A magnetic topological semimetal Sr1-yMn1-zSb2 (y, z < 0.1).

Weyl (WSMs) evolve from Dirac semimetals in the presence of broken time-reversal symmetry (TRS) or space-inversion symmetry. The WSM phases in TaAs-class materials and photonic crystals are due to the loss of space-inversion symmetry. For TRS-breaking WSMs, despite numerous theoretical and experimental efforts, few examples have been reported. In this Article, we report a new type of magnetic semimetal Sr1-yMn1-zSb2 (y, z < 0.1) with nearly massless relativistic fermion behaviour (m∗ =  0.04 - 0.05m0, where m0 is the free-electron mass). This material exhibits a ferromagnetic order for 304 K  <  T  <  565 K, but a canted antiferromagnetic order with a ferromagnetic component for T  <  304 K. The combination of relativistic fermion behaviour and ferromagnetism in Sr1-yMn1-zSb2 offers a rare opportunity to investigate the interplay between relativistic fermions and spontaneous TRS breaking.

Molecular identification and seasonal infections of species of Fasciola in ruminants from two provinces in China.

We determined the prevalence and seasonality of infections by Fasciola of goats and bovine species (cattle and water buffalo) in Hubei and Anhui provinces of China. Faecal samples were collected at 2- to 3-month intervals from 200 goats in Hubei province and from 152 bovine species in Anhui province. All faecal samples were examined for the presence of parasites. We determined the nucleotide sequences of the first and second internal transcribed spacers (ITS-1 and ITS-2) of the nuclear ribosomal DNA (rDNA) of 39 Fasciola worms from Anhui province. The prevalence of Fasciola infection in goats ranged between 3.5 and 37.0%, with mean eggs per gram (EPG) ranging between 29.0 and 166.0. Prevalence and EPG exhibited downward trends over time with significant differences. The prevalence of Fasciola infection in cattle ranged between 13.3 and 46.2% (mean EPG, 36.4-100.0), and that of water buffalo ranged between 10.3 and 35.4% (mean EPG, 25.0-89.6), with a higher prevalence of infection and EPG from June to October compared with December to March. Analysis of ITS-1 and ITS-2 sequences revealed that F. hepatica and F. gigantica were present in all bovine species of Anhui province and that F. gigantica mainly infected water buffalo. This is the first demonstration of Fasciola infection in Hubei province and detection of F. hepatica and F. gigantica in Anhui province. The present study of Hubei province shows that mass treatment of livestock with closantel sodium injections in April and August/September controlled Fasciola infection effectively.

Apoptosis induction in duck tissues during duck hepatitis A virus type 1 infection.

To investigate the role of apoptosis in duck viral hepatitis pathogenesis, 4- and 21-d-old ducks were inoculated with duck hepatitis A virus serotype 1 and killed at 2, 6, 12, 24, and 48 h postinfection. TdT-mediated dUTP nick-end labeling was used to detect apoptosis cells. Expression profiles of apoptosis-related genes including caspase-3, -8, -9, and Bcl-2 in spleen, bursa of Fabricius, liver, and the quantity of virus in blood were examined using real-time PCR. The TdT-mediated dUTP nick-end labeling analysis indicated there was a significant difference of apoptotic cells between treatments and controls. The same difference also appeared in virus amount variation in blood during infection. Gene expression analysis revealed that the apoptosis-related gene expression profile was different in the 2 groups, and also different between various organs. This study suggested that apoptosis may play an important role in duck hepatitis A virus serotype 1 infection, and apoptosis suppression might facilitate virus multiplication, resulting in the highest virus concentration in the host.

Cytokine gene expression in the livers of ducklings infected with duck hepatitis virus-1 JX strain.

