Hearing Loss and Sixth Cranial Nerve Paresis after COVID-19.

An 80-year-old patient was admitted to the internal medicine department for binocular diplopia and hearing loss with sudden onset. The patient had presented with SARS-CoV-2 infection 3 weeks previously and had been admitted to hospital. Complete work-up including autoimmunity, serum and LCR viral serology and MRI did not allow a diagnosis to be established. The hypothesis of a microvascular origin or the previous SARS-CoV-2 infection was considered. The latter was retained in light of the temporal relationship, the absence of other pathologies after exhaustive work-up, and the clinical evolution. LEARNING POINTS: A temporal relationship between SARS-CoV-2 infection and symptoms in the absence of other pathologies is important for diagnosis.Mid or long-term follow-up is necessary in patients with unexplained symptoms after SARS-CoV-2 infection.

αN-Acetyl ß-Endorphin Is an Endogenous Ligand of σ1Rs That Regulates Mu-Opioid Receptor Signaling by Exchanging G Proteins for σ2Rs in σ1R Oligomers.

The opioid peptide ß-endorphin coexists in the pituitary and brain in its αN-acetylated form, which does not bind to opioid receptors. We now report that these neuropeptides exhibited opposite effects in in vivo paradigms, in which ligands of the sigma type 1 receptor (σ1R) displayed positive effects. Thus, αN-acetyl ß-Endorphin reduced vascular infarct caused by permanent unilateral middle cerebral artery occlusion and diminished the incidence of N-methyl-D-aspartate acid-promoted convulsive syndrome and mechanical allodynia caused by unilateral chronic constriction of the sciatic nerve. Moreover, αN-acetyl ß-Endorphin reduced the analgesia of morphine, ß-Endorphin and clonidine but enhanced that of DAMGO. All these effects were counteracted by ß-Endorphin and absent in σ1R-/- mice. We observed that σ1Rs negatively regulate mu-opioid receptor (MOR)-mediated morphine analgesia by binding and sequestering G proteins. In this scenario, ß-Endorphin promoted the exchange of σ2Rs by G proteins at σ1R oligomers and increased the regulation of G proteins by MORs. The opposite was observed for the αN-acetyl derivative, as σ1R oligomerization decreased and σ2R binding was favored, which displaced G proteins; thus, MOR-regulated transduction was reduced. Our findings suggest that the pharmacological ß-Endorphin-specific epsilon receptor is a σ1R-regulated MOR and that ß-Endorphin and αN-acetyl ß-Endorphin are endogenous ligands of σ1R.

The σ1 Receptor and the HINT1 Protein Control α2δ1 Binding to Glutamate NMDA Receptors: Implications in Neuropathic Pain.

Nerve injury produces neuropathic pain through the binding of α2δ1 proteins to glutamate N-methyl-D-aspartate receptors (NMDARs). Notably, mice with a targeted deletion of the sigma 1 receptor (σ1R) gene do not develop neuropathy, whereas mice lacking the histidine triad nucleotide-binding protein 1 (Hint1) gene exhibit exacerbated allodynia. σ1R antagonists more effectively diminish neuropathic pain of spinal origin when administered by intracerebroventricular injection than systemically. Thus, in mice subjected to unilateral sciatic nerve chronic constriction injury (CCI), we studied the participation of σ1Rs and HINT1 proteins in the formation of α2δ1-NMDAR complexes within the supraspinal periaqueductal gray (PAG). We found that δ1 peptides required σ1Rs in order to interact with the NMDAR NR1 variant that contains the cytosolic C1 segment. σ1R antagonists or low calcium levels provoke the dissociation of σ1R-NR1 C1 dimers, while they barely affect the integrity of δ1-σ1R-NR1 C1 trimers. However, HINT1 does remove δ1 peptides from the trimer, thereby facilitating the subsequent dissociation of σ1Rs from NMDARs. In σ1R-/- mice, CCI does not promote the formation of NMDAR-α2δ1 complexes and allodynia does not develop. The levels of α2δ1-σ1R-NMDAR complexes increase in HINT1-/- mice and after inducing CCI, degradation of α2δ1 proteins is observed. Notably, σ1R antagonists but not gabapentinoids alleviate neuropathic pain in these mice. During severe neuropathy, the metabolism of α2δ1 proteins may account for the failure of many patients to respond to gabapentinoids. Therefore, σ1Rs promote and HINT1 proteins hinder the formation α2δ1-NMDAR complexes in the PAG, and hence, the appearance of mechanical allodynia depends on the interplay between these proteins.

