summarizes the role and potential applications of histone acetylation in sepsis, providing new ideas for the treatment of sepsis.
Sepsis/metabolism* ; Acetylation ; Humans ; Histones/metabolism* ; Histone Acetyltransferases/metabolism* ; Histone Deacetylase Inhibitors ; Epigenesis, Genetic ; Histone Deacetylases/metabolism* ; Signal Transduction ; NF-kappa B/metabolism* ; Animals

Acute pancreatitis(AP)is a common and severe digestive disease in dogs,characterized by a high recurrence rate and complications that significantly impact canine health.This study in-vestigates the mechanism by which adipose-derived stem cells(ADSCs)regulate the CHOP/Bcl-2 pathway to mitigate acute pancreatic injury in dogs.Twenty Beagle dogs were randomly divided in-to four groups:a Sham group,an AP model group,an ADSCs treatment group,and a conditioned medium(CM)treatment group.The AP model was established by injecting a mixed solution of trypsin and sodium taurocholate into the AP model group.The ADSCs treatment group received intravenous injections of ADSCs immediately following surgery,while the CM treatment group re-ceived conditioned medium preparations.Pancreatic tissue was collected 24 hours post-surgery,and changes in the CHOP/Bcl-2 pathway were assessed using histopathology,transmission electron microscopy,western blotting,fluorescence quantification,immunofluorescence,and TUNEL stai-ning.The results indicated that AP induced significant interstitial edema,hemorrhage,inflammato-ry cell infiltration,chromatin contraction,and endoplasmic reticulum swelling,the expression lev-els of GRP78 and CHOP were found to be elevated,whereas the expression of Bcl-2 was downreg-ulated.Additionally,the expression levels of BAX,JNK,Caspase-3,and Caspase-12 increased,leading to an increased rate of cell apoptosis.Such changes result in an elevated apoptosis rate and a further decrease in Bcl-2 expression.Both ADSCs and CM therapy were found to alleviate the path-ological damage in pancreatic tissue,resulting in downregulation of CHOP and apoptosis-related markers,upregulation of Bcl-2,and a reduction in the apoptosis rate.The results of this study sug-gest that ADSCs may mitigate acute pancreatic injury induced by trypsin and sodium taurocholate in AP dogs by modulating the CHOP/Bcl-2 pathway.Targeted modulation of the transcriptional activity of CHOP may offer novel therapeutic approaches for AP.

Objective To analyze the application value of assisted compressed sensing(ACS)combined with deep reconstruction(DR)(ACS+DR)algorithm in MR abdominal T2WI.Methods A total of 60 patients were prospectively selected to undergo three types of respiratory-triggered transverse T2 sequence scans:fast spin echo(FSE),propeller scanning(ARMS),and ACS+DR.Two radiologists independently evaluated the images for respiratory motion artifacts,gastrointestinal peristalsis artifacts,sharpness of intrahepatic vessel and bile duct,lesion clarity,and overall image quality.Additionally,the signal-to-noise ratio(SNR),contrast-to-noise ratio(CNR),and contrast ratio(CR)between lesions and liver parenchyma signal intensity were calculated.Wilcoxon and independent sample Mann-Whitney U tests were used to compare objective scores and subjective evaluations among different groups.Results The scan time for the ACS+DR sequence was 35 s,for the ARMS sequence 180 s,and for the FSE sequence 210 s.The ACS+DR sequence showed superior performance over the other sequences in terms of scan time,respiratory motion artifacts,intrahepatic vessel and bile duct sharpness,lesion clarity,and overall image quality(P＜0.05).Compared with FSE sequence,the ARMS and ACS+DR sequences exhibited higher SNR,CNR,and CR(P＜0.05).The ACS+DR sequence showed better SNR and CNR than the ARMS sequence(P＜0.05);however,there was no significant difference between the two sequences in CR(P＞0.05).No significant difference was found among the three sequences in the number of detected lesions(P＞0.05).Conclusion The ACS+DR reconstruction algorithm for upper abdominal imaging not only ensures high image quality but also significantly improves scan speed,making it valuable for clinical application.

