Unbiased quantification of the spatial distribution of murine cells using point pattern analysis.

CNS injuries are associated with profound changes in cell organization. This protocol presents a stepwise approach to quantitatively describe the spatiotemporal changes in glial cell rearrangement in the injured murine brain, which is applicable to other biological contexts. Herein, we apply common immunolabeling of neurons and glial cells and wide-field microscopy imaging. Then, we employ computational tools for alignment to the Allen Brain Atlas, unbiased/automatic detection of cells, generation of point patterns, and data analysis. For complete details on the use and execution of this protocol, please refer to Manrique-Castano et al.1.

Tenascin-C restricts reactive astrogliosis in the ischemic brain.

Cellular responses in glia play a key role in regulating brain remodeling post-stroke. However, excessive glial reactivity impedes post-ischemic neuroplasticity and hampers neurological recovery. While damage-associated molecular patterns and activated microglia were shown to induce astrogliosis, the molecules that restrain astrogliosis are largely unknown. We explored the role of tenascin-C (TnC), an extracellular matrix component involved in wound healing and remodeling of injured tissues, in mice exposed to ischemic stroke induced by transient intraluminal middle cerebral artery occlusion. In the healthy adult brain, TnC expression is restricted to neurogenic stem cell niches. We previously reported that TnC is upregulated in ischemic brain lesions. We herein show that the de novo expression of TnC post-stroke is closely associated with reactive astrocytes, and that astrocyte reactivity at 14 days post-ischemia is increased in TnC-deficient mice (TnC-/-). By analyzing the three-dimensional morphology of astrocytes in previously ischemic brain tissue, we revealed that TnC-/- reduces astrocytic territorial volume, branching point number, and branch length, which are presumably hallmarks of the homeostatic regulatory astrocyte state, in the post-acute stroke phase after 42 days. Interestingly, TnC-/- moderately increased aggrecan, a neuroplasticity-inhibiting proteoglycan, in the ischemic brain tissue at 42 days post-ischemia. In vitro in astrocyte-microglia cocultures, we showed that TnC-/- reduces the microglial migration speed on astrocytes and elevates intercellular adhesion molecule 1 (ICAM1) expression. Post-stroke, TnC-/- did not alter the ischemic lesion size or neurological recovery, however microglia-associated ICAM1 was upregulated in TnC-/- mice during the first week post stroke. Our data suggest that TnC plays a central role in restraining post-ischemic astrogliosis and regulating astrocyte-microglial interactions.

Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors.

Vascular dementia (VaD) constitutes the second most prevalent cause of dementia in the world after Alzheimer's disease (AD). VaD regroups heterogeneous neurological conditions in which the decline of cognitive functions, including executive functions, is associated with structural and functional alterations in the cerebral vasculature. Among these cerebrovascular disorders, major stroke, and cerebral small vessel disease (cSVD) constitute the major risk factors for VaD. These conditions alter neurovascular functions leading to blood-brain barrier (BBB) deregulation, neurovascular coupling dysfunction, and inflammation. Accumulation of neurovascular impairments over time underlies the cognitive function decline associated with VaD. Furthermore, several vascular risk factors, such as hypertension, obesity, and diabetes have been shown to exacerbate neurovascular impairments and thus increase VaD prevalence. Importantly, air pollution constitutes an underestimated risk factor that triggers vascular dysfunction via inflammation and oxidative stress. The review summarizes the current knowledge related to the pathological mechanisms linking neurovascular impairments associated with stroke, cSVD, and vascular risk factors with a particular emphasis on air pollution, to VaD etiology and progression. Furthermore, the review discusses the major challenges to fully elucidate the pathobiology of VaD, as well as research directions to outline new therapeutic interventions.

Inhibitory control in neuronal networks relies on the extracellular matrix integrity.

