摘要:

Summary1. A mode of origin of cephalopod buoyancy, by withdrawal of the animal from the apex of the shell followed by withdrawal of liquid from the resulting space, is suggested.2. Buoyancy, once evolved, gave cephalopods an immediate advantage over contemporary animals and evolutionary radiation in the early Ordovician was a consequence of this.3. The earliest cephalopods probably had curved (cyrtocone) shells. Tightly coiled shells evolved from cyrtocones in at least two separate lineages and were in the first place adapted to a benthonic existence. Straight shells (orthocones) were adapted for efficient swimming. They usually had apical counterweights to maintain a horizontal position, but in forms without counterweights, liquid‐filled chambers could have served the same purpose.4. Six evolutionary branches are described, which were distinct by the end of the Canadian (Lower Ordovician). Each branch is believed to be monophyletic, and up to a point each is characterized by certain structures or trends.5. Increased efficiency in jet propulsion became possible in one orthocone group, consequent on loss of the ventral wall of the body‐chamber, so that the mantle cavity wall could become muscular and contractile. This group gave rise to the living di‐branchiates, or Coleoidea.6. The primitive septum, which was concave forwards, remained standard in most orthocones and in some coiled shells. Folded septal edges, giving rise to more or less complex septal sutures, evolved independently in a number of coiled lineages. Their significance is unknown.7. The siphuncle is simple and small in all coiled shells and in some orthocones. In some cyrtocones and other orthocones large siphuncles of complex structure were evolved. They usually contain deposits which are interpreted as counterweights.8. Existing classifications of cephalopoda stem from subdivisions recognized in the nineteenth century when knowledge of fossils was inadequate. They are ill‐balanced and should be abandoned.9. A classification based on phylogeny is now possible. The six branches already described may be regarded as major subdivisions. In addition, it may be desirable to subdivide branches on the basis of important evolutionary changes. The strongest case is for the separation of Coleoidea on the grounds of the loss of th

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1964.tb01160.x

出版商:Blackwell Publishing Ltd    

年代:1964

数据来源: WILEY

摘要:

SummaryThe radiosensitivity of germ cells depends on (a) the criterion by which it is assessed, and (b) the developmental stage at the time of irradiation. For any given parameter and cell‐type, the final effect exerted by ionizing radiations depends on the genetic make‐up and age of the organism; type of irradiation; method of irradiation (acute, fractionated, chronic at different dose rates); oxygen tension; and temperature. Variations between different developmental stages may be due to inherent changes in oxygenation, metabolic activity, chromosomal configuration; and other factors, as yet to be determined, are probably also involved. The yield of mutations observed after irradiation of different developmental stages may be at least partly determined by the selective elimination, during subsequent development, of cells sensitive to immediate or delayed cell‐death.In general, mitotically active gonia, particularly in mammals, are highly sensitive to cell‐killing. In some species, inhibition of mitosis may play a considerable part in the final expression of radiation damage. Paradoxically, permanent sterilization in male rodents is most readily achieved by irradiating mitotically inactive primordial germ cells before or shortly after birth. In adult males of all species, permanent sterilization only occurs if all the primary gonia are destroyed. The last pre‐meiotic generation of spermatogonia appears to be more sensitive to cell‐death than are earlier generations; the difference is correlated with the relative durations of theG1, Sand G2periods, at least in adult mice. It is possible that mammalian pre‐meiotic oogonia are also more sensitive than preceding generations. Interpretation of observations on insects is complicated by radiation‐damage to nurse cells which may secondarily hamper the development of the germ cells.The incidence of chromosomal aberrations and mutations following gonial irradiation is relatively low, possibly due to selective elimination. A proportion of gonia which survive to give rise to differentiated gametes may carry a variety of mutations, including dominant lethals (of a special type). The claim that a reduction in dose rate lowers the yield of mutations following gonial irradiation in the male mouse has so far not been confirmed by studies onDrosophila.Primary meiocytes are relatively insensitive to cell‐killing. Cells irradiated as spermatocytes may fail, or be slow to complete normal maturation division(s), or they may give rise to morphologically abnormal spermatids. The effect depends upon the phase of meiosis at irradiation. In both sexes, sensitivity to cell‐death appears to decrease more or less progressively as meiotic prophase advances; in most female mammals, the trend is sharply reversed at early diplotene, when the oocytes become enveloped within primordial follicles. As the oocyte enters upon its rapid phase of growth which, in many species, is associated with vitellogenesis, sensitivity decreases again. Growing oocytes at the diplotene stage are relatively resistant to cell‐killing in almost all species investigated. Due to the brief duration of subsequent stages of meiosis (diakinesis, metaphase I), sensitivity to cell‐death is difficult to establish. As judged by the induction of dominant lethals, sensitivity of oocytes increases sharply between diplotene and metaphase I; in rodents, the rise becomes manifest a few hours before the onset of diakinesis. Increases of the same magnitude in the incidence of chromosomal aberrations at anaphase I and II have been scored for microsporocytes. Corresponding data for spermatocytes are less reliable, but there is some evidence indicating the same trend.In general, sensitivity to the induction of mutations is greater in meiocytes than in gonia. The yields of some mutations in the female have been shown to rise as meiotic prophase proceeds; but the relative increase as metaphase I approaches is not always as striking as that recorded for dominant lethals. Differential sensitivity to mutagenesis in spermatocytes at various stages of meiotic prophase has not been fully documented. There is some reason to believe that spermatocytes at early stages of meiotic prophase are less susceptible to mutation induction than those nearing the end of prophase.The sensitivity of secondary meiocytes has not been quantitatively assessed except by the incidence of chromosomal aberrations and dominant lethality. In both plants and animals, cells at metaphase II appear to be somewhat less sensitive than those at metaphase I.Spermatids, whose homologous stage is absent in the female, are apparently highly resistant to the induction of morphological abnormalities or cell‐death, In contrast, they are highly sensitive to the induction of dominant lethals and a variety of mutations; those at early stages of spermiogenesis appear to be more susceptible than those approaching full differentiation. Corresponding changes are less readily induced in fully differentiated spermatozoa. Anoxia during irradiation diminishes the difference between spermatids and spermatozoa, without however abolishing it. Spermatozoa irradiated after insemination are more sensitive to mutagenesis than are those retained within the testes or the male genital ducts.Irradiation of differentiated gametes of either sex shortly before fertilization induces a delay in subsequent cleavage. While eggs undergo some spontaneous recovery if the period between irradiation and fertilization is prolonged, spermatozoa do not.There is at present no single working hypothesis to account for all the s

