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Background Many solid tumors rely heavily on the regulation and organization of leader and follower cells during the collective invasion. However, leader cells’ specific biomarkers and mechanisms in colorectal cancer (CRC) collective invasion are unclear. This study aimed to identify the specific biomarkers of leader cells and reveals their molecular mechanisms during CRC collective invasion and metastasis. Methods The 3D photoconvertible CRC spheroid model in vitro was constructed to isolate leader cells and follower cells. The RNA-Seq, functional, and animal experiments revealed that GLUT1, PLOD2, and CCL5 in leader cells were required for CRC collective invasion. Results CCL5 up-regulated the expression of GLUT1 and PLOD2 through PI3K/Akt signaling in leader cells. Moreover, GLUT1 and CCL5 could be used as specific biomarkers for leader cells in CRC collective invasion, and their co-expression was associated with poor prognosis of CRC patients. Notably, blocking GLUT1 and CCL5-CCR5 effectively inhibited CRC collective invasion. Conclusions Our findings illustrate that CCL5 and GLUT1 may define leader cells and are required for CRC collective invasion as a potential key regulator of hypoxia-induced metabolic shifts and collagen deposition.

Study objective: To investigate the effects of epidural dexmedetomidine infusion on perioperative hemodynamics in patients. Design: Randomized, interventional, blinded clinical trial. Setting: An operating room and postoperative period in university-affiliated teaching hospital. Patients: 90 patients aged 18~65 years, of ASA status I/II, posted for elective saphenous vein peeling or aspiration surgery. Interventions: Patients were randomly divided into 0.5 μg/kg dexmedetomidine combined with 0.67% ropivacaine epidural infusion group (ED group), 0.5 μg/kg dexmedetomidine intravenous infusion combined with 0.67% ropivacaine epidural infusion group (VD group), and 0.67% ropivacaine plus isovolumic saline epidural infusion group (NS group), with 30 cases in each group. Measurements: The primary outcome was the systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) at before dexmedetomidine infusion (T0), 5 min (T1), 15 min (T2), 30 min (T3), 1 h (T4), 2 h (T5), 4 h (T6), 6 h (T7), 8 h (T8) after the start of dexmedetomidine infusion. The secondary outcomes included plasma norepinephrine (NE) concentration, myocardial oxygen consumption (MVO2), the Ramsay sedation score, the Visual Analogue Scale (VAS) score, anesthetic efficiency between three groups, patient's satisfaction with postoperative anesthesia and the occurrence of adverse reactions. Main results: Compared with NS group, SBP at T3-7 and DBP at T4-5 and T7 were significantly decreased in ED group (P＜0.05 or 0.005), SBP and DBP at T1-8 were lower in VD group (P＜0.05 or 0.005). SBP and DBP at T1-2 in ED group were higher than that in VD group (P＜0.05 or 0.005). The heart rate at T3-4 and T6-7 was lower in ED group than in NS group (P＜0.05 or 0.005). Compared with VD group, the heart rate in ED group at T7 was significantly decreased (P＜0.001). The plasma NE concentration in ED and VD groups at T3-7 was dramatically decreased compared with NS group (P＜0.05 or 0.005). The plasma NE concentration in ED group was considerably increased at T3-4 and reduced at T6 compared with VD group (P＜0.005). MVO2 was lower in both ED and VD groups than in NS group (P＜0.05 or 0.005). The anesthesia efficiency was significantly enhanced in ED group compared with VD and NS groups (P＜0.05 or 0.005). Compared with NS group, the anesthesia satisfaction score was higher in ED and VD groups (P＜0.001). The incidence of dizziness in ED group and the incidence of hypotension and dizziness in VD group were higher than that in NS group (P＜0.05 or 0.005), and the occurrence of hypotension was less common in ED group than in VD group (P=0.003). Conclusion: 0.5 μg/kg dexmedetomidine epidural infusion can provide more stable perioperative hemodynamics for patients with varicose vein surgery under epidural anesthesia, with lower incidence of hypotension and significantly advanced efficiency of epidural anesthesia.

