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The Hemipteran predator, Cyrtorhinus lividipennis, feeds on the eggs and nymphs of rice planthoppers and leafhoppers. We previously demonstrated that sublethal concentrations of imidacloprid stimulated the reproduction of C. lividipennis. Considering the essential roles of juvenile hormone (JH) in insect reproduction, we speculated that sublethal concentrations of imidacloprid may stimulate the reproduction of C. lividipennis by regulating JH level. To test this, we cloned C. lividipennis JH acid methyl transferase (ClJHAMT) and JH esterase (ClJHE), which are responsible for JH biosynthesis and degradation genes, respectively. We then knocked down ClJHAMT by injecting dsRNA into C. lividipennis nymphs and found that emerging female adults exhibited 88.8% lower expression of the vitellogenin gene (ClVg) and the number of eggs was reduced by 41.5% as compared with controls. Silencing ClJHE increased ClVg mRNA expression by 275.0% but did not affect fecundity. A sublethal concentration of imidacloprid (LC20) increased the JH titer in females by 35.3% and 60.6% at 24 and 48 h post-emergence, respectively. In treatments containing both imidacloprid and dsJHAMT, the silencing of CLJHAMT reduced the number of eggs produced by adult females by 21.4% as compared to the control (imidacloprid + dsGFP). Our results indicated that sublethal concentration of imidacloprid may induce C. lividipennis reproduction by upregulating JH level via JHAMT. The finding could provide valuable information for improved integration of C. lividipennis and insecticides in pest management.

Cytorhinus lividipennis is a natural enemy of rice planthoppers and leafhoppers. Improving the fecundity of C. lividipennis will be helpful to improve its control effect on pests. However, little is known about the hormonal regulatory mechanism of reproduction in C. lividipennis. In the current study, we examined the role of 20-hydroxyecdysone (20E) biosynthesis relative gene Shadow in the reproduction of C. lividipennis. The complementary DNA sequence of ClSad is 2018 -bp in length with an open reading frame of 1398-bp encoding 465 amino acid residues. ClSad was readily detected in nymphal and adult stages, and highly expressed in the adult stage. ClSad was highly expressed in the midgut and ovaries of adult females. Moreover, RNA interference-mediated knockdown of ClSad reduced the 20E titers and ClVg transcript level, resulting in fewer fully developed eggs and a decrease in the number of eggs laid by dsSad-injected adult females within 15 days. These results suggest that ClSad plays a critical role in the reproduction of C. lividipennis. The present study provides insights into the molecular mechanism of the ClSad gene for the reproduction of C. lividipennis.

An integrated aptamer macroarray functionalized with reduced graphene oxide (rGO) to specifically capture and sensitively detect cancer cells is reported. The capture for cancer cells is based on effective recognition of the modified rGO surface through the aptamer against epithelial cell adhesion molecule (EpCAM). The rough structure of rGO enhances morphologic interactions between rGO film interface and the cancer cells, while super-hydrophilicity of modified rGO hinders nonspecific cell capture. The synergistic interactions offer the aptamer macroarray high efficiency of cancer cell capture. By means of a turn-on fluorescence strategy based on the conformation change of the aptamer induced by the target recognition, the enriched cancer cells can be directly read out at excitation/emission wavelengths of 550/680 nm without washing, separation, and dying steps. The working range is 1 × 102 to 2 × 104 cells per mL with a detection limit of 22 cells per mL. The results indicate that the aptamer macroarray has a considerable foreground for early diagnosis, therapy, and monitoring of cancer.

Sensitive detection, especially in situ monitoring of intracellular MMP-2, is extremely desirable for cancer early diagnosis, evaluation of therapy, and discovery of the new anti-cancer drug. Herein, a programmed microcapsule-type MMP-2 responsive nanosensor based on mesoporous silica nanoparticles (MSN) is developed to realize in situ imaging monitoring of intracellular MMP-2. In the wrapping anti-MMP-2 antibody sealed microcapsule-type nanosensor, a black hole fluorescence quencher (BHQ-3) is covalently combined onto the inner walls of the MSN mesopores, and the fluorescein Cy5 is loaded in the cavity of MSN, resulting in fluorescence “OFF” state. With the existence of MMP-2, the anti-MMP-2 antibody which acts as a “bio-lid” could detach from the surface of the nanosensor owing to the binding MMP-2 with the antibody, leading to the release of the fluorescein Cy5 to produce fluorescence “ON” state. The prepared programmed microcapsule-type MMP-2 responsive nanosensor is capable of sensitive in situ imaging monitoring of intracellular MMP-2 and is further verified by tracking the change of intracellular MMP-2 level in response to MMP-2-repressive drugs. Thus, the nanosensor give a platform for in vivo detection of biomarkers for diagnosis, evaluation of therapy, and discovery of the new anti-cancer drug.

