Aberrant Human Epididymal Protein 4 in Heart Failure Patients' Serum and its Association with C-Reactive Protein, Uric Acid and Homocysteine.

BACKGROUND: The goal was to explore the aberrant human epididymal protein 4 (HE4) in chronic heart failure (CHF) patients and its association with C-reactive protein (CRP), uric acid (UA), and homocysteine (HCY). METHODS: Analysis of serum HE4 and its relevance with associated indexes in 117 CHF patients was implemented. RESULTS: Serum HE4 in CHF patients was linked with the disease's severity and CRP, UA, and HCY. An assessment value was provided for it (p < 0.05). CONCLUSIONS: HE4 is aberrant in CHF patients' serum and is associated with the disease's severity and CRP, UA, and HCY's indexes.

[17-year study on the curative effect of treatment to prevent the recurrence of hepatitis B in different risk groups after liver transplantation].

Objective: To observe the recurrence condition of hepatitis B in different risk groups after liver transplantation in an attempt to provide useful information on whether to discontinue hepatitis B immunoglobulin (HBIG) in the future at an early stage. Methods: The patient population was divided into high, low-risk, and special groups [especially primary hepatocellular carcinoma (HCC)] according to the guidelines for the prevention and treatment of hepatitis B recurrence after liver transplantation. The recurrence condition and risk factors in this population were observed for hepatitis B. Measurement data were analyzed using a t-test and a rank-sum test. Count data were compared using a χ(2) test between groups. Results: This study finally included 532 hepatitis B-related liver transplant cases. A total of 35 cases had HBV recurrence after liver transplantation, including 34 cases that were HBsAg positive, one case that was HBsAg negative, and 10 cases that were hepatitis B virus (HBV) DNA positive. The overall HBV recurrence rate was 6.6%. The recurrence rate of HBV was 9.2% and 4.8% in the high- and low-risk HBV DNA positive and negative groups before surgery (P = 0.057). Among the 293 cases diagnosed with HCC before liver transplantation, 30 had hepatitis B recurrence after surgery, with a recurrence rate of 10.2%. The independent related factors for the recurrence of hepatitis B in patients with HCC after liver transplantation were HCC recurrence (HR =181.92, 95%CI 15.99~2 069.96, P < 0.001), a high postoperative dose of mycophenolate mofetil dispersible tablets (MMF) ( HR =5.190, 95%CI 1.289~20.889, P = 0.020), and a high dosage of HBIG (HR = 1.012, 95%CI 1.001~1.023, P = 0.035). Among the 239 cases who were non-HCC before liver transplantation, five cases (recurrence rate of 2.1%) arouse postoperative hepatitis B recurrence. Lamivudine was used in all cases, combined with on-demand HBIG prophylaxis after surgery. There was no hepatitis B recurrence in non-HCC patients who treated with entecavir combined with HBIG after surgery. Conclusion: High-barrier-to-resistance nucleotide analogues combined with long-term HBIG have a good effect on preventing the recurrence of hepatitis B after liver transplantation. The discontinuation of HBIG may be considered at an early stage after administration of a high-barrier-to-resistance nucleotide analogue in low-risk patients. Domestically, the HBV infection rate is high, so further research is still required to explore the timing of HBIG discontinuation for high-risk patients, especially those with HCC.

Structural features of subchondral bone cysts and adjacent tissues in hip osteoarthritis.

OBJECTIVE: Focal lesions within the subchondral bone, termed subchondral bone cysts (SBCs), are clinically accepted radiographic markers of advanced osteoarthritis (OA), but their etiology in the hip is not well understood. DESIGN: This study used micro-computed tomography (µCT), and histological and immunocytological analysis to examine the prevalence, size, location, and morphological and cellular features of SBCs found within 34 femoral heads (14 male, 20 female; age range = 43-80 years) obtained from total hip arthroplasty procedures. RESULTS: SBCs were common-present in 91% of the femoral heads examined-and frequently commuted with the surface of the femoral head, but otherwise showed no preferred anatomical location. Few associations were found between SBC features and patient characteristics such as BMI, age and sex. SBCs were also heterogenous in composition, ranging from fibrous (most common) to predominantly fatty (least common) and often containing vasculature, nerve fibers, cartilage islands, and bony spicules. Despite this heterogeneity, focal abnormalities in bone density and cartilage thickness were consistently observed. Bone adjacent to SBCs was denser than that in the primary compressive group, and cartilage thickness in regions overlying SBCs was lower than in non-overlying regions. In contrast to these local bony changes, µCT-based finite element analyses indicated that the stiffness of the primary compressive group was only mildly affected by SBCs. CONCLUSIONS: These findings indicate that SBCs in the femoral head involve extensive perturbations in cellular activity, culminating in myriad skeletal tissue types and spatially heterogenous changes in bone and cartilage morphology that are likely to affect OA progression.

