Audiovisuals Reviews

Book reviewed in this article:
Vagrant Woman . A film by JOHN MARSHALL
A Forty Dollar Misunderstanding . A film by JOHN MARSHALL
Two Brothers . A film by JOHN MARSHALL
Wrong Kid . A film by JOHN MARSHALL
The Informant . A film by JOHN MARSHALL
After the Game . A film by JOHN MARSHALL
901/904 . A film by JOHN MARSHALL
An Investigation of a Hit and Run . A film by JOHN MARSHALL
A Legal Discussion of a Hit and Run . A film by JOHN MARSHALL
Nothing Hurt but My Pride . A film by JOHN MARSHALL
Youth and the Man of Property . A film by JOHN MARSHALL
Manifold Controversy . A film by JOHN MARSHALL
Appitsch and the Drunk . A film by JOHN MARSHALL
Henry is Drunk . A film by JOHN MARSHALL
T-Group . A film by JOHN MARSHALL
You Wasn't Loitering . A film by JOHN MARSHALL     

Reviews of publications

Principles of Crop Improvement, by N. W. Simmonds
Marine Organisms – Genetics, Ecology & Evolution, edited by B. Battaglia & J. A. Beardrnore
Arthropod Phytogeny, edited by A. P. Gupta. Van Nostrand Reinhold
Field Guide to the Land Snails of Britain and North-west Europe, by M. P. Kernev & R. A. D. Cameron; illustrated by Gordon Riley
Key to the Fishes of Northern Europe, by Alwync Wheeler; illustrated by Peter Stebbing; maps by F. Rodney Fraser
Penguin Nature Guides: The Biology of Flowers, by Eigil Holm; illustrated by Thomas BredsdorfT; translated by Joan Tate; edited & adapted by Ronald Melville
Penguin Nature Guides: Orchids of Northern Europe, by Sven Nilsson; illustrated by Bo Mossberg; edited & adapted by P. Francis Hunt
A New Look at the Dinosaurs, by Alan Charig. Heinemann     

PHARMACOLOGICAL STUDIES ON THE STIMULATION OF THE PHOSPHOLIPASE A2-ACYLATION SYSTEM OF SYNAPTIC MEMBRANES OF BRAIN, BY NEUROTRANSMITTERS AND OTHER AGONISTS

Methacholine, nicotine and succinylcholine stimulated the phospholipase A2-acylation system of synaptic membranes isolated from the cerebral cortex of guinea pig. Stimulation by acetylcholine was partially blocked by atropine and by D-tuberocurarine respectively, indicating both muscarinic and nicotinic stimulation. Muscarinic stimulation by acetylcholine was greater than -isotinic stimulation, and stimulation by acetylcholine was completely blocked by a combip, or;. and n-tuberocurarine. The phospholipase A2-acylat tem was stimulated by phenylcphrine., id. Cqxoterenoi. Stimulation by noradrenaline was J-. tidlr, by phenoxybenzamine and pindalol i:spectively, indicating both 8-adrenergic and P-adrenergic ztimulation. n-Adrenergic stimulation by noradrenaline was greater than P-adrenergic-stimulation. 5 -mlation by noradrenaline was completely blocked by a combination of phenoxybenzamins and pindalol. Stimulation of both acylation and phospholipid hydrolysis, by 5-hydroxytryptamine and histamine were partially blocked by methysergide and diphenhydramine respectively. Stimulation by dopamine was blocked by halopcridol. Stimulation by y-aminobutyric acid was partially blocked by strychnine and by picrotoxin. Dichloroisoproterenol, atropine, methysergidr, diphenhydramine, strychnine, picrotoxin and eserine, at relatively high concentrations (1 mM), stimuhted the phospholipase A2-acylation system. Synergistic stimulations of both acylatior, and hydrolysis of phosphatidylcholine, were observed by adenosine combined with noradrenaline, 5-hydroxytryptamine, histamine, dopamine or yaminobutyric acid, respectively. In the presence of ATP-MgCI, synergistic stimulations of the hydrolysis of phosphatidyicholine were observed after 30 s by noradrenaline combined with 5-hydroxytryptamine, histamine, dopamine, aminobutyric acid or carbamoylcholine respectively. In the presence of GTP-MgC12 synergistic stimulations were obtained by cdrbamoylcholine combined with noradrenaline. 5-hydroxytryptamine. histamine, dopamine or y-aminobutyric acid, respectively. In the presence of ATP-MgC12 plus GTP-MgC12, stimulation by noradrenaline and one other agonist including 5-hydroxytryptamine, histamine, dopamine, y-aminobutyric acid or carbamoylcholine were close to additive.     

