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This is a response to Robert Buzzanco's article, "Fear and (Self) Loathing in Lubbock," which argued against views expressed by the author about the US-Vietnam War. This essay emphasizes the perspective of anticommunist Vietnamese, suggests a rationale for American policy decisions, and contextualizes the outcome of the war with human choices rather than with a scheme of historical inevitability.

Viruses have long been considered a major environmental factor in the aetiology of Type I (insulin-dependent) diabetes mellitus and recent work has greatly confirmed and extended this role. In addition to the enteroviruses, there are several other viruses which, from time to time, have been considered potential causal agents for human diabetes. With the exception of rubella, their role is not clear. The relation of enteroviruses with Type I diabetes has only been properly clarified by the use of new technologies, especially those based on polymerase chain reaction methods to identify them in blood. It is now evident from studies in several countries that enterovirus infection accompanies or precedes the onset of diabetes in many children. It is less certain whether this is true for older persons or for other types of diabetes. Enterovirus infection in pregnancy has also been suggested to cause diabetes in children. The infection with enteroviruses seems to be linked to the induction of islet-cell autoantibodies as well as to the expression of interferon-alpha. Both of these events are connected with islet-cell destruction. It has become increasingly important to establish the nature of the infecting virus in the early stages of diabetes. It seems likely that a number of viruses of the coxsackie or echovirus type are involved, although the nature of the nucleotide sequences responsible for diabetogenicity remains elusive.

If we can clear our minds of “Vietnameseness” as the object of our knowledge and instead look carefully at what the peoples we call Vietnamese were doing at particular times and places, then we begin to see that beneath the veneers of shared fields of sounds and marks, or of however one may refer to mutually intelligible languages and writings, lay quite different kinds of peoples whose views of themselves and of others was significantly grounded in the particular times and terrains where they dwelled and in the material and cultural exchanges available in those times and terrains. If we speak of these peoples as oriented toward the surfaces of their times and places rather than as oriented toward an imagined unifying depth, we will shift the effects of our ideological intent upon the archive away from the figurations both of univocal national narratives and of multivocal regional narratives contextualized by the nation. In this essay, I am interested in how the archive can be read to disperse the coherencies of Vietnamese histories as epistemological or hermeneutical categories, whether they be conceived as national histories or as regional histories. Rather than simply opposing regional histories to a dominant national narrative, I believe that regional and national narratives are “cofigured” in ways similar to how Naoki Sakai has written of desires for Japanese originality in realms of language, literature, and national identity being mimetically cofigured with desires for the West (Sakai 1997, 15-16, 21-22, 51-52). Posing a regional identity does not erase or diminish the potency of a national identity but rather mimetically reinforces it in a schema of cofiguration. I endeavor an orientation toward the surface of time and place as a way of thinking beyond histories of region and nation.

Many different viruses belonging to several genera have the potential to damage beta cells. The mechanisms they employ are varied, and infection may result in either a direct destruction of islets and rapid insulin deficiency, or in a more gradual loss of functioning islets with the onset of diabetes many years later. Several case histories involving extensive cytolysis of beta cells can be directly linked to viral infection, whilst an example of diabetes occurring many years after viral infection is found in individuals who had a congenital infection with rubella virus. Here, the virus induces an autoimmune reaction against beta cells. Autoimmune phenomena have also been observed in islets following infections with viruses other than rubella, and thus activation of autoimmune mechanisms leading to beta-cell destruction may be a relatively frequent occurrence. Recent evidence shows that picornaviruses are not exclusively lytic, and can induce more subtle, long-term changes in beta cells, which may be important in the aetiology of diabetes. The exact mechanisms involved are not known, but it is clear that several viruses can directly inhibit insulin synthesis and induce the expression of other proteins such as interferons, and the HLA antigens. Strain differences in viruses are important since not all variants are tropic for the beta cells. Several laboratories are in the process of identifying the genetic determinants of tropism and diabetogenicity, especially amongst the Coxsackie B (CB) virus group. The sequence of one such diabetogenic CB4 strain virus has been determined. It is clear therefore that there are many viruses with the potential to induce diabetes, and a viral involvement in the pathogenesis of diabetes has been established in some instances. Further research work at both a fundamental and epidemiological level is now urgently needed to define the nature of the interaction of such viruses with the beta cell.

