The moth Hylesia metabus and French Guiana lepidopterism: centenary of a public health concern.

The females of the moths Hylesia metabus have their abdomens covered by urticating hairs looking like micro-arrows and causing a puriginous dermatitis to humans known as "papillonite" in French Guiana and also called yellowtail moth dermatitis or Caripito itch. The densities of the moths show great seasonal and annual variations depending on mechanisms mostly unknown. When H. metabus infestations occur, numerous cases of dermatologic manifestations are reported from people living near the mangrove swamps where the moths are developing. One hundred years after the first "papillonite" epidemic reported from French Guiana in 1912, the data presented herein summarize the actual state of knowledge on H. metabus biology and ecology and on the lepidopterism. Some recommendations are proposed for the surveillance and warning systems of H. metabus infestations and to avoid contact with the moths. Research priorities are suggested to improve the control against this problem emerging between nuisance and public health.

[Lessons from the Malaria Vector Control Program Based on Indoors Residual Spraying with DDT or Dieldrin in the Pilot Zone of Bobo-Dioulasso: Failure or Success?] / Les Leçons du Programme de Lutte Contre les Vecteurs du Paludisme Par Aspersions Intradomiciliaires de DDT ou de Dieldrine dans la Zone Pilote de Bobo-Dioulasso: Échec ou Succès?

During five years, from 1953, a village scale indoors residual spraying (IRS) was done in the pilot zone of Bobo-Dioulasso, Burkina Faso, with DDT or dieldrin (DLN) or even HCH with a conceptually both entomological and parasitological evaluation [18].Compared to the control area, DDT induced an approximatively 95% and 67% reduction in the landing rate of Anopheles gambiae, respectively inside and outside human houses but due to its irritant action, DDT greatly increased their exophagic behaviour. However, DLN had no impact on the landing rate of An. gambiae either indoors or outdoors due to the already noticed resistance of this species to this insecticide. The sporozoitic index of An. gambiae was reduced by 96% in the DDT treated areas and by 70% in the DLN treated area.DDT reduced the landing rates of Anopheles funestus by 98% and 91%, inside and outside treated houses respectively. With DLN, these reductions were 98% and 97%, respectively. The sporozoitic index of An. funestus was reduced by 95% in areas treated with DDT.Thus, vector control has reduced malaria transmission due to the two main vectors, An. gambiae and An. funestus, by some 99.8% in DDT treated villages compared to control villages. DLN reduced transmission from An. funestus by 99.9%, but almost not from An. gambiae . Overall, the implementation of vector control based on indoor residual spraying with DDT or DLN reduced by 99.9% the transmission of human Plasmodium in the villages of the pilot zone and therefore the program can be considered as entomologically successful.In children aged 2-9 years (target group for endemicity indices) the splenic index was 84.3% (n = 979) in the control area and 44.4% (n = 8920) in the treated areas (difference -47.3%), the plasmodial prevalence was 60.6% (n = 946) in the control zone and 38.0% (n = 7242) in the treated zones (difference - 37%) but the relatively high level of plasmodic or splenic index in treated villages showed that transmission was maintained at such a level that the program could be considered as a "semi-failure".Besides, the gametocytic indices remained at the same levels (3.28%, n = 946 in the control zone and 3.04%, n = 7242 in the treated zones) indicating the maintenance of the "reservoir of parasites" and the remaining possibilities of transmission.Compared to the control area, the index of new contamination was significantly lower in infants 0-3 months and 4 to 6 months in DDT treated villages but not in infants 7 to 12 months demonstrating that the control vector had some efficacy in the prevention of plasmodial infection but "all newborns were infected within one year" demonstrating that P. falciparum transmission was not completely stopped.In spite of its striking drop, the transmission was not fully stopped, and the programme was considered as a "semi-failure" or even a "failure" and inducing a complete shift in malaria control policy from vector control to mass drug chemotherapy (with several drugs, chloroquine, primaquine, pyriméthamine etc) without complete stop of transmission either. In fact, such vector control operations by DDT may have different analysis; in one side they can be considered an entomological success but, in another side, the actual reduction of plasmodic and splenic indices was not enough to be considered as successful. It was clear that both vector and parasite must be implemented in an integrated programme taking care of insecticide and drug resistance. Nevertheless, such programme, even not as successful as expected, could be considered as encouraging and not "disappointing" as it was. Important lessons can be learned from such large-scale field trial in spite of several methodological and operational issues.

