The LiCl effect on the conformation of lentinan in DMSO.

Lentinan (β-(1→3)-D-glucan) was found to be successfully fractionated by the mixture of dimethyl sulfoxide (DMSO) and lithium chloride (LiCl) as a solvent and acetone as a precipitant. Light scattering and viscosity measurements were made on solutions of fractionated samples in pure DMSO and 0.2M LiCl/DMSO in the range of the molecular weight M(w) from 21.

Comparison of neurobehavioral effects of methylmercury exposure in older and younger adult zebrafish (Danio rerio).

It is widely recognized that the nature and severity of responses to toxic exposure are age-dependent. Using active avoidance conditioning as the behavioral paradigm, the present study examined the effect of short-term methylmercury (MeHg) exposure on two adult age classes, 1- and 2-year-olds to coincide with zebrafish in relatively peak vs. declining health conditions.

Disruption of Contactin 4 in two subjects with autism in Chinese population.

Autism is a heterogeneous childhood neurodevelopmental disorder that is characterised by deficits in verbal communication, impaired social interactions, restricted interests and repetitive behaviours. Using an Illumina HumanCNV370-Quad BeadChip, we identified two Han Chinese individuals with autism and large duplications (~1.6 Mb and ~2.

β-Glucan from Saccharomyces cerevisiae reduces lipopolysaccharide-induced inflammatory responses in RAW264.7 macrophages.

Background: β-Glucans obtained from fungi, such as baker's yeast (Saccharomyces cerevisiae)-derived β-glucan (BBG), potently activate macrophages through nuclear factor κB (NFκB) translocation and activation of its signaling pathways. The mechanisms by which β-glucans activate these signaling pathways differ from that of lipopolysaccharide (LPS). However, the effects of β-glucans on LPS-induced inflammatory responses are poorly understood.

A novel splicing mutation in COL1A1 gene caused type I osteogenesis imperfecta in a Chinese family.

Osteogenesis imperfect (OI) is a heritable connective tissue disorder with bone fragility as a cardinal manifestation, accompanied by short stature, dentinogenesis imperfecta, hyperlaxity of ligaments and skin, blue sclerae and hearing loss. Dominant form of OI is caused by mutations in the type I procollagen genes, COL1A1/A2. Here we identified a novel splicing mutation c.

Loss-of-function mutations in filaggrin gene associate with psoriasis vulgaris in Chinese population.

Loss-of-function mutations in filaggrin gene (FLG; OMIM #135940) have been reported to cause the semi-dominant keratinizing disorders such as ichthyosis vulgaris (IV; OMIM #146700) and atopic dermatitis (AD; OMIM #605803). Recent linkage analysis and immunohistochemical studies suggest the possible contribution of FLG to psoriatic susceptibility. However, no susceptibility variant in FLG gene associated with psoriasis (OMIM #177900) has been identified.

Mutation analysis of the NRXN1 gene in a Chinese autism cohort.

Autism is a brain developmental disorder characterized by impaired social interaction and communication, as well as restricted and repetitive behaviors. The neurexin-1(NRXN1) gene mapped on chromosome 2p16.3 encodes neurexin, a cell adhesion molecule and receptor in the vertebrate nervous system.

Branching structure and chain conformation of water-soluble glucan extracted from Auricularia auricula-judae.

A water-soluble neutral polysaccharide (AF1) was extracted from Auricularia (A.) auricula-judae with 0.15 M aqueous NaCl at 80-100 °C.

How does the neck flexion affect the cervical MRI features of Hirayama disease?

Although flexion cervical MRI has been recommended for the diagnosis of Hirayama disease (HD), no study focused on the MR features at different neck flexion angles. Moreover, no uniform flexion angle has been confirmed in clinical practice. The purpose of this study is to quantitatively investigate the MRI typical signs of HD patients in different neck flexion degree and gives a suggestion to the MR scanning.

β-Glucan from Lentinus edodes inhibits nitric oxide and tumor necrosis factor-α production and phosphorylation of mitogen-activated protein kinases in lipopolysaccharide-stimulated murine RAW 264.7 macrophages.

