Miracle-dz/UniFAR-FTUs huggingface dataset:
Impacts of soybean agriculture on the resistome of the Amazonian soil

The soils of the Amazon are complex environments with different organisms cohabiting in continuous adaptation processes; this changes significantly when these environments are modified for the development of agricultural activities that alter the chemical, macro, and microbiological compositions. The metagenomic variations and the levels of the environmental impact of four different soil samples from the Amazon region were evaluated, emphasizing the resistome. Soil samples from the organic phase from the different forest, pasture, and transgenic soybean monocultures of 2–14 years old were collected in triplicate at each site. The samples were divided into two groups, and one group was pre-treated to obtain genetic material to perform sequencing for metagenomic analysis; another group carried out the chemical characterization of the soil, determining the pH, the content of cations, and heavy metals; these were carried out in addition to identifying with different databases the components of the microbiological communities, functional genes, antibiotic and biocide resistance genes. A greater diversity of antibiotic resistance genes was observed in the forest soil. In contrast, in monoculture soils, a large number of biocide resistance genes were evidenced, highlighting the diversity and abundance of crop soils, which showed better resistance to heavy metals than other compounds, with a possible dominance of resistance to iron due to the presence of the acn gene. For up to 600 different genes for resistance to antibiotics and 256 genes for biocides were identified, most of which were for heavy metals. The most prevalent was resistance to tetracycline, cephalosporin, penam, fluoroquinolone, chloramphenicol, carbapenem, macrolide, and aminoglycoside, providing evidence for the co-selection of these resistance genes in different soils. Furthermore, the influence of vegetation cover on the forest floor was notable as a protective factor against the impact of human contamination. Regarding chemical characterization, the presence of heavy metals, different stress response mechanisms in monoculture soils, and the abundance of mobile genetic elements in crop and pasture soils stand out. The elimination of the forest increases the diversity of genes for resistance to biocides, favoring the selection of genes for resistance to antibiotics in soils.
Different stages of chronic kidney disease are associated with physical performance in adults over 60 years

Objective: The purpose of this study was to determine the association between different stages of chronic kidney disease (CKD) and sarcopenia and its components in the Chinese older population. Methods The study comprised of 2,213 participants aged ≥ 60 years (1,025 men; mean age: 70.7 years) recruited from Shanghai who were invited to participate in a comprehensive geriatric assessment. Sarcopenia was defined according to the AWGS 2019 consensus update on sarcopenia diagnosis criteria. The glomerular filtration rate (GFR) was estimated using the equation that originated from the CKD-EPI equation, the stages of CKD are classified according to the Kidney Disease—Improving Global Outcomes (KDIGO). Results The overall prevalence of sarcopenia was 19.0%, which increased with the severity of CKD. The prevalence of sarcopenia in patients with CKD 3–4 and kidney failure was significantly higher than that in normal and CKD 1–2 (p < 0.05). In logistic regression analysis model, compared with normal and CKD 1 patients, kidney failure was significantly associated with the increased risk of sarcopenia and low grip strength (p < 0.05); CKD 2, CKD 3–4 and kidney failure groups were significantly associated with an increased risk of low walking speed (p < 0.05), respectively; while the association between CKD and muscle mass was not shown. Conclusions In our study, only decreased physical performance, as represented by walking speed, was significantly associated with increased CKD severity. This may improve the evidence for the prevention and intervention of sarcopenia in patients with CKD.
The privacy and control paradoxes in the context of smartphone apps

This research examines how various factors, such as the degree of e-privacy concerns and control over data access permissions, can influence a user's intention to install a smartphone app. We conducted two survey-based experiments with 441 participants. In each experiment, we manipulated the degree of control over the number and type of data access permissions granted to different fictional apps. In Study 1, participants were informed about the set of permissions the apps required. In Study 2, participants indicated which individual permissions they were willing to grant to the apps. In both experiments, we assessed the level of e-privacy concerns, perceived app importance, and the intention to install the apps. The results suggest that the type of app plays a central role in determining both the perceived benefit of installing the app and the level of e-privacy concerns. The intention to install an app is more strongly associated with perceived app importance than with e-privacy concerns (especially when app importance is high, and users have explicit control over which specific data access permissions they want to grant). The implications of these results are discussed regarding psychological factors involved in app installation decision-making process and the importance of promoting data protection by design.
Visually driven functional MRI techniques for characterization of optic neuropathy

