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Biomedical subjects

D Yu

Publications and source records attributed to D Yu.

At least 253 records · Page 14Linked to original sources
PubMed1994

Heat-treatment-induced reduction in the apparent solubility of human dental enamel.

Holcomb and Young (1980) have shown a significant increase in human dental enamel (HE) structural order resulting from heat treatment in the temperature range of from 275 to 400 degrees C. Also, previous work in our laboratory had shown dramatic decreases in the initial dissolution rates (IDRs) of both carbonated apatite (CAP) heated at similar temperatures (from 300 to 500 degrees C) and HE exposed to CO2 laser irradiation for which calculated surface temperatures were in this same range. We hypothesize that thermal treatment shifts the apparent solubility distribution profile of HE toward lower apparent solubilities, paralleling the observed increased in crystal structural order and the decrease in IDRs. Powdered HE was heated in a furnace at temperatures ranging from 150 to 500 degrees C for 24 hours. The apparent solubility distributions of both heated and unheated HE powders were measured by equilibration for 24 hours in a series of partially saturated solutions simulating various amounts of HE dissolved in a pH 4.5 dissolution medium. The apparent solubility distribution for the unheated HE showed a peak at KHAP [the ion activity product based on the Ca10(PO4)6(OH)2 stoichiometry] of 10(121.0). Heat treatment shifted the apparent solubility distribution to lower solubilities. The peak KHAP values were approximately 10(124.8) at 200 degrees C; approximately 10(127.8) at 300 degrees C; and approximately 10(-129.1) from 400 to 500 degrees C. This approximately 8 orders of magnitude decrease in KHAP for HE heated at from 400 to 500 degrees C correlates with the previously observed reduction in the IDR driving force for laser-treated HE experiencing a similar surface temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

Apatites↗
PubMed1994

[Study on the invasive properties of cloned human nasopharyngeal carcinoma CNE2Z variants using organ culture in vitro].

Using limiting dilution assay, variants were cloned from the CNE-2Z cell line. The variants CNE2L2, CNE2H2, CNE2L4 and CNE2M2, with cell electrophoresis rates which differed greatly, were assayed for their invasive capabilities by observing their ability to invade preculture embryonic chicken heart fragment (PHF) in organ culture using a gyrotory shaker system. The results indicated that CNE2L2 variant cells invaded 9-day-old chicken embryonic heart fragments at a rate significantly higher than those seen using CNE2L4 and CNE2M2 in 7-day assay. Computer image analysis showed that the CNE2L2 cells occupied 80.2% of the PHF area much greater than that occupied by CNE2L4 (46.5%) or CNE2M2 (36.5%). This experiment also showed that the electrophoresis rate of the CNE2Z variants was positively related to their invasive capabilities in vitro.

Animals↗
PubMed1994

Enterprise-based sheltered workshops in Nanjing. A new model for the community rehabilitation of mentally ill workers.

This paper describes the development of community mental health services in Nanjing and reports on a retrospective study that compared the two-year outcome for 78 schizophrenic patients who attended four enterprise-based sheltered workshops (experimental group) with that of 78 schizophrenic patients who attended an out-patient clinic (control group). Despite having a longer course of illness and more prior hospital admissions than patients in the control group, at the end of the two years patients treated in enterprise-based sheltered workshops had significantly less psychosocial dysfunction (mean Social Dysfunction Screening Schedule score 3.4 (s.d. 0.2) v. 7.4 (s.d. 0.7), t = 49.2, d.f. 154, P < 0.001) and less severe psychiatric symptomatology (mean Brief Psychiatric Rating Scale score 33.1 (s.d. 2.7) v. 54.1 (s.d. 2.9), t = 47.0, d.f. 154, P < 0.001). Moreover, compared with the control group, over the two year period a smaller proportion of the experimental group experienced a clinical relapse (14.1% v. 38.5%, chi 2 = 5.10, d.f. 1, P < 0.05) or hospital readmission (7.7% v. 21.8%, chi 2 = 10.7, d.f. 1, P < 0.01). We conclude that the organisation of on-site sheltered workshops for mentally ill factory workers is an effective model for promoting community mental health that merits widespread application in China.

Adult↗
PubMed1994

Transcriptional regulation of neu by RB and E1A in rat-1 cells.

