Detection and monitoring of SARS coronavirus in the plasma and peripheral blood lymphocytes of patients with severe acute respiratory syndrome.
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Adolescent↗
Biomedical subjects
Haibin Wang
Publications and source records attributed to Haibin Wang.
Immunization against endogenous inhibin increases normal oocyte/embryo production in adult mice.
The objectives of the present study were to induce super-ovulation in adult mice by immunoneutralization of endogenous inhibin and to investigate embryo development in vivo and in vitro. Adult female mice of the ddY strain at 3 mo of age were superovulated with a single ip injection of inhibin antiserum (inhibin-AS; 50, 100, or 200 micro L) at 12:00 h on metestrus of the 4-d estrous cycle. The control group was treated with 100 micro L normal goat serum (control serum). Five mice were sacrificed every 6 h and blood samples were collected for hormonal assay. Individual female mice were bred in the afternoon of proestrus with individual fertile males. Embryos were collected at 08.00 h on d 2 post-coitus and cultured in KSOM solution. Treatment with inhibin-AS significantly increased the concentrations of plasma FSH. Furthermore, there was a significant elevation in plasma concentrations of estradiol-17beta and progesterone in the inhibin-immunized groups in comparison with controls. The superovulated oocytes that were fertilized normally in vivo were able to develop normally to blastocysts in vitro. The number of oocytes and blastocysts developed in animals treated with inhibin-AS was significantly higher than that for mice treated with control serum. Moreover, the rate of fertilization and the rate of blastocyst development were similar in inhibin-AS treated and control groups. These results indicate that immunoneutralization of endogenous inhibin induces superovulation in adult mice without additional treatment with human chorionic gonadotropin (hCG). In addition, the superovulated oocytes obtained by administration of inhibin-AS have normal embryonic developmental competence.
Animals↗
Effects of the Chinese drugs for activating blood circulation on plasma TXB2 and 6-keto-PGF1alpha contents in rabbits with glucocorticoid-induced femoral head necrosis.
In the femoral head necrosis model rabbit induced by endotoxin combined with methylprenisolone, the dynamical changes of plasma TXB2 and 6-keto-PGF1alpha contents were observed. As a result, microscopic examination showed that in the model group, bone trabeculae became fine, empty bone lacunae increased, and osteoblasts in number decreased; the ratio of TXB2 and 6-keto-PGF1alpha was out of balance, and these changes worsened gradually with the lapse of time; Compound Sheng Mai Cheng Gu Capsules could reverse femoral head necrosis, protect the vascular endothelial cells, recover the balance of TXB2 and 6-keto-PGF1alpha. It is concluded that the hormone-induced femoral head necrosis is closely related with blood stasis, and that the Chinese drugs for activating blood circulation and removing blood stasis can prevent the femoral head from development of necrosis.
6-Ketoprostaglandin F1 alpha↗
[Separation and identification of red pigments in natural red yolk of duck's eggs by HPLC-MS-MS].
The natural red yolk of duck's eggs is produced by the laying duck in the lake areas in southward of China. In the laying duck breeding areas such as Honghu, Jianli, Xiantao, Tianmen and Hanchuan citys in Hubei Province, the culturists are used to feeding fresh pondweeds to the laying ducks. The yolk of duck's eggs is natural red with the chrominance reaching up to and/or above RCF (Roche Yolk Color Fan) 15. The red pigment components of natural red yolk of duck's eggs were separated and identified by thin layer chromatography (TLC), high performance liquid chromatography-mass spectrometry-mass spectrometry (HPLC-MS-MS) and high resolution electron impact-mass spectrometry (EI-MS). Four isomers of red pigments were separated by HPLC on a RP-C18 column with methanol-water (99.5:0.5, v/v) as mobile phase. The lambda(max) of the four components were 482, 488, 496, 501 nm, respectively, and all of them were single peak on chromatogram. They had the same molecular mass (Mr = 562), and had the same fragment peaks of MS2 with rhodoxanthin. The molecular formula of red pigments was determined as C40H50O2 by high resolution EI-MS. The results indicate that the red pigment is rhodoxanthin, and they are all cis-isomers of rhodoxanthin.
