Biomedical subjects

Y Huang

Publications and source records attributed to Y Huang.

At least 37 records · Page 2Linked to original sources

PubMed2006

Reporter gene recombination in juxtaglomerular granular and collecting duct cells by human renin promoter-Cre recombinase transgene.

To assess the feasibility of using the renin promoter for expressing Cre recombinase in juxtaglomerular (JG) cells only, we generated five independent transgenic mouse lines (designated hRen-Cre) expressing Cre recombinase under control of a 12.2-kb human renin promoter. In the kidneys of adult mice Cre mRNA (RT-PCR) was found in the renal cortex, with Cre protein (immunohistochemistry) being localized in afferent arterioles and to a lower degree in interlobular arteries. Cre mRNA levels were regulated in a renin-typical fashion by changes in oral salt intake, water restriction, or isoproterenol infusion, indicating the presence of key regulatory elements within 12.2 kb of the 5'-flanking region of the human renin gene. hRen-Cre mice were interbred with both the ROSA26-EGFP and ROSA26-lacZ reporter strains to assess renin promoter activity from Cre-mediated excision of a floxed stop cassette and subsequent enhanced green fluorescent protein (EGFP) and beta-galactosidase (beta-gal) detection. In adult mice, beta-gal staining and EGFP were observed in afferent arterioles and interlobular arteries, overlapping with Cre protein expression. In addition, intense beta-gal staining was found in cortical and medullary collecting ducts where Cre expression was minimal. In embryonic kidneys, beta-gal staining was detected in the developing collecting duct system beginning at embryonic day 12, showing substantial activity of the human renin promoter in the branching ureteric bud. Our data indicate that besides its well-known activity in JG cells and renal vessels the human renin promoter is transiently active in the collecting duct system during kidney development, complicating the use of this approach for JG cell-specific excision of floxed targets.

Animals↗

PubMed2006

Preparation of bioactive nanotitania ceramics with biomechanical compatibility.

In this article, bioactive nanotitania ceramics with biomechanical compatibility was prepared by using an additive of hydroxyapatite or MgO as particle growth inhibitor. After sintering at 1000 degrees C, the particle size of nanotitania ceramics prepared by using HA as additive (HT) was much smaller than that prepared by using MgO as additive (MT). In simulated body fluid (SBF), HT could induce apatite formation in 4 days, while no apatite could be found on MT even after it was soaked in SBF for 14 days. After Ros17/28 osteoblasts were cultured on the materials for 1, 4, and 6 days, MTT results showed that the osteoblasts on the HT differentiated faster than that on the MT. Mechanical tests results showed that the bending and compressive strength of HT were 160 and 200 MPa, while those of MT were 70 and 88 MPa, respectively. These results demonstrated that it is suitable to prepare bioactive nanotitania ceramics, with biomechanical compatibility, by using HA as particle growth inhibitor.

Animals↗

PubMed2006

Protein kinase C can inhibit TRPC3 channels indirectly via stimulating protein kinase G.

There are two known phosphorylation-mediated inactivation mechanisms for TRPC3 channels. Protein kinase G (PKG) inactivates TRPC3 by direct phosphorylation on Thr-11 and Ser-263 of the TRPC3 proteins, and protein kinase C (PKC) inactivates TRPC3 by phosphorylation on Ser-712. In the present study, we explored the relationship between these two inactivation mechanisms of TRPC3. HEK cells were first stably transfected with a PKG-expressing construct and then transiently transfected with a TRPC3-expressing construct. Addition of 1-oleoyl-2-acetyl-sn-glycerol (OAG), a membrane-permeant analog of diacylglycerol (DAG), elicited a TRPC3-mediated [Ca2+]i rise in these cells. This OAG-induced rise in [Ca2+]i could be inhibited by phorbol 12-myristate 13-acetate (PMA), an agonist for PKC, in a dose-dependent manner. Importantly, point mutations at two PKG phosphorylation sites (T11A-S263Q) of TRPC3 markedly reduced the PMA inhibition. Furthermore, inhibition of PKG activity by KT5823 (1 microM) or H8 (10 microM) greatly reduced the PMA inhibition of TRPC3. These data strongly suggest that the inhibitory action of PKC on TRPC3 is partly mediated through PKG in these PKG-overexpressing cells. The importance of this scheme was also tested in vascular endothelial cells, in which PKG plays a pivotal functional role. In these cells, OAG-induced [Ca2+]i rise was inhibited by PMA, which activates PKC, and by 8-BrcGMP and S-nitroso-N-acetylpenicillamine (SNAP), both of which activate PKG. Importantly, the PMA inhibition on OAG-induced [Ca2+]i rise was significantly reduced by PKG inhibitor KT5823 (1 microM) or DT-3 (500 nM), suggesting an important role of PKG in the PMA-induced inhibition of TRPC channels in native endothelial cells.

