2023: A year of accomplishments for the 13 Science Citation Index Expanded- and Emerging Sources Citation Index-indexed Baishideng journals.

In 2023, Baishideng Publishing Group (Baishideng) routinely published 47 open-access journals, including 46 English-language journals and 1 Chinese-language journal. Our successes were accomplished through the collective dedicated efforts of Baishideng staffs, Editorial Board Members, and Peer Reviewers. Among these 47 Baishideng journals, 7 are included in the Science Citation Index Expanded (SCIE) and 6 in the Emerging Sources Citation Index (ESCI). With the support of Baishideng authors, company staffs, Editorial Board Members, and Peer Reviewers, the publication work of 2023 is about to be successfully completed. This editorial summarizes the 2023 activities and accomplishments of the 13 SCIE- and ESCI-indexed Baishideng journals, outlines the Baishideng publishing policy changes and additions made this year, and highlights the unique advantages of Baishideng journals.

Cyclic tensile strain facilitates proliferation and migration of human aortic smooth muscle cells and reduces their apoptosis via miRNA-187-3p.

The cardiovascular is a system that contains extremely complex mechanical factors, in which the circulatory flow of blood has rich mechanical laws. Many studies have revealed that mechanical factors play a very important role in the process of revascularization. Hence, it is essential to investigate the mechanical factors in the process of revascularization in depth. A cyclic tensile strain (CTS) was applied to human aortic smooth muscle cells (HASMCs) at a frequency of 1 Hz and amplitudes of 5%, 10% and 15%, respectively. SmallRNA-seq was used to identify differentially expressed miRNAs (DE-miRNAs) responding to CTS in HASMCs. Starbase database predicted the target genes of DE-miRNAs. Metascape was applied for GO and KEGG pathway enrichment analysis and protein-protein interaction network construction. The proliferation and migration of CTS-treated HASMCs were significantly enhanced, and apoptosis were significantly reduced compared to the control group. SmallRNA-seq results demonstrated that 55, 16 and 16 DE-miRNAs were present in 5%, 10% and 15% CTS-treated HASMCs, respectively. Compared to controls, with miR-26a-2-3p and miR-187-3p being the intersection of these DE-miRNAs. Starbase database identified 189 common target genes for miR-26a-2-3p and miR-187-3p. Common target genes are mainly enriched in the basolateral plasma membrane and endocytosis. Further, in vitro experiments exhibited that CTS upregulated miR-187-3p expression, and miR-187-3p enhanced the proliferation and migration of HASMCs and reduced their apoptosis. It is suggested that miR-187-3p may be an important target for CTS participate in the process of cardiovascular disease.[Figure: see text].

Integrated Analysis of lncRNAs and mRNAs Identifies a Potential Driver lncRNA FENDRR in Lung Cancer in Xuanwei, China.

This study was to screen out potential driver long non-coding RNAs (lncRNAs) in lung cancer in Xuanwei (LCXW) differently expressed mRNAs and lncRNAs were detected by gene expression microarrays in 23 paired lung adenocarcinoma and adjacent tissues. Combined bioinformatics analysis was performed to identify potential driver lncRNAs and their potential regulatory relationships. Transcriptome and clinical data in TCGA-LUAD were used as comparison and validation dataset. The comparison of LCXW and TCGA-LUAD revealed significant differences in expression of some genes, signaling pathways affected by differentially expressed genes, and the 5-year survival rate of patients. We identified 14 consistently deregulated mRNAs and 5 lncRNAs as candidate genes, which affected multiple cancer-related pathways and influenced patients' overall survival. By combined bioinformatics analysis, we further identified a potential driver lncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) and proposed its possible regulation mechanism. The low expression of FENDRR was positively correlated with Krüppel-like factor4 (KLF4), KLF4 down-regulation may loss the activation function of cyclin-dependent kinase inhibitor 1A (CDKN1A) and cyclin-dependent kinase inhibitor 1C (CDKN1C) and the inhibition function of CyclinB1 (CCNB1), eventually cause excessive cell cycle activation and lead to lung cancer. This study revealed a potential FENDRR-KLF4-cell cycle regulation axis. These results lay an important foundation for further research on the pathogenesis of LCXW and identification of potential novel biomarkers or therapeutic targets.

Analysis of circular RNA expression profiles of lung cancer in Xuanwei, China.

