The early years of the Lycée and the Lycée des Arts. A chapter in the lives of A. L. Lavoisier and A. F. de Fourcroy

The first professors at the newly-established London University (later University College London) were appointed in 1827, but a chair in geology was not created there until 1841. In the intervening years, teaching in geology and palaeontology was included in other natural science courses. Early in 1831, John Phillips, keeper of the Yorkshire Museum at York, was prompted to give a formal course of geological lectures and subsequently he was informally offered the professorship, which he declined.     

Division ofEntamoeba invadens Rodhain, 1934, in cultures

Zusammenfassung BeiEntamoeba invadens wurde eine ungleiche zellplasmatische Teilung beobachtet. Ein entsprechender Teilungsmodus gilt auch fürE. ranarum undE. moshkovskii.

---

---

This work was done in the Department of Zoology, University of London, King's College, London WC2, England.     

Reelin is a platelet protein and functions as a positive regulator of platelet spreading on fibrinogen

Abnormalities of platelet functions have been linked to reelin-impaired neuronal disorders. However, little attention has been given to understanding the interplay between reelin and platelet. In this study, reelin was found to present in the human platelets and megakaryocyte-like leukemic cells. Reelin-binding assays revealed that extracellular reelin can interact with platelets through the receptor belonging to the low density lipoprotein receptor gene family. The reelin-to-platelet interactions enhance platelet spreading on fibrinogen concomitant with the augmentation of lamellipodia formation and F-actin bundling. In contrast, reelin has no effect on integrin αIIbβ3 activation and agonist-induced platelet aggregation. Molecular analysis revealed that the up-regulation of Rac1 activity and the inhibition of protein kinase C δ-Thr505 phosphorylation are important for reelin-mediated enhancement of platelet spreading on fibrinogen. These findings demonstrate for the first time that reelin is present in platelets and the reelin-to-platelet interactions play a novel role in platelet signaling and functions.     

Glycoprotein IIb/IIIa blockade inhibits platelet aminophospholipid exposure by potentiating translocase and attenuating scramblase activity

The present study investigated the mechanisms underlying the inhibition of platelet phosphatidylserine (PS) exposure by GPIIb/IIIa blockade. Platelet PS exposure induced by thrombin stimulation was cell-cell contact dependent. GPIIb/IIIa blockade by c7E3 or SR121566 inhibited thrombin-induced platelet PS exposure. Thrombin stimulation induced mild, while A23187 induced extensive platelet-derived microparticle (PDMP) generation. Thrombin-induced PDMP generation was not inhibited by GPIIb/IIIa blockade. Aminophospholipid translocase activity was reduced upon platelet activation by thrombin. The reduction of non-PS-exposing platelets was attenuated by GPIIb/IIIa blockade, while little translocase activity was seen in PS-exposing platelets. Thrombin increased scramblase activity slightly in non-PS-exposing platelets, which was inhibited by GPIIb/IIIa blockade, and markedly enhanced scramblase activity in PS-exposing platelets. Activation of platelet calpain and caspase-3 or cytosolic calcium mobilization were not altered by GPIIb/IIIa inhibition. Thus, GPIIb/IIIa blockade inhibits platelet PS exposure by enhancing translocase activity and attenuating scramblase activity, but does not inhibit PDMP generation. Received 13 December 2006; received after revision 5 February 2007; accepted 9 March 2007     

