Hybrid source translation scanning mode for interior tomography.

Interior tomography is a promising technique that can be used to image large objects with high acquisition efficiency. However, it suffers from truncation artifacts and attenuation value bias due to the contribution from the parts of the object outside the ROI, which compromises its ability of quantitative evaluation in material or biological studies. In this paper, we present a hybrid source translation scanning mode for interior tomography, called hySTCT-where the projections inside the ROI and outside the ROI are finely sampled and coarsely sampled respectively to mitigate truncation artifacts and value bias within the ROI. Inspired by our previous work-virtual projection-based filtered backprojection (V-FBP) algorithm, we develop two reconstruction methods-interpolation V-FBP (iV-FBP) and two-step V-FBP (tV-FBP)-based on the linearity property of the inverse Radon transform for hySTCT reconstruction. The experiments demonstrate that the proposed strategy can effectively suppress truncated artifacts and improve the reconstruction accuracy within the ROI.

LncRNA RP11-620J15.3 promotes HCC cell proliferation and metastasis by targeting miR-326/GPI to enhance glycolysis.

BACKGROUND: Accumulating studies have demonstrated that the Warburg effect plays a central role in the occurrence and development of hepatocellular carcinoma (HCC), albeit the role of non-coding RNA (lncRNA) in its association remains unclear. METHODS: The Zhengzhou University People's Hospital kindly provided 80 pairs of HCC tissues and their matched paracancerous tissues for this study. Bioinformatics analysis, real-time quantitative polymerase chain reaction, Western blotting, and oncology functional assays were performed to determine the contribution of RP11-620J15.3 to the development of HCC. The mechanism of co-immunoprecipitation and a luciferase reporter gene was employed to ascertain how RP11-620J15.3 interacts with important molecular targets. RESULTS: Our results revealed that a lncRNA termed RP11-620J15.3 was overexpressed in HCC and was substantially associated with the tumor size. A high expression of RP11-620J15.3 mRNA was found to be significantly associated with worsening prognosis in HCC patients. We discovered that RP11-620J15.3 stimulated the glycolytic pathway in HCC cells by RNA-sequencing (RNA-seq) and metabolomics analyses. Mechanistically, RP11-620J15.3 acted as a competitive endogenous RNA to regulate the GPI expression by sponging miR-326 in HCC. In addition, TBP acted as a transcription factor for RP11-620J15.3, which contributed to the high expression of RP11-620J15.3 in HCC cells. CONCLUSION: Based on our findings, lncRNA RP11-620J15.3 is a novel LncRNA that positively regulates tumor progression. Specifically, RP11-620J15.3/miR-326/GPI pathway promotes HCC malignant progression by regulating glycolysis, thereby providing novel targets for HCC treatment and drug development.

LINC01419 Promotes the Proliferation of Hepatoma Cells by Recruiting XRCC5 and Regulating Its Phosphorylation to Repair DNA Damage.

Background: Hepatocellular carcinoma (HCC) is one of the most common and fatal malignancies in human beings. Studies have shown that long non-coding RNAs (lncRNAs) play key parts in the occurrence and development of HCC. Although many lncRNAs have been studied in the HCC specifically for DNA damage repair, the role of LINC01419 in cellular DNA damage repair has not yet been studied. Objective: This study is aimed at exploring the biological role of LINC01419 and its potential mechanism in HCC. Methods: qRT-PCR was used to detect the expression level of LINC01419 in HCC tissues and cells, the proteins which were involved were detected by Western blot. Effect of LINC01419 knockdown on cell cycle, apoptosis, DNA damage, cell proliferation, wound healing, colony formation, and migration of HCC cells was studied in vitro. Results: The analysis showed that LINC01419 was overexpressed in HCC tissues and cells. Silencing of LINC01419 expression significantly inhibited the proliferation and migration ability of the HCC cells and resulted in cell cycle arrest at G0/G1 phase. Furthermore, the knockdown of LINC01419 increased the DNA damage, and to some extent, promoted sensitivity of HCC cells to doxorubicin. In addition, we performed RIP analysis which showed XRCC5 as a potential protein related to DNA damage repair in hepatoma cells. Conclusion: In conclusion, the LINC01419 acts as an oncogene in HCC and regulates DNA damage repair through XRCC5 in HCC cells.

Does City Public Service Distance Increase Sense of Gain to Public Health Service? Evidence from 1394 Migrant Workers in Six Provinces.

