Search, Seizure and (False?) Arrest: An Analysis of Fourth Amendment Remedies when Police can Plant Evidence

The Fourth Amendment prohibits unreasonable searches and seizures in criminal investigations. The Supreme Court has interpreted this to require that police obtain a warrant prior to search and that illegally seized evidence be excluded from trial. A consensus has developed in the law and economics literature that tort liability for police officers is a superior means of deterring unreasonable searches. We argue that this conclusion depends on the assumption of truth-seeking police, and develop a game-theoretic model to compare the two remedies when some police officers (the bad type) are willing to plant evidence in order to obtain convictions, even though other police (the good type) are not (where this type is private information). We characterize the perfect Bayesian equilibria of the asymmetric-information game between the police and a court that seeks to minimize error costs in deciding whether to convict or acquit suspects. In this framework, we show that the exclusionary rule with a warrant requirement leads to superior outcomes (relative to tort liability) in terms of truth-finding function of courts, because the warrant requirement can reduce the scope for bad types of police to plant evidence

The role of deregulated E2F1 expression in brain tumors

Mutations disabling the retinoblastoma (Rb) pathway are among the most common in human cancers, including brain cancer. These mutations promote tumor development through deregulated control of the E2F family of transcription factors. E2F1 belongs to a class of E2F's identified as transcriptional activators and involved in the G1/S phase transition of the cell. However, E2F-1 presents with a paradox as it is considered to have membership in two gene classes, functioning as both an oncogene and a tumor suppressor. This unusual trait generates a degree of uncertainty on the role that E2F1 plays in the development or maintenance of any given tumor. Here we show that E2F1 functions as an oncogene in brain tumors through the generation of mice engineered to overexpress E2F1 specifically within glial cells and neuronal progenitors as directed by the GFAP promoter. Mice carrying the transgene develop with high penetrance a phenotype characterized by neurological deficits including paresia, ataxia, head tilt and seizures. MRI imagining of the tgE2F1 mice reveals a low incidence of mild hydrocephalus, and most notably, histological analysis demonstrates that 25% of tgE2F1 mice present with the spontaneous formation of malignant brain tumors. Overall these neoplasms show histological features from a wide range of aggressive brain cancers including medulloblastoma, choroid plexus carcinoma, primary neuroectodermic tumor and malignant gliomas. Isolation and characterization of astrocytes from the tgE2F1 animal reveals a highly proliferative population of cells with 55% ± 2.5 of the tgE2F1astrocytes, 35% ± 3.4 normal mouse astrocytes in S-phase and the acquired capacity to grow in anchorage independent conditions. Additionally tgE2F1 astrocytes show an aberrant phenotype with random chromosomal fusions and nearly all cells demonstrating polyploidy. Taken together, this model forces a comparison to human brain tumor formation. Mouse age as related to tumoral mimics the human scenario with juvenile tgE2F1 mice presenting embryonal tumors typically identified in children, and older tgE2F1 mice demonstrating gliomas. In this regard, this study suggests a global role for E2F1 in the formation and maintenance of multilineage brain tumors, irrefutably establishing E2F1 as an oncogene in the brain. ^

Abnormal expression of E2F1 and E2F4 results in hyperproliferation of the ependyma and lethal hydrocephalus

