No seroconversion among healthcare workers exposed to SARS-CoV-2 during the early phase of the pandemic / Ausencia de seroconversión en trabajadores de la salud expuestos a SARS-CoV-2 durante la primera fase de la pandemia

BACKGROUND: The SARS-CoV-2 pandemic is associated with morbidity, hospitalizations, absenteeism, and mortality among healthcare workers (HCW). AIM: To evaluate the seroconversion rate in HCW exposed to SARS-CoV-2 in the early pandemic phase in 2020 at a regional reference hospital. MATERIAL AND METHODS: One hundred seventy-nine HCW working at a regional hospital were invited to a longitudinal study performed between April-July 2020. A serological analysis by ELISA IgG for viral nucleoprotein and protein S with a secondary analysis by ELISA IgG protein S1/S2 for samples with positive or doubtful result was carried out together with a complementary online survey to inquire about occupational or community exposures to SARS-CoV-2. RESULTS: Two cases with baseline infection were detected (1.1%, one symptomatic and one asymptomatic) and no cases of seroconversion were detected. During the study period, there were 136 patients hospitalized with COVID-19, and regional weekly COVID-19 incidence ranged from 2.7 to 24.4 per 100,000 inhabitants. No SARS-CoV-2 cases were detected by PCR among 27 HCW who consulted for respiratory symptoms in the period. Online surveys confirmed direct care of COVID-19 patients and also detected a high degree of unprotected social interaction at work. CONCLUSIONS: There was no evidence of seroconversion in this group of HCW exposed to the risk of infection by SARS-CoV-2 during the onset of the COVID-19 pandemic. Personal protective equipment and other measures used by the HCW were extremely useful for their protection in the initial phase of the pandemic.

ANTECEDENTES: La pandemia de SARS-CoV-2 está asociada a morbilidad, hospitalizaciones, ausentismo y mortalidad entre el personal de salud (PS). OBJETIVO: Evaluar la tasa de seroconversión en el PS expuesto al SARS-CoV-2 en la fase pandémica inicial el 2020 en un hospital regional de referencia. MATERIAL Y MÉTODOS: Ciento setenta y nueve trabajadores de la salud fueron invitados a un estudio longitudinal realizado entre abril-julio de 2020. Se efectuó un análisis serológico por ELISA IgG para nucleoproteína viral y proteína S con un análisis secundario por ELISA IgG proteína S1 / S2 para muestras con resultado positivo o dudoso junto a encuestas complementarias en línea para preguntar sobre exposiciones ocupacionales o comunitarias al SARS-CoV-2. RESULTADOS: Se detectaron dos casos con infección basal (1,1%, uno sintomático y uno asintomático) sin casos de seroconversión. Durante el período de estudio, hubo 136 pacientes hospitalizados con COVID-19, y la incidencia semanal regional de COVID-19 osciló entre 2,7 y 24,4 por 100.000 habitantes. No se detectaron casos de SARS-CoV-2 por PCR entre los 27 funcionarios que consultaron por síntomas respiratorios en este período. Las encuestas en línea confirmaron la atención directa de los pacientes con COVID-19 y también detectaron un alto grado de interacción social desprotegida en el trabajo. CONCLUSIONES: No hubo evidencia de seroconversión en un grupo de funcionarios expuestos al riesgo de infección por SARS-CoV-2 durante el inicio de la pandemia de COVID-19. Los equipos de protección personal y otras medidas utilizadas por el PS fueron de suma utilidad para su protección en la fase inicial de la pandemia.

Prolactin Attenuates Neuroinflammation in LPS-Activated SIM-A9 Microglial Cells by Inhibiting NF-κB Pathways Via ERK1/2.