Hematological metastasis was the main metastatic method of colorectal cancer and the main reason for failure of radical surgery. Vascular endothelial cells played an important role in tumor hematologic metastasis. We previously performed RNA-Seq on primary and metastatic colorectal carcinoma (CRC) tissues and then identified GPR63 as a potential metastasis-promoting gene, but its role and mechanisms in the interaction between cancer cells and vascular endothelial cells were still unknown. In this study, GPR63 was significantly elevated in CRC tissues compared with paracarcinoma tissues. GPR63 expression was closely related to lymph node metastasis and distant metastasis in 147 CRC tissues. GPR63 promoted cell migration and stemness. Moreover, endothelial cell-derived S1P enhanced the migration and sphere-forming ability of CRC through activation of GPR63. Mechanistically, S1P promoted GPR63 binding to Src to activate JAK2/STAT3 pathway, and therefore promoted CRC cell migration. Our study revealed a novel mechanism by which endothelial cells promoted metastasis of CRC cells, which might have potential as a promising target for CRC therapy.

Background Circular RNAs (circRNAs) are involved in diverse processes that drive cancer development. However, the expression landscape and mechanistic function of circRNAs in osteosarcoma (OS) remain to be studied. Methods Bioinformatic analysis and high-throughput RNA sequencing tools were employed to identify differentially expressed circRNAs between OS and adjacent noncancerous tissues. The expression level of circ_001422 in clinical specimens and cell lines was measured using qRT-PCR. The association of circ_001422 expression with the clinicopathologic features of 55 recruited patients with OS was analyzed. Loss- and gain-of-function experiments were conducted to explore the role of circ_001422 in OS cells. RNA immunoprecipitation, fluorescence in situ hybridization, bioinformatics database analysis, RNA pulldown assays, dual-luciferase reporter assays, mRNA sequencing, and rescue experiments were conducted to decipher the competitive endogenous RNA regulatory network controlled by circ_001422. Results We characterized a novel and abundant circRNA, circ_001422, that promoted OS progression. Circ_001422 expression was dramatically increased in OS cell lines and tissues compared with noncancerous samples. Higher circ_001422 expression correlated with more advanced clinical stage, larger tumor size, higher incidence of distant metastases and poorer overall survival in OS patients. Circ_001422 knockdown markedly repressed the proliferation and metastasis and promoted the apoptosis of OS cells in vivo and in vitro, whereas circ_001422 overexpression exerted the opposite effects. Mechanistically, competitive interactions between circ_001422 and miR-195-5p elevated FGF2 expression while also initiating PI3K/Akt signaling. These events enhanced the malignant characteristics of OS cells. Conclusions Circ_001422 accelerates OS tumorigenesis and metastasis by modulating the miR-195-5p/FGF2/PI3K/Akt axis, implying that circ_001422 can be therapeutically targeted to treat OS.

Background Our objective was to observe the effects of extracorporeal circulation (ECC) with different time on platelet count in patients undergoing cardiac surgery. Methods A total of 427 patients who underwent elective cardiac surgery under ECC in affiliated hospital of north Sichuan medical college from January 1, 2018 to July 31, 2021 were divided into three groups according to ECC time. Their data were collected from the Do care and electronic medical record information system. All authors confirm that all methods were performed in accordance with the relevant guidelines and regulations. Results At the end of operation, platelet count was significantly lower in group C than in group A (p< 0.05); on the first day after operation, platelet count was significantly higher in groups A and B than in group C (p< 0.05); compared with group A, platelet count on the second day and the fifth day after operation were significantly lower in groups B and C (p< 0.05). The mean platelet volume (MPV) was significantly reduced at the end of operation in each group (p< 0.05). The absolute monocyte count at the end of operation was significantly higher in group C than in groups A and B (p< 0.05). The volume of blood loss and plasma transfusion were significantly lower in group A than in groups B and C (p< 0.05). Conclusion Platelet count in patients undergoing cardiac surgery after ECC was reduced significantly, which was more serious with the extension of ECC time. The recovery level and speed of platelet count in patients with long ECC time were lower than those with short ECC time.