Arthropod-borne viruses transmitted by Phlebotomine sandflies in Europe: a review.

Phlebotomine sandflies are known to transmit leishmaniases, bacteria and viruses that affect humans and animals in many countries worldwide. These sandfly-borne viruses are mainly the Phlebovirus, the Vesiculovirus and the Orbivirus. Some of these viruses are associated with outbreaks or human cases in the Mediterranean Europe. In this paper, the viruses transmitted by Phlebotomine sandflies in Europe (Toscana virus, Sicilian virus, sandfly fever Naples virus) are reviewed and their medical importance, geographical distribution, epidemiology and potential spreading discussed. Data on vertebrate reservoirs is sparse for sandfly fever viruses. The factor currently known to limit the spread of diseases is mainly the distribution areas of potential vectors. The distribution areas of the disease may not be restricted to the areas where they have been recorded but could be as wide as those of their vectors, that is to say Larroussius and P. papatasi mainly but not exclusively. Consequently, field work in form of viral isolation from sandflies and possible reservoirs as well as laboratory work to establish vectorial competence of colonised sandflies need to be encouraged in a near future, and epidemiological surveillance should be undertaken throughout the European Union.

Horse-, bird-, and human-seeking behavior and seasonal abundance of mosquitoes in a West Nile virus focus of southern France.

After 35 yr of disease absence, West Nile virus (family Flaviviridae, genus Flavivirus, WNV) circulation has been regularly detected in the Camargue region (southern France) since 2000. WNV was isolated from Culex modestus Ficalbi, which was considered the main vector in southern France after horse outbreaks in the 1960s. Recent WNV transmissions outside of the Cx. modestus distribution suggested the existence of other vectors. To study potential WNV vectors, horse- and bird-baited traps and human landing collections of mosquitoes were carried out weekly from May to October 2004 at two Camargue sites: one site in a wet area and the other site in a dry area, both chosen for their past history of WNV transmission. At the wet site, the most abundant species in bird-baited traps were Culex pipiens L. and Cx. modestus; both species also were found in lower proportions on horses and humans. The most abundant species in horse-baited traps and human landing collections were Aedes caspius (Pallas), Aedes vexans (Meigen), and Anopheles hyrcanus (Pallas) sensu lato; some of these species were occasionally collected with avian blood at the end of the summer. Anopheles maculipennis Meigen sensu lato was an abundant horse feeder, but it was rarely collected landing on human bait and never contained avian blood. At the dry site, Cx. pipiens was the most abundant species in bird- and horse-baited traps. The seasonal and circadian dynamics of these species are analyzed, and their potential in WNV transmission in Camargue discussed.

Characterization of a liver low Michaelis-Menten constant 3',5'-cyclic adenosine monophosphate phosphodiesterase activity sensitive to thyroid status.

