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“We know for at least the first few months after symptomatic because levels of natural immunity tend to differ from person to person. Mercs in Spies Vs Mercs also have first person view. This is like putting a t-Rex against a chicken. - Callinater. Timothy Ray Brown, the first person cured of H.I.V., in he underwent a procedure in which stem cells harvested from blood and.
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History of the discovery of the malaria parasites and their vectors

Parasites & Vectorsvolume 3, Article number: 5 () Cite this article

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Abstract

Malaria is caused by infection with protozoan parasites belonging to the genus Plasmodium transmitted by female Anopheles species mosquitoes. Our understanding of the malaria parasites begins in with the discovery of the parasites in the blood of malaria patients by Alphonse Laveran. The sexual stages in the blood were discovered by William MacCallum in birds infected with a related haematozoan, Haemoproteus columbae, in and the whole of the transmission cycle in culicine mosquitoes and birds infected with Plasmodium relictum was elucidated by Ronald Ross in In the Italian malariologists, Giovanni Battista Grassi, Amico Bignami, Giuseppe Bastianelli, Angelo Celli, Camillo Golgi and Ettore Marchiafava demonstrated conclusively that human malaria was also transmitted by mosquitoes, in this case anophelines. The discovery that malaria parasites developed in the liver before entering the blood stream was made by Henry Shortt and Cyril Garnham in and the final stage in the life cycle, the presence of dormant stages in the liver, was conclusively demonstrated in by Wojciech Krotoski. This article traces the main events and stresses the importance of comparative studies in that, apart from the initial discovery of parasites in the blood, every subsequent discovery has been based on studies on non-human malaria parasites and related organisms.

Background

Malaria is an ancient disease and references to what was almost certainly malaria occur in a Chinese document from about BC, clay tablets from Mesopotamia from BC, Egyptian papyri from BC and Hindu texts as far back as the sixth century BC. Such historical records must be regarded with caution but moving into later centuries we are beginning to step onto firmer ground. The early Greeks, including Homer in about BC, Empedocles of Agrigentum in about BC and Hippocrates in about BC, were well aware of the characteristic poor health, malarial fevers and enlarged spleens seen in people living in marshy places. For over years the idea that malaria fevers were caused by miasmas rising from swamps persisted and it is widely held that the word malaria comes from the Italian mal'aria meaning spoiled air although this has been disputed. With the discovery of bacteria by Antoni van Leeuwenhoek inand the incrimination of microorganisms as causes of infectious diseases and the development of the 1st person to see cells theory of infection by Louis Pasteur and Robert Koch inthe search for the cause of malaria intensified. Scientific studies only became possible after the discovery of the parasites themselves by Charles Louis Alphonse Laveran in and the incrimination of mosquitoes as the vectors, first for avian malaria by Ronald Ross in and then for human malaria by the Italian scientists Giovanni Battista Grassi, Amico Bignami, Giuseppe Bastianelli, Angelo Celli, Camillo Golgi and Ettore Marchiafava between and Excellent histories of this disease include those by Celli [1], Stephens [2], Scott [3], Russell [4], Foster [5], Garnham [6, 7], Harrison [8], Bruce-Chwatt [9], Desowitz [10], McGregor [11], Poser & Bruyn [12] and Schlagenhauf [13].

The life cycle of the malaria parasites, Plasmodium spp

In order to understand the historical events it is necessary to summarise briefly our current state of knowledge. Malaria is caused by infection with five species of Plasmodium the life cycles of which are very similar (Figure 1).

Schematic life cycle ofPlasmodiumspp.

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Infection begins when (1) sporozoites, the infective stages, are injected by a mosquito and are carried around the body until they invade liver hepatocytes where (2) they undergo a phase of asexual multiplication (exoerythrocytic schizogony) resulting in the production of many uninucleate merozoites. These merozoites flood out into the blood and invade red blood cells where (3) they initiate a second phase of asexual multiplication (erythrocytic schizogony) resulting in the production of about merozoites which invade new red blood cells. This process is repeated almost indefinitely and is responsible for the disease, malaria. As the infection progresses, some young merozoites develop into male and female gametocytes that circulate in the peripheral blood until they are (4) taken up by a female anopheline mosquito when it feeds. Within the mosquito (5) the gametocytes mature into male and female gametes, fertilization occurs and a motile zygote (ookinete) is formed within the lumen of the mosquito gut, the beginning of a process known as sporogony. The ookinete penetrates the gut wall and becomes a conspicuous oocyst within which another phase of multiplication occurs resulting in the formation of sporozoites that migrate to the salivary glands of a mosquito and are injected when the mosquito feeds on a new host.

The malaria parasites

Our understanding of the life cycle of the malaria parasites did not proceed in the logical order just outlined but more like a jigsaw in which the various pieces were painstakingly put into place and, like a jigsaw, often involved mistakes and false starts. The story begins with the discovery of the stages in the blood. Many textbooks merely state that 'in Laveran discovered the malaria parasite' words that do not give this discovery the credit it deserves. In order to understand the background of this discovery it is necessary to go back to the s. The discoveries of Pasteur and Koch had precipitated a search for a bacterial cause for many diseases including malaria. By the miasma theory was going out of favour and the two theories vying for contention were whether the microorganisms responsible were transmitted (1) by air and inhalation or (2) by water and ingestion. The leading theory was that proposed by the Italian Corrado Tommasi-Crudeli and the German, Theodor Albrecht Edwin Klebs, an eminent microbiologist who had been the first person to see the bacteria responsible for typhoid and diphtheria. Tommasi-Crudeli and Klebs claimed that they had isolated from the waters of the Pontine Marshes, where malaria was prevalent, a bacterium, Bacillus malariae, which when isolated in culture and injected into rabbits caused febrile infections accompanied by enlarged spleens reminiscent of malaria [14]. It was against this background that Charles Louis Alphonse Laveran, an unknown French army officer working in Algeria, challenged the perceived wisdom and began in his own words 'to follow the pigment'. Beginning with the known fact that the spleens of malaria patients contained pigment he began to look for pigment in the fresh unstained blood 1st person to see cells patients and observed it first in leucocytes and then in or on red blood cells. Looking more carefully, he observed several different forms of erythrocytic organism including crescents, spherical motionless bodies with pigment, spherical moving bodies with pigment and bodies that extruded flagella-like structures all of which he thought were on the outside of the red cells. These observations are particularly interesting because Laveran not only used fresh blood but also a dry objective with a maximum magnification of × diameters. He also suggested a course of events that began with clear spots that grew, acquired pigment and filled the corpuscle which then burst coinciding with the fevers associated with malaria. Laveran meticulously examined the blood of patients and in observed the crescentic bodies in all cases of malaria but never in those without malaria. He also noted that quinine removed these stages from the blood. Laveran quickly realised that he had found a parasitic protozoan which he called Oscillaria malariae. He presented his findings to the French Academy of Medical Sciences in December [15] but failed to persuade any of the eminent microbiologists, zoologists or malariologists of the day that he was seeing anything other than disintegrating red blood cells. Nevertheless he persevered and by had convinced the leading Italian malariologists including Bignami, Golgi and Marchiafava that malaria was caused by a protozoan and not a bacterium [16]. His biggest triumph came in the same year when he also convinced the more cynical microbiologists Louis Pasteur, Charles Edouard Chamberland and Pierre Paul Émile Roux. Robert Koch, one of the most influential microbiologists of his time, however, remained sceptical until Nevertheless in some quarters the miasma theory persisted and as late as the American R. C. Newton, a supporter of Tommasi-Crudeli, wrote that 'Aerial and aquatic transportation of malaria has been proved' [17]. (This paper is worth reading in full because, although based on what we now know to be false premises, it contains a mass of interesting information about the prevention of malaria such as the use of screens or mosquito nets to exclude insects, closing doors at night and lighting fires out of doors). Laveran was awarded the Nobel Prize for Medicine in and his discoveries are described in some detail by the Sergent brothers [18] and Bruce-Chwatt [19] as well as in the various histories of malaria listed above.

