Psoriasis comorbid with atherosclerosis meets in lipid metabolism.

Psoriasis (PSO) is a common skin disease affecting approximately 1%-3% of the population, and the incidence rate is increasing yearly. PSO is associated with a dramatically increased risk of cardiovascular disease, the most common of which is atherosclerosis (AS). In the past, inflammation was considered to be the triggering factor of the two comorbidities, but in recent years, studies have found that lipid metabolism disorders increase the probability of atherosclerosis in patients with psoriasis. In this review, we discuss epidemiological studies, clinical treatment methods, risk factors, and lipid metabolism of psoriasis and atherosclerosis comorbidities.

Anti-breast cancer-induced cardiomyopathy: Mechanisms and future directions.

With the progression of tumor treatment, the 5-year survival rate of breast cancer is close to 90%. Cardiovascular toxicity caused by chemotherapy has become a vital factor affecting the survival of patients with breast cancer. Anthracyclines, such as doxorubicin, are still some of the most effective chemotherapeutic agents, but their resulting cardiotoxicity is generally considered to be progressive and irreversible. In addition to anthracyclines, platinum- and alkyl-based antitumor drugs also demonstrate certain cardiotoxic effects. Targeted drugs have always been considered a relatively safe option. However, in recent years, some random clinical trials have observed the occurrence of subclinical cardiotoxicity in targeted antitumor drug users, which may be related to the effects of targeted drugs on the angiotensin converting enzyme, angiotensin receptor and ß receptor. The use of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and beta-blockers may prevent clinical cardiotoxicity. This article reviews the toxicity and mechanisms of current clinical anti-breast cancer drugs and proposes strategies for preventing cardiovascular toxicity to provide recommendations for the clinical prevention and treatment of chemotherapy-related cardiomyopathy.

Bisdemethoxycurcumin suppresses the progression of atherosclerosis and VSMC-derived foam cell formation by promoting lipophagy.

Vascular smooth muscle cells (VSMCs) are one of the sources of foam cells in atherosclerosis. However, the mechanism of VSMC-derived foam cell formation remain largely unknown. Bisdemethoxycurcumin (BDMC) is considered to possess diverse pharmacological properties, including anti-inflammation and anti-oxidation. However, the effects of BDMC on atherosclerosis remain unclear. Here, we established an in vitro foam cell model by culturing VSMCs with oxidized low-density lipoprotein (ox-LDL). The results show that BDMC reduced lipid droplets in ox-LDL-stimulated VSMCs. In addition, BDMC promotes autophagy by suppressing PDK1/Akt/mTOR signaling pathway. In vivo, BDMC alleviates inflammatory responses and lipid accumulation in in apoe-/- mice. Above all, the results from the present study suggested that BDMC may be used as a therapeutic agent for the prevention and treatment of atherosclerosis.

Research on weed identification method in rice fields based on UAV remote sensing.

Rice is the world's most important food crop and is of great importance to ensure world food security. In the rice cultivation process, weeds are a key factor that affects rice production. Weeds in the field compete with rice for sunlight, water, nutrients, and other resources, thus affecting the quality and yield of rice. The chemical treatment of weeds in rice fields using herbicides suffers from the problem of sloppy herbicide application methods. In most cases, farmers do not consider the distribution of weeds in paddy fields, but use uniform doses for uniform spraying of the whole field. Excessive use of herbicides not only pollutes the environment and causes soil and water pollution, but also leaves residues of herbicides on the crop, affecting the quality of rice. In this study, we created a weed identification index based on UAV multispectral images and constructed the WDVI NIR vegetation index from the reflectance of three bands, RE, G, and NIR. WDVI NIR was compared with five traditional vegetation indices, NDVI, LCI, NDRE, and OSAVI, and the results showed that WDVI NIR was the most effective for weed identification and could clearly distinguish weeds from rice, water cotton, and soil. The weed identification method based on WDVI NIR was constructed, and the weed index identification results were subjected to small patch removal and clustering processing operations to produce weed identification vector results. The results of the weed identification vector were verified using the confusion matrix accuracy verification method and the results showed that the weed identification accuracy could reach 93.47%, and the Kappa coefficient was 0.859. This study provides a new method for weed identification in rice fields.

Designer Functional Nanomedicine for Myocardial Repair by Regulating the Inflammatory Microenvironment.

