Environmental justice and power plant emissions in the Regional Greenhouse Gas Initiative states.

Policies to reduce greenhouse gases associated with electricity generation have been a major focus of public policy in the United States, but their implications for achieving environmental justice among historically overburdened communities inappropriately remains a marginal issue. In this study we address research gaps in historical and current ambient air emissions burdens in environmental justice communities from power plants participating in the Regional Greenhouse Gases Initiative (RGGI), the country's first market-based power sector emissions reduction program. We find that in RGGI states the percentage of people of color that live within 0-6.2 miles from power plants is up to 23.5 percent higher than the percent of the white population that lives within those same distance bands, and the percentage of people living in poverty that live within 0-5 miles from power plants is up to 15.3 percent higher than the percent of the population not living in poverty within those same distance bands. More importantly, the transition from coal to natural gas underway before RGGI formally started resulted in large increases in both the number of electric-generating units burning natural gas and total net generation from natural gas in environmental justice communities hosting electric-generating units, compared to other communities. Our findings indicate that power sector carbon mitigation policies' focusing on aggregate emissions reductions have largely benefitted non-environmental justice communities and have not redressed the fundamental problem of disparities in pollutant burdens between EJ and non-EJ communities. These must be directly addressed in climate change and carbon emissions mitigation policy.

Urinary Nicotine Metabolites and Self-Reported Tobacco Use Among Adults in the Population Assessment of Tobacco and Health (PATH) Study, 2013-2014.

INTRODUCTION: The Population Assessment of Tobacco and Health (PATH) Study is a longitudinal cohort study on tobacco use behavior, attitudes and beliefs, and tobacco-related health outcomes, including biomarkers of tobacco exposure in the U.S. population. In this report we provide a summary of urinary nicotine metabolite measurements among adult users and non-users of tobacco from Wave 1 (2013-2014) of the PATH Study. METHODS: Total nicotine and its metabolites including cotinine, trans-3'-hydroxycotinine (HCTT), and other minor metabolites were measured in more than 11 500 adult participants by liquid chromatography tandem mass spectrometry methods. Weighted geometric means (GM) and least square means from statistical modeling were calculated for non-users and users of various tobacco products. RESULTS: Among daily users, the highest GM concentrations of nicotine, cotinine and HCTT were found in exclusive smokeless tobacco users, and the lowest in exclusive e-cigarette users. Exclusive combustible product users had intermediate concentrations, similar to those found in users of multiple products (polyusers). Concentrations increased with age within the categories of tobacco users, and differences associated with gender, race/ethnicity and educational attainment were also noted among user categories. Recent (past 12 months) former users had GM cotinine concentrations that were more than threefold greater than never users. CONCLUSIONS: These urinary nicotine metabolite data provide quantification of nicotine exposure representative of the entire US adult population during 2013-2014 and may serve as a reference for similar analyses in future measurements within this study. IMPLICATIONS: Nicotine and its metabolites in urine provide perhaps the most fundamental biomarkers of recent nicotine exposure. This report, based on Wave 1 of the Population Assessment of Tobacco and Health (PATH) Study, provides the first nationally representative data describing urinary nicotine biomarker concentrations in both non-users, and users of a variety of tobacco products including combustible, e-cigarette and smokeless products. These data provide a urinary biomarker concentration snapshot in time for the entire US population during 2013-2014, and will provide a basis for comparison with future results from continuing, periodic evaluations in the PATH Study.

Targeted implementation of cool roofs for equitable urban adaptation to extreme heat.