The effects of a diabetogenic strain of encephalomyocarditis (EMC) virus on total protein and insulin biosynthesis in mouse islets of Langerhans have been studied in tissue culture. In dispersed mouse islets, the rates of protein biosynthesis were assessed by measuring the incorporation of [3H]leucine into proteins. In infected dispersed islets incubated in 20 mM-glucose, both insulin and total protein biosynthesis were decreased at 6 h; only insulin biosynthesis was significantly decreased at 3 h. In whole islets, EMC virus brought about a decrease in glucose-stimulated protein and insulin biosynthesis as early as 2 h after infection without concomitant effects on insulin release. This inhibition of protein biosynthesis was still apparent at 20 h post-infection, at which time insulin release was found to be markedly elevated, and the islet insulin content was moderately decreased. At 44 h post-infection, glucose-induced insulin biosynthesis was preferentially inhibited. Infected islets at this later time point also displayed elevated levels of insulin release, and a marked loss of islet insulin content. When insulin mRNA and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA levels were assessed by dot-blot hybridization using appropriate cDNA probes, levels of insulin mRNA were shown to decrease steadily during the first 20 h of infection, in contrast with the levels of GAPDH mRNA. At 44 h post-infection, both types of mRNA were markedly decreased. It is suggested that there is an initial early ‘shut-off’ of protein synthesis without other detectable changes in islet function. This is followed by a phase where both insulin mRNA levels and insulin synthesis are dramatically decreased.

Infections with Coxsackie viruses (especially Coxsackie B4) are thought to be involved in the pathogenesis of diabetes. Many interdependent variables determine the outcome of an infection with a Coxsackie virus, one of them being the tropism of the virus for a specific tissue. The extent to which Beta cell tropic variants of Coxsackie B4 virus occur naturally was assessed. Human isolates of this virus were tested in an in vitro system in which elevated insulin release from infected islets incubated at a non-stimulatory (2 mmol/l) glucose concentration appears to be related to viral attack. Using this technique, 8/24 isolates tested, impaired secretory function in mouse islets. Some strains of Coxsackie B4 virus, therefore, will directly infect mouse islets in vitro leading to changes in islet cell function. In conclusion, these findings confirm that variants of Coxsackie B4 virus with the potential to damage Beta cells occur quite frequently in the natural population. In certain circumstances the damage they inflict on Beta cells may cause destruction of these cells, or precipitate overt diabetes.

Skin lipids and pH are two factors classically considered of importance in homeostatic characteristics of skin. Skin physiology in cats has received little attention. The aim of this study was to evaluate the long-term influence of sex, sexual status, season, and dietary fat and energy on these parameters. Twenty-four European short-haired laboratory cats, 14 months of age, were followed over a 1-year period. They were divided into 8 groups of three, according to: sex (12 males and 12 females), sexual status (intact or neutered) and diets [(high energy 4300 kcal/kg as fed, 21% fat) vs. (moderate energy 3500 kcal/kg as fed, 10% fat)]. Both diets were fed to all cats for 6 months following a cross-over design. Parameters regularly evaluated were skin pH and hair total lipid content (extraction from samples of 0.6–1.2 g of clipped hairs). The pH of the skin varied from 6.6–6.8 initially to 7.2–7.4 at the end of the study. This increase was significant only in intact animals (male and female). The dietary changes did not affect skin pH. Hair total lipid content was not affected by sex or the diets but slightly increased in all groups over the study period from 1.5–2.4 to 2.4–3.3%. In conclusion, skin pH appeared to be potentially modified by sexual status, but not by sex or dietary lipids and energy. Hair lipids do not appear to be affected by sex or increases in dietary lipids and energy. The slight increase in pH and hair lipids during the study was attributed to the change from young adult to adult stage of all cats. Funding: Royal Canin.

