The Role of Forecasting in Crop Protection Decision Making: an Economic Viewpoint1

In making crop protection decisions, farmers have to answer two questions: what type of control measure(s) should I adopt? How should I apply this (these) measure (s), when, how frequently, etc.? The answer to these questions will depend upon: a) the dimensions of pest attack and the damage it causes, b) farmers' goals, c) the range of protection measures available to them which they can use, and d) the information available, in the form of monitored and forecast information. It is within this context that the role of forecasting is considered. An analysis is made of the possible impact that forecast infomation can have on farmer decision-making, particularly with regard to the accuracy of the forecast and the time at which it is available. This leads on to the problem of assessing the value of a forecast at a regional level, against which the costs of providing such information can be set. Finally, situations in which forecast information is likely to be of greatest value (and of least value) are identified, and implications are drawn concerning the institutional and other changes that could be taken to allow better use to be made of forecast information. Lorsque les agriculteurs decident de proteger leurs cultures, ils doivent repondre aux deux questions suivantes: quel est le mode d'intervention a choisir et comment, quand et a frequence faut-il intervenir. La reponse dependra notamment: de I'etendue de I'infestation et de L'importance des deglts; des buts que s'est assignes L'arboriculteur; de la gamme de methodes dont il dispose; des previsions qui lui sont fournies. La prevision est condideree dans ce cadre, puisqu'elle est susceptible d'infuler sur les decisions de L'agriculteur dans la mesure ou elle est etablie avec precision et au bon moment. I1 est donc utile d'evaluer L'inter6t economique d'une prevision regionale en faisant intervenir le cofit de celle-ci. Enfin, il est fait etat de situations dans lesquelles la prevision est profitable ou non. Suivant les cas, certaines modifications structurelles peuvent s'imposer afin de mieux tirer benefice des previsions.     

Insect epoxide hydrolase: Properties of a purified enzyme from the southern armyworm (Spodoptera eridania)

An epoxide hydrolase purified from midgut microsomes of southern armyworm (Spodoptera eridania) larvae exhibited high activity toward monosubstituted epoxides (1,2-epoxyoctane, 1,2-epoxypropane, and styrene oxide) and lower activity toward cis-1,2-disubstituted epoxides (cyclohexene oxide, and the cyclodienes HEOM, HCE, and chlordene epoxide). Trisubstituted epoxides (2-methyl-2,3-epoxyheptane and JH-1) as well as several cyclodiene insecticides (dieldrin, endrin, endo-epoxyaldrin, and anti-heptachlor epoxide) were refractory to enzymatic attack. It is concluded that both lipophilic and steric factors dictate the substrate specificity of the enzyme. With cyclohexene oxide the enzyme yields the 1R, 2R enantiomer of the trans-diol. The purified enzyme is inhibited by several epoxides and mixed-function oxidase inhibitors and the potency of 3,3,3-trichloro-1,2-epoxypropane and sodium picrylsulfonate suggest the importance of electronic factors in the inhibitory mechanism. Studies with specific amino acid modifiers suggest the presence of an essential lysine or histidine residue at the active site and indicate that the enzyme lacks a metal ion requirement and an essential cysteine residue. The purified enzyme has a molecular weight of 46,000 daltons and amino acid analysis and immunochemical studies show it to be very similar to, but not identical with, the epoxide hydrolase from mammalian liver microsomes.     

Localizing the action of two thiadiazolyl herbicidal derivatives

Enzymatically isolated leaf cells from navy beans (Phaseolus vulgaris L., cv. “Tuscola”) were used to study the effect of buthidazole (3-[5-(1,1-dimethylethyl)-1,3,4-thiadiazol-2-yl]-4-hydroxy-1-methyl-2-imidazolidinone) and tebuthiuron (N-[5-(1,1-dimethylethyl)-1,3,4-thiadiazol-2-yl]-N,N′-dimethylurea) on photosynthesis, protein, ribonucleic acid (RNA), and lipid synthesis. The incorporation of NaH¹⁴CO₃, [¹⁴C]leucine, [¹⁴C]uracil, and [¹⁴C]acetic acid as substrates for the respective metabolic process was measured. Time-course and concentration studies included incubation periods of 30, 60, and 120 min and concentrations of 0.1, 1, 10, and 100 μM of both herbicides. Photosynthesis was very sensitive to both buthidazole and tebuthiuron and was inhibited in 30 min by 0.1 μM concentrations. RNA and lipid syntheses were inhibited 50 and 87%, respectively, by buthidazole and 42 and 64%, respectively, by tebuthiuron after 120 min at 100 μM concentration. Protein synthesis was not affected by any herbicide at any concentration or any exposure time period. The inhibitory effects of buthidazole and tebuthiuron on RNA and lipid syntheses may be involved in the ultimate herbicidal action of these herbicidal chemicals.     

The relationship between the pharmacokinetics of intravenous cismethrin and bioresmethrin and their mammalian toxicity

The distribution and excretion of [¹⁴C]alcohol-labeled cismethrin and bioresmethrin was determined after intravenous administration to rats. Initially the label distribution of both isomers was similar, but differences occurred at later times mainly due to the retention of 5-benzyl-3-furylcarboxylic acid, a metabolite of bioresmethrin, in high concentration in the blood. Retention of this metabolite accounted for the slower excretion of bioresmethrin label compared to cismethrin. After administration of either isomer, parent pyrethroid was rapidly cleared from the blood and liver, and both isomers rapidly entered the central nervous system reaching peak concentrations within 2–5 min. Brain cismethrin concentrations exceeding 3.5 nmol/g were associated only with animals showing tremors. These levels of cismethrin are maintained for up to 30 min but bioresmethrin was depleted more rapidly possibly due to brain metabolism. It is concluded that the low toxicity of bioresmethrin is possibly due to the inability of this isomer to interact with the site of action in the central nervous system and not, as previously suggested, primarily because of more rapid metabolism in the liver.