Bilateral Bow Hunter Syndrome Associated with Loss of Cervical Physiological Curvature.

BACKGROUND Bow hunter syndrome is a rare disease that is often overlooked. It presents with complex and variable clinical symptoms and causes, making diagnosis and treatment challenging. This case report focuses on a young patient with bilateral bow hunter syndrome, possibly caused by the loss of cervical physiological curvature. The aim is to enhance understanding and awareness of the disease. It is important to consider the possibility of bow hunter syndrome in young patients with long-term poor neck posture and symptoms such as dizziness, nausea, vomiting, and neck rotation-related symptoms. In such cases, thorough examination of posterior circulation hemodynamics and vascular morphology is recommended. CASE REPORT A 25-year-old woman was admitted to the hospital mainly because of "dizziness for 10 hours." The dizziness was aggravated when the right side of the neck was turned and the body position changed. This was accompanied by visual rotation, nausea, and vomiting. Bow hunter syndrome was diagnosed based on the clinical symptoms and hemodynamic examination of the posterior circulation. The patient was given a cervical collar to limit excessive twisting of the neck and instructed to avoid large-angle deflection of the neck after discharge. During the 3-month follow-up, no characteristic symptoms (such as dizziness) reappeared. CONCLUSIONS Bow hunter syndrome is a rare clinical posterior circulation compression syndrome with complex etiology. This case suggests that the simple disappearance of cervical curvature may be related to the occurrence of bow hunter syndrome. The dynamic monitoring of blood flow by color Doppler ultrasound and transcranial Doppler in different head positions provides clear clues to suspected bow hunter syndrome. With the help of computed tomography angiography, the diagnosis of bow hunter syndrome may be obtained by noninvasive examination.

Ultimate Strength Study of Structural Bionic CFRP-Sinker Bolt Assemblies Subjected to Preload under Three-Point Bending.

Countersunk head bolted joints are one of the main approaches to joining carbon fiber-reinforced plastics, or CFRP. In this paper, the failure mode and damage evolution of CFRP countersunk bolt components under bending load are studied by imitating water bears, which are born as adult animals and have strong adaptability to life. Based on the Hashin failure criterion, we establish a 3D finite element failure prediction model of a CFRP-countersunk bolted assembly, benchmarked with the experiment. The analysis shows that the simulation results under specified parameters have a good correlation with the experimental results, and can better reflect the three-point bending failure and fracture of the CFRP-countersunk bolted assembly. Based on the specified parameter of the carbon lamina material change, we used the countersunk bolt preload to investigate the stress distribution near the counterbore zone, and to investigate the effect of bolt load on the three-point bending limit load. The results obtained using FEA calculations indicate that the stress distribution around the countersunk hole is related to the laminate direction. The bolt preloading force increasing reduces the load value at the initial damage, and the appropriate preload force will increase the ultimate load of the joint.

Investigation of CFRP-Countersunk Bolted Assembly Fatigue Damage under Three-Point Bending via Experimental and Numerical Analysis.

In this research, the fatigue damage behavior under three-point bending of a composite joint incorporating a single countersunk fastener is investigated. Firstly, a self-developed fatigue test system was set up to test the fatigue characteristics of CFRP-countersunk bolted assembly under the displacement amplitude cycles of 103 to 106 to study the formation and expansion rule of damage and cracks. It found two typical damage processes, both of which involve some formal interface damage between fiber and matrix. Based on the experiment, a finite element fatigue damage analysis on this assembly was carried out according to the Hashin failure criterion. The simulation result shows an identical fatigue damage location and fatigue life with the experimental phenomenon. Moreover, it predicted the final fatigue life of the specimen under 10 hz cyclic loading with 1 mm displacement and 10 Nm bolt preloading. This research provides guidance for the engineering fatigue issues of single-bolted joint composite connection structures and provides a reference for the corresponding technical specifications formulation.

Droplet rolling angle model of micro-nanostructure superhydrophobic coating surface.