Skin physiology in cats has received little attention. The aim of this study was to evaluate the long-term influence of sex, time and the level of dietary fat and energy on the dynamics and qualities of the hair coat. Twenty-four European short-haired laboratory cats were followed over a 1-year period. They were divided into eight groups of three, according to: sex (12 males and 12 females), sexual status (intact or neutered) and diets [(high energy 4300 kcal/kg as fed, 21% fat) vs. (moderate energy 3500 kcal/kg as fed, 10% fat)]. Both diets were fed for 6 months to all cats following a cross-over design. The following parameters were evaluated throughout the study: thickness of hair coat and hair lengths (neck, rump, lateral, flank), hair regrowth (after periodic clippings of 25 cm2 areas), and telogen/anagen ratio. The thickness of the hair coat initially varied from 1.2–1.7 cm on the neck, 1–1.4 cm on the rump, 1.8–2.5 cm on the flank, and hair shaft lengths were 1.7–2.5, 3.7–3.9 and 2.5–3.2 cm, respectively. Comparison of values revealed few statistical differences: increase of the thickness of hair coat in neutered cats (male and female) during the study, and increase of the length of lateral hairs in all groups during the study. Over all periods and in all groups, the curve of growth was similar (rapid then slower). Some transient variations were attributed to temporary changes in ambient conditions. In conclusion, neither sex, nutrition or season (in housed cats) influenced the general quality of hair coat, in particular hair regrowth. Funding: Royal Canin.

Ketone bodies promote insulin secretion from isolated rat pancreatic islets in the presence of 5 mM-glucose, but are ineffective in its absence. At concentrations of 10 mM or less, the relative abilities of the ketone bodies to potentiate release are in the order D-3-hydroxybutyrate greater than DL-3-hydroxybutyrate greater than acetoacetate. The response curve relating insulin release to D-3-hydroxybutyrate concentration displays a threshold at 1 mM and a maximum at 10 mM. D-3-Hydroxybutyrate (5 mM, but not 10 mM) promotes insulin secretion in the presence of 5 mM concentrations of both L-arginine and DL-glyceraldehyde, but not with L-leucine, L-alanine, L-glutamate or 4-methyl-2-oxopentanoate. The oxidation rates of the exogenous ketone bodies do not correlate well with their capacities to promote insulin release. Moreover, the oxidation of 5 mM-D-3-hydroxybutyrate can be inhibited by 25% with methylmalonate (10 mM) without any diminution of release. The potentiation with D-3-hydroxybutyrate occurs without an observable increase in total islet cyclic AMP. However, a small net efflux matches the relative abilities of the ketone bodies to promote insulin release. With islets from 48 h-starved animals the insulin response is both diminished and less sensitive than in fed animals, since insulin secretion is not significantly raised until a threshold of 5 mM-D-3-hydroxybutyrate is reached. These results suggest that, in the rat at least, there should be a reappraisal of the physiological role of ketone bodies in the promotion of insulin release.

1. Rabbit islets of Langerhans were disrupted by ultrasonic methods and the sonicated preparations were used to study proinsulin biosynthesis. 2. When [3h]leucine is incubated in such preparations, incorporation takes place into proinsulin, as evidenced by characterization on polyacrylamide gels, and by the conversion of this labelled material into insulin, by using trypsin. 3. The labelled proinsulin may also be purified by antiinsulin antibody bound to Sepharose. 4. With the broken-cell preparation it was shown that incorporation of leucine is accelerated by increasing the glucose content of the medium from 2mM to 16mM. However, 16mM-galactose or -sucrose did not stimulate incorporation significantly from basal values. This effect of glucose was abolished by cycloheximide. 5. The significance of these findings in relation to the mechanism of glucose stimulation of proinsulin biosynthesis is discussed.

