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Qing Luo

Publications and source records attributed to Qing Luo.

At least 19 recordsLinked to original sources
PubMed2025

A chromosome-level reference genome assembly of the Small snakehead (Channa asiatica).

The Small snakehead (Channa asiatica) is an economically important species in both aquaculture and ornamental trade, mainly distributed in South China and Southeast Asia. Despite its significance, limited genomic resources have impeded in-depth genetic studies and breeding programs. In this study, we used PacBio HiFi long-read sequencing, Illumina short-read sequencing, and Hi-C technologies to generate a high-quality chromosome-level genome of the C. asiatica. The final genome spans 659.44 Mb, with an impressive 98.18% anchored to 23 chromosomes. Notably, the contig N50 and scaffold N50 are 23.92 Mb and 29.61 Mb, validated by a BUSCO completeness score of 98.93%. Genome annotation identified 26,603 protein-coding genes, 99.29% of which were confirmed by BUSCO analysis, and 93.68% were functionally annotated. Approximately 27.72% of the genome sequences were classified as repeat elements. This high-fidelity genome assembly provides a robust foundation for advancing molecular breeding, comparative genomics, and evolutionary studies of C. asiatica and related species.

Animals↗
PubMed2006

Transport of ions through the oil phase of W(1)/O/W(2) double emulsions.

Using a capillary video microscopy technique, the ion transport at liquid-liquid interfaces and through a surfactant-containing emulsion liquid membrane was visually studied by preparing a double emulsion globule within the confined space of a thin-walled, transparent, cylindrical microtube. NaCl and AgNO(3) were selected as the model reactants and were prepared to form a NaCl/AgNO(3) pair across the oil film. By observing and measuring the formed AgCl deposition, it was found that both Cl(-) and Ag(+) could transport through a thick oil film and Ag(+) was transported faster than Cl(-). Interestingly, the ion transport was significantly retarded when the oil film became extremely thin (<1 microm). The results suggested that the transport of ions mainly depends on the "reverse micelle transport" mechanism, in which reverse micelles with entrapped ions and water molecules can be formed in a thick oil film and their construction will get impeded if the oil film becomes extremely thin, leading to different ion transport rates in these two cases. The direction of ion transport depends on the direction of the osmotic pressure gradient across the oil film and the ion transport is independent of the oil film thickness in the investigated thick range. Ions with smaller Pauling radii are more easily entrapped into the formed reverse micelles and therefore will be transported faster through the oil film than bigger ions. Oil-soluble surfactants facilitate ion transport; however, too much surfactant in the oil film will slow down the ion migration. In addition, this study showed no support for the "molecular diffusion" mechanism of ion transport through oils.

Journal Article↗
PubMed2006

Effects of oxymatrine on proliferation and apoptosis in human hepatoma cells.

Oxymatrine, a natural quinolizidine alkaloid, has been known having cytotoxic and chemopreventive effects on various cancer cells. To investigate the possible mechanism of oxymatrine's role on cancer cells, in the present study, we examined further the effects of oxymatrine on the growth, proliferation, apoptosis and expression of bcl-2 and p53 gene in human hepatoma SMMC-7721 cells in vitro. Our results show that oxymatrine notably inhibits the growth and proliferation of SMMC-7721 cells and it present a dose-dependence and time-dependence manner within definite reacting dose and time. Oxymatrine block SMMC-7721 cells in G2/M and S phase; prevent cells entering into G0/G1 phase. It results in an obvious accumulation of G2/M and S phase cells while decrease of G0/G1 phase cells. Oxymatrine induce apoptosis of SMMC-7721 cells and apoptotic rate amount to about 60% after treatment with 1.0 mg/ml oxymatrine for 48 h. We also find that oxymatrine down-regulate expression of bcl-2 gene while up-regulate expression of p53 gene. These results demonstrate that oxymatrine inhibit the proliferation and induce apoptosis of human hepatoma SMMC-7721 cells, and suggest that this effect was mediated probably by a significant cell cycle blockage in G2/M and S phase, down-regulation of bcl-2 and up-regulation of p53.

Alkaloids↗
PubMed2006

Resistance to fracture of two all-ceramic crown materials following endodontic access.

