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The immune mechanisms underlying the pathogenesis of severe pneumonia associated with the A/H1N1 virus are not well known. The objective of this study was to determine whether severe A/H1N1-associated pneumonia can be explained by the emergence of particular T-cell subsets and the cytokines/chemokines they produced, as well as distinct responses to infection. T-cell subset distribution and cytokine/chemokine levels in peripheral blood and bronchoalveolar lavage (BAL) were determined in patients with severe A/H1N1 infection, asymptomatic household contacts, and healthy controls. Cytokine and chemokine production was also evaluated after in vitro infection with seasonal H1N1 and pandemic A/H1N1 strains. We found an increase in the frequency of peripheral Th2 and Tc2 cells in A/H1N1 patients. A trend toward increased Tc1 cells was observed in household contacts. Elevated serum levels of IL-6, CXCL8, and CCL2 were found in patients and a similar cytokine/chemokine profile was observed in BAL, in which CCL5 was also increased. Infection assays revealed that both strains induce the production of several cytokines/chemokines at 24 and 72 h, however, IL-6, CCL3, and CXCL8 were strongly up-regulated in 72-h cultures in presence of the A/H1N1 virus. Several inflammatory mediators are up-regulated in peripheral and lung samples from A/H1N1-infected patients who developed severe pneumonia. In addition, the A/H1N1 strain induces higher levels of pro-inflammatory cytokines and chemokines than the seasonal H1N1 strain. These findings suggest that it is possible to identify biomarkers of severe pneumonia and also suggest the therapeutic use of immunomodulatory drugs in patients with severe pneumonia associated with A/H1N1 infection.

For an ideal I of a nonassociative algebra A, the π-closure of I is defined by \(\overline{I} = {\rm Ann}({\rm Ann} (I))\), where Ann(I) denotes the annihilator of I, i.e., the largest ideal J of A such that IJ = JI = 0. An algebra A is said to be π-complemented if for every π-closed ideal U of A there exists a π-closed ideal V of A such that A = U ⊕ V. For instance, the centrally closed semiprime ring, and the AW∗-algebras (or more generally, boundedly centrally closed C∗-algebras) are π-complemented algebras. In this paper we develop a structure theory for π-complemented algebras by using and revisiting some results of the structure theory for pseudocomplemented lattices.

The impact of adult scoliosis on pain, function and health-related quality of life (QOL) has not been clearly defined. A population-based study using widely applied screening tools could better reflect the impact of adult scoliosis. In this study, a visual analog pain scale assessment (VAS) for lumbar and leg pain, an Oswestry disability index (ODI) and a standard version of the Medical Outcome Study Short Form-36 (SF-36) questionnaire were sent by mail to 261 women of age 50 years and older, consecutively evaluated with dual-energy radiograph absorptiometry (DXA) scan images. 138 patients (32 with lumbar curves 10° or bigger) returned the questionnaires. Differences in lumbar VAS, leg VAS, ODI and SF-36 values between groups of patients with curves

We show the primeness of the multiplication algebra of the two prime degenerate Jordan algebras constructed by Skosyrskiĭ.

SummaryDengue fever (DF) is the most prevalent arthropod-borne viral disease of humans. No safe vaccine is available, there is no experimental animal model and no specific treatment (antiviral) for Dengue virus (DV) infection exists. The pathogenic mechanisms of the severe forms of the disease, such as Dengue shock syndrome (DSS) and Dengue haemorrhagic fever (DHF), in which endothelial damage is the pathognomonic sign, are not fully understood. Clinical observations have revealed significant abnormalities in the coagulation and inflammation systems, with increased levels of soluble thrombomodulin (sTM) in the plasma of patients with DHF/DSS (grade III or IV). Blood sTM was proposed as an early predictor of DSS during the febrile stage. However, the role of the DV in endothelial injury during DSS is unclear. Here, we present novel insights into the participation of DV in the downregulation of the thrombomodulin-thrombin-protein C complex formation at the endothelial surface, with a reduction in activated protein C (APC). APC is the most important vasoprotective protein because it downregulates thrombin generation (by the inactivation of procoagulant factors Va and VIIIa) and has anti-inflammatory, antiapoptotic, and barrier protection properties. These biological functions of APC are associated with the endothelial protein C receptor (EPCR) and pro-tease-activated receptor 1 (PAR-1) signalling pathways, which link the coagulation-inflammation responses. We found alterations in the antithrombotic and cytoprotective protein C pathways during DV infection of human endothelial vascular cells, which may explain the vasculopathy observed during DHF/DSS. Clarification of the basic principles that underlie these processes has important implications for the design of new therapeutic strategies for DHF/DSS.