Animals↗

PubMed2006

Effects of recombinant human growth hormone on acute lung injury in endotoxemic rats.

OBJECTIVE: To investigate the effects of recombinant human growth hormone (rhGH) on rat acute lung injury (ALI). METHODS: ALI was mimicked by intraperitoneal (i. p.) injection of E. coli. Female Sprague-Dawley rats were randomized into three groups: control group, injected with physiologic saline (i. p.); ALI group, received a bolus injection of E. coli (1 x 10(10) cfu/l, 15 ml/kg, i. p.) followed by intramuscular physiologic saline injection; and ALI + GH group, received a bolus administration of E. coli, and then treated with intramuscular rhGH injection (2.25 U/kg/d). ALI group and ALI + GH group were subdivided into day 1 and day 3 subgroups, respectively. Left lungs were lavaged and bronchial alveolar lavage fluid (BALF) was harvested. Lung injury score, lung wet-to-dry weight (W/D) ratio, percentage of neutrophils (PMNs) in BALF, lung permeability index (LPI), intercellular adhesion molecule-1(ICAM-1) expression and activation of nuclear factor-kappa B (NF-kappaB) in the lungs were determined. RESULTS: (1) On day 1 and day 3, the lung injury score, lung W/D ratio, LPI and protein content in BALF were significantly higher in the ALI group than in the control and ALI + GH groups. rhGH attenuated lung injuries significantly. (2) Compared with the control group, the percentage of PMNs in BALF was elevated significantly in the ALI and ALI + GH groups, especially in ALI group. (3) Nuclear positive rate of NF-kappaB and ICAM-1 expression at the levels of protein and mRNA in the lung in the ALI group on day 1 and day 3 were higher than in the control group. rhGH diminished activation of NF-kappaB and expression of ICAM-1 in the lung markedly. CONCLUSIONS: Treatment with rhGH can significantly attenuate lung injury in the endotoxemic rats, which may be attributed to the reduction of the expression of ICAM-1, the influence on the adhesion and activation of PMNs, the inhibition of the activation of NF-kappaB and the regulation of the transcription of certain proinflammatory cytokines.

Animals↗

PubMed2006

Renin increases mesangial cell transforming growth factor-beta1 and matrix proteins through receptor-mediated, angiotensin II-independent mechanisms.

Recent evidence suggesting a strong interplay between components of the renin-angiotensin system and key mediators of fibrosis led us to hypothesize that renin, independent of its enzymatic action to enhance angiotensin (Ang) II synthesis, directly increases production of the fibrogenic cytokine transforming growth factor (TGF)-beta. Human or rat mesangial cells (MCs) were treated with human recombinant renin (HrRenin) or rat recombinant renin (RrRenin) and the effects on TGF-beta1, plasminogen activator inhibitor-type 1 (PAI-1), fibronectin (FN) and collagen 1 mRNA and protein were investigated. Blockade of the rat MC renin receptor was achieved using siRNA. HrRenin or RrRenin, at doses shown to be physiologically relevant, induced marked dose- and time-dependent increases in TGF-beta1. These effects were not altered by adding an inhibitor of renin's enzymatic action (RO 42-5892), the Ang II receptor antagonist losartan or the Ang-converting enzyme inhibitor enalapril. RrRenin also induced PAI-1, FN and collagen 1 mRNA and PAI-1 and FN protein in a dose-dependent manner. Neutralizing antibodies to TGF-beta partially blocked these effects. Supernatant and cell lysate Ang I and Ang II levels were extremely low. MC angiotensinogen mRNA was undetectable both with and without added renin. Targeting of the rat renin receptor mRNA with siRNA blocked induction of TGF-beta1. We conclude that renin upregulates MC TGF-beta1 through a receptor-mediated mechanism, independent of Ang II generation or action. Renin-induced increases in TGF-beta1 in turn stimulate increases in PAI-1, FN and collagen I. Thus, renin may contribute to renal fibrotic disease, particularly when therapeutic Ang II blockade elevates plasma renin.