The proliferative role of E2F has been under investigation for several years. However, while it is known that E2F1 and E2F4 play a part in development and differentiation, research has not been centered on determining the exact functions these E2Fs play in brain development, given there high expression levels throughout embryogenesis. A GFAP-E2F1 mouse model directing human E2F1 transgene expression to glial cells, such as ependymal cells, was used in the present study in combination with an E2F4 mutant mouse model. Interestingly, 20% of tgE2F1; E2F4 null mice developed a phenotype consisting of domed head, hunched posture, seizures, tremors, hyperactivity or hypeactivity, dysnea, and low body weight. These mice died during the first three weeks of severe hydrocephalus. Similarly, tgE2F1; E2F4 heterozygous mice also develop severe hydrocephalus, although this occurs at 6 weeks at a 2% frequency. Pathological examination of the brains of those animals uncovered enlarged cerebral ventricles with marked thinning of the cerebral cortices, confirming the diagnosis of three-ventricle hydrocephalus, and the absence of tumors. Careful examination of the aqueduct shows an excess of proliferating cells that may cause a blockage of CSF. Of significance, 44% of ependymal cells in hydrocephalic tgE2F1;E2F4-/- mouse brains were positive for BrdU incorporation. Studies determining the molecular rationale for the hydrocephalic phenotype suggest proliferative ependymal cells may not be exclusively related to dysregulated cell cycle in conjuction with E2F activity. Due in part to the deficiency of E2F4 in this mouse model, we find that differentiation of these ependymal cells is not complete and instead undergoes maturation arrest. This suggestion is confirmed by the expression of genes found in neural stem cells or precursor cell populations, in the ependymal cell region of tgE2F1; E2F4-/-. Therefore, from this study, we conclude that dysregulated E2F1 expression in combination with deficient E2F4 expression results in an undifferentiated ependymal cell population that is hyperproliferative in the ventricular system causing an impediment of CSF circulation. It is further concluded that normal E2F1 and E2F4 expression in brain development is crucial for the proper formation and function of the ventricular system.^

Defining barriers in caring for seriously-ill children in a resource-limited setting: An observational study of 2 children's hospitals in Haiti

Background. According to the WHO 2007 country report, Haiti lags behind the Millennium Development Goal of reducing child mortality and maintains the highest under-5 mortality rate in the Western hemisphere. 3 Overall, few studies exist that seek to better grasp barriers in caring for a seriously ill child in a resource-limited setting and only a handful propose sustainable, effective interventions. ^ Objectives. The objectives of this study are to describe the prevalence of serious illnesses among children hospitalized at 2 children's hospitals in Port au Prince, to determine the barriers faced when caring for seriously ill children, and to report hospital outcomes of children admitted with serious illnesses. ^ Methods. Data were gathered from 2 major children's hospitals in Port au Prince, Haiti (Grace Children's Hospital [GCH] and Hopital d l'Universite d'Etat d'Haiti [HUEH]) using a triangulated approach of focus group discussions, physician questionnaires, and retrospective chart review. 23 pediatric physicians participated in focus group discussions and completed a self-administered questionnaire evaluating healthcare provider knowledge, self-efficacy, and perceived barriers relating to the care of seriously ill children in a resource-limited setting. A sample of 240 patient charts meeting eligibility criteria was abstracted for pertinent elements including sociodemographics, documentation, treatment strategies, and outcomes. Factors associated with mortality were analyzed using χ2 test and Fisher exact test [Minitab v.15]. ^ Results. The most common primary diagnoses at admission were gastroenteritis with moderate dehydration (35.5%), severe malnutrition (25.8%), and pneumonia (19.3%) for GCH, and severe malnutrition (32.6%), sepsis (24.7%), and severe respiratory distress (18%) for HUEH. Overall, 12.9% and 27% of seriously ill patients presented with shock to GCH and HUEH, respectively. ^ Shortage of necessary materials and equipment represented the most commonly reported limitation (18/23 respondents). According to chart data, 9.4% of children presenting with shock did not receive a fluid bolus, and only 8% of patients presenting with altered mental status or seizures received a glucose check. 65% of patients with meningitis did not receive a lumbar puncture due to lack of materials. ^ Hospital mortality rates did not differ by gender or by institution. Children who died were more likely to have a history of prematurity (OR 4.97 [95% CI 1.32-18.80]), an incomplete vaccination record (OR 4.05 [95% CI 1.68-9.74]), or a weight for age ≤3rd percentile (OR 6.1 [95% CI 2.49-14.93]. Case-fatality rates were significantly higher among those who presented with signs of shock compared with those who did not (23.1% vs. 10.7%, RR=2.16, p=0.03). Caregivers did not achieve shock reversal in 21% of patients and did not document shock reversal in 50% of patients. ^ Conclusions. Many challenges face those who seek to optimize care for seriously ill children in resource-limited settings. Specifically, in Haiti, qualitative and quantitative data suggest major issues with lack of supplies, pre-hospital factors, including malnutrition as a comorbidity, and early recognition and management of shock. A tailored intervention designed to address these issues is needed in order to prospectively evaluate improvements in child mortality in a high-risk population.^

Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane

Lindane, or γ-hexachlorocyclohexane, is a chlorinated hydrocarbon pesticide that was banned from U.S. production in 1976, but until recently continued to be imported and applied for occupational and domestic purposes. Lindane is known to cause central nervous system (CNS), immune, cardiovascular, reproductive, liver, and kidney toxicity. The mechanism for which lindane interacts with the CNS has been elucidated, and involves antagonism of the γ-aminobutyric acid/benzodiazepine (GABAA/BZD) receptor. Antagonism of this receptor results in the inhibition of Cl- channel flux, with subsequent convulsions, seizures, and paralysis. This response makes lindane a desirable defense against arthropod pests in agriculture and the home. However, formulation and application of this compound can contribute to human toxicity. In conjunction with this exposure scenario, workers may be subject to both heat and physical stress that may increase their susceptibility to pesticide toxicity by altering their cellular stress response. The kidneys are responsible for maintaining osmotic homeostasis, and are exposed to agents that undergo urinary excretion. The mechanistic action of lindane on the kidneys is not well understood. Lindane, in other organ systems, has been shown to cause cellular damage by generation of free radicals and oxidative stress. Previous research in our laboratory has shown that lindane causes apoptosis in distal tubule cells, and delays renal stress response under hypertonic stress. Characterizing the mechanism of action of lindane under conditions of physiologic stress is necessary to understand the potential hazard cyclodiene pesticides and other organochlorine compounds pose to exposed individuals under baseline conditions, as well as under conditions of physiologic stress. We demonstrated that exposure to lindane results in oxidative damage and dysregulation of glutathione response in renal distal tubule (MDCK) cells. We showed that under conditions of hypertonic stress, lindane-induced oxidative stress resulted in early onset apoptosis and corresponding down-regulated expression of the anti-apoptotic protein, Bcl-xL. Thus, the interaction of lindane with renal peripheral benzodiazepine receptors (PBR) is associated with attenuation of cellular protective proteins, making the cell more susceptible to injury or death. ^

The relationship between premature rupture of the membranes and sepsis in preterm neonates

This investigation was designed as a hospital-based, historical cohort study. The objective of the study was to determine the association between premature rupture of the membranes (PROM) and its duration on neonatal sepsis, infection, and mortality. Neonates born alive with gestational ages between 25 and 35 weeks from singleton pregnancies complicated by PROM were selected. Each of the 507 neonates was matched on gestational age, gender, ethnicity, and month of birth with a neonate without the complication of PROM.^ Data were abstracted from deliveries between January 1979 and December 1985 describing the mother's demographics, labor and delivery treatments and complications, the neonate's demographics, infection status, and medical care. The matched pairs analysis reveals a significant increase in risk of neonatal sepsis (RR = 3.5) and neonatal infection (RR = 2.4) among preterm births complicated by PROM, with a PROM exposure contributing an excess 4 to 5 cases of sepsis per 100 infants (RD = 0.04 for infection and RD = 0.05 for sepsis). Generally PROM remains an important risk factor for sepsis and infection when controlling for various other characteristics, and the risk difference remains constant.^ PROM was not significantly associated with neonatal mortality (RR = 1.02). There is an increase in risk difference for mortality associated with PROM among septic and infected infants, but it is not significant.^ A clear increase in risk of sepsis and infection from PROM occurs when durations of PROM are long (more than 48 hours), e.g., for sepsis the RR is 2.42 for short durations and RR is 6.0 for long durations. No such risk with long duration appears for neonatal mortality.^ This study indicates the importance of close observation of neonates with PROM for sepsis and infection so treatment can be initiated early. However, prematurity is the major risk for sepsis and the practice of early delivery to avoid prolonged durations of PROM does not alter the magnitude of risk. The greatest protection against these infection complications was provided when the neonate weighed over 1500 grams or had more than 33 weeks gestation. ^