Optic neuropathies are conditions that cause disease to the optic nerve, and can result in loss of visual acuity and/or visual field defects. An improved understanding of how these conditions affect the entire visual system is warranted, to better predict and/or restore the visual loss. In this article, we review visually-driven functional magnetic resonance imaging (fMRI) studies of optic neuropathies, including glaucoma and optic neuritis (ON); we also discuss traumatic optic neuropathy (TON). Optic neuropathy-related vision loss results in fMRI deficit within the visual cortex, and is often strongly correlated with clinical severity measures. Using predominantly flickering checkerboard stimuli, glaucoma studies indicated retinotopic-specific cortical alteration with more prominent deficits in advanced than in early glaucoma. Some glaucoma studies indicate a reorganized visual cortex. ON studies have indicated that the impacted cortical areas are briefly hyperactive. For ON, brain deficits are greater in the acute stages of the disease, followed by (near) normalization of responses of the LGN, visual cortex, and the dorsal visual stream, but not the ventral extrastriate cortex. Visually-driven fMRI is sensitive, at least in ON, in discriminating patients from controls, as well as the affected eye from the fellow eye within patients. The use of a greater variety of stimuli beyond checkerboards (e.g., visual motion and object recognition) in recent ON studies is encouraging, and needs to continue to disentangle the results in terms of change over time. Finally, visually-driven fMRI has not yet been applied in TON, although preliminary efforts suggest it may be feasible. Future fMRI studies of optic neuropathies should consider using more complex visual stimuli, and inter-regional analysis methods including functional connectivity. We suggest that a more systematic longitudinal comparison of optic neuropathies with advanced fMRI would provide improved diagnostic and prognostic information.
Pan-cancer analysis of CREB3L1 as biomarker in the prediction of prognosis and immunotherapeutic efficacy

Background: CAMP response element binding protein 3-like 1 (CREB3L1) has been indicated as a critical biomarker and can modulate multifaced behaviors of tumor cells in diverse cancers. However, a systematic assessment of CREB3L1 in pan-cancer is of absence, and the predictive value of CREB3L1 in cancer prognosis, the tumor immune microenvironment and the efficacy of immunotherapy remains unexplored. Methods: CREB3L1 expression in 33 different cancer types was investigated using RNAseq data from The Cancer Genome Atlas (TCGA) database. The characteristics of CREB3L1 alternations were illustrated in cBioPortal database. The prognostic and clinicopathological value of CREB3L1 was analyzed through clinical data downloaded from the TCGA database. The potential role of CREB3L1 in the tumor immune microenvironment was illustrated by utilizing CIBERSORT and ESTIMATE algorithms, and TISIDB online database. The associations between CREB3L1 expression and tumor mutation burden (TMB), and microsatellite instability (MSI) were assessed by spearman’s rank correlation coefficient. Furthermore, Gene Set Enrichment Analysis (GSEA) was conducted to explore the potential biological functions and downstream pathways of CREB3L1 in different human cancers. The correlations of CREB3L1 expression with PD-1/PD-L1 inhibitors efficacy and drug sensitivity were also investigated. Results: The expression of CREB3L1 was abnormally high or low in several different cancer types, and was also strictly associated with the prognosis of cancer patients. CREB3L1 expression levels have a strong relationship with infiltrating immune cells, including regulatory T cells, CD8+ T cells, macrophages, B naïve cells, dendritic cells and mast cells. CREB3L1 expression was also correlated with the expression of multiple immune-related biomolecules, TMB, and MSI in several cancers. Moreover, CREB3L1 had promising applications in predicting the immunotherapeutic benefits and drug sensitivity in cancer management. Conclusions: Our results highlight the value of CREB3L1 as a predictive biomarker for the prognosis and immunotherapy efficacy in multiple cancers, and CREB3L1 seems to play key roles in the tumor immune microenvironment, suggesting the role of CREB3L1 as a promising biomarker for predicting the prognosis and immune-related signatures in diverse cancers.
Bacterial outer membrane vesicles as a candidate tumor vaccine platform

