Large deletions and splicing-site mutations in the STK11 gene in Peutz-Jeghers Chilean families.

Peutz-Jeghers syndrome (PJS) is an autosomal dominant disorder characterized by mucocutaneous melanocytic macules, gastrointestinal hamartomatous polyposis and an increased risk of various neoplasms. Germline mutations in the serine/threonine kinase 11 (STK11) gene have been identified as a cause for PJS. The aim of this study was to characterize the genotype of Chilean PJS patients. Mutation screening of 13 patients from eight PJS families was performed using a single strand conformation polymorphism analysis, DNA sequencing and multiplex ligation-dependent probe amplification assay. The breakpoints of the genomic rearrangements were assessed by a long-range polymerase chain reaction and sequencing. The results revealed the existence of seven different pathogenic mutations in STK11 gene in seven unrelated families, including three point mutations and four large genomic deletions. Three of these point mutations (43%, 3/7) may be considered as novel. Our results showed that a germline mutation is present in STK11 in 88% of probands fulfilling the diagnostic criteria of PJS. In this study, the combination of two different experimental approaches in the screening of the STK11 in PJS, led to a higher percentage of mutation detection.

Hepatitis C virus quasispecies in plasma and peripheral blood mononuclear cells of treatment naïve chronically infected patients.

Peripheral blood mononuclear cells (PBMCs) from 45 treatment naïve, HIV-negative, chronically hepatitis C virus (HCV)-infected patients were analyzed for the presence of HCV RNA. Viral RNA was detected in 73% of the studied patients. Single-strand conformation polymorphism assays and sequence analysis of the HCV 5'untranslated regions amplified from RNA recovered from both Plasma and PBMCs suggested virus compartmentalization in 57.6% of patients studied. In summary, our study presents evidence that HCV RNA can be found in PBMCs of treatment naïve chronically infected patients that are not immunocompromised or co-infected with the human immunodeficiency virus.

Novel sites of expression of functional angiotensin II receptors in the late gestation fetus.

In the adult, the peptide hormone angiotensin II (AII) is primarily known as a regulator of circulatory homeostasis, but recent evidence also suggests a role in cell growth. This study of AII in late gestation rat fetuses revealed the unexpected presence of receptors in skeletal muscle and connective tissue, in addition to those in recognized adult target tissues. The AII receptors in this novel location decreased by 80 percent 1 day after birth and were almost undetectable in the adult. Studies in fetal skin fibroblasts showed that the receptors were coupled to phospholipid breakdown, with concomitant increases in inositol phosphate and cytosolic calcium. The abundance, timing of expression, and unique localization of functional AII receptors in the fetus suggest a role for AII in fetal development.

Protein kinase C mediates the effect of vasopressin in pituitary corticotrophs.

The role of protein kinase C (PKC) on vasopressin (VP) action was investigated by inhibition of endogenous PKC using prolonged incubation of the cells with phorbol ester, and by direct measurement of PKC activity in pituitary cells. Preincubation of the cells for 6 h with 100 nM TPA at 37 C resulted in a 90% decrease in total PKC activity. In the PKC-depleted cells, cAMP responses to stimulation with 100 nM CRF for 30 min were normal, but the potentiating effects of VP and PMA on CRF-stimulated cAMP production were abolished. The stimulation of ACTH secretion by VP and PMA alone was also abolished in PKC- depleted cells. PKC activity in cytosolic and detergent-solubilized membrane fractions from enriched pituitary corticotrophs obtained by centrifugal elutriation, was directly measured by enzymatic assays and by immunoblotting techniques. Basal PKC activity was higher in the cytosol than in the membranes (8.43 +/- 0.47 and 1.93 +/- 0.11 pmol 32P incorporated/10 min, respectively). After incubation of the cells with VP for 15 min or [3H] phorbol-12-myristate-13-acetate (PMA) for 30 min, PKC activity in cytosol was decreased by 40% and 89%, respectively, while the activity in the membrane was increased by 138% and 405%, respectively. Such VP- and PMA-induced translocation of PKC was also observed when the enzyme content in the cytosol and the membranes was measured by immunoblotting using a specific anti-PKC antibody and [125I]protein A. Autoradiographic analysis of immunoblots revealed an 80 kilodalton band characteristic of PKC, with OD higher in the cytosolic than in the membrane fractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of protein kinase C on the steroidogenic effect of angiotensin II in the rat adrenal glomerulosa cell.

