Traumatologia da Articulação de Lisfranc

As lesões do complexo articular de Lisfranc são frequentes e muitas vezes subdiagnosticadas em desportistas. São lesões com tempo prolongado de recuperação e que muitas vezes colocam a carreira desportiva em risco, na medida em que a maioria evolui rapidamente para osteoartrose sintomática. Um nível elevado de suspeita de reconhecimento dos sinais clínicos de lesão e uso dos exames de imagem adequados são críticos para um diagnóstico correto e precoce, de modo a se conseguir um tratamento adequado e garantir rápido regresso à atividade desportiva. Os tratamentos ideais para as lesões de Lisfranc são controversos e devem ser adequados ao tipo de lesão, estadio e características do atleta. Este artigo apresenta uma revisão da atual evidência científica em relação aos princípios de diagnóstico e tratamento das lesões do complexo articular de Lisfranc na população praticante de desporto.info:eu-repo/semantics/publishedVersio

Síndrome do osso trígono

A causa mais frequente da síndrome de conflito posterior do tornozelo envolve o osso trígono e o processo talar, chamando-se síndrome do osso trígono à compressão sintomática de tecidos moles e osso a nível do intervalo calcâneo-tibial. Trata-se de uma entidade controversa, atualmente ainda com evidência limitada na literatura. A presença do osso trígono é na maior parte dos casos apenas um achado imagiológico sem tradução clínica, no entanto o seu traumatismo, agudo ou crónico, em movimentos de flexão plantar forçada pode ser responsável pela sua lesão e conversão sintomática. O diagnóstico é feito pela clínica e pela evidência imagiológica e é frequentemente subdiagnosticado ou tem diagnóstico tardio. É necessário um nível elevado de suspeição para diagnóstico precoce, que é fundamental não só para iniciar rapidamente o tratamento adequado para alívio sintomático, como também em termos de prognóstico. O tratamento pode ser conservador ou cirúrgico, envolvendo a ressecção deste ossículo acessório, por técnicas de cirurgia aberta ou minimamente invasivas de artroscopia ou endoscopia. O presente trabalho faz uma revisão da literatura científica existente sobre este tema. Introduzimos com a definição da síndrome, noções anatómicas e fisiopatológicas, seguindo-se a apresentação dos sinais e sintomas clínicos e dos meios complementares de diagnóstico e finalizando com as várias abordagens terapêuticas, tanto conservadora como cirúrgica. São descritas e comparadas entre si as três técnicas cirúrgicas mais praticadas atualmente, a cirurgia aberta, a artroscópica subtalar e a endoscópica

