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Biomedical subjects

D Henley

Publications and source records attributed to D Henley.

11 recordsLinked to original sources
PubMed2006

Paclitaxel induced apoptosis in breast cancer cells requires cell cycle transit but not Cdc2 activity.

PURPOSE: Paclitaxel (PTX) is a widely used chemotherapy agent and may cause cell death by apoptosis subsequent to microtubule (MT) disruption. In this paper, we have investigated whether cell cycle transit and or Cdc2 (Cdk1) activity is required for the apoptosis induced by PTX. METHODS: Cell cycle was analyzed by flow cytometry, Cdc2 was assayed bio chemically. Cdc2 activity was decreased by siRNA and dominant negative (dn) Cdc2 expression. Cells were arrested by chemical or biological inhibitors in a G1 or S phase. Apoptosis was measured by DNA fragmentation and examination of nuclei by microscopy. JNK and AKT activations were assessed as well. RESULTS: Cell cycle inhibition was highly effective in decreasing PTX induced apoptosis. MT morphology was not altered by these inhibitors. PTX induced JNK activity or AKT mediated BAD phosphorylation was unaffected by cell cycle inhibitors. Abrogation of Cdc 2 activity was without effect on PTX induced apoptosis. CONCLUSIONS: While cell cycle transit is required for PTX induced apoptosis; Cdc2 activity is not required.

Antineoplastic Agents, Phytogenic↗
PubMed2005

Symptomatic hypocalcaemia and renal impairment associated with bisphosphonate treatment in patients with multiple myeloma.

We report three cases of severe hypocalcaemia associated with i.v. bisphosphonate treatment in patients with multiple myeloma. All patients had symptomatic hypocalcaemia, including a tonic-clonic seizure and tachyarrhythmia in one case. Two cases were associated with the development of acute renal failure, whereas the third patient had pre-existing renal impairment. We recommend that bisphosphonates be used with caution in patients with myeloma and renal impairment, that vitamin D deficiency be corrected prior to treatment (to reduce the risk of hypocalcaemia) and that serum calcium and renal function be monitored during treatment.

Acute Kidney Injury↗
PubMed2001

Malaria past and present: the case of North Sulawesi, Indonesia.

The incidence and impact of malaria in North Sulawesi have declined both in the short term during the 1990s, and over a much longer timespan (though perhaps less continuously) since the end of the colonial period. The improvement already seems to have been well underway before deliberate vector control activities became extensive in the second half of the 1970s, and environmental changes affecting the Anopheles mosquito fauna, in particular the replacement of primary and secondary forest by permanent farmland, are probably the principal reasons for the long-term trend; other possible factors include the increasing use of antimalarial drugs. The well-documented decline in malaria incidence over the years 1991-1997, nevertheless, probably reflects the unprecedented scale of residual insecticide spraying in the province during that period, while the slight resurgence of the disease in the last three years corresponds to the subsequent cessation of house spraying as a result of the current economic crisis. Despite the evident importance of environmental change as a factor ameliorating the malaria situation in the long term, experience from the colonial era suggests that the prospects for deliberate environmental management (species sanitation) as an alternative malaria control strategy are poor.

Animals↗
PubMed1997

Estrogenic and DNA-damaging activity of Red No. 3 in human breast cancer cells.

Exposure to pesticides, dyes, and pollutants that mimic the growth promoting effects of estrogen may cause breast cancer. The pesticide DDT and the food colorant Red No. 3 were found to increase the growth of HTB 133 but not estrogen receptor (ER) negative human breast cells (HTB 125) or rat liver epithelial cells (RLE). Red No. 3, beta-estradiol, and DDT increase ER site-specific DNA binding to the estrogen response element in HTB 133 cells and increase cyclin-dependent kinase 2 activity in MCF-7 breast cancer cells. Site-specific DNA binding by p53 in RLE, HTB 125, HTB 133, and MCF-7 cells was increased when they were treated with Red No. 3, which suggests that cellular DNA was damaged by this colorant. Red No. 3 increased binding of the ER from MCF-7 cells to the estrogen-responsive element. Consumption of Red No. 3, which has estrogenlike growth stimulatory properties and may be genotoxic, could be a significant risk factor in human breast carcinogenesis.

Animals↗
PubMed1996

Carcinogenic potential of benzene and toluene when evaluated using cyclin-dependent kinase activation and p53-DNA binding.