Infection of DBA2 mice with the M strain of EMC virus was used to study the effects of virusinduced diabetes on the A and B cells of the islets of Langerhans. A transient hypoglycaemia was seen in 48% of mice 2–3 days after infection and probably resulted from increased serum insulin concentrations together with inhibition of glucagon secretion at that time. Islets from hypoglycaemic mice showed no significant alterations from control level in basal or fluoride-stimulated adenylate cyclase activity. Overall, 70% of infected mice became hyperglycaemic with a maximum incidence 6 days after infection. Hyperglycaemia was accompanied by a dramatic reduction in the total pancreatic insulin content and in insulin secretory responses to glucose and theophylline, while A-cell structure and function appeared relatively unaffected in diabetic animals. Basal adenylate cyclase activity was increased in hyperglycaemic mice at 7 days after infection, while fluoride-stimulated adenylate cyclase activity was normal throughout the course of infection. Ultrastructural alterations were observed in a small proportion of B cells from two days after infection and included abnormalities of mitochondrial structure and increased electron opacity of the cytoplasm of affected cells, which subsequently led to complete necrosis. The results suggest that EMC virus specifically affects the B cells of the islets and that disturbances of A cell function may be secondary to B cell damage.

Diabetes was induced in 20–30% of adult CD1 mice 15–20 days after infection by a tissue culture propagated strain of Coxsackie B4 virus. Serum insulin and insulin release from isolated islets indicated a relative insulin deficiency in diabetic animals. In some animals diabetes appeared to be permanent whilst in many it was of a temporary nature. Histology showed only slight damage in both islet and acinar tissue. Infection with pancreas and heart adapted strains of Coxsackie B3 virus failed to produce diabetes in mice and, in contrast to the effects of Coxsackie B4, severe acinar cell damage was seen.

Blood insulin, blood glucose and the biosynthesis and release of insulin have been studied in mice made obese with a single injection of gold thioglucose. In such mice, blood glucose levels were normal, though serum insulin rose in parallel with the development of obesity. When compared with controls, insulin secretion and synthesis were increased in isolated islets of Langerhans from obese mice, over a wide range of glucose concentrations. However, in obese animals, insulin biosynthesis was augmented above control levels at 2 mmol/l glucose, whilst the increase in insulin secretion accompanying obesity only became evident at glucose concentrations greater than 5 mmol/l. After 2 min incubation, cyclic AMP rose more in islets from obese mice than in controls, though cyclic AMP levels did not significantly differ in either group after 10 min incubation with glucose. Glucose oxidation was also increased in islets of Langerhans from obese mice. It seems possible that changes in glucose oxidation, as well as in cyclic AMP levels, contribute to the alteration in the B cell response in this type of obesity.

Our chief sources of information about Vietnam until the middle of the tenth century are the dynastic histories and related writings of China. This is because, from the beginning of recorded history in Vietnam until then, Vietnam was, for the most part, under the authority of Chinese governors or people who posed as Chinese-style governors. By the end of the tenth century, an independent Vietnamese monarchy was established, and historical information was being independently preserved by the Vietnamese; this information was eventually incorporated into the Vietnamese historiographical tradition as it developed in later centuries. Consequently, the historian of tenth-century Vietnam finds two streams of information, one coming from a wellestablished viewpoint from which Vietnam was a remote frontier district at the edge of the horizon, the other coming from the Vietnamese themselves as they worked toward a standpoint from which to remember their past.

Modern Vietnamese history is generally considered to begin with the seventeenth century. The final destruction of the Cham kingdom and the concurrent territorial expansion presided over by the Nguyễn lords of Hue increased the visibility of the Vietnamese people along the South China Sea and attracted the attention of refugees, merchants, and missionaries from China, Japan, and Europe. These foreign contacts were symptomatic of basic changes occurring in Vietnam; they were not the cause. From the decline of the Lê dynasty early in the sixteenth century, political life was dominated by militarized family alliances. By the second quarter of the seventeenth century, the two most successful families in the competition for power were locked in a grim testing of wills. Mutually aggressive policies remained inconclusive after half a century of warfare, however, and were eventually abandoned by both parties. This resulted from the rise of new interests tied to the internal social, political, and economic conditions of Vietnam. The rise of these new interests was the most significant development in the seventeenth century.

