Exploring the potential of Artificial Intelligence in Traumatology: Conversational answers to specific questions. / Explorando el potencial de la inteligencia artificial en traumatología: respuestas conversacionales a preguntas específicas.

INTRODUCTION: Generative Artificial Intelligence is a technology that provides greater connectivity with people through conversational bots («chatbots¼). These bots can engage in dialogue using natural language indistinguishable from humans and are a potential source of information for patients.The aim of this study is to examine the performance of these bots in solving specific issues related to orthopedic surgery and traumatology using questions from the Spanish MIR exam between 2008 and 2023. MATERIAL AND METHODS: Three «chatbot¼ models (ChatGPT, Bard and Perplexity) were analyzed by answering 114 questions from the MIR. Their accuracy was compared, the readability of their responses was evaluated, and their dependence on logical reasoning and internal and external information was examined. The type of error was also evaluated in the failures. RESULTS: ChatGPT obtained 72.81% correct answers, followed by Perplexity (67.54%) and Bard (60.53%).Bard provides the most readable and comprehensive responses. The responses demonstrated logical reasoning and the use of internal information from the question prompts. In 16 questions (14%), all 3 applications failed simultaneously. Errors were identified, including logical and information failures. CONCLUSIONS: While conversational bots can be useful in resolving medical questions, caution is advised due to the possibility of errors. Currently, they should be considered as a developing tool, and human opinion should prevail over Generative Artificial Intelligence.

Vertebral fractures are increased in rheumatoid arthritis despite recent therapeutic advances: a case-control study.

Prevalence and risk factors of vertebral fractures in postmenopausal RA women were assessed in 323 patients and compared with 660 age-matched women. Of patients, 24.15% had at least one vertebral fracture vs.16.06% of controls. Age, glucocorticoids and falls were the main fracture risks. Vertebral fractures were associated with disease severity. INTRODUCTION: There is little quality data on the updated prevalence of fractures in rheumatoid arthritis (RA) that may have changed due to advances in the therapeutic strategy in recent years. This study was aimed at analysing the prevalence and risk factors of vertebral fractures in postmenopausal women with RA and comparing it with that of the general population. METHODS: We included 323 postmenopausal women diagnosed with RA from 19 Spanish Rheumatology Departments, randomly selected and recruited in 2018. Lateral radiographs of the thoracic and lumbar spine were obtained to evaluate morphometric vertebral fractures and the spinal deformity index. We analysed subject characteristics, factors related to RA, and fracture risk factors. The control group consisted of 660 age-matched Spanish postmenopausal women from the population-based Camargo cohort. RESULTS: Seventy-eight (24.15%) RA patients had at least one vertebral fracture. RA patients had increased fracture risk compared with controls (106 of 660, 16.06%) (p = 0.02). Logistic regression analysis showed that age (OR 2.17; 95% CI 1.27-4.00), glucocorticoids (OR 3.83; 95% CI 1.32-14.09) and falls (OR 3.57; 95% CI 1.91-6.86) were the independent predictors of vertebral fractures in RA patients. The subgroup with vertebral fractures had higher disease activity (DAS28: 3.15 vs. 2.78, p = 0.038) and disability (HAQ: 0.96 vs. 0.63, p = 0.049), as compared with those without vertebral fractures. CONCLUSION: The risk of vertebral fracture in RA is still high in recent years, when compared with the general population. The key determinants of fracture risk are age, glucocorticoids and falls. Patients with vertebral fractures have a more severe RA.

Abstract and experiential thinking differentially account for anomalous perception of reality in people with or without schizophrenia.

repetitive thinking is often increased in various psychopathological conditions. However, evidence for its possible contribution to psychotic symptoms relies only on correlational analysis and has not been experimentally tested within the psychotic continuum. This research aims to examine whether repetitive thinking about a negative past experience using concrete versus abstract processing might modify the reporting of anomalous sensory experiences. 89 patients with schizophrenia and 89 matched controls were asked to reflect on their most negative Self-Defining Memory during a thirty-minute period. By means of a written script, half of the participants were instructed to remember thoughts, feelings and sensations associated with the event in an abstract mode, while the other half followed an equivalent script but with concrete questions. After induced concrete-experiential thinking, both controls and patients significantly reduced self-reported anomalous reality perception. However, participants in the induced abstract-analytical thinking condition increased anomalous experience, especially sensory experience from an unexplained source. Multigroup path analyses showed that involvement in abstract-analytical thinking during the task significantly mediated the relationship between pre-test and post-test anomalous perception scores, but only in the patient group. These results suggest that abstract thinking contributes to distorted sensory experiences. In contrast, training in a concrete processing mode of past experiences may be a useful tool to reduce subjective anomalous perceptions.