Animals↗
Rescue of female infertility from the loss of cyclooxygenase-2 by compensatory up-regulation of cyclooxygenase-1 is a function of genetic makeup.
Cyclooxygenase-2 (COX-2), an inducible rate-limiting enzyme in prostaglandin biosynthesis, is implicated in various physiological and pathological processes including female fertility, renal function, angiogenesis, inflammation, and tumorigenesis. We showed previously that targeted deletion of Ptgs2 encoding COX-2, but not Ptgs1 encoding COX-1, in C57BL/6J/129 mice produces complete female infertility resulting from multiple reproductive failures spanning ovulation, fertilization, and implantation. Here we show that Ptgs2 null mice on a CD1 background have dramatically improved female fertility including ovulation, fertilization, and implantation, giving rise to live births. We provide evidence that this improved fertility in CD1 Ptgs2 null mice is the result of a compensatory up-regulation of Ptgs1 which does not occur in C57BL/6J/129 mice missing Ptgs2. These results clearly demonstrate for the first time that COX-1 can replace specific functions of COX-2 in vivo in the context of genetic disparity. In light of this finding, the therapeutic use and efficacy of COX-2-specific inhibitors among human populations without regard for genetic and ethnic diversities should be revisited.
Animals↗
Differential G protein-coupled cannabinoid receptor signaling by anandamide directs blastocyst activation for implantation.
Mammalian fertility absolutely depends on synchronized development of the blastocyst to the stage when it is competent to implant, and the uterus to the stage when it is receptive to implantation. However, the molecular basis for the reciprocal interaction between the embryo and the uterus remains largely unexplored. One potentially important mechanism involves signaling between an evolutionarily conserved G protein-coupled protein cannabinoid receptor, CB1, that is expressed at high levels on the surface of the trophectoderm and anandamide (N-arachi-donoylethanolamine), an endocannabinoid ligand found to be produced at higher levels by the uterus before implantation and then down-regulated at the time of implantation. Using genetic, pharmacological, and physiological approaches, we show here that anandamide within a very narrow range regulates blastocyst function and implantation by differentially modulating mitogen-activated protein kinase signaling and Ca2+ channel activity via CB1 receptors. Anandamide at a low concentration (7 nM) induces extracellular regulated kinase phosphorylation and nuclear translocation in trophectoderm cells without influencing Ca2+ channels, and renders the blastocyst competent for implantation in the receptive uterus. In contrast, anandamide at a higher concentration (28 nM) inhibits Ca2+ channel activity and blastocyst competency for implantation without influencing mitogen-activated protein kinase signaling. Besides uncovering a potentially important regulatory mechanism for synchronizing blastocyst and uterine competency to implantation, this observation has high clinical relevance, because elevated levels of anandamide induce spontaneous pregnancy loss in women.
Animals↗
Differential expression of ezrin/radixin/moesin (ERM) and ERM-associated adhesion molecules in the blastocyst and uterus suggests their functions during implantation.