Frostbite and Cold Agglutinin Disease: Coexistence of Two Entities Leading to Poor Clinical Outcomes.

An 83-year-old woman was admitted to the emergency department for a 7-day history of fatigue and progressive cyanosis in the feet and hands after cold exposure despite physical protective measures. Upon arrival, the patient presented with necrotic cutaneous lesions in both hands and distal lower extremities. Upon admission, hemoglobin was 7.6 g/dL and laboratory tests were consistent with cold agglutinin disease (CAD), the presence of monoclonal IgM, and flow cytometry consistent with lymphoplasmacytic lymphoma, but MYD88 L265P mutation was negative. The patient required blood transfusion, resulting in stabilized hemoglobin and a decrease in markers of hemolysis. Treatment with aspirin 250 mg daily and intravenous iloprost 0.5 mL/h was initiated with a poor clinical response at day 4. Amputation was required. Plasma exchange was performed and chemotherapy with rituximab and bendamustine was initiated. The clinical course was marked by further necrosis, prompting discussions regarding an additional amputation that was not performed considering the high surgical risk and refusal by the patient. Supportive treatment was initiated, and the patient expired one month after hospital admission.

Spinal Cord Compression Secondary to a Spontaneous Spinal Haematoma in a Patient Newly Treated with Rivaroxaban.

A 74-year-old patient anticoagulated with rivaroxaban for chronic atrial fibrillation presented to the emergency department with acute lumbar pain with progressive weakness of the lower limbs and inability to stand up. No previous trauma was reported. Neurological examination was consistent with a complete spinal cord syndrome at the level of T6. Magnetic resonance imaging showed the presence of spinal cord compression associated with signs of extensive intramedullary inflammation secondary to a haematoma. The patient underwent thoracic laminectomy with evacuation of an intradural haematoma. No intraoperative complications were described, but no clinical improvement had been achieved 15 days after the surgical intervention. LEARNING POINTS: Apixaban could be preferred as the first choice for direct oral anticoagulation (DOAC) in older patients.DOACs can have important side effects even if the switch from vitamin K antagonist to this group is correctly carried out.

Acute Confusional State Revealing Moyamoya Disease in the Emergency Department: A Rare Entity.

A 54-year-old woman was admitted to the emergency department for an acute, fluctuating altered mental status and reduced perceptual awareness of her surroundings as well as disorganized thinking. Blood tests, including for drugs, were normal. A CT scan of the brain was normal. Magnetic resonance imaging and CT angiography of the supra-aortic vessels were both were consistent with moyamoya disease. The patient was hospitalized for further investigations. LEARNING POINTS: Moyamoya disease should be considered in the differential diagnosis of middle-aged patients presenting with an acute confusional state of unknown aetiology in the emergency department.The absence of focal examination findings does not exclude neurological disease as the cause of acute confusion, requiring further neuroimaging tests.

Human HINT1 Mutant Proteins that Cause Axonal Motor Neuropathy Exhibit Anomalous Interactions with Partner Proteins.

The 14 kDa histidine triad nucleotide-binding protein 1 (HINT1) is critical to maintain the normal function of motor neurons. Thus, a series of human HINT1 mutants cause autosomal recessive axonal neuropathy with neuromyotonia. HINT1 establishes a series of regulatory interactions with signaling proteins, some of which are enriched in motor neurons, such as the type 1 sigma receptor or intracellular domain (ICD) of transmembrane teneurin 1, both of which are also implicated in motor disturbances. In a previous study, we reported the capacity of HINT1 to remove the small ubiquitin-like modifier (SUMO) from a series of substrates and the influence of HINT1 mutants on this activity. We now report how human HINT1 mutations affect the interaction of HINT1 with the regulator of its SUMOylase activity, calcium-activated calmodulin, and its substrate SUMO. Moreover, HINT1 mutants exhibited anomalous interactions with G protein coupled receptors, such as the mu-opioid, and with glutamate N-methyl-D-aspartate receptors as well. Additionally, these HINT1 mutants showed impaired associations with transcriptional regulators such as the regulator of G protein signaling Z2 protein and the cleaved N-terminal ICD of teneurin 1. Thus, the altered enzymatic activity of human HINT1 mutants and their anomalous interactions with partner proteins may disrupt signaling pathways essential to the normal function of human motor neurons.