Currently, nanosphere-based ligand fishing cannot be accomplished with imaging processing, although this step is important for real-time identification. Herein, a ligand fishing technique combined with real-time imaging is presented for the identification of ligands for heat shock protein 90α (Hsp 90α) from a complex matrix, Alisma plantago-aquatica Linn. crude extract, using Hsp 90α-functionalized mesoporous silica nanoparticle (MSN)-InP/ZnS quantum dot (QD) nanocomposites as a support material. Twenty ligands for Hsp 90α were screened, and their structures were identified by mass spectrometry. The activities of the ligands were verified by real-time imaging of cells apoptotic morphological changes. Quantitative analysis showed that Alisma plantago-aquatica Linn contained 8.19μg/g Alisol F, which regarded as one typical component of Alisma plantago-aquatica Linn, and the extraction ratio of Alisol F was 76.2%. The precision for five replicate measurements was 7.0% (RSD). The prepared nanocomposites were also used to screen proteins from a mixture of cellular extracts, and five proteins from HeLa cells were identified as potential client proteins of Hsp 90α.

A new rearranged lignan, asasiebolin (1), was isolated from a kind of traditional Chinese medicine Asarum sieboldii, together with two known lignans, L-sesamin and L-asarinin. Asasiebolin (1) contained a benzo[d][1,3]dioxole-5-carboxyl moiety linked to a hydroxymethyl at C-3 of the tetrahydrofuran core, which might be rearranged after a cleavage from C-4. The structure with relative configuration was elucidated by in-depth spectral methods.

Plants are known for their capacity to regenerate the whole body through de novo formation of apical meristems from a mass of proliferating cells named callus. Exogenous cytokinin and auxin determine cell fate for the establishment of the stem cell niche, which is the vital step of shoot regeneration, but the underlying mechanisms remain unclear. Here, we show that type-B ARABIDOPSIS RESPONSE REGULATORs (ARRs), critical components of cytokinin signaling, activate the transcription of WUSCHEL (WUS), which encodes a key regulator for maintaining stem cells. In parallel, type-B ARRs inhibit auxin accumulation by repressing the expression of YUCCAs, which encode a key enzyme for auxin biosynthesis, indirectly promoting WUS induction. Both pathways are essential for de novo regeneration of the shoot stem cell niche. In addition, the dual regulation of type-B ARRs on WUS transcription is required for the maintenance of the shoot apical meristem in planta. Thus, our results reveal a long-standing missing link between cytokinin signaling and WUS regulator, and the findings provide critical information for understanding cell fate specification.

A rolling-mediated cascade (RMC) amplification strategy is described for improved visualization of profiling glycans of mucin 1 (MUC 1) on cell surfaces. CdTe quantum dots (QDs) are used as fluorescent labels. The RMC based amplification allows even distinct glycoforms of MUC1 to be visualized on the surface of MCF-7 cell via an amplified Förster resonance energy transfer (FRET) imaging strategy that works at excitation/emission wavelengths of 345/610 nm. This is achieved by utilizing antibody against MUC1 modified with the fluorescent label 7-amino-4-methylcoumarin-3-acetic acid (AMCA) as the energy donor in FRET. The QDs (used to label surface glycans) act as acceptors. N-Azidoacetylgalactosamine-Acetylated (Ac4GalNAz) as a non-natural azido sugar, can be incorporated into the glycans of the cell surface, which can promote further labeling. The method has the advantage of only requiring a small amount of non-natural sugar to be introduced in metabolic glycan labeling since too much of an artificial sugar will interfere with the physiological functions of cells. Graphical abstract Schematic for the DNA rolling-mediated cascade (RMC)-assisted metabolic labeling of cell surface glycans by using CdTe quantum dots as labels and an intramolecular amplified FRET strategy for imaging glycans on a specific glycosylated protein, MUC1.