Inhibitory control is essential for the regulation of neuronal network activity, where excitatory and inhibitory synapses can act synergistically, reciprocally, and antagonistically. Sustained excitation-inhibition (E-I) balance, therefore, relies on the orchestrated adjustment of excitatory and inhibitory synaptic strength. While growing evidence indicates that the brain's extracellular matrix (ECM) is a crucial regulator of excitatory synapse plasticity, it remains unclear whether and how the ECM contributes to inhibitory control in neuronal networks. Here we studied the simultaneous changes in excitatory and inhibitory connectivity after ECM depletion. We demonstrate that the ECM supports the maintenance of E-I balance by retaining inhibitory connectivity. Quantification of synapses and super-resolution microscopy showed that depletion of the ECM in mature neuronal networks preferentially decreases the density of inhibitory synapses and the size of individual inhibitory postsynaptic scaffolds. The reduction of inhibitory synapse density is partially compensated by the homeostatically increasing synaptic strength via the reduction of presynaptic GABAB receptors, as indicated by patch-clamp measurements and GABAB receptor expression quantifications. However, both spiking and bursting activity in neuronal networks is increased after ECM depletion, as indicated by multi-electrode recordings. With computational modelling, we determined that ECM depletion reduces the inhibitory connectivity to an extent that the inhibitory synapse scaling does not fully compensate for the reduced inhibitory synapse density. Our results indicate that the brain's ECM preserves the balanced state of neuronal networks by supporting inhibitory control via inhibitory synapse stabilization, which expands the current understanding of brain activity regulation.

Tenascin-C preserves microglia surveillance and restricts leukocyte and, more specifically, T cell infiltration of the ischemic brain.

As an endogenous activator of toll-like receptor-4 (Tlr4), the extracellular matrix glycoprotein tenascin-C (TnC) regulates chemotaxis, phagocytosis and proinflammatory cytokine production in microglia. The role of TnC for ischemic brain injury, post-ischemic immune responses and stroke recovery has still not been evaluated. By comparing wild type and TnC-/- mice exposed to transient intraluminal middle cerebral artery occlusion (MCAO), we examined the effects of TnC deficiency for ischemic injury, neurological deficits, microglia/macrophage activation and brain leukocyte infiltration using behavioural tests, histochemical studies, Western blot, polymerase chain reaction and flow cytometry. Histochemical studies revealed that TnC was de novo expressed in the ischemic striatum, which contained the infarct core, and overlapped with the area of strongest accumulation of Iba1 + microglia/macrophages. TnC deficiency increased overall Iba1 immunoreactivity in the perilesional cortex, suggesting that TnC might restrict the distribution of microglial cells to the infarct core. By analysing microglial morphology in 3D we found that the post-ischemic loss of microglial cell territory, branching and volume at 3 and 7 days post-ischemia was amplified in the brains of TnC deficient compared with wild type mice. Microglial cell number was not different between genotypes. Hence, TnC deficiency reduced tissue surveillance by microglial cells. Concomitantly, the number of infiltrating leukocytes and, more specifically, T cells was increased in the ischemic brain parenchyma of TnC deficient compared with wild type mice. Ischemic injury and neurological deficits were not affected by TnC deficiency. We propose that the reduced microglia surveillance in TnC deficient mice might favour leukocyte accumulation in the ischemic brain.

Deactivation of ATP-Binding Cassette Transporters ABCB1 and ABCC1 Does Not Influence Post-ischemic Neurological Deficits, Secondary Neurodegeneration and Neurogenesis, but Induces Subtle Microglial Morphological Changes.

