Analysis of Ultrasonic Machining Characteristics under Dynamic Load.

This research focuses on the load characteristics of piezoelectric transducers in the process of longitudinal vibration ultrasonic welding. We are primarily interested in the impedance characteristics of the piezoelectric transducer during loading, which is studied by leveraging the equivalent circuit theory of piezoelectric transducers. Specifically, we propose a cross-value mapping method. This method can well map the load change in ultrasonic welding to the impedance change, aiming to obtain an equivalent model of impedance and load. The least-squares strategy is used for parameter identification during data fitting. Extensive simulations and physical experiments are conducted to verify the proposed model. As a result, we can empirically find that the result from our model agrees with the impedance characteristics from the real-life data measured by the impedance meter, indicating its potential for real practice in controller research and transducer design.

Effect of different factors on treatment of oily wastewater by TiO2/Al2O3-PVDF ultrafiltration membrane.

An ultrafiltration membrane developed by our research group was applied to treat simulated emulsified oil wastewater. ATR-FTIR, SEM, TEM, and Zeta potential analyzes demonstrated that the modified ultrafiltration membrane (MM) has excellent stability and anti-fouling capacity than origin membrane (OM), which possesses a pure water flux of 260 L·m-2·h-1 and oil/water (o/w) rejection of 98.5 ± 0.33%. Inorganic salt CaCl2 has more considerable influence than MgSO4 and NaCl under the same mass concentration in the two membranes UF process. Along with concentration increasing, flux sharply reduces; meanwhile, the rejection has an opposite trend. Moreover, permeation flux has a maximum value, and the rejection also gets its optimal state under neutral conditions during the pH value of 2-12. The membrane also exhibits excellent anti-fouling performance and anti- o/w adsorption properties with an adsorption rate below 0.8% compared with OM, which has an adsorption rate of nearly 2.1%, respectively. A kind of new UF membrane developed by our research group was applied to treat simulated o/w. ATR-FTIR, SEM, TEM, and Zeta potential analyzes demonstrated that PVDF-Al2O3/TiO2 material has excellent stability and anti-fouling capacity. CaCl2 has the greatest influence than MgSO4 and NaCl under the same mass concentration. Moreover, permeation flux has maximum value and the rejection also gets its optimal state under neutral conditions during pH 2-12. The membrane also exhibits excellent anti-fouling performance and anti-O/W adsorption properties with adsorption rate below 0.8% compared with OM which has an adsorption rate nearly 2.1%, respectively.

Correction to: Mild endoplasmic reticulum stress ameliorates lipopolysaccharide-induced neuroinflammation and cognitive impairment via regulation of microglial polarization.

An amendment to this paper has been published and can be accessed via the original article.

Preoperative Sleep Disturbance Exaggerates Surgery-Induced Neuroinflammation and Neuronal Damage in Aged Mice.

Postoperative cognitive dysfunction (POCD) is defined as new cognitive impairment (memory impairment and impaired performance) after surgery, especially in aged patients. Sleep disturbance is a common phenomenon before surgery that has been increasingly thought to affect patient recovery. However, little is known about the functional impact of preoperative sleep disturbance on POCD. Here, we showed that tibial fracture surgery induced cognitive deficit and production of proinflammatory cytokines interleukin-6 (IL-6) and IL-1ß, along with microglia and astrocyte activation, neuronal damage, and blood-brain barrier (BBB) disruption. Preoperative sleep disturbance enhanced the surgery-induced neuroinflammation, neuronal damage, BBB disruption, and memory impairment 24 h after surgery. Taken together, these results demonstrated that preoperative sleep disturbance aggravated postoperative cognitive function in aged mice and the mechanism may be related to central nervous system (CNS) inflammation and neuronal damage.

IL-17A contributes to perioperative neurocognitive disorders through blood-brain barrier disruption in aged mice.

