Heart rate regularisation in patients with permanent atrial fibrillation implanted with a VVI(R) pacemaker.

Irregularity of ventricular cycles is a cause of haemodynamic impairment and symptoms in patients with atrial fibrillation (AF). AIM OF THE STUDY: Aim of the study was to determine the optimal pacing rate to stabilise ventricular cycle length at rest in patients with chronic AF, bradycardiac symptoms and VVI pacing. METHODS: The compensatory pause (CP) in AF, as defined by Langendorf, was used as a reference value in pacing the heart. The spontaneous mean heart rate (MHR) was assessed with the PM OFF. The CP was then calculated with the pacing rate programmed at 40 bpm. Four pacing rates were tested: rate of the CP (RCP), RCP + 5 bpm, RCP - 5 bpm and RCP - 10 bpm. RESULTS: RCP provided a good estimate of the MHR (r = 0.92). Pacing percentage (P%) was 24 +/- 15% at the pacing rate of RCP - 10 bpm, 39 +/- 19% at RCP - 5 bpm, 63 +/- 17% at RCP, and 79 +/- 19% at RCP + 5 bpm (p < 0.001). The corresponding HR modestly increased from 65 +/- 13 bpm to 66 +/- 13 bpm (p = NS), 68 +/- 13 bpm (p < 0.001) and 71 +/- 13 bpm (p < 0.001), respectively. CONCLUSION: The RCP estimates, during pacing, what the spontaneous MHR would be. Ventricular stimulation at the RCP causes a high P%, stabilising cardiac cycles with a modest increase in HR.     

MiR-205 is downregulated in hereditary hemorrhagic telangiectasia and impairs TGF-beta signaling pathways in endothelial cells

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by arteriovenous malformations and hemorrhages. This vascular disease results mainly from mutations in 2 genes involved in the TGF-β pathway (ENG and ALK1) that are exclusively expressed by endothelial cells. The present study identified miR-27a and miR-205 as two circulating miRNAs differentially expressed in HHT patients. The plasma levels of miR-27a are elevated while those of miR-205 are reduced in both HHT1 and HHT2 patients compared to healthy controls. The role of miR-205 in endothelial cells was further investigated. Our data indicates that miR-205 expression displaces the TGF-β balance towards the anti-angiogenic side by targeting Smad1 and Smad4. In line, overexpression of miR-205 in endothelial cells reduces proliferation, migration and tube formation while its inhibition shows opposite effects. This study not only suggests that detection of circulating miRNA (miR-27a and miR-205) could help for the screening of HHT patients but also provides a functional link between the deregulated expression of miR-205 and the HHT phenotype.     

Self-perceived public health competency among recent dental graduates

The aim of this study was to assess the level of self-perceived competency in dental public health in recent graduates from the Faculty of Stomatology of the Universidad Peruana Cayetano Heredia. One hundred and nineteen graduates (28.6 percent males and 71.4 percent females) were asked to rate their self-perception of proficiency on each of the twenty-one dental public health functions identified in a dental practice competency matrix. Students assessed their competence in these dental public health functions using a three-point ordinal scale with 0 indicating "not at all competent," 1 indicating "competent," and 2 indicating "very competent." Males scored themselves higher than females for items concerning "design, develop, and evaluate community restorative interventions," "apply basic maintenance to dental equipment and instruments," and "participate in an epidemiological surveillance system." However, there were no significant differences for any item according to age. A confirmatory factorial analysis provided two factors with Eigenvalues greater than one (13.09 and 1.53, respectively), which explained 62.3 percent and 7.3 percent of the variance in the graduates' responses respectively. However, the fact that all twenty-one dental public health functions loaded higher than 0.55 on the first factor led to the conclusion that the dental public health competency is perceived by students to be a one-dimensional construct. Graduates perceived themselves as very competent for solving dental health needs at the community level. This study also provided further evidence in support of the rationale for the competency-based dental curriculum of the Faculty of Stomatology of the Universidad Peruana Cayetano Heredia.     

Estimating arch length discrepancy through Little's Irregularity Index for epidemiological use

The objective of this study was to evaluate the diagnostic capability of Little's Irregularity Index (LII) in order to estimate the arch length discrepancy (ALD) in a dental arch. Dental casts with a full permanent dentition, excluding third molars, from 200 12- to-16-year-old schoolchildren from a representative high school located in Lima, Peru, were used. Incisal irregularity was measured using the LII, whereas ALD was calculated as the difference between available and required space in each dental arch anterior to the first permanent molars. The receiver-operator characteristic (ROC) curve was used to contrast the LII with three different dichotomized ALDs and locate optimized cut-off points. Correlation between ALD and LII was -0.68 (P < 0.001). According to ROC curves, LIIs of 2.45, 4.00, and 4.55 mm were the optimized cut-off points to estimate negative ALDs higher than 0, 3, and 6 mm, respectively. LII's highest diagnostic capability was found for estimating negative ALD greater than 3 mm with a sensibility of 0.78 and a specificity of 0.76. Based on the present findings, LII could potentially be used in epidemiological surveys as a valid and less time-consuming measurement of crowding compared with ALD; however, further studies are needed to test the reliability of this approach in field settings.     

