APbI3-A2AgBiI6 Double-Layer Perovskite Film for a Self-Powered and High-Stability X-ray Detector.

The development of lead halide perovskite X-ray detectors has promising applications in medical imaging and security inspection but is hindered by poor long-term stability and drift of the dark current and photocurrent. Herein, we design a (Cs0.05MA0.65FA0.3)PbI3-(Cs0.1MA1.3FA0.6)AgBiI6 double-layer perovskite film to assemble a self-powered flat-panel X-ray detector. The demonstrated X-ray detector achieves an outstanding self-powered sensitivity of 80 µC Gyair-1 cm-2 under a 0 V bias. More importantly, owing to the inhibition of the phase transition process and ion migration of (Cs0.05MA0.65FA0.3)PbI3 by the (Cs0.1MA1.3FA0.6)AgBiI6 layer, the device exhibits excellent continuous operating stability with a retention rate of 99% dark current and photocurrent over X-ray pulses of up to 4000 s and excellent long-term stability without a loss of the original response current after 150 days in an air environment. The strategy of double-layer perovskites improves the stability and sensitivity of devices, which paves a path for the industrial application of lead halide perovskite X-ray detectors.

The protein phosphatase qGL3/OsPPKL1 self-regulates its degradation to orchestrate brassinosteroid signaling in rice.

Brassinosteroids (BRs) are a class of phytohormones that regulate plant growth and development. In previous studies, we cloned and identified PROTEIN PHOSPHATASE WITH KELCH-LIKE1 (OsPPKL1) as the causal gene for the quantitative trait locus GRAIN LENGTH3 (qGL3) in rice (Oryza sativa). We also showed that qGL3/OsPPKL1 is mainly located in the cytoplasm and nucleus and negatively regulates BR signaling and grain length. Because qGL3 is a negative regulator of BR signaling, its turnover is critical for rapid response to changes in BRs. Here, we demonstrate that qGL3 interacts with the WD40-domain-containing protein WD40-REPEAT PROTEIN48 (OsWDR48), which contains a nuclear export signal (NES). The NES signal is crucial for the cytosolic localization of OsWDR48 and also functions in the self-turnover of qGL3. We show that OsWDR48 physically interacts with and genetically acts through qGL3 to modulate BR signaling. Moreover, qGL3 may indirectly promote the phosphorylation of OsWDR48 at the Ser-379 and Ser-386 sites. Substitutions of both phosphorylation sites in OsWDR48 to non-phosphorylatable alanine enhanced the strength of the OsWDR48-qGL3 interaction. Furthermore, we found that brassinolide can promote the accumulation of non-phosphorylated OsWDR48, leading to strong interaction intensity between qGL3 and OsWDR48. Taken together, our results show that OsWDR48 facilitates qGL3 retention and induces degradation of qGL3 in the cytoplasm. These findings suggest that qGL3 self-modulates its turnover by binding to OsWDR48 to regulate its cytoplasmic localization and stability, leading to efficient orchestration of BR signal transduction in rice.

OsBAK2/OsSERK2 expression is repressed by OsBZR1 to modulate brassinosteroid response and grain length in rice.

