HHL1 and SOQ1 synergistically regulate nonphotochemical quenching in Arabidopsis.

Nonphotochemical quenching (NPQ) is an important photoprotective mechanism that quickly dissipates excess light energy as heat. NPQ can be induced in a few seconds to several hours; most studies of this process have focused on the rapid induction of NPQ. Recently, a new, slowly induced form of NPQ, called qH, was found during the discovery of the quenching inhibitor suppressor of quenching 1 (SOQ1). However, the specific mechanism of qH remains unclear. Here, we found that hypersensitive to high light 1 (HHL1)-a damage repair factor of photosystem II-interacts with SOQ1. The enhanced NPQ phenotype of the hhl1 mutant is similar to that of the soq1 mutant, which is not related to energy-dependent quenching or other known NPQ components. Furthermore, the hhl1 soq1 double mutant showed higher NPQ than the single mutants, but its pigment content and composition were similar to those of the wildtype. Overexpressing HHL1 decreased NPQ in hhl1 to below wildtype levels, whereas NPQ in hhl1 plants overexpressing SOQ1 was lower than that in hhl1 but higher than that in the wildtype. Moreover, we found that HHL1 promotes the SOQ1-mediated inhibition of plastidial lipoprotein through its von Willebrand factor type A domain. We propose that HHL1 and SOQ1 synergistically regulate NPQ.

Ultra-high Q resonances based on zero group-velocity modes accompanied by bound states in the continuum in 2D photonic crystal slabs.

Optical resonators made of 2D photonic crystal (PhC) slabs provide efficient ways to manipulate light at the nanoscale through small group-velocity modes with low radiation losses. The resonant modes in periodic photonic lattices are predominantly limited by nonleaky guided modes at the boundary of the Brillouin zone below the light cone. Here, we propose a mechanism for ultra-high Q resonators based on the bound states in the continuum (BICs) above the light cone that have zero-group velocity (ZGV) at an arbitrary Bloch wavevector. By means of the mode expansion method, the construction and evolution of avoided crossings and Friedrich-Wintgen BICs are theoretically investigated at the same time. By tuning geometric parameters of the PhC slab, the coalescence of eigenfrequencies for a pair of BIC and ZGV modes is achieved, indicating that the waveguide modes are confined longitudinally by small group-velocity propagation and transversely by BICs. Using this mechanism, we engineer ultra-high Q nanoscale resonators that can significantly suppress the radiative losses, despite the operating frequencies above the light cone and the momenta at the generic k point. Our work suggests that the designed devices possess potential applications in low-threshold lasers and enhanced nonlinear effects.

[Improvement effect of cinnamaldehyde on reserpine-induced Parkinson's disease rat model].

In order to study the neuroprotective mechanism of cinnamaldehyde on reserpine-induced Parkinson's disease(PD) rat models, 72 male Wistar rats were randomly divided into blank group, model group, Madopar group, and cinnamaldehyde high-, medium-, and low-dose groups. Except for the blank group, the other groups were intraperitoneally injected with reserpine of 0.1 mg·kg~(-1) once every other morning, and cinnamaldehyde and Madopar solutions were gavaged every afternoon. Open field test, rotarod test, and oral chewing movement evaluation were carried out in the experiment. The brain was taken and fixed. The positive expression of dopamine receptor D1(DRD1) was detected by TSA, and the changes in neurotransmitters such as dopamine(DA) and 3,4-dihydroxyphenylacetic acid(DOPAC) in the brain were detected by enzyme-linked immunosorbent assay(ELISA). The protein and mRNA expression levels of tyrosine hydroxylase(TH) and α-synuclein(α-Syn) in substantia nigra(SN) were detected by RT-PCR and Western blot. The results showed that after the injection of reserpine, the hair color of the model group became yellow and dirty; the arrest behavior was weakened, and the body weight was reduced. The spontaneous movement and exploration behavior were reduced, and the coordination exercise ability was decreased. The number of oral chewing was increased, but the cognitive ability was decreased, and the proportion of DRD1 positive expression area in SN was decreased. The expression of TH protein and mRNA was down-regulated, and that of α-Syn protein and mRNA was up-regulated. After cinnamaldehyde intervention, it had an obvious curative effect on PD model animals. The spontaneous movement behavior, the time of staying in the rod, the time of movement, the distance of movement, and the number of standing times increased, and the number of oral chewing decreased. The proportion of DRD1 positive expression area in SN increased, and the protein and mRNA expression levels of α-Syn were down-regulated. The protein and mRNA expression levels of TH were up-regulated. In addition, the levels of DA, DOPAC, and homovanillic acid(HVA) neurotransmitters in the brain were up-regulated. This study can provide a new experimental basis for clinical treatment and prevention of PD.