ATP-binding cassette (ABC) transporters prevent the access of pharmacological compounds to the ischemic brain, thereby impeding the efficacy of stroke therapies. ABC transporters can be deactivated by selective inhibitors, which potently increase the brain accumulation of drugs. Concerns have been raised that long-term ABC transporter deactivation may promote neuronal degeneration and, under conditions of ischemic stroke, compromise neurological recovery. To elucidate this issue, we exposed male C57BL/6 mice to transient intraluminal middle cerebral artery occlusion (MCAO) and examined the effects of the selective ABCB1 inhibitor tariquidar (8 mg/kg/day) or ABCC1 inhibitor MK-571 (10 mg/kg/day), which were administered alone or in combination with each other over up to 28 days, on neurological recovery and brain injury. Mice were sacrificed after 14, 28, or 56 days. The Clark score, RotaRod, tight rope, and open field tests revealed reproducible motor-coordination deficits in mice exposed to intraluminal MCAO, which were not influenced by ABCB1, ABCC1, or combined ABCB1 and ABCC1 deactivation. Brain volume, striatum volume, and corpus callosum thickness were not altered by ABCB1, ABCC1 or ABCB1, and ABCC1 inhibitors. Similarly, neuronal survival and reactive astrogliosis, evaluated by NeuN and GFAP immunohistochemistry in the ischemic striatum, were unchanged. Iba1 immunohistochemistry revealed no changes of the overall density of activated microglia in the ischemic striatum of ABC transporter inhibitor treated mice, but subtle changes of microglial morphology, that is, reduced microglial cell volume by ABCB1 deactivation after 14 and 28 days and reduced microglial ramification by ABCB1, ABCC1 and combined ABCB1 and ABCC1 deactivation after 56 days. Endogenous neurogenesis, assessed by BrdU incorporation analysis, was not influenced by ABCB1, ABCC1 or combined ABCB1 and ABCC1 deactivation. Taken together, this study could not detect any exacerbation of neurological deficits or brain injury after long-term ABC transporter deactivation in this preclinical stroke model.

Noninvasive Localized Cold Therapy: A New Mode of Bone Repair Enhancement.

IMPACT STATEMENT: A variety of biological, mechanical, and physical therapeutic modalities of varying complexity, efficacy, cost, and safety profile have been developed to enhance bone healing. There have been sporadic reports of spontaneous bone formation after repeated cold exposure. In this study we report for the first time, the anabolic effect of cold exposure on bone healing in vivo resulting in a doubling of bone volume. Although the precise mechanism is not fully understood, cold is well known to stimulate osteoclastogenesis and modulate inflammation. The impact of this finding is considerable for tissue regeneration because cold application is noninvasive, safe, and easily implemented.

Topological remodeling of cortical perineuronal nets in focal cerebral ischemia and mild hypoperfusion.

Despite the crucial role of perineuronal nets (PNNs) in neural plasticity and neurological disorders, their ultrastructural organization remains largely unresolved. We have developed a novel approach combining superresolution structured illumination microscopy (SR-SIM) and mathematical reconstruction that allows for quantitative analysis of PNN topology. Since perineuronal matrix is capable to restrict neural plasticity but at the same time is necessary to maintain synapses, we hypothesized that a beneficial post stroke recovery requires a reversible loosening of PNNs. Our results indicated that focal cerebral ischemia induces partial depletion of PNNs and that mild hypoperfusion not associated with ischemic injury can induce ultra-structural rearrangements in visually intact meshworks. In line with the activation of neural plasticity under mild stress stimuli, we provide evidence that topological conversion of PNNs can support post stroke neural rewiring.

Role of immune responses for extracellular matrix remodeling in the ischemic brain.

Neuroinflammation is one of the key components contributing to the devastating outcome of ischemic stroke. Starting with stroke onset, inflammatory processes contribute both to cell damage and tissue remodeling. The early release of alarmins triggers the upregulation of multiple proinflammatory cytokines, resulting in the compromised integrity of the blood-brain barrier. From this moment on, the infiltration of peripheral immune cells, reactive gliosis and extracellular matrix (ECM) alterations become intricately intertwined and act as one unit during the tissue remodeling. While the mechanisms of leukocyte and glia activation are amply reviewed, the field of ECM modification remains as yet under explored. In this review, we focus on the interplay between neuroinflammatory cascades and ECM in the ischemic brain. By summarizing the currently available evidence obtained by in vitro research, animal experimentation and human studies, we aim to propose a new direction for the future investigation of stroke recovery.

Assessment transcallosal Diaschisis in a model of focal cerebral ischemia in rats.

