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Las contracciones ventriculares prematuras (CVP o PVC) son activaciones eléctricas originadas en un foco ectópico del miocardio ventricular o del sistema de Purkinje. Sus mecanismos incluyen automatismo anormal, actividad desencadenada y reentrada (PMID: 37689374). Aunque pueden aparecer de forma idiopática en personas sin cardiopatía demostrable, también se asocian con enfermedad estructural o isquémica, inflamación y fibrosis miocárdica, alteraciones genéticas y del sistema de conducción, trastornos metabólicos, hipoxia, sustancias, medicamentos y activación simpática. La carga elevada y persistente puede contribuir a una miocardiopatía inducida por CVP. La relevancia clínica depende de la frecuencia, los síntomas, la relación con el ejercicio y la presencia de enfermedad cardíaca subyacente.
Question: CUÁLES SONLAS CAUSAS QUE GENERAN CONTRACCIONES VENTRICULARES PREMATURAS?
Read the full reviewThe Circle of Willis is an arterial anastomotic ring at the brain’s base that connects the anterior and posterior cerebral circulations. Through its communicating vessels, it offers a potential route for collateral blood flow when a major feeding artery is narrowed or occluded, although this protection depends on the completeness, symmetry, and caliber of its component vessels. Anatomical variation is common, with reported frequencies differing according to population, developmental stage, imaging method, and definitions of completeness. Studies have documented diverse configurations, frequent posterior communicating artery hypoplasia or aplasia, and lower completeness of the posterior than anterior portion. Embryonic development, vessel dimensions, and the balance between carotid and vertebrobasilar flow contribute to this variability. These features are relevant to cerebral ischemia, cerebrovascular disease, neurovascular imaging, and neurosurgical or endovascular planning.
Question: circle of willis
Read the full reviewLipophagy protects cells from lipotoxicity by selectively delivering lipid droplets (LDs) to lysosomes, where stored triacylglycerols are degraded and fatty acids become available for controlled oxidation, export, or re-esterification. This process limits the accumulation of excess LDs, nonesterified fatty acids, acylcarnitines, and other toxic lipid intermediates that can promote oxidative and endoplasmic-reticulum stress, mitochondrial dysfunction, inflammation, membrane injury, and cell death. Evidence from hepatocytes, cardiomyocytes, and macrophage-like cells identifies coordinated regulation by AMPK–ULK1, mTORC1–PLIN3, SIRT3, ATGL–SIRT1–PPARα, and lysosomal pathways. Lipophagy can also redirect mobilized fatty acids toward temporary triacylglycerol storage, thereby preserving mitochondrial integrity. However, protection requires complete autophagic flux and adequate oxidation or re-esterification; excessive mobilization or defective lysosomal degradation may instead worsen lipid stress.
Question: How lipophagy protect cell against lipitoticity
Read the full reviewLa néphrostomie percutanée peut être réalisée sous guidage échographique, fluoroscopique ou combiné. L’échographie fournit une visualisation anatomique en temps réel, permet d’éviter les structures adjacentes et n’expose ni le patient ni l’équipe aux rayonnements. La fluoroscopie complète cette approche en contrôlant la progression du guide, la dilatation du trajet et le positionnement final du cathéter, mais implique une irradiation et nécessite souvent un produit de contraste. Les données disponibles rapportent des taux élevés de succès pour les techniques échoguidées et combinées, avec une réduction des tentatives, du temps opératoire et de l’exposition aux rayons dans plusieurs contextes. La combinaison échographie–fluoroscopie est particulièrement utile lorsque l’anatomie est complexe, que le système collecteur est peu dilaté ou qu’une confirmation radiologique est nécessaire.
Question: Nephrostomie percutané échographie fluoroscopie
Read the full reviewAcute kidney injury (AKI) management is primarily supportive and centers on promptly identifying and reversing the precipitating disorder, restoring adequate renal perfusion, preventing additional injury, monitoring complications, and providing renal replacement therapy (RRT) when clinically necessary. Fluid therapy should be individualized because both inadequate resuscitation and fluid overload may be harmful. Medication review, renal dose adjustment, selective diuretic use, nutritional support, and close assessment of electrolytes, acid–base status, urine output, and fluid balance are essential. RRT is indicated for life-threatening or medically refractory complications rather than for an isolated creatinine concentration or AKI stage. Intermittent and continuous modalities are established options, with selection determined by hemodynamic stability, fluid and solute removal needs, clinical urgency, resources, and expertise. Evidence remains uncertain regarding optimal timing, dose, anticoagulation, and discontinuation, requiring frequent reassessment and individualized clinical judgment (PMID: 28284300; PMID: 33334463).