Dental morphology and crowding. A multivariate approach

The objective of this study was to compare, combined and individually, the mesiodistal (MD) and buccolingual (BL) tooth sizes as well as their respective crown proportions in the permanent dentition in dental arches with moderate, mild, and no crowding. Dental casts from two-hundred 12 to 16-year-old school children from a typical high school from Lima, Peru, were used. The MD and BL tooth sizes of all permanent teeth except second and third molars were measured, and their crown proportion (MD/BL ratio) was estimated. Each dental arch was classified as presenting moderate (-5.1 mm or more of discrepancy), mild (-0.1 and -5 mm of discrepancy), and no crowding (zero or a positive discrepancy). Combined and tooth-specific comparisons among the crowding groups for the tooth sizes as well as crown proportions were performed with a multivariate analysis of variance (MANOVA, using Wilks lambda). Combined MD tooth sizes and crown proportions differed among crowding groups. Subsequent individual comparisons indicated differences for MD tooth size of all upper teeth and for lower premolars and central incisors. Differences were also detected for crown proportions of the upper second premolar, canine, and both incisors; as well as for the lower first premolar, canine, and central incisor. No differences were found for the BL tooth sizes among crowding groups. MD tooth sizes and crown proportions from specific teeth are significantly different between dental arches with moderate, mild, and noncrowded arches. This study helps to understand the odontometric component of the dental crowding multifactorial origin.     

Neuronal regeneration partially compensates the delayed neuronal cell death observed in the hippocampal CA1 field of soman-poisoned mice

Soman poisoning induces long-term neuropathology characterized by the presence of damaged neurons up to 2 months after exposure in various central brain areas, especially the hippocampal CA1 layer. Rapid depletion of this layer could therefore be expected. Surprisingly, the CA1 layer remained consistently visible, suggesting delayed death of these damaged neurons, potentially accompanied by neuronal regeneration. To address this issue, mice were exposed to a convulsive dose of soman (110 microg/kg followed by 5.0mg/kg of atropine methyl nitrate (MNA) 1 min later) and brains were collected from day 1 to day 90 post-exposure. Damaged and residual healthy neurons were quantified on brain sections using hemalun-phloxin and fluorojade staining or neuronal nuclei antigen (NeuN) immunohistochemistry. On post-soman day 1, a moderate neuronal cell death was noticed in the hippocampal CA1 layer. In this area, an important and steady quantity of damaged neurons (about 48% of the whole pyramidal neurons) was detected from post-soman day 1 to day 30. Thus, throughout this period, damaged neurons seemed to survive, as confirmed by the unmodified depth of the hippocampal CA1 layer. The dramatic disappearance of the damaged neurons occurred only later during the experiment and was almost complete at day 90 after soman exposure. Interestingly, between day 30 and day 90 following poisoning, an increase in the number of residual healthy pyramidal neurons was observed. These different kinetic patterns related to the density of total, damaged and residual healthy neurons after soman poisoning demonstrate that neuronal regeneration is delayed in the hippocampal CA1 layer and is concomitant to the death of damaged neurons.     

A role for endoglin as a suppressor of malignancy during mouse skin carcinogenesis

Endoglin is a membrane glycoprotein that acts as a coreceptor for transforming growth factor-beta. We and others have previously suggested a function of endoglin as a tumor suppressor in epithelial cancer. Here, we study the expression of endoglin during chemical mouse skin carcinogenesis. We find that shedding of membrane endoglin, allowing the secretion of a soluble endoglin form, is a late event associated with progression from squamous to spindle cell carcinomas. Knockdown of endoglin in transformed keratinocytes activates the Smad2/3 signaling pathway resulting in cell growth arrest, delayed tumor latencies, and a squamous to spindle phenotypic conversion. Forced expression of the long endoglin isoform in spindle carcinoma cells blocks transforming growth factor-beta1 stimulation of Smad2/3 signaling and prevents tumor formation. In contrast, expression of the short endoglin isoform has no effect on spindle cell growth in vitro or in vivo. Our results show that endoglin behaves as a suppressor of malignancy during the late stages of carcinogenesis. Therefore, disruption of membrane endoglin emerges as a crucial event for progression to spindle cell carcinomas.