47 research outputs found

    High Thermoelectric Performance in Supersaturated Solid Solutions and Nanostructured nâ Type PbTeâ GeTe

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    Sbâ doped and GeTeâ alloyed nâ type thermoelectric materials that show an excellent figure of merit ZT in the intermediate temperature range (400â 800 K) are reported. The synergistic effect of favorable changes to the band structure resulting in high Seebeck coefficient and enhanced phonon scattering by point defects and nanoscale precipitates resulting in reduction of thermal conductivity are demonstrated. The samples can be tuned as singleâ phase solid solution (SS) or twoâ phase system with nanoscale precipitates (Nano) based on the annealing processes. The GeTe alloying results in band structure modification by widening the bandgap and increasing the densityâ ofâ states effective mass of PbTe, resulting in significantly enhanced Seebeck coefficients. The nanoscale precipitates can improve the power factor in the low temperature range and further reduce the lattice thermal conductivity (κlat). Specifically, the Seebeck coefficient of Pb0.988Sb0.012Teâ 13%GeTeâ Nano approaches â 280 µV Kâ 1 at 673 K with a low κlat of 0.56 W mâ 1 Kâ 1 at 573 K. Consequently, a peak ZT value of 1.38 is achieved at 623 K. Moreover, a high average ZTavg value of â 1.04 is obtained in the temperature range from 300 to 773 K for nâ type Pb0.988Sb0.012Teâ 13%GeTeâ Nano.Both supersaturated solid solutions and nanostructured nâ type Pb1â xGexTe systems with excellent thermoelectric performance can be prepared via a nonequilibrium process. The nanostructured sample enhances the figure of merit ZT via reducing the lattice thermal conductivity. A ZTavg of â 1.04 is obtained, which is among the highest ZTavg values for nâ type PbTe materials reported so far.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/145314/1/adfm201801617-sup-0001-S1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/145314/2/adfm201801617.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/145314/3/adfm201801617_am.pd

    Generation and Role of Oscillatory Contractions in Mouse Airway Smooth Muscle

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    Background/Aims: Tetraethylammonium chloride (TEA) induces oscillatory contractions in mouse airway smooth muscle (ASM); however, the generation and maintenance of oscillatory contractions and their role in ASM are unclear. Methods: In this study, oscillations of ASM contraction and intracellular Ca2+ were measured using force measuring and Ca2+ imaging technique, respectively. TEA, nifedipine, niflumic acid, acetylcholine chloride, lithium chloride, KB-R7943, ouabain, 2-Aminoethoxydiphenyl borate, thapsigargin, tetrodotoxin, and ryanodine were used to assess the mechanism of oscillatory contractions. Results: TEA induced depolarization, resulting in activation of L-type voltage-dependent Ca2+ channels (LVDCCs) and voltage-dependent Na+ (VNa) channels. The former mediated Ca2+ influx to trigger a contraction and the latter mediated Na+ entry to enhance the contraction via activating LVDCCs. Meanwhile, increased Ca2+-activated Cl- channels, inducing depolarization that resulted in contraction through LVDCCs. In addition, the contraction was enhanced by intracellular Ca2+ release from Ca2+ stores mediated by inositol (1,4,5)-trisphosphate receptors (IP3Rs). These pathways together produce the contractile phase of the oscillatory contractions. Furthermore, the increased Ca2+ activated the Na+-Ca2+ exchanger (NCX), which transferred Ca2+ out of and Na+ into the cells. The former induced relaxation and the latter activated Na+/K+-ATPase that induced hypopolarization to inactivate LVDCCs causing further relaxation. This can also explain the relaxant phase of the oscillatory contractions. Moreover, the depolarization induced by VNa channels and NCX might be greater than the hypopolarization caused by Na+/K+-ATPase alone, inducing LVDCC activation and resulting in further contraction. Conclusions: These data indicate that the TEA-induced oscillatory contractions were cooperatively produced by LVDCCs, VNa channels, Ca2+-activated Cl- channels, NCX, Na+/K+ ATPase, IP3Rs-mediated Ca2+ release, and extracellular Ca2+

    Semen cassiae Extract Inhibits Contraction of Airway Smooth Muscle

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    β2-adrenoceptor agonists are commonly used as bronchodilators to treat obstructive lung diseases such as asthma and chronic obstructive pulmonary disease (COPD), however, they induce severe side effects. Therefore, developing new bronchodilators is essential. Herbal plants were extracted and the extracts’ effect on airway smooth muscle (ASM) precontraction was assessed. The ethyl alcohol extract of semen cassiae (EESC) was extracted from Semen cassia. The effects of EESC on the ACh- and 80 mM K+-induced sustained precontraction in mouse and human ASM were evaluated. Ca2+ permeant ion channel currents and intracellular Ca2+ concentration were measured. HPLC analysis was employed to determine which compound was responsible for the EESC-induced relaxation. The EESC reversibly inhibited the ACh- and 80 mM K+-induced precontraction. The sustained precontraction depends on Ca2+ influx, and it was mediated by voltage-dependent L-type Ca2+ channels (LVDCCs), store-operated channels (SOCs), TRPC3/STIM/Orai channels. These channels were inhibited by aurantio-obtusin, one component of EESC. When aurantio-obtusin removed, EESC’s action disappeared. In addition, aurantio-obtusin inhibited the precontraction of mouse and human ASM and intracellular Ca2+ increases. These results indicate that Semen cassia-contained aurantio-obtusin inhibits sustained precontraction of ASM via inhibiting Ca2+-permeant ion channels, thereby, which could be used to develop new bronchodilators