Brassinosteroids (BRs) are a class of polyhydroxylated steroidal phytohormones that are essential for plant growth and development. Rice BRASSINOSTEROID-INSENSITIVE1 (BRI1)-ASSOCIATED RECEPTOR KINASES (OsBAKs) are plasma membrane-localized receptor kinases belonging to the subfamily of leucine-rich repeat receptor kinases. It has been found that in Arabidopsis, BRs induce the formation of a BRI1-BAK1 heterodimer complex and transmit the cascade signal to BRASSINAZOLE RESISTANT1/bri1-EMS-SUPPRESSOR1 (BZR1/BES1) to regulate BR signaling. Here, in rice (Oryza sativa ssp. japonica), we found that OsBZR1 binds directly to the promoter of OsBAK2, but not OsBAK1, and represses the expression of OsBAK2 to form a BR feedback inhibition loop. Additionally, the phosphorylation of OsBZR1 by OsGSK3 reduced its binding to the OsBAK2 promoter. The osbak2 mutant displays a typical BR-deficiency phenotype and negative modulates the accumulation of OsBZR1. Interestingly, the grain length of the osbak2 mutant was increased whereas in the cr-osbak2/cr-osbzr1 double mutant, the reduced grain length of the cr-osbzr1 mutant was restored, implying that the increased grain length of osbak2 may be due to the rice somatic embryogenesis receptor kinase-dependent pathway. Our study reveals a novel mechanism by which OsBAK2 and OsBZR1 engage in a negative feedback loop to maintain rice BR homeostasis, facilitating a deeper understanding of the BR signaling network and grain length regulation in rice.

qGL3/OsPPKL1 induces phosphorylation of 14-3-3 protein OsGF14b to inhibit OsBZR1 function in brassinosteroid signaling.

Brassinosteroids (BRs) play essential roles in regulating plant growth and development, however, gaps still remain in our understanding of the BR signaling network. We previously cloned a grain length quantitative trait locus qGL3, encoding a rice (Oryza sativa L.) protein phosphatase with Kelch-like repeat domain (OsPPKL1), that negatively regulates grain length and BR signaling. To further explore the BR signaling network, we performed phosphoproteomic analysis to screen qGL3-regulated downstream components. We selected a 14-3-3 protein OsGF14b from the phosphoproteomic data for further analysis. qGL3 promoted the phosphorylation of OsGF14b and induced the interaction intensity between OsGF14b and OsBZR1. In addition, phosphorylation of OsGF14b played an important role in regulating nucleocytoplasmic shuttling of OsBZR1. The serine acids (Ser258Ser259) residues of OsGF14b play an essential role in BR-mediated responses and plant development. Genetic and molecular analyses indicated that OsGF14b functions as a negative regulator in BR signaling and represses the transcriptional activation activity of OsBZR1. Collectively, these results demonstrate that qGL3 induces the phosphorylation of OsGF14b, which modulates nucleocytoplasmic shuttling and transcriptional activation activity of OsBZR1, to eventually negatively regulate BR signaling and grain length in rice.

The phosphoproteomic and interactomic landscape of qGL3/OsPPKL1-mediated brassinosteroid signaling in rice.

Oryza sativa L. (rice) is one of the most important crops in the world, and grain size is a major component determining rice yield. Recent studies have identified a number of grain size regulators, which are involved in phytohormone signaling, G protein signaling, the mitogen-activated protein kinase signaling pathway, the ubiquitin-proteasome pathway or transcriptional regulation. In a previous study, we cloned qGL3/OsPPKL1 encoding a rice protein phosphatase that negatively modulates brassinosteroid (BR) signaling and grain length. Here, to further explore the qGL3-mediated BR signaling network, we performed phosphoproteomic screenings using two pairs of rice materials: the indica rice cultivar 9311 and its near-isogenic line NILqgl3 and the japonica rice cultivar Dongjin and its qGL3 knockout mutant m-qgl3. Together with qGL3-interacting proteins, we constructed the qGL3-mediated network, which reveals the relationships between BR signaling and other critical signaling pathways. Transgenic plants of these network components showed BR-related alterations in plant architecture. From this network, we validated a qGL3-interacting protein, O. sativa VERNALIZATION INSENSITIVE 3-LIKE 1 (OsVIL1), and demonstrated that qGL3 dephosphorylates OsVIL1 to modulate BR signaling. The qGL3-dependent network uncovered in this study increases our understanding of BR signaling and provides a profound foundation for addressing how BR modulates plant architecture in rice.

An Adenylate Kinase OsAK3 Involves Brassinosteroid Signaling and Grain Length in Rice (Oryza sativa L.).