Acute pancreatitis(AP)is a common and severe digestive disease in dogs,characterized by a high recurrence rate and complications that significantly impact canine health.This study in-vestigates the mechanism by which adipose-derived stem cells(ADSCs)regulate the CHOP/Bcl-2 pathway to mitigate acute pancreatic injury in dogs.Twenty Beagle dogs were randomly divided in-to four groups:a Sham group,an AP model group,an ADSCs treatment group,and a conditioned medium(CM)treatment group.The AP model was established by injecting a mixed solution of trypsin and sodium taurocholate into the AP model group.The ADSCs treatment group received intravenous injections of ADSCs immediately following surgery,while the CM treatment group re-ceived conditioned medium preparations.Pancreatic tissue was collected 24 hours post-surgery,and changes in the CHOP/Bcl-2 pathway were assessed using histopathology,transmission electron microscopy,western blotting,fluorescence quantification,immunofluorescence,and TUNEL stai-ning.The results indicated that AP induced significant interstitial edema,hemorrhage,inflammato-ry cell infiltration,chromatin contraction,and endoplasmic reticulum swelling,the expression lev-els of GRP78 and CHOP were found to be elevated,whereas the expression of Bcl-2 was downreg-ulated.Additionally,the expression levels of BAX,JNK,Caspase-3,and Caspase-12 increased,leading to an increased rate of cell apoptosis.Such changes result in an elevated apoptosis rate and a further decrease in Bcl-2 expression.Both ADSCs and CM therapy were found to alleviate the path-ological damage in pancreatic tissue,resulting in downregulation of CHOP and apoptosis-related markers,upregulation of Bcl-2,and a reduction in the apoptosis rate.The results of this study sug-gest that ADSCs may mitigate acute pancreatic injury induced by trypsin and sodium taurocholate in AP dogs by modulating the CHOP/Bcl-2 pathway.Targeted modulation of the transcriptional activity of CHOP may offer novel therapeutic approaches for AP.

Cardiac arrest most commonly occurs outside of the hospital, known as out-of-hospital cardiac arrest (OHCA), and is an important global health problem. Approximately 40% of cardiac arrest has no clear cause. Hereditary arrhythmias and cardiomyopathies factors contribute to cardiac arrest. The identification of genetic factors for cardiac arrest after its occurrence is of great value not only for the individual, but also for relatives who may be at risk for the disease in their family. In the United States, there are over 350?000 cases of OHCA and over 200?000 cases of in-hospital cardiac arrest (IHCA) each year, and in Western Europe, cardiac arrest accounts for 15%-20% of all adult natural deaths and 50% of all cardiovascular deaths. In order to reduce the burden caused by cardiac arrest within society, it is essential to further understand its etiological factors, such as incidence in different regions, risk factors, and populations at higher risk. For each individual, cardiac arrest is the result of a complex interaction of genetic and acquired factors. Understanding the complex interplay of pathogenic factors in cardiac arrest and the development of individualized prevention and treatment approaches requires the collection of clinical data from cardiac arrest populations and multimodal analysis in order to identify epidemiological features and risk factors for cardiac arrest. Recently, cardiac arrest-related data are being collected and integrated in Europe in different regions and populations. As a result of the commitment to the creation of large datasets of clinical information on cardiac arrest populations, the knowledge of the pathology of cardiac arrest pathogenesis as well as risk factors is steadily increasing. This article reviews the epidemiologic data of cardiac arrest in recent years and the associated risk factors, thus providing ideas for developing better strategies for the prevention and treatment of cardiac arrest.

Pyroptosis is a programmed death of inflammatory cells triggered by pathogen invasion,dependent on caspase activation,through both classical and non-classical pyroptosis pathways.Cell pyroptosis is related to the occurrence and development of a variety of animal infectious diseases caused by microbial infection.After microorganisms invading,cells are stimulated by pathology-re-lated molecular patterns,causing strong immune response,stimulating inflammatory signaling pathways,and then activating inflammasome,leading to pyroptosis.The immune system has e-volved multiple mechanisms to fight microbial infections and regulate inflammatory responses.The innate immune system,by recognizing microbial molecules in pathogens and responding quickly by producing inflammasome and activating pyroptosis,helps clear pathogens to prevent infection and maintain the normal functioning of the body.A thorough study of the pathogenesis and immune es-cape mechanism of cell pyroptosis in animal infectious diseases will provide a new direction for the treatment of animal infectious diseases.

