Search

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.

This paper argues that use of the term Muong to designate an ethnic minority in Vietnam began in the early twentieth century as a product of French colonial efforts to apply modern social scientific description to form knowledge of upland peoples adjacent to and linguistically related to Vietnamese speakers in the lowlands. Subsequently, Vietnamese speakers adopted this usage to designate a national minority. A local text from the turn of the century is used to suggest an alternative way of viewing these peoples based on pre-French experience.

Summary Aims This study was designed to assess further the possible links between enterovirus infection and Type 1 diabetes mellitus (DM). Methods Sera from 110 children in the age range 0–15 years was obtained shortly after the diagnosis of Type 1 DM, in paediatric centres throughout the UK. They were tested for the presence of enteroviral sequences by the polymerase chain reaction (PCR) of the 5′ nontranslated region (5′ NTR). One hundred and eighty-two controls tested were matched for age, geographical location and time of year. Results A significantly greater number of diabetic children (27% vs. 4.9%, P

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.

Between north and south The country that appeared at the beginning of the nineteenth century stretching from the southern border of China to the eastern border of Cambodia had never existed before. The name Vietnam can be found in some earlier Vietnamese texts, and the Qing court used this name when recognizing the new country as a vassal kingdom, but it was not commonly used until the twentieth century. The Qing continued to routinely refer to this place as An Nam, a name that dated from the Tang dynasty and that later became the French name for the central part of the country. In 1802, Vietnamese envoys to the Qing court were instructed to propose Nam Viet as the name of their new country. The message sent with the envoys cited the ancient kingdom of Nam Viet founded by Zhao To in Guangdong and Guangxi at the beginning of the Han dynasty as an auspicious precedent because it had pacified and civilized all the southern territories. Furthermore, the message gave the name a new contemporary meaning as representing the unification of all the Vietnamese lands: “Now, the South (Nam) has been swept of rebels and the whole realm of Viet has been restored to normalcy.” The Qing court, however, objected to the name Nam Viet for the very same reason proposed in its favor by the Vietnamese. In imperial historiography, contrary to Vietnamese historical tradition, Zhao To’s kingdom was an inauspicious rather than an auspicious precedent because it had rebelled against the Han dynasty. Arguments about the name shuttled between Hue and Beijing for nearly a year before the Qing court finally turned the name to Viet Nam, thereby avoiding the unpropitious connotation of insubordination and separatism in the name Nam Viet. The name Vietnam eventually entered popular usage with the spread of alphabetic literacy and nationalist ideas in the 1910s, 1920s, and 1930s.

The empire comes south After conquering the Yangtze River basin and proclaiming the Qin Empire in 221 bce , Qin Shi Huang, “The First Emperor of China,” sent thousands of his soldiers over the mountains into the valleys and coastlands of what is now South China. He also sent convicts and women to establish a population of northerners there. After years of hard fighting against local people, Qin commanders built a city on the site of modern Guangzhou (Canton), the main seaport for trade into the southern seas. When the Qin Empire collapsed after Qin Shi Huang’s death in the year 210 bce , this coastal outpost became the center of a regional kingdom ruled by the senior commanding officer, Zhao To. As armies fought for control of the empire in the north, Zhao To proclaimed himself King of Nan Yue (Southern Yue). Zhao To is among the first historical figures with a role in Vietnamese history. Sometime during the first quarter of the second century bce , he extended his authority over the people living in the Red River plain of northern Vietnam. Yue had been the name of a state on the south-central coast of China (the modern province of Zhejiang) during the sixth to fourth centuries bce . It was appropriated by Zhao To and eventually applied to the Red River plain by ancient Chinese dynasties; in Vietnamese, it is pronounced Viet.

Saigon After Bao Dai went to France in late 1953 to pursue possibilities for negotiating full independence with the Laniel government, Ngo Dinh Diem departed the United States for Europe, sensing that he may find a role in the changing situation. Ngo Dinh Diem’s youngest brother, Ngo Dinh Luyen (1914–1990), was a childhood friend of Bao Dai from their schoolboy days in France and served as a go-between. Although Bao Dai had never been comfortable with Ngo Dinh Diem’s strong anti-French attitude, in May 1954 he turned to him because there was no other person of his stature and reputation as an uncompromising nationalist. Furthermore, Ngo Dinh Nhu’s emergence as a political figure in Saigon the previous year suggested that Ngo Dinh Diem had a point of access into the political world of the State of Vietnam. Two other considerations were apparently on Bao Dai’s mind. Ngo Dinh Diem’s appointment would apply pressure on the French to sign the independence treaty, and no other Vietnamese politician was likely to elicit the American assistance that would be necessary for the future of his government. However, Bao Dai soon realized that with the appointment of Ngo Dinh Diem he had ended his role in the political life of his country, and he never returned to Vietnam. In the summer of 1954, Ngo Dinh Diem was seemingly without any firm source of support. The United States was beginning to provide institutional assistance but was non-committal regarding Ngo Dinh Diem himself, being unsure of whether he would be able to surmount the daunting situation in Saigon. The French army had regrouped to southern Vietnam and was still the pre-eminent military force in the country. The French military commander and commissioner in Vietnam was General Paul Henri Romuald Ely (1897–1975), who made no secret of his opinion that Ngo Dinh Diem should be replaced.