What was remarkable about Laveran's discovery was that it was without precedent as no protozoan had previously been found inhabiting any kind of youtube video embed responsive code blood cell. Unbeknown to Laveran or the Italian malariologists, however, the Russian physiologist, Vassily Danilewsky had been examining the blood of birds and reptiles in the Ukraine and had discovered a number of parasites including trypanosomes and others that he identified as 'pseudovacules'. Anyone who has studied blood parasites will immediately recognise his description of 'pseudovacuoles' as unstained malaria parasites. By Danilewsky had recognised the three most common genera of intraerythrocytic blood parasites of birds now known as Plasmodium, Haemoproteus and Leucocytozoon but, as he had published much of his work in Russian, it was not until his three volume book La Parasitologie Comparée du Sang had been published in French in that this information became widely available [20]. Thereafter there began searches for other malaria parasites in reptiles, birds and mammals and this was facilitated by the accidental discovery of a methylene blue-eosin stain by Dimitri Leonidovitch Romanowsky in [6]. Romanowsky's stains became popular at the beginning of the twentieth century and remain the basis of blood stains such as Leishman's, Giemsa's and Wright's to the present day. These stains colour the nucleus of the parasite red and the cytoplasm blue permitting their easy identification and are used not only for malaria parasites but also for trypanosomes, leishmanias and filarial worms. Romanowsky's discovery is one of the most significant technical advances in midland theater tickets history of parasitology.

Meanwhile the Italian workers, now convinced that malaria was caused by a parasite, took up the challenge with vigour and Marchiafava and Bignami, using a combination of eosin-based blood stains and the oil-immersion microscope objective developed by the Carl Zeiss Company inobserved amoeboid movement of the organism. This left them in no doubt that they were dealing with a protozoan parasite that invaded red blood cells, grew within the cells and produced daughter cells that invaded fresh blood cells [21]. Thereafter the Italian views dominated malaria research and, based on observations of the erythrocytic stages of the parasite, Golgi between differentiated between tertian (48 hour periodicity) and quartan (72 hour periodicity) malaria [22] and in Golgi and Marchiafava further described the differences between mild Spring malaria (benign tertian) and severe Summer-Autumn (malignant tertian) malaria [23].

By this time it had also become clear that the paroxsms characteristic of malaria coincided with the bursting of infected red blood cells and the release of the products of multiplication something that Laveran, who had also realised that in the case of malignant tertian malaria the brain was involved, had proposed [24]. Thus by it was known that malaria was caused by a protozoan parasite that invaded and multiplied in red blood cells and, after a lot of confusion, that there were three species with specific periodicities and other characteristics responsible for benign tertian (Haemamoeba vivax), malignant tertian (Laverania malariae) and quartan (Haemamoeba malariae) malaria now respectively Plasmodium vivax, P. falciparum and P. malariae. The situation as it existed in is beautifully summarised by Grassi in his monograph, Studi di uno Zoologo Sulla Malaria[25] and, although more details have since been added, this work remains as relevant today as it was years ago. InJohn Stephens, working in West Africa, discovered a fourth species which resembled P. vivax which he described as P. ovale in [26].

The sexual stages

The action now moves to Canada in and to the United States a year later where a medical student, William MacCallum, and his colleague, Eugene Opie, while examining the blood of crows infected with Haemoproteus columbae, a haematozoan closely 1st person to see cells to the malaria parasites, observed flagellated structures which they described in detail and also recorded how the flagellated bodies fused with non-motile bodies to form a vermicule (now called an ookinete) [27]. MacCallum suggested that he was witnessing sexual reproduction that paralleled that in mammals (and, it should be noted, related sporozoans that were already familiar to European zoologists [28, 29]) and that the flagellated forms were male gametes, the non-motile forms female gametes and the vermicule the zygote. MacCallum's findings are very significant as he realised that: 'Have we not herea sexual processthe result of which is the motile vermiculus? This is a process which we might have expected and which I am confident will be found to occur in the case of the human malaria parasites' [30]. The significance of this observation initially eluded Ronald Ross (see below) something that remained with him for the rest of his life [31] but was not missed by Patrick Manson who wrote to Ross that 'MacCallum's observation on Halteridium; if it is correct, it is of the greatest importance' [31, 32]. Here MacCallum reached a dead end because he believed that the vermicule then invaded cells of the vertebrate host but was unable to pursue this line of investigation.