BACKGROUND: Mounting evidence indicates that circular RNAs (circRNAs) could play a pivotal role in cancers. However, due to the lack of sensitive biomarkers, most lung cancer in Xuanwei (LCXW) patients are still diagnosed at an advanced stage accompany with distant metastasis. METHODS: According to the stage of LCXW patients and tissue sources, circRNAs microarray detection was carried out in six groups. Considering fold change, raw intensity, the length of circRNAs, and P-value, we selected eightcircRNAs for further study. A total of 50 paired LCXW tissues were carried out real-time quantitative polymerase chain reaction (RT-qPCR) in order to extended sample size to verify the expression of these circRNAs. RESULTS: We designed 13 617 human circRNA probes for the human circular RNA microarray, detected 10 819 circRNA in six groups of samples; 537 circRNAs were differentially expressed consistently in every stage. Through RT-qPCR, we selected 8 circRNAs, three of which were upregulated (hsa_circ_0005927, hsa_circ_0069397 and hsa_circ_0000937) and five were downregulated (hsa_circ_0001936, hsa_circ_0005255, hsa_circRNA_406010, hsa_circ_0007064, hsa_circ_0000907) in tumor tissues, only hsa_circ_0001936 showed the opposite expression between microarray and RT-qPCR, others were consistent. Additionally, hsa_circ_0005927 and hsa_circ_0001936 were significantly correlated with tumor size, and hsa_circRNA_406010 was related to the prognosis of LCXW patients. CONCLUSION: Together, these results suggest that hsa_circ_0005927, hsa_circ_0001936, and hsa_circRNA_406010 may serve as the novel potential biomarkers for LCXW. Moreover, these results may provide a new insight for the pathogenesis of LCXW.

Comprehensive analyses of T-UCR expression profiles and exploration of the efficacy of uc.63- and uc.280+ as biomarkers for lung cancer in Xuanwei, China.

OBJECTIVES: Lung cancer in Xuanwei (LCXW), China, is known worldwide for occurring frequently with high morbidity and mortality, which necessitates research to determine its pathogenesis. This study attempted to screen potential transcribed ultraconserved region (T-UCR) biomarkers related to LCXW. METHODS: We performed T-UCR microarrays on 26 paired lung adenocarcinoma and adjacent tissues to explore the T-UCR expression profile of LCXW. Then, bioinformatics analysis was carried out to identify potential T-UCRs, which were further validated by real-time quantitative PCR (RT-qPCR). Then, clinical relevance analysis and Kaplan-Meier tests were performed on 50 paired tissues. RESULTS: T-UCRs and RNA transcripts whose transcription units overlap UCRs (RTOUs) were significantly dysregulated in LCXW tissues compared with the corresponding noncancerous lung (NCL) tissues and presented an increasing trend from stage I to III. The expression between T-UCRs and host genes or flanking genes presented a positive or negative correlation. RT-qPCR analysis showed that uc.63- and uc.280+ were significantly up-regulated in LCXW tissues (P < 0.05). Uc.63- up-regulation was associated with tumor stage and poor prognosis of patients (P < 0.05), and uc.280+ up-regulation was associated with patient age (P < 0.05). Bioinformatics analysis of RTOUs showed that the transcripts of XPO1, uc002sbh and uc002sbg, were potentially regulated targets of uc.63-. Gene Ontology and pathway analyses showed XPO1 was involved in many important biological functions. CONCLUSION: This study depicted T-UCR and RTOU expression profiling of LCXW and revealed some potential T-UCR biomarkers that may be involved in the carcinogenesis of LCXW.

Validation of thwaites' diagnostic scoring system for the differential diagnosis of tuberculous meningitis and bacterial meningitis.

To compare the clinical features of patients with tuberculous meningitis (TBM) and bacterial meningitis (BM) and to validate Thwaites' diagnostic scoring system for the differential diagnosis of TBM and BM, a retrospective review of 211 patients with TBM or BM who were admitted to Huashan Hospital, Fudan University, from 2007 to 2012 was conducted. The clinical characteristics and laboratory data were compared, and Thwaites' diagnostic scores were assessed at the time of admission for the differential diagnosis of TBM and BM. Significant differences were observed between the 2 groups in general information, clinical features, and cerebrospinal fluid characteristics. The sensitivity and specificity of Thwaites' diagnostic scoring system for the differential diagnosis of TBM and BM were found to be 98.2% and 43.6%, respectively, with positive and negative predictive values being 65.9% and 95.8%, respectively. The sensitivity and specificity for the differential diagnosis of TBM and initially treated BM were 98.2% and 82.9%, respectively, but were only 98.2% and 24.2% for that of TBM and partially treated BM, respectively. Thus, Thwaites' diagnostic scoring system was found to be highly effective for the differential diagnosis of TBM and initially treated BM but was found to be less effective for that of TBM and partially treated BM.

