10,969 research outputs found
Use of Diagnosis-Based Risk Adjustment Models to Predict Individual Healthcare Expenditure under the National Health Insurance in Taiwan
No full textTransposon mutagenesis and cloning of the genes encoding the enzymes of fengycin biosynthesis in Bacillus subtilis.
No full textStructural requirements of mastoparan for activation of membrane-bound guanylate-cyclase.
No full textStatistical optimization of medium components for the production of Antrodia cinnamomea AC0623 in submerged cultures.
No full text
Dinuclear niobium(III), tantalum(III) and tantalum(IV) complexes with thioether and selenoether ligands
Full text linkMagnesium reduction of MCl5 (M = Nb or Ta) in the presence of R2S (R = Me or nBu) affords the complexes [M2Cl4(R2S)2(μ-Cl)2(μ-R2S)]. The X-ray structures of those complexes where M = Nb or Ta, R = nBu2S, and of a new polymorph of [Ta2Cl4(Me2S)2(μ-Cl)2(μ-Me2S)], show that they have confacial bi-octahedral structures with M=M double bonds. The reactions of [Nb2Cl4(R2S)2(μ-Cl)2(μ-R2S)] with MeSCH2CH2SMe, MeSeCH2CH2SeMe or MeSeCH2CH2CH2SeMe produce the edge-linked dimers [Nb2Cl4(MeSCH2CH2SMe)2(μ-Cl)2] and [Nb2Cl4{MeSe(CH2)nSeMe}2(μ-Cl)2], all with M=M double bonds (M26+). The tantalum diselenoether complex, [Ta2Cl4(MeSeCH2CH2SeMe)2(μ-Cl)2], is similar. Two “dimer of dimers”, [{Nb2Cl4(μ-Cl)2(μ-Me2S)}2(μ-MeSeCH2CH2CH2SeMe)2] and [{Ta2Cl4(μ-Cl)2(μ-Me2S)}2(μ-nBuSeCH2CH2CH2SenBu)2], containing confacial bi-octahedra linked by diselenoether bridges, were obtained as minor by-products and were identified via their X-ray crystal structures. The xylyl-linked diselenoether, o-C6H4(CH2SeMe)2, gave a complex mixture of products, including [Ta2Cl4{o-C6H4(CH2SeMe)2}2(μ-Se)2]. The complexes were characterised by microanalysis, IR and UV–visible spectroscopy. X-ray crystal structures are reported for [Nb2Cl6(nBu2S)3], [Ta2Cl6(nBu2S)3], [Ta2Cl8(Me2S)2], [Ta2Cl6(Me2S)3], [Ta2Cl4{o-C6H4(CH2SeMe)2}2(Se)2], [{Ta2Cl6(Me2S)(nBuSeCH2CH2CH2SenBu)}2] and [Ta2Cl4(Me2S)4(S)2]
Outcome and prognostic factors in critically ill patients with systemic lupus erythematosus: a retrospective study.
No full textDifferential Regulation of Ca2+-Activated Cl− Channel TMEM16A Splice Variants by Membrane PI(4,5)P2
Full text linkTMEM16A is a Ca2+-activated Cl− channel that controls broad cellular processes ranging from mucus secretion to signal transduction and neuronal excitability. Recent studies have reported that membrane phospholipid phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is an important cofactor that allosterically regulates TMEM16A channel activity. However, the detailed regulatory actions of PIP2 in splice variants of TMEM16A remain unclear. Here, we demonstrated that the attenuation of membrane phosphoinositide levels selectively inhibited the current amplitude of the TMEM16A(ac) isoform by decreasing the slow, but not instantaneous, Cl− currents, which are independent of the membrane potential and specific to PI(4,5)P2 depletion. The attenuation of endogenous PI(4,5)P2 levels by the activation of Danio rerio voltage-sensitive phosphatase (Dr-VSP) decreased the Cl− currents of TMEM16A(ac) but not the TMEM16A(a) isoform, which was abolished by the co-expression of PIP 5-kinase type-1γ (PIPKIγ). Using the rapamycin-inducible dimerization of exogenous phosphoinositide phosphatases, we further revealed that the stimulatory effects of phosphoinositide on TMEM16A(ac) channels were similar in various membrane potentials and specific to PI(4,5)P2, not PI4P and PI(3,4,5)P3. Finally, we also confirmed that PI(4,5)P2 resynthesis is essential for TMEM16A(ac) recovery from Dr-VSP-induced current inhibition. Our data demonstrate that membrane PI(4,5)P2 selectively modulates the gating of the TMEM16A(ac) channel in an agonistic manner, which leads to the upregulation of TMEM16A(ac) functions in physiological conditions
- …