Any nonassociative algebra A, regarded as a left module over its multiplication algebra M ( A ) , can be endowed with a natural closure: the e-closure. The e-closed ideals of A form a complete lattice L ( A ) with e-continuous product. The algebra A is said to be e-decomposable if A is the joint of its atoms in L ( A ) , i.e., A is the e-closure of the sum of its minimal e-closed ideals. A distinguished atom is the annihilator Ann ( A ) of A, whenever it is nonzero. The main result of the paper proves that A is e-decomposable if, and only if, M ( A ) is semiprime and any e-closed ideal U of A, with U ≠ Ann ( A ) , contains a minimal e-closed ideal B ≠ Ann ( A ) . Another characterization of e-decomposability is also provided, one which involves the notion of e-radical (the intersection of all maximal e-closed ideals). This result extends both a Jacobson's theorem for finite-dimensional algebras and a previous one by the authors for algebras with zero annihilator. Moreover, it has well-known precedents (Yood's theorem) in the theory of complete normed algebras.

Let A be an algebra whose multiplication algebra M(A) is semiprime. We prove that, except in an exceptional case, the proper closed prime ideals of A are the maximal closed ideals of A, for the closure operations π and ϵ. In fact, these sets agree for both closures. The same can be said in M(A) for the closure operations π and ϵ′. Moreover, we establish the relationships between the proper closed prime ideals of A and the ones of the algebras M(A),U and A/U, for a given ideal U of A.

We introduce and study weak-2-local symmetric maps between C ⁎ -algebras A and B as not necessarily linear, nor continuous, maps Δ : A → B such that for each a , b ∈ A and ϕ ∈ B ⁎ , there exists a symmetric linear map T a , b , ϕ : A → B , depending on a, b and ϕ, satisfying ϕ Δ ( a ) = ϕ T a , b , ϕ ( a ) and ϕ Δ ( b ) = ϕ T a , b , ϕ ( b ) . We prove that every weak-2-local symmetric map between C ⁎ -algebras is a linear map. Among the consequences we show that every weak-2-local ⁎-derivation on a general C ⁎ -algebra is a (linear) ⁎-derivation. We also establish a 2-local version of the Kowalski–Slodkowski theorem for general C ⁎ -algebras by proving that every 2-local ⁎-homomorphism between C ⁎ -algebras is a (linear) ⁎-homomorphism.

Overproduction of pro-inflammatory cytokines and chemokines is frequently associated with severe clinical manifestations in patients infected with influenza A/H1N1 virus. Micro-RNAs (miRNAs) are highly conserved small non-coding RNA molecules that post-transcriptionally regulate gene expression and are potential biomarkers and therapeutic targets in different inflammatory conditions.We studied the circulating and miRNA profiles in critically ill A/H1N1 patients, A/H1N1 patients with milder disease, asymptomatic housemates and healthy controls. Cytokine, chemokine and growth factors that were potential targets of differentially expressed miRNAs were assessed. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and interactome analysis of these miRNAs were also performed.Critically ill patients exhibited a significant over-expression of circulating miR-150 (p0.005) when compared to patients with milder disease. miR-29c, miR-145 and miR-22 were differentially expressed in patients with severe A/H1N1 disease whereas miR-210, miR-126 and miR-222 were downregulated in individuals exposed to the A/H1N1 virus. Significant correlations (p0.05) between circulating levels of miR-150 with IL-1ra, IL-2, IL-6, CXCL8, IFN-γ, CXCL10 and G-CSF were detected, particularly in critically ill patients.The up-regulation of miR-150 is associated with poorer outcomes of A/H1N1 infection. The differential expression of miRNAs related with immune processes in severe A/H1N1 disease supports the potential role of these miRNAs as biomarkers of disease progression.

We prove that, for every complex Hilbert space $H$ , every weak 2-local derivation on $B(H)$ or on $K(H)$ is a linear derivation. We also establish that every weak 2-local derivation on an atomic von Neumann algebra or on a compact C $^{*}$ -algebra is a linear derivation.

