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Abstract: Stearns‐Noechel model was utilized as a primary reference to study color matching principles of digital rotor spun yarn. Three primary colored (red, yellow and blue) cotton fibers were used to spin blended yarns. Spectral reflectance of the two‐component and three‐component samples was measured with data color spectrophotometer. For these samples, the Stearns‐Noechel model parameter M was determined. Four methods were employed to calculate the M value to improve accuracy of the model, 1.Classical method, named as M1; 2.Optimizing the M1 value obtained by the classical method considering the wavelength factor, named as M2; 3.Simplified M2 according to the linear correlation with the wavelength, named as M3; 4. Simplified M2 according to the segmentation correlation with the wavelength, named as M4. The study shows that average color difference of the two‐component decreases from 2.7 to 1.48, and for three‐component samples from 3.32 to 1.66, by using M2 instead of M1. While calculated using M3, the color difference of the two types of samples will be 1.73 and 2.19, correspondingly. This cannot meet color matching needs. As for M4, the average color difference of the two categories will be 1.54 and 1.91, better than the result obtained using M1 and M3, worse than M2. [ABSTRACT FROM AUTHOR]

Abstract: Previous research has demonstrated that diabetes induced learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Sprague–Dawley rats were used in the present study to investigate the effect of streptozotocin (STZ)-induced diabetes on spatial learning and memory with the Morris water maze. The excitability of CA1 pyramidal neurons in hippocampus was also examined. Diabetes impaired spatial learning and memory of rats. Diabetes decreased the membrane excitability of CA1 pyramidal neurons, effects which may contribute to the behavioral deficits. To investigate the further ionic mechanisms, the sodium currents and the potassium currents were detected. Diabetes decreased both transient and persistent sodium currents, and increased both transient and sustained potassium currents, which leads to the reduction of neuron excitability and to the increase of firing accommodation. The results of the present study suggested that sodium and potassium currents contributed to the inhibitory effect of diabetes on neuron excitability, further influencing learning and memory processing. Modulating the ion channels and increasing the membrane excitability are possible candidates for preventing the impairments of diabetes on hippocampal function. [Copyright &y& Elsevier]

Abstract: It has been confirmed that sleep has a key role in learning and memory. Our previous study indicated that paradoxical sleep deprivation (PSD) impairs spatial learning ability of rats, and the decrease in membrane excitability of CA1 pyramidal neurons contributes to deficits in performing a spatial learning task. To investigate the further ionic mechanisms, the persistent sodium currents (I NaP), the hyperpolarization-activated cation current (I h), and their roles in neuron excitability were detected. PSD decreased I NaP and suppressed spike ADP, which leads to the reduction of neuron excitability and to the increase of firing accommodation. In addition, PSD reduced the I h amplitude and the rebound excitability of CA1 pyramidal neurons. The results of the present study suggested that I h and I NaP contributed to the inhibitory effect of PSD on neuron excitability, further influencing learning and memory processing. Modulating the ion channels and increasing the membrane excitability of hippocampal neurons are possible targets for preventing the effects of paradoxical sleep deprivation. [Copyright &y& Elsevier]

Abstract: It has been confirmed that the voltage-gated persistent sodium currents mediate the generation of subthreshold membrane potential oscillations (SMPOs) and contribute to shaping repetitive firing. Our previous study indicated that gabapentin (GBP) administration induced a dose-dependent inhibition of SMPO in chronically compressed dorsal root ganglion (CCD) neurons. To investigate the mechanisms and possible site(s) of action of GBP, the persistent sodium currents (I NaP) were measured and the effects of GBP on I NaP were examined in CCD neurons electrophysiologically in vitro. DRG neurons possess slow TTX-sensitive inactivating sodium currents that significantly contribute to the generation of membrane oscillations by amplifying the resonance behavior. GBP reduced the resonant amplitude of DRG neurons as well as inhibiting the firing and SMPO induced by injection current, which was strongly due to the inhibitory effect on persistent sodium currents. Furthermore, we found that GBP (1–20μM) administration inhibited the persistent sodium currents in dose-dependent manner, while the changes of K+ and Ca2+ current minimally contributed to the effect of GBP on oscillation and resonant behavior of DRG neurons. In contrast, the amplitude and voltage-dependence of transient sodium current were unchanged by GBP. The results suggest that GBP decreased the amplitude of resonance and abolished the SMPO of A-type DRG neurons through the inhibition of I NaP, and thus inhibited the SMPO dependent repetitive and bursting firings. [Copyright &y& Elsevier]