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1964.tb01161.x

出版商:Blackwell Publishing Ltd    

年代:1964

数据来源: WILEY

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1964.tb01162.x

出版商:Blackwell Publishing Ltd    

年代:1964

数据来源: WILEY

摘要:

SummaryIn reviewing a problem such as atherogenesis in man and animals, it is easy to overemphasize one particular aspect of the pathogenesis and to ignore or discredit other equally well‐substantiated factors. A multitude of atherogenic mechanisms have been advanced in the literature—some reasonably well proven and some quite tentative—but, rather than ignore or arbitrarily reject a number of these concepts, it will be assumed that each is a lesser or greater particle in the complex jigsaw of atherogenesis. A speculative diagram of the interrelationship of various atherogenic and anti‐atherogenic mechanisms is presented in Text‐fig. 4.In human atherosclerosis the initiating factor appears to be intimal thickening of the artery induced by encrustations of mural thrombus and fine films of fibrin. This mechanism has, however, only been observed on one occasion in spontaneous atherosclerosis of animals. Whether the failure to observe it in mammals and birds is due to insufficient search or whether the pathogenesis of the animal disease is different in this respect from human atherosclerosis is uncertain.It is postulated that hyperlipaemia and hypertension increase respectively the amount and rate of lipid transport across the arterial wall. From studies on the effects of feeding a cholesterol‐enriched diet to the experimental animal and on the fate of subcutaneously injected cholesterol, it is concluded that accumulation of cholesterol in the tunica intima promotes proliferation of connective tissues, sclerosis and intimal thickening in the arteries in man, other mammals and birds. In man, haemorrhage into the vascularized and thickened tunica intima appears to provoke further organization and thickening. Mechanical strains on the human arterial wall are exaggerated by hypertension and, by inducing reparative changes, contribute to intimal thickening. Such strains are held to be responsible for the severity of atherosclerosis at certain sites of greatest mechanical stress, such as bends, bifurcations and orifices in arteries. Likewise, focal accentuation of experimental atheroma occurs after local application of a variety of physical and chemical insults to the arterial wall.It is suggested that intimal thickening of the human artery, caused by the three mechanisms of encrustation, lipid accumulation and mechanical stress, precipitates ischaemia of the middle zone of the tunica media. Such ischaemia would interfere with the local synthesis of lipotrophic factors required to transport lipid across the human arterial wall and would lead to further accumulation of lipid in its inner layers. A self‐perpetuating circle would be set up, whereby intimal thickening encourages further mural thrombosis and lipid accumulation which, in turn, lead to further intimal thickening.In this explanation for the lipid accumulation seen in human atherosclerosis, as much emphasis has been placed on metabolic impairment of the normal outward flow of lipid through the arterial wall as on increased entry of lipid through the endo‐thelium from the blood. Conversely, in experimental atheroma produced by feeding cholesterol, the accumulation of lipid in the artery appears to be a result of gross overloading of an otherwise intact system for lipid transport in the arterial wall.Hyperlipaemia has the other important atherogenic role of accelerating fibrin deposition over the arterial wall and, at the same time, inhibiting serum fibrinolytic activity. Experimental evidence suggests that hyperlipaemia with high levels of triglyceride promotes thrombosis, presumably by increasing platelet adhesiveness and the coagulability of the blood. Some hormones act against hyperlipaemia either by increasing the catabolic breakdown and excretion of lipid or by diverting metabolites away from lipid synthesis towards protein and carbohydrate metabolism. Excess lipid can also be eliminated from plasma and tissue by the action of clearing factor or lipo‐lytic systems. Acid mucopolysaccharide—a component of these clearing systems—is synthesized in the atherosclerotic plaque and may, thus, contribute towards the local degradation of atheroma lipids.It can be argued, however, that it is not hyperlipaemia that is directly responsible for the deposition of lipid in human and animal arteries but, rather, an associated instability of the suspension of lipid in plasma and tissue fluid. Such instability may result from a deficiency of phospholipid and an excess of hydrophobic triglycerides, cholesterol and cholesterol esters in the β‐lipoprotein molecule and other vehicles for lipid transport. Hydrophilic surface‐active agents, such as phospholipid and the detergents Tritons and Tweens, appear to stabilize lipoprotein and shift the partition of lipids away from the arterial wall towards plasma. Furthermore, the arterial wall in both man and the experimental animal reacts to lipid infiltration by synthesis of phospholipid, in an apparent endeavour to stabilize infiltrated lipoprotein and to d

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1964.tb01163.x

出版商:Blackwell Publishing Ltd    

年代:1964

数据来源: WILEY