β-defensins are a family of antimicrobial molecules involved in inflammatory processes and infections. In human airways, β-defensin-2 (hβD-2) is the best characterized in bacterial and fungal infections; however, it has been insufficiently studied in viral infections. The respiratory syncytial virus (RSV) and adenoviruses (ADV) are important agents of acute respiratory infections. The aim of this study was to measure in vitro the production and antiviral activity of hβD-2 in HEp-2 cells and A549 cells infected with ADV and RSV; hβD-2 production at different times was assessed by RT-PCR, and its presence by immunodetection assay (Western blot) using antibodies anti-hβD-2. The effect of this defensin on viral replication was determined using recombinant hβD-2 in plaque assays. The results revealed that in the cell lines production of hβD-2is up regulated after ADV or RSV infection, in direct proportion to the exposure time to each virus. The use of a high concentration of recombinant hβD-2 resulted in less deleterious viral effect on the cells. The results suggest that both viruses induce hβD-2 production, no matter if the virus is enveloped or not, and that presence of hβD-2 reduces replication and cytopathic in vitro effect of RSV and ADV. The hβD-2 production by low pathogenicity viruses or live viral vaccines can be useful as therapeutic tools in some infectious diseases.

Dengue fever (DF) is the most prevalent arthropod-borne viral disease which affects humans. DF is caused by the four dengue virus (DENV) serotypes, which are transmitted to the host by the mosquitoAedes aegyptithat has key roles in DENV infection, replication, and viral transmission (vector competence). Mosquito saliva also plays an important role during DENV transmission. In this study, we detected the presence of sialic acid (Sia) inAedes aegyptitissues, which may have an important role during DENV-vector competence. We also identified genome sequences encoding enzymes involved in Sia pathways. The cDNA forAedes aegyptiCMP-Sia synthase (CSAS) was amplified, cloned, and functionally evaluated via the complementation of LEC29.Lec32 CSAS-deficient CHO cells.AedesCSAS-transfected LEC29.Lec32 cells were able to express Sia moieties on the cell surface. Sequences related toα-2,6-sialyltransferase were detected in theAedes aegyptigenome. Likewise, we identified Sia-α-2,6-DENV interactions in different mosquito tissues. In addition, we evaluated the possible role of sialylated molecules in a salivary gland extract during DENV internalization in mammalian cells. The knowledge of early DENV-host interactions could facilitate a better understanding of viral tropism and pathogenesis to allow the development of new strategies for controlling DENV transmission.

Background Coccidioides spp. is the ethiological agent of coccidioidomycosis, an infection that can be fatal. Its diagnosis is complicated, due to that it shares clinical and histopathological characteristics with other pulmonary mycoses. Coccidioides spp. is a dimorphic fungus and, in its saprobic phase, grows as a mycelium, forming a large amount of arthroconidia. In susceptible persons, arthroconidia induce dimorphic changes into spherules/endospores, a typical parasitic form of Coccidioides spp. In addition, the diversity of mycelial parasitic forms has been observed in clinical specimens; they are scarcely known and produce errors in diagnosis. Methods We presented a retrospective study of images from specimens of smears with 15% potassium hydroxide, cytology, and tissue biopsies of a histopathologic collection from patients with coccidioidomycosis seen at a tertiary-care hospital in Mexico City. Results The parasitic polymorphism of Coccidioides spp. observed in the clinical specimens was as follows: i) spherules/endospores in different maturation stages; ii) pleomorphic cells (septate hyphae, hyphae composed of ovoid and spherical cells, and arthroconidia), and iii) fungal ball formation (mycelia with septate hyphae and arthroconidia). Conclusions The parasitic polymorphism of Coccidioides spp. includes the following: spherules/endospores, arthroconidia, and different forms of mycelia. This knowledge is important for the accurate diagnosis of coccidioidomycosis. In earlier studies, we proposed the integration of this diversity of forms in the Coccidioides spp. parasitic cycle. The microhabitat surrounding the fungus into the host would favor the parasitic polymorphism of this fungus, and this environment may assist in the evolution toward parasitism of Coccidioides spp.