Cancer represents a serious concern for human life and health. Due to drug resistance and the easy metastasis of tumors, there is urgent need to develop new cancer treatment methods beyond the traditional radiotherapy, chemotherapy, and surgery. Bacterial outer membrane vesicles (OMVs) are a type of double-membrane vesicle secreted by Gram-negative bacteria in the process of growth and life, and play extremely important roles in the survival and invasion of those bacteria. In particular, OMVs contain a large number of immunogenic components associated with their parent bacterium, which can be used as vaccines, adjuvants, and vectors to treat diseases, especially in presenting tumor antigens or targeted therapy with small-molecule drugs. Some OMV-based vaccines are already on the market and have demonstrated good therapeutic effect on the corresponding diseases. OMV-based vaccines for cancer are also being studied, and some are already in clinical trials. This paper reviews bacterial outer membrane vesicles, their interaction with host cells, and their applications in tumor vaccines.
Hepatic damage caused by long-term high cholesterol intake induces a dysfunctional restorative macrophage population in experimental NASH

Excessive dietary cholesterol is preferentially stored in the liver, favoring the development of nonalcoholic steatohepatitis (NASH), characterized by progressive hepatic inflammation and fibrosis. Emerging evidence indicates a critical contribution of hepatic macrophages to NASH severity. However, the impact of cholesterol on these cells in the setting of NASH remains elusive. Here, we demonstrate that the dietary cholesterol content directly affects hepatic macrophage global gene expression. Our findings suggest that the modifications triggered by prolonged high cholesterol intake induce long-lasting hepatic damage and support the expansion of a dysfunctional pro-fibrotic restorative macrophage population even after cholesterol reduction. The present work expands the understanding of the modulatory effects of cholesterol on innate immune cell transcriptome and may help identify novel therapeutic targets for NASH intervention.
Functional consequence of myeloid ferritin heavy chain on acute and chronic effects of rhabdomyolysis-induced kidney injury

Acute kidney injury (AKI) is a serious complication of rhabdomyolysis that significantly impacts survival. Myoglobin released from the damaged muscle accumulates in the kidney, causing heme iron-mediated oxidative stress, tubular cell death, and inflammation. In response to injury, myeloid cells, specifically neutrophils and macrophages, infiltrate the kidneys, and mediate response to injury. Ferritin, comprised of ferritin light chain and ferritin heavy chain (FtH), is vital for intracellular iron handling. Given the dominant role of macrophages and heme-iron burden in the pathogenesis of rhabdomyolysis, we studied the functional role of myeloid FtH in rhabdomyolysis-induced AKI and subsequent fibrosis. Using two models of rhabdomyolysis induced AKI, we found that during the acute phase, myeloid FtH deletion did not impact rhabdomyolysis-induced kidney injury, cell death or cell proliferation, suggesting that tubular heme burden is the dominant injury mechanism. We also determined that, while the kidney architecture was markedly improved after 28 days, tubular casts persisted in the kidneys, suggesting sustained damage or incomplete recovery. We further showed that rhabdomyolysis resulted in an abundance of disparate intra-renal immune cell populations, such that myeloid populations dominated during the acute phase and lymphoid populations dominated in the chronic phase. Fibrotic remodeling was induced in both genotypes at 7 days post-injury but continued to progress only in wild-type mice. This was accompanied by an increase in expression of pro-fibrogenic and immunomodulatory proteins, such as transforming growth factor-β, S100A8, and tumor necrosis factor-α. Taken together, we found that while the initial injury response to heme burden was similar, myeloid FtH deficiency was associated with lesser interstitial fibrosis. Future studies are warranted to determine whether this differential fibrotic remodeling will render these animals more susceptible to a second AKI insult or progress to chronic kidney disease at an accelerated pace.
SNAI1-dependent upregulation of CD73 increases extracellular adenosine release to mediate immune suppression in TNBC