Cities are facing the twin pressures of greenhouse gas driven climatic warming and locally induced urban heating. These pressures are threatening populations that are sensitive to extreme heat due to sociodemographic factors including economic means. Heat-reducing infrastructure adaptation measures such as reflective "cool" materials can reduce urban temperatures. Here we examine the needs-based equity implications associated with heat-reducing cool roofing in Maricopa County, Arizona through application of high-resolution urban-atmospheric simulations. We simulate heatwave conditions and evaluate the air temperature reduction arising from uniform cool roof implementation (i.e., the entire urbanized county), and contrast results against simulated cooling impacts of needs-based targeted cool roof implementation in sociodemographically heat sensitive areas. We find that installing cool roofs uniformly, rather than in a targeted fashion, provides on average 0.66 °C reduction in the highest heat sensitivity area and 0.39 °C temperature reduction in the lowest heat sensitivity area due in part to a higher roof area density in the heat sensitive area. Targeting cool roof implementation yields 0.45 °C cooling in the most sensitive areas compared to 0.22 °C cooling in the least sensitive areas, meaning that needs-based targeted cool roofs in high sensitivity areas provide more relief than cool roofs targeted at low sensitivity areas, thus providing more cooling where it is most needed. Needs-based targeted implementation has the dual benefits of concurrently producing more than twice as much cooling and reducing heat exposure for the largest absolute number of individuals in the densely populated, highly heat sensitive areas. Targeting cool roof implementation to high heat sensitivity areas, however, does not achieve thermally equal temperatures in Maricopa County because the high sensitivity areas were substantially warmer than low sensitivity areas prior to implementation. This study illustrates the utility of a new "Targeted Urban Heat Adaptation" (TUHA) framework to assess needs-based equity implications of heat-reducing strategies and underscores its importance by examining the impacts of cooling interventions across sociodemographically heterogeneous urban environments.

Hazardous air pollutant emissions implications under 2018 guidance on U.S. Clean Air Act requirements for major sources.

On January 25, 2018, the United States Environmental Protection Agency withdrew a 1995 policy that mandates the use of maximum achievable control technology (MACT) to regulate emissions from major sources of hazardous air pollutants (HAPs), a category of toxic chemicals that may be carcinogenic, mutagenic, or cause other adverse health effects. To better understand the implications and scope of the change in regulatory guidance for HAP emissions of major sources that may reclassify as area sources, the increase in emissions that could legally occur under the new policy is assessed here. Based on facility-level data from a 2014 HAP national emissions inventory, it is estimated that 70% of major sources of HAPs qualify for reclassification as area sources, which could result in a maximum of 35,030 tons per year (tpy) of additional HAP emissions if all sources successfully reclassified. This amount would nearly triple the total volume of HAPs that qualifying major sources emitted in 2014. On average, qualifying sources could emit individually an additional 18.4 tpy. In the 21 states and territories that follow only federal guidelines for controlling HAPs, it is more likely that the estimates presented here could materialize compared to states that have additional guidelines for area sources of HAPs. The quantitative analysis of the potential emission changes resulting from regulatory change is instructive for industry, state and federal decisionmakers, and interested members of the public looking to understand and anticipate how relevant stakeholders will be affected by this policy change.Implications: Withdrawal of a U.S. Environmental Protection Agency policy that mandates the use of maximum achievable control technology (MACT) to regulate emissions from major sources of hazardous air pollutants (HAPs) could result in higher emissions of toxic chemicals that may be carcinogenic, mutagenic, or cause other adverse health effects. Analysis of potential emission changes resulting from regulatory change is instructive for industry, state, and federal decisionmakers, and interested members of the public looking to understand and anticipate how relevant stakeholders will be affected by this policy change.

Valores de referencia pediátricos de cromo y mercurio en orina del área de la Ciudad de Buenos Aires y alrededores / Pediatric reference values for chromium and mercury in urine in the City of Buenos Aires and Greater Buenos Aires

