990 resultados para Indian art -- North America -- Exhibitions
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v.35:no.3(1954)
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v.71(1978)
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v.47:no.2(1957)
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no.8(1923)
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v.20-21 (1897) plates
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no.15(1924)
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no.6 (1979)
Impact of low-level viremia on clinical and virological outcomes in treated HIV-1-infected patients.
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BACKGROUND: The goal of antiretroviral therapy (ART) is to reduce HIV-related morbidity and mortality by suppressing HIV replication. The prognostic value of persistent low-level viremia (LLV), particularly for clinical outcomes, is unknown. OBJECTIVE: Assess the association of different levels of LLV with virological failure, AIDS event, and death among HIV-infected patients receiving combination ART. METHODS: We analyzed data from 18 cohorts in Europe and North America, contributing to the ART Cohort Collaboration. Eligible patients achieved viral load below 50 copies/ml within 3-9 months after ART initiation. LLV50-199 was defined as two consecutive viral loads between 50 and 199 copies/ml and LLV200-499 as two consecutive viral loads between 50 and 499 copies/ml, with at least one between 200 and 499 copies/ml. We used Cox models to estimate the association of LLV with virological failure (two consecutive viral loads at least 500 copies/ml or one viral load at least 500 copies/ml, followed by a modification of ART) and AIDS event/death. RESULTS: Among 17 902 patients, 624 (3.5%) experienced LLV50-199 and 482 (2.7%) LLV200-499. Median follow-up was 2.3 and 3.1 years for virological and clinical outcomes, respectively. There were 1903 virological failure, 532 AIDS events and 480 deaths. LLV200-499 was strongly associated with virological failure [adjusted hazard ratio (aHR) 3.97, 95% confidence interval (CI) 3.05-5.17]. LLV50-199 was weakly associated with virological failure (aHR 1.38, 95% CI 0.96-2.00). LLV50-199 and LLV200-499 were not associated with AIDS event/death (aHR 1.19, 95% CI 0.78-1.82; and aHR 1.11, 95% CI 0.72-1.71, respectively). CONCLUSION: LLV200-499 was strongly associated with virological failure, but not with AIDS event/death. Our results support the US guidelines, which define virological failure as a confirmed viral load above 200 copies/ml.
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This research paper seeks to bring into view the present-day situation of Native-American narrative in English. It is divided into four chapters. The first deals with the emergence of what we might call a Native-American narrative style and its evolution from 1900 up until its particularly forceful expression in 1968 with the appearance of N. Scott Momaday’s novel House Made of Dawn. To trace this evolution, we follow the chronology set forth by Paula Gunn Allen in her anthology Voice of the Turtle: American Indian Literature 1900-1970. In the second chapter we hear various voices from contemporary Native-American literary production as we follow Simon J. Ortiz’s anthology Speaking for the Generations: Native Writers on Writing. Noteworthy among these are Leslie Marmon Silko and Gloria Bird, alongside new voices such as those of Esther G. Belin and Daniel David Moses, and closing with Guatemalan-Mayan Victor D. Montejo, exiled in the United States. These writers’ contributions gravitate around two fundamental notions: the interdependence between human beings and the surrounding landscape, and the struggle for survival, which of necessity involves the deconstruction of the (post-)colonial subject. The third chapter deals with an anthology of short stories and poems by present-day Native-American women writers, edited by Joy Harjo and Gloria Bird and entitled Reinventing the Enemy’s Language: Contemporary Native Women’s Writings of North America. It too exemplifies personal and cultural reaffirmation on a landscape rich in ancestral elements, but also where one’s own voice takes shape in the language which, historically, is that of the enemy. In the final chapter we see how translation studies provide a critical perspective and fruitful reflection on the literary production of Native-American translative cultures, where a wide range of writers struggle to bring about the affirmative deconstruction of the colonialised subject. Thus there comes a turnaround in the function of the “enemy’s language,” giving rise also to the question of cultural incommensurability.