STATEMENT OF PROBLEM: There is currently no protocol for managing endodontic access openings for all-ceramic crowns. A direct restorative material is generally used to repair the access opening, rendering a repaired crown as the definitive restoration. This endodontic procedure, however, may weaken the restoration or initiate microcracks that may propagate, resulting in premature failure of the restoration. PURPOSE: The purpose of this in vitro study was to evaluate how an endodontic access opening prepared through an all-ceramic crown altered the structural integrity of the ceramic, and the effect of a repair of this access on the load to failure of an all-ceramic crown. MATERIAL AND METHODS: Twenty-four alumina (Procera) and 24 zirconia (Procera) crowns were fabricated and cemented (Rely X Luting Plus Cement) onto duplicate epoxy resin dies. Twelve crowns of each were accessed to simulate root canal treatment therapy. Surface defects of all accessed specimens were evaluated with an environmental scanning electron microscope. The specimens were repaired with a porcelain repair system (standard adhesive resin/composite resin protocol) and were loaded to failure in a universal testing machine. Observations made visually and microscopically noted veneer delamination from the core, core fracture, shear within the veneer porcelain, or a combination thereof. A Kruskal-Wallis test was used to determine if a significant difference (alpha=.05) in load to failure existed between the 4 groups, and a Mann-Whitney test with a Bonferroni correction (P<.0125) was used for multiple comparisons. A Weibull analysis was also used to estimate the Weibull modulus and characteristic failure for each group. RESULTS: All specimens exhibited edge chipping around the access openings. Some displayed larger chips within the veneering porcelain, and 4 zirconia crowns showed radial crack formation. There was a significant difference in load to failure among all groups with the exception of the alumina intact and repaired specimens (P=.695). The alumina crowns generally showed fracture of the coping with the veneering porcelain still bonded to the core, whereas the zirconia copings tended not to fracture but experienced veneering porcelain delamination. CONCLUSION: Endodontic access through all-ceramic crowns resulted in a significant loss of strength in the zirconia specimens but not in the alumina specimens.

Aluminum Oxide↗
PubMed2006

CCN1/Cyr61 is regulated by the canonical Wnt signal and plays an important role in Wnt3A-induced osteoblast differentiation of mesenchymal stem cells.

Marrow mesenchymal stem cells are pluripotent progenitors that can differentiate into bone, cartilage, muscle, and fat cells. Wnt signaling has been implicated in regulating osteogenic differentiation of mesenchymal stem cells. Here, we analyzed the gene expression profile of mesenchymal stem cells that were stimulated with Wnt3A. Among the 220 genes whose expression was significantly changed by 2.5-fold, we found that three members of the CCN family, CCN1/Cyr61, CCN2/connective tissue growth factor (CTGF), and CCN5/WISP2, were among the most significantly up-regulated genes. We further investigated the role of CCN1/Cyr61 in Wnt3A-regulated osteogenic differentiation. We confirmed that CCN1/Cyr61 was up-regulated at the early stage of Wnt3A stimulation. Chromatin immunoprecipitation analysis indicates that CCN1/Cyr61 is a direct target of canonical Wnt/beta-catenin signaling. RNA interference-mediated knockdown of CCN1/Cyr61 expression diminished Wnt3A-induced osteogenic differentiation. Furthermore, exogenously expressed CCN1/Cyr61 was shown to effectively promote mesenchymal stem cell migration. These findings suggest that tightly regulated CCN1/Cyr61 expression may play an important role in Wnt3A-induced osteoblast differentiation of mesenchymal stem cells.

Adenoviridae↗
PubMed2006

[Mechanical properties of rat HCC adhesion to collagen I and its relationship with cell cycle].

The mechanical properties of tumor cells adhering to extracellular matrix (ECM) are closely related with their invasion and metastesis. In this study we investigated the adhesive mechanical properties between hepatocellular carcinoma cells(HCC) and the collagen I coated surfaces from the viewpoint of cell cycle by coupling cellular biology and cellular mechanics, using micropipette aspiration and cell synchronization technique. The results showed that the synchronous G1 and S phase HCC cells were achieved by use of thymine-2-desoryriboside, colchicines sequential blockage method and double thymine-2-desoryriboside blockage method, and that the synchronous rates of G1 and S phase HCC amounted to 74.09% and 90.39% respectively. Within the ranges of dosing and timing in this study, the adhesion of HCC cells to collagen I displayed dose dependent and time dependent patterns. S phase cells had small force of adhesion to collagen I as compared with G1 phase and controlled cells(P<0.001), which suggested that G1 phase HCC may play an important role in the step of invading interstitial connective tissue in the metastasis pathway of HCC through blood circulation. These are of significance to unveiling the mechanism of HCC metastasis.

