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ObjectiveTo compare the diagnostic effectiveness of the Gynecologic Imaging Reporting and Data System (GI-RADS) and Neoplasias in the Adnexa (ADNEX) model for the diagnosis of benign and malignant ovarian tumors by junior physicians.MethodsThe sonographic data of 634 patients with ovarian tumors confirmed by pathology in our hospital over 4 years were analyzed retrospectively by junior doctors. The diagnostic efficacy of the GI-RADS and ADNEX models was compared based on pathology.Results(1) Regarding the diagnostic efficacy of the GI-RADS and ADNEX models, the sensitivity was 90.15% and 84.85%, the specificity was 87.65% and 85.86%, the accuracy rates were 88.17% and 85.65%, and the Youden Indices were 0.778 and 0.707, respectively. The areas under the receiver operating characteristic (ROC) curves were 0.924 (95% CI: 0.900-0.943) and 0.933 (95% CI: 0.911-0.951), respectively. The GI-RADS classification was equivalent to that of the ADNEX model in the diagnosis of adnexal tumors (P>0.05). These findings were highly consistent with the pathological results (Kappa values were 0.684 and 0.691, respectively). (2) When differentiating between different pathological types of adnexal tumors, the ADNEX model had the best diagnostic value for distinguishing between benign tumors and stage II-IV ovarian cancer (AUC=0.990, 95% CI: 0.978-0.997).Conclusions(1) The diagnostic efficacy of the GI-RADS and ADNEX models in the diagnosis of benign and malignant ovarian tumors by junior physicians is excellent and comparable. (2) The ADNEX model shows good value for differentiating ovarian tumors of different pathological types by junior physicians.

BackgroundDiabetic peripheral neuropathy (DPN) is one of the most common chronic complications of diabetes and the strongest initiating risk factor for diabetic foot ulceration. Early diagnosis of DPN through screening measures is, therefore, of great importance for diabetic patients. Recently, shear wave elastography (SWE) has been used as a method that is complementary to neuroelectrophysiological examination in the diagnosis of DPN. We aimed to conduct a meta-analysis based on currently available data to evaluate the performance of tibial nerve stiffness on SWE for diagnosing DPN.MethodsBoth PubMed, EMBASE, the Cochrane Library, and Web of Science were searched for studies that investigated the diagnostic performance of SWE for DPN up to March 1th, 2022. Three measures of diagnostic test performance, including the summary area under receiver operating characteristics curve (AUROC), the summary sensitivity and specificity, and the summary diagnostic odds ratios were used to assess the diagnostic accuracy of SWE. All included studies were published between 2017 and 2021.ResultsSix eligible studies (with 170 DPN patients, 28 clinically defined DPN patients, 168 non-DPN patients, and 154 control participants) that evaluated tibial nerve stiffness were included for meta-analysis. The summary sensitivity and specificity of SWE for tibial nerve stiffness were 75% (95% confidence interval [CI]: 68–80%) and 86% (95% CI: 80–90%), respectively, and the summary AUROC was 0.84 (95% CI: 0.81–0.87), for diagnosing DPN. A subgroup analysis of five two-dimensional SWE studies revealed similar diagnostic performance, showing the summary sensitivity and specificity of 77% (95% CI: 69–83%) and 86% (95% CI: 79–91%), respectively, and a summary AUROC value of 0.86 (95% CI: 0.83–0.89).ConclusionsSWE is found to have good diagnostic accuracy for detecting DPN and has considerable potential as an important and noninvasive adjunctive tool in the management of patients with DPN.

BackgroundMeasurement of hepatic venous pressure gradients is the gold standard for assessing portal hypertension (PH) but is invasive with potential complications. We aimed to assess the performance in liver and spleen stiffness measurement (LSM and SSM, respectively) by two-dimensional shear wave elastography (2D-SWE) and composite scores including liver stiffness-spleen diameter to platelet ratio score (LSPS), platelet (PLT) count/spleen diameter ratio (PSR), aspartate aminotransferase (AST)/alanine aminotransferase ratio (AAR), and AST-to-PLT ratio index (APRI) for diagnosing PH in nonalcoholic fatty liver disease (NAFLD) rat models.MethodsAnimal models with PH in NAFLD were established in 65 rats, which then underwent 2D-SWE measurements. Morphological and biological parameters were collected for calculation of four composite scores. Correlations of noninvasive methods with portal venous pressure were evaluated by Spearman correlation analysis. The area under the receiver operating characteristic curve (AUC) was used to assess the performance of noninvasive methods in predicting PH.ResultsLSM and SSM were significantly associated with portal venous pressure (r = 0.636 and 0.602, respectively; all P < 0.001). The AUCs of LSM and SSM in the diagnosis of PH were 0.906 (95% confidence interval [CI]:0.841–0.97) and 0.87 (95% CI:0.776–0.964), respectively, and were significantly higher than those in composite scores. The AUCs for LSPS, PSR, AAR, and APRI were 0.793, 0.52, 0.668, and 0.533, respectively, for diagnosing PH. The AUCs of the combined models of LSM and SSM, LSM and PLT, SSM and PLT, and LSM, SSM and PLT were 0.923, 0.913, 0.872, and 0.923, respectively. The four combined models showed no statistical differences compared to LSM and SSM in evaluating PH (all P > 0.05).ConclusionsLSM and SSM by 2D-SWE can be used as promising noninvasive parameters for diagnosing PH in NAFLD and have higher accuracy than composite scores. The combined models, compared to LSM and SSM, did not significantly improve the performance in diagnosing PH.