Introduction Etomidate has been advocated to be used in anesthesia of the elderly and the critically ill patients due to its faint effect on cardiovascular system. But the dose-dependent suppression of etomidate on adrenal cortex function leads to the limitation of its clinical application. Clinical research shows that dexmedetomidine can reduce the dose requirements for intravenous or inhalation anesthetics and opioids, and the hemodynamics is more stable during the operation. The objective is to observe the effect of etomidate combined with dexmedetomidine on adrenocortical function in elderly patients. Methods 180 elder patients scheduled for elective ureteroscopic holmium laser lithotripsy were randomly allocated to PR group anesthetized with propofol- remifentanil, ER group anesthetized with etomidate-remifentanil, and ERD group anesthetized with dexmedetomidine combined with etomidate-remifentanil. Patients in each group whose operation time was less than or equal to 1h were incorporated into short time operation group (PR1 group, ER1 group and ERD1 group), and whose operation time was more than 1h were incorporated into long time operation group (PR2 group, ER2 group and ERD2 group). The values of SBP, DBP, HR and SpO2 were recorded at T0, T1, T2, T3, T4, T5, T6 and T7.The time of operation, the dosage of etomidate and remifentanil administrated during surgery, the time to spontaneous respiration, recovery and extubation, and the duration of stay in the PACU were recorded. The serum cortisol and ACTH concentration was measured at t0, t1, t2, t3, t4 and t5. Results The dosage of etomidate was significantly lower in ERD1 group and ERD2 group compared with ER1 group and ER2 group(P < 0.05), respectively. The SBP in ER2 and ERD2 group were higher at T1 and T3 compared to PR2 group (P < 0.05). The DBP in ER1 and ERD1 group were higher at T1compared to PR1 group (P < 0.05). The Serum cortisol concentration were higher at t1 ~ 2 in ERD1 group compared to ER1 group (P < 0.05). The Serum cortisol concentration were higher at t1 ~ 3 in ERD2 group compared to ER2 group (P < 0.05).The Serum ACTH concentration were lower at t1 ~ 2 in ERD1 group compared to ER1 group (P < 0.05). The Serum ACTH concentration were lower at t1 ~ 3 in ERD2 group compared to ER2 group (P < 0.05). Conclusion The administration of dexmedetomidine combined with etomidate can attenuate the inhibition of etomidate on adrenocortical function in elderly patients and maintain intraoperative hemodynamic stability.

One of the malignant transformation hallmarks is metabolism reprogramming, which plays a critical role in the biosynthetic needs of unchecked proliferation, abrogating cell death programs, and immunologic escape. However, the mechanism of the metabolic switch is not fully understood. Here, we found that the S-nitrosoproteomic profile of endogenous nitrogen oxide in ovarian cancer cells targeted multiple components in metabolism processes. Phosphofructokinase (PFKM), one of the most important regulatory enzymes of glycolysis, was S-nitrosylated by nitric oxide synthase NOS1 at Cys351. S-nitrosylation at Cys351 stabilized the tetramer of PFKM, leading to resist negative feedback of downstream metabolic intermediates. The PFKM-C351S mutation decreased the proliferation rate of cultured cancer cells, and reduced tumor growth and metastasis in the mouse xenograft model. These findings indicated that S-nitrosylation at Cys351 of PFKM by NOS1 contributes to the metabolic reprogramming of ovarian cancer cells, highlighting a critical role of endogenous nitrogen oxide on metabolism regulations in tumor progression.

BackgroundCircular RNAs (circRNAs) are involved in diverse processes that drive cancer development. Nevertheless, the expression landscape and mechanistic function of circRNAs in osteosarcoma (OS) remain to be studied.MethodsBioinformatics analysis and high-throughput RNA sequencing tools were employed to determine differentially expressed circRNAs between OS and adjacent healthy tissues. The expression levels of circ_001422 in clinical specimens and cell lines were measured using qRT-PCR. A total of 55 OS patients were recruited to analyze the association of circ_001422 expression with clinicopathologic features. Loss- and gain-of-function tests were conducted to explore the role of circ_001422 in OS cells. RNA immunoprecipitation, fluorescent in situ hybridization, bioinformatics databases, RNA pull-down assay, dual-luciferase reporter assay, mRNA sequencing, and rescue experiments were conducted to decipher the competitive endogenous RNAs regulatory network dominated by circ_001422.ResultsWe characterized a novel and abundant circRNA, circ_001422, which promoted the progression of OS. Circ_001422 expression was dramatically higher in OS cell lines and tissues relative to normal samples. Increased circ_001422 correlated with more advanced clinical stage, larger tumor size, more distant metastases and poorer overall survival of OS patients. Knockdown of circ_001422 markedly repressed proliferation and metastasis and promoted apoptosis of OS cells in vivo and in vitro, whereas overexpression of circ_001422 exerted an opposite effect. Mechanistically, competitive interactions between circ_001422 and miR-195-5p elevated the expression of FGF2 while also initiating the PI3K/Akt signaling pathway. These events enhanced the malignant characteristics of OS cells.Conclusions Circ_001422 accelerates OS tumorigenesis and metastasis through modulating the miR-195-5p/FGF2/PI3K/Akt axis, implying that circ_001422 could be therapeutically targeted to treat OS patients.

