Glutamatergic neurons in the paraventricular hypothalamic nucleus regulate isoflurane anesthesia in mice.

The glutamatergic-mediated excitatory system in the brain is vital for the regulation of sleep-wake and general anesthesia. Specifically, the paraventricular hypothalamic nucleus (PVH), which contains mainly glutamatergic neurons, has been shown to play a critical role in sleep-wake. Here, we sought to explore whether the PVH glutamatergic neurons have an important effect on the process of general anesthesia. We used c-fos staining and in vivo calcium signal recording to observe the activity changes of the PVH glutamatergic neurons during isoflurane anesthesia and found that both c-fos expression in the PVH and the calcium activity of PVH glutamatergic neurons decreased in isoflurane anesthesia and significantly increased during the recovery process. Chemogenetic activation of PVH glutamatergic neurons prolonged induction time and shortened emergence time from anesthesia by decreasing the depth of anesthesia. Using chemogenetic inhibition of PVH glutamatergic neurons under isoflurane anesthesia, we found that inhibition of PVH glutamatergic neurons facilitated the induction process and delayed the emergence accompanied by deepening the depth of anesthesia. Together, these results identify a crucial role for PVH glutamatergic neurons in modulating isoflurane anesthesia.

Syndiospecific Copolymerization of Styrene with para-Methoxystyrene Catalyzed by Functionalized Fluorenyl-Ligated Rare-Earth Metal Complexes.

The development of efficient catalysts for the copolymerization of nonpolar monomers with polar monomers remains a great challenging task in polymer synthesis. A one-pot reaction of anhydrous LnCl3 with pyridyl-methylene-functionalized octamethylfluorenyl lithium OctFlu-CH2PyLi in a 1:1 molar ratio, followed by alkylation with 2 equiv of LiCH2SiMe3 in THF afforded the fluorenyl-ligated rare-earth metal bis(alkyl) complexes (OctFlu-CH2Py)Ln(CH2SiMe3)2(THF) [Ln = Sc (1), Y (2)]. Both complexes were isolated as neutral species and were characterized by NMR spectrum and elemental analysis. Complex 2 was subjected to single-crystal X-ray diffraction, which showed that the whole modified fluorenyl ligand was coordinated to Y3+ in the η5/κ1 mode to form a constrained geometry configuration. In the presence of excess AliBu3, and on activation with 1 equiv of [Ph3C][B(C6F5)4] in toluene, complexes 1 and 2 became active for both styrene (St) and para-methoxystyrene (pMOS) polymerization, giving polymers with high syndiotacticity (rrrr > 99%) without solvent extraction. Moreover, the ternary catalyst system composed of complex 2/AliBu3/[Ph3C][B(C6F5)4] was highly effective for the syndiospecific copolymerization of styrene with pMOS, producing random copolymers with high molecular weights and narrow molecular weight distributions. The contents of pMOS in the copolymers could be easily tuned in a wide range (11-93 mol %) by simply changing the pMOS-to-St feed ratios.

Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.

BACKGROUND: Neuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models. METHODS: We first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and IL-1ß. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays. RESULTS: Our findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL-6, IL-1ß and TNF-α in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats. CONCLUSION: DLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.

Icariin, a flavonoid with anti-cancer effects, alleviated paclitaxel-induced neuropathic pain in a SIRT1-dependent manner.