Photoelectron Migration Boosted by Hollow Double-Shell Dyads Based on Covalent Organic Frameworks for Highly Efficient Photocatalytic Hydrogen Generation.

Photocatalytic hydrogen production based on noble metal-free systems is a promising technology for the conversion of solar energy into green hydrogen, it is pivotal and challenging to tailor-make photocatalysts for achieving high photocatalytic efficiency. Herein, we reported a hollow double-shell dyad through uniformly coating covalent organic frameworks (COFs) on the surface of hollow Co9S8. The double shell architecture enhances the scattering and refraction efficiency of incident light, shortens the transmission distance of the photogenerated charge carriers, and exposes more active sites for photocatalytic conversion. The hydrogen evolution rate is as high as 23.15 mmol g-1 h-1, which is significantly enhanced when compared with that of their physical mixture (0.30 mmol g-1 h-1) and Pt-based counterpart (11.84 mmol g-1 h-1). This work provides a rational approach to the construction of noble-metal-free photocatalytic systems based on COFs to enhance hydrogen evolution performance.

Hydrogen alleviated cognitive impairment and blood‒brain barrier damage in sepsis-associated encephalopathy by regulating ABC efflux transporters in a PPARα-dependent manner.

Hydrogen (H2) can protect against blood‒brain barrier (BBB) damage in sepsis-associated encephalopathy (SAE), but the mechanism is still unclear. We examined whether it is related to PPARα and its regulatory targets, ABC efflux transporters. After injection with DMSO/GW6471 (a PPARα inhibitor), the mice subjected to sham/caecal ligation and puncture (CLP) surgery were treated with H2 for 60 min postoperation. Additionally, bEnd.3 cells were grown in DMSO/GW6471-containing or saline medium with LPS. In addition to the survival rates, cognitive function was assessed using the Y-maze and fear conditioning tests. Brain tissues were stained with TUNEL and Nissl staining. Additionally, inflammatory mediators (TNF-α, IL-6, HMGB1, and IL-1ß) were evaluated with ELISA, and PPARα, ZO-1, occludin, VE-cadherin, P-gp, BCRP and MRP2 were detected using Western blotting. BBB destruction was assessed by brain water content and Evans blue (EB) extravasation. Finally, we found that H2 improved survival rates and brain dysfunction and decreased inflammatory cytokines. Furthermore, H2 decreased water content in the brain and EB extravasation and increased ZO-1, occludin, VE-cadherin and ABC efflux transporters regulated by PPARα. Thus, we concluded that H2 decreases BBB permeability to protect against brain dysfunction in sepsis; this effect is mediated by PPARα and its regulation of ABC efflux transporters.

c-Jun N-terminal kinase activation contributes to improving low temperature tolerance via regulating apoptosis in the Pacific white shrimp Penaeus vannamei.

Temperature is an essential environmental factor for the survival of aquatic animals. Low temperature stress can induce mitochondria to produce excessive ROS and free radicals, and destroy homeostasis. c-Jun N-terminal kinase (JNK) is involved in regulating various physiological processes, including inflammatory responses, cell cycle, reproduction, and apoptosis. Here, we investigated the mechanism of ROS/JNK pathway under low temperature stress both in vitro and in vivo. In this study, transcriptome analysis revealed that apoptosis, autophagy, calcium channel, and antioxidant were involved in the mediation of low temperature tolerance in Pacific white shrimp (penaeus vannamei). PvJNK was activated in response to low temperature stress. Treatments with different temperature caused oxidative stress as demonstrated by increased intensity of the ROS indicator H2DCF-DA, and induced apoptosis as confirmed by indicator FITC. Pretreatment with N-acetylcysteine, an ROS scavenger, attenuated low temperature induced apoptosis, and inhibited the expression of PvJNK. In addition, we demonstrate that mediator PvJNK translocated to nuclear through interacting with PvRheb. By using flow cytometry, inhibiting PvJNK can increase the expression of apoptosis related genes, accelerate tissue damage, and induce ROS and cell apoptosis. The ultimate inhibition of PvJNK accelerates the mortality of shrimp under low temperature stress. Overall, these findings suggest that during low temperature stress, PvJNK was activated by ROS to regulates apoptosis via interacting with PvRheb to promote PvJNK into the nucleus and to improve low temperature tolerance of shrimp.