Introducción. Debido a la fuerte industrialización de la Ciudad de Buenos Aires y alrededores, la población podría estar expuesta a metales. Para poder evaluar el nivel de exposición de los niños al cromo y al mercurio, es fundamental tener valores de referencia (VR) propios. El objetivo fue determinar los VR pediátricos para cromo y mercurio en la muestra aislada de orina. Población y métodos: Se incluyeron niños y niñas no expuestos a los contaminantes evaluados que concurrieron al Servicio de Bajo Riesgo y al Consultorio del Jardín Maternal del Hospital de Pediatría S.A.M.I.C. "Prof. Dr. Juan P. Garrahan". Se cuantificó cromo (UCr), mercurio (UHg) y creatinina urinarios. Se calcularon los p95 con su intervalo de confianza del 95 % [IC 95 %] según el concepto para VR de la German Human Biomonitoring Commission. Resultados: Se incluyeron 160 pacientes en el estudio. Se obtuvieron 144 muestras de niños y niñas de entre 1 y 17 años (mediana: 7 años). Se cuantificó UCr a 137 muestras y UHg a 129. La mediana y rango de cromo fue 0,54 (indetectable -3,06) µg/g de creatinina y la de mercurio fue 0,49 (indetectable -7,57) µg/g de creatinina.Conclusiones: Los VR fueron, para UCr, hasta 1,5 µg/l [1,2-2,8] y hasta 2,2 µg/g de creatinina [1,8-3,0] y para UHg, hasta 2,5 µg/l [1,8-4,8] y 3,2 µg/g de creatinina [2,5-4,7

Introduction. Due to the heavy industrialization of the Autonomous City of Buenos Aires and Greater Buenos Aires, the population may have become exposed to metals.To assess the level of exposure to chromium and mercury in children, it is critical to have local reference values (RVs). Our objective was to determine pediatric RVs for chromium and mercury in a single urine sample.Population and methods: Children who were not exposed to the studied contaminants and who attended the Department of Low Risk Conditions and the Daycare Center Office of Hospital de Pediatría S.A.M.I.C. "Prof. Dr. Juan P. Garrahan" were included. Urinary chromium (UCr), urinary mercury (UHg), and urinary creatinine were measured. The p95 and its corresponding 95 % confidence interval (CI) were estimated based on the RV concept proposed by the German Human Biomonitoring Commission.Results: The study included 160 patients. A total of 144 samples from children aged 1-17 years (median: 7 years) were collected. UCr was measured in 137 samples and UHg, in 129 samples. The median value of chromium was 0.54 µg/g of creatinine (range, undetectable to 3.06), while that of mercury was 0.49 µg/g of creatinine (range, undetectable to 7.57). Conclusions: The RVs for UCr were up to 1.5 µg/L [1.2-2.8] and up to 2.2 µg/g of creatinine [1.8-3.0], and for UHg, up to 2.5 µg/L [1.8-4.8] and 3.2 µg/g of creatinine [2.5-4.7]

Pediatric reference values for chromium and mercury in urine in the City of Buenos Aires and Greater Buenos Aires. / Valores de referencia pediátricos de cromo y mercurio en orina del área de la Ciudad de Buenos Aires y alrededores.

INTRODUCTION: Due to the heavy industrialization of the Autonomous City of Buenos Aires and Greater Buenos Aires, the population may have become exposed to metals. To assess the level of exposure to chromium and mercury in children, it is critical to have local reference values (RVs). Our objective was to determine pediatric RV s for chromium and mercury in a single urine sample. POPULATION AND METHODS: Children who were not exposed to the studied contaminants and who attended the Department of Low Risk Conditions and the Daycare Center Office of Hospital de Pediatría S.A.M.I.C. "Prof. Dr. Juan P. Garrahan" were included. Urinary chromium (UCr), urinary mercury (UHg), and urinary creatinine were measured. The p95 and its corresponding 95 % confidence interval (CI) were estimated based on the RV concept proposed by the German Human Biomonitoring Commission. RESULTS: The study included 160 patients. A total of 144 samples from children aged 1-17 years (median: 7 years) were collected. UCr was measured in 137 samples and UHg, in 129 samples. The median value of chromium was 0.54 µg/g of creatinine (range, undetectable to 3.06), while that of mercury was 0.49 µg/g of creatinine (range, undetectable to 7.57). CONCLUSIONS: The RVs for UCr were up to 1.5 µg/L [1.2-2.8] and up to 2.2 µg/g of creatinine [1.8-3.0], and for UHg, up to 2.5 µg/L [1.8-4.8] and 3.2 µg/g of creatinine [2.5-4.7].