Duck hepatitis virus type 1 (DHV-1) causes a highly contagious disease in ducklings and is often associated with liver necrosis, hemorrhages, and high mortality. In the current study, the expression levels of gene transcripts encoding proinflammatory cytokines and the virus were measured by quantitative reverse-transcription PCR in duck livers after infection with a DHV-1 JX isolate obtained from natural cases in Hubei Province, China. In addition, sera IL-1ß, IL-6, and alanine aminotransferase levels were quantified. Liver histopathology was examined following DHV-1 infection. The ducklings died within 1 to 2 d postinfection (d.p.i.) because of typical liver degeneration, hemorrhage, necrosis, and bile-duct epithelial cell proliferation. Transcripts of the cytokines IFN-α, IL-6, TNF-α, and IL-10 decreased by 0.5 d.p.i. and then gradually increased at 1 d.p.i. Similarly, DHV-1 JX 3D gene levels in the liver sharply increased at 1 d.p.i. and then maintained a high level. In contrast, liver TNF-α and IL-1ß transcripts showed no increased expression of the cytokine gene postinfection and significantly decreased compared with the expression at 0.25 d.p.i., only the expression of IFN-α transcripts increased 128-fold by 1 d.p.i. Changes in the serum IL-6 level remained relatively stable postinfection and not significantly different compared with that of the control (P > 0.05), whereas serum levels of IL-1ß significantly decreased at 0.5 d.p.i. and increased from 1 d.p.i. onwards (P < 0.05). Serum alanine aminotransferase levels significantly increased 2 d.p.i. compared with that of the control group (P < 0.01), which seemed to keep with the number of dead ducks. The cytokines exhibited a biphasic pattern following DHV-1 JX infection. Taken together, the data indicated that duckling liver inflammatory responses were produced following experimental DHV-1 JX infection involving multiple cytokines.

Mössbauer study of superconducting NdFeAsO(0.88)F(0.12) and its parent compound NdFeAsO.

(57)Fe Mössbauer spectroscopy has been used to investigate the magnetic order of non-superconducting NdFeAsO (T(N) = 140 K) and superconducting NdFeAsO(0.88)F(0.12) (T(c) = 45 K). A magnetic hyperfine field B(hf) was observed at the (57)Fe nucleus below T(N)∼140 K for NdFeAsO. Below ∼2 K an increase of B(hf) relative to the saturation value was attributed to the transferred B(hf) at the Fe site resulting from the collinear antiferromagnetic (AF) spin structure of the Nd moments. The analysis of the spectra is consistent with a commensurate AF order of Fe spins. No  B(hf) is observed in superconducting NdFeAsO(0.88)F(0.12) down to 1.5 K.

Role of interleukin-6 in the pathogenesis of an avian model of Staphylococcus aureus arthritis.

To evaluate the role of interleukin-6 (IL-6) in arthritis induced by Staphylococcus aureus, a chicken model was developed for study. A total of 120 healthy broilers (8 wk old) were randomly divided into 4 groups. Two groups were injected with 0.35 mL of Staph. aureus (7.1x10(9) cfu/mL) into the right hock joints and the other 2 were injected with 0.35 mL of sterile saline into the same joints. One group of each of the 2 treatment groups was fed levofloxacin at a dose of 5 mg/kg of BW on the third day postinoculation for 4 successive days. Chicken blood samples were obtained on d 0, 1, 4, 7, 14, 21, 28, and 35 postinoculation. Chicken IL-6 (chIL-6) activities and concentrations in serum were quantified by B9 bioassay and human IL-6 ELISA, respectively. The results showed that chIL-6 activities and concentrations were reduced (P<0.05) in the serum of infected broilers treated with levofloxacin compared with birds injected only with Staph. aureus. Levofloxacin treatment had no effect on IL-6 activities and concentrations in uninfected broilers. There was a strong correlation (r=0.91) between serum chIL-6 activities by the B9 bioassay and serum IL-6 concentrations determined by the human IL-6 ELISA. We concluded that chIL-6 is involved in the progression of chicken arthritis induced by Staph. aureus, and that it contributes to disease incidence and mortality.