Increasing the well-being of migrant workers is one of the key objectives of promoting equality and safe, people-oriented, and sustainable social development, as well as inclusive globalization. With the equalization reform of the public health system and the reduction of frictions between cities, the well-being of the sense of gain to public health service (SGPHS) of migrant workers has attracted widespread attention. Based on the migrant worker thematic survey data in 2017 and the city statistical data in six destination cities, this study constructed and measured the sense of gain to public health service index and city public service distance index, and then studied the effects of city public service distance on the SGPHS of migrant workers and the heterogeneous effect. The results showed that the SGPHS of Chinese migrant workers is at a moderate level and presents spatial differences. Under the dual mechanism of preference reinforcement effect and public service discount effect, the effect of city public service distance on the SGPHS of migrant works shows an inverted U-shaped relationship, and the results of the endogeneity test by the generalized propensity score matching model are robust. The city public service distance has a significant non-linear effect on the public health service accessibility and provision for migrant workers, as well as on second-generation, low-income migrant workers, and migrant workers in central and western regions. The results provide beneficial insights for the formulation of rational public service policies.

A Metastatic Intrahepatic Cholangiocarcinoma With HPCs Features: Report of a Case.

Intrahepatic cholangiocarcinoma (ICC) is a highly lethal hepatobiliary neoplasm, which originates from the bile ducts proximal to the second-order division. ICC can be anatomically divided into two subtypes: the large duct type (mucin-production ICC, muc-ICC) and the small duct type (mixed-ICC) origins from hepatic progenitor cells (HPCs). The immunoreactivity of S100P and neural cell adhesion molecule (NCAM) are useful biomarkers to distinguish the two subtypes. In this study, we report a difficult-to-diagnose case of metastatic retroperitoneal tumor of occult hepatolithiasis-associated ICC. Besides, this case was both positive for S100P and NCAM, considered as a rare muc-ICC with the HPCs features. Tumor whole exome sequencing detection results by Genetron (China) revealed that there were 41 gene mutations in this patient. The SMAD4-p.His530ThrfsTer47 and KRAS-p.Gly12Val mutation might promote the occurrence and distant metastasis of the tumor.

miR-199a-5p inhibits the proliferation of hepatocellular carcinoma cells by regulating CDC25A to induce cell cycle arrest.

BACKGROUND: Hepatocellular carcinoma (HCC) has been verified as a really common cancer worldwide. Several studies have suggested that the suppression of malignancy growth can be traced to miR-199a-5p. Even though CDC25A could activate the tumorigenesis of various cancer by modulating cell cycle, the modulation of the miR-199a-5p/CDC25A axis is still not clear in HCC. Our aim is to identify the modulation of the miR-199a-5p/CDC25A axis in HCC. METHODS: The expression of CDC25A and miR-199a-5p in HCC cells and tissues was assessed using qRT-PCR. After using western blot assay to confirm the protein level, luciferase reporter and RNA pull-down assays were performed to explore the relation between CDC25A and miR-199a-5p. Functional assays such as CCK8 assay, BrdU proliferation assay and flow cytometry analysis identified the cell progression. RESULTS: Experimental findings indicated the downregulation of miR-199a-5p in HCC samples. It was also found that miR-199a-5p overexpression declined the development of the cells with HCC and that it could bind to CDC25A to suppress the progression of HCC. CONCLUSION: Research suggested that miR-199a-5p could restrain the proliferation ability of HCC cells by regulating CDC25A, thus inducing cell-cycle arrest.

Long noncoding RNA EPIC1 interacts with YAP1 to regulate the cell cycle and promote the growth of pancreatic cancer cells.

Pancreatic cancer (PC) is a fatal disease; most patients are asymptomatic before the disease enters the advanced stage, but molecular mechanisms of early PC that can be exploited for diagnosis are not clear. Long noncoding RNAs (lncRNAs) play key roles in the progression of PC. In this study, we found that the expression of the lncRNA EPIC1 (Lnc-EPIC1) is high in PC and closely related to tumor size, TNM staging and lymph node metastasis status. Silencing Lnc-EPIC1 by siRNA targeting could significantly inhibit the cell growth and colony formation ability of PC cells and induced G1/S cell cycle arrest and apoptosis in PC cells. Lnc-EPIC1-specific siRNAs could downregulate the expression of cyclins and CDKs, such as CDC20, CDK4 and Cyclin A1. Knocking out YAP1 with the CRISPR/Cas-9 gene editing method recapitulated the effects of the Lnc-EPIC1-specific siRNAs on cell growth, colony formation ability and apoptosis in PC cells. In addition, the Lnc-EPIC1-specific siRNAs did not further inhibit cell growth or promote apoptosis in YAP1-knockout (YAP1-KO) cells. RNA immunoprecipitation (RIP) results showed that there was a direct interaction between Lnc-EPIC1 and YAP1. An Lnc-EPIC1-overexpressing lentiviral vector promoted the growth of PC cells. The results show that Lnc-EPIC1 interacts with YAP1 to promote the progression of PC.

