E3 ubiquitin ligase RNF114 promotes vesicular stomatitis virus replication via inhibiting type I interferon production.

As a single-stranded RNA virus, vesicular stomatitis virus (VSV) causes influenza-like clinical symptoms in infected individuals. Type-I interferon signaling pathway plays a vital role in inhibiting VSV replication. It has been shown that RNF114 (RING finger protein 114) acts as an E3 ubiquitin ligase to regulate the type-I interferon signaling pathway. In contrast, the effects of RNF114 from Chinese sturgeon or sea perch remain controversial. In the present study, we reported the effect of human RNF114 on VSV infection. Overexpression of RNF114 promoted VSV replication, while depletion of RNF114 reduced viral replication. We further found that RNF114 inhibited type-I interferon production via interacting with mitochondrial antiviral signaling protein (MAVS). Moreover, in vivo experiments demonstrated that RNF114 could also accelerate VSV replication and virus-induced inflammation in lung tissues. Collectively, our findings supported that RNF114 negatively regulated the type-I interferon signaling pathway during VSV replication, providing novel and favorable insights into clinical treatment of VSV infection.

Effect of Different Heat Treatments on the Quality and Flavor Compounds of Black Tibetan Sheep Meat by HS-GC-IMS Coupled with Multivariate Analysis.

There are limited reports about the effect of different heat treatments on the quality and flavor of Black Tibetan sheep meat. The current study examined the effect of pan-frying, deep-frying, baking, and boiling treatment on the quality of Black Tibetan sheep meat; the amino acid, fatty acid, and volatile flavor compounds (VFCs) were investigated by a texture analyzer, ultra-high-performance liquid chromatography (UHPLC), gas chromatography (GC), and headspace-gas chromatography-ion mobility (HS-GC-IMS). The key VFCs were identified through orthogonal partial least squares discrimination analysis (OPLS-DA), and variable importance projection (VIP) values. In addition, Pearson's correlations between meat quality parameters and key VFCs were examined. The sensory scores, including texture, color, and appearance, of baked and pan-fried meat were higher than those of deep-fried and boiled meat. The protein (40.47%) and amino acid (62.93 µmol/g) contents were the highest in pan-fried meat (p < 0.05). Additionally, it contained the highest amounts of monounsaturated and polyunsaturated fatty acids, such as oleic, linoleic, and α-linolenic acids (p < 0.05). Meanwhile, pan-fried and deep-fried meat had higher amounts of VFCs than baked meat. The OPLS-DA similarity and fingerprinting analyses revealed significant differences between the three heat treatment methods. Aldehydes were the key aroma compounds in pan-fried meat. Importantly, 3-methylbutyraldehyde and 2-heptanone contents were positively correlated with eicosenoic, oleic, isooleic, linoleic, α-Linolenic, and eicosadiene acids (p < 0.05). To sum up, pan-fried Black Tibetan sheep meat had the best edible, nutritional, and flavor quality.

Identification of the association of CD28+ CD244+ Tc17/IFN-γ cells with chronic hepatitis C virus infection.

CD8+ T cells play multiple and complex immunological roles including antiviral, regulatory, and exhaustive effects in hepatitis C virus (HCV) infected patients. Some CD8+ T-cell subsets were confirmed to be closely related to HCV infection such as TCM , TEM , TEM RA, Tc17, and CD8+ Treg. Herein, we report a new subset of interleukin (IL)-17/interferon (IFN)-γ producing CD8+ T (Tc17/IFN-γ) cells that markedly correlate with CD28+ CD244+ cells, IL-17 levels, and HCV RNA in HCV patients. During early treatment with peg-IFN-a2a plus ribavirin, the imbalance of these Tc17/IFN-γ cells could be partially restored, together with normalized serum alanine aminotransferase but not aspartate transaminase. Also, we analyzed the dynamic change of the percentage of this T cells subset in patients with different outcome after 4-week course of treatment with peg-IFN-a2a plus ribavirin and found that the percentage of CD8+ CD28+ CD244+ T cells significantly decreased in recovered patients but not in nonrecovered patients. In vitro, CD28+ CD244+ T cells were the only CD8+ T-cell group that secreted both IL-17 and IFN-γ in this axis and blockade with anti-CD244 antibodies significantly reduced cytokine production. Taken together, this study demonstrates that the frequency and regulatory functions of CD28+ CD244+ Tc17/IFN-γ cells may play an important role in persistent HCV infection.

