Microscopic mechanism of tunable thermal conductivity in carbon nanotube-geopolymer nanocomposites

Geopolymer has been considered as a green and low-carbon material with great potential application due to its simple synthesis process, environmental protection, excellent mechanical properties, good chemical resistance and durability. In this work, the molecular dynamics simulation is employed to investigate the effect of the size, content and distribution of carbon nanotubes on the thermal conductivity of geopolymer nanocomposites, and the microscopic mechanism is analyzed by the phonon density of states, phonon participation ratio and spectral thermal conductivity, etc. The results show that there is a significant size effect in geopolymer nanocomposites system due to the carbon nanotubes. In addition, when the content of carbon nanotubes is 16.5%, the thermal conductivity in carbon nanotubes vertical axial direction (4.85 W/(mk)) increases 125.6% compared with the system without carbon nanotubes (2.15 W/(mk)). However, the thermal conductivity in carbon nanotubes vertical axial direction (1.25 W/(mk)) decreases 41.9%, which is mainly due to the interfacial thermal resistance and phonon scattering at the interfaces. The above results provide theoretical guidance for the tunable thermal conductivity in carbon nanotube-geopolymer nanocomposites

Production of Ds0∗(2317)D^*_{s0}(2317) and Ds1(2460)D_{s1}(2460) in BB decays as D(∗)KD^{(*)}K and Ds(∗)ηD^{(*)}_s\eta molecules

The molecular nature of $D_{s0}^{\ast}(2317)$ and $D_{s1}(2460)$ have been extensively studied from the perspective of their masses, decay properties, and production rates. In this work, we study the weak decays of $B \to \bar{D}^{(\ast)}D_{s0}^{*}(2317)$ and $B \to \bar{D}^{(\ast)}D_{s1}(2460)$ by invoking triangle diagrams where the $B$ meson first decays weakly into $\bar{D}^{(\ast)}D_{s}^{(\ast)}$ and $J/\psi K$($\eta_{c}K$), and then the $D_{s0}^{\ast}(2317)$ and $D_{s1}(2460)$ are dynamically generated by the final-state interactions of $D_{s}^{(\ast)}\eta$ and $D^{(\ast)}K$ via exchanges of $\eta$ and $D^{(\ast)}$ mesons. The obtained absolute branching fractions of Br$[B \to \bar{D}^{(\ast)}D_{s0}^{*}(2317)]$ are in reasonable agreement with the experimental data, while the branching fractions of Br$[B \to \bar{D}^{(\ast)}D_{s1}(2460)]$ are smaller than the experimental central values by almost a factor of two to three. We tentatively attribute such a discrepancy to either reaction mechanisms missing in the present work or the likely existence of a relatively larger $c\bar{s}$ component in the $D_{s1}(2460)$ wave function.Comment: 17 pages, 4 figure

Rapamycin sensitizes T-ALL cells to dexamethasone-induced apoptosis

<p>Abstract</p> <p>Background</p> <p>Glucocorticoid (GC) resistance is frequently seen in acute lymphoblastic leukemia of T-cell lineage (T-ALL). In this study we investigate the potential and mechanism of using rapamycin to restore the sensitivity of GC-resistant T-ALL cells to dexamethasone (Dex) treatment.</p> <p>Methods</p> <p>Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay. Fluorescence-activated cell sorting (FACS) analysis was used to analyze apoptosis and cell cycles. Western blot analysis was performed to test the expression of the downstream effector proteins of mammalian target of rapamycin (mTOR), the cell cycle regulatory proteins, and apoptosis associated proteins.</p> <p>Results</p> <p>10 nM rapamycin markedly increased GC sensitivity in GC-resistant T-ALL cells and this effect was mediated, at least in part, by inhibition of mTOR signaling pathway. Cell cycle arrest was associated with modulation of G₁-S phase regulators. Both rapamycin and Dex can induce up-regulation of cyclin-dependent kinase (CDK) inhibitors of p21 and p27 and co-treatment of rapamycin with Dex resulted in a synergistic induction of their expressions. Rapamycin did not obviously affect the expression of cyclin A, whereas Dex induced cyclin A expression. Rapamycin prevented Dex-induced expression of cyclin A. Rapamycin had a stronger inhibition of cyclin D1 expression than Dex. Rapamycin enhanced GC-induced apoptosis and this was not achieved by modulation of glucocorticoid receptor (GR) expression, but synergistically up-regulation of pro-apoptotic proteins like caspase-3, Bax, and Bim, and down-regulation of anti-apoptotic protein of Mcl-1.</p> <p>Conclusion</p> <p>Our data suggests that rapamycin can effectively reverse GC resistance in T-ALL and this effect is achieved by inducing cell cycles arrested at G₀/G₁phase and activating the intrinsic apoptotic program. Therefore, combination of mTOR inhibitor rapamycin with GC containing protocol might be an attracting new therapeutic approach for GC resistant T-ALL patients.</p