Introducción. Debido a la fuerte industrialización de la Ciudad de Buenos Aires y alrededores, la población podría estar expuesta a metales. Para poder evaluar el nivel de exposición de los niños al cromo y al mercurio, es fundamental tener valores de referencia (VR) propios. El objetivo fue determinar los VR pediátricos para cromo y mercurio en la muestra aislada de orina. Población y métodos: Se incluyeron niños y niñas no expuestos a los contaminantes evaluados que concurrieron al Servicio de Bajo Riesgo y al Consultorio del Jardín Maternal del Hospital de Pediatría S. A. M. I. C. "Prof. Dr. Juan P. Garrahan". Se cuantificó cromo (UCr), mercurio (UHg) y creatinina urinarios. Se calcularon los p95 con su intervalo de confianza del 95 % [IC 95 %] según el concepto para VR de la German Human Biomonitoring Commission. Resultados: Se incluyeron 160 pacientes en el estudio. Se obtuvieron 144 muestras de niños y niñas de entre 1 y 17 años (mediana: 7 años). Se cuantificó UCr a 137 muestras y UHg a 129. La mediana y rango de cromo fue 0,54 (indetectable -3,06) µg/g de creatinina y la de mercurio fue 0,49 (indetectable -7,57) µg/g de creatinina. Conclusiones: Los VR fueron, para UCr, hasta 1,5 µg/l [1,2-2,8] y hasta 2,2 µg/g de creatinina [1,8-3,0] y para UHg, hasta 2,5 µg/l [1,8-4,8] y 3,2 µg/g de creatinina [2,5-4,7].

Balancing Protein Stability and Activity in Cancer: A New Approach for Identifying Driver Mutations Affecting CBL Ubiquitin Ligase Activation.

Oncogenic mutations in the monomeric Casitas B-lineage lymphoma (Cbl) gene have been found in many tumors, but their significance remains largely unknown. Several human c-Cbl (CBL) structures have recently been solved, depicting the protein at different stages of its activation cycle and thus providing mechanistic insight underlying how stability-activity tradeoffs in cancer-related proteins-may influence disease onset and progression. In this study, we computationally modeled the effects of missense cancer mutations on structures representing four stages of the CBL activation cycle to identify driver mutations that affect CBL stability, binding, and activity. We found that recurrent, homozygous, and leukemia-specific mutations had greater destabilizing effects on CBL states than random noncancer mutations. We further tested the ability of these computational models, assessing the changes in CBL stability and its binding to ubiquitin-conjugating enzyme E2, by performing blind CBL-mediated EGFR ubiquitination assays in cells. Experimental CBL ubiquitin ligase activity was in agreement with the predicted changes in CBL stability and, to a lesser extent, with CBL-E2 binding affinity. Two thirds of all experimentally tested mutations affected the ubiquitin ligase activity by either destabilizing CBL or disrupting CBL-E2 binding, whereas about one-third of tested mutations were found to be neutral. Collectively, our findings demonstrate that computational methods incorporating multiple protein conformations and stability and binding affinity evaluations can successfully predict the functional consequences of cancer mutations on protein activity, and provide a proof of concept for mutations in CBL.

KLF13 cooperates with c-Maf to regulate IL-4 expression in CD4+ T cells.

Kruppel-like factor (KLF) 13 is a transcription factor that positively regulates expression of the chemokine RANTES 3-5 d after activation of T cells. In this study, we document a key role for KLF13 in the expression of IL-4 in CD4(+) T cells. Gene expression analysis in activated T cells from Klf13(-/-) mice showed that IL-4, along with other Th2 cytokine genes, was downregulated when compared with cells from wild-type mice. The decreased levels of IL-4 were not associated with changes in expression of the Th2-inducing transcription factors GATA3 or c-Maf. Additional analysis revealed that KLF13 directly binds to IL-4 promoter regions and synergizes with c-Maf to positively regulate IL-4 expression. These results indicate that KLF13 is a positive regulator for differentiation of Th2 cells, as part of the transcriptional machinery that regulates IL-4 production in Th2 cells.

Pharmacometabolomic signature of ataxia SCA1 mouse model and lithium effects.

