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Biomedical subjects

S Yu

Publications and source records attributed to S Yu.

At least 91 records · Page 5Linked to original sources
PubMed2001

[The relationship between cyanotoxin (microcystin, MC) in pond-ditch water and primary liver cancer in China].

OBJECTIVE: To explore the relationship between primary liver cancer (PLC) and MC in drinking pond-ditch water. METHODS: Epidemiological and ecological assays, Meta-analysis and risk assessment were used in this study. Cyanotoxin (Microcystin, MC) in the water of different sources was detected by ELISA. The F344 and HBVx transgenic mice were used to confirm the promotion effect on PLC and the synthetically carcinogenic effect of HBV, aflatoxin and MC. RESULTS: Using Meta-analysis the results of six case-control studies showed that the pooled odds ratio (OR) was 2.46 (95% CI 1.69-2.59), population attributable rick (PAR) was 30.39% (95% CI, 23.30%-37.47%), heterogeneity test P > 0.05. Eutrophication led to cyanobacterial bloom in the pond-ditch water. Cyanotoxin released from dead cyanobacteria was hepatotactic tumor promoter. In HBVx transgenic rats, hepatocellular carcinoma was induced by the joint administration of aflatoxin B1 and cyanotoxin. Epidemiological study showed that the recombined index of HBsAg, aflatoxin-albumin adducts and drinking of pond-ditch water correlated with PLC mortalities in 13 townships. CONCLUSION: Microcystin in the pond-ditch water is a hepatotactic toxin which can induce hepatitis and promote development of hepatocellular carcinoma. The combined effect of microcystin, HBV and aflatoxin may be responsible for the endemicity of PLC.

Aflatoxin B1↗
PubMed2001

[Postoperative follow-up of mural ameloblastoma].

OBJECTIVE: To investigate the determinant of recurrence in mural ameloblastoma. METHODS: Forty-four cases of mural ameloblastoma were followed up postoperatively for 1 year to 25 years and 4 months (mean of 5.7 years). RESULTS: 1. The recurrence is more likely to recur in curettage group (8/35) than in radical surgery group (1/9); 2. The recurrence is more in intramural (4/7) and complex (3/4) group more than in intracavity group (0/15) after curettage treatment; 3. Those with honeycomb appearance (3/3) recurred more than those with unilocular appearance (1/20); 4. It recurred mostly within 2 years postoperatively (7 recurrences in 5 cases); 5. Recurrent cases were susceptible to repeated recurrence after recurettage. CONCLUSIONS: 1. The lesion with honeycomb appearance should be treated with radical surgery; 2. The follow-up should be emphasized for those with intramural or complex feature; 3. The curettage cases should be followed routinely for 5 years postoperatively.

Ameloblastoma↗
PubMed2001

[The treatment of osteoporosis and bone resorption of alveoli with alendronate in rat model].

OBJECTIVE: To evaluate the anti-osteoporosis effect of alendronate on bone in rat model. METHODS: The osteoporosis and alveolar bone resorption animal model were established in rats. The experimental groups were given alendronate in 5 mg/kg BW by subcutaneous injection after first day of ovariectomy and dental ligature, three times a week for 6 weeks. All the animals were sacrifised 12 weeks after the operation. The blood samples were collected for determination of biochemical indices. The left femora and jaw bones were processed for histomorphometry. The right femora and mendibles were prepared for determination of bone density and bone biodynamics. RESULTS: As compared with the control groups(without alendronate), the values of experimental groups (with alendronate) were all significantly improved on bone density, bone anti-flexure ability and body weight. The alkaline phosphatase, calcium in serum of ovariectomy groups(without alendronate) were obviously increased. In the experimental group, however, these indices were close to normal levels. In histomorphometry, there were little inflammation in gingiva and no obvious bone resorption in the alveolar crests of the experimental groups; but there were obvious gingivitis and alveolar crests resorption of the control groups. CONCLUSIONS: Alendronate can effectively prevent bone loss to reduce osteoporosis in ovariectomized rats and prohibit pathological alveolar bone resorption.

Alendronate↗
PubMed2001

[Alteration of Fas/FasL gene expression in oral squamous cell carcinoma cell line Tca83 by retinoid acid].

