RESUMO
Offsets are a novel conservation tool, yet using them to achieve no net loss of biodiversity is challenging. This is especially true when using conservation offsets (i.e., protected areas) because achieving no net loss requires avoiding equivalent loss. Our objective was to determine if offsetting the impacts of mining achieves no net loss of native vegetation in Brazil's largest iron mining region. We used a land-use change model to simulate deforestation by mining to 2020; developed a model to allocate conservation offsets to the landscape under 3 scenarios (baseline, no new offsets; current practice, like-for-like [by vegetation type] conservation offsetting near the impact site; and threat scenario, like-for-like conservation offsetting of highly threatened vegetation); and simulated nonmining deforestation to 2020 for each scenario to quantify avoided deforestation achieved with offsets. Mines cleared 3570 ha of native vegetation by 2020. Under a 1:4 offset ratio, mining companies would be required to conserve >14,200 ha of native vegetation, doubling the current extent of protected areas in the region. Allocating offsets under current practice avoided deforestation equivalent to 3% of that caused by mining, whereas allocating under the threat scenario avoided 9%. Current practice failed to achieve no net loss because offsets did not conserve threatened vegetation. Explicit allocation of offsets to threatened vegetation also failed because the most threatened vegetation was widely dispersed across the landscape, making conservation logistically difficult. To achieve no net loss with conservation offsets requires information on regional deforestation trajectories and the distribution of threatened vegetation. However, in some regions achieving no net loss through conservation may be impossible. In these cases, other offsetting activities, such as revegetation, will be required.
Assuntos
Biodiversidade , Conservação dos Recursos Naturais/métodos , Mineração , Brasil , Conservação dos Recursos Naturais/legislação & jurisprudênciaRESUMO
The serum complement activities of a 1-year-old infant with recurrent life-threatening bacterial infections and persistent C3-Coombs-positive red blood cells were investigated. The patient's serum had a depressed serum level of CH50, C3, factor B, and factor H as well as undetectable antigenic or functional factor I. The complement profile of the parents was normal, with the exception of factor I, which was approximately 50% of normal in each parent. The Coombs positivity of the patient's red blood cells could be reversed in vitro by incubation with normal serum containing factor I. Infusion of normal plasma into the patient resulted in increased levels of CH50, with concomitant increases in serum C3, factor B, and factor H levels. The patient's red blood cells became transiently Coombs negative. At no time after plasma infusion was factor I detectable in the patient's serum. All complement functions and the C3 Coombs reactivity of the patient's red blood cells returned to preinfusion levels within 14 days. These findings are consistent with an inherited deficiency of factor I and emphasize the critical role this protein plays in the regulation of the alternative complement pathway. Plasma therapy may be an adjunct to the management of acute infection in patients with factor I deficiency.
Assuntos
Afibrinogenemia/terapia , Transfusão de Sangue , Plasma , Afibrinogenemia/imunologia , Infecções Bacterianas/etiologia , Via Alternativa do Complemento , Via Clássica do Complemento , Proteínas do Sistema Complemento/análise , Teste de Coombs , Feminino , Fibrinogênio/análise , Humanos , Lactente , RecidivaRESUMO
Sjögren syndrome, consisting of keratoconjunctivitis sicca and xerostomia with or without another autoimmune disease, is uncommon in children. We describe our retrospective experience with eight pediatric patients with SS. All had recurrent parotid enlargement and abnormal salivary gland biopsies, six had keratoconjunctivitis sicca, and five had other autoimmune manifestations, although only two of these had other clearly defined autoimmune disorders (mixed connective tissue disease and hypergammaglobulinemic purpura). Our patients had a higher incidence of primary SS, parotid enlargement, and hematologic abnormalities than did children previously reported with SS. Children with SS demonstrate a clinical heterogeneity comparable to that seen in adults.
Assuntos
Síndrome de Sjogren/diagnóstico , Adolescente , Doenças Autoimunes/diagnóstico , Criança , Pré-Escolar , Feminino , Humanos , Ceratoconjuntivite/diagnóstico , Masculino , Doenças Parotídeas/diagnóstico , Estudos Retrospectivos , Doenças das Glândulas Salivares/diagnósticoRESUMO
Reconstruction of the T-cell immune defect in patients with the DiGeorge syndrome has been accomplished in the past by fetal thymus transplantation. Because of the risk of fatal graft-versus-host reaction with fetal thymus transplantation in patients with abnormal T-cell immunity, we have examined the effects of a thymus tissue extract, thymosin fraction 5, on the in vitro and in vivo immune function in children with the DiGeorge syndrome. T-cell numbers were increased with thymosin F5 in vitro in three of five patients. T-cell number and function was improved in three of four patients treated with thymosin F5 in vivo. Spontaneous improvement in the immune function of these patients cannot be excluded. These results suggest, however, that further trials with thymosin F5 therapy may be indicated in patients with the DiGeorge syndrome.