We have shown that lithium treatment improves motor coordination in a spinocerebellar ataxia type 1 (SCA1) disease mouse model (Sca1(154Q/+)). To learn more about disease pathogenesis and molecular contributions to the neuroprotective effects of lithium, we investigated metabolomic profiles of cerebellar tissue and plasma from SCA1-model treated and untreated mice. Metabolomic analyses of wild-type and Sca1(154Q/+) mice, with and without lithium treatment, were performed using gas chromatography time-of-flight mass spectrometry and BinBase mass spectral annotations. We detected 416 metabolites, of which 130 were identified. We observed specific metabolic perturbations in Sca1(154Q/+) mice and major effects of lithium on metabolism, centrally and peripherally. Compared to wild-type, Sca1(154Q/+) cerebella metabolic profile revealed changes in glucose, lipids, and metabolites of the tricarboxylic acid cycle and purines. Fewer metabolic differences were noted in Sca1(154Q/+) mouse plasma versus wild-type. In both genotypes, the major lithium responses in cerebellum involved energy metabolism, purines, unsaturated free fatty acids, and aromatic and sulphur-containing amino acids. The largest metabolic difference with lithium was a 10-fold increase in ascorbate levels in wild-type cerebella (p<0.002), with lower threonate levels, a major ascorbate catabolite. In contrast, Sca1(154Q/+) mice that received lithium showed no elevated cerebellar ascorbate levels. Our data emphasize that lithium regulates a variety of metabolic pathways, including purine, oxidative stress and energy production pathways. The purine metabolite level, reduced in the Sca1(154Q/+) mice and restored upon lithium treatment, might relate to lithium neuroprotective properties.

Neighborhood effects on heat deaths: social and environmental predictors of vulnerability in Maricopa County, Arizona.

BACKGROUND: Most heat-related deaths occur in cities, and future trends in global climate change and urbanization may amplify this trend. Understanding how neighborhoods affect heat mortality fills an important gap between studies of individual susceptibility to heat and broadly comparative studies of temperature-mortality relationships in cities. OBJECTIVES: We estimated neighborhood effects of population characteristics and built and natural environments on deaths due to heat exposure in Maricopa County, Arizona (2000-2008). METHODS: We used 2000 U.S. Census data and remotely sensed vegetation and land surface temperature to construct indicators of neighborhood vulnerability and a geographic information system to map vulnerability and residential addresses of persons who died from heat exposure in 2,081 census block groups. Binary logistic regression and spatial analysis were used to associate deaths with neighborhoods. RESULTS: Neighborhood scores on three factors-socioeconomic vulnerability, elderly/isolation, and unvegetated area-varied widely throughout the study area. The preferred model (based on fit and parsimony) for predicting the odds of one or more deaths from heat exposure within a census block group included the first two factors and surface temperature in residential neighborhoods, holding population size constant. Spatial analysis identified clusters of neighborhoods with the highest heat vulnerability scores. A large proportion of deaths occurred among people, including homeless persons, who lived in the inner cores of the largest cities and along an industrial corridor. CONCLUSIONS: Place-based indicators of vulnerability complement analyses of person-level heat risk factors. Surface temperature might be used in Maricopa County to identify the most heat-vulnerable neighborhoods, but more attention to the socioecological complexities of climate adaptation is needed.

Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua.

Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.

ATXN1 protein family and CIC regulate extracellular matrix remodeling and lung alveolarization.

Although expansion of CAG repeats in ATAXIN1 (ATXN1) causes Spinocerebellar ataxia type 1, the functions of ATXN1 and ATAXIN1-Like (ATXN1L) remain poorly understood. To investigate the function of these proteins, we generated and characterized Atxn1L(-/-) and Atxn1(-/-); Atxn1L(-/-) mice. Atxn1L(-/-) mice have hydrocephalus, omphalocele, and lung alveolarization defects. These phenotypes are more penetrant and severe in Atxn1(-/-); Atxn1L(-/-) mice, suggesting that ATXN1 and ATXN1L are functionally redundant. Upon pursuing the molecular mechanism, we discovered that several Matrix metalloproteinase (Mmp) genes are overexpressed and that the transcriptional repressor Capicua (CIC) is destabilized in Atxn1L(-/-) lungs. Consistent with this, Cic deficiency causes lung alveolarization defect. Loss of either ATXN1L or CIC derepresses Etv4, an activator for Mmp genes, thereby mediating MMP9 overexpression. These findings demonstrate a critical role of ATXN1/ATXN1L-CIC complexes in extracellular matrix (ECM) remodeling during development and their potential roles in pathogenesis of disorders affecting ECM remodeling.

