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Biomedical subjects

Yan Zhao

Publications and source records attributed to Yan Zhao.

At least 145 records · Page 8Linked to original sources

Environmentally responsive molecular baskets: unimolecular mimics of both micelles and reversed micelles.

[structure: see text] When four facially amphiphilic cholate derivatives are attached to a tetraaminocalixarene scaffold, the resulting molecule responds to environmental changes by rotation of the cholate units. In polar solvents, the molecule adopts a micellelike conformation with the hydrophilic alpha-faces of the cholates pointing outward. In nonpolar solvents, it turns inside out, assuming a reversed micellelike conformation with the hydrophobic beta-faces pointing outward. Switching between the two conformations is driven by solvophobic interactions and is fully reversible.

Calixarenes↗

Early diagnosis of bacterial and fungal infection in chronic cholestatic hepatitis B.

AIM: To investigate the early diagnostic methods of bacterial and fungal infection in patients with chronic cholestatic hepatitis B. METHODS: One hundred and one adult in-patients with chronic hepatitis B were studied and divided into 3 groups: direct bilirubin (DBil)/total bilirubin (TBil) > or = 0.5, without bacterial and fungal infection (group A, n=38); DBil/TBil <0.5, without bacterial and fungal infection (group B, n=23); DBil/TBil> or = 0.5, with bacterial or fungal infection (group C, n=40). The serum biochemical index and pulse rate were analyzed. RESULTS: Level of TBil, DBil, alkaline phosphatase (ALP) and DBil/ALP in group A increased compared with that in group B. The level of ALP in group C decreased compared with that in group A, whereas the level of TBil, DBil and DBil/ALP increased (ALP: 156+/-43, 199+/-68, respectively, P<0.05; TBil: 370+/-227, 220+/-206, respectively, P<0.01; DBil: 214+/-143, 146+/-136, respectively, P<0.01; DBil/ALP: 1.65+/-1.05, 0.78+/-0.70, respectively, P<0.001). The level of DBil and infection affected DBil/ALP. Independent of the effect of DBil, infection caused DBil/ALP to rise (P<0.05). The pulse rate in group A decreased compared with that in group B (63.7+/-6.4, 77.7+/-11.4, respectively, P<0.001), and the pulse rate in group C increased compared with that in group A (81.2+/-12.2, 63.7+/-6.4, respectively, P<0.001). The equation (infection=0.218 pusle rate +1.064 DBil/ALP -16.361), with total accuracy of 85.5%, was obtained from stepwise logistic regression. Pulse rate (> or =80/min) and DBil/ALP (> or =1.0) were used to screen infection. The sensitivity was 62.5% and 64.7% respectively, and the specificity was 100% and 82.8% respectively. CONCLUSION: Bacterial and fungal infection deteriorate jaundice and increase pulse rate, decrease serum ALP and increase DBil/ALP. Pulse rate, DBil/ALP and the equation (infection=0.218 pusle rate+1.064 DBil/ALP-16.361) are helpful to early diagnosis of bacterial and fungal infection in patients with chronic cholestatic hepatitis B.

Bacterial Infections↗

Transgene expression in strawberries driven by a heterologous phloem-specific promoter.

Strawberry is susceptible to diseases caused by phytoplasmas, mycoplasma-like prokaryotes restricted to sieve elements in the phloem tissue of infected plants. One strategy to improve strawberry resistance to phytoplasmas involves transgenic expression of anti-microbial peptide genes in phloem. For targeted phloem-specific expression, we constructed a binary vector with an expression cassette bearing the beta-glucuronidase (GUS) reporter gene (uidA) under control of the Arabidopsis sucrose-H+ symporter gene (AtSUC2) promoter. Transgenic strawberry lines were generated with high efficiencies by a modified transformation protocol, which combines the adoption of a 3-day pre-selection period following transformation, and the addition of 10-microM thidiazuron to the regeneration medium. Histological GUS activity indicated that the reporter gene was expressed specifically in phloem of leaves, petioles, and roots of transgenic plants. The results suggest that the transformation protocol and the AtSUC2 promoter may be useful for engineering phytoplasma-resistant transgenic strawberries.

