Thrips (Thysanoptera: Thripidae, Phlaeothripidae) damaging peach in Paranapanema, São Paulo State, Brazil

Seeking to identify thrips species associated to peach and the injuries they cause, plants of Aurora and Tropic Beauty cultivars were weekly monitored, from May to August of 2005, in Holambra II district, in Paranapanema, SP. Flowers and fruits from six plants per hectare were sampled by the hitting technique. Frankliniella occidentalis (Pergande), F. schultzei (Trybom), F. gardenia (Moulton), F. condei John, F. insularis (Franklin) and Thrips tabaci Lindeman, in Thripidae, and Haplothrips gowdeyi (Franklin), in Phlaeothripidae were identified. F. occidentalis was dominant, comprising 55.7% of the total specimens sampled. Slight and severe injuries were registered in fruits.     

The search for non-chordate retinoic acid signaling: lessons from chordates

Signaling by retinoic acid (RA) is an important pathway in the development and homeostasis of vertebrate and invertebrate chordates, with a critical role in mesoderm patterning. Classical studies on the distribution of nuclear receptors of animals suggested that the family of RA receptors (RARs/NR1B) was restricted to chordates, while the family of RA X receptors (RXR/NR2B) was distributed from cnidarians to chordates. However, the accumulation of data from genome projects and studies in non-model species is questioning this traditional view. Here we discuss the evidence for non-chordate RA signaling systems in the light of recent advances in our understanding of carotene (pro-Vitamin A) metabolism and of the identification of potential RARs and members of the NR1 family in echinoderms and lophotrochozoan trematodes, respectively. We conclude, as have others before (Bertrand et al., 2004. Mol Biol Evol 21(10):1923-1937), that signaling by RA is more likely an ancestral feature of bilaterians than a chordate innovation.     

Greigite magnetosome membrane ultrastructure in 'Candidatus Magnetoglobus multicellularis'

The ultrastructure of the greigite magnetosome membrane in the multicellular magnetotactic bacteria 'Candidatus Magnetoglobus multicellularis' was studied. Each cell contains 80 membrane-enclosed iron-sulfide magnetosomes. Cytochemistry methods showed that the magnetosomes are enveloped by a structure whose staining pattern and dimensions are similar to those of the cytoplasmic membrane, indicating that the magnetosome membrane likely originates from the cytoplasmic membrane. Freeze-fracture showed intramembrane particles in the vesicles surrounding each magnetosome. Observations of cell membrane invaginations, the trilaminar membrane structure of immature magnetosomes, and empty vesicles together suggested that greigite magnetosome formation begins by invagination of the cell membrane, as has been proposed for magnetite magnetosomes.     

Mechanistic insights and new products of the reaction of steroid sapogenins with NaNO2 and BF3.Et2O in acetic acid

A detailed analysis of the course of the reaction of steroid sapogenins with NaNO(2) and BF(3).Et(2)O in acetic acid is presented and some evidences on the involved mechanism are provided. Two new products of the studied reaction were isolated and unambiguously characterized with the aid of NMR and single crystal X-ray diffraction.     

Leuprolide acetate reduces both in vivo and in vitro ovarian steroidogenesis in infertile women undergoing assisted reproduction

Despite the probable inhibitory effects of GnRH analogues on ovarian steroidogenesis in vitro, their association with assisted reproduction protocols shows favorable results. This suggests that there are important differences in the behaviors of these drugs when administered in vivo versus in vitro. To clarify these differences, this study was designed to analyze the effect of leuprolide acetate (LA) on ovarian steroidogenesis in women undergoing In Vitro Fertilization (IVF). A prospective, randomized open label study was conducted on 14 women (26-35 years): seven receiving only gonadotrophins (Group 1) and seven receiving gonadotrophin plus LA at 1mg/day (Group 2). The LA in vivo effect was determined with serum and follicular fluid (FF) samples and via luteinized granulosa cell cultivation (GCC), where cells were obtained during oocyte retrieval after ovarian hyperstimulation. In vitro analysis was performed via addition of LA to GCC only for Group 1 (without LA) at progressively higher concentrations (0, 10(-12), 10(-9) and 10(-6)M). In vivo, the main observation was a reduction in androgen production in Group 2, represented by lower androstenedione production in FF (G1=6479+/-3458; G2=3021+/-1119 ng/ml; p=0.04) and a lower testosterone peak in GC at 96h (G1=0.64+/-0.12 ng/ml; G2=0.50+/-0.19 ng/ml; P=0.02), but a higher fertilization rate (G1=67%; G2=83%; p=0.009). In vitro, testosterone, estradiol and progesterone were also reduced by LA, even though this reduction occurred for progesterone only at the highest LA dosage (10(-6)M; 606.0+/-114.3 ng/ml versus 1524.0+/-246.5 ng/ml; p=0.02). Results show that LA reduces ovarian steroidogenesis in vivo by essentially inhibiting androgen synthesis; whereas, in vitro, ovarian steroidogenesis is reduced overall.     