BACKGROUND: Grain size is one of the major determinants of cereal crop yield. As a class of plant polyhydroxysteroids, brassinosteroids (BRs) play essential roles in the regulation of grain size and plant architecture in rice. In a previous research, we cloned qGL3/OsPPKL1 encoding a protein phosphatase with Kelch-like repeat domains, which negatively regulates BR signaling and grain length in rice. RESULTS: Here, we screened qGL3-interacting proteins (GIPs) via yeast two-hybrid assay and analyzed the phenotypes of the T-DNA insertion mutants of GIPs. Among these mutants, mutant osak3 presents shorter grain length and dwarfing phenotype. OsAK3 encodes an adenylate kinase, which regulates grain size by controlling cell expansion of rice spikelet glume. Overexpression of OsAK3 resulted in longer grain length. OsAK3 interacts with qGL3 in vivo and in vitro. Lamina inclination, coleoptile elongation and root inhibition experiments showed that the osak3 mutant was less sensitive to exogenous brassinolide (BL) treatment. The transcriptional level of OsAK3 was up-regulated under BL induction. In addition, RNA-Seq data indicate that OsAK3 is involved in a variety of biological processes that regulate BR signaling and grain development in rice. CONCLUSIONS: Our study reveals a novel BR signaling component OsAK3 in the regulation of grain length, and provides novel clues for uncovering the potential functions of OsAK3 in rice growth and development.

A Cys2/His2 Zinc Finger Protein Acts as a Repressor of the Green Revolution Gene SD1/OsGA20ox2 in Rice (Oryza sativa L.).

Gibberellins (GAs) play important roles in the regulation of plant growth and development. The green revolution gene SD1 encoding gibberellin 20-oxidase 2 (GA20ox2) has been widely used in modern rice breeding. However, the molecular mechanism of how SD1/OsGA20ox2 expression is regulated remains unclear. Here, we report a Cys2/His2 zinc finger protein ZFP207 acting as a transcriptional repressor of OsGA20ox2. ZFP207 was mainly accumulated in young tissues and more specifically in culm nodes. ZFP207-overexpression (ZFP207OE) plants displayed semidwarfism phenotype and small grains by modulating cell length. RNA interference of ZFP207 caused increased plant height and grain length. The application of exogenous GA3 could rescue the semidwarf phenotype of ZFP207OE rice seedlings. Moreover, ZFP207 repressed the expression of OsGA20ox2 via binding to its promoter region. Taken together, ZFP207 acts as a transcriptional repressor of SD1/OsGA20ox2 and it may play a critical role in plant growth and development in rice through the fine-tuning of GA biosynthesis .

Integration of Transcriptional Repression and Polycomb-Mediated Silencing of WUSCHEL in Floral Meristems.

Arabidopsis (Arabidopsis thaliana) floral meristems terminate after the carpel primordia arise. This is achieved through the temporal repression of WUSCHEL (WUS), which is essential for stem cell maintenance. At floral stage 6, WUS is repressed by KNUCKLES (KNU), a repressor directly activated by AGAMOUS. KNU was suggested to repress WUS through histone deacetylation; however, how the changes in the chromatin state of WUS are initiated and maintained to terminate the floral meristem remains elusive. Here, we show that KNU integrates initial transcriptional repression with polycomb-mediated stable silencing of WUS After KNU is induced, it binds to the WUS promoter and causes eviction of SPLAYED, which is a known activator of WUS and can oppose polycomb repression. KNU also physically interacts with FERTILIZATION-INDEPENDENT ENDOSPERM, a key polycomb repressive complex2 component, and mediates the subsequent deposition of the repressive histone H3 lysine 27 trimethylation for stable silencing of WUS This multi-step silencing of WUS leads to the termination of floral stem cells, ensuring proper carpel development. Thus, our work describes a detailed mechanism for heritable floral stem cell termination in a precise spatiotemporal manner.

