STK25: a viable therapeutic target for cancer treatments?

Serine/threonine protein kinase 25 (STK25) is a critical regulator of ectopic lipid storage, glucose and insulin homeostasis, fibrosis, and meta-inflammation. More and more studies have revealed a strong correlation between STK25 and human diseases. On the one hand, STK25 can affect glucose and fatty acid metabolism in normal cells or tumors. On the other hand, STK25 participates in autophagy, cell polarity, cell apoptosis, and cell migration by activating various signaling pathways. This article reviews the composition and function of STK25, the energy metabolism and potential drugs that may target STK25, and the research progress of STK25 in the occurrence and development of tumors, to provide a reference for the clinical treatment of tumors.

Microtubule affinity regulating kinase 4: A promising target in the pathogenesis of atherosclerosis.

Microtubule affinity regulating kinase 4 (MARK4), an important member of the serine/threonine kinase family, regulates the phosphorylation of microtubule-associated proteins and thus modulates microtubule dynamics. In human atherosclerotic lesions, the expression of MARK4 is significantly increased. Recently, accumulating evidence suggests that MARK4 exerts a proatherogenic effect via regulation of lipid metabolism (cholesterol, fatty acid, and triglyceride), inflammation, cell cycle progression and proliferation, insulin signaling, and glucose homeostasis, white adipocyte browning, and oxidative stress. In this review, we summarize the latest findings regarding the role of MARK4 in the pathogenesis of atherosclerosis to provide a rationale for future investigation and therapeutic intervention.

Monocular Depth Estimation with Self-Supervised Learning for Vineyard Unmanned Agricultural Vehicle.

To find an economical solution to infer the depth of the surrounding environment of unmanned agricultural vehicles (UAV), a lightweight depth estimation model called MonoDA based on a convolutional neural network is proposed. A series of sequential frames from monocular videos are used to train the model. The model is composed of two subnetworks-the depth estimation subnetwork and the pose estimation subnetwork. The former is a modified version of U-Net that reduces the number of bridges, while the latter takes EfficientNet-B0 as its backbone network to extract the features of sequential frames and predict the pose transformation relations between the frames. The self-supervised strategy is adopted during the training, which means the depth information labels of frames are not needed. Instead, the adjacent frames in the image sequence and the reprojection relation of the pose are used to train the model. Subnetworks' outputs (depth map and pose relation) are used to reconstruct the input frame, then a self-supervised loss between the reconstructed input and the original input is calculated. Finally, the loss is employed to update the parameters of the two subnetworks through the backward pass. Several experiments are conducted to evaluate the model's performance, and the results show that MonoDA has competitive accuracy over the KITTI raw dataset as well as our vineyard dataset. Besides, our method also possessed the advantage of non-sensitivity to color. On the computing platform of our UAV's environment perceptual system NVIDIA JETSON TX2, the model could run at 18.92 FPS. To sum up, our approach provides an economical solution for depth estimation by using monocular cameras, which achieves a good trade-off between accuracy and speed and can be used as a novel auxiliary depth detection paradigm for UAVs.

Progress in Research on CNPY2 in Diseases.