Role of the Met(287)Thr polymorphism in the AS3MT gene on the metabolic arsenic profile

Chronic exposure to arsenic involves a biotransformation process leading to the excretion of methylated metabolites, such as monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA), as well as the parental inorganic species (As(III) and As(V)). Inter-individual variations in arsenic biotransformation have been reported and polymorphisms affecting the genes involved in arsenic biotransformation have been considered as one of the plausible explanations for this variation. Coding and flanking regions of the human arsenic methyltransferase (AS3MT) gene have been analysed in 50 Chilean men exposed to arsenic. Nine polymorphisms were found, including one non-synonymous SNP at exon 9 (Met(287)Thr) with an allele frequency of 0.14. Other four changes occurred at potentially regulatory regions: a variable number of tandem repeats (VNTR) at the 5'-untranslated region (UTR5'), a G/C substitution at the promoter region, a GC/AT substitution inside the VNTR, and a G/A substitution at the 3'-untranslated region (UTR3'). The rest of polymorphisms were located in non-coding regions: a T/G substitution in intron 1, a CTC deletion in intron 2 and a TTT and ATT insertions in intron 5. In addition, the individual urinary arsenic profiles were analysed. Our results indicate that genetic polymorphisms in AS3MT contribute to inter-individual variation in arsenic biotransformation and, therefore, may contribute to inter-individual variations in risk of arsenic toxicity and arsenic carcinogenesis. Individuals with the Met(287)Thr polymorphism displayed increased arsenic methylation and might be at increased risk for toxic and genotoxic effects of arsenic exposure if, as the classical arsenic metabolic pathway indicates, methylation enhances toxicity.     

Tetraflavonoid and biflavonoids from Aristolochia ridicula

Biflavones, a chalcone-flavone, and a tetraflavonoid with a new carbon skeleton were isolated from the leaves of Aristolochia ridicula. Their structures were determined by chemical derivatizations and spectrometric analyses.     

Hypothalamic angiotensinergic-noradrenergic systems interaction in fructose induced hypertension

OBJECTIVE: Several studies suggest the importance of the interaction between the renin angiotensin and sympathetic nervous systems in blood pressure control, especially in clinical situations such as the metabolic syndrome. Previously, we have demonstrated changes in noradrenergic hypothalamic control of blood pressure in an animal model of insulin resistance and hypertension. The aim of the present study was to evaluate the effects of the interaction between the noradrenergic and angiotensinergic systems on hypothalamic blood pressure regulation in fructose hypertensive rats. METHODS: In control (C) and fructose-fed hypertensive (F) rats, we studied: 1) the effects of hypothalamic perfusion of irbesartan (AT(1) angiotensin receptor antagonist, 50 and 500 microg ml(-1)) and metoprolol (beta(1) adrenergic receptor antagonist, 10 and 100 microg ml(-1)) on blood pressure, heart rate and noradrenaline intrahypothalamic levels, by means of the microdialysis technique; and 2) the effects of intrahypothalamic microinjection of angiotensin II alone or after metoprolol pre-administration, on blood pressure and heart rate. RESULTS: Meanwhile irbesartan perfusion did not modify neither mean arterial pressure (MAP) nor heart rate or noradrenaline hypothalamic levels in the C group, its highest dose diminished MAP (DeltaMAP: F: - 16.3+/-1 mm Hg, p<0.05) and noradrenaline levels (% of basal levels: 58+/-7%, p<0.05) in the F group, without affecting heart rate. Intrahypothalamic perfusion of metoprolol diminished MAP only in the F group (DeltaMAP: F: -12.1+/-1.1 mm Hg, p<0.05), but did not modify heart rate in both groups. On the other hand, it diminished noradrenaline hypothalamic levels in C (% of basal levels: 53+/-6%, p<0.05) but not in the F group. The pressor response to angiotensin II microinjection was increased in F rats (DeltaMAP: F: 13.3+/-1.5 mm Hg vs. C: 6.9+/-1.8 mm Hg; p<0.05). Previous administration of metoprolol markedly abolished this increment. CONCLUSIONS: Our results suggest the existence of an increase in AT(1) and beta(1) adrenergic receptors tone in the hypothalamus of F rats, which could be related to the increase in blood pressure present in this experimental model. On the other hand, considering that the enhanced pressor response to angiotensin II intrahypothalamic injection in F rats was abolished by previous administration of a beta(1) adrenergic receptor antagonist, these results would indicate that beta(1) adrenergic receptors activation participates in the pressor response to angiotensin II in this experimental model of insulin resistance and hypertension.     

Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein

Neurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.     

Anti-plasmodium activity of angiotensin II and related synthetic peptides

Plasmodium species are the causative agents of malaria, the most devastating insect-borne parasite of human populations. Finding and developing new drugs for malaria treatment and prevention is the goal of much research. Angiotensins I and II (ang I and ang II) and six synthetic related peptides designated Vaniceres 1-6 (VC1-VC6) were assayed in vivo and in vitro for their effects on the development of the avian parasite, Plasmodium gallinaceum. Ang II and VC5 injected into the thoraces of the insects reduced mean intensities of infection in the mosquito salivary glands by 88% and 76%, respectively. Although the mechanism(s) of action is not completely understood, we have demonstrated that these peptides disrupt selectively the P.gallinaceum cell membrane. Additionally, incubation in vitro of sporozoites with VC5 reduced the infectivity of the parasites to their vertebrate host. VC5 has no observable agonist effects on vertebrates, and this makes it a promising drug for malaria prevention and chemotherapy.