Transmission

Despite all their accumulated knowledge and skills no malariologists could explain how the parasite spread from one human to another. The clues were, however, in place. Over the centuries, circumstantial evidence had accumulated that suggested that mosquitoes might somehow be connected with malaria and by the American physician, Albert King, had assembled the mass of evidence that was to become known as the mosquito-malaria doctrine [33]. Between andLaveran, Manson (who in had demonstrated that the filarial worms responsible for lymphatic filariasis were transmitted by mosquitoes [34]), and the Italian malariologists, had become increasingly convinced that mosquitoes were involved in the transmission of malaria. Thereafter opinions differed with some observers, including Manson, believing that humans became infected by drinking water contaminated by infected mosquitoes while others thought that the infection was acquired by inhaling dust from dried-up ponds in which infected mosquitoes had died, in other words, variations on the water and ingestion and air and inhalation theories proposed by Tommasi-Crudeli and Klebs in Manson also toyed with the idea that transmission might be mechanical, i.e. the parasites were passively carried from host to host on the proboscis of a mosquito.

By Manson, who had spent much of his working life in Taiwan and was then in his 50s and in an established medical practice in London, turned his attention to the possibility of mosquito transmission of malaria but, as he was unable to go to malarious countries himself, he needed someone to carry out the necessary investigations and experiments for him. His colleague-to-be was an unlikely choice, Ronald Ross (Figure 2).

Ronald Ross . Photograph by courtesy of the Royal Society of Tropical Medicine and Hygiene. Portraits of other scientists who were involved in the elucidation of the life cycle of the malaria parasites can be found elsewhere [9, 40].

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Ronald Ross In Ronald Ross working in India discovered that culicine mosquitoes transmitted the avian malaria parasite Plasmodium relictum and suggested that human malaria parasites might also be transmitted by mosquitoes. Later, when working in Sierra Leone inhe demonstrated that the human malaria parasites were indeed transmitted by anopheline mosquitoes. In the meantime, however, several Italian scientists had already shown that this was the case.

Ross then aged 37 was an established army surgeon working in India who did not believe that malaria was caused by a blood parasite but thought that it was an intestinal infection. Throughout the second half ofManson worked on Ross, showed him blood slides containing malaria parasites and convinced him that incriminating a mosquito vector of malaria was a goal worth aiming for. Ross returned to India and over the next four years Manson directed operations at a distance and we are fortunate to have an almost complete collection of the letters that passed between the two men [32]. This was not an easy relationship partly because Ross's first priorities were his military commitments and these inevitably delayed the work he was doing with malaria and partly because, from time to time, Ross seemed more interested in writing poetry and novels. Nevertheless, the cooperation reached a satisfactory conclusion but later ended in acrimony.

Manson, who had access to malaria patients in London, had observed that it was only when blood taken from such patients began to cool that the flagellated forms and subsequent fertilization, as described by MacCallum, appeared and concluded that further development must occur outside the human body in another host, probably a mosquito. Ross, having returned to India, examined several thousand mosquitoes from endemic areas without any success but, remembering Laveran's dictum 'follow the pigment' and Manson's advice to 'follow the flagellum', a reference to the flagella of the male gamete, he eventually found pigmented bodies, which he called spores, on the stomach wall of a mosquito experimentally fed on an infected patient. Ross was no entomologist (in fact the only book he had on entomology was one written for anglers) so he classified the mosquitoes he was studying as grey or barred-back (A), brindled (B), and dappled-winged (C). We now know that the grey mosquitoes were culicines and that the dappled-winged mosquitoes were anophelines. Grey mosquitoes were very common but never walking the west highland way in 4 days the pigmented spores. On the other hand the rarer 'dapple-winged' mosquitoes, after being fed on a malaria patient, were found to contain pigmented bodies that ruptured releasing 'rods' that invaded the mosquito's salivary glands. Ross had now made the crucial break-through and had found developmental stages of human malaria parasites in anopheline mosquitoes and, in his letters, he calls August 20th 'Mosquito day' [31, 32]. Ross was on the brink of demonstrating that anopheline mosquitoes could transmit human malaria but unfortunately he was not able to complete his studies because at this crucial stage he was posted to Calcutta where there was very little malaria [31]. He did, however, have access to laboratory facilities and, remembering that in Manson had mentioned the possibility of using malaria parasites of birds in his investigations, he turned his attention to an avian malaria parasite, Proteosoma relictum (now called Plasmodium relictum), common in many species of birds including crows and sparrows. This parasite, he discovered, was transmitted by his 'grey' (culicine) mosquitoes, probably Culex fatigans. Of 'grey' mosquitoes fed on infected birds, developed pigmented spores. Ross concluded that mosquitoes fed on infected birds took up male and female gametocytes which fertilized in the mosquito gut and developed into spores on the surface of the mosquito's gut within which rod-like structures were produced that invaded the mosquito's salivary glands and were injected into a new host when the infected mosquito fed. His results were made public in [35, 36]. Ross surmised correctly that human malaria was probably transmitted in the same way and later wrote that 'The triumph of 20 August was now completed and crowned by that of 9 July ' [31]. These experiments finally convinced Manson, that malaria was transmitted through the bite of a mosquito contrary to his earlier opinion that the infective stages were discharged into water. He nevertheless still thought that discharge of infective stages into water was the way that filiarial worms were transmitted until it was shown that they too were transmitted via the bite of a mosquito by George Carmichael Low in [37].

Although Ross had elucidated the whole of life cycle of Plasmodium relictum in culicine mosquitoes and had come tantalizingly close to completing the mosquito stages of the human malaria parasites the actual proof of the transmission of human malaria by anopheline mosquitoes still remained unresolved. Ross recorded that one single experiment could bring about the life cycle of human malaria [31] but his military duties took precedence and he was sent to work on an epidemic of plague that was then spreading across India and was not allowed to test his hypothesis because of the plague.

In the meantime several Italian workers were already on the trail. Bignami had suggested in that mosquitoes might transmit malaria by inoculation but it wasn't until that he and Grassi, who were fortunate to have access to sites where malaria was present near Rome and in Sicily, produced the final proof when they fed local Anopheles claviger mosquitoes on infected patients and subsequently transmitted the infection to uninfected individuals via the bite of these mosquitoes [38]. Over the next two years the Italians proved that only female Anopheles mosquitoes could transmit malaria and methodically consolidated their findings and described the whole blood-mosquito life cycles of P. vivax, P. falciparum and P. malariae (see Grassi's classical monograph, Studi di uno Zoologo Sulla Malaria[25]). Ross, in 1st person to see cells meantime, had been posted to Sierra Leone where within a few weeks after his arrival in he had demonstrated the development of P. falciparum, P. vivax and P. malariae in anopheline mosquitoes. Meanwhile, in London, Manson persuaded Bignami and Bastianelli to send him A. maculipennis mosquitoes infected with benign tertian malaria which he used to infect his medial student son, Patrick Thurburn, and another volunteer thus completing this part of the story. More detailed accounts of these discoveries can be found in reviews by Ascenzi [39], Dobson [40] and Fantini [41] which were published together in the proceedings of a meeting held in Rome to commemorate one hundred years of malariology.