Acute myocardial infarction is a major global health problem, and the repair of damaged myocardium is still a major challenge. Myocardial injury triggers an inflammatory response: immune cells infiltrate into the myocardium while activating myofibroblasts and vascular endothelial cells, promoting tissue repair and scar formation. Fragments released by cardiomyocytes become endogenous "danger signals", which are recognized by cardiac pattern recognition receptors, activate resident cardiac immune cells, release thrombin factors and inflammatory mediators, and trigger severe inflammatory responses. Inflammatory signaling plays an important role in the dilation and fibrosis remodeling of the infarcted heart, and is a key event driving the pathogenesis of post-infarct heart failure. At present, there is no effective way to reverse the inflammatory microenvironment in injured myocardium, so it is urgent to find new therapeutic and diagnostic strategies. Nanomedicine, the application of nanoparticles for the prevention, treatment, and imaging of disease, has produced a number of promising applications. This review discusses the treatment and challenges of myocardial injury and describes the advantages of functional nanoparticles in regulating the myocardial inflammatory microenvironment and overcoming side effects. In addition, the role of inflammatory signals in regulating the repair and remodeling of infarcted hearts is discussed, and specific therapeutic targets are identified to provide new therapeutic ideas for the treatment of myocardial injury.

Immunity: Psoriasis comorbid with atherosclerosis.

Psoriasis is an immune-mediated, persistent inflammatory disease with a genetic predisposition, and the involvement of multiple organs in psoriasis remains indicative of systemic disease. Atherosclerosis (AS) is a common complication of patients with severe or prolonged psoriasis. The specific pathogenesis of psoriasis is still unclear. Current studies suggest that psoriasis is a polygenic genetic disease with the interaction of multiple factors such as heredity and environment. Keratinocytes are proliferated through immune-mediated inflammatory pathway, which leads to cell activation, infiltration of dermis cells and release of inflammatory factors. Activation of inflammatory cells and pro-inflammatory factors play an important role in the progression of psoriasis and atherosclerosis. Studies have found that there is a close relationship between psoriasis and atherosclerosis, and systemic inflammation may be the common feature of psoriasis and AS. This paper attempts to explore the possibility of the relationship between psoriasis and atherosclerotic comorbidities from the aspects of potential epidemiology and immune mechanism, in order to provide some reference for the subsequent scientific research.

Schisandrin B ameliorates high-glucose-induced vascular endothelial cells injury by regulating the Noxa/Hsp27/NF-κB signaling pathway.

BACKGROUND: To address the molecular mechanism of the anti-inflammation effects of schisandrin B (Sch B) in atherosclerosis, we examined injured HMEC-1, HBMEC, and HUVEC-12 cells induced by high glucose (HG). METHODS: Western blot was performed to detect the levels of the proteins Hsp27, Noxa, TLR5, p-IκBα, and p-p65 in HG-induced cells, while ELISA was used to analyze the inflammatory cytokines TNF-α, IL-6, MCP-1, and IL-1ß in cells with Hsp27 or Noxa stable expression. RESULTS: Overexpression of Hsp27 upregulated the inflammatory cytokines and the release of IκBα, promoted transportation of p65 into the nucleus, and lastly, affected the inflammation process, while Sch B counteracted the upregulation. In addition, the effect of Noxa overexpression, which is different from Hsp27 overexpression, was consistent with that of Sch B treatment. CONCLUSIONS: Sch B may inhibit the inflammatory cascade and alleviate the injury to HMEC-1, HBMEC, and HUEVC-12 cells caused by HG by regulating the Noxa/Hsp27/NF-κB signaling pathway.

Schisandrin B inhibits LPS-induced inflammatory response in human umbilical vein endothelial cells by activating Nrf2.

Schisandrin B (SchB), an active ingredient extracted from Schisandra chinensis (Turcz.) Baill, has been known to have anti-oxidant and anti-inflammatory activities. In this study, we investigated the anti-inflammatory effects and mechanism of SchB in LPS-stimulated human umbilical vein endothelial cells (HUVECs). The effects of SchB on VCAM-1, ICAM-1, NF-κB and Nrf2 expression were detected by western blot analysis. The effects of SchB on TNF-α and IL-8 production were detected by ELISA. The results showed that SchB strongly suppressed the production of TNF-α and IL-8 in HUVECs stimulated with LPS. SchB also inhibited LPS-induced VCAM-1 and ICAM-1 expression. Furthermore, SchB blocked the activation of NF-κB induced by LPS. In addition, SchB increased the expression of Nrf2 and HO-1 in a concentration-dependent manner. And the inhibition of TNF-α and IL-8 production by SchB was blocked by transfection with Nrf2 siRNA. Our findings showed that SchB inhibited LPS-induced inflammation in HUVECs by activating Nrf2 signaling pathway.

Doxycycline affects gene expression profiles in aortic tissues in a rat model of vascular calcification.