A report of clinical diagnosis and treatment of nine cases of coronavirus disease 2019.

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 has become an important public health issue in the world. More than 118 000 cases were confirmed around the world. The main clinical manifestations were respiratory symptoms and occasional gastrointestinal symptoms. However, there is no unified standard for the diagnosis and treatment of COVID-19. In the retrospective analysis, we report nine cases of COVID-19, describe the history of contact, clinical manifestations, the course of diagnosis and clinical treatment before, during and after treatment.

Chemical renal denervation-induced upregulation of the ACE2/Ang (1-7)/Mas axis attenuates blood pressure elevation in spontaneously hypertensive rats.

OBJECTIVE: Evidence has shown that the ACE2/Ang (1-7)/Mas axis plays an important role in the control of hypertension. Thus, we hypothesized that chemical renal denervation (RDN) could reduce blood pressure by regulating the ACE2/Ang (1-7)/Mas axis in spontaneously hypertensive rats. METHODS: Twelve rats were randomly divided into sham group and chemical RDN group. All the rats were sacrificed 4 weeks later. Plasma samples were collected to measure the renin-angiotensin system (RAS) activities and reactive oxygen species levels by radioimmunoassay, chromatometry and ELISA. Paraventricular nucleus (PVN) tissues were collected to examine the expression of the components of the ACE2/Ang (1-7)/Mas axis by western bolt and immunofluorescence. RESULTS: The systolic blood pressure (169.33 ± 7.50 vs 182.67 ± 7.00 mmHg, p < .05) and the diastolic blood pressure (97.50 ± 4.68 vs 109.33 ± 4.41 mmHg, p < .05) in the RDN group were obviously lower than the baseline levels, whereas the opposite results were observed in the sham group. The RDN group exhibited a significant reduction in the plasma ROS (91.59 ± 13.12 vs 72.34 ± 11.76 U/ml, p < .05) and NADPH oxidase (171.86 ± 1.14 vs 175.75 ± 1.74 nmol/ml, p < .001) compared with the sham group, while the plasma eNOS (3.47 ± 0.42 vs 2.49 ± 0.51 U/ml, p < .05) and NO (55.92 ± 8.10 vs 43.53 ± 4.58 µmol/L, p < .05) were increased. The expression of the components of the ACE2/Ang (1-7)/Mas axis was upregulated while the expression of the components of the ACE/Ang II/AT1 R axis was downregulated in the plasma and PVN in the RDN group. CONCLUSION: Our findings suggested that the reduction in blood pressure was regulated by chemical RDN-induced upregulation of the components of the ACE2/Ang (1-7)/Mas axis.

Early Serum HBsAg Drop Is a Strong Predictor of HBeAg Seroconversion and HBsAg Loss to Pegylated Interferon Alfa-2a in Chronic Hepatitis B Patients with Prior Nucleos(t)ide Analogue Exposure.