Partial loss of ataxin-1 function contributes to transcriptional dysregulation in spinocerebellar ataxia type 1 pathogenesis.

Spinocerebellar ataxia type 1 (SCA1) is a dominantly inherited neurodegenerative disease caused by expansion of a CAG repeat that encodes a polyglutamine tract in ATAXIN1 (ATXN1). Molecular and genetic data indicate that SCA1 is mainly caused by a gain-of-function mechanism. However, deletion of wild-type ATXN1 enhances SCA1 pathogenesis, whereas increased levels of an evolutionarily conserved paralog of ATXN1, Ataxin 1-Like, ameliorate it. These data suggest that a partial loss of ATXN1 function contributes to SCA1. To address this possibility, we set out to determine if the SCA1 disease model (Atxn1(154Q/+) mice) and the loss of Atxn1 function model (Atxn1-/- mice) share molecular changes that could potentially contribute to SCA1 pathogenesis. To identify transcriptional changes that might result from loss of function of ATXN1 in SCA1, we performed gene expression microarray studies on cerebellar RNA from Atxn1-/- and Atxn1(154Q/+) cerebella and uncovered shared gene expression changes. We further show that mild overexpression of Ataxin-1-Like rescues several of the molecular and behavioral defects in Atxn1-/- mice. These results support a model in which Ataxin 1-Like overexpression represses SCA1 pathogenesis by compensating for a partial loss of function of Atxn1. Altogether, these data provide evidence that partial loss of Atxn1 function contributes to SCA1 pathogenesis and raise the possibility that loss-of-function mechanisms contribute to other dominantly inherited neurodegenerative diseases.

Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1.

Spinocerebellar ataxia type 1 (SCA1) is a dominantly inherited neurodegenerative disease caused by expansion of a glutamine-encoding repeat in ataxin 1 (ATXN1). In all known polyglutamine diseases, the glutamine expansion confers toxic functions onto the protein; however, the mechanism by which this occurs remains enigmatic, in light of the fact that the mutant protein apparently maintains interactions with its usual partners. Here we show that the expanded polyglutamine tract differentially affects the function of the host protein in the context of different endogenous protein complexes. Polyglutamine expansion in ATXN1 favours the formation of a particular protein complex containing RBM17, contributing to SCA1 neuropathology by means of a gain-of-function mechanism. Concomitantly, polyglutamine expansion attenuates the formation and function of another protein complex containing ATXN1 and capicua, contributing to SCA1 through a partial loss-of-function mechanism. This model provides mechanistic insight into the molecular pathogenesis of SCA1 as well as other polyglutamine diseases.

Regulation of RNA splicing by the methylation-dependent transcriptional repressor methyl-CpG binding protein 2.

Rett syndrome (RTT) is a postnatal neurodevelopmental disorder characterized by the loss of acquired motor and language skills, autistic features, and unusual stereotyped movements. RTT is caused by mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MeCP2). Mutations in MECP2 cause a variety of neurodevelopmental disorders including X-linked mental retardation, psychiatric disorders, and some cases of autism. Although MeCP2 was identified as a methylation-dependent transcriptional repressor, transcriptional profiling of RNAs from mice lacking MeCP2 did not reveal significant gene expression changes, suggesting that MeCP2 does not simply function as a global repressor. Changes in expression of a few genes have been observed, but these alterations do not explain the full spectrum of Rett-like phenotypes, raising the possibility that additional MeCP2 functions play a role in pathogenesis. In this study, we show that MeCP2 interacts with the RNA-binding protein Y box-binding protein 1 and regulates splicing of reporter minigenes. Importantly, we found aberrant alternative splicing patterns in a mouse model of RTT. Thus, we uncovered a previously uncharacterized function of MeCP2 that involves regulation of splicing, in addition to its role as a transcriptional repressor.

