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Biomedical subjects

J J Yu

Publications and source records attributed to J J Yu.

45 records · Page 3Linked to original sources
PubMed1992

Oxygen-evolving photosystem II preparation from wild type and photosystem II mutants of Synechocystis sp. PCC 6803.

We present here a simple and rapid method which allows relatively large quantities of oxygen-evolving photosystem II- (PS-II-) enriched particles to be obtained from wild-type and mutants of the cyanobacterium Synechocystis 6803. This method is based on that of Burnap et al. [Burnap, R., Koike, H., Sotiropoulou, G., Sherman, L. A., & Inoue, Y. (1989) Photosynth. Res. 22, 123-130] but is modified so that the whole preparation, from cells to PS-II particles, is achieved in 10 h and involves only one purification step. The purified preparation exhibits a 5-6-fold increase of O2-evolution activity on a chlorophyll basis over the thylakoids. The ratio of PS-I to PS-II is about 0.14:1 in the preparation. The secondary quinone electron acceptor, QB, is present in this preparation as demonstrated by thermoluminescence studies. These PS-II particles are well-suited to spectroscopic studies as demonstrated by the range of EPR signals arising from components of PS-II that are easily detectable. Among the EPR signals presented are those from a formal S3-state, attributed to an oxidized amino acid interacting magnetically with the Mn complex in Ca(2+)-deficient PS-II particles, and from S2 modified by the replacement of Ca2+ by Sr2+. Neither of these signals has been previously reported in cyanobacteria. Their detection under these conditions indicates a similar lesion caused by Ca2+ depletion in both plants and cyanobacteria. The protocol has also been applied to mutants which have site-specific changes in PS-II. Data are presented on mutants having changes on the electron donor (Y160F) and electron acceptor (G215W) side of the D2 polypeptide.

Chlorophyll↗
PubMed1991

Cloning of the psbK gene from Synechocystis sp. PCC 6803 and characterization of photosystem II in mutants lacking PSII-K.

We cloned and sequenced the psbK gene, coding for a small photosystem II component (PSII-K), from the transformable cyanobacterium, Synechocystis sp. PCC 6803, and determined the N-terminal sequence of mature PSII-K. The psbK gene product is processed by cleaving off eight amino acid residues from the N terminus. A mutant lacking psbK was constructed; this mutant grew photoautotrophically, but its growth rate was reduced. The number of photosystem II reaction centers on a chlorophyll basis was decreased by less than a factor of 2 in the psbK-deletion mutant. In Synechocystis sp. PCC 6803, the psbK gene is transcribed as a single gene and is not part of an operon. Single-site mutations were introduced into psbK leading to early termination or deletion of the presequence. The phenotype of these mutants strongly resembles that of the psbK deletion mutant, indicating that indeed the change in phenotype in the deletion mutant is directly correlated with PSII-K. PSII-K is not essential for photosystem II assembly or activity but is needed for optimal photosystem II function.

Amino Acid Sequence↗
PubMed1990

A comparison of smoking patterns in the People's Republic of China with the United States. An impending health catastrophe in the middle kingdom.

Half of the global increase in tobacco use from 1976 to 1986 occurred in the People's Republic of China. In 1984, the first national smoking survey was conducted in China, involving over a half-million subjects. Sixty-one percent of Chinese males over age 15 smoke, with higher rates in all occupational groups than for corresponding groups in the United States. Current smoking patterns in China are similar to those in the United States during the 1950s, and these patterns forecast a steadily increasing epidemic of smoking-related deaths. It is estimated that by 2025, two million Chinese men will die annually from smoking. Foreign tobacco companies are mounting massive production and advertising campaigns in China. Government health education programs lack funds to counter these influences with sustained and comprehensive educational and interventional campaigns. To avert an impending national health catastrophe, China must launch a comprehensive smoking-control initiative aimed at public education, cessation, and legislation and policy.

Adolescent↗
PubMedDate not supplied

Costs of polio immunization days in China: implications for mass immunization campaign strategies.