BACKGROUND High rates of HBeAg and/or HBsAg seroconversion or clearance have been achieved in chronic hepatitis B (CHB) patients receiving pegylated interferon (pegIFN) in addition to ongoing nucleos(t)ide analogue (NUC) treatment. In the present study, we aimed to evaluate HBsAg kinetics to predict HBeAg seroconversion and HBsAg clearance in these patients. MATERIAL AND METHODS A total of 33 HBeAg-positive and 17 HBeAg-negative patients were enrolled between January 2010 and January 2018. At the end of pegIFN treatment, 9 of 50 patients achieved HBsAg clearance, and 9 of 33 HBeAg-positive patients achieved HBeAg seroconversion. RESULTS The cutoff value of 0.41 log10 IU/mL in HBsAg decline at week 12 had a positive predictive value (PPV) of 58.3% and a negative predictive value (NPV) of 94.6% for HBsAg clearance. The cutoff value of 1.94 log10 IU/mL in HBsAg decline at week 24 had a PPV of 80.0% and an NPV of 97.5% for HBsAg clearance. The cutoff value of 0.47 log10 IU/mL in HBsAg decline at week 12 had a PPV of 83.3% and an NPV of 85.2% for HBeAg seroconversion. The cutoff value of 1.29 log10 IU/mL in in HBsAg decline at week 24 had a PPV of 85.7% and an NPV of 88.5% for HBeAg seroconversion. CONCLUSIONS Early HBsAg drop has a high predictive value for HBsAg clearance and HBeAg seroconversion in patients who were treated with combination therapy of pegIFN and NUCs.

AMPK/NF-κB signaling pathway regulated by ghrelin participates in the regulation of HUVEC and THP1 Inflammation.

Endothelial inflammation and monocyte plays an essential role in the initiation and progression of atherosclerosis. Ghrelin is beneficial for atherosclerosis progression. However, the detailed and precise molecular mechanisms of how ghrelin regulates endothelial inflammation are not clear. In this study, we investigated the regulation mechanism of ghrelin on TNF-α-activated endothelial inflammation and monocyte adhesion. It was found that TNF-α-induced monocyte adhesion on HUVEC was significantly attenuated by ghrelin. Furthermore, we found that ghrelin effectively suppressed TNF-α-induced inflammatory factors' (including ICAM-1, VCAM-1, MCP-1, and IL-1ß) expression through inhibiting AMPK phosphorylation and p65 expression both in HUVEC and THP-1. This phenomenon was further demonstrated by using AMPK agonist AICAR and inhibitor compound C, respectively. Our findings suggest that ghrelin may mediate TNF-α-induced endothelial inflammation and monocyte adhesion, in part via AMPK/NF-κB signaling pathway. These novel anti-inflammatory and immunoregulatory actions of ghrelin may play a certain role in understanding the formation and development of atherosclerosis.

CYP2C19 and ABCB1 genetic polymorphisms correlate with the recurrence of ischemic cardiovascular adverse events after clopidogrel treatment.

BACKGROUND: This study was aimed to investigate the correlation between CYP2C19 and ABCB1 polymorphisms and the recurrence of ischemic cardiovascular adverse events in patients with coronary artery disease treated with clopidogrel. METHODS: A total of 168 patients with coronary heart disease who underwent PCI operation and received clopidogrel treatment were enrolled. Dual antiplatelet therapy was applied to the treatment of patients for 2 years. Thromboelastography was used to test the efficiency of blood coagulation. Polymerase chain reaction (PCR) was used to detect CYP2C19 and ABCB1 3435CT polymorphisms. One-year follow-up visit was carried out to record the incidence of cardiovascular adverse events after drug-eluting stent implantation was inset. RESULTS: Follow-up visit results suggested that the patients with high on-treatment platelet reactivity (HPR) had a higher recurrence rate of cardiovascular adverse events after PCI operation and clopidogrel treatment. Gene polymorphism testing results indicated that patients with CYP2C19*3 had a significantly higher incidence of HPR, whereas CYP2C19*2 and ABCB1 3435CT were not significantly correlated with HPR. Multivariable logistic regression analysis showed that CYP2C19*3 might be an independent predictive factor of post-PCI HPR. In addition, CYP2C19*3 as well as post-PCI HPR could function as independent predictive factors of cardiovascular adverse events. CONCLUSION: CYP2C19*3 polymorphism could be an important predictive factor of HPR and ischemic cardiovascular adverse events after clopidogrel treatment.