Development of the blastocyst to implantation competency, differentiation of the uterus to the receptive state, and a cross talk between the implantation-competent blastocyst and the uterine luminal epithelium are all essential to the process of implantation. In the present investigation, we examined the possibility for a potential cross talk between the blastocyst and uterus involving the ezrin/radixin/moesin (ERM) proteins and ERM-associated cytoskeletal cross-linker proteins CD43, CD44, ICAM-1, and ICAM-2. In normal Day 4 blastocysts and after rendering dormant blastocysts to implantation-competent by estrogen in vivo (activated), the outer surface of mural trophectoderm cells showed much higher levels of radixin as compared to those in the polar trophectoderm cells, inner cell mass (ICM), and primitive endoderm. In contrast, ezrin was present on both the mural and the polar trophectoderm cell surfaces of normal Day 4 and activated blastocysts at higher intensity than dormant blastocysts. A distinct localization was noted in the primitive endoderm of dormant blastocysts that was not apparent in activated or normal Day 4 blastocysts. The expression of moesin was modestly higher at the mural trophectoderm of implantation-competent blastocysts, while the localization appeared to be present primarily on the polar trophectoderm cell surface of Day 4 blastocysts. The localization of ERM-associated adhesion molecules CD43, CD44, and ICAM-2 was more intense in the implantation-competent blastocysts compared with the dormant blastocysts. However, while CD44 was present both in the trophectoderm and in ICM, CD43 and ICAM-2 were localized primarily to the trophectoderm. The signal for ICAM-1 was very intense in the ICM but was modest in the trophectoderm. No significant changes in fluorescence intensity were noted between activated and dormant blastocysts. In the receptive uterus on Day 4 of pregnancy, ERM proteins were localized to the uterine epithelium, while on Day 5 the localization, especially of radixin and moesin, extended to the stroma surrounding the implantation chamber. With respect to ERM-associated adhesion molecules, while CD44 and ICAM-1 were exclusively localized in the stroma on Day 4, CD43 and ICAM-2 were localized to the epithelium. On Day 5, the localization of CD44 and ICAM-1 became highly concentrated in the antimesometrial stroma of the implantation chamber. The localization of CD43 and ICAM-2 remained mostly epithelial, although some stromal localization of CD43 was noted on Day 5. These results suggest that differential expression and distribution of ERM proteins and ERM-associated adhesion molecules are involved in the construction of the cellular architecture necessary for blastocyst activation and uterine receptivity leading to successful implantation.
Animals↗
Protein kinase C phosphorylation sensitizes but does not activate the capsaicin receptor transient receptor potential vanilloid 1 (TRPV1).
Protein kinase C (PKC) modulates the function of the capsaicin receptor transient receptor potential vanilloid 1 (TRPV1). This modulation manifests as increased current when the channel is activated by capsaicin. In addition, studies have suggested that phosphorylation by PKC might directly gate the channel, because PKC-activating phorbol esters induce TRPV1 currents in the absence of applied ligands. To test whether PKC both modulates and gates the TRPV1 function by direct phosphorylation, we used direct sequencing to determine the major sites of PKC phosphorylation on TRPV1 intracellular domains. We then tested the ability of the PKC-activating phorbol 12-myristate 13-acetate (PMA) to potentiate capsaicin-induced currents and to directly gate TRPV1. We found that mutation of S800 to alanine significantly reduced the PMA-induced enhancement of capsaicin-evoked currents and the direct activation of TRPV1 by PMA. Mutation of S502 to alanine reduced PMA enhancement of capsaicin-evoked currents, but had no effect on direct activation of TRPV1 by PMA. Conversely, mutation of T704 to alanine had no effect on PMA enhancement of capsaicin-evoked currents but dramatically reduced direct activation of TRPV1 by PMA. These results, combined with pharmacological studies showing that inactive phorbol esters also weakly activate TRPV1, suggest that PKC-mediated phosphorylation modulates TRPV1 but does not directly gate the channel. Rather, currents induced by phorbol esters result from the combination of a weak direct ligand-like activation of TRPV1 and the phosphorylation-induced enhancement of the TRPV1 function. Furthermore, modulation of the TRPV1 function by PKC appears to involve distinct phosphorylation sites depending on the mechanism of channel activation.
Animals↗
Bd-->phi KS CP asymmetries as an important probe of supersymmetry.