Abstract: Previous research has demonstrated that paradoxical sleep has a key role in learning and memory, and sleep deprivation interferes with learning and memory. However, the mechanism of memory impairment induced by sleep deprivation is poorly understood. The present study investigated the effect of paradoxical sleep deprivation (PSD) on spatial learning and memory using the Morris Water Maze. Effects of PSD on CA1 pyramidal neurons in hippocampus were also examined. PSD impaired spatial learning of rats. PSD induced translocation of Bax to mitochondria and cytochrome c release into the cytoplasm, and decreased the membrane excitability of CA1 pyramidal neurons, effects which may contribute to the deficits in learning behavior. These results may partially explain the mechanism of the effect of PSD on learning. Modulating the excitability of hippocampal neurons and protecting mitochondrial function are possible targets for preventing the effects of paradoxical sleep deprivation. [Copyright &y& Elsevier]

Ectopic spontaneous discharges play a critical role for both initiation and maintenance of the neuropathic pain state. Gabapentin (GBP) has been shown to be effective in animal models of neuropathic pain as well as in chronic pain patients. To investigate the peripheral mechanisms of GBP, the effects of GBP on spontaneous discharges and subthreshold membrane potential oscillation (SMPO) of chronically compressed dorsal root ganglion (DRG) were examined electrophysiolocally in vitro. The rate of spontaneous discharges was transitorily enhanced when GBP was applied to the DRG. When the concentration was under 5microM, only enhanced effect was observed, while spontaneous discharges were completely suppressed when the concentration of GBP was beyond 5microM. The similar doses of GBP blocking the spontaneous discharges failed to block the propagation of impulses by electrical nerve stimulation. Furthermore, we found that the SMPO of injured DRG cells can be selectively abolished by GBP without interrupting spike propagation. The results suggest that the inhibitory effect of GBP on SMPO might be one of the membrane mechanisms of action of GBP. This may partially explain the antinociceptive action of GBP by directly suppression nociceptive afferent input to the spinal cord. [ABSTRACT FROM AUTHOR]

Abstract: Ectopic spontaneous discharges play a critical role for both initiation and maintenance of the neuropathic pain state. Gabapentin (GBP) has been shown to be effective in animal models of neuropathic pain as well as in chronic pain patients. To investigate the peripheral mechanisms of GBP, the effects of GBP on spontaneous discharges and subthreshold membrane potential oscillation (SMPO) of chronically compressed dorsal root ganglion (DRG) were examined electrophysiolocally in vitro. The rate of spontaneous discharges was transitorily enhanced when GBP was applied to the DRG. When the concentration was under 5μM, only enhanced effect was observed, while spontaneous discharges were completely suppressed when the concentration of GBP was beyond 5μM. The similar doses of GBP blocking the spontaneous discharges failed to block the propagation of impulses by electrical nerve stimulation. Furthermore, we found that the SMPO of injured DRG cells can be selectively abolished by GBP without interrupting spike propagation. The results suggest that the inhibitory effect of GBP on SMPO might be one of the membrane mechanisms of action of GBP. This may partially explain the antinociceptive action of GBP by directly suppression nociceptive afferent input to the spinal cord. [Copyright &y& Elsevier]

Abstract: A nonlinear oscillator is established for the rotor-spun composite yarn spinning process. The oscillating frequencies in vertical and horizontal directions are obtained approximately using the variational iteration method. The condition for resonance is obtained. The presented study sheds light on the optimal design of the system. [Copyright &y& Elsevier]

Abstract: A nonlinear dynamic model is proposed for the rotor-spun composite yarn spinning process. The position of a convergent point and the section area can be easily determined using the proposed model. Trajectories and phase diagrams can be obtained for different spinning parameters. [Copyright &y& Elsevier]