OBJECTIVE: To evaluate transcallosal changes after a local ischemic injury in rats by using the monoclonal marker anti-NeuN (Mouse anti-neuronal nuclei). METHODS: Twenty-eight adult, male, Wistar rats were subjected to focal injury in the right hemisphere. The technique used was the experimental model of focal ischemic injury through intraluminal suture of the middle cerebral artery. Analyses were made for the five groups: after the lesion (control), at 24 h, 96 h, 10 days and 20 days. Exofocal neuronal damage was inferred from neuronal immunoreactivity changes to NeuN. RESULTS: In the cortex contralateral to the lesion, immunoreactivity was diminished. This finding was most notable in the supra-granular sheets 24 h post ischemia. After 96 h, there was a generalized diminishment of the inmmunoreactivity in the supra and infra-granular sheets. At 10 and 20 days, the tissue recovered some immunoreactivity to NeuN, but there were some changes in the VI layer. CONCLUSION: The immunoreactive changes to NeuN support the process of inter-hemispheric diaschisis. Changes in immunoreactivity could indicate metabolic stress secondary to the disruption in connectivity to the site of lesion.

OBJETIVO: Evaluar los cambios exofocales transcallosos después de lesión isquémica focal en ratas, mediante marcación inmunohistoquímica con el anticuerpo monoclonal anti-NeuN (Mouse Anti-Neuronal Nuclei). MÉTODOS: Se intervinieron 28 ratas machos Wistar adultas. Mediante el modelo experimental de isquemia cerebral focal del territorio de la arteria cerebral media por filamento intraluminal, se les ocasionó una lesión focal en el hemisferio derecho. Posteriormente se evaluó el hemisferio contralateral, marcando la población neuronal con el anticuerpo monoclonal anti-NeuN. Se definieron cinco grupos de evaluación: uno de control, 24 horas, 96 horas, 10 días y 20 días. Se evaluaron los cambios neuronales exofocales después de la lesión con base en la observación de los cambios en la inmunoreactividad de las neuronas al NeuN. RESULTADOS: Se redujo la inmunoreactividad en la corteza contralateral a la lesión. Este fenómeno fue más notable en las capas supragranulares después de 24 h post isquemia. Después de 96 h hubo una disminución generalizada de la inmmunoreactivity en las capas supra e infragranulares. A los 10 y 20 días, el tejido recobró alguna inmunoreactividad NeuN, estos cambios se dieron en la capa VI. CONCLUSIONES: Los cambios inmunorreactivos a NeuN apoyan el proceso de diasquisis interhemisférica. Los cambios en la inmunorreactividad podrían indicar estrés metabólico secundario a la interrupción en la conectividad con el sitio de la lesión.

Assessment transcallosal Diaschisis in a model of focal cerebral ischemia in rats / Evaluación de la diásquisis transcallosa en un modelo de isquemia cerebral focal en ratas

Objective: To evaluate transcallosal changes after a local ischemic injury in rats by using the monoclonal marker anti-NeuN (Mouse anti-neuronal nuclei). Methods: Twenty eight adult, male, Wistar rats were subjected to focal injury in the right hemisphere. The technique used was the experimental model of focal ischemic injury through intraluminal suture of the middle cerebral artery. Analyses were made for the five groups: and after the lesion (control), at 24 h, 96 h, 10 days and 20 days. Exofocal neuronal damage was inferred from neuronal immunoreactivity changes to NeuN. Results: In the cortex contralateral to the lesion, immunoreactivity was diminished. This was most notable in the supragranular layers 24 h post ischemia. After 96 h, there was a generalized diminishment of the inmmunoreactivity in supra and infragranular layers. At 10 and 20 days, the tissue recovered some NeuN immunoreactivity, but there were set changes in the VI layer. Conclusion: The immunoreactive changes to NeuN support the process of interhemispheric diaschisis. Changes in immunoreactivity could indicate metabolic stress secondary to the disruption in connectivity to the site of lesion.

