PubMed Health⌕ Search

Biomedical subjects

C Lin

Publications and source records attributed to C Lin.

At least 109 records · Page 6Linked to original sources

A model and its implications for denitrification in soil environment.

We analyzed the mechanisms of a soil nitrogen (N) sub-model, which is a subroutine of the Crop-Environment Resources Synthesis (CERES)-maize; a model which was originally designed to simulate crop yield and has been calibrated and validated in Taiwan. Some experiments designed specifically for testing the N sub-model proved the capability of the model in reflecting field observations. With the mechanisms, we could write computer programs for calculating the relative sensitivities of major parameters in the model, and for simulating different treatments of organic matter. The purposes were to find how they affected N transformations, especially the processes of denitrification, which are considered to be responsible for N losses in upland soils and are an important environmental issue related to human disturbance of the N cycle. The results implied that soil water content and temperature were, respectively, the first and second dominant factors. They were much more sensitive than any other parameters, such as the decomposition rate coefficients, soil pH and bulk density. Decomposition of organic matter could slow down if organic matter with different carbon/nitrogen (C/N) ratios were treated in fractions. This treatment could also decrease the process of denitrification unless the organic matter was extremely large in quantity and has a high C/N ratio.

Calibration↗

Multistep signaling and transcriptional requirements for pituitary organogenesis in vivo.

During development of the mammalian pituitary gland, specific hormone-producing cell types, critical in maintaining homeostasis, emerge in a spatially and temporally specific fashion from an ectodermal primordium. We have investigated the molecular basis of generating diverse cell phenotypes from a common precursor, providing in vivo and in vitro evidence that development of these cell types involves at least four sequential phases of signaling events and the action of a gradient at an ectodermal boundary. In the first phase, we hypothesize that this notochord induces invagination of Rathke's pouch from the oral ectoderm. This is followed by appearance of an ectodermal boundary, formed with exclusion of Shh from the nascent pouch. Next, signals from the ventral diencephalon--expressing BMP4, Wnt5a, FGF10, and FGF8--in concert with Shh represent critical in vivo signals for pituitary determination. Subsequently, a dorsal-ventral BMP2 signal gradient emanates from a ventral pituitary organizing center, forming at the boundary to oral ectoderm region from which Shh expression is selectively excluded. In concert with a dorsal FGF8 signal, this creates opposing gradients that generate overlapping patterns of specific transcription factors that underlie cell lineage specification events. The mechanisms by which these transient gradients of signaling molecules lead to the appearance of four ventral pituitary cell types appear to involve the reciprocal interactions of two transcription factors, Pit-1 and GATA-2, which are epistatic to the remainder of the cell type-specific transcription programs and serve as a molecular memory of the transient signaling events. Unexpectedly, this program includes a DNA-binding-independent function of Pit-1, suppressing the ventral GATA-2-dependent gonadotrope program by inhibiting GATA-2 binding to gonadotrope- but not thyrotrope-specific genes. This indicates that both DNA-binding-dependent and-independent actions of abundant determining factors contribute to generate distinct cell phenotypes. In the fourth phase, temporally specific loss of the BMP2 signal is required to allow terminal differentiation. The consequence of these sequential organ and cellular determination events is that each of the pituitary cell types--gonadotropes, thyrotropes, somatotropes, lactotropes, corticotropes, and melanotropes appears to be determined, in a ventral to dorsal gradient, respectively, apparently based on a combinatorial code of transcription factors induced by the gradient of specific signaling molecules.

Animals↗

[Quantitative characteristics of rare and endangered Castanopsis kawakamii population].

In this paper, a new self-adaptive model for population growth, i.e. S = exp(alpha ln2(1 + ce-rt) + beta ln(1 + ce-rt) + gamma) was established, which combined Logistic, Smith, Gompertz, Gui-Lawson, Zhang-Logistic and Liu-Logistic models. Estimations with genetic algorithm showed that the new model was more suitable than other models to simulate the actual growth trend of Castanopsis kawakamii population.