These studies were undertaken to assess the subcellular distribution and some biochemical properties of the hepatic cAMP phosphodiesterase(s) whose activity is modulated by the thyroid status in the rat. Thyroidectomy led to a 2-fold increase in low Michaelis-Menten constant (Km) cAMP phosphodiesterase activity in Golgi-endosomal fractions, but little affected this activity in crude particulate fractions. On analytical sucrose density gradients, an increase in cAMP phosphodiesterase activity in particulate elements which equilibrated at densities 1.17-1.22 was also observed. Acute insulin treatment did not further increase cAMP phosphodiesterase activity in Golgi-endosomal fractions of thyroidectomized rats. Up to 75% of the cAMP phosphodiesterase activity associated with Golgi-endosomal fraction of euthyroid and hypothyroid rats was inhibited by cGMP (IC50, 10 microM and 1 microM, respectively). Activity was also potently inhibited by griseolic acid, cilostamide, and cilostazole (IC50, less than 1 microM) but was much less sensitive to R0-20-1724 (IC50, 1 mM). Treatment of Golgi-endosomal fractions by a hypotonic extract of rat liver lysosomes led to the solubilization of 50% of low Km cAMP phosphodiesterase activity. On sucrose density gradients, the solubilized activity migrated as a slightly asymmetrical peak with a sedimentation coefficient of 6 S in euthyroid rats and 6.9 S in hypothyroid rats. On nondenaturing polyacrylamide gel electrophoresis, the activity migrated as two majors peaks with Rf values of 0.23 and 0.50; only the activity associated with the fast-moving peak was increased by thyroidectomy. On diethylaminoethyl-Sephacel chromatography, four peaks of cAMP phosphodiesterase activity, two of which were cGMP-inhibitable, were resolved. Thyroidectomy increased the activity associated with one of the cGMP-inhibitable peaks (eluted at 0.7-0.9 M sodium acetate) and led to the appearance of a new peak of activity (eluted at 0.4 M), which was not sensitive to cGMP. These results show that the low Km phosphodiesterase activity associated with liver Golgi-endosomal fractions, previously shown to be increased in hyperinsulinemic rats, is also increased in hypothyroid animals. They also suggest that, based on pharmacological and physical criteria, the enzyme species affected by the thyroid status belongs to the cGMP-and cilostamide-inhibited subclass of low Km cAMP phosphodiesterases.

Pyruvate dehydrogenase activity is stimulated by growth hormone (GH) in human mononuclear cells: a new tool to measure GH responsiveness in man.

Human peripheral mononuclear cells (PMC) were used to examine the effects of hGH and insulin on the activity of the pyruvate dehydrogenase (PDH) complex. Incubation of PMC with 10(-7) mol/L hGH or insulin increased basal PDH activity. Hormonal effects were maximal (50-60% above control values) at 15 min. Later on, activation progressively decreased and was no longer detectable at 30 min. Total PDH activity was unaffected by hormonal treatment. PMC were subfractionated into lymphocytes and monocytes to assess the sensitivity of each cell types to the hormones. hGH significantly increased basal PDH activity in lymphocytes and monocytes (38% and 70% above control values, respectively), whereas insulin increased basal PDH activity only in monocytes (151% above control value). PMC from healthy subjects aged 1-45 yr were incubated for 15 min with 10(-7) mol/L hGH or insulin before PDH measurement. An increase of enzyme activity higher than 20% was observed in 26 patients out of 29 with hGH, and in 15 out of 18 with insulin. In conclusion, hGH is able to stimulate PDH activity of human mononuclear cells. This hormonal effect allows rapid evaluation of the cellular responsiveness of hGH in various pathophysiologic situations.

Triggering by Paf-acether and adrenaline of cyclo-oxygenase-independent platelet aggregation.

Platelet-activating factor (Paf-acether, 1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine) induced full aggregation and a limited release reaction of human platelets in plasma or in blood. Cyclo-oxygenase inhibition with aspirin only reduced aggregation when induced by threshold amounts of Paf-acether, whereas higher concentrations surmounted inhibition whether tested in citrated or in heparinized platelet-rich plasma or blood. Aspirin-induced inhibition of platelet secretion by Paf-acether was insurmountable and independent of the anti-coagulant used. Paf-acether and adrenaline acted synergistically in inducing aggregation in citrate and heparin. Aspirin in vitro or after oral ingestion at doses that suppressed aggregation induced by arachidonic acid alone, failed to reduce significantly the synergized aggregation induced by Paf-acether alone or combined with adrenaline. Twenty-four hours after the oral ingestion of aspirin, when aggregation by arachidonic acid remained blocked, a slight inhibitory activity on the effect of Paf-acether noted 4 h after aspirin, had ceased. This was probably accounted for by the synthesis of thromboxane A2 by newly formed platelets, since the in vitro addition of aspirin, or of the thromboxane/endoperoxide receptor inhibitor 13-azaprostanoic acid caused the 24 h platelets to behave in a manner similar to platelets collected 4 h after aspirin. The alpha 2-adrenoceptor inhibitor, yohimbine, blocked the direct effect of adrenaline as well as its synergism with Paf-acether. Since the synergistic effect of Paf-acether and adrenaline was maintained when thrombin-degranulated platelets were used, and aspirin remained ineffective against it, it is clear that the augmented platelet responsiveness is not accounted for by the platelet release reaction. 6 Paf-acether and adrenaline act synergistically and stimulate platelets by cyclo-oxygenaseindependent mechanisms, which may be relevant in human physiopathological conditions.