Screening Serum Biomarkers for Rats Preconditioned with Hyperbaric Oxygen: Potential of Predicting Prognosis for Stroke.

BACKGROUND: Stroke is a major health concern and a leading cause of mortality and morbidity. We and other groups have documented that hyperbaric oxygen preconditioning could significantly alleviate neuronal damage in ischemia‒reperfusion models through various mechanisms. However, we found that some of the subjects did not benefit from preconditioning with hyperbaric oxygen. The preconditioning phenomenon is similar to vaccination, in which the endogenous survival system is activated to fight against further injuries. However, with vaccine inoculations, we could test for specific antibodies against the pathogens to determine if the vaccination was successful. Likewise, this experiment was carried out to explore a biomarker that can reveal the effectiveness of the preconditioning before neuronal injury occurs. METHODS: Middle cerebral artery occlusion (MCAO) was used to induce focal cerebral ischemia-reperfusion injury. 2D-DIGE-MALDI-TOF-MS/MS proteomic technique was employed to screen the differentially expressed proteins in the serum of rats among the control (Con) group (MCAO model without hyperbaric oxygen (HBO) preconditioning), hyperbaric oxygen protective (HBOP) group (in which the infarct volume decreased after HBO preconditioning vs. Con), and hyperbaric oxygen nonprotective (HBOU) group (in which the infarct volume remained the same or even larger after HBO preconditioning vs. Con). Candidate biomarkers were confirmed by western blot and enzyme linked immunosorbent assay (ELISA), and the relationship between the biomarkers and the prognosis of cerebral injury was further validated. RESULTS: Among the 15 differentially expressed protein spots detected in the HBOP group by Two-dimensional fluorescence difference gel electrophoresis (2D-DIGE), 3 spots corresponding to 3 different proteins (haptoglobin, serum albumin, and haemopexin) products were identified by MALDI-TOF-MS/MS. Serum albumin and haemopexin were upregulated, and haptoglobin was downregulated in the HBOP group (p < 0.05 vs. Con and HBOU groups). After the western blot study, only the changes in haemopexin were validated and exhibited similar changes in subjects from the HBOP group in accordance with MALDI-TOF-MS/MS proteomic analysis and enzyme linked immunosorbent assay (ELISA) analysis. The serum level of the hemopexin (HPX) at 2 h after HBO preconditioning was correlated with the infarct volume ratio after MCAO. CONCLUSIONS: Haemopexin may be developed as a predictive biomarker that indicated the effectiveness of a preconditioning strategy against cerebral ischaemic injury.

Phosphorylation-mediated PI3K-Art signalling pathway as a therapeutic mechanism in the hydrogen-induced alleviation of brain injury in septic mice.

Our previous studies illustrated that 2% H2 inhalation can protect against sepsis-associated encephalopathy (SAE) which is characterized by high mortality and has no effective treatment. To investigate the underlying role of protein phosphorylation in SAE and H2 treatment, a mouse model of sepsis was constructed by caecal ligation and puncture (CLP), then treated with H2 (CLP + H2 ). Brain tissues of the mice were collected to be analysed with tandem mass tag-based quantitative proteomics coupled with IMAC enrichment of phosphopeptides and LC-MS/MS analysis. In proteomics and phosphoproteomics analysis, 268 differentially phosphorylated proteins (DPPs) showed a change in the phosphorylated form in the CLP + H2 group (p < 0.05). Gene ontology analysis revealed that these DPPs were enriched in multiple cellular components, biological processes, and molecular functions. KEGG pathway analysis revealed that they were enriched in glutamatergic synapses, tight junctions, the PI3K-Akt signalling pathway, the HIF-1 signalling pathway, the cGMP-PKG signalling pathway, the Rap1 signalling pathway, and the vascular smooth muscle contraction. The phosphorylated forms of six DPPs, including ribosomal protein S6 (Rps6), tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma (Ywhag/14-3-3), phosphatase and tensin homologue deleted on chromosome ten (Pten), membrane-associated guanylate kinase 1 (Magi1), mTOR, and protein kinase N2 (Pkn2), were upregulated and participated in the PI3K-Akt signalling pathway. The WB results showed that the phosphorylation levels of Rps6, Ywhag, Pten, Magi1, mTOR, and Pkn2 were increased. The DPPs and phosphorylation-mediated molecular network alterations in H2 -treated CLP mice may elucidate the biological roles of protein phosphorylation in the therapeutic mechanism of H2 treatment against SAE.