Background One of the most common side effects of paclitaxel was dosage-dependently painful neuropathy. Various reports indicated that spinal neuroinflammation was involved in paclitaxel-induced neuropathic pain. This study investigated the effect of icariin on paclitaxel-induced neuroinflammation and peripheral neuropathy in rats. Methods Two parts were included in this study. In part one, the effect of icariin on paclitaxel-induced neuropathic pain was investigated. Mechanical thresholds were measured as primary outcomes. Production of proinflammatory factors (tumor necrosis factor-α, interleukin-1 ß, and interleukin-6), activation of nuclear factor-κB (NF-κB(p65)) signal, and activation of astrocytes were detected as secondary outcomes. Spinal Sirtuin 1 (SIRT1) expression, H4 acetylation, and NAD+ content were measured to investigate the effect of icariin on spinal SIRT1 signal pathway. In part two, the role of SIRT1 signal on icariin-induced effect in rats was investigated, and EX527, a SIRT1 inhibitor, was employed. Results The results showed paclitaxel treatment induced significant decrease in mechanical thresholds. Paclitaxel treatment also induced NF-κB(p65) activation and upregulation of proinflammatory factors (TNF-α, IL-1ß, and IL-6). Paclitaxel also induced astrocyte activation in the spinal cord. However, 100 mg/kg icariin treatment significantly alleviated paclitaxel-induced mechanical allodynia and spinal neuroinflammation. Furthermore, icariin treatment dosage-dependently reversed paclitaxel-induced SIRT1 downregulation and H4 acetylation. EX527, a selective SIRT1 inhibitor, completely reversed icariin-induced anti-neuroinflammation and anti-allodynia effects in paclitaxel-induced neuropathic pain rats. Conclusions This meant that spinal SIRT1 activation was involved in icariin-induced effects in paclitaxel-induced neuropathic pain rats. Icariin could be a potential agent for the treatment of paclitaxel-induced neuropathic pain.

Investigating the Thermal Stability of Organic Thin-Film Transistors and Phototransistors Based on [1]-Benzothieno-[3,2-b]-[1]-benzothiophene Dimeric Derivatives.

Two new highly thermally stable [1]benzothieno[3,2-b][1]benzothiophene (BTBT) dimeric derivatives, namely 1,4-bis([1]benzothieno[3,2-b][1]benzothiophene-2-yl)benzene (BTBT-Ph-BTBT) and 4,4'-bis([1]benzothieno[3,2-b][1]benzothiophene-2-yl)-1,1'-biphenyl (BTBT-DPh-BTBT), were synthesized by combining two simple fragment structures. Compared to the monomer compound 2-phenyl[1]benzothieno[3,2-b][1]benzothiophene (Ph-BTBT, µmax =3.4×10-2  cm2 V-1 s-1 ), the organic thin-film transistors (OTFTs) based on BTBT-Ph-BTBT and BTBT-DPh-BTBT showed significantly higher mobility (up to 2.5 and 3.6 cm2 V-1 s-1 for BTBT-Ph-BTBT and BTBT-DPh-BTBT, respectively). The mobility of OTFTs based on BTBT-Ph-BTBT was kept at a high value (2.4×10-1  cm2 V-1 s-1 ) after the devices were thermally annealed at 350 °C. Furthermore, the organic phototransistors (OPTs) based on BTBT-Ph-BTBT and BTBT-DPh-BTBT displayed high photosensitivities in a range of 250-400 nm with a low intensity, making these materials potentially applicable for sensitive optoelectronic devices.

α-Asarone Alleviated Chronic Constriction Injury-Induced Neuropathic Pain Through Inhibition of Spinal Endoplasmic Reticulum Stress in an Liver X Receptor-Dependent Manner.

