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PubMed1998

The 18th C.L. Oakley Lecture. Pathogenicity of enteropathogenic Escherichia coli.

Enteropathogenic Escherichia coli (EPEC) remain an important world-wide cause of diarrhoeal disease and mortality of infants and young children. Research programmes around the world have, in recent times, made enormous strides towards a better understanding of EPEC pathogenesis, yielding unique insights into the molecular intercourse between host and pathogen. Recombinant DNA and cell biology techniques have provided powerful tools, giving the first intriguing glimpses of a wealth of bacterial products mediating complex host:pathogen interactions involving the subversion of normal host signalling processes. Much has been discovered since 1945, when E. coli was first implicated as a cause of diarrhoea. However, many questions remain unanswered and many more remain unasked. Much remains to be discovered, especially in the area of molecular interactions between host and pathogen and how they relate to the manifestation of disease in the patient.

Child, Preschool↗
PubMed2003

Richard P. Bunge memorial lecture. Nerve injury and repair--a challenge to the plastic brain.

Repair and reconstruction of major nerve trunks in the upper extremity is a very challenging surgical problem. Today, there is no surgical repair technique that can assure recovery of tactile discrimination in the hand of an adult patient following nerve repair. In contrast, young individuals usually attain a complete recovery of functional sensibility. The outcome from nerve repair depends mainly on central nervous system factors including functional cortical reorganizational processes caused by misdirection in axonal outgrowth. Deafferentation due to local anesthetic block, amputation or nerve transection in the upper extremity leads to very rapid cortical synaptic remodeling, resulting in a distorted cortical hand representation as well as in enlarged and overlapping cortical receptive fields. Sensory relearning programs are aimed at refinement of these receptive fields to normalize the distorted hand map and improve processing at a high-order cortical level in the context of the 'new language spoken by the hand'. As peripheral nerve repair techniques cannot be further refined, there is a need for new and improved strategies for sensory relearning following nerve repair. We propose the utilization of multimodal capacity of the brain, using another sense (hearing) to substitute for lost hand sensation and to provide an alternate sensory input from the hand early after transection. The purpose was to modulate cortical reorganizations due to deafferentation to preserve cortical hand representation. Preliminary results from a prospective clinical randomized study indicate that the use of a Sensor Glove System, which stereophonically transposes the friction sound elicited by active touch, results in improved recovery of tactile discrimination in the nerve-injured hand. Future strategies for treatment of nerve injuries should promote cellular methods to minimize post-traumatic nerve cell death and to improve axonal outgrowth rate and orientation, but high on the agenda are new strategies for refined sensory relearning following nerve repair.

Adolescent↗
PubMed1997

Dohi memorial lecture. Clinical implications of basic research on heritable skin diseases.

Spectacular success has recently been made in understanding the molecular basis of various heritable skin diseases. A prototype of such conditions is epidermolysis bullosa (EB), a heterogenous group of mechano-bullous disorders, characterized by fragility of the skin and other specialized epithelia. The fragility of the skin in EB results from defective attachment of the epidermis to the underlying dermis due to genetic lesions within molecules of the basement membrane zone (BMZ) at the dermal-epidermal junction. Specifically, distinct mutations have been disclosed thus far in ten different genes encoding the macromolecular components of the BMZ, and the combinations and the types of mutations as well as their positions along the altered gene products collectively reflect the phenotypic variability observed in this group of heritable skin diseases. This information has major implications for genetic counseling of families at risk for recurrence of EB in subsequent pregnancies and in future generations. Furthermore, examination of specific mutations in an affected newborn allows prognostication of the severity of the clinical outcome. Finally, mutation analyses have provided the basis to develop DNA-based prenatal testing by chorionic villus sampling or early aminocentesis during the first trimester of gestation. Collectively, the advances on EB exemplify the potential of molecular biology for improved diagnosis and patient care of genetic skin disorders.

Amino Acid Sequence↗
PubMed2002

Dohi Memorial Lecture. New aspects of cutaneous mosaicism.

The concept of cutaneous mosaicism has today been proven at the cellular level in at least fifteen different skin disorders. We can distinguish five different patterns of mosaicism, including the phylloid pattern and the lateralization pattern. Etiologically, cutaneous mosaics can be divided into two large categories, epigenetic mosaicism and genomic mosaicism. All forms of epigenetic mosaicism known so far, including the various patterns of X-inactivation, appear to be caused by the action of retrotransposons. A new concept is functional autosomal mosaicism transmittable through the action of retrotransposons, which has been described in mice and dogs and may explain, for example, the familial occurrence of pigmentary mosaicism along the Blaschko lines in human skin. Among the examples of mosaicism of autosomal lethal mutations, phylloid hypomelanosis is a recently recognized neurocutaneous entity caused by mosaic trisomy 13. Possible examples of a type 2 segmental manifestation now include at least fifteen different autosomally dominant skin disorders. This phenomenon is most frequently found in glomangiomatosis, cutaneous leiomyomatosis, and disseminated superficial actinic porokeratosis. Recently proposed examples of didymosis (twin spotting) include cutis tricolor, paired patches of excessive or absent involvement in Darier disease, and didymosis aplasticosebacea characterized by coexistent aplasia cutis congenita and nevus sebaceus. To the list of possible examples of paradominant inheritance, cutis marmorata telangiectatica congenita and speckled lentiginous nevus syndrome have now been added. Revertant mosaicism giving rise to unaffected skin areas in autosomally recessive cutaneous traits will certainly likewise be recognized more often when clinicians are bearing this concept in mind. Such cases can be taken as examples of "natural gene therapy".