Spinal NLRP3 inflammasome activation mediates IL-1ß release and contributes to remifentanil-induced postoperative hyperalgesia by regulating NMDA receptor NR1 subunit phosphorylation and GLT-1 expression in rats.

BACKGROUND: Trafficking and activation of N-methyl-D-aspartate (NMDA) receptors play an important role in initiating and maintaining postoperative remifentanil-induced hyperalgesia (RIH). Activation of the NOD-like receptor protein 3 (NLRP3) inflammasome has been linked to the development of inflammatory and neuropathic pain. We hypothesized that activation of NLRP3 inflammasome mediates IL-1ß release and contributes to RIH in rats by increasing NMDA receptor NR1 (NR1) subunit phosphorylation and decreasing glutamate transporter-1 (GLT-1) expression. METHODS: Acute exposure to remifentanil (1.2 µg/kg/min for 60 min) was used to establish RIH in rats. Thermal and mechanical hyperalgesia were tested at baseline (24 h before remifentanil infusion) and 2, 6, 24, and 48 h after remifentanil infusion. The levels of IL-1ß, GLT-1, phosphorylated NR1 (phospho-NR1), and NLRP3 inflammasome activation indicators [NLRP3, Toll-like receptor 4 (TLR4), P2X purinoceptor 7 (P2X7R), and caspase-1] were measured after the last behavioral test. A selective IL-1ß inhibitor (IL-1ß inhibitor antagonist; IL-1ra) or three different selective NLRP3 inflammasome activation inhibitors [(+)-naloxone (a TLR4 inhibitor), A438079 (a P2X7R inhibitor), or ac-YVADcmk (a caspase-1 inhibitor)] were intrathecally administered immediately before remifentanil infusion into rats. RESULTS: Remifentanil induced significant postoperative hyperalgesia, increased IL-1ß and phospho-NR1 levels and activated the NLRP3 inflammasome by increasing TLR4, P2X7R, NLRP3, and caspase-1 expression, but it decreased GLT-1 expression in the L4-L6 spinal cord segments of rats, which was markedly improved by intrathecal administration of IL-1ra, (+)-naloxone, A438079, or ac-YVADcmk. CONCLUSION: NLRP3 inflammasome activation mediates IL-1ß release and contributes to RIH in rats by inducing NMDA receptor NR1 subunit phosphorylation and decreasing GLT-1 expression. Inhibiting the activation of the NLRP3 inflammasome may be an effective treatment for RIH.

Bismuth Gadolinium Oxychloride with a Remarkable Visible-Light-Responsive O2 Evolution Activity Promoted by Iodine Doping.

Visible-light-responsive bismuth-based oxyhalide has recently attracted extensive attention, however, the promotion of its charge separation is still challenging. Herein, we introduce iodine into Bi2 GdO4 Cl to synthetize I-doped Bi2 GdO4 Cl (denoted as yI-Bi2 GdO4 Cl, 0≤y≤2). The incorporation of I- ions is found to enhance light absorption and to accelerate charge separation by combining various characterizations such as density functional theory calculation, photoelectrochemical test, electrochemical impedance spectroscopy, photoluminescence spectrum, and open-circuit voltage decay. The O2 -evolving performances of 1I-Bi2 GdO4 Cl with optimized dopant concentration of I- ion and IrO2 loaded 1I-Bi2 GdO4 Cl are tremendously enhanced by ca. 4 and 45 times compared to pristine Bi2 GdO4 Cl. Notably, The O2 evolution rate reaches as high as 154.8 µmol ⋅ h-1 with an apparent quantum efficiency of ∼1.1 % at 420 nm. The synthetic iodine-doped photocatalyst remains stable after long-term photoreaction, demonstrating its potential in the field of photocatalysis.

Hydrogen alleviates cell damage and acute lung injury in sepsis via PINK1/Parkin-mediated mitophagy.