OBJECTIVE: To study the induction of apoptosis by retinoid acid(RA) in Tca83 cell line and the expression of correlative Fas/FasL gene. METHODS: Apoptosis of Tca83 was detected by TUNEL, the expression of Fas/FasL-mRNA was detected by RT-PCR and cell immunohistochemical technique. RESULTS: The cell apoptosis number of Tca83 in RA group was significantly higher than that in non-RA groupe on day 5(P < 0.05). The expression of Fas-mRNA in RA group was also much higher than that in non-RA group on day 5(P < 0.05), but the level of FasLmRNR had no change. Immunohistochemistry also showed, after RA treatment, the Fas stain was enhanced. CONCLUSION: The result suggests that apoptosis induced by RA may be resulted from the enhancement of Fas gene transcription and translation.

Antineoplastic Agents↗
PubMed2001

Response of cancer cells to molecular interruption of the CK2 signal.

Protein kinase CK2 is one of the key cellular signals for cell survival, growth, and proliferation. It is has been observed to be elevated in various cancers that have been examined. Various observations suggest that moderate dysregulation of CK2 may profoundly influence the cell response. We have examined the effects of interfering with the CK2 signal in various cancer cell lines by employing antisense oligodeoxynucleotides (ODN) against the alpha and beta subunits of CK2. Our results demonstrate that antisense CK2-alpha and antisense CK2-beta ODNs markedly influence cell viability of these cancer cells in a dose and time-dependent manner. Antisense CK2-alpha was slightly more effective than antisense CK2-beta in most of the cells tested. The efficacy of the antisense ODN seemed to vary with the cell type; however, in all cases potent induction of apoptosis was observed. Significantly, the effects of the antisense ODN on the CK2 activity in the nuclear matrix were relatively small compared to the much stronger induction of apoptosis in cells. This suggests that modest downregulation of CK2 can evoke a much greater apoptotic response in cancer cells.

Apoptosis↗
PubMed2001

Consequences of CK2 signaling to the nuclear matrix.

Protein kinase CK2 is recognized as one of the key cellular signals for cell growth and proliferation. Its nuclear targeting appears to be critical to its role in these functions. In the nucleus, nuclear matrix (NM) which plays a major role in growth-related activities is a primary locus for CK2 signaling. A variety of growth stimuli evoke a rapid translocation of the CK2 to the NM whereas removal of these factors has the opposite effect. These studies, employing various experimental models of cell growth (involving different growth-stimulatory factors), have suggested that rapid shuttling of CK2 to the NM is a key feature of early growth control. By contrast, removal of growth-stimulatory factors leading to the loss of cell viability is associated with early loss of CK2 from the NM (and chromatin). This indicates that absence of CK2 from the nuclear compartment is contributory to induction of cell death via apoptosis, implying a protective role for CK2 against cell death. Here, we review the evidence that suggests that CK2 signaling in the NM is not only involved in cell growth but also in cell survival.

Active Transport, Cell Nucleus↗
PubMed2001

Trauma-related xanthogranulomatous interstitial nephritis: a clinicopathological analysis.

OBJECTIVE: To investigate the pathogenesis, exact nature, histologic feature of xanthogranulomatous interstitial nephritis (XGIN) as well as its significance in clinical medicine. METHODS: The medical histories concerned were collected with diagnostic images including CT scanning, ultrasonography, intravenous urography (IVU) and laboratory data being synthesized by comparison with what was discover ed during operations and pathologic examinations. RESULTS: All patients were ever struck on their loins or backs by blunt violence over 4-12 years. The diseases were clinically diagnosed as "renal cancer" before, during and after operations, and treated with ra dic al nephrectomy. Located at cortical parts, the tumor focus had penetrated the renal capsules and invaded other organs. However, immunohistochemistry demonstrated that the lesions were xanthogranulomas, not tumors, in which there were stacks of foam cells and lymphocytes with vast extends of fibrotic tissues obliterating the cortical interstitial structures. Urinary tracts yielded no bacterium, obstruction or calculus. CONCLUSIONS: XGIN is likely to be one kind of immunologic mediated granuloma following blunt renal trauma. It is imperative to clarify pathogenesis and character of this lesion so as to find out any approach to diagnosis and cure of such an unusual nephropathy.

Adult↗
PubMed2001

[Investigation on root-knot diseases of medicinal plants in Yunnan].