Purification and characterization of a new peptide with analgesic effect from the scorpion Buthus martensi Karch.

Anew peptide, designated as Buthus martensi Karch (BmK) AngM1, with an isoelectric point (pI) of 5.8 was purified and characterized from the venom of Buthus martensi Karch. The molecular mass was calculated as 7040.5 Da from multiple-charged ions by elelctrospray ionization mass spectroscopy (ESI/MS). The complete amino acid sequence of BmK AngM1 of 64 amino acid residues was determined by automatic sequencing of N-terminal part of the native peptide and the fragments of reduced and S-carboxymethylated (RCM)-peptide degraded by Staphylococcus aureaus V(8) protease and TPCK(N-p-Tosyl-L-phenylalanine chloromethyl ketone)-treated trypsin. Bioactivity tested using mouse-twisting model showed an evident analgesic effect with 63.0% (P < 0.001) inhibition efficiency at the dose of 0.8 mg/kg, but the LD(50) was larger than 50 mg/kg. Electrophysiological studies showed that BmK AngM1 at the concentration of 1 microm obviously inhibit voltage-dependent Na(+) current (I(Na)) and voltage-dependent delayed rectifier K(+) current (I(K)) but had no effects on transient K(+) current.

Anti-inflammatory tetramers of resveratrol from the roots of Vitis amurensis and the conformations of the seven-membered ring in some oligostilbenes.

Five resveratrol tetramers, amurensins I-M, were isolated from the roots of Vitis amurensis (Rupr.), together with five known resveratrol tetramers, (+)-hopeaphenol, isohopeaphenol, vitisin A, (+)-vitisifuran A, and heyneanol A. Their structures and stereochemistry were determined by chemical and spectroscopic methods, especially by use of 2D NMR analysis. Some of them had an ampelopsin A or a balanocarpol unit, in which the conformations of the seven-membered carbon ring were described for the first time. The anti-inflammatory activities of the tetramers were also tested. Among them, (+)-hopeaphenol, isohopeaphenol, vitisin A, (+)-vitisifuran A and heyneanol A showed potent inhibition on the biosynthesis of leukotriene B4 (LTB4), and amurensins I and L showed strong antagonism of the histamine acceptor.

[Effects of musk glucoprotein on the function of rat polymorphonuclear leukocytes activated by IL-8 in vitro].

OBJECTIVE: To investigate the effects of musk-1, a glucoprotein component isolated from the water extract of musk, on some functions of rat polymorphonuclear leukocytes activated by IL-8 in vitro. METHOD: An in vitro incubation system was used. Superoxide anion production was determined by cytochrome C reduction. beta-glucuronidase and lysozyme release was quantitated by enzyme reactions in which phenolph-thaleinglucuronic acid and Micrococcus Lysodeikticus were as the substrates, respectively. RESULTS: In comparison with control, musk-1 at concentration 1-100 micrograms.ml-1 can increase superoxide anion production by 91.7%-291%, and decrease beta-glucuronidase and lysozyme release by 2.2%-58.1% and 3.9%-39.8%, respectively. CONCLUSION: Inhibition of lysosomel enzyme release might be considered as one of mechanisms of antiinflammatory action of musk.

[Effect of stilbene polymer (Gn-3) on experimental liver injuries in mice].

AIM: To study the protective effect of Gn-3 (a stilbene polymer isolated from Gnetum parvifolium) against liver injury induced by CCl4, N-acetyl-p-aminophenol (APAP) and Bacillus Calmette-Guerin (BCG) plus bacterial lipopolysaccharide (LPS) in mice. METHODS: The experimental model of liver injury were induced by 0.1% CCl4 i.p. (10 mL.kg-1.d-1 for 3d), APAP i.p. (150 mg.kg-1) or BCG (5 mg) plus LPS (7.5 micrograms) in mice. The levels of ALT in serum, MDA and GSH in liver tissues were detected. The histopathologic changes were observed by light microscope. RESULTS: Gn-3 was shown to markedly reduce the elevated serum ALT levels, liver tissue MDA and improve the histopathological changes in all the three experimental liver injury models. No effect of Gn-3 was observed on the liver GSH level in liver injury mice. CONCLUSION: Gn-3 was found to inhibit the development of liver injury caused by CCl4, APAP, or BCG plus LPS. This means that Gn-3 has liver protective effects.

