PubMed Health⌕ Search

Biomedical subjects

Q Qin

Publications and source records attributed to Q Qin.

At least 37 records · Page 2Linked to original sources
PubMed1998

Modulation of human epidermal cell response to 2,3,7,8-tetrachlorodibenzo-p-dioxin by epidermal growth factor.

Cultured human epidermal cells were treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the presence or absence of epidermal growth factor (EGF). In both normal keratinocytes and a spontaneously immortalized keratinocyte (SIK) line, TCDD treatment in the absence of EGF induced a marked reduction in colony size and cell number, and it perturbed colony morphology. These effects were largely prevented by EGF, indicating that growth factor action in the cellular microenvironment may considerably modify TCDD action in target cells. Both TCDD and EGF substantially reduced expression of the differentiation markers keratin 1 and keratin 10 in the normal and immortalized cells, and did so in an additive fashion. The cells did not display a general loss of differentiated function, since several other markers, including involucrin, were little affected. EGF dramatically stimulated telomerase activity in SIK cultures, and TCDD prevented this action but not by reducing cell growth. However, EGF did not stimulate telomerase activity in normal human epidermal cells despite an evident increase in their growth. The growth factor stimulation of telomerase in the minimally deviated SIK line suggests that derepression of enzyme activity in normal cells may occur in a stepwise fashion during neoplastic progression. TCDD could act as a late stage tumor promoter by selecting for variants in which telomerase is constitutively active.

Cell Differentiation↗
PubMed1997

Dual-label time-resolved immunofluorometric assay for simultaneous determination of pregnancy-associated plasma protein A and free beta-subunit of human chorionic gonadotrophin.

Using time-resolved fluorometry, a simple one-step dual-label immunometric assay has been developed, which allows simultaneous determination of pregnancy-associated plasma protein A (PAPP-A) and free beta-subunit of human chorionic gonadotrophin (beta-hCG) in first-trimester maternal serum samples. Two monoclonal antibodies were biotinylated and immobilized onto the surface of streptavidin-coated microtitration plates, and used to capture PAPP-A and beta-hCG. respectively. Europium (Eu) and Samarium (Sm) chelates were conjugated to two additional monoclonal antibodies acting as detection antibodies for PAPP-A and beta-hCG. The assay was performed using a 4-h one-step format. The within-run precision with buffer-based calibrators was below 8% over the working range of PAPP-A (40-10000 mIU/l) and beta-hCG (7.3-525 micrograms/l) and no hook effect was observed. The intra- and inter-assay coefficients of variation were below 7.1% for serum samples. PAPP-A and beta-hCG concentrations measured by the dual assay in 39 first-trimester serum samples correlated excellently with those obtained by DELFIA single-label PAPP-A (r = 0.997) and the beta-hCG part (r = 0.993) of the DELFIA AFP/beta hCG dual-label assay.

Antibodies, Monoclonal↗
PubMed1997

Randomized trial of breast self-examination in Shanghai: methodology and preliminary results.

BACKGROUND: The efficacy of breast self-examination in helping to reduce mortality from breast cancer has not been rigorously demonstrated. PURPOSE: To assess efficacy, a large, randomized trial was initiated in Shanghai, China. METHODS: From October 1989 to October 1991, 267040 current and retired female employees associated with 520 factories in the Shanghai Textile Industry Bureau were randomly assigned on the basis of factory to either a self-examination instruction group (133375 women) or a control group (133665 women). The women were born within the period from 1925 through 1958. Women in the instruction group were given intensive training in breast self-examination, including the use of silicone breast models and personalized instruction, plus two subsequent reinforcement sessions and multiple reminders to practice the technique. Women in the control group were asked to attend training sessions on the prevention of low back pain. All women have been followed for the development of breast diseases and for death from breast cancer. RESULTS: A high level of participation during the first 4-5 years of the trial was documented among women in the instruction group. Randomly sampled women in this group demonstrated greater proficiency in detecting lumps in breast models than did randomly sampled women in the control group. Approximately equal numbers of breast cancers were detected in the two groups (331 in the instruction group and 322 in the control group) through 1994, which is the last year for which case-finding efforts have been completed. The breast cancers detected in the instruction group were not diagnosed at an appreciably earlier stage or smaller size than those in the control group. More benign breast lesions were detected in the instruction group than in the control group (1457 versus 623, respectively), suggesting a higher index of suspicion for women who received training. Cumulative breast cancer mortality rates through 5 years from entry into the study were nearly equivalent for the two groups. CONCLUSIONS: Breast self-examination has not led to a reduction in mortality from breast cancer in this study cohort in the first several years since the trial began. A shift toward the diagnosis of disease at a less advanced stage in women given instruction has also not been demonstrated. Longer follow-up of participants in this trial is required before final assessment can be made of the efficacy of breast self-examination. IMPLICATIONS: At this time, there is insufficient evidence to recommend for or against the teaching of breast self-examination.

