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PubMed2006

Fred Hollows lecture: hypertensive retinopathy - a journey from fundoscopy to digital imaging.

Hypertensive retinopathy refers to a spectrum of retinal microvascular signs that develop in response to elevated blood pressure. These signs are broadly divided into localized signs (focal retinal arteriolar narrowing, arteriovenous nicking, retinal haemorrhages, cotton wool spots, hard exudates and microaneurysms) and diffuse signs (generalized retinal arteriolar narrowing, arterial wall opacification and optic disc oedema). Although their association with systemic morbidity was recognized more than a century ago, the prognostic significance of hypertensive retinopathy has not received much attention. In large part, this is because clinical assessment of hypertensive retinopathy signs with the direct fundoscopy has proven imprecise. Data from large population-based studies in the past decade, using retinal photographic methods to define hypertensive retinopathy signs, have provided new insights into the epidemiology, systemic associations and clinical significance of hypertensive retinopathy. These studies show that hypertensive retinopathy signs are common (up to 14% of adults aged 40 years and older, even in those without clinical diabetes or hypertension) and are strongly associated with blood pressure. Various retinopathy signs predict the risk of stroke, congestive heart failure and cardiovascular mortality, independent of blood pressure and other risk factors. These data suggest that patients with hypertensive retinopathy signs may benefit from a careful cardiovascular evaluation, and appropriate risk reduction therapy if indicated. Future advances in digital retinal imaging technology will allow researchers and clinicians to better chart and monitor the vascular effects of hypertension.

Humans↗
PubMed2006

The Gordon Gordon-Taylor Memorial Lecture: surgical giants and giants among surgeons--the case of Abraham Colles.

Sir Gordon Gordon-Taylor was a surgical giant and a giant among surgeons. There's a distinction between the two. Surgical giants are technical geniuses who pave the way for others and set the standards against which others can measure their performance. Giants among surgeons contribute other things to the science and practice of surgery and sometimes to fields outside surgery. By these measures, Abraham Colles was not a surgical giant. He thought, wrote and taught about his interests. He enhanced the reputation of Irish surgery. In retrospect, his science and his ethics seem flawed by modern standards, but by the measures of his own time he was a model investigator and a man of outstanding moral probity. He is remembered for the eponymous Colles's fracture and for Colles's fascia and ligament. He held the Chair of Anatomy and Surgery in Dublin for 32 years and drew the admiration and affection of his contemporaries, colleagues and students. He was a giant among surgeons, and his name deserves commemoration.

Anatomy↗
PubMed2001

Chien-Tien Hsu Memorial Lecture. Fertility and gynaecologic malignancies.

Fertility and gynaecological malignancies have an important relationship. A clear inverse relationship exists between family size and the incidence of ovarian and endometrial cancer. Current methods of fertility control have an influence on subsequent development of various gynaecological malignancies. A slightly increased risk of breast cancer has been reported in current users and those who had used hormonal contraceptives (OCs) within 10 years; this risk declined with time and disappeared after 10 years. Women who started OC before age 20 had a higher relative risk; the disease did not spread beyond the breast in the majority. Most studies found OC to reduce the risk of ovarian and endometrial cancer. The relative risks of squamous cell carcinoma and adenomatous carcinoma of the cervix have been reported to be 1.3 and 1.5, respectively in ever-users of OCs; however, the aetiology of cervical cancer is multifactoral. Several reports suggest the beneficial effect of tubal ligation and breast feeding in reducing the risk of ovarian cancer. Therapy of gynaecological malignancies may have an influence on subsequent fertility. Amenorrhoea developing after treatment of hydatidiform mole may be due to choriocarcinoma, recurrent mole or a normal pregnancy. Choriocarcinoma can also develop after a partial mole. The risk of fetal teratogenicity from chemotherapy is present only if conception occurs during or immediately following the treatment cycles. Fertility is not impaired following chemotherapy. Successful pregnancies have occurred in women who have had widespread GTD including cerebral metastases. In the young patient with gynaecological malignancy preservation of fertility is possible. Fertility-sparing surgery may be safe in early ovarian epithelial cancers and even in advanced germ cell tumours. Recently, the fertility-sparing surgery of radical trachelectomy and pelvic lymphadenectomy has been carried out for early invasive cervical cancer in young women. Gynaecological cancer occurring in pregnancy is uncommon; it presents the clinician with a difficult situation to manage. In most instances the cancer is treated as though the patient is not pregnant; the timing and mode of delivery needs individualization. The overall prognosis for breast cancer complicating pregnancy is poor. Survival in cervical cancers diagnosed antepartum is similar to the non-pregnant patient. Ovarian cancer in pregnancy has a good prognosis because of the early stage at diagnosis.