Lentinan (LNT), a β-glucan from the fruiting bodies of Lentinus edodes, is well known to have immunomodulatory activity. NO and TNF-α are associated with many inflammatory diseases. In this study, we investigated the effects of LNT extracted by sonication (LNT-S) on the NO and TNF-α production in LPS-stimulated murine RAW 264.

The coordination polymer poly[bis[μ2-2-(2,2'-bi-1H-imidazol-1-yl)acetato]cadmium].

The title compound, [Cd(C(8)H(7)N(4)O(2))(2)](n), crystallizes in the centrosymmetric triclinic space group P1 with an asymmetric unit consisting of a bivalent Cd(II) atom and two 2-(2,2'-bi-1H-imidazol-1-yl)acetate (BDAC(-)) anions. Two inversion-related BDAC(-) ligands are oppositely arranged and bind two Cd(II) ions to form a [Cd(2)(BDAC)(2)] rhomboid subunit which is bridged by another BDAC(-) ligand to form an infinite ladder along the a direction containing parallelogram grids. The three-dimensional supramolecular architecture is formed by hydrogen bonds and C-H···π and π-π interactions.

Electrotransformation of Haemophilus parasuis with in vitro modified DNA based on a novel shuttle vector.

The objective of the present study was to establish a valid transformation method of Haemophilus parasuis, the causative agent of Glässer's disease in pigs, using a novel H. parasuis-Escherichia coli shuttle vector. A 4.

Immunomodulatory beta-glucan from Lentinus edodes activates mitogen-activated protein kinases and nuclear factor-kappaB in murine RAW 264.7 macrophages.

Lentinan, a cell wall β-glucan from the fruiting bodies of Lentinus edodes, is well known to be a biological defense modifier, but the signal transduction pathway(s) induced by Lentinan have not been elucidated. In this study, we extracted Lentinan (LNT-S) by ultrasonication from Lentinus edodes and report that, in murine RAW 264.7 macrophages, LNT-S glucan activated NF-κB p65 and triggered its nuclear translocation as determined by Western blotting.

Mutation-linked defective interdomain interactions within ryanodine receptor cause aberrant Ca²⁺release leading to catecholaminergic polymorphic ventricular tachycardia.

Background: The molecular mechanism by which catecholaminergic polymorphic ventricular tachycardia is induced by single amino acid mutations within the cardiac ryanodine receptor (RyR2) remains elusive. In the present study, we investigated mutation-induced conformational defects of RyR2 using a knockin mouse model expressing the human catecholaminergic polymorphic ventricular tachycardia-associated RyR2 mutant (S2246L; serine to leucine mutation at the residue 2246).

Methods And Results: All knockin mice we examined produced ventricular tachycardia after exercise on a treadmill.

Identification and analysis of potential virulence-associated genes in Haemophilus parasuis based on genomic subtraction.

Haemophilus parasuis is a commensal bacterium in the swine upper respiratory tract, but virulent strains can invade host and cause Glässer's disease under certain conditions. In order to explore the virulence difference in H. parasuis strains, a virulent isolate, SH0165 (serotype 5), and an avirulent isolate, 7140 (serotype 4), were selected to investigate genetic differences by genomic subtraction.

Triple helical polysaccharide-induced good dispersion of silver nanoparticles in water.

Silver nanoparticles were constructed by using triple helical polysaccharide (lentinan) dissolved in water as matrix for the first time. The structure, morphology, and size of the nanocomposites in the polysaccharide aqueous solutions were investigated with UV-visible spectroscopy (UV-vis), transmission electron microscopy (TEM), and dynamic laser light scattering (DLS). The results revealed that the silver nanoparticles were attached to the polysaccharide chains through the strong noncovalent interactions, leading to the good dispersion of silver nanoparticles with mean radius of 6 nm in water.

A novel nonsense mutation in the NDP gene in a Chinese family with Norrie disease.

