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Portal vein thrombosis （PVT） is one of the common complications during the natural course of liver cirrhosis and has an important influence on the progression of liver cirrhosis. This article mainly summarizes the research advances in the risk factors for PVT. There are many risk factors for PVT， and Virchow’s triad， namely venous stasis， hypercoagulability， and vascular endothelial injury and systemic inflammation caused by surgery or trauma， are considered the main reasons for the development and progression of PVT. At present， more prospective studies are still needed to validate the predictive models for the risk of PVT that have certain application prospects in clinical practice. Cirrhotic patients with PVT tend to have a poor prognosis， and complete obstructive PVT is associated with increased mortality after liver transplantation. Recent studies have shown that prophylactic anticoagulant therapy is safe and effective in patients with liver cirrhosis and can thus help with the prevention and treatment of PVT.
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Objective:To analyze the correlation between serum bile acid and glycolipid metabolism in patients with type 2 diabetic mellitus (T2DM) and metabolically associated fatty liver disease (MAFLD).Methods:A total of 387 T2DM patients hospitalized in Jinan Central Hospital in Shandong Province from July 2020 to November 2021 were selected, including 140 T2DM patients (T2DM group) and 247 T2DM patients with MAFLD (T2DM with MAFLD group). Clinical data were collected of all patients for retrospective analysis and compare the differences in clinical datas in the T2DM group and the T2DM with MAFLD group. Analyze the influencing factors of T2DM with MAFLD. The serum total bile acid (S-TBA) of the T2DM with MAFLD group was divided into T1, T2 and T3 groups by the method of trisection. Triglyceride glucose index (TyG) and hemoglobin glycation index (HGI) were divided into low TyG group, high TyG group and low HGI group, high HGI group by their median values. The incidence of hyperlipidemia, degree of insulin resistance and glycosylated hemoglobin variation was compared among the three groups. To analyze the influencing factors of TyG and HGI. The measurement data conforming to the normal distribution were compared between two groups by independent sample t-test, the comparison between multiple groups by ANOVA, the comparison between two groups of measurement data not conforming to the normal distribution by Mann Whitney U test, and the comparison between multiple groups by Kruskal Wallis H test, χ 2 test was used for comparison of count data between groups. The influencing factors of T2DM with MAFLD and high HGI were analyzed by multivariate binary Logistic regression. The influencing factors of TyG were analyzed using multiple stepwise linear regression. Results:There was no significant difference between the S-TBA of T2DM group and T2DM with MAFLD group ( P>0.05). TyG ( OR=1.788, 95% CI: 1.223-2.614), superoxide dismutase (SOD) ( OR=1.019, 95% CI: 1.009-1.030) and VFA (visceral fat area) ( OR=1.021, 95% CI: 1.013-1.028) were risk factors for the occurrence of T2DM with MAFLD ( P values are 0.003, 0.001 and 0.001, respectively). The incidence of high TyG in T3 group (61.0% (50/82)) as higher than that in T1 group (40.0% (32/80)), the incidence of high HGI in T3 group (61.0% (50/82)) was higher than that in T2 group (41.2% (35/85)), the morbidity of hypercholesterolemia in T3 group (15.9% (13/82)) was higher than that in T2 group (4.7% (4/85)), the differences were statistically significant (χ 2 values were 7.13, 6.55, 5.67; the P values were 0.008, 0.011, 0.017). S-TBA, hepatic steatosis index (HSI) and VFA were independent influencing factors of TyG (the P values were 0.003, <0.001, <0.001). S-TBA ( OR=0.940, 95% CI:0.887-0.997) and fasting C peptide ( OR=0.454, 95% CI:0.219-0.940) were protective factors for the occurrence of high HGI (the P values were 0.039, 0.034). Conclusion:S-TBA was positively correlated with the degree of insulin resistance and incidence of hypercholesterolemia in patients with T2DM and MAFLD, negatively correlated with the degree of glycated hemoglobin variation.