During 1994-1997, the damage levels about root-knot diseases on 52 medicinal plants were investigated and analyzed. 185 samples were collected from more than 20 counties or cities in Yunnan province. The results showed that 76 specimens were infected by root-knot nematode, which are Meloidogyne incognita (Kofoid and White 1919, Chitwood 1949), M. javanice (Trenb 1855, Chitwood 1949), M. arenaria (Neal 1889, Chitwood 1949) and M. halpa (Chitwood 1949). They infected 21 medicinal plants. The paper describes the damage levels and the distribution about these root-knot diseases of medicinal plants.

Animals↗
PubMed2001

[Culture and cryopreservation of human mandibular condylar cartilage cells].

OBJECTIVE: To establish an effective way in cryopreserving mandibular condylar cartilage cells. METHODS: Human mandibular condylar cartilage (MCC) cells were harvested and amplified by microcarrier culture technique. MCC cells were preserve in liquid nitrogen. The biological properties of cryopreserved MCC cells were investigated. RESULTS: Cells from liquid nitrogen preservation kept their phenotypic, proliferative an metabolic characteristics of MCC cells in vivo. CONCLUSIONS: Cryopreservation of MCC cells can supply adequate qualified cells for repairing the defects of mandibular condyle cartilage and temporomandibular joint disk.

Cartilage↗
PubMed2000

Early requirement for B cells for development of spontaneous autoimmune thyroiditis in NOD.H-2h4 mice.

B cells are known to play an important role in the pathogenesis of several autoimmune diseases. NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and anti-mouse thyroglobulin (MTg) autoantibodies, the levels of which correlate closely with the severity of thyroid lesions. NOD.H-2h4 mice genetically deficient in B cells (NOD.Kmu(null)) or rendered B cell-deficient by treatment from birth with anti-IgM develop minimal SAT. B cells were required some time in the first 4-6 wk after birth, because NOD.Kmu(null) or NOD.H-2h4 mice did not develop SAT when they were reconstituted with B cells as adults. The requirement for B cells was apparently not solely to produce anti-MTg autoantibodies, because passive transfer of anti-MTg Ab did not enable B cell-deficient mice to develop SAT, and mice given B cells as adults produced autoantibodies but did not develop SAT. B cell-deficient mice developed SAT if their T cells developed from bone marrow precursors in the presence of B cells. Because B cells are required early in life and their function cannot be replaced by anti-MTg autoantibodies, B cells may be required for the activation or selection of autoreactive T cells. These autoreactive T cells are apparently unable to respond to Ag if B cells are absent in the first 4-6 wk after birth.

Animals↗
PubMed2000

Identification, expression, and substrate specificity of a mammalian beta-carotene 15,15'-dioxygenase.

We have identified from mouse the first mammalian beta-carotene 15,15'-dioxygenase (beta-CD), a crucial enzyme in development and metabolism that governs the de novo entry of vitamin A from plant-derived precursors. beta-CD is related to the retinal pigment epithelium-expressed protein RPE65 and belongs to a diverse family that includes the plant 9-cis-epoxycarotenoid dioxygenase and bacterial lignostilbene dioxygenases. beta-CD expression in Escherichia coli cells engineered to produce beta-carotene led to the accumulation of all-trans-retinal at the expense of beta-carotene, confirming that beta-CD catalyzed the central cleavage of this vitamin A precursor. Purified recombinant beta-CD protein cleaves beta-carotene in vitro with a V(max) of 36 pmol of retinal/mg of enzyme/min and a K(m) of 6 microm. Non-provitamin A carotenoids were also cleaved, although with much lower activity. By Northern analysis, a 2.4-kilobase (kb) message was observed in liver, kidney, small intestine, and testis, tissues important in retinoid/carotenoid metabolism. This message encoded a 63-kDa cytosolic protein expressed in these tissues. A shorter transcript of 1.8 kb was found in testis and skin. Developmentally, the 2.4-kb mRNA was abundant at embryonic day 7, with lower expression at embryonic days 11, 13, and 15, suggesting a critical role for this enzyme in gastrulation. Identification of beta-CD in an accessible model organism will create new opportunities to study vitamin A metabolism.

Amino Acid Sequence↗
PubMed2000

Lysophosphatidic acid prevents apoptosis in fibroblasts via G(i)-protein-mediated activation of mitogen-activated protein kinase.

