Outbreak of enteric cryptosporidiosis in cockatiels (Nymphicus hollandicus).
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Animals↗
Biomedical subjects
Y K Kwon
Publications and source records attributed to Y K Kwon.
Determination of the subthreshold state contribution in 13C(alpha,n)16O, the main neutron-source reaction for the s process.
The reaction rate of the stellar reaction 13C(alpha,n)16O, which is currently considered to be the main neutron source for the slow (s) process at low energies, has been rederived using the direct alpha-transfer reaction 13C(6Li,d)17O leading to the subthreshold state at 6.356 MeV in 17O. The contribution of the subthreshold state is found to be much smaller than the currently accepted predictions for the main neutron source of the s process, indicating less of a role of this reaction as the neutron source for the s-process scenario in low-mass stars at the asymptotic giant branch.
Journal Article↗
Temporal and spatial expression of neurotrophins and their receptors during male germ cell development.
Spermatogenesis is a stepwise cellular differentiation process involving proliferation and commitment to differentiate in spermatogonia, meiosis in spermatocytes, and morphological changes in round spermatids. The whole process is regulated by intercellular communication between the germ cells and the supporting cells. In order to investigate whether neurotrophin family and their receptors contribute to the intercellular communication, we examined the expression of neurotrophins and their receptors in testis during spermatogenesis. One of neurotrophin family, NT-3 was expressed in spermatocytes and spermatogonia while its high affinity receptor, TrkC was found mainly in late spermatids and their low affinity receptor, TrkA in spermatocytes and round spermatids. On the other hand, BDNF immunoreactivity was found in Sertoli cells while its high affinity receptor, TrkB was found in spermatogonia. The temporally and spatially regulated expression of neurotrophins, NT-3 and BDNF, and their receptors, TrkC and TrkB, during male germ cell development suggests that neurotrophins play as the paracrine factors in the intercellular communication between the germ cells and the supporting somatic cells to control germ cell development.
Animals↗
Inhibition of neuronal nitric oxide synthase enhances cell proliferation in the dentate gyrus of the adrenalectomized rat.
Recent studies have demonstrated that the elimination of adrenal steroids by an adrenalectomy (ADX) increases the expression of neuronal nitric oxide synthase (NOS), and that it increases cell proliferation in the rat dentate gyrus. However, no evidence has been presented to date which indicates that NO regulates cell proliferation in the dentate gyrus of the adult rats. In this study, the effect of blocking NO production on ADX-induced increase of cell proliferation and serotonergic innervation was examined in the rat dentate gyrus. 7-nitroindazole (7-NI; 30 mg/kg, intraperitoneally), a selective inhibitor of neuronal NOS, was injected 1 day before an ADX and then once every 24 h for 4 days after the ADX subsequently. The proliferating cells were identified with 5-bromo-2-deoxyuridine (BrdU) immunostaining. Long-term inhibition of the neuronal NOS by 7-NI markedly increased the BrdU-labeled cell population density 4-18-fold in the dentate gyrus of the adrenalectomized rats compared to that in the vehicle-injected adrenalectomized rats. Immunoreactivity of serotonin, known as a mediator of granule cell genesis, was detected only in the dentate gyrus of 7-NI-injected adrenalectomized rats. These results indicate that NO may be involved in the cell proliferation in the dentate gyrus of the adrenalecomized rat and that serotonin may mediate the regulatory effect of NO on the cell proliferation in rat dentate gyrus.
Adrenal Cortex↗
FLASH coordinates NF-kappa B activity via TRAF2.
FLASH is a protein recently shown to interact with the death effector domain of caspase-8 and is likely to be a component of the death-inducing signaling complex in receptor-mediated apoptosis. Here we show that antisense oligonucleotide-induced inhibition of FLASH expression abolished TNF-alpha-induced activation of NF-kappaB in HEK293 cells, as determined by luciferase reporter gene expression driven by a NF-kappaB responsive promoter. Conversely, overexpression of FLASH dose-dependently activated NF-kappaB, an effect suppressed by dominant negative mutants of TRAF2, NIK, and IKKalpha, and partially by those of TRAF5 and TRAF6. TRAF2 was co-immunoprecipitated with FLASH from the cell extracts of HEK293 cells or HeLa cells stably expressing exogenous FLASH (HeLa/HA-FLASH). Furthermore, serial deletion mapping demonstrated that a domain spanning the residues 856-1191 of FLASH activated NF-kappaB as efficiently as the full-length and could directly bind to TRAF2 in vitro and in the transfected cells. Taken together, these results suggest that FLASH coordinates downstream NF-kappaB activity via a TRAF2-dependent pathway in the TNF-alpha signaling.
Animals↗
Effect of van der Waals interactions on the Raman modes in single walled carbon nanotubes.