Rice qGL3/OsPPKL1 Functions with the GSK3/SHAGGY-Like Kinase OsGSK3 to Modulate Brassinosteroid Signaling.

Brassinosteroids (BRs) are steroid hormones that play essential roles in plant growth and development. We previously cloned qGL3, a major quantitative trait locus regulating grain length in rice (Oryza sativa). The O. sativa japonica var N411 has extra-large grains compared with the O. sativa indica var 9311, and the recessive qgl3 allele from N411 contributes positively to grain length. qGL3 encodes a putative protein phosphatase with Kelch-like repeat domains, an ortholog of Arabidopsis (Arabidopsis thaliana) brassinosteroid-insensitive1 SUPPRESSOR1 (BSU1). BSU1 positively regulates BR signaling, while overexpression of qGL3 induced BR loss-of-function phenotypes. Both qGL3N411 and qGL39311 physically interact with the rice glycogen synthase kinase 3 (GSK3)/SHAGGY-like kinase 3 (OsGSK3), an ortholog of Arabidopsis BR INSENSITIVE2 (BIN2). qGL39311 dephosphorylates OsGSK3, but qGL3N411 lacks this activity. Knocking out OsGSK3 enhances BR signaling and induces nuclear localization of O. sativa BRASSINAZOLE RESISTANT1 (OsBZR1). Unlike the dephosphorylation of BIN2 (which leads to protein degradation) in Arabidopsis, qGL3 dephosphorylates and stabilizes OsGSK3 in rice. These results demonstrate that qGL3 suppresses BR signaling by regulating the phosphorylation and stability of OsGSK3, which modulates OsBZR1 phosphorylation and subcellular distribution. Our study clarifies the role of qGL3 in the regulation of grain length and provides insight into BR signaling, including the differences between rice and Arabidopsis.

Interaction between tissue factor pathway inhibitor-2 gene polymorphisms and environmental factors associated with coronary atherosclerosis in a Chinese Han.

To investigate the association of single nucleotide polymorphisms (SNPs) within tissue factor pathway inhibitor-2 (TFPI-2) gene polymorphisms and additional gene-environment interaction with coronary atherosclerosis risk. Generalized multifactor dimensionality reduction (GMDR) was used to screen the best interaction combination among 4 SNPs, smoking and alcohol drinking. Logistic regression was performed to investigate association between 4 SNPs within TFPI-2 gene and coronary atherosclerosis risk. Coronary atherosclerosis risk was significantly higher in carriers with the A allele of rs34489123 within TFPI-2 gene than those with GG genotype (GA+AA versus GG), adjusted OR (95% CI) = 1.70 (1.20-2.31), and was also higher in carriers with the G allele of rs4264 within TFPI-2 gene than those with AA genotype (AG+GG versus AA), adjusted OR (95% CI) = 1.62 (1.21-2.11). GMDR model shown the best models for gene-environment interaction were rs34489123 and smoking after adjusting the covariates, which scored 10 out of 10 for cross-validation consistency and 0.0010 for the sign test. Heavy LD was found for SNPs rs34489123 and rs59805398 (D' value was more than 0.8). Compared to control individuals, the AG haplotypes appeared to be significantly associated with increased coronary atherosclerosis risk, OR (95% CI) = 1.73 (1.22-2.32). We found that the A allele of rs34489123 and the G allele of rs4264 within TFPI-2 gene, interaction between rs34489123 and smoking and AG haplotypes were all associated with increased coronary atherosclerosis risk.

Acute intravenous glucose load impairs early insulin secretion and insulin content in islet ß cells in mice.