MicroRNA-212 inhibits osteosarcoma cells proliferation and invasion by down-regulation of Sox4.

BACKGROUND: Multiple MicroRNAs (miRNAs) have been identified in the development and progression of osteosarcoma. However, the expression and roles of miR-212 in osteosarcoma remain largely undefined. METHODS: Real-time PCR assays were used to detect the expression of miR-212 in human osteosarcoma tissues. MiR-212 mimics were introduced into MG63 and U2OS cells. Bioinformatic prediction was used to identify the potential targets of miR-212. Protein expression analysis, luciferase assays and rescue assays were used to confirm the substrate of miR-212. RESULTS: miR-212 was significantly down-regulated in human osteosarcoma tissues, compared with adjacent normal tissues. Introduction of miR-212 mimics into MG63 and U2OS cells inhibited cell proliferation and invasion. Besides, miR-212 overexpression could also inhibit tumor growth in the nude mice. Additionally, bioinformatic prediction suggested that the sex-determining region Y-box 4 (Sox4) is a target gene of miR-212. Sox4 inhibition phenocopied the roles of miR-212, while restored expression of Sox4 dampened miR-212-mediated suppression of tumor progression. CONCLUSION: The miR-212/Sox4 interaction plays an important role of in the osteosarcoma progression.

Automated nanomanipulation for nanodevice construction.

Nanowire field-effect transistors (nano-FETs) are nanodevices capable of highly sensitive, label-free sensing of molecules. However, significant variations in sensitivity across devices can result from poor control over device parameters, such as nanowire diameter and the number of electrode-bridging nanowires. This paper presents a fabrication approach that uses wafer-scale nanowire contact printing for throughput and uses automated nanomanipulation for precision control of nanowire number and diameter. The process requires only one photolithography mask. Using nanowire contact printing and post-processing (i.e. nanomanipulation inside a scanning electron microscope), we are able to produce devices all with a single-nanowire and similar diameters at a speed of ~1 min/device with a success rate of 95% (n = 500). This technology represents a seamless integration of wafer-scale microfabrication and automated nanorobotic manipulation for producing nano-FET sensors with consistent response across devices.

Classification of cell types using a microfluidic device for mechanical and electrical measurement on single cells.

This paper presents a microfluidic system for cell type classification using mechanical and electrical measurements on single cells. Cells are aspirated continuously through a constriction channel with cell elongations and impedance profiles measured simultaneously. The cell transit time through the constriction channel and the impedance amplitude ratio are quantified as cell's mechanical and electrical property indicators. The microfluidic device and measurement system were used to characterize osteoblasts (n=206) and osteocytes (n=217), revealing that osteoblasts, compared with osteocytes, have a larger cell elongation length (64.51 ± 14.98 µm vs. 39.78 ± 7.16 µm), a longer transit time (1.84 ± 1.48 s vs. 0.94 ± 1.07 s), and a higher impedance amplitude ratio (1.198 ± 0.071 vs. 1.099 ± 0.038). Pattern recognition using the neural network was applied to cell type classification, resulting in classification success rates of 69.8% (transit time alone), 85.3% (impedance amplitude ratio alone), and 93.7% (both transit time and impedance amplitude ratio as input to neural network) for osteoblasts and osteocytes. The system was also applied to test EMT6 (n=747) and EMT6/AR1.0 cells (n=770, EMT6 treated by doxorubicin) that have a comparable size distribution (cell elongation length: 51.47 ± 11.33 µm vs. 50.09 ± 9.70 µm). The effects of cell size on transit time and impedance amplitude ratio were investigated. Cell classification success rates were 51.3% (cell elongation alone), 57.5% (transit time alone), 59.6% (impedance amplitude ratio alone), and 70.2% (both transit time and impedance amplitude ratio). These preliminary results suggest that biomechanical and bioelectrical parameters, when used in combination, could provide a higher cell classification success rate than using electrical or mechanical parameter alone.