The discovery of the role of mosquitoes in the transmission of malaria provided malariologists with a new weapon against this ancient disease. In a classical experiment, Grassi dispatched volunteers to the Capaccio Plains, a malarious area in Italy, protected them from mosquito bites between dusk and dawn and found that only five succumbed to the disease compared with unprotected volunteers who all contracted malaria [25]. Thus the possibility of controlling the disease by reducing contact with infected mosquitoes had been demonstrated. Over the next decades, methods to prevent mosquito biting by avoidance, screening and mosquito proofing dwellings and anti mosquito measures such as by the use of oils and larvivorous fish and draining mosquito habitats had become commonplace [9].

One surprising aspect of this whole story is that some of the clues about arthropod-transmission of blood-inhabiting protozoa were available several years before Ross and the Italian scientists began their investigations. In the American microbiologists Theobald Smith and Frederick Kilborne had observed that young ticks taken from cattle infected with the piroplasm Babesia bigemina, an intraerythrocytic protozoan resembling a malaria parasite, could infect susceptible animals and this was confirmed in a series of meticulously controlled experiments over the next two years [42]. It is strange that none of the participants in the malaria story seemed to be aware of these discoveries, probably because they were published in an American Government Agricultural document. How differently things might have turned out if they had been aware of these discoveries is a matter of speculation.

Exoerythrocytic development

The life cycle in humans, however, remained incompletely understood and nobody knew where the parasites developed during the first 10 days or so after infection during which they could not be seen in the blood. Grassi was the first to suggest that there must be some developmental stage in cells other than red blood cells, possibly white blood cells [25]. This theory was elaborated by Grassi and his colleagues from and onwards but was later abandoned mainly due to too much reliance on a mistake by the influential German scientist Fritz Schaudinn who, indescribed the direct penetration of red blood cells by the infective sporozoites of P. vivax[43]. No one else was able to confirm these observations and the phenomenon is now referred to among malariologists unkindly as 'Schaudinn's fallacy'. Nevertheless Schaudinn's ideas were adopted by such authorities as Grassi and dominated scientific opinion for over forty years. Meanwhile evidence that there was a phase of multiplication preceding that in the blood was accumulating from another source, the avian malarias. MacCallum in had observed developmental stages of P. relictum in the liver and spleen of infected birds [30] and thereafter there were numerous somewhat inadequate descriptions of exoerythrocytic development of a number of avian malaria parasites [6, 44]. In Sydney James and Parr Tate conclusively demonstrated that in sporozoite-induced P. gallinaceum infections in chickens there was phase of multiplication between the injection of sporozoites and the appearance of parasites in the blood and that this occurred in cells of the reticuloendothelial system [45].

By the late s there was no doubt that in all the avian malaria parasites studied there was a phase of multiplication in various nucleated cells before (and after) parasites appeared in the blood and over the next decade the complete life cycles of a number of avian Plasmodium and Haemoproteus species, differing only in detail particularly relating to the types of cells involved which varied from species to species, had been worked out. What happened in primates was not so clear and during the s and s there were sporadic reports of parasites in the tissues, particularly in the brain and nervous system, of animals infected with primate and bat malarias. After the end of the Second World War in malaria research throughout the world intensified and a number of workers became convinced that that there must be an exoerythrocytic stage in the life cycle of the primate malarias but what form this took was not known. This question was not resolved until when Henry Shortt and Cyril Garnham, working in London, showed that a phase of division in the liver preceded the development of parasites in the blood [46]. The crucial clues came from studies on Hepatocystis kochi, another parasite of monkeys first identified by Laveran as Haemamoeba kochi. Hepatocystis spp. are related to malaria parasites but do not have an erythrocytic stage in their life cycles so these parasites must have only an exoerythrocytic stage which in H. kochi is in the parenchyma cells of the liver [47]. This suggested to Shortt, Garnham and their colleagues that the liver might be the place to look for the elusive exoerythrocytic stages of primate malaria parasites and selected P. cynomolgi in rhesus monkeys for their investigations. Previous attempts by other workers had failed to find any liver forms so Shortt and Garnham decided to use infected A. maculipennis atroparvus, a massive dose of sporozoites, and found exoerythrocytic stages seven days later [48]. Shortly afterwards Shortt, Garnham and their co-workers found exoerythrocytic forms of P. vivax in human volunteers [49] and subsequently in volunteers infected with P. falciparum in [50] and P. ovale in [51]. In the meantime the same team had also demonstrated exoerythrocytic stages of P. inui, a quartan form of primate malaria. The exoerythrocytic stages of P. malariae were more elusive and it was not until that Robert (Bill) Bray demonstrated their presence in experimentally infected chimpanzees [52]. The story of the discovery of the exoerythrocytic forms of malaria parasites until is told in some detail by Bray [44] and updated until by Garnham [6].

The story of the life cycle of the human malaria parasites was almost complete and had taken nearly 70 years to elucidate. There remained, however, one further question; what caused the long prepatent period between infection and the appearance and reappearance of parasites in the blood seen in some temperate strains of P. vivax? This led to the discovery of dormant exoerythrocytic stages, hypnozoites, by Wojciech Krotoski, working with Garnham's team, in [53].