We have measured the Raman spectrum of individual single walled carbon nanotubes in solution and compare it to that obtained from the same starting material where the tubes are present in ordered bundles or ropes. Interestingly, the radial mode frequencies for the tubes in solution are found to be approximately 10 cm (-1) higher than those observed for tubes in a rope, in apparent contradiction to lattice dynamics predictions. We suggest that there is no such contradiction, and propose that the upshift is due rather to a decreased energy spacing of the Van Hove singularities in isolated tubes over the spacings in a rope, thereby allowing the same laser excitation to excite different diameter tubes in these two samples.
Journal Article↗
Proapoptotic effects of tau cleavage product generated by caspase-3.
Using an in vitro translation assay to screen a human brain cDNA library, we isolated the microtubule-associated protein Tau and determined it to be a caspase-3 substrate whose C-terminal cleavage occurred during neuronal apoptosis. DeltaTau, the 50-kDa cleavage product, was detected by Western blot in apoptotic cortical cells probed with anti-PHF-1 and anti-Tau-5 antibodies, but not anti-T-46 antibody which recognizes the C-terminus. Overexpression of DeltaTau in SK-N-BE2(C) cells significantly increased the incidence of cell death. Staurosporine-induced Tau cleavage was blocked by 20 microM z-Asp-Glu-Val-Asp-chloromethylketone, a caspase-3 inhibitor, and in vitro, Tau was selectively cleaved by caspase-3 or calpain, a calcium-activated protease, but not by caspases-1, -8, or -9. (D421E)-Tau, a mutant in which Asp421 was replaced with a Glu, was resistant to cleavage by caspase-3 and tended to suppress staurosporine-induced cell death more efficiently than did wild-type Tau in both transient and stable expression systems. Finally, the incidence of DeltaTau-induced cell death was augmented by expression of Abeta precursor protein (APP) or Swedish APP mutant. Taken together, these results suggest that the caspase-3 cleavage product of Tau may contribute to the progression of neuronal cell death in Alzheimer's disease.
Amyloid beta-Protein Precursor↗
Differential activation of phospholipases by mitogenic EGF and neurogenic PDGF in immortalized hippocampal stem cell lines.
In several neuronal systems, nerve growth factor (NGF) and platelet-derived growth factor (PDGF) act as neurogenic agents, whereas epidermal growth factor (EGF) acts as a mitogenic agent. Hippocampal stem cell lines (HiB5) immortalized by the expression of a temperature-sensitive SV40 large T antigen also respond differentially to EGF and PDGF. While EGF treatment at the permissive temperature induces proliferation, the addition of PDGF induces differentiation at the non-permissive temperature. However, the mechanism responsible for these different cellular fates has not been clearly elucidated. In order to clarify possible critical signaling events leading to these distinct cellular outcomes, we examined whether either EGF or PDGF differentially induces the activation of phospholipases, such as phospholipase A(2) (PLA(2)), C (PLC), or D (PLD). Although EGF stimulation did not induce phospholipases, PDGF caused a rapid and transient activation of PLC and PLD, but not PLA(2). When the activation of PLC or PLD was blocked, the neurite outgrowth induced by PDGF was significantly inhibited. Although the activation of PLD occurred faster than PLC, blocking of PLD activity by transient expression of lipase-inactive mutants did not inhibit the induction of PLC activity by PDGF. These results suggest that the differential activation of phospholipases may play an important role in signal transduction by mitogenic EGF and neurotrophic PDGF in HiB5 neuronal hippocampal stem cells. In particular, the activation of phospholipase C and D may contribute to neuronal differentiation by neurogenic PDGF in the HiB5 cells.
Animals↗
Activation of retinoic acid receptor gamma induces proliferation of immortalized hippocampal progenitor cells.
In the present study, we report evidence that activation of RARgamma promotes cell proliferation in immortalized hippocampal progenitor cell line HiB5. We found that treatment of HiB5 cells with all-trans- (all-trans-RA) or 9-cis-retinoic acid (9-cis-RA) significantly increased the number of dead floating cells as well as viable cells in serum-free defined medium (N2). Flow cytometric analysis of DNA contents revealed that the proportion of apoptotic cells over the whole cell population was not affected by both retinoids. Instead, the proportion of S phase cells was significantly increased by retinoids. Under this condition, bcl-2 mRNA levels were significantly increased over time by retinoid treatment, whereas bax mRNA levels were not affected. This suggests that retinoids increase viable cells by enhancing proliferation rather than by suppressing apoptosis. In an attempt to dissect the molecular mechanism underlying retinoid-induced HiB5 cell proliferation, we examined the expression patterns of retinoid receptors following retinoid treatment. Retinoids induced RARgamma mRNA, which paralleled the increase in the transactivation of strong retinoic acid response element (RARE) reporter construct. Accordingly, treatment of HiB5 cells with RARgamma-selective agonist (CD666) increased HiB5 cell number in a dose-dependent manner, which was blocked by co-treatment with RARgamma-selective antagonist (CD2665). Taken together, these data clearly indicate that activation of RARgamma increases proliferation of immortalized hippocampal progenitor cells.
