Sequential sampling plans to Orthezia praelonga Douglas (Hemiptera: Sternorrhyncha, Ortheziidae) in citrus

The sequential sampling is characterized by using samples of variable sizes, and has the advantage of reducing sampling time and costs if compared to fixed-size sampling. To introduce an adequate management for orthezia, sequential sampling plans were developed for orchards under low and high infestation. Data were collected in Mat?o, SP, in commercial stands of the orange variety 'Pêra Rio', at five, nine and 15 years of age. Twenty samplings were performed in the whole area of each stand by observing the presence or absence of scales on plants, being plots comprised of ten plants. After observing that in all of the three stands the scale population was distributed according to the contagious model, fitting the Negative Binomial Distribution in most samplings, two sequential sampling plans were constructed according to the Sequential Likelihood Ratio Test (SLRT). To construct these plans an economic threshold of 2% was adopted and the type I and II error probabilities were fixed in alpha = beta = 0.10. Results showed that the maximum numbers of samples expected to determine control need were 172 and 76 samples for stands with low and high infestation, respectively.     

Advantages and disadvantages of cytidine deamination

Cytidine deamination of nucleic acids underlies diversification of Ig genes and inhibition of retroviral infection, and thus, it would appear to be vital to host defense. The host defense properties of cytidine deamination require two distinct but homologous cytidine deaminases-activation-induced cytidine deaminase and apolipoprotein B-editing cytidine deaminase, subunit 3G. Although cytidine deamination has clear benefits, it might well have biological costs. Uncontrolled cytidine deamination might generate misfolded polypeptides, dominant-negative proteins, or mutations in tumor suppressor genes, and thus contribute to tumor formation. How cytidine deaminases target a given nucleic acid substrate at specific sequences is not understood, and what protects cells from uncontrolled mutagenesis is not known. In this paper, I shall review the functions and regulation of activation-induced cytidine deaminase and apolipoprotein B-editing cytidine deaminase, subunit 3G, and speculate about the basis for site specificity vis-à-vis generalized mutagenesis.     

Genotoxic effects of rotenone on cultured lymphocytes

Rotenone is a heterocyclic compound widely used as an insecticide, acaricide and piscicide. Its toxicity is mainly caused by the inhibition of mitochondrial respiratory processes and ATP production, resulting in the generation of reactive oxygen species. Reactive oxygen species can interact with DNA, RNA and proteins, leading to cell damage, followed by death. We used the Comet assay, and we analyzed chromosome aberrations, in order to evaluate the genotoxic and clastogenic effects of rotenone on the different phases of the cell cycle. Cultured human lymphocytes were treated with 1.0, 1.5 and 2.0 microg/mL rotenone during the G1, G1/S, S (pulses of 1 and 6 h), and G2 phases of the cell cycle. Rotenone induced DNA damage and was clastogenic, but the clastogenicity was detected only with treatments conducted during the G1/S and S phases of the cell cycle. Rotenone also induced endoreduplication and polyploidy in treatments made during G1, while it significantly reduced the mitotic index in all phases of the cell cycle.     

An unusual presentation of paracoccidioidomycosis in an AIDS patient: A case report

A case of paracoccidioidomycosis presenting as a solitary pulmonary nodular lesion in a patient with acquired immunodeficiency syndrome (AIDS) is presented. This case illustrates that restricted lung lesions can also be found and diagnosed in immunodeficient patients. This revised version was published online in June 2006 with corrections to the Cover Date.     

The effect of adrenaline and Walker‐256 tumour‐induced cachexia upon Kupffer cell metabolism

Kupffer cells (KC), the liver macrophages, are able to produce PGE₂, which is involved in immune suppression and in the aggravation of cancer cachexia due to interference with lipid metabolism in the liver. Since tumour‐bearing (TB) rats present high plasma epinephrine levels, and this hormone is able to affect macrophage metabolism and function, we have assessed the effect of epinephrine (5 nm ) upon Kupffer cell PGE₂ production. Epinephrine induced increased production of PGE₂ both by control (3·5‐fold) and TB rats (27 per cent) KC, an effect blocked by propranolol. Enhancement of cAMP content in the cells by addition of isoproterenol (0·1 μm ) to the incubations, however, failed to induce the same response in the cells. Nevertheless, when phenylephrine (1 μm ) was added to the incubation, a similar pattern of PGE₂ production to that observed for epinephrine was found for control and TB rat KC. We propose that the effect of epinephrine upon KC PGE₂ production is mediated by α‐adrenergic receptors and that Ca²⁺ is involved in the response, since increasing concentrations of the ion added to the incubation medium (0·25, 0·5 and 1·0 mm ) enhanced the eicosanoid production, while EDTA abolished the response. Copyright © 1999 John Wiley & Sons, Ltd.     

