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Ischemic stroke is a prevalent form of cerebrovascular accident, with its pathogenesis involving the intricate interplay between neuroinflammation and energy metabolism. Cerebral ischemia disrupts oxygen and energy supply, triggering metabolic dysregulation and activating neuroinflammatory responses, ultimately resulting in cellular damage. This review provides an exhaustive analysis of the complex mechanisms of ischemic stroke, with a particular focus on the interaction between neuroinflammation and energy metabolism. The interruption of oxygen and energy supply due to cerebral ischemia initiates metabolic dysregulation and activates neuroinflammatory responses, including the release of inflammatory cytokines and the activation of immune cells, contributing to cellular damage and further metabolic disturbances. Studies indicate that dysregulation of energy metabolism significantly impairs neural cell function and interacts with neuroinflammation, exacerbating ischemic brain injury. Therapeutic strategies primarily concentrate on modulating energy metabolism and suppressing neuroinflammatory responses, emphasizing the importance of in-depth research into their interaction to provide a theoretical foundation for new treatment strategies for ischemic stroke. Future research should focus on how to balance anti-inflammatory treatment with energy regulation to minimize neural damage and promote recovery.

Identification of high consequence areas is an important task in pipeline integrity management. However, traditional identification methods are generally characterized by low efficiency, high cost and low accuracy. For this reason, this paper proposes a recognition method based on the improved algorithm Mask Region-based Convolutional Neural Network. Coordinate attention mechanism module is introduced into the traditional Mask R-CNN algorithm to improve the recognition accuracy and reduce the training time. For the identification results, GIS tools are utilized to establish high consequence zones along both sides of the pipeline, and the grade and scope of the high consequence zones are determined according to relevant specifications.In this paper, this method is used to identify the high-consequence area of a pipeline section in Guangdong Province, the results show that: 1, the improved algorithm in the identification of densely populated, geologic hazards, flammable and explosive high consequence zones of the average accuracy of the identification of 1.7%, 3.4%, 3.9%. 2, The method in this paper identifies 8 more building elements and 0.311 more kilometers of pipeline mileage compared to traditional identification methods. The method of this paper can provide a reference for the early identification of high consequence areas of pipelines.

Astrocytes (AST) are abundant glial cells in the human brain, accounting for approximately 20–50% percent of mammalian central nervous system (CNS) cells. They display essential functions necessary to sustain the physiological processes of the CNS, including maintaining neuronal structure, forming the blood–brain barrier, coordinating neuronal metabolism, maintaining the extracellular environment, regulating cerebral blood flow, stabilizing intercellular communication, participating in neurotransmitter synthesis, and defending against oxidative stress et al. During the pathological development of brain tumors, stroke, spinal cord injury (SCI), neurodegenerative diseases, and other neurological disorders, astrocytes undergo a series of highly heterogeneous changes, which are called reactive astrocytes, and mediate the corresponding pathophysiological process. However, the pathophysiological mechanisms of reactive astrocytes and their therapeutic relevance remain unclear. The microRNAs (miRNAs) are essential for cell differentiation, proliferation, and survival, which play a crucial role in the pathophysiological development of CNS diseases. In this review, we summarize the regulatory mechanism of miRNAs on reactive astrocytes in CNS diseases, which might provide a theoretical basis for the diagnosis and treatment of CNS diseases.

Farnesoid X receptor (FXR) is a nuclear receptor known to play protective roles in anti-hepatocarcinogenesis and regulation of the basal metabolism of glucose, lipids, and bile acids. FXR expression is low or absent in HBV-associated hepatocarcinogenesis. Full-length HBx and HBx C-terminal truncation are frequently found in clinical HCC samples and play distinct roles in hepatocarcinogenesis by interacting with FXR or FXR signaling. However, the impact of C-terminal truncated HBx on the progression of hepatocarcinogenesis in the absence of FXR is unclear. In this study, we found that one known FXR binding protein, a C-terminal truncated X protein (HBx C40) enhanced obviously and promoted tumor cell proliferation and migration by altering cell cycle distribution and inducing apoptosis in the absence of FXR. HBx C40 enhanced the growth of FXR-deficient tumors in vivo. In addition, RNA-sequencing analysis showed that HBx C40 overexpression could affect energy metabolism. Overexpressed HSPB8 aggravated the metabolic reprogramming induced by down-regulating glucose metabolism-associated hexokinase 2 genes in HBx C40-induced hepatocarcinogenesis. Overall, our study suggests that C-terminal truncated HBx C40 synergizes with FXR deficiency by altering cell cycle distribution as well as disturbing glucose metabolism to promote HCC development.