BACKGROUND: Multiple organ failure (MOF) is the main cause of early death in septic shock. Lungs are among the organs that are affected in MOF, resulting in acute lung injury. Inflammation is an important factor that causes immune cell dysfunction in the pathogenesis of sepsis. Autophagy is involved in the process of inflammation and also occurs in response to cell and tissue injury in several diseases. We previously demonstrated that hydrogen alleviated the inflammation-induced cell injury and organ damage in septic mice. AIM: The focus of the present study was to elucidate whether mitophagy mediates the inflammatory response or oxidative injury in sepsis in vitro and in vivo. Furthermore, we evaluated the role of mitophagy in the protective effects of hydrogen against cell injury or organ dysfunction in sepsis. METHOD: RAW 264.7 macrophages induced by lipopolysaccharide (LPS) were used as an in vitro model for inflammation, and cecal ligation and puncture (CLP)-induced acute lung injury mice were used as an in vivo model for sepsis. The key protein associated with mitophagy, PTEN-induced putative kinase 1 (PINK1), was knocked down by PINK1 shRNA transfection in RAW 264.7 macrophages or mice. RESULTS: Hydrogen ameliorated cell injury and enhanced mitophagy in macrophages stimulated by LPS. PINK1 was required for the mitigation of the cell impairment in LPS-stimulated macrophages by hydrogen treatment. PINK1 knockdown abrogated the beneficial effects of hydrogen on mitophagy in LPS-stimulated macrophages. Hydrogen inhibited acute lung injury in CLP mice via activation of PINK1-mediated mitophagy. CONCLUSION: These results suggest that PINK1-mediated mitophagy plays a key role in the protective effects of hydrogen against cell injury in LPS-induced inflammation and CLP-induced acute lung injury.

P2Y1 Purinergic Receptor Contributes to Remifentanil-Induced Cold Hyperalgesia via Transient Receptor Potential Melastatin 8-Dependent Regulation of N-methyl-d-aspartate Receptor Phosphorylation in Dorsal Root Ganglion.

BACKGROUND: Remifentanil can induce postinfusion cold hyperalgesia. N-methyl-d-aspartate receptor (NMDAR) activation and upregulation of transient receptor potential melastatin 8 (TRPM8) membrane trafficking in dorsal root ganglion (DRG) are critical to cold hyperalgesia derived from neuropathic pain, and TRPM8 activation causes NMDAR-dependent cold response. Contribution of P2Y1 purinergic receptor (P2Y1R) activation in DRG to cold pain hypersensitivity and NMDAR activation induced by P2Y1R upregulation in neurons are also unraveled. This study explores whether P2Y1R contributes to remifentanil-induced cold hyperalgesia via TRPM8-dependent regulation of NMDAR phosphorylation in DRG. METHODS: Rats with remifentanil-induced cold hyperalgesia were injected with TRPM8 antagonist or P2Y1R antagonist at 10 minutes before remifentanil infusion. Cold hyperalgesia (paw lift number and withdrawal duration on cold plate) was measured at -24, 2, 6, 24, and 48 hours following remifentanil infusion. After the last behavioral test, P2Y1R expression, TRPM8 expression and membrane trafficking, and NMDAR subunit (NR1 and NR2B) expression and phosphorylation in DRG were detected by western blot, and colocalization of P2Y1R with TRPM8 was determined by double-labeling immunofluorescence. Two-way repeated measures analysis of variance (ANOVA) or 2 × 2 factorial design ANOVA with repeated measures was used to analyze behavioral data of cold hyperalgesia. One-way ANOVA followed by Bonferroni post hoc comparisons was used to analyze the data in western blot and immunofluorescence. RESULTS: Remifentanil infusion (1 µg·kg-1·min-1 for 60 minutes) induced cold hyperalgesia (hyperalgesia versus control, paw lift number and withdrawal duration on cold plate at 2-48 hours, P < .0001) with upregulated NR1 (hyperalgesia versus naive, 48 hours, mean ± standard deviation [SD], 114.00% ± 12.48% vs 41.75% ± 5.20%, P < .005) and NR2B subunits expression (104.13% ± 8.37% vs 24.63% ± 4.87%, P < .005), NR1 phosphorylation at Ser896 (91.88% ± 7.08% vs 52.00% ± 7.31%, P < .005) and NR2B phosphorylation at Tyr1472 (115.75% ± 8.68% vs 59.75% ± 7.78%, P < .005), TRPM8 expression (115.38% ± 9.27% vs 40.50% ± 4.07%, P < .005) and membrane trafficking (112.88% ± 5.62% vs 48.88% ± 6.49%, P < .005), and P2Y1R expression (128.25% ± 14.86% vs 45.13% ± 7.97%, P < .005) in DRG. Both TRPM8 and P2Y1R antagonists attenuated remifentanil-induced cold hyperalgesia and downregulated increased NR1 and NR2B expression and phosphorylation induced by remifentanil (remifentanil + RQ-00203078 versus remifentanil + saline, NR1 phosphorylation, 69.38% ± 3.66% vs 92.13% ± 4.85%; NR2B phosphorylation, 72.25% ± 6.43% vs 111.75% ± 11.00%, P < .0001). NMDAR activation abolished inhibition of TRPM8 and P2Y1R antagonists on remifentanil-induced cold hyperalgesia. P2Y1R antagonist inhibited remifentanil-evoked elevations in TRPM8 expression and membrane trafficking and P2Y1R-TRPM8 coexpression (remifentanil + 2'-deoxy-N6-methyl adenosine 3',5'-diphosphate [MRS2179] versus remifentanil + saline, coexpression, 8.33% ± 1.33% vs 22.19% ± 2.15%, P < .0001). CONCLUSIONS: Attenuation of remifentanil-induced cold hyperalgesia by P2Y1R inhibition is attributed to downregulations in NMDAR expression and phosphorylation via diminishing TRPM8 expression and membrane trafficking in DRG.