Adult↗
PubMed1997

Arsenate suppression of human keratinocyte programming.

The human keratinocyte line SCC-9 has been used as a model for arsenate-induced perturbations of differentiation. Growth of these cells in 10 microM arsenate permitted the cultures to reach confluence, but prevented expression of 6 markers of suprabasal differentiation (involucrin, loricrin, filaggrin, spr 1, keratin 1 and keratin 10) as assayed by Northern blotting. By contrast, only slight alterations in mRNA levels were observed for one differentiation marker (keratinocyte transglutaminase) and for keratin 5, keratin 14, AP2 or glyceraldehyde phosphate dehydrogenase. The transition metal oxyanions vanadate and chromate had essentially the same suppressive effect on these markers as arsenate, while chronic treatment with tetradecanoylphorbol acetate was generally less effective in suppressing differentiation. To determine whether the previously observed arsenate-mediated alteration in AP1 and AP2 activities could account for the suppression of involucrin, a promoter analysis was conducted. Putative AP1 and AP2 response elements were identified in regions important for transcriptional activity of the 5'-flanking DNA. Mutations in two AP1 sites and one AP2 site were observed to decrease promoter activity significantly, and in combination, to reduce it to approximately 10% of that conferred by the native sequence. These results lend support to the working hypothesis that arsenate suppresses involucrin expression, and, more generally, keratinocyte programming, by altering the transcription factors AP1 and AP2.

Arsenates↗
PubMed1997

[Design of CA-1680 biochemical analyzer].

The paper provides the design idea structure of key parts software and hardware of microprocessor of CA-1680 Biochemical Analyzer. The instrument uses the specific flow cell high properties photodiode and programmable amplifier. The 16 bit programmable A/D conversion is completed with V/F convertor and programmable counter. Logarithm conversion is completed with software. On Using these methods, the instrument has not only simpler circuit, better reliability, but also the characteristics of accuracy, precision and widely linearity.

Biochemistry↗
PubMed1995

Keratinocyte transglutaminase promoter analysis. Identification of a functional response element.

Keratinocyte transglutaminase catalyzes isopeptide bond formation to yield the highly insoluble cross-linked envelope during terminal differentiation of epidermal cells. Transcriptional response elements were identified in the 5'-flanking DNA of the gene for this enzyme by a combination of transient transfection and electrophoretic mobility shift analyses. Since human keratinocytes transcribed ineffectively transfected transglutaminase flanking DNA, a key feature of these experiments was the use of rat bladder epithelial cells as recipients. Serial deletion experiments identified by transient transfection an important response region containing three putative AP2-like response elements approximately 0.5 kilobases from the transcription initiation site. Oligonucleotides, each containing a single one of the elements, formed specific complexes with keratinocyte nuclear proteins. Two of the response elements were found to be functional by transfection in site-specific deletion experiments. Of these one formed specific DNA-protein complexes with nuclear proteins only from cells exhibiting keratinocyte differentiation. UV cross-linking experiments estimated the protein component of the complex to be approximately 85 kDa. This response element alone increased substantially the transcription of a minimal transglutaminase promoter in transient transfections. Further characterization of the putative transcription factor binding to this response element may provide insight into the regulation of keratinocyte transglutaminase.

Animals↗
PubMed1994

Chromium-induced early changes in renal function among ferrochromium-producing workers.

Urinary biochemical indicators of renal injury were examined in 84 male and 38 female ferrochromium-producing workers exposed to water-soluble chromium compounds [Cr(VI)]. The indicators examined included urinary chromium (U-Cr), alkaline phosphatase (ALP), gamma-glutamyl transferase (gamma-GT), glutamic-oxalacetic and glutamic-pyruvic transaminases (GOT & GPT), lactate dehydrogenase (LDH), N-acetyl-beta-D-glucosaminidase (NAG), total protein (TPr) and beta 2-microglobulin (beta 2-MG). The U-Cr levels in the exposed group were approximately 1.8 times that of the control group. Compared to controls, the activities of gamma-GT, NAG, ALP, GOT and LDH in the urine of workers were significantly increased whenever U-Cr concentration exceeded 45 microgram/g creatinine. The activities of gamma-GT, GOT and NAG were elevated in workers employed for longer than ten years. However, no clear dose-response relationships nor time-effect relationships were found. The present results suggest that long-term exposure to water-soluble chromium [Cr(VI)] produces chronic renal injury. The site of the injury appears to mainly involve the proximal tubule. U-Cr concentrations of > 15 microgram/g creatinine can be proposed as a threshold dosage for nephrotoxicity, and gamma-GT, NAG and ALP are early sensitive indicators of the most valuable for evaluating the renal injury.

