Psilídeos no Brasil: 9 - Tuthillia myrcianthes (Hemiptera: Psylloidea) em Myrcianthes pungens (Myrtaceae).

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Potential Geographic Distribution of Brown Marmorated Stink Bug Invasion (Halyomorpha halys)

BACKGROUND: The Brown Marmorated Stink Bug (BMSB), Halyomorpha halys (Stål) (Hemiptera: Pentatomidae), native to Asia, is becoming an invasive species with a rapidly expanding range in North America and Europe. In the US, it is a household pest and also caused unprecedented damage to agriculture crops. Exploring its climatic limits and estimating its potential geographic distribution can provide critical information for management strategies. METHODOLOGY/PRINCIPALS: We used direct climate comparisons to explore the climatic niche occupied by native and invasive populations of BMSB. Ecological niche modelings based on the native range were used to anticipate the potential distribution of BMSB worldwide. Conversely, niche models based on the introduced range were used to locate the original invasive propagates in Asia. Areas with high invasion potential were identified by two niche modeling algorithms (i.e., Maxent and GARP). CONCLUSIONS/SIGNIFICANCE: Reduced dimensionality of environmental space improves native model transferability in the invade area. Projecting models from invasive population back to native distributional areas offers valuable information on the potential source regions of the invasive populations. Our models anticipated successfully the current disjunct distribution of BMSB in the US. The original propagates are hypothesized to have come from northern Japan or western Korea. High climate suitable areas at risk of invasion include latitudes between 30°-50° including northern Europe, northeastern North America, southern Australia and the North Island of New Zealand. Angola in Africa and Uruguay in South America also showed high climate suitability

Genetic Diversity of EBV-Encoded LMP1 in the Swiss HIV Cohort Study and Implication for NF-Κb Activation

Epstein-Barr virus (EBV) is associated with several types of cancers including Hodgkin's lymphoma (HL) and nasopharyngeal carcinoma (NPC). EBV-encoded latent membrane protein 1 (LMP1), a multifunctional oncoprotein, is a powerful activator of the transcription factor NF-κB, a property that is essential for EBV-transformed lymphoblastoid cell survival. Previous studies reported LMP1 sequence variations and induction of higher NF-κB activation levels compared to the prototype B95-8 LMP1 by some variants. Here we used biopsies of EBV-associated cancers and blood of individuals included in the Swiss HIV Cohort Study (SHCS) to analyze LMP1 genetic diversity and impact of sequence variations on LMP1-mediated NF-κB activation potential. We found that a number of variants mediate higher NF-κB activation levels when compared to B95-8 LMP1 and mapped three single polymorphisms responsible for this phenotype: F106Y, I124V and F144I. F106Y was present in all LMP1 isolated in this study and its effect was variant dependent, suggesting that it was modulated by other polymorphisms. The two polymorphisms I124V and F144I were present in distinct phylogenetic groups and were linked with other specific polymorphisms nearby, I152L and D150A/L151I, respectively. The two sets of polymorphisms, I124V/I152L and F144I/D150A/L151I, which were markers of increased NF-κB activation in vitro, were not associated with EBV-associated HL in the SHCS. Taken together these results highlighted the importance of single polymorphisms for the modulation of LMP1 signaling activity and demonstrated that several groups of LMP1 variants, through distinct mutational paths, mediated enhanced NF-κB activation levels compared to B95-8 LMP1

A whole-genome association study of major determinants for host control of HIV-1

Understanding why some people establish and maintain effective control of HIV-1 and others do not is a priority in the effort to develop new treatments for HIV/AIDS. Using a whole-genome association strategy, we identified polymorphisms that explain nearly 15% of the variation among individuals in viral load during the asymptomatic set-point period of infection. One of these is found within an endogenous retroviral element and is associated with major histocompatibility allele human leukocyte antigen (HLA)-B*5701, whereas a second is located near the HLA-C gene. An additional analysis of the time to HIV disease progression implicated two genes, one of which encodes an RNA polymerase I subunit. These findings emphasize the importance of studying human genetic variation as a guide to combating infectious agents

Growth inhibition of human colorectal-carcinoma cells by interleukin-4 and expression of functional interleukin-4 receptors

The growth-inhibitory effect of interleukin-4 (IL-4) was investigated in a panel of 7 human colorectal-carcinoma cell lines. In 5 cell lines (HT29, WiDr, LS411N, LS513, LS1034) a dose-dependent reduction of proliferation was documented. At 100 U/ml, IL-4 inhibited thymidine incorporation between 45 and 75% and MTT conversion (26 to 41%). The ability of LS513 and WiDr cells to form colonies after IL-4 treatment was reduced by 85 and 62% respectively. LS513 was the most sensitive cell line, with IL-4 inducing half-maximal inhibition at 5 to 6 U/ml. The inhibitory effect of IL-4 was completely neutralized by anti-IL-4 antibodies. Northern-blot analysis revealed the presence of IL-4-receptor (IL-4R) mRNA in all cell lines. The membrane expression of the 130-kDa IL-4R was assessed by FACS, utilizing an anti-IL-4R monoclonal antibody and was confirmed by biotinylated IL-4 binding. Our results attribute an important role for IL-4 as a negative regulator of colorectal-carcinoma cell growth, thus indicating a possible avenue for intervention in this disease

Promoter polymorphisms and allelic imbalance in ABCB1 expression

OBJECTIVE: The ABCB1 (MDR1) gene, encoding the transporter P-glycoprotein, is known to act on a broad range of prescription medicines. For this reason a large number of studies have assessed the functional consequences of variation in this gene. Particular attention has focused on the ABCB1_3435C>T polymorphism, an exonic variant resulting in a synonymous change. This variant has been associated with mRNA, protein and serum levels, and with responses to a number of medicines. The results of association studies have, however, been variable and it is not currently clear whether this polymorphism is functional or is in linkage disequilibrium with functionally distinct alleles. RESULTS: To identify functional variation in the ABCB1 gene we assessed allelic imbalance by pyrosequencing cDNA from 80 lymphoblastoid B cell lines from the Centre d'Etude du Polymorphisme Humain (CEPH) collection, including 74 individuals heterozygous for 3435C>T. We found that the degree of ABCB1 allelic imbalance differed among B-cell lines. In an effort to fine-map variants that influence the proportion of the two allelic mRNA species we genotyped representative common variations near the 3435C>T polymorphism by using a tagging single nucleotide polymorphism (SNP) approach. In one approach, we assessed in segregating families the impact of cis-acting variants on mRNA levels by using allelic imbalance as the phenotype in a regression analysis that distinguishes the coupling arrangements (phase) among alleles. In a second approach, we assessed allelic imbalance levels in lymphoblastoid B-cell lines from unrelated HapMap individuals, and performed an association using tagSNPs in a 5-Mb region surrounding the gene. Two potential cis-acting variants, a promoter rs28656907/rs28373093 dinucleotide polymorphism (P=0.007) and the rs10245483 SNP (P=0.0003) located 2 Mb upstream from the gene, were predictors of ABCB1 expression. CONCLUSIONS: The study outlines a general experimental approach for fine mapping gene variants that influence mRNA expression by using cultured cell lines