The role of protein kinase C (PKC) in the steroidogenic action of angiotensin II (AII) was investigated by depletion of endogenous PKC using prolonged incubation with phorbol ester and direct measurement of PKC in isolated rat adrenal glomerulosa cells. PKC activity was measured by incorporation of 32P from [gamma 32P]ATP into histone in the presence of cytosolic and detergent-solubilized membrane fractions purified by diethylaminoethyl cellulose chromatography. Basal PKC activity was higher in cytosol than in membranes (1,000 +/- 57 and 413 +/- 14 pmol P incorporated/mg.min, respectively). After incubation of the cells with AII for 5, 15, 30, and 60 min, PKC activity in the cytosol decreased by 5, 18, 25, and 27%, respectively, while in the membrane there was a transient increase of 15% at 15 min returning to basal by 60 min. Incubation of the cells with 100 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in transient translocation of PKC activity to the membrane (15 min) which was followed by a 64% decrease in total cellular enzyme activity after 3 h. In PKC-depleted cells, the aldosterone response to ACTH was increased by 25% but AII-stimulated steroidogenesis was unchanged. In contrast, in cells in which PKC was translocated to the membrane by a 15 min preincubation with TPA, aldosterone response to AII was enhanced by 40%, while the response to ACTH was reduced by 30%; under these conditions membrane PKC levels rapidly returned to basal. However, the changes in aldosterone response were still evident when addition of AII or ACTH was delayed for up to 30 min after removal of TPA, indicating a persistent modification in the cell membrane secondary to PKC activation. Aldosterone responses to potassium were not altered by preincubation of the cells with TPA. The inactive phorbol ester analog, 4 alpha-hydroxyphorbol-12,13-dibutyrate, had no effect on the steroid responses to either stimulus. The small but significant translocation of PKC activity from cytosol to membrane after treatment of rat adrenal glomerulosa cells with AII suggests that AII activates PKC. However, the fact that aldosterone responses to AII are potentiated during TPA-induced PKC translocation to the membrane suggests that AII and phorbol esters do not share the same mechanism of action in the regulation of steroidogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Interleukin-1beta (IL-1beta) is a modulator of human luteal cell steroidogenesis: localization of the IL type I system in the corpus luteum.

The present investigation examined the effect of interleukin-1beta (IL-1beta) on progesterone production by human luteal cells and the expression and localization of the IL-1 system in the human corpus luteum (CL). Luteal cells were isolated from corpora lutea collected throughout the luteal phase. After dispersion, luteal cells were treated with a panel of monoclonal antibodies directed to leukocyte-specific molecules. The leukocytes were isolated with immunomagnetic beads. Leukocyte-free luteal cells exhibited greater steroidogenic responsiveness to hCG toward the end of the luteal phase. The treatment of mixed luteal cells (total luteal cells) with IL-1beta inhibited by 60% hCG-stimulated progesterone production. Interestingly, the treatment of leukocyte-free luteal cells with IL-1beta did not affect progesterone production. In addition, the treatment of mixed luteal cells with monoclonal antibodies against IL-1 receptor type I (IL-1RtI) resulted in a 2.5-fold increase in the hCG-supported progesterone production. IL-1RtI and IL-1 receptor antagonist were localized by immunohistochemistry in both somatic and immune cells of the CL. Flow cytometric analysis indicated that both nonleukocyte luteal cells and leukocyte-luteal cells exhibited IL-1Rt-I positive cells, representing 56% and 31% of the total luteal cells, respectively. However, 13% of nonleukocyte luteal cells did not express IL-1Rt-I. Northern analysis demonstrated the presence of the 5.1-kb IL-1RtI messenger ribonucleic acid transcript in CL of different ages. RT-PCR indicated that both leukocyte-free luteal cells and luteal leukocytes express IL-1RtI messenger ribonucleic acid. We conclude that 1) luteal leukocytes have an inhibitory effect on hCG-stimulated progesterone production; 2) IL-1beta inhibits hCG-stimulated progesterone production only in mixed luteal cell cultures, indicating that leukocytes mediate the effect; 3) the somatic and immune cells of the CL are sites of action and expression of the IL-1 system; and 4) interaction between the steroidogenic and immune cells of the CL suggests a functional intraovarian role for IL-1beta in CL physiology.