A descriptive study of the sociodemographic, health and developmental factors associated with slow learning in children from upper to middle social class families in Texas

"Slow Learners" is a term used to describe children with an IQ range of 70-89 on a standardized individual intelligence test (i.e. with a standard deviation of either 15 or 16). They have above retarded, but below average intelligence and potential to learn. If the factors associated with the etiology of slow learning in children can be identified, it may be possible to hypothesize causal relationships which can be tested by intervention studies specifically designed to prevent slow learning. If effective, these may ultimately reduce the incidence of school dropouts and their cost to society. To date, there is little information about variables which may be etiologically significant. In an attempt to identify such etiologic factors this study examines the sociodemographic characteristics, prenatal history (hypertension, smoking, infections, medication, vaginal bleeding, etc.), natal history (length of delivery, Apgar score, birth trauma, resuscitation, etc.), neonatal history (infections, seizures, head trauma, etc.), developmental history (health problems, developmental milestones and growth during infancy and early childhood), and family history (educational level of the parents, occupation, history of similar condition in the family, etc.) of a series of children defined as slow learners. The study is limited to children from middle to high socioeconomic families in order to exclude the possible confounding variable of low socioeconomic status, and because a descriptive study of this group has not been previously reported. ^

A case-control study of the risk factors for eclampsia

Objective. To study the risk factors for eclampsia, a rare but significant complication of pregnancy.^ Target population. All deliveries at or after the 20th week of gestation that took place between January 1, 1977 and March 1992, and between January 1990 and April 1992 at two hospitals in Houston, Texas, respectively.^ Study population. Sixty-six confirmed cases of eclampsia, and 2 groups of randomly selected controls: Non-preeclamptic and preeclamptic deliveries matched to cases on hospital and month of delivery on a 1:4 ratio.^ Exclusions. Women with chronic hypertension, gestational epilepsy, a previous history of epilepsy, and convulsions attributed to encephalitis, meningitis, cerebral tumor, and intracerebral bleeding, and women without a definite diagnosis of preeclampsia/eclampsia.^ Results. Eclampsia developed in 0.52-0.93/1000 deliveries. Fifty-six percent of seizures occurred in the antepartum period, 2% as early as 20 weeks of gestation and 39% between 37 and 42 weeks. Twenty-nine percent and 15% occurred in the postpartum and late postpartum periods, respectively, 8% as late as one week postpartum. A different set of risk factors was involved in the development of eclampsia in non-preeclamptic women than in the progression from preeclampsia to eclampsia. Factors involved in the development of eclampsia included, in addition to twin pregnancy and family history of pregnancy-induced hypertension, fewer than 3 prenatal care visits, urinary tract infections, primigravidity, obesity, black ethnicity, diabetes mellitus, and age $\le$20 years. Risk factors involved in the progression from preeclampsia to eclampsia included fewer than 3 of prenatal care visits, and age $\le$20 years. Protective factors were magnesium sulfate administration prior to seizure, history of abortions and longer gestational age. Having less than 3 prenatal care visits and being less than or equal to 20 years of age were predictors of eclampsia, whether of its development or progression from preeclampsia. Once preeclampsia is diagnosed, primigravid, diabetic, black, or obese women and those with urinary tract infections did not appear to exhibit any increased risk for the progression to eclampsia. The administration of magnesium sulfate was especially protective, followed by a positive history of abortions, 3 or more prenatal care visits, and longer gestational age. The protective effect of MgSO$\sb4$ was only slightly diminished when cases were restricted to the 65% who had a diagnosis of preeclampsia. The progression from preeclampsia to eclampsia may be largely preventable through adequate prenatal care and presumably the administration of magnesium sulfate. (Abstract shortened by UMI.) ^