Arabidopsis↗

c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells.

AIM: To investigate the roles of c-Jun N-terminal kinase (JNK) signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS: Human gastric cancer cell lines (SGC-7901) were treated with vitamin E succinate (VES) at 5, 10, 20 mg/L. Succinic acid and vitamin E were used as vehicle controls and condition medium only as an untreated (UT) control. Apoptosis was observed by 4', 6-diamidine-2'-phenylindole dihydrochloride (DAPI) staining for morphological changes and by DNA fragmentation for biochemical alterations. Western blot analysis was applied to measure the expression of JNK and phosphorylated JNK. After the cells were transiently transfected with dominant negative mutant of JNK (DN-JNK) followed by treatment of VES, the expression of JNK and c-Jun protein was determined. RESULTS: The apoptotic changes were observed after VES treatment by DNA fragmentation. DNA ladder in the 20 mg/L VES group was more clearly seen than that in 10 mg/L VES group and was not detected following treatment of UT control, succinate and vitamin E. VES at 5, 10 and 20 mg/L increased the expression of p-JNK by 2.5-, 2.8- and 4.2-fold, respectively. VES induced the phosphorylation of JNK beginning at 1.5 h and produced a sustained increase for 24 h with the peak level at 12 h. Transient transfection of DN-JNK blocked VES-triggered apoptosis by 52%. DN-JNK significantly increased the level of JNK, while decreasing the expression of VES-induced c-Jun protein. CONCLUSION: VES-induced apoptosis in human gastric cancer SGC-7901 cells involves JNK signaling pathway via c-Jun and its downstream transcription factor.

Apoptosis↗

Interferon-alpha 2a up-regulated thymidine phosphorylase and enhanced antitumor effect of capecitabine on hepatocellular carcinoma in nude mice.

PURPOSE: To investigate the antitumor effect of interferon-alpha 2a (IFN-alpha2a) combined with capecitabine on hepatocellular carcinoma (HCC) in nude mice in relation to thymidine phosphorylase (TP) expression. METHODS: Thirty nude mice bearing orthotopic xenografts of a human HCC tumor (LCI-D20) were divided into control, capecitabine, IFN-alpha2a, and combination (capecitabine plus IFN-alpha2a) groups. Tumor growth was determined by measuring the tumor volume. An enzyme-linked immunosorbent assay (ELISA) was used to study the TP expression in the cancer tissues of the liver. RESULTS: IFN-alpha2a enhanced the sensitivity of the LCI-D20 tumor response to capecitabine treatment. The tumor volume was significantly reduced in the capecitabine (455+/-236 mm(3)), IFN-alpha2a (248 +/- 114 mm(3)) or combination (46 +/- 29 mm(3)) treatment groups as compared to the control (1,033 +/- 146 mm(3)) (P < 0.01). A significant difference was also found between the single treatment (capecitabine or interferon) and combination treatment group (P < 0.01 and P < 0.05, respectively). IFN-alpha2a up-regulated TP expression in LCI-D20 tumor. An approximate 1.5-fold increase in TP expression was observed in the mice which received IFN-alpha2a treatment compared to the control mice. CONCLUSION: IFN-alpha2a enhanced the antitumor effect of capecitabine on HCC in nude mice, which might be ascribed to the up-regulation of TP expression in liver cancer tissues by IFN-alpha2a.

Animals↗

Nanoprobe implantation into mammalian cells by cationic transfection.

Submicron-sized Au particles and Au/SiO(2) nanocomposites (superparticles) as large as 670 nm have been introduced into tsA201 cells with minimal cell trauma by cationic transfection systems. Successful implantations can be characterized by the expression of co-transfected DNA.

Animals↗

Nuclear translocation of EGF receptor regulated by Epstein-Barr virus encoded latent membrane protein 1.

Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) is considered to be the major oncogenic protein of EBV encoded proteins, and also it has always been the core of the oncogenic mechanism of EBV. Traditional receptor theory demonstrates that cell surface receptors exert biological functions on the membrane, which neither enter into the nucleus nor directly affect the transcription of the target genes. But, advanced studies on nuclear translocation of the epidermal growth factor receptor (EGFR) family have greatly developed our knowledge of the biological function of cell surface receptors. In this study, we used Tet-on LMP1 HNE2 cell line as a cell model, which is a dual-stable LMP1 integrated NPC cell line and the expression of LMP1 in which could be regulated by Tet system. We found that LMP1 could regulate the nuclear translocation of EGFR in a dose-dependent manner from both quantitative and qualitative levels through the Western blot analysis and the immunofluorescent analysis with a laser scanning confocal microscope. We further demonstrated that the nuclear localization sequence of EGFR played some roles in the location of the protein within the nucleus under LMP1 regulation, and the nuclear accumulation of EGFR regulated by LMP1 was in a ligand-independent manner. These findings provide a novel view that the regulation of LMP1 on the nuclear translocation of EGFR is critical for the process of nasopharyngeal carcinoma.

Active Transport, Cell Nucleus↗

Antisense Tcf inhibits the neoplastic growth of liver cancer cells.

PURPOSE: T cell transcription factors are nuclear effectors of the Wnt signaling transduction pathway and play crucial roles in embryonic and malignant development. Our previous study showed increased expression level of Tcf mRNA in liver cancer. In the present paper, antisense Tcf RNA was used to explore the possible therapeutic effect on liver cancer cells by interrupting the abnormal Wnt pathway. METHODS: Antisense expression vectors containing the conserved sequence of Tcf cDNA were constructed and transfected into a human liver cancer cell line SMMC-7721. Tumorigenic potential was determined by cellular growth assay and tumor growth in nude mice. RESULTS: The stable transfection of anti-sense Tcf in SMMC-7721 cells significantly reduced Tcf expression at both mRNA and protein levels compared with parental and mock-transfected cells. Antisense-mediated suppression of Tcf inhibited the in vitro proliferation and in vivo tumor formation ability. Furthermore, the apoptosis rate of antisense transfected cells was significantly higher than that of control, indicating that antisense RNA suppressed malignant growth by induction of apoptosis. CONCLUSION: Our studies demonstrate the critical role of Wnt signaling pathway in the neoplastic growth of liver cancer cells and suggest that inhibition of Tcf activity with antisense Tcf RNA may be a potential new gene therapy method for liver cancer.

Cell Proliferation↗

Blockade of ionotropic glutamatergic transmission in the ventral tegmental area attenuates the physical signs of morphine withdrawal in rats.

The present study sought to assess whether the blockade of ionotropic glutamate receptors in the ventral tegmental area (VTA) could modulate the morphine withdrawal in male Sprague-Dawley rats. The effects of dizocilpine (MK-801) or 6,7-dinitroquinnoxaline-2,3-dione (DNQX), ionotropic glutamate receptor antagonists, microinjected unilaterally into the VTA 30 min before naloxone [2 mg/kg, intraperitoneally (i.p.)] administration on the morphine withdrawal were assessed. Morphine dependence was developed with increasing morphine injection (i.p.), and morphine withdrawal was induced by injection of naloxone (2 mg/kg, i.p.). Jumping, wet-dog shakes, writhing posture, wall clamber, weight loss and Gellert-Holtzman scale were used as the indices to evaluate the intensity of morphine withdrawal. The results showed that unilateral microinjection of MK-801 or DNQX into the VTA significantly increased the incidence of wall clamber, had no effect on weight loss, and reduced all other symptoms of morphine withdrawal. These data suggest that the ionotropic glutamate receptors in the VTA are involved in mediating naloxone-precipitated opiate withdrawal.

Animals↗

Induction of apoptosis by epigallocatechin-3-gallate via mitochondrial signal transduction pathway.