Angiotensin II↗

PubMed2006

Perspectives on blockade of TGFbeta overexpression.

Many approaches to blocking profibrotic TGFbeta overexpression are under way. Therapeutic targeting of TGFbeta-Smad signaling holds promise for slowing or halting progressive renal disease. In this issue, Fukasawa et al., using the unilateral ureteral obstruction model, provide a new target for therapeutic intervention by identifying loss of the Smad corepressors Ski and SnoN as a mechanism that amplifies the profibrotic actions of TGFbeta.

Animals↗

PubMed2006

Effects of alveolar macrophage depletion on liposomal vaccine protection against respiratory syncytial virus (RSV).

Little is known about the identities and roles of antigen-presenting cells upon exposure to antigens of respiratory syncytial virus (RSV). Here, we focused on elucidating the importance of alveolar macrophages in conferring protective immunity in mice administered a liposome-encapsulated recombinant fragment of the RSV G protein. Mice were depleted of alveolar macrophages by intranasal inoculation of liposome-encapsulated dichloromethylenediphosphonic acid (DMDP). Mice depleted of alveolar macrophages prior to immunization developed reduced levels of serum RSV-neutralizing antibody and showed dramatically impaired protection against RSV challenge. The severity of interstitial inflammation was also markedly reduced in macrophage-depleted mice. In conclusion, this study demonstrates a pivotal role for alveolar macrophages during exposure to liposome-encapsulated RSV antigen in initiating both protective and histopathological responses against RSV.

Animals↗

PubMed2006

Infection with a periodontal pathogen induces procoagulant effects in human aortic endothelial cells.

BACKGROUND: Multiple studies have demonstrated a link between periodontal infections and vascular disease. Porphyromonas gingivalis, a major periodontal pathogen, has been shown to adhere to and invade endothelial cells. OBJECTIVE: In order to dissect mechanisms underlying these observations, we assessed the role of P. gingivalis infection in modulating properties of endothelial cells linked to atherothrombosis. METHODS: Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. Markers of coagulation and thrombosis were assessed 8 h and 18 h postinfection in cell lysates and supernatants. RESULTS: Infection with P. gingivalis 381 significantly enhanced tissue factor expression and activity, and suppressed levels of tissue factor pathway inhibitor. Furthermore, P. gingivalis infection decreased levels and activity of tissue plasminogen activator, and enhanced plasminogen activator inhibitor-1 antigen and activity. Consistent with an important role for bacterial adhesion/invasion in this setting, infection with DPG3 failed to induce procoagulant properties in HAEC. Most of the above effects of P. gingivalis 381 were more apparent at the later time point (18 h postinfection). This suggests that P. gingivalis infection, rather than having an immediate and direct effect, might activate pathways that, in turn, trigger endothelial procoagulant mechanisms. CONCLUSIONS: Taken together these data demonstrate for the first time that infection with a periodontal pathogen induces procoagulant responses in HAEC.

Aorta↗

PubMed2006

Apolipoprotein (apo) E4 and Alzheimer's disease: unique conformational and biophysical properties of apoE4 can modulate neuropathology.

The unique structural and biophysical features of apolipoprotein (apo) E4 - domain interaction and molten globule formation - have been correlated with the detrimental effects of apoE4 in neuropathology. Two examples of how the structure of apoE4 determines the pathological outcome in neurons include apoE4 potentiation of amyloid beta-induced lysosomal leakage and apoptosis and the proteolytic cleavage of apoE synthesized by neurons. Thus, a new therapeutic target is to identify small molecules to modulate the inherent neuropathological structure of apoE4, i.e. to prevent domain interaction and to convert apoE4 to an apoE3-like molecule. A second therapeutic target is to inhibit the apoE-cleaving enzyme. This would prevent the generation of the reactive carboxyl-terminal fragments of apoE that enter the cytosol, disrupt the cytoskeleton, and cause neurodegeneration. ApoE4 is more susceptible than apoE3 to proteolytic cleavage and is thus more likely to cause detrimental effects in the central nervous system. It is predictable that apoE4 acts through various pathways to cause cognitive decline and neurodegeneration.

Alzheimer Disease↗

PubMed2006

Dissociation of food and opiate preference by a genetic mutation in zebrafish.