Canopy FGF signaling regulator 2 (CNPY2) is a novel angiogenic growth factor. In recent years, increasing evidence highlights that CNPY2 has important functions in health and disease. Many new blood vessels need to be formed to meet the nutrient supply in the process of tumor growth. CNPY2 can participate in the development of tumors by promoting angiogenesis. CNPY2 also enhances neurite outgrowth in neurologic diseases and promotes cell proliferation and tissue repair, thereby improving cardiac function in cardiovascular diseases. Regrettably, there are few studies on CNPY2 in various diseases. At the same time, its biological function and molecular mechanism in the process and development of disease are still unclear. This paper reviews the recent studies on CNPY2 in cervical cancer, renal cell carcinoma, prostate cancer, colorectal cancer, lung cancer, gastric cancer, hepatocellular carcinoma, cerebral ischemia-reperfusion injury, spinal cord ischemia-reperfusion injury, Parkinson's disease, ischemic heart disease, myocardial ischemiareperfusion injury, myocardial infarction, heart failure, and non-alcoholic fatty liver disease. The biological function and molecular mechanism of CNPY2 in these diseases have been summarized in this paper. Many drugs that play protective roles in tumors, cardiovascular diseases, non-alcoholic fatty liver disease, and neurologic diseases by targeting CNPY2, have also been summarized in this paper. In addition, the paper also details the biological functions and roles of canopy FGF signaling regulator 1 (CNPY1), canopy FGF signaling regulator 3 (CNPY3), canopy FGF signaling regulator 4 (CNPY4), and canopy FGF signaling regulator 5 (CNPY5). The mechanism and function of CNPY2 should be continued to study in order to accelerate disease prevention in the future.

Dauricine: Review of Pharmacological Activity.

Background: Dauricine is an important natural organic compound in Menispermum dauricum, which often has significant biological activity. Purpose: The purpose of this review is to systemically summarize and discuss the pharmacological activity and underlying mechanisms of dauricine in recent years. Methods: Web of Science (121 articles) and PubMed databases (97 articles) were used to search for articles related to "dauricine" published from 2000 to 2024. Meanwhile, we classified the pharmacological activity of dauricine by screening these articles. Results: Emerging evidence suggests that dauricine possesses numerous pharmacological activities, including neuroprotection, anti-cancer, anti-arrhythmia, anti-inflammatory and anti-diabetes. Conclusion: Dauricine has a potential value in the treatment of many diseases. We hope that this review will contribute to therapeutic development and future studies of dauricine.

Mini-review: research and progress of oxeiptosis in diseases.

Oxeiptosis is a novel cell death pathway that was introduced in 2018. As a form of regulated cell death, it operates independently of caspases and is induced by ROS. Distinguished from other cell death pathways such as apoptosis, necroptosis, pyroptosis, and ferroptosis, oxeiptosis features unique damage causes pivotal genes, and signaling pathways (KEAP1/PGAM5/AIFM1). Emerging studies indicate that oxeiptosis plays a significant role in the progression of various diseases and its regulation could serve as a promising therapeutic target. However, the precise molecular mechanisms underlying oxeiptosis remain to be fully elucidated. In this mini-review, we systematically summarize the latest developments in oxeiptosis-related diseases while detailing the molecular mechanisms and regulatory networks of oxeiptosis. These insights offer a foundation for a deeper understanding of oxeiptosis.

The roles of E2F7 in cancer: Current knowledge and future prospects.

Background: E2F7 is a recently discovered member of the E2F family. Investigating the function and mechanism of E2F7 in the growth of tumors is significant for the clinical diagnosis and therapy of these malignancies. Objective: The purpose of this review is to provide theoretical basis for the diagnosis and treatment of malignant tumors by exploring E2F7. Methods: The relevant information was collected through the PubMed database using keyword searches "E2F7" and "cancer". Results: On the one hand, E2F7 plays an essential role in embryonic development, angiogenesis, and the nervous system. On the other hand, E2F7 is also linked to the occurrence and growth of various malignant tumors. Conclusion: E2F7 has potential as a therapeutic target in future cancer treatments.

Ophiopogonin D: review of pharmacological activity.

Background: Ophiopogon D is an important natural organic compound in Ophiopogon japonicus, which often has significant biological activity. Purpose: The purpose of this review is to systemically summarize and discuss the pharmacological activity and underlying mechanisms of OP-D in recent years. Method: PubMed and Web of Science were searched with the keywords:"Ophiopogon japonicus", "Ophiopogon D" "pharmacology", and "pharmacokinetics". There was no restriction on the publication year, and the last search was conducted on 1 Jan 2024. Results: Emerging evidence suggests that OP-D possess numerous pharmacological activities, including bone protection, cardiovascular protection, immune regulation, anti-cancer, anti-atherosclerosis, anti-inflammatory and anti-NAFLD. Conclusion: OP-D has a potential value in the prevention and treatment of many diseases. We hope that this review will contribute to therapeutic development and future studies of OP-D.