China↗

Overexpression of Bcl-2 partly inhibits apoptosis of human cervical cancer SiHa cells induced by arsenic trioxide.

OBJECTIVE: To study the biological effect of arsenic trioxide (As2O3) on human cervical cancer SiHa cells and SiHa cells overexpressing bcl-2 gene. METHODS: SiHa cells with overexpression of Bcl-2 (SiHa-Bcl2 cells) were established by transfecting SiHa cells with Bcl-2 expression vector. The sensitivities of SiHa and SiHa-Bcl2 cells to As2O3 were determined using MTT (Thiazolyl blue) reduction and colony forming ability assay, morphological analysis, flow cytometric analysis, DNA agarose gel electrophoresis, in situ cell death detection (TUNEL), Northern blot, RT-PCR and Western blot. RESULTS: As2O3 inhibited the growth of SiHa cells and induced G2/M arrest and apoptosis of the cells. RT-PCR and Western blot analysis revealed that As2O3 induced SiHa cell apoptosis possibly via inhibiting the expression of HPV16 E7 and decreasing the expression of c-myc. However, we found that SiHa-Bcl2 cells partly resisted As2O3 induced apoptosis, which might be related to the prevention of the down-regulation of HPV16 E7 and c-myc gene expression. Nevertheless, As2O3 at a high concentration could still induce apoptosis of SiHa-Bcl2 cells mainly via decreasing Bcl-2 expression and slightly inhibiting viral gene expression. CONCLUSION: As2O3 is an inducer of the apoptosis of human cervical carcinoma cells and the cells overexpressing Bcl-2 can partly resist As2O3 induced apoptosis, but the exact mechanism is unclear.

Antineoplastic Agents↗

[Safety evaluation of Ad-ASmyc in vitro and in vivo].

OBJECTIVE: To assess the safety of adenovirus-mediated transfer of anti-sense c-myc (Ad-ASmyc). METHODS: RT-PCR was used to detect the transcription of Ad-ASmyc in HeLa cells infected with extracts from HeLa cells previously infected with Ad-ASmyc. Cell count was used to observe the effects of Ad-ASmyc on the growth of normal human fetal lung diploid cell line 2BS. Ad-ASmyc was given to 2 groups of Balb/c mice by intraperitoneal injection at a dosage of 10(7) pfu and 10(9) pfu respectively. Blood samples were obtained from the mice for liver and renal function tests. PCR was used to screen the vital organs for the presence of adenovirus DNA. Microscopic examination of the vital organs was performed to observe the pathogenicity of Ad-ASmyc. RESULTS: As a replication-defective virus, Ad-ASmyc could infect 2BS cells effectively, but did not inhibit 2BS cell growth. No mouse died and no signs of general toxicity following intraperitoneal injection of Ad-ASmyc were observed. In mice injected with 10(9) pfu Ad-ASmyc, the adenoviral vector was found in the liver, spleen, kidney, and stomach. On day 6 and day 12 after injection, mild inflammatory infiltration of mononuclear cells was observed. CONCLUSION: The use ofadenoviral vector for antisense c-myc gene transfer in vitro and in vivo is considered to be safe for clinical trial.

Adenoviridae↗

[The effects of RA538 and antisense c-myc on cervical cancer cell lines with high expression of bcl-2 gene].