A microfluidic device for simultaneous electrical and mechanical measurements on single cells.

This paper presents a microfluidic device for simultaneous mechanical and electrical characterization of single cells. The device performs two types of cellular characterization (impedance spectroscopy and micropipette aspiration) on a single chip to enable cell electrical and mechanical characterization. To investigate the performance of the device design, electrical and mechanical properties of MC-3T3 osteoblast cells were measured. Based on electrical models, membrane capacitance of MC-3T3 cells was determined to be 3.39±1.23 and 2.99±0.82 pF at the aspiration pressure of 50 and 100 Pa, respectively. Cytoplasm resistance values were 110.1±37.7 kΩ (50 Pa) and 145.2±44.3 kΩ (100 Pa). Aspiration length of cells was found to be 0.813±0.351 µm at 50 Pa and 1.771±0.623 µm at 100 Pa. Quantified Young's modulus values were 377±189 Pa at 50 Pa and 344±156 Pa at 100 Pa. Experimental results demonstrate the device's capability for characterizing both electrical and mechanical properties of single cells.

Recombinant antibody libraries and selection technologies.

Active immunization has benefited human health perhaps more than any other biomedical advancement. Today, passive immunization is profoundly changing the practice of medicine by enabling antibody targeting of toxic, self, and other antigens not conducive to active immunization. Recombinant antibody libraries have contributed greatly to this progress and will continue to do so. The ability to construct and display a variety of antibody libraries, including naive, immune, semi-synthetic, and synthetic ones coupled with rapid screening and selection technologies, is in large measure responsible for the thousands of monoclonal antibody therapeutics in development.

[Prenatal diagnosis of a fetus in a family with mandibulofacial dysostosis].

OBJECTIVE: To measure the feasibility of application of comparative genomic hybridization technique in the prenatal diagnosis of fetus with mandibulofacial dysostosis. METHODS: A pregnant woman having a fetus with mandibulofacial dysostosis diagnosed by prenatal ultrasound test was selected. The amniotic fluid and blood of the pregnant and blood of her husband were collected and conventional cytogenetic analysis was performed. The whole genome was scanned by array comparative genomic hybridization assay (array-CGH). Reverse transcription fluorescence quantitative PCR (RT-qPCR) analysis was used to verify the result of array-CGH. RESULTS: No abnormality was found in conventional cytogenetic analysis while a duplicated region in 1p36.33 was detected by array-CGH assay. The region spans 722 kb and contains two genes, VWA1 and PYGO2, which play roles in the development of cartilage. The result of array-CGH was confirmed by the RT-qPCR assay. The diagnosis of mandibulofacial dysostosis was confirmed after birth. CONCLUSION: Author diagnosed a fetus with mandibulofacial dysostosis by array-CGH assay and found two candidate genes related to the development of craniofacial bone: VWA1 and PYGO2.

Apparent PKA activity responds to intermittent hypoxia in bone cells: a redox pathway?

We studied hypoxia-induced dynamic changes in the balance between PKA and PKA-counteracting phosphatases in the microfluidic environment in single cells using picosecond fluorescence spectroscopy and intramolecular fluorescence resonance energy transfer (FRET)-based sensors of PKA activity. First, we found that the apparent PKA activity in bone cells (MC3T3-E1 cells) and endothelial cells (bovine aortic endothelial cells) is rapidly and sensitively modulated by the level of O(2) in the media. When the O(2) concentration in the glucose-containing media was lowered due to O(2) consumption by the cells in the microfluidic chamber, the apparent PKA activity increases; the reoxygenation of cells under hypoxia leads to a rapid ( approximately 2 min) decrease of the apparent PKA activity. Second, lack of glucose in the media led to a lower apparent PKA activity and to a reversal of the response of the apparent PKA activity to hypoxia and reoxygenation. Third, the apparent PKA activity in cells under hypoxia was predominantly regulated via a cAMP-independent pathway since 1) changes in the cAMP level in the cells were not detected using a cAMP FRET sensor, 2) the decay of cAMP levels was too slow to account for the fast decrease in PKA activity levels in response to reoxygenation, and 3) the response of the apparent PKA activity due to hypoxia/reoxygenation was not affected by an adenylate cyclase inhibitor (MDL-12,330A) at 1 mM concentration. Fourth, the immediate onset of ROS accumulation in MC3T3-E1 cells subjected to hypoxia and the sensitivity of the apparent PKA activity to redox levels suggest that the apparent PKA activity change during hypoxia and reoxygenation in this study can be linked to a redox potential change in response to intermittent hypoxia through the regulation of activities of PKA-counteracting phosphatases such as protein phosphatase 1. Finally, our results suggest that the detection of PKA activity could be used to monitor responses of cells to hypoxia in real time.