[Arthroscopic treatment of Hill-Sachs lesions in glenohumeral instability. "Remplissage" technique]. / Tratamiento artroscópico de las lesiones de Hill-Sachs en la inestabilidad glenohumeral. Técnica de "remplissage".

Hill-Sachs lesion is a defect of the posterosuperior aspect of the humeral head that occurs during an episode of instability. Under abduction and external rotation, this lesion may engage the anterior glenoid border, thus favoring instability. It may be the cause of many failed surgical stabilization procedures. We herein describe the arthroscopic remplissage technique, which consists of filling the lesion through capsulotenodesis of the infraspinatus tendon. This maneuver should be always be performed together with anterior capsulolabral repair. The results obtained by the authors and published in the literature are good, with a loss of mobility similar to the one resulting from the isolated arthroscopic Bankart technique. We recommend performing remplissage together with Bankart repair in patients with glenohumeral instability with significant Hill-Sachs lesions without a glenoid defect or with defects less than 25%.

Filogenia de la articulación de la cadera. Plasticidad del fenotipo. ¿Paradigma Lamarckiano o Darwiniano? Parte II / Hip Joint phylogenesis. Phenotypic plasticity. Lamarckian or Darwinian paradigm? Part II

Objetivo. El objetivo de este trabajo es analizar el origen de los cambios plásticos del fenotipo en una estructura biológica, en nuestro caso la cadera. Como hipótesis de trabajo se presenta la posibilidad de que los cambios se puedan interpretar según el paradigma Lamarckiano, en contraposición al paradigma Darwiniano. La sección material y método del trabajo se menciona en la parte I. Se han añadido estudios de plantas y peces. Discusión. Los resultados muestran que el diseño de la cadera, como relación de bola y cuenco, no cambia. El fenotipo, en los elementos que costituyen los tejidos de la articulación de la cadera, muestra cambios plásticos significativos. Conclusión. Sugerimos: que los cambios de la plasticidad del fenotipo de la cadera son inmanentes al fenotipo, y no se interpretan según el paradigma Lamarckiano ni Darwiniano (AU)

Objective. The aim of this work is to analyse the origin of phenotypic plastic changes into a biologic structure, in this case the hip. As a hypothesis of the work, the possibility that changes could be explained following the Lamarckian paradigm, opposed to the Darwinian paradigm, is shown. The section material and methods of this work have been published in part I. Studies in plants and fish have been added. Discussion. Results showed that the ball-and-socket design of the hip joint remains unchanged. Phenotype in the elements that form the hip joint tissues showed significant plastic changes. Conclusion. Interpretation of our results suggest that changes in phenotype plasticity of the hip joint are immanent to phenotype and cannot be explained by following Lamarck's or Darwin's paradigm (AU)

[Hip Joint phylogenesis. Phenotypic plasticity. Lamarckian or Darwinian paradigm? Part II]. / Filogenia de la articulación de la cadera. Plasticidad del fenotipo. ¿Paradigma Lamarckiano o Darwiniano? Parte II.

OBJECTIVE: The aim of this work is to analyse the origin of phenotypic plastic changes into a biologic structure, in this case the hip. As a hypothesis of the work, the possibility that changes could be explained following the Lamarckian paradigm, opposed to the Darwinian paradigm, is shown. The section material and methods of this work have been published in part I. Studies in plants and fish have been added. DISCUSSION: Results showed that the ball-and-socket design of the hip joint remains unchanged. Phenotype in the elements that form the hip joint tissues showed significant plastic changes. CONCLUSION: Interpretation of our results suggest that changes in phenotype plasticity of the hip joint are immanent to phenotype and cannot be explained by following Lamarck's or Darwin's paradigm.