Effects of public health policies on the health status and medical service utilization of Chinese internal migrants.

This paper examines the effects of the "Equalization Program of Basic Public Health and Family Planning Services for Migrants" (EHFPSM), a novel internal migrant-targeted public health policy, of China implemented in 2013. By combining the individual-level data from the "China Migrants Dynamic Survey" and city-level statistical data, we find that EHFPSM contributes to a 6.9% statistically significant increase in the probability of electronic health records coverage and a 7.2% increase in the probability of reimbursement in the last inpatient visit, as well as a 1.2% decrease in the probability of one-year prevalence. The mechanism test shows that this program promotes the migrants' understanding of the policies and social insurance coverage to enhance their health status. EHFPSM brings about more significant decreases in disease prevalence for male and less-educated migrants, and higher reimbursement probability for urban hukou migrants. Our paper facilitates better understanding of the role of public health policies in promoting the internal migrants' health from the perspective of China.

Emerging Roles Of hsa-circ-0046600 Targeting The miR-640/HIF-1α Signalling Pathway In The Progression Of HCC.

PURPOSE: Circular RNAs (circRNAs) play important roles in the development and progression of various human cancers. hsa-circ-0046600 is a circRNA of unknown function. The purpose of this study was to investigate the biological function of hsa-circ-0046600 in hepatocellular carcinoma (HCC) and elucidate the possible molecular mechanisms of this circRNA. MATERIALS AND METHODS: GSE97332, quantitative reverse transcription polymerase chain reaction (qRT-PCR) and fluorescence in situ hybridization (FISH) were used to detect the expression of hsa-circ-0046600 in HCC tissues and cells. A dual-luciferase reporter assay was used to confirm the interaction between hsa-circ-0046600 and miR-640, and a meta-analysis confirmed the expression of miR-640 in HCC. Bioinformatics was used for the functional analysis of miR-640 target genes. N-cadherin and HIF-1α expression was measured by Western blot analysis. RESULTS: The expression level of hsa-circ-0046600 in HCC tissue was significantly higher than that in adjacent normal tissue (P < 0.05) and was associated with tumour size, TNM stage and pathological vascular invasion. Moreover, the downregulated expression of hsa-circ-0046600 significantly inhibited the migration of HepG2 and SK-HEP-1 cells. hsa-circ-0046600 is present mainly in the cytoplasm and promotes the expression of proteins such as HIF-1α by competitively binding to miR-640 in HCC, thereby affecting the malignant biological behaviour of liver cancer cells. CONCLUSION: hsa-circ-0046600 can be used as a new biomarker for HCC diagnosis and disease progression and provides a potential target for targeted therapy.

Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells.

AIM: To elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22. METHODS: One hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis. An amylase assay kit was used to measure the amylase expression level in the supernatant. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-22 expression. We used online tools to predict the potential transcription promoter of miR-22 and the binding sites, which was further identified by using luciferase reporter analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR assays. Then, a mimic of miR-22, Nr3c1 plasmid encoding the glucocorticoid receptor (GR), and si-Nr3c1 were used to transfect AR42J cells, respectively. The mRNA expression of miR-22, Nr3c1, and Erb-b2 receptor tyrosine kinase 3 (ErbB3) was confirmed by qRT-PCR and the apoptosis rate of AR42J cells was detected by flow cytometry analysis. Western blot was used to detect the expression of ErbB3, GR, PI3k, PI3k-p85α, Akt, p-Akt, Bad, Bax, Bcl-xl, Bcl-2, and cleaved caspase3. RESULTS: After inducing apoptosis of AR42J cells in vitro, the expression of miR-22 was significantly increased by 2.20 ± 0.26 and 4.19 ± 0.54 times, respectively, at 3 h and 6 h in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-22 was 78.25 ± 6.61 times higher in the miR-22 mimic group relative to the miRNA control group, accompanied with an obviously increased acinar cell apoptosis rate (32.53 ± 1.15 vs 18.07 ± 0.89, P = 0.0006). The upregulation of miR-22 could suppress its target gene, ErbB3, and the phosphorylation of PI3k and Akt. Furthermore, we predicted the potential transcription promoter of miR-22 and the binding sites using online tools. Luciferase reporter analysis and site-directed mutagenesis indicated that the binding site (GACAGCCATGTACA) of the GR, which is encoded by the Nr3c1 gene. Downregulation of the expression of GR could upregulate the expression of miR-22, which further promoted the apoptosis of AR42J cells. CONCLUSION: GR transcriptionally represses the expression of miR-22, which further promotes the apoptosis of pancreatic acinar cells by downregulating the downstream signaling pathway.