1. The effects of azaserine and nicotinamide, agents which inhibit and stimulate hepatic NAD synthesis respectively, on the content of NAD+ and NADH in isolated rat islets of Langerhans incubated in vitro were studied. The effects of these compounds on the rates of insulin release, from isolated islets incubated in vitro, in response to various secretagogues were also measured. 2. Preincubation of islets in the presence of azaserine (0.3mm) caused a marked depletion of the normal islet-cell content of both NAD+ and NADH and prevented the secretion of insulin in response to stimulatory concentrations of d-glucose, xylitol, d-xylulose, l-arginine hydrochloride and l-leucine. 3. Preincubation of islets in the presence of nicotinamide (2mm) increased the islet content of NAD+ and enhanced the rate of release of insulin in response to d-glucose. Also when nicotinamide was present the inhibitory effect of azaserine on insulin release and the azaserine-induced depletion of the islet content of NAD+ and NADH was prevented. 4. Preincubation with azaserine was without effect on the stimulation of insulin release caused by theophylline or dibutyryl cyclic AMP. 5. It is suggested that insulin release caused by sugars and amino acids is dependent on the maintenance of NAD concentrations, though this may not be the case for release due to theophylline and dibutyryl cyclic AMP.

LET ME begin with three assertions. First, causal analysis is an important and viable method for theory construction in sociology. Second, the Merton variety of functional analysis in sociology is a unique method of theory construction and is the major alternative to causal analysis. Third, inherent methodological difficulties in Mertonian functional ananalysis in sociology argument for its abandonment. The first of the above assertions constitutes my reason for this attempt to spell out a notion of causal analysis as a method for theory construction in sociology. The appreciation of the second and third assertions requires some discussion of the work of Robert K. Merton and Kingsley Davis. Merton's classic methodological paradigm for functional analysis was put forth in Social Theory and Social Structure in 1949. A number of assertions prior to the statement of the paradigm imply that Merton saw functional analysis as a unique method of theory construction. He claimed that much had been accomplished with its use and much more could be expected. The paradigm was offered as an explicit codification of the procedures used by several sociologists and anthropologists. In this light, then, it is interesting to find that ten years later the president of the American Sociological Association was claiming that the uniqueness of functional analysis in sociology was a myth. In the paper titled "The Myth of Functional Analysis as a Special Method in Sociology and Anthropology," Kingsley Davis (1959) argued that "the definitions most commonly agreed upon make functionalism synonymous with sociological analysis and make non-functionalism synonymous with either reductionist theories or pure description." Davis went on to claim that the ambiguities of the special terminology of functionalism "make the myth that it is a special method a liability," and that the myth should be abandoned. Davis' argument is essentially that of parsimony. If it can be shown that there are no differences between functional analysis and any other kind of analysis in sociology then it is clearly parsimonious to abandon

INTRODUCTION THE western regions of the United States are relatively deficient in poultry feedstuffs containing high-quality carbohydrate. As the result corn is shipped from the Midwest at high cost to producers and consumers of poultry products. Growers could produce much larger amounts of sugar beets than are allowed under the quota system of the Sugar Act. If sugar beets could be used in feeds, they could be produced on non-quota acres and possibly serve as a replacement crop on surplus land. Sucrose, as refined product and in various raw materials, has been fed to livestock for many years. Beet varieties such as Mangold are used widely for silage. Recently pig starter rations (Lewis et al., 1955) have included generous levels of sucrose. Feeding it to hogs and steers prior to slaughter (Greenwood et al., 1953) results in heavier carcasses and more palatable livers. The use of refined sucrose in poultry …

In a number of important aspects Canadian war-time price controls were a pioneering venture and for this reason have aroused considerable interest both at home and abroad. It is too soon to present a considered appraisal of these policies and procedures—indeed the operation has not yet been concluded—but it is perhaps not too soon to record in a broad way what was done and why.When war broke out in September, 1939 Canada, in common with most other countries, was emerging uncertainly from a decade of economic depression. Prices were low, unemployment was high, and the costs of relief were still a heavy charge on federal, provincial, and municipal budgets. The general index of wholesale prices was 28 per cent below 1926 and only 9 points above the low point of the depression in 1933. The iron and steel industry was operating at 20 per cent below 1928-9, and probably not in excess of 50 per cent of capacity. Recorded unemployed formed 12 per cent of the normal working force, and under-employment affected a further large percentage. Nearly a million persons were on direct relief and the fully employable persons on direct urban relief numbered nearly 200,000. In brief we entered the war with a high proportion of idle and underemployed resources.We also entered the war with a sound and reasonably well thought out conception of overall war-time economic policy, but, excepting foreign exchange control which had been carefully prepared in detail well in advance, with very little organization for carrying it out and no very clear notion of what kind of a war it would be and along what lines our major contributions would, lie. The Defence Purchasing Board, predecessor of the Department of Munitions and Supply, began operations in July, 1939, but the organization of price and supply controls received detailed consideration only a few weeks before hostilities broke out. The Wartime Prices and Trade Board was created on September 3, 1939, and within a few weeks was actively involved in half a dozen commodity fields.