Lysophosphatidic acid (LPA) is a naturally occurring phospholipid with multiple biological functions. In the present study, we demonstrate that, besides its mitogenic activity, LPA is a potent survival factor, preventing serum-deprivation-induced apoptosis in fibroblasts and other cell types. Both the proliferative effect and survival activity of LPA are sensitive to the action of pertussis toxin (PTX), indicating that both processes are mediated by G(i) protein(s). We therefore focused on the role of G(i)-protein-mediated signalling events in the promotion of cell survival by LPA. In addition to activation of mitogen-activated protein kinase (MAPK), LPA stimulates a modest PTX-sensitive phosphorylation/activation of the serine/threonine kinase Akt, a survival mediator downstream of phosphoinositide 3-kinase (PI3K). Inhibition of PI3K with LY 294002 or wortmannin resulted in a marked inhibition of LPA-induced DNA synthesis, and yet the survival activity of LPA decreased by only 20-30%, suggesting a limited input of the PI3K-Akt cascade in LPA-induced cell survival. In contrast, inhibition of MAPK activation by the MEK-1 inhibitor, PD 98059, blocked both the proliferative and survival effects of LPA. These results indicate that LPA promotes cell survival largely via G(i)-protein-mediated activation of ERK1/ERK2, or other PD 98059-sensitive member(s) of the MAPK family.

3T3 Cells↗
PubMed2000

A potential role of nuclear matrix-associated protein kinase CK2 in protection against drug-induced apoptosis in cancer cells.

Protein kinase CK2 (CK2) has long been implicated in the regulation of cell growth and proliferation. Its activity is generally elevated in rapidly proliferating tissues, and nuclear matrix (NM) is an important subnuclear locale of its functional signaling. In the prostate, nuclear CK2 is rapidly lost commensurate with induction of receptor-mediated apoptosis after growth stimulus withdrawal. By contrast, chemical-induced apoptosis in prostate cancer and other cells (by etoposide and diethylstilbestrol) evokes an enhancement in CK2 associated with the NM that appears to be because of translocation of CK2 from the cytoplasmic to the nuclear compartment. This shuttling of CK2 to the NM may reflect a protective response to chemical-mediated apoptosis. Supporting evidence for this was obtained by employing cells that were transiently transfected with various expression plasmids of CK2 (thereby expressing additional CK2) prior to treatment with etoposide or diethylstilbestrol. Cells transfected with the CK2alpha or CK2alphabeta showed significant resistance to chemical-mediated apoptosis commensurate with the corresponding elevation in CK2 in the NM. Transfection with CK2beta did not demonstrate this effect. These results suggest, for the first time, that besides the commonly appreciated function of CK2 in cell growth, it may also have a role in protecting cells against apoptosis.

Adenocarcinoma↗
PubMed2000

TIMP-3 binds to sulfated glycosaminoglycans of the extracellular matrix.

Of the four known tissue inhibitors of metalloproteinases (TIMPs), TIMP-3 is distinguished by its tighter binding to the extracellular matrix. The present results show that glycosaminoglycans such as heparin, heparan sulfate, chondroitin sulfates A, B, and C, and sulfated compounds such as suramin and pentosan efficiently extract TIMP-3 from the postpartum rat uterus. Enzymatic treatment by heparinase III or chondroitinase ABC also releases TIMP-3, but neither one alone gives complete release. Confocal microscopy shows colocalization of heparan sulfate and TIMP-3 in the endometrium subjacent to the lumen of the uterus. Immunostaining of TIMP-3 is lost upon digestion of tissue sections with heparinase III and chondroitinase ABC. The N-terminal domain of human TIMP-3 was expressed and found to bind to heparin with affinity similar to that of full-length mouse TIMP-3. The A and B beta-strands of the N-terminal domain of TIMP-3 contain two potential heparin-binding sequences rich in lysine and arginine; these strands should form a double track on the outer surface of TIMP-3. Synthetic peptides corresponding to segments of these two strands compete for heparin in the DNase II binding assay. TIMP-3 binding may be important for the cellular regulation of activity of the matrix metalloproteinases.

Alkylation↗
PubMed2000

The upstream region of the Rpe65 gene confers retinal pigment epithelium-specific expression in vivo and in vitro and contains critical octamer and E-box binding sites.