BACKGROUND: Neuropathic pain is an intractable and complex disease. Recent studies have shown a close relationship between endoplasmic reticulum (ER) stress and neuropathic pain. Here, we investigated the effect of α-asarone, an ER stress inhibitor, on chronic constriction injury (CCI)-induced neuropathic pain. METHODS: Two parts were included in this study. In part 1, rats were assigned to 7 groups: the sham group, the sham + α-asarone 20 mg/kg group, the CCI group, the CCI + vehicle group, the CCI + α-asarone 5 mg/kg group, the CCI + α-asarone 10 mg/kg group, and the CCI + α-asarone 20 mg/kg group. After surgery, the rats were treated with α-asarone or normal saline daily. Pain thresholds were measured, and samples of the L3-6 spinal cord were taken for western blotting and immunofluorescence on day 7. In part 2, rats were intrathecally implanted with PE-10 tubes and divided into 4 groups: the CCI + α-asarone 20 mg/kg group, the CCI + α-asarone 20 mg/kg + vehicle group, the CCI + α-asarone 20 mg/kg + SR9243 group, and the CCI group. Five rats in each group were separated for behavioral tests 1 hour after intrathecal injection. The rest of them were killed for western blotting on day 7. RESULTS: In this study, CCI surgery significantly induced mechanical allodynia and thermal hyperalgesia. CCI surgery significantly induced activation of ER stress (PERK-eIF2α, IRE1α, CHOP, and XBP-1s) in rats. However, treatment with 20 mg/kg of α-asarone significantly alleviated CCI-induced activation of ER stress. Behavioral results showed that daily treatment with 20 mg/kg of α-asarone significantly alleviated CCI-induced nociceptive behaviors, on day 7 (mechanical allodynia, P = .016, 95% confidence interval, 0.645-5.811; thermal hyperalgesia, P = .012, 95% confidence interval, 0.860-6.507). Furthermore, α-asarone induced upregulated expression of liver X receptor ß (LXRß) and downstream proteins in the spinal cord. The LXR antagonist SR9243 completely inhibited the anti-ER stress and antinociceptive effects of α-asarone in rats. CONCLUSIONS: α-Asarone relieved CCI-induced neuropathic pain in an LXR-dependent manner. α-Asarone may be a potential agent for treatment of neuropathic pain.

Systemic LPS resulted in a transient hippocampus malfunction but a prolonged corpus callosum injury.

BACKGROUND: To investigate the effect of systemic lipopolysaccharide (LPS) on function of hippocampus and corpus callosum (CC) in adult rats. METHODS: Adult rats with mature white matter tract were divided into systemic LPS and saline injection groups. Animal were euthanized following 3 daily injections (day 3) and 3-day after cessation of injections (day 6). At both time points, hippocampal long term potentiation (LTP) and CC compound action potentials (CAP) were recorded, beta amyloid precursor protein (ß-APP) level in CC tissue was measured by Western blot, and microglia activation was examined by immunostaining and proportional area analysis. RESULTS: Systemic LPS significantly decreased amplitude of both post tetanic potentiation (PTP) and LTP at day 3, but PTP and LTP turned to be normal at day 6. CAP was significantly declined at day 3 but was further declined at day 6. The ß-APP levels in CC tissues of LPS injected rats were significantly higher than that of saline group at both time-points. Interestingly, proportional area measurement disclosed that microglial areas in both hippocampus and CC significantly expanded at day3, but at the day 6, microglial area decreased in hippocampus but further increased in CC. CONCLUSION: Systemic LPS resulted in a transient hippocampus malfunction but a prolonged CC injury. Microglia activation may correlate with such LPS induced white matter injury.

Endogenous CBS-H2S Pathway Contributes to the Development of CCI-Induced Neuropathic Pain.

Studies showed a complex relationship between hydrogen sulfide (H2S) and neuropathic pain. In this study, the relationship between endogenous CBS-H2S pathway in L4-6 spinal cord and neuropathic pain was explored. A total of 163 adult Kunming mice were used in this study. CBS expression and H2S formation in L4-6 spinal cord were detected in the development of neuropathic pain firstly. Then, effect of AOAA, an CBS inhibitor, on treatment of neuropathic pain by chronic construction injury surgery (CCI) was detected. Pain thresholds and activation of NF-κB(p65), ERK1/2 and CREB were measured as biomarks of neuropathic pain. Results showed that CCI surgery significantly upregulated protein expression of CBS and H2S formation. Correlation analysis showed pain thresholds had negative relationships with protein expression of CBS and H2S formation. Treatment with AOAA, a CBS inhibitor, inhibited CCI-induced upregulation of CBS expression and H2S formation (P < 0.05). Further, AOAA significantly decreased activation of NF-κB(p65), ERK1/2 and CREB pathway, and reversed CCI-induced allodynia (P < 0.05). This indicated that CBS-H2S pathway promoted the development of neuropathic pain. CBS-H2S pathway could be a promising target for treatment of neuropathic pain.

Efficacy of a single low dose of esketamine after childbirth for mothers with symptoms of prenatal depression: randomised clinical trial.