Triple-negative subtype of breast cancer (TNBC) is hallmarked by frequent disease relapse and shows highest mortality rate. Although PD-1/PD-L1 immune checkpoint blockades have recently shown promising clinical benefits, the overall response rate remains largely insufficient. Hence, alternative therapeutic approaches are warranted. Given the immunosuppressive properties of CD73-mediated adenosine release, CD73 blocking approaches are emerging as attractive strategies in cancer immunotherapy. Understanding the precise mechanism regulating the expression of CD73 is required to develop effective anti-CD73-based therapy. Our previous observations demonstrate that the transcription factors driving epithelial-to-mesenchymal transition (EMT-TF) can regulate the expression of several inhibitory immune checkpoints. Here we analyzed the role of the EMT-TF SNAI1 in the regulation of CD73 in TNBC cells. We found that doxycycline-driven SNAI1 expression in the epithelial -like TNBC cell line MDA-MB-468 results in CD73 upregulation by direct binding to the CD73 proximal promoter. SNAI1-dependent upregulation of CD73 leads to increased production and release of extracellular adenosine by TNBC cells and contributes to the enhancement of TNBC immunosuppressive properties. Our data are validated in TNBC samples by showing a positive correlation between the mRNA expression of CD73 and SNAI1. Overall, our results reveal a new CD73 regulation mechanism in TNBC that participates in TNBC-mediated immunosuppression and paves the way for developing new treatment opportunities for CD73-positive TNBC.
Fucoxanthin prevents breast cancer metastasis by interrupting circulating tumor cells adhesion and transendothelial migration

Metastasis is the leading cause of cancer-related death and a critical challenge in improving cancer treatment today. Circulating tumor cells (CTCs) adhesion to and across the vascular endothelium are critical steps in the establishment of micrometastatic foci away from the primary tumor. Therefore, we believe that interrupting CTCs adhesion to endothelium and transendothelial migration may efficiently prevent cancer metastasis. Fucoxanthin (Fx) is an algal carotenoid widely distributed in brown algae, macroalgae, and diatoms. Previous studies have found that Fx has various pharmacological activities, including antidiabetic, antioxidant, anti-inflammatory, anti-obesity, antimalarial, anticancer, and so on. However, it remains unclear whether Fx has a preventive effect on cancer metastasis. Here, we found that Fx interrupts breast cancer cells MCF-7 adhesion to endothelium and transendothelial migration, thus inhibiting CTCs-based pulmonary metastasis in vivo. The hetero-adhesion assay showed that Fx significantly inhibited the expression of inflammatory factor-induced cell adhesion molecules (CAMs) and the resulting adhesion between MCF-7 cells and endothelial cells. The wound-healing and transwell assays showed that Fx significantly inhibited the motility, invasion, and transendothelial migration abilities of MCF-7 cells. However, the same concentration of Fx did not significantly alter the cell viability, cell cycle, apoptosis, and ROS of breast cancer cells, thus excluding the possibility that Fx inhibits MCF-7 cell adhesion and transendothelial migration through cytotoxicity. Mechanistically, Fx inhibits the expression of CAMs on endothelial cells by inhibiting the NF-кB signaling pathway by down-regulating the phosphorylation level of IKK-α/β, IкB-α, and NF-кB p65. Fx inhibits transendothelial migration of MCF-7 cells by inhibiting Epithelial-to-mesenchymal transition (EMT), PI3K/AKT, and FAK/Paxillin signaling pathways. Moreover, we demonstrated that Fx significantly inhibits the formation of lung micrometastatic foci in immunocompetent syngeneic mouse breast cancer metastasis models. We also showed that Fx enhances antitumor immune responses by substantially increasing the subsets of cytotoxic T lymphocytes in the peripheral immune system. This new finding provides a basis for the application of Fx in cancer metastatic chemoprevention and suggests that interruption of the CTCs adhesion to endothelium and transendothelial migration may serve as a new avenue for cancer metastatic chemoprevention.
Artificial intelligence in the pediatric echocardiography laboratory: Automation, physiology, and outcomes