Depth-Resolved Magnetization Dynamics Revealed by X-Ray Reflectometry Ferromagnetic Resonance.

Magnetic multilayers offer diverse opportunities for the development of ultrafast functional devices through advanced interface and layer engineering. Nevertheless, a method for determining their dynamic properties as a function of depth throughout such stacks has remained elusive. By probing the ferromagnetic resonance modes with element-selective soft x-ray resonant reflectivity, we gain access to the magnetization dynamics as a function of depth. Most notably, using reflectometry ferromagnetic resonance, we find a phase lag between the coupled ferromagnetic layers in [CoFeB/MgO/Ta]_{4} multilayers that is invisible to other techniques. The use of reflectometry ferromagnetic resonance enables the time-resolved and depth-resolved probing of the complex magnetization dynamics of a wide range of functional magnetic heterostructures with absorption edges in the soft x-ray wavelength regime.

Alteration of liver-infiltrated and peripheral blood double-negative T-cells in primary biliary cholangitis.

BACKGROUND & AIMS: Double-negative (DN) T-cell is a unique regulatory T-cell, which is essential for maintaining immune system homoeostasis. However, the role of DN T-cells in the pathogenesis of primary biliary cholangitis (PBC) is still unknown. METHODS: We investigated the number and function of DN T-cells in peripheral blood and liver biopsy specimens of PBC patients. RESULTS: The number and frequency of DN T-cells significantly decreased in peripheral blood and liver tissue of PBC patients. Furthermore, the frequency of DN T-cells in PBC was negatively correlated with disease severity and positively correlated with ursodeoxycholic acid response. In vitro assays showed that perforin expression and the suppressive capability of DN T-cells on the proliferation of CD4+ and CD8+ T-cells were impaired in PBC. Finally, lithocholic acid, the most hydrophobic acid, could downregulate the proliferation and perforin expression of DN T-cells. CONCLUSIONS: Decreased quantity and function of DN T-cells in PBC may result in the loss of immune regulations on effector CD4+ and cytotoxic CD8+ T-cells, and thereby may break the immune tolerance and promote the pathogenesis of PBC.

Aberrant hippocampal Atp8a1 levels are associated with altered synaptic strength, electrical activity, and autistic-like behavior.

Type IV ATPases are putative aminophospholipid translocases (APLTs), more commonly known as flippases. A pronounced induction of the flippase Atp8a1 was observed in post-mortem tissue homogenates from the hippocampus and temporal lobe of juvenile autistic subjects compared to age-matched controls. In order to simulate the human data, C57BL/6 mice were allowed to develop after intra-hippocampal injection of recombinant lentivirus expressing Atp8a1 at the early developmental stage of postnatal day 6 (P6). Transmission electron microscopy (TEM) analysis of the lentivirus-Atp8a1 treated (Atp8a1+) mice in adulthood revealed fewer and weaker excitatory synapses in the hippocampal CA1 region compared to mice injected with empty virus. Significant inhibition of the Schaffer collateral pathway was observed in the Atp8a1+ mice in paired-pulse recording (PPR) at 20-ms inter-stimulus interval. In the three-chambered sociability test, the Atp8a1+ mice displayed no preference for an encaged stranger mouse over a novel object, which is a characteristic autistic-like behavior. In sharp contrast, Atp8a1 (-/-) mice displayed a preference for a stranger mouse over the novel object, which is characteristic of neurotypical mouse behavior. However, similar to the Atp8a1+ mice, the Atp8a1 (-/-) mice harbored fewer and weaker excitatory synapses in CA1 compared to wild-type controls, and displayed inhibition at 20-ms inter-stimulus interval in PPR. These findings suggest that both elevated and diminished levels of Atp8a1 during early development are detrimental to brain connectivity, but only elevated Atp8a1 is associated with aberrant social behavior. Mice with augmented levels of Atp8a1 may therefore serve as a potential model in autism research.