Necrostatin-1: a promising compound for neurological disorders.

Necrostatin-1, a small molecular alkaloid, was identified as an inhibitor of necroptosis in 2005. Investigating the fundamental mechanism of Necrostatin-1 and its role in various diseases is of great significance for scientific and clinical research. Accumulating evidence suggests that Necrostatin-1 plays a crucial role in numerous neurological disorders. This review aims to provide a comprehensive overview of the potential functions of Necrostatin-1 in various neurological disorders, offering valuable insights for future research.

The role and mechanism of various trace elements in atherosclerosis.

Atherosclerosis is a slow and complex disease that involves various factors, including lipid metabolism disorders, oxygen-free radical production, inflammatory cell infiltration, platelet adhesion and aggregation, and local thrombosis. Trace elements play a crucial role in human health. Many trace elements, especially metallic ones, not only maintain the normal functions of organs but also participate in basic metabolic processes. The latest studies have revealed a close correlation between trace elements and the occurrence and progression of atherosclerosis. The imbalance of these trace elements can induce atherosclerosis or accelerate its progression through various mechanisms, which poses a significant threat to human health. Therefore, exploring the specific mechanism of trace elements on atherosclerosis is highly significant. In this review, we summarized the roles and mechanisms of iron, copper, zinc, magnesium, and selenium homeostasis and imbalance in atherosclerosis development, in order to identify novel targets and therapeutic strategies for treating atherosclerosis.

Mechanism of efferocytosis in atherosclerosis.

Atherosclerosis (AS) is a chronic inflammatory vascular disease that occurs in the intima of large and medium-sized arteries with the immune system's involvement. It is a common pathological basis for high morbidity and mortality of cardiovascular diseases. Abnormal proliferation of apoptotic cells and necrotic cells leads to AS plaque expansion, necrotic core formation, and rupture. In the early stage of AS, macrophages exert an efferocytosis effect to engulf and degrade apoptotic, dead, damaged, or senescent cells by efferocytosis, thus enabling the regulation of the organism. In the early stage of AS, macrophages rely on this effect to slow down the process of AS. However, in the advanced stage of AS, the efferocytosis of macrophages within the plaque is impaired, which leads to the inability of macrophages to promptly remove the apoptotic cells (ACs) from the organism promptly, causing exacerbation of AS. Moreover, upregulation of CD47 expression in AS plaques also protects ACs from phagocytosis by macrophages, resulting in a large amount of residual ACs in the plaque, further expanding the necrotic core. In this review, we discussed the molecular mechanisms involved in the process of efferocytosis and how efferocytosis is impaired and regulated during AS, hoping to provide new insights for treating AS.

Feasibility of using wire-guided needle-knife electrocautery for refractory biliary and pancreatic strictures.

BACKGROUND: Endoscopic management of biliary or pancreatic strictures by stent insertion is well established. However, some high-grade strictures are refractory to dilation and stent placement with conventional methods. OBJECTIVE: To evaluate the safety and efficacy of the wire-guided electrotomy technique in dilating stiff biliary and/or pancreatic stenoses when ordinary methods failed. DESIGN: Retrospective analysis of a prospective database. SETTING: Tertiary referral university hospital. PATIENTS: This study involved 279 patients with biliary or pancreatic strictures who underwent ERCP for stenting. INTERVENTION: After conventional dilation failed, wire-guided needle-knife electrocautery was attempted to facilitate insertion of the dilating devices and eventually endoprosthesis. MAIN OUTCOME MEASUREMENTS: The successful treatment and drainage of biliary or pancreatic strictures. RESULTS: With wire-guided needle-knife cauterization, the success rate of stricture dilatation increased from 95.7% (267 of 279 patients) to 98.9% (276 of 279 patients). Dilation of stenoses was successful in 9 of 10 patients (90%) by using electrocautery with the wire-guided needle-knife technique. Postprocedure adverse events included self-limited bleeding, mild acute pancreatitis, hyperamylasemia, cholangitis, and biliary perforation. No procedure-related death occurred. LIMITATIONS: Retrospective, single-center study and small sample size. CONCLUSIONS: Wire-guided needle-knife electroincision appears to be effective for traversing refractory biliary or pancreatic strictures and can be considered as an alternative approach to conventional methods. However, the safety of such a technique needs to be further evaluated.