[Cytogenetic and molecular characterization of partial trisomy 4q and partial monosomy 10q in a patient].

OBJECTIVE: To ascertain the karyotype of a girl with moderate mental retardation and growth retardation, perform correlation analysis between chromosomal variation and phenotype, and investigate the application and superiority of array-based comparative genomic hybridization (array-CGH) in clinical cytogenetic diagnosis. METHODS: G-banded chromosome analysis, array-CGH, fluorescence in situ hybridization (FISH) and real-time quantitative PCR (RQ-PCR) were used to ascertain the karyotype of the patient and her relatives. RESULTS: G-banding analysis of the patient showed a derivative chromosome 10 with an extra fragment on its long arm terminal, both her father and grandmother had an apparently balanced translocation t(4;10)(q25;q26). Array-CGH revealed that the breakpoint on chromosome 4 was located at 4q26. In addition, a microdeletion of about 0.54 Mb del(10)(q26.3) was identified from the patient. FISH and RQ-PCR confirmed that the del(10)(q26.3) was also present in both her father and grandmother. CONCLUSION: No recognizable phenotype was associated with del(10)(q26.3). The abnormal phenotypes presented in the patient may be ascribed to the 4q26-q35.2 triplication. Further more, compared with conventional cytogenetic analysis, array-CGH is of high resolution and high accuracy.

Mechanical stimulus alters conformation of type 1 parathyroid hormone receptor in bone cells.

The molecular mechanisms by which bone cells transduce mechanical stimuli into intracellular biochemical responses have yet to be established. There is evidence that mechanical stimulation acts synergistically with parathyroid hormone PTH(1-34) in mediating bone growth. Using picosecond time-resolved fluorescence microscopy and G protein-coupled receptor conformation-sensitive fluorescence resonance energy transfer (FRET), we investigated conformational transitions in parathyroid hormone type 1 receptor (PTH1R). 1) A genetically engineered PTH1R sensor containing an intramolecular FRET pair was constructed that enabled detection of conformational activity of PTH1R in single cells. 2) The nature of ligand-dependent conformational change of PTH1R depends on the type of ligand: stimulation with the PTH(1-34) leads to conformational transitions characterized by decrease in FRET efficiency while NH(2)-terminal truncated ligand PTH(3-34) stimulates conformational transitions characterized by higher FRET efficiencies. 3) Stimulation of murine preosteoblastic cells (MC3T3-E1) with fluid shear stress (FSS) leads to significant changes in conformational equilibrium of the PTH1R in MC3T3-E1 cells, suggesting that mechanical perturbation of the plasma membrane leads to ligand-independent response of the PTH1R. Conformational transitions induced by mechanical stress were characterized by an increase in FRET efficiency, similar to those induced by the NH(2)-terminal truncated ligand PTH(3-34). The response to the FSS stimulation was inhibited in the presence of PTH(1-34) in the flow medium. These results indicate that the FSS can modulate the action of the PTH(1-34) ligand. 4) Plasma membrane fluidization using benzyl alcohol or cholesterol extraction also leads to conformational transitions characterized by increased FRET levels. We therefore suggest that PTH1R is involved in mediating primary mechanochemical signal transduction in MC3T3-E1 cells.

Membrane activity of an amphiphilic alpha-helical membrane-proximal cytoplasmic domain of the MoMuLV envelope glycoprotein.