Human parainfluenza virus type 1 (HPIV-1) is the most common cause of croup in infants. The aim of this study was to describe molecular mechanisms associated with IL-8 production during HPIV-1 infection and the role of viral replication in MAPK synthesis and activation. Anin vitromodel of HPIV-1 infection in the HEp-2 and A549 cell lines was used; a kinetic-based ELISA for IL-8 detection was also used, phosphorylation of the mitogen-activated protein kinases (MAPKs) was identified by Western blot analysis, and specific inhibitors for each kinase were used to identify which MAPK was involved. Inactivated viruses were used to assess whether viral replication is required for IL-8 production. Results revealed a gradual increase in IL-8 production at different selected times, when phosphorylation of MAPK was detected. The secretion of IL-8 in the two cell lines infected with the HPIV-1 is related to the phosphorylation of the MAPK as well as viral replication. Inhibition of p38 suppressed the secretion of IL-8 in the HEp-2 cells. No kinase activation was observed when viruses were inactivated.

Letr, s ∈ ]0, 1]. We prove that a Banach spaceXsatisfies theM(r, s)-inequality (i.e.,[formula]where π is the canonical projection ofX*** ontoX*) wheneverr + s/2 > 1 and there exists a norm one projectionPon L (X)* with Ker P = K (X) ⊥ satisfying[formula]We characterize the last property of K (X) in L (X) by a strong version of the metric compact approximation property ofX. Our results extend some well-known results onM-ideals.

The object of this paper is to investigate JB∗-triples which are M-ideals in their biduals. M-ideals in their biduals is a subject of current interest (see [9], [10], [11], [12], [14]), c0 and the compact operators on a Hilbert space being representative examples. Let us recall that a Banach space X is an M-ideal in its bidual (in short, M-ideal) if ‖φ‖ = ‖π(φ)‖+ ‖φ− π(φ)‖, for all φ ∈ X∗∗∗, where π is the canonical projection of X . M-ideals can also be characterized by intersection properties of balls. For further information we refer to [2]. In particular, A. Lima proved (see e.g. [12, p. 43] that a Banach space X is M-ideal in its bidual if, and only if, X has the 2-ball property in its bidual. On the other hand, it is known (see [14, Theorem 2.6]) that Banach spaces which are M-ideals in their biduals are Asplund spaces (see [5, Chapter VII, Section 5] for a definition). A JB∗-triple is a complex Banach space J together with a continuous triple product {., ., .} : J × J × J −→ J , which satisfies: 1. {x, y, z} is bilinear and symmetric in x and z and conjugate-linear in y. 2. The Jordan identity {a, b, {x, y, z}} = {{a, b, x}, y, z}− {x, {b, a, y}, z}+ {x, y, {a, b, z}}. 3. For each x ∈ J , the operator x∆x : J −→ J defined by x∆x(y) = {x, x, y} is a hermitian operator with non-negative spectrum. 4. ‖x∆x‖ = ‖x‖2, for each x ∈ J . As an example, any C∗-algebra with the triple product {x, y, z} = 12 (xy∗z+zy∗x) is a JB∗-triple. We recall that the bidual J∗∗ of a JB∗-triple J is in a natural way a JB∗-triple containing J as a subtriple (see [6]). An (algebraic) ideal in a JB∗-triple J is a complex subspace F satisfying {x, y, F} ⊆ F and {x, F, y} ⊆ F , for all x, y ∈ J . Observe that it is enough to take x = y in this definition. Received by the editors July 19, 1995 and, in revised form, January 2, 1997. 1991 Mathematics Subject Classification. Primary 46B20; Secondary 17C65. This research was partially supported by M.E.C., Project No. PB96/1406. c ©1998 American Mathematical Society

Speaking of viral pathogenesis, it must describe the features and factors of viral pathogen, hosts and environment. Over its lifetime, an individual is exposed to many infectious agents, however, in most situations does not develop a disease thanks to factors such as physical and chemical host barriers. In other cases, pathogens circumvent these barriers and cause infection; however, a “biological war” will start between the determinants of pathoge‐ nicity and early host defenses. If the virus is able to overcome these first lines of defense, a type of highly specialized and specific protection will be activated. This defense will ach‐ ieve, in most situations, the infection control and subsequent eradication of the disease. Fur‐ thermore, this process will initiate the generation of the immunological memory, enabling the individual with a more quickly and effectively response at the next contact with the same agent. On the contrary, if the foreign agent can overcome both defenses, the result is disease. In certain cases, the line of defense, when triggered, can also cooperate with the damage instead of healing, making the disease more severe. Thus, the immunopathology vi‐ ral respiratory infection is a frequent consequence of the immune response against many of respiratory pathogens. Furthermore, if the infection is established, the factors or viral viru‐ lence determinants and physiological conditions of the host cell will determine which direc‐ tion the infection will take. A virus is pathogenic when it is able to infect and cause disease in a host, while it is virulent when it causes more severe disease than another virus of a dif‐ ferent strain, although both remain pathogens. Each virus can cause different cytopathic ef‐ fects in the host cell, which may lead to several symptoms and disease. In addition, developing a disease reflects the existence of an abnormality of the host, either structural or functional, induced by the invading virus.