Functional inactivation of the tumor-suppressing retinoblastoma gene (Rb) is involved in the etiology of many types of human cancers, including hereditary retinoblastomas. The neu gene is a dominant transforming oncogene, and we previously found that the Rb-encoded protein (RB) suppresses neu-induced transformation in NIH3T3 cells by repressing transcription of the neu oncogene. We report here that RB was unable to repress neu oncogene transcription in Rat-1 cells but could functionally antagonize transcriptional repression of neu by the adenovirus E1A. Mutant forms of RB that have mutations in either the E1A-binding or carboxy-terminal regions had less or no antagonizing effects on E1A-mediated repression of neu in Rat-1 cells. Results of focus-formation assays showed that the transformation activity of the neu oncogene in Rat-1 cells could be regulated by E1A and RB in accordance with their transcriptional regulation activities. The data demonstrate that RB can regulate transcription of neu in a negative or positive manner depending on the cell type. Carboxy terminus of RB as well as the E1A-binding region can mediate transcriptional regulation. Based on these results, we propose a model for the complex transcriptional regulation of neu by RB and E1A.

Adenoviridae↗
PubMed1993

Reexpression of neu-encoded oncoprotein counteracts the tumor-suppressing but not the metastasis-suppressing function of E1A.

By transfecting the adenovirus 5 E1A gene into neu-transformed NIH3T3 cells, we previously showed that E1A can dramatically repress neu-encoded p185 expression and, concomitantly, suppress the features of transformation and metastasis of neu+E1A transfectants. From these results we concluded that suppression of transformation and metastasis by E1A in neu-transformed cells may be through repression of neu gene expression. However, E1A has recently been shown to also repress the transformation features of other human cancer cells that do not overexpress neu. This observation raised a possibility that repression of neu gene expression in our neu+E1A cells might not be the only mechanism for transformation and metastasis suppression. To study whether other molecular mechanisms might be involved in suppression of transformation and metastasis by E1A in our neu+E1A cells, we reexpressed p185 oncoprotein in the neu+E1A cells by transfecting them with a plasmid containing activated rat neu complementary DNA and we examined whether E1A can suppress transformation and metastasis when the neu-encoded p185 protein is reexpressed. All the features of transformed cells including cell morphology, DNA synthesis rate, colony formation in soft agar, and tumorigenicity in nu/nu mice were restored in the cell lines that reexpressed neu. In addition, the levels of neu reexpression corresponded to the degree of malignant transformation. However, the in vivo metastatic tumor formation by these p185 reexpressing cells was still significantly inhibited by E1A. When metastasis-associated properties were examined in the cell lines that reexpressed p185, we found that cell motility was recovered by reexpression of p185 to the degree corresponding to the p185 reexpression level, but secretion of membrane-degrading gelatinases and invasion through the basement membrane preparation Matrigel by these cells were still inhibited by E1A. The data demonstrated that reexpression of p185 in neu+E1A cells can counteract the tumor-suppressing function of E1A but not completely recover the neu-induced metastatic phenotype. We conclude from these results that (a) repression of neu oncogene expression was indeed the molecular mechanism by which E1A suppressed tumor formation in neu-transformed 3T3 cells, and (b) suppression of metastasis by E1A in neu-transformed 3T3 cells was via multiple molecular mechanisms in addition to repressing neu. Our model system clearly demonstrated that tumorigenicity and metastasis are related but separable phenomena.

3T3 Cells↗
PubMed1993

Enhanced c-erbB-2/neu expression in human ovarian cancer cells correlates with more severe malignancy that can be suppressed by E1A.