Single-Cell Non-coding RNA in Embryonic Development.

Non-coding RNAs (ncRNAs) have significant regulatory functions on the regulation of gene expression of various life activities after transcription, even though they do not encode proteins. During the development of embryos, ncRNAs, such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs), circular RNAs (circRNAs), small nucleolar RNAs (snoRNAs), and Piwi-interacting RNAs (piRNAs), have been widely proven as key regulators. The emerging single-cell RNA sequencing technique is powerful for profiling "cell-to-cell" variability at the genomic level. It has been applied to detect the expression of ncRNAs during embryo development. In this chapter, we pay close attention to single-cell ncRNA expression and summarize their roles in embryo development.

NLRP3 Deficiency Alleviates Severe Acute Pancreatitis and Pancreatitis-Associated Lung Injury in a Mouse Model.

The rapid production and release of a large number of inflammatory cytokines can cause excessive local and systemic inflammation in severe acute pancreatitis (SAP) and multiple organ dysfunction syndrome (MODS), especially pancreatitis-associated acute lung injury (P-ALI), which is the main cause of early death in patients with SAP. The NLRP3 inflammasome plays an important role in the maturation of IL-1ß and the inflammatory cascade. Here, we established a model of SAP using wild-type (NLRP3+/+) and NLRP3 knockout (NLRP3-/-) mice by intraperitoneal injections of caerulein (Cae) and lipopolysaccharide (LPS). Pathological injury to the pancreas and lungs, the inflammatory response, and neutrophil infiltration were significantly mitigated in NLRP3-/- mice. Furthermore, INF-39, an NLRP3 inflammasome inhibitor, could reduce the severity of SAP and P-ALI in a dose-dependent manner. Our results suggested that SAP and P-ALI were alleviated by NLRP3 deficiency in mice, and thus, reducing NLRP3 expression may mitigate SAP-associated inflammation and P-ALI.

miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene.

AIM: To investigate the expression of miR-29a in rat acute pancreatitis and its functional role in AR42J cell apoptosis. METHODS: Twelve SD rats were divided into a control group and an acute edematous pancreatitis (AEP) group randomly. AEP was induced by intraperitoneal injection of L-arginine (150 mg/kg) in the AEP group and equal volume of 0.9% NaCl was injected in the control group. The apoptosis of acinar cells in pancreatic tissue was determined by TUNEL assay. miRNA chip assay was performed to examine the expression of miRNAs in two groups. Besides, to further explore the role of miR-29a in apoptosis in vitro, recombinant rat TNF-α (50 ng/mL) was administered to treat the rat pancreatic acinar cell line AR42J for inducing AR42J cell apoptosis. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-29a expression. Then, miRNA mimic, miRNA antisense oligonucleotide (AMO) and control vector were used to transfect AR42J cells. The expression of miR-29a was confirmed by qRT-PCR and the apoptosis rate of AR42J cells was detected by flow cytometry analysis. Western blot was used to detect the expression of activated caspase3. Moreover, we used bioinformatics software and luciferase assay to test whether TNFRSF1A was the target gene of miR-29a. After transfection, qRT-PCR and Western blot was used to detect the expression of TNFRSF1A in AR42J cells after transfection. RESULTS: The expression of miR-29a was much higher in the AEP group compared with the control group as displayed by the miRNA chip assay. After inducing apoptosis of AR42J cells in vitro, the expression of miR-29a was significantly increased by 1.49 ± 0.04 times in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-29a was 2.68 ± 0.56 times higher in the miR-29a mimic group relative to the control vector group, accompanied with an obviously increased acinar cell apoptosis rate (42.83 ± 1.25 vs 24.97 ± 0.15, P < 0.05). Moreover, the expression of miR-29a in the miRNA AMO group was 0.46 ± 0.05 times lower than the control vector group, and the cell apoptosis rate was much lower accordingly (17.27 ± 1.36 vs 24.97 ± 0.15, P < 0.05). The results of bioinformatics software and luciferase assay showed that TNFRSF1A might be a target gene of miR-29a. TNFRSF1A expression was up-regulated in the miR-29a mimic group, while the miR-29a AMO group showed the reverse trend. CONCLUSION: miR-29a might promote the apoptosis of AR42J cells via up-regulating the expression of its target gene TNFRSF1A.