Other malaria parasites

It has already been noted that malaria-like parasites are commonly found in birds, mammals and reptiles and studies on many of these have contributed to our overall understanding of human malaria. Malaria-like parasites belonging to the genus Hepatocystis in non-human primates were first recognised by Laveran in but true malaria parasites, Plasmodium spp., were not identified with certainty until with the independent discoveries of P. cynomolgi, P. inui, and P. pitheci in monkeys imported into Germany from Java [6]. Throughout the s and s there were increasing numbers of reports of new species from wild-caught primates including P. knowlesi in [6, 54]. During the s, there were occasional reports of accidental infections with P cynomolgi, P. inui and P. knowlesi in humans suggesting that some primates might act as reservoirs for human malaria but it appeared that the chances of such naturally acquired infections were very remote. However it is now known that humans are at risk from infection with P. knowlesi, a malaria parasite with a 24 hour erythrocytic cycle, in Southeast Asia where its natural hosts are macaque and leaf monkeys. Until there had only been two authenticated cases of naturally acquired human infections with P. knowlesi both in peninsular Malaysia. No other cases were recorded until when a focus of human infections was identified in Sarawak, Malaysian Borneo [55]. Since then there have been several hundred reports of human infections in the region and there is now overwhelming evidence that P. knowlesi is a zoonosis involving macaque (Macaca spp.) and leaf (Presbytis spp.) monkeys as reservoir hosts with mosquitoes belonging to the Leucosphyrus group of Anopheles mosquitoes as the vectors in Malaysia and elsewhere in Southeast Asia [56]. Retrospective examination of blood films and the application of the polymerase chain reaction (PCR) and other molecular techniques have revealed that a number of malaria cases previously attributed to P. malariae in Malaysia were misidentified and that they were in all probability due to P. knowlesi[57].

The first avian malaria parasites were discovered at about the same time as the human species and there are now about 24 species including P. relictum, which has contributed most to our understanding of the transmission of human malaria parasites, and P. gallinaceum which not only contributed to our understanding of the exoerythrocytic phases of the malaria life cycle but also, because it could easily be maintained and mosquito-transmitted in chickens, served at the main model for chemotherapeutic studies until the discovery of rodent malarias.

The first rodent malaria parasite, P. berghei, was identified and isolated from wild rodents in Central Africa by Ignace Vincke and Marcel Lips in and subsequently adapted to mice, rats, hamsters and gerbils and easily maintained laboratory-bred mosquitoes such as A. stephensi[58]. Since then three other species, P. yoelii, P. vinckei and P. chabaudi, of which there are a number of subspecies and strains, have been identified, isolated and adapted to laboratory rodents and have become the mainstay of studies on chemotherapy and have served as surrogate models of human malaria in the fields of immunology, genetics, molecular biology and biochemistry [59].

In vitro cultivation

One of the most important breakthroughs in malaria research was the development of techniques that enabled scientists to grow the erythrocytic stages of malaria parasites in continuous culture pioneered by William Trager and J.B. Jensen [60] thus freeing investigators from the need to use animals for chemotherapeutic and biochemical studies. The importance of this discovery cannot be overemphasised. For the first time, scientists had access to unlimited quantities of human malaria parasites, particularly P. falciparum, thus reducing their dependence on laboratory animals and blood taken from humans. The ease with which the erythrocytic stages could be grown in bulk made it possible not only to test the effects of drugs directly but also to isolate and purify parasite components in order to identify biochemical pathways and molecules of potential use in the development of vaccines and chemotherapy. The cultivation of sexual stages provided insights into the genetics of human malaria parasites and the development of drug resistance. The cultivation of liver stages, although more difficult to achieve, made it possible to develop and test drugs against these stages and provided vital information about the immune responses in the liver. Finally, the food bank of central and eastern nc greenville of sporogonic stages has enabled scientists to discover what happens to the parasite in its mosquito vector.

The final [?] step

The final stage in the story of our understanding of the malaria parasites that began when an unknown French scientist, working by himself in Algeria with a crude microscope, noticed that the blood of patients suffering from malaria contained organisms that he identified as parasitic protozoa culminated years later when union savings bank mt washington massive team of investigators determined the compete genome of Plasmodium falciparum[61] since when the genomes of other malaria parasites have also been published [62].

Conclusions

Over a century later it seems appropriate to attribute the various discoveries concerning the malaria parasites and their transmission as follows. Laveran was the first person to find parasites in the blood of patients infected with malaria inMacCullum was the first to observe the sexual stages of a malaria-like parasite, Haemoproteus columbae, in birds inRoss was the first to show that any malaria parasite, in this case the avian Plasmodium relictum, was transmitted by the bite of infected mosquitoes in and, by implication, that this would be the case for human malarias and in Grassi, Bignami and Bastienelli were the first to demonstrate that human malaria parasites were actually transmitted in this way. The most far-reaching discovery made by Ross, and one that is frequently ignored, was that a blood-sucking insect could not only take up infective organisms from an infected individual but could also transmit them some time later when it fed on an uninfected host something that was completely contrary to the received opinion of the time. It took a long time before other investigators realised the universal importance of this discovery and it was not until the first decades of the twentieth century that diseases such as African trypanosomiasis, leishmaniasis, filariasis and loaiasis were discovered to be transmitted by the bites of infected insects. This discovery was not missed by virologists who, after the discovery of viruses, soon established the concept of arthropod-borne or arboviruses or by bacteriologists looking for the mode of transmission of the plague bacillus. The tissues stages in the blood were discovered half a century later, inby Shortt and Garnham and the final mystery, the persistence of liver stages was established by Krotoski in The story of the elucidation of the complex life cycle of the malaria parasites was only possible because the various scientists involved were able to transfer knowledge gleaned from non-human malarias in birds and primates to the problem of human malaria thus emphasising the importance of comparative studies in the investigation of human diseases.

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There is someone alive today who will live to be 1, years old: Why we are living longer than ever?

“The first person to live to be 1, years old is alive today.” I read that sentence two years ago and it set me off on a voyage of discovery. Since then I’ve been finding out what is known about longevity, the time that each of us are allotted to live our lives. I’m not going to live to be 1, but could my granddaughter?

We live in unprecedented times and the pace of change and innovation is explosive. Unlike any other era, mankind has the means to destroy the world completely and in so many ways. If mankind does not succumb to man-made or natural disasters, and continues to progress exponentially, it becomes difficult to predict the next years, let alone peer darkly into the distant future.

Mankind’s curiosity has taken us to the stage when we can start to answer some of the fundamental questions about ourselves, why we are here and what are the mechanisms that got us to this point. I believe that we stand on the threshold where this understanding can be translated into the most extraordinary and wonderful changes in the human condition.

A few generations ago death was a familiar event. Death was capricious, visiting the young as well as the old, the hale as well as the infirm, the rich as well as the poor. It was an accepted and everyday occurrence over which man had little influence. No wonder that it was often seen as beyond man’s control.