Animals↗
PubMed2006

Therapeutic efficacy and bone marrow protection of the mdr1 gene and over-dose chemotherapy with doxorubicin for rabbits with VX2 hepatocarcinoma.

BACKGROUND: Malignant tumors are common diseases threatening to the health and life of human being. Clinically, the multidrug resistance of tumor cells and bone marrow depression caused by chemotherapeutic agents are the main obstacles to the treatment of tumors, and both are related to the mdr1 gene. The over expression of the mdr1 gene in tumor cells contributes to the multidrug resistance of malignant tumor cells. With little expression of the mdr1 gene, bone marrow cells particularly susceptible to multidrug resistance-sensitive agents, which cause serious toxicity in bone marrow. This study was undertaken to assess therapeutic efficacy of transplantation of bone marrow mononuclear cells transferred with the mdr1 gene and over-dose chemotherapy with doxorubicin for VX2 hepatocarcinoma of rabbits. METHODS: The mdr1 gene was transferred into the bone marrow mononuclear cells of rabbits, which was co-cultured with retroviral vector-containing supernatant, and the cells were autotransplanted into a rabbit model with VX2 hepatocarcinoma. After chemotherapy with doxorubicin, the protective effects of the mdr1 gene and therapeutic efficacy of over-dose chemotherapy were observed. RESULTS: The mdr1 gene was transferred successfully into the bone marrow mononuclear cells, with a transduction efficiency of 35%. After autotransplantation, the mdr1 gene was expressed functionally in bone marrow with a positive rate of 8%, indicating that the gene played an important role in bone marrow protection. The rabbits with VX2 hepatocarcinoma, which had received the mdr1 gene-transduced cells, survived after chemotherapy with a 3-fold dose of adriamycin, and their white blood cell counts were (4.26 +/- 1.03) x 10(4)/L. Since hepatocarcinoma cells were eradicated, the survival time (97.00 +/- 46.75 d) of the rabbits was extended (P<0.05) and the healing rate of the tumor was increased (P<0.05). CONCLUSIONS: The transferring of the mdr1 gene into bone marrow mononuclear cells could confer chemoprotection to bone marrow, and over-dose chemotherapy could be prescribed for the treatment of malignant tumors.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Brönsted and Lewis acidity of the BF3/gamma-Al2O3 alkylation catalyst as revealed by solid-state NMR spectroscopy and DFT quantum chemical calculations.

Multinuclear solid-state NMR techniques and DFT quantum chemical calculations were employed to investigate the detailed structure of acid sites on the BF3/gamma-Al2O3 alkylation catalyst. The NMR experiment results indicate that gaseous BF3 is able to react with the hydroxyl groups present on the surface of gamma-Al2O3, leading to the formation of new Brönsted and Lewis acid sites. The 1H/11B and 1H/27Al TRAPDOR (TRAnsfer of Population in DOuble Resonance) experiments suggest that the 3.7 ppm signal in 1H NMR spectra of the BF3/gamma-Al2O3 catalyst is due to a bridging B-OH-Al group that acts as a Brönsted acid site of the catalyst. On the other hand, a Lewis acid site on the surface of the catalysts, as revealed by 31P MAS and 31P/27Al TRAPDOR NMR of adsorbed trimethylphosphine, is associated with three-coordinate -OBF2 species. 13C NMR of adsorbed 2-13C-acetone indicates that the Brönsted acid strength of the catalyst is slightly stronger than that of zeolite HZSM-5 but still weaker than that of 100% H2SO4, which is in good agreement with theoretical prediction. In addition, DFT calculations also reveal the detailed structure of various acid sites formed on the BF3/gamma-Al2O3 catalyst and the interaction of probe molecules with these sites.

Journal Article↗
PubMed2005

Adhesion of different cell cycle human hepatoma cells to endothelial cells and roles of integrin beta1.