IL-35 inhibits HBV antigen-specific IFN-γ-producing CTLs in vitro.

Interleukin (IL)-35 is an inhibitory cytokine consisting of IL-12A and Epstein-Barr virus-induced gene 3 (Ebi3) and is required by regulatory T-cells (Tregs) for maximal activity. During chronic hepatitis B virus (HBV) infection, Tregs have immunosuppressive effects on HBV-specific T helper (Th) cells, yet little is known about the complex regulation of Tregs and their contribution to the inadequate immune system response to the virus. In the present study, we investigated whether IL-35 is involved in HBV-related cellular immune responses. Cluster of differentiation (CD)4(+) T-cells from peripheral blood were derived from healthy volunteers, resolved HBV individuals and chronic active hepatitis B patients and stimulated with CD3/28-conjugated beads. We analysed mRNA and protein levels of IL-35 and assessed the inhibitory effect of IL-35 on HBV core antigen-specific cytotoxic T lymphocytes (CTLs), dendritic cells (DCs) and effector T-cells (Teffs). Correlation analyses between liver inflammation and HBV DNA load were conducted. Results show that chronic HBV patients harbour significantly higher levels of Ebi3 mRNA and protein in CD4(+) T-cells compared with healthy volunteers and resolved HBV individuals. IL-35 suppressed the proliferation of HBV antigen-specific CTLs and interferon (IFN)-γ production in vitro. Ex vivo, IL-35 decreased the proliferation of CD4(+)CD45RA(+) naïve T-cells, especially in CD4(+)CD25(-)CD45RA(+) naïve Teffs. IL-35 inhibited the expansion of CD11c(+) DCs. Our data indicate that IL-35 is highly expressed in chronic HBV CD4(+) T-cells and plays an important role in the inhibition of the cellular immune response in chronic HBV.

Glatiramer acetate ameliorates inflammatory bowel disease in mice through the induction of Qa-1-restricted CD8⁺ regulatory cells.

Inflammatory bowel diseases (IBDs) are complex multifactorial immunological disorders characterized by dysregulated immune reactivity in the intestine. Here, we investigated the contribution of Qa-1-restricted CD8(+) Treg cells in regulating experimental IBD in mice. We found that CD8(+) T cells induced by T-cell vaccination ameliorated the pathological manifestations of dextran sulfate sodium induced IBD when adoptively transferred into IBD mice. In addition, CD8(+) cell suppressive activity was induced by vaccination with glatiramer acetate (GA), an FDA-approved drug for multiple sclerosis (MS). We next showed that GA-induced CD8(+) Treg cells worked in a Qa-1-dependent manner and their suppressive activity depends on perforin-mediated cytotoxicity. Finally, we confirmed the role of CD4(+) T cells in dextran sulfate sodium induced colitis progression, and clarified that GA-induced CD8(+) T cells exerted their therapeutic effects on colitis by targeting pathogenic CD4(+) T cells. Our results reveal a new regulatory role of Qa-1-restricted CD8(+) Treg cells in IBD and suggest their induction by GA vaccination as a potential therapeutic approach to IBD.

Pancreatic Injury Is Associated with Poor Prognosis in Severe Fever with Thrombocytopenia Syndrome.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease. Previous studies have primarily focused on the epidemiological and clinical characteristics of patients with SFTS, whereas pancreatic injury has received little attention. This study investigated the effects of pancreatic injury on the prognosis of patients with SFTS. A total of 156 patients diagnosed with SFTS between April 2016 and April 2022 were included in the analysis. Multivariate logistic regression analysis showed that pancreatic injury (odds ratio [OR] = 3.754, 95% confidence interval [CI]: 1.361-79.036, P = 0.024) and neurological symptoms (OR = 18.648, 95% CI: 4.921-70.668, P < 0.001) were independent risk factors for mortality. The receiver operating characteristic curve indicated that serum pancreatic enzymes were predictive of progression to death in patients with SFTS. The area under the curve (AUC) for amylase was 0.711, with an optimal cutoff value of 95.5 U/L, sensitivity of 96.4%, and specificity of 35.9%. Lipase had an AUC of 0.754, an optimal cutoff value of 354.75 U/L, sensitivity of 75%, and specificity of 67.2%. Thus, pancreatic injury was associated with a poor prognosis of SFTS and can be used as an important reference for SFTS determination and prognostic assessment.