Effect of Preoperative Oral Carbohydrate Administration on Patients Undergoing Cesarean Section with Epidural Anesthesia: A Pilot Study.

PURPOSE: The aim of this study was to evaluate the effect of preoperative oral carbohydrate administration on patients undergoing Cesarean section with epidural anesthesia. DESIGN: Randomized controlled clinical study. METHODS: A total of 75 patients undergoing Cesarean section (American Society of Anesthesiologists physical status grade I-II) were randomized to preparation with a carbohydrate drink (CHO group), flavored water (placebo group), or to the fasting group. The CHO and placebo groups were double-blinded and given 300 mL of the drink 2 hours before surgery. Visual analog scores of the patient were assessed to evaluate thirst, hunger, and anxiety level, and the gastric antral cross-sectional areas were recorded by ultrasonography during the operative period. Insulin resistance was calculated on the basis of the blood glucose and insulin levels assessed before administration and after surgery. FINDINGS: The CHO and placebo groups did not show an increase in gastric fluid volumes in terms of gastric antral cross-sectional area, and there were no adverse events. The visual analog scale scores at preoperative baseline were not different between groups . During the preoperative waiting period, preparation with CHO reduced not only thirst and anxiety more efficiently than water (placebo) but also hunger (P < .05), whereas water did not. No difference was observed in insulin resistance between groups before intake of the drink. Compared with the preoperative levels, insulin resistance showed a statistically significant increase in all groups (P < .05); however, the increase was significantly higher in the fasting and placebo groups than in the CHO group (P < .05). CONCLUSIONS: Preoperative administration of CHO decreases postoperative insulin resistance and enhances pregnant women's comfort, leading to a reduced sense of thirst, hunger, and anxiety during the preoperative period for Cesarean section.

Polymorph selection during melt crystallization of the isotactic polybutene-1 homopolymer depending on the melt state and crystallization pressure.

This work investigated the crystalline forms obtained from melt crystallization in the isotactic polybutene-1 (iPB-1) homopolymer via manipulation of the temperature at which samples were melted (Tmelt) and crystallization pressure (Pcry). Unlike the results under atmospheric conditions where the molten sample crystallized into the pure form II and the crystallization temperature and kinetics were affected obviously by Tmelt, the melted sample crystallized into forms II or I' under high pressure, depending on Tmelt and Pcry. The content of form I' decreases with increasing Tmelt or decreasing Pcry. Meanwhile, the critical pressure for the formation of pure form I' increases with increasing Tmelt. The formation of form I' is attributed to the memory effect of the melt which preserved some ordered sequence of crystal and the high pressure (Pcry) which suppressed the nucleation and growth of the kinetically favored form II, which results in the formation of form I'. In addition, the melt crystallized form II transforms to form I under high pressure conditions; thus forms I, I' and II are observed. The relative contents of the three crystalline forms on samples for different Tmelt and Pcry are obtained in this work. The result shows that the crystalline forms in melt crystallization of iPB-1 can be customized by regulating the melt state and crystallization conditions.

Early menarche is associated with insulin resistance in advanced maternal age before delivery.