Chemistry and Chemists at the London Institution 1807-1912

The London Institution, established in the City of London in 1807, was devoted, as its full title proclaimed, to the 'advancement of Literature and the Diffusion of Useful Knowledge'. With its extensive lecture programme, splendid reference library, reading rooms, laboratory and other amenities, it provided for its members a scientific and cultural centre, modelled on the highly successful and fashionable Royal Institution in London's West End. Among its scientific activities, chemistry long maintained a leading role, in terms of both the sheer volume and variety of its presentations, and the high standing of its lecturers; they included Faraday, Playfair, Hofmann, Roscoe, Odling, Norman Lockyer, Meldola, and Sir William Ramsay, as well as other visiting lecturers, specially selected for their ability to present their subject in an interesting and attractive fashion to a wider lay public. The laboratory of the Institution, although limited in size and facilities, was the scene of instruction in practical chemistry, and between 1863 and 1884 attained the reputation of a significant centre of chemical research during the successive tenure of the professorship in chemistry by J. A. Wanklyn and H. E. Armstrong. Their publications, appearing under the device 'From the Laboratory of the London Institution', were a frequent feature of the leading chemical periodicals. Thus, within its many-sided activities, the Institution promoted significantly the public appreciation of the function of chemistry, as a contributor both to pure knowledge, and to technical and economic progress. It achieved this in an environment of influential City merchants, manufacturers and financiers and doubtless led to beneficient, if unrecorded, consequences. It was only towards the close of the nineteenth century, when the universities had become increasingly concerned with the systematic study of the discipline, that chemistry lost its direct impact in the London Institution, but continued to maintain a presence within its cultural framework.     

Platelet–bacterial interactions

Many bacteria are capable of interacting with platelets and inducing platelet aggregation. This interaction may be a direct interaction between a bacterial surface protein and a platelet receptor or may be an indirect interaction where plasma proteins bind to the bacterial surface and subsequently bind to a platelet receptor. However, these interactions usually do not trigger platelet activation as a secondary co-signal is also required. This is usually due to specific antibody bound to the bacteria interacting with FcγRIIa on the platelet surface. Secreted bacterial products such as gingipains and lipopolysaccharide may also be capable of triggering platelet activation.     

Human platelet 5-hydroxytryptamine receptors: binding of [3H]-lysergic acid diethylamide (LSD). Effects of chronic neuroleptic and antidepressant drug administration

Chronic treatment with phenothiazines and thioxanthenes has been found to enhance 5-HT-induced aggregation of human platelets. A method has been developed to study 5-HT2 receptor binding sites on platelets utilising [3H]-LSD and more recently 125I/LSD. Results are presented which suggest that the LSD binding site is indeed the 5-HT2 binding site and that the LSD binding characterises the specific receptor responsible for 5-HT-induced shape change and aggregation. In a group of patients receiving phenothiazines or thioxanthenes, the Bmax of LSD binding was increased. The mean binding affinity was decreased possibly due to a persistence of neuroleptic in the platelet membrane preparation. Analysis showed that this was not the reason why the mean binding capacity was increased. The results show that chronic phenothiazine and thioxanthene delta treatment 'up-regulates' platelet 5-HT2 binding sites and that this may be accompanied by increased sensitivity to platelet aggregation by 5-HT. In normal subjects desipramine treatment increased the Bmax of platelet LSD binding and this was accompanied by an increased prolactin response to tryptophan which is thought to be mediated by central 5-HT function.     

A comparison of the effects of the optical isomers of isoproterenol on energy metabolism in a mouse sarcoma

Summary Disturbance to energy production in the S180 sarcoma (CB) by optical isomers of isoproterenol was assessed from altered adenine nucleotide levels at 1 h. The L-isomer almost halved the ATP level and lowered the energy charge significantly; the D-isomer was inactive. Dependence of tumor injury on cytochrome P-450 activity appears unlikely.One of us (GRNJ) thanks the Department of Surgery, Medical School, Kings's College Hospital, London, England, for the provision of experimental facilities; the Institute of Biochemistry, German Cancer Research Centre, Heidelberg, FRG, for permitting the measurement of metabolites; the Cancer Research Campaign, London, UK, for a part-time grant; and Zyma GmbH, München, FRG, and the estate of the late Dr Lucie Polak for additional financial support.     