Background In this work, we aimed to demonstrate how to utilize the lab test results and other clinical information to support precision medicine research and clinical decisions on complex diseases, with the support of electronic medical record facilities. We defined “clinotypes” as clinical information that could be observed and measured objectively using biomedical instruments. From well-known ‘omic’ problem definitions, we defined problems using clinotype information, including stratifying patients—identifying interested sub cohorts for future studies, mining significant associations between clinotypes and specific phenotypes-diseases, and discovering potential linkages between clinotype and genomic information. We solved these problems by integrating public omic databases and applying advanced machine learning and visual analytic techniques on two-year health exam records from a large population of healthy southern Chinese individuals (size n = 91,354). When developing the solution, we carefully addressed the missing information, imbalance and non-uniformed data annotation issues. Results We organized the techniques and solutions to address the problems and issues above into CPA framework (Clinotype Prediction and Association-finding). At the data preprocessing step, we handled the missing value issue with predicted accuracy of 0.760. We curated 12,635 clinotype-gene associations. We found 147 Associations between 147 chronic diseases-phenotype and clinotypes, which improved the disease predictive performance to AUC (average) of 0.967. We mined 182 significant clinotype-clinotype associations among 69 clinotypes. Conclusions Our results showed strong potential connectivity between the omics information and the clinical lab test information. The results further emphasized the needs to utilize and integrate the clinical information, especially the lab test results, in future PheWas and omic studies. Furthermore, it showed that the clinotype information could initiate an alternative research direction and serve as an independent field of data to support the well-known ‘phenome’ and ‘genome’ researches.

Tempol (4-hydroxy-2,2,6,6-Tetramethylpiperidine-1-oxyl, TPL), a nitroxide compound, inhibits proliferation and increases the vulnerability of cancer cells to apoptosis induced by cytotoxic agents. However, the molecular mechanism of TPL inhibiting cancer cell proliferation has not been fully understood. In this study, we evaluated the metabolic effect of TPL on cancer cells and explored its cancer therapeutic potential. Extracellular flow assays showed that TPL inhibited cellular basal and maximal oxygen consumption rates of mitochondrial. 13C metabolic flux analysis showed that TPL treatment had minimal effect on glycolysis. However, we found that TPL inhibits glutamine metabolism by interfering with the oxidative tricarboxylic acid cycle (TCA) process and reductive glutamine process. We found that the inhibitory effect of TPL on metabolism occurs mainly on the step from citrate to α-ketoglutarate or vice versa. We also found that activity of isocitrate dehydrogenase IDH1 and IDH2, the key enzymes in TCA, were inhibited by TPL treatment. In xenograft mouse model, TPL treatment reduced tumor growth by inhibiting cellular proliferation of xenograft tumors. Thus, we provided a mechanism of TPL inhibiting cancer cell proliferation by interfering with glutamine utilization that is important for survival and proliferation of cancer cells. The study may help the development of a therapeutic strategy of TPL combined with other anticancer medicines.

BackgroundThe dysfunction of type I interferon (IFN) signaling is an important mechanism of immune escape and metastasis in tumors. Increased NOS1 expression has been detected in melanoma, which correlated with dysfunctional IFN signaling and poor response to immunotherapy, but the specific mechanism has not been determined. In this study, we investigated the regulation of NOS1 on the interferon response and clarified the relevant molecular mechanisms.MethodsAfter stable transfection of A375 cells with NOS1 expression plasmids, the transcription and expression of IFNα-stimulated genes (ISGs) were assessed using pISRE luciferase reporter gene analysis, RT-PCR, and western blotting, respectively. The effect of NOS1 on lung metastasis was assessed in melanoma mouse models. A biotin-switch assay was performed to detect the S-nitrosylation of HDAC2 by NOS1. ChIP-qPCR was conducted to measure the binding of HDAC2, H4K16ac, H4K5ac, H3ac, and RNA polymerase II in the promoters of ISGs after IFNα stimulation. This effect was further evaluated by altering the expression level of HDAC2 or by transfecting the HDAC2-C262A/C274A site mutant plasmids into cells. The coimmunoprecipitation assay was performed to detect the interaction of HDAC2 with STAT1 and STAT2. Loss-of-function and gain-of-function approaches were used to examine the effect of HDAC2-C262A/C274A on lung metastasis. Tumor infiltrating lymphocytes were analyzed by flow cytometry.ResultsHDAC2 is recruited to the promoter of ISGs and deacetylates H4K16 for the optimal expression of ISGs in response to IFNα treatment. Overexpression of NOS1 in melanoma cells decreases IFNα-responsiveness and induces the S-nitrosylation of HDAC2-C262/C274. This modification decreases the binding of HDAC2 with STAT1, thereby reducing the recruitment of HDAC2 to the ISG promoter and the deacetylation of H4K16. Moreover, expression of a mutant form of HDAC2, which cannot be nitrosylated, reverses the inhibition of ISG expression by NOS1 in vitro and decreases NOS1-induced lung metastasis and inhibition of tumor infiltrating lymphocytes in a melanoma mouse model.ConclusionsThis study provides evidence that NOS1 induces dysfunctional IFN signaling to promote lung metastasis in melanoma, highlighting NOS1-induced S-nitrosylation of HDAC2 in the regulation of IFN signaling via histone modification.

