We investigated the relationship between basilar artery (BA) atherosclerotic stenosis features and vertebral artery (VA) stenosis and explored whether BA stenosis features are associated with perforator stroke after stenting.Patients with BA stenosis who underwent HRMRI and DSA were recruited. Patients were divided into proximal BA stenosis and middle-or-distal BA stenosis groups, and then subgroup analyses were performed based on whether they had VA stenosis. BA plaque features were evaluated by HRMRI. Artery stenosis was measured by DSA. The incidence of perforator stroke after BA stenting was recorded, and the potential association between BA stenosis features and perforator stroke was analyzed.One hundred and seventy-four patients were consecutively enrolled. Patients with proximal BA stenosis had a higher proportion of severe stenosis than those with middle-or-distal BA stenosis (P = 0.027). In the subgroup analysis, this difference mainly existed in patients complicated with VA stenosis (P = 0.023). Patients with proximal BA stenosis had a higher proportion of strong plaque enhancement than those with middle-or-distal BA stenosis (P < 0.001), especially in those with vertebrobasilar junction (VBJ) stenosis (P < 0.001). Perforator stroke after BA stenting occurred in five patients, of whom four had lateral wall BA plaques, four had plaque enhancement and four had proximal BA stenosis.Patients with proximal BA stenosis had a higher proportion of severe stenosis and strong plaque enhancement, particularly in patients complicated with VA stenosis and VBJ stenosis. Perforator stroke after BA stenting may be related to distribution, burden and characteristics of BA lesions.
Gallbladder perforation can be caused by delayed diagnosis of cholecystitis and, more rarely, trauma. Despite advancements in imaging modalities, diagnosis is often challenging, leading to further delays in diagnosis and increased morbidity and mortality. In this report, we discuss a 49-year-old Caucasian male who presented to the emergency department with severe, out-of-proportion pain and fevers following a mechanical fall. Blood tests were unremarkable, but portal venous contrast-enhanced CT of the abdomen-pelvis showed a thickened gallbladder with perihepatic fluids, and CT of the chest revealed bilateral lobar atelectasis. After a period of conservative management, the patient eventually underwent diagnostic laparoscopy, revealing a perforated gallbladder with biliary peritonitis.
Abstract This case reports a patient with IgG4 related (IgG4-RD) lung disease who exhibited two different pathological manifestations during the disease process. IgG4 related diseases are a newly defined immune-mediated chronic inflammatory fibrosis disease in recent years. The most common clinical symptoms of this disease are a significant increase in serum IgG4 levels and a mass like lesion.IgG4 RD may have different pathological changes at different stages of the disease, mainly following two stages of development. Its characteristic is the "inflammation" stage, which ultimately leads to "fibrosis" results. Histopathology plays an extremely important role in disease diagnosis. Compared with imaging, it may detect the trend of pulmonary fibrosis earlier to better guide the diagnosis and treatment of IgG4 RD.
Abstract Background Kidney renal papillary cell carcinoma (KIRP) is the second most prevalent malignant cancer originating from the renal epithelium. Nowadays, cancer stem cells (CSC) and stemness-related genes (SRGs) are constantly revealed to play important roles in carcinogenesis and metastasis of various tumors. In the present study, we aim to investigate the underlying mechanisms of stemness-related genes (SRGs) in carcinogenesis and metastasis of KIRP. Methods RNA-seq profiles of 141 KIRP samples were downloaded from the TCGA database, which was used to identify differentially expressed genes (DEGs). The univariate Cox analysis was used to identify the significant stemness-related genes (SRGs) with prognostic value, based on which we calculated the risk score and established a prognostic model by multivariate Cox regression in KIRP patients. In addition, the regulatory network of SRGs, upstream transcription factors (TFs), and downstream signaling pathways was constructed by the Pearson correlation analysis. Results In total, 1124 genes were characterized as DEGs between low- and high-stemness groups. Based on six prognostic SRGs, a prediction model was established with an AUC of 0.861. Furthermore, the transcription factor CBX2 was co-expressed with the stemness-related gene ASPH (R = 0.46, P < 0.001), and ASPH had a significant co-expression pattern with the Notch signaling pathway (R = 0.42, P < 0.001). Meanwhile, we also found that resveratrol might be a potential inhibitor for KIRP. Conclusions We suggested that CBX2 regulated ASPH through activation of Notch signaling pathway, which might be correlated with the carcinogenesis, development, and unfavorable prognosis of KIRP.
This paper describes how to seek the superior in fuzzy controller using the genetic algorithm. Efficiency of fuzzy control depends on several key parameters: membership function, fuzzy control rule and so forth. In this paper a method based on binary-code for parameters of membership function is provided, which only select two parameters of each variables. The result of simulation and real time control experiment show that this method is effective and applicatory.
Aging is a major risk factor for cerebrovascular disease; however, the molecular mechanisms of cerebrovascular aging remain to be clarified. The aim of this study was to reveal the molecular signaling pathways involved in cerebrovascular aging. This study used high-resolution liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS), in combination with quantitative 6-plex tandem mass tag labeling, to profile protein changes in brain vessels from three groups of healthy rhesus macaques (3-years, 6-years, and 20-years). Western blot analyses were used to validate the proteomic data. A total of 2,934 proteins were identified and analyzed. Twenty-two proteins were continuously downregulated with increasing age, while three proteins were continuously upregulated. When comparing Group C vs. Group B, 270 proteins were downregulated, while 73 proteins were upregulated. All these 368 significantly changed proteins were used for further analysis. Bioinformatic analysis showed that the changed proteins were involved in several signaling pathways during cerebrovascular aging. Proteins in the NRF2 pathway, such as Glutathione S-transferase Mu (GSTM), were consistently downregulated especially after 6-years old, whereas proteins related to miRNA targets in the extracellular matrix (ECM) and membrane receptors were upregulated. Protein-protein interaction networks demonstrated that disorders of energy pathways and serine/threonine kinases were critical during cerebrovascular aging. Data are available via ProteomeXchange under the identifier PXD012306. Our results indicated that during aging, the disorders of energy metabolism and dysfunction of antioxidant activity caused over-production of reactive oxygen species (ROS) may exacerbate cerebrovascular aging. In addition, accumulation of ECM proteins during aging might be closely associated with age-related arterial stiffening and decreased compliance.
