Actin-binding proteins (ABPs), by interacting with actin, regulate the polymerization, depolymerization, bundling, and cross-linking of actin filaments, directly or indirectly, thereby mediating the maintenance of cell morphology, cell movement, and many other biological functions. Consequently, these functions of ABPs help regulate cancer cell invasion and metastasis when cancer occurs. In recent years, a variety of ABPs have been found to be abnormally expressed in various cancers, indicating that the detection and interventions of unusual ABP expression to alter this are available for the treatment of cancer. The early stages of most cancer development involve long-term chronic inflammation or repeated stimulation. This is the case for breast cancer, gastric cancer, lung cancer, prostate cancer, liver cancer, esophageal cancer, pancreatic cancer, melanoma, and colorectal cancer. This article discusses the relationship between chronic inflammation and the above-mentioned cancers, emphatically introduces relevant research on the abnormal expression of ABPs in chronic inflammatory diseases, and reviews research on the expression of different ABPs in the above-mentioned cancers. Furthermore, there is a close relationship between ABP-induced inflammation and cancer. In simple terms, abnormal expression of ABPs contributes to the chronic inflammation developing into cancer. Finally, we provide our viewpoint regarding these unusual ABPs serving as potential biomarkers for chronic inflammation-induced cancer diagnosis and therapy, and interventions to reverse the abnormal expression of ABPs represent a potential approach to preventing or treating the corresponding cancers.

Hedysari Radix Praeparata Cum Melle (HRPCM) and Astragali Radix Praeparata Cum Melle (ARPCM) are used interchangeably in clinics to treat spleen-qi deficiency (SQD) symptom mainly including gastroi...

Background: Identifying risk factors associated with cardiac intensive care unit (CICU) patients’ prognosis can help clinicians intervene earlier and thus improve their prognosis. The correlation between the geriatric nutrition risk index (GNRI), which reflects nutritional status, and in-hospital mortality among CICU patients has yet to be established.Method: The present study retrospectively enrolled 4,698 CICU patients. Based on the nutritional status, the participants were categorized into four groups. The primary endpoint was in-hospital mortality. The length of hospital stay and length of CICU stay were the secondary endpoints. To explore the correlation between nutritional status and in-hospital mortality, a logistic regression analysis was conducted. The nonlinear associations of GNRI with in-hospital mortality were evaluated using restricted cubic spline (RCS). Furthermore, subgroup analyses were conducted to evaluate the effect of the GNRI on in-hospital mortality across different subgroups, with calculation of the p for interaction.Result: A higher risk of malnutrition was significantly linked to an increased incidence of in-hospital mortality (High risk vs. No risk: 26.2% vs. 4.6%, p < 0.001), as well as a longer length of hospital stay (High risk vs. No risk: 15.7, 9.1–25.1 vs. 8.9, 6.9–12.9, p < 0.001) and CICU stay (High risk vs. No risk: 6.4, 3.8–11.9 vs. 3.2, 2.3–5.1, p < 0.001). An elevated GNRI was significantly associated with an increased risk of in-hospital mortality even after controlling for pertinent confounding factors (High risk vs. No risk: OR, 95% CI: 2.37, 1.67–3.37, p < 0.001, p for trend <0.001). Additionally, the RCS model showed a linear relationship between GNRI and in-hospital mortality, with the risk of in-hospital mortality significantly decreasing as GNRI increased (non-linear p = 0.596). Furthermore, in the subgroups of hypertension, ventricular arrhythmias, cardiac arrest, shock, and chronic kidney disease, there was a significant interaction between nutritional status and in-hospital mortality.Conclusion: Among CICU patients, a low GNRI was a significant predictor of in-hospital mortality. Furthermore, patients with a higher risk of malnutrition, as indicated by low GNRI values, experienced significantly longer hospital and CICU stays.

Objective. To compare the changes of chemical components of Hedysari Radix (HR) before and after honey‐processing, and to explore the material basis of the difference between HR and honey‐processed Hedysari Radix (HPHR) in Buzhong Yiqi. Methods. Different compounds in aqueous extracts of HR and HPHR were analysed by UPLC‐MS. A rat model of spleen qi deficiency was established. The rats were treated with different doses of water extracts of HR or HPHR, and pathological differences in spleen tissue, serum levels of D‐xylose, gastrin (GAS) and amylase (AMS) interleukin‐2 (IL)‐2 and tumour necrosis factor‐α (TNF‐α), as well as spleen and thymus indices, were used as indicators. Differences in the efficacy of HR and HPHR in Buzhong Yiqi were studied. Results. The research showed that compared with the blank group, the spleen tissue of rats in the model group showed spleen tissue damage, which mainly manifested as unclear boundaries between red pulp and white pulp, irregular spleen morphology and irregular arrangement, and the structure of white pulp destruction, less lymphocytes, the number of germinal centers decreased or atrophied. Compared with the model group, the middle and high dose groups of HR and HPHR had protective effects on spleen tissue of spleen‐qi deficiency rats, and HPHR had a stronger effect; compared with those in the model group, rats in each treatment group showed remarkably higher serum D‐xylose, GAS and AMS levels and thymus and spleen indices, and remarkably lower serum IL‐2 and TNF‐α levels, among which HPHR group showed better regulation effect than HR group. A total of 16 differential compounds were found in the aqueous extracts of HR and HPHR, of which 10 compounds in HPHR were up regulated, while 6 compounds were down regulated compare to HR. Conclusion. The results indicated that both HR and HPHR can improve spleen qi deficiency syndrome of rats, the pharmacodynamic effect of the latter was better than the former. Differences in components of HR and HPHR potentially leading to variations in efficacy.