Cirugía en sitio erróneo / Wrong site surgery

El término "cirugía en sitio erróneo" engloba aquella cirugía que es realizada en el lado erróneo, en una zona anatómica errónea, en el paciente erróneo o en la que se realiza un procedimiento diferente al planeado. Pese a estar claramente poco comunicada, es una complicación frecuente en la vida profesional de un cirujano, siendo la cirugía ortopédica la especialidad con mayor riesgo. La repercusión mediática aumenta la desconfianza en el sistema sanitario y las consecuencias legales para el cirujano son la norma. En la actualidad hay varios protocolos, entre ellos los propuestos para evitar esta complicación por la American Academy of Orthopaedic Surgeons (AAOS) y la Joint Comission on Accreditation of Healthcare Organizations (JCAHO), de fácil aplicación. Consisten básicamente en comprobar los datos del paciente, marcar la zona que se va a operar y realizar un “tiempo muerto”, una comprobación final, justo antes de iniciar la cirugía. Es fundamental su implantación en los centros de España, con la colaboración de los diferentes estamentos, para una prevención efectiva de este problema(AU)

The term "wrong site surgery" refers to surgery carried out on the wrong side, in the wrong anatomical area or in the wrong patient. It can also indicate that the surgical procedure employed was not the one intended. In spite of being a rather neglected topic, wrong site surgery is a fairly usual complication in a surgeon's professional life – orthopaedic surgery being the speciality most at risk. Media reports on this subject undermine the general public's distrust of the health care system, surgeons more often than not having to face serious legal consequences. There are at present several easy-to-apply protocols, among them those proposed by the American Academy of Orthopaedic Surgeons (AAOS) and the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), which can help preventing these unfortunate occurrences. They basically consist in checking the patient's details, marking the area to be operated and performing a final run-through just before starting the surgical procedure. It is of essence to introduce such a protocol in our own hospitals, with the support of all parties involved, in order to effectively address this problem(AU)

Metabolismo de las hormonas tiroideas y el yodo en el embarazo / Thyroid hormone and iodine metabolism in pregnancy

El yodo es un micronutriente esencial necesario para que la glándula tiroides sintetice 2 hormonas yodadas: la tetrayodotironina (tiroxina, T4) y la 3’,3,5-triyodotironina (T3), con 4 y 3 átomos de yodo respectivamente. Son necesarias durante toda la vida, especialmente la T4 para el desarrollo de la corteza cerebral, desde el primer trimestre del embarazo. La necesidad de un aporte adecuado de yodo se reconoce entre los Derechos de la Infancia, ya que su deficiencia es, después de la inanición extrema, la causa nutricional más frecuente de retraso mental prevenible en el mundo. Aquí desarrollamos varios puntos: ¿son equivalentes la T4 y la T3 para el cerebro en desarrollo?; ¿qué ocurre con la T4 en condiciones de yodo deficiencia?; ¿qué cambios impone el feto mismo a la función tiroidea de la madre?; ¿qué ocurre cuando hay yodo deficiencia durante el embarazo?; ¿y la lactancia? Contestarlos explica por qué se duplican las necesidades de yodo desde el comienzo mismo del embarazo. Incluso en situaciones de yodo deficiencia leve-moderada, prevalentes todavía en España, se requiere la suplementación diaria con al menos (..) (AU)

Iodine is an essential micronutrient without which the thyroid is unable to synthesize and secrete its two iodine-containing hormones, tetra-iodo-thyronine or thyroxine (T4) and 3’, 3, 5-tri-iodothyronine (T3),containing, respectively, 4 and 3 iodine atoms per molecule. Both hormones are needed throughout life, with T4 being especially important for the development of the cerebral cortex as early as during the first trimester of pregnancy. The need for adequate iodine intake is recognized among the Rights of the Child, since, after starvation, iodine deficiency is the most frequent nutritional cause worldwide of preventable mental retardation. The present article discusses several questions: are T4and T3 equivalent for the developing brain? What happens to T4 during iodine deficiency? What changes are imposed on maternal thyroid function by the fetus? What happens when a pregnant woman is iodine deficient? What effect does breastfeeding have on iodine status? The answers to the above questions explain why iodine requirements are doubled from the very onset of pregnancy. Even in conditions of mild-moderate iodine deficiency, which still prevail throughout Spain, daily supplementation of at least (..) (AU)

Ontogenesis of thyroid function and interactions with maternal function.