Acetylglucosaminidase↗
PubMed1994

Arsenate perturbation of human keratinocyte differentiation.

Treatment of cultured malignant human keratinocytes with sodium arsenate greatly suppressed expression of involucrin, a specific marker of keratinocyte differentiation. This action was primarily attributable to inhibition of involucrin transcription according to message run-on and stability measurements. Involucrin was suppressed in nontumorigenic keratinocytes as well, although the efficacy of suppression was less dramatic in cells derived from clinically normal epidermis. Several transition metal oxyanions (vanadate, molybdate, and tungstate) also substantially suppressed involucrin expression, but okadaic acid was ineffective. Immunoblotting detected marked increases in tyrosine phosphorylation of several proteins as a consequence of arsenate treatment of the cultures, while mobility shift analysis revealed a dramatic loss of DNA binding by the transcription factor AP2. These findings support a proposed role for altered levels of protein tyrosine phosphorylation in keratinocyte differentiation. They also suggest that arsenate perturbs the differentiation program in target cells by altering this phosphorylation level and transcription factor activity.

Arsenates↗
PubMed1993

Keratinocyte transglutaminase membrane anchorage: analysis of site-directed mutants.

Keratinocyte transglutaminase is anchored on the cytosolic side of the plasma membrane by fatty acid thioesterification near the amino terminus, a process which is seen to occur within 30 min of synthesis. The importance of a cluster of five cysteines (residues 47, 48, 50, 51, and 53) where acylation was presumed to occur is now demonstrated by site-directed mutagenesis. Transglutaminase mutants in which the cluster is deleted or the cysteines are all converted to alanine or serine are cytosolic. Partial replacement of the cluster, leaving two contiguous cysteines, is sufficient to confer membrane anchorage, while a single cysteine is only partially effective. As demonstrated with a soluble transglutaminase mutant, membrane anchorage confers susceptibility of the amino-terminal region to phorbol ester-stimulated phosphorylation. Attachment of 105 residues from the transglutaminase amino terminus to involucrin, a highly soluble protein, results in membrane anchorage of the hybrid protein. Attachment of the cysteine cluster alone does not result in membrane attachment of involucrin, but a 32-residue segment containing this cluster is sufficient. Stable transfectants of the human transglutaminase in mouse 3T3 cells are membrane-bound, indicating the fatty acid transacylation is not keratinocyte-specific.

3T3 Cells↗
PubMed1993

Elevation of cell cycle control proteins during spontaneous immortalization of human keratinocytes.

A human line of spontaneously immortalized keratinocytes (SIK cells) has been derived from ostensibly normal epidermis and has proven useful in dissecting molecular changes associated with immortalization. The original cultures had a normal karyotype and a colony forming efficiency of approximately 3% through 10 passages. At passage 15, after which normal strains ordinarily senesce, these cells continued vigorous growth and gradually increased in colony forming efficiency, stabilizing at approximately 30% by passage 40. During the early stage of increasing colony forming efficiency, the cells acquired a single i(6p) chromosomal aberration and 5- to 10-fold increases in expression of the cell-cycle control proteins cyclin A, cyclin B, and p34cdc2. Additional chromosomal aberrations accumulated at later passages (i(8q) and +7), but the i(6p) and the increased expression of cell-cycle proteins were maintained, raising the possibility that these features were important for immortalization. Regulation of cell growth and differentiation in the cultures appeared minimally altered compared with normal keratinocytes as judged by their microscopic appearance and generation of abortive colonies, sensitivity to growth suppression by transforming growth factor-beta and tetradecanoylphorbol acetate, and dependence upon epidermal growth factor for progressive growth.

CDC2 Protein Kinase↗
PubMed1992

Keratinocyte differentiation markers: involucrin, transglutaminase, and toxicity.

Studies of three keratinocyte differentiation markers are described. First, the involucrins of several mammals are identified, facilitating use of this marker in animal models of human disease. The rapid evolution of involucrin has prevented its routine immunochemical identification beyond the primates, but its unusual solubility and its labeling by transglutaminase have permitted detection in rats, cats, and sheep. Second, the re-expression of keratinocyte transglutaminase in carcinoma cells lacking the enzyme is demonstrated. Lack of this enzyme expression has been observed previously in squamous cell carcinomas. The present finding suggests genomic hypermethylation could contribute to this phenomenon and offers an approach to analyzing transcriptional features of the enzyme regulation. Third, the sensitivity of keratinocytes to growth suppression by aflatoxin B1 is reported. The observed toxicity appears to be mediated by aryl hydrocarbon hydroxylase, a metabolic enzyme inducible in keratinocytes by environmental agents. Such expression may be relevant to carcinogenesis in tissues subject to squamous metaplasia as well as in other exposed cell types stimulated to express this biotransformation enzyme.

Aflatoxins↗