Reviews of publications

Book reviewed in this article:
The Voyage of Charles Darwin: His Autobiographical writings, selected and arranged by Christopher Railing.
Penguin Nature Guides: Fungi of Northern Europe, Vols I & II, by S. Nilsson &; O. Persson; illustrated by B. Mossberg
Penguin Nature Guides: Plant Communities, by Anned Biilow-Olsen, illustrated by Susanne Larsen; translated from the Danish by Joan Tate; edited and adapted by Francis Rose.
Penguin Nature Guides: Fishes of the British and Northern European Seas, by J. Moller Christensen; illustrated by Bente Nystrom; translated from the Danish by Gwynne Vevers; edited and adapted by Gwynne Vevers and Philip Orkin.
Birds of Wood, Park and Garden, text and illustrations by Lars Jonsson; translated from the Swedish by Roger Tanner
Birds of Sea and Coast, text and illustrations by Lars Jonsson; translated from the Swedish by Roger Tanner     

Different types of ADP-ribose protein bonds formed by botulinum C2 toxin, botulinum ADP-ribosyltransferase C3 and pertussis toxin

We attempted to characterize ADP-ribose-amino acid bonds formed by various bacterial toxins. The ADP-ribose-arginine bond formed by botulinum C2 toxin in actin was cleaved with a half-life of about 2 h by treatment with hydroxylamine (0.5 M). In contrast, the ADP-ribose-cysteine bond formed by pertussis toxin in transducin and the ADP-ribose-amino acid linkage formed by botulinum ADP-ribosyltransferase C3 in platelet cytosolic proteins were not affected by hydroxylamine. HgCl2 cleaved the ADP-ribose-amino acid bond formed by pertussis toxin in transducin but not those formed by botulinum C2 toxin or botulinum ADP-ribosyltransferase C3 in actin and platelet cytosolic proteins, respectively. NaOH (0.5 M) cleaved the ADP-ribose-amino acid bonds formed by botulinum C2 toxin and pertussis toxin but not the one formed by botulinum ADP-ribosyltransferase C3. The data indicate that the ADP-ribose bond formed by botulinum ADP-ribosyltransferase C3 differs from those formed by the known bacterial ADP-ribosylating toxins.     

Relationship between ion requirements for respiration and membrane transport in a marine bacterium.

Intact cells of the marine bacterium Alteromonas haloplanktis 214 oxidized NADH, added to the suspending medium, by a process which was stimulated by Na+ or Li+ but not K+. Toluene-treated cells oxidized NADH at three times the rate of untreated cells by a mechanism activated by Na+ but not by Li+ or K+. In the latter reaction, K+ spared the requirement for Na+. Intact cells of A. haloplanktis oxidized ethanol by a mechanism stimulated by either Na+ or Li+. The uptake of alpha-aminoisobutyric acid by intact cells of A. haloplanktis in the presence of either NADH or ethanol as an oxidizable substrate required Na+, and neither Li+ nor K+ could replace it. The results indicate that exogenous and endogenous NADH and ethanol are oxidized by A. haloplanktis by processes distinguishable from one another by their requirements for alkali metal ions and from the ion requirements for membrane transport. Intact cells of Vibrio natriegens and Photobacterium phosphoreum oxidized NADH, added externally, by an Na+-activated process, and intact cells of Vibrio fischeri oxidized NADH, added externally, by a K+-activated process. Toluene treatment caused the cells of all three organisms to oxidize NADH at much faster rates than untreated cells by mechanisms which were activated by Na+ and spared by K+.     

Involvement of transforming growth factor-alpha secreted by macrophages in metallothionein induction by endotoxin

The mechanism of metallothionein (MT) induction of the liver by endotoxin, which is mediated by a factor secreted by endotoxin-stimulated macrophages, was studied in vitro. MT induction of the liver cells by the endotoxin-stimulated macrophage conditioned medium was inhibited by a monoclonal antiepidermal growth factor (EGF) / transforming growth factor-alpha (TGF-alpha) receptor antibody, which acts as an antagonist of EGF and TGF-alpha. MT was induced by the substance, which was adsorbed by polyclonal antibody to TGF-alpha, but not by a monoclonal antibody to EGF, in the conditioned medium of endotoxin-stimulated macrophages. These results suggest that TGF-alpha secreted by macrophages is involved in MT induction by endotoxin.     