Vitamin D3-induced vascular calcification (VC) in rats shares many phenotypical similarities with calcification occurring in human atherosclerosis, diabetes mellitus and chronic kidney disease, thereby it is a reliable model for identifying chemopreventive agents. Doxycycline has been shown to effectively attenuated VC. This study aimed to explore the effects of doxycycline on gene expression profiles in VC rats. The model of VC in rats was established by subcutaneous injection of vitamin D3 for 3days. Doxycycline at 120mgkg-1day-1 was given via subcutaneous injection for 14days. Rat pathological changes, calcium deposition and calcium content in aortic tissues were measured by Hematoxylin-eosin, von Kossa staining and colorimetry, respectively. The gene change profile of aortic tissues after doxycycline treatment was assessed by Gene Microarray analysis using the Agilent Whole Rat Genome Oligo Microarray. The results showed that doxycycline significantly decreased the deposition of calcium, reduced the relative calcification area and alleviated pathological injury in aortic tissues. In addition, doxycycline treatment altered 88 gene expressions compared with untreated VD group. Of these, 61 genes were down-regulated and 27 genes were up-regulated. The functions of differentially expressed (DE) genes were involved in neutrophil chemotaxis, chronic inflammatory response, negative regulation of apoptotic process, cellular response to mechanical stimulus and immune response, etc. In conclusions, this study might provide the potential novel insights into the molecular mechanisms of doxycycline on VC.

Inhibition of eukaryotic initiation factor 4E phosphorylation by cercosporamide selectively suppresses angiogenesis, growth and survival of human hepatocellular carcinoma.

Mnk kinase is required for the phosphorylation and activation of the eukaryotic initiation factor 4E (eIF4E), which regulates translation of proteins involve in important aspects of hepatocellular carcinoma (HCC). Here we investigated whether an antifungal agent, cercosporamide, which had been recently identified as a potent Mnk inhibitor, is active against HCC and angiogenesis. We showed that cercosporamide significantly inhibited growth and induced caspase-dependent apoptosis on numerous HCC cell lines, while sparing normal liver cells. In addition, cercosporamide impaired HCC angiogenesis via inhibiting HCC-endothelial cells (HCC-EC) capillary network formation, migration, proliferation and survival. Importantly, cercosporamide sensitized HCC cells to cisplatin in in vitro cell culture and in vivo HCC xenograft mouse model. Cercosporamide blocked the phosphorylation of eIF4E but not Erk or p38 in a dose- and time-dependent manner in HCC and HCC-EC cells, suggesting that suppression of eIF4E phosphorylation was the result of inhibition of Mnk but not Mnk upstream pathways. Overexpression of constitutively active eIF4E (S209D) but not the nonphosphorylatable eIF4E (S209A) abolished the inhibitory effects of cercosporamide in HepG2 cells. Altogether, our work demonstrates that cercosporamide acts as a Mnk inhibitor through blockage of eIF4E phosphorylation and selectively exhibits anti-HCC activities. Our work suggests that targeting MNK-eIF4E pathway represents a therapeutic strategy to overcome chemo-resistance for HCC treatment.

Clinical implication of long non-coding RNA NEAT1 expression in hepatocellular carcinoma patients.

UNLABELLED: Hepatocellular carcinoma (HCC), a primary malignancy of the liver, is associated with high mortality rate and poor prognosis. Emerging evidence showed that novel biomarkers are required toward a better understanding of the biological mechanisms of HCC. NEAT1 (nuclear paraspeckle assembly transcript 1, also known as MENε/ß), a novel long non-coding RNA (lncRNA), serves as a crucial regulator in several cancers. However, the correlation between NEAT1 expression with tumorigenesis and metastasis in HCC tissues remains out of the question so far. In the current study, the aim was to evaluate the potential role of NEAT1 expression in HCC tissues and its relationship with clinicopathological parameters. METHOD: The expression of NEAT1 was detected by qRT-PCR, in 95 cases of adjacent non-cancerous liver and their paired HCC tissues, respectively. The associations of NEAT1 with clinicopathological features and other biological factors were further analyzed. RESULT: Our results revealed that NEAT1 appeared to have higher expression in the HCC tissues, compared with the adjacent non-cancerous liver tissues. High levels of NEAT1 promoted the clinical features of HCC, including the number of tumor nodes, metastasis, clinical TNM stage, the status of portal vein tumor embolus, vaso-invasion and the infiltration of tumor cells. Additionally, high NEAT1 expression levels were significantly associated with the expression level of MDTH, NM23 and MALAT1. CONCLUSION: Our study demonstrates that NEAT1 acts as a pivotal player in tumorigenesis and metastasis of hepatocellular carcinoma.