Both natural rewards and addictive substances have the ability to reinforce behaviors. It has been unclear whether identical neural pathways mediate the actions of both. In addition, little is known about these behaviors and the underlying neural mechanisms in a genetically tractable vertebrate, the zebrafish Danio rerio. Using a conditioned place preference paradigm, we demonstrate that wildtype zebrafish exhibit a robust preference for food as well as the opiate drug morphine that can be blocked by the opioid receptor antagonist naloxone. Moreover, we show that the too few mutant, which disrupts a conserved zinc finger-containing gene and exhibits a reduction of selective groups of dopaminergic and serotonergic neurons in the basal diencephalon, displays normal food preference but shows no preference for morphine. Pretreatment with dopamine receptor antagonists abolishes morphine preference in the wildtype. These studies demonstrate that zebrafish display measurable preference behavior for reward and show that the preference for natural reward and addictive drug is dissociable by a single-gene mutation that alters subregions of brain monoamine neurotransmitter systems. Future genetic analysis in zebrafish shall uncover further molecular and cellular mechanisms underlying the formation and function of neural circuitry that regulate opiate and food preference behavior.

Analysis of Variance↗

PubMed2006

Increased HO-1 expression and decreased iNOS expression in the hippocampus from adult spontaneously hypertensive rats.

Brain expression of heme oxygenase (HO) and nitric oxide synthase (NOS) in hypertension may participate in the pathogenesis of hypertension-related neuronal disorders, such as vascular dementia. In the present study, expression levels of HO and NOS in spontaneously hypertensive rats (SHR) were investigated using Western immunoblotting assay. Expression level of inducible HO-1 in hippocampus of 4-wk prehypertensive SHR was about twofold of that in age-matched Sprague-Dawley (SD) rats (p < 0.01). In 23-wk SHR with fully developed hypertension, hippocampal HO-1 level was significantly greater than that of age-matched SD rats (p < 0.05), but not different from 4-wk SHR. There was no difference in expression levels of hippocampal HO-2 between SHR and SD rats at different ages. Total enzymatic activity of hippocampal HO was significantly greater in 23-wk SHR than in age-matched SD rats or 4-wk SD/SHR (p < 0.01). Although hippocampal expression of nNOS protein was relatively unchanged, iNOS expression in 23-wk SHR was about fourfold lower than that in age-matched SD rats and 4-wk SD/SHR (p < 0.01). Total enzymatic activity of hippocampal NOS was significantly lower in 23-wk SHR than in age-matched SD rats or 4-wk SD/SHR (p < 0.01). Significantly suppressed Morris water maze performance was found in 23-wk SHR in comparison with age-matched SD rats. Because SHR has been used as a model of vascular dementia and hippocampus is essential for spatial learning and memory, understanding of altered HO/CO and NOS/NO systems in the hippocampus of adult SHR may shed light on the pathogenic development of memory deficits associated with vascular dementia.

Aging↗

PubMed2005

Impaired transforming growth factor beta signalling in Barrett's carcinogenesis due to frequent SMAD4 inactivation.

BACKGROUND AND AIMS: Transforming growth factor beta (TGF-beta) is frequently involved in gastrointestinal carcinogenesis although its contribution to oesophageal adenocarcinoma (AC) and its precursor Barrett's oesophageal epithelium (BE) metaplasia are unclear. METHODS: Expression of TGF-beta signalling components was assessed by reverse transcription-polymerase chain reaction (PCR), western blot, and immunohistochemistry in oesophageal endoscopic biopsies and cell lines. Genomic alterations in SMAD4 were characterised by fluorescence in situ hybridisation, methylation specific PCR, and sequencing. Functional integrity of TGF-beta signalling was assessed by characterisation of p21 and proliferation status. Smad4 negative BIC-1 cells were transiently transfected with smad4 and TGF-beta responsiveness evaluated. RESULTS: smad4 mRNA expression was progressively reduced in the metaplasia-dysplasia-adenocarcinoma sequence (p<0.01). A quarter of AC samples displayed an abnormal Smad4 protein isoform, with no corresponding changes in gene sequence or organisation. Methylation of smad4 has not been described previously but we found promoter methylation in 70% of primary AC samples. In 6/8 oesophageal cell lines, chromosomal rearrangements affected the smad4 locus. Lack of smad4 expression in BIC-1 cells occurred secondary to loss of one copy and extensive deletion of the second allele's promoter region. TGF-beta dependent induction of p21 and downregulation of minichromosome maintenance protein 2 was lost in >80% of BE and AC. TGF-beta failed to inhibit proliferation in 5/8 oesophageal cell lines. In BIC-1, the antiproliferative response was restored following transient transfection of smad4 cDNA. CONCLUSIONS: In BE carcinogenesis, downregulation of Smad4 occurs due to several different mechanisms, including methylation, deletion, and protein modification. Frequent alterations in TGF-beta signalling lead to a functionally significant impairment of TGF-beta mediated growth suppression.