Functional role of MicroRNA-19b in acinar cell necrosis in acute necrotizing pancreatitis.

The expression of microRNA-19b (miR-19b) in acute necrotizing pancreatitis (ANP) and its functional role in acinar cell necrosis of SD rats were investigated. Twelve SD rats were divided into two groups randomly, including control group and ANP group. The rat ANP models were established by intraperitoneal injection of L-arginine (2400 mg/kg body weight), and equal volume of 0.9% NaCl was injected in the control group. MiRNA chip assay was performed to examine the expression of miRNAs in the pancreas in two different groups. Besides, to further explore the role of miR-19b in ANP in vitro, taurolithocholic acid 3-sulfate disodium salt (TLC-S) (200 µmol/L) was administrated to treat the rat pancreatic acinar cell line, AR42J, for establishing the ANP cells model. The quantitative real-time PCR (qRT-PCR) was adopted to measure the miR-19b expression. Moreover, the mimic miRNA, miRNA antisense oligonucleotide (AMO) and control vector were used to transfect AR42J cells, the expression of miR-19b was confirmed by qRT-PCR and the necrotizing rate of AR42J cells was detected with AO/EB method. The expression of miR-19b was significantly higher in ANP group than in control group as displayed by the miRNA chip assay. Furthermore, after inducing necrosis of AR42J cells in vitro, the expression of miR-19b was significantly increased by 2.51±0.14 times in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-19b was 5.94±0.95 times higher in the mimic miRNA group than in the control vector group, companied with an obviously increased acinar cell necrotizing rate (50.3%±1.5% vs. 39.6%±2.3%, P<0.05). Moreover, the expression of miR-19b in the miRNA AMO group was 0.38±0.15 times lower than in the control vector group, and the cell necrosis rate was much lower accordingly (23.1%±3.3% vs. 39.6%±2.3%, P<0.05). Besides, there was no significant difference between the control vector cells and the cells without treatment (P>0.05). The expression of miR-19b was significantly induced in ANP. In addition, up-regulation of miR-19b could promote the necrosis of pancreatic acinar cells and miR-19b deficiency could decrease the rate of pancreatic acinar cell necrosis.

In Situ Raman Spectroscopic Study of Barite as a Pressure Gauge Using a Hydrothermal Diamond Anvil Cell.

In situ Raman measurements of barite were performed at temperatures in the range of 298-673 K and pressures in the range of 105-1217 MPa using a hydrothermal diamond anvil cell combined with laser Raman spectroscopy. The Raman frequency and the full width at half maximum (FWHM) of the most intense ν1 Raman peak for barite as a function of pressure and temperature were obtained. In the experimental P-T ranges, the ν1Raman band systematically shifted toward low wavenumbers with increasing pressure and temperature. The positive pressure dependence of ν1Raman frequency indicates stress-induced shortening of the S-O bond, whereas the negative temperature dependence shows temperature-induced expansion of the S-O bond. In contrast, the observed ν1Raman band became broadened, which should be attributed to the reduced ordering of molecular structure. Based on the obtained data, the established relationships among the Raman shift or the FWHM, pressure and temperature can be used to obtain good estimates of the internal pressure in natural barite-bearing fluid inclusions or hydrothermal diamond anvil cell. This is a sensitive and reliable approach to the accurate determination of geological pressure.

Expressions of miR-22 and miR-135a in acute pancreatitis.