AIM: To investigate the adhesive mechanical properties of different cell cycle human hepatoma cells (SMMC-7721) to human umbilical vein endothelial cells (ECV-304), expression of adhesive molecule integrinbeta1 in SMMC-7721 cells and its contribution to this adhesive course. METHODS: Adhesive force of SMMC-7721 cells to endothelial cells was measured using micropipette aspiration technique. Synchronous G1 and S phase SMMC-7721 cells were achieved by thymine-2-deoxyriboside and colchicines sequential blockage method and double thymine-2-deoxyriboside blockage method, respectively. Synchronous rates of SMMC-7721 cells and expression of integrinbeta1 in SMMC-7721 cells were detected by flow cytometer. RESULTS: The percentage of cell cycle phases of general SMMC-7721 cells was 11.01% in G2/M phases, 53.51% in G0/G1 phase, and 35.48% in S phase. The synchronous rates of G1 and S phase SMMC-7721 cells amounted to 74.09% and 98.29%, respectively. The adhesive force of SMMC-7721 cells to endothelial cells changed with the variations of adhesive time and presented behavior characteristics of adhesion and de-adhesion. S phase SMMC-7721 cells had higher adhesive forces than G1 phase cells ((307.65+/-92.10) x 10(-10) N vs (195.42+/-60.72) x 10(-10) N, P<0.01). The expressive fluorescent intensity of integrinbeta(1) in G(1) phase SMMC-7721 cells was depressed more significantly than the values of S phase and general SMMC-7721 cells. The contribution of adhesive integrinbeta1 was about 53% in this adhesive course. CONCLUSION: SMMC-7721 cells can be synchronized preferably in G1 and S phases with thymine-2-deoxyriboside and colchicines. The adhesive molecule integrinbeta1 expresses a high level in SMMC-7721 cells and shows differences in various cell cycles, suggesting integrin beta1 plays an important role in adhesion to endothelial cells. The change of adhesive forces in different cell cycle SMMC-7721 cells indicates that S phase cells play predominant roles possibly while they interact with endothelial cells.

Carcinoma, Hepatocellular↗
PubMed2005

An orthotopic model of human osteosarcoma growth and spontaneous pulmonary metastasis.

Osteosarcoma is the most common primary malignancy of bone and patients often develop pulmonary metastases. In order to investigate the pathogenesis of human osteosarcoma, there is a great need to develop a clinically relevant animal model. Here we report the development of an osteosarcoma animal model using three related human osteosarcoma lines, the parental TE-85 and two derivative lines MNNG/HOS and 143B. In vitro characterization demonstrated that the 143B line had the greatest cell migration and the least cell adhesion activities among the three lines. The 143B line also exhibited the greatest ability for anchorage independent growth. When GFP-tagged osteosarcoma cells were injected into the proximal tibia of athymic mice, we found that 143B cells were highly tumorigenic and metastatic, and MNNG/HOS cells were tumorigenic but significantly less metastatic. TE85 cells were neither tumorigenic nor metastatic. The number of pulmonary metastases was found 50-fold higher in 143B injected animals than that in MNNG/HOS injected mice. No pulmonary metastases were detected in TE85 injected animals for up to 8 weeks. Primary tumors formed by MNNG/HOS and 143B cells could be visualized by whole body fluorescence imaging, while the pulmonary metastases were visualized on the necropsied samples. The GFP tagged 143B cells (and to a lesser extent, MNNG/HOS cells) were readily recovered from lung metastases. This clinically relevant model of human osteosarcoma provides varying degrees of tumor growth at the primary site and metastatic potential. Thus, this orthotopic model should be a valuable tool to investigate factors that promote or inhibit osteosarcoma growth and/or metastasis.

Animals↗
PubMed2005

Unambiguously distinguishing Si[3Si,1Al] and Si[3Si,1OH] stuctural units in zeolite by 1H/29Si/27Al triple resonance solid state NMR spectroscopy.