OBJECTIVE: To study the effects of recombinant adenovirus with RA538 or antisense c-myc insert on cervical cancer cell lines with high expression of bcl-2 gene. METHODS: Cervical cancer cell lines HeLa and SiHa were transduced with full length bcl-2 cDNA by lipofectin and cell clones with stable expression of bcl-2 were selected. They were then transfected with recombinant adenovirus containing RA538 (Ad-RA538), antisense c-myc (Ad-ASc-myc) or LacZ (Ad-LacZ) gene. Morphologic and molecular changes of the transfected cancer cells were examined by light microscopy, MTT, RT-PCR and Northern blot. RESULTS: The bcl-2 cDNA was successfully transferred into HeLa and SiHa cells. Two cell lines, called HeLa-bcl2 and SiHa-bcl2 with high expression of bcl-2 gene were generated. Ad-RA538 and Ad-ASc-myc transfection both could inhibit cell growth and induce apoptosis of HeLa and SiHa cells, and inhibit their expression of c-myc and bcl-2 genes. However, although Ad-RA538 and Ad-ASc-myc had some inhibitory effect on bcl-2 and c-myc gene expression by HeLa-bcl2 and SiHa-bcl2 cells, they could only slightly inhibit cell growth and weakly induce apoptosis. CONCLUSION: Ad-RA538 and Ad-ASc-myc can to certain extent inhibit cell growth and induce apoptosis of two cervical cancer cell lines. They have little such effect when these cell lines have over-expressed bcl-2 by transduction of exogenous bcl-2 gene.

Antineoplastic Agents↗

[The use of gene gun in cancer gene therapy].

OBJECTIVE: With Helios gene gun, the report genes EGFP and Lac-Z were transfected to several cultured mammalian tumor cell lines in vitro and mice skin in vivo, respectively. A stable long time exogene's expression were got. Then, the pWRG3142, which carried mGM-CSF gene was delivered to the abdominal skin of C57BL/6 mice using gene gun. Pathological sections showed the local transproteins' expression companying with a profound inflammation reaction characterized by neutrophilic infiltration. ELISA assay of transfected mouse's serum sample indicated a high improvement of transgenic proteins level, which demonstrated that transgenic GM-CSF secreted from treated skin into the bloodstream effectively. In B16 melanoma tumor model, mice immunized with mGM-CSF expression plasmids could be partially protected from 1 x 10(5) B16 cells challenge and exhibited a drastically reduced tumor growth rate. Finally, we conclucled that exogenes could be transfected into cultured cell lines and mice skin effectively by gene gun technology, and gene gun mediated in vivo delivery of GM-CSF cDNA should be further developed for potential clinical testing as an approach for human cancer gene therapy.

Animals↗

[Experimental study on combination of Ad-p53 with CDDP or As(2)O(3) in human lung adenocarcinoma cell line GLC-82].

OBJECTIVE: To evaluate the therapeutic efficiency of combining p53-expressing adenovirus with chemotherapy agents on GLC-82 human lung adenocarcinoma cells. METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)). The cell growth, morphological changes, cell cycle, apoptosis and molecular changes were measured using cell counting, reversmicroscope, flow cytometry, TUNEL, RT-PC, immunocytochemical assays, and in vivo therapy experiments to evaluate the therapeutic efficiency of such combined regimen. RESULTS: Ad-p53 transfer and CDDP (or As(2)O(3)) administration to GLC-82 cells could exertubstantially stronger therapeutic effects than the single agent treatment. Especially in in vivo experiments, combined administration of Ad-p53 and CDDP induced almost complete tumor remission (89.0%) compared to the partial tumor remission induced by single agent (43.9% or 57.3%). Moreover, delivery of Ad-p53, or administration of minimal-dose CDDP or As(2)O(3) or combined regimen could induce massive apoptosis of GLC-82 cells. Cell cycle analysis demonstrated that administration of CDDP or As(2)O(3) remarkably arrested GLC-82 cells in G(2)/M prior to apoptotic cell death. When treated with combined regimen, cells were arrested in G(2)/M to a greater extent prior to apoptotic cell death. CONCLUSION: After introduced into GLC-82 cells, Ad-p53 shows enhanced therapeutic efficiency for GLC-82 cells when combined with CDDP or As(2)O(3).

Adenocarcinoma↗

[Expression of tumor metastasis gene MTA 1 in hepatocellular carcinoma: clinical implications].

