LncRNA XIST: A Breakthrough in Inflammation-related Diseases.

BACKGROUND: Long non-coding RNA (LncRNA) is a type of non-coding RNA that plays an important role in the body and accounts for the majority of RNA, and this non-coding RNA can regulate disease onset and progression with its wide range of functions. LncRNA Xist, also known as the long non-coding RNA X inactive specific transcript, is a member of them. It can regulate the development of organismal diseases by acting downstream on specific target genes. In addition to this, it can also influence disease onset and progression by acting on apoptosis, migration, invasion, and other processes. It has been shown that XIST plays an important role in the development of inflammation. OBJECTIVE: To explore the role played by XIST in inflammation-related diseases and to explore its mechanism of action. METHODS: This paper summarizes and analyzes the role played by XIST in inflammation- related diseases by conducting a search in PubMed. CONCLUSION: In this paper, we summarize the mechanism of action of XIST in different types of inflammation-related diseases and propose new protocols for the future clinical treatment of these diseases.

Salivary and serum biomarkers to evaluate psychological disorders in burning mouth syndrome: A systematic review and meta-analysis.

BACKGROUND: Burning mouth syndrome is a chronic pain syndrome mainly characterized by an intensive burning sensation of tongue. Previous studies have suggested that saliva/serum biomarkers in burning mouth syndrome might be associated with psychological disorders. The aim of systematic review was to observe whether the biomarkers in serum/saliva could be an alternative method to evaluate the psychological disorders in patients with burning mouth syndrome. MATERIALS AND METHODS: The PubMed, Embase, and Cochrane Library databases were searched for papers published up to March 15, 2023. Risk of bias was measured by using the Newcastle-Ottawa Scale. RevMan was used for meta-analysis. RESULTS: A total of 467 articles were screened, which of 12 studies were included. These studies collected 43 different biomarkers in saliva and 35 in serum. Of these biomarkers, only three (cortisol, α-amylase, and IL-6) were analyzed in two or more studies. Only salivary cortisol levels were significantly higher in the patient group compared to the controls (Mean Difference = 1.39; 95% CI [0.80-1.97]; p < 0.001). Moreover, cortisol might be relevant to psychological scores, especially anxiety. CONCLUSION: Different papers have investigated salivary and serum biomarkers in burning mouth syndrome patients with controversial results. This meta-analysis showed that cortisol levels in saliva may be a potential biomarker to assess the psychological disorders in burning mouth syndrome patients.

Brucella-driven host N-glycome remodeling controls infection.

Many powerful methods have been employed to elucidate the global transcriptomic, proteomic, or metabolic responses to pathogen-infected host cells. However, the host glycome responses to bacterial infection remain largely unexplored, and hence, our understanding of the molecular mechanisms by which bacterial pathogens manipulate the host glycome to favor infection remains incomplete. Here, we address this gap by performing a systematic analysis of the host glycome during infection by the bacterial pathogen Brucella spp. that cause brucellosis. We discover, surprisingly, that a Brucella effector protein (EP) Rhg1 induces global reprogramming of the host cell N-glycome by interacting with components of the oligosaccharide transferase complex that controls N-linked protein glycosylation, and Rhg1 regulates Brucella replication and tissue colonization in a mouse model of brucellosis, demonstrating that Brucella exploits the EP Rhg1 to reprogram the host N-glycome and promote bacterial intracellular parasitism, thereby providing a paradigm for bacterial control of host cell infection.

LncRNA Gm15232 Promotes Lipogenesis in Aging Mice Through the miR-192-3p/GCR Pathway.

