Laboratory Estimation of Field Resistance of Potato to Late Blight

Based on quantitative measurement of components of field resistance of potatoes to late blight, a multiple linear regression equation is derived for laboratory estimation of Area Under Disease Progress Curve. The equation accounts for 82% of variation in Area Under Disease Progress Curve. Transformation of data or inclusion of more terms do not improve the equation significantly. The method is suggested as a replacement or supplement to field testing.     

Preliminary X-ray investigation of a bifunctional inhibitor from Indian finger millet (ragi).

A bifunctional alpha-amylase/trypsin inhibitor that has two binding sites has been purified from ragi. The inhibitor has been crystallized from its ammonium sulphate solution by the vapour diffusion method. The crystals belong to the orthogonal space group P2(1)2(1)2(1) with unit cell dimensions a = 30.49 A, b = 56.30 A, c = 73.65 A and Z = 4.     

Life cycle changes during 12 successive generations of laboratory colonisation of the leafroller Cnephasia jactatana (Walker) (Lepidoptera: Tortricidae) on artificial diet

Abstract

Close monitoring of the lepidopteran leafroller Cnephasia jactatana under laboratory colonisation revealed few distinct effects of successive rearing on artificial diet on the life cycle. The second laboratory generation had a prolonged development time and altered sex synchronism in pupation and eclosion patterns. Some deleterious changes were observed in later generations, including decreases in fertility, egg hatch and sperm motility, failure of mating adults to separate, and pupal and adult malformations. These changes were not adaptive, but were due to incompatibility with the general purpose diet (GPD) used; they were absent under sub-colonisation on a sheepnut-bean based diet (SBD). Success in the laboratory colonisation of C. jactatana is attributed to a random mating protocol, choice of environmental conditions representing the wild habitat, and a rapid rate of population growth.     

Molecular mimicry between a uveitopathogenic site of S-antigen and viral peptides. Induction of experimental autoimmune uveitis in Lewis rats.

S-Antigen (S-Ag) is a well characterized 45,000 m.w. photoreceptor cell protein. When injected into susceptible animal species, including primates, it induces an experimental autoimmune uveitis, a predominantly T cell-mediated autoimmune disease of the retina and uveal tract of the eye, and of the pineal gland. In this study we found an amino acid sequence homology between a uveitopathogenic site of S-Ag, several viral proteins and one additional nonviral protein. An experimental autoimmune uveitis and pinealitis was induced in Lewis rats with these different synthetic peptides, corresponding to the amino sequence of hepatitis B virus DNA polymerase, gag-pol polyprotein of Baboon endogenous virus and gag-pol polyprotein of AKV murine leukemia virus and potato proteinase inhibitor IIa, which contain three or more consecutive amino acids identical to peptide M in S-Ag. Lymph node cells from rats immunized with either peptide M or the different synthetic peptides showed a significant degree of cross-reaction. Mononuclear cells from monkeys (Macaca fascicularis) immunized with peptide M also showed significant proliferation when incubated with either peptide M or synthetic peptides as measured by in vitro lymphocyte mitogenesis assay using [3H]TdR. Based on our findings we conclude that a viral infection may sensitize the mononuclear cells that can cross-react with self proteins by a mechanism termed molecular mimicry. Tissue injury from the resultant autoantigenic event can take place in the absence of the infectious virus that initiated the immune response.     

Metabolic Syndrome Is Associated with Increased Oxo-Nitrative Stress and Asthma-Like Changes in Lungs

Epidemiological studies have shown an increased obesity-related risk of asthma. In support, obese mice develop airway hyperresponsiveness (AHR). However, it remains unclear whether the increased risk is a consequence of obesity, adipogenic diet, or the metabolic syndrome (MetS). Altered L-arginine and nitric oxide (NO) metabolism is a common feature between asthma and metabolic syndrome that appears independent of body mass. Increased asthma risk resulting from such metabolic changes would have important consequences in global health. Since high-sugar diets can induce MetS, without necessarily causing obesity, studies of their effect on arginine/NO metabolism and airway function could clarify this aspect. We investigated whether normal-weight mice with MetS, due to high-fructose diet, had dysfunctional arginine/NO metabolism and features of asthma. Mice were fed chow-diet, high-fat-diet, or high-fructose-diet for 18 weeks. Only the high-fat-diet group developed obesity or adiposity. Hyperinsulinemia, hyperglycaemia, and hyperlipidaemia were common to both high-fat-diet and high-fructose-diet groups and the high-fructose-diet group additionally developed hypertension. At 18 weeks, airway hyperresponsiveness (AHR) could be seen in obese high-fat-diet mice as well as non-obese high-fructose-diet mice, when compared to standard chow-diet mice. No inflammatory cell infiltrate or goblet cell metaplasia was seen in either high-fat-diet or high-fructose-diet mice. Exhaled NO was reduced in both these groups. This reduction in exhaled NO correlated with reduced arginine bioavailability in lungs. In summary, mice with normal weight but metabolic obesity show reduced arginine bioavailability, reduced NO production, and asthma-like features. Reduced NO related bronchodilation and increased oxo-nitrosative stress may contribute to the pathogenesis.     

Survival and virulence of copper- and chlorine-stressed Yersinia enterocolitica in experimentally infected mice

The effect of gastric pH on the viability and virulence of Yersinia enterocolitica O:8 after exposure to sublethal concentrations of copper and chlorine was determined in mice. Viability and injury were assessed with a nonselective TLY agar (tryptic soy broth containing lactose, yeast extract, and agar) and two selective media, TLYD agar (TLY agar plus sodium deoxycholate) and CIN agar (cefsulodin-Irgasan-novobiocin agar). Both copper and chlorine caused injury which was manifested by the inability of the cells to grow on selective media. CIN agar was more restrictive to the growth of injured cells than TLYD agar. Injury of the exposed cells was further enhanced in the gastric environment of mice. Besides injury, the low gastric pH caused extensive loss of viability in copper-exposed cells. Lethality in the chlorine-exposed cells was less extensive, and a portion of the inoculum (5.2 X 10(5) of 1 X 10(7) inoculated cells) reached the small intestine 5 min postinoculation. No adverse effect on the injured cells was apparent in the small intestine, and a substantial revival (approximately 70%) of the injury occurred in 3 to 4 h after intraluminal inoculation. The virulence of chlorine-stressed Y. enterocolitica in orally inoculated mice was similar to that of the control culture, but copper-stressed cells showed reduced virulence. Virulence was partly restored by oral administration of sodium bicarbonate before the inoculation of copper-exposed cells. Neutralization of gastric acidity had no effect on the virulence of the control or chlorine-stressed cells. The results of this study indicate that the extensive injury caused by the low gastric pH does not affect the virulence potential of chlorine-exposed cells. However, extensive cell death in the mouse stomach is responsible for the reduced virulence of the copper-stressed bacteria.