Fetal and neonatal development of thyroid function involves the embryogenesis, differentiation and maturation of the thyroid gland, of the hypothalamic-pituitary-thyroid axis and of the systems controlling thyroid hormone metabolism. We focus here on aspects related to neurodevelopment. Throughout gestation, thyroxine (T4) transferred from the mother, present in embryonic fluids by 4 weeks, protects the fetal brain. Free T4 (FT4) in fetal fluids increases rapidly, approaching adult levels by midgestation, in concentrations that are determined by the maternal serum T4. T3 remains very low throughout pregnancy. In the cerebral cortex T3, generated from T4, reaches adult values by midgestation and is partly bound to specific nuclear receptor isoforms. The iodothyronine deiodinases are important for the spatial and temporal presence of T3 in different fetal brain areas. After onset of fetal thyroid secretion at midgestation, maternal transfer of T4 continues to contribute importantly to fetal serum T4, protecting neurodevelopment until birth. In rats, even a transient period of maternal hypothyroxinemia disrupts neurodevelopment irreversibly, supporting epidemiological evidence for its negative role in human neurodevelopment. The prompt treatment of maternal hypothyroidism or hypothyroxinemia should mitigate negative effects on neurodevelopment. Neurodevelopmental deficits of preterm infants might also result from an untimely interruption of the maternal transfer of T4 [Morreale de Escobar et al: J Clin Endocrinol Metab 2000;85:3975-3987; Best Pract Res Clin Endocrinol Metab 2004;18:225-248; Eur J Endocrinol 2004;151(suppl 3):U25-U37].

El yodo durante la gestación, lactancia y primera infancia. Cantidades mínimas y máximas: de microgramos a gramos / Iodine during pregnancy, lactation and infancy. Minimum and maximum doses: From micrograms to grams

Una deficiencia de yodo durante el período fetal y posnatal puede dar lugar a déficit de desarrollo mental y psicomotor, tanto más graves cuanto mayor sea la deficiencia de yodo y cuantos antes se haya padecido. Muchos déficit se han hecho irreversibles antes de la mitad de la gestación, por lo que hay que asegurar una ingesta adecuada de yodo (250-300 μg/día) mediante medidas de suplementación desde el comienzo del embarazo. Preferiblemente desde antes de su comienzo.Por elevada que sea la ingesta basal de yodo de la mujer la suplementación diaria con 250-300 μg de yodo no resulta nociva para la madre, el feto ni para el lactante.Hay un amplio margen de seguridad de dos a tres órdenes de magnitud entre las cantidades de yodo beneficiosas durante la gestación y primera infancia y las que pueden ser nocivas. Estas últimas son 500 a 3.000 veces superiores a las que se ingieren habitualmente, incluso cuando se toman suplementos. Las cantidades nocivas de yodo se relacionan invariablente con el uso de medicamentos, de antisépticos yodados (p. ej., povidona yodada) o de medios de contraste radiológicos. No hay actualmente excusa alguna para seguir usando antisépticos que, aunque normalmente inocuos en el adulto, son muy peligrosos durante el embarazo, parto y postparto. Su uso debe quedar terminantemente prohibido, sobre todo considerando que pueden ser sustituidos con eficacia por otros preparados no yodados, como clorhexidina al 0,05%. No debe olvidarse que el feto y el neonato, sobre todo si prematuro, carecen aún de los mecanismos de autorregulación tiroidea del adulto. Como consecuencia, ante un exceso de yodo se produce un un bloqueo del tiroides del feto y del neonato, sobre todo cuando éste es prematuro. Este hipotiroidismo iatrogénico puede dar lugar a defectos irreversibles de maduración cerebral, ya las consecuencias serían las mismas que las que se observan en niños con hipotiroidismo congénito, que no se han tratado a tiempo con tiroxina