Intake of trans fatty acids during gestation and lactation leads to hypothalamic inflammation via TLR4/NFκBp65 signaling in adult offspring

We examined whether feeding pregnant and lactating rats with hydrogenated vegetable fats rich in trans fatty acids led to an increase in serum endotoxin levels and inflammation and to impaired satiety-sensing pathways in the hypothalamus of 90-day-old offspring. Pregnant and lactating Wistar rats were fed either a standard chow (Control) or one enriched with hydrogenated vegetable fat (Trans). Upon weaning, the male offspring were divided in two groups: Control-Control (CC), mothers and offspring fed the control diet; and Trans-Control (TC), mothers fed the trans diet, and offspring fed the control diet. The offspring's food intake and body weight were quantified weekly and the offspring were killed on the 90th day of life by decapitation. The blood and hypothalamus were collected from the offspring. Food intake and body weight were higher in the TC rats than in the CC rats. TC rats had increased serum endotoxin levels and increased hypothalamic cytokines, IL-6, TNF-α and IL1-β, concentrations (P<.05). TLR4, NFκBp65 and MyD88 were higher (P<.05) in the TC rats than in the CC rats. AdipoR1 was lower in the TC rats than in the CC rats. Thus, the present study shows that the mothers' hydrogenated vegetable fat intake during pregnancy and lactation led to hypothalamic inflammation and impaired satiety-sensing, which promotes deleterious metabolic consequences such as obesity, even after the withdrawal of the causal factor. In other words, the effect remains after the consumption of the standard chow by offspring.     

Transforming growth factor β and apoptosis in leprosy skin lesions: possible relationship with the control of the tissue immune response in the Mycobacterium leprae infection

The course of leprosy depends of the host immune response which ranges from the lepromatous pole (LL) to the tuberculoid pole (TT). A comparative study was conducted in 60 patients with the LL and TT. The results showed a mean expression of TGF-β of 339 ± 99.4 cells/field for TT and of 519.2 ± 68.2 cells/field for LL. Frequency of apoptosis was 6.3 ± 1.8 in TT and 14.0 ± 6.1 in LL. A correlation (p = 0.0251) between TGF-β and caspase-3 in the LL was found. This finding indicates a role of TGF-β and apoptosis in the immune response in leprosy.     

Citral and eugenol modulate DNA damage and pro-inflammatory mediator genes in murine peritoneal macrophages

Citral and eugenol have been broadly studied because of their anti-inflammatory, antioxidant and antiparasitic potentials. In this study, the effects of citral (25, 50 and 100 µg/mL) and eugenol (0.31, 0.62, 1.24 and 2.48 µg/mL) on the expression (RT-PCR) of the pro-inflammatory mediator genes NF-κB1, COX-2 and TNF-α were evaluated in mouse peritoneal macrophages with or without activation by a bacterial lipopolysaccharide (LPS). Additionally, the genotoxic potentials of two compounds and their capacities to modulate the DNA damage induced by doxorubicin (DXR) were investigated using the comet assay. The data revealed that neither citral nor eugenol changed COX-2, NF-κB1 or TNF-α expression in resting macrophages. However, in LPS-activated cells, citral induced the hypoexpression of COX-2 (100 µg/mL) and TNF-α (50 and 100 µg/mL). Hypoexpression of TNF-α was also detected after cellular exposure to eugenol at the highest concentration (2.48 µg/mL). Both compounds exhibited genotoxic potential (citral at 50 and 100 µg/mL and eugenol at all concentrations) but also showed chemopreventive effects, in various treatment protocols. Both citral and eugenol might modulate inflammatory processes and DXR-induced DNA damage, but the use of these compounds must be viewed with caution because they are also able to induce primary DNA lesions.