The effect of orbital-lattice coupling on the electrical resistivity of YBaCuFeO5 investigated by X-ray absorption.

Temperature-dependent X-ray absorption near-edge structures, X-ray linear dichroism (XLD) and extended X-ray absorption fine structure (EXAFS) spectroscopic techniques were used to investigate the valence state, preferred orbital and local atomic structure that significantly affect the electrical and magnetic properties of a single crystal of YBaCuFeO5 (YBCFO). An onset of increase of resistivity at ~180 K, followed by a rapid increase at/below 125 K, is observed. An antiferromagnetic (AFM)-like transition is close to the temperature at which the resistivity starts to increase in the ab-plane and is also observed with strong anisotropy between the ab-plane and the c-axis. The XLD spectra at the Fe L3,2-edge revealed a change in Fe 3d eg holes from the preferential [Formula: see text] orbital at high temperature (300-150 K) to the [Formula: see text] orbital at/below 125 K. The analysis of the Fe K-edge EXAFS data of YBCFO further revealed an unusual increase in the Debye-Waller factor of the nearest-neighbor Fe-O bond length at/below 125 K, suggesting phonon-softening behavior, resulting in the breaking of lattice symmetry, particularly in the ab-plane of Fe-related square pyramids. These findings demonstrate a close correlation between electrical resistivity and coupling of the preferred Fe 3d orbital with lattice distortion of a single crystal of YBCFO.

Anisotropy in the magnetic interaction and lattice-orbital coupling of single crystal Ni3TeO6.

This investigation reports on anisotropy in the magnetic interaction, lattice-orbital coupling and degree of phonon softening in single crystal Ni3TeO6 (NTO) using temperature- and polarization-dependent X-ray absorption spectroscopic techniques. The magnetic field-cooled and zero-field-cooled measurements and temperature-dependent Ni L3,2-edge X-ray magnetic circular dichroism spectra of NTO reveal a weak Ni-Ni ferromagnetic interaction close to ~60 K (TSO: temperature of the onset of spin ordering) with a net alignment of Ni spins (the uncompensated components of the Ni moments) along the crystallographic c-axis, which is absent from the ab-plane. Below the Néel temperature, TN~ 52 K, NTO is stable in the antiferromagnetic state with its spin axis parallel to the c-axis. The Ni L3,2-edge X-ray linear dichroism results indicate that above TSO, the Ni 3d eg electrons preferentially occupy the out-of-plane 3d3z2-r2 orbitals and switch to the in-plane 3dx2-y2 orbitals below TSO. The inherent distortion of the NiO6 octahedra and anisotropic nearest-neighbor Ni-O bond lengths between the c-axis and the ab-plane of NTO, followed by anomalous Debye-Waller factors and orbital-lattice in conjunction with spin-phonon couplings, stabilize the occupied out-of-plane (3d3z2-r2) and in-plane (3dx2-y2) Ni eg orbitals above and below TSO, respectively.

CARMA3 regulates the invasion, migration, and apoptosis of non-small cell lung cancer cells by activating NF-кB and suppressing the P38 MAPK signaling pathway.

In our previous study, CARMA3 overexpression in lung cancer cells promoted cell proliferation and invasion; however, the mechanism underlying the role of CARMA3 in cancer cell invasion remained unclear. In the present study, knockdown of CARMA3 in A549 and H1299 cells suppressed cell invasion and migration, and downregulated matrix metalloprotease 9 expression at the protein and mRNA levels, as shown by Western blotting and real-time PCR. CARMA3 knockdown increased cell apoptosis, as shown by flow cytometry, increased the mRNA and protein expression levels of Bax and Caspase3, and downregulated Bcl-2 in A549 and H1299 cells. Phosphorylated P38 levels increased and NF-кB activation decreased following knockdown of CARMA3. SB203580, a P38 MAPK inhibitor, activated NF-кB, increased cell migration, and inhibited cell apoptosis after knockdown of CARMA3 compared to knockdown of CARMA3 without SB203580. These findings indicate that CARMA3 may suppress the activation of the P38 MAPK signaling pathway to regulate invasion, migration and apoptosis of lung cancer cells by activating NF-кB (P65) in the nucleus.