Question: How to treat aki
Read the full reviewLa sindrome di Fanconi è una disfunzione generalizzata, completa o parziale, del tubulo prossimale renale, con perdita urinaria combinata di bicarbonato, fosfato, glucosio, aminoacidi, acido urico, elettroliti, acqua e proteine a basso peso molecolare. Il quadro tipico comprende glicosuria normoglicemica, fosfaturia, aminoaciduria, proteinuria tubulare e acidosi metabolica ipercloremica a gap anionico normale; possono inoltre comparire ipokaliemia, poliuria, disidratazione, rachitismo, osteomalacia e progressione della malattia renale. La sindrome è un quadro fisiopatologico comune a numerose condizioni ereditarie o acquisite. Nei bambini predominano cistinosi e altre malattie metaboliche o genetiche, mentre negli adulti sono rilevanti farmaci nefrotossici, metalli pesanti, gammopatie monoclonali e mieloma multiplo. La diagnosi richiede la dimostrazione di più difetti di riassorbimento prossimale e la ricerca della causa. Il trattamento combina reintegro delle perdite, gestione delle complicanze e terapia eziologica, con monitoraggio prolungato della funzione renale, dell’equilibrio elettrolitico e della salute ossea (PMID: 36729281; PMID: 30454741; PMID: 21252524).
Question: Tutto sulla sindrome di fanconi
Read the full reviewReverse-genetics technology has contributed to the development and manufacture of several viral vaccines, but the supplied evidence varies in its ability to link specific products directly to the method. The clearest evidence concerns influenza vaccines, particularly live attenuated influenza vaccines (LAIVs) and other reassortant or recombinant preparations. These products can be generated by combining hemagglutinin and neuraminidase genes from relevant circulating strains with the six internal gene segments of an attenuated master donor virus. Reverse genetics also supported the construction of Dengvaxia, a tetravalent live-attenuated chimeric dengue vaccine based on yellow fever 17D backbones expressing dengue structural proteins. Evidence concerning rotavirus and other viral vaccines indicates contributions from reverse-genetics or recombinant systems, but does not consistently establish direct derivation of each licensed product. Several experimental influenza and arenavirus candidates should not be classified as approved vaccines. Overall, reverse genetics is best understood as an enabling technology for defined vaccine-virus construction, strain updating, and vaccine development rather than as evidence that a particular product was approved exclusively through this method.
Question: approved viral vaccines developed through reverse genetics technology
Read the full reviewBK polyomavirus (BKV) and JC polyomavirus (JCV) are ubiquitous human polyomaviruses that usually cause asymptomatic primary infection followed by latent persistence. Reported prevalence differs according to population, age, geographic region, specimen type, detection method, and whether infection is assessed by serology or viral DNA. BKV seroprevalence is generally high, ranging from approximately 65% to 99% across the supplied studies, whereas JCV seroprevalence is more variable and generally lower, with a meta-analytic estimate of 61%. Viral DNA detection is less frequent and varies substantially by specimen and population. Available data do not establish reliable prevalence estimates for BKV genotypes I–IV, although genotype III was identified among urinary BKV-positive samples in one study. Reactivation is clinically important in immunocompromised populations, particularly because BKV is associated with BK polyomavirus–associated nephropathy and JCV with progressive multifocal leukoencephalopathy (PMID: 40509546; PMID: 31911182).
Question: Prevalence of BKV I-IV, JCV
Read the full reviewLong COVID, also termed post-COVID-19 condition or post-acute sequelae of SARS-CoV-2 infection (PASC), comprises symptoms and health complications that persist, recur, or newly develop after acute COVID-19. It can follow severe or mild infection, including infection managed without hospitalization, and affects adults and children. Manifestations span respiratory, cardiovascular, neurological, musculoskeletal, gastrointestinal, psychological, and autonomic domains, with fatigue, post-exertional worsening, dyspnea, cognitive difficulties, pain, palpitations, sleep disturbance, and altered smell or taste among commonly reported symptoms (PMID: 34024217; PMID: 34163217; PMID: 34265229). Long COVID is biologically heterogeneous and may reflect overlapping tissue injury, viral persistence or remnants, persistent inflammation, immune dysregulation, autoimmunity, endothelial or microvascular abnormalities, and autonomic dysfunction (PMID: 35874958; PMID: 35272932; PMID: 37351054). Its symptoms may last beyond a year and impair daily functioning, education, employment, and quality of life. Diagnosis and care therefore require individualized, multidisciplinary assessment, while disease-specific treatments and reliable biomarkers remain insufficiently established.
Question: longcovid
Read the full reviewLa evidencia disponible indica que la tiroiditis subaguda y las alteraciones transitorias de la función tiroidea pueden aparecer después de la infección por SARS-CoV-2 y, con menor frecuencia, tras la vacunación contra COVID-19. Los datos sobre AstraZeneca (ChAdOx1/AZD1222/Vaxzevria) proceden principalmente de informes y series de casos, con escasos estudios observacionales y sin comparaciones directas adecuadas con la infección. La presentación posvacunal suele corresponder a una fase hipotiroidea transitoria de una tiroiditis subaguda, precedida por tirotoxicosis. Aunque se han descrito casos de hipotiroidismo manifiesto y exacerbación de enfermedad tiroidea previa, no se ha demostrado causalidad individual ni un riesgo específico superior al asociado con SARS-CoV-2. La mayoría de los casos evoluciona favorablemente, pero puede requerirse seguimiento de TSH y T4 libre.
Question: Hipotiroidismo post vacunación vs. COVID29 con vacuna Astra Zeneca
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