PURPOSE: To elucidate the apoptosis induction of Epigallocatechin-3-gallate (EGCG) on nasopharyngeal carcinoma (NPC) cells via mitochondrial signal transduction pathway regulated by EB-virus-encoded latent membrane protein 1 (LMP1). METHODS: The survival rates of pTet-on-LMP1 HNE2 cells after the EGCG treatment were determined by MTT assay. Induction of apoptosis in pTet-on-LMP1 HNE2 cells after the EGCG treatment was analyzed by agarose gel electrophoresis. The activity of caspase-9 was determined by ApoAlert Caspase-9 Fluorescent Assay kit after the EGCG treatment. The protein expressions of cytochrome c and Bcl-2 were analyzed by Western blotting after the EGCG treatment. RESULTS: EGCG inhibited the survival rates of pTet-on-LMP1 HNE2 cells and induced apoptosis of pTet-on-LMP1 HNE2 cells. EGCG raised the activities of caspase-9, enhanced the releasing of cytochrome c from the mitochondria, and suppressed the protein expression of Bcl-2. These are the key targets on the mitochondrial signal transduction pathway in apoptosis. CONCLUSIONS: EGCG inhibited the survival rate of NPC cells and induced apoptosis of NPC cells via the mitochondrial signal transduction pathway. This study suggests that the interference effect of EGCG on targets of the mitochondrial signal transduction pathway plays an important role in the anticancer function.

Anticarcinogenic Agents↗

Eicosapentaenoic acid prevents LPS-induced TNF-alpha expression by preventing NF-kappaB activation.

BACKGROUND: Many studies have shown that fish oil supplementation inhibits tumor necrosis factor-alpha (TNF-alpha) production in mice and human subjects; however, the mechanisms remain unclear. Nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays an important role in controlling the expression of pro-inflammatory genes including TNF-alpha. Activation of NF-kappaB has been shown to mediate the maximal expression of TNF-alpha in human monocytes. NF-kappaB is kept in an inactive form in the cytoplasm by IkappaB, the inhibitory subunit of NF-kappaB complex. Phosphorylation and subsequent degradation of IkappaB lead to NF-kappaB activation. OBJECTIVES: The effect of eicosapentaenoic acid (EPA), a major n-3 fatty acid in fish oil, on the lipopolysaccharide (LPS)-induced expression of TNF-alpha and activation of NF-kappaB were investigated. The mechanism underlying EPA modulation of NF-kappaB activation was also studied. METHODS: Human monocytic THP-1 cells were pre-incubated with EPA and stimulated with LPS. The levels of secreted TNF-alpha were determined by ELISA. The DNA binding activity of NF-kappaB was analyzed by EMSA. The degradation and phosphorylation of IkappaB-alpha were examined by Western blot analysis. RESULTS: TNF-alpha production and expression induced by LPS were significantly decreased in cells pre-incubated with EPA. LPS-induced NF-kappaB activation, translocation of p65 subunit to the nucleus, phosphorylation and degradation of IkappaB-alpha were partially prevented by EPA. CONCLUSIONS: The results suggest that suppression of the TNF-alpha expression by EPA is partly attributed to its inhibitory effect on NF-kappaB activation. EPA appears to prevent NF-kappaB activation by preventing the phosphorylation of IkappaB-alpha.

Blotting, Western↗

Cell division gene cluster in Spiroplasma kunkelii: functional characterization of ftsZ and the first report of ftsA in mollicutes.

Spiroplasma kunkelii is a helical, wall-less bacterium that causes corn stunt disease. In adaptation to its phloem-inhabiting parasitic lifestyle, the bacterium has undergone a reductive evolutionary process and, as a result, possesses a compact genome with a gene set approaching the minimal complement necessary for multiplication and pathogenesis. We cloned a much-reduced cell division gene cluster from S. kunkelii and functionally characterized the key division gene, ftsZ(sk). The 1236-bp open reading frame of ftsZ(sk) is capable of encoding a protein with a calculated molecular mass of 44.1 kDa. Protein sequence alignment revealed that FtsZ(sk) is remarkably similar to FtsZ proteins from other eubacteria, and possesses the conserved GTP-binding and hydrolyzing motifs. We demonstrated that overexpression of ftsZ(sk) in Escherichia coli causes transgression of the host cell division, resulting in a filamentous phenotype. We also report, for the first time, the presence of a ftsA gene in the cell division cluster of a mollicute species.

Amino Acid Sequence↗

[Effects of Radix Salviae Miltiorrhizae on the PMN-EC adhesion in vitro at the early stage of endotoxemia].