Hepatitis C virus-induced myeloid-derived suppressor cells regulate T-cell differentiation and function via the signal transducer and activator of transcription 3 pathway.

T cells play a pivotal role in controlling viral infection; however, the precise mechanisms responsible for regulating T-cell differentiation and function during infections are incompletely understood. In this study, we demonstrated an expansion of myeloid-derived suppressor cells (MDSCs), in particular the monocytic MDSCs (M-MDSCs; CD14(+) CD33(+) CD11b(+) HLA-DR(-/low) ), in patients with chronic hepatitis C virus (HCV) infection. Notably, HCV-induced M-MDSCs express high levels of phosphorylated signal transducer and activator of transcription 3 (pSTAT3) and interleukin-10 (IL-10) compared with healthy subjects. Blocking STAT3 signalling reduced HCV-mediated M-MDSC expansion and decreased IL-10 expression. Importantly, we observed a significant increase in the numbers of CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells following incubation of healthy peripheral blood mononuclear cells (PBMCs) with MDSCs derived from HCV-infected patients or treated with HCV core protein. In addition, depletion of MDSCs from PBMCs led to a significant reduction of Foxp3(+) Treg cells developed during chronic HCV infection. Moreover, depletion of MDSCs from PBMCs significantly increased interferon-γ production by CD4(+) T effector (Teff) cells derived from HCV patients. These results suggest that HCV-induced MDSCs promote Treg cell development and inhibit Teff cell function, suggesting a novel mechanism for T-cell regulation and a new strategy for immunotherapy against human viral diseases.

Hepatitis C virus-induced reduction in miR-181a impairs CD4(+) T-cell responses through overexpression of DUSP6.

UNLABELLED: T cells play a crucial role in viral clearance or persistence; however, the precise mechanisms that control their responses during viral infection remain incompletely understood. MicroRNA (miR) has been implicated as a key regulator controlling diverse biological processes through posttranscriptional repression. Here, we demonstrate that hepatitis C virus (HCV)-mediated decline of miR-181a expression impairs CD4(+) T-cell responses through overexpression of dual specific phosphatase 6 (DUSP6). Specifically, a significant decline of miR-181a expression along with overexpression of DUSP6 was observed in CD4(+) T cells from chronically HCV-infected individuals compared to healthy subjects, and the levels of miR-181a loss were found to be negatively associated with the levels of DUSP6 overexpression in these cells. Importantly, reconstitution of miR-181a or blockade of DUSP6 expression in CD4(+) T cells led to improved T-cell responses including enhanced CD25 and CD69 expression, increased interleukin-2 expression, and improved proliferation of CD4(+) T cells derived from chronically HCV-infected individuals. CONCLUSION: Since a decline of miR-181a concomitant with DUSP6 overexpression is the signature marker for age-associated T-cell senescence, these findings provide novel mechanistic insights into HCV-mediated premature T-cell aging through miR-181a-regulated DUSP6 signaling and reveal new targets for therapeutic rejuvenation of impaired T-cell responses during chronic viral infection.

KLRG1 impairs CD4+ T cell responses via p16ink4a and p27kip1 pathways: role in hepatitis B vaccine failure in individuals with hepatitis C virus infection.