Study of GH sensitivity in chilean patients with idiopathic short stature.

We hypothesized that some children with idiopathic short stature in Chile might bear heterozygous mutations of the GH receptor. We selected 26 patients (3 females, 23 males) from 112 patients who consulted for idiopathic short stature at the University of Chile. Their chronological age was 8.3 +/- 1.9, and bone age was 6.1 +/- 1.0 yr. Their height was -3.0 +/- 0.7 SDS; IGF-I, -1.2 +/- 1.1 SD; IGF binding protein 3, -0.7 +/- 2.0 SDS; and GH binding protein, 0.4 +/- 0.8 SDS. Patients were admitted, and blood samples were obtained every 20 min to determine GH concentrations overnight. Coding sequences and intron-exon boundaries of exons 2-10 of GH receptor gene were amplified by PCR and subsequently analyzed through single-strand conformational analysis. Mean serum GH concentration, over 12-h, was 0.20 +/- 0.08 nM; pulse amplitude, 0.40 +/- 0.15 nM; number of peaks, 5.8 +/-1.5 peaks/12 h; peak value of GH during the 12-h sampling, 1.03 +/- 0.53 nM; and area under the curve, 151.4 +/- 56.1 nM/12 h. There were positive correlations between mean GH vs. area under the curve (P < 0.001) and GH peak (P < 0.01). The single-strand conformational analysis of the GH receptor gene showed abnormal migration for exon 6 in 9 patients and for exon 10 in 9 patients, which (by sequence analysis) corresponded to 2 polymorphisms of the GH receptor gene: an A-to-G transition in third position of codon 168 in exon 6 and a C-to-A transversion in the first position of codon 526 in exon 10. We further sequenced all coding exons and intron-exon boundaries in the most affected patients (nos. 6, 9, 11, 14, 15, 16, and 23). This analysis revealed a C-to-T transition in codon 161 of exon 6 in patient 23, which results in an amino acid change (Arg to Cys) in an heterozygous form in the patient and his father. In conclusion, the results of our study suggest that, in Chilean patients with idiopathic short stature, GH receptor gene mutations are uncommon, although we cannot exclude mutations that were missed by single-strand conformational analysis or mutations within introns or in the promoter regions of the GH receptor gene.

Expression of steroidogenic acute regulatory protein in the human corpus luteum throughout the luteal phase.

The expression of the steroidogenic acute regulatory protein (StAR) in the human corpus luteum (CL) was examined throughout the luteal phase. The primary 1.6-kb StAR transcript was in greater abundance in early (3.1-fold) and mid (2.2-fold) luteal phase CL compared with late luteal phase CL. The larger StAR transcript (4.4 kb) was found in early and midluteal phase CL, but was not detected in late luteal phase specimens. Mature StAR protein (30 kDa) was present in lower amounts within late CL compared with early and midluteal phase CL. The StAR preprotein (37 kDa) was also detected in greater abundance in early and midluteal CL. Immunohistochemistry revealed that StAR staining was most prominent in thecal-lutein cells throughout the luteal phase. The intensity of the signal for StAR exhibited significant changes throughout the luteal phase, being most intense during the midluteal phase and least during the late luteal phase. Plasma progesterone concentrations were highly correlated (r = 0.73 and r = 0.79) with luteal expression of the preprotein and mature StAR isoforms, respectively, throughout the luteal phase. To examine the LH dependency of StAR expression, the GnRH antagonist, Cetrorelix, was administered during the midluteal phase. Cetrorelix caused a decline in serum LH levels within 2 h, which, in turn, caused a pronounced decline in plasma progesterone within 6 h. The StAR 4.4-kb transcript was not detectable, and the 1.6-kb transcript was reduced by approximately 50% within 24 h of Cetrorelix treatment. The mature 30-kDa StAR protein level declined approximately 30% after Cetrorelix treatment. We conclude that 1) StAR mRNA and protein are highly expressed in early and midluteal phase CL; 2) StAR protein is present in both thecal-lutein and granulosa-lutein cells throughout the luteal phase; 3) StAR protein levels in the CL are highly correlated with plasma progesterone levels; 4) declining StAR mRNA and protein levels are characteristic of late luteal phase CL; and 5) suppression of LH levels during the midluteal phase results in a marked decline in plasma progesterone and a diminished abundance of StAR transcripts in the CL without a corresponding significant decline in StAR protein. Collectively, these data are consistent with the idea that StAR gene expression is a key determinant of luteal progesterone during the normal menstrual cycle. However, the pharmacologically induced withdrawal in the midluteal phase of LH support diminishes luteal progesterone output by mechanisms others than reduced StAR protein levels.