Amplification or overexpression of c-erbB-2/neu protooncogene, or both, occur frequently in many different types of human cancers and have been shown to correlate with decreased survival in ovarian cancer patients. We have previously found that the ovarian carcinoma cell line SK-OV-3 overexpresses c-erbB-2/neu mRNA. To further study the biological effect of c-erbB-2/neu overexpression in SK-OV-3 cells, we injected such cells i.p. into female nu/nu mice and found that this cell line forms extensive abdominal tumors and ascites. From the ascites in an injected mouse, we established the SKOV3.ip1 cell line and found that it expressed 2-fold more c-erbB-2/neu-encoded p185 proteins than the parental SK-OV-3 cells. When transformation phenotypes of SK-OV-3 and SKOV3.ip1 cells were compared, SKOV3.ip1 cells showed higher cell growth and DNA synthesis rates, formed more colonies in soft agar, produced larger s.c. tumors, and resulted in shorter survival of nu/nu mice after i.p. injection. These data indicate that the level of c-erbB-2/neu overexpression may correlate with the degree of malignancy in these ovarian carcinoma cells. Since we had previously shown that the adenovirus 5 E1A gene product can suppress transformation and metastatic properties induced by mutation-activated rat neu oncogene in mouse embryo fibroblast cells, we further examined whether E1A can abrogate malignancy in c-erbB-2/neu-overexpressing human ovarian cancer cells. We introduced the E1A gene into c-erbB-2/neu-overexpressing SKOV3.ip1 cells and found that the E1A-expressing ovarian cancer cell lines had decreased c-erbB-2/neu-encoded p185 expression and reduced malignancy, including a decreased ability to induce tumors in nu/nu mice. Therefore, we concluded that E1A is a tumor suppressor gene for c-erbB-2/neu-overexpressing human ovarian cancer cells and may be useful in developing therapeutic reagents for these human cancers.

Adenovirus E1A Proteins↗
PubMed1993

Comparison of three lasers on dental pulp chamber temperature change.

Previous studies have reported dental pulp chamber temperature changes using only one beam size per laser. This study was designed to evaluate the effects of beam size, wattage, and energy density on pulp chamber temperature changes of extracted human teeth for three lasers (CO 2, Argon, Nd:YAG). During laser irradiation of the outer enamel surface, a thermocouple was placed in the pulp chamber which measured and recorded the temperature changes. This was done for each combination of lasing dosimetry parameters. In all cases the recorded temperatures increased with the increase in beam size for a given energy density (J/cm 2) and wattage. Also, the recorded temperatures increased with increased energy density for a given wattage and beam size.

Dental Pulp Cavity↗
PubMed1993

Synthesis of the prototype DNA-protein cross-link, 1-(guan-1-yl)-2-(cysteine-S-yl)ethane, and its role in the reactions of the haloethylnitrosoureas.

The haloethylnitrosoureas form a cytotoxic DNA cross-link in a series of reactions which involves initial alkylation of the O6 position of guanine and rearrangement to the intermediate, 1,O6-ethanoguanine; 1,O6-ethanoguanine then reacts with a neighboring cytosine base. O6-Alkylguanine-DNA alkyltransferase can interrupt this process after the initial alkylation step by removing the alkyl group from the O6 position of guanine. Recent evidence suggests that the O6-alkylguanine-DNA alkyltransferase also recognizes 1,O6-ethanoguanine as a substrate, becoming bound to DNA when it interacts with that intermediate. It has also been shown that glutathione becomes bound to haloethylnitrosourea-treated DNA, apparently through chemical interaction with 1,O6-ethanoguanine. Since both of these reactions involve the thiol group of cysteine, we have examined the reaction of cysteine with 1,O6-ethanoguanine, characterizing the prototype DNA-protein cross-link, 1-(3-cytosinyl),2-(1-guanyl)ethane, which is formed in this reaction. These results establish a competitive reaction with 1,O6-ethanoguanine as a likely route to protein-DNA cross-linking.

Cross-Linking Reagents↗
PubMed1993

Optimal conditions of chemotherapeutic sensitivity in K562 cell line using tetrazolium dye assay.

Ten antineoplastic agents were used on K562 cell lines with the tetrazolium salts (MTT) assay to investigate optimal conditions of the chemotherapeutic sensitivity. The doubling time of K562 cell was 20.4 h in 96-well microtitre plates. The optical density in MTT assay of the no-drug controls was 0.77 (n = 45). A 70% reduction (IC70) in absorbance compared with control values using an ELISA reader at 570 nm was referred to as drug sensitive and < 70% (IC70) was referred to as resistant. The inhibitory effect of the theoretical maximal plasma drug concentration (Cmax) in plasma was compared with that of 10% Cmax drug concentration. At 10% Cmax after a 2-d drug exposure to daunorubicin and homoharringtonine, or after 5 d to epirubicin, 5-fluorouracil, cytarabine hydrochloride, and doxorubicin, significant cytotoxicities were shown. There were little time-dependent effects after 2-5 d drug exposure for 4 out of the 10 tested drugs, and mild or marked time- and dose-dependent effect for others.