Ethnopharmacological relevance: Curcumin is a bright yellow chemical produced by plants of the Curcuma longa species. Chemically, curcumin is a diarylheptanoid, belonging to the group of curcuminoids. The therapeutic potential of curcumin has been widely investigated, including its utilization in various of cardiovascular diseases. However, its effect in cardiac remodeling post myocardial infarction and underlying mechanism remains to be uncover.Aim: To evaluate the therapeutic effect and underlying mechanism of curcumin on cardiac fibrosis after myocardial infarction via macrophage-fibroblast crosstalk.Methods: Male C57BL/6 (C57) mice were subjected to left anterior descending coronary artery ligation to establish myocardial infarction and intragastrically fed vehicle or curcumin (50 mg/kg or 100 mg/kg) for 4 weeks. In parallel, neonatal rat cardiac fibroblasts were isolated and co-cultured with liposaccharide (LPS− or LPS+) curcumin-treated macrophages, followed by TGF-β stimulation for 24 h. Cardiac function was determined by 2-dimensional echocardiography, and cardiac fibrosis was measured by picrosirius red staining. Apoptosis of macrophages was investigated by flow cytometry; all pro-fibrotic protein expression (EDA-Fibronectin, Periostin, Vimentin, and α-SMA) as well as TGF-βR1 downstream signaling activation reflected by phosphorylated SMAD2/3 (p-SMAD2 and p-SMAD3) were demonstrated by western blotting.Results: Curcumin significantly ameliorated the inflammation process subsequent to myocardial infarction, reflected by decreased expression of CD68+ and CD3+ cells, accompanied by dramatically improved cardiac function compared with the placebo group. In addition, cardiac fibrosis is inhibited by curcumin administration. Interestingly, no significant reduction in fibrotic gene expression was observed when isolated cardiac fibroblasts were directly treated with curcumin in vitro; however, pro-fibrotic protein expression was significantly attenuated in CF, which was co-cultured with LPS-stimulated macrophages under curcumin treatment compared with the placebo group. Mechanistically, we discovered that curcumin significantly downregulated pro-inflammatory cytokines in macrophages, which in turn inhibited IL18 expression in co-cultured cardiac fibroblasts using bulk RNA sequencing, and the TGF-β1-p-SMAD2/3 signaling network was also discovered as the eventual target downstream of IL18 in curcumin-mediated anti-fibrosis signaling.Conclusion: Curcumin improves cardiac function and reduces cardiac fibrosis after myocardial infarction. This effect is mediated by the inhibition of macrophage-fibroblast crosstalk in the acute phase post-MI and retrained activation of IL18-TGFβ1-p-SMAD2/3 signaling in cardiac fibroblasts.

This study describes the dynamics and complexity of microbial communities producing hydrogen-rich fermentation gas from sugar-beet molasses in five packed-bed reactors (PBRs). The bioreactors constitute a part of a system producing hydrogen from the by-products of the sugar-beet industry that has been operating continuously in one of the Polish sugar factories. PBRs with different working volumes, packing materials, construction and inocula were tested. This study focused on analysis (based on 16S rRNA profiling and shotgun metagenomics sequencing) of the microbial communities selected in the PBRs under the conditions of high (>100 cm3/g COD of molasses) and low (

Autoimmune diseases can be chronic with relapse of inflammatory symptoms, but it can be also acute and life-threatening if immune cells destroy life-supporting organs, such as lupus nephritis. The etiopathogenesis of autoimmune diseases has been revealed as that genetics and environmental factors-mediated dysregulated immune responses contribute to the initiation and development of autoimmune disorders. However, the current understanding of pathogenesis is limited and the underlying mechanism has not been well defined, which lows the development of novel biomarkers and new therapeutic strategies for autoimmune diseases. To improve this, broadening and deepening our understanding of pathogenesis is an unmet need. As genetic susceptibility cannot explain the low accordance rate of incidence in homozygous twins, epigenetic regulations might be an additional explanation. Therefore, this review will summarize current progress of studies on epigenetic dysregulations contributing to autoimmune diseases, including SLE, rheumatoid arthritis (RA), psoriasis, type 1 diabetes (T1D), and systemic sclerosis (SSc), hopefully providing opinions on orientation of future research, as well as discussing the clinical utilization of potential biomarkers and therapeutic strategies for these diseases.