Structure and sequence of an intronless gene for human casein kinase II-alpha subunit.

Using sixteen different primers based on the cDNA sequence of the human casein kinase II-alpha subunit, different fragments of this gene were amplified by PCR from human genomic DNA. The sizes of these fragments were identical to amplified cDNA, which suggests the existence of an intronless genomic gene. The amplification was carried out on whole blood genomic DNA from three different individuals. The total sequence of the amplified casein kinase II-alpha gene showed more than 99% homology to the cDNA. The gene contains a noninterrupted open reading frame, as expected for the homolog cDNA. Although the gene sequence is complete, four point mutations were found. Since there are no interruptions of the open reading frame, this intronless gene might be expressed.

Interaction of protein synthesis initiation factor 2 from Xenopus laevis oocytes with GDP and GTP analogs.

The structural specificity of the purified protein synthesis initiation factor 2 (eIF-2) from X. laevis ovary towards analogs of GTP and GDP was studied. The relative affinity of the structural analogs was measured by their capacity to inhibit the formation of the [3H]GDP X eIF-2 binary complex. The results obtained demonstrate that modifications in the ribose moiety are well tolerated by eIF-2 which binds dGTP, 2',3'-dialdehyde GTP (oGTP) and 2',3'-dialdehyde GDP (oGDP) and even the dinucleotide cytidylyl(5'-3')guanosine 5'-triphosphate (pppGpC). Substitution in the polyphosphate chain by phosphorothioate groups in the beta and gamma positions (GDP beta S or GTP gamma S) does not abolish the affinity for the nucleotides and the presence of an imido group between the beta and gamma phosphates in guanyl-5'-yl imidodiphosphate (GppNHp) still permits a weaker but significant binding. Guanine 5'-O-(2-fluorodiphosphate) (GDP beta F) has an affinity considerably lower than GDP beta S. Methylation of position 7 of the guanine (7-m GDP), however, completely eliminates the interaction of GDP with eIF-2. The analogs tested can be listed in the following order of descending affinities: GDP greater than GDP beta S greater than oGDP greater than or equal to GTP gamma S greater than GDP beta F greater than pppGpC greater than GTP greater than GppNHp greater than oGTP much greater than 7-m GDP. Assays of the capacity of GTP analogs to form a ternary complex of the type met-tRNAi X GTP X eIF-2 or of GDP analogs to inhibit the formation of this complex reflect, in general, the same order of relative affinities except for pppGpC, which is weaker in its capacity to form a ternary complex than GppNHp or oGTP, although it has a higher affinity than these compounds in the formation of a binary complex.

Cloning of a Xenopus laevis muscarinic receptor encoded by an intronless gene.

The Xenopus laevis oocyte has endogenous sites that bind muscarinic agonists, which have been pharmacologically characterized as M3 and/or M1 receptor subtypes. In order to define the molecular identify of the receptor protein we have analyzed a Xenopus oocyte cDNA library and cloned a 2.9 kb cDNA fragment encoding a muscarinic receptor (xMR). The deduced amino acid sequence reveals a protein of 484 residues with an apparent molecular weight of 54,188 Da. Amino acid comparison with previously cloned mammalian muscarinic receptors showed a 78% identity with the human m4 subtype, presenting at the same time clustered differences within the amino-terminal region and third intracellular loop Genomic Southern analysis displayed the presence of one main gene belonging to this subtype, and the PCR analysis revealed an intronless gene.

Characterization of protein synthesis initiation factor 2 from Xenopus laevis oocytes.