Background In April 2009, public health surveillance detected an increased number of influenza-like illnesses in Mexico City’s hospitals. The etiological agent was subsequently determined to be a spread of a worldwide novel influenza A (H1N1) triple reassortant. The purpose of the present study was to demonstrate that molecular detection of pandemic influenza A (H1N1) 2009 strains is possible in archival material such as paraffin-embedded lung samples. Methods In order to detect A (H1N1) virus sequences in archived biological samples, eight paraffin-embedded lung samples from patients who died of pneumonia and respiratory failure were tested for influenza A (H1N1) Neuraminidase (NA) RNA using in situ RT-PCR. Results We detected NA transcripts in 100% of the previously diagnosed A (H1N1)-positive samples as a cytoplasmic signal. No expression was detected by in situ RT-PCR in two Influenza-like Illness A (H1N1)-negative patients using standard protocols nor in a non-related cervical cell line. In situ relative transcription levels correlated with those obtained when in vitro RT-PCR assays were performed. Partial sequences of the NA gene from A (H1N1)-positive patients were obtained by the in situ RT-PCR-sequencing method. Sequence analysis showed 98% similarity with influenza viruses reported previously in other places. Conclusions We have successfully amplified specific influenza A (H1N1) NA sequences using stored clinical material; results suggest that this strategy could be useful when clinical RNA samples are quantity limited, or when poor quality is obtained. Here, we provide a very sensitive method that specifically detects the neuraminidase viral RNA in lung samples from patients who died from pneumonia caused by Influenza A (H1N1) outbreak in Mexico City.

Borrelia burgdorferi sensu lato (s.l.), transmitted by Ixodes spp. ticks, is the causative agent of Lyme disease. Although Ixodes spp. ticks are distributed in both Northern and Southern Hemispheres, evidence for the presence of B. burgdorferi s.l. in South America apart from Uruguay is lacking. We now report the presence of culturable spirochetes with flat-wave morphology and borrelial DNA in endemic Ixodes stilesi ticks collected in Chile from environmental vegetation and long-tailed rice rats (Oligoryzomys longicaudatus). Cultured spirochetes and borrelial DNA in ticks were characterized by multilocus sequence typing and by sequencing five other loci (16S and 23S ribosomal genes, 5S-23S intergenic spacer, flaB, ospC). Phylogenetic analysis placed this spirochete as a new genospecies within the Lyme borreliosis group. Its plasmid profile determined by polymerase chain reaction and pulsed-field gel electrophoresis differed from that of B. burgdorferi B31A3. We propose naming this new South American member of the Lyme borreliosis group B. chilensis VA1 in honor of its country of origin.

Infection with pandemic (pdm) A/H1N1 virus induces high levels of pro-inflammatory mediators in blood and lungs of experimental animals and humans.To compare the involvement of seasonal A/PR/8/34 and pdm A/H1N1 virus strains in the regulation of inflammatory responses, we analyzed the changes in the whole-genome expression induced by these strains in macrophages and A549 epithelial cells. We also focused on the functional implications (cytokine production) of the differential induction of suppressors of cytokine signaling (SOCS)-1, SOCS-3, retinoid-inducible gene (RIG)-I and interferon receptor 1 (IFNAR1) genes by these viral strains in early stages of the infection.We identified 130 genes differentially expressed by pdm A/H1N1 and A/PR/8/34 infections in macrophages. mRNA levels of SOCS-1 and RIG-I were up-regulated in macrophages infected with the A/PR/8/34 but not with pdm A/H1N1 virus. mRNA levels of SOCS-3 and IFNAR1 induced by A/PR/8/34 and pdm A/H1N1 strains in macrophages, as well as in A549 cells were similar. We found higher levels of IL-6, TNF-α, IL-10, CCL3, CCL5, CCL4 and CXCL8 (p0.05) in supernatants from cultures of macrophages infected with the pdm A/H1N1 virus compared to those infected with the A/PR/8/34 strain, coincident with the lack of SOCS-1 and RIG-I expression. In contrast, levels of INF-α were higher in cultures of macrophages 48h after infection with the A/PR/8/34 strain than with the pdm A/H1N1 virus.These findings suggest that factors inherent to the pdm A/H1N1 viral strain may increase the production of inflammatory mediators by inhibiting SOCS-1 and modifying the expression of antiviral immunity-related genes, including RIG-I, in human macrophages.