Recent scientific studies have highlighted the importance of long-chain noncoding RNAs (lncRNAs) in a variety of metabolic diseases, but the specific functions and mechanisms of lncRNAs in aberrant lipid synthesis associated with aging are unknown. In this work, we inspected the effects of lncRNAs on the lipid metabolism in aging mice, as substantial evidence suggests that aging disturbs lipid metabolism. The results revealed that the expression of lncRNA Gm15232 was significantly elevated in the epididymal white adipose tissue of aging mice compared to adult mice. This upregulation of Gm15232 functioned as a competitive endogenous RNA by inhibiting the expression of miR-192-3p, and the ensuing downregulation of miR-192-3p increased the expression of the glucocorticoid receptor gene, which ultimately stimulated fat synthesis. The upregulation of Gm15232 thus increased lipogenesis through this mechanism. This study reveals a potential target for the treatment of age-related abnormalities of lipid metabolism.

Immunoprotective effect of silybin through blocking p53-driven caspase-9-Apaf-1-Cyt c complex formation and immune dysfunction after difenoconazole exposure in carp spleen.

As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important secondary lymphoid organ in carp. In this study, we assessed the protective impact of silybin as a dietary additive on spleen tissues of carp during exposure to difenoconazole. Sixty carp were separated into four groups for this investigation including control group, difenoconazole group, silybin group, and silybin and difenoconazole group. By hematoxylin-eosin staining, dihydroethidium staining, immunohistochemical staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, quantitative real-time PCR assay, Western blot analysis, biochemical assays, and immune function indicator assays, we found that silybin could prevent difenoconazole-induced spleen tissue damage, oxidative stress, and immune dysfunction, and inhibited apoptosis of carp spleen tissue cells by suppressing the formation of p53-driven caspase-9-apoptotic protease activating factor-1-cytochrome C complex. The results suggested that silybin as a dietary additive could improve spleen tissue damage and immune dysfunction induced by difenoconazole in aquaculture carp.

Pesticide avermectin-induced hepatotoxicity and growth inhibition in carp: Ameliorative capacity and potential mechanisms of quercetin as a dietary additive.

Flavonoid quercetin (QUE) has biological activities of anti-oxidation, anti-inflammation and anti-apoptosis, however, its protective effects against avermectin (AVM) induced liver toxicity in carp remains unclear. The objective of this research is to explore the biologically potent effects of QUE in AVM-induced hepatotoxicity in carp and its underlying mechanism. Therefore, we established a liver injury model in carp induced by AVM to evaluate QUE against AVM induced liver toxicity in carp. In this investigation, AVM dosage was determined as 2.404 µg/L for both groups, and an experimentation of 30 days duration was carried out. Various methods including hematoxylin and eosin (H&E) staining, biochemical kits, real-time quantitative PCR (qRT-PCR), western blotting, TUNEL, reactive oxygen species (ROS) staining, immunofluorescence (Hoseinifar, et al.,), and oil red O staining were used in this study. Results showed that the growth inhibition of carp was relieved in the QUE treatment group comparing to the AVM group. In the QUE treatment group, there was a significant decrease in the levels of ALT and AST in carp liver tissue. Additionally, the histopathological damage and lipid accumulation were alleviated compared to the AVM group. Moreover, QUE prevented AVM induced decrease in the activities of antioxidant enzymes of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), glutathione (GSH), catalase (CAT) and the accumulation of reactive oxygen species (ROS), but reduced accumulation of malondialdehyde (MDA). In addition, the mRNA levels of liver pro-inflammatory factors of tumor necrosis factor-α (TNF-α), interleukin-1ß (iL-1ß), interleukin-6 (iL-6), interleukin-10 (iL-10) and the protein levels of NOD-like receptor protein 3 (NLRP3) inflammasome were significantly down-regulated in the QUE treatment group in comparison to the AVM group. We also found that QUE could affect the expression of Bcl2-associated x (Bax), B-cell lymphoma-2 (Bcl-2), cleaved-cysteinyl aspartate specific proteinase (CCaspase3) key apoptotic proteins and TUNEL-labeled apoptotic hepatocytes by regulating SIRT1/FOXO3a signal pathway. In summary, QUE alleviated the growth inhibition, liver oxidative damage, lipid accumulation, inflammatory response, and apoptosis of carp induced by AVM. QUE is a potential protective agent against liver injury induced by AVM in carp.