Antineoplastic Agents↗
PubMed1993

A study and analysis of the deaths due to advanced Schistosoma japonicum infection in the Dongting Lake area of China.

This study collected records of 245 cases of death due to advanced schistosomiasis japonica in the eastern Dongting Lake area between 1985 and 1990. The mean survival of the patients was 5.16 years. The patients with ascitic type had a shorter expected life while the life span of splenomegalic type patient markedly improved after splenectomy. The HBsAg positive rate was 43.64%; the rate of those complicated with carcinoma of liver was 19.18%. The latter group had a HBV infection rate as high as 61.70%.

Adolescent↗
PubMed1992

Identification of the cross-link between human O6-methylguanine-DNA methyltransferase and chloroethylnitrosourea-treated DNA.

Chloroethylnitrosoureas induce reactive O6-guanine adducts in DNA that can form either interstrand cross-links or a covalent complex with the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT). To test our hypothesis that these end-products are formed from the common precursor, 1-O6-ethanoguanine, we compared the kinetics of interstrand cross-link formation with those of decay of MGMT complex forming capacity. The half-lives of these processes were identical. Our hypothesis also predicts that the linkage between DNA and MGMT is 1-(guan-1-yl)-2-(cystein-S-yl)ethane. This notion was tested by forming the complex with 35S-labeled recombinant human MGMT and a chloroethylnitrosourea-treated oligodeoxynucleotide. After degradation by depurination and proteolytic digestion, the identity of the [35S]cysteine-guanine linkage was confirmed by comparison with the synthetic marker compound using high performance liquid chromatography and UV spectrometry. These results strengthen the hypothesis that DNA interstrand cross-links and DNA-MGMT complex both arise from the same precursor. The data also suggest that 1-O6-ethanoguanine is a good substrate for MGMT such that, under certain conditions in vivo, DNA-MGMT complex formation may constitute a significant secondary lesion.

Antineoplastic Agents↗
PubMed1992

The retinoblastoma gene product suppresses neu oncogene-induced transformation via transcriptional repression of neu.

The retinoblastoma susceptibility gene (Rb) is a tumor suppressor gene involved in the etiology of many types of human cancers. However, the molecular mechanisms involved in tumor suppression by Rb are largely unknown. The neu gene is a dominant transforming oncogene and a member of the growth factor receptor tyrosine kinase gene family. Both inactivation of the Rb gene and overexpression of the neu gene are involved in human breast and lung cancers. Therefore, it is of interest and importance to investigate the potential interactions between Rb and neu. Here we show that Rb suppresses neu-induced transformation by focus formation assays. This transformation suppression by Rb was further shown to be due to transcriptional repression of neu using Rb expressing effector plasmid and neu promoter-chloramphenicol acetyltransferase reporter gene. The cis-acting element conferring Rb-mediated repression was mapped to a recently identified novel enhancer in the neu promoter. The data indicate that the growth factor receptor neu is a target for the Rb gene product and transcriptional repression of a dominant oncogene expression may be one of the molecular mechanisms of Rb-mediated tumor suppression.

3T3 Cells↗
PubMed1992

Self-setting hydroxyapatite cement: a novel skeletal drug-delivery system for antibiotics.

A novel approach using a self-setting hydroxyapatite (HAP) cement as a skeletal drug-delivery system has been proposed to solve the problem of delivering drugs to skeletal tissue at sufficiently high local concentrations for desirable therapeutic effects. HAP cements loaded with antibiotics can be formed in situ and can be used as bonding materials between bone and prostheses, as well as drug-release devices. The cement also possesses sufficient mechanical strength to be a potential bone grafting material. Using cephalexin and norfloxacin as model drugs, we observed continuous in vitro release profiles of these compounds from cement pellets loaded 0.9-4.8% by weight with one of the drugs. This drug-release pattern correlated well with the Higuchi model. This hydroxyapatite cement drug-delivery system can be applied in the treatment of osteomyelitis and infected compound fractures.

Anti-Bacterial Agents↗