Reviews of publications

Book reviewed in this article:
Taxonomy of Economic Seaweeds: With reference to some Pacific and Caribbean Species, 2 edited by Isabella A. Abbott. La Jolla
Botanic Gardens and the World Conservation Strategy edited by D. Bramwell, O. Hamann, V. Heywood & H. Synge
Introduction to Ecological Biochemistry 3rd ed., by J. B. Harborne
A monographic study of the genus Rosularia (Crassulaceae) by Urs Eggli
The Photographic Guide to Identify Mediterranean Wild Flowers by Roger Phillips assisted by Martin Rix and Nicky Fox
The Photographic Guide to Identify Mediterranean Wild Flowers by Roger Phillips assisted by Martin Rix and Nicky Fox
Conserving the Wild Relatives of Crops by Erich Hoyt.
Somatic Cell Genetics of Woody Plants edited by M. R. Ahuja
Indian Journal of Natural Rubber Research
Dictionary of Weeds of Eastern Europe by G. Williams and K. Hunyadi
Nutrition of the Angiosperm Embryo by David R. Murray.
Plant Pigments edited by T. W. Goodwin.
Panbiogeography edited by R. Craw & G. Sermonti
Saxifrages of Europe: with notes on African, American and some Asiatic species by D. A. Webb & R. J. Gornall     

植物生长调节物质IP－1号对木薯产量及其生物性状的影响

１９９０和１９９１年在木薯（ＭａｎｉｈｏｔｅｓｃｕｌｅｎｔａＣｒａｎｔｚ）生长期以植物生长调节物质ＩＰ－１号０,２０,３０和４０ｐｐｍ进行叶面喷洒,结果表明：３０ｐｐｍ处理可使木薯块根产量平均增加５４．４４％,块根淀粉含量平均提高２０．８１％。单株最大薯重提高３１．５５％,块根数增加２１．１７％,块根长度增长１７．６２％,地上部鲜重增加３４．３６％,植株高度增加４．３６％,植株收获期保留青叶数增加１９．４２％,主茎直径增加６．２６％,块根直径增加２．５８％,叶片的叶绿素和蛋白质含量分别提高５．５７％和２５．９６％,叶片光合作用强度提高１５．８６％,而对主茎高度、主茎节数没有明显影响。     

The regulation of rat liver tryptophan pyrrolase activity by reduced nicotinamide-adenine dinucleotide (phosphate). Experiments with glucose and nicotinamide.

1. Chronic administration of glucose or nicotinamide in drinking water inhibits the activity of rat liver tryptophan pyrrolase, and subsequent withdrawal causes an enhancement. The enzyme activity is also inhibited by administration in drinking water of sucrose, but not fructose, which is capable of preventing the glucose effect. 2. The inhibition by glucose or nictinamide is not due to a defective apoenzyme synthesis nor a decreased cofactor availability. 3. The inhibition by nicotinamide is reversed by regeneration of liver NAD+ and NADP+ in vivo by administration of fructose, pyruvate or phenazine methosulphate. Inhibition by glucose is also reversed by the above agents and by NH4Cl. Reversal of inhibition by glucose or nicotinamide is also achieved in vitro by addition of NAD+ or NADP+. 4. Glucose or nicotinamide increases liver [NADPH]. [NADP+] is also increased by nicotinamide. [NADPH] is also increased by sucrose, but not by fructose, which prevents the glucose effect. Phenazine methosulphate prevents the increase in [NADPH] caused by both glucose and nicotinamide. 5. It is suggested that the inhibition of tryptophan pyrrolase activity by glucose or nicotinamide is mediated by both NADPH and NADH.     