Diabetes mellitus is a common metabolic disease in human beings with characteristic symptoms of hyperglycemia, chronic inflammation and insulin resistance. One of the most common complications of early-onset diabetes mellitus is peripheral diabetic neuropathy, which is manifested either by loss of nociception or by allodynia and hyperalgesia. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown the potential of anti-inflammation and modulating neuron excitability. The present study investigated the effects of docosahexaenoic acid (DHA) on the excitability of dorsal root ganglion (DRG) neurons in streptozotocin (STZ)-induced diabetes rats. The effects of DHA on the allodynia and hyperalgesia of diabetic rats were also evaluated. Dietary DHA supplementation effectively attenuated both allodynia and hyperalgesia induced by STZ injection. DHA supplementation decreased the excitability of DRG neurons by decreasing the sodium currents and increasing potassium currents, which may contribute to the effect of alleviating allodynia and hyperalgesia in diabetic rats. The results suggested that DHA might be useful as an adjuvant therapy for the prevention and treatment of painful diabetic neuropathy. [ABSTRACT FROM AUTHOR]

In this paper, a dynamic model coupled with linear and nonlinear stiffness is proposed for nonlinear cushioning packaging system based on critical component. The approximate analytical solution for the nonlinear free vibration of the coupled system is derived by applying He's variational iteration method. And the maximum dropping shock response of the critical component is obtained, based on which, the dropping damage evaluation parameters for cushioning packaging system are predicted, agreeing well with the reported experiment results. The results may lead to thorough understanding of the dropping damage mechanism of packaged products based on critical components. [ABSTRACT FROM AUTHOR]

Abstract: A dynamic model is proposed for a tangent cushioning packaging system based on critical components. Conditions for resonance are obtained by applying He’s variational iteration method, which should be avoided in the cushioning packaging design. The results help us to understand the dropping damage mechanism of packaged products based on critical components. [Copyright &y& Elsevier]

Abstract: Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. The present study investigated the effect of streptozotocin (STZ)-induced diabetes on spatial learning and memory using the Morris Water Maze. The effects of diabetes on CA1 pyramidal neurons in hippocampus were also examined. Diabetes impaired spatial learning and memory of rats. Diabetes induced the apoptosis of neurons and translocation of Bax from cytoplasm to mitochondria. On the contrary, diabetes induced cytochrome c release into the cytoplasm from mitochondria. Release of Cyt-c from mitochondria into cytoplasm may play a role in apoptosis of the CA1 pyramidal neurons, which resulted in a decrease of the number of neurons in hippocampus and impaired the performance function. These results partially explain the mechanism of the effect of diabetes on learning and memory. To protect mitochondrial function is possible candidate for preventing the impairments of diabetes on hippocampal function. [Copyright &y& Elsevier]

Abstract: A new chelating radical ligand NIT-1′-MeBzIm (1) (NIT-1′-MeBzIm=2-{2′-[(l’-methyl)benzimidazolyl]}-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide) and three corresponding complexes [M(NIT-1′-MeBzIm)2(NO3)(CH3OH)]·(NO3)(CH3OH) (M=Ni (2), Co (3)), [Zn(NIT-1′-MeBzIm)2(CH3OH)2]·(ClO4)2(H2O)2(CH3OH) (4) have been prepared and structurally characterized by X-ray diffraction method and variable-temperature magnetic susceptibility measurements. In the crystal structures, radical 1, complexes 3 and 4 crystallize isomorphously in monoclinic, with the space groups are P2(1)/n, P2(1)/c, and P2(1), respectively. Complex 2 crystallizes in orthorhombic space group Pna2(1). The metal ions of the three complexes embed in distorted octahedron geometry centers and coordinated by two NIT-1′-MeBzIm radicals from the equatorial positions to form trans configuration, the axial positions are occupied by one methanol molecule and one nitrate anion for 2 and 3, but by two methanol molecules for 4. Magnetic measurement demonstrates that the intramolecular exchange couplings in 2 and 3 are antiferromagnetic with J =−41.25 and −38.1cm−1, where the spin Hamiltonian is defined as Ĥ =−2J(Ŝ rad1 Ŝ M + Ŝ M Ŝ rad2) based on the molecular structure of radical-metal-radical, while that in 4 is weak ferromagnetic with J =1.65cm−1 where the spin Hamiltonian is defined as Ĥ =−2JŜ 1 Ŝ 2 within the complexes. Intermolecular exchange couplings in 1 is also weak ferromagnetic with J =1.32cm−1 where the spin Hamiltonian is defined as Ĥ =−2JŜ 1 Ŝ 2 between radical and radical. Compounds 2–4 exhibit intermolecular antiferromagnetic interaction with the zJ′=−0.52cm−1, θ =−0.75K and zJ′=−0.49cm−1 for compounds 2, 3 and 4, respectively, which should ascribe to the weak interactions. The crystal structures for 1–4 have intermolecular hydrogen bonding interactions (and π–π piling interactions for 1 and 3) which form the single crystals into 1-D, 2-D, 3-D structures and seems to play an important role in molecular packing and in magnetic coupling. [Copyright &y& Elsevier]