Selective inhibition of adrenaline-induced human platelet aggregation by the structurally related Paf antagonist Ro 19-3704.

1. Two non-lipid antagonists of platelet-activating factor acether (Paf), BN 52021 and WEB 2086, at concentrations which completely blocked Paf-induced platelet aggregation, failed to interfere with aggregation by adrenaline. In contrast, Ro 19-3704, a structurally related antagonist of Paf, inhibited concentration-dependently aggregation induced by adrenaline or by the simultaneous addition of submaximal concentrations of adrenaline and Paf. Reversal of aggregation was obtained when Ro 19-3704 was added to the platelet suspension after adrenaline. 2. Ro 19-3704 was selective for Paf and adrenaline since it failed to interfere with platelet aggregation induced by arachidonic acid or ADP. CV-3988, an antagonist of Paf structurally similar to Ro 19-3704, also inhibited adrenaline-induced aggregation. However, a morpholine analogue (MA) of Paf, which has no anti-Paf activity, failed to interfere with the aggregation induced by adrenaline. This suggests that the effect of Ro 19-3704 and CV-3988 on adrenaline is not simply due to their lipid structure. 3. Experiments on plasma membrane preparations showed that Ro 19-3704 inhibited [3H]-yohimbine binding with an inhibition constant (Ki) of 7 +/- 3 microM. In contrast, BN 52021 and MA did not interfere with [3H]-yohimbine binding. Equilibrium binding experiments showed that Ro 19-3704 increased the apparent KD of [3H]-yohimbine binding from 2.02 +/- 0.15 to 7.3 +/- 0.4 nM. The Paf antagonist Ro 19-3704 interacts specifically with the alpha 2-adrenoceptor and may thus prevent the early steps involved in the mechanism of adrenaline-induced platelet activation.

Characterization of insulin degradation products generated in liver endosomes: in vivo and in vitro studies.

The degradation products generated from A14 and B26 125I-labelled insulins in liver endosomes in vivo and in vitro have been isolated by high-performance liquid chromatography and cleavages in the B chain have been identified by automated radiosequence analysis. In rats sacrificed various times after injection of each of the 125I-labelled insulins, two major degradation products slightly less hydrophobic than intact iodoinsulins were identified; these accounted, at 8 min. for about 45% (A14 125I-labelled insulin) and 15% (B26 125I-labelled insulin) of the total radioactivity recovered, respectively. The products generated from A14 125I-labelled insulin contained an intact A chain, whereas those generated from B26 125I-labelled insulin contained a B chain cleaved at the B16-B17 bond. With B26 125I-labelled insulin, two minor products, with cleavages at the B23-B24 and B24-B25 bonds, were also observed. In vivo chloroquine treatment did not alter the nature but caused a decrease in the amount of insulin degradation products associated with endosomes. When endosomal fractions isolated from iodoinsulin injected rats were incubated at 30 degrees C in isotonic KCl, a rapid degradation of iodoinsulin, maximal at pH 6, was observed. With A14 125I-labelled insulin, the two major degradation products identified in vivo were generated along with monoiodotyrosine, but with B26 125I-labelled insulin monoiodotyrosine was the main product formed. Addition of ATP, presumably by decreasing the endosomal pH, shifted the medium pH for maximal iodoinsulin degradation to about 7-8. These studies have allowed a direct identification of two previously suggested cleavage sites in the B chain. They have also shown that the degradation products generated in cell-free endosomes under conditions that promote endosomal acidification are similar to those identified in vivo.

Longitudinal study of tissue- and subunit-specific obesity-induced regulation of the pyruvate dehydrogenase complex.