The decay B(d)-->phi K(S) is a special probe of physics beyond the standard model (SM), since it has no SM tree level contribution. Motivated by recent data suggesting a deviation from the SM for its time-dependent CP asymmetry, we examine supersymmetric explanations. Chirality preserving contributions are generically small, unless gluino is relatively light. Higgs contributions are also too small to explain a large asymmetry. Chirality flipping LR and RL gluino contributions actually can provide sizable effects without conflict with all related results. We discuss how various insertions can be distinguished, and argue the needed sizes of mass insertions are reasonable.
Journal Article↗
cAMP-dependent protein kinase regulates desensitization of the capsaicin receptor (VR1) by direct phosphorylation.
The capsaicin receptor, VR1 (also known as TRPV1), is a ligand-gated ion channel expressed on nociceptive sensory neurons that responds to noxious thermal and chemical stimuli. Capsaicin responses in sensory neurons exhibit robust potentiation by cAMP-dependent protein kinase (PKA). In this study, we demonstrate that PKA reduces VR1 desensitization and directly phosphorylates VR1. In vitro phosphorylation, phosphopeptide mapping, and protein sequencing of VR1 cytoplasmic domains delineate several candidate PKA phosphorylation sites. Electrophysiological analysis of phosphorylation site mutants clearly pinpoints Ser116 as the residue responsible for PKA-dependent modulation of VR1. Given the significant roles of VR1 and PKA in inflammatory pain hypersensitivity, VR1 phosphorylation at Ser116 by PKA may represent an important molecular mechanism involved in the regulation of VR1 function after tissue injury.
Amino Acid Sequence↗
Dual source and target of heparin-binding EGF-like growth factor during the onset of implantation in the hamster.
Heparin binding EGF-like growth factor (HB-EGF), encoded by the Hegfl gene, is considered as an important mediator of embryo-uterine interactions during implantation in mice. However, it is unknown whether HB-EGF is important for implantation in species with different steroid hormonal requirements. In mice and rats, maternal ovarian estrogen and progesterone (P(4)) are essential to implantation. In contrast, blastocyst implantation can occur in hamsters in the presence of P(4) alone. To ascertain whether HB-EGF plays any role in implantation in hamsters, we examined the expression, regulation and signaling of HB-EGF in the hamster embryo and uterus during the periimplantation period. We demonstrate that both the blastocyst and uterus express HB-EGF during implantation. Hegfl is expressed solely in the uterine luminal epithelium surrounding the blastocyst prior to and during the initiation of implantation. Hypophysectomized P(4)-treated pregnant hamsters also showed a similar pattern of implantation-specific Hegfl expression. These results suggest that uterine Hegfl expression at the implantation site is driven by either signals emanating from the blastocyst or maternal P(4), but not by maternal estrogen. However, in ovariectomized hamsters, uterine induction of Hegfl requires the presence of estrogen and activation of its nuclear receptor (ER), but not P(4). This observation suggests an intriguing possibility that an estrogenic or unidentified signal from the blastocyst is the trigger for uterine HB-EGF expression. An auto-induction of Hegfl in the uterus by blastocyst-derived HB-EGF is also a possibility. We further observed that HB-EGF induces autophosphorylation of ErbB1 and ErbB4 in the uterus and blastocyst. Taken together, we propose that HB-EGF production and signaling by the blastocyst and uterus orchestrate the 'two-way' molecular signaling to initiate the process of implantation in hamsters.
Animals↗
[Simulation study of Kubicek formula for cardiac stroke volume calculation by 3-dimensional finite element method].
This paper deals with the clinical application value of Kubicek formula for cardiac stroke volume calculation from the angle of Kubicek model simulation by 3-dimensional finite element method. In the process of computer simulation, we have made a comparison between the result of model simulation, the specific value of Kubicek formula for cardiac stroke volume calculation, and the theoretical value of the prescribed model. The simulation results showed that an approximately linear relationship exists between the impedance change and the blood volume change of the aorta in the model, which has proved that Kubicek formula for cardiac stroke volume calculation has great clinical application value. On the other hand, the new method has opened up a path for studying the basic theory of impedance cardiography.
Algorithms↗