Pé de Charcot – Um caso clínico

A artropatia neuropática de Charcot é uma doença osteoarticular primária progressiva que atinge mais frequentemente o pé e tornozelo. Trata-se de uma patologia característica de doentes diabéticos de longa evolução e com mau controlo glicémico. Aceita-se hoje em dia que esta condição tem origem numa combinação de hiperémia/inflamação óssea, osteopénia e défices sensitivo-motores, ou seja, uma combinação das clássicas teorias neuro-traumática e neuro-vascular, com a nova teoria inflamatória. A doença pode estar na fase aguda, activa ou inflamatória, verificando-se um pé edemaciado, com calor e eritema, ou na fase crónica ou inactiva, onde são características deformidades acentuadas devido a luxações e fracturas. O diagnóstico faz-se sobretudo pela clínica, podendo a radiografia, a ressonância magnética e a cintigrafia óssea serem úteis, nomeadamente em termos de diagnóstico diferencial. Os objectivos do tratamento são analgesia, estabilidade articular, pé plantígrado, marcha e prevenção de úlceras, deformidades e amputação. A opção de tratamento depende da fase de doença, local, gravidade e grau de ulceração. Para a fase aguda reserva-se imobilização com bota gessada por 2-4 meses e descarga, enquanto na fase crónica está indicada imobilização com ortóteses tornozelo-pé ou calçado especializado ou correcção cirúrgica das deformidades em casos específicos. Casos de dor incapacitante, exostose, úlcera recorrente, deformidades acentuadas e luxações ou fracturas, têm indicação de correcção cirúrgica, que pode ir desde exostosectomia, a artrodese ou mesmo amputação. Apresenta-se um caso clínico de um caso de pé de Charcot com evolução rápida de destruição osteo-articular em 6meses. Quanto a classificações trata-se de Sanders-Frykberg grau III-IV (sub-talar, médiotársica),Brodsky grau II (sub-talar, talo-navicular, calcâneo-cuboideia) e Eichenholtz grau III (estadio crónico/consolidação - Deformidade). Face a deformidade acentuada instável e dor incapacitante, opta-se por tratamento cirúrgico com artrodese tripla do tornozelo com encavilhamento calcâneo-tibial retrógrado. Intraoperatoriamente verifica-se destruição osteo-articular necrótica acentuada do astrágalo e parcial do calcâneo, é então feita astragalectomia, encavilhamento calcâneo-tibial retrógrado e artrodese com 2 parafusos canulados: calcâneo-tibial e fíbulo-tíbio-navicular, bem como aplicação de aloenxerto. É feita imobilização com bota gessada, que é renovada em consulta a cada 2 semanas sob vigilância. A imobilização e descarga são mantidas até sinais deconsolidação. Quanto a prognóstico é conhecida a taxa elevada de complicações deste tipo de procedimento no pé de Charcot, estando relatadas percentagens superiores a 70%, nomeadamente de infecção, mau posicionamento de material cirúrgico, úlcera recorrente e fractura. São fundamentais para boa evolução manter a descarga e imobilização prolongada, a renovação de imobilização e inspecção frequente do pé e um bom controlo da glicémia. Face à localização e presença de deformidade acentuada e lesão cutânea, este caso clínico apresenta um prognóstico reservado, podendo eventualmente por complicações progredir para amputação

Peripheral biomarkers to diagnose obstructive sleep apnea in adults: A systematic review and meta-analysis

Background: Obstructive Sleep Apnea (OSA) has been recognized as a major health concern worldwide, given its increasing prevalence, difficulties in diagnosis and treatment, and impact on health, economy, and society. Clinical guidelines highlight the need of biomarkers to guide OSA clinical decision-making, but so far, without success. In this systematic review and meta-analysis, registered on the International Prospective Register of Systematic Reviews database (ID CRD42020132556), we proposed to gather and further explore candidates identified in the literature as potential OSA biomarkers. Methods: Search strategies for eight different databases (PubMed/Medline, Cochrane Library, Biblioteca Virtual da Saúde, Web of Science, EMBASE, World Intellectual Property Organization database, and bioRxiV and medRxiV Preprint Servers) were developed. We identified studies exploring potential biomarkers of OSA, in peripheral samples of adults, with and without OSA, with no comorbidities defined in study inclusion criteria, published after the last systematic review and meta-analysis conducted on OSA biomarkers, until May 31st, 2020. Risk of bias was assessed through the 14-item Quality Assessment Tool for Diagnostic Accuracy Studies. Demographic, clinical, and candidate biomarkers' data were collected and analyzed via random effects meta-analyses. Findings: Among the 1512 unique studies screened, 120 met the inclusion criteria and 16 studies with low risk of bias were selected for meta-analyses. The selected 16 studies enrolled a total of 2156 participants, from which 1369 were diagnosed with OSA and 787 were disease-free controls. The assessed variables showed high heterogeneity. From the 38 biomarker candidates evaluated, only two were evaluated in more than one study. Most studies pinpointed candidates with more potential for OSA prognosis. ADAM29, FLRT2 and SLC18A3 mRNA levels in PBMCs, Endocan and YKL-40 levels in serum, and IL-6 and Vimentin levels in plasma revealed the most promising candidates for OSA diagnosis. Interpretation: Although the current systematic review and meta-analysis allowed us to identify candidates to further explore as potential biomarkers in future studies, it is evident that OSA biomarkers research is still at an early stage. Most findings derive from small-size single-center study cohorts and single-candidate studies. We point several gaps in current OSA biomarker research that may guide into new directions and approaches towards the identification of OSA biomarkers.info:eu-repo/semantics/publishedVersio