Two series of proteolysis targeting chimeras (PROTACs) containing the phthalimide degrons with different linker were identified. Compound A16 displayed the most potent inhibition against LNCaP and showed excellent AR degradation efficacy at 30 μM. [Display omitted] • Two series of novel PROTACs and androgen receptor degradation efficacy have been discovered. • The best compound A16 displayed excellent binding affinity and AR degradation activity. • Molecular docking analysis illustrates the possible dual mechanism actions of these compounds with AR and E3 ligase. As a continuation of our research on developing potent and potentially safe androgen receptor (AR) degrader, a series of novel proteolysis targeting chimeras (PROTACs) containing the phthalimide degrons with different linker were designed, synthesized and evaluated for their AR degradation activity against LNCaP (AR+) cell line. Most of the synthesized compounds displayed moderate to satisfactory AR binding affinity and might lead to antagonist activity against AR. Among them, compound A16 exhibited the best AR binding affinity (85%) and degradation activity against AR. Due to the strong fluorescence properties of pomalidomide derivatives, B10 was found to be effectively internalized and visualized in LNCaP (AR +) cells than PC-3 (AR-) cells. Moreover, the molecular docking of A16 with AR and the active site of DDB1-CRBN E3 ubiquitin ligase complex provides guidance to design new PROTAC degrons targeting AR for prostate cancer therapy. These results represent a step toward the development of novel and improved AR PROTACs. [ABSTRACT FROM AUTHOR]

Abstract As a continuation of our research on developing potent and potentially safe anti-proliferative agents, two series of novel Jiyuan Oridonin A-1,2,3-triazole-azole hybrids were designed, synthesized and evaluated for their anti-proliferative activity against four selected cancer cell lines (MGC-803, MCF-7, PC-3, Eca-109). Some compounds with better growth inhibitory effects were chosen to carry out further studies in A549 and SMMC-7721. Most of the synthesized compounds exhibited moderate to good activity against all the cancer cell lines selected. Particularly, the most active agent 8b showed high potency against human cancer cells with IC 50 ranging from 0.2 ± 0.0 to 5.0 ± 0.9 μM. Cellular mechanism studies elucidated compound 8b arrests cell cycle at G1 phase and induce a strong apoptotic response in SMMC-7721 cells. Furthermore, 8b could inhibit the colony formation and migration via Wnt signaling pathway in SMMC-7721 cells. For all these reasons, compound 8b holds promising potential as anti-proliferative agent. Graphical abstract A focused library of Jiyuan Oridonin A-1,2,3-triazole-azole derivatives were designed and synthesis. Compound 8b displayed the most potent inhibition against SMMC-7721 cells, inhibited colony formation and migration of SMMC-7721, as well as induced apoptosis. Image 1 Highlights • Jiyuan Oridonin A-1,2,3-triazole-azole hybrids inhibited proliferation of cancer cells. • Compound 8b exerted the most potent and broad-spectrum antiproliferative activity. • Compound 8b inhibited growth and migration of SMMC-7721 cells and induced apoptosis. [ABSTRACT FROM AUTHOR]