Endotoxin, also known as lipopolysaccharide (LPS), can induce strong immune response that causes casualties annually. This number may be greatly reduced if specific, robust, sensitive and more capable of clearance LPS biosensor existed. By introducing a LPS specific binding peptide to a typical aggregation induced emission (AIE) fluorophore, 1-(4-carboxylbenzene)-1,2,2-triphenyl (CTPY), a robust, sensitive and specific “OFF-ON” fluorescent biosensor was developed. The biosensor can achieve LPS sensing of a linear relationship in the concentration range of 0.1–1 μM with a detection limit of 6.97 nM. Moreover, a rapid clearance of LPS is simultaneous realized by integration of mesoporous silica nanospheres with a LPS recognition peptide. Such robust biosensor with highly specific detection and rapid clearance based on LPS specific binding peptide hold considerable promise in diverse clinical and biological applications.

Gout is a genetic or acquired metabolic disease caused by increase of uric acid synthesis resulted from purine metabolic abnormalities. Whether cGMP-dependent protein kinase 2 (cGKII/PRKG2) is correlated with gout remains controversial. The objective of the present study was to investigate whether there is a correlation between polymorphism of cGKII/PRKG2 and gout susceptibility of Han population in northern China. Four hundred and five male patients with gout in the case group and 429 controls in the control group were collected from the Department of Endocrinology and Metabolic Disease, the Fourth Affiliated Hospital of Harbin Medical University. A case-control study method was used to study the correlation between cGKII/PRKG2 polymorphism rs7688672 and rs10033237 and gout susceptibility. The genotype frequencies of rs7688672 and rs10033237 polymorphisms of cGKII/PRKG2 in the case group and the control group both were in accordance with Hardy-Weinberg equilibrium. There were significant differences of rs10033237 in the allele frequencies and genotype distributions (P

Summary Introduction The upregulation of Nav1.8 in primary afferents plays a critical role in the development and persistence of neuropathic pain. The mechanisms underlying the upregulation are not fully understood. Aims The present study aims to investigate the regulatory effect of histamine on the expression of Nav1.8 in primary afferent neurons and its involvement in neuropathic pain. Results Histamine at 10−8 M increased the expression of Nav1.8 in cultured DRG neurons. This effect could be blocked by H2 receptor antagonist cimetidine or famotidine, but not by H1 receptor antagonist pyrilamine or dual H3/H4 antagonist thioperamide. Peri-sciatic administration of histamine increased Nav1.8 expression in the sciatic nerve and L4/L5 DRG neurons in a dose-dependent manner, accompanied with remarkable mechanical allodynia and heat hyperalgesia in the ipsilateral hindpaw. Famotidine but not pyrilamine or thioperamide inhibited Nav1.8 upregulation and pain hypersensitivity. In addition, famotidine (40 mg/kg, i.p.) not only suppressed autotomy behavior in the rat neuroma model of neuropathic pain but also attenuated mechanical allodynia and thermal hyperalgesia following partial sciatic nerve ligation. Moreover, famotidine inhibited Nav1.8 upregulation in the neuroma and ligated sciatic nerve. Conclusions Our findings indicate that histamine increases Nav1.8 expression in primary afferent neurons via H2 receptor-mediated pathway and thereby contributes to neuropathic pain. H2 receptor antagonists may potentially be used as analgesics for patients with neuropathic pain.

Summary Aims To explore the role of histamine in acute pain perception and its possible mechanisms. Methods Pain-like behaviors induced by four types of noxious stimuli (hot-plate, tail-pressure, acetic acid, and formalin) were accessed in mice. Nav1.8 expression and functions in primary afferent neurons were compared between histidine decarboxylase knockout (HDC−/−) mice and their wild-types. Results HDC−/− mice, lacking in endogenous histamine, showed elevated sensitivity to all these noxious stimuli, as compared with the wild-types. In addition, a depletion of endogenous histamine with α-fluoromethylhistidine (α-FMH), a specific HDC inhibitor, or feeding mice a low-histamine diet also enhanced nociception in the wild-types. Nav1.8 expression in primary afferent neurons was increased both in HDC−/− and in α-FMH-treated wild-type mice. A higher Nav1.8 current density, a lower action potential (AP) threshold, and a higher firing rate in response to suprathreshold stimulation were observed in nociception-related small DRG neurons of HDC−/− mice. Nav1.8 inhibitor A-803467, but not TTX, diminished the hyperexcitability and blocked repetitive AP firing of these neurons. Conclusion Our results indicate that histamine participates in acute pain modulation in a dose-related manner. The regulation of Nav1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.