Prolactin (PRL) is a pleiotropic hormone with multiple functions in several tissues and organs, including the brain. PRL decreases lesion-induced microgliosis and modifies gene expression related to microglial functions in the hippocampus, thereby providing a possible mechanism through which it might participate in neuroimmune modulatory responses and prevent neuronal cell damage. However, the direct contribution of microglial cells to PRL-mediated neuroprotection is still unclear and no studies have yet documented whether PRL can directly activate cellular pathways in microglial cells. The aim of this study is to elucidate in vitro actions of PRL on the immortalized SIM-A9 microglia cell line in basal and LPS-stimulated conditions. PRL alone induced a time-dependent extracellular signal-regulated kinase 1/2 (ERK1/2) activation. Pretreatment with PRL attenuated LPS (200 ng/ml) stimulated pro-inflammatory markers: nitric oxide (NO) levels, inducible nitric oxide synthase (iNOS), interleukins (IL)-6, -1ß and tumor necrosis factor (TNF-α) expression at 20 nM dosage. PRL suppressed LPS-induced nuclear factor (NF)-κappaB (NF-κB) p65 subunit phosphorylation and its upstream p-ERK1/2 activity. In conclusion, PRL exhibits anti-inflammatory effects in LPS-stimulated SIM-A9 microglia by downregulating pro-inflammatory mediators corresponding to suppression of LPS-activated ERK1/2 and NF-κB phosphorylation.

Sexually dimorphic effects of prolactin treatment on the onset of puberty and olfactory function in mice.

The onset of puberty is associated with the psychophysiological maturation of the adolescent to an adult capable of reproduction when olfactory signals play an important role. This period begins with the secretion of the gonadotropin-releasing hormone (GnRH) from GnRH neurons within the hypothalamus. This is regulated by kisspeptin neurons that express high levels of transmembrane prolactin receptors (PRLR) that bind to and are activated by prolactin (PRL). The elevated levels of serum PRL found during lactation, or caused by chronic PRL infusion, decreases the secretion of gonadotropins and kisspeptin and compromised the estrous cyclicity and the ovulation. In the present work, we aimed to evaluate the effects of either increased or decreased PRL circulating levels within the peripubertal murine brain by administration of PRL or treatment with cabergoline (Cab) respectively. We showed that either treatment delayed the onset of puberty in females, but not in males. This was associated with the augmentation of the PRL receptor (Prlr) mRNA expression in the arcuate nucleus and decreased Kiss1 expression in the anteroventral periventricular zone. Then, during adulthood, we assessed the activation of the mitral and granular cells of the main (MOB) and accessory olfactory bulb (AOB) by cFos immunoreactivity (ir) after the exposure to soiled bedding of the opposite sex. In the MOB, the PRL treatment promoted an increased cFos-ir of the mitral cells of males and females. In the granular cells of male of either treatment an augmented activation was observed. In the AOB, an impaired cFos-ir was observed in PRL and Cab treated females after exposure to male soiled bedding. However, in males, only Cab impaired its activation. No effects were observed in the AOB-mitral cells. In conclusion, our results demonstrate that PRL contributes to pubertal development and maturation of the MOB-AOB during the murine juvenile period in a sex-dependent way.

Fatherhood diminishes the hippocampal damaging action of excitotoxic lesioning in mice.

Parental experience imposes neuroplasticity in the hippocampus of females and males. In lactating rat dams, the hippocampus is protected against excitotoxic damage by kainic acid lesioning, although it is still unknown whether paternity can provide such protection to male rodents. To evaluate the protective effects of fatherhood against excitotoxic lesions, we paired male mice with females and co-housed them until the day of parturition (PPD0), when we randomly assigned them to two groups: (i) the pregnancy group (males housed individually overnight and injected i.c.v. with 100 ng per 1 µL of kainic acid or vehicle on PPD1) and (ii) the sire group (males housed with the dam and pups until PPD8, when injected i.c.v. after evaluation of parental behaviour). Individually housed virgin adult male mice formed the control group. Markers of neurodegeneration (NeuN, Fluoro-Jade C) and astrogliosis (glial fibrillary acidic protein) were evaluated in fixed cerebral tissue containing the dorsal CA1, CA3 and CA4 hippocampal subfields. The CA1 subfield did not suffer damage in any of the experimental groups. The sire group exhibited less neurodegeneration and astrogliosis in the CA3 and CA4 subfields compared to their respective controls, independently of the expression of parental behaviour. Western blot analysis was conducted for prolactin (PRL), PRL receptor and related intracellular pathways. Monomeric PRL was lower in the hippocampus of sires in the first week postpartum with a parallel rise of a 48-kDa dimerised isoform compared to virgin controls. The long isoform of PRL receptor did not change, and signal transducer and activator of transcription 5 (STAT5) was not detected in the hippocampus. However, a sustained rise in pAkt, a signalling molecule that participates in cell survival, was observed in the sire group. These results indicate that the hippocampus of sires housed with the dam and pups is less sensitive to neurotoxic injury, which might not be primarily regulated by PRL-STAT5-modulated mechanisms.