In Mexico, Influenza virus infections occur more frequently during the winter with small peaks throughout the year. In April 2009, an epidemic arose from the emergence of a new Influenza A virus, whose devastating effect reflected significantly in Mexico city. Numerous patients with Influenza-like severe symptoms were attended at the Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico (INER) and in many cases required hospitalization. The INER, in collaboration with the Direccion General de Epidemiologia (Mexico) and the Instituto Nacional de Referencia Epidemiologica, Mexico (INDRE) marked the first guidelines for the management, diagnosis and treatment of Influenza-illness in Mexico. The INER is considered one of the leading centers for the care of critically respiratory-ill patients, and was one of the first institutions to describe the clinical presentation and death in the initial period of outbreak (Acuna, 2010; Manjarrez et al., 2003). The pandemic that occurred in 2009 in Mexico, took a different tack in contrast to other countries with respect to the frequency, severity and number hospitalized patients with mortality and greater affection in healthy young people. Influenza is a respiratory illness caused by viruses of the same name. Each year, seasonal flu viruses originate occasional epidemics. The name "influenza" comes from the belief that disease was caused by a negative supernatural influence, that is, a malign influence, or that the stars have influence on the occurrence of the disease (Acuna, 2010; Manjarrez & Arenas 1999).

The world is experiencing an increase in emergent infections as a result of anthropogenic changes of the biosphere and globalization. Global warming unrestricted exploitation of natural resources such as forests and fisheries, urbanization, human migration, and industrialization of animal husbandry cause environmental destruction and fragmentation. These changes of the biosphere favor local emergence of zoonoses from their natural biotopes and their interaction with domestic animals and human populations. Subsequently, international commerce, human and animal migration and travel, favor the dissemination of these zoonotic pathogens worldwide. Chile is undergoing an important degradation of many wild-life biotopes, affecting their diversity and contributing to the dissemination of zoonoses such as Chagas disease, Hantavirus, rabies, fish tapeworms, and marine vibriosis. Moreover, agents of many other zoonoses such as inverted exclamation markeptospirosis, hydatidosis, salmonellosis, rabies, brucellosis and anthrax have been detected in different wild-life environments in the country. The intensification and accelerations of the anthropogenic deterioration of the biosphere in Chile, as results of the unrestricted utilization of natural resources and global climate change, suggests that emergence of new zoonoses in the near future will lead to important public health and economic problems. Forestalling of these problems will require active epidemiológica! surveillance of wild and domestic animals with a wide range of modern molecular and ancillary epidemiológica! tools. This also demands government and private sector (i.e., animal husbandry) intervention, funding and the collaboration of professionals in human and veterinary medicine with those in the environmental sciences including ecology, climatology and oceanography.

SummaryDengue fever is the most prevalent viral disease transmitted by vectors (Aedes aegypti, Aedes albopictus) in worldwide. More than 100 million cases occur annually with a mortality rate of 5% and no safe vaccine is available. The pathogenesis of Dengue, where host and viral factors participate in the establishment of Dengue haemorrhagic fever (DHF) and Dengue shock syndrome (DSS) remains unresolved. Clinical observations have revealed significant abnormalities in coagulation and inflammation systems, with increased levels of tissue factor (TF) and the chemokine IL-8, correlating with the severity of the disease and implicating damage to endothelial vascular cells (EVC). Here we present novel insights concerning the crosstalk between the regulatory signaling pathways of the coagulation-inflammation processes, during Dengue virus (DV) infection of EVC. We found that DV up-regulates Protease Activated receptor type-1 (inflammation) and TF (coagulation) receptors, via the phosphorylation of p38 and ERK1/2 MAPKs, which favor the activation of NF-κB transcription factor. This induces pro-inflammatory (IL-8) or pro-adhesive (VCAM-1) gene expression which may lead to EVC activation. The elucidation of the basic principles that signal these processes has important implications for the design of new therapeutic strategies for DHF/DSS.