BACKGROUND: Perioperative neurocognitive disorders (PND) occur frequently after surgery, especially in aged patients. Surgery-induced neuroinflammation and blood-brain barrier (BBB) dysfunction play a crucial role in the pathogenesis of PND. Interleukin-17A (IL-17A) increases after surgical stress and will be involved in BBB dysfunction. However, the effect of IL-17A on BBB function during PND remains poorly understood. METHODS: Male wild-type C57BL/6J mice (15 months old) received tibial fracture surgery and fixation to establish the PND model. All the mice were injected intraperitoneally with an IL-17A-neutralizing antibody (Abs) or isotype-control Abs 30 min before tibial fracture surgery. Animal behaviour tests conducted 24 h after surgery included the contextual fear conditioning and Y maze tests. Serum and hippocampus IL-17A levels and hippocampus IL-6 and IL-1ß levels were detected by ELISA. BBB function was detected by Evans blue (EB) test. Hippocampus matrix metalloproteinase-2 (MMP-2)- and MMP-9-positive cells were detected by immunohistochemistry. Hippocampus albumin, occludin, claudin-5 and IL-17A receptors were detected by Western blot. For the in vitro experiment, bEnd.3 cells were incubated with IL-17A. Cell IL-17A receptors were detected by immunofluorescence. Cellular MMP-2, MMP-9, occludin, and claudin-5 were detected by Western blot. RESULTS: Tibial fracture surgery promoted memory impairment, increased levels of IL-17A and IL-17A receptors, inflammatory factor production and BBB dysfunction. IL-17A Abs inhibited this effect, including improving memory function, decreasing inflammatory factor production and alleviating BBB disruption, indicated by decreased tight junctions (TJs) and increased MMPs after surgery. The in vitro study suggested that recombinant IL-17A could upregulate the expression of IL-17A receptors, decrease TJs and increase the level of MMPs in bEnd.3 cells. CONCLUSIONS: Our results suggested that IL-17A-promoted BBB disruption might play an important role in the pathogenesis of PND.

Effect of tryptase on mouse brain microvascular endothelial cells via protease-activated receptor 2.

BACKGROUND: Mast cells (MCs), the 'first responders' in brain injury, are able to disrupt the blood-brain barrier (BBB), but the underlying mechanism is not well understood. Tryptase is the most abundant MC secretory product. Protease-activated receptor 2 (PAR-2) has been identified as a specific receptor for tryptase, which is abundantly expressed in brain microvascular endothelial cells. The BBB comprises brain microvascular endothelial cells that display specialised molecular properties essential for BBB function and integrity. Therefore, the purpose of the present study was to investigate the effects of tryptase on mouse brain microvascular endothelial cell line bEnd3 and its potential mechanisms of action. METHODS: Induction of mouse brain microvascular endothelial cell activation by tryptase was examined. Then, mouse brain microvascular endothelial cells were pretreated with a PAR-2 antagonist and stimulated with tryptase. Cellular activation, proinflammatory cytokine production, expression of PAR-2, Toll-like receptors (TLRs) and mitogen-activated protein kinases (MAPK), nuclear factor kappa B (NF-kappa B) phosphorylation were assessed. RESULTS: Tryptase upregulated the production of VCAM-1, MMPs (MMP9 and MMP2), TLR4 and TNF-α and downregulated the expression of the tight junction proteins occludin and claudin-5 in mouse brain microvascular endothelial cell. Among the MAPK and NF-kappa B pathway, ERK and NF-kappa B were activated by tryptase. All of these effects could be eliminated by the PAR-2 inhibitor. CONCLUSION: Based on our findings, we conclude that tryptase can trigger brain microvascular endothelial cell activation and proinflammatory mediator release. These findings may further clarify the involvement and mechanism of tryptase in BBB disruption.

Mild Endoplasmic Reticulum Stress Protects Against Lipopolysaccharide-Induced Astrocytic Activation and Blood-Brain Barrier Hyperpermeability.