1. Insulin secretion was studied in isolated islets of Langerhans obtained by collagenase digestion of rat pancreas. In addition to responding to glucose and mannose as do whole pancreas and pancreas slices in vitro, isolated rat islets also secrete insulin in response to xylitol, ribitol and ribose, but not to sorbitol, mannitol, arabitol, xylose or arabinose. 2. Xylitol and ribitol readily reduce NAD+ when added to a preparation of ultrasonically treated islets. 3. Adrenaline (1μm) inhibits the effects of glucose and xylitol on insulin release. Mannoheptulose and 2-deoxy-glucose, however, inhibit the response to glucose but not that to xylitol. 4. The intracellular concentration of glucose 6-phosphate is increased when islets are incubated with glucose but not with xylitol, suggesting that xylitol does not promote insulin release by conversion into glucose 6-phosphate. 5. Theophylline (5mm) potentiates the effect of 20mm-glucose on insulin release from isolated rat islets of Langerhans, but has no effect on xylitol-mediated release. These results indicate that xylitol does not stimulate insulin release by alterations in the intracellular concentrations of cyclic AMP. 6. A possible role for the metabolism of hexoses via the pentose phosphate pathway in the stimulation of insulin release is discussed.

Whatever may be regarded as the immediate motives which impelled the Price Spreads investigation it will be generally agreed that a careful examination of the Canadian economy as a whole is long overdue, and that present conditions and current trends require the formulation of intelligent and co-ordinated economic policies. We are now in the sixth year of a major industrial depression and, while there has been a substantial measure of recovery from the low points of 1933, there is no clear indication of continued improvement and there is at least a possibility of the crumbling of the statistical ledge to which we have been rather precariously and nervously clinging for the past twelve months. Canada, with its large measure of dependence on the exports of two or three staple products, has always been in a vulnerable position, but this has been greatly accentuated by the widespread trend towards economic nationalism and self-sufficiency. Our professional optimists to the contrary, Canada has been one of the heaviest sufferers during the past five years and the outlook for the future is still uncertain and still threatening.It is not necessary to elaborate the familiar problems of the Canadian economy: an income that fluctuates violently with the volume and value of our exports, and expenses that are made highly rigid by the dominating factors of heavy overhead costs; the wide differences in the technological problems of the several major industries; the concentration of staple industries in specialized geographical areas and the growing political and cultural domination of metropolitan centres which accentuate political and economic sectionalism, and at the same time a high degree of concentration of the control of finance, commerce, and manufacturing on a national scale—a concentration to which it is difficult to apply social regulation and control within the present framework of the British North America Act.

1. The release of growth hormone from isolated fragments of rat anterior pituitary tissue incubated in vitro was studied by employing a double-antibody radioimmunoassay. 2. In the absence of added stimuli, two phases of hormone release could be distinguished, an early phase of 2h duration and a subsequent late phase. In the early phase, hormone release was rapid but could be significantly decreased by calcium depletion and by 2,4-dinitrophenol whereas the rate of release in the late phase was uninfluenced by these incubation conditions. These results have been interpreted as indicating the existence of a secretory component in the early phase of release. 3. In subsequent experiments, the effects of various agents on the rate of hormone output during the late phase of incubation were investigated. Hormone release was increased by theophylline and by dibutyryl cyclic AMP (N6-2′-O-dibutyryl-adenosine 3′:5′-cyclic monophosphate), the response to both of these agents being related to the concentration of the stimulant employed. 4. The stimulation of growth hormone output by theophylline was significantly decreased by calcium deprivation and by 2,4-dinitrophenol. The response to dibutyryl cyclic AMP was diminished by 2,4-dinitrophenol, iodoacetate and 2-deoxyglucose but not by malonate or colchicine. 5. Arginine, β-hydroxybutyrate, albumin-bound palmitate and variation in the glucose concentration of the incubation medium over a wide range were without any statistically significant effect on the rate of hormone release from either control pituitary fragments or those subject to secretory stimulation by dibutyryl cyclic AMP. 6. It is suggested that the regulation of growth hormone secretion is mediated by cyclic AMP (adenosine 3′:5′-cyclic monophosphate). The secretion observed in response to cyclic AMP requires the presence of ionized calcium and a source of metabolic energy but is independent of pituitary protein synthesis de novo. The integrity of the glycolytic pathway of glucose metabolism appears to be essential for cyclic AMP-stimulated growth hormone secretion to occur.