Deciphering the Role of the Gut Microbiota in Exposure to Emerging Contaminants and Diabetes: A Review.

Emerging pollutants, a category of compounds currently not regulated or inadequately regulated by law, have recently become a focal point of research due to their potential toxic effects on human health. The gut microbiota plays a pivotal role in human health; it is particularly susceptible to disruption and alteration upon exposure to a range of toxic environmental chemicals, including emerging contaminants. The disturbance of the gut microbiome caused by environmental pollutants may represent a mechanism through which environmental chemicals exert their toxic effects, a mechanism that is garnering increasing attention. However, the discussion on the toxic link between emerging pollutants and glucose metabolism remains insufficiently explored. This review aims to establish a connection between emerging pollutants and glucose metabolism through the gut microbiota, delving into the toxic impacts of these pollutants on glucose metabolism and the potential role played by the gut microbiota.

Insulin resistance and coronary inflammation in patients with coronary artery disease: a cross-sectional study.

BACKGROUND: Insulin resistance (IR) is associated with coronary artery disease (CAD) severity. However, its underlying mechanisms are not fully understood. Therefore, our study aimed to explore the relationship between IR and coronary inflammation and investigate the synergistic and mediating effects of coronary inflammation on the association between IR and CAD severity. METHODS: Consecutive patients with CAD who underwent coronary angiography and coronary computed tomography angiography between April 2018 and March 2023 were enrolled. The triglyceride-glucose index (TyG index) and peri-coronary adipose tissue (PCAT) attenuation around the proximal right coronary artery (RCA) were used to evaluate IR and coronary inflammation, respectively. The correlation between the TyG index and PCAT attenuation was analyzed using linear regression models. Logistic regression models were further used for investigating the correlation of the TyG index and PCAT attenuation with CAD severity. A mediation analysis assessed the correlation between IR and CAD severity mediated by coronary inflammation. RESULTS: A total of 569 participants (mean age, 62 ± 11 years; 67.8% men) were included in the study. PCAT attenuation was positively associated with the TyG index (r = 0.166; P < 0.001). After adjusting for potential confounders, the per standard deviation increment in the TyG index was associated with a 1.791 Hounsfield unit (HU) increase (95% confidence interval [CI], 0.920-2.662 HU; P < 0.001) in the PCAT attenuation. In total, 382 (67.1%) patients had multivessel CAD. The patients in the high-TyG index/high PCAT attenuation group had approximately 3.2 times the odds of multivessel CAD compared with those in the low-TyG index/low PCAT attenuation group (odds ratio, 3.199; 95%CI, 1.826-5.607; P < 0.001). Mediation analysis indicated that PCAT attenuation mediated 31.66% of the correlation between the TyG index and multivessel CAD. CONCLUSIONS: The TyG index positively correlated with PCAT attenuation in patients with CAD. The TyG index and PCAT attenuation showed a synergistic correlation with multivessel CAD. Furthermore, PCAT attenuation partially mediated the relationship between the TyG index and CAD severity. Controlling inflammation in patients with high IR and coronary inflammation may provide additional benefits.

Assessment of Individual and Mixed Effects of Six Minerals on Thyroid Hormones in Chinese Pregnant Women.

The biosynthesis of thyroid hormones is essential for brain and neurological development. It requires iodine as a key component but is also influenced by other nutrients. Evidence for the combined nutrient status in relation to thyroid hormones during pregnancy is limited. We aimed to investigate the joint associations of iodine, selenium, zinc, calcium, magnesium and iron with maternal thyroid functions in 489 pregnant women from Hangzhou, China. Serum levels of six essential minerals and thyroid function parameters were measured during the first antenatal visit. Linear regression, quantile g-computation and Bayesian kernel machine regression were used to explore the individual and joint relationships between the six minerals and thyroid hormones. Linear regression analyses revealed that calcium was positively associated with free triiodothyronine (FT3). Zinc was positively associated with free thyroxine (FT4). Iodine was negatively associated with thyroid-stimulating hormone (TSH) and positively associated with FT3 and FT4. The quantile g-computation and BKMR models indicated that the joint nutrient concentration was negatively associated with TSH and positively associated with FT3 and FT4. Among the six minerals, iodine contributed most to thyroid function. The findings suggested that maintaining the appropriate concentration of minerals, either as individuals or a mixture, is important for thyroid health during pregnancy.

eIF4E plays the role of a pathogenic gene in psoriasis, and the inhibition of eIF4E phosphorylation ameliorates psoriasis-like skin damage.