RPE65 is essential for all-trans- to 11-cis-retinoid isomerization, the hallmark reaction of the retinal pigment epithelium (RPE). Here, we identify regulatory elements in the Rpe65 gene and demonstrate their functional relevance to Rpe65 gene expression. We show that the 5' flanking region of the mouse Rpe65 gene, like the human gene, lacks a canonical TATA box and consensus GC and CAAT boxes. The mouse and human genes do share several cis-acting elements, including an octamer, a nuclear factor one (NFI) site, and two E-box sites, suggesting a conserved mode of regulation. A mouse Rpe65 promoter/beta-galactosidase transgene containing bases -655 to +52 (TR4) of the mouse 5' flanking region was sufficient to direct high RPE-specific expression in transgenic mice, whereas shorter fragments (-297 to +52 or -188 to +52) generated only background activity. Furthermore, transient transfection of analogous TR4/luciferase constructs also directed high reporter activity in the human RPE cell line D407 but weak activity in the non-RPE cell lines HeLa, HepG2, and HS27. Functional binding of potential transcription factors to the octamer sequence, AP-4, and NFI sites was demonstrated by directed mutagenesis, electrophoretic mobility shift assay, and cross-linking. Mutations of these sites abolished binding and corresponding transcriptional activity and indicated that octamer and E-box transcription factors synergistically regulate the RPE65 promoter function. Thus, we have identified the regulatory region in the Rpe65 gene that accounts for tissue-specific expression in the RPE and found that octamer and E-box transcription factors play a critical role in the transcriptional regulation of the Rpe65 gene.

5' Untranslated Regions↗
PubMed2000

Characterization of a nuclear factor that binds to AP1-like element in the rat p53 promoter during liver regeneration.

The transcription level of the rat p53 gene increases at 5-12 h in the regenerating liver after partial hepatectomy. It was previously reported that an activator protein 1 (AP1)-like element (-264--284) mediated the induced transcription of the rat p53 gene during liver regeneration. In this study, we characterize the protein binding to the AP1-like element by various methods. Oligonucleotide competition assays showed that the binding protein did not require AP1 consensus sequence. Therefore, the binding protein is not an AP1 family protein. Zn(2+) was required for maximum DNA-binding activity of the protein, suggesting that the binding protein contains zinc fingers. The binding protein was highly resistant to denaturant. Even 1.8 M urea did not eliminate the protein-DNA complexes. In addition, the binding protein was stable up to 55 degrees C. The protein-DNA complexes were abolished in the presence of 0.6 M NaCl and higher. Protease clipping assay showed that the protein had a protease-resistant core DNA binding domain. These results provided new insights into the structure of the protein that binds to the AP1-like element of the p53 promoter during liver regeneration.

Animals↗
PubMed2000

1,5-Anhydro-D-fructose increases glucose tolerance by increasing glucagon-like peptide-1 and insulin in mice.

Besides being degraded to glucose-6-phosphate and to free glucose, glycogen is degraded by alpha-1,4-glucan lyase to 1, 5-anhydro-D-fructose. We examined the influence of 1, 5-anhydro-D-fructose on glucose-stimulated insulin secretion in vivo and in vitro in mice. When administered together with i.v. glucose (1 g/kg), 1,5-anhydro-D-fructose did not affect (at 0.2 g/kg) or inhibited (at 1 g/kg) insulin secretion without affecting glucose elimination. When incubated with isolated islets, 1, 5-anhydro-D-fructose at <16.7 mmol/l, did not affect glucose (11.1 mM)-stimulated insulin secretion but inhibited insulin secretion at 16.7 mmol/l. When given through a gastric gavage (150 mg/mouse) together with glucose (150 mg/mouse), 1,5-anhydro-D-fructose increased glucose tolerance and insulin secretion. Furthermore, 1, 5-anhydro-D-fructose potentiated the increase in plasma levels of the gut hormone, glucagon-like peptide-1 (GLP-1). We therefore conclude that when given enterally, but not parenterally, 1, 5-anhydro-D-fructose increases glucose tolerance in mice by increasing insulin secretion due to increased plasma levels of GLP-1. The sugar may therefore be explored for increasing endogenous GLP-1 secretion in the treatment of type 2 diabetes.

Animals↗