Calmodulin Supports TRPA1 Channel Association with Opioid Receptors and Glutamate NMDA Receptors in the Nervous Tissue.

Transient receptor potential ankyrin member 1 (TRPA1) belongs to the family of thermo TRP cation channels that detect harmful temperatures, acids and numerous chemical pollutants. TRPA1 is expressed in nervous tissue, where it participates in the genesis of nociceptive signals in response to noxious stimuli and mediates mechanical hyperalgesia and allodynia associated with different neuropathies. The glutamate N-methyl-d-aspartate receptor (NMDAR), which plays a relevant role in allodynia to mechanical stimuli, is connected via histidine triad nucleotide-binding protein 1 (HINT1) and type 1 sigma receptor (σ1R) to mu-opioid receptors (MORs), which mediate the most potent pain relief. Notably, neuropathic pain causes a reduction in MOR antinociceptive efficacy, which can be reversed by blocking spinal NMDARs and TRPA1 channels. Thus, we studied whether TRPA1 channels form complexes with MORs and NMDARs that may be implicated in the aforementioned nociceptive signals. Our data suggest that TRPA1 channels functionally associate with MORs, delta opioid receptors and NMDARs in the dorsal root ganglia, the spinal cord and brain areas. These associations were altered in response to pharmacological interventions and the induction of inflammatory and also neuropathic pain. The MOR-TRPA1 and NMDAR-TRPA1 associations do not require HINT1 or σ1R but appear to be mediated by calcium-activated calmodulin. Thus, TRPA1 channels may associate with NMDARs to promote ascending acute and chronic pain signals and to control MOR antinociception.

The Sigma 2 receptor promotes and the Sigma 1 receptor inhibits mu-opioid receptor-mediated antinociception.

The Sigma-1 receptor (σ1R) has emerged as an interesting pharmacological target because it inhibits analgesia mediated by mu-opioid receptors (MOR), and also facilitates the development of neuropathic pain. Based on these findings, the recent cloning of the Sigma-2 receptor (σ2R) led us to investigate its potential role as a regulator of opioid analgesia and of pain hypersensitivity in σ2R knockout mice. In contrast to σ1R deficient mice, σ2R knockout mice developed mechanical allodynia following establishment of chronic constriction injury-induced neuropathic pain, which was alleviated by the σ1R antagonist S1RA. The analgesic effects of morphine, [D-Ala, N-MePhe, Gly-ol]-encephalin (DAMGO) and ß-endorphin increased in σ1R-/- mice and diminished in σ2R-/- mice. The analgesic effect of morphine was increased in σ2R-/- mice by treatment with S1RA. However, σ2R-/- mice and wild-type mice exhibited comparable antinociceptive responses to the delta receptor agonist [D-Pen2,5]-encephalin (DPDPE), the cannabinoid type 1 receptor agonist WIN55,212-2 and the α2-adrenergic receptor agonist clonidine. Therefore, while σR1 inhibits and σ2R facilitates MOR-mediated analgesia these receptors exchange their roles when regulating neuropathic pain perception. Our study may help identify new pharmacological targets for diminishing pain perception and improving opioid detoxification therapies.

The ALS-related σ1R E102Q Mutant Eludes Ligand Control and Exhibits Anomalous Response to Calcium.

Sigma receptor type 1 (σ1R) is a transmembrane protein expressed throughout the central nervous system and in certain peripheral tissues. The human σ1R E102Q mutation causes juvenile amyotrophic lateral sclerosis (ALS), likely by inducing a series of alterations in calcium efflux from the endoplasmic reticulum (ER) to mitochondria that affects calcium homeostasis and cellular survival. Here, we report the influence of calcium on σ1R E102Q associations with glutamate N-methyl-D-aspartate receptors (NMDARs), binding immunoglobulin protein (BiP), and transient receptor potential calcium channels A1, V1, and M8. The mutant protein inhibited the binding of calmodulin to these calcium channels and interacted less with BiP than wild-type σ1R, thereby contributing to calcium homeostasis dysfunction. Mutant σ1R, but not wild-type σ1R, strongly bound to histidine triad nucleotide binding protein 1, which regulates neuromuscular synaptic organization and target selection through teneurin 1. While ligands regulated the association of σ1R wild-type with NMDARs and BiP, they failed to modulate the interaction between these proteins and the σ1R E102Q mutant. Thus, the σ1R E102Q mutant exhibited an anomalous response to cytosolic calcium levels, altered affinity for target proteins, and a loss of response to regulatory ligands. We believe that these modifications may contribute to the onset of juvenile ALS.

