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A conditionally pathogenic bacterium called Bibersteinia trehalosi inhabits the upper respiratory tract of ruminants and is becoming a significant cause of pneumonia, especially in goats. In this study, we identified a gram-negative bacteria strain isolated from dead goat's lungs, which was named M01. By integrating the outcomes of its morphological and biochemical characterization with the investigation of the 16S rRNA gene sequence analysis, the isolate was identified as B. trehalosi. Based on antibiotic susceptibility tests, the isolate was shown to be resistant to β-lactams, tetracyclines, and amphenicols. Its genome was discovered to comprise 2115 encoded genes and a circular chromosome measuring 2,345,568 bp using whole genome sequencing. Annotation of the VFBD database revealed that isolate M01 had four virulence genes encoding three virulence factors. The CARD database revealed that its genome has two antibiotic-resistance genes. Based on pathogenicity testing, isolate M01 was highly pathogenic to mice, primarily causing pneumonia, with an LD50 of 1.31 × 107 CFU/ml. Moreover, histopathology showed loss of alveolar structure and infiltration of lung inflammatory cells. Hence, the current study could provide sufficient information for prevention and control strategies for future epidemics of B. trehalosi in goat species. • Bibersteinia trehalosi M01 is resistant to β-Lactam, Tetracyclines and Amphenicols. • Bibersteinia trehalosi M01 has four virulence genes, which are cyll, wbaP/rfbP, wbbM, and wbbN. • The LD50 of Bibersteinia trehalosi M01 in mice is 1.31*107 CFU/ml. • This is a rare study of Bibersteinia trehalosi , which is important for the control of Bibersteinia trehalosi in China. [ABSTRACT FROM AUTHOR]

• The alterations in dFC and SC networks unveil distinct characteristics associated with cLBP. • The enhanced connectivity between the FPN, SMN and thalamus signifies the most relevant changes in brain networks associated with cLBP. • The integration of different features effectively enhances the classification accuracy between cLBP patients and HC. The prolonged duration of chronic low back pain (cLBP) inevitably leads to changes in the cognitive, attentional, sensory and emotional processing brain regions. Currently, it remains unclear how these alterations are manifested in the interplay between brain functional and structural networks. This study aimed to predict the Oswestry Disability Index (ODI) in cLBP patients using multimodal brain magnetic resonance imaging (MRI) data and identified the most significant features within the multimodal networks to aid in distinguishing patients from healthy controls (HCs). We constructed dynamic functional connectivity (dFC) and structural connectivity (SC) networks for all participants (n = 112) and employed the Connectome-based Predictive Modeling (CPM) approach to predict ODI scores, utilizing various feature selection thresholds to identify the most significant network change features in dFC and SC outcomes. Subsequently, we utilized these significant features for optimal classifier selection and the integration of multimodal features. The results revealed enhanced connectivity among the frontoparietal network (FPN), somatomotor network (SMN) and thalamus in cLBP patients compared to HCs. The thalamus transmits pain-related sensations and emotions to the cortical areas through the dorsolateral prefrontal cortex (dlPFC) and primary somatosensory cortex (SI), leading to alterations in whole-brain network functionality and structure. Regarding the model selection for the classifier, we found that Support Vector Machine (SVM) best fit these significant network features. The combined model based on dFC and SC features significantly improved classification performance between cLBP patients and HCs (AUC=0.9772). Finally, the results from an external validation set support our hypotheses and provide insights into the potential applicability of the model in real-world scenarios. Our discovery of enhanced connectivity between the thalamus and both the dlPFC (FPN) and SI (SMN) provides a valuable supplement to prior research on cLBP. [ABSTRACT FROM AUTHOR]

• We investigated sex-dependent associations between behavioral inhibition and resting-state brain function as well as their underlying molecular mechanisms. • A negative correlation between behavioral inhibition and functional connectivity density in the left superior parietal lobule was found in females but not males. • The female-specific neural correlates of behavioral inhibition were associated with expression of specific gene categories and the serotonergic system. • Our findings may provide a critical context for understanding how biological sex might contribute to variation in behavioral inhibition and its related disease risk. Previous literature has established the presence of sex differences in behavioral inhibition as well as its neural substrates and related disease risk. However, there is limited evidence that speaks directly to the question of whether or not there are sex-dependent associations between behavioral inhibition and resting-state brain function and, if so, how they are modulated by the underlying molecular mechanisms. We computed functional connectivity density (FCD) using resting-state functional MRI data to examine their associations with behavioral inhibition ability measured using a Go/No-Go task across a large cohort of 510 healthy young adults. Then, we examined the spatial relationships of the FCD correlates of behavioral inhibition with gene expression and neurotransmitter atlases to explore their potential genetic architecture and neurochemical basis. A significant negative correlation between behavioral inhibition and FCD in the left superior parietal lobule was found in females but not males. Further spatial correlation analyses demonstrated that the identified neural correlates of behavioral inhibition were associated with expression of gene categories predominantly implicating essential components of the cerebral cortex (glial cell, neuron, axon, dendrite, and synapse) and ion channel activity, as well as were linked to the serotonergic system. Our findings may not only yield important insights into the molecular mechanisms underlying the female-specific neural substrates of behavioral inhibition, but also provide a critical context for understanding how biological sex might contribute to variation in behavioral inhibition and its related disease risk. [ABSTRACT FROM AUTHOR]

Obesity is a risk factor for cerebrovascular diseases. Accumulating evidence has revealed that gut dysbiosis plays an important role in the pathophysiology of cerebrovascular diseases. However, little is known about the role of gut dysbiosis in stroke in obesity. In this study, we established a rodent middle cerebral artery occlusion (MCAO) model to investigate whether obesity-induced gut dysbiosis exacerbates cerebral ischemic injury and the role of the bile salt sequestrant cholestyramine resin (CR) in gut microbiota and stroke outcome in obese mice. Long-term 45% high-fat diet (HFD) diet (8 weeks) induced an obesity phenotype and caused gut dysbiosis, resulting in a larger infarct volume and higher serum levels of inflammatory cytokines after stroke, compared to those in the lean counterparts. LC-MS/MS and GC analysis revealed that obese mice with stroke developed an obviously perturbed bile acid (BA) profile characterized by higher levels of deoxycholic acid and its conjugated forms, and lower levels of butyrate in the cecal content. CR administration improved the obesity-induced dysbiotic microbiome, attenuated ischemic brain injury and modulated the stroke-perturbed BA profile. Furthermore, fecal microbiota transplantation (FMT) experiments revealed that the impact of obesity on stroke and the neuroprotective effects of CR were mediated by gut microbiota. In conclusion, Obesity induces gut dysbiosis, worsens stroke outcomes, and perturbs the BA profile. The dysbiotic microbiome is an important linkage between obesity and stroke. CR confers metabolic benefits and neuroprotective effects in obesity, perhaps by modulating gut microbial composition and BA metabolism. • Long-term high-fat diet induced obesity and gut dysbiosis. • Obesity aggravated cerebral ischemic injury and intestinal barrier disruption. • Cholestyramine resin improved stroke outcome in obesity mice. • Gut microbiota was an important linkage between obesity and stroke. [ABSTRACT FROM AUTHOR]