OBJECTIVE: To investigate the effect of the chemoprotectant tempol on the anti-tumor activity of cisplatin (DDP). METHODS: The cellular toxicity of tempol in human colon cancer SW480 cells and mouse colon cancer CT26 cells were evaluated using MTT and cell counting kit-8 assays. CalcuSyn software analysis was used to determine the interaction between tempol and DDP in inhibition of the cell viability. A subcutaneous homograft mouse model of colon cancer was established. The mice were randomly divided into control group, tempol group, cisplatin group and tempol + DDP treatment group with intraperitoneal injections of the indicated agents. The tumor size, body weight and lifespan of the mice were measured, and HE staining was used to analyze the cytotoxic effect of the agents on the kidney and liver. Immunohistochemistry and Western blotting were performed to detect the expression of Bax and Bcl2 in the tumor tissue, and TUNEL staining was used to analyze the tumor cell apoptosis. The level of reactive oxygen species (ROS) in the tumor tissue was determined using flow cytometry. RESULTS: Tempol showed inhibitory effects on the viability of SW480 and CT26 cells. CalcuSyn software analysis showed that tempol had a synergistic anti-tumor effect with DDP (CI < 1). In the homograft mouse model, tempol treatment alone did not produce obvious anti-tumor effect. HE staining showed that the combined use of tempol and DDP alleviated DDP-induced fibrogenesis in the kidneys, but tempol also reduced the anti-tumor activity of DDP. Compared with the mice treated with DDP alone, the mice treated with both tempol and DDP had a significantly larger tumor size (P < 0.01) and a shorter lifespan (P < 0.05). Tempol significantly reversed DDP-induced expression of Bax and Bcl2 in the tumor tissue and tumor cell apoptosis (P < 0.001), and obviously reduced the elevation of ROS level in the tumor tissue induced by DDP treatment (P < 0.05). CONCLUSION: Tempol can attenuate the anti-tumor effect of DDP while reducing the side effects of DDP. Caution must be taken and the risks and benefits should be carefully weighed when considering the use of tempol as an anti-oxidant to reduce the toxicities of DDP.

Microcystins-LR (MC-LR), a cyanobacterial toxins, initiate apoptosis in normal and tumor cells. Nitric oxide produced by iNOS is necessary for MC-LR-induced apoptosis. However, the underlying mechanism of NO mediated MC-LR cytotoxicity remains unclear. Here, we performed in vitro experiments on MC-LR cytotoxicity associated with NO induced S-nitrosyation of GAPDH in human colon cancer cells SW480. MTT assay indicated that MC-LR decreased the cellular viability by high concentration (>1 μM). Flow cytometer assay revealed that apoptosis was core mode for MC-LR cytotoxicity. Griess assay showed that MC-LR exposure increased the release of NO through the function of NOS1 and NOS2 in SW480 cells. In turn, NO stress induced the S-nitrosylated modification of GAPDH leading to its nuclear translocation following Siah1 binding. CHIP assay showed that the nuclear GADPH increased P53 transcript of a panner of apoptosis related genes. Moreover, apoptosis induced by MC-LR could be reduced by GAPDH or si-Siah1 or NOSs inhibitor, L-NAME. Thus, our study verified a molecular mechanism of NO/GAPDH/Siah1 cascade in MC-LR mediated apoptosis in colorectal cancer cells, providing a further understanding the in vitro molecular mechanism of MC-LR colorectal toxicity.