Alitretinoin↗
Effective gene transfer into regenerating sciatic nerves by adenoviral vectors: potentials for gene therapy of peripheral nerve injury.
Replication defective adenoviral vectors have been demonstrated as an effective method for delivering genes into a variety of cell types and tissues both in vivo and in vitro. Transfecting genes into neuronal cells has proven to be difficult because of their lack of cell division. Since the major problem in neurological disease is the degeneration of the terminally differentiated neuronal cells, the adenoviral vector's ability to transfer genes into differentiated post-mitotic cells makes them advantageous for a gene delivery system for the nervous system. Here we showed that a replication defective recombinant adenovirus carrying the lacZ gene could infect the neuronal stem cells and even the differentiated neuronal cells derived from the central nervous system. The lacZ gene delivered into the neuronal cells was expressed efficiently. In addition, the recombinant virus also infected Schwann cells in intact and injured nerves in vivo. The expression of the lacZ gene lasted for 5 weeks, within which nerve regeneration is accomplished in the rat. Adenoviral vectors might thus be used to modulate Schwann cell gene expression for treating peripheral nerve injury or peripheral neuropathy.
Adenoviridae↗
Sustained formation of focal adhesions with paxillin in morphological differentiation of PC12 cells.
Differentiation of PC12 cells triggered by nerve growth factor (NGF) is characterized by several well-defined events including induction of a set of neuron-specific genes, gain of membrane excitability, and morphological changes such as neurite outgrowth. Here we report that K252a, a protein kinase inhibitor, converts the proliferation signal of epidermal growth factor (EGF) into the morphological differentiation signal without inducing the sustained activation of ERK and the expression of neurofilament. Major effects of EGF/K252a, found also in the NGF-treated cells, are the sustained mobility shift of paxillin in SDS-PAGE and the promoted association of Crk-II with paxillin. These effects explain the prominent and robust development of peripheral focal adhesion assembly and stress fiber-like structures observed in the early stages of PC12 cell differentiation. These results suggest a model that cytoskeletal reorganization via focal adhesion assembly triggered by NGF provides a signal required for the morphological differentiation of PC12 cells.
Actin Cytoskeleton↗
Phytochrome signalling is mediated through nucleoside diphosphate kinase 2.
Because plants are sessile, they have developed intricate strategies to adapt to changing environmental variables, including light. Their growth and development, from germination to flowering, is critically influenced by light, particularly at red (660 nm) and far-red (730 nm) wavelengths. Higher plants perceive red and far-red light by means of specific light sensors called phytochromes(A-E). However, very little is known about how light signals are transduced to elicit responses in plants. Here we report that nucleoside diphosphate kinase 2 (NDPK2) is an upstream component in the phytochrome signalling pathway in the plant Arabidopsis thaliana. In animal and human cells, NDPK acts as a tumour suppressor. We show that recombinant NDPK2 in Arabidopsis preferentially binds to the red-light-activated form of phytochrome in vitro and that this interaction increases the activity of recombinant NDPK2. Furthermore, a mutant lacking NDPK2 showed a partial defect in responses to both red and farred light, including cotyledon opening and greening. These results indicate that NDPK2 is a positive signalling component of the phytochrome-mediated light-signal-transduction pathway in Arabidopsis.
Arabidopsis↗
Neuregulin stimulates myogenic differentiation in an autocrine manner.
During myogenesis, mononucleated myoblasts form multinucleated myotubes by membrane fusion. Efficiency of this intercellular process can be maximized by a simultaneous progress, with a time window, of other neighboring myoblasts in the differentiation program. This phenomenon has been described as the community effect. It proposes the existence of a molecule that acts as a differentiation-inducing signal to a group of identical cells. Here, we show that neuregulin is a strong candidate for this molecule in myoblast differentiation. The expression of neuregulin increased rapidly but transiently at early stage of differentiation of rat L6 cells. Neuregulin showed a potent differentiation-promoting activity in membrane fusion and expression of myosin heavy chain. The antibodies raised against neuregulin and its cognate receptor ErbB3, which were capable of neutralizing the signal pathway, inhibited myotube formation and expression of myosin heavy chain in both L6 cells and primary rat myoblasts. The progress of differentiation was mostly halted after the expression of myogenin and cell cycle arrest. These results suggest that the activation of an autocrine signaling of neuregulin may provide a basic mechanism for the community effect observed in the differentiation of the embryonic muscle cells.
