Party System Institutionalization and Reliance on Personal Income Tax in Developing Countries

This paper explores the effect of party system institutionalization on the relevance of the personal income tax in the tax composition. Based on a fiscal contractualism approach, it is argued that institutionalized political party systems increase the capacity of political actors to credibly commit to fiscal contracts agreed with wealthy taxpayers. Consequently, in countries characterized by institutionalized political party systems wealthy taxpayers accept paying a bigger share of the tax burden, as reflected in a greater relevance of progressive tax types. The analysis of panel data for more than 90 countries from 1990 to 2010 supports this hypothesis, showing that party system institutionalization has an especially significant and strong positive effect on the relevance of the personal income tax where bureaucratic capacity is low. At high levels of bureaucratic capacity the effect disappears. The findings strongly support the claim that, particularly in developing countries, where bureaucratic capacity tends to be limited, taxation is best understood as a problem of credible commitment

Presencia de huevos de Toxocara spp. en el pelaje de caninos callejeros y domésticos

Toxocara canis and Toxocara cati are the etiologic agents of a zoonotic disease with a broad distribution: human toxocariasis. Toxocara spp. eggs on the hair of dogs could be a route of transmission. The objective was to determine the presence of Toxocara spp. eggs in canine fur, according to dog type and age. We analyzed hairs from 148 dogs classified by their type in stray dogs (56) or domestic (92) and by age in puppy (20), juvenile (39) or adult (89). Eggs were detected in 8 stray dogs (14.3%) and in 1 domestic dog (1.1%). We found positive samples in 5 puppies (25%), 3 juveniles (8%) and 1 adult (1%). Being stray and less than one year were risk factors for the presence of eggs in dogs hair (OR=15,17 (IC 1,84-124,85); p=0,0018, y OR=13,80 (IC 1,67-113,55); p=0,0028, respectively). Amongst the 213 eggs found from all the samples, we detected 60 (28.1%) non viable, 79 (37.1%) viable, 73 (34.3%) embryonating and 1 (0.5%) embryonated. Canine hair with Toxocara spp. eggs could represent a secondary transmission route.Fil: Sierra, M.F. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias. Cátedra de Salud Pública. Buenos Aires, ArgentinaFil: Daprato, B. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias. Cátedra de Salud Pública. Buenos Aires, ArgentinaFil: Kunic, M. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias. Cátedra de Salud Pública. Buenos Aires, ArgentinaFil: López, C.M. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias. Cátedra de Salud Pública. Buenos Aires, ArgentinaFil: Sommerfelt, I.E. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias. Cátedra de Salud Pública. Buenos Aires, ArgentinaToxocara canis y Toxocara cati son los agentes etiológicos de una zoonosis parasitaria ampliamente distribuida: la Toxocariasis humana. Una vía de transmisión de Toxocara spp. podría ser a través del pelaje de los caninos que tengan huevos del parásito adheridos al mismo. El objetivo fue establecer presencia de huevos de Toxocara spp. en el pelaje de caninos según origen y edad de los animales. Se analizaron pelos de 148 perros clasificados según origen, callejeros (56) y domésticos (92) y, según edad, cachorros (20), juveniles (39) y adultos (89). Se encontraron huevos en pelo de 8 callejeros (14,3%) y 1 doméstico (1,1%). Según edad en 5 cachorros (25%), 3 juveniles (8%) y 1 adulto (1%). Ser callejero y menor de un año resultaron factores de riesgo para la presencia de huevos en el pelaje de perros (OR=15,17 (IC 1,84-124,85); p=0,0018, y OR=13,80 (IC 1,67 113,55); p=0,0028, respectivamente). Se observaron 213 huevos, no viables 60 (28,1%), viables 79 (37,1%), embrionados 73 (34,3%) y larvados 1 (0,5%). El pelo de los caninos con huevos de Toxocara spp. podría ser una vía secundaria de transmisión

Risk factors associated with Toxoplasma gondii seroprevalence in domestic pig farms in Argentina