We present an experimentally feasible triple-resonance NMR method that establishes the correlation among three different nuclei, avoiding the difficulty to directly explore the weak coupling between two NMR nuclei, such as (29)Si and (27)Al. Using this method, we are able to give an unambiguous assignment to the various peaks in (29)Si CP NMR spectrum of MCM-22 zeolite and discriminate (29)Si signals from SiOHAl and SiOH groups. In addition, in combination with (1)H/(27)Al double-resonance technique, the (1)H/(27)Al/(29)Si triple-resonance experiment suggests the presence of two different kinds of Brönsted acid sites in H-MCM-22 zeolite.

Journal Article↗
PubMed2005

Gene therapy for bone regeneration.

Efficacious bone regeneration could revolutionize the clinical management of many bone and musculoskeletal disorders. Bone has the unique ability to regenerate and continuously remodel itself throughout life. However, clinical situations arise when bone is unable to heal itself, as with segmental bone loss, fracture non-union, and failed spinal fusion. This leads to significant morbidity and mortality. Current attempts at improved bone healing have been met with limited success, fueling the development of improved techniques. Gene therapy in many ways represents an ideal approach for augmenting bone regeneration. Gene therapy allows specific gene products to be delivered to a precise anatomic location. In addition, the level of transgene expression as well as the duration of expression can be regulated with current techniques. For bone regeneration, the gene of interest should be delivered to the fracture site, expressed at appropriate levels, and then deactivated once the fracture has healed. Delivery of biological factors, mostly bone morphogenetic proteins (BMPs), has yielded promising results both in animal and clinical studies. There has also been tremendous work on discovering new growth factors and exploring previously defined ones. Finally, significant advances are being made in the delivery systems of the genes, ranging from viral and non-viral vectors to tissue engineering scaffolds. Despite some public hesitation to gene therapy, its use has great potential to expand our ability to treat a variety of human bone and musculoskeletal disorders. It is conceivable that in the near future gene therapy can be utilized to induce bone formation in virtually any region of the body in a minimally invasive manner. As bone biology and gene therapy research progresses, the goal of successful human gene transfer for augmentation of bone regeneration draws nearer.

Animals↗
PubMed2005

Is cytomegalovirus associated with human colorectal tumorigenesis?

Despite the rapid advance in the understanding of molecular pathways underlying human colorectal tumorigenesis, the causes that initiate dysregulation of the pathways remain largely unknown. Human cytomegalovirus (CMV) has been implicated as a potential etiopathogenetic agent. To further investigate whether CMV participates in human colorectal tumorigenesis, we examined 23 colorectal hyperplastic polyps, 65 colorectal adenomas, and 51 colorectal adenocarcinomas by immunohistochemical analysis using 2 antibody mixtures that recognize CMV immediate early, early, and delayed gene products. The results show that while typical nuclear staining (with or without cytoplasmic positivity) was observed in control cases of CMV colitis, no nuclear positivity was detected in any cases studied. Focal and weak cytoplasmic staining was noted in a subset of cases, particularly when a higher antibody concentration was used. This staining was believed to be nonspecific, however, because it also was observed in normal-appearing colonic mucosa. In addition, polymerase chain reaction failed to detect the presence of CMV DNA in 24 selected cases showing nonspecific cytoplasmic immunostaining. These observations demonstrate an absence of CMV proteins and DNA in human colorectal adenocarcinomas and their precursor lesions.

Adenocarcinoma↗
PubMed2004

Connective tissue growth factor (CTGF) is regulated by Wnt and bone morphogenetic proteins signaling in osteoblast differentiation of mesenchymal stem cells.

Osteoblast lineage-specific differentiation of mesenchymal stem cells is a well regulated but poorly understood process. Both bone morphogenetic proteins (BMPs) and Wnt signaling are implicated in regulating osteoblast differentiation and bone formation. Here we analyzed the expression profiles of mesenchymal stem cells stimulated with Wnt3A and osteogenic BMPs, and we identified connective tissue growth factor (CTGF) as a potential target of Wnt and BMP signaling. We confirmed the microarray results, and we demonstrated that CTGF was up-regulated at the early stage of BMP-9 and Wnt3A stimulations and that Wnt3A-regulated CTGF expression was beta-catenin-dependent. RNA interference-mediated knockdown of CTGF expression significantly diminished BMP-9-induced, but not Wnt3A-induced, osteogenic differentiation, suggesting that Wnt3A may also regulate osteoblast differentiation in a CTGF-independent fashion. However, constitutive expression of CTGF was shown to inhibit both BMP-9- and Wnt3A-induced osteogenic differentiation. Exogenous expression of CTGF was shown to promote cell migration and recruitment of mesenchymal stem cells. Our findings demonstrate that CTGF is up-regulated by Wnt3A and BMP-9 at the early stage of osteogenic differentiation, which may regulate the proliferation and recruitment of osteoprogenitor cells; however, CTGF is down-regulated as the differentiation potential of committed pre-osteoblasts increases, strongly suggesting that tight regulation of CTGF expression may be essential for normal osteoblast differentiation of mesenchymal stem cells.