OBJECTIVE: To determine whether a single low dose of esketamine administered after childbirth reduces postpartum depression in mothers with prenatal depression. DESIGN: Randomised, double blind, placebo controlled trial with two parallel arms. SETTING: Five tertiary care hospitals in China, 19 June 2020 to 3 August 2022. PARTICIPANTS: 364 mothers aged ≥18 years who had at least mild prenatal depression as indicated by Edinburgh postnatal depression scale scores of ≥10 (range 0-30, with higher scores indicating worse depression) and who were admitted to hospital for delivery. INTERVENTIONS: Participants were randomly assigned 1:1 to receive either 0.2 mg/kg esketamine or placebo infused intravenously over 40 minutes after childbirth once the umbilical cord had been clamped. MAIN OUTCOME MEASURES: The primary outcome was prevalence of a major depressive episode at 42 days post partum, diagnosed using the mini-international neuropsychiatric interview. Secondary outcomes included the Edinburgh postnatal depression scale score at seven and 42 days post partum and the 17 item Hamilton depression rating scale score at 42 days post partum (range 0-52, with higher scores indicating worse depression). Adverse events were monitored until 24 hours after childbirth. RESULTS: A total of 364 mothers (mean age 31.8 (standard deviation 4.1) years) were enrolled and randomised. At 42 days post partum, a major depressive episode was observed in 6.7% (12/180) of participants in the esketamine group compared with 25.4% (46/181) in the placebo group (relative risk 0.26, 95% confidence interval (CI) 0.14 to 0.48; P<0.001). Edinburgh postnatal depression scale scores were lower in the esketamine group at seven days (median difference -3, 95% CI -4 to -2; P<0.001) and 42 days (-3, -4 to -2; P<0.001). Hamilton depression rating scale scores at 42 days post partum were also lower in the esketamine group (-4, -6 to -3; P<0.001). The overall incidence of neuropsychiatric adverse events was higher in the esketamine group (45.1% (82/182) v 22.0% (40/182); P<0.001); however, symptoms lasted less than a day and none required drug treatment. CONCLUSIONS: For mothers with prenatal depression, a single low dose of esketamine after childbirth decreases major depressive episodes at 42 days post partum by about three quarters. Neuropsychiatric symptoms were more frequent but transient and did not require drug intervention. TRIAL REGISTRATION: ClinicalTrials.gov NCT04414943.

A new low-bandgap polymer containing benzene-fused quinoxaline: significantly enhanced performance caused by one additional benzene ring.

Two new alkoxy-substituted quinoxaline (Qx)-based copolymers, PBDTQx and PBDTPz, are designed and synthesized. The only difference between these two polymers is that two methyl groups of the Qx are replaced by one additional fused benzene ring. The UV-Vis absorptions, thermal stability, energy levels, field-effect carrier mobility, and photovoltaic characteristics of the two copolymers are systematically evaluated to understand the relationships between the polymer structure at the molecular level and the photovoltaic performances. Photovoltaic cells based on the PBDTPz with a structure of ITO/PEDOT:PSS/Polymer:PC(71) BM/PEO/Ca/Al exhibit a promising efficiency of 4.40%, while that of PBDTQx is relatively much poorer.

Low-dose esketamine with sufentanil for postcesarean analgesia in women with gestational diabetes mellitus: a prospective, randomized, double-blind study.