Brain volume decrease in the anterior cingulate cortex (ACC) after lead (Pb) exposure has been linked to persistent impairment of attention behavior. However, the precise structural change and molecular mechanism for the Pb-induced ACC alteration and its contribution to inattention have yet to be fully characterized. The present study determined the role of miRNA regulated synaptic structural and functional impairment in the ACC and its relationship to attention deficit disorder in Pb exposed mice. Results showed that Pb exposure induced presynaptic impairment and structural alterations in the ACC. Furthermore, we screened for critical miRNA targets responsible for the synaptic alteration. We found that miR-130, which regulates presynaptic vesicle releasing protein SNAP-25, was responsible for the presynaptic impairment in the ACC and attention deficits in mice. Blocking miR-130 function reversed the Pb-induced decrease in the expression of its presynaptic target SNAP-25, leading to the redistribution of presynaptic vesicles, as well as improved presynaptic function and attention in Pb exposed mice. We report, for the first time, that miR-130 regulating SNAP-25 mediates Pb-induced presynaptic structural and functional impairment in the ACC along with attention deficit disorder in mice. [Display omitted] • Low level lead (Pb) exposure is related to the occurrence of attention deficit. • Pb exposure-induced presynaptic structural and functional alteration in anterior cingulate cortex (ACC). • miR-130/SNAP-25 axis is responsible for Pb induced presynaptic structural change. • Blocking miR-130 can alleviate Pb-induced presynaptic alteration and attention deficit. [ABSTRACT FROM AUTHOR]

One of the most common complications of early-onset diabetes mellitus is peripheral diabetic neuropathy, which is manifested either by loss of nociception or by allodynia and hyperalgesia. Diabetes mellitus is a common metabolic disease in human beings with characteristic symptoms of hyperglycemia, chronic inflammation and insulin resistance. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown anti-inflammatory role in various experimental conditions. The present study investigated the effects of fish oil supplementation on the inflammation in the dorsal root ganglion (DRG) of streptozotocin (STZ)-induced diabetes rats. The effects of diabetes and fish oil treatment on the allodynia and hyperalgesia were also evaluated. Dietary fish oil effectively attenuated both allodynia and hyperalgesia induce by STZ injection. Along with the behavioral findings, DRG from fish oil-treated diabetic rats displayed a decrease in inflammatory cytokines and the expression of nuclear factor-κB (NF-κB) compared with untreated diabetic rats. Fish oil supplementation also increased the phosphorylation of AKT in DRG of diabetic rats. These results suggested that dietary fish oil-inhibited allodynia and hyperalgesia in diabetic rats may stem from its anti-inflammatory potential by regulating NF-κB and AKT. Fish oil might be useful as an adjuvant therapy for the prevention and treatment of diabetic complications. [ABSTRACT FROM AUTHOR]

Dietary ratios of n-3/n-6 polyunsaturated fatty acids (PUFAs) have been implicated in controlling markers of metabolic disorders, including obesity, insulin resistance (IR), inflammation, and lipid profiles, which are also presumed to be partly related to type 2 diabetes mellitus (T2DM). However, molecular mechanisms of the different PUFAs related to metabolic disorders have not been systematically addressed. The present study aimed to investigate the impact of dietary n-3/n-6 PUFA ratios on obesity and IR and, further, to determine the underlying mechanisms. For 16 weeks, 32 SD male rats, randomly divided into four groups (n = 8 per group), received one of the following diets: normal chow, high saturated fatty acid (SFA), high n-3/n-6 PUFA ratio (1∶1, PUFA1:1), or low n-3/n-6 PUFA ratio (1∶4, PUFA1:4). Following the experimental diet period, metabolic parameters related to obesity and IR were measured. Compared to SFA diet-fed rats, PUFA1:1 diet-fed rats exhibited decreased body and visceral fat weight, lowered blood lipids, and improved glucose tolerance and insulin sensitivity. Interestingly, these changes were accompanied with decreased expression levels of circulating pro-inflammatory cytokines, including tumor necrosis factor α, interleukin-6, and C-reactive protein. Moreover, the TLR4 protein and mRNA levels were markedly down-regulated by PUFA1:1 compared with SFA; however, PUFA1:4 diet-fed rats failed to exhibit these changes. Cumulatively, our data highlight a role for a PUFA1:1 diet in the prevention of obesity and related metabolic disorders by suppressing the activation of TLR4, a critical modulator of pro-inflammatory cytokines. [Copyright &y& Elsevier]