Adenocarcinoma↗

PubMed2005

In vitro and in vivo characterization of recombinant human butyrylcholinesterase (Protexia) as a potential nerve agent bioscavenger.

Previous studies in rodents and nonhuman primates have demonstrated that pretreatment with cholinesterases can provide significant protection against behavioral and lethal effects of nerve agent intoxication. Human butyrylcholinesterase (HuBuChE) purified from plasma has been shown to protect against up to 5 x LD50s of nerve agents in guinea pigs and non-human primates, and is currently being explored as a bioscavenger pretreatment for human use. A recombinant form of HuBuChE has been expressed in the milk of transgenic goats as a product called Protexia. Protexia was supplied by Nexia Biotechnologies (Que., Canada) as a purified solution with a specific activity of 600 U/mg. Initial in vitro studies using radiolabeled 3H-soman or 3H-DFP (diisopropyl fluorophosphate) demonstrated that these inhibitors specifically bind to Protexia. When Protexia was mixed with soman, sarin, tabun or VX using varying molar ratios of enzyme to nerve agent (8:1, 4:1, 1:1 and 1:4, respectively), the data indicated that 50% inhibition of enzyme activity occurs around the 1:1 molar ratio for each of the nerve agents. Protexia was further characterized for its interaction with pyridostigmine bromide and six unique carbamate inhibitors of cholinesterase. IC50 and Ki values for Protexia were determined to be very similar to those of HuBuChE purified from human plasma. These data suggest that Protexia has biochemical properties very similar to those HuBuChE when compared in vitro. Together these data the continued development of the goat milk-derived recombinant HuBuChE Protexia as a potential bioscavenger of organophosphorus nerve agents.

Animals↗

PubMed2005

Human airway smooth muscle cells express eotaxin in response to signaling following mast cell contact.

BACKGROUND: Asthma is a chronic inflammatory disease of the airways. Mast-cell (MC)-derived cytokines may mediate both airway inflammation and remodeling. It has also been shown that airway smooth muscle cells (ASMC) can be a source of proinflammatory cytokines. In the human airways, MC-ASMC cell interactions may have pivotal effects on modulating inflammation. OBJECTIVES: We wanted to know whether the production of eotaxin, an important proinflammatory cytokine, through a cell-to-cell contact mechanism of human ASMC activation by MC was mediated by p38 MAPK. METHODS: We cocultured normal humanASMC with a human MC line (HMC-1) and assayed for the production of eotaxin. RESULTS: When cultured together, human ASMC and HMC-1 contact induced eotaxin secretion. Separation of HMC-1 and human ASMC by a porous membrane inhibited this induction. Coculturing of human ASMC with HMC-1 induced increased expression of eotaxin gene mRNA. HMC-1-derived cellular membranes caused an increase in eotaxin production in human ASMC. Activation of p38 MAPK was also seen in cocultures by Western blot, whereas eotaxin production in cocultures was significantly inhibited by the p38 inhibitor SB203580. CONCLUSION: These novel studies reveal the importance of cell-to-cell interactions in the complex milieu of airway inflammation.

Blotting, Western↗

PubMed2005

Reduced autoregulatory effectiveness in adenosine 1 receptor-deficient mice.

Adjustments of renal vascular resistance in response to changes in blood pressure are mediated by an interplay between the myocyte-inherent myogenic and the kidney-specific tubuloglomerular feedback (TGF) mechanisms. Using mice with deletion of the A(1) adenosine receptor (A1AR) gene, we tested the prediction that the absence of TGF, previously established to result from A1AR deficiency, is associated with a reduction in the efficiency of autoregulation. In anesthetized wild-type (A1AR+/+) and A1AR-deficient mice (A1AR-/-), glomerular filtration rate (GFR) and renal blood flow (RBF) were determined before and after reducing renal perfusion pressure through a suprarenal aortic clamp. In response to a blood pressure reduction by 15.9 +/- 1.34 mmHg in A1AR-/- (n = 9) and by 14.2 +/- 0.9 mmHg in A1AR+/+ mice (n = 8; P = 0.31), GFR fell by 187.9 +/- 37 mul/min and by 72.3 +/- 10 mul/min in A1AR-/- and A1AR+/+ mice, respectively (P = 0.013). Similarly, with pressure reductions of 14.8 +/- 1.1 and 13.3 +/- 1.5 mmHg in A1AR-/- (n = 9) and wild-type mice (n = 8), respectively (P = 0.43), RBF fell by 0.17 +/- 0.02 ml/min in A1AR-/- mice and by only 0.08 +/- 0.02 ml/min in wild-type animals (P = 0.0039). Autoregulatory indexes for both GFR and RBF were significantly higher in A1AR-/- compared with A1AR+/+ mice, indicating reduced regulatory responsiveness in the knockout animals. We conclude that autoregulation of renal vascular resistance is less complete in A1AR-deficient mice, an effect that is presumably related to absence of TGF regulation in these animals.