Breast Neoplasms↗
PubMed2002

Wellcome Prize Lecture. Cell surface, ion-sensing receptors.

Changes in extracellular calcium (Ca(2+)o) concentration ([Ca2+]o) affect kidney function both under basal and hormone-stimulated conditions. The molecular identification of an extracellular Ca(2+)-sensing receptor (CaR) has confirmed a direct role of Ca(2+)o on parathyroid and kidney function (i.e. independent of calciotropic hormones) as a modulator of Ca2+ homeostasis. In addition, evidence accumulated over the last 10 years has shown that CaR is also expressed in regions outside the calcium homeostatic system where its role is largely undefined but seems to be linked to regulation of local ionic homeostasis. The parathyroid and kidney CaRs are 1081 and 1079 amino acids long, respectively, and belong to the type III family of G protein-coupled receptors (GPCRs), which includes other CaRs, metabotropic glutamate receptors and putative vomeronasal organ receptors. For the CaR, its low (millimolar) affinity for Ca2+, its positive cooperativity and its large ion-sensing extracellular domain, indicate that the receptor is more sensitive to changes in net cationic charge rather than to a specific ligand. Mg2+, trivalent cations of the lanthanide series and polyvalent cations such as spermine and aminoglycoside antibiotics can all activate the receptor in vitro with EC50 values in the micromolar range for trivalent and polyvalent cations or in the millimolar range for Ca2+ and Mg2+. In addition to true CaR agonists, CaR sensitivity to Ca(2+)o is also susceptible to allosteric modulation by ionic strength, L-amino acids and by pharmacological agents. This review will address endogenous and exogenous CaR agonists, the role of the receptor in the calcium homeostatic system and some speculation on possible role(s) of the CaR in regions not involved in mineral ion homeostasis.

Awards and Prizes↗
PubMed2002

The G. L. Brown Prize Lecture. Hypoxic regulation of ion channel function and expression.

Acute hypoxia regulates the activity of specific ion channels in a rapid and reversible manner. Such effects underlie appropriate cellular responses to hypoxia which are designed to initiate cardiorespiratory reflexes and contribute importantly to other tissue responses, all of which are designed to improve tissue O2 supply. These responses include excitation of chemoreceptors as well as pulmonary vasoconstriction and systemic vasodilatation. However, such responses may also contribute to the adverse responses to hypoxia, such as excitotoxicity in the central nervous system. Whilst numerous ion channel types are known to be modulated by acute hypoxia, the nature of the O2 sensor in most tissues remains to be identified. Prolonged (chronic) hypoxia regulates functional expression of ion channels, and so remodels excitability of various cell types. Whilst this may contribute to adaptive responses such as high-altitude acclimatization, such altered channel expression may also contribute to the onset of pathological disorders, including Alzheimer's disease. Indeed, evidence is emerging that production of pathological peptides associated with Alzheimer's disease is increased during prolonged hypoxia. Such effects may account for the known increased incidence of this disease in patients who have previously endured hypoxic episodes, such as congestive heart failure and stroke. Identification of the mechanisms coupling hypoxia to the increased production of these peptides is likely to be of therapeutic benefit.

Animals↗
PubMed1996

The Emanuel Miller Memorial Lecture 1995. Children's relationships: bridging the divide between cognitive and social development.

Recent research that bridges the divide between cognitive and social development in early childhood illuminates, but also sets challenges, for both fields. The implications of recent studies of children's social interactions for research on cognitive development--in particular, the development of understanding mind and emotion--are considered, then the implications of new cognitive research for understanding social development are discussed. An example of longitudinal research on children's relationships with family and friends between 2 and 7 years is described, highlighting links between individual differences in cognitive and social development.