Animals↗
Cholesterol-lowering activity of naringenin via inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase and acyl coenzyme A:cholesterol acyltransferase in rats.
The effects of dietary supplementation of a citrus bioflavonoid, naringenin, on the cholesterol metabolism were studied. For 42 days male rats were fed a 1% (wt/wt) high-cholesterol diet with or without a naringenin supplementation (0.1%, wt/wt) to study its effect on plasma lipid levels, hepatic lipid contents, activities of hepatic acyl coenzyme A:cholesterol O-acyltransferase (ACAT) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and the excretion of fecal neutral sterols. Naringenin did not significantly alter the concentration of plasma triglycerides, but lowered the plasma cholesterol (3.80 vs. 3.12 mmol/l) concentration and the hepatic cholesterol content (70.3 vs. 54.0 mg/g) significantly (p < 0.05) compared to those of the controls. HMG-CoA reductase (1,879.0 vs. 1,715.0 pmol/min/mg) and ACAT activities (806.0 vs. 563.0 pmol/min/mg) were significantly lower in the naringenin-supplemented group than in controls. Naringenin supplementation caused a marked decrease in the excretion of fecal neutral sterols (242.9 mg/day) compared to the controls (521.9 mg/day). These results show that naringenin lowers the plasma and hepatic cholesterol concentrations by suppressing HMG-CoA reductase and ACAT in rats fed a high-cholesterol diet.
Animals↗
Assignment of apoptotic protease activating factor-1 gene (APAF1) to human chromosome band 12q23 by fluorescence in situ hybridization.
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Apoptotic Protease-Activating Factor 1↗
Activation of ErbB2 during wallerian degeneration of sciatic nerve.
We used anti-phosphopeptide-immunodetecting antibodies as immunohistochemical reagents to define the location and activity state of p185(erbB2) during Wallerian degeneration. Nerve damage induces a phosphorylation event at Y1248, a site that couples p185(erbB2) to the Ras-Raf-MAP kinase signal transduction pathway. Phosphorylation of p185(erbB2) occurs within Schwann cells and coincides in time and space with Schwann cell mitotic activity, as measured by bromodeoxyuridine uptake. These visual images of receptor autophosphorylation link activation of p185(erbB2) to the Schwann cell proliferation that accompanies nerve regeneration.
Animals↗
Detection of activated platelet-derived growth factor receptors in human meningioma.
The beta receptor subunit of platelet-derived growth factor (PDGF) and its corresponding ligand (PDGF-BB) are coordinately expressed in fresh surgical isolates of human meningioma. These observations imply that PDGF autocrine loops are engaged in human meningioma and suggest that activated PDGF-beta receptors might contribute to the pathology of this common brain neoplasm. The study of PDGF autocrine loops and human meningioma has been slowed by the scarcity of meningioma cell culture model systems. Furthermore, in meningioma tumor tissue, the activation state of PDGF receptors is difficult to assess with conventional reagents, because the tumor is intermixed with normal stroma. In fact, there is no evidence that PDGF receptors within the tumor are activated by ligand. We used a synthetic tyrosine phosphopeptide to raise an antibody that reports the phosphorylation state of tyrosine 751 in the human PDGF-beta receptor. Phosphorylated tyrosine 751 is a recognition site for phosphatidylinositol 3'-kinase, a cytoplasmic effector of PDGF-induced mitogenesis, chemotaxis, and membrane ruffling. Immunoblotting and immunostaining analyses with this antibody show that the PDGF-beta receptor is constitutively phosphorylated at tyrosine 751 within multiple fresh surgical isolates of human meningioma. These findings are consistent with a role for activated PDGF receptors in the proliferation of human meningiomas.
3T3 Cells↗
Expression of brain-derived neurotrophic factor mRNA stimulated by basic fibroblast growth factor and platelet-derived growth factor in rat hippocampal cell line.
Brain-derived neurotrophic factor (BDNF) promotes neuronal cell survival and differentiation in the central nervous system. BDNF mRNA is expressed at high levels in hippocampus and BDNF serves as a trophic factor in primary cultures of rat hippocampus. A hippocampal stem cell line HIB5, which is immortalized by the temperature sensitive SV 40 T antigen, undergoes neuronal differentiation at non-permissive temperatures. During the differentiation process, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) facilitate cell survival and differentiation in HiB5 cells as well as in primary cultures of rat embryonic hippocampal cells. This report demonstrates that HiB5 cells express a functionally active PDGF beta receptor and that PDGF and bFGF stimulate the expression of BDNF within 2 h. These results propose that BDNF is a candidate mediator of trophic effects of PDGF and bFGF in the hippocampal stem cell line HiB5.
Animals↗