Exogenous fibronectin modifies the aggregation of collagen-stimulated human platelets

Fibronectins (FN) are adhesive glycoproteins whose role in platelet aggregation is unclear. Addition of 3, 6 and 12 micrograms/ml of human plasma FN in vitro to isolated human platelets, which had been freed from plasma FN by gel filtration and subsequently stimulated with collagen, inhibited the last stage of platelet aggregation. With 3 and 6 micrograms/ml of FN a shortening of the lag-time was also observed. These data showed that FN may play a role in platelet-collagen interaction as well as in platelet-platelet interaction.     

Is prostacyclin subserving a vasodilator effect of methoxamine involving alpha adrenoreceptors?

The influence of methoxamine on the contractile tension of isolated rat abdominal aorta, and on its capacity to produce a platelet antiaggregating substance, were explored. Methoxamine stimulated platelet antiaggregation and diminished arterial tone. The last action was blocked by phentolamine as well as by inhibitors of cyclo-oxygenase and prostacyclinsynthetase.     

Newly synthesized elastin is associated with neoplastic epithelial cells in human mammary carcinoma

Summary Indirect immunofluorescence with a purified antiserum to human foetal elastin has identified newly synthesized elastin on the membranes of neoplastic epithelial cells in human mammary carcinoma.This research was supported by a project grant from the Medical Research Council, London.     

Platelets and viruses: an ambivalent relationship

Thrombocytopenia is a frequent complication of viral infections providing evidence that interaction of platelets with viruses is an important pathophysiological phenomenon. Multiple mechanisms are involved depending on the nature of the viruses involved. These include immunological platelet destruction, inappropriate platelet activation and consumption, and impaired megakaryopoiesis. Viruses bind platelets through specific receptors and identified ligands, which lead to mutual alterations of both the platelet host and the viral aggressor. We have shown that HIV-1 viruses are internalized specifically in platelets and megakaryocytes, where they can be either sheltered, unaltered (with potential transfer of the viruses into target organs), or come in contact with platelet secretory products leading to virus destruction and facilitated platelet clearance. In this issue, we have reviewed the various pathways that platelets use in order to interact with viruses, HIV and others. This review also shows that more work is still needed to precisely identify platelet roles in viral infections, and to answer the challenge of viral safety in platelet transfusion.     

Low-density lipoprotein and its effect on human blood platelets

Events leading to hyperactivity of human blood platelets are accompanied by an enhanced risk of atherosclerosis and arterial thrombosis. Lipoprotein disorders affect platelet functions, and hypersensitive platelets are observed in various stages of hyperlipidemia. Low-density lipoprotein (LDL), a circulating complex of lipids and proteins that is increased in hypercholesterolemia, enhances platelet function and increases sensitivity of platelets to several naturally occurring agonists. LDL sensitizes platelets via binding of apoB-100 to a receptor on the platelet membrane and via transfer of lipids to the platelet membrane. The receptor that mediates binding of LDL to the platelet and initiates subsequent intracellular signaling cascades has not yet been identified. Modification of native LDL generates a platelet-activating particle, and this interaction might contribute to the development of the atherosclerotic plaque. Lysophosphatidic acid is formed upon mild oxidation of LDL and is responsible for subsequent platelet activation induced by the modified LDL particle. Thus, LDL changes the functions of platelets via a broad spectrum of interactions.     

Effect of catecholamines on ADP aggregation of rat platelets in vivo

Summary The influence of catecholamines on the platelet count was studied in an in vivo experimental model obtained with cannulation of the carotid and of the femoral vein. The i.v. infusion of epinephrine and l-norepinephrine induces a low drop in the platelet count and also potentiate aggregation by ADP.     

Effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7-ethoxycarbonylmethoxy coumarin) on cyclic nucleotide phosphodiesterases in human platelets

Summary The effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7-ethoxycarbonylmethoxy coumarin), an inhibitor of platelet aggregation, on cyclic nucleotide metabolism was investigated. AD6 inhibited selectively human platelet cyclic GMP phosphodiesterase, which was separated from cyclic AMP phosphodiesterase by DEAE-cellulose chromatography. Addition of AD6 to washed platelets increased cyclic GMP levels significantly in two minutes. These results could be useful in elucidating the action of AD6 on intact platelets.     

Effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7-ethoxycarbonylme tho xy coumarin) on cyclic nucleotide phosphodiesterases in human platelets

The effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7-ethoxycarbonylmeth oxy coumarin), an inhibitor of platelet aggregation, on cyclic nucleotide metabolism was investigated. AD6 inhibited selectively human platelet cyclic GMP phosphodiesterase, which was separated from cyclic AMP phosphodiesterase by DEAE-cellulose chromatography. Addition of AD6 to washed platelets increased cyclic GMP levels significantly in two minutes. These results could be useful in elucidating the action of AD6 on intact platelets.     

Prostaglandin-like substances inPropionibacterium acnes. V. Activity profiles using cascade superfusion bioassay and platelet aggregation

Summary The activity spectrum of prostaglandin-like substances (PLS) fromP. acnes was investigated with cascade superfusion technique and by platelet aggregation assay. The biological activity of PLS resembles that of PGI₂: both relax bovine coronary artery, rabbit mesentric and coeliac arteries; both contract the rat stomach strip as well as both typically inhibit spontaneous movements of isolated guinea pig ileum. Also, similarly to PGI₂, PLS inhibits platelet aggregation regardless the inducer used. However, PLS possesses a specific antiaggregatory pattern on platelet, which indicates that these compounds are not indentical with primary prostaglandins or PGI₂.     

Activated scramblase and inhibited aminophospholipid translocase cause phosphatidylserine exposure in a distinct platelet fraction

Platelet procoagulant activity is mainly determined by the extent of surface-exposed phosphatidylserine (PS), controlled by the activity of aminophospholipid translocase and phospholipid scramblase. Here, we studied both transport activities in single platelets upon stimulation with various agonists. Besides the formation of procoagulant microparticles, the results show that a distinct fraction of the platelets exposes PS when stimulated. The extent of PS exposure in these platelet fractions was similar to that in platelets challenged with Ca²⁺-ionophore, where all cells exhibit maximal attainable PS exposure. The size of the PS-exposing fraction depends on the agonist and is proportional to the platelet procoagulant activity. Scramblase activity was observed only in the PS-exposing platelet fraction, whereas translocase activity was exclusively detectable in the fraction that did not expose PS. We conclude that, irrespective of the agonist, procoagulant platelets exhibit maximal surface exposure of PS by switching on scramblase and inhibiting translocase activity.Received 8 March 2005; received after revision 19 April 2005; accepted 13 May 2005     

Comparative platelet anti-aggregant activity of D-cysteinolic acid analogues

D-Cysteinolic acid (1) analogues with an S-C-C-N skeleton showed increased platelet anti-aggregant activity in the following order: 2-aminoethanesulfonic acids, thiazolidines, 2-aminoethanethiols and 2-aminoethyl disulfides. Methyl substitutions at the 2-position potentiated the activity. Of these analogues, bis [(R)-2-aminopropyl] disulfide was the most potent inhibitor of platelet aggregation, with about 600-fold the activity of (1).     

A phenomenological solution to the measurement problem? Husserl and the foundations of quantum mechanics

The London and Bauer monograph occupies a central place in the debate concerning the quantum measurement problem. Gavroglu has previously noted the influence of Husserlian phenomenology on London's scientific work. However, he has not explored the full extent of this influence in the monograph itself. I begin this paper by outlining the important role played by the monograph in the debate. In effect, it acted as a kind of ‘lens’ through which the standard, or Copenhagen, ‘solution’ to the measurement problem came to be perceived and, as such, it was robustly criticized, most notably by Putnam and Shimony. I then spell out the Husserlian understanding of consciousness in order to illuminate the traces of this understanding within the London and Bauer text. This, in turn, yields a new perspective on this ‘solution’ to the measurement problem, one that I believe has not been articulated before and, furthermore, which is immune to the criticisms of Putnam and Shimony.