Coinfection of hepatitis B virus (HBV) with hepatitis C virus (HCV) is quite common, leading to an increase in morbidity and mortality. As such, HBV vaccination is recommended in HCV-infected individuals. However, HBV vaccine responses in HCV-infected individuals are often blunted compared with uninfected populations. The mechanism for this failure of vaccine response in HCV-infected subjects remains unclear. In this study, we investigated the expression and function of an inhibitory receptor, killer cell lectin-like receptor subfamily G member 1 (KLRG1), in the regulation of CD4(+) T cells and HBV vaccine responses during HCV infection. We demonstrated that KLRG1 was overexpressed on CD4(+) T cells from HCV-infected, HBV vaccine nonresponders compared with HBV vaccine responders. The capacity of CD4(+) T cells to proliferate and secrete IL-2 cytokine was inversely associated with the level of KLRG1 expression. Importantly, blocking KLRG1 signaling resulted in a significant improvement in CD4(+) T cell proliferation and IL-2 production in HCV-infected, HBV vaccine nonresponders in response to TCR stimulation. Moreover, blockade of KLRG1 increased the phosphorylation of Akt (Ser(473)) and decreased the expression of cell cycle inhibitors p16(ink4a) and p27(kip1), which subsequently enhanced the expression of cyclin-dependent kinase 2 and cyclin E. These results suggest that the KLRG1 pathway impairs CD4(+) T cell responses to neoantigen and induces a state of immune senescence in individuals with HCV infection, raising the possibility that blocking this negative-signaling pathway might improve HBV vaccine responses in the setting of chronic viral infection.

MicroRNA-155 regulates interferon-γ production in natural killer cells via Tim-3 signalling in chronic hepatitis C virus infection.

Host immune responses must be tightly regulated by an intricate balance between positive and negative signals while fighting pathogens; persistent pathogens may usurp these regulatory mechanisms to dampen host immunity to facilitate survival in vivo. Here we report that Tim-3, a negative signalling molecule expressed on monocytes and T cells, is up-regulated on natural killer (NK) cells in individuals chronically infected with hepatitis C virus (HCV). Additionally, the transcription factor T-bet was also found to be up-regulated and associated with Tim-3 expression in NK cells during chronic HCV infection. MicroRNA-155 (miR-155), an miRNA that inhibits signalling proteins involved in immune responses, was down-regulated in NK cells by HCV infection. This Tim-3/T-bet over-expression and miR-155 inhibition were recapitulated in vitro by incubating primary NK cells or NK92 cell line with Huh-7 hepatocytes expressing HCV. Reconstitution of miR-155 in NK cells from HCV-infected patients led to a decrease in T-bet/Tim-3 expression and an increase in interferon-γ production. Blocking Tim-3 signalling also enhanced interferon-γ production in NK cells by improving signal transducer and activator of transcription-5 phosphorylation. These data indicate that HCV-induced, miR-155-regulated Tim-3 expression regulates NK cell function, suggesting a novel mechanism for balancing immune clearance and immune injury during chronic viral infection.

An insecticide-treated bed-net campaign and childhood malaria in Burkina Faso.

OBJECTIVE: To investigate if the first national insecticide-treated bed-net campaign in Burkina Faso, done in 2010, was followed by a decrease in childhood malaria in a district with high baseline transmission of the disease. METHODS: We obtained data on the prevalence of Plasmodium falciparum parasitaemia in children aged 2 weeks to 36 months from malaria surveys in 2009 and 2011. We assessed morbidity in children younger than 5 years by comparing data from the Nouna health district's health management information system before and after the campaign in 2010. We analysed mortality data from 2008 to 2012 from Nouna's health and demographic surveillance system. FINDINGS: The bed-net campaign was associated with an increase in the reported use of insecticide-treated nets. In 2009, 73% (630/869) of children reportedly slept under nets. In 2011, 92% (449/487) did. The campaign had no effect on the proportion of young children with P. falciparum parasitaemia after the rainy season; 52% (442/858) in 2009 and 53% (263/499) in 2011. Cases of malaria increased markedly after the campaign, as did the number of children presenting with other diseases. The campaign was not associated with any changes in child mortality. CONCLUSION: The 2010 insecticide-treated net campaign in Burkina Faso was not associated with a decrease in care-seeking for malaria or all-cause mortality in children younger than 5 years. The most likely explanation is the high coverage of nets in the study area before the campaign which could have had an effect on mosquito vectors, limiting the campaign's impact.

KLRG1 negatively regulates natural killer cell functions through the Akt pathway in individuals with chronic hepatitis C virus infection.

In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1(+) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1(-) NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection.

Decolorization of methylene blue in aqueous suspensions of gold nanoparticles using parallel nanosecond pulsed laser.