The tissue-specific expression of the mitochondrial pyruvate dehydrogenase complex (PDHc) has been studied in an animal model of obesity with hyperinsulinemia, the obese (fa/fa) Zucker rat. Liver and heart were obtained from 4 and 8 week-old obese rats and age-matched lean animals, and in each tissue the following parameters were analyzed: (1) total activity of the mitochondrial PDHc; (2) abundance of the mitochondrial PDHc subunits on Western blots; and (3) abundance of the E1alpha and E1beta subunit mRNAs on Northern blots and semi-quantitative RT-PCR. Regardless of age, obese rats showed an increase in liver total PDHc activity and a coordinate increase in liver E1alpha and E1beta PDHc subunit abundance. At 4 weeks, obese rats also showed an increase in liver PDH E1alpha mRNA level, but regardless of age E1beta mRNA level was unchanged. In contrast, neither total PDHc activity nor the concentration of its protein subunits were increased in heart of obese rats. Thus, obese Zucker rats display a liver-specific early increase in PDHc which results from a selective up-regulation of the E1alpha gene expression.

Detection of Bordetella bronchiseptica by the polymerase chain reaction.

Polymerase chain reaction (PCR) assays were developed that enabled not only discriminative detection of three Bordetella species, B. pertussis, B. parapertussis, and B. bronchiseptica (Bspp PCR), but also specific detection of B. bronchiseptica (Bb PCR). An upstream sequence of the flagellin gene was used as a target DNA region. This sequence contained differences in B. pertussis, B. parapertussis, and B. bronchiseptica DNA. These species could then be differentiated using two different sets of primers, Bspp and Bb. When oligonucleotide Bspp primers were used, PCR products were obtained from the three species of Bordetella. A fragment of the expected size (164 bp) was amplified using B. bronchiseptica and B. parapertussis DNA, but a fragment with a distinct molecular weight was amplified with B. pertussis DNA (195 bp). This Bspp PCR was specific and sensitive, but it could not differentiate between B. parapertussis and B. bronchiseptica. When Bb primers were used, a 237-bp PCR product was detected only from B. bronchiseptica DNA. No PCR products were identified after Bb PCR amplification of DNAs either from B. parapertussis isolates or B. pertussis isolates, nor from other respiratory pathogen DNAs tested. This second PCR assay had a sensitivity limit of less than 10 organisms of B. bronchiseptica after detection with a specific probe. The specificity and the sensitivity of the fla PCR assay were evaluated with purified DNA, as was its capacity for detecting the bacteria in human clinical samples and in lungs of infected mice.

Evidence for a role of protein kinase C in the activation of the pyruvate dehydrogenase complex by insulin in Zajdela hepatoma cells.

The signal transduction pathway involved in the activation of pyruvate dehydrogenase (PDH) by insulin is still unknown. In this study, we have examined the possible involvement of protein kinase C (PKC) in the process. In addressing this question, we examined (1) the insulin-like effects of the PKC activator 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) on the PDH complex, (2) the effects of various PKC inhibitors on the PDH activation by insulin, and (3) the response of PKC-depleted cells to insulin. We used as an experimental model Zajdela hepatoma cultured (ZHC) cells, which have been demonstrated to be responsive to physiological doses of insulin. Half-maximal and maximal stimulations of the PDH complex by insulin were observed at 0.05 and 5 nmol/L, respectively. Stimulation of PDH activity by insulin (5 nmol/L) occurred within 5 minutes of incubation and was maximal (+70%) at 7.5 minutes. In the presence of PMA (162 nmol/L), enzyme activity increased within 30 seconds, was maximal (+90%) at 5 minutes, and was no longer detectable after 10 minutes. Total PDH activity was unchanged by insulin or PMA treatment. The effects of PMA and insulin on basal PDH activity were not additive. Moreover, various inhibitors of PKC--staurosporine, sphingosine, acridine orange--completely blocked the stimulation of PDH activity induced by insulin or PMA. A 17-hour treatment of ZHC cells with 500 nmol/L PMA efficiently downregulated PKC, as attested by the marked decrease in the enzyme activity and the loss of phorbol 12,13-dibutyrate binding to intact cells.(ABSTRACT TRUNCATED AT 250 WORDS)

The iodine content of amniotic fluid and placental transfer of iodinated drugs.