In the Moloney murine leukemia virus (MoMuLV) envelope glycoprotein (Env) we identified a membrane-proximal cytoplasmic domain (residues 598-616) that facilitates the Env incorporation into virions and Env-mediated fusion [Rozenberg, Y., Conner, J., Aguilar-Carreno, H., Chakraborti, S., Dimiter, D.S., Anderson, W.F., 2008. Viral entry: membrane-proximal cytoplasmic domain of MoMuLV envelope tail facilitates fusion. In the same issue. (accompanying paper)]. By biophysical methods (CD, EPR) a corresponding peptide (membrane-proximal peptide, 598-616) was demonstrated to form a membrane-parallel amphiphilic alpha-helix in the presence of membranes. Electrophysiological studies with planar bilayers and liposomes indicate that the membrane-proximal peptide is membrane destabilizing. This peptide and the fusion peptide from the MoMuLV transmembrane (TM) ectodomain were tested for their effect on the bilayer for hexagonal phase transition temperature of dipalmitoleoylphosphatidylethanolamine (T(H)). Importantly, the external fusion peptide and the internal membrane-proximal peptides of MoMuLV env exert opposite effects on membrane curvature. The fusion peptide lowers T(H) while the membrane proximal peptide raises it. These effects on T(H) correlate with the ability of these peptides to induce lipid mixing in large unilamellar vesicles composed of dioleoylphosphatidylethanolamine: dioleoylphosphatidylcholine:cholesterol (1:1:1 mol). When added externally to preformed liposomes, the N-terminal fusion peptide promotes lipid mixing while the cytoplasmic membrane-proximal peptide inhibits this effect. These finding indicate a possible mechanism by which the membrane-proximal domain in MoMuLV Env may affect the formation of membrane fusion intermediates.

G protein-coupled receptors sense fluid shear stress in endothelial cells.

Hemodynamic shear stress stimulates a number of intracellular events that both regulate vessel structure and influence development of vascular pathologies. The precise molecular mechanisms by which endothelial cells transduce this mechanical stimulus into intracellular biochemical response have not been established. Here, we show that mechanical perturbation of the plasma membrane leads to ligand-independent conformational transitions in a G protein-coupled receptor (GPCR). By using time-resolved fluorescence microscopy and GPCR conformation-sensitive FRET we found that stimulation of endothelial cells with fluid shear stress, hypotonic stress, or membrane fluidizing agent leads to a significant increase in activity of bradykinin B2 GPCR in endothelial cells. The GPCR conformational dynamics was detected by monitoring redistribution of GPCRs between inactive and active conformations in a single endothelial cell under fluid shear stress in real time. We show that this response can be blocked by a B(2)-selective antagonist. Our data demonstrate that changes in cell membrane tension and membrane fluidity affect conformational dynamics of GPCRs. Therefore, we suggest that GPCRs are involved in mediating primary mechanochemical signal transduction in endothelial cells. We anticipate our experiments to be a starting point for more sophisticated studies of the effects of changes in lipid bilayer environment on GPCR conformational dynamics. Furthermore, because GPCRs are a major target of drug development, a detailed characterization of mechanochemical signaling via the GPCR pathway will be relevant for the development of new antiatherosclerosis drugs.

Laurdan fluorescence senses mechanical strain in the lipid bilayer membrane.

The precise molecular mechanisms by which cells transduce a mechanical stimulus into an intracellular biochemical response have not yet been established. Here, we show for the first time that the fluorescence emission of an environment-sensitive membrane probe Laurdan is modulated by mechanical strain of the lipid bilayer membrane. We have measured fluorescence emission of Laurdan in phospholipid vesicles of 30, 50, and 100 nm diameter to show that osmotically induced membrane tension leads to an increase in polarity (hydration depth) of the phospholipid bilayer interior. Our data indicate that the general polarization of Laurdan emission is linearly dependent on membrane tension. We also show that higher membrane curvature leads to higher hydration levels. We anticipate that the proposed method will facilitate future studies of mechanically induced changes in physical properties of lipid bilayer environment both in vitro and in vivo.

[Anti-stokes blue fluorescence and stark splitting of 3H4 in Pr3+:Y2SiO5 (YSO)].

In the Pr3+ -doped Y2SiO5, the population in 1D2 of Pr3+ can be transferred to 3P0 state via non-radiative energy transfer by the laser excitation in resonance with 3H4-->1D2 , and we can experimentally study the Stark splitting of 3H4 energy level via 3P0 -->3H4 anti-Stokes emission spectra. Because the anti-Stokes emission spectra can avoid the energy transfer between different crystallographic site 1D2 energy levels, the above splitting lines attribution is more accurate than the assignment via 1D2-->3H4 Stokes spectra by the laser excitation in resonance with 3H4-->1D2. In addition, the character of the anti-Stokes fluorescence decay time was observed.