Using 532 nm parallel nanosecond pulsed laser, the decolorization of methylene blue (MB) in aqueous suspensions of gold nanoparticles (GNPs) was studied. The effects of various experimental parameters, such as irradiation time, laser energy, and initial MB concentration on the decolorization rate were investigated. Experiments using real samples of textile dyeing wastewater were also carried out to examine the effectiveness of the method in more complex samples. From the results, the following conclusions may be drawn: (i) Under the optimum conditions (pH 7.19, 135 mJ laser energy, 4 mg/L MB concentration, and 11.6 mg/L GNP concentration), the rate of MB decolorization could reach 94% in 15 min. The decolorization follows pseudo-first-order kinetics; (ii) The amount of MB decreased rapidly during the decolorization. No intermediates of the decolorization could be detected by high-performance liquid chromatography. These observations indicate that MB was decolorized through a very rapid degradation mechanism; (iii) The rate of MB decolorization increased with the increase in laser energy (at laser energies of 0 to 135 mJ); and, (iv) The efficient decolorization of MB in real samples of textile dyeing wastewater was achieved at a decolorization rate of about 85% in 15 min.

Developmental origin of preBötzinger complex respiratory neurons.

A subset of preBötzinger Complex (preBötC) neurokinin 1 receptor (NK1R) and somatostatin peptide (SST)-expressing neurons are necessary for breathing in adult rats, in vivo. Their developmental origins and relationship to other preBötC glutamatergic neurons are unknown. Here we show, in mice, that the "core" of preBötC SST(+)/NK1R(+)/SST 2a receptor(+) (SST2aR) neurons, are derived from Dbx1-expressing progenitors. We also show that Dbx1-derived neurons heterogeneously coexpress NK1R and SST2aR within and beyond the borders of preBötC. More striking, we find that nearly all non-catecholaminergic glutamatergic neurons of the ventrolateral medulla (VLM) are also Dbx1 derived. PreBötC SST(+) neurons are born between E9.5 and E11.5 in the same proportion as non-SST-expressing neurons. Additionally, preBötC Dbx1 neurons are respiratory modulated and show an early inspiratory phase of firing in rhythmically active slice preparations. Loss of Dbx1 eliminates all glutamatergic neurons from the respiratory VLM including preBötC NK1R(+)/SST(+) neurons. Dbx1 mutant mice do not express any spontaneous respiratory behaviors in vivo. Moreover, they do not generate rhythmic inspiratory activity in isolated en bloc preparations even after acidic or serotonergic stimulation. These data indicate that preBötC core neurons represent a subset of a larger, more heterogeneous population of VLM Dbx1-derived neurons. These data indicate that Dbx1-derived neurons are essential for the expression and, we hypothesize, are responsible for the generation of respiratory behavior both in vitro and in vivo.

Association of endothelial nitric oxide synthase and mitochondrial dysfunction in the hippocampus of scrapie-infected mice.

The elevation of nitric oxide (NO) within the central nervous system (CNS) is known to be associated with the pathogenesis of neurodegenerative diseases such as HIV-associated dementia (HAD), brain ischemia, Parkinson's disease, and Alzheimer's disease. NO is enzymatically formed by the enzyme nitric oxide synthase (NOS). There are two forms of NOS, the constitutive and the inducible form. The constitutive form is present in endothelial cells (eNOS) and neurons (nNOS). The inducible form (iNOS) is expressed in various cell types including astroglia and microglia of the CNS. Using an animal model, we investigated the involvement of eNOS in the pathology of prion disease. We showed dramatic upregulation of eNOS immunoreactivity in reactive astroglial cells in the hippocampus in the prion disease animal model, scrapie in mice. Expression of eNOS was upregulated in cytosolic and mitochondrial fractions of whole brain. In the hippocampal region, eNOS was widely overexpressed in various components of the cell. We found that eNOS dramatically accumulated in hippocampal mitochondria and was particularly prevalent in structurally dysfunctional mitochondria. In association with the accumulation of eNOS in mitochondria, we showed that mitochondrial superoxide dismutase (Mn-SOD or SOD2), cytochrome c, and ATP activity were downregulated both in whole brain and in the hippocampal region. These results indicate that eNOS plays a role in the development of dysfunctional mitochondria and this, in turn, could induce some of the histopathological changes seen in prion diseases.