OBJECTIVE: To evaluate the effects of Radix Salviae Miltiorrhizae (RSM) on the PMN-EC adhesion in vitro at the early stage of endotoxemia, and to probe into the mechanism there in involved. METHODS: The rabbit endotoxemia model was made, and one group was treated with RSM injection (2 ml/kg) instantly and 24 h after the modeling of endotoxemia. PMN-EC adhesion rate, adhesion molecule (CD11a/CD18 and CD11b/CD18) and TNF-alpha level were measured instantly, 2 h, 4 h, 8 h, 16 h, 24 h and 48 h after endotoxemia modeling. RESULTS: It was found that after the modeling of endotoxemia, the levels of CD11a/CD18, CD11b/CD18 and PMN-EC adhesion rate instantly increased in the endotoxemia group and RSM group, they went up to the peak at 4 h in the endotoxemia group, and at 2 h, 4 h, 8 h, 16 h, 24 h and 48 h, they were markedly lower in the RSM group than in the endotoxemia group (P < 0.05). The TNF-alpha level in the endotoxemia group began to increase 2 h after the modeling and reached to the peak at 8 h, with its level still higher than normal at 48 h, while the RSM group had lower level of TNF-alpha at all time-points(P < 0.05). CONCLUSION: The data from this animal experiment indicate that Radix Salviae Miltiorrhizae can decrease PMN-EC adhesion rate and the levels of CD11a/CD18, CD11b/CD18 and TNF-alpha in case of endotoxemia so as to improve the microcirculation.

Animals↗

[Analysis of the efficiency of transcervical resection of endometrium for treating dysfunctional uterine bleeding and factors reducing the efficiency of the operation].

OBJECTIVE: To investigate the efficiency and factors related to the recurrence of transcervical resection of endometrium (TCRE) in treating women with dysfunctional uterine bleeding (DUB). METHODS: Two hundred and twenty women with DUB were selected for TCRE. Specimens from removed endometrium were obtained during the procedures and their menstruation and menorrhagia after the operations were followed up. We also studied the uterine specimens obtained from the recurrent cases undergoing hysterectomies. The specimens were stained by hematoxylin-eosin and immuno-histochemistry respectively to evaluate the depth of removed myometrium and the histopathologic changes in relapsed cases. RESULTS: The follow up period after operation was 24 to 114 months. (1) Overall effective rate was 94.5%, in which amenorrhea rate was 25.9%, menstruation reduction rate was 68.6%. (2) The effective rate of corrective anemia was 97.3% and the satisfaction rate for the operation was 92.3%. (3) Thirty-eight cases required subsequent treatment as a result of recurrence, of which 10 cases underwent hysterectomy and 3 cases underwent repeat TCRE and 25 cases were given medicine treatment. (4) The average depth of myometrium in removed endometrium strip was 2.12 approximately 3.26 mm. (5) Endometrium regrowth was seen in the resected uterine specimens from relapsed cases and adenomyosis was also found in the intra-uterine wall in some cases. CONCLUSIONS: (1) TCRE is a safe and effective alternative treatment for DUB. (2) The main factor reducing the efficiency is either incomplete removal of endometrium or adenomyosis. (3) Standardizing the procedures and strengthening postoperative management are essential requirements for improving the efficiency of TCRE.

Adult↗

[Clinical features of primary Sjögren's syndrome in childhood].

OBJECTIVE: To assess the clinical features of primary Sjgren's syndrome (pSS) in childhood and adult patients to understand the differences between them. METHOD: Data of 21 childhood and 400 adult patients with definite primary Sjgren's syndrome were analyzed retrospectively. RESULTS: In adult patients, initial clinical symptoms were various, dry mouth and dry eyes, arthritis and arthralgia, parotid swelling, renal tubular abnormalities (RTA) were more common. Compared with adult patients, RTA, parotid swelling and rash were more common in childhood, pulmonary abnormalities and neurologic system involvement were less common. The frequency of renal tubular abnormalities (52.4%) and rash (47.6%) in childhood pSS were higher than those of adults, but the frequencies of dry eyes (61.0%) and pulmonary interstitial fibrosis (25.2%) in adults pSS were higher than those in childhood (P < 0.01); serum rheumatoid factor (RF) and gamma-globulin were higher in all childhood patients (P < 0.01). Anti-nuclear antibody (ANA), anti-SSA and anti-SSB antibodies, and IgG were significantly higher in childhood cases than in adult patients (P < 0.05 or 0.01). CONCLUSION: The major clinical characteristics of childhood pSS cases included: (1) RTA, parotid swelling and rash which appeared earlier, but dry mouth and dry eyes appeared later and were mild. (2) The frequency of pulmonary abnormalities, nervous system involvement and Raynaud's phenomenon were less commonly seen. (3) Positivity of RF, anti-SSA and anti-SSB antibodies, and serum IgG were higher.