I’m now retired but I spent many years looking after seriously ill patients as director of intensive care at the Royal London hospital. In a previous age I might not have survived this long, let alone enjoy an active physical and mental existence. Over the last years, improved nutrition, clean water, better sanitation and the application of medical science have been remarkably successful in tackling disease and allowing most people to reach their potential lifespan. Because of these advances millions of people are alive today who would have died not so many years ago.

In recent years the search for ways to achieve an extended lifespan has moved out of the realm of fantasy and science fiction to become a legitimate scientific pursuit. Death has moved from being inevitable, to a technical hitch amenable to intervention and prevention.

Even in the s the squalor of places such as the Gorbals, in Glasgow, was not conducive to a long life expectancy

For most of recorded human history average life expectancy has been between 20 and 40 years. In Britain it was only in the mids that this figure consistently rose above 40 years. Today in the UK average life expectancy is about 80 years. The main reason for this extraordinary advance is the fall in infant mortality. In one-third of British children died before their fifth birthday. Today that figure is less than one per cent. The big killers used to be infectious diseases such as tuberculosis, scarlet fever, smallpox, influenza, typhoid and cholera. If progress at reducing mortality continues then many children born since the year will live to celebrate their th birthday.

Psalm in the Bible concedes a natural life span of three score years and 10, or fourscore for the fortunate. Living to 70 or 80 years of age was not unusual in historical times. For example, Michelangelo died in three weeks before his 89th birthday. Worldwide there are thought to be about people older than years, and more than 90 per cent of them are women. The oldest reliably documented person was a Hdfc forex prepaid card net banking login woman called Jeanne Calment who died in at the age of A healthy, non-smoking lifestyle involving exercise, good nutrition and rewarding social interactions will maximise the chances of achieving your potential lifespan. I can’t tell you how to live for hundreds of years, but at the moment bank snb south hutchinson ks can.

Natural selection is the key mechanism in evolution. We can’t rely on this to extend life as there is little evolutionary pressure once we have had children and passed on our genes. If humans are to live longer than anyone has before then medical science will have to up its game.

Frenchwoman Jeanne Calment lived to see her rd year 

All living organisms use the same chemical building blocks and the same cellular organisation. That is why it is said that we share 50 per cent of our genetic material with a banana plant. If other creatures can live extraordinary long lives, regenerate limbs or spend winters in hibernation, then why can’t we?

Ageing is common to almost all creatures but occurs at vastly different rates and in different ways. Interventions have already been demonstrated that substantially extend the lifespans of yeasts, worms, fruit flies and small mammals. Successful techniques include genetic manipulation, calorie restriction and therapy with drugs that slow ageing. Researchers are getting a better understanding of the ageing process and thus the ways in which it could be slowed, halted or even reversed.

Ageing Japan: Robots' role in future of elderly care

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Some off the wall solutions to extending lifespan have been described. These include freezing the dead to be reanimated in the future, head transplants and uploading to a computer. More mainstream approaches, all in their infancy, probably have a better chance of prolonging human life. These are the application of technology to replace and enhance human functions, regeneration and stem cell therapy, and genetic manipulation.

Humans share 50 per cent of our genetic material with a banana plant

Medical innovations have already walmart eye center mexico mo the lives of millions of people. My working lifetime saw the introduction of CT and other imaging, non-invasive surgery, and endoscopy made possible by fibreoptics and cameras on microchips. In the UK more thancataract replacements are performed each year inserting an artificial lens into the eye. The near future will probably see the wide application of smart health monitors, brain stimulators, replacement organs grown in the laboratory or in donor animals, artificial intelligence to diagnose and treat disease, and nanomedibots in the bloodstream programmed to search out and destroy harmful viruses and cancers.

*Longevity: Why we are living longer than ever and the discoveries that may allow us to live to by Dr David Goldhill is available from Amazon for £10 as a book or £ for the Kindle edition.

A human foetus in the womb can regenerate a damaged fingertip. After birth the capacity for repair and regrowth is rapidly lost. Across the animal kingdom there is a huge range in the ability to regenerate tissues and organs with some adult animals retaining the ability to regrow limbs, heart muscle, brain and spinal cord.

Stem cells may provide the answer to regeneration. These cells contain all the genetic information to become any other type of cell. During development the embryonic cell differentiates and turns into the specialised cell that is its destiny. We now know that these specialised cells can be rejuvenated back into pluripotent stem cells with the potential to turn into almost any other cell. These cells could be used to replace those lost or damaged and be used to build new organs without the risk of rejection. They are being investigated to replace or renew damaged tissue in brain and spinal cord, in the heart, to replace teeth, restore vision and transplant new 1st person to see cells cells to produce insulin.

With a few exceptions, each and every one of the 30 trillion cells that are your body contains a full set of DNA. This genetic material contains all the information needed to build and maintain an individual. The molecular structure of DNA was only identified in Inafter 13 years of work and at a cost of $bn (£bn), the more than 3 billion base pairs of the human genome were described for the first time. This was one of the most important discoveries that mankind has ever made.

Using a technique called CRISPR it is now theoretically possible to go to any strand of DNA from any life form, snip it in a precise location and then add or remove DNA. In humans this is the equivalent of taking volumes of the complete works of Shakespeare and purposefully editing one specific letter. Diseases such as Haemophilia B and sickle cell disease are already being treated with gene therapy. Genes from one species have been successfully inserted into another.

This creates novel changes impossible in nature. We already know that small genetic changes can profoundly affect longevity. In the future gene manipulation may directly introduce alterations in DNA to cure ageing and prolong life.

I was 26 when my grandfather died aged When he was born in the population of the world was about billion. I came along in by which time it had grown to billion. By the time of my granddaughter’s birth in the number of people on our planet had swollen to billion. The world my granddaughter was born into would be unrecognisable to the horse-drawn, steam-powered world of my grandfather’s birth. My grandchild can reasonably expect to live well into the 22nd century. But that is without accounting for medical progress. I stand as the link between my grandfather and my granddaughter. What will her world look like, and that of her grandchildren? Maybe she will be the first person to live to be 1, I celebrated the coming of the second millennia. Perhaps she will be around for the third?