AIMS: To investigate insulin secretion and content in islet ß cells after intravenous glucose load in mice. MATERIALS AND METHODS: Acute hyperglycemia (≥16.7 mmol/L) in C57BL/J6 mice was achieved by hyperglycemic clamp. Mice were divided into four groups: a 2-hour and a 4-hour high glucose-infusion (2 h-HG and 4 h-HG) with 25% dextrose groups and control groups with saline infusion of the same duration. Insulin levels and response were measured using intraperitoneal glucose tolerance test (IPGTT) in mice and glucose-stimulated insulin secretion (GSIS) for isolated islets after overnight culture. Immunohistochemistry and electron microscopy (EM) for islet ß cells were used after the hyperglycemic clamp to study morphologic changes of insulin granules and to assess the impact of acute glucose load on islet histology. KEY FINDINGS: Blood glucose at 15, 30, 60 and 120 min was significantly higher in 4 h-HG compared with the other groups. Serum plasma insulin significantly decreased only at 15 min as a first-phase insulin response (FPIR). Insulin secretion at 2.8 and 16.7 mmol/L glucose stimulus in 4 h-HG group decreased 77% and 64% more than those in 2 h-HG, respectively (P<0.05). Similarly, residual insulin content in islet ß cells after 2.8 and 16.7 mmol/L glucose challenge decreased 30% and 43% more than those in 2 h-HG, respectively (P<0.05). EM showed decreased insulin granules in islet cells and swollen mitochondria only in 4 h-HG. SIGNIFICANCE: Short time intravenous glucose load blunted FPIRs and decreased insulin content of islet ß cells.

Moderate calorie restriction to achieve normal weight reverses ß-cell dysfunction in diet-induced obese mice: involvement of autophagy.

BACKGROUND: Severe calorie restriction (CR) is shown to improve or even reverse ß-cell dysfunction in patients with obesity and type 2 diabetes mellitus. However, whether mild to moderate CR can reverse ß-cell dysfunction induced by obesity and the underlying mechanism remain unclear. Autophagy plays an important role in maintaining mass, architecture and function of ß-cells. While the impact of CR on ß-cell autophagy is unknown. This study aims to investigate the effects of moderate CR on ß-cell function and autophagy activity in diet-induced obese (DIO) mice. METHODS: DIO C57BL/6 mice were subjected to 3 weeks of switching to normal chow (HF → NC group) or normal chow with 40 % CR (HF → NC CR group). Then hematoxylin-eosin and immunohistochemistry staining were performed to observe ß-cell morphology. ß-cell function was evaluated by intraperitoneal glucose tolerance test in vivo and static GSIS (glucose-stimulated insulin secretion) in isolated islets. ß-cell autophagy activity was determined by transmission electron microscope and western blot. RESULTS: In the HF → NC CR group, CR normalized body weights, completely restored glucose tolerance, early-phase and second-phase insulin secretion, insulin sensitivity, and islet size. CR also normalized insulin content and glucose-stimulated insulin secretion in isolated islets in vitro. Furthermore, ß-cell autophagy level was increased in the HF → NC CR group, but AMPK phosphorylation remained unchanged. Although HF → NC mice achieved moderate weight loss and normal glucose tolerance, their insulin secretion was not improved compared with obese control mice, and additionally, ß-cell autophagy was not activated in these mice. CONCLUSIONS: Moderate (40 %) CR to achieve normal weight reversed ß-cell dysfunction and insulin resistance, and restored glucose homeostasis in DIO mice. Furthermore, the up-regulation of ß-cell autophagy may play a role in this process, independent of AMPK activation.

The additive effects of GS3 and qGL3 on rice grain length regulation revealed by genetic and transcriptome comparisons.