Schizophrenia and depression, two poles of endocannabinoid system deregulation.

The activity of certain G protein-coupled receptors (GPCRs) and of glutamate N-Methyl-D-aspartate receptors (NMDARs) is altered in both schizophrenia and depression. Using postmortem prefrontal cortex samples from subjects with schizophrenia or depression, we observed a series of opposite changes in the expression of signaling proteins that have been implicated in the cross-talk between GPCRs and NMDARs. Thus, the levels of HINT1 proteins and NMDAR NR1 subunits carrying the C1 cytosolic segment were increased in depressives and decreased in schizophrenics, respect to matched controls. The differences in NR1 C1 subunits were compensated for via altered expression of NR1 subunits lacking the C1 segment; thus, the total number of NR1 subunits was comparable among the three groups. GPCRs influence the function of NR1 C1-containing NMDARs via PKC/Src, and thus, the association of mu-opioid and dopamine 2 receptors with NR1 C1 subunits was augmented in depressives and decreased in schizophrenics. However, the association of cannabinoid 1 receptors (CB1Rs) with NR1 C1 remained nearly constant. Endocannabinoids, via CB1Rs, control the presence of NR1 C1 subunits in the neural membrane. Thus, an altered endocannabinoid system may contribute to the pathophysiology of schizophrenia and depression by modifying the HINT1-NR1 C1/GPCR ratio, thereby altering GPCR-NMDAR cross-regulation.

Increased PKC activity and altered GSK3ß/NMDAR function drive behavior cycling in HINT1-deficient mice: bipolarity or opposing forces.

Mice with histidine triad nucleotide-binding protein 1 (HINT1) deletion exhibit manic-like symptoms that evolve into depressive-like behavior in response to stressful paradigms. Molecular and electrophysiological studies have indicated that HINT1-/- mice exhibit increased PKC, PKA, and GSK3ß activities, as well as glutamate N-methyl-D-aspartate receptor (NMDAR)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor (AMPAR) and NR2B/NR2A subunit ratios. Pharmacological interventions stabilized their behavior but through different mechanisms. GSK3ß inhibitors and valproate directly attenuated the expression of the manic-like symptoms, whereas PKC inhibition, lamotrigine, or risperidone promoted NMDAR-mediated depressive-like behaviors that counterbalanced the preexisting manic-like symptoms. Naïve HINT1-/- mice exposed to stressful paradigms rapidly manifested depressive-like behaviors in subsequent stressful situations, a capacity that persisted for a couple of weeks thereafter. During the depressive-like phase, citalopram, amitriptyline and MK801 precipitated manic-like behaviors in stressed HINT1-/- mice. Notably, the antagonism of NMDARs prevented HINT1-/- mice from alternating behaviors in response to stress. A comparison with "manic" Black Swiss mice indicated that in HINT1-/- mice, PKC supports manic-like symptoms and reduces the expression of depressive-like behaviors via activation of GSK3ß and regulation of NR2B-enriched NMDARs. HINT1-/- mice represent a suitable model for studying human BPD and may facilitate the identification of novel targets and drugs to treat this mental disorder.

Endocannabinoid control of glutamate NMDA receptors: the therapeutic potential and consequences of dysfunction.