Biomedical informatics applications for epilepsy management: A systematic review

Epilepsy is a very complex disease which can have a variety of etiologies, co-morbidities, and a long list of psychosocial factors4. Clinical management of epilepsy patients typically includes serological tests, EEG's, and imaging studies to determine the single best antiepileptic drug (AED). Self-management is a vital component of achieving optimal health when living with a chronic disease. For patients with epilepsy self-management includes any necessary actions to control seizures and cope with any subsequent effects of the condition9; including aspects of treatment, seizure, and lifestyle. The use of computer-based applications can allow for more effective use of clinic visits and ultimately enhance the patient-provider relationship through focused discussion of determinants affecting self-management. ^ The purpose of this study is to conduct a systematic literature review on informatics application in epilepsy self-management in an effort to describe current evidence for informatics applications and decision support as an adjunct to successful clinical management of epilepsy. Each publication was analyzed for the type of study design utilized. ^ A total of 68 publications were included and categorized by the study design used, development stage, and clinical domain. Descriptive study designs comprised of three-fourths of the publications and indicate an underwhelming use of prospective studies. The vast majority of prospective studies also focused on clinician use to increase knowledge in treating patients with epilepsy. ^ Due to the chronic nature of epilepsy and the difficulty that both clinicians and patients can experience in managing epilepsy, more prospective studies are needed to evaluate applications that can effectively increase management activities. Within the last two decades of epilepsy research, management studies have employed the use of biomedical informatics applications. While the use of computer applications to manage epilepsy has increased, more progress is needed.^

Neocortical hyperexcitability defect in a mutant mouse model of spike-wave epilepsy, {\it stargazer}

Single-locus mutations in mice can express epileptic phenotypes and provide critical insights into the naturally occurring defects that alter excitability and mediate synchronization in the central nervous system (CNS). One such recessive mutation (on chromosome (Chr) 15), stargazer(stg/stg) expresses frequent bilateral 6-7 cycles per second (c/sec) spike-wave seizures associated with behavioral arrest, and provides a valuable opportunity to examine the inherited lesion associated with spike-wave synchronization.^ The existence of distinct and heterogeneous defects mediating spike-wave discharge (SWD) generation has been demonstrated by the presence of multiple genetic loci expressing generalized spike-wave activity and the differential effects of pharmacological agents on SWDs in different spike-wave epilepsy models. Attempts at understanding the different basic mechanisms underlying spike-wave synchronization have focused on $\gamma$-aminobutyric acid (GABA) receptor-, low threshold T-type Ca$\sp{2+}$ channel-, and N-methyl-D-aspartate receptor (NMDA-R)-mediated transmission. It is believed that defects in these modes of transmission can mediate the conversion of normal oscillations in a trisynaptic circuit, which includes the neocortex, reticular nucleus and thalamus, into spike-wave activity. However, the underlying lesions involved in spike-wave synchronization have not been clearly identified.^ The purpose of this research project was to locate and characterize a distinct neuronal hyperexcitability defect favoring spike-wave synchronization in the stargazer brain. One experimental approach for anatomically locating areas of synchronization and hyperexcitability involved an attempt to map patterns of hypersynchronous activity with antibodies to activity-induced proteins.^ A second approach to characterizing the neuronal defect involved examining the neuronal responses in the mutant following application of pharmacological agents with well known sites of action.^ In order to test the hypothesis that an NMDA receptor mediated hyperexcitability defect exists in stargazer neocortex, extracellular field recordings were used to examine the effects of CPP and MK-801 on coronal neocortical brain slices of stargazer and wild type perfused with 0 Mg$\sp{2+}$ artificial cerebral spinal fluid (aCSF).^ To study how NMDA receptor antagonists might promote increased excitability in stargazer neocortex, two basic hypotheses were tested: (1) NMDA receptor antagonists directly activate deep layer principal pyramidal cells in the neocortex of stargazer, presumably by opening NMDA receptor channels altered by the stg mutation; and (2) NMDA receptor antagonists disinhibit the neocortical network by blocking recurrent excitatory synaptic inputs onto inhibitory interneurons in the deep layers of stargazer neocortex.^ In order to test whether CPP might disinhibit the 0 Mg$\sp{2+}$ bursting network in the mutant by acting on inhibitory interneurons, the inhibitory inputs were pharmacologically removed by application of GABA receptor antagonists to the cortical network, and the effects of CPP under 0 Mg$\sp{2+}$aCSF perfusion in layer V of stg/stg were then compared with those found in +/+ neocortex using in vitro extracellular field recordings. (Abstract shortened by UMI.) ^