The protein synthesis initiation factor 2 (eIF2) from Xenopus laevis oocytes has been extensively purified and characterized. Depending upon the purification scheme, eIF2 containing three subunits (alpha, beta and gamma) with Mr of 160,000, or two subunits (alpha and gamma) with Mr 90,000 can be obtained. The key step for obtaining the three subunit factor is the addition of 30 mM benzamidine to the initial homogenization, since this compound protects the highly sensitive beta subunit from proteolytic degradation. Subunit alpha of the oocyte eIF2 can be phosphorylated by the specific kinase from rabbit reticulocytes, whereas subunit beta is phosphorylated by oocyte casein kinase II. The oocyte eIF2 has a KD of 7.2 X 10(-8) M for GDP and 3.8 X 10(-6) M for GTP. The purified three subunit eIF2 has 0.4 mol of GDP bound/mol of factor. The crude preparations of eIF2 are not affected by Mg2+ in their exchange of guanine nucleotides or in the formation of ternary complexes with GTP and methionyl-tRNA, but these reactions are strongly inhibited by Mg2+ when the highly purified preparations are used.

Tc45, a dimorphic Trypanosoma cruzi immunogen with variable chromosomal localization, is calreticulin.

We demonstrate that Tc45, a polypeptide described as an immunogenetically restricted Trypanosoma cruzi antigen in mice, is calreticulin, a dimorphic molecule encoded by genes with variable chromosomal distribution. Previously we showed that IgG from A.SW (H2s) mice immunized with T. cruzi trypomastigotes or epimastigotes and sera from infected humans recognize Tc45, a 45 kD parasite polypeptide. Herein we describe the cloning, sequencing, and expression of the Tc45 gene. A 98% homology in the deduced amino acid sequence was found with a T. cruzi calreticulin-like molecule and 41% with Leishmania donovani and human calreticulin. In the T. cruzi CL Brener clone and in the Tulahuén strain, the gene is located in two and four chromosomes, respectively. Calreticulin was detected in several T. cruzi clones, in the Tulahuén strain, and in T. rangeli, displaying alternative 43 and 46 kD forms.

Physicochemical characterization of corticotrophin releasing factor receptor in rat pituitary and brain.

The physicochemical characteristics of solubilized crosslinked CRF receptor-ligand complexes were studied in the anterior and intermediate pituitary lobes and brain of the rat. In all tissues studied, there was a major labeled band with a molecular weight of 72 +2- 3.5 kDa, (n = 15), 71 +/- 1.3 (n = 6), 73 +2- 2.5 (n = 7) and 75 +2- 3.5 (n = 7) kDa in the anterior and intermediate lobes of the pituitary, amygdala and cerebral cortex, respectively. The density of this band was inhibited by CRF analogs, but not by unrelated peptides. This is consistent with the comparable binding properties of CRF in membrane preparations of these tissues. These results suggest that differences in receptor regulation and the reported ability of CRF to stimulate cAMP is due to differences in ligand receptor processing and coupling to membrane transduction systems, rather than to major differences in the binding protein.

Origin and evolutionary relationships of native Andean populations.

This paper represents an effort to explore the origin and the evolutionary relationships of native Andean populations using a multidisciplinary approach. Archeological and linguistic evidence is briefly reviewed. A genetic distance analysis among major linguistic groupings and among Andean and Amazonian native populations, together with information obtained from archaeological and linguistic sources was used to generate a migration model. It is suggested that in the late Pleistocene a group of nomadic hunters entered South America through the Isthmus of Panama and split afterwards into two groups, one moving southward into the central and south Andean areas and after crossing the Colombian, Equador and Peruvian highlands to people northwestern Argentina, the open park country of east Brazil and the Argentine Pampas. The second group migrated eastwards into Venezuela and Guyana and later southward, peopling the Brazilian Amazon. Following available waterways the Amazonian Indians expanded east and west arriving probably at the eastern slopes of the Andes some 3,500 years ago. It is hypothesized that present day Andean natives are descendants of the Amazonian groups that migrated eastwards.