Adult↗

[Epigallocatechin-3-gallate interferes with EBV-encoding AP-1 signal transduction pathway].

OBJECTIVE: To elucidate the interference effect of Epigallocatechin-3-Gallate (EGCG) on targets of Activator Protein-1 (AP-1) signal transduction pathway activated by EB virus encoded latent membrane protein 1 in nasopharyngeal carcinoma (NPC) cell lines. METHODS: Survival rate of cells was determined by MTT assay. AP-1 and CyclinD1 activation were analyzed by promoter luciferase reporter system. Nuclear translocation of JNK was analyzed by indirect immunofluorescence. Protein expression and phosphorylation were observed by Western blot. RESULTS: EGCG inhibited the survival of CNE1 and CNE-LMP1 cells and the activity of AP-1 caused by LMP1 in CNE-LMP1 cells. EGCG also inhibited the nuclear translocation of JNK and the phosphorylation of c-Jun. It also inhibited cyclinD1 promoter activity and cyclinD1 expression. CONCLUSION: EGCG inhibits AP-1, JNK, c-Jun and cyclinD1 which are key targets on AP-1 signal transduction pathway. The results may explain the molecular mechanism of action of EGCG against nasopharyngeal carcinoma.

Carcinoma, Squamous Cell↗

[Clinical analysis of 50 cases of cytomegalovirus disease].

OBJECTIVES: To investigate the clinical features, diagnostic methods, therapeutic approaches, outcomes and the alterations of peripheral lymphocyte subsets in cytomegalovirus (CMV) diseases. METHODS: From August 2000 to October 2002, 50 cases of CMV diseases were treated in Peking Union Medical College Hospital. The diagnosis were made by their symptoms and positive CMV pp65 antigen or/and CMV specific IgM. Of the 50 patients, 15 were male, and 35 female. Their age was (35.5 +/- 16.2) years. Their clinical data were collected, and their peripheral lymphocyte subsets were measured at the time when they were first diagnosed as CMV disease. The lymphocyte subsets of 51 healthy blood donors were tested as normal controls. The lymphocyte subsets were compared between those who had an immunocompromising underlying disease and those who had not. RESULTS: (1) CMV disease occurred in 39 patients who had immunocompromising underlying diseases, and in 11 patients who had not; (2) CMV disease caused various symptoms, most of them were nonspecific. Fever (100%), hematological abnormalities (96%) and abnormal liver function test (30%) were the most common manifestations. 3 cases of CMV retinitis were acquired immune deficiency syndrome patients with CD4+ T cell count less than 50/ microl; 2 patients developed multiple organ failure; (3) The positive rates of CMV pp65 antigen and specific IgM assays were 85.3% and 68.3%, respectively; (4) Comparing with normal controls, all patients with CMV disease had decreased B cell and nature killer cells, increased CD8+ T cell percentage and a reversed CD4+/CD8+ ratio; further more, the patients with underlying diseases had lower CD4+ T-cell and CD8+ T-cell counts than those without underlying diseases. CONCLUSIONS: CMV disease occurred in patients with or without underlying diseases. Their clinical manifestations were heterogeneous and non-specific, therefore, special laboratory tests were necessary to confirm the diagnosis. pp65 antigen assay had more diagnostic value than IgM assay. The dramatic changes in lymphocyte subsets suggest CMV disease has a immunological pathogenesis.

Adolescent↗