The history of Vietnam prior to the nineteenth century is rarely examined in any detail. In this groundbreaking work, K. W. Taylor takes up this challenge, addressing a wide array of topics from the earliest times to the present day - including language, literature, religion, and warfare - and themes - including Sino-Vietnamese relations, the interactions of the peoples of different regions within the country, and the various forms of government adopted by the Vietnamese throughout their history. A History of the Vietnamese is based on primary source materials, combining a comprehensive narrative with an analysis which endeavours to see the Vietnamese past through the eyes of those who lived it. Taylor questions long-standing stereotypes and clichés about Vietnam, drawing attention to sharp discontinuities in the Vietnamese past. Fluently written and accessible to all readers, this highly original contribution to the study of Southeast Asia is a landmark text for all students and scholars of Vietnam.

This report describes classical Type 1 insulin deficient diabetes mellitus (DM) arising in twins aged 14 months, both of whom had evidence of enterovirus infection. The diagnosis of Type 1 DM was made in the second twin within 12 days of the first. Enterovirus infection was detected in each twin at diagnosis by polymerase chain reaction (PCR). Both twins were negative for enterovirus by PCR 5 months following diagnosis, although both were then positive for islet cell antibodies. Sequencing of the amplicons produced by PCR suggested that the viruses from each twin were not the same but that they were both variants related to echovirus 6. © 1998 John Wiley & Sons, Ltd.

This report describes classical Type 1 insulin deficient diabetes mellitus (DM) arising in twins aged 14 months, both of whom had evidence of enterovirus infection. The diagnosis of Type 1 DM was made in the second twin within 12 days of the first. Enterovirus infection was detected in each twin at diagnosis by polymerase chain reaction (PCR). Both twins were negative for enterovirus by PCR 5 months following diagnosis, although both were then positive for islet cell antibodies. Sequencing of the amplicons produced by PCR suggested that the viruses from each twin were not the same but that they were both variants related to echovirus 6.

Immunoglobulin (Ig) fractions from the plasma of a group of newly diagnosed insulin-dependent diabetes mellitus (type 1) patients and set of control subjects were assessed for their effects on isolated mouse islet function. It was found that Igs from type 1 patients caused a significant inhibitory effect on insulin secretion when incubated with mouse islets as compared with controls (25.6 +/- 2.9 pg islet-1 h-1 vs 44.7 +/- 7.7 pg islet-1 h-1, P0.05). The plasma samples from which the Igs were obtained were then tested for the presence of antibodies to the mouse islet cell surface (ICSA). Four of the nine patients were positive for ICSA, and plasma samples from eight control subjects were all negative. ICSA-positive samples appeared to have the greatest inhibitory effect on insulin secretion when compared with their respective controls (53.3 +/- 7.0 pg insulin islet -1 min-1 vs 30.9 +/- 3.7 pg insulin islet -1 min-1, (P0.05). In contrast, it was also found that ICSA-positive Ig fractions had no significant effect on glucose oxidation when co-incubated with mouse islets as compared with the controls (11.3 +/- 2.3 pmol islet-1 h-1 vs 11.2 +/- 2.9 pmol islet-1 h-1). These studies suggest that Igs from newly diagnosed type 1 patients containing ICSA may impair insulin secretion from isolated mouse islets by mechanisms which do not involve the inhibition of B-cell glucose metabolism.

The aqueous degradation of the carbacephalosporin loracarbef under moderately acidic conditions (pH range, 2.7-4.3) is described. Structures of a total of 10 compounds isolated by preparative reversed-phase HPLC have been proposed. Five of these 10 degradation compounds arose from hydrolysis of the beta-lactam ring followed by structural changes in the six-membered heterocyclic ring. Four compounds form from intermolecular reactions of loracarbef to form dimeric structures with peptide linkages. The remaining compound resulted from oxidation of the primary amine to a hydroxylamine. Pathways for the formation of these compounds from the parent loracarbef are proposed.

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.

1. β-Cell function in human islets derived from a number of kidney donors was investigated by using various types of islet preparations. 2. With fresh islets, both insulin release and biosynthesis were increased by raising glucose concentrations, although the response was a variable one. 3. In fresh islets, the effects of 5 mmol of glucose/l on release were potentiated by 10 mmol of d-3-hydroxybutyrate/l. 4. Insulin release at 20 mmol of glucose/l was inhibited by adrenaline (0.1 mmol/l), and potentiated by theophylline (10 mmol/l) in the presence of 5 mmol of glucose/l, in islets cultured for 4 days. 5. After culture for 8 days, islets still showed an increase in insulin release and biosynthesis in response to glucose. 6. Pancreas slices derived from fresh human tissue also responded to increasing concentrations of glucose with a sigmoidal curve for insulin release.

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.