Efecto terapéutico de los exosomas en el ACV isquémico en animales de experimentación / Therapeutic effect of exosomes on ischemic stroke in experimental animals

La posibilidad de que los exosomas funcionen como una nueva forma de comunicación intercelular para establecer y mantener circuitos cerebrales está comenzando a ser explorada. Los exosomas son liberados desde células e interactúan con otras células receptoras para mediar cambios fisiológicos. Todas las células cerebrales liberan exosomas incluyendo las celulas madre neuronales, las neuronas, astrocitos, microglia, oligodendrocitos y las celulas endoteliales. El objetivo de esta revisión es reunir evidencia actualizada sobre las funciones de protección, antiinflamación y regeneración de los exosomas en el ataque cerebrovascular (ACV) isquémico en ratas. Se realizó una búsqueda sistemática de la literatura sensible y específica en base de datos Medline, EMBASE, Web of Science, Scopus, TRIP database, SciELO y LILACS con términos libres y meSH. Los exosomas generados de CSMs pueden ser utilizados para el tratamiento del ACV. Los exosomas de oligodendrocitos también ejercen una variedad de efectos sobre las neuronas receptoras e influencian un amplio espectro de la fisiología neuronal. En conjunto estos resultados sugieren que los exosomas de las CSMs mediados con miR-133b se transfieren a astrocitos y neuronas, las que regulan la expresión génica, beneficiando tanto la remodelación de neuritas, como la recuperación funcional despues de un ACV. Sería importante en el futuro desarrollar métodos para cuantificar y caracterizar los exosomas en el cerebro con isquemia. Esto permitiría correlacionar entre la cantidad de exosomas en el cerebro y la recuperación funcional entregando información sobre sus mecanismos de acción.

The possibility that exosomes function as a new form of inter cellular communication to establish and maintain brain circuits is beginning to be investigated. Exosomes are released from cells and interact with other receptor cells to mediate physiological changes. All brain cells release exosomes including neural stem cells, neurons, astrocytes, microglia, oligodendrocytes and endothelial cells. The aim of this review is to gather current evidence on the protective, anti-inflammatory and regenerative functions of exosomes in ischemic stroke in rats. A systematic search of sensitive and specific literature was carried out in the following database search engines: Medline, EMBASE, Web of Science, Scopus, TRIP database, SciELO and LILACS with free and MeSH terms data. MSC generated exosomes can be used in the treatment of stroke. Oligodendrocyte exosomes also exert a variety of effects on receptor neurons and influence a wide spectrum of neuronal physiology. Together these results suggest that MSC exosome-mediated transfer of miR-133b to astrocytes and neurons, thus regulating gene expression, benefiting both neurite remodeling, such as functional recovery following a stroke. It would be important in the future to develop methods to quantify and characterize exosomes in brain ischemia. This would allow correlation between the amount of exosomes in the brain and functional recovery providing information relevant to its action mechanisms.

Oclusión de la arteria cerebral media en ataque cerebrovascular isquémico agudo / Middle cerebral artery occlusion in acute ischaemic cerebrovascular attack

El ataque cerebrovascular isquémico (ACV) es una de las principales causas de morbimortalidad a nivel mundial y nacional. Se estudiaron 35 pacientes identificándose que las arterias que presentaron mayor frecuencia de oclusión en el ACV isquémico agudo fueron la arteria cerebral media y la arteria cerebral posterior. Consideramos necesario que los especialistas puedan localizaran atómicamente los ACV para la aplicación de terapias neuroprotectoras mejorando las opciones de tratamiento y previniendo obstrucciones secundarias.

Ischaemic stroke (CVA) is one of the leading causes of morbidity and mortality at a global and national level. We studied 35 patients, determined the arteries that presented a higher frequency of occlusion in acute ischemic stroke and identified the middle cerebral artery and the posterior cerebral artery. We consider it necessary that specialists can locate anatomically strokes in order to apply neuroprotective therapies to improve treatment options and preventing secondary obstructions.