The present study was designed to investigate the ef- fects of histamine on spontaneous neuropathic pain (NP) induced by peripheral axotomy. Rats and mice were subjected to complete transection of the left sciatic and saphenous nerves to induce spontaneous NP (the neuroma model). Rats were then treated with drugs once daily for 30 days (histidine and loratadine, i.p.) or 21 days (histamine, i.c.v.). Autotomy behavior was scored daily until day 50 post-operation (PO). On days 14 to 21 PO, some rats in the control group were subjected to single-fiber recording. Autotomy behavior was also monitored daily in histidine decar- boxylase (the key enzyme for histamine synthesis) knockout (HDC -/- ) and wild-type mice for 42 days. We found that both histidine (500 mg/kg) (a precur- sor of histamine that increases histamine levels in the tissues) and histamine (50 µg/5 µL) significantly suppressed autotomy behavior in rats. HDC -/- mice lacking endogenous histamine showed higher levels of autotomy than the wild-type. In addition, the an- algesic effect of histidine was not antagonized by loratadine (a peripherally-acting H1 receptor antago- nist), while loratadine alone significantly suppressed autotomy. Electrophysiological recording showed that ectopic spontaneous discharges from the neuroma were blocked by systemic diphenhydramine (an H1 receptor antagonist). Our results suggest that hista- mine plays an important role in spontaneous NP. It is likely that histamine in the central nervous system is analgesic, while in the periphery, via H1 receptors, it is algesic. This study justifies the avoidance of a his- tamine-rich diet and the use of peripherally-acting H1 receptor antagonists as well as agents that improve histamine action in the central nervous system in pa- tients with spontaneous NP.

Background It is known that histamine participates in pain modulation. However, the effect of central histamine on neuropathic pain is not fully understood. Here, we report a critical time window for the analgesic effect of central histamine in the partial sciatic nerve ligation model of neuropathic pain. Methods Neuropathic pain was induced by partial sciatic nerve ligation (PSL) in rats, wild-type (C57BL/6J) mice and HDC−/− (histidine decarboxylase gene knockout) and IL-1R−/− (interleukin-1 receptor gene knockout) mice. Histidine, a precursor of histamine that can increase the central histamine levels, was administered intraperitoneally (i.p.). Histidine decarboxylase (HDC) enzyme inhibitor α-fluoromethylhistidine was administered intracerebroventricularly (i.c.v.). Histamine H1 receptor antagonist mepyramine and H2 receptor antagonist cimetidine were given intrathecally (i.t.) and intracisternally (i.c.). Withdrawal thresholds to tactile and heat stimuli were measured with a set of von Frey hairs and infrared laser, respectively. Immunohistochemistry and Western blot were carried out to evaluate the morphology of microglia and IL-1β production, respectively. Results Histidine (100 mg/kg, i.p.) administered throughout days 0–3, 0–7, or 0–14 postoperatively (PO) alleviated mechanical allodynia and thermal hyperalgesia in the hindpaw following PSL in rats. Intrathecal histamine reversed PSL-induced thermal hyperalgesia in a dose-dependent manner and intracisternal histamine alleviated both mechanical allodynia and thermal hyperalgesia. Moreover, α-fluoromethylhistidine (i.c.v.) abrogated the analgesic effect of histidine. However, histidine treatment initiated later than the first postoperative day (treatment periods included days 2–3, 4–7, and 8–14 PO) did not show an analgesic effect. In addition, histidine treatment initiated immediately, but not 3 days after PSL, inhibited microglial activation and IL-1β upregulation in the lumbar spinal cord, in parallel with its effects on behavioral hypersensitivity. Moreover, the inhibitory effects on pain hypersensitivity and spinal microglial activation were absent in HDC−/− mice and IL-1R−/− mice. H1 receptor antagonist mepyramine (200 ng/rat i.t. or i.c.), but not H2 receptor antagonist cimetidine (200, 500 ng/rat i.t. or 500 ng/rat i.c.), blocked the effects of histidine on pain behavior and spinal microglia. Conclusions These results demonstrate that central histamine is analgesic within a critical time window in the PSL model of neuropathic pain via histamine H1 receptors. This effect may partly relate to the inhibition of microglial activation and IL-1β production in the spinal cord following nerve injury. Electronic supplementary material The online version of this article (doi:10.1186/s12974-016-0637-0) contains supplementary material, which is available to authorized users.

