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To better conserve the ecology of the wild Rhododendron mucronulatum range, we studied the rhizosphere microenvironment of R. mucronulatum in Beijing’s Yunmeng Mountain National Forest Park. R. mucronulatum rhizosphere soil physicochemical properties and enzyme activities changed significantly with temporal and elevational gradients. The correlations between soil water content (SWC), electrical conductivity (EC), organic matter content (OM), total nitrogen content (TN), catalase activity (CAT), sucrose-converting enzyme activity (INV), and urease activity (URE) were significant and positive in the flowering and deciduous periods. The alpha diversity of the rhizosphere bacterial community was significantly higher in the flowering period than in the deciduous period, and the effect of elevation was insignificant. The diversity of the R. mucronulatum rhizosphere bacterial community changed significantly with the change in the growing period. A network analysis of the correlations revealed stronger linkages between the rhizosphere bacterial communities in the deciduous period than in the flowering period. Rhizomicrobium was the dominant genus in both periods, but its relative abundance decreased in the deciduous period. Changes in the relative abundance of Rhizomicrobium may be the main factor influencing the changes in the R. mucronulatum rhizosphere bacterial community. Moreover, the R. mucronulatum rhizosphere bacterial community and soil characteristics were significantly correlated. Additionally, the influence of soil physicochemical properties on the rhizosphere bacterial community was larger than that of enzyme activity on the bacterial community. We mainly analyzed the change patterns in the rhizosphere soil properties and rhizosphere bacterial diversity of R. mucronulatum during temporal and spatial variation, laying the foundation for further understanding of the ecology of wild R. mucronulatum.

Introduction: Hemodynamic diagnosis indexes (HDIs) can comprehensively evaluate the health status of the cardiovascular system (CVS), particularly for people older than 50 years and prone to cardiovascular disease (CVDs). However, the accuracy of non-invasive detection remains unsatisfactory. We propose a non-invasive HDIs model based on the non-linear pulse wave theory (NonPWT) applied to four limbs.Methods: This algorithm establishes mathematical models, including pulse wave velocity and pressure information of the brachial and ankle arteries, pressure gradient, and blood flow. Blood flow is key to calculating HDIs. Herein, we derive blood flow equation for different times of the cardiac cycle considering the four different distributions of blood pressure and pulse wave of four limbs, then obtain the average blood flow in a cardiac cycle, and finally calculate the HDIs.Results: The results of the blood flow calculations reveal that the average blood flow in the upper extremity arteries is 10.78 ml/s (clinically: 2.5–12.67 ml/s), and the blood flow in the lower extremity arteries is higher than that in the upper extremity. To verify model accuracy, the consistency between the clinical and calculated values is verified with no statistically significant differences (p < 0.05). Model IV or higher-order fitting is the closest. To verify the model generalizability, considering the risk factors of cardiovascular diseases, the HDIs are recalculated using model IV, and thus, consistency is verified (p < 0.05 and Bland-Altman plot).Conclusion: We conclude our proposed algorithmic model based on NonPWT can facilitate the non-invasive hemodynamic diagnosis with simpler operational procedures and reduced medical costs.

BackgroundPatients in minimally conscious state (MCS) exist measurable evidence of consciousness. The frontal lobe is a crucial part of the brain that encodes abstract information and is closely related to the conscious state. We hypothesized that the disturbance of the frontal functional network exists in MCS patients.MethodsWe collected the resting-state functional near-infrared spectroscopy (fNIRS) data of fifteen MCS patients and sixteen age- and gender-matched healthy controls (HC). The Coma Recovery Scale-Revised (CRS-R) scale of MCS patients was also composed. The topology of the frontal functional network was analyzed in two groups.ResultsCompared with HC, the MCS patients showed widely disrupted functional connectivity in the frontal lobe, especially in the frontopolar area and right dorsolateral prefrontal cortex. Moreover, the MCS patients displayed lower clustering coefficient, global efficiency, local efficiency, and higher characteristic path length. In addition, the nodal clustering coefficient and nodal local efficiency in the left frontopolar area and right dorsolateral prefrontal cortex were significantly reduced in MCS patients. Furthermore, the nodal clustering coefficient and nodal local efficiency in the right dorsolateral prefrontal cortex were positively correlated to auditory subscale scores.ConclusionThis study reveals that MCS patients’ frontal functional network is synergistically dysfunctional. And the balance between information separation and integration in the frontal lobe is broken, especially the local information transmission in the prefrontal cortex. These findings help us to understand the pathological mechanism of MCS patients better.