Ten provinces of China were selected to estimate the cost per immunization of the 1994-95 national immunization days (NIDs) at five levels (e.g. province, prefecture, county, township and village). Personnel costs accounted for the largest overall share of costs (39 per cent), followed by publicity and promotion costs (27 per cent), and logistic costs (15 per cent). Without consideration of vaccine costs, the major part of NID expenses were shouldered at the township level, which paid for 47 per cent of all incremental costs, while county and village level covered 28 per cent and 18 per cent respectively. Estimation of average costs per immunization was 2.86 RMB yuan, or $0.34, including vaccine costs, buildings and equipment amortization and salaries at all levels. The factors affecting average cost of NID included the output volume, socio-economic development and geographic features. Various approaches were recommended: to intensify the productivity of time and staff, to employ alternative inexpensive manpower resources, to make the best use of publicity and social promotion, the expansion of the age groups and utilization of multi-intervention strategies. Good planning at township level was a decisive factor to ensure an effective NID conducted in an efficient manner. The average cost of China's NID was the lowest among all mass immunization campaigns ever documented. Much of the reduced average cost was attributable to economies of scale.

Catchment Area, Health↗
PubMedDate not supplied

Evidence for in the appearance of mRNAs of nucleotide excision repair genes, in human ovarian cancer tissues.

Nucleotide excision repair (NER) is the DNA repair pathway through which cisplatin-DNA intrastrand adduct is repaired. Clinical studies have shown that increased mRNA expression of selected genes involved in the rate-limiting step of NER, appear to be closely associated with clinical resistance to platinum agents. These specific studies have led to the possibility of an assessment of the order in which, the appearance of mRNAs of selected NER genes may occur. Included in this assessment are ERCC1, XPB, CSB, and XPA, studied in 28 ovarian cancer tumor tissue specimens. The study of these four genes, in pairs, from 28 ovarian cancer specimens, results in 168 separate observations. Based on the mRNA expression patterns of these genes in these tissues, it is suggested that ERCC1 mRNA may appear before the mRNA of any of the other genes, in an obligate fashion. This is followed by XPB mRNA; which appears before the mRNA of XPA; which in turn, may appear before CSB. This pattern is consistent with what we have reported previously, in non-malignant human bone marrow specimens from a cohort of 52 patients.

Adenocarcinoma↗
PubMedDate not supplied

Association between the level of ERCC-1 expression and the repair of cisplatin-induced DNA damage in human ovarian cancer cells.

Nucleotide excision repair (NER) is responsible for the repair of platinum-DNA lesions. ERCC-1 is a critical gene within the NER pathway, and cells without a functional ERCC-1 do not repair cisplatin-caused DNA damage. The present study was therefore designed to evaluate the relationship between the expression of ERCC-1 and the repair of cisplatin-induced DNA adducts in human ovarian cancer cells in vitro. One hour exposure of MCAS cells to cisplatin yielded an approximately two-fold increment in the levels of ERCC-1 mRNA and ERCC-1 protein, as determined, respectively, by Northern and Western blottings. In addition, nuclear run-on assay showed that ERCC-1 gene transcription rate was increased to about the same extent as steady-state ERCC-1 mRNA and protein, in response to cisplatin treatment. However, the levels of ERCC-1 mRNA, ERCC-1 protein, and ERCC-1 transcript in MCAS cells are two-fold lower than those in A2780/CP70 cells, as previously reported. Furthermore, the repair of cisplatin-DNA adducts in MCAS cells, as measured by atomic absorption spectrometry, is also nearly two-fold less than that in A2780/CP70 cells, indicating a strong association between the level of ERCC-1 expression and the activity of excision repair in these two human ovarian tumor cell lines. These results suggest that ERCC-1 may be a useful marker to monitor the repair of platinum-DNA damage in tumor cells, and further highlight that potential pharmacological approaches which specifically inhibit ERCC-1 expression may increase cellular sensitivity to cisplatin.

Cell Nucleus↗
PubMedDate not supplied

Tumor necrosis factor-alpha-based gene therapy enhances radiation cytotoxicity in human prostate cancer.

The purpose of the present study was to determine the therapeutic potential of combining radiotherapy with tumor necrosis factor (TNF)-alpha-based gene therapy in the human prostate cancer PC-3 xenograft. PC-3 cells are highly resistant to TNF-alpha-induced cytotoxicity in vitro. A modest enhancement of radiation killing was observed with the addition of TNF-alpha in clonogenic survival assays. Combined treatment with Ad.Egr-TNF, a replication-deficient adenovirus modified to express TNF-alpha following the exposure of infected cells to ionizing radiation (40 Gy administered at 5 Gy per fraction) in vivo, resulted in increased tumor control, as defined by a reduction of tumor volume, when compared with treatment with Ad.Egr-TNF alone or with radiation alone (P < .03). The improvement in tumor control was achieved without increasing acute normal tissue damage when compared with tissue injury from radiation alone. The results of these studies support further development and clinical application of genetic radiotherapy for human prostate cancer.

Adenoviridae↗