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Depression is a common psychiatric disease that seriously affects the physical and mental health and quality of life of patients， and has become one of the major global disease burdens. The etiology of depression is intricate， and despite extensive research， its pathogenesis remains inconclusive， resulting in various hypotheses of its onset mechanisms. Presently， the primary approach for clinically treating depression involves the utilization of selective inhibitors targeting the reuptake of monoamine neurotransmitters within the central nervous system. However， these drugs are generally characterized by delayed onset of action， limited efficacy and obvious resistance. Recently， researchers have gradually turned their attention to the development of antidepressant drugs with novel mechanisms. Notably， as a category of abundantly available active ingredients in Chinese medicine， numerous pharmacological studies have demonstrated that oligosaccharides and polysaccharides possess promising antidepressant properties， such as Morindae Officinalis Radix oligosaccharides， Polygalae Radix oligosaccharide esters， Poria polysaccharides and Astragali Radix polysaccharides. Their pharmacological mechanisms are various， including enhancing the levels of monoamine neurotransmitters in the brain， inhibiting the hyperactivation of the hypothalamic-pituitary-adrenal axis（HPA axis）， increasing the expression of neurotrophic factors（NTF）， regulating immune-inflammatory responses and modulating the microbiota-gut-brain axis. Therefore， oligosaccharides and polysaccharides from Chinese medicine have become a vital source of safe and effective novel antidepressant candidates due to the potential to improve depression through integrated regulatory effects. This article aims to provide a comprehensive and systematic review of recent progress to contribute to the elucidation of the mechanisms underlying the antidepressant effects of oligosaccharides and polysaccharides derived from Chinese medicine.
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Epidermal growth factor receptor exon 20 insertion (EGFR ex20ins) is one of the earliest driver gene activation mutations in non-small cell lung cancer (NSCLC). However, due to the unique structure of protein variation caused by this mutation, most patients with EGFR ex20ins mutation (except A763_Y764insFQEA) have poor response to the launched first/second/third generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs). With the successive approval of new specific targeted drugs for EGFR ex20ins in Food and Drug Administration (FDA) and other national regulatory agencies, the development and clinical research of targeted drugs for EGFR ex20ins in China have also developed rapidly and Mobocertinib has been approved recently in China. It is worth noting that EGFR ex20ins is a variant type with strong molecular heterogeneity. How to detect it comprehensively and accurately in clinical practice, so as to enable more patients to benefit from targeted therapy, is a very important and urgent problem to be solved. This review introduces the molecular typing of EGFR ex20ins, then discusses the importance of EGFR ex20ins detection and the differences of various detection methods, and summarizes the research and development of new drugs progress of EGFR ex20ins, in order to optimize the diagnosis and treatment path of EGFR ex20ins patients by selecting accurate, rapid and appropriate detection methods, so as to improve the clinical benefits of the patients. .
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Humanos , Estados Unidos , Carcinoma de Pulmón de Células no Pequeñas , Mutagénesis Insercional , Neoplasias Pulmonares , Receptores ErbB , ExonesRESUMEN
The incidence rate of nonalcoholic fatty liver disease (NAFLD) continues to rise around the world, and due to its complex pathogenesis, there is still a lack of effective treatment drugs. If NAFLD is not treated in time, it may increase the risk of related metabolic diseases such as diabetes and hyperlipidemia and even lead to liver fibrosis and liver cirrhosis. Glucagon-like peptide-1 is a hormone secreted by L-shaped cells of the small intestine and can regulate glucose-dependent stimulation of insulin secretion, reduce gastric emptying, and inhibit food intake. This article reviews the effect of glucagon-like peptide-1 receptor agonist in the treatment of NAFLD and related mechanism.
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Hepatocellular carcinoma (HCC) is a primary malignant tumor of the liver and has a complex pathogenesis. At present, the oxidative stress theory is one of the many important theories for the mechanism of the development and progression of this disease. Autophagy is an important way for cells to clear misfolded proteins or damaged organelles and maintain homeostasis of the internal environment. An increasing number of evidence has shown that autophagy plays an important role in liver fibrosis and HCC and is closely associated with oxidative stress. With reference to the latest research findings around the world, this article analyzes the interaction between autophagy and oxidative stress in the pathogenesis of HCC from the aspect of their relationship with HCC. It is pointed out that the molecular mechanism by which autophagy regulates oxidative stress in the development of HCC may become a research hotspot in the future; it may provide a new means for the early diagnosis and treatment of HCC to activate or block a key pathway through which autophagy regulates oxidative stress.
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A large number of studies have shown that berberine exerts an anti-tumor effect mainly by inhibiting cancer cell proliferation, inducing cancer cell death, inhibiting cancer cell metastasis and invasion, regulating the expression of endogenous oncogenes and tumor suppressor genes, affecting the activity of cancer-related enzymes, exerting an anti-oxidative stress effect, correcting abnormal glucose metabolism, and inhibiting the activity of nuclear factor-kappa B and its pathways. In vivo and in vitro studies have shown than berberine has a marked clinical effect in the treatment of hepatocellular carcinoma with various pharmacological actions and molecular regulatory mechanisms. This article reviews the role and mechanism of berberine, an active component of traditional Chinese medicines including Coptis chinensis, in the treatment of hepatocellular carcinoma and thus reveals the clinical effect of berberine in the treatment of hepatocellular carcinoma. In future, new dosage forms should be developed to improve its bioavailability and form effective therapeutic regimens for clinical application.