Awareness↗
PubMed1997

The Emanuel Miller Memorial Lecture 1994. Depressive disorders in childhood: an impressionistic landscape.

To convey an impressionistic landscape of depressive disorders in childhood, studies of clinically referred and diagnosed patients as well as community samples, and data from experimental investigations are used to consider five questions: Are depressive syndromes morbid states in childhood? Should we be concerned about depression in childhood? How do very early-onset depressions arise? What happens to depressed children as they grow up? And how can we help youngsters who suffer from depression? The information is discussed with respect to its implications for the management of clinically depressed children, as well as the prevention of very early-onset depressive disorders.

Adolescent↗
PubMed2006

The Emanuel Miller Memorial Lecture 2006: adoption as intervention. Meta-analytic evidence for massive catch-up and plasticity in physical, socio-emotional, and cognitive development.

BACKGROUND: Adopted children have been said to be difficult children, scarred by their past experiences in maltreating families or neglecting orphanages, or by genetic or pre- and perinatal problems. Is (domestic or international) adoption an effective intervention in the developmental domains of physical growth, attachment security, cognitive development and school achievement, self-esteem, and behaviour problems? METHOD: Through a series of meta-analyses on more than 270 studies that include more than 230,000 adopted and non-adopted children and their parents an adoption catch-up model was tested. RESULTS: Although catch-up with current peers was incomplete in some developmental domains (in particular, physical growth and attachment), adopted children largely outperformed their peers left behind. Adoptions before 12 months of age were associated with more complete catch-up than later adoptions for height, attachment, and school achievement. International adoptions did not lead to lower rates of catch-up than domestic adoptions in most developmental domains. CONCLUSIONS: It is concluded that adoption is an effective intervention leading to massive catch-up. Domestic and international adoptions can be justified on ethical grounds if no other solutions are available. Humans are adapted to adopt, and adoption demonstrates the plasticity of child development.

Achievement↗
PubMed1996

The 1996 RSA Distinguished Research Award Lecture. A genetic animal model of alcohol withdrawal.

Work with genetic animal models has a long history in alcohol research. No attempt has been made here to acknowledge the contributions of the many other long-standing projects in the area. Rather, I have tried to give a capsule view of one such project, and to indicate some areas of future direction. It seems clear that the expression of molecular biological tools will greatly expand our capabilities in the immediate future. The field is well-situated to take advantage of this situation, as it has achieved much progress during the "dark ages," where the study of genetic influence was inferential: that is, we were limited to studying genes we could not identify. The future will surely lead us to the identification and study of specific genes of importance.

Alcohol Withdrawal Delirium↗
PubMed1996

Long reflections on the QT interval: the sixth annual Gordon K. Moe Lecture.

This review of accumulated knowledge about the long QT syndromes begins with an iteration of the original papers and then proceeds to a broader historic reflection that includes my personal work as well as many studies by others. Next come reflections upon the current status of knowledge on the subject, combined with comments about remaining challenges and questions grouped as follows: (1) morphologic abnormalities of the cardiac conduction system and their pathophysiologic significance in the long QT syndromes; (2) cardioneuropathy in the pathogenesis of long QT syndromes; (3) variability of QT prolongation, including consideration of peripheral and central dysautonomic conditions with certain diagnostic and therapeutic implications; (4) some caveats about the popular use of left cervical sympathectomy to treat symptomatic individuals with long QT syndrome, emphasizing hazards for future electrical instability of the heart; (5) consideration of genetic influences in the long QT syndromes, a field holding great promise as well as fraught with many puzzling dilemmas; and (6) apoptosis and the pathogenesis of the long QT syndromes, based upon personal observations previously made with electron microscopic studies of the sinus node and now including new immunohistochemical evidence expanding the relevance of this novel view-point. These intentionally provocative presentations are made to stimulate physicians and other scientists to consider these several different perspectives in planning future studies aimed at better understanding of one of the most challenging medical entities facing cardiology today.

Apoptosis↗