Objective     To analyze the clinical intervention effect of multi-disciplinary team (MDT) nursing mode on patients after transcatheter aortic valve implantation (TAVI). Methods     A total of 89 patients who were admitted to our hospital and underwent TAVI surgery from April to December 2021 were selected, including 64 males and 25 females, with an average age of 64.7±11.8 years. The subjects were divided into a MDT intervention group (n=42) and a control group (n=47) according to different postoperative nursing intervention methods. Clinical effectivenesses were compared between the two groups. Results     The left ventricular ejection fraction in the two groups significantly increased on the 7th day after the operation, and the increase in the MDT intervention group was more obvious, with no statistical  difference between the two groups (P=0.14). On the 7th day after surgery, forced vital capacity/predicated value and forced expiratory volume in one second/predicated value significantly decreased, and decreased more significantly in the control group than those in the MDT intervention group with statistical differences (P=0.01). The ICU stay time (P=0.01), hospital stay time (P<0.01) and total postoperative pulmonary complications rate (P=0.03) in the MDT intervention group were significantly shorter or lower than those in the control group The evaluation results of the anxiety and depression status of the patients before and after nursing intervention showed that the scores of anxiety and depression in the two groups were significantly lower than before, and the scores of each scale in the MDT intervention group were lower. The score of quality of life of the two groups significantly improved at the end of 6 months after surgery, and in the MDT intervention group it was significantly higher than that in the control group (P=0.02). Conclusion     MDT intervention mode can promote the rapid recovery of patients after TAVI, effectively reduce the risk of postoperative pulmonary complications, and improve the postoperative quality of life.

Cardiac fibrosis is a cause of morbidity and mortality in people with heart disease. Anti-fibrosis treatment is a significant therapy for heart disease, but there is still no thorough understanding of fibrotic mechanisms. This study was carried out to ascertain the functions of cytokine receptor-like factor 1 (CRLF1) in cardiac fibrosis and clarify its regulatory mechanisms. We found that CRLF1 was expressed predominantly in cardiac fibroblasts. Its expression was up-regulated not only in a mouse heart fibrotic model induced by myocardial infarction, but also in mouse and human cardiac fibroblasts provoked by transforming growth factor-‍β1 (TGF‍-‍β1). Gain- and loss-of-function experiments of CRLF1 were carried out in neonatal mice cardiac fibroblasts (NMCFs) with or without TGF-‍β1 stimulation. CRLF1 overexpression increased cell viability, collagen production, cell proliferation capacity, and myofibroblast transformation of NMCFs with or without TGF‍-‍β1 stimulation, while silencing of CRLF1 had the opposite effects. An inhibitor of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and different inhibitors of TGF-‍β1 signaling cascades, comprising mothers against decapentaplegic homolog (SMAD)‍-dependent and SMAD-independent pathways, were applied to investigate the mechanisms involved. CRLF1 exerted its functions by activating the ERK1/2 signaling pathway. Furthermore, the SMAD-dependent pathway, not the SMAD-independent pathway, was responsible for CRLF1 up-regulation in NMCFs treated with TGF-‍β1. In summary, activation of the TGF-‍β1/SMAD signaling pathway in cardiac fibrosis increased CRLF1 expression. CRLF1 then aggravated cardiac fibrosis by activating the ERK1/2 signaling pathway. CRLF1 could become a novel potential target for intervention and remedy of cardiac fibrosis.
Animals ; Humans ; Mice ; Disease Models, Animal ; Fibroblasts/metabolism* ; Fibrosis ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase 3/metabolism* ; Myocardial Infarction/metabolism* ; Receptors, Cytokine/metabolism* ; Signal Transduction ; Transforming Growth Factor beta1/pharmacology*