The association of maternal exposure to selective serotonin reuptake inhibitors (SSRIs) or serotonin and norepinephrine reuptake inhibitors (SNRIs) with the risk of system-specific congenital malformations in offspring remains unclear. We conducted a meta-analysis to examine this association and the risk difference between these two types of inhibitors. A literature search was performed from January 2000 to May 2023 using PubMed and Web of Science databases. Cohort and case-control studies that assess the association of maternal exposure to SSRIs or SNRIs with the risk of congenital abnormalities were eligible for the study. Twenty-one cohort studies and seven case-control studies were included in the meta-analysis. Compared to non-exposure, maternal exposure to SNRIs is associated with a higher risk of congenital cardiovascular abnormalities (pooled OR: 1.64 with 95% CI: 1.36, 1.97), anomalies of the kidney and urinary tract (pooled OR: 1.63 with 95% CI: 1.21, 2.20), malformations of nervous system (pooled OR: 2.28 with 95% CI: 1.50, 3.45), anomalies of digestive system (pooled OR: 2.05 with 95% CI: 1.60, 2.64) and abdominal birth defects (pooled OR: 2.91 with 95%CI: 1.98, 4.28), while maternal exposure to SSRIs is associated with a higher risk of congenital cardiovascular abnormalities (pooled OR: 1.25 with 95%CI: 1.20, 1.30), anomalies of the kidney and urinary tract (pooled OR: 1.14 with 95%CI: 1.02, 1.27), anomalies of digestive system (pooled OR: 1.11 with 95%CI: 1.01, 1.21), abdominal birth defects (pooled OR: 1.33 with 95%CI: 1.16, 1.53) and musculoskeletal malformations (pooled OR: 1.44 with 95%CI: 1.32, 1.56). SSRIs and SNRIs have various teratogenic risks. Clinicians must consider risk-benefit ratios and patient history when prescribing medicines.

Myocardial ischemia/reperfusion (I/R) injury is a potential complication of ischemic heart disease after recanalization. One of the primary reasons for I/R injury is the excessive accumulation of reactive oxygen species (ROS) in cardiomyocytes. Verapamil, a classic calcium channel blocker, has the potential to mitigate I/R-evoked oxidative stress. However, the underlying mechanisms have not been fully elucidated. SIRT1 is an essential regulator of I/R and offers resistance to oxidative stress arising from I/R. It is still inconclusive if verapamil can reduce myocardial I/R-triggered oxidative damage through modulating SIRT1 antioxidant signaling. To verify our hypothesis, the H9c2 cardiomyocytes and the mice were treated with verapamil and then exposed to hypoxia/reoxygenation (H/R) or I/R in the presence or absence of the SIRT1 inhibitor EX527. As expected, verapamil stimulated SIRT1 antioxidant signaling evidenced by upregulation of SIRT1, FoxO1, SOD2 expressions and downregulation of Ac-FoxO1 expression in vitro and in vivo . In addition, verapamil remarkably suppressed H/R and I/R-induced oxidative stress proven by declined ROS level and MDA content. The cardioprotective actions of verapamil via SIRT1 were further confirmed in the experiments with the presence of the specific SIRT1 inhibitor EX527. We demonstrated that verapamil alleviated myocardial I/R-evoked oxidative stress partially via activation of SIRT1 antioxidant signaling. Subsequently, verapamil protected against cardiac dysfunction and myocardial infarction accompanied by oxidative stress.

Autosomal recessive bestrophinopathy (ARB) comprises remarkable retinal dystrophy characterized by yellowish subretinal lesions scattered in the posterior pole and is always accompanied with refractory angle-closure glaucoma (ACG). The treatment of ACG patients with ARB is a major challenge for all ophthalmologists. A 12-year-old female child was diagnosed with ARB and ACG and presented with discrete, round, yellow-white deposits of variable sizes scattered in the retina, retinoschisis in the macular, shallow anterior chamber depth and angle closure with uncontrolled intraocular pressure (IOP). Micropulse transscleral cyclophotocoagulation (MP-TCP) successfully deepened anterior chamber, lowered IOP and resolved retinoschisis. However, the postoperative deepening of the anterior chamber began to regress 12 days after surgery and stabilized 142 days after surgery, the retinoschisis reoccurred 67 days after surgery. This case revealed that changes in vitreous condition may play an important role in the formation of retinoschisis. MP-TCP, which induces vitreous compression and increases osmotic pressure on the retina, could be used to treat young ACG patients with ARB to avoid other complicated surgeries and vision-threatening postoperative complications. However, the theory needs to be confirmed by further studies.