Additional file 1: Sequences of siRNA and primer used in this study. Table S1. Primer sequences for RT-PCR. Table S2. The sequences of siRNA. Table S3. Primer sequences for ChIP-qPCR

Elbow joint stiffness is critical to positioning the hand. Abnormal elbow joint stiffness may affect a person's ability to participate in activities of daily living. In this work, elbow joint stiffness was measured in ten healthy young adults with a device adapted from one previously used to measure stiffness in other joints. Measurements of elbow stiffness involved applying a constant-velocity rotational movement to the elbow and measuring the resultant displacement, torque, and acceleration. Elbow stiffness was then computed using a previously-established model for joint stiffness. Measurements were made at two unique elbow joint angles, two speeds, and two forearm muscle contraction levels. The results indicate that the elbow joint stiffness is significantly affected by both rotational speed and forearm muscle contraction level.

In this work, we constructed diabetes predictive models using electronic health record data, which could potentially have better preventive power than other diabetes predictive models known according to our knowledge. Diabetes is one of the most common, costly and complicated diseases all over the world, including China. To tackle the complexity of diabetes, electronic health record has been widely used to support physicians in integrated care. However, diabetes predictive models using electronic health record may lack of preventive power when the clinical measurements directly related to diabetes diagnosis criteria are used. To overcome this limitation, we did not use glucose, insulin, C-peptide and HbA1C clinical measurements in classifying diabetes patients. We used decision-table and support vector machine algorithm to build predictive models. As the result, our decision-table-based model achieves accuracy of 0.879, AUC of 0.921, precision of 0.898 and recall of 0.904, which is comparable with any known definition to diabetes. Our support-vector-machine-based model achieves accuracy of 0.660, AUC of 0.584, precision of 0.652 and recall of 0.939. We also found 37 measurements significantly associated to diabetes, which are not directly related to diabetes diagnosis criteria.

The elbow joint is critical for positioning the hand to carry out activities of daily living. Deficits in elbow joint range of motion, torque production capabilities, or alterations in elbow joint stiffness affect the ability to successfully carry out feeding, grooming, and other essential activities [1]. Thus quantifying elbow joint stiffness is desirable. Quantifying elbow joint stiffness could help diagnose, monitor and rehabilitate elbow impairments if its relationship to them is known. Ultimately, accurate measurements of joint stiffness can also impact the design of artificial limbs and human motor system control and simulation. The long-term research goal is to quantify how elbow stiffness changes with elbow joint flexion angles, movement speeds, muscle contraction, and injury or disease. The immediate goal was to validate that a recently-modified Stiffness Tester measures elbow stiffness values within the range of those previously reported. The expectation was that muscle contraction level and joint position would influence the elbow stiffness values.Copyright © 2013 by ASME

Liquid level detection (LLD) is necessary for eliminating carry-over of needle's outside by limiting the depth the needle probes into liquid in auto clinical laboratory analyzers. This paper listed various demands of liquid-handling system under different situations; reviewed various LLD techniques, such as capacitive, air pressure, mechanical vibration, ultrasound, light reflection, CCD imaging etc.; briefly introduced the working principles, features, and limitation of the LLDs; and recapitulated the characteristics of contact and non-contact LLDs. Lastly, the next generation technique of LLD is prospected.

It is well know that nanoscale rare earth compounds can increase luminescent quantum efficiency and display resolution. To improve luminescent properties of nanocrystalline phosphors and obtain the nanocrystals with different morphology, many preparation methods have been used, such as hydrothermal approach, sol-gel technique and ultrasonic method, etc. In this paper, the LaPO 4 : Eu 3+ nanocrystals were prepared via the ultrasonic method. There were two series prepared, by changing ultrasonic time, using polyvinglpyrrolidone (PVP) and cetyltrimethylammonium bromide (CTAB) as template, respectively. The morphology, structure and spectra properties of the products were characterized by scanning electron microscopy (SEM), X-ray diffraction (XRD), Fourier transform infrared (FT-IR) and fluorescence spectrum (FS). The results show that all the LaPO 4 nanocrystals have a hexagonal structure, and without other impurity phase appearance. All the samples obtained are nanoparticles in the range of 50-120 nm, which indicates that there are almost no effectives on the morphology of the nanocrystals with the change of template kinds and ultrasonic time. But their luminescent properties depend on the kinds of template. When the ultrasonic time is 1h, the luminescent intensity of the obtained sample using PVP as template is much stronger than that using CTAB, but the 5 D 0 energy level fluorescence lifetime of the Eu 3+ in the sample using PVP template is shorter than that using CTAB. In addition, in the two series, luminescent intensity increases at first, then decreases with the growth of ultrasonic time, but the 5 D 0 energy level lifetime of Eu 3+ shows no regulation.