Objetivo: Evaluar los cambios exofocales transcallosos después de lesión isquémica focal en ratas, mediante marcación inmunohistoquímica con el anticuerpo monoclonal anti-NeuN (Mouse Anti-Neuronal Nuclei). Métodos: Se intervinieron 28 ratas machos Wistar adultas. Mediante el modelo experimental de isquemia cerebral focal del territorio de la arteria cerebral media por filamento intraluminal, se les ocasionó una lesión focal en el hemisferio derecho. Posteriormente se evaluó el hemisferio contralateral, marcando la población neuronal con el anticuerpo monoclonal anti-NeuN. Se definieron cinco grupos de evaluación: uno de control, 24 h, 96 h, 10 días y 20 días. Se evaluaron los cambios neuronales exofocales después de la lesión con base en la observación de los cambios en la inmunoreactividad de las neuronas al NeuN. Resultados: Se redujo la inmunoreactividad en la corteza contralateral a la lesión. Este fenómeno fue más notable en las capas supragranulares después de 24 h post isquemia. Después de 96 h hubo una disminución generalizada de la inmmunoreactivity en las capas supra e infragranulares. A los 10 y 20 días, el tejido recobró alguna inmunoreactividad NeuN, estos cambios se dieron en la capa VI. Conclusiones: Los cambios inmunorreactivos a NeuN apoyan el proceso de diasquisis interhemisférica. Los cambios en la inmunorreactividad podrían indicar estrés metabólico secundario a la interrupción en la conectividad con el sitio de la lesión.

El problema de la consciencia y su brecha explicativa en la psicología / The Problem of Consciousness and its Explanatory Gap in Psychology

El presente artículo plantea una reflexión sobre la brecha explicativa en la dificultad de la consciencia en el marco del problema mente-cuerpo y su estudio en la psicología. A pesar de los desarrollos teóricos en múltiples disciplinas, la consciencia sigue escapando a la mirada de la ciencia. Particularmente se puede sustentar que la psicología ha dejado el tema de lado, y al respecto, se ha enfrascado en la investigación de fenómenos subordinados a la consciencia. Por tal motivo, se espera que en los próximos años el conjunto de la ciencia en general, pueda pensar el problema de una nueva forma y abrirse paso hacia el objeto que ha cautivado desde el antiguo filósofo hasta el científico actual.

This article reflects on the explanatory gap in the problem of consciousness within the mind-body problem. Despite the theoretical developments in multiple disciplines, consciousness still eludes the gaze of science. Particularly, it can be argued that psychology has left the issue aside, and has been engaged in the investigation of phenomena subordinate to consciousness. Therefore, it is expected that in coming years the whole of science in general, thinks the problem in a new way and breaks through to the object that has captivated from the old philosopher to the current scientific.

Glutathione Peroxidase and Superoxide Dismutase activities in blood and seminal plasma in colombian stallions / Actividad de la Glutatión Peroxidasa y la Superóxido Dismutasa en sangre y plasma seminal en caballos colombianos / Atividade das enzimas antioxidantes: glutationa peroxidase e superóxido dismutase no sangue e plasma em cavalos colombiano

Objective: to measure the activity of the antioxidant enzymes Glutathione Peroxidase (GSH-Px; EC 1.11.1.9) and Superoxide Dismutase (SOD; EC 1.15.1.1) in blood and seminal plasma of Colombian Stallions from four farms and to relate them to changes in semen quality. Methods: semen was collected from 25 horses using an artificial vagina. Blood was collected in EDTA vacutaniers by yugular venipuncture. Basic semen analysis included individual and mass motility, morphology, and sperm concentration. A sub sample was centrifuged to obtain seminal plasma for the evaluating GSH and SOD. Results: mean GSH- Px activity was 514.8 ± 22.4 U/g Hb and 0.55 ± 0.05 U/mL in blood and seminal plasma, respectively. Mean SOD activity was 1877 ± 188 U/g Hb in blood, and 86 ± 7.1 U/mL in seminal plasma. No correlation was found between the enzyme activities in seminal plasma and blood. However, seminal plasma GSH- Px activity was correlated with sperm concentration. Similarly, GSH-Px activity in blood was correlated to the proportion of sperm cells with progressive motility and morphologically normal. Conclusions: the absence of correlation found between enzymatic activity in blood and seminal plasma suggests that both antioxidant systems are independent.