Legumain: a potential biomarker for atherosclerosis.

Atherosclerosis is a lipid-driven chronic inflammatory disease that poses a serious threat to health. Legumain (LGMN), also known as asparagine endonuclease, is a new type of cysteine proteases that can specifically hydrolyze substrate molecules containing asparagine residues. It has anti-apoptotic effects in mammals and plays an antigen-presenting role in inflammatory response. Several studies have found that LGMN can activate multiple signal pathways to promote cell apoptosis and migration, inflammatory response, and the development of atherosclerosis. Importantly, LGMN exerts pro-atherogenic effects by participating in a variety of pathophysiological mechanisms of atherosclerosis, including vascular remodeling, inflammatory response, plaque stability, and the degradation of extracellular matrix. In the present review, we describe the LGMN distribution, structure, generation, and functional partners. Furthermore, we summarize the relationship between LGMN and atherosclerosis. Based on the relationship between LGMN and atherosclerosis, LGMN may be a potential biomarker for atherosclerosis.

Salusins: advance in cardiovascular disease research.

Salusins are discovered in 2003 and divided into salusin-α and salusin-ß, which are bioactive peptides with hemodynamic and mitotic activity and mainly distributed in plasma, urine, endocrine glands and kidneys. A large number of studies have shown that salusins can regulate lipid metabolism, inflammatory response and vascular proliferation. Despite the profound and diverse physiological properties of salusins, the exact mechanism of their cardiovascular effects remains to be determined. The potential mechanisms of action of salusins in cardiovascular-related diseases such as atherosclerosis, hypertension, heart failure, myocardial infarction and myocarditis, and their use as biomarkers of cardiovascular disease are discussed. This review aims to provide a new strategy for the diagnosis and prevention of clinical cardiovascular diseases.

Research and Progress of Probucol in Nonalcoholic Fatty Liver Disease.

With the development of the social economy over the last 30 years, non-alcoholic fatty liver disease (NAFLD) is affected by unhealthy living habits and eating styles and has gradually become an increasingly serious public health problem. It is very important to investigate the pathogenesis and treatment of NAFLD for the development of human health. Probucol is an antioxidant with a bis-phenol structure. Although probucol is a clinically used cholesterol-lowering and antiatherosclerosis drug, its mechanism has not been elucidated in detail. This paper reviews the chemical structure, pharmacokinetics and pharmacological research of probucol. Meanwhile, this paper reviews the mechanism of probucol in NAFLD. We also analyzed and summarized the experimental models and clinical trials of probucol in NAFLD. Although current therapeutic strategies for NAFLD are not effective, we hope that through further research on probucol, we will be able to find suitable treatments to solve this problem in the future.

Research and progress of inflammasomes in nonalcoholic fatty liver disease.

With the development of the social economy, unhealthy living habits and eating styles are gradually affecting people's health in recent years. As a chronic liver disease, NAFLD is deeply affected by unhealthy living habits and eating styles and has gradually become an increasingly serious public health problem. As a protein complex in clinical research, the inflammasomes play a crucial role in the development of NAFLD, atherosclerosis, and other diseases. This paper reviews the types, composition, characteristics of inflammasomes, and molecular mechanism of the inflammasome in NAFLD. Meanwhile, the paper reviews the drugs and non-drugs that target NLRP3 inflammasome in the treatment of NAFLD in the past decades. we also analyzed and summarized the related experimental models, mechanisms, and results of NAFLD. Although current therapeutic strategies for NAFLD are not effective, we expect that we will be able to find an appropriate treatment to address this problem in the future with further research on inflammasome.