Tratamiento quirúrgico de la hemorragia del tubo digestivo bajo. Experiencia en el Instituto Nacional de Ciencias MÚdicas y Nutrición Salvador Zubirán / Surgical treatment of lower digestive tract hemorrhage. Experience at the Instituto Nacional de Ciencias MÚdicas y Nutrición Salvador Zubirán

BACKGROUND: Lower gastrointestinal bleeding is usually self-limiting in about 80 of cases; however, surgical treatment may be required in selected cases. Preoperative precise identification of the bleeding source is crucial for a successful outcome. OBJECTIVE: To determine the most frequent diagnoses, as well as short and long-term results in a series of patients who underwent a surgical procedure for lower gastrointestinal bleeding. MATERIAL AND METHODS: Retrospective analysis of 39 patients operated upon for lower gastrointestinal bleeding from 1979 through 1997 in a referral center. Demographic data, history, physical examination, laboratory tests, resuscitative measures, preoperative work-up for identification of bleeding source, definitive cause of bleeding, surgical procedure, operative morbidity and mortality, as well as long-term status and recurrence of bleeding were recorded. RESULTS: There were 54 women and 46 men. Mean age was 56 years (range, 15-92). Most patients presented hematochezia (69). Colonoscopy was the most used diagnostic procedure (69). The bleeding source was located in 90 of patients. Diverticular disease was the most frequent cause of bleeding. A segmental bowel resection was the treatment in 97 of cases. Morbidity was 23 with 18 of mortality. Recurrence occurred in 9 of survivors. CONCLUSIONS: Morbidity and mortality were high. Patients who require a surgical operation should be carefully selected and evaluated with a complete work-up to determine the site and cause of bleeding.

[Quality of life after ileo-anal anastomosis]. / Calidad de vida posterior a la anastomosis íleo-anal.

BACKGROUND: The ileo-anal pouch is the surgical procedure of choice for patients with Ulcerative Colitis or Familial Adenomatous Polyposis, but has functional limitations such as a higher frequency of bowel movements, anal leakage, and sometimes the necessity of a protective anal pad. OBJECTIVE: To analyze the functional results and quality of life after the pelvic pouch. MATERIAL AND METHODS: This is a descriptive, prolective, and cross-sectional study that analyzes the clinical variables, functional results and self-reported quality of life of patients after an ileo-anal pouch. A correlation between postoperative clinical variables and quality of life was searched. RESULTS: Twenty-seven patients were included. Mean age was 36 years. Surgical indications for the ileo-anal pouch were Ulcerative Colitis in 17 (63%), Familial Adenomatous Polyposis in 9 (33%) and a colo-rectostomy stricture in 1 (4%). Mean number of bowel movements was 4 at day and 1 at night. Eighteen percent of patients referred anal leakage, 11% had pouchitis, and 11% small bowel obstruction. Most of the patients reported high scores in all evaluated quality of life scales. There was a correlation between lower scores of quality of life and a higher number of bowel movements. CONCLUSIONS: The majority of patients reported an adequate quality of life after the ileo-anal pouch; there was a correlation between lower scores of quality of life and a higher number of bowel movements.

Evaluación clínica y bacteriológica de infecciones en miembros inferiores de pacientes diabéticos / Clinical and bacteriological evaluation of infections in low extremities of diabetic patients

Se evaluaron 22 pacientes diabéticos con infecciones en miembros inferiores; 66,66% presentaron lesiones ulcerativas. La mayoría (90.9%). Mostró descompensación metábolica al ingreso, con algún grado de detonemia en el 54,55%. Todos presentaron alteración radiológica. La neuropatía periferica fue la patología asociada, más frecuente. En la evaluación microbiológica aeróbica se demostraron cultivos polimicrobianos en una alta proporción, siendo los gérmenes más encontrados: Staphilococcus aureus, Klebsiella pneumoniae. Pseadomona aeruginosa, Escherichia Coli y especies de proteus. Hubo buena correlación entre los resultados de sensibilidad antibiótica para los cultivos de secreción superficial y aspirados en tejidos profundos