Toxoplasmosis is a worldwide parasitic zoonosis caused by Toxoplasma gondii. Pigs can become infected by consuming water or food contaminated with sporulated oocysts, or by carnivorism (like the consumption of infected rodents). In pigs most infections are asymptomatic. In certain countries, pig meat containing tissue cysts is a major source of infection for human beings. The aims of this study were to estimate the seroprevalence of toxoplasmosis and to identify which factors were related with the increase of the risk of infection in Argentina. The seroprevalence of T. gondii was determined in 240 pigs from 27 farms in the central-western area of Buenos Aires province, Argentina. Serum samples were analyzed using indirect fluorescent antibody test (IFAT) and enzyme-linked immunosorbent assay (ELISA) techniques. Prevalence determined was 53.33% and 32.08% by IFAT and ELISA, respectively. Results showed that 81.5% (22/27) of the farms were seropositive to T. gondii. Seropositivity for T. gondii was related with the following risk factors (p value ≤0.05): presence of felids and rodents in the farms, feeding with waste of human food and storage of food outdoors with free access to felids and to the reservoirs when applying both serological techniques. Our results strongly suggest that the risk of infection with T. gondii in pigs is related to the outdoor/extensive type of production system with low infrastructure conditions, which allows both felids and rodents to have free access to pigs and stored food. Also, the high seroprevalence detected in the present study could indicate a potential role of pork in human infections in the region.Fil: Kunic, J. M.. Universidad de Buenos Aires; ArgentinaFil: Bernstein, Mariana. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Epizootiología y Salud Pública. Laboratorio de Inmunoparasitología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Venturini, María Cecilia. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Epizootiología y Salud Pública. Laboratorio de Inmunoparasitología; ArgentinaFil: Pardini, Lais Luján. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Epizootiología y Salud Pública. Laboratorio de Inmunoparasitología; ArgentinaFil: Sommerfelt, I. E.. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias; Argentin

Calmodulin mutations associated with recurrent cardiac arrest in infants.

Background-Life-threatening disorders of heart rhythm may arise during infancy and can result in the sudden and tragic death of a child. We performed exome sequencing on 2 unrelated infants presenting with recurrent cardiac arrest to discover a genetic cause. Methods and Results-We ascertained 2 unrelated infants (probands) with recurrent cardiac arrest and dramatically prolonged QTc interval who were both born to healthy parents. The 2 parent-child trios were investigated with the use of exome sequencing to search for de novo genetic variants. We then performed follow-up candidate gene screening on an independent cohort of 82 subjects with congenital long-QT syndrome without an identified genetic cause. Biochemical studies were performed to determine the functional consequences of mutations discovered in 2 genes encoding calmodulin. We discovered 3 heterozygous de novo mutations in either CALM1 or CALM2, 2 of the 3 human genes encoding calmodulin, in the 2 probands and in 2 additional subjects with recurrent cardiac arrest. All mutation carriers were infants who exhibited life-threatening ventricular arrhythmias combined variably with epilepsy and delayed neurodevelopment. Mutations altered residues in or adjacent to critical calcium binding loops in the calmodulin carboxyl-terminal domain. Recombinant mutant calmodulins exhibited several-fold reductions in calcium binding affinity. Conclusions-Human calmodulin mutations disrupt calcium ion binding to the protein and are associated with a life-threatening condition in early infancy. Defects in calmodulin function will disrupt important calcium signaling events in heart, affecting membrane ion channels, a plausible molecular mechanism for potentially deadly disturbances in heart rhythm during infancy

Long QT syndrome-associated mutations in intrauterine fetal death.