Abstract: Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. The present study investigated the effects of fish oil supplementation on the neuron apoptosis in the hippocampus of streptozotocin (STZ)-induced diabetes rats. The effects of diabetes and fish oil treatment on the spatial learning and memory were also evaluated using the Morris Water Maze. Diabetes impaired spatial learning and memory of rats. Diabetes increased the expression of Bax and caspase-3, which led the apoptosis of the CA1 pyramidal neurons, and further contributed to the deficits in learning and memory processing. Fish oil dietary supplementation in diabetic rats conducts neuron-protective function through an anti-apoptotic pathway and significantly improves the ability of learning and memory. These results partially explain the mechanism of the effect of diabetes and fish oil treatment on learning and memory, supporting a potential role for fish oil as an adjuvant therapy for the prevention and treatment of diabetic complications. [Copyright &y& Elsevier]

Targeted protein degradation using small molecules is a novel strategy for drug development. In order to solve the problem of drug resistance in the treatment of prostate cancer, proteolysis-targeting chimeras (PROTAC) was introduced into the design of anti-prostate cancer derivatives. In this work, we synthesized two series of selective androgen receptor degraders (SARDs) containing the hydrophobic degrons with different linker, and then investigated the structure-activity relationships of these hybrid compounds. Most of the synthesized compounds exhibited moderate to good activity against all the cancer cell lines selected. Among them, compound A9 displayed potent inhibitory activity against LNCaP prostate cancer cell line with IC 50 values of 1.75 μM, as well as excellent AR degradation activity. Primary mechanism studies elucidated compound A9 arrested cell cycle at G0/G1 phase and induced a mild apoptotic response in LNCaP cells. Further study indicated that the degradation of AR was mediated through proteasome-mediated process. For all these reasons, compound A9 held promising potential as anti-proliferative agent for the development of highly efficient SARDs for drug-resistance prostate cancer therapies. Two series of selective androgen receptor degraders (SARDs) containing the hydrophobic degrons with different linker were identified. Compound A9 displayed the most potent inhibition against LNCaP and showed excellent AR degradation efficacy. Image 1 • Two series of novel SARDs with hydrophobic tagging have been discovered. • The best compound A9 displayed potent inhibitory activity against LNCaP cell lines and excellent AR degradation activity. • Primary mechanism study indicated that the degradation of AR is mediated throughproteasome-mediated process. [ABSTRACT FROM AUTHOR]

As our research focus on anticancer drugs, two series of novel derivatives of Flexicaulin A (FA), an ent -kaurene diterpene, condensation with amino acid trifluoroacetate were synthesized, and their anti-proliferative activity against four human cancer cell lines (TE-1, MCF-7, A549 and MGC-803) were evaluated. Compared with FA, the anticancer activity and solubility of most derivatives were significantly improved. Among them, compound 6d had the best activity, and its IC 50 value against Esophageal cancer cells (TE-1) was up to 0.75 μM. Subsequent cellular mechanism studies showed that compound 6d could inhibit the proliferation of cancer cells, the formation of cell colonies, and increase the level of ROS on TE-1 cells. In addition, 6d could up-regulate the expressions of SAPK/JNK pathway-associated proteins (p-ASK1, p-MKK4 and p-JNK) and pro-apoptotic proteins (Bak, Bad and Noxa), remarkably increase the ratio of Bax to Bcl-2 and activate Cleaved Caspase-3/9/PARP. These results indicate that compound 6d induces apoptosis through the ROS/JNK/Bcl-2 pathway and holds promising potential as an anti-proliferative agent. The schematic diagram shown the possible pathway for 6d induced apoptosis on TE-1 cells. Image 1 • Two series of novel derivatives of Flexicaulin A were discovered as potential anti-proliferative agent. • Most of the derivatives showed improved solubility and enhanced anti-proliferative activity. • Compound 6d exerted the best anti-proliferative activity against TE-1 cells. • Compound 6d could inhibit the formation of cell colonies and increase the level of ROS on TE-1 cells. • Compound 6d could induce cell apoptosis of TE-1 cells through the ROS/JNK/Bcl-2 pathway. [ABSTRACT FROM AUTHOR]