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S Eastwood

Publications and source records attributed to S Eastwood.

8 recordsLinked to original sources

Ocular lens gap junctions: protein expression, assembly, and structure-function analysis.

Recent advances in understanding lens fiber gap junction formation are reviewed. These include studies of junctional protein expression in the embryonic lens, and of age related changes affecting gap junction structure and composition in the adult lens. An in vitro assembly system based on detergent solubilized pore complexes and endogenous lipids has been developed to provide information on the molecular interactions involved in gap junction formation and to provide material for structure analysis. Important information on the electrical properties of lens gap junction channels is obtained using electrophysiological techniques including planar lipid bilayer analysis and patch clamping.

Animals

Gap junction formation during development of the mouse lens.

We have identified a 60 kDa membrane protein (MP60) as a component of the mouse cortical lens fiber gap junction and a monoclonal antibody recognizing this protein has been used to establish the temporal and spatial patterns of gap junction formation during development of the mouse lens. The initial expression of MP60 during embryonic development of the mouse lens correlates with primary fiber elongation and is first seen on the luminal aspect of the extending cells. About 2 days after birth, the relatively large, antibody-positive macular structures characteristic of late embryonic fiber cells begin to disperse into progressively smaller structures within a centrally located region of the lens. This change in the staining pattern with antibody directed against MP60 is consistent with the dispersion of gap junction plaques as confirmed by freeze fracture analysis. Around 5 days after birth, the 60 kDa gap junctional protein in this central region of the lens undergoes a modification resulting in the alteration to the epitope for the monoclonal antibody and a consequent loss of immunorecognition. Our results suggest that gap junctions in the central region of the developing mouse lens undergo sequential changes in immunoreactivity which may reflect potentially distinct functional phases of intercellular communication.

Age Factors

Familial systemic lupus erythematosus: evidence for separate loci controlling C4 deficiency and formation of antibodies to DNA, nRNP, Ro and La.

A family has been identified in the Canadian province of Prince Edward Island in which 2 sisters have systemic lupus erythematosus in a sibship of 14. Studies are reported on 11 of the siblings and 16 other family members. The affected siblings, and 4 other members of their sibship, are halfnull homozygotes for the C4A component of complement. We studied the distribution in family members of antibodies to ss and dsDNA, and to Ro(SSA), La(SSB), Sm and nRNP. Eight of 11 members of the affected sibship are antibody producers, compared to only 3 of 13 members of the parental generation. Our study provides further evidence for an association between null genes for C4A and familial lupus, and suggests, in an unusually large kindred, that several other genetic factors are involved in the production of antinuclear antibodies.

Adult

Arterial eicosanoid production following chronic exposure to a periarterial haematoma.

Cisternal and lumbar cerebrospinal fluid obtained some days following a subarachnoid haemorrhage contains abnormally large quantities of various prostanoids; some may be partly the result of abnormal production by the cerebral arteries. The extra-arterial and intra-arterial production of 6 oxo PGF1 alpha (prostacyclin metabolite), PGE2, PGF2 alpha and TXB2 were measured in perfused rabbit common carotid arteries taken both from normal rabbits and from rabbits in which the arteries had been ensheathed by blood clot in vivo for 7 days using two techniques. Prostaglandin production by control arteries was highest during the first hour of perfusion but declined or increased marginally (PGE2) during the succeeding three hours. Arteries exposed to a periarterial haematoma for 7 days produced prostaglandins at a high rate throughout the 4 hours of study, and there was a progressive and marked increase in PGE2 production. The disproportionate increase in the cerebral vasoconstrictor PGE2 may reflect the inflammatory response which occurred in the adventitia of the vessels. Increased prostanoid production by cerebral arteries probably does contribute to the increased levels in CSF after subarachnoid haemorrhage.

6-Ketoprostaglandin F1 alpha

Effects of subarachnoid haemorrhage on intracranial prostaglandins.

Prostaglandins E2, F2 alpha, 6 oxo F1 alpha and thromboxane B2 increased in cisternal CSF following mock subarachnoid haemorrhage in dogs, particularly PGE2 (X25.5). Concentrations were increased also in lumbar CSF of five patients some 8 days after subarachnoid haemorrhage. Subarachnoid haemorrhage did not alter the production of prostaglandins by dog whole cortex or choroid plexuses in vitro, but production by pooled dissected cerebral arteries of PGE2 was increased and of 6 oxo F1 alpha was decreased. Intravenous indomethacin decreased prostaglandin production by cerebral tissues, and caused a marked decrease in the prostacyclin metabolite in CSF. The implications of our findings for the aetiology of cerebral vasospasm are discussed.

6-Ketoprostaglandin F1 alpha

[Improving the quality of reports on randomized controlled trials. Recommendations of the CONSORT Study Group].

This summary corresponds to the translation into Spanish of the Special Communication published in the Journal of the American Medical Association in August 1996, along with the editorial published in the same issue "How to report Randomized Controlled Trials. The Consort Statement". It describes the Consolidated Standards for Preparation of Controlled Clinical Trials, prepared by a work group made up of members of the SORT Group and of the Asilomar Work Group, along with the director of a magazine and the author of the report on a clinical trial. The work was carried out by means of a Delphi process and the result was a check list and a process diagram. The check list is made up of 21 items that mainly refer to methods, results and discussions on the report of a controlled clinical trial, identifying the necessary information in order to be able to evaluate the internal and external value of the report, judging the improvement to be positive for the patient, the editors and the reviewers of the magazines.

Delphi Technique