Psoriasis is a complex inflammatory skin disease with uncertain pathogenesis. eIF4E (eukaryotic translation initiation factor 4E) and its phosphorylation state p-eIF4E are highly expressed in psoriatic tissues. However, the role eIF4E played in psoriasis is still unclear. To investigate the function of eIF4E and p-eIF4E in psoriasis and to figure out whether eFT-508 (Tomivosertib, eIF4E phosphorylation inhibitor) can relieve the disease severity and become a promising candidate for the psoriasis treatment. We first verified the expression of eIF4E and p-eIF4E in psoriasis patients' lesional skin. Then, we demonstrated the effect of eIF4E and p-eIF4E on the abnormal proliferation and inflammatory state of keratinocytes by using eIF4E-specific small interfering RNA (si-eIF4E) and eFT-508. In this study, all cell experiments were performed under the psoriasis-model condition. Moreover, the external application of eFT-508 on imiquimod (IMQ)-induced psoriasis mice was performed to explore its potential clinical value. Results showed that eIF4E and p-eIF4E were significantly overexpressed in skin lesions of psoriasis patients. Knocking down eIF4E or adding eFT-508 can relieve the abnormal proliferation and the excessive inflammatory state of keratinocytes by reducing the expression of cyclin D1, IL-1ß, CXCL10, IL23, Wnt 5a, NBS1 and p-AKT from mRNA or protein levels. Furthermore, these results were consistent with those obtained from the in vitro experiments. Then, we conclude that eIF4E plays the role of the pathogenic gene in psoriasis, and eFT-508 may be a promising candidate for anti-prosoriasis drugs.

Emerging Contaminants: An Emerging Risk Factor for Diabetes Mellitus.

Emerging contaminants have been increasingly recognized as critical determinants in global public health outcomes. However, the intricate relationship between these contaminants and glucose metabolism remains to be fully elucidated. The paucity of comprehensive clinical data, coupled with the need for in-depth mechanistic investigations, underscores the urgency to decipher the precise molecular and cellular pathways through which these contaminants potentially mediate the initiation and progression of diabetes mellitus. A profound understanding of the epidemiological impact of these emerging contaminants, as well as the elucidation of the underlying mechanistic pathways, is indispensable for the formulation of evidence-based policy and preventive interventions. This review systematically aggregates contemporary findings from epidemiological investigations and delves into the mechanistic correlates that tether exposure to emerging contaminants, including endocrine disruptors, perfluorinated compounds, microplastics, and antibiotics, to glycemic dysregulation. A nuanced exploration is undertaken focusing on potential dietary sources and the consequential role of the gut microbiome in their toxic effects. This review endeavors to provide a foundational reference for future investigations into the complex interplay between emerging contaminants and diabetes mellitus.

TRPV4 blockade alleviates endoplasmic reticulum stress mediated apoptosis in hypoxia-induced cardiomyocyte injury.