Metallothionein inhibits peroxynitrite-induced DNA and lipoprotein damage

Previous studies have demonstrated that metallothionein functions as an antioxidant that protects against oxidative DNA, protein, and lipid damage induced by superoxide anion, hydrogen peroxide, hydroxyl radical, and nitric oxide. The present study was undertaken to test the hypothesis that metallothionein also protects from DNA and lipoprotein damage induced by peroxynitrite, an important reactive nitrogen species that causes a diversity of pathological processes. A cell-free system was used. DNA damage was detected by the mobility of plasmid DNA in electrophoresis. Oxidation of low density lipoprotein was measured by a thiobarbituric acid-reactive substance, which was confirmed by lipid hydroperoxide assay. Plasmid DNA damage and low density lipoprotein oxidation were induced by 3-morpholinosydnomine, which produces peroxynitrite through the reaction between nitric oxide and superoxide anion or by synthesized peroxynitrite directly. DNA damage by 3-morpholinosydnomine was prevented by both metallothionein and superoxide dismutase, whereas the damage caused by peroxynitrite was prevented by metallothionein only. The oxidation of low density lipoprotein by 3-morpholinosydnomine and peroxynitrite was also significantly inhibited by metallothionein. This study thus demonstrates that metallothionein may react directly with peroxynitrite to prevent DNA and lipoprotein damage induced by this pathological reactive nitrogen species.     

Interactions of acetate, propionate and butyrate in sheep liver mitochondria

1. Interactions in the rates of consumption of acetate, propionate and butyrate in sheep liver mitochondria were examined in the presence and absence of l-malate and alpha-oxoglutarate. 2. Acetate was not consumed in absence of ancillary substrate but utilization of acetate (7.2nmol/min per mg of protein) occurred in the presence of alpha-oxoglutarate. This consumption was abolished by propionate or butyrate but the presence of acetate did not affect consumption of propionate or butyrate. 3. Propionate consumption (10.1nmol/min per mg of protein) was unaffected by malate but was stimulated by 63% by butyrate or by 180% by alpha-oxoglutarate. 4. Butyrate consumption (3.3nmol/min per mg of protein) was stimulated by 117% by malate, by 151% by propionate and by 310% by alpha-oxoglutarate. 5. In the absence of ancillary substrates the maximum rate of total volatile fatty acid utilization (24.7nmol/min per mg of protein) occurred with a mixture of propionate and butyrate. When both propionate and butyrate were present total consumption was not affected by malate but was stimulated by 24% by alpha-oxoglutarate. With alpha-oxoglutarate present, propionate and butyrate each decreased the other's consumption by about 26%, but the total utilization was the greatest observed. 6. The inhibition of acetate consumption by propionate or butyrate is unexplained, but the remaining effects are consistent with an interaction of propionate and butyrate through oxaloacetate together with a general limitation imposed by a need for GTP to rephosphorylate AMP formed during activation of the volatile fatty acids.     

Reviews of Publications

Book reviewed in this article:
Flowers of the Himalaya , by Oleg Polunin and Adam Stainton.
A Guide to the Vegetation of Britain and Europe , by Oleg Polunin and Martin Walters.
The Experimental Biology of Bryophytes, edited by A. F. Dyer & J. G. Duckett.
A Birdwatcher's Miscellany, edited by Rob Hume.
The Moths and Butterjlies of Great Britain and Ireland, Volume 10, Noctuidae (Part II) and Agaristidae, edited by J. Heath.
Atlas of Butterjlies in Britain and Ireland, by J. Heath, E. Pollard & J. A. Thomas.
Colour Identification Guide to Butterjlies of the British Isles, revised edition by T. G. Howarth.
The World of Butterjlies, An Illustrated Encyclopaedia, by V. Sbordoni & S.Forestiero.
Colour Identijcation Guide to Moths of the British Isles, by Bernard Skinner.
The Biology of Buttegies, edited by R. I. Vane-Wright & P. R. Ackery.
Australian Grasses, by Nancy T. Burbidge, revised by Surrey W. L. Jacobs.
Collins Guide to Grasses, Sedges, Rushes and Ferns, by R. Fitter & A. Fitter. Collins.
Grasses of the Soviet Union, by N. N. Tsvelev, edited by A. A. Fedorov.
The European Garden Flora, Volume 2, Monocotyledons (Part ZZ), edited by S. M Walters et al.
Grasses, 3rd edition, by C. E. Hubbard, revised by J. C. E. Hubbard.     

Body composition techniques and the four-compartment model in children.