Background: Pregnant women with gestational diabetes mellitus (GDM) require more analgesics after cesarean delivery than those who do not have GDM. Uncontrolled pain following cesarean delivery is a major problem in women with GDM. We investigate the efficacy of low-dose esketamine combined with sufentanil intravenous patient-controlled analgesia (PCA)for postcesarean analgesia in women with GDM. Methods: One hundred forty pregnant women with GDM were enrolled participate in this randomized controlled trial and were randomized into two groups (70 in each group). The esketamine (S) group was given esketamine +sufentanil + ondansetron, and the control (C) group was given sufentanil +ondansetron. The primary outcome is sufentanil consumption at 24 hours postoperatively, the secondary outcomes are sufentanil consumption at 6 hours postoperatively, pain scores at 6, 24 and 48 hours postoperatively. Results: Compared with group C, group S had significantly lower sufentanil consumption at 6 and 24 hours postoperatively (P= 0.049 and P<0.001), significantly lower activities VAS(pain during activities)scores at 6 hours postoperatively, rest and activities VAS (pain at rest and pain during activities)scores at 24 hours postoperatively, and activities VAS scores at 48 hours postoperatively(P=0.022, P =0.002, P=0.001 and P=0.007). Compared to group C, the time to bowel function return was significantly shorter in group S. There was no significant difference in rest VAS (pain at rest) scores at 6 and 48 hours postoperatively (P>0.05). The time to first lactation was not significantly different between the two groups (P>0.05). There was no significant difference in neonatal neurobehavioral scores between the two groups (P>0.05). Conclusion: Compared to sufentanil PCA, adding low dose of esketamine significantly reduced the consumption of sufentanil while providing equally effective post cesarean analgesia in the patients with gestational diabetes.

Dual Targeting of Autophagy and NF-κB Pathway by PPARγ Contributes to the Inhibitory Effect of Demethoxycurcumin on NLRP3 Inflammasome Priming.

BACKGROUND: Demethoxycurcumin (DMC), a natural derivative of curcumin, has anti-inflammatory activities. However, the mechanism has not been fully elucidated. OBJECTIVE: The aim of the current study was to investigate the role of DMC on NLRP3 inflammasome priming. METHODS: Protein expression was quantified by western blotting. Inflammatory cytokines were measured by ELISA. Autophagosomes were evaluated by transmission electron microscopy. RESULTS: DMC inhibited LPS-stimulated NLRP3, pro-caspase-1, and pro-IL-1ß expression. Meanwhile, DMC diminished NLRP3-dependent IL-1ß maturation, caspase-1 activation, IL-1ß, and IL-18 production caused by LPS plus ATP. Moreover, DMC induced autophagy and autophagy inhibitor 3-MA abrogated the role of DMC on NLRP3 inflammasome priming and subsequent activation. DMC also inhibited LPS-stimulated phosphorylation and nuclear translocation of p65 NF-κB. Additionally, DMC significantly increased the PPARγ expression, and the effects of DMC in NF- κB inhibition, autophagy, and NLRP3 inflammasome priming were abrogated by specific PPARγ antagonist T0070907. CONCLUSION: The evidence presented here has confirmed that DMC increases PPARγ expression, resulting in autophagy and NF-κB inhibition, and subsequently inhibits LPS-induced NLRP3 inflammasome priming and subsequent activation.

Bexarotent Attenuated Chronic Constriction Injury-Induced Spinal Neuroinflammation and Neuropathic Pain by Targeting Mitogen-Activated Protein Kinase Phosphatase-1.

It is widely accepted that neuroinflammation in the spinal cord contributes to the development of central sensitization in neuropathic pain. Mitogen-activated protein kinase (MAPK) activation plays a vital role in the development of neuroinflammation in the spinal cord. In this study, we investigated the effect of bexarotene (bex), a retinoid X receptor agonist, on MAPKs activation in chronic constriction injury (CCI)-induced neuropathic pain. The data showed that daily treatment with bex 50 mg/kg significantly alleviated CCI-induced nociceptive hypersensitivity in rats. Bex 50 mg/kg/day inhibited CCI-induced MAPKs (p38MAPK, ERK1/2, and JNK) activation and upregulation of proinflammatory factors (IL-1ß, tumor necrosis factor-α and IL-6). Bex also reversed CCI-induced microglia activation in the ipsilateral spinal cord. Furthermore, bex treatment significantly upregulated MKP-1 in the spinal cord. These effects were completely abrogated by MKP-1 inhibitor BCI. These results indicated that bex relieved CCI-induced neuroinflammation and neuropathic pain by targeting MKP-1. Therefore, bex might be a potential agent for the treatment of neuropathic pain. PERSPECTIVE: Bex could relieve neuropathic pain behaviors in animals by reversing MKP-1 downregulation and MAPKs activation in the spinal cord. Therapeutic applications of bex may be extended beyond cutaneous T-cell lymphoma.