OBJECTIVE: To evaluate the relevance of the expression of tumor metastasis gene metastasis-associated 1 (MTA 1) to HCC metastasis. METHODS: A fragment of MTA 1 cDNA was synthesized by reverse transcription (RT)-PCR. A DIG-labeled method of in situ hybridisation (ISH) was used to measure semiquantitatively MTA 1 mRNA in formalin-fixed, paraffin-embedded sections. RESULTS: Most of MTA 1 mRNA positive cells were located on the border of the tumor in some invasive HCC. High MTA 1 expression was found to correlate significantly with portal venous invasion, intrahepatic metastasis, tumor size or distant metastasis (P < 0.05), but not with gender, cirrhosis or AFP level. It also significantly predicted a shorter survival (P < 0.05). CONCLUSION: The overexpression of MTA 1 correlates closely with the invasion process of HCC.

Adult↗

[Investigation on E. coli O157 in Fujian, China].

OBJECTIVES: To understand the distribution of Escherichia coli O157 (E. coli O157) in human beings, livestock and fowls in Fujian Province, and biological features of the isolated strains. METHODS: Fecal specimens from diarrheal patients, livestock and fowls and meat specimens in Putian and Fuzhou were collected for detection of E. coli O157 during 1997 - 1998. RESULTS: A total of 2,725 specimens were detected, and 76 strains of E. coli O157 were isolated from pigs, pigeons, cattle, chickens, ducks, et al., as well as from the diarrheal patients. These strains could be classified into three types according to their serological tests, including 33 strains of O157: H7, 21 strains of O157: NM, and 22 strains of O157: H?. Detecting rate of E. coli O157 from pigs was the highest. The isolated strains could cause diarrhea in human and obvious pathological changes in the intestines of mice, but could not produce cytotoxin Vero, or heat-stable or heat-liable enterotoxin LT or ST. CONCLUSIONS: There were three types of E. coli O157 in Fujian. But, pathogenic factors of O157: H7 and O157: NM were different from those reported abroad. It suggested that there possibly existed some new pathogenic factors.

Animals↗

[The changes in serum antibody level after immunization with HFRS vaccine].

OBJECTIVES: To observe the changes in serum antibody level after mass immunization with vaccine against hemorrhagic fever with renal syndrome (HFRS) and to evaluate its efficacy and effectiveness in the prevalent areas. METHODS: Healthy people aged 16 to 60 years in the villages were recruited as study subjects, excluding those suffered from HFRS previously, going out for more than nine months and those with contraindications, and were randomly allocated into immunization and control groups with 10,460 and 16,159 persons, respectively. Specific IgG antibody was determined with indirect immunofluorescent assay (IFA) and neutralizing antibody (NA) was determined with micro CPE method. RESULTS: Two weeks after the full-course immunization, sero-conversion rate for IFA reached 100% in those sero-negative before immunization, with a 95% confidence interval of 96.3 - 100.0%, and that for NA 44.4%, with a 95% CI of 22.0% - 69.0%. Geometric mean titer (GMT) were 72.1 and 4.6 for IFA and NA, respectively. Booster immunization was provided for them one year later. Positivity of IFA and NA was 28.6%, 83.3%, 75.0%, 53.1%, 22.6% and 14.8%, 55.6%, 35.0%, 31.3%, 26.0%, before booster immunization, two weeks, one year, one and a half years, two years after booster immunization, respectively. CONCLUSION: HFRS vaccine had good immunogenicity, but its duration of serum antibody sustenance was relatively short.

Adolescent↗

[The development of immune-mediated aplastic anemia in mice can be blocked by cimetidine].