Animals↗

PubMed2005

Vasoconstrictor and vasodilator effects of adenosine in the mouse kidney due to preferential activation of A1 or A2 adenosine receptors.

The present experiments in mice were performed to determine the steady-state effects of exogenous adenosine on the vascular resistance of the whole kidney, of superficial blood vessels, and of afferent arterioles. The steady-state effect of an intravenous infusion of adenosine (5, 10, and 20 microg/min) in wild-type mice was vasodilatation as evidenced by significant reductions of renal and superficial vascular resistance. Resistance decreases were augmented in adenosine 1 receptor (A1AR) -/- mice. Renal vasodilatation by the A2aAR agonist CGS 21680A [2-p-(2-carboxyethyl)phenethyl-amino-5'-N-ethylcarboxamido-adenosine hydrochloride] (0.25, 0.5, and 1 microg/kg/min) and inhibition of adenosine-induced relaxation by the A2aAR antagonist ZM-241385 [4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-yl-amino]ethyl)phenol] (20 mg/kg) suggests that the reduction of renovascular resistance was largely mediated by A2aAR. After treatment with Nomega-nitro-L-arginine methyl ester (L-NAME) adenosine was unable to alter superficial blood flow and resistance significantly indicating that adenosine-induced dilatation is NO-dependent. Absence of a dilatory effect in endothelial nitric-oxide synthase (NOS) -/- mice suggests endothelial NOS as the source of NO. When infused into the subcapsular interstitium, adenosine reduced superficial blood flow through A1AR activation. Adenosine (10(-7) M) constricted isolated perfused afferent arterioles when added to the bath but not when added to the luminal perfusate. Luminal adenosine caused vasoconstriction in the presence of L-NAME or the A2AR antagonist 3,7-dimethyl-1-(2-propynyl)xanthine. Our data show that global elevation of renal adenosine causes steady-state vasorelaxation resulting from adenosine 2 receptor (A2AR)-mediated generation of NO. In contrast, selective augmentation of adenosine around afferent arterioles causes persistent vasoconstriction, indicating A1AR dominance. Thus, adenosine is a renal constrictor only when it can interact with afferent arteriolar A1AR without affecting the bulk of renal A2AR at the same time.

Adenosine↗

PubMed2005

From Al4B2O9 nanowires to BN-coated Al18B4O33 nanowires.

A novel route was proposed to completely coat aluminum borate nanowires by in situ providing the precursor for BN coating. Uniformly BN-coated Al18B4O33 nanowires could be obtained by the reaction of Al4B2O9 nanowires with ammonia at high temperature. The high-temperature unstable Al4B2O9 nanowires were converted into Al18B4O33 nanowires, simultaneously evaporated boron oxide. The reaction between the in situ generated vapors and ammonia ensures that the BN layers are attached tightly on the surface of the as-formed Al18B4O33 nanowires.

Letter↗

PubMed2005

Phylogenetic and recombination analysis of coronavirus HKU1, a novel coronavirus from patients with pneumonia.

Phylogenetic trees constructed using predicted amino acid sequences of putative proteins of coronavirus HKU1 (CoV-HKU1) revealed that CoV-HKU1 formed a distinct branch among group 2 coronaviruses. Of the 14 trees from p65 to nsp10, nine showed that CoV-HKU1 was clustered with murine hepatitis virus. From nsp11, the topologies of the trees changed dramatically. For the eight trees from nsp11 to N, seven showed that the CoV-HKU1 branch was the first branch. The codon usage patterns of CoV-HKU1 differed significantly from those in other group 2 coronaviruses. Split decomposition analysis revealed that recombination events had occurred between CoV-HKU1 and other coronaviruses.

Codon↗