Purpose: With the wide implementation of the universal two-child policy in China, the number of pregnant women in advanced maternal age (AMA) will increase gradually. We aimed to assess the association between age at menarche (AAM) and insulin resistance (IR) before delivery in AMA. Methods: A total of 80 pregnant women in AMA were consecutively enrolled before delivery in Zhongda hospital. Pregnant women were stratified into early menarche group and late menarche group according to the age of regular menstruation (about 13 years). At delivery, serum glucose and lipid levels were measured. IR was calculated by the method of homeostasis model assessment 2(HOMA2). Results: The fasting blood insulin (17.68(9.72-36.71) and 10.35(7.76-15.10), respectively; p = .006) and HOMA-IR (2.08(1.18-4.37) and 1.24(0.89-1.78), respectively; p = .005) were higher in early menarche group than in late menarche group. AAM was inversely associated with HOMA-IR in AMA (r= -0.27, p = .014). In the multivariable analysis, AAM in late menarche group was negatively related to the level of HOMA-IR compared to those in early menarche group (ß= -2.275, p≤.0001). Conclusions: Taken together, our findings suggest that AAM was inversely associated with HOMA-IR in AMA. Furthermore, pregnant women in AMA with early menarche might have higher HOMA-IR levels than those with late menarche. Clinical trial registration: Chinese Clinical Trial Registry (No. ChiCTR-RRC-16008714), retrospectively registered.

The role of PI3K-mediated AMPA receptor changes in post-conditioning of propofol in brain protection.

BACKGROUND: We aimed to study the role of amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) glutamate receptor 2 (GluR2) subunit trafficking, and activity changes in short-term neuroprotection provided by propofol post-conditioning. We also aimed to determine the role of phosphoinositide-3-kinase (PI3K) in the regulation of these processes. METHODS: Rats underwent 1 h of focal cerebral ischemia followed by 23 h of reperfusion were randomly divided into 6 groups (n = 36 per group): sham- operation (S), ischemia-reperfusion (IR), propofol (P group, propofol 20 mg/kg/h at the onset of reperfusion for 2 h after 60 min of occlusion), and LY294002 (PI3K non-selective antagonist) + sham (L + S, LY294002 of 1.5 mg/kg was infused 30 min before sham operation), LY294002+ ischemia-reperfusion (L + IR, LY294002 of 1.5 mg/kg was infused 30 min before middle cerebral artery occlusion), LY294002 + IR + propofol (L + P, LY294002 of 1.5 mg/kg was infused 30 min before middle cerebral artery occlusion and propofol 20 mg/kg/h at the onset of reperfusion for 2 h after 60 min of occlusion). RESULTS: Compared with group IR, rats in group P had significant lower neurologic defect scores and infarct volume. Additionally, consistent with enhanced expression of PI3K-AMPAR GluR2 subunit complex substances in ipsilateral hippocampus, GluR2 subunits showed increased levels in both the plasma and postsynaptic membranes of neurons, while pGluR2 expression was reduced in group P. Furthermore, LY294002, the PI3K non-selective antagonist, blocked those effects. CONCLUSION: These observations demonstrated that propofol post-conditioning revealed acute neuroprotective role against transient MCAO in rats. The short-term neuroprotective effect was contributed by enhanced GluR2 subunits trafficking to membrane and postsynaptic membranes of neurons, as well as down-regulated the expression of pGluR2 in damaged hippocampus. Finally, the above-mentioned protective mechanism might be contributed by increased combination of PI3K to AMPAR GluR2 subunit, thus maintained the expression and activation of AMPAR GluR2 in the ipsilateral hippocampus.

The relationship between vitamin D and insulin resistance before delivery in advanced maternal age.