Benzene is carcinogenic, whereas toluene is thought to have little carcinogenic potential. Benzene and toluene were found to activate cyclin-dependent kinase 2 in rat liver epithelial (RLE) and HL60 cells. pRb105 was hyperphosphorylated in RLE cells treated with either solvent. Kinase activation and subsequent hyperphosphorylation of pRb105 and p53 by benzene or toluene may be responsible for their growth promotional effects, but it does not account for increased potential of benzene to induce cancer. Therefore, we examined the ability of these solvents to increase p53-DNA site-specific binding in RLE cells. Benzene increased p53-DNA site-specific DNA binding in RLE cells compared to control levels or the effects of toluene. Increased p53-DNA site-specific binding by benzene may be caused by damage to cellular DNA. If so, although both solvents appear to have promotional activity, the increased potential of benzene to damage DNA may be responsible to the difference in the ability of benzene to cause cancer.

Animals↗
PubMed1996

Effects of 60-Hz fields, estradiol and xenoestrogens on human breast cancer cells.

If exposure to xenoestrogens or electromagnetic fields (EMFs) such as 60 Hz contributes to the etiology of breast cancer, it is likely that they must stimulate the growth of breast cells, damage genetic material or enhance the effects of other mitogenic or mutagenic agents (co-promotion). Therefore, the ability of xenoestrogens or exposure to 60-Hz fields to stimulate the entry of growth-arrested human breast cancer cells into the cell cycle was determined using cyclin-dependent kinase 2 (Cdk2) activity, synthesis of cyclin D1 and cdc2 activity. Exposure of estrogen receptor-positive MCF-7 or T-47D cells to estrogen and xenoestrogens (DDT and Red No. 3) increased Cdk2 and cyclin B1-cdc2 activity and cyclin D1 synthesis. Exposure of breast cancer cells to 12 mG or 1 or 9 G electromagnetic fields at 60 Hz failed to stimulate Cdk2 or cyclin B1-cdc2 activity or cyclin D1 synthesis. Simultaneous co-exposure of cells to 60-Hz fields and chemical promoters did not enhance Cdk2 activation above the levels produced by the chemical promoter alone. Estrogen and xenoestrogens also stimulated binding of the estrogen receptor to the estrogen receptor element but the EMF did not. Phorbol 12-myristate 13-acetate (PMA) induced phosphorylation of p53 and pRb1O5 in MCF-7 cells, but EMF exposure had no effect. DNA-damaging chemotherapeutic agents and Red Dye No. 3 were found to increase p53 site-specific DNA binding in breast cancer cells, but EMF exposure did not. Differential display analysis failed to detect any effect of EMF exposure on gene expression in MCF-7 cells, whereas the effects of estradiol were detected. These studies suggest that estrogen and xenoestrogens stimulate growth-arrested breast cancer cells to enter the growth cycle, but EMF exposure does not. Site-specific p53-DNA binding was increased in MC F-7 cells treated with DNA-damaging agents, but not by EMF exposure. EMF exposure does not appear to act as a promoter or DNA-damaging agent for human breast cancer cells in vitro.

Base Sequence↗
PubMed1982

Measles encephalopathy during immunosuppression: failure of interferon treatment.

Measles encephalopathy during immunosuppression (MEI) occurs in patients with immunologic defects and is fatal. The course of the disease in 2 children, 4 and 5 years old, in the remission phase of acute lymphatic leukemia is presented. Diagnosis was possible, post-mortem, by recognition of measles virus antigen in brain tissue and in one patient by demonstration of intrathecal production of measles antibodies. Treatment with interferon did not improve the condition. Preventive measures primarily by early immunization of the childhood population against measles is stressed.

Antibodies, Viral↗
PubMed1977

Psychometric modeling of consumer decisions in primary health care.

A psychometric technique, functional measurement, was used to measure the preferences of 77 persons for hypothetical health care providers identified by various levels of cost, travel time, and waiting time; responses were subjected to analysis of variance and graphic analysis to determine the functional relation by which respondents combined the three attributes in arriving at their preferences. Both modes of analysis suggested multiplicative decision models, but these yielded lower values of R2 than did linear models derived for comparison. Respondents were grouped by the proportion of response variance that was explained by each of the three attributes, and decision models were derived for each group. Discriminant analysis of socioeconomic characteristics of the respondents identified the variables that distinguished the groups and contributed to forming their preferences.

Community Participation↗