Reperfusion strategies on the clinical outcomes of ST-elevation myocardial infarction patients over 80 years old in China.

BACKGROUNDS AND AIMS: This study aims to explore the efficacy of reperfusion strategies on the clinical outcomes of ST-elevation myocardial infarction (STEMI) patients over 80 years old in China. METHODS: A retrospective cohort study was performed on STEMI patients over 80 years old who underwent reperfusion strategies and no reperfusion between January 2014 and December 2021 based on the China Cardiovascular Association (CCA) Database-Chest Pain Center. RESULTS: This study included a total of 42,699 patients (mean age 84.1 ± 3.6 years, 52.2% male) among which 19,280 (45.2%) underwent no reperfusion, 20,924 (49.0%) underwent primary percutaneous coronary intervention (PCI), and 2,495 (5.8%) underwent thrombolytic therapy. After adjusting for potential confounders, multivariable logistic regression analysis revealed that patients who underwent primary PCI strategy showed a significantly lower risk of in-hospital mortality (OR = 0.62, 95% CI: 0.57-0.67, P < 0.001) and the composite outcome (OR = 0.83, 95% CI: 0.79-0.87, P < 0.001) compared to those received no reperfusion. In contrast, patients with thrombolytic therapy exhibited a non-significantly higher risk of in-hospital mortality (OR = 0.99, 95% CI: 0.86-1.14, P = 0.890), and a significantly elevated risk of the composite outcome (OR = 1.15, 95% CI: 1.05-1.27, P = 0.004). During a median follow-up of 6.7 months post-hospital admission, there was a percentage 31.4% of patients died and patients in the primary PCI group consistently demonstrated a reduced incidence of all-cause mortality (HR = 0.58, 95% CI: 0.56-0.61, P < 0.001). CONCLUSION: STEMI patients over 80 years old who underwent the primary PCI strategy are more likely to have favorable clinical outcomes compared to those who received no reperfusion, whereas, thrombolytic therapy warrants careful assessment and monitoring.

Improvement in the performance of an autoantibody panel in combination with heat shock protein 90a for the detection of early­stage lung cancer.

The early diagnosis of lung cancer is closely associated with the decline of mortality. A panel consisting of seven lung cancer-related autoantibodies (7-AABs) has been shown to be a reliable and specific indicator for the early detection of lung cancer, with a specificity of ~90% and a positive predictive value of ~85%. However, its low sensitivity and negative predictive value limit its wide application. To improve its diagnostic value, the diagnostic efficiencies of 7-AABs in combination with non-specific tumor markers were retrospectively investigated for the detection of early-stage lung cancer. A total of 217 patients with small lung nodules who presented with ground-glass opacity or solid nodules as well as 30 healthy controls were studied. The concentrations of 7-AABs and heat shock protein 90a (HSP90a) were assessed using ELISA. Automated flow fluorescence immune analysis was used for the assessment of CEA, CYFRA21-1, CA199 and CA125 levels. The results showed that 7-AABs + HSP90a possessed a remarkably improved diagnostic efficiency for patients with small pulmonary nodules or for patients with lung nodules of different types, which suggested that 7-AABs in combination with HSP90a could have a high clinical value for the improvement of the diagnostic efficiency of early-stage lung cancer.

A Novel Spatial Position Prediction Navigation System Makes Surgery More Accurate.