The droplet rolling angle is one of the important indicators to measure the coating's hydrophobic performance, but the specific factors affecting the droplet rolling angle on the micro-nanostructured superhydrophobic coating surface are not yet known. Based on the rolling mechanism of droplets on rough surfaces, and from the perspective of coating microscopic energy conservation, this paper points out that the micron-scale morphology and the nanoscale morphology can comprehensively affect the droplet rolling angle. From the above perspective, a mathematical model of the droplet rolling angle on the micro-nanostructure superhydrophobic coating surface was established. The model shows that the droplet rolling angle is positively correlated with the ratio of nano-sized pillar width to spacing, the ratio of micron-sized papilla radius to spacing, and the liquid-gas interfacial tension, and is negatively correlated to the droplet intrinsic contact angle, droplet volume and droplet density. The droplet rolling angle calculated by the presented model is in good agreement with the experimentally tested results. This model can provide good accuracy in predicting the droplet rolling angle on the micro-nanostructured superhydrophobic coating surface.

Knockdown of long non-coding RNA TUG1 depresses apoptosis of hippocampal neurons in Alzheimer's disease by elevating microRNA-15a and repressing ROCK1 expression.

OBJECTIVE: Many studies have already suggested the role of long non-coding RNAs (lncRNAs) in Alzheimer's disease (AD), but the functions of lncRNA Taurine Upregulated Gene 1 (TUG1) in AD have been scarcely discussed. This study aims to verify how TUG1 affects hippocampal neurons in AD through modulation of microRNA-15a (miR-15a)/Rho-associated protein kinase 1 (ROCK1). METHOD: AD mice was modeled through injection of ß-amyloid 25-35 (Aß25-35) into the lateral ventricle. After modeling, the mice were injected with altered TUG1 and/or miR-15a agomir lentiviruses. The spatial learning ability and memory ability of mice were detected through Morris water maze test. Hippocampal neuronal apoptosis and oxidative stress indicators in AD mice were then detected. The hippocampal neuron AD model was induced by Aß25-35. Next, the neurons were, respectively, transfected with altered TUG1 vector and/or miR-15a mimics to determine the proliferation inhibition and apoptosis of hippocampal neurons. The interactions between TUG1 and miR-15a, and between miR-15a and ROCK1 were assessed using bioinformatic prediction, dual luciferase reporter gene assay and RNA-pull-down assay. RESULTS: In the animal models, Aß25-35-induced mice exhibited decreased spatial learning and memory ability, obvious pathological injury, promoted hippocampal neuronal apoptosis and decreased antioxidant ability. TUG1 silencing and miR-15a elevation improved spatial learning ability and memory ability, ameliorated pathological injury, depressed neuronal apoptosis, and strengthened antioxidant ability of hippocampal neurons in AD mice. In cellular models, Aß25-35-treated hippocampal neurons presented inhibited neuronal viability and promoted neuronal apoptosis. TUG1 silencing and miR-15a elevation increased viability and limited apoptosis of Aß25-35-treated hippocampal neurons. TUG1 specifically bound to miR-15a, and miR-15a targeted ROCK1. CONCLUSION: Collectively, this study reveals that TUG1 knockdown restricts apoptosis of hippocampal neurons in AD by elevating miR-15a and suppressing ROCK1 expression, and provides a new therapeutic target for AD treatment.

Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13.

Ischemic stroke represents a major cause of adult physical disability, which is triggered by cerebral artery occlusion induced blood flow blockage. MiR-874-3p has been reported to be down-regulated in the brain injury induced by ischemia-reperfusion (I/R), but the direct evidence associated with injury of I/R remains unknown. In this study, we found that miR-874-3p levels significantly decreased in rat I/R brain induced by middle cerebral artery occlusion/reperfusion (MCAO/R) and SH-SY5Y cells following oxygen-glucose deprivation and reperfusion (OGD/R) treatment. Upregulation of miR-874-3p reduced infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining, as well as increased proliferation and inhibited apoptosis in OGD/R induced SH-SY5Y cells by CCK-8, Edu staining and flow cytometry analysis. Mechanistically, bioinformatics analysis and luciferase reporter assay confirmed BCL-2-modifying factor (BMF) and Bcl-2 family protein Bcl-rambo (BCL2L13) were the direct targets of miR-874-3p. Furthermore, BMF or BCL2L13 knockdown also provided significant protection against OGD/R induced injury, while their overexpression reversed the protective effects of miR-874-3p on SH-SY5Y cells following OGD/R. In summary, our results suggest that miR-874-3p attenuated ischemic injury by negatively regulating BMF and BCL2L13, highlighting a novel therapeutic target for ischemic stroke.