Advanced Glycation End Products Induce PeroxisomeProliferator-Activated Receptor c Down-Regulation-Related Inflammatory Signals in Human Chondrocytesvia Toll-Like Receptor-4 and Receptor for AdvancedGlycation End Products

Accumulation of advanced glycation end products (AGEs) in joints is important in the development of cartilage destruction and damage in age-related osteoarthritis (OA). The aim of this study was to investigate the roles of peroxisome proliferator-activated receptor γ (PPARγ), toll-like receptor 4 (TLR4), and receptor for AGEs (RAGE) in AGEs-induced inflammatory signalings in human OA chondrocytes. Human articular chondrocytes were isolated and cultured. The productions of metalloproteinase-13 and interleukin-6 were quantified using the specific ELISA kits. The expressions of related signaling proteins were determined by Western blotting. Our results showed that AGEs enhanced the productions of interleukin-6 and metalloproteinase-13 and the expressions of cyclooxygenase-2 and high-mobility group protein B1 and resulted in the reduction of collagen II expression in human OA chondrocytes. AGEs could also activate nuclear factor (NF)-κB activation. Stimulation of human OA chondrocytes with AGEs significantly induced the up-regulation of TLR4 and RAGE expressions and the down-regulation of PPARγ expression in a time- and concentration-dependent manner. Neutralizing antibodies of TLR4 and RAGE effectively reversed the AGEs-induced inflammatory signalings and PPARγ down-regulation. PPARγ agonist pioglitazone could also reverse the AGEs-increased inflammatory signalings. Specific inhibitors for p38 mitogen-activated protein kinases, c-Jun N-terminal kinase and NF-κB suppressed AGEs-induced PPARγ down-regulation and reduction of collagen II expression. Taken together, these findings suggest that AGEs induce PPARγ down-regulation-mediated inflammatory signalings and reduction of collagen II expression in human OA chondrocytes via TLR4 and RAGE, which may play a crucial role in the development of osteoarthritis pathogenesis induced by AGEs accumulation

Excitatory and inhibitory effects of prolactin release activated by nerve stimulation in rat anterior pituitary

<p>Abstract</p> <p>Background</p> <p>A series of studies showed the presence of substantial amount of nerve fibers and their close relationship with the anterior pituitary gland cells. Our previous studies have suggested that aside from the classical theory of humoral regulation, the rat anterior pituitary has direct neural regulation on adrenocorticotropic hormone release. In rat anterior pituitary, typical synapses are found on every type of the hormone-secreting cells, many on lactotrophs. The present study was aimed at investigating the physiological significance of this synaptic relationship on prolactin release.</p> <p>Methods</p> <p>The anterior pituitary of rat was sliced and stimulated with electrical field in a self-designed perfusion chamber. The perfusate was continuously collected in aliquots and measured by radioimmunoassay for prolactin levels. After statistic analysis, differences of prolactin concentrations within and between groups were outlined.</p> <p>Results</p> <p>The results showed that stimulation at frequency of 2 Hz caused a quick enhancement of prolactin release, when stimulated at 10 Hz, prolactin release was found to be inhibited which came slower and lasted longer. The effect of nerve stimulation on prolactin release is diphasic and frequency dependent.</p> <p>Conclusions</p> <p>The present in vitro study offers the first physiological evidence that stimulation of nerve fibers can affect prolactin release in rat anterior pituitary. Low frequency stimulation enhances prolactin release and high frequency mainly inhibits it.</p