Anorexia increases microglial density and cytokine expression in the hippocampus of young female rats.

Anorexia by osmotic dehydration is an adaptive response to hypernatremia and hyperosmolaemia induced by ingestion of a hypertonic solution. Dehydration-induced anorexia (DIA) reproduces weight loss and avoidance of food, despite its availability. By using this model, we previously showed increased reactive astrocyte density in the rat dorsal hippocampus, suggesting a pro-inflammatory environment where microglia may play an important role. However, whether such anorexic condition increases a pro-inflammatory response is unknown. The aim of this study was to test if DIA increases microglial density in the dorsal hippocampus, as well as the expression of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin 1 beta (IL-1ß) in the hippocampus of young female rats. Our results showed that DIA significantly increased microglial density in CA2-CA3 and dentate gyrus (DG) but not in CA1. However, forced food restriction (FFR) only increased microglial density in the DG. Accordingly, the activated/resting microglia ratio was significantly increased in CA2-CA3 and DG, in DIA and FFR groups. Finally, western blot analysis showed increased expression of IBA1, TNF-α, IL-6 and IL-1ß in the hippocampus of both experimental groups. We conclude that anorexia triggers increased reactive microglial density and expression of TNF-α, IL-6 and IL-1ß; this environment may result in hippocampal neuroinflammation.

Prolactin released in vitro from the pituitary of lactating, pregnant, and steroid-treated female or male rats stimulates prolactin secretion from pituitary lactotropes of male rats.

We have previously shown that soluble factor(s) in conditioned media (CM) from the central and peripheral regions of the anterior pituitary (AP) gland of lactating rats promoted the in vitro dose-related release of prolactin (PRL) from pituitary glands of male rats. In the present experiments we sought to determine whether CM from rats in different physiological states provoked similar effects (like those of lactating rats), and the nature of the factors, whether 23K PRL or other variants of the hormone, were responsible for these effects. Stimulatory effects were induced by CM from pregnant females and steroid-treated castrated males or females, but not from untreated castrated rats, intact males, or by a PRL standard. More potent effects occurred with CM from APs of early- than from mid- or late-lactating rats, and from rats unsuckled for 8 or 16 h than from those unsuckled for 32 h. With respect to the nature of factor(s) responsible for these effects, immunoprecipitation of PRL from the CM of lactating females and of steroid-treated, castrated males eliminated, whereas dephosphorylation or deglycosylation of CM of lactating rats greatly increased its effects upon PRL release. Also, electrophoretic analysis and Western blotting of the CM proteins under native and denaturing conditions revealed a variety of PRL variants, ranging from 14 to <90 kDa, in CM from lactating rats, and the main effects on PRL release were provoked by the 23- to 46-kDa PRL variants. These results indicate that specific effects upon male rat lactotropes may be exerted by PRL variants released from APs of lactating and non-lactating rats.

[Clinical guideline for the diagnosis and treatment of subclinical thyroid dysfunction in pregnancy. Working Group on Subclinical Thyroid Dysfunction of the Spanish Endocrinology Society]. / Guía clínica para el diagnóstico y el tratamiento de la disfunción tiroidea subclínica en la gestación. Grupo de Trabajo sobre la Disfunción Tiroidea Subclínica de la Sociedad Española de Endocrinología.

Subclinical thyroid disease is a biochemical diagnosis and is common during pregnancy. Because of the physiological hormonal changes that take place during pregnancy and the absence of normal ranges for thyroid hormones during this period, subclinical thyroid disease is difficult to interpret during pregnancy. Subclinical hyperthyroidism during pregnancy has few clinical consequences and no treatment is required. In contrast, subclinical hypothyroidism seems to improve with thyroxine treatment. Iodine supplements during pregnancy and lactation, even in iodine-sufficient areas, are also indicated.

Estrogen receptors increased expression during hippocampal neuroprotection in lactating rats.