IntroductionThe endometrial microbiota plays an essential role in the health of the female reproductive system. However, the interactions between the microbes in the endometrium and their effects on adenomyosis remain obscure.Materials and methodsWe profile endometrial samples from 38 women with (n=21) or without (n=17) adenomyosis to characterize the composition of the microbial community and its potential function in adenomyosis using 5R 16S rRNA gene sequencing.ResultsThe microbiota profiles of patients with adenomyosis were different from the control group without adenomyosis. Furthermore, analysis identified Lactobacillus zeae, Burkholderia cepacia, Weissella confusa, Prevotella copri, and Citrobacter freundii as potential biomarkers for adenomyosis. In addition, Citrobacter freundii, Prevotella copri, and Burkholderia cepacia had the most significant diagnostic value for adenomyosis. PICRUSt results identified 30 differentially regulated pathways between the two groups of patients. In particular, we found that protein export, glycolysis/gluconeogenesis, alanine, aspartate, and glutamate metabolism were upregulated in adenomyosis. Our results clarify the relationship between the endometrial microbiota and adenomyosis.DiscussionThe endometrial microbiota of adenomyosis exhibits a unique structure and Citrobacter freundii, Prevotella copri, and Burkholderia cepacia were identified as potential pathogenic microorganisms associated with adenomyosis. Our findings suggest that changes in the endometrial microbiota of patients with adenomyosis are of potential value for determining the occurrence, progression, early of diagnosis, and treatment oadenomyosis.

Hemodynamic prediction of carotid artery stenosis (CAS) is of great clinical significance in the diagnosis, prevention, and treatment prognosis of ischemic strokes. While computational fluid dynamics (CFD) is recognized as a useful tool, it shows a crucial issue that the high computational costs are usually required for real-time simulations of complex blood flows. Given the powerful feature-extraction capabilities, the deep learning (DL) methodology has a high potential to implement the mapping of anatomic geometries and CFD-driven flow fields, which enables accomplishing fast and accurate hemodynamic prediction for clinical applications. Based on a brain/neck CT angiography database of 280 subjects, image based three-dimensional CFD models of CAS were constructed through blood vessel extraction, computational domain meshing and setting of the pulsatile flow boundary conditions; a series of CFD simulations were undertaken. A DL strategy was proposed and accomplished in terms of point cloud datasets and a DL network with dual sampling-analysis channels. This enables multimode mapping to construct the image-based geometries of CAS while predicting CFD-based hemodynamics based on training and testing datasets. The CFD simulation was validated with the mass flow rates at two outlets reasonably agreed with the published results. Comprehensive analysis and error evaluation revealed that the DL strategy enables uncovering the association between transient blood flow characteristics and artery cavity geometric information before and after surgical treatments of CAS. Compared with other methods, our DL-based model trained with more clinical data can reduce the computational cost by 7,200 times, while still demonstrating good accuracy (error

BackgroundNeural reorganization occurs after a stroke, and dynamic functional network connectivity (dFNC) pattern is associated with cognition. We hypothesized that dFNC alterations resulted from neural reorganization in post-stroke cognitive impairment (PSCI) patients, and specific dFNC patterns characterized different pathological types of PSCI.MethodsResting-state fMRI data were collected from 16 PSCI patients with hemorrhagic stroke (hPSCI group), 21 PSCI patients with ischemic stroke (iPSCI group), and 21 healthy controls (HC). We performed the dFNC analysis for the dynamic connectivity states, together with their topological and temporal features.ResultsWe identified 10 resting-state networks (RSNs), and the dFNCs could be clustered into four reoccurring states (modular, regional, sparse, and strong). Compared with HC, the hPSCI and iPSCI patients showed lower standard deviation (SD) and coefficient of variation (CV) in the regional and modular states, respectively (p < 0.05). Reduced connectivities within the primary network (visual, auditory, and sensorimotor networks) and between the primary and high-order cognitive control domains were observed (p < 0.01).ConclusionThe transition trend to suboptimal states may play a compensatory role in patients with PSCI through redundancy networks. The reduced exploratory capacity (SD and CV) in different suboptimal states characterized cognitive impairment and pathological types of PSCI. The functional disconnection between the primary and high-order cognitive control network and the frontoparietal network centered (FPN-centered) incomplete compensation may be the pathological mechanism of PSCI. These results emphasize the flexibility of neural reorganization during self-repair.