Glutamate is probably the most important excitatory neurotransmitter in the brain. The glutamate N-methyl-D-aspartate receptor (NMDAR) is a calcium-gated channel that coordinates with G protein-coupled receptors (GPCRs) to establish the efficiency of the synaptic transmission. Cross-regulation between these receptors requires the concerted activity of the histidine triad nucleotide-binding protein 1 (HINT1) and of the sigma receptor type 1 (σ1R). Essential brain functions like learning, memory formation and consolidation, mood and behavioral responses to exogenous stimuli depend on the activity of NMDARs. In this biological context, endocannabinoids are released to retain NMDAR activity within physiological limits. The efficacy of such control depends on HINT1/σ1R assisting in the physical coupling between cannabinoid type 1 receptors (CB1Rs) and NMDARs to dampen their activity. Subsequently, the calcium-regulated HINT1/σ1R protein tandem uncouples CB1Rs to prevent NMDAR hypofunction. Thus, early recruitment or a disproportionate cannabinoid induced response can bring about excess dampening of NMDAR activity, impeding its adequate integration with GPCR signaling. Alternatively, this control circuit can apparently be overridden in situations where bursts of NMDAR overactivity provoke convulsive syndromes. In this review we will discuss the possible relevance of the HINT1/σ1R tandem and its use by endocannabinoids to diminish NMDAR activity and their implications in psychosis/schizophrenia, as well as in NMDAR-mediated convulsive episodes.

The ON:OFF switch, σ1R-HINT1 protein, controls GPCR-NMDA receptor cross-regulation: implications in neurological disorders.

In the brain, the histidine triad nucleotide-binding protein 1 (HINT1) and sigma 1 receptors (σ1Rs) coordinate the activity of certain G-protein coupled receptors (GPCRs) with that of glutamate N-methyl-D-aspartate receptors (NMDARs). To determine the role of HINT1-σ1R in the plasticity of GPCR-NMDAR interactions, substances acting at MOR, cannabinoid CB1 receptor, NMDAR and σ1R were injected into mice, and their effects were evaluated through in vivo, ex vivo, and in vitro assays. It was observed that HINT1 protein binds to GPCRs and NMDAR NR1 subunits in a calcium-independent manner, whereas σ1R binding to these proteins increases in the presence of calcium. In this scenario, σ1R agonists keep HINT1 at the GPCR and stimulate GPCR-NMDAR interaction, whereas σ1R antagonists transfer HINT1 to NR1 subunits and disengage both receptors. This regulation is lost in σ1R-/- mice, where HINT1 proteins mostly associate with NMDARs, and GPCRs are physically and functionally disconnected from NMDARs. In HINT1-/- mice, ischemia produces low NMDAR-mediated brain damage, suggesting that several different GPCRs enhance glutamate excitotoxicity via HINT1-σ1R. Thus, several GPCRs associate with NMDARs by a dynamic process under the physiological control of HINT1 proteins and σ1Rs. The NMDAR-HINT1-σ1R complex deserves attention because it offers new therapeutic opportunities.

Grupos sobre alimentación saludable en Facebook: características y contenidos / Healthy eating support groups on Facebook: Content and features

Objetivo: Conocer las características de los grupos de Facebook relacionados con la alimentación saludable. Método: Estudio observacional transversal en Internet. Mediante el API de Facebook se seleccionaron los grupos abiertos en español relacionados con alimentación saludable. Variables estudiadas: nombre, descripción, categoría, número y sexo de los usuarios, fecha de creación, número de posts, contenido de los primeros 20 posts y última actualización. Resultados: Se identificaron 281 grupos abiertos, pero se excluyeron 125 por no haber posts en el muro o no estar relacionados con alimentación saludable. Finalmente se incluyeron 156 grupos con 14.619 usuarios (10.373 mujeres [71%] y 3919 hombres [26,8%]). El 40% de los grupos promocionaban productos dietéticos. Conclusiones: Facebook se utiliza como medio de comunicación y para compartir información sobre alimentación. Se encontró un gran número de grupos que promocionan la venta de productos dietéticos, que hacen dudar de su utilidad para la educación en salud. Las entidades sanitarias deberían participar en las redes sociales (AU)

Objective: To determine the features and use of groups related to healthy eating on Facebook. Method: We carried out a cross-sectional study through the Internet. Using the API on Facebook, we included open groups related to healthy eating in the Spanish language. The variables studied were name, description, category, the number and gender of users, date of creation, number of posts, content of the first 20 posts, and the most recent update. Results: We selected 281 open groups for inclusion in the study. Of these, 125 were excluded because the content was unrelated to healthy eating. Finally 156 groups were studied with 14,619 users (10,373 women [71%] and 3,919 men [26.8%]). Dietary products were promoted by 40% of the groups. Conclusions: Facebook is used as a means of communication and for sharing health information. Because many of these groups promote dietary products, their usefulness for health education is doubtful. Health organizations should participate in social media (AU)

Using experts feedback in clinical case resolution and arbitration as accuracy diagnosis methodology.