Ischemic preconditioning protects against cerebral ischemia. Recent investigations indicated that acidic preconditioning (APC) protects against ischemia-induced cardiomyocytes injury. However, it is not clear whether APC can protect against cerebral ischemia. To address this issue, C57BL/6 mice were exposed 3 times at 10-min intervals to a normoxic atmosphere containing 20% CO(2) for 5 min before being further subjected to bilateral common carotid artery occlusion. APC reversed the ischemia-induced brain injury as revealed by improved performance in passive avoidance experiments and decreased neuron loss in the hippocampal CA1 region. Consistently, both APC-treated brain slices and primary cultured neurons were more resistant to oxygen-glucose-deprivation (OGD)-induced injury, in a pH- and time-dependent manner, as revealed by reversed cell/tissue viability. In addition, the APC treatment prevented OGD-induced mitochondrial transmembrane potential loss and apoptosis, which was inhibited by the mitochondrial permeability transport pore opener atractyloside. Taken together, these findings indicated that APC protects against ischemia-induced neuronal injury. The beneficial effects may be attributed, at least in part, to decreased mitochondria-dependent neuronal apoptosis.

Hydroxyapatite (HAP) urchins were synthesized by a facile hydrothermal method using calcium nitrate, ammonium dihydrogen phosphate, diamine tetraacetic acid disodium salt as complexing agent and ethonalamine as alkaline source. The influence of hydrothermal time on crystallinity and morphology of HAP have been investigated. The results indicate that well-crystallized HAP urchins can be synthesized at 180°C for 24h. SEM images show a large area of urchin-like microspheres consisted of a number of ribbons with lengths ranging from 2 to 5μm. Based on XRD and SEM results, the formation mechanism of HAP crystals has been discussed. A typical anti-inflammatory drug, ibuprofen, was used for drug loading, and the release behaviors of ibuprofen in a simulated body fluid (SBF) were studied. The results indicate that HAP urchins showed a favorable sustained release property for ibuprofen.

Calcium sulfate nanorods, nanowires, nanobelts and sheets had been synthesized via a facile solution reaction of CaCl2 and H2SO4 in mixed solvents of ethanol/N, N-dimethylformamide and deionized water at 35°C. The results indicated that well-crystallized CaSO4 nanomaterials with different morphology were obtained by adjusting the volume ratio of ethanol/N, N-dimethylformamide to deionized water and the reaction time. Samples prepared at 35°C in mixed solvents of 50 mL ethanol and 30 mL water for 1 min and 2 h showed nanowire and sheet morphology, respectively. While increasing the volume ratio of ethanol to deionized water to 78/2, only nanorods were obtained. When N, N-dimethylformamide was employed to substitute ethanol, the sample heating at 35°C for 2 h was composed of nanowires in 50 mL N, N-dimethylformamide and 30 mL water. Higher volume ratio of N, N-dimethylformamide to deionized water caused the formation of nanorods.

ZnSn(OH)6hierarchical cubes and Zn2SnO4octahedra have been synthesized through a rapid, template-free, one-pot hydrothermal approach using zinc acetate, tin chloride and sodium hydroxide. ZnSn(OH)6aggregates with cubic morphology and uniform size distribution have been successfully synthesized via aggregation-mediated crystallization. Through adjusting the hydrothermal parameters, Zn2SnO4octahedra were obtained at a higher temperature. The formation of Zn2SnO4 octahedra undergone a transformation from ZnSn(OH)6cubes. The as-synthesized products were characterized by powder X-ray diffraction (XRD), scanning electron microscopy (SEM) and differential scanning calorimetric analysis (DSC) and thermogravimetric analysis (TG).