An ionic molecular glass as electron injection layer for efficient polymer light-emitting diode.

An ionic molecular glass based on a dendronized monoammonium salt has been facilely synthesized and utilized as an interfacial electron-injection layer in a light-emitting diode (LED). The characterization of a yellow-green LED that involves an Al cathode and a thin layer of the new compound spin cast from a methanol solution has shown device performances comparable to those obtained with a Ba/Al cathode. Photovoltaic measurements under white light irradiation reveal that a thin layer of the new compound can significantly increase the built-in potential and thus facilitate electron injection from an Al cathode. Furthermore, it is interesting to observe that the new ionic salt could undergo reorganization on the emissive conjugated polymer layer, which leads to the formation of nearly uniform nanoaggregates.

Low-Voltage, High-Performance Flexible Organic Field-Effect Transistors Based on Ultrathin Single-Crystal Microribbons.

Organic field-effect transistors (OFETs) have acquired increasing attention because of their wide range of potential applications in electronics; nevertheless, high operating voltage and low carrier mobility are considered as major bottlenecks in their commercialization. In this work, we demonstrate low-voltage, flexible OFETs based on ultrathin single-crystal microribbons. Flexible OFETs fabricated with 2,7-dioctylbenzothieno[3,2-b]benzothiophene (C8-BTBT) based solution-processed ultrathin single-crystal microribbon as the semiconductor layer and high-k polymer, polysiloxane-poly(vinyl alcohol) composite as an insulator layer manifest a significantly low operating voltage of -4 V, and several devices showed a high mobility of >30 cm2 V-1 s-1. Besides, the carrier mobility of the fabricated devices exhibits a slight degradation in static bending condition, which can be retained by 83.3% compared with its original value under a bending radius of 9 mm. As compared to the bulk C8-BTBT single-crystal-based OFET, which showed a large crack only after 50 dynamic bending cycles, our ultrathin single-crystal-based counterpart demonstrates a much better dynamic force stability. Moreover, under a 20 mm bending radius, the mobility of the device decreased by only 11.7% even after 500 bending cycles and no further decrease was observed until 1000 bending cycles. Our findings reveal that ultrathin C8-BTBT single-crystal-based flexible OFETs are promising candidates for various high-performance flexible electronic devices.

Methyl cinnamate alleviated CCI-induced upregualtion of spinal AMPA receptors and pain hypersensitivity by targeting AMPK.

Various studies proved spinal AMPA receptors were involved in the formation of neuropathic pain. In this study, we investigated the effect of methyl cinnamate (MC), a flavoring agent widely used in food and commodity industry, on CCI-induced upregulation of spinal AMPARs and pain hypersensitive behaviors. Results indicated that MC treatment dosage-dependently inhibited CCI-induced mechanical and thermal hypersensitivity. To further investigate the effect of MC after the formation of neuropathic pain, MC at the dosage of 100 mg/kg was administrated on day 7-14 on CCI rats. Results showed that MC treatment for seven days alleviated CCI-induced pain hypersensitivity after the formation of neuropathic pain. MC treatment reversed CCI-induced upregulation of GluR2, GluR3 and phosphorylation of GluR1. Further, MC dosage-dependently alleviated CCI-induced activation of mTOR and the downstream p70s6k. MC dosage-dependently induced activation of AMPK. All the MC-induced effects in CCI rats were completely reversed by Compound C, a AMPK inhibitor. These results meant MC treatment mitigated CCI-induced upregualtion of spinal AMPA receptors and pain hypersensitive behaviors through actviation of AMPK.

Effects of p-(Trifluoromethoxy)benzyl and p-(Trifluoromethoxy)phenyl Molecular Architecture on the Performance of Naphthalene Tetracarboxylic Diimide-Based Air-Stable n-Type Semiconductors.