Digallate dimers of (-)-epigallocatechin gallate inactivate herpes simplex virus.

Topical microbicides are potentially an alternative method to vaccines for reducing the spread of herpes simplex virus (HSV). We have previously shown (S. Liu et al., Biochim. Biophys. Acta 1723:270-281, 2005) that the catechin (-)-epigallocatechin gallate (EGCG) inactivates HSV at neutral pH; however, to function in the female genital tract EGCG must also be effective at acidic pH. EGCG inactivated HSV-1 and HSV-2 at pH 8.0 by 3 log(10) to 4 log(10) but was ineffective at pH 5.7. The EGCG digallate dimers theasinensin A, P2, and theaflavin-3,3'-digallate (TF-3) inactivated both viruses by 3 log(10) to 4 log(10) at pH 5.7 and as much as 5 log(10) at pH 8.0. TF-3 inactivated HSV-1 and HSV-2 by 4 to 5 log(10) in the pH range of 4.0 to 5.7. Dimers with one gallate moiety had antiviral activity intermediate between the activities of EGCG and digallate dimers. Confocal and electron microscopy showed that theasinensin A did not damage Vero cells. All EGCG dimers inactivated enveloped viruses with class I, class II, and class III (HSV-1, HSV-2) fusion proteins more effectively than did monomeric EGCG. EGCG had no activity against the nonenveloped viruses tested, but TF-3 reduced the titer of 4 of 5 nonenveloped viruses by ≅2 to 3.5 log(10). Results also showed that HSV-1 glycoprotein B (gB) was aggregated more rapidly by theasinensin A than EGCG, which, when taken together with the nonenveloped virus data, suggests that dimers may inhibit the function of viral proteins required for infectivity. Digallate dimers of EGCG appear to have excellent potential as microbicidal agents against HSV at acidic and neutral pHs.

Lesions of nucleus accumbens affect morphine-induced release of ascorbic acid and GABA but not of glutamate in rats.

Our previous studies have shown that local perfusion of morphine causes an increase of extracellular ascorbic acid (AA) levels in nucleus accumbens (NAc) of freely moving rats. Lines of evidence showed that glutamatergic and GABAergic were associated with morphine-induced effects on the neurotransmission of the brain, especially on the release of AA. In the present study, the effects of morphine on the release of extracellular AA, γ-aminobutyric acid (GABA) and glutamate (Glu) in the NAc following bilateral NAc lesions induced by kainic acid (KA) were studied by using the microdialysis technique, coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD) and fluorescent detection (HPLC-FD). The results showed that local perfusion of morphine (100 µM, 1 mM) in NAc dose-dependently increased AA and GABA release, while attenuated Glu release in the NAc. Naloxone (0.4 mM) pretreated by local perfusion to the NAc, significantly blocked the effects of morphine. After NAc lesion by KA (1 µg), morphine-induced increase in AA and GABA were markedly eliminated, while decrease in Glu was not affected. The loss effect of morphine on AA and GABA release after KA lesion could be recovered by GABA agonist, musimol. These results indicate that morphine-induced AA release may be mediated at least by µ-opioid receptor. Moreover, this effect of morphine possibly depend less on the glutamatergic afferents, but more on the GABAergic circuits within this nucleus. Finally, AA release induced by local perfusion of morphine may be GABA-receptor mediated and synaptically localized in the NAc.

The OPR gene family in watermelon: Genome-wide identification and expression profiling under hormone treatments and root-knot nematode infection.

The enzyme 12-oxo-phytodienoic acid reductase (OPR) is important in the jasmonic acid (JA) biosynthesis pathway and thus plays a vital role in plant defence. However, systematic and comprehensive analyses of OPR genes in watermelon and their roles in defence responses are extremely limited. The physicochemical properties, phylogenetic tree, gene structure and cis-acting elements of watermelon OPR genes were analysed using bioinformatics, and qRT-PCR and RNA-Seq were applied to assay expression of OPR genes in watermelon. A total of five OPR family genes were identified in watermelon, which were unevenly distributed across the four chromosomes. Phylogenetic analysis assigned OPR members from different plant species to five subfamilies (OPRI-OPRV). The motif compositions of OPR members were relatively conserved. Expression analysis using qRT-PCR revealed that ClOPR genes, except for ClOPR5, were highly expressed in the flower and fruit. RNA-seq analysis showed that the ClOPR genes had different expression patterns during flesh and rind development. Furthermore, the ClOPR genes, particularly ClOPR2 and ClOPR4, were significantly upregulated by exogenous JA, salicylic acid (SA) and ethylene (ET) treatments. In addition, red light induced expression of ClOPR2 and ClOPR4 in leaves and roots of root-knot nematode (RKN)-infected watermelon plants, suggesting their involvement in red light-induced defence against RKN. These results provide a theoretical basis for elucidating the diverse functions of OPR family genes in watermelon.