Determinations of total iodine content, levels of thyroxine (T4) and triiodothyronine (T3), and protein concentrations were made on amniotic fluid. A total of 218 samples obtained at various stages of pregnancy, from both normal and pathological pregnancies, were studied. Normal values for the iodine and hormone concentrations are presented. Several amniotic fluid samples showed greatly elevated iodine levels, thought to be the result of maternal iodine intake. This study demonstrated that such elevated levels can be produced by urography with an iodinated medium, by thyroid extract therapy, and by vaginal therapy with an iodinated agent. Levels of T4 and T3 in amniotic fluid decreased slightly from the second to the third trimester and were unrelated to the total iodine levels. Despite reports in the literature of fetal hypothyroidism produced by amniography with a fat-soluble medium, no thyroid defect was observed in this series in the presence of elevated amniotic fluid iodine levels or when a water-soluble iodinated medium was used for amniography.

Potentiation and inhibition by clonidine of PAF-acether-induced human platelet activation.

PAF-acether (platelet-activating factor) and adrenaline synergized to induce aggregation of human platelets in whole blood and in platelet-rich plasma (PRP) irrespective of the use of citrate, of heparin or acid-citrate dextrose (ACD) as anticoagulants, whereas the partial adrenoceptor agonist clonidine imitated adrenaline in a limited number of cases and only when blood was collected in ACD. Whether added to ACD-PRP or ingested by the blood donors, aspirin suppressed the synergic effect of clonidine plus PAF-acether in plasma but failed to block the potentiated aggregation of adrenaline plus PAF-acether. Clonidine alone had no effect on plasma-free platelet suspensions and also failed to synergize with PAF-acether under conditions where the latter's association to adrenaline consistently induced full aggregation. Added before adrenaline or before adrenaline plus PAF-acether, clonidine reduced the aggregation to the level of that due to PAF-acether alone irrespective of cyclooxygenase inhibition with aspirin. The alpha 2-adrenoceptor antagonist yohimbine blocked the synergistic effects of adrenaline or clonidine associated to PAF-acether, reducing aggregation to that due to PAF-acether alone. Clonidine has dual effects on human platelets, since it can imitate adrenaline and synergize with PAF-acether in some subjects, and can also block aggregation induced by adrenaline alone or in combination with PAF-acether.

Mechanisms of bronchoconstriction and of thrombocytopenia induced by collagen in the guinea pig.

Collagen injected to guinea pigs i.v. increased the pulmonary resistance to inflation (bronchoconstriction) and induced thrombocytopenia. Immune platelet depletion protected against the effects of collagen, and has been shown not to prevent bronchoconstriction induced by the prostaglandin/thromboxane A2 precursor arachidonic acid. Use of inhibitors demonstrated that histamine, serotonin, acetylcholine and bradykinin were not involved with the effects of collagen in the guinea pig. Aspirin and indomethacin inhibited collagen-induced bronchoconstriction completely and thrombocytopenia partly, supporting the hypothesis that the former is prostaglandin cyclo-oxygenase dependent, whereas the latter has a thromboxane A2-independent mechanism as well. Carrageenan, heparin and reserpine inhibited the in vivo effects of collagen to various extents, but their precise mechanism of action could not be discovered. Collagen-induced bronchoconstriction is strictly platelet and thromboxane A2-dependent.

Adrenaline and PAF-acether synergize to trigger cyclooxygenase-independent activation of plasma-free human platelets.

Platelet-activating factor (PAF-acether, 1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine), a potent aggregating agent for the platelets in plasma, induced only a moderate aggregation of plasma-free suspensions of human platelets. By contrast, addition of PAF-acether plus adrenaline or ADP to the platelet suspension was followed by full aggregation, accompanied by a moderate secretion of ATP. This synergism was observed better in the presence of fibrinogen, but was also seen in its absence when using the combination of PAF-acether with adrenaline. Aspirin failed to interfere with the synergized aggregation, ruling out a role for cyclooxygenase. The order of addition of adrenaline and of PAF-acether to the platelets was critical. When the former was added first to the platelets suspension, aggregation was induced by the latter even if added after one hour. Conversely, aggregation was only induced by adrenaline added after PAF-acether, if the interval between both was of around one minute. Removal of ADP with the scavenging system creatine phosphate/creatine phosphokinase prevented the synergism between PAF-acether plus ADP, but failed to interfere with that induced by PAF-acether plus adrenaline. The synergized aggregation induced by adrenaline or ADP and PAF-acether may represent a novel mechanism, accounting for the increased aggregability under various physiopathological conditions.