The world is experiencing an increase in emergent infections as a result of anthropogenic changes of the biosphere and globalization. Global warming unrestricted exploitation of natural resources such as forests and fisheries, urbanization, human migration, and industrialization of animal husbandry cause environmental destruction and fragmentation. These changes of the biosphere favor local emergence of zoonoses from their natural biotopes and their interaction with domestic animals and human populations. Subsequently, international commerce, human and animal migration and travel, favor the dissemination of these zoonotic pathogens worldwide. Chile is undergoing an important degradation of many wild-life biotopes, affecting their diversity and contributing to the dissemination of zoonoses such as Chagas disease, Hantavirus, rabies, fish tapeworms, and marine vibriosis. Moreover, agents of many other zoonoses such as inverted exclamation markeptospirosis, hydatidosis, salmonellosis, rabies, brucellosis and anthrax have been detected in different wild-life environments in the country. The intensification and accelerations of the anthropogenic deterioration of the biosphere in Chile, as results of the unrestricted utilization of natural resources and global climate change, suggests that emergence of new zoonoses in the near future will lead to important public health and economic problems. Forestalling of these problems will require active epidemiologica! surveillance of wild and domestic animals with a wide range of modern molecular and ancillary epidemiologica! tools. This also demands government and private sector (i.e., animal husbandry) intervention, funding and the collaboration of professionals in human and veterinary medicine with those in the environmental sciences including ecology, climatology and oceanography.

El síndrome de muerte súbita infantil es causa significativa de mortalidad infantil en Chile y otros países. Un factor de riesgo conocido es colocar lactantes en prono para dormir. Un estudio reciente realizado en Estados Unidos demostró fallas al respecto ya que en 49% de salas cuna encuestadas lactantes dormían en prono. Objetivo: conocer las conductas que dice adoptar el personal de una muestra de salas cuna de Santiago, respecto de la posición en que son colocados a dormir lactantes menores. Pacientes y Método: realizamos una encuesta telefónica a 126 salas cuna de Santiago para determinar la posición al dormir de los lactantes. No se visitó las salas cuna para validar las respuestas. Resultados: Obtuvimos respuesta de 91 en que dijeron atender lactantes menores. Sesenta y tres declararon tener normas sobre el tema, pero solamente 20 eran escritas (22%). Entre las salas cuna que dijeron tener norma, 38% incluía la posición prona como única o como alternativa. Cincuenta y siete salas cuna (63%) declararon tener lactantes menores durmiendo en prono y en 17 (19%) exclusivamente en prono. Conclusión: Un alto porcentaje de salas cuna mantienen el factor de riesgo para muerte súbita "posición prona al dormir" presente en la práctica diaria. Se debe mejorar la información sobre el tema para disminuir este factor de riesgo de muerte súbita Sudden infant death syndrome (SIDS) is a major cause of infant mortality in Chile and other countries. A significant risk factor is placing infants to sleep in the prone position. A recent survey carried out in Washington D.C. found that 43% of day care centers were unaware of the association between SIDS and sleep position, and that in 49% of centers infants were sometimes placed prone. Our purpose was to obtain information about conducts related to sleeping position of infants that attend a sample of day care centers in Santiago. Methods: We performed a telephonic survey of 126 day care centers in Santiago. The centers were not visited by the authors to validate the answers. Results: 91 centers looking after infants of less than 12 months took part. 63 (69%) said that they had policies about sleeping position but only 20 (22%) had a written policy. 24 centers contested that their policy stated prone as the preferred or alternative position. 57 (63%) contested that some infants slept prone, and in 17 all the infants did. Conclusions: A high percentage of day care centers use this risk factor in their routine. More information is needed for Chilean child care providers about the association between sleep position and SIDS

An ideal I of a (non-associative) algebra A is dense if the multiplication algebra of A acts faithfully on I, and is complementedly dense if it is a direct summand of a dense ideal. We prove that every complementedly dense ideal of a semiprime algebra is a semiprime algebra, and determine its central closure and its extended centroid. We also prove that a semiprime algebra is an essential subdirect product of prime algebras if and only if, its extended centroid is a direct product of fields. This result is applied to discuss decomposable algebras with respect to some familiar closures for ideals.