Effects of dietary allicin on health and growth performance of weanling piglets and reduction in attractiveness of faeces to flies.

To investigate the effect of dietary allicin on health and growth performance of weanling piglets, at 21 days of age. Two hundred and twenty-five piglets were weaned and randomly allocated into five groups. Piglets in the control group were fed diets supplemented with antibiotics. Those in the treatment groups were fed diets without antibiotics, but supplemented with allicin product (25% pure allicin oil) in the proportion of 0.10 g/kg, 0.15 g/kg, 0.20 g/kg and 0.25 g/kg in the diet, respectively. During the 28 days of the experiment, average daily weight gain increased linearly (P < 0.0001) and quadratically (P = 0.0014) as the level of dietary allicin increased. The feed gain ratio decreased linearly (P < 0.0001) and quadratically (P < 0.0001). As the dietary allicin level increased, the incidence of diarrhoea in the treatment piglets, especially female piglets decreased linearly (P = 0.0003) and tended to decrease quadratically (P = 0.0716). The number of flies alighting on the surface of the faeces of the piglets at each counting time point decreased linearly (P < 0.0001), quadratically (P < 0.0001) and cubically (P < 0.0001) as the dietary allicin level increased. In conclusion, supplementation of the diet with allicin may improve growth performance, reduce the incidence of diarrhoea and possibly improve their local environmental conditions by reducing the attractiveness of faeces to flies.

Association study between adolescent idiopathic scoliosis and the DPP9 gene which is located in the candidate region identified by linkage analysis.

BACKGROUND: It has been recognised that genetic or hereditary factors may contribute to the aetiology of adolescent idiopathic scoliosis (AIS). Recently, two linkage analyses have identified 19p13.3 as the candidate region for AIS. The dipeptidyl peptidase 9 (DPP9) gene is located on chromosome 19p13.3. OBJECTIVE: To investigate whether DPP9 gene polymorphisms are associated with the occurrence or curve severity of AIS. METHODS: 571 girls with AIS and 236 normal controls were recruited. Using the Chinese data from the HapMap project, a set of tagging single-nucleotide polymorphisms (tagSNPs) were defined for the DPP9 gene. Five SNPs were genotyped by PCR restriction fragment length polymorphism. Statistical analysis of genotype frequencies between cases and controls was performed by the chi2 test. One-way analysis of variance was used to compare mean maximum Cobb angles with different genotypes in case-only analysis. RESULTS: Genotype frequencies were comparable between cases and controls for all five polymorphisms (p>0.05). The mean maximum Cobb angles of different genotypes were similar to each other for all five polymorphisms. CONCLUSIONS: The DPP9 gene is not associated with the occurrence or curve severity of AIS. It is neither a disease-predisposition nor a disease-modifying gene of AIS.

The role of melatonin receptor 1B gene (MTNR1B) in adolescent idiopathic scoliosis--a genetic association study.

UNLABELLED: Many studies have demonstrated the role of melatonin in the etiology of AIS. Previous studies have shown that there is no evidence of mutations in the melatonin receptor 1A gene in AIS patients. In this study, we have examined the role of melatonin receptor 1B in predisposition for AIS. Using haplotype block tagging technique, a set of tagging SNPs were defined for MTNR1B from the Han Chinese data of the International HapMap project. The association between the tagging of single nucleotide polymorphisms (tSNPs) in MTNR1B region and the occurrence of AIS was studied. METHOD: 473 AIS girls and 311 normal controls were recruited. The age range of the patients was between 10 and 18 years old. The maximum Cobb was recorded at latest follow-up in AIS patients. Three of five tSNPs were studied; they were all located within the coding region of the MTNR1B gene. RESULTS: There was no significant difference in the genotype or allelic frequencies (AF) of the 3 tSNPs between AIS and controls. In a case-only analysis, no difference in curve severity in AIS patients was found among patients with different genotypes (by one-way ANOVA). DISCUSSION: The 3 tSNPs showed no association with either the occurrence of AIS or the maximum Cobb angle within AIS girls. Further analysis of the remaining tSNPs within the regulatory region of the MTNR1B gene and other related genes in the melatonin signaling pathway may provide further information on the role of the melatonin in AIS girls.