Simulating development and survival of Aedes vexans (Diptera: Culicidae) preimaginal stages under field conditions.

Ecology and population dynamics of Aedes vexans (Meigen), were studied for 3 yr in southern Switzerland. Demographic data were compiled into single and multicohort stage-frequency lifetables that indicated variability in individual developmental times and losses caused by mortality. The structure of life table matrices suggested an analysis using a timevarying distributed delay model with attrition. Field data then were used to construct and validate a simulation model that input the number of 1st instars and output the number of emerging adults. The delay was the time required to complete development and attrition corresponded to mortality. Under optimal food supply, temperature was the most important driving variable. The model was parameterized with data obtained from laboratory experiments and evaluated with field data. Development and survival of preimaginal Ae. vexans were simulated reasonably well under 2 different pool habitats. Addition of a hydrology component to the model would enhance control operations by predicting hatch rates in the field.

First-month variations in total iodine content of human breast milks.

In 183 samples of breast milk from 23 young mothers we found the mean total iodine content to be 47 ng/ml, a value that is not dependent on length of gestation. There is a progressive increase in iodine concentration from colostrum to transitional and mature milk. The results show that breast milk sometimes contains an amount of iodine barely necessary to make thyroid hormones, which is around 10 micrograms in the first days of life rising to about 15-20 micrograms after four weeks. Secondly, nursing mothers should be watched, because if their daily breast milk contains more than 50 micrograms iodine for several consecutive days, they may be on a negative balance.

Carrageenan-induced activation of human platelets is independent of phospholipase A2 and of formation of thromboxanes.

Aggregation of washed rabbit platelets by thrombin and by carrageenan is accompanied by the activation of phospholipase A2 and by the synthesis of thromboxanes. Accordingly, aggregation, the accompanying release reaction and the activation of phospholipase are blocked by p-bromophenacyl bromide and by CB 874 (2,3-dibromo (4'-cyclohexyl-3'-chloro)-phenyl-4-oxo-butyric acid), two recognized inhibitors of the enzyme. Since these two reagents also inhibit aggregation and the release reaction induced by thrombin and by carrageenan on washed human platelets, it might have been anticipated that the mechanisms of aggregation of the platelets from the two species are similar. Nevertheless, no thromboxanes A2 or B2, nor activation of phospholipase A2 could be demonstrated with the use of carrageenan on human platelets, under conditions where thrombin was effective. It is concluded that carrageenan activates the human platelets by phospholipase A2- and thromboxane A2-independent mechanisms, and that the inhibitors of phospholipase A2 may block platelet functions by mechanisms other than inhibition of the expected enzyme.

Residual activity of Bacillus thuringiensis serovars medellin and jegathesan on Culex pipiens and Aedes aegypti larvae.

Bacillus thuringiensis serovar medellin strain 163-131 and Bacillus thuringiensis serovar jegathesan (B.t.jeg.) strain 367 are very toxic to mosquito larvae. However, they are 10 times less toxic than Bacillus thuringiensis var. israelensis (B.t.i.) to mosquito larvae under laboratory conditions. Lyophilized powders were produced from these strains and their toxicities were compared to that of powder produced from the B.t.i. strain. Larvicidal activity was titrated using Aedes aegypti (Bora-Bora strain) larvae, with IPS82 powder as the standard. The efficacy of these powders in the field was determined using Culex pipiens (Montpellier strain) in Paris, France, and Ae. aegypti larvae (French Guiana strain) in Cayenne, French Guiana, in standardized conditions. Residual activity was also assessed in the laboratory, using Cx. pipiens (SLAB strain), in Montpellier, France. Any negative effect of direct sunlight, soil, or polluted water on the residual activity of the 3 powders was recorded. Increasing bacterial concentration by a factor of 8 had little effect on the duration of larvicidal activity, except in the presence of polluted water and when substrate was added. All powders had similar initial efficacies against both types of mosquito larvae, in all conditions except water rich in organic matter. Bacillus thuringiensis serovar medellin had the lowest residual activity, both in the laboratory and in the field, whereas B.t.jeg. remained toxic for as long as B.t.i.