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Tuberculosis is a prehistoric American human disease. This paper reviews the literature and discusses hypotheses for origins and epidemiological patterns of prehistoric tuberculosis. From the last decades, 24 papers about prehistoric tuberculosis were published and 133 cases were reviewed. In South America most are isolated case studies, contrary to North America where more skeletal series were analyzed. Disease was usually located at the deserts of Chile and Peru, Central Plains in USA, and Lake Ontario in Canada. Skeletal remains represent most of the cases, but 16 mummies have also been described. Thirty individuals had lung disease, 19 of them diagnosed by the ribs. More then 100 individuals had osseous tuberculosis and 26 also had it in other organs. As today, transmission of the infection and establishment of the disease were favored by cultural and life-style changes such as sedentarization, crowding, undernutrition, use of dark and insulated houses, and by the frequency of interpersonal contacts. The papers confirm that despite previous perceptions, tuberculosis seems to have occured in America for millennia. It only had epidemiological expression when special conditions favored its expansion. Occurring as epidemic bursts or low endemic disease, it had differential impact on groups or social segments in America for at least two millennia.
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Aspects related to hatching, lifetime, number of blood meals for molting, mortality, feeding time, and postfeeding defecation delay were evaluated and compared in each instar of three North American Triatominae: Triatoma gerstaeckeri, Triatoma lecticularia and Triatoma protracta, all of them fed on rabbits. No significant differences (p > 0.05) were found among the three species regarding mean hatching rate, which was close to 20 days. Egg-to-adult development times were significantly shorter (p < 0.05) for T. lecticularia. Number of blood meals for molting to next instar ranged from one to five for T. protracta, and from one to six for T. gerstaeckeri and T. lecticularia. Mortality rates were higher in younger nymphs of T. lecticularia and T. protracta, while rates in T. gerstaeckeri were higher in fifth-instar nymphs. Mean feeding time was longest in T. gerstaeckeri, followed by T. lecticularia. More than twice the number of T. gerstaeckeri nymphs completed the development process, if compared to the nymphs from the other two species. Defecation delay was less than 10 min for T. lecticularia, T. protracta and the youngest nymphs of T. gerstaeckeri. Results point out that these three species may be important potential vectors of Trypanosoma cruzi for human populations, in areas of Mexico where these species are currently present.
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Retinitis pigmentosa (RP) is a hereditary disease that leads to the progressive degeneration of retinal photoreceptor cells and to blindness. It is caused by mutations in several distinct genes, including the ciliary gene FAM161A, which is associated with a recessive form of this disorder. Recent investigations have revealed that defects in FAM161A represent a rather prevalent cause of hereditary blindness in Israel and the Palestinian territories, whereas they seem to be rarely present within patients from Germany. Genetic or clinical data are currently not available for other countries. In this work, we screened a cohort of patients with recessive RP from North America to determine the frequency of FAM161A mutations in this ethnically-mixed population and to assess the phenotype of positive cases. Out of 273 unrelated patients, only 3 subjects had defects in FAM161A. A fourth positive patient, the sister of one of these index cases, was also identified following pedigree analysis. They were all homozygous for the p.T452Sfx3 mutation, which was previously reported as a founder DNA variant in the Israeli and Palestinian populations. Analysis of cultured lymphoblasts from patients revealed that mutant FAM161A transcripts were actively degraded by nonsense-mediated mRNA decay. Electroretinographic testing showed 30 Hz cone flicker responses in the range of 0.10 to 0.60 microvolts in all cases at their first visit (age 12 to 23) (lower norm = 50 μV) and of 0.06 to 0.32 microvolts at their most recent examination (age 27 to 43), revealing an early-onset of this progressive disease. Our data indicate that mutations in FAM161A are responsible for 1% of recessive RP cases in North America, similar to the prevalence detected in Germany and unlike the data from Israel and the Palestinian territories. We also show that, at the molecular level, the disease is likely caused by FAM161A protein deficiency.