Estrogen receptor (ER)-mediated neuroprotection has been demonstrated in both in vitro and in vivo model systems. Two types of estrogen receptors, ERalpha and ERbeta, are the major mediators of the biological functions of estrogens. In the hippocampus, ERbeta is prevalent over ERalpha. Recently, we reported that during the final phase of lactation there is a neuroprotective mechanism in the hippocampus of the adult female rat against neuronal damage induced by systemic kainic acid administration vs. virgin (metestrus) rats. In this study, we assessed differential ER expression and localization in CA1, CA3 and dentate gyrus regions of dorsal hippocampus of metestrus and lactating adult rats at day 19 of lactation, during basal conditions (metestrus and L19, respectively) and 24h after systemic kainate administration. ERs were assessed by western blot and immunohistochemistry. We found a significant increase in the expression of ERs in the hippocampus during lactation as compared with metestrus. ERbeta was significantly increased in the CA1 and CA3 of lactating rats after the kainic acid insult. In addition, we observed a relocalization of ERbeta from the cytoplasm to the nucleus of neuronal cells. Our results suggest that there is a strong correlation between expression of ERs, especially ERbeta, in lactating CA1 and CA3 hippocampus regions in response to kainate administration, and neuroprotection observed during this reproductive period. This may be one of the mechanisms involved in the protection of the maternal brain to ensure offspring survival.

Fos expression induced by milk ingestion in the caudal brainstem of neonatal rats.

Prominent Fos expression in the nucleus of the solitary tract (NTS) related to feeding has been reported in the brainstem of adult animals. In this study, we used a Fos-guided immunohistochemical approach to determine the brainstem areas activated specifically in response to milk ingestion in rat pups at two different ages. Rats at 9 or 18 days postpartum were isolated from the mother for a 6-h period, after which they were returned to the mother for a suckling period of either 5 or 90 min and then perfused at 90 min after the beginning of suckling. Control groups were sacrificed before or after the 6-h-deprivation period and showed little or no Fos-ir. In contrast, a 90-min-suckling episode after 6 h of deprivation induced strong Fos-ir in the caudal regions of the NTS and in the spinal nucleus of the trigeminal (SPV). Moderate expression was observed in the rostral NTS and in the nucleus raphé obscurus. In rat pups that suckled for only 5 min, the main area activated was the SPV. Fos immunostaining was detected in only 1% of the catecholaminergic neurons from the NTS after milk ingestion. The experimental design employed here allowed us to distinguish brainstem areas activated by milk ingestion from those activated by suckling action in rat pups. In contrast to adult rats, catecholaminergic neurons from the caudal NTS seem to contribute little to the regulation of feeding at this age.

Suckling-induced oxytocin increase in the spinal cord of the rat.

Oxytocin (OT) is essential for parturition and milk ejection, and OT-containing fibers are present in several regions of the brain and in the spinal cord. During lactation, activation of spinal cord neurons by suckling stimulation involves deep laminae III-X including sympathetic preganglionic neurons of the intermedio-medial cell column. In the present study, experiments were designed to determine if the suckling provided by the litter increased OT levels in the spinal cord of dams, as determined by competitive immunoassay. In addition, we investigated if OT fibers reach neurons of the spinal cord that are known to respond to suckling. The OT content was higher in the hypothalamus than in the spinal cord in animals from all experimental groups. After 6 h of pup separation, OT levels decreased and suckling for 5 min induced a significant increase of OT levels in the spinal cord. Double immunostaining for Fos and OT showed OT-positive fibers adjacent to neurons that had Fos-positive nuclei, located mostly in laminae III, IV, and X. The present data support the notion that OT is released within the spinal cord in response to suckling, suggesting a role for this peptide in modulating the afferent and/or efferent responses generated by suckling.

Vesicular release of prolactin from preformed prolactin granules is stimulated by soluble factor(s) from the anterior pituitary of lactating rats.

This study demonstrates that conditioned media (CM) from the anterior pituitary gland (AP) of lactating rats contains soluble factors that promote in vitro prolactin (PRL) release from the pituitary glands of male rats. CM-induced PRL release was confirmed by polyacrylamide gel electrophoresis, ELISA and bioassay. In cultured AP cells challenged with CM, increased intracellular staining with the dye FM1-43 was observed, suggesting vesicular PRL release and subsequent endocytosis. The percentage and hormone content of PRL-containing cells but not of growth hormone-containing cells increased in cultured male AP cells when exposed to CM. When the release of PRL, prelabeled with [3H] leucine for 30 min to 24 h was examined, no stimulatory effect of CM was observed, suggesting that released PRL originates from hormone synthesized more than 24 h earlier. Accordingly, the PRL content of mature granules from male pituitary tissues decreased after CM treatment. These findings were confirmed by electron microscopy immunogold PRL labeling. Treatment with inhibitors of protein synthesis or vesicle trafficking between the endoplasmic reticulum and the Golgi complex did not prevent the stimulatory effect of CM on PRL release. However, blockage of traffic to the plasma membrane completely abolished the effect of CM. These results suggest that CM from the AP of lactators contains soluble factor(s) capable of inducing rapid vesicular release of PRL in the male AP, which originates from preformed, mature granules by mechanisms independent of protein synthesis.