[Effects of ginkgolide B on arachidonic acid metabolizing enzymes and level of intracellular calcium in rat polymorphonuclear leukocytes].

AIM: To investigate the effects of ginkgolide B on arachidonic acid (AA) metabolizing enzymes and the level of intracellular calcium in rat polymorphonuclear leukocytes. METHODS: Intracellular free calcium was quantitated by Fura-2 fluorescence technique. Phospholipase A2 (PLA2) activity was determined by incorporating 3H-arachidonic acid in leukocytes. 5-Lipoxygenase (5-LO) activity was evaluated by RP-HPLC. RESULTS: In comparison with control, ginkgolide B at final concentration of 0.1-10 mumol.L-1 inhibited A23187 induced AA release by 10.9%-22.2%; at final concentration of 0.1-50 mumol.L-1, ginkgolide B inhibited LTB4 and 5-HETE synthesis stimulated by PAF by 29.4%-88.8% and 26.2%-89.3% respectively. At the final concentration of 0.1-100 mumol.L-1, ginkgolide B decreased the rise of intracellular calcium level induced by pletelet activating factor (PAF) and N-formyl-methionine-leucine-phenglalanine (fMLP) by 13.9%-51.4% and 2.2%-36.6%, respectively. CONCLUSION: Ginkgolide B was found to significantly inhibit PLA2 and 5-LO activities, as well as the increase of the intracellular calcium induced by PAF.

[Inhibitory effects of benzoisoselenothiazolidone sulfonamide derivatives on cyclooxygenase].

AIM: To study the inhibitory effects of benzisoselenothiazolidone sulfonamide derivatives on cyclooxygenase. METHODS: 6-Keto-PGF1 alpha and PGE2 were assayed by radioimmunoassay (RIA) method; mRNA expression of COX-1 and COX-2 were assayed by reverse transcription-polymerase chain reaction (RT-PCR) method. RESULTS: Compound A [N-4-(4-methoxyphenyl-aminosulfonyl)-benziososelenothiazolidone] and B [N-4-(4-fluorophenyl-aminosulfonyl)-benzoisoselenothiazolidone] were two benzoisoselenothiazolidone sulfonamide derivatives, which can inhibit COX activity with IC50 of 1.5 x 10(-8) mol.L-1 and 5.0 x 10(-8) mol.L-1 for COX-2, as well as IC50 of 1.5 x 10(-5) mol.L-1 and 2.8 x 10(-5) mol.L-1 for COX-1. The ratio of IC50 COX-1/IC50 COX-2 of compound A and B are 1,000 and 560, respectively. They both can inhibit COX-2 mRNA expression in cultured rat peritoneal macrophages stimulated with LPS (1 microgram.mL-1), and have no effect on COX-1 mRNA expressions. CONCLUSION: Compound A and B, two benzoisoselenothiazolidone sulfonamide derivatives, both are selective inhibitory agents of COX-2, and possess inhibitory effects on 5-lipoxygenase and cyclooxygenase.

[Inhibitory effects of indomethacin and meloxicam on NF-kappa B in mouse peritoneal macrophages].