BACKGROUND: Hypoxia-induced myocardial injury remains to be a huge health issue worldwide. Transient receptor potential vanilloid 4 (TRPV4) is a high-flux Ca2+ channel that is involved in numerous cardiovascular diseases. However, the role of TRPV4 in myocardial hypoxic injury remains unclear. Accordingly, this study aimed to investigate the antiapoptotic activity of TRPV4 inhibition and elucidate the underlying mechanisms in myocardial hypoxic injury. METHODS: The ability of TRPV4 to modulate the endoplasmic reticulum stress (ERS) and apoptosis was assessed in vitro through the administration of the TRPV4 antagonist HC-067047 or the agonist GSK1016790A. Additionally, intracellular Ca2+ concentration was measured by Fluo-4 AM. RESULTS: TRPV4 expression was significantly upregulated in hypoxic H9c2 cells compared with that in normoxic cardiomyocytes, accompanied with increased intracellular Ca2+ levels. Conversely, TRPV4 inhibition alleviated ERS in hypoxic H9c2 cells and prevented apoptosis, whereas TRPV4 agonist exacerbated such events. Furthermore, H9c2 cell apoptosis was attenuated with the administration of 4-PBA, an ERS inhibitor. CONCLUSION: TRPV4 inhibition alleviates hypoxia-induced H9c2 cell apoptosis by mitigating ERS.

Liensinine alleviates mouse intestinal injury induced by sepsis through inhibition of oxidative stress, inflammation, and cell apoptosis.

Sepsis is a clinical syndrome triggered by an imbalanced host response to pathogens that can lead to multiple organ dysfunction. The immune response and barrier function of the gut play an important role in the pathogenesis and progression of sepsis. This study aimed to explore the potential role of natural alkaloid Liensinine in the treatment of intestinal injury caused by sepsis and its possible molecular mechanism. In this study, a mouse model of sepsis was established by injecting LPS to explore the protective effect of Liensinine on intestinal injury in sepsis. The results showed that Liensinine could reduce the intestinal damage caused by LPS and increase the number of goblet cells. Furthermore, it decreased the release of inflammatory cytokines by inhibiting NF-kB phosphorylation and NLRP3 inflammasome synthesis. Liensinine also reduced the oxidative stress and ROS accumulation caused by LPS, and played an anti-oxidative stress role by regulating the Nrf2/keap1 signaling pathway. In addition, Liensinine alleviated the inhibition of intestinal autophagy caused by LPS by inhibiting the PI3K/Akt/mTOR pathway. And then it reduced the excessive apoptosis of intestinal cells. This study provides valuable insights for sepsis prevention and treatment, offering a potential therapeutic candidate to protect against intestinal injury and regulate the inflammatory response in sepsis.

Monotropein induces autophagy through activation of the NRF2/PINK axis, thereby alleviating sepsis-induced colonic injury.

Sepsis is a systemic inflammatory disease that is caused by a dysregulated host response to infection and is a life-threatening organ dysfunction that affects many organs, which includes the colon. Mounting evidence suggests that sepsis-induced colonic damage is a major contributor to organ failure and cellular dysfunction. Monotropein (MON) is the major natural compound in the iris glycoside that is extracted from Morendae officinalis radix, which possesses the potent pharmacological activities of anti-inflammatory and antioxidant properties. This research evaluated whether MON is able to alleviate septic colonic injury in mice by cecal ligation and puncture. Colonic tissues were analyzed using histopathology, immunofluorescence, quantitative real-time polymerase chain reaction, and Western blot methods. It was initially discovered that MON reduced colonic damage in infected mice, in addition to inflammation, apoptosis, and oxidative stress in colonic tissues, while it activated autophagy, with the NRF2/keap1 and PINK1/Parkin pathways also being activated. Through the stimulation of NCM460 cells with lipopolysaccharides, an in vitro model of sepsis was created as a means of further elucidating the potential mechanisms of MON. In the in vitro model, it was found that MON could still activate the NRF2/keap1, PINK1/Parkin, and autophagy pathways. However, when MON was paired with the NRF2 inhibitor ML385, it counteracted MON-induced activation of PINK1/Parkin and autophagy, while also promoting inflammatory response and apoptosis in NCM460 cells. Therefore, the data implies that MON could play a therapeutic role through the activation of the NFR2/PINK pathway as a means of inducing autophagy to alleviate the oxidative stress in colonic tissues that is induced by sepsis, which will improve inflammation and apoptosis in colonic tissues.