A Targeted Constitutive Mutation in the Apc Tumor Suppressor Gene Underlies Mammary But Not Intestinal Tumorigenesis

Germline mutations in the adenomatous polyposis coli (APC) gene are responsible for familial adenomatous polyposis (FAP), an autosomal dominant hereditary predisposition to the development of multiple colorectal adenomas and of a broad spectrum of extra-intestinal tumors. Moreover, somatic APC mutations play a rate-limiting and initiating role in the majority of sporadic colorectal cancers. Notwithstanding its multifunctional nature, the main tumor suppressing activity of the APC gene resides in its ability to regulate Wnt/β-catenin signaling. Notably, genotype–phenotype correlations have been established at the APC gene between the length and stability of the truncated proteins encoded by different mutant alleles, the corresponding levels of Wnt/β-catenin signaling activity they encode for, and the incidence and distribution of intestinal and extra-intestinal tumors. Here, we report a novel mouse model, Apc1572T, obtained by targeting a truncated mutation at codon 1572 in the endogenous Apc gene. This hypomorphic mutant allele results in intermediate levels of Wnt/β-catenin signaling activation when compared with other Apc mutations associated with multifocal intestinal tumors. Notwithstanding the constitutive nature of the mutation, Apc+/1572T mice have no predisposition to intestinal cancer but develop multifocal mammary adenocarcinomas and subsequent pulmonary metastases in both genders. The histology of the Apc1572T primary mammary tumours is highly heterogeneous with luminal, myoepithelial, and squamous lineages and is reminiscent of metaplastic carcinoma of the breast in humans. The striking phenotype of Apc+/1572T mice suggests that specific dosages of Wnt/β-catenin signaling activity differentially affect tissue homeostasis and initiate tumorigenesis in an organ-specific fashion

Emerging Infectious Disease leads to Rapid Population Decline of Common British Birds

Emerging infectious diseases are increasingly cited as threats to wildlife, livestock and humans alike. They can threaten geographically isolated or critically endangered wildlife populations; however, relatively few studies have clearly demonstrated the extent to which emerging diseases can impact populations of common wildlife species. Here, we report the impact of an emerging protozoal disease on British populations of greenfinch Carduelis chloris and chaffinch Fringilla coelebs, two of the most common birds in Britain. Morphological and molecular analyses showed this to be due to Trichomonas gallinae. Trichomonosis emerged as a novel fatal disease of finches in Britain in 2005 and rapidly became epidemic within greenfinch, and to a lesser extent chaffinch, populations in 2006. By 2007, breeding populations of greenfinches and chaffinches in the geographic region of highest disease incidence had decreased by 35% and 21% respectively, representing mortality in excess of half a million birds. In contrast, declines were less pronounced or absent in these species in regions where the disease was found in intermediate or low incidence. Also, populations of dunnock Prunella modularis, which similarly feeds in gardens, but in which T. gallinae was rarely recorded, did not decline. This is the first trichomonosis epidemic reported in the scientific literature to negatively impact populations of free-ranging non-columbiform species, and such levels of mortality and decline due to an emerging infectious disease are unprecedented in British wild bird populations. This disease emergence event demonstrates the potential for a protozoan parasite to jump avian host taxonomic groups with dramatic effect over a short time period

The role of steroids in the management of brain metastases: a systematic review and evidence-based clinical practice guideline