OBJECTIVE: To investigate the effect of H(2) receptor antagonist cimetidine on the development of immune-mediated aplastic anemia (AA) in mice. METHODS: The immune-mediated aplastic anemia mice model was induced by irradiation and half-matched allogeneic lymphocytes transfusion (ALT). The mice were divided into 3 groups: the irradiation alone control group, the irradiation + ALT group (AA group) and the irradiation + ALT + cimetidine group. In cimetidine group, each mouse was intraperitoneally injected cimetidine at different doses once a day for 8 days. On day 14, the bone marrow histology was examined. RESULTS: In 0.5 mg, 1.0 mg and 2.0 mg x (10g)(-1) x d(-1) cimetidine groups, the percentages of hematopoietic tissue volume in bone marrow were (46.58 +/- 20.41)%, (51.88 +/- 24.94)% and (59.12 +/- 32.48)%, respectively, and all much higher than that in AA group [(19.99 +/- 10.98)%, P < 0.01], but were not different from that in irradiated control group [(53.81 +/- 31.72)%, P > 0.05]. CONCLUSION: The development of immune-mediated aplastic anemia in irradiated mice by half-matched allogeneic lymphocytes transfusion was blocked by H(2) receptor antagonist cimetidine.

Anemia, Aplastic↗

[Alloreactive helper T cell responses in kidney transplant patients].

OBJECTIVE: To study allo-specific immune responses of CD4+ helper T lymphocytes (Th) in patients with long-term and well-functioning renal grafts. METHODS: Peripheral blood mononuclear cells (PBMC) were collected from 16 patients with long-term (3-15 years) and well-functioning live-related renal grafts. Donor-specific Th precursor (Th-p) frequencies in the PBMC were determined by limiting dilution analysis(LDA). RESULTS: Eight out of the 16 patients showed donor-specific hyporesponsiveness. Donor-specific Th-p from the other 8 patients was susceptible to anti-CD4 inhibition. CONCLUSION: Some of the patients carrying long-term and well-functioning renal grafts had become immunologic tolerant to donor cells. Donor-specific Th-p from patients who did not show donor-specific hyporesponsiveness were of low avidity type.

Adult↗

[Arsenic trioxide induced human esophageal cancer Ec109 cell apoptosis with downregulation of c-myc gene expression].

OBJECTIVE: To study effect of downregulation of c-myc gene expression with As2O3 on inducing Ec109 cell apoptosis. METHODS: MTT reduction assay, flowcytometric analysis, DNA gel electrophoresis, Western blot and in situ cell death detection (TUNEL). RESULTS: The viability of the cells treated with As2O3 was decreased. The cells treated with As2O3 showed a typical apoptotic morphology and hypodiploid peak before G1 phase. DNA of treated Ec109 cells appeared a ladder pattern characteristic of apoptosis. TUNEL detection analysis also revealed the DNA fragmentation and As2O3 decreased c-myc gene expression was observed. CONCLUSIONS: As2O3 can induce Ec109 cell apoptosis with downregulation of c-myc gene expression.

Antineoplastic Agents↗

[Arsenic trioxide induces human tumor cell apoptosis and G2 + M arrest whereas causes HPV16 DNA immortalized cervical epithelial cells G1 block].

OBJECTIVE: To investigate whether As2O3 induces tumor cell apoptosis and cell cycle arrest. METHODS: DNA agarose gel electrophoresis, flowcytometry analysis, RT-PCR, and Western blot. RESULTS: As2O3 induced G2 + M arrest of tumor cells such as GLC-82, MGC-803, SGC-7901, Eca109 and HeLa cells before inducing apoptosis and decreased c-myc gene expression, whereas caused G1 block of HPV16 DNA immortalized cervical epithelial HCE16/3 cells and did not affect c-myc expression. CONCLUSIONS: As2O3 caused apoptosis was related with cell cycle arrest. However, the phase of arrest of tumor cells was different from the pre-tumor cell HCE16/3 cells, which could be related to the change of c-myc gene expression.

Apoptosis↗

[Studies on the gas phase reaction of ablated Ni+ with molecular flows of alcohols in the time-of-flight mass spectrometer].

A apparatus combining molecular flows, laser ablation and time-of-flight mass spectrometer was first designed, in which the gas phase reactions of metal ions with organic compounds were realized. In a small quartz cell of it, laser ablated Ni+ meet and react with molecular flows of alcohols, and their product ions were detected by the time-of-flight mass spectrometer. The gas phase reactions of Ni+ with C2-C6 alcohols were studied. All of which can be explained by the following mechanism: (1) Insertion of Ni+ into bonds of alcohols; (2)Following each insertion, a beta-hydrogen shift onto Ni+ to produce intermediate; (3) Dessociation of each intermediate by loss of neutral molecular to give product ion.