Objetivo: determinar la actividad de las enzimas antioxidantes Glutatión Peroxidasa (GSH-Px; EC 1.11.1.9) y Superóxido Dismutasa (SOD; EC 1.15.1.1) en sangre y plasma seminal de 25 caballos reproductores criollos colombianos, clínicamente sanos, pertenecientes a cuatro criaderos y alimentados con concentrado comercial. Métodos: a cada caballo se le tomó un eyaculado mediante vagina artificial. Previa centrifugación del semen para obtener el plasma seminal, se evaluaron las características seminales (volumen, motilidad masal, motilidad individual, concentración espermática). Resultados: el promedio para GSH-Px fue 514.8 ± 22.4 U/g Hb y 0.55 ± 0.05 U/mL en sangre y plasma seminal, respectivamente. La actividad de SOD fue 1877 ± 188 U/g Hb en sangre y 86 ± 7.1 U/mL en plasma seminal. No se encontró correlación entre la actividad de las enzimas estudiadas en el plasma seminal con la actividad sanguínea. Sin embargo la actividad de GSH-Px en plasma seminal se correlacionó significativamente con la concentración espermática. Así mismo GSH-Px en sangre se correlacionó con el porcentaje de espermatozoides con movimiento individual progresivo y con el porcentaje de espermatozoides normales. La SOD no tuvo ninguna correlación con las variables espermáticas analizadas. Conclusiones: La falta de correlación entre la actividad enzimática en ambos sistemas sugiere que serían sistemas antioxidantes independientes.

Objetive: o objetivo deste estudo foi determinar a atividade de enzimas antioxidantes glutationa peroxidase (GSH-Px, EC 1.11.1.9) e superóxido dismutase (SOD, EC 1.15.1.1) no sangue e plasma seminal de 25 cavalos reprodutores crioulo colombiano, clinicamente saudáveis , provenientes de quatro fazendas e alimentados com ração comercial. Métodos: cada cavalo foi levado por ejaculado vagina artificial. Após a centrifugação do sêmen para a obtenção do plasma seminal, foram avaliados as características seminais (volume, turbilhonamento, motilidade individual, a concentração de espermatozóides). Resultados: a média de GSH-Px foi de 514.8 ± 22.4 U / g Hb e 0.55 ± 0.05 U / mL no plasma sanguíneo e seminal, respectivamente. Atividade da SOD foi 1877 ± 188 U / g Hb no sangue e 86 ± 7.1 U / mL no plasma seminal. Não houve correlação entre a atividade das enzimas estudadas no plasma seminal para a atividade de sangue. No entanto, a atividade de GSH-Px no plasma seminal se correlacionaram significativamente com a concentração de espermatozoides. Também a GSH-Px no sangue foi correlacionada com a percentagemde espermatozoides com movimento individual progressiva e o percentual de espermatozoides normais. SOD não teve correlação com variáveis analisadas no esperma. Conclusões: A falta de correlação entre a atividade da enzima em ambos os sistemas sugere que os sistemas antioxidantes são independentes.

[Prevalence of Helicobacter pylori infection in physicians in Medellín, Colombia]. / Prevalencia de la infección por Helicobacter pylori en médicos de Medellín, Colombia.

UNLABELLED: Infection by Helicobacter pylori (H. pylori) and its associated complications, such as gastric cancer, constitute a true public health problem due to the high morbidity and mortality rates in Colombia and Latin America, where it is highly prevalent. OBJECTIVE: To characterize the prevalence of H. pylori infection in the medical population ofMedellin, Colombia. METHODS: A transversal-cut observational epidemiological study was done, 342 physicians were included. The presence of H. pylori infection, diagnosed with carbon 13-labelled urea breath test, and its association with personal aspects, history of gastric disease and clinical manifestations was evaluated. RESULTS: The general prevalence of H. pylori infection was found to be 77.2% (CI 95%: 72.4% to 81.5%). Discriminating by gender, it represents a prevalence of 78.4% in men and 72.6% in women, without any significant association (chi-square, p = 0.37). Of the total 342 participants, 183 (53.5%) presented at least one suspected episode of gastric disease, and of these, 141 (77%) were positive and 42 (23%) were negative for H. pylori; of the 264 H. pylori positive participants, 141 (53.4%) had history of gastric disease and 123 (46.6%) were asymptomatic. CONCLUSIONS: Prevalence of H. pylori infection in the medical population in Medellin, Colombia, is 77.2% (CI 95%: 72.4% to 81.5%), in accordance to the epidemiologic profile of the region. Also, 46.6% of individuals infected by H. pylori were asymptomatic and with no history or symptoms suggestive of the presence of the bacteria, which is only possible to determine after appropriate testing of the individuals.