During intravascular interventional surgery, the 3D surgical navigation system can provide doctors with 3D spatial information of the vascular lumen, reducing the impact of missing dimension caused by digital subtraction angiography (DSA) guidance and further improving the success rate of surgeries. Nevertheless, this task often comes with the challenge of complex registration problems due to vessel deformation caused by respiratory motion and high requirements for the surgical environment because of the dependence on external electromagnetic sensors. This article proposes a novel 3D spatial predictive positioning navigation (SPPN) technique to predict the real-time tip position of surgical instruments. In the first stage, we propose a trajectory prediction algorithm integrated with instrumental morphological constraints to generate the initial trajectory. Then, a novel hybrid physical model is designed to estimate the trajectory's energy and mechanics. In the second stage, a point cloud clustering algorithm applies multi-information fusion to generate the maximum probability endpoint cloud. Then, an energy-weighted probability density function is introduced using statistical analysis to achieve the prediction of the 3D spatial location of instrument endpoints. Extensive experiments are conducted on 3D-printed human artery and vein models based on a high-precision electromagnetic tracking system. Experimental results demonstrate the outstanding performance of our method, reaching 98.2% of the achievement ratio and less than 3 mm of the average positioning accuracy. This work is the first 3D surgical navigation algorithm that entirely relies on vascular interventional robot sensors, effectively improving the accuracy of interventional surgery and making it more accessible for primary surgeons.

A Comparison of Dynamic SPECT Coronary Flow Reserve with TIMI Frame Count in the Treatment of Non-Obstructive Epicardial Coronary Patients.

Background: Microvascular dysfunction in patients with non-obstructive epicardial coronary may aggravate patient's symptoms or lead to various clinical events. Objective: To investigate the correlation between dynamic single photon emission computed tomography (D-SPECT) derived coronary flow reserve (CFR) and TIMI frame count (TFC) in patients with non-obstructive epicardial coronary patients. Methods: Patients with suspected or known stable CAD who were recommended to undergo invasive coronary angiography were prospectively enrolled in this study. Those who had non-obstructive coronary received TIMI frame count (TFC) and D-SPECT. A cut-off value of >40 was defined as slow flow referred to TFC. Results: A total of 47 patients diagnosed with non-obstructive coronary were enrolled. The mean age of patients was 66.09 ± 8.36 years, and 46.8% were male. Dynamic SPECT derived coronary flow reserve (CFR) was significantly correlated with TIMI frame count in 3 epicardial coronary (LAD: r=-0.506, P = 0.0003; LCX: r= -0.532, P = 0.0001; RCA: r= -0.657, P < 0.0001). The sensitivity and specificity of CFR in identifying abnormal TIMI frame count < 40 was 100.0% and 57.6% in LAD, 62.5% and 87.0% in LCX, 83.9% and 75.0% in RCA, respectively. The optimal CFR cut-off values were 2.02, 2.47, and 1.96 among the three vessels. Conclusion: In patients with non-obstructive coronary, CFR derived from D-SPECT was strongly correlated with TFC. This study demonstrates that that CFR may be an alternative non-invasive method for identifying slow flow in non-obstructive coronary.

Pyruvate dehydrogenase kinase supports macrophage NLRP3 inflammasome activation during acute inflammation.

Activating the macrophage NLRP3 inflammasome can promote excessive inflammation with severe cell and tissue damage and organ dysfunction. Here, we show that pharmacological or genetic inhibition of pyruvate dehydrogenase kinase (PDHK) significantly attenuates NLRP3 inflammasome activation in murine and human macrophages and septic mice by lowering caspase-1 cleavage and interleukin-1ß (IL-1ß) secretion. Inhibiting PDHK reverses NLRP3 inflammasome-induced metabolic reprogramming, enhances autophagy, promotes mitochondrial fusion over fission, preserves crista ultrastructure, and attenuates mitochondrial reactive oxygen species (ROS) production. The suppressive effect of PDHK inhibition on the NLRP3 inflammasome is independent of its canonical role as a pyruvate dehydrogenase regulator. Our study suggests a non-canonical role of mitochondrial PDHK in promoting mitochondrial stress and supporting NLRP3 inflammasome activation during acute inflammation.