This article is an extract from ‘Longevity: Why We are Living Longer than Ever and the Discoveries that May Allow Us to Live to ’ by Dr David Goldhill, which is available from Amazon in paperback (£10) and Kindle (£)

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The History Behind the Invention of the First Cell Phone

While cell phones are a fairly modern invention — if you consider modern — the idea of a telephone that could travel with you is as old as the telephone itself. For decades though, the best anyone could offer were bulky, two-way radio devices that were essentially walkie-talkies that filled the trunk of your car. However, a couple of key engineering developments and a classic tale of American business rivalry would help lay the foundation for the device that revolutionized the way people communicate.

Earliest Mobile Communications Devices

Since the turn of the 20th century, people have envisioned a world where they would be able to have a means of communication with each other continuously, free from the restricting wires and cables. With the introduction of radio communications in the early s, and the introduction of landline telephone services, it wasn’t hard to see why people would think that the invention of real mobile phones as we know them today would happen much sooner than it did.

RELATED: THE WORLD AT YOUR FINGERTIPS: A BRIEF HISTORY OF MOBILE DISPLAY TECHNOLOGY

For amazon fire stick 4k sound out of sync of their history, "mobile" phones were mostly two-way radios that you installed on something that moved. In the s, German railroad operators began testing wireless telephones in their train cars, starting with military trains on a limited number of lines, before spreading to public trains a few years later.

InZugtelephonie AG was founded as a supplier of mobile telephone equipment for use in trains, and the following year saw the first public introduction of wireless telephones for first-class passengers on major rail lines between Berlin and Hamburg.

The Second World War saw major advances in radio technology, with handheld farmers state bank cedar rapids coming into widespread use. These advances placed mobile radio systems in military vehicles around the same time, but technological limitations limited the quality of the systems significantly.

This didn't stop companies from offering mobile telephone systems designed for use in automobiles in the s and s in America and elsewhere. However, like their military counterparts, they came with serious drawbacks. They were large systems that required a lot of power, had limited coverage, and the networks weren't able to support more than a few active connections at a time. These limitations would hamper mobile phone technology for decades and put a ceiling on how fast the technology could be adopted by the public.

Major Developments Towards Modern Mobile Phone Systems

In response to this growing demand for better mobile telephony, AT&T’s Bell Labs went to work developing a system for placing and receiving telephone calls inside automobiles that allowed for a greater number of calls to be placed in a given area at the same time.

They introduced their mobile service inwhich AT&T commercialized in as the Mobile Telephone Service. The service was slow to take off, however, with only a few thousand customers in about localities in total. The system required an operator at a switchboard to set up a connection and the users had to push a button to talk and let go of it to listen, making it more like a military radio than the existing telephone system that people were used to.

The service was also expensive, and the number of channels available for active connections remained limited to as little as three channels in some places, and with a conversation taking up the entire channel for the duration of the call, there could never be more active conversations than there were available channels.

Bell Labs engineers were working on a new system that would 1st person to see cells the efficiency of these channels in the s. However, Douglas Ring and W. Rae Young proposed the idea of a network of ‘cells’ to help manage the reuse of channels and reduce 1st person to see cells as early as The technology just wasn’t there union savings bank mt washington the time, however, and it would be another couple of decades before a pair of Bell Labs engineers, Richard Frenkiel and Philip Porter, would build out this concept of cells into a more detailed plan for a mobile telephone network for automobiles. By this time, AT&T had already pushed the Federal Communications Commission to make more of the frequency spectrum available for radiotelephones, providing more channels for them to use.

Other significant developments in the s enabled automatic cell switching and signaling systems that allowed for devices to maintain a connection as they moved from one cell to another, expanding the area that mobile telephone networks could service. But all of these developments were put to use developing mobile phones in automobiles. It would take an upstart to give us the first hand-held cell phone, as we know bike repair at home near me today.

Motorola's Martin Cooper Invents The First Hdfc forex prepaid card net banking login Phone

While Bell Labs was working to develop the system that would become the cellular networks we are all familiar with, they weren’t having as much success in building an actual portable, handheld telephone. They had spent much of their efforts developing what we used to call the car phone. Though not anymore, since those aren’t really a thing now that everyone has hand-held phones.

The reason we don't all have car phones today was because of the work of a small company called Motorola, and a man named Marty Https www suntrust online banking.

“We believed people didn't want to talk in cars and that people wanted to talk to other people,” Cooper told the BBC in a interview, “and the only way we at Motorola, this little company, could prove this to the world was to actually show we could build a cellular telephone, a personal telephone.”

Build it they did. With encouragement from his boss, Motorola’s chief of portable communication products John Mitchell, Cooper, and the engineers at Motorola produced the working prototype for the first cell phone. On April 3,before stepping into a news conference in Manhattan to demonstrate the new device that would go on to revolutionize communications, Cooper tested it by placing the first public cellular phone call in history.

“I called my counterpart at Bell Labs, Pauls valley first united bank Engel,” Cooper said, “and told him: ‘Joel, I'm calling you from a “real” cellular telephone. A portable handheld telephone.’”

Beating AT&T to the punch was a thrilling experience for the upstart Motorola. They had taken on a company that at that time exercised monopoly power over American telephone systems.

“When you are a competitive entity like we were,” Cooper said, “it's one of the great satisfactions in life.

The Invention of the Cell Phone Was a Multi-Generational Effort

While demonstrated init would be another decade of development before Motorola’s cell phone — the world’s first — made it to market, and commercial cellular service for handheld cell phones began. Selling for about $3, at the time, no one — not even Cooper — saw Motorola’s DynaTAC x as the first step towards a communications revolution to come.

“I have to confess that [the widespread global use of cell phones] would have been a stretch at the time and in those first phones cost $3,, which is the equivalent of $7, today,” Cooper said in “But we did envision that someday the phone would be so small that you could hang it on your food stamp office houston or even have it embedded under your skin.”

As for whether Cooper accepted the title given to him by history, Father of the Cell Phone, he felt that the honor should be shared. “Even though I conceived of it,” he said, “it really took teamwork, and literally hundreds of people ended up creating the vision of what cellular is today, which by the way is not complete. We are still working on it and still trying to make it better.”

For a more comprehensive look at the history behind the cell phone, you can also check out our video below. 

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Living to 1, The man who says science will soon defeat ageing

Dr Aubrey de Grey is a Cambridge-affiliated biomedical gerontologist who believes ageing can be postponed for hundreds of years

Aubrey de Grey is one of the world’s leading – and most talked-about – biomedical gerontologists

Ageing can be rendered almost irrelevant if we decode the genetic markers that pre-dispose us to illnesses

Meet the man who believes that the first person to live to 1, years of age has already been born.