Abstract Objective: We developed a predictive model associated with ferroptosis to provide a more comprehensive view of kidney renal clear cell carcinoma (KIRC) immunotherapy. Methods: Gene expression data and corresponding clinical outcomes were obtained from the GEO and The Cancer Genome Atlas (TCGA) databases, and a ferroptosis-related gene set was obtained from the FerrDb database. Results: We identified 17 ferroptosis-related genes that were differentially expressed, including enrichment in genes involved in the immune system process. We established a ferroptosis-related gene-based prognostic model based on the results of univariate Cox regression and multivariate Cox regression analyses, with an area under the curve (AUC) of 0.644 (3 years). We found that the higher exprssion of MT1G, LAMP2 and MIOX showed a higher proportion of CD8+ T cells, CD4+ memory activated T cells, etc. Finally, a predictive ferroptosis-related prognostic nomogram, which included the predictive values of age, gender, grade, TNM stage, and risk score, was established to predict overall survival. Conclusions: In sum, we developed a ferroptosis-related gene-based prognostic model that provides novel insights into the prediction of KIRC prognosis and identifies the relevance of the immune microenvironment for patient outcomes.
AbstractBackground: Burns are extremely destructive injuries to the human body. Once a major burn occurs, it can lead to long-term disabilities, psychological burdens, and significant loss of human resources and economic losses. Extensive burns can cause severe oxidative stress, systemic inflammatory response, and a hypermetabolic state. Besides traditional symptomatic treatment, there is an urgent need for new approaches to address oxidative stress and internal environment disturbance in burn injuries. Methods: Based on the GEO database and the Limma R package, differential gene expression analysis was performed to identify genes differentially expressed in severe burns and genes associated with oxidative stress. The Gene Ontology (GO) database was used to analyze the cellular functions of these oxidative stress-related genes, and weighted gene co-expression networks analysis (WGCNA) and protein-protein interaction (PPI) networks were constructed. Receiver operating characteristic (ROC) curves were then constructed to identify hub genes in the networks. A diagnostic model based on these central genes was established using the least absolute shrinkage and selection operator (LASSO) analysis and ROC analysis. Immune-related functions were assessed by evaluating the correlation between the expression of hub genes and immune cell infiltration scores. Additionally, drug-gene interaction databases were used to predict target drugs, and miRNet was used to predict the regulation of miRNA and transcription factors. Results: Through differential analysis, a total of 2,899 differentially expressed genes, 4,936 WGCNA module genes, and 437 oxidative stress-related genes were identified, resulting in 44 candidate genes. Ten hub genes (GCLM, MMP9, BCL2, IL10, SIRT1, NME8, PINK1, GCLC, EPAS1, PARK7) were identified. These central genes were found to be enriched in GO annotations related to “starch and sugar metabolism,” “lysosomes,” and “actin cytoskeleton regulation.” Additionally, it is predicted that 78 drugs can target GCLM, MMP9, BCL2, IL10, SIRT1, NME8, PINK1, GCLC, EPAS1, PARK7, including cisplatin, curcumin, and bevacizumab. A hub gene-miRNA regulatory network with 168 miRNAs and a hub gene-transcription factor (TF) network with 15 TFs were also constructed. These hub genes may serve as biomarkers for the assessment and treatment of oxidative stress in major burns, and provide clues for potential new therapeutic targets. Conclusion: Based on the common genes associated with major burns and oxidative stress in this study, 10 target genes were proposed. These candidate genes may provide new insights into potential mechanisms for exploring the increased risk of burn severity changes caused by oxidative stress at the transcriptional level.
The protective role of intracranial primary collaterals on plaque vulnerability is not well established. We aimed to explore the association of intracranial collateral status with arterial wall features including arterial remodeling and culprit plaque features in severe symptomatic intracranial vertebrobasilar atherosclerosis (sIVBAS). Posterior circulation stroke or TIA patients owing to sIVBAS from a three-dimensional high-resolution MRI (3D HRMRI) prospective observational study was included for current analysis. Participants were dichotomized into poor and good collateral groups according to a modified semiquantitative grading system for primary collateral of posterior circulation. Differences of arterial remodeling, culprit plaque distribution, enhancement, intraplaque hemorrhage (IPH), and calcification on HRMRI were compared between the two groups. Seventy-four eligible patients were included, wherein 39 in poor collateral group and 35 in good collateral group. The average age was 57.0 ± 9.0 years, 65 (87.8%) were male, 62 (83.8%) were diagnosed with ischemic stroke and 12 (16.2%) with TIA. Patients with good collateral had lower occurrence of arterial positive remodeling and plaque diffuse distribution, enhancement (Adjusted OR = 0.17 [0.05–0.54], p 0.05). Intracranial good collateral of posterior circulation may be associated with lower risk of arterial positive remodeling and culprit plaque diffuse distribution, plaque enhancement in patients with severe sIVBAS. clinicaltrials.gov Identifier: NCT02705599.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)