Defect of TIMP4 Is Associated with High Myopia and Participates in Rat Ocular Development in a Dose-Dependent Manner.

Thinning of the sclera happens in myopia eyes owing to extracellular matrix (ECM) remodeling, but the initiators of the ECM remodeling in myopia are mainly unknown. The matrix metalloproteinase (MMPs) and tissue inhibitors of matrix metalloproteinase (TIMPs) regulate the homeostasis of the ECM. However, genetic studies of the MMPs and TIMPs in the occurrence of myopia are poor and limited. This study systematically investigated the association between twenty-nine genes of the TIMPs and MMPs families and early-onset high myopia (eoHM) based on whole exome sequencing data. Two TIMP4 heterozygous loss-of-function (LoF) variants, c.528C>A in six patients and c.234_235insAA in one patient, were statistically enriched in 928 eoHM probands compared to that in 5469 non-high myopia control (p = 3.7 × 10-5) and that in the general population (p = 2.78 × 10-9). Consequently, the Timp4 gene editing rat was further evaluated to explore the possible role of Timp4 on ocular and myopia development. A series of ocular morphology abnormalities in a dose-dependent manner (Timp4-/- < Timp4+/- < Timp4+/+) were observed in a rat model, including the decline in the retinal thickness, the elongation in the axial length, more vulnerable to the form deprivation model, morphology changes in sclera collagen bundles, and the decrease in collagen contents of the sclera and retina. Electroretinogram revealed that the b-wave amplitudes of Timp4 defect rats were significantly reduced, consistent with the shorter length of the bipolar axons detected by HE and IF staining. Heterozygous LoF variants in the TIMP4 are associated with early onset high myopia, and the Timp4 defect disturbs ocular development by influencing the morphology and function of the ocular tissue.

Thyroglobulin as a Sensitive Biomarker of Iodine Status in Mildly and Moderately Iodine-Deficient Pregnant Women.

Pregnant women are more susceptible to iodine deficiency. However, there are limitations in existing indicators for the evaluation of iodine nutrition in pregnant women. The study aimed to explore whether thyroglobulin (Tg) can be used as a more sensitive biomarker for pregnant women with mild and moderate iodine deficiency. A repeated-measure study was conducted among 1332 pregnant women in Zhejiang Province, China. Serum and urine specimens were collected at a mean of 10, 17, and 32 weeks of pregnancy, respectively; thyroid-stimulating hormone (TSH), Tg, and urinary iodine concentrations were measured. Linear mixed effects models were used to determine the associations between interaction of iodine concentrations and increasing gestation week and TSH and Tg, where participants were divided by urinary iodine concentration (UIC). The median Tg concentration was 11.56, 11.45, and 12.43 µg/L in the first, second, and third trimesters, respectively. After controlling the covariates, the interaction effects between the iodine status and gestation week were significant for both TSH and Tg (p = 0.038 and p = 0.007, respectively). TSH increased with the week of gestation in both iodine concentration groups. Tg increased with advancing pregnancy in the iodine-deficient group whereas it did not in the iodine-sufficient group. There was no significant variation in TSH at each trimester, and Tg was higher in the iodine-deficient group than in the iodine-sufficient group. Tg may be a more sensitive iodine status biomarker than TSH for pregnant women with mild-to-moderate iodine insufficiency.

Double Hyperautofluorescence Rings as a Sign of CFAP410-related Retinopathy.