BACKGROUND: Grain length, as a critical trait for rice grain size and shape, has a great effect on grain yield and appearance quality. Although several grain size/shape genes have been cloned, the genetic interaction among these genes and the molecular mechanisms of grain size/shape architecture have not yet to be explored. RESULTS: To investigate the genetic interaction between two major grain length loci of rice, GS3 and qGL3, we developed two near-isogenic lines (NILs), NIL-GS3 (GS3/qGL3) and NIL-qgl3 (gs3/qgl3), in the genetic background of 93-11 (gs3/qGL3) by conventional backcrossing and marker-assisted selection (MAS). Another NIL-GS3/qgl3 (GS3/qgl3) was developed by crossing NIL-GS3 with NIL-qgl3 and using MAS. By comparing the grain lengths of 93-11, NIL-GS3, NIL-qgl3 and NIL-GS3/qgl3, we investigated the effects of GS3, qGL3 and GS3 × qGL3 interaction on grain length based on two-way ANOVA. We found that GS3 and qGL3 had additive effects on rice grain length regulation. Comparative analysis of primary panicle transcriptomes in the four NILs revealed that the genes affected by GS3 and qGL3 partially overlapped, and both loci might be involved in brassinosteroid signaling. CONCLUSION: Our data provide new information to better understand the rice grain length regulation mechanism and help rice breeders improve rice yield and appearance quality by molecular design breeding.

Association of chemerin mRNA expression in human epicardial adipose tissue with coronary atherosclerosis.

BACKGROUND: Growing evidence suggests that epicardial adipose tissue (EAT) may play a key role in the pathogenesis and development of coronary artery disease (CAD) by producing several inflammatory adipokines. Chemerin, a novel adipokine, has been reported to be involved in regulating immune responses and glucolipid metabolism. Given these properties, chemerin may provide an interesting link between obesity, inflammation and atherosclerosis. In this study, we sought to determine the relationship of chemerin expression in EAT and the severity of coronary atherosclerosis in Han Chinese patients. METHODS: Serums and adipose tissue biopsies (epicardial and thoracic subcutaneous) were obtained from CAD (n = 37) and NCAD (n = 16) patients undergoing elective cardiac surgery. Gensini score was used to assess the severity of CAD. Serum levels of chemerin, adiponectin and insulin were measured by ELISA. Chemerin protein expression in adipose tissue was detected by immunohistochemistry. The mRNA levels of chemerin, chemR23, adiponectin and TNF-alpha in adipose tissue were detected by RT-PCR. RESULTS: We found that EAT of CAD group showed significantly higher levels of chemerin and TNF-alpha mRNA, and significantly lower level of adiponectin mRNA than that of NCAD patients. In CAD group, significantly higher levels of chemerin mRNA and protein were observed in EAT than in paired subcutaneous adipose tissue (SAT), whereas such significant difference was not found in NCAD group. Chemerin mRNA expression in EAT was positively correlated with Gensini score (r = 0.365, P < 0.05), moreover, this correlation remained statistically significant (r = 0.357, P < 0.05) after adjusting for age, gender, BMI and waist circumference. Chemerin mRNA expression in EAT was also positively correlated with BMI (r = 0.305, P < 0.05), waist circumference (r = 0.384, P < 0.01), fasting blood glucose (r = 0.334, P < 0.05) and negatively correlated with adiponectin mRNA expression in EAT (r = -0.322, P < 0.05). However, there were no significant differences in the serum levels of chemerin or adiponectin between the two groups. Likewise, neither serum chemerin nor serum adiponectin was associated with Gensini score (P > 0.05). CONCLUSIONS: The expressions of chemerin mRNA and protein are significantly higher in EAT from patients with CAD in Han Chinese patients. Furthermore, the severity of coronary atherosclerosis is positive correlated with the level of chemerin mRNA in EAT rather than its circulating level.

Theoretical studies of lattice distortions around the impurity ions in V2+ doped CdCl2, CdI2 and PbI2.

The lattice distortions around the impurity ions in V(2+) doped CdCl(2), CdI(2) and PbI(2) are theoretically studied from the perturbation formulas of the spin Hamiltonian (SH) parameters zero-field splitting, g factors and the hyperfine structure constants for a 3d(3) ion in trigonal symmetry based on the cluster approach. In these formulas, the contributions from the s-orbitals of the ligands are taken into account. Based on the studies, it is found that the local angles beta (between the impurity-ligand bonding lengths and the C(3) axis) in the impurity centers are smaller than the angles beta(H) in the hosts. The calculated SH parameters based on the above local angles beta show better agreement than those on neglecting of the ligand s-orbital contributions (and those on the host angles beta(H)) with the experimental data.