Enhanced inhibitory avoidance learning prevents the memory-impairing effects of post-training hippocampal inactivation.

Rats were trained on an inhibitory avoidance task to study the effects of post-training administration of tetrodotoxin (TTX, which temporarily inactivates neural activity) on memory consolidation. During training, independent groups of rats received either a mild foot shock (0.8 mA) or a stronger (1.0 mA) foot shock. TTX was administered bilaterally into the dorsal hippocampus immediately after training, and memory of the task was measured 48 h later. We corroborated the typical amnesic effect of intrahippocampal infusions of TTX in those rats trained with the mild-intensity foot shock. More importantly, with the stronger foot shock, the same treatment was ineffective in producing amnesia. These results suggest that, after an enhanced learning experience, other brain regions are also activated, which may compensate for the amnesic effect of TTX infusions into the hippocampus.

Progesterone receptor gene and protein expression in the anterior preoptic area and hypothalamus of defeminized rats.

Progesterone receptor (PR) plays an important role during sexual differentiation of the rat brain. The objective of the present study was to determine PR protein and gene expression pattern in preoptic-anterior hypothalamic area (POA-AHA) and hypothalamus (HYP), after estradiol or testosterone treatment during the postnatal critical period of sexual differentiation of the rat brain (defeminized animals). Three-day-old female rats were subcutaneously (s.c.) injected with a single dose of 17beta-estradiol (200 microg), or testosterone enanthate (200 microg), or vehicle (corn oil). POA-AHA and HYP were dissected 3 h, 24 h, and 14 days, as well as on the day of vaginal opening (VO) after treatments. Other animals, previously treated as above, were acutely injected with 17beta-estradiol (5 microg) on the day of VO; POA-AHA and HYP were obtained 3 h later. Total RNA was extracted and processed for semiquantitative RT-PCR and tissue slices were prepared for protein detection by immunohistochemistry. We observed that PR mRNA expression was increased in POA-AHA and HYP of the animals treated with estradiol or testosterone 3 hours after treatments, compared with the vehicle-treated control group. We also found a significant increase in PR mRNA and protein expression in POA-AHA and HYP on the day of VO in both estradiol and testosterone defeminized rats. Interestingly, the acute administration of estradiol on the day of VO (VO + E(2)) did not increase PR mRNA or protein expression in POA-AHA and HYP of either estradiol or testosterone defeminized animals, as opposed to the marked induction observed in the intact animals of the control group. The overall results suggest that estradiol and testosterone treatment during the postnatal critical period of sexual differentiation of the brain modifies the regulation of the PR mRNA and protein expression during early onset of maturity.

Suckling-induced activation of neural c-fos expression at lower thoracic rat spinal cord segments.

Suckling stimulation is essential for neuroendocrine and sympathetic reflex activation during lactation. In the present study, the induction of c-fos gene expression was used to identify neuronal populations in the spinal cord activated by acute 5 min suckling or by electrical stimulation of the central stump of the first abdominal mammary nerve in lactating rats previously separated from their litters for 6 or 18 h. In addition, to investigate whether spinal sympathetic preganglionic neurons are activated by suckling, dual immunostaining (Fos and choline acetyltransferase) was performed. Fos was expressed at low levels in continuously suckled and 6 h nonsuckled mothers, but no expression was found after 18 h of nonsuckling. On the other hand, in 6 h nonsuckled rats, significant increments in Fos expression occurred in several regions after acute suckling and after electrical stimulation. Also, the pattern of Fos expression in each spinal laminae was different for the two stimuli, i.e. more intense effects of suckling in deep laminae V-X and more intense effects in laminae I-IV with electrical stimulation. Double-labeling after suckling was found only in sympathetic preganglionic neurons from the intermedio-medial cell column, whereas after electrical stimulation, double label was observed only in neurons from the intermedio-lateral cell column. On the other hand, no effect upon Fos protein expression was observed after suckling and only a minor effect after electrical stimulation of mammary nerve in 18 h nonsuckled rats. These results are consistent with previous findings on the sympathetic reflex regulation of the mammary gland, as well as on the importance of the nonsuckling interval for optimal functioning of lactation.