Plant pathogens are increasingly considered as important agents in promoting plant coexistence, while plant symbionts like ectomycorrhizal fungi (EMF) can facilitate plant dominance by helping conspecific individuals to defend against plant pathogens. However, we know little about their relationships with plants at large scales. Here, using soil fungal data collected from 28 forest reserves across China, we explored the latitudinal diversity gradients of overall fungi and different fungal functional guilds, including putative plant pathogens, EMF, and saprotrophic fungi. We further linked the spatial patterns of alpha diversities of putative plant pathogens and EMF to the variation of plant species richness. We found that the relationships between latitude and alpha diversities of putative plant pathogens and EMF were region-dependent with sharp diversity shifts around the mid-latitude (~35°N), which differed from the unimodal diversity distributions of the overall and saprotrophic fungi. The variations in the diversities of putative plant pathogens and EMF were largely explained by the spatial regions (south vs. north/subtropical zone vs. temperate zone). Additionally, the alpha diversities of these two fungal guilds exhibited opposing trends across latitude. EMF could alter the relationship between diversities of putative plant pathogens and plants in the south/subtropical region, but not vice versa. We also found that the ratio of their alpha diversities (EMF to putative plant pathogens) was negatively related to plant species richness across the spatial regions (north to south), and explained ~10% of the variation of plant species richness. Overall, our findings suggest that plant-microbe interactions not only shape the local plant diversity but also may have non-negligible contributions to the large-scale patterns of plant diversity in forest ecosystems.

Autophagy is a complicated cellular mechanism that maintains cellular and tissue homeostasis and integrity via degradation of senescent, defective subcellular organelles, infectious agents, and misfolded proteins. Accumulating evidence has shown that autophagy is involved in numerous immune processes, such as removal of intracellular bacteria, cytokine production, autoantigen presentation, and survival of lymphocytes, indicating an apparent and important role in innate and adaptive immune responses. Indeed, in genome-wide association studies, autophagy-related gene polymorphisms have been suggested to be associated with the pathogenesis of several autoimmune and inflammatory disorders, such as systemic lupus erythematosus, psoriasis, rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis. In addition, conditional knockdown of autophagy-related genes in mice displayed therapeutic effects on several autoimmune disease models by reducing levels of inflammatory cytokines and autoreactive immune cells. However, the inhibition of autophagy accelerates the progress of some inflammatory and autoimmune diseases via promotion of inflammatory cytokine production. Therefore, this review will summarize the current knowledge of autophagy in immune regulation and discuss the therapeutic and pathogenic role of autophagy in autoimmune diseases to broaden our understanding of the etiopathogenesis of autoimmune diseases and shed light on autophagy-mediated therapies.

Understanding microbial interactions is essential to decipher the mechanisms of community assembly and their effects on ecosystem functioning, however, the conservation of species- and trait-based network interactions along environmental gradient remains largely unknown. Here, by using the network-based analyses with three paralleled data sets derived from 16S rRNA gene pyrosequencing, functional microarray, and predicted metagenome, we test our hypothesis that the network interactions of traits are more conserved than those of taxonomic measures, with significantly lower variation of network characteristics along the environmental gradient in acid mine drainage. The results showed that although the overall network characteristics remained similar, the structural variation was significantly lower at trait levels. The higher conserved individual node topological properties at trait level rather than at species level indicated that the responses of diverse traits remained relatively consistent even though different species played key roles under different environmental conditions. Additionally, the randomization tests revealed that it could not reject the null hypothesis that species-based correlations were random, while the tests suggested that correlation patterns of traits were non-random. Furthermore, relationships between trait-based network characteristics and environmental properties implied that trait-based networks might be more useful in reflecting the variation of ecosystem function. Taken together, our results suggest that deterministic trait-based community assembly results in greater conservation of network interaction, which may ensure ecosystem function across environmental regimes, emphasizing the potential importance of measuring the complexity and conservation of network interaction in evaluating the ecosystem stability and functioning.

Estimating the species richness of microorganisms is of great importance in predicting, maintaining and managing microbial communities. Although the roles of environmental heterogeneity and geographical distance in structuring soil microbial communities have been studied intensively, the effects of environmental and spatial variation on the species richness estimation have not been examined. To this end, we have explored their effects on estimating the belowground soil bacterial species richness within a 50 ha forest dynamic plot (FDP) using a published massive sequencing dataset with intensive sampling scheme. Our resampling analyses showed that, for a given sequencing depth, increasing the sample size could significantly enhance the detection of rare species by capturing more of the environmental and spatial variation, thus obtaining higher observed and estimated species richness. Additionally, the estimates of bacterial species richness were significantly and positively correlated with environmental variation among samples, indicating that environmental filtering was the main mechanism driving the processes of community assembly for belowground soil bacterial communities in the plot. Moreover, this effect of environmental variation could be markedly alleviated when the sample size was higher than 450, and thus we predicted that there were at least 42,866 soil bacterial species based on 8,296,878 sequences from 550 samples in the whole 50 ha FDP. Furthermore, we built a power law environmental heterogeneity equation (EHE) as a decision-tool to determine an approximate sample size for comprehensively capturing the environmental gradient within a given habitat. Collectively, this work further links the inherent environmental and spatial variation to the estimation of soil bacterial species richness within a given region, and provides a useful tool of sampling design for a better understanding of microbial biogeographic patterns and estimation of microbial biodiversity. [ABSTRACT FROM AUTHOR]