Comparison of sevoflurane volatile induction/maintenance anaesthesia and propofol-remifentanil total intravenous anaesthesia for rigid bronchoscopy under spontaneous breathing for tracheal/bronchial foreign body removal in children.

BACKGROUND AND OBJECTIVE: Foreign body aspiration is a life-threatening condition, with children under 3 years of age most at risk. This study was designed to compare the clinical characteristics of sevoflurane volatile induction/maintenance anaesthesia (VIMA) and propofol-remifentanil total intravenous anaesthesia (TIVA) for children undergoing rigid bronchoscopy under spontaneous breathing for tracheal/bronchial foreign body removal. METHODS: Sixty-four children undergoing rigid bronchoscopy were allocated randomly to receive sevoflurane (Group VIMA; n = 32) or propofol-remifentanil (Group TIVA, n = 32) between 2007 and 2009. Respiratory rate, heart rate and mean blood pressure were compared at the time points including baseline level (T 0); laryngoscopy (T lary); insertion of rigid bronchoscope (T bron); 5, 10 and 20 min during procedure (T 5 min, T 10 min, T 20 min); the end of procedure (Tend) and discharge (T dis). Induction time, emergence time, intubating condition scores and the incidence of adverse events were compared. RESULTS: Time for loss of consciousness (Group VIMA 95.6 ± 15.2 s vs. Group TIVA 146.2 ± 26.9 s, P < 0.05), time of Bispectral Index value decreased to 40 (Group VIMA 115.3 ± 16.5 s vs. Group TIVA 160.4 ± 25.8 s, P < 0.05) and emergence time (Group VIMA 10.5 ± 2.6 min vs. Group TIVA 16.9 ± 3.1 min, P < 0.05) in Group VIMA were significantly shorter than those in Group TIVA. Intubating condition scores between the two groups were comparable (8.1 ± 0.9 in Group VIMA vs. 8.1 ± 1.0 in Group TIVA). The incidence rates of breath holding (Group VIMA 6.25% vs. Group TIVA 31.25%, P < 0.05) and desaturation (Group VIMA 15.63% vs. Group TIVA 37.50%, P < 0.05) in Group VIMA were significantly lower than those in Group TIVA. Heart rate, mean blood pressure and respiratory rate were significantly higher in Group VIMA than in Group TIVA. CONCLUSION: Compared with propofol-remifentanil TIVA, sevoflurane VIMA provides more stable haemodynamics and respiration, faster induction and recovery and higher incidence of excitement in paediatric patients undergoing tracheal/bronchial foreign body removal under spontaneous breathing.

Spin-orbit torque switching in a T-type magnetic configuration with current orthogonal to easy axes.

Different symmetry breaking ways determine various magnetization switching modes driven by spin-orbit torques (SOT). For instance, an applied or effective field parallel to applied current is indispensable to switch magnetization with perpendicular anisotropy by SOT. Besides of this mode, here we experimentally demonstrate a distinct field-free switching mode in a T-type magnetic system with structure of MgO/CoFeB/Ta/CoFeB/MgO where a perpendicular layer with tilted easy axis was coupled to an in-plane layer with a uniaxial easy axis. Current was applied orthogonal to both easy axes and thus also normal to an in-plane effective field experienced by the perpendicular layer. Dynamic calculation shows perpendicular layer could be switched at the same time as the in-plane layer is switched. These field-free switching modes realized in the same T-type magnetic system might expedite the birth of multi-state spin memories or spin logic devices which could be operated by all electric manners.