    Upregulation of TLR2/4 Expression in Mononuclear Cells in Postoperative Systemic Inflammatory Response Syndrome after Liver Transplantation

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    Background. To explore the relationship between Toll-like rpheral blood mononuclear cells (PBMC) and systemic inflammatory response syndrome (SIRS) in postoperative patients of liver transplantation (LT). Methods. Blood samples of 27 patients receiving LT were collected at T1 (after induction of anaesthesia), T2 (25 minutes after the beginning of anhepatic phase), T3 (3 hours after graft reperfusion), and T4 (24 hours after graft reperfusion). The expression of TLR2/4 on PBMC and serum concentration of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-8 were measured. The patients were divided into SIRS group (n=12) and non-SIRS group (n=15) for analysis. Results. Blood loss and transfusion were higher in the SIRS group than in the non-SIRS group. Both the preanhepatic and anhepatic phase were significantly longer in the SIRS group. The TLR2/4 expression on PBMC as well as serum TNF-α, IL-1β, and IL-8 were significantly higher at T3 and T4 than that at T1 and T2 in the SIRS patients. The expression of TLR4 on PBMC is positively correlated to serum TNF-α, IL-8. Expression of TLR2/4 on PBMC and serum concentrations of TNF-α, IL-1β, did not differ among the 4-time points in non-SIRS patients. Conclusions. Upregulation of TLR2/4 expression on PBMC may contribute to the development of postoperative SIRS during perioperative period of LT

    Downregulation of Lung Toll-Like Receptor 4 Could Effectively Attenuate Liver Transplantation-Induced Pulmonary Damage at the Early Stage of Reperfusion

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    Acute lung injury (ALI) is a severe complication of orthotopic liver transplantation (OLT) with unclear underline mechanism. Toll-like receptor 4 (TLR4) has been identified as a key receptor mediating inflammation. We hypothesized that TLR4-mediated pulmonary inflammation may contribute to development of ALI during OLT. Patients with or without ALI were observed for serum cytokines and expression of TLR4 on peripheral blood polymorphonuclear leukocytes (PMNs). Next, rats which underwent orthotopic autologous liver transplantation (OALT) were divided into sham and model groups. Pulmonary function and the level of TLR4 expression and cytokines were analyzed. Furthermore, the role of TLR4 in OALT-mediated ALI was assessed in rats treated with TLR4-siRNA before OALT. The PMNs TLR4 expression and the serum TNF-α and IL-β level were higher in patients with ALI than those with non-ALI. Interestingly, lung TLR4 expression was significantly increased after 8 hours of OALT with increased levels of TNF-α and IL-β, which lead to lung pathological damage and an increase of lung myeloperoxidase content. Moreover, knockdown of TLR4 reduced lung cytokines release and reversed the above pathologic changes after OALT and finally improved rats’ survival rate. In conclusion, TLR4 overexpression, potentially by stimulating proinflammatory cytokine overproduction, contributes to the development of ALI after OLT

    Protective role of nitric oxide donors on endothelium in ischemia-reperfusion injury: a meta-analysis of randomized controlled trials

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    Abstract Background Decreased bioavailability of nitric oxide (NO) under hypoxic conditions can lead to endothelial dysfunction. NO supplementation may protect endothelial function in ischemia-reperfusion (IR) injury. Therefore, a meta-analysis of randomized controlled trials (RCTs) was performed to verify the protective effect of NO donors on endothelium in IR injury. Methods Medline, Embase, Cochrane Library, and Web of Science databases were searched from inception to April 1, 2023. The specific inclusion criteria were as follows: (1) RCTs; (2) trials comparing NO donors with placebo control groups; and (3) trials reporting the effects of these interventions on vascular endothelial functional outcomes in IR injury. Random-effects models were used to assess pooled effect sizes, which were expressed as standardized mean differences (SMD). Results Seven studies satisfied the inclusion criteria and consisted of a total of 149 participants. NO donors were protective of endothelial function in IR injury (SMD: − 1.60; 95% confidence interval [CI]: − 2.33, − 0.88, P < 0.0001; heterogeneity [I2 = 66%, P = 0.001]). Results of the subgroup analysis showed the following: absence of protective effect of NO donor use following ischemia on endothelial function in IR injury − 1.78 (95% CI: − 2.50, − 1.07) and loss of protective effect on endothelial function after prolonged NO donor use − 0.89 (95% CI: − 2.06, 0.28). Conclusion The short-period use of NO donors before the onset of ischemia can protect endothelial function in IR injury
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