Theoretical studies of the spin Hamiltonian parameters and local structures for Cs3CoX5 (X = Cl, Br).

The spin Hamiltonian (SH) parameters (zero-field splitting D and anisotropic g factors g(||) and g( perpendicular)) and local structures for Cs(3)CoX(5) (X = Cl, Br) are theoretically studied from the perturbation formulas of the SH parameters for a 3d(7) ion in tetragonally distorted tetrahedra based on the cluster approach. In these formulas, both the contributions from the crystal-field (CF) mechanism and those from the charge-transfer (CT) mechanism are taken into account. It is found that the [CoX(4)](2-) clusters are slightly elongated and the tetragonal distortion angles Deltatheta(=theta-theta(0), where theta(0) equals to approximately 54.74 degrees is the bonding angle related to the C(4)-axis in regular tetrahedra) are about -1.68 degrees and -1.71 degrees for X = Cl and Br, respectively. The calculated SH parameters as well as the effective magnetic moments based on the above angles are in reasonable agreement with the observed values. From the studies, the importance of the contributions to the SH parameters from the CT mechanism increases with increasing the spin-orbit coupling coefficient of the ligand, i.e., Cl(-) < Br(-). The results are compared with those obtained from the conventional crystal-field model in the previous works.

Theoretical studies of the local structure for the trigonal Ti(3+) center in LiF crystal.

The local structure of the trigonal Ti(3+) center in LiF crystal is theoretically investigated by using the perturbation formulas of the anisotropic g factors and g(//) and g(/_) for a 3d(1) ion in trigonally distorted octahedra based on the cluster approach. From the studies on the basis of various possible structure models, the local structure of the trigonal Ti(3+) center may be characterized as [TiF(3)O(3)](6-) cluster (or model I). In this model, the impurity Ti(3+) is expected to substitute for the host Li(+) ion and shift away from its regular lattice site along the [111] (or C(3)) axis by about 0.19 A due to the strong electrostatic attraction of the O(2-) triangle replacing the original F(-) triangle. The magnitude of the above displacement obtained in this work is comparable with that ( approximately 0.2-0.3A) given by ENDOR experiment. Moreover, the cubic field parameter Dq (approximately 1497 cm(-1)) based on the above structure model is also in agreement with that (approximately 1500 cm(-1)) obtained from the experimental optical spectra of the studied system. The theoretical investigations of the local structure in this work may be useful to understand optical properties of Ti-doped LiF.

Theoretical studies of the spin Hamiltonian parameters and the local structures for M2+ (M=Co, Mn, V and Ni) ions in CsMgCl3.

The spin Hamiltonian parameters (zero-field splitting D, g factors g parallel, g perpendicular and hyperfine structure constants A parallel, A perpendicular) for M2+ (M=Co, Mn, V and Ni) ions in CsMgCl3 are studied by using the perturbation formulas of the spin Hamiltonian parameters for 3dn (n=7, 5, 3, 8) ions in trigonal symmetry based on the cluster approach. In these formulas, the contributions to the spin Hamiltonian parameters from the admixture of d orbitals of the central ions with the p orbitals of the ligands and from the trigonal distortion are included and the parameters related to these effects can be obtained from the optical spectra and the local structures of the studied systems. Based on the studies, it is found that the local trigonal distortion angle beta in the M2+ impurity center is unlike that betaH (approximately 51.71 degrees) in the host CsMgCl3. The spin Hamiltonian parameters for these divalent ions in CsMgCl3 are also satisfactorily explained by using the local angle beta. The validity of the results is discussed.