N,N'-Bis(4-trifluoromethoxyphenyl) naphthalene-1,4,5,8-tetracarboxylic acid diimide (NDI-POCF3) and N,N'-bis(4-trifluoromethoxybenzyl) naphthalene-1,4,5,8-tetracarboxylic acid diimide (NDI-BOCF3) have similar optical and electrochemical properties with a deep LUMO level of approximately 4.2 eV, but exhibit significant differences in electron mobility and molecular packing. NDI-POCF3 exhibits nondetectable charge mobility. Interestingly, NDI-BOCF3 shows air-stable electron transfer performance with enhanced mobility by increasing the deposition temperature onto the octadecyltrichlorosilane (OTS)-modified SiO2/Si substrates and achieves electron mobility as high as 0.7 cm(2) V(-1) s(-1) in air. The different mobilities of those two materials can be explained by several factors including thin-film morphology and crystallinity. In contrast to the poor thin-film morphology and crystallinity of NDI-POCF3, NDI-BOCF3 exhibits larger grain sizes and improved crystallinities due to the higher deposition temperature. In addition, the theoretical calculated transfer integrals of the intermolecular lowest unoccupied molecular orbital (LUMO) of the two materials further show that a large intermolecular orbital overlap of NDI-BOCF3 can transfer electron more efficiently than NDI-POCF3 in thin-film transistors. On the basis of fact that the theoretical calculations are consistent with the experimental results, it can be concluded that the p-(trifluoromethoxy) benzyl (BOCF3) molecular architecture on the former position of the naphthalene tetracarboxylic diimides (NDI) core provides a more effective way to enhance the intermolecular electron transfer property than the p-(trifluoromethoxy) phenyl (POCF3) group for the future design of NDI-related air-stable n-channel semiconductor.

[Studies of Calotes versicolor on the sexual function amelioration mechanism by hypothalamus inhibition in immature male rats].

OBJECTIVE: To study the amelioration mechanism of Calotes versicolor petroleum ether extracts (CVPEE) on hypothalamus inhibition sexual function induced by morphine in immature male rats. METHODS: The hypothalamus inhibition induced by morphine in immature male rats was used as model of the testis reproductive functional disturbance. The rats was given CVPEE for 21 days. The levels of testosterone (T) and follicle stimulating hormone (FSH) in serum were determined by the radio-immunoassay. The nitrogen monoxide (NO) contents in serum and penis tissue were determined by nitrate reductase method. The sexual organ and auxiliary sexual organ coefficient were calculated and the histopathological changes in the testes and epididymides were observed with microscope. RESULTS: CVPEE groups (low and high dosage groups) significantly enhanced the level of serum T, compared with model group (P < 0.05); the low dosage group decreased obviously the level of FSH. CVPEE had the tendency to increase NO contents in serum and penile tissue. The microscopic examination results showed that the testis tissue in CVPEE group was damaged more gently than those in model group. CONCLUSION: CVPEE can enhance the level of serum T and NO contents in penile tissue, improve the sexual functional disturbance in hypothalamus inhibition induced by morphine in immature male rats. It indicated that CVPEE had the effects by the hypothalamus-hypophysis-gonad axial function.

Involvement of AMPK/SIRT1 pathway in anti-allodynic effect of troxerutin in CCI-induced neuropathic pain.

Neuropathic pain was regarded as a main form of chronic pain condition that remains difficult to treat. Conventional pharmacotherapy for neuropathic pain responsed vary and side effects limited their compliance. These prompted us to find new alternatives. In this study, we investigated the effect of troxerutin on treatment of CCI-induced neuropathic pain. Results showed that troxerutin significantly reversed mechanical allodynia and thermal hyperalgesia. In L4-6 spinal cord, troxerutin reduced the expression of INF-γ, IL-1ß, TNF-α, and activation of NF-κB(p65). Immunofluorescence results showed that troxerutin significantly inhibited microglia activation induced by CCI surgery. Further, troxerutin treatment significantly induced AMPK activation and inhibited CCI-induced SIRT1 decrease. However, AMPK inhibitor compound C and SIRT1 inhibitor EX527 inhibited analgesic effect of troxerutin in CCI mice. This demonstrated the involvement of AMPK/SIRT1 pathway in anti-allodynic effect of troxerutin in CCI mice. Troxerutin could be developed as a potential therapeutic agent for neuropathic pain.