An insufficient iodine intake during fetal and postnatal development often results in disorders of mental and psicomotor development, which are the more severe, the greater the degree of iodine deficiency and the earlier it is suffered during development. Many of these disorders have become irreversible by midgestation, and it is necessary to ensure the mother with an intake of 250- 300 μg I/day, from the beginning of the pregnancy or, preferably, before its onset, and throughout lactation. When the pregnancy is planned, supplementation ought to start before conception.Even if the basal iodine intake of the pregnant woman is more than adequate, supplementation with 250- 300 μg I/day is safe for her, the fetus and the newborn.There is a great margin of safety between the amounts of iodine which are beneficia, and those which are dangerous, as the latter are 2 to 3 orders of magnitude higher than the former. The amounts of iodine which may be harmful are 500-3,000 times higher than those we receive through food, even when dietary supplements are added. Harmful doses of iodine are invariably associated with the use of some medicines and drugs, mainly of iodinated disinfectants, or of radiological contrast agents. The damage results from the lack of maturation in fetuses and neonates, of thyroid autorregulatory mechanisms that protect the adult thyroid from the blocking effects of an iodine excess. There is at present no excuse for not totally banning, completely and permanently, the use of such disinfectants, especially during delivery, and the newborn period. Other disinfectants, such a clorhexidine, are equally effective without increasing the risk of inducing iatrogenic hypothyroidism during important phases of human brain development. It should continuously be born in mind that thyroid failure of the fetus and newborn, especially if preterm, may result in irreversible brain damage, whether its cause, is congenital or iatrogenic

Aplasia medular. Descripción de un caso / Medullary aplasia. Description of a case

Presentamos el caso de un paciente con antecedentes personales de hipertensión arterial e infarto agudo de miocardio, que de forma brusca presenta un cuadro de hemorragia digestiva alta, detectándose en los análisis presencia de anemia y trombopenia. Se realiza un aspirado de médula ósea, observándose una celularidad polimorfa con presencia de megacariocitos de morfología normal diagnosticándose como púrpura trombopénica idiopática. Al no obtener respuesta al tratamiento con corticoides, se realiza nuevo aspirado de médula que pone de manifiesto unas preparaciones normo-hipocelulares sin megacariocitos y un aumento porcentual de linfocitos. Se realiza posteriormente un aspirado-biopsia de médula ósea que confirmó el diagnóstico de aplasia medular. Se inicia tratamiento con Globulina antitimocítica, con buena evolución clínica y analítica. Se describen exploraciones complementarias, evolución y tratamiento (AU)

Leucemia de células plasmáticas. Descripción de un caso / Plasma cell leukaemia: a case study

La leucemia de células plasmáticas (LCP) es una patología infrecuente con pobres resultados, asociados a resistencia al tratamiento y a una supervivencia corta. No está bien definido el tipo óptimo de tratamiento. Presentamos un nuevo caso de LCP con factores de muy mal pronóstico y una buena respuesta a la quimioterapia. Este hecho es poco frecuente y hay pocos casos en la literatura (AU)

Analysis of 41 kb of the DNA sequence from the right arm of chromosome II of Schizosaccharomyces pombe.

We report the complete sequence of cosmid c18A7 (41 046 bp insert), located on the right arm of chromosome II of the Schizosaccharomyces pombe genome. The sequence, which partially overlaps with cosmids SPBC4F6 and SPBC336, contains 16 open reading frames (ORFs) capable of coding for proteins of at least 100 amino acid residues in length (one partial) and one small nucleolar RNA (snoRNA). Four known genes were found: swi10 (encoding a mating-type switching protein also involved in nucleotide excision repair); dim1 (encoding a dimethyladenosine transferase); arf1 (encoding ADP-ribosylation factor 1); and pol3 (cdc6) the partial fragment, encoding the 125 kDa catalytic subunit of the DNA polymerase type B. Six ORFs similar to known proteins were found. They include a transporter of the major facilitator superfamily class, a vacuolar sorting protein, an asparagine synthase, a nuclear protein, a reticulum oxidoreductin and a heat shock protein. Each protein product of the other six ORFs has conserved domains and can be assigned a molecular, but not a biological, function. The sequence has been submitted to the EMBL database under Accession No. AL080287.