This paper proposes a new methodology for assessing the efficiency of medical diagnostic systems and clinical decision support systems by using the feedback/opinions of medical experts. The methodology behind this work is based on a comparison between the expert feedback that has helped solve different clinical cases and the expert system that has evaluated these same cases. Once the results are returned, an arbitration process is carried out in order to ensure the correctness of the results provided by both methods. Once this process has been completed, the results are analyzed using Precision, Recall, Accuracy, Specificity and Matthews Correlation Coefficient (MCC) (PRAS-M) metrics. When the methodology is applied, the results obtained from a real diagnostic system allow researchers to establish the accuracy of the system based on objective facts. The methodology returns enough information to analyze the system's behavior for each disease in the knowledge base or across the entire knowledge base. It also returns data on the efficiency of the different assessors involved in the evaluation process, analyzing their behavior in the diagnostic process. The proposed work facilitates the evaluation of medical diagnostic systems, having a reliable process based on objective facts. The methodology presented in this research makes it possible to identify the main characteristics that define a medical diagnostic system and their values, allowing for system improvement. A good example of the results provided by the application of the methodology is shown in this paper. A diagnosis system was evaluated by means of this methodology, yielding positive results (statistically significant) when comparing the system with the assessors that participated in the evaluation process of the system through metrics such as recall (+27.54%) and MCC (+32.19%). These results demonstrate the real applicability of the methodology used.

[Healthy eating support groups on Facebook: content and features]. / Grupos sobre alimentación saludable en Facebook: características y contenidos.

OBJECTIVE: To determine the features and use of groups related to healthy eating on Facebook. METHOD: We carried out a cross-sectional study through the Internet. Using the API on Facebook, we included open groups related to healthy eating in the Spanish language. The variables studied were name, description, category, the number and gender of users, date of creation, number of posts, content of the first 20 posts, and the most recent update. RESULTS: We selected 281 open groups for inclusion in the study. Of these, 125 were excluded because the content was unrelated to healthy eating. Finally 156 groups were studied with 14,619 users (10,373 women [71%] and 3,919 men [26.8%]). Dietary products were promoted by 40% of the groups. CONCLUSIONS: Facebook is used as a means of communication and for sharing health information. Because many of these groups promote dietary products, their usefulness for health education is doubtful. Health organizations should participate in social media.

Membrane perforation in sinus floor elevation - piezoelectric device versus conventional rotary instruments for osteotomy: an experimental study.

PURPOSE: Sinus membrane perforation is the most common intraoperative complication of maxillary sinus floor elevation (MSFE) procedures and frequently causes postoperative problems. Piezoelectric devices have been claimed to reduce the frequency of membrane perforations although no clear evidence supports this view. MATERIALS AND METHODS: Ten surgeons with different expertise levels performed 80 MSFEs in selected lamb heads, with rotary and piezoelectric instruments following standard protocols. After the procedures, specimens were coded and perforations or tears determined through a microscope. RESULTS: No significant differences in terms of thickness either of the sinus lateral wall (xi -xj = 73.2; 95% confidence interval [CI] = 45.3-191.8) or the membrane (xi -xj = 24.2; 95% CI = -29.4 to 77.9) were identified between the specimens allocated to each group. Nine membrane perforations (11.2%) occurred during the study, all within the lower expertise group. Membrane elevation by hand instruments caused five perforations (40%) in the rotary instrument group and one in the piezoelectric group. Expert surgeons produced no membrane perforations, the size of the antrostomy that was smaller in the piezoelectric group being the only significant difference between the rotary and piezoelectric groups. CONCLUSIONS: The use of piezoelectric material for MSFE reduces the frequency of membrane perforation among surgeons with a limited experience.