1. Concentrations of glucose 6-phosphate and 6-phosphogluconate were studied in islets of Langerhans isolated from rat pancreas and incubated in the presence of various agents that induce insulin release. 2. In response to rising concentrations of extracellular glucose (2–10mm) there is a linear increase in the intracellular concentration of glucose 6-phosphate, though this is not the case for 6-phosphogluconate, the intracellular concentration of which only increases when the external glucose concentration exceeds 5mm. 3. Tolbutamide, octanoate and citrate, all of which promote insulin secretion from isolated islets, increase the intracellular concentrations of glucose 6-phosphate and 6-phosphogluconate. The results obtained in the presence of octanoate and citrate are compatible with an inhibitory effect of citrate on islet-cell phosphofructokinase. 4. Theophylline and glucagon when incubated with islets in vitro promote insulin release and cause a rise in 6-phosphogluconate concentration and not in that of glucose 6-phosphate. 5. It is suggested that the further metabolism of glucose 6-phosphate through a pathway other than glycolysis is essential for insulin release. One such pathway involves its oxidation to 6-phosphogluconate, which seems to be a necessary accompaniment of insulin secretion due to glucose. The possibility that agents other than glucose promote insulin release by enhancing the oxidation of glucose 6-phosphate through this pathway is discussed.

Economics first appeared in a Canadian university curriculum more than eighty years ago; thirty years later several universities were offering groups of courses in economics that could qualify a student for the equivalent of an honours degree in economics; but it is only in the past thirty-five years that a steady flow of scholarly writing in Canadian economics has developed. The twenty-fifth anniversary of the founding of this Journal provides an appropriate occasion to review briefly the expansion of economic scholarship in Canada.The first university course in political economy to be offered in Canada was in 1878 when the Department of Philosophy at Queen's University introduced a course of lectures based on Adam Smith, Mill, and Jevons. Ten years later, in 1888, Adam Shortt was appointed lecturer in political economy and in 1891 he became the Sir John A. Macdonald Professor of Political Science. The University of Toronto appointed its first professor of political science in 1888, and (Sir) William Ashley gave lectures in both political economy and constitutional history. McGill entered the field in 1899 when Dr. LeRossignol of Colorado was appointed visiting professor for one year. In 1900 Stephen Leacock was appointed lecturer in political science, and in 1901 (Sir) William Flux was brought over from England to occupy McGill's first chair in economics. The succeeding chairs of political economy in Canadian universities were occupied by A. L. McCrimmon at McMaster in 1904, E. Bouchette at Montreal in 1907, and A. B. Clark at Manitoba in 1909.

1. The concentrations of cyclic AMP were compared in islets of Langerhans isolated from the pancreases of normal female and pregnant rats and were higher in islets in pregnancy. 2. There was also a significant increase in adenylate cyclase activity in homogenates of islets from pregnant rats compared with those from normal rats. 3. Increased cyclic AMP concentration in islets from pregnant rats was reflected in increased protein kinase activity. When the cyclic AMP-dependent protein kinase activity was increased by 3-isobutyl-1-methylxanthine this stimulated activity was significantly greater in pregnancy. 4. Insulin-secretion studies with islets from normal and pregnant rats showed that theophylline or 3-isobutyl-1-methylxanthine, which raise intracellular cyclic AMP concentrations, caused a significantly greater insulin secretion in pregnancy. 5. It was also found that in the presence of a glucose concentration too low to stimulate insulin secretion, the latter could be induced if the cyclic AMP concentrations were raised sufficiently with 3-isobutyl-1-methylxanthine. 6. It is suggested that the higher cyclic AMP concentrations observed in islets in pregnancy mediate the greater insulin-secretory capacity, as well as the greater sensitivity of these islets to low glucose concentrations.