Modulation of the Leishmania donovani peroxin 5 quaternary structure by peroxisomal targeting signal 1 ligands.

The import of proteins containing the peroxisomal targeting signal 1 (PTS1) into the Leishmania glycosome is dependent on the docking of the PTS1-loaded LdPEX5 cytosolic receptor with LdPEX14 on the glycosome surface. Here we show that, in the absence of PTS1, LdPEX5 is a tetramer that is stabilized by two distinct interaction domains; the first is a coiled-coil motif encompassing residues 277 to 310, whereas the second domain is localized to residues 1 to 202. By using microcalorimetry, surface plasmon resonance, and size exclusion chromatography techniques, we show that PTS1 peptide binding to LdPEX5 tetramers promotes their dissociation into dimeric structures, which are stabilized by a coiled-coil interaction. Moreover, we demonstrated that the resulting LdPEX5-PTS1 complex is remarkably stable and exhibits extremely slow dissociation kinetics. However, binding of LdPEX14 to LdPEX5 modulates the LdPEX5-PTS1 affinity as it decreases the thermodynamic dissociation constant for this latter complex by 10-fold. These changes in the oligomeric state of LdPEX5 and in its affinity for PTS1 ligand upon LdPEX14 binding may explain how, under physiological conditions, LdPEX5 can function to deliver and unload its cargo to the protein translocation machinery on the glycosomal membrane.

Light activates binding of membrane proteins to chloroplast RNAs in Chlamydomonas reinhardtii.

Several membrane proteins were previously shown to bind to the 5' leader of the chloroplast psbC mRNA in the unicellular eukaryotic alga Chlamydomonas reinhardtii. This study showed that these proteins have affinity for AU-rich RNAs, as determined by competition experiments. In addition, their binding activities are enhanced 13-15-fold by light, and a 46 kDa protein is activated within 1-10 min. This activation could be mediated by the modulation of ADP pools by the light-dependent reactions of photosynthesis and ATP synthase because (1) two inhibitors that block ATP synthesis also prevent this activation and (2) ADP inhibits the RNA-binding activity of this protein in vitro. An inhibitor of Photosystem II diminishes this induction, suggesting that reducing potential generated by the photosynthetic electron transport chain modulates this RNA-binding activity. The RNA-binding activities of two proteins (of 46 and 47 kDa) are inhibited by Mg-protoporphyrin IX methyl ester in vitro suggesting they could be regulated by these intermediates in the chlorophyll biosynthetic pathway.

[Control of Thrombopoietin Expression by Doxycycline in CHO Cells]

To control thrombopoietin (TPO) expression by doxycycline in CHO cells, Tet-On gene expression system was used. Recombinant plasmid pTRE-TPO was successfully constructed. pTRE-TPO and pTK-Hyg were cotransfected into CHO-Tet-On cells. Cells resistant to hygromycin were cloned, high expression and low background clone was selected, and named as CHO-Tet-On-TPO. There was no significant TPO expression in the absence of doxycycline, the TPO level in the cell culture supernatant was 0.1 micro g/L. After exposure to 2 mg/L doxycycline, TPO expression was greatly increased, the TPO level in the cell culture supernatant reached 10.8 micro g/L. Tet-On gene expression system is a ready access to the tight-regulated and high-level gene expression system. It is likely to provide a safe and regulatable way for TPO gene therapy.