Prevalencia de la infección por Helicobacter pylori en médicos de Medellín, Colombia / Prevalence of Helicobacter pylori infection in physicians in Medellín, Colombia

La infección por Helicobacter pylori (H. pylori) y las omplicaciones asociadas, como el cáncer gástrico, representan un verdadero problema de salud pública porque lideran las tasas de morbilidad y mortalidad en Colombia y Latinoamérica, en donde es altamente prevalente. Objetivo: caracterizar la prevalencia de la infección por H. pylori en la población médica de Medellín, Colombia. Métodos: se realizó un estudio epidemiológico bservacional transversal donde se incluyeron 342 médicos. Se evaluó la presencia de la infección por H. pylori mediante la prueba de aliento con urea marcada con carbono 13 y su asociación con aspectos personales, antecedentes de enfermedad gástrica y manifestaciones clínicas. Resultados: se encontró una prevalencia general de infección por H. pylori de 77.2% (IC 95%: 72.4% a 81.5%), que discriminada por género epresenta una prevalencia de 78.4% en hombres y 72.6% en mujeres, sin asociación significativa (Chi- –cuadrado p= 0.37). Del total de los 342 participantes, 183 (53.5%) presentaron al menos un evento sospechoso de enfermedad gástrica y de éstos, 141 (77%) fueron positivos y 42 (23%) negativos para H. pylori; de los 264 participantes H. pylori positivos, 141 (53.4%) presentaban antecedentes de enfermedad gástrica y 123 (46.6%) fueron asintomáticos. Conclusiones: la prevalencia de la infección por H. pylori en lapoblación médica de Medellín, Colombia, es de 77.2% (IC 95%: 72.4% a 81.5%), acorde con el perfil epidemiológico de la región. Además, el 46.6% de los individuos infectados por H. pylori fueron asintomáticos y no hay antecedentes ni síntomas que permitan sospechar la presencia de la bacteria, la cual sólo es posible determinar tras el estudio apropiado de los individuos.

Infection by Helicobacter pylori (H. pylori) and its associated complications, such as gastric cancer, constitute a true public health problem due to the high morbidity and mortality rates in Colombia and Latin America, where it is highly prevalent. Objective: To characterize the prevalence of H. pylori infection in the medical population of Medellín, Colombia. Methods: A transversal-cut observational epidemiological study was done, 342 physicians were included. The presence of H. pylori infection, diagnosed with carbon 13-labelled urea breath test, and its association with personal aspects, history of gastric disease and clinical manifestations was evaluated. Results: The general prevalence of H. pylori infection was found to be 77.2% (CI 95%: 72.4% to 81.5%). Discriminating by gender, it represents a prevalence of 78.4% in men and 72.6% in women, without any significant association (chisquare, p=0.37). Of the total 342 participants, 183 (53.5%) presented at least one suspected episode of gastric disease, and of these, 141 (77%) were positive and 42 (23%) were negative for H. pylori; of the 264 H. pylori positive participants, 141 (53.4%) had history of gastric disease and 123 (46.6%) were asymptomatic. Conclusions: Prevalence of H. pylori infection in the medical population in Medellín, Colombia, is 77.2% (CI 95%: 72.4% to 81.5%), in accordance to the epidemiologic profile of the region. Also, 46.6% of individuals infected by H. pylori were asymptomatic and with no history or symptoms suggestive of the presence of the bacteria, which is only possible to determine after appropriate testing of the individuals.