For a nonassociative algebra A, by considering A as a left module over its multiplication algebra M ( A ) , a closure operation (termed the e-closure) appears on the lattice I A of all ideals of A. For an ideal U of A, the e-closure of U is the largest ideal of A which satisfies the same “multiplicative identities” as U. An algebra A is said to be e-complemented if for every e-closed ideal U of A there exists an e-closed ideal V of A such that A = U ⊕ V . What is termed the e ′ -closure appears in a dual fashion in I M ( A ) and the e ′ -complementarity can be considered in M ( A ) . This paper provides different characterizations of both complementarities. Moreover, we determine the relation between these concepts, the classical complementarity, and the complementarity for the π-closure. We also develop a structure theory for e-complemented algebras.

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Eight of 27 rodents, Octodon degus, collected 30 km southwest of Santiago, Chile, harbored Trichuris bradleyi sp. n. These whipworms lack a true spicular tube and the spicule is contained within the cloaca, thus differentiating the species from all others described from rodents. The species shows some similarity to T. sylvilagi Tiner 1950, especially in the length of the spicule and shape of the cloacal tube. Between July-August 1974, in the area of "Quebrada de la Plata," approximately 30 km southwest of Santiago, Chile, a biological survey was undertaken. The collection location is mountainous with steep slopes (30 to 50% grades and approximately 500-m elevation) covered by a coarse colluvial soil. The prevailing vegetation is savannah dominated by Acacia caven, although significant differences are apparent due to slope exposure. For example, north-facing slopes are covered with xerophytic vegetation (thorny shrub and Puya trichocereus association), whereas south-facing slopes are covered by a mosaic of xerophytic forest which has been degraded by human activity. The mean yearly temperature and rainfall is 14.5 C and 400 mm, respectively (Di Castri, 1968). MATERIALS AND METHODS Twenty-seven degu rodents, Octodon degus, were collected. The animals were obtained using snap-traps with oats as bait. Helminths were obtained, with some modification, employing the method described by Tagle-Villarroel (1956). They were stored in alcohol-formalin-acetic acid (AFA) solution and all nematodes were studied after clearing in lactophenol.

El virus de influenza H1N1 (2009), es considerado una emergencia sanitaria a nivel mundial; se ha descrito que durante el 2009 ocasionó 151,700 a 575,400 muertes en todo el mundo afectando mayoritariamente a personas menores de 65 años. El virus de Influenza comúnmente infecta el tracto superior respiratorio resultando en una infección limitada, sin embargo en casos severos puede llegar al aparato respiratorio bajo, y ocasionar neumonía. Este proceso genera daño severo a la microvasculatura pulmonar, el daño a endotelio da inicio a la cascada de coagulación por la exposición del factor tisular (FT), causando edema, hipoxemia y falla respiratoria. Así mismo en pacientes con influenza severa, se ha descrito la presencia de tormenta de citocinas en casos fatales, y falla multiorgánica. En estos procesos inflamatorios los receptores activados por proteasas (PAR´s), juegan una papel determínate, debido a que su actividad está directamente relacionada con procesos involucrados en, citoprotección, regulación de la cascada de coagulación e inflamación. PAR-1 es un receptor presente en la microvasculatura del endotelio y su participación en la activación de genes inflamatorios a través de proteínas G, es determinante para la translocación de NF-NB al núcleo, que regula la expresión de dichos genes. Influenza A virus H1N1 (2009) is considered a global health emergency; it has been described that during 2009 caused between 151,700 and 575,400 deaths worldwide, affecting mostly people under 65 years. Influenza viruses commonly infect the upper respiratory tract resulting in a limited infection, but in severe cases the viruses can reach the lower respiratory tract and cause pneumonia. In this type of infections a severe damage is generated in the pulmonary microvasculature, damaged endothelium initiates the blood coagulation by the exposure of tissue factor (TF), causing edema, hypoxemia and respiratory failure. Also in patients with severe influenza, it has been described an increase in proinflmatory cytokines denominated “cytokine storm” causing fatal cases, and multiorgan failure. In these inflammatory processes protease activated receptors (PARs), play a determinant role because its activity is directly involved in cytoprotection, regulation of the coagulation cascade and inflammatory processes. PAR-1 is a receptor present in the microvasculature endothelium and its participation in the activation of inflammatory genes through G proteins, is decisive for the translocation of NF-NB to the nucleus, which regulates the expression of such genes. Currently there is not clear information on the participation of PAR-1 during infection of the vascular endothelium with influenza A virus.