AIM: To study the inhibitory effects of indomethacin and meloxicam on NF-kappa B from lipopolysaccharide (LPS) stimulated peritoneal macrophages of mice. METHODS: NF-kappa B was measured with the method of electrophoretic mobility shift assay (EMSA). RESULTS: After induction by LPS at the concentrations of 1 and 3 micrograms.mL-1, the NF-kappa B content of the mouse peritoneal macrophages increased markedly. Indomethacin and meloxicam, at the concentrations of 10(-7)-10(-5) mol.L-1, decreased the activation of NF-kappa B at the concentrations of 1 and 3 micrograms.mL-1 in activated mouse peritoneal macrophages induced with LPS at the concentrations of 1 and 3 micrograms.mL-1. CONCLUSION: The inhibitory effects of indomethacin and meloxicam on NF-kappa B activation may be one of their mechanisms of antiinflammatory actions.

[Inhibitory effects of hydrocortisone on human polymorphonuclear leukocyte adhesion to human synovial cell].

AIM: To investigate the inhibitory effects of hydrocortisone on human polymorphonuclear leukocyte (PMN) adhesion to human synovial cell (HSC), and to explore its mechanism. METHODS: MTT colorimetry was used to determine the adhesion effect of PMN to HSC. Cell-ELISA and RT-PCR methods were used to determine the expression of adhesion molecular ICAM-1 and VCAM-1. EMSA method was also used to observe the activity of nucleus transcription factor-kappa B (NF-kappa B). RESULTS: Hydrocortisone inhibited TNF-alpha (50 U.mL-1 for 12 hours) and IL-1 beta (50 U.mL-1 for 12 hours)-induced adhesion of PMN to HSC (IC50 2.05 x 10(-6) mol.L-1 and 2.13 x 10(-7) mol.L-1, respectively) in a concentration-dependent manner. Adhesion molecular VCAM-1 and ICAM-1 protein and mRNA (rather than ICAM-1) expression in HSC induced by TNF-alpha (50 U.mL-1) were inhibited significantly by hydrocortisone at 1 x 10(-6)-10(-5) mol.L-1. The activity of NF-kappa B was also extensively inhibited by hydrocortisone at 1 x 10(-6)-10(-5) mol.L-1. CONCLUSION: Hydrocortisone inhibited TNF-alpha-stimulated PMN-HSC adhesion, and expression of VCAM-1 by suppressing the activity of NF-kappa B.

[Inhibitory effects of isorhapotigenin on IL-8 production and mRNA expression induced with TNF alpha in normal human synovial cells].

AIM: To study the effects of isorhapotigenin (Iso) on interleukin-8 (IL-8) production and mRNA expression in normal human synovial cells (HSC) induced with TNF alpha. METHODS: IL-8 were assayed with RIA method. The mRNA expression of IL-8 was detected by RT-PCR method. RESULTS: It was shown that TNF alpha at concentrations of 0.05 to 0.5 U.mL-1 for 24 h significantly increased IL-8 production. The expression of IL-8 mRNA was also promoted by TNF alpha (0.25 U.mL-1) for 6 h. Iso at the concentrations of 1 x 10(-6) mol.L-1 to 1 x 10(-5) mol.L-1 showed inhibitory effects on IL-8 production induced with TNF alpha (0.25 U.mL-1). The further study indicated that Iso at the concentrations of 1 x 10(-6) mol.L-1 to 1 x 10(-5) mol.L-1 inhibited IL-8 mRNA expression in HSC induced with TNF alpha (0.25 U.mL-1). CONCLUSION: TNF alpha promoted IL-8 production and mRNA expression in HSC. Iso inhibited IL-8 production and mRNA expression induced by TNF alpha (0.25 U.mL-1). This might be one of the anti-inflammatory mechanisms of Iso.

Regulation of murine interleukin-10 production by dehydroepiandrosterone.