Adenoviridae↗
PubMed2004

Inhibitor of DNA binding/differentiation helix-loop-helix proteins mediate bone morphogenetic protein-induced osteoblast differentiation of mesenchymal stem cells.

Bone morphogenetic proteins (BMPs) belong to the TGF-beta superfamily and play an important role in development and in many cellular processes. We have found that BMP-2, BMP-6, and BMP-9 induce the most potent osteogenic differentiation of mesenchymal stem cells. Expression profiling analysis has revealed that the Inhibitors of DNA binding/differentiation (Id)-1, Id-2, and Id-3 are among the most significantly up-regulated genes upon BMP-2, BMP-6, or BMP-9 stimulation. Here, we sought to determine the functional role of these Id proteins in BMP-induced osteoblast differentiation. We demonstrated that the expression of Id-1, Id-2, and Id-3 genes was significantly induced at the early stage of BMP-9 stimulation and returned to basal levels at 3 days after stimulation. RNA interference-mediated knockdown of Id expression significantly diminished the BMP-9-induced osteogenic differentiation of mesenchymal progenitor cells. Surprisingly, a constitutive overexpression of these Id genes also inhibited osteoblast differentiation initiated by BMP-9. Furthermore, we demonstrated that BMP-9-regulated Id expression is Smad4-dependent. Overexpression of the three Id genes was shown to promote cell proliferation that was coupled with an inhibition of osteogenic differentiation. Thus, our findings suggest that the Id helix-loop-helix proteins may play an important role in promoting the proliferation of early osteoblast progenitor cells and that Id expression must be down-regulated during the terminal differentiation of committed osteoblasts, suggesting that a balanced regulation of Id expression may be critical to BMP-induced osteoblast lineage-specific differentiation of mesenchymal stem cells.

Adenoviridae↗
PubMed2004

Expression of integrin beta1 and its roles on adhesion between different cell cycle hepatocellular carcinoma cells (SMMC-7721) and human umbilical vein endothelial cells.

To investigate expression of integrin beta1 and its roles on adhesion between different cell cycle hepatocellular carcinoma cell (HCC) and human umbilical vein endothelial cells (HUVEC), the synchronous G1 and S phase HCC were achieved through thymine-2-deoxyriboside and colchicines sequential blockage method and double thymine-2-deoxyriboside blockage method, respectively. Expression of integrin beta1 on hepatocellular carcinoma cells was detected with flow cytometer. Further, the adhesive force of HCC to HUVEC and the role of integrin beta1 in this adhesive course were studied by micropipette aspiration technique. The results showed that percentage of each cyclic phases of the controlled HCC (non-synchronous) are: G2 + M phase, 11%; G1 phase, 54%; S phase, 36%; the synchronous rates of G1 and S phase HCC amount to 74 and 98%, respectively. The expressive fluorescent intensity of integrin beta1 in G1 phase HCC is depressed significantly than the values of S phase and controlled HCC. Accordingly, the adhesive forces of G1 phase HCC to HUVEC was significantly lower than the value of S phase cells (P < 0.01), but it has no remarkable difference when compared the adhesive force values of S phase HCC with control; the contribution of integrin beta1 was about 50% in the adhesion of HCC to HUVEC. It suggested that HCC would be synchronized preferably in G1 and S phase with thymine-2-deoxyriboside and colchicines, the adhesive molecule integrin beta1 expressed in a high lever in HCC and presented differences in vary cell cycle, and integrin beta1 played an important roles in adhesion of HCC to HUVEC. Possibly, S phase HCC take a great action in this adhesive course.

Antibodies, Monoclonal↗