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion.

The benefits of renal sympathetic denervation (RDN) on blood pressure have been proved in a large number of clinical trials in recent years. However, the regulatory mechanism of RDN on hypertension remains elusive. Thus, it's essential to establish a simpler RDN model in mice. In this study, osmotic mini pumps filled with Angiotensin II were implanted in 14-week-old C57BL/6 mice. One week after the implantation of the mini-osmotic pump, a modified RDN procedure was performed on bilateral renal arteries of the mice using phenol. Age-sex-matched mice were given saline and served as sham group. Blood pressure was measured at baseline and every week subsequently for 21 days. Then, renal artery, abdominal aorta and heart were collected for histological examination using H&E and Masson staining. In this study, we present a simple, practical, repeatable, and standardized RDN model, which can control hypertension and alleviate cardiac hypertrophy. The technique can denervate peripheral renal sympathetic nerves without renal artery damage. Compared to previous models, the modified RDN facilitates the study of the pathobiology and pathophysiology of hypertension.

Secoisolariciresinol diglucoside ameliorates high fat diet-induced colon inflammation and regulates gut microbiota in mice.

Secoisolariciresinol diglucoside (SDG) has a strong anti-inflammatory effect, which depends partly on the participation of gut microbiota. We studied the effect of SDG on colonic inflammation caused by a common poor diet, high-fat diet (HFD), and the regulation of gut microbiota as well as its metabolites. Considering the difference of sources, prices, and possible bioactivity, we compared the effects of a single compound and the extract of SDG on colon inflammation. The results displayed that both the single compound and the extract ameliorated morphologic damage of the colon and improved intestinal barrier integrity. In addition, SDG suppressed the mRNA expressions of inflammatory cytokines in the colon, and the inhibitory effect of a single compound was stronger than that of the extract. The results of 16S rRNA sequencing showed that SDG altered the diversity and composition of gut microbiota, particularly the abundance of inflammation-related bacteria, and the effect of the extract was greater than that of a single compound. The analysis of short-chain fatty acids (SCFAs) manifested the improved concentration with the intervention of SDG. These results confirmed that SDG, including a single compound and extract, exerted protective effects against colon inflammation, which might be partly explained by the gut microbiome. Our research could provide a positive nutritional intervention for chronic intestinal inflammation.

Ascending aortic perivascular adipose tissue inflammation associates with aortic valve disease.

BACKGROUND: Ascending aortic perivascular adipose tissue (AA-PVAT) mainly comprises brown adipose tissue (BAT), originates from neural crest cells that derive from ectoderm, and plays important role in angiotensin II-induced vascular inflammation and remodeling in mice. However, the characterization and function of human AA-PVAT remains highly unclear. METHODS: Patients with coronary artery disease (CAD) (n = 20) and aortic valve disease (AVD) (n = 23) who underwent cardiac surgery consented to take part in transcriptome and histological studies. Paired samples of AA-PVAT, epicardial adipose tissue (EAT), and subcutaneous adipose tissue (SAT) were obtained. RNA sequencing, histological analysis, quantitative reverse transcription polymerase chain reaction and western blot studies were performed on those samples. RESULTS: Human AA-PVAT exhibited smaller adipocyte morphology and high expression of brown adipocyte marker. Transcriptome analysis revealed that AA-PVAT showed unique transcriptome characteristics compared with EAT and SAT. While comparing CAD and AVD patients, AA-PVAT exhibited a decreasing brown phenotype and higher inflammatory response in AVD patients. Gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that the differentially expressed genes in AA-PVAT between CAD and AVD patients were involved mainly in the processes of inflammation and metabolism regulation. CONCLUSIONS: Human AA-PVAT is a BAT-like adipose tissue with unique transcriptome characteristics, and exhibits a weakened brown phenotype and an enhanced inflammation response in AVD patients.