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Biomedical subjects

R J Daly

Publications and source records attributed to R J Daly.

At least 55 records · Page 3Linked to original sources
PubMed1991

Ability of Anopheles gambiae mosquitoes to transmit malaria during the dry and wet seasons in an area of irrigated rice cultivation in The Gambia.

The seasonality of malaria transmission was studied in a Gambian village situated in an area where rice was cultivated. Observations were made during two dry seasons, when pump-fed irrigation was used to grow rice, and in the intervening rainy season, when rice was cultivated using a combination of irrigated and rain-fed paddies. Clinical episodes of malaria were mainly confined to the months during and soon after the rainy season. In the wet season the prevalence of parasitaemia was higher in febrile subjects than in afebrile controls but the reverse applied during the dry seasons. However, the biting rates of Anopheles gambiae complex mosquitoes in the two dry seasons (2.5 and 0.8 bites/child/night respectively) were greater than or similar to that in the rainy season (0.6 bites/child/night). The proportion of human bloodmeals (0.53 vs 0.75) and the survival of mosquitoes (parity rates of 0.41 vs 0.58) were both lower in the dry seasons than in the rains. The low prevalence of morbidity due to malaria in the dry season and the observed fall in the sporozoite rate may therefore have been due to a reduction in the vectorial capacity of the An. gambiae population. However, reduced transmission in the dry season may also have been due to the direct effect of high temperatures on the parasite in the vector.

Age Factors↗
PubMed1990

Transition of human breast cancer cells from an oestrogen responsive to unresponsive state.

An in vitro model system is described for studying the problem of loss of steroid sensitivity in breast cancer cells. Growth of cloned oestrogen-sensitive human breast cancer cells in the long-term absence of steroid gives rise to a population of oestrogen-insensitive cells. In ZR-75-1 cells, the effect is clonal but occurs at high frequency suggesting a mechanism affecting a wide proportion of the cell population synchronously. This does not involve any reduction in oestrogen receptor number. Furthermore, there is no coordinated loss of oestrogen-sensitive molecular markers, showing that oestrogen receptors remain not only present but functional. These growth changes are not accompanied by any loss of growth inhibition by antioestrogen. Although steroid deprivation does not result in loss of oestrogen-sensitive markers, this does not hold true for other steroids. There was a reduction in progestin, androgen and glucocorticoid regulation on transfected LTRs. Loss of steroid-sensitive growth was accompanied by changes in response to exogenous growth factors and altered endogenous growth factor mRNA production. Steroid-deprived T-47-D cells acquire sensitivity to stimulation by TGF beta and have raised TGF beta 1 and TGF beta 2 mRNA levels. ZR-75-1 cells are growth inhibited by TGF beta and have reduced TGF beta 1 mRNA levels. In MCF-7 cells, increased IGFII mRNA, following transfection, can result in an increased basal cell growth rate in the absence of steroid. These findings are discussed in relation to possible autocrine mechanisms in the loss of steroid sensitivity of breast cancer cells.

Breast Neoplasms↗
PubMed1990

Cellular and molecular events in loss of estrogen sensitivity in ZR-75-1 and T-47-D human breast cancer cells.

When deprived of steroid in the long term, both estrogen-dependent (ZR-75-1) and estrogen-responsive (T-47-D) human breast cancer cells lose estrogen regulation of cell growth in a reproducible time course using both stock lines and recloned cells. The estrogen-stimulated growth rate was unaffected by such treatment, but there was an increase in the basal growth rate without steroid. For ZR-75-1 cells, the effects are clonal but occur at high frequency (1 in 1000 cells) and synchronously between clones, suggesting a phenotypic mechanism. These changes in cell growth occur without any coordinated loss of estrogen sensitivity of molecular markers (pS2 mRNA, progesterone receptor protein) showing that functional estrogen receptors remain present throughout. The constitutive expression of progesterone receptor in one clone of steroid-deprived ZR-75-1 cells does suggest, however, that alterations in expression of individual estrogen-sensitive genes can occur. Loss of estrogen-stimulated growth was not accompanied by loss of growth inhibition by antiestrogen, and the latter effect remained reversible by estradiol. In an attempt to understand the molecular mechanisms underlying the loss of steroid sensitivity in the two cell lines, growth factor gene expression was investigated. Progression to steroid autonomy in T-47-D cells was accompanied by an upregulation of transforming growth factor (TGF) alpha, TGF beta 1, and TGF beta 2 mRNA. However, TGF beta 1 mRNA was downregulated in two ZR-75-1 steroid-deprived clones. These findings are discussed in relation to possible autocrine mechanisms in the loss of steroid sensitivity of breast cancer cells.

Breast Neoplasms↗
PubMed1990

Interaction of growth factors during progression towards steroid independence in T-47-D human breast cancer cells.

When deprived of steroid in the long term, T-47-D human breast cancer cells lose estrogen sensitivity of cell growth. This loss of response results from an increased basal growth rate in the absence of steroid, not from a loss of estrogen-stimulated growth, and it occurs without any loss of estrogen receptor number or function. Growth factor gene expression and sensitivity have been investigated in this model system in an attempt to unravel the molecular mechanisms underlying the progression to steroid autonomy. The transition was accompanied by a decreased dependence on added serum and by a loss of the stimulatory effects of insulin and basic fibroblast growth factor, but also by an acquired sensitivity to stimulation by transforming growth factor-beta (TGF-beta). An increase in TGF-beta 1 mRNA was detected following loss of steroid sensitivity. There was no increase in epidermal growth factor (EGF) receptor number. These findings are discussed in relation to current knowledge concerning the mechanisms by which estrogens stimulate breast cancer cell proliferation.