Artificial intelligence (AI) is frequently used in non-medical fields to assist with automation and decision-making. The potential for AI in pediatric cardiology, especially in the echocardiography laboratory, is very high. There are multiple tasks AI is designed to do that could improve the quality, interpretation, and clinical application of echocardiographic data at the level of the sonographer, echocardiographer, and clinician. In this state-of-the-art review, we highlight the pertinent literature on machine learning in echocardiography and discuss its applications in the pediatric echocardiography lab with a focus on automation of the pediatric echocardiogram and the use of echo data to better understand physiology and outcomes in pediatric cardiology. We also discuss next steps in utilizing AI in pediatric echocardiography.
A predictive hemodynamic model based on risk factors for ruptured mirror aneurysms

Objectives To identify hemodynamic risk factors for intracranial aneurysm rupture and establish a predictive model to aid evaluation. Methods We analyzed the hemodynamic parameters of 91 pairs of ruptured mirror aneurysms. A conditional univariate analysis was used for the continuous variables. A conditional multivariate logistic regression analysis was performed to identify the independent risk factors. Differences where p < 0.05 were statistically significant. A predictive model was established based on independent risk factors. Odds ratios (ORs) were used to score points. The validation cohort consisted of 189 aneurysms. Receiver operating characteristic curves were generated to determine the cutoff values and area under the curves (AUCs) of the predictive model and independent risk factors. Results The conditional multivariate logistic analysis showed that the low shear area (LSA) (OR = 70.322, p = 0.044, CI = 1.112–4,445.256), mean combined hemodynamic parameter (CHP) (>0.087) (OR = 3.171, p = 0.034, CI = 1.089–9.236), and wall shear stress gradient (WSSG) ratio (>893.180) (OR = 5.740, p = 0.003, CI = 1.950–16.898) were independent risk factors. A prediction model was established: 23*LSA + 1*CHP mean (>0.087: yes = 1, no = 0) + 2 * WSSG ratio (>893.180: yes = 1, no = 0). The AUC values of the predictive model, LSA, mean CHP (>0.087), and WSSG ratio (>893.180) were 0.748, 0.700, 0.654, and 0.703, respectively. The predictive model and LSA cutoff values were 1.283 and 0.016, respectively. In the validation cohort, the predictive model, LSA, CHP (>0.087), and WSSG ratio (>893.180) were 0.736, 0.702, 0.689, and 0.706, respectively. Conclusions LSA, CHP (>0.087), and WSSG ratio (>893.180) were independent risk factors for aneurysm rupture. Our predictive model could aid practical evaluation.
Exploring neurometabolic alterations in bipolar disorder with suicidal ideation based on proton magnetic resonance spectroscopy and machine learning technology

Bipolar disorder (BD) is associated with a high risk of suicide. We used proton magnetic resonance spectroscopy (1H-MRS) to detect biochemical metabolite ratios in the bilateral prefrontal white matter (PWM) and hippocampus in 32 BD patients with suicidal ideation (SI) and 18 BD patients without SI, identified potential brain biochemical differences and used abnormal metabolite ratios to predict the severity of suicide risk based on the support vector machine (SVM) algorithm. Furthermore, we analyzed the correlations between biochemical metabolites and clinical variables in BD patients with SI. There were three main findings: (1) the highest classification accuracy of 88% and an area under the curve of 0.9 were achieved in distinguishing BD patients with and without SI, with N-acetyl aspartate (NAA)/creatine (Cr), myo-inositol (mI)/Cr values in the bilateral PWM, NAA/Cr and choline (Cho)/Cr values in the left hippocampus, and Cho/Cr values in the right hippocampus being the features contributing the most; (2) the above seven features could be used to predict Self-rating Idea of Suicide Scale scores (r = 0.4261, p = 0.0302); and (3) the level of neuronal function in the left hippocampus may be related to the duration of illness, the level of membrane phospholipid catabolism in the left hippocampus may be related to the severity of depression, and the level of inositol metabolism in the left PWM may be related to the age of onset in BD patients with SI. Our results showed that the combination of multiple brain biochemical metabolites could better predict the risk and severity of suicide in patients with BD and that there was a significant correlation between biochemical metabolic values and clinical variables in BD patients with SI.