The purpose of this study was to compare the accuracy, precision, and bias of fat mass (FM) as assessed by dual-energy X-ray absorptiometry (DXA), hydrostatic weighing (HW), air-displacement plethysmography (PM) using the BOD POD body composition system and total body water (TBW) against the four-compartment (4C) model in 25 children (11.4 +/- 1.4 yr). The regression between FM by the 4C model and by DXA deviated significantly from the line of identity (FM by 4C model = 0.84 x FM by DXA + 0.95 kg; R(2) = 0.95), as did the regression between FM by 4C model and by TBW (FM by 4C model = 0. 85 x FM by TBW - 0.89 kg; R(2) = 0.98). The regression between FM by the 4C model and by HW did not significantly deviate from the line of identity (FM by 4C model = 1.09 x FM by HW + 0.94 kg; R(2) = 0. 95) and neither did the regression between FM by 4C (using density assessed by PM) and by PM (FM by 4C model = 1.03 x FM by PM + 0.88; R(2) = 0.97). DXA, HW, and TBW all showed a bias in the estimate of FM, but there was no bias for PM. In conclusion, PM was the only technique that could accurately, precisely, and without bias estimate FM in 9- to 14-yr-old children.     

Possible involvement of eicosanoids in the zymosan and arachidonic-acid-induced oxygen uptake, glycogenolysis and Ca2+ mobilization in the perfused rat liver

Exposure of perfused rat livers to zymosan, arachidonic acid and phenylephrine, but not to latex particles, induces pronounced oxygen uptake, glycogenolysis and Ca2+ mobilization. The oxygen uptake induced by arachidonic acid and by zymosan remains elevated even after the agents have been removed. NaN3 was found to be much more effective in inhibiting the oxygen uptake induced by phenylephrine than that induced by zymosan or arachidonic acid. Glucose release induced by zymosan and by arachidonic acid reaches a maximum after about 2 min and then declines very rapidly even while the agents are still being infused. In contrast, glucose release induced by phenylephrine remains elevated for the duration of the infusion. Ca2+ fluxes induced by arachidonic acid are similar to those induced by phenylephrine in that efflux occurs when the agent is administered and influx occurs only when the agent is removed. This contrasts to the Ca2+ flux changes induced by zymosan where both Ca2+ efflux and Ca2+ influx occur even while zymosan is still being infused. Glucose release induced by zymosan is inhibited by bromophenacylbromide and nordihydroguaiaretic acid, but not by indomethacin. Indomethacin, however inhibits the arachidonic-acid-induced glucose release which is also inhibited by nordihydroguaiaretic acid but not by bromophenacylbromide. Indomethacin inhibits also the arachidonic-acid-induced Ca2+ flux changes whereas the zymosan- and the phenylephrine-induced Ca2+ flux changes are not inhibited by the cyclooxygenase inhibitor. The data presented in this paper suggest that in the perfused rat liver the zymosan-induced glycogenolysis, as well as the Ca2+ flux changes and glycogenolysis induced by arachidonic acid, are mediated by eicosanoids.     

Resistin release by human adipose tissue explants in primary culture

Resistin, also known as Fizz3 or ADSF, is a protein found in murine adipose tissue and inflammatory lung exudates. The present studies found that resistin was released by explants of human adipose tissue but the release was quite variable ranging from 3 to 158 ng/g over 48 h. The release of resistin was 250% greater by explants of omental than by explants of human subcutaneous abdominal adipose tissue. Resistin release by adipocytes was negligible as compared to that by the non-fat cells of adipose tissue. Leptin formation by adipocytes was 8-fold greater than its formation by the non-fat cells, while the formation of PAI-1 by adipocytes was 38% of that by the non-fat cells. The conversion of glucose to lactate as well as the formation of PGE(2) and IL-8 was approximately 15% of that by the non-fat cells. In contrast the release of IL-6 and IL-1beta by adipocytes was 4-7% of that by the non-fat cells while the formation of resistin and IL-10 by adipocytes was 2% of that by non-fat cells. The release of adiponectin by explants ranged from 1000 to 5000 ng/g over 48 h but did not correlate with that of resistin. The present data suggest that resistin release by explants of human adipose tissue in primary culture is largely derived from the non-fat cells present in the explants.     