Dehydroepiandrosterone (DHEA), one of the predominant androgens secreted by the adrenal cortex, is a potential immunologic regulator. In this report, the effect of DHEA on interleukin-10 (IL-10) production was studied in vivo. Mice were injected s.c. with DHEA or DHEA-sulfate (DHEAS) ranging from 50 microg to 500 microg/g body weight. The serum was collected, and the spleen cells were isolated 48 h after treatment. Results indicate that treatment with DHEA or DHEAS significantly increases the serum level of IL-10. The spleen cells isolated from the DHEA-treated or DHEAS-treated mice also showed an increase in IL-10 secretion and mRNA expression after the cells were activated by concanavalin A (ConA). The maximal dose of DHEA for inducing IL-10 production was 250 microg/g body weight. As IL-10 is a potent differentiation factor of B lymphocytes, the possible role of DHEA in regulation of immunoglobulin (Ig) production was studied in vivo. Results indicated a significant increase in both serum level of Ig (IgG, IgM, IgA) and Ig secretion by spleen cells after the mice were treated with DHEA or DHEAS. Mice injected with both DHEA (250 microg/g body weight) and anti-IL-10 antibody (0.5 mg/g body weight) showed a significantly reduced DHEA-mediated increase in Ig production. Thus, DHEA might affect the function of B lymphocytes via stimulating IL-10 production.

[Effects of baicalin on liver microsomal cytochrome P450 system].

AIM: To investigate the effect of baicalin on liver microsomal cytochrome P450 system and the mechanism of liver protective action of baicalin. METHODS: Liver microsomal cytochrome P450, b5, aminopyrin N-demethylase (ADM), 7-ethoxycoumarin O-deethylase (ECD) and benzopyrene hydroxylase (AHH) activity were quantitated by UV chromatography. Activities of six cytochrome P450 isoforms were assayed with Western Blotting. RESULTS: Baicalin increased liver microsomal cytochrome. P450 level and ADM, ECD and AHH activity significantly. The three P450 isoforms, 1A1, 2B1 and 2C11, were also induced selectively by baicalin, but the b5 level, 3A2, 2D1 and 2E1 were not induced. CONCLUSION: Baicalin increases liver microsomal cytochrome P450 level and induces selectively 1A1, 2B1 and 2C11 of P450 isoforms in mice.

[Effects of musk glucoprotein on PAF production and cytosolic Ca2+ level in rat polymorphonuclear leukocytes in vitro].

OBJECTIVE: To investigate the effects of Musk glucoprotein on platelet activating factor (PAF) production and the concentration of cytosolic free Ca2+ in polymorphonuclear leukocytes of rat. METHODS: An in vitro incubation system was used, production of PAF and activity of acetyl transferase were measured by isotope incorporation, the concentration of cytosolic free Ca2+ was quantitated using the fluorescent Ca2+ indicator Fura-2. RESULTS: Musk-1 at concentration of 1-100 micrograms.ml-1 can significantly inhibit production of PAF, activity of acetyl transferase and the increase of cytosolic Ca2+ concentration in polymorphonuclear leukocytes of rat. CONCLUSION: Part of mechanisms underlying antiinflammatory action of Musk-1 is through inhibiting the synthesis of PAF and the increase of cytosolic Ca2+ level.

Inhibitory effect of resveratrol on interleukin 6 release by stimulated peritoneal macrophages of mice.

In the present investigation, interleukin 6 (IL-6) activity in the supernatant of cultured mouse peritoneal macrophages was monitored using a sensitive bioassay involving the IL-6-dependent murine hybridoma B9 cell line. The effects of resveratrol on Il-6 release by mouse peritoneal macrophages stimulated with calcium ionophore A23187 and fMLP were explored. Resveratrol, at a concentration range from 5 x 10(-6) to 4 x 10(-5) mol.l-1, was found to dose-dependently inhibit IL-6 release by cultured macrophages induced by A23187 and fMLP, and showed no direct cytotoxic effect, but induced proliferation of cultured mouse thymus cells. Resveratrol, at a concentration range from 10(-8) to 10(-5) mol.l-1, was shown to dose-dependently inhibit calcium ion influx into the cells with the stimulation of fMLP (10(-6) mol.l-1). These results suggest that the blocking of calcium ion influx into cells by reveratrol is one of the possible mechanisms of the IL-6 biosynthesis inhibitory action of resveratrol.