Adolescent↗
PubMed2006

Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.

The risk of venous or arterial thrombosis is routinely assessed by clinical variables (risk factors) supplemented by measurement of blood lipids and glucose for arterial thrombotic events. Haematological tests that might play a role in risk prediction include haemostatic variables, haematocrit and inflammatory markers (erythrocyte sedimentation rate, plasma viscosity, white cell count). Recent epidemiological studies of these phenotypes and related genotypes are reviewed. For the risk prediction of first venous thrombosis, screening for thrombophilias in 'high-risk' situations does not appear clinically effective or cost-effective; with the possible exception of women considering oral hormone replacement therapy. General screening after a first venous event to predict recurrence (or risk in asymptomatic relatives) does not appear effective; with the possible exception of d-dimer, which requires further study. For risk prediction of first arterial thrombosis, screening adds little to prediction by current clinical risk scores. Screening of persons after a first arterial event, or with atrial fibrillation (e.g. with D-dimer for stroke prediction), requires further study. In conclusion, haematological tests have very limited roles in the prediction of cardiovascular risk, and should only be used according to evidence-based guidelines. The need for management studies is highlighted.

Biomarkers↗
PubMed2006

Jacques Benoit Lecture. Information processing in the hypothalamus: peptides and analogue computation.

Peptides in the hypothalamus are not like conventional neurotransmitters; their release is not particularly associated with synapses, and their long half-lives mean that they can diffuse to distant targets. Peptides can act on their cells of origin to facilitate the development of patterned electrical activity, they can act on their neighbours to bind the collective activity of a neural population into a coherent signalling entity, and the co-ordinated population output can transmit waves of peptide secretion that act as a patterned hormonal analogue signal within the brain. At their distant targets, peptides can re-programme neural networks, by effects on gene expression, synaptogenesis, and by functionally rewiring connections by priming activity-dependent release.

Animals↗
PubMed1996

Review. David Oppenheimer Memorial Lecture 1995: Some neuropathological aspects of Alzheimer's disease and its relevance to other disciplines.

Recent studies of diffuse A beta plaques point to the neurons as a source of A beta in diffuse plaques. The neuritic (primitive and classical) plaques appear to be the product of microglia and the myocytes are the source of amyloid deposits in the meningeal and cortical vessels. Dyshoric angiopathy is associated with deposits of amyloid by perivascular cells. Fibrillization of the neuron-derived diffuse, thioflavine-negative or benign plaques is poor or undetectable by current morphological methods including ultrastructural immunocytochemistry. It appears that fibrillization depends on the length of the A beta peptides and on the presence of amyloid-associated proteins. Four genes are now tightly linked with Alzheimer's disease (AD) and they are located on chromosomes 21, 19, 14 and 1. Therefore, AD should be considered a polyaetiological disease or syndrome. There are currently five transgenic mouse models overexpressing beta-APP. There is also a myocyte tissue culture model in which both soluble and fibrillized A beta are found. The relationship between A beta and neurofibrillary pathology is not clear and the current cascade hypothesis proposing that A beta pathology drives the formulation of neurofibrillary tangles is being questioned. There is growing evidence that it is not the A beta hypothesis, but the co-existing A beta neurofibrillary tangle pathology hypothesis which will be the basis for AD neuropathology.

Alzheimer Disease↗
PubMed1996

Norman MacAlister Gregg Lecture. The pathogenesis of diabetic retinopathy.

Diabetic retinopathy remains a major cause of loss of vision. The Diabetes Control and Complications Trial (DCCT) has implicated hyperglycaemia as a probable major direct causative factor in the pathogenesis of diabetic retinopathy. There are several plausible mechanisms by which high glucose concentrations could lead to the functional and later structural changes characterising diabetic retinopathy. These include increased activity of the aldose reductase pathway, increase de novo synthesis of diacylglycerol from glucose, causing protein kinase C activation, increased non-enzymatic glycation and increased oxidative damage. The demonstration of the potential roles of these pathways and the subsequent effects of growth factors in enhancing angiogenesis provide potential new approaches to the prevention and treatment of diabetic retinopathy.

Aldehyde Reductase↗
PubMed1996

Ida Mann Lecture. Transduction in human photoreceptors.

Phototransduction (the process by which light triggers a neural response in retinal rod and cone photoreceptors) is now understood at a molecular level. Indeed, the G-protein cascade of phototransduction is one of the best understood of all biological signalling pathways. The diffusional interactions of the proteins underlying the cascade are described and are briefly analysed. In response to a single activated rhodopsin (R*), formed as a result of a single photon hit, it can be shown that molecules of the G-protein will be activated (to G*) at an approximately constant rate. This, in turn, will cause the number of activated molecules of the third protein (the effector protein, E*, a phosphodiesterase) also to rise linearly with time. These kinetics of protein activation lead to an accurate description of the time-course of the rising phase of the photoreceptor's electrical response, both in single-cell recordings and also in recordings of the human electroretinogram (ERG). By analysing the a-wave of the ERG it is possible to determine the 'amplification' of transduction within living photoreceptors, and to begin to localise the molecular site of dysfunction is cases of photoreceptor abnormality.

Electroretinography↗