BackgroundStroke is an important cause of cognitive impairment. Rich club organization, a highly interconnected network brain core region, is closely related to cognition. We hypothesized that the disturbance of rich club organization exists in patients with post-stroke cognitive impairment (PSCI).MethodsWe collected data on resting-state functional magnetic resonance imaging (rs-fMRI) with 21 healthy controls (HC), 16 hemorrhagic stroke (hPSCI), and 21 infarct stroke (iPSCI). 3D shape features and first-order statistics of stroke lesions were extracted using 3D slicer software. Additionally, we assessed cognitive function using the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE).ResultsNormalized rich club coefficients were higher in hPSCI and iPSCI than HC at low-degree k-levels (k = 1–8 in iPSCI, k = 2–8 in hPSCI). Feeder and local connections were significantly decreased in PSCI patients versus HC, mainly distributed in salience network (SN), default-mode network (DMN), cerebellum network (CN), and orbitofrontal cortex (ORB), especially involving the right and left caudate with changed nodal efficiency. The feeder and local connections of significantly between-group difference were positively related to MMSE and MoCA scores, primarily distributed in the sensorimotor network (SMN) and visual network (VN) in hPSCI, SN, and DMN in iPSCI. Additionally, decreased local connections and low-degree ϕnorm(k) were correlated to 3D shape features and first-order statistics of stroke lesions.ConclusionThis study reveals the disrupted low-degree level rich club organization and relatively preserved functional core network in PSCI patients. Decreased feeder and local connections in cognition-related networks (DMN, SN, CN, and ORB), particularly involving the caudate nucleus, may offer insight into pathological mechanism of PSCI patients. The shape and signal features of stroke lesions may provide an essential clue for the damage of functional connectivity and the whole brain networks.

Stroke causes alterations in local spontaneous neuronal activity and related networks functional connectivity. We hypothesized that these changes occur in patients with post-stroke cognitive impairment (PSCI). Fractional amplitude of low-frequency fluctuations (fALFF) was calculated in 36 patients with cognitive impairment, including 16 patients with hemorrhagic stroke (hPSCI group), 20 patients with ischemic stroke (iPSCI group). Twenty healthy volunteers closely matched to the patient groups with respect to age and gender were selected as the healthy control group (HC group). Regions with significant alteration were regarded as regions of interest (ROIs) using the one-way analysis of variance, and then the seed-based functional connectivity (FC) with other regions in the brain was analyzed. Pearson correlation analyses were performed to investigate the correlation between functional indexes and cognitive performance in patients with PSCI. Our results showed that fALFF values of bilateral posterior cingulate cortex (PCC)/precuneus and bilateral anterior cingulate cortex in the hPSCI group were lower than those in the HC group. Compared with the HC group, fALFF values were lower in the superior frontal gyrus and basal ganglia in the iPSCI group. Correlation analysis showed that the fALFF value of left PCC was positively correlated with MMSE scores and MoCA scores in hPSCI. Besides, the reduction of seed-based FC values was reported, especially in regions of the default-mode network (DMN) and the salience network (SN). Abnormalities of spontaneous brain activity and functional connectivity are observed in PSCI patients. The decreased fALFF and FC values in DMN of patients with hemorrhagic and SN of patients with ischemic stroke may be the pathological mechanism of cognitive impairment. Besides, we showed how to use fALFF values and functional connectivity maps to specify a target map on the cortical surface for repetitive transcranial magnetic stimulation (rTMS).

Objective: Peritonitis is a severe complication in peritoneal dialysis (PD). This study was performed to identify predictors and establish a risk score for treatment failure in peritonitis patients.Methods: A single-center, retrospective observational study was conducted. The basic demographic characteristics, clinical and laboratory data of all patients with peritonitis during the study period were documented and analyzed. Multivariate logistic regression was applied to examine independent predictors of treatment failure, and a risk prediction score was established.Results: Three hundred fourteen episodes experienced by 241 patients were included in the final analysis. Logistic regression analysis indicated that PD duration (OR 1.017; P 0.005), fibrinogen (OR 1.327; P 0.021), high-density lipoprotein (OR 0.443; P 0.032), fungal infection (OR 63.413; P < 0.001), intestinal obstruction (OR 5.186, P 0.007), and diabetes mellitus (OR 2.451; P 0.018), hemodialysis history (OR 2.804, P 0.006) were independent predictors of treatment failure. The risk prediction score system showed a good calibration (P > 0.05) and discrimination (AUROC 0.80, P < 0.001).Conclusions: Fibrinogen, PD duration, fungal infection, hemodialysis history, concurrent intestinal obstruction, or diabetes mellitus were independent risk factors for a poor peritonitis outcome, while the high-density lipoprotein was a protective factor. This novel risk prediction score system may be used to predict a high risk of treatment failure effectively.