The adsorption mechanism of Zn2+ by triclinic birnessite and the mechanism.

In this paper, the reaction mechanism for the adsorption of Zn2+ by synthetic triclinic Na-birnessite was studied by reacting synthetic triclinic Na-birnessite with Zn2+ in solution, thereby providing a theoretical basis for the purification of heavy metal ions in acid soil and water by triclinic birnessite. The adsorption effect of Zn2+ on Na-birnessite enhances with an increase in either reaction time or Na-birnessite dosage, as well as decrease of pH. Na-birnessite can effectively adsorb Zn2+ in acidic solutions without any secondary pollution, and the stronger the acidity, the better the treatment effect. In acidic conditions, H+ in solution exchanges with Na+ in the interlayer of triclinic Na-birnessite, then a small part of Zn2+ in solution exchanges with the Mn2+ produced during the triclinic-to-hexagonal phase transformation, and most of the Zn2+ forms a complex with OH- on the octahedral layer, which loses protons due to the consumption of H+ ions. Finally, Zn2+ adsorbs above and below octahedral vacancies in hexagonal birnessite in either an octahedral or tetrahedral coordination.

A novel antireflux metal stent for the palliation of biliary malignancies: a pilot feasibility study (with video).

BACKGROUND: Antireflux stents that prevent duodenal biliary reflux may improve biliary drainage and prolong stent patency. However, the use of antireflux metal stents (ARMSs) in the human biliary system has not been reported. OBJECTIVE: To evaluate the safety and efficacy of ARMSs for the palliation of unresectable distal biliary malignancies. DESIGN AND SETTING: A retrospective case series in a tertiary referral center. PATIENTS: From August 2007 to April 2009, a total of 23 patients with unresectable nonhilar malignant biliary obstruction. INTERVENTION: Endoscopic placement of an ARMS. MAIN OUTCOME MEASUREMENTS: Technical success and early complications with follow-up of stent patency and patient survival. RESULTS: Placement of an ARMS was successful on the first attempt in all patients. There were no procedure-related complications. Follow-up was obtained in 22 cases. Serum bilirubin level returned to normal within 1 month of stenting in 20 patients. Six stent malfunctions occurred as a result of tumor ingrowth (1 patient), tumor overgrowth (2 patients), and stent migration (3 patients). The remaining patients were free of biliary symptoms until death or final follow-up. The median duration of stent patency of ARMSs was 14 months, with cumulative patency rates at 3, 6, and 12 months of 95%, 74%, and 56%, respectively. The median survival of the patients was 7.9 months (range, 1-14 months). LIMITATIONS: Small number of patients in single endoscopy center. CONCLUSIONS: Endoscopic insertion of an ARMS is technically feasible, safe, and effective in patients with distal malignant biliary obstruction. The impact of ARMSs in prolonging stent patency and life expectancy deserves further randomized evaluation.

Nesfatin-1 in lipid metabolism and lipid-related diseases.

Nesfatin-1, an anorexic neuropeptide discovered in 2006, is widely distributed in the central nervous system and peripheral tissues. It has been shown to be involved in the regulation of food intake and lipid metabolism, inhibiting fat accumulation, accelerating lipid decomposition, and in general, inhibiting the development of lipid-related diseases, such as obesity and metabolic syndrome. Potential mechanisms of Nesfatin-1 action in lipid metabolism and lipid-related diseases will be discussed as well as its role as a biomarker in cardiovascular disease. This review expected to provide a new strategy for the diagnosis and prevention of clinically related diseases.