This study examined the expressions of miR-22 and miR-135a in rats with acute edematous pancreatitis (AEP) and their target genes in order to shed light on the involvement of miR-22 and miR-135a in the pathogenesis of acute pancreatitis (AP). The in vivo model of AEP was established by introperitoneal injection of L-arginine (150 mg/kg) in rats. The miRNA microarray analysis was used to detect the differential expression of miRNAs in pancreatic tissue in AEP and normal rats. The in vitro AEP model was established by inducing the rat pancreatic acinar cell line (AR42J) with 50 ng/mL recombinant rat TNF-α. Real-time quantitative RT-PCR was employed to detect the expression of miR-22 and miR-135a in AR42J cells. Lentiviruses carrying the miRNA mimic and anti-miRNA oligonucleotide (AMO) of miR-22 and miR-135a were transfected into the AR42J cells. The AR42J cells transfected with vehicle served as control. Western blotting was used to measure the expression of activated caspase3 and flow cytometry analysis to detect the apoptosis of AR42J cells. Targets of miR-22 and miR-135a were predicted by using TargetScan, miRanda, and TarBase. Luciferase reporter assay and quantitative real-time RT-PCR were performed to confirm whether ErbB3 and Ptk2 were the target gene of miR-22 and miR-135a, respectively. The results showed that the expression levels of miR-22 and miR-135a were obviously increased in AEP group compared with the control group in in-vivo and in-vitro models. The expression levels of miR-22 and miR-135a were elevated conspicuously and the expression levels of their target genes were reduced significantly in AR42J cells transfected with lentiviruses carrying the miRNA mimic. The apoptosis rate was much higher in the TNF-α-induced cells than in non-treated cells. The AR42J cells transfected with miRNA AMOs expressed lower level of miR-22 and miR-135a and had lower apoptosis rate, but the expression levels of ErbB3 and Ptk2 were increased obviously. It was concluded that the expression levels of miR-22 and miR-135a were elevated in AEP. Up-regulating the expression of miR-22 and miR-135a may promote the apoptosis of pancreatic acinar cells by repressing ErbB3 and Ptk2 expression in AEP.

[In situ experimental study of phase transition of calcite by Raman spectroscopy at high temperature and high pressure].

The phase transitions of calcite at high temperature and high pressure were investigated by using hydrothermal diamond anvil cell combined with Raman spectroscopy. The result showed that the Raman peak of 155 cm(-1) disappeared, the peak of 1 087 cm(-1) splited into 1083 and 1 090 cm(-1) peaks and the peak of 282 cm(-1) abruptly reduced to 231 cm(-1) at ambient temperature when the system pressure increased to 1 666 and 2 127 MPa respectively, which proved that calcite transformed to calcite-II and calcite-III. In the heating process at the initial pressure of 2 761 MPa and below 171 degrees C, there was no change in Raman characteristic peaks of calcite-III. As the temperature increased to 171 degrees C, the color of calcite crystal became opaque completely and the symmetric stretching vibration peak of 1 087 cm(-1), in-plane bending vibration peak of 713 cm(-1) and lattice vibration peaks of 155 and 282 cm(-1) began to mutate, showing that the calcite-III transformed to a new phase of calcium carbonate at the moment. When the temperature dropped to room temperature, this new phase remained stable all along. It also indicated that the process of phase transformation from calcite to the new phase of calcium carbonate was irreversible. The equation of phase transition between calcite-III and new phase of calcium carbonate can be determined by P(MPa) = 9.09T x (degrees C) +1 880. The slopes of the Raman peak (v1 087) of symmetrical stretching vibration depending on pressure and temperature are dv/dP = 5.1 (cm(-1) x GPa(-1)) and dv/dT = -0.055 3(cm(-1) x degrees C(-1)), respectively.

[Raman spectra study of barite at the pressure of 0-1 GPa and ambient temperature].

The variation characters of Raman spectra of S-O symmetric stretching vibration v987 and symmetric bending vibration v452 and V462 of barite at high pressure were studied using moissanite anvil cell. The experimental results show that barite is stable at the pressure of 0-1 GPa and ambient temperature, and the Raman peak positions of barite shift to higher frequency with increasing pressure. The relations between the Raman shifts and system pressure are given as follows: v987 = 0.004 4p+987.42, v452 = 0.002 3p+452.6, v462 = 0.001 8p+ 462.42, and that stretching vibrations are more affected by pressure than bending vibrations. The intensity of 987 cm(-1) Raman peak of barite is six times greater than that of 464 cm(-1) Raman peak of quartz, so barite can be used as a good pressure gauge. Besides, the relation between the system pressure and Raman shift of 987 cm(-1) peak position of barite is given as follows: p(MPa) = 223.16 X (deltav(p))987 -90.35 (987 cm(-1) < v(p) < 992 cm(-1)). The difference in the measured relative pressure-shift of the Raman line of the symmetric stretching vibration among various sulfate minerals shows the compressibility and strength of the S-O bond in the SO4 group.