Blotting, Northern↗
PubMed1989

Approaches to studying the role of growth factors in the progression of breast tumours from the steroid sensitive to insensitive state.

Progression from steroid sensitive to autonomous proliferation can be modelled in several cultured mammary tumour cell lines by long-term withdrawal of steroids. A feature of all the four systems studied thus far is that the basal growth in the absence of steroid increases with duration of steroid withdrawal until it reaches that obtained in the presence of steroid. It cannot be assumed that the increased proliferation in the absence of steroid is modulated by the same pathways as those stimulated by steroids in sensitive cells. Therefore, we feel that mechanisms of progression can best be studied via cell behaviour in the absence of steroid. With both the mouse S115 and human T-47-D systems, changes in sensitivity to several growth factors accompany progression; responses to TGF beta 1 are of particular interest in the T-47-D cells where this growth factor becomes stimulatory in the steroid insensitive state. This is accompanied by upregulation of TGF beta 1 mRNA. This upregulation of TGF beta agrees with the finding that ER - PR - primary human breast tumours contain more TGF beta 1 than do ER + PR + tumours; TGF alpha has the opposite pattern. Furthermore, only 40 and 30 kDa TGF beta species have been detected within cultured cells and primary tumours; TGF alpha exists in a 30 kDa form. The functions of these large forms of TGF alpha and TGF beta are unclear. Our conclusions from these experiments is that the increased proliferation in the absence of steroid accompanying progression may not be mediated by the same pathways as those perturbed by steroids in sensitive cells. Furthermore, TGF beta 1 may have different effects in steroid responsive and unresponsive cells.

Animals↗
PubMed1988

Effects of oestrogen on the expression of a 4.4 kb mRNA in the ZR-75-1 human breast cancer cell line.

A cDNA library has been constructed from the poly(A)+ mRNA of oestrogen-stimulated ZR-75-1 human breast cancer cells. Screening by differential hybridization has identified eight clones which are stimulated between 4- and 16-fold by oestrogen. Two clones (pLIV-1) that are stimulated 4-fold, hybridize to three different mRNA species. A further five recombinants encode for a mRNA 600 bp long which is induced greater than 16-fold and have been shown to cross-hybridize to the oestrogen-responsive clone, pS2, isolated from the MCF-7 breast cancer cell line. Oestradiol was shown to be without detectable effect upon the expression of mRNA for dihydrofolate reductase, which is reported to be oestrogen regulated in MCF-7 cells. Actin gene expression is also unresponsive to oestradiol in ZR-75-1 cells. These results suggest that pLIV-1 represents a previously unidentified mRNA that may be involved in the oestrogen-regulated growth of ZR-75-1 human breast cancer cells.

Breast Neoplasms↗
PubMed1987

Interpersonal problem-solving deficits in self-poisoning patients.

Self-poisoning patients (n = 40) were compared with psychiatric patients (n = 40) and nonpatient controls (n = 20) on measures of interpersonal problem-solving skills and locus of control in an effort to determine the importance of these cognitive and personality variables in self-poisoning behavior. The psychiatric and self-poisoning groups showed deficits on measures assessing interpersonal problem solving when compared with nonpatient controls. The self-poisoning group performed below the level of the psychiatric patients on all except one test, on which they performed at the level of the psychiatric group. Locus of control did not differentiate self-poisoning patients from nonpatient controls, and it was concluded that this variable is not an important factor in self-poisoning behavior.

Adolescent↗
PubMed1987

Plasma levels of beta-endorphin in depressed patients with and without pain.

We studied 27 patients who complained of pain, for which no organic basis could be found, and 11 patients without pain. All patients were depressed according to clinical diagnosis and Beck Depression Inventory (BDI) scores. Plasma beta-endorphin levels were found not to differ between the two groups or across other variables. The patients who complained of pain had significantly higher scores on the BDI.

Adolescent↗
PubMed1986

Liaison psychiatry in an Irish hospital: a survey of a year's experience.

A brief summary of the pattern of mental illness in Ireland is given and the work of a psychiatric consultation-liaison service in a general hospital in the southern part of the country is discussed in this context. The referral rates to the service mirror the referral rates in the United Kingdom more than those in the United States. The high rates of alcoholism and functional psychosis found in referred patients probably reflect the increased prevalence of these conditions in the general community. In Ireland, as elsewhere, the rate of referral of general hospital inpatients to a psychiatric consultation-liaison service is below the rate of psychiatric illness found in hospital inpatients.

Adult↗
PubMed1983

Samuel Pepys and post-traumatic stress disorder.

Samuel Pepys's diary allows us an opportunity to see how a man of acknowledged ability and stability coped with the severe psychological trauma of being involved in the Great Fire of London in 1666. His self-monitoring provides an excellent record of the development of post-traumatic stress disorder and an account of his coping behaviour. Despite being one of the newest categories of mental disorder in the official nomenclature, post-traumatic stress disorder has obviously had a long existence.

Fires↗
PubMed1970

Reported sleep on maintenance haemodialysis.

Subjective estimates of sleep in patients undergoing maintenance haemodialysis at home showed significant differences between dialysis nights and other nights; both patients and spouses lost sleep on dialysis nights. The sleep debt thus accumulated was not so well repaid in spouses as in patients. No pronounced differences were found between sleep on various forms of maintenance haemodialysis, and sleep did not show a consistent change over the three days between dialyses. The findings are interpreted as indicating the importance of functional rather than physical causes of insomnia in dialysis patients.

Family↗