The abnormal diameter of the coronary artery is twice or more than the normal diameter, which is a coronary artery aneurysm (CAA). According to the clinical statistics, CAA shows high occurrence on right coronary artery (RCA). The most common cause of CAA in adults is atherosclerosis, which destroys the elastic fibers in the middle layer of the blood vessel. Under the intravascular pressure, the weak wall bulges outward and form CAA. This article aims to explain the hemodynamic mechanism of coronary artery aneurysm shows high occurrence on RCA. Occurrence of CAA was simulated by the volume growth of coronary artery. Firstly, a 0–3D multi-scale model of normal coronary artery was constructed to obtain the hemodynamic environments of coronary artery. Then, fluid-structure interaction of normal and atherosclerotic blood vessel was performed to obtain volume growth rate of the coronary artery. Atherosclerosis was simulated by modifying Young’s modulus in middle layer of the blood vessel. Finally, creep simulation was performed to compare the deformation of the blood vessels under the accumulation of time. Under normal condition, the volume growth rate of the RCA is 2.28 times and 1.55 times of the LAD and the LCX. After atherosclerosis, the volume growth rate of the RCA was 2.69 times and 2.12 times of the LAD and the LCX. And the volume growth rate of the RCA was 3.85 times and 3.45 times of the LAD and the LCX after further deepening of atherosclerosis. The expansion time above the average volume growth rate of the RCA, the LAD and the LCX respectively were 0.194, 0.168 and 0.179 s. The RCA is 2.06 times the original, the LAD and LCX are 1.53 times and 1.56 times after 10 years in creep simulation. It can be concluded that the RCA is more prone to aneurysms originated from the larger expansion of the RCA under normal physiological condition, and the larger expansion is magnified under atherosclerosis condition with destroyed vessel elasticity, and further magnified during the time accumulated viscoelastic creep to develop to aneurysm eventually.

NFAT activating protein with ITAM motif 1 (NFAM1) is an ITAM bearing-transmembrane receptor that has been reported to play a role in B cell signaling and development. We performed expression analysis of NFAM1 using publicly available gene expression data sets and found that NFAM1 expression is significantly induced in intestinal biopsies from Crohn’s disease (CD) and ulcerative colitis (UC) patients. At the cellular level, we further observed high expression of NFAM1 in monocytes and neutrophils, and low expression in B and T cells. To explore the role of NFAM1 in multiple immune cells and its potential role in IBD, we generated NFAM1-/- mice. In contrast with previous reports using NFAM1-transgenic mice, NFAM1-/- mice have no obvious defects in immune cell development, or B cell responses. Interestingly, NFAM1-/- monocytes produce reduced levels of TNF-α in response to activation by multiple IBD-relevant stimuli, including CD40L, TLR ligands and MDP. Additional cytokines and chemokines such as IL-6, IL-12, CCL3 and CCL4 are also reduced in CD40L stimulated NFAM1-/- monocytes. Collectively, these findings indicate that NFAM1 promotes monocyte activation, thereby amplifying the response to diverse stimuli. Similarly, we observed that deletion of NFAM1 in human monocytes reduces expression of CD40L-induced CCL4. Lastly, to assess the role of NFAM1 in IBD, we compared development of anti-CD40 induced colitis in NFAM1+/+ and NFAM1-/- mice. We found that although NFAM1 deletion had no impact on development of gut pathology, we did observe a decrease in serum TNF-α, confirming that NFAM1 promotes pro-inflammatory cytokine production in vivo. Taken together, we conclude that NFAM1 functions to amplify cytokine production and should be further evaluated as a therapeutic target for treatment of autoimmune disease. [ABSTRACT FROM AUTHOR]

NFAT activating protein with ITAM motif 1 (NFAM1) is an ITAM bearing-transmembrane receptor that has been reported to play a role in B cell signaling and development. We performed expression analysis of NFAM1 using publicly available gene expression data sets and found that NFAM1 expression is significantly induced in intestinal biopsies from Crohn’s disease (CD) and ulcerative colitis (UC) patients. At the cellular level, we further observed high expression of NFAM1 in monocytes and neutrophils, and low expression in B and T cells. To explore the role of NFAM1 in multiple immune cells and its potential role in IBD, we generated NFAM1-/- mice. In contrast with previous reports using NFAM1-transgenic mice, NFAM1-/- mice have no obvious defects in immune cell development, or B cell responses. Interestingly, NFAM1-/- monocytes produce reduced levels of TNF-α in response to activation by multiple IBD-relevant stimuli, including CD40L, TLR ligands and MDP. Additional cytokines and chemokines such as IL-6, IL-12, CCL3 and CCL4 are also reduced in CD40L stimulated NFAM1-/- monocytes. Collectively, these findings indicate that NFAM1 promotes monocyte activation, thereby amplifying the response to diverse stimuli. Similarly, we observed that deletion of NFAM1 in human monocytes reduces expression of CD40L-induced CCL4. Lastly, to assess the role of NFAM1 in IBD, we compared development of anti-CD40 induced colitis in NFAM1+/+ and NFAM1-/- mice. We found that although NFAM1 deletion had no impact on development of gut pathology, we did observe a decrease in serum TNF-α, confirming that NFAM1 promotes pro-inflammatory cytokine production in vivo. Taken together, we conclude that NFAM1 functions to amplify cytokine production and should be further evaluated as a therapeutic target for treatment of autoimmune disease.