Do steroids improve neurologic symptoms in patients with metastatic brain tumors compared to no treatment? If steroids are given, what dose should be used? Comparisons include: (1) steroid therapy versus none. (2) comparison of different doses of steroid therapy. Target population These recommendations apply to adults diagnosed with brain metastases. Recommendations Steroid therapy versus no steroid therapy Asymptomatic brain metastases patients without mass effect Insufficient evidence exists to make a treatment recommendation for this clinical scenario. Brain metastases patients with mild symptoms related to mass effect Level 3 Corticosteroids are recommended to provide temporary symptomatic relief of symptoms related to increased intracranial pressure and edema secondary to brain metastases. It is recommended for patients who are symptomatic from metastatic disease to the brain that a starting dose of 4–8 mg/day of dexamethasone be considered. Brain metastases patients with moderate to severe symptoms related to mass effect Level 3 Corticosteroids are recommended to provide temporary symptomatic relief of symptoms related to increased intracranial pressure and edema secondary to brain metastases. If patients exhibit severe symptoms consistent with increased intracranial pressure, it is recommended that higher doses such as 16 mg/day or more be considered. Choice of Steroid Level 3 If corticosteroids are given, dexamethasone is the best drug choice given the available evidence. Duration of Corticosteroid Administration Level 3 Corticosteroids, if given, should be tapered slowly over a 2 week time period, or longer in symptomatic patients, based upon an individualized treatment regimen and a full understanding of the long-term sequelae of corticosteroid therapy. Given the very limited number of studies (two) which met the eligibility criteria for the systematic review, these are the only recommendations that can be offered based on this methodology. Please see “Discussion” and “Summary” section for additional details

Molecular and phenotypic characterisation of paediatric glioma cell lines as models for preclinical drug development.

Although paediatric high grade gliomas resemble their adult counterparts in many ways, there appear to be distinct clinical and biological differences. One important factor hampering the development of new targeted therapies is the relative lack of cell lines derived from childhood glioma patients, as it is unclear whether the well-established adult lines commonly used are representative of the underlying molecular genetics of childhood tumours. We have carried out a detailed molecular and phenotypic characterisation of a series of paediatric high grade glioma cell lines in comparison to routinely used adult lines

Adhesive capsulitis and dynamic splinting: a controlled, cohort study

<p>Abstract</p> <p>Background</p> <p>Adhesive Capsulitis (AC) affects patient of all ages, and stretching protocols are commonly prescribed for this condition. Dynamic splinting has been shown effective in contracture reduction from pathologies including Trismus to plantar fasciitis. The purpose of this study was to examine the efficacy of dynamic splinting on patients with AC.</p> <p>Methods</p> <p>This controlled, cohort study, was conducted at four physical therapy, sports medicine clinics in Texas and California. Sixty-two patients diagnosed with Stage II Adhesive Capsulitis were grouped by intervention. The intervention categories were as follows: Group I (Control); Group II (Physical Therapy exclusively with standardized protocols); Group III; (Shoulder Dynasplint system exclusively); Group IV (Combined treatment with Shoulder Dynasplint and standardized Physical Therapy). The duration of this study was 90 days for all groups, and the main outcome measures were change in active, external rotation.</p> <p>Results</p> <p>Significant difference was found for all treatment groups (p < 0.001) following a one-way ANOVA. The greatest change with the smallest standard deviation was for the combined treatment group IV, (mean change of 29°).</p> <p>Conclusion</p> <p>The difference for the combined treatment group was attributed to patients' receiving the best PT combined with structured "home therapy" that contributed an additional 90 hours of end-range stretching. This adjunct should be included in the standard of care for adhesive Capsulitis.</p> <p>Trial Registration</p> <p><b>Trial Number</b>: NCT00873158</p

VISMapper: ultra-fast exhaustive cartography of viral insertion sites for gene therapy

Background -- The possibility of integrating viral vectors to become a persistent part of the host genome makes them a crucial element of clinical gene therapy. However, viral integration has associated risks, such as the unintentional activation of oncogenes that can result in cancer. Therefore, the analysis of integration sites of retroviral vectors is a crucial step in developing safer vectors for therapeutic use. Results -- Here we present VISMapper, a vector integration site analysis web server, to analyze next-generation sequencing data for retroviral vector integration sites. VISMapper can be found at: http://vismapper.babelomics.org. Conclusions -- Because it uses novel mapping algorithms VISMapper is remarkably faster than previous available programs. It also provides a useful graphical interface to analyze the integration sites found in the genomic context