Background  Mitral valve prolapse (MVP) is an etiologically heterogeneous disorder. Early diagnosis and prompt treatment of the underlying disease are of great significance. Herein, we present a rare case of MVP caused by anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Case presentation A 22-year-old female presented with a 16-year history of anterior mitral leaflet prolapse. However, she had never experienced any discomfort before. At a routine follow-up, a transthoracic echocardiogram showed anterior mitral leaflet prolapse (A2) with moderate mitral regurgitation, and a retrograde blood flow from an extremely dilated left coronary artery (LCA). Further coronary angiography and coronary computed tomography angiography confirmed the diagnosis of ALCAPA. She subsequently underwent successful LCA reimplantation and concomitant mitral valve replacement. Intraoperatively, her mitral annulus was mildly dilated, anterior mitral valve leaflet appeared markedly thickened with rolled edges, and a chordae tendineae connecting the anterior leaflet (A2) was ruptured and markedly shortened. Conclusions ALCAPA is a rare and potentially life-threatening congenital coronary artery anomaly that may cause mitral valve prolapse. Echocardiogram is an important screening tool for this disorder.

Microglia are the primary immunocompetent cells in brain tissue and microglia-mediated inflammation is associated with the pathogenesis of various neuronal disorders. Recently, many studies have shown that mesenchymal stem cells (MSCs) display a remarkable ability to modulate inflammatory and immune responses through the release of a variety of bioactive molecules, thereby protecting the central nervous system. Previously, we reported that MSCs have the ability to modulate inflammatory responses in a traumatic brain injury model and that the potential mechanisms may be partially attributed to upregulated TNF-α stimulated gene/protein 6 (TSG-6) expression. However, whether TSG-6 exerts an anti-inflammatory effect by affecting microglia is not fully understood. In this study, we investigated the anti-inflammatory effects of MSCs and TSG-6 in an in vitro lipopolysaccharide (LPS)-induced BV2 microglial activation model. We found that MSCs and TSG-6 significantly inhibited the expression of pro-inflammatory mediators in activated microglia. However, MSC effects on microglia were attenuated when TSG-6 expression was silenced. In addition, we found that the activation of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) pathways in LPS-stimulated BV2 microglial cells was significantly inhibited by TSG-6. Furthermore, we found that the presence of CD44 in BV2 microglial cells was essential for MSC- and TSG-6-mediated inhibition of pro-inflammatory gene expression and of NF-κB and MAPK activation in BV2 microglial cells. The results of this study suggest that MSCs can modulate microglia activation through TSG-6 and that TSG-6 attenuates the inflammatory cascade in activated microglia. Our study indicates that novel mechanisms are responsible for the immunomodulatory effect of MSCs on microglia and that MSCs, as well as TSG-6, might be promising therapeutic agents for the treatment of neurotraumatic injuries or neuroinflammatory diseases associated with microglial activation.

Gobi spans a large area of China, surpassing the combined expanse of mobile dunes and semi-fixed dunes. Its presence significantly influences the movement of sand and dust. However, the complex origins and diverse materials constituting the Gobi result in notable differences in saltation processes across various Gobi surfaces. It is challenging to describe these processes according to a uniform morphology. Therefore, it becomes imperative to articulate surface characteristics through parameters such as the three-dimensional (3D) size and shape of gravel. Collecting morphology information for Gobi gravels is essential for studying its genesis and sand saltation. To enhance the efficiency and information yield of gravel parameter measurements, this study conducted field experiments in the Gobi region across Dunhuang City, Guazhou County, and Yumen City (administrated by Jiuquan City), Gansu Province, China in March 2023. A research framework and methodology for measuring 3D parameters of gravel using point cloud were developed, alongside improved calculation formulas for 3D parameters including gravel grain size, volume, flatness, roundness, sphericity, and equivalent grain size. Leveraging multi-view geometry technology for 3D reconstruction allowed for establishing an optimal data acquisition scheme characterized by high point cloud reconstruction efficiency and clear quality. Additionally, the proposed methodology incorporated point cloud clustering, segmentation, and filtering techniques to isolate individual gravel point clouds. Advanced point cloud algorithms, including the Oriented Bounding Box (OBB), point cloud slicing method, and point cloud triangulation, were then deployed to calculate the 3D parameters of individual gravels. These systematic processes allow precise and detailed characterization of individual gravels. For gravel grain size and volume, the correlation coefficients between point cloud and manual measurements all exceeded 0.9000, confirming the feasibility of the proposed methodology for measuring 3D parameters of individual gravels. The proposed workflow yields accurate calculations of relevant parameters for Gobi gravels, providing essential data support for subsequent studies on Gobi environments.