Processos de democracia direta: sim ou não? Os argumentos clássicos à luz da teoria e da prática

Regularmente surgem controvérsias sobre os processos de democracia direta, dos quais os mecanismos mais frequentes são a iniciativa popular, o plebiscito e o referendo. Por um lado, há autores que defendem a posição de que essas instituições tornam o jogo político mais lento, caro, confuso e ilegítimo; outros defendem a posição contrária e argumentam que processos de democracia direta são fundamentais para os cidadãos e a qualidade da democracia. O presente estudo analisa esse tema em torno de sete questões, baseadas em considerações teóricas e pesquisas empíricas: 1. A questão entre o minimalismo e o maximalismo democrático; 2. A concorrência entre maioria e minoria; 3. A concorrência entre as instituições representativas e os processos de democracia direta; 4. A questão da competência dos cidadãos; 5. A questão dos efeitos colaterais dos processos de democracia direta; 6. A questão do tamanho do eleitorado; 7. A questão dos custos dos processos de democracia direta. As sete questões são analisadas a partir de uma revisão bibliográfica que considera tanto fontes nacionais como internacionais. O estudo mostra que os processos de democracia direta podem ser um complemento para as instituições representativas em um sistema democrático. O bom desempenho dos plebiscitos, referendos e iniciativas populares depende tanto da regulamentação destes como também do desempenho das outras instituições políticas e da situação socioeconômica de um país. O estudo permite ampliar e aprofundar o debate sobre processos de democracia direta no Brasil

Effects of chemical carcinogens on hemopoiesis, immunopoiesis and viral oncogenesis. Three year technical progress report, February 1, 1977-September 30, 1979. [MMS; BP; DMBA; propane sultone; MCA; mice]

Studies were initiated to evaluate in an in vitro system selected chemical carcinogens derived from energy producing hydrocarbons for their effect on the hematopoietic and immune systems. Studies were also conducted to determine whether the selected carcinogens could interact with leukemogenic virus to produce leukemia in mice. Five compounds have been investigated thus far: (1) methylmethane sulfonate (MMS); (2) benzo(a)pyrene (BP); (3) 7,12 dimethylbenz(a)anthracene (DMBA); (4) propane sultone (PS); and (5) 20-methylcholanthrene (MCA). MMS inhibited both the colony forming ability of CFU-S and the immune response of PFC. MMS also potentiated the development of Friend viral leukemia when given to mice before the virus. The observed potentiation did not appear to correlate with the suppressed antibody formation response of the PFC. Good temporal correlation was found between leukemia potentiation and suppression of the colony forming ability of the CFU-S. DNA synthetic activity was also increased without a substantial increase in the number of CFU-S over that found for normal mice. BP also inhibited colony forming by the CFU-S. Effects of BP on PFC response were of a mixed nature, varying as a function of time. When given in conjunction with Friend leukemia virus, a potentiation of leukemia development was observed. To date no suppressive effect of DMBA on PFC response has been observed. The results on potentiation of viral leukemogenesis are also varied. With a high virus dose, DMBA inhibited leukemia development. However, when a subthreshold dose of virus was employed, injections of DMBA resulted in potentiation. Studies with MCA and PS were only recently begun. The effects of PS on PFC response were measured at selected dates. Suppression was found only at one time. Initial data suggests that MCA may potentiate the development of viral leukemogenesis when given before the virus. (ERB

Effects of chemical carcinogens of hemopoiesis, immunopoiesis and viral oncogenesis. Technical progress report, December 1, 1977--September 30, 1978. [Mechanisms of potentiation of viral leukemogenesis by MMS, benzopyrene, and DMBA]

During the past year we have concentrated on defining the circumstances under which methyl methanesulfonate (MMS), benzo(a) pyrene (BP), and 7,12-dimethylbenz(a)anthracene (DMBA) interact with Friend virus (FLV) to produce leukemia. The optimum scheduling for each and also the effective dose levels of the chemicals have been partially determined. There are at least three critical factors which govern whether or not a leukemogenic interaction can be shown between the chemical agents and the virus. These are chemical dose, virus dose, and their relative time of administration. The most critical of these is virus dose. The optimum virus dose is that which results in between 25 and 40% incidence of leukemia within 40 days after virus infection when virus is given alone. The chemical carcinogens have a lower dose threshold, below which no significant potentiating effect can be observed. The only upper limit would appear to be acute drug toxicity. The third element, timing, is equally critical and varies according to the chemical. This variation may reflect different mechanisms of action by the chemical agents and/or different pharmacology. Data on the effects of MMS, BP, and DMBA on the immune system have indicated that the viral enhancement is probably not dependent on this function. Further enhancement of the potentiation of viral leukemogenesis was observed using benzo(a)pyrene and caffeine, indicating that the inhibition by caffeine of DNA repair may be an important factor in virus potentiation. (ERB