Degradation of angiotensin I to [des-Asp1]angiotensin I by a novel aminopeptidase in the rat hypothalamus.

The particulate enzyme that degrades angiotensin I (ANG I) to [des-aspartate1]angiotensin I ([des-Asp1]ANG I) in the hypothalamic homogenate of the rat has been established as a specific aminopeptidase. The major characteristics is its resistance to inhibition by 10(-4) M amastatin, bestatin and EDTA. Among the four amino acyl-beta-naphthylamides (aspartyl, glutamyl-, arginyl- and leucyl-beta-naphthylamide), aspartyl-beta-naphthylamide is the most susceptible substrate of the enzyme; being degraded at twice the rate of arginyl-, and leucyl-beta-naphthylamide, and six times that of glutamyl-beta-naphthylamide. Although the precise role of this aminopeptidase has yet to be determined, its presence establishes the existence of a specific pathway for the degradation of ANG I that bypasses the formation of ANG II. The relationship between degradation and hypertension is shown by our recent findings that the formation of [des-Asp1]ANG I form ANG I in the hypothalamic homogenate of the spontaneously hypertensive rat (SHR) is significantly enhanced, and the findings of other investigators that the production of ANG II by neuronal cultures of the SHR is significantly decreased.

Formation of des-Asp-angiotensin I in the hypothalamic extract of normo- and hypertensive rats.

Exogenous angiotensin I (ANG I) was degraded to mainly des-Asp-ANG I instead of ANG II in the hypothalamic homogenate of the Sprague Dawley (SD), Wistar Kyoto (WKY), left renal artery stenosed hypertensive SD (LRAS), deoxycorticosterone acetate/salt-induced hypertensive SD (DOCA-salt) and spontaneously hypertensive rats (SHR). In the same homogenate, ANG II was degraded to ANG III and ANG III remained unchanged during the first 10 min of incubation. However, all the homogenates were able to catalyse hippuryl-L-histidyl-L-leucine to hippuric acid and the catalysis was completely inhibited by 3 microM captorpil. The data show that the angiotensin converting enzyme present in the hypothalamus when extracted by the normal laboratory procedures is not able to hydrolyse ANG I to ANG II. In addition, the aminopeptidase that degraded ANG I to des-Asp-ANG I was not inhibited by amastatin, bestatin and EDTA, indicating that it is not aminopeptidase A or B. The formation of hippuric acid was significantly higher in the homogenate of the LRAS whilst the SHR and DOCA-salt showed significant higher rate of des-Asp-ANG I formation than in the normotensive control rats.

[Bronchial carcinoids: report of 17 cases].

Seventeen cases of bronchial carcinoids were treated surgically from 1967 to 1989. Of these, 11 were female and 6 were male. The age ranged from 15 to 58 years and 11 cases (64.7%) were under 40 years of age. The peak incidence differs markedly form that of bronchogenic carcinoma. Bronchial carcinoid is a primary bronchial tumor of low malignancy, they may have lymphatic metastases and recurrence after operation. Surgical resection is the main treatment. Local resection was performed in one, enucleation in 3, wedge resection in 4, lobectomy in 7 and bronchoplastic lobectomy in 2.5-year survival rate was 93%. The indications for each mode of resection are discussed and the principles of complete eradication of tumor with maximal reservation of functioning lung are emphasized.