Purpose: Norrie disease (ND), a rare X-linked recessive disorder, is characterized by congenital blindness and, occasionally, mental retardation and hearing loss. ND is caused by the Norrie Disease Protein gene (NDP), which codes for norrin, a cysteine-rich protein involved in ocular vascular development. Here, we report a novel mutation of NDP that was identified in a Chinese family in which three members displayed typical ND symptoms and other complex phenotypes, such as cerebellar atrophy, motor disorders, and mental disorders.

Dantrolene, a therapeutic agent for malignant hyperthermia, inhibits catecholaminergic polymorphic ventricular tachycardia in a RyR2(R2474S/+) knock-in mouse model.

Background: Dantrolene, a specific agent for the treatment of malignant hyperthermia, was found to inhibit Ca(2+) leak through not only the skeletal ryanodine receptor (RyR1), but also the cardiac ryanodine receptor (RyR2) by correcting the defective inter-domain interaction between N-terminal (1-619 amino acid) and central (2,000-2,500 amino acid) domains of RyRs. Here, the in vivo anti-arrhythmic effect of dantrolene in a human catecholaminergic polymorphic ventricular tachycardia (CPVT)-associated RyR2(R2474S/+) knock-in (KI) mouse model was investigated.

Methods And Results: ECG was monitored in KI mice (n=6) and wild-type (WT) mice (n=6), before and after an injection of epinephrine (1.

Looking for high energy density compounds applicable for propellant among the derivatives of DPO with -N3, -ONO2, and -NNO2 groups.

The derivatives of DPO (2,5-dipicryl-1,3,4-oxadiazole) are optimized to obtain their molecular geometries and electronic structures at the DFT-B3LYP/6-31G* level. The bond length is focused to primarily predict thermal stability and the pyrolysis mechanism of the title compounds. Detonation properties are evaluated using the modified Kamlet-Jacobs equations based on the calculated densities and heats of formation.

The increased range of cervical flexed motion detected by radiographs in Hirayama disease.

Purpose: Cervical flexion movement is supposed to play an important role in the pathogenesis of Hirayama disease. But there is no report on the range of cervical flexed motion in this disease. The purpose of current study was to compare the range of cervical flexed motion in patients with Hirayama disease with the one in healthy controls using conventional lateral flexion radiographs of the cervical spine, and to investigate the diagnostic value of radiographs for Hirayama disease.

[Imaging and quantitative measurement of brain extracellular space using MRI Gd-DTPA tracer method].

Objective: To observe the diffusion of Gd-DTPA in brain extracellular space (ECS) by magnetic resonance imaging(MRI) and investigate the feasibility of ECS measurement by using MRI tracer method in vivo.

Methods: 2 microL Gd-DTPA was introduced into ECS by caudate nucleus according to stereotaxic atlas in 8 Sprague Dawley(SD) rats (male, 280-320 g). The MRI scans were performed at 1 h, 3 h, 6 h, 9 h and 12 h respectively after administration.

Dissociation of calmodulin from cardiac ryanodine receptor causes aberrant Ca(2+) release in heart failure.

Aims: Calmodulin (CaM) is well known to modulate the channel function of the cardiac ryanodine receptor (RyR2). However, the possible role of CaM on the aberrant Ca(2+) release in diseased hearts remains unclear. In this study, we investigated the state of RyR2-bound CaM and channel dysfunctions in pacing-induced failing hearts.

Defective calmodulin binding to the cardiac ryanodine receptor plays a key role in CPVT-associated channel dysfunction.

Calmodulin (CaM), one of the accessory proteins of the cardiac ryanodine receptor (RyR2), is known to play a significant role in the channel regulation of the RyR2. However, the possible involvement of calmodulin in the pathogenic process of catecholaminergic polymorphic ventricular tachycardia (CPVT) has not been investigated. In this study, we investigated the state of RyR2-bound CaM and channel dysfunctions using a knock-in (KI) mouse model with CPVT-linked RyR2 mutation (R2474S).