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Objective To evaluate the prognostic accuracy of the score of toxic epidermal necrolysis (SCORTEN) scoring system in patients with toxic epidermal necrolysis (TEN) or Stevens-Johnson syndrome (SJS).Methods Clinical data were collected from 39 patients with SJS/TEN hospitalized in Peking Union Medical College Hospital during April 1992 and March 2014,and retrospectively analyzed.Among the 39 patients,13 had died,and the other 26 patients,who were matched to the dead patients in a ratio of 2:1 for age,all had a definite diagnosis and were discharged with improved conditions.The SCORTEN scoring system was used to evaluate the 39 patients with SJS/TEN and calculate expected mortality.The expected mortality and actual mortality were compared between different groups stratified by age in the 39 patients.The receiver operating characteristic (ROC) curve was drawn to assess the prognostic accuracy of the SCORTEN scoring system.Results According to the SCORTEN scoring system,15 out of the 39 patients scored 1 point,14 scored 2 points,6 scored 3 points,and 4 scored 4 points.The total number of expected deaths was 6.808,while that of actual deaths was 13.There was no significant difference between the expected mortality and actual mortality in every SCORTEN score-based group.The area under curve (AUC) was 0.832 8,indicating a good predictive ability of the SCORTEN scoring system.Conclusion The SCORTEN scoring system can predict mortality in TEN/SJS patients at early stage.
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Aim To investigate the effect of the total flaconoids extracted from Xiaobuxin-Tan g ( XBXT-2 ) on the hyperactivity of hypothalamic-pituitary-adrenal axis in mouse learned helplessness model. Methods Learned helplessness was induced by inescapable foot shock stress over 1h session for 5 days. After screen-ing, we divided learned helplessness mice into five groups:IS, inescapable shock;Dlx, dulxetine(20 mg ·kg-1);XBXT-2(25,50 mg·kg-1). Latency to es-cape shocks and escape failure had been recorded. During the test, Dlx(20 mg·kg-1 ) and XBXT-2(25, 50 mg·kg-1 ) were administered intragastrically once daily for four days. Serum corticosterone level and ad-renocorticotropic hormone ( ACTH ) level were meas-ured by ELISA, and expression of glucocorticoids re-ceptor ( GR) α/β and brain-derived neurotrophic fac-tor ( BDNF ) in hippocampus was determined using Western blot method. Results XBXT-2 (25,50 mg· kg-1 ) or duloxetine treatment showed antidepressant effect in mouse learned helplessness model, as demon-strated by the decreased escape failure and escape la-tency. Our ELISA results showed that XBXT-2 or du-loxetine significantly decreased serum corticosterone level and its upstream stress hormone ACTH level in learned helplessness mice. Furthermore, Western blot result demonstrated XBXT-2 treatment increased GRs and BDNF expression in hippocampus. Conclusions XBXT-2 produces significant antidepressant effect on learned helplessness mice. In addition, the modulation of HPA axis produced by XBXT-2 may be important mechanism underlying its antidepressant-like effect in mouse learned helplessness model.
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Aiming at the present situation that the students of traditional Chinese college usually have relatively weak background knowledge in western medicine, we proposed that pharmacological teaching should improve teaching quality by explaining the profound knowledge in simple terms, focusing on key-point knowledge, contacting clinical practice ,and making full use of multimedia.
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Hepatocellular carcinoma (HCC) is a primary malignant tumor of the liver and has a complex pathogenesis. At present, the oxidative stress theory is one of the many important theories for the mechanism of the development and progression of this disease. Autophagy is an important way for cells to clear misfolded proteins or damaged organelles and maintain homeostasis of the internal environment. An increasing number of evidence has shown that autophagy plays an important role in liver fibrosis and HCC and is closely associated with oxidative stress. With reference to the latest research findings around the world, this article analyzes the interaction between autophagy and oxidative stress in the pathogenesis of HCC from the aspect of their relationship with HCC. It is pointed out that the molecular mechanism by which autophagy regulates oxidative stress in the development of HCC may become a research hotspot in the future; it may provide a new means for the early diagnosis and treatment of HCC to activate or block a key pathway through which autophagy regulates oxidative stress.