Recent research has revealed that uncontrolled chronic neuroinflammation is closely associated with diverse neurodegenerative diseases, by impairing blood-brain barrier (BBB) function and astrocytic reaction. Endoplasmic reticulum (ER) stress is conventionally linked to the loss of neuronal structure and function and should be widely attenuated. This notion has been questioned by recent experimental studies, which have shown that non-harmful levels of ER stress had numerous beneficial roles against neurodegeneration, including neuroprotection and inhibition of cytokine production. Here, we investigated the mild ER stress-based regulation of LPS-induced inflammatory responses in astrocytes. Primary astrocytes were exposed to tunicamycin (TM), a compound that activates ER stress, with or without the ER-stress inhibitor sodium 4-phenylbutyrate (4-PBA) before LPS treatment. Astrocytic activation, proinflammatory factor production, and the extent of ER stress were assessed. In addition, the effect of mild ER stress on astrocytes and BBB function was determined in vivo. Male Sprague-Dawley rats received intracerebroventricular injections of TM with or without intraperitoneal 4-PBA before LPS administration. The levels of astrocytic activation and BBB permeability were measured after treatment. Our results showed that lower doses of TM resulted in a mild ER-stress response without inducing cytotoxicity and tissue toxicity. Non-toxic ER-stress preconditioning ameliorated LPS-induced overactivation and inflammatory responses in astrocytes. Moreover, pre-exposure to non-lethal doses of TM improved LPS-induced BBB impairment and cognitive ability dysfunction in rats. However, 4-PBA, reversed the protective effect of TM preconditioning in vitro and in vivo. We conclude that mild ER stress ("preconditioning") can alleviate LPS-induced astrocytic activation and BBB disruption. Our findings provide a better understanding for the regulatory role of ER stress in neuroinflammation and indicate that mild ER stress might have therapeutic value for the treatment of neurodegenerative diseases.

Mild endoplasmic reticulum stress ameliorates lipopolysaccharide-induced neuroinflammation and cognitive impairment via regulation of microglial polarization.

BACKGROUND: Neuroinflammation, which ultimately leads to neuronal loss, is considered to play a crucial role in numerous neurodegenerative diseases. The neuroinflammatory process is characterized by the activation of glial cells such as microglia. Endoplasmic reticulum (ER) stress is commonly associated with impairments in neuronal function and cognition, but its relationship and role in neurodegeneration is still controversial. Recently, it was confirmed that nonharmful levels of ER stress protected against experimental Parkinson's disease. Here, we investigated mild ER stress-based regulation of lipopolysaccharide (LPS)-driven neuroinflammation in rats and in primary microglia. METHODS: Male Sprague-Dawley (SD) rats received the intracerebroventricular injection of the ER stress activator tunicamycin (TM) with or without intraperitoneal injection of the ER stress stabilizer sodium 4-phenylbutyrate (4-PBA) 1 h before LPS administration. The levels of neuroinflammation and memory dysfunction were assessed 24 h after treatment. In addition, the effect of mild ER stress on microglia was determined in vitro. RESULTS: Here, we found that low doses of TM led to mild ER stress without cell or organism lethality. We showed that mild ER stress preconditioning reduced microglia activation and neuronal death as well as improved LPS-induced memory impairment in rats. In addition, pre-exposure to nonlethal doses of TM in microglia showed significant protection against LPS-induced proinflammatory cytokine production and M1/2b polarization. However, sodium 4-PBA, a compound that ameliorates ER stress, ablated this protective effect in vivo and in vitro. CONCLUSIONS: Based on our findings, we conclude that the mild ER stress not only limits the accumulation of misfolded proteins but also protects tissues from harmful endotoxemia insults. Therefore, ER stress preconditioning has potential therapeutic value for the treatment of neurodegenerative diseases.

The influence of Sr and H3PO4 concentration on the hydration of SrCaHA bone cement.

Sr-contained calcium hydroxyapatite (SrCaHA) cement is a potential biomaterial for in vivo bone repair and surgery fixation due to its excellent biodegradability, bioactivity, biocompatibility, easily shaping and self-hardening. We had ever reported the in vitro physiochemical properties, biocompatibility and in vivo degradability of the SrCaHA cement obtained by mixing a cement powder of Ca(4)(PO(4))(2)O/CaHPO(4)/SrHPO(4) and a cement liquid of diluted H(3)PO(4) aqueous solution. In the present study, we intensively studied the influences of both Sr content and H(3)PO(4) concentration in diluted phosphoric acid aqueous solution on the setting time, hydration heat-liberation behaviours, and real-time microstructure and phase evolutions of the SrCaHA cement. The results show that both PO(4)(3-) and H(+) ions in PA solution attended the hydration reaction as reactants, and thus the increase of the PA concentration not only promoted the dissolution of Ca(4)(PO(4))(2)O but also pushed the hydration progress of SrCaHA bone cement. Sr content exhibits a remarkable retardation role on the apatite transformation of the SrCaHA cement pastes which probably attributed to its higher degree of supersaturation for yielding apatite crystals and lower transformation rate when exposed to the Sr(2+)-containing hydration system. This present results contribute to a better understanding on the hydration mechanism of the new SrCaHA cement and help to the more precisely controlling of its hydration process.