Effect of acetaldehyde and cyanamide on the metabolism of formaldehyde by hepatocytes, mitochondria, and soluble supernatant from rat liver

Formaldehyde can be metabolized primarily by two different pathways, one involving oxidation by the low-Km mitochondrial aldehyde dehydrogenase, the other involving a specific, glutathione-dependent, formaldehyde dehydrogenase. To estimate the roles played by each enzyme in formaldehyde metabolism by rat hepatocytes, experiments with acetaldehyde and cyanamide, a potent inhibitor of the low-Km aldehyde dehydrogenase were carried out. The glutathione-dependent oxidation of formaldehyde by 100,000g rat liver supernatant fractions was not affected by either acetaldehyde or by cyanamide. By contrast, the uptake of formaldehyde by intact mitochondria was inhibited 75 to 90% by cyanamide. Acetaldehyde inhibited the uptake of formaldehyde by mitochondria in a competitive fashion. Formaldehyde was a weak inhibitor of the oxidation of acetaldehyde by mitochondria, suggesting that, relative to formaldehyde, acetaldehyde was a preferred substrate. In isolated hepatocytes, cyanamide, which inhibited the oxidation of acetaldehyde by 75 to 90%, produced only 30 to 50% inhibition of formaldehyde uptake by cells as well as of the production of 14CO2 and of formate from [14C]formaldehyde. The extent of inhibition by cyanamide was the same as that produced by acetaldehyde (30-40%). In the presence of cyanamide, acetaldehyde was no longer inhibitory, suggesting that acetaldehyde and cyanamide may act at the same site(s) and inhibit the same formaldehyde-oxidizing enzyme system. These results suggest that, in rat hepatocytes, formaldehyde is oxidized by cyanamide- and acetaldehyde-sensitive (low-Km aldehyde dehydrogenase) and insensitive (formaldehyde dehydrogenase) reactions, and that both enzymes appear to contribute about equally toward the overall metabolism of formaldehyde.     

Induction of the non-selective mitochondrial pore in lymphoid cells. 1. Permeabilized rat thymocytes.

The opening of the cyclosporin-sensitive pore in the inner membrane of mitochondria in rat thymocytes was studied. In thymocytes with digitonin-permeabilized plasma membrane, the mitochondrial pore was induced by Ca2+ overload, by uncoupling, by oxidation or cross-linking of membrane dithiols, and by atractyloside, a specific inhibitor of the adenine nucleotide transporter. Pore opening was prevented by cyclosporin A (CsA) and by its non-immunosuppressive analog MeVal-CsA. The sensitivity of the pore to CsA was decreased by atractyloside and practically disappeared when it was added in combination with uncoupler. The main properties of the pore in mitochondria from thymocytes and from hepatocytes are the same. Release of Ca2+ from thymocyte mitochondria induced by uncoupling is mediated by a specific uniporter and by the pore with similar rates.     

Response of larch species to climate changes

Global warming has changed the distributions of forests of northeastern China. Larix are very important species in this area. Predicting the potential distributions of Larix species and their responses to climate change would attract more and more attention.This paper predicted the potential distributions of three Larix species based on 'climatic-topographic' relationships by logistic regression. The results showed that L. gmelinii is predicted to retreat northwestward by 220 km by 2050 and by 270 km more by 2100; L. olgensis var. changpaiensis is predicted to retreat northwestward by 200 km by 2050 and by 190 to 300 km more by 2100; L. principis-rupprechtii is predicted to retreat northeastward by 200 km by 2050 and by 250 to 400 km more by 2100. This indicated that L. gmelinii could have its optimum latitude moved into Russia, L. olgensis var. changpaiensis could move to the Small Xing'an Mountains and L. principis-rupprechtii would move to the middle part of the Great Xing'an Mountains.     

Reviews of publications

Book reviewed in this article:
A World Like Our Own—Man and Nature in Madagascar , by Alison Jolly.
Vertebrate Limb Regeneration , by H. Wallace.
Statistical Methods in Biology , by N. T.J. Bailey
Conservation and Evolution , by O. H. Frankel & M. E. Soule
Evolution in Age-structured Populations by B. Charlesworth
Essential Biology , by Herbert T. Hendrickson
Flora Suzakiensis , edited by Biological Laboratory, Imperial Household
Phylogenetic Patterns and the Evolutionary Process , by N. Eldredge & J. Cracraft
Excursion Flora of the British Isles , by A. R. Clapham, T. G. Tutin & E. F. Warburg
Whales , by W. N. Bonner
Les Chevaux, Fossiles et Actuels , by V. Eisenmann
Freshwater Snails of Africa and their Medical Importance , by David S. Brown
Symbiosis in Cell Evolution , by Lynn Margulis
Vegetation Dynamics , by J. Miles