Prevalencia de la infección por Helicobacter pylori en médicos de Medellín, Colombia / Prevalence of Helicobacter pylori infection in physicians in Medellín, Colombia

La infección por Helicobacter pylori (H. pylori) y las omplicaciones asociadas, como el cáncer gástrico, representan un verdadero problema de salud pública porque lideran las tasas de morbilidad y mortalidad en Colombia y Latinoamérica, en donde es altamente prevalente. Objetivo: caracterizar la prevalencia de la infección por H. pylori en la población médica de Medellín, Colombia. Métodos: se realizó un estudio epidemiológico bservacional transversal donde se incluyeron 342 médicos. Se evaluó la presencia de la infección por H. pylori mediante la prueba de aliento con urea marcada con carbono 13 y su asociación con aspectos personales, antecedentes de enfermedad gástrica y manifestaciones clínicas. Resultados: se encontró una prevalencia general de infección por H. pylori de 77.2% (IC 95%: 72.4% a 81.5%), que discriminada por género epresenta una prevalencia de 78.4% en hombres y 72.6% en mujeres, sin asociación significativa (Chi- ¹cuadrado p= 0.37). Del total de los 342 participantes, 183 (53.5%) presentaron al menos un evento sospechoso de enfermedad gástrica y de éstos, 141 (77%) fueron positivos y 42 (23%) negativos para H. pylori; de los 264 participantes H. pylori positivos, 141 (53.4%) presentaban antecedentes de enfermedad gástrica y 123 (46.6%) fueron asintomáticos. Conclusiones: la prevalencia de la infección por H. pylori en lapoblación médica de Medellín, Colombia, es de 77.2% (IC 95%: 72.4% a 81.5%), acorde con el perfil epidemiológico de la región. Además, el 46.6% de los individuos infectados por H. pylori fueron asintomáticos y no hay antecedentes ni síntomas que permitan sospechar la presencia de la bacteria, la cual sólo es posible determinar tras el estudio apropiado de los individuos.(AU)

Infection by Helicobacter pylori (H. pylori) and its associated complications, such as gastric cancer, constitute a true public health problem due to the high morbidity and mortality rates in Colombia and Latin America, where it is highly prevalent. Objective: To characterize the prevalence of H. pylori infection in the medical population of Medellín, Colombia. Methods: A transversal-cut observational epidemiological study was done, 342 physicians were included. The presence of H. pylori infection, diagnosed with carbon 13-labelled urea breath test, and its association with personal aspects, history of gastric disease and clinical manifestations was evaluated. Results: The general prevalence of H. pylori infection was found to be 77.2% (CI 95%: 72.4% to 81.5%). Discriminating by gender, it represents a prevalence of 78.4% in men and 72.6% in women, without any significant association (chisquare, p=0.37). Of the total 342 participants, 183 (53.5%) presented at least one suspected episode of gastric disease, and of these, 141 (77%) were positive and 42 (23%) were negative for H. pylori; of the 264 H. pylori positive participants, 141 (53.4%) had history of gastric disease and 123 (46.6%) were asymptomatic. Conclusions: Prevalence of H. pylori infection in the medical population in Medellín, Colombia, is 77.2% (CI 95%: 72.4% to 81.5%), in accordance to the epidemiologic profile of the region. Also, 46.6% of individuals infected by H. pylori were asymptomatic and with no history or symptoms suggestive of the presence of the bacteria, which is only possible to determine after appropriate testing of the individuals.(AU)

Robust regression of scattered data with adaptive spline-wavelets.

A coarse-to-fine data fitting algorithm for irregularly spaced data based on boundary-adapted adaptive tensor-product semi-orthogonal spline-wavelets has been proposed in Castaño and Kunoth, 2003. This method has been extended in Castaño and Kunoth, 2005 to include regularization in terms of Sobolev and Besov norms. In this paper, we develop within this least-squares approach some statistical robust estimators to handle outliers in the data. Our wavelet scheme yields a numerically fast and reliable way to detect outliers.