The insulin-like growth factor binding proteins in uncultured human cartilage: increases in insulin-like growth factor binding protein 3 during osteoarthritis.

OBJECTIVE: To assess changes in the insulin-like growth factor binding proteins (IGFBPs) in uncultured cartilage during stages of osteoarthritis (OA), and to determine if OA cartilage is capable of autocrine secretion of IGFBPs. METHODS: Articular cartilage was dissected from fibrillated and nonfibrillated sites of 11 human femoral heads, and extracted in buffer containing 8M urea. IGFBPs were identified by immunoprecipitation and subsequent analysis by (125)I-IGF-2 Western ligand blotting (WLB), radioimmunoassay, or 2-site immunoradiometric assay (IRMA). IGFBPs were assessed in cartilage extracts by WLB. IGFBP-3 content was determined by IRMA and synthesis by metabolic labeling with (35)S-cysteine in organ cultures. RESULTS: Sample grouping into 3 distinct OA strata was supported by gross pathology of the femoral heads, histologic grading of cartilage slices, and biochemical analysis of the glycosaminoglycan and protein content of the extracts. Group I was normal/mild OA, group II was intermediate OA, and group III was severe OA. IGFBP-2 was present in all samples, IGFBP-4 in sporadic samples, and BP-3 in group II-III samples. By IRMA, group I had a mean +/- SD of 6.26 +/- 2.6 ng IGFBP-3/mg soluble protein (IGFBP-3) (n = 6), group II had a mean +/- SD 14 +/- 7.5 IGFBP-3 (n = 10), and group III had a mean +/- SD 17.03 +/- 8.94 IGFBP-3 (n = 6). Analysis of variance showed group differences (F[3,19] = 3.84, P = 0.04), and post hoc tests revealed that IGFBP-3 levels were higher for group III versus group I (P = 0.04). OA cartilage synthesized IGFBP-3. CONCLUSION: Increases in net cartilage content of IGFBP-3 occurred in intact OA cartilage, reaching statistically significant elevation in severe disease. There was autocrine IGFBP-3 production in OA cartilage.

Sistema de vigilancia de las complicaciones neurológicas de la parotiditis en Cuba / System for the surveillance of neurologic complications due to parotiditis in Cuba

Se describe el comportamiento de la morbilidad por parotiditis en los últimos 25 años. Se precisa el porcentaje de complicaciones neurológicas en el país durante los 3 años en conjunto desde 1982 a 1984. Las complicaciones neurológicas de las parotiditis son más frecuentes en el sexo masculino que en el femenino; esta diferencia es más marcada en los niños que en los adultos. El grupo de edad de mayor riesgo lo constituye el de 5 a 9 años. Las complicaciones se producen con más frecuencia durante los meses de febrero a junio

Normas de la escala de Wechsler para preprimaria en niños de 5 años de Ciudad Habana / Wechsler scale patterns for kinder-garten children of 5 years old of Habana City

Se aplicó el Test de WPPSI a una muestra representativa de 89 niños (44 varones y 45 hembras) del Municipio Playa de Ciudad Habana. Se siguieron las normas y procedimientos de puntuación establecidos por Wechsler. La media obtenida en la Escala Global fue de 100 y la desviación standard de 18. La media del CI Verbal fue de 101, con desviación standard de 16. La media del CI Ejecutivo fue de 100, con una desviación de 19 puntos. No hubo diferencias significativas entre las medidas de nuestra muestra y las proporcionadas por el autor del Test. El número de niños con diferencias entre escalas de 15 puntos o más fue de 30. De estos casos, sólo uno fue diagnosticado Perturbación Simple de la Actividad y de la Atención. Los otros 2 niños diagnosticados D.C.M. en la muestra, tenían diferencias entre escalas de 3 y 4 puntos. Estos resultados apoyan los obtenidos en un trabajo anterior de los mismos autores y en trabajos recientes de otros investigadores. Se dan los índices de Bannatyne obtenidos para esta muestra y se hacen consideraciones sobre su utilidad