Sera from 123 patients with diabetes mellitus of recent onset, 155 patients with diabetes of more than two years' duration, and 250 normal persons were collected over a period of two and a half years. All sera were tested for neutralizing antibody to Coxsackie virus types B1-6, and a sample was tested for complement-fixing antibody to a number of viral, rickettsial, and mycoplasmal antigens.In diabetics of recent onset no evidence was found of any excess of antibodies to mumps virus or some common respiratory viruses. Insulin-dependent diabetes within three months of onset were found to have higher antibody titres to Coxsackie B virus, particularly of type B4, than either normal subjects or patients with diabetes of longer duration.

I deeply appreciate the honour which the Canadian Political Science Association has done me by inviting me to fill this vacant place in the programme of these meetings. More than most of those present, I profoundly regret the necessity for the invitation which was extended to me. Professor William Burton Hurd, the president of the Canadian Political Science Association for 1949-50, had been one of my close friends for twenty-five years. We had worked together on various research projects and we were colleagues at McMaster University. The severe illness which came upon him more than a year ago, against which he maintained a gallant struggle, but which terminated in his death last February, cut short a career of distinguished research, of brilliant teaching, and of effective university administration at a time when it had reached the height of its power. In terms of the normal span of life we had the right to expect another dozen or fifteen productive years of maturing wisdom and scholarship. The deprivation we have sustained is a serious loss to Canadian thought and life.I do not know what topic or what aspect of his work Professor Hurd would have chosen for his presidential address this evening, but it is natural that I should turn to a field of study in which we were both deeply interested, but which I have been forced to relinquish for the past twelve years. Our interests in population studies were different but complementary. Professor Hurd was trained and took his first degree in mathematics and, as an adolescent and as a young man, he witnessed the great wave of population movement which during the half-dozen years preceding the First World War poured more than a million migrants through the portal city of Winnipeg. It was natural, therefore, that after serving with distinction in the Canadian army overseas, and after turning to economics during his deferred tenure of a Rhodes scholarship at Oxford, he should develop a special interest in the statistical analysis of Canadian population trends with particular reference to their growth factors, our absorptive capacity, and the problems of assimilation into a developing Canadian culture.

Inosine is a potent simulant of insulin release from rat but not from rabbit islets of Langerhans. Further investigation showed that nucleoside phosphorylase activity is exceptionally low in rabbit islets. The ability of inosine to promote insulin release seems to be related to islet nucleoside phosphorylase activity, which can display marked species differences.

The intraperitoneal inoculation of CD(1) mice with Coxsackie virus B(4) resulted in the raising of blood sugar levels to diabetic values 12 days after the administration of the virus. Serum insulin remained inappropriately low. Light microscopy changes in the islets of Langerhans showed mononuclear cell infiltration of the islets and marked degranulation of the beta cells. The acinar tissue appeared to be little changed. It is concluded that Coxsackie B(4) virus may cause a diabetic state compatible with islet cell damage.

Glucose tolerance with serum insulin assay has been carried out in 24 apparently unaffected identical twins of diabetics. Glucose values were significantly higher and insulin values significantly lower than in control subjects, but there was considerable individual variation and in half the cases glucose tolerance was normal. There was no case of increased insulin response. In these twins glucose tolerance and insulin response were not correlated with weight, family history of diabetes, age at diagnosis of diabetes in the affected twin, time since that diagnosis, nor with age at testing the unaffected twin. On retesting 12 of the twins after two years no significant differences were found from the first testing.We conclude that not all these twins are likely to develop diabetes, that the assumption that identical twins of diabetics are necessarily "prediabetic" is probably erroneous, and that factors other than genetic ones are important in the aetiology of diabetes.