BACKGROUND: With the widely implementation of universal two-child policy, the number of pregnant women in advanced maternal age (AMA) will increase gradually. We aimed to assess the association of vitamin D levels and insulin resistance (IR) during the late pregnancy in AMA. METHODS: A total of 80 pregnant women were consecutively enrolled in the cross-sectional study before delivery from the August 2016 to June 2017 at the department of gynecology and obstetrics in the hospital of ZhongDa, affiliated to Southeast University. At delivery, serum 25(OH) D and metabolism parameters including glucose and lipid levels were measured. IR was calculated by the method of homeostasis model assessment 2(HOMA2). RESULTS: Pregnant women in AMA with vitamin D deficiency have higher fasting insulin (14.70(8.76-34.65) and 10.89(7.15-16.12), respectively, P = 0.031) and HOMA-IR indices (1.78(1.07-4.14) and 1.30(0.83-1.89), respectively, P = 0.024) than those with vitamin D non-deficiency. Serum 25(OH) D levels were inversely associated with HOMA-IR indices (r = - 0.25, P = 0.025). In multivariable analysis for adjusting confounder factors, vitamin D non-deficiency was also negatively correlated with HOMA-IR compared to vitamin D deficiency (ß = - 1.289, P = 0.026). CONCLUSIONS: Taken together, our findings suggest that serum 25(OH) D levels were inversely associated with HOMA-IR in AMA. Furthermore, pregnant women in AMA with vitamin D deficiency might have higher HOMA-IR levels than those with vitamin D non-deficiency. TRIAL REGISTRATION: Chinese Clinical Trial Registry (No. ChiCTR-RRC-16008714). retrospectively registered.

Vitamin B6 Intake and Pancreatic Carcinoma Risk: A Meta-Analysis.

Objectives: There are conflicting results for the association between vitamin B6 intake with reduced pancreatic carcinoma risk. Thus, a meta-analysis was performed to summarize the evidences from epidemiological studies. Methods: We searched documents from PubMed-Medline, Web of Science, and Cochrane Library. The results were analyzed by using Stata software. Results: A total of nine studies were included. The multivariate-adjusted results found that the total RR values of pancreatic carcinoma was 0.65 (95% CI: 0.53-0.80) for the highest vitamin B6 intake vs the lowest vitamin B6 intake, and there was no significant heterogeneity among studies (I2 = 42.0%, P = 0.087). Sensitivity analysis indicated that no single study leaded to an excessive change for the relation between vitamin B6 intake and pancreatic carcinoma risk. Conclusions: This meta-analysis suggested that vitamin B6 intake could significantly decrease pancreatic carcinoma risk. However, further study is needed based on the limitations of the current analysis.

Particulate Oxynitride Photoanodes Assembled with Transparent Electron-Collecting Oxide Nanorod Arrays.

The collection of photogenerated electrons is commonly a bottleneck in photoelectrochemical water oxidation on a particulate photoanode. Herein, a new strategy called "array insertion" for particulate photoanode preparation is proposed to improve electron collection. ZnO nanorod arrays are inserted between LaTiO2N particles and Al-doped ZnO (AZO) substrates via epitaxial electrodeposition, which make electronic connections. Using this methodology, charge separation efficiency is improved drastically, and the photocurrent at 1.23 VRHE is enhanced by more than 1 order of magnitude, because the obstacle of electron collection in the particulate LaTiO2N photoanodes is overcome.

Hemopexin alleviates cognitive dysfunction after focal cerebral ischemia-reperfusion injury in rats.

BACKGROUND: Ischemia-reperfusion (I/R) is a critical pathophysiological basis of cognitive dysfunction caused by ischemia stroke. Heme-oxygenase-1 (HO-1) is the rate-limiting enzyme for the elimination of excessive free heme by combining with hemopexin (HPX), a plasma protein that contributes to eliminating excessive free heme during ischemia stroke. This study aimed to elucidate whether HPX could alleviate cognitive dysfunction in rats subjected to cerebral I/R. METHODS: Rats were randomly divided into five groups: sham, MCAO, Vehicle, HPX and HPX + protoporphyrin IX (ZnPPIX). Cerebral I/R was induced by MCAO. Saline, vehicle, HPX and HPX + ZnPPIX were injected intracerebroventricularly at the moment after reperfusion. Morris water maze (MWM) test was used to detect the learning and cognitive function. Western blot was used to detect the expression of HO-1 in ischemic penumbra. CD31/vWF double labeling immunofluorescence was used to detect the neovascularization in the penumbra hippocampus. The structure and function of blood-brain barrier (BBB) was detected by the permeability of Evans Blue (EB), water content of the brain tissue, the Ang1/Ang2 and VE-cadherin expression. RESULTS: Our study verified that HPX improved the learning and memory capacity. Hemopexin up-regulated HO-1 protein expression, the average vessel density in the penumbra hippocampus and the VE- cadherin expression but decreased the permeability of EB, the water content of brain tissue and the ratio of Ang1/Ang2. The effects were reversed by ZnPPIX, an inhibitor of HO-1. CONCLUSION: HPX can maintain the integrity of the blood-brain barrier and alleviate cognitive dysfunction after cerebral I/R through the HO-1 pathway.