Aubrey de Grey is one of the chief proponents of research utilising genomics to explore longevity.

An Englishman living in California, Dr de Grey is a biomedical gerontologist who co-founded the SENS (Strategies for Engineered Negligible Senescence) Research Foundation in It explores the use of regenerative medicine to repair the damage underlying the diseases of ageing. Doing so, it is hoped, will improve our ‘healthspan’ – the length of time for which we enjoy good health.

Dr de Grey is listed at the University of Cambridge’s Centre for Science and Policy as the chief scientific officer for the SENS Foundation. He received a BA in Computer Science in and a Ph.D. in Biology from the University of Cambridge inand organised a series of conferences on longevity in the city in

Dr Aubrey de Greys theories on ageing are discussed in a wide variety of ways

He tells the Cambridge Independent: “SENS Research Foundation has a couple of dozen employees and other dependents, such as PhD students who depend on us for their salaries. Our mission is clear: the medical defeat of ageing via damage repair.”

The longevity theory is essentially about preventing people from getting sick. The model takes an engineering approach to human life. The aim is to use rejuvenation biotechnologies directly to remove, repair, replace, or render harmless the cellular and molecular damage caused by the biological ageing process.

And if you can reduce the process of degradation to the point where it never crosses the threshold of causing a life-threatening disease, we could effectively defeat ageing – and live to 1, or perhaps longer.

“The 1,year number is purely a ball-park estimate of the average lifespan – and even then, it’s in the context of today’s risk of death from causes that don’t arise from ageing, so it’s almost certainly very conservative,” Dr de Grey says.

Genetic theory is revealing a number of insights about the human condition that would have been unthinkable even a few decades ago

Would he want to live that long?

“I don’t want to get sick, and I don’t expect ever to want to get sick, however long I live,” he replies. “What I can’t imagine is ever basing my view of how bad it would be to get suntrust bank routing number for direct deposit on how long ago I was born.

“As for what other people can imagine, well, that’s rather dictated by whether the media remind them that long life can and will only happen as a side-effect of staying truly youthful, as opposed to focusing on the longevity side-effect as if it were the goal in and of itself.”

Explaining his motives for wanting to solve ageing in his TED Talk, Dr de Grey put it succinctly: “Getting frail and miserable and dependent is no fun.”

He believes we’re in a trance if we believe otherwise. And he dealt with those who suggest living to 1, might be boring, cause starvation and put dictators in charge for ever, not to mention play havoc with our pensions, with this verdict on such arguments: “These are completely crazy when you remember your sense of proportion. Are these so bad that they outweigh condemningpeople a day to an unnecessarily early death?”

What of overpopulation though?

Dr de Grey acknowledges that humanity will face a dilemma. We’ll need to decide whether to have a low birth rate or maintain a high death rate by 1st person to see cells such therapies. But there is a third way, he suggests.

“I believe that we will reduce the impact of the average person on the environment far faster than we increase global population, even without continued reductions in birth rate.”

So does he believe it would be possible to turn off the menopause?

“The ovary is just another organ – and indeed there has already been plenty of progress in ovary reconstruction and rejuvenation,” he points out. Failure to explore the potential of longevity, he argues, would be immoral.

He describes ageing as the result of our metabolism – the hugely complex set of homeostatic processes that keep us alive from day to day – eventually causing pathology, the hugely complex set of anti-homeostatic processes that kill us. In other words, our self-repair processes are not perfect.

While geriatricians will look to deal with pathology and try to hold back the sands of time, gerontologists aim to work with metabolism on the basis that prevention is better than cure.

Dr de Grey says we have discovered only seven types of damage that lead to pathology – such as cell loss and mutations in chromosomes. In principle, he says we know how to fix these in mice with a range of techniques, like cell therapy, growth factors and the expression of proteins.

Given sufficient funding, which he describes as the biggest challenge, he believes it will be possible to rejuvenate an ageing mouse within a decade. Fifteen years from that point, he argues the first therapies could be available within humans.

Bad news for somethings: the initial experimental therapies we’re about to invent will be too late for you, he suggests. But if you’re only 50 “then there’s a chance you may be able to pull out of the dive”.

And intriguingly, he believes the first person to live to be 1, will probably only be 10 years younger than the first year-old.

“It’s all about what I’ve called ‘longevity escape velocity’,” he tells us. This refers to the fact that ultimately technological advances will increase life expectancy more than the year that just went by.

In other words, Dr de Grey is clear that we’re not about to invent some incredible therapy that will enable us live to 1, But if we can deliver therapies that give a middle-aged person an extra 30 years of life expectancy, then by the time they get there, we’ll have further therapies to extend their life again. That’s how we’ll continue to stay ahead of the ageing process and, thanks to this incremental progress, he believes the first people who will live to 1, are already breathing.

There is considerable focus today on epigenetics – changes in gene expression that don’t affect our underlying DNA code. So is this part of the plan? Walmart eye center mexico mo so much, apparently.

“Epigenetic changes during ageing tend to be good things – deliberate changes that cells make, in order to minimise and delay the impact of other types of damage,” says Dr de Grey says. “Our work focuses on eliminating that damage; once we do so, the epigenetic changes will become unnecessary and will probably reverse themselves spontaneously.”

Nor is what we eat a particularly significant factor in defeating ageing, he suggests.

“Diets are really not very important in all this. One may be able to obtain a very modest postponement of ageing by dietary choices, but only very modest relative to just basically doing what your mother said – not getting seriously overweight, and being reasonably varied in terms of fruit and veg. I don’t follow any special diet,” he adds.

Let’s assume he’s right, then, and humans start living to 1, Won’t we run out of food for us all?

“The elimination of age-related ill-health will not make problems for the food supply, because other technologies, such as renewable energy and artificial meat and desalination, will be well-established years before the end of ageing,” he suggests.

Living to 1, – or more – raises all sorts of philosophical questions about what it means to be human, but Dr de Grey says: “I find so-called philosophical discussions of this issue to be a wholly counter-productive distraction, founded not in philosophy but psychology, ie the fear of believing that this time, finally, after so many false dawns throughout the history of civilisation, we may finally be about to overcome our oldest and most formidable adversary.”


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