English Abstract↗

HCPTPA, a protein tyrosine phosphatase that regulates vascular endothelial growth factor receptor-mediated signal transduction and biological activity.

Angiogenesis is a tightly controlled process in which signaling by the receptors for vascular endothelial growth factor (VEGF) plays a key role. In order to define signaling pathways downstream of VEGF receptors (VEGFR), the kinase domain of VEGFR2 (Flk-1) was used as a bait to screen a human fetal heart library in the yeast two-hybrid system. One of the signaling molecules identified in this effort was HCPTPA, a low molecular weight, cytoplasmic protein tyrosine phosphatase. Although HCPTPA possesses no identifiable phosphotyrosine binding domains (i.e. SH2 or phosphotyrosine binding domains), it bound specifically to active, autophosphorylated VEGFR2 but not to a mutated, kinase-inactive VEGFR2. Recombinant VEGFR2 and endogenous VEGFR2 were substrates for recombinant HCPTPA, and HCPTPA was co-expressed with VEGFR2 in endothelial cell lines, suggesting that HCPTPA may be a negative regulator of VEGFR2 signal transduction. To pursue this possibility, an adenovirus directing the expression of HCPTPA was constructed. When used to infect cultured endothelial cells, this adenovirus directed high level expression of HCPTPA that resulted in impairment of VEGF-mediated VEGFR2 autophosphorylation and mitogen-activated protein kinase activation. Adenovirus-mediated overexpression of HCPTPA also inhibited VEGF-induced cellular responses (endothelial cell migration and proliferation) and inhibited angiogenesis in the rat aortic ring assay. Taken together, these findings indicate that HCPTPA may be an important regulator of VEGF-mediated signaling and biological activity. Potential interactions with other signaling pathways and possible therapeutic implications are discussed.

Animals↗

Luteolytic effects of DL111-IT in pregnant rats.

The present studies were conducted to evaluate the effects of DL111-IT [3-(2-ethyl phenyl)-5-(3-methoxy phenyl)-1H-1,2,4 triazol] on ovaries of pregnant rats. Pregnant rats were i.m. treated with DL111-IT 2.5 mg kg(-1) day(-1) or camellia oleum (vehicle control) 0.2 ml/day from day 6 of pregnancy for 1, 3 or 5 days. Blood and ovaries were collected 24 h after the last injection. Ovarian fresh weight and protein contents, activities of the 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) in ovaries, and cell apoptosis of corpus luteum (including hematoxylin-eosine stain, in situ 3'-end labeling and nucleosomal banding) were estimated. Compared with that in the control group, ovarian fresh weight declined 11% and 22% after DL111-IT-3 days and -5 days; protein content dropped 29% after 5-day administration. DL111-IT for 3 days provoked a marked decrease of serum progesterone, by 31% of the control; the activity of 3beta-HSD decreased 34.4% after i.m. DL111-IT for 5 days, while that of 20alpha-HSD increased dramatically after only one injection of DL111-IT (P < 0.01). Histological analysis and in situ 3'-end DNA labeling indicated that DL111-IT induced the pyknosis of cells and the formations of apoptotic bodies and intense oligonucleosomes in luteal cells of pregnant rats. The cell apoptosis induced by DL111-IT was further confirmed by evaluation of nucleosomal DNA fragmentation by agarose gel electrophoresis in cultured luteal cells exposed to DL111-IT for 24 h. In conclusion, all results, including shrunken luteal cells, decreased concentration of protein content and serum progesterone, changed activities of 3beta-HSD and 20alpha-HSD and formation of DNA fragments in luteal cells, showed the luteolytic effect of DL111-IT in pregnant rats.

20-Hydroxysteroid Dehydrogenases↗