Purpose: Variants in CFAP410 have been reported to cause retinal dystrophy with or without systemic symptoms. This study was designed to characterize the fundus changes of patients with biallelic variants in CFAP410. Methods: Variants in CFAP410 were identified through whole exome sequencing and targeted exome sequencing of 10,530 probands. Biallelic variants in CFAP410 were evaluated by comprehensive in silico analysis and confirmed by Sanger sequencing and segregation analysis. Ocular phenotypes including fundus photographs, scanning laser ophthalmoscopy, autofluorescence images, ERG, and optical coherence tomography were characterized. Results: Nine patients from eight families were homozygotes or compound heterozygotes for a total of four variants in CFAP410, including c.144-6_159del (novel), c.340_351dup, c.347C>T, and c.545+1G>A. Three patients were diagnosed with cone-rod dystrophy, and the remaining six patients with RP. Among eight patients performed with ultra-wide scanning laser ophthalmoscopy, double hyperautofluorescence rings inside and outside of the macular vascular arcades were observed in six patients, and the remaining two older patients demonstrated single hyperautofluorescence ring surrounded by pigmentation. CFAP410-associated retinopathy in early stage was generally tapetoretinal degeneration without noticeable bone spicule pigmentation, with more severe degeneration in the inferior nasal retina. ERG recordings delineated a severely reduced cone response and mildly to severely reduced rod response. Posterior staphyloma was seen in seven patients who underwent optical coherence tomography examinations. Conclusions: The present study demonstrates the fundus characteristics of patients with biallelic variants in CFAP410 and expands the genotype-phenotype spectrum of CFAP410-related retinal degeneration, in which posterior staphyloma together with double hyperautofluorescence rings might be common peculiar signs.

Machine-Learning-Assisted Procoagulant Extracellular Vesicle Barcode Assay toward High-Performance Evaluation of Thrombosis-Induced Death Risk in Cancer Patients.

Venous thromboembolism (VTE) is the most fatal complication in cancer patients. Unfortunately, the frequent misdiagnosis of VTE owing to the lack of accurate and efficient evaluation approaches may cause belated medical intervention and even sudden death. Herein, we present a rapid, easily operable, highly specific, and highly sensitive procoagulant extracellular vesicle barcode (PEVB) assay composed of TiO2 nanoflower (TiNFs) for visually evaluating VTE risk in cancer patients. TiNFs demonstrate rapid label-free EV capture capability by the synergetic effect of TiO2-phospholipids molecular interactions and topological interactions between TiNFs and EVs. From ordinary plasma samples, the PEVB assay can evaluate potential VTE risk by integrating TiNFs-based EV capture and in situ EV procoagulant ability test with machine-learning-assisted clinical data analysis. We demonstrate the feasibility of this PEVB assay in VTE risk evaluation by screening 167 cancer patients, as well as the high specificity (97.1%) and high sensitivity (96.8%), fully exceeding the nonspecific and posterior traditional VTE test. Together, we proposed a TiNFs platform allowing for highly accurate and timely diagnosis of VTE in cancer patients.

LncRNA MEG3: Targeting the Molecular Mechanisms and Pathogenic causes of Metabolic Diseases.

BACKGROUND: Non-coding RNA is a type of RNA that does not encode proteins, distributed among rRNA, tRNA, snRNA, snoRNA, microRNA and other RNAs with identified functions, where the Long non-coding RNA (lncRNA) displays a nucleotide length over 200. LncRNAs enable multiple biological processes in the human body, including cancer cell invasion and metastasis, apoptosis, cell autophagy, inflammation, etc. Recently, a growing body of studies has demonstrated the association of lncRNAs with obesity and obesity-induced insulin resistance and NAFLD, where MEG3 is related to glucose metabolism, such as insulin resistance. In addition, MEG3 has been demonstrated in the pathological processes of various cancers, such as mediating inflammation, cardiovascular disease, liver disease and other metabolic diseases. OBJECTIVE: To explore the regulatory role of lncRNA MEG3 in metabolic diseases. It provides new ideas for clinical treatment or experimental research. METHODS: In this paper, in order to obtain enough data, we integrate and analyze the data in the PubMed database. RESULTS: LncRNA MEG3 can regulate many metabolic diseases, such as insulin resistance, NAFLD, inflammation and so on. CONCLUSION: LncRNA MEG3 has a regulatory role in a variety of metabolic diseases, which are currently difficult to be completely cured, and MEG3 is a potential target for the treatment of these diseases. Here, we review the role of lncRNA MEG3 in mechanisms of action and biological functions in human metabolic diseases.