Intrauterine fetal death or stillbirth occurs in approximately 1 out of every 160 pregnancies and accounts for 50\% of all perinatal deaths. Postmortem evaluation fails to elucidate an underlying cause in many cases. Long QT syndrome (LQTS) may contribute to this problem.To determine the spectrum and prevalence of mutations in the 3 most common LQTS susceptible genes (KCNQ1, KCNH2, and SCN5A) for a cohort of unexplained cases.In this case series, retrospective postmortem genetic testing was conducted on a convenience sample of 91 unexplained intrauterine fetal deaths (mean [SD] estimated gestational age at fetal death, 26.3 [8.7] weeks) that were collected from 2006-2012 by the Mayo Clinic, Rochester, Minnesota, or the Fondazione IRCCS Policlinico San Matteo, Pavia, Italy. More than 1300 ostensibly healthy individuals served as controls. In addition, publicly available exome databases were assessed for the general population frequency of identified genetic variants.Comprehensive mutational analyses of KCNQ1 (KV7.1, LQTS type 1), KCNH2 (HERG/KV11.1, LQTS type 2), and SCN5A (NaV1.5, LQTS type 3) were performed using denaturing high-performance liquid chromatography and direct DNA sequencing on genomic DNA extracted from decedent tissue. Functional analyses of novel mutations were performed using heterologous expression and patch-clamp recording.The 3 putative LQTS susceptibility missense mutations (KCNQ1, p.A283T; KCNQ1, p.R397W; and KCNH2 [1b], p.R25W), with a heterozygous frequency of less than 0.05\% in more than 10 000 publicly available exomes and absent in more than 1000 ethnically similar control patients, were discovered in 3 intrauterine fetal deaths (3.3\% [95\% CI, 0.68\%-9.3\%]). Both KV7.1-A283T (16-week male) and KV7.1-R397W (16-week female) mutations were associated with marked KV7.1 loss-of-function consistent with in utero LQTS type 1, whereas the HERG1b-R25W mutation (33.2-week male) exhibited a loss of function consistent with in utero LQTS type 2. In addition, 5 intrauterine fetal deaths hosted SCN5A rare nonsynonymous genetic variants (p.T220I, p.R1193Q, involving 2 cases, and p.P2006A, involving 2 cases) that conferred in vitro electrophysiological characteristics consistent with potentially proarrhythmic phenotypes.In this molecular genetic evaluation of 91 cases of intrauterine fetal death, missense mutations associated with LQTS susceptibility were discovered in 3 cases (3.3\%) and overall, genetic variants leading to dysfunctional LQTS-associated ion channels in vitro were discovered in 8 cases (8.8\%). These preliminary findings may provide insights into mechanisms of some cases of stillbirth

Calmodulin mutations associated with recurrent cardiac arrest in infants.

Background-: Life-threatening disorders of heart rhythm may arise during infancy and can result in the sudden and tragic death of a child. We performed exome sequencing on 2 unrelated infants presenting with recurrent cardiac arrest to discover a genetic cause. Methods and Results-: We ascertained 2 unrelated infants (probands) with recurrent cardiac arrest and dramatically prolonged QTc interval who were both born to healthy parents. The 2 parent-child trios were investigated with the use of exome sequencing to search for de novo genetic variants. We then performed follow-up candidate gene screening on an independent cohort of 82 subjects with congenital long-QT syndrome without an identified genetic cause. Biochemical studies were performed to determine the functional consequences of mutations discovered in 2 genes encoding calmodulin. We discovered 3 heterozygous de novo mutations in either CALM1 or CALM2, 2 of the 3 human genes encoding calmodulin, in the 2 probands and in 2 additional subjects with recurrent cardiac arrest. All mutation carriers were infants who exhibited life-threatening ventricular arrhythmias combined variably with epilepsy and delayed neurodevelopment. Mutations altered residues in or adjacent to critical calcium binding loops in the calmodulin carboxyl-terminal domain. Recombinant mutant calmodulins exhibited several-fold reductions in calcium binding affinity. Conclusions-: Human calmodulin mutations disrupt calcium ion binding to the protein and are associated with a life-threatening condition in early infancy. Defects in calmodulin function will disrupt important calcium signaling events in heart, affecting membrane ion channels, a plausible molecular mechanism for potentially deadly disturbances in heart rhythm during infancy