Estimates of hospital and physician costs of epilepsy in the United States for 1995 comparing the provider -based survey method and a patient -based medical charts and billing method

This investigation compares two different methodologies for calculating the national cost of epilepsy: provider-based survey method (PBSM) and the patient-based medical charts and billing method (PBMC&BM). The PBSM uses the National Hospital Discharge Survey (NHDS), the National Hospital Ambulatory Medical Care Survey (NHAMCS) and the National Ambulatory Medical Care Survey (NAMCS) as the sources of utilization. The PBMC&BM uses patient data, charts and billings, to determine utilization rates for specific components of hospital, physician and drug prescriptions. ^ The 1995 hospital and physician cost of epilepsy is estimated to be $722 million using the PBSM and $1,058 million using the PBMC&BM. The difference of $336 million results from $136 million difference in utilization and $200 million difference in unit cost. ^ Utilization. The utilization difference of $136 million is composed of an inpatient variation of $129 million, $100 million hospital and $29 million physician, and an ambulatory variation of $7 million. The $100 million hospital variance is attributed to inclusion of febrile seizures in the PBSM, $−79 million, and the exclusion of admissions attributed to epilepsy, $179 million. The former suggests that the diagnostic codes used in the NHDS may not properly match the current definition of epilepsy as used in the PBMC&BM. The latter suggests NHDS errors in the attribution of an admission to the principal diagnosis. ^ The $29 million variance in inpatient physician utilization is the result of different per-day-of-care physician visit rates, 1.3 for the PBMC&BM versus 1.0 for the PBSM. The absence of visit frequency measures in the NHDS affects the internal validity of the PBSM estimate and requires the investigator to make conservative assumptions. ^ The remaining ambulatory resource utilization variance is $7 million. Of this amount, $22 million is the result of an underestimate of ancillaries in the NHAMCS and NAMCS extrapolations using the patient visit weight. ^ Unit cost. The resource cost variation is $200 million, inpatient is $22 million and ambulatory is $178 million. The inpatient variation of $22 million is composed of $19 million in hospital per day rates, due to a higher cost per day in the PBMC&BM, and $3 million in physician visit rates, due to a higher cost per visit in the PBMC&BM. ^ The ambulatory cost variance is $178 million, composed of higher per-physician-visit costs of $97 million and higher per-ancillary costs of $81 million. Both are attributed to the PBMC&BM's precise identification of resource utilization that permits accurate valuation. ^ Conclusion. Both methods have specific limitations. The PBSM strengths are its sample designs that lead to nationally representative estimates and permit statistical point and confidence interval estimation for the nation for certain variables under investigation. However, the findings of this investigation suggest the internal validity of the estimates derived is questionable and important additional information required to precisely estimate the cost of an illness is absent. ^ The PBMC&BM is a superior method in identifying resources utilized in the physician encounter with the patient permitting more accurate valuation. However, the PBMC&BM does not have the statistical reliability of the PBSM; it relies on synthesized national prevalence estimates to extrapolate a national cost estimate. While precision is important, the ability to generalize to the nation may be limited due to the small number of patients that are followed. ^

Parámetros biológicos y demograficos de áfidos (Hemiptera: aphididae) en variedades de colza canola (Brassica napus L.)