Trastornos de los linfocitos. Leucemia linfática crónica y otros síndromes linfoproliferativos crónicos

A lo largo de estos años se han realizado diversas clasificaciones de los síndromes linfoproliferativos. Sin embargo, la más aceptada hoy día es la clasificación REAL. Mencionamos en primer lugar la leucemia linfática crónica tipo B que es la forma más frecuente de todas las leucemias; los pacientes suelen tener una edad media de 65 años. Su frecuencia ha aumentado hoy día, debido al alargamiento de la edad media. Recientemente se han alcanzado importantes avances terapéuticos, sobre todo con la aparición de los análogos de las purinas. Comentaremos también avances terapéuticos en otros síndromes linfoproliferativos como leucemia prolifoncítica, tricoleucemia y síndrome de Sézary (AU)

A genomic approach for the identification and classification of genes involved in cell wall formation and its regulation in Saccharomyces cerevisiae.

Using a hierarchical approach, 620 non-essential single-gene yeast deletants generated by EUROFAN I were systematically screened for cell-wall-related phenotypes. By analyzing for altered sensitivity to the presence of Calcofluor white or SDS in the growth medium, altered sensitivity to sonication, or abnormal morphology, 145 (23%) mutants showing at least one cell wall-related phenotype were selected. These were screened further to identify genes potentially involved in either the biosynthesis, remodeling or coupling of cell wall macromolecules or genes involved in the overall regulation of cell wall construction and to eliminate those genes with a more general, pleiotropic effect. Ninety percent of the mutants selected from the primary tests showed additional cell wall-related phenotypes. When extrapolated to the entire yeast genome, these data indicate that over 1200 genes may directly or indirectly affect cell wall formation and its regulation. Twenty-one mutants with altered levels of beta1,3-glucan synthase activity and five Calcofluor white-resistant mutants with altered levels of chitin synthase activities were found, indicating that the corresponding genes affect beta1,3-glucan or chitin synthesis. By selecting for increased levels of specific cell wall components in the growth medium, we identified 13 genes that are possibly implicated in different steps of cell wall assembly. Furthermore, 14 mutants showed a constitutive activation of the cell wall integrity pathway, suggesting that they participate in the modulation of the pathway either directly acting as signaling components or by triggering the Slt2-dependent compensatory mechanism. In conclusion, our screening approach represents a comprehensive functional analysis on a genomic scale of gene products involved in various aspects of fungal cell wall formation.

Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia?

Several recent publications have drawn attention to the role of the thyroid hormone status of the mother on the future neuropsychological development of the child. The screening of pregnant women for clinical or subclinical hypothyroidism based on second trimester elevated maternal TSH values has been proposed. Here, we have summarized present epidemiological and experimental evidence strongly suggesting that conditions resulting in first trimester hypothyroxinemia (a low for gestational age circulating maternal free T4, whether or not TSH is increased) pose an increased risk for poor neuropsychological development of the fetus. This would be a consequence of decreased availability of maternal T4 to the developing brain, its only source of thyroid hormone during the first trimester; T4 is the required substrate for the ontogenically regulated generation of T3 in the amounts needed for optimal development in different brain structures, both temporally and spatially. Normal maternal T3 concentrations do not seem to prevent the potential damage of a low supply of T4, although they might prevent an increase in circulating TSH and detection of the hypothyroxinemia if only TSH is measured. Hypothyroxinemia seems to be much more frequent in pregnant women than either clinical or subclinical hypothyroidism and autoimmune thyroid disease, especially in regions where the iodine intake of the pregnant woman is inadequate to meet her increased needs for T4. It is proposed that the screening of pregnant women for thyroid disorders should include the determination of free T4 as soon as possible during the first trimester as a major test, because hypothyroxinemia has been related to poor developmental outcome, irrespective of the presence of high titers of thyroid autoantibodies or elevated serum TSH. The frequency with which this may occur is probably 150 times or more that of congenital hypothyroidism, for which successful screening programs have been instituted in many countries.