Estrés post-traumático post terremoto 27F en cuidadores de niños preescolares. Factores asociados del cuidador, de la familia y la crianza / Post-traumatic stress disorder after 27/F earthquake in caregivers of preschool children. Factors associated with the caregiver, family and parenting

Objetivos: Describir la frecuencia de estrés postraumático posterior al terremoto de Chile del 27 de febrero de 2010, en cuidadores de niños prescolares y su asociación con el reporte del desarrollo de los niños, como también de las actitudes respecto de la crianza. Metodología: El estudio fue ejecutado seis meses después de acontecido el terremoto. Se realizó un diseño transversal en 1.625 cuidadores de niños entre 30 y 48 meses, que recibían atención en centros de salud públicos. Se evaluó el trastorno mediante la escala auto-administrada de trauma de Davidson. Adicionalmente se midieron las características sociodemográficas, de salud física y mental de los cuidadores, el desarrollo de los niños y crianza. Resultados: La frecuencia del trastorno de estrés postraumático fue de 7,3%. No se encontraron asociaciones significativas entre estrés postraumático en el cuidador y desarrollo infantil. Hubo asociaciones estadísticamente significativas con funcionamiento familiar (p<0,05) y creencias coercitivas respecto de la educación de los niños (p < 0,05), entre otras. Conclusiones: La presencia de este trastorno en el cuidador podría ser un marcador de riesgo para el cuidado infantil, por lo que, resulta fundamental su detección y tratamiento tempranos post desastre mediante un abordaje familiar.

Objectives: To describe the PTSD frequency, following the February 27, 2010 (27-F) earthquake in Chile, in preschool caregivers and its association with child development reports and parenting attitudes. Methodology: The study was carried out six months after the earthquake. A cross-sectional survey design was performed in 1625 caregivers of children between 30 and 48 months old, who received care at public health centers. Disorders were evaluated by the self-administered Davidson trauma scale. Additionally, sociodemographic, physical and mental health of caregivers, child development and parenting characteristics were measured. Results: The frequency of PTSD was 7.3%. There were no significant associations between post-traumatic stress in the caregiver and child development. There were statistically significant associations with family functioning (p < 0.05) and enforced beliefs regarding the education of children (p < 0.05), among others. Conclusions: The presence of this disorder in the caregiver may be a risk marker for child care; therefore, after the disaster and through a familiar approach, detection and early treatment are essential.

Estrés post-traumático post terremoto 27F en cuidadores de niños preescolares: factores asociados del cuidador, de la familia y la crianza / Post-traumatic stress disorder (PTSD) after 27/F earthquake in caregivers of preschool children. Factors associated with the caregiver, family and parenting

Objectives: to describe the PTSD frequency, following the february 27, 2010 (27-F) earthquake in Chile, in preschool caregivers and its association with child development reports and parenting attitudes. Methodology: the study was carried out six months after the earthquake. A cross-sectional survey design was performed in 1625 caregivers of children between 30 and 48 months old, who received care at public health centers. Disorders were evaluated by the self-administered Davidson trauma scale. Additionally, sociodemographic, physical and mental health of caregivers, child development and parenting characteristics were measured. Results: the frequency of PTSD was 7.3 percent. There were no significant associations between post-traumatic stress in the caregiver and child development. There were statistically significant associations with family functioning (p < 0.05) and enforced beliefs regarding the education of children (p < 0.05), among others. Conclusions: the presence of this disorder in the caregiver may be a risk marker for child care; therefore, after the disaster and through a familiar approach, detection and early treatment are essential.

Objetivos: describir la frecuencia de estrés postraumático posterior al terremoto de Chile del 27 de febrero de 2010, en cuidadores de niños prescolares y su asociación con el reporte del desarrollo de los niños, como también de las actitudes respecto de la crianza. Metodología: el estudio fue ejecutado seis meses después de acontecido el terremoto. Se realizó un diseño transversal en 1.625 cuidadores de niños entre 30 y 48 meses, que recibían atención en centros de salud públicos. Se evaluó el trastorno mediante la escala auto-administrada de trauma de Davidson. Adicionalmente se midieron las características sociodemográficas, de salud física y mental de los cuidadores, el desarrollo de los niños y crianza. Resultados: la frecuencia del trastorno de estrés postraumático fue de 7,3 por ciento. No se encontraron asociaciones significativas entre estrés postraumático en el cuidador y desarrollo infantil. Hubo asociaciones estadísticamente significativas con funcionamiento familiar (p<0,05) y creencias coercitivas respecto de la educación de los niños (p < 0,05), entre otras. Conclusiones: la presencia de este trastorno en el cuidador podría ser un marcador de riesgo para el cuidado infantil, por lo que, resulta fundamental su detección y tratamiento tempranos post desastre mediante un abordaje familiar.