Análisis de la composición química de los cementos tipo MTA y PORTLAND tipo I / Comparative chemical analysis of MTA and PORTLAND i cements

El propósito de este estudio es evaluar la composición química de tres cementos: Portland tipo I (CEMEX Samper , Cundinamarca, Colombia), Portland tipo I (CEMEX-Diamante, Ibagué, Colombia) y ProRoot MTA (Dentsply-Maillefer, Ballaigues, Suiza). Se utilizó una muestra probabilística de 17 pastillas para cada tipo de cemento. El análisis se llevó a cabo con la microsonda EDAX (Mahwah, NJ, USA) del microscopio de barrido electrónico SEM FEI (Quanta 200, Hillsboro, Oregon USA), bajo condiciones estandarizadas de lectura de las muestras. Se hicieron cuatro lecturas por muestra, para un subtotal de 68 lecturas por cada tipo de cemento y un total de 208 lecturas. Los resultados se obtuvieron en porcentaje de peso sólido por elemento. Los datos generales fueron analizados por las pruebas ANOVA, comparaciones múltiples de Tukey y t de Student. Se observaron tres elementos comunes entre los tres cementos: Ca, Si y Al, pero se encontraron diferencias estadísticamente significativas de los elementos comunes entre el cemento ProRoot MTA y los cementos Portland I. El Bi solo se encontró en el ProRoot MTA y el S solo se encontró en los cementos Portland tipo I. Se concluye que la composición de los tres cementos es similar. Sin embargo, es necesario evaluar el impacto que puede tener, tanto la presencia de S en los cementos Portland I, como la diferencia de concentraciones de los elementos que fueron comunes en los tres cementos en cuanto a biocompatibilidad y efectividad clínica.

The objective of this study is to evaluate the chemical composition of three cements: Portland Type I (CEMEXSamper , Cundinamarca, Colombia), Portland Type I (CEMEX-Diamante, Ibague, Colombia) and Pro Root MTA (Dentsply-Maillefer, Ballaigues, Switzerland). A probabilistic sample of 17 tablets for each type of cement was used. The analysis was carried out with energy dispersive analysis with x-rays (EDAX) (Mahwah, NJ, USA) in the scanning electron microscope (SEM) FEI (Quanta 200, Hillsboro, Oregon, USA) under standard sample reading conditions. Four readings per sample were carried out for a total of 68 readings per cement, and a grand total of 208 readings. The results were obtained as a percentage of solid weight per element. General data was analyzed with the ANOVA test, and Tukey and t of Student multiple comparison tests. Three common elements were observed between the three cements: Ca, Si, and Al, but there were significant statistical differences between the common elements of the ProRoot MTA and the Portland cements I. The Bi was found only in the ProRoot MTA, and the S only in the Portland type I cements. It can be concluded then that the composition of the three cements is similar; however, it is necessary to evaluate the impact that the presence of S in the Portland I cements as well as the difference in concentrations of the three common elements may have in the biocompatibility and clinical effectiveness.

Simulation for training in sinus floor elevation: New surgical bench model

Objectives: to describe a bench model (workshop of abilities) for sinus floor elevation (SFE) training that simulates the surgical environment and to assess its effectiveness in terms of trainees’ perception.Study design: thirty-six randomly selected postgraduate students entered this cross-sectional pilot study and asked to fill in an anonymous, self-applied, 12-item questionnaire about a SFE workshop that included a study guide containing the workshop’s details, supervised practice on a simulated surgical environment, and assessment by means of specific check-lists. Results: Thirtiy-six fresh sheep heads were prepared to allow access to the buccal vestible. Using the facial tuber, third premolar and a 3D-CT study as landmarks for trepanation, the sinus membrane was lifted, the space filled with ceramic material and closed with a resorbable membrane. The participants agreed on their ability to perform SFE in a simulated situation (median score= 4.5; range 2-5) and felt capable to teach the technique to other clinicians or to undertake the procedure for a patient under supervision of an expert surgeon (median= 4; range 1-5 ). There were no differences on their perceived ability to undertake the technique on a model or on a real patient under supervision of an expert surgeon (p=0.36). Conclusions: Clinical abilities workshops for SFE teaching are an essential educational tool but supervised clinical practice should always precede autonomous SFE on real patients. Simulation procedures (workshop of abilities) are perceived by the partakers as useful for the surgical practice. However, more studies are needed to validate the procedure and to address cognitive and communication skills, that are clearly integral parts of surgical performance (AU)