Myzus persicae (Sulz.), Brevicoryne brassicae L. y Lipaphis erysimi (Kalt.) constituyen plagas del cultivo de colza canola, Brassica napus L., y de otras crucíferas cultivadas. Los pulgones fueron colectados en un cultivo de canola y se multiplicaron en un insectario. Para el estudio se criaron 2 cohortes de 20 hembras neonatas, para cada especie de áfido y cultivar de colza, a 20 ± 1°C, 60-70% de humedad relativa y 14:10 horas de fotofase. Las principales diferencias entre especies de pulgones se observaron en la duración de los períodos reproductivo y post-reproductivo, la longevidad y la fecundidad. M. persicae fue el áfido más longevo y fecundo en Impact, mientras que en Teddy el más fecundo fue L. erysimi y el más longevo M. persicae. Con respecto a los parámetros poblacionales, la mayor tasa de incremento poblacional (R0) fue de 58,43 (♀/♀/generación) para M. persicae en Impact. En cambio en Teddy la mayor R0 (63,17) fue para L. erysimi. La tasa intrínseca de crecimiento natural (rm) más elevada fue para L. erysimi en Teddy (0,29 ♀/♀/día) y para M. persicae en Impact (0,24 ♀/♀/día). Estos estudios indican que, de acuerdo con el cultivar de colza empleado, teniendo en cuenta la tasa de crecimiento poblacional de las diferentes especies de pulgones, se podría inferir cuál será la especie dominante y el daño potencial que ocasionarían al cultivo.

Las confiscaciones y embargos de Rosas en Chascomús, 1840-1852

En este trabajo, a partir de la identificación de los propietarios afectados, se analiza el impacto local de las confiscaciones y embargos de Rosas. Se estimará la importancia de los muebles y útiles rematados y se considerará la magnitud del ganado bovino, ovino y equino extraído por los alcaldes locales para destinarlo a los ejércitos de frontera y de Santos Lugares. Además se indagará acerca de la época de los desembargos para comprobar si luego de los mismos los estancieros de Chascomús retomaron sus actividades y siguieron con la propiedad de sus estancias, tema éste directamente relacionado con un proyecto de más largo aliento que estudia la transmisión de la propiedad rural al noreste del río Salado y la constitución de un mercado de tierras entre fines del siglo XVIII y fines del XIX

Las confiscaciones y embargos de Rosas en Chascomús, 1840-1852

En este trabajo, a partir de la identificación de los propietarios afectados, se analiza el impacto local de las confiscaciones y embargos de Rosas. Se estimará la importancia de los muebles y útiles rematados y se considerará la magnitud del ganado bovino, ovino y equino extraído por los alcaldes locales para destinarlo a los ejércitos de frontera y de Santos Lugares. Además se indagará acerca de la época de los desembargos para comprobar si luego de los mismos los estancieros de Chascomús retomaron sus actividades y siguieron con la propiedad de sus estancias, tema éste directamente relacionado con un proyecto de más largo aliento que estudia la transmisión de la propiedad rural al noreste del río Salado y la constitución de un mercado de tierras entre fines del siglo XVIII y fines del XIX

Las confiscaciones y embargos de Rosas en Chascomús, 1840-1852

En este trabajo, a partir de la identificación de los propietarios afectados, se analiza el impacto local de las confiscaciones y embargos de Rosas. Se estimará la importancia de los muebles y útiles rematados y se considerará la magnitud del ganado bovino, ovino y equino extraído por los alcaldes locales para destinarlo a los ejércitos de frontera y de Santos Lugares. Además se indagará acerca de la época de los desembargos para comprobar si luego de los mismos los estancieros de Chascomús retomaron sus actividades y siguieron con la propiedad de sus estancias, tema éste directamente relacionado con un proyecto de más largo aliento que estudia la transmisión de la propiedad rural al noreste del río Salado y la constitución de un mercado de tierras entre fines del siglo XVIII y fines del XIX