2-(2-Hydroxy­ethyl­amino)-3-phenyl-1-benzofuro[3,2-d]pyrimidin-4(3H)-one dichloro­methane hemisolvate

In the title compound, C18H15N3O3·0.5CH2Cl2, the fused ring benzofuro[2,3-d]pyrimidine system is essentially planar [maximum deviation 0.029 (1) Å]. The planes of the pyrimidinone and phenyl rings are nearly perpendicular [dihedral angle = 87.50 (14)°]. The packing of the mol­ecules in the crystal structure is governed mainly by inter­molecular O—H⋯O and N—H⋯O hydrogen-bonding inter­actions and inter­molecular π–π inter­actions between benzofuro[3,2-d]pyrimidine units [the interplanar distances are ca 3.4 and 3.5 Å, and the distances between adjacent ring centroids are in the range 3.64 (1)–3.76 (1) Å]. The dichloromethane solvent molecule lies on a special position

2-Benzyl-6-benz­yloxypyridazin-3(2H)-one

In the title compound, C18H16N2O2, the central pyridazine ring forms dihedral angles of 77.08 (5)° and 84.62 (5)° with the two benzene rings. The dihedral angle between the two benzene rings is 68.18 (4)°. A very weak intra­molecular C—H⋯N hydrogen bond and an intra­molecular C—H⋯π inter­action occur. The crystal structure is stabilized by weak inter­molecular C—H⋯O hydrogen bonds and weak C—H⋯π and π–π stacking inter­actions [centroid–centroid distance = 3.6867 (10) Å]

Output entanglement and squeezing of two-mode fields generated by a single atom

A single four-level atom interacting with two-mode cavities is investigated. Under large detuning condition, we obtain the effective Hamiltonian which is unitary squeezing operator of two-mode fields. Employing the input-output theory, we find that the entanglement and squeezing of the output fields can be achieved. By analyzing the squeezing spectrum, we show that asymmetric detuning and asymmetric atomic initial state split the squeezing spectrum from one valley into two minimum values, and appropriate leakage of the cavity is needed for obtaining output entangled fields

Preoperative ultrasound identification and localization of the inferior parathyroid glands in thyroid surgery

IntroductionThe parathyroid glands are important endocrine glands for maintaining calcium and phosphorus metabolism, and they are vulnerable to accidental injuries during thyroid cancer surgery. The aim of this retrospective study was to investigate the application of high-frequency ultrasound imaging for preoperative anatomical localization of the parathyroid glands in patients with thyroid cancer and to analyze the protective effect of this technique on the parathyroid glands and its effect on reducing postoperative complications.Materials and methodsA total of 165 patients who were operated for thyroid cancer in our hospital were included. The patients were assigned into two groups according to the time period of surgery: Control group, May 2018 to February 2021 (before the application of ultrasound localization of parathyroid in our hospital); PUS group, March 2021 to May 2022. In PUS group, preoperative ultrasound was used to determine the size and location of bilateral inferior parathyroid glands to help surgeons identify and protect the parathyroid glands during operation. We compared the preoperative ultrasound results with the intraoperative observations. Preoperative and first day postoperative serum calcium and PTH were measured in both groups.ResultsOur preoperative parathyroid ultrasound identification technique has more than 90% accuracy (true positive rate) to confirm the location of parathyroid gland compared to intraoperative observations. Postoperative biochemical results showed a better Ca2+ [2.12(0.17) vs. 2.05(0.31), P=0.03] and PTH [27.48(14.88) vs. 23.27(16.58), P=0.005] levels at first day post-operation in PUS group compared to control group. We also found a reduced risk of at least one type of hypoparathyroidism after surgery in control group:26 cases (31.0%) vs. 41 cases (50.6%), p=0.016.ConclusionUltrasound localization of the parathyroid glands can help in the localization, identification and in situ preservation of the parathyroid glands during thyroidectomy. It can effectively reduce the risk of hypoparathyroidism after thyroid surgery