Spontaneous pneumomediastinum is a rare disease with a benign course, which should be treated conservatively unless a complication mandates an invasive procedure. An algorithm for diagnosis and treatment is offered, based on the available evidence.
Alpha-synuclein (α-syn) is localized in cellular organelles of most neurons, but many of its physiological functions are only partially understood. α-syn accumulation is associated with Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy as well as other synucleinopathies; however, the exact pathomechanisms that underlie these neurodegenerative diseases remain elusive. In this review, we describe what is known about α-syn function and pathophysiological changes in different cellular structures and organelles, including what is known about its behavior as a prionlike protein. We summarize current knowledge of α-syn and its pathological forms, covering its effect on each organelle, including aggregation and toxicity in different model systems, with special interest on the mitochondria due to its relevance during the apoptotic process of dopaminergic neurons. Moreover, we explore the effect that α-syn exerts by interacting with chromatin remodeling proteins that add or remove histone marks, up-regulate its own expression, and resume the impairment that α-syn induces in vesicular traffic by interacting with the endoplasmic reticulum. We then recapitulate the events that lead to Golgi apparatus fragmentation, caused by the presence of α-syn. Finally, we report the recent findings about the accumulation of α-syn, indirectly produced by the endolysosomal system. In conclusion, many important steps into the understanding of α-syn have been made using in vivo and in vitro models; however, the time is right to start integrating observational studies with mechanistic models of α-syn interactions, in order to look at a more complete picture of the pathophysiological processes underlying α-synucleinopathies.
Mirizzi syndrome, known as extrinsic bile compression syndrome, is a rare complication of cholecystitis and chronic cholelithiasis, secondary to the obliteration of the infundibulum of the gallbladder or cystic duct caused by the impact of one or more calculations in these anatomical structures, which leads to compression of the adjacent bile duct, resulting in partial or complete obstruction of the common hepatic duct, triggering liver dysfunction. Our aim is to identify and describe the current epidemiology, diagnostic methods, and treatment of Mirizzi syndrome. A literature search was performed using different databases, including Medline, Cochrane, Embase, Medscape, PubMed, using keywords: Mirizzi syndrome, epidemiology, markers, pathophysiology, clinical presentation, diagnosis, and treatment. Selected original articles, review articles or case reports from 1997 to 2015 were collected, written in English or Spanish. The endoscopic retrograde cholangiopancreatography (ERCP) is the most accurate diagnostic method. The traditional treatment has been surgery and involves an incision at the bottom of the gallbladder and calculus removal. If fistulas are observed, it is performed a partial cholecystectomy; otherwise, a cholecystocholedochoduodenostomy is an alternative. Endoscopic treatment includes biliary drainage and stone extraction. Many surgeons claim that laparoscopic cholecystectomy is contraindicated in Mirizzi syndrome because of the presence of inflammatory tissue and adhesions in the Calot's triangle. If dissection is attempt, it can cause unnecessary injury to the bile duct. However, other surgeons consider the laparoscopic approach is feasible, although technically challenging. Currently, laparoscopic cholecystectomy for this condition is considered controversial and technically challenging; however, it has shown that with the right skills and equipment, it is a safe and feasible way to treat some cases of Mirizzi syndrome type I and II.
In this low socioeconomic status patient population, descending necrotizing mediastinitis below the carina causes high morbidity and mortality, the latter particularly associated with age, complications, diabetes mellitus and other comorbidities.
Dysfunction of cellular homeostasis can lead to misfolding of proteins thus acquiring conformations prone to polymerization into pathological aggregates. This process is associated with several disorders, including neurodegenerative diseases, such as Parkinson’s disease (PD), and endoplasmic reticulum storage disorders (ERSDs), like alpha-1-antitrypsin deficiency (AATD) and hereditary hypofibrinogenemia with hepatic storage (HHHS). Given the shared pathophysiological mechanisms involved in such conditions, it is necessary to deepen our understanding of the basic principles of misfolding and aggregation akin to these diseases which, although heterogeneous in symptomatology, present similarities that could lead to potential mutual treatments. Here, we review: (i) the pathological bases leading to misfolding and aggregation of proteins involved in PD, AATD, and HHHS: alpha-synuclein, alpha-1-antitrypsin, and fibrinogen, respectively, (ii) the evidence linking each protein aggregation to the stress mechanisms occurring in the endoplasmic reticulum (ER) of each pathology, (iii) a comparison of the mechanisms related to dysfunction of proteostasis and regulation of homeostasis between the diseases (such as the unfolded protein response and/or autophagy), (iv) and clinical perspectives regarding possible common treatments focused on improving the defensive responses to protein aggregation for diseases as different as PD, and ERSDs.
Peripheral blood mononuclear cells (PBMCs) contain a cell fraction of mononuclear progenitor cells (MPCs), which own significant angiogenic potential. Autologous transplant of PBMC and/or platelet-rich plasma (PRP) promotes endothelial cells differentiation in experimental lower limb ischemia, which is considered a safe and effective strategy to support revascularization, either in animal models or clinical trials. In addition, thrombin has been proposed to enrich biological scaffolds, hence increasing MPC viability after intramuscular administration, whereas proangiogenic mediators such as vascular endothelial growth factor (VEGF), tumor necrosis factor alpha (TNF-α), inhibitor of the plasminogen activator-1 (PAI-1), and chemokine (CXCL1; GRO-α) participate in the endothelial response to ischemia, through their proangiogenic effects over endothelial cells proliferation, survival, migration, endothelial integrity maintenance, and physiologic vascular response to injury. In the present study, we describe the effect of autologous PBMCs transplant and PRP, either with or without thrombin, over proangiogenic mediators (measured by enzyme-linked immunosorbent assay) and revascularization response (angiographic vascular pattern at 30 days after vascular occlusion) in a rat model of lower limb ischemia. The group treated with PBMC + PRP significantly induced PAI-1, an effect that was prevented by the addition of thrombin. Furthermore, treatment with PBMC + PRP + thrombin resulted in the induction of VEGF. GRO-α showed a sensitive induction of all proangiogenic mediators. All treatments significantly stimulated revascularization, according to angiographic assessment, whereas higher effect was observed with PBMC + PRP treatment (p < .0001). In conclusion, autologous PBMC transplant stimulates revascularization during experimental ischemia of the lower limb, whereas
A 58-year-old man with a history of Ludwig's angina was admitted with a spinal cord abscess at the level of C2-T1 and associated osteomyelitic destruction of vertebral bodies, spinal cord compression, and secondary quadriparesis, followed by descending mediastinitis. A right posterolateral thoracotomy and a cervicotomy drained purulent exudates. A tracheostomy was performed, and the patient was discharged after 84 days.
Resultados: 1) La tasa de donación cadavérica de México en 2007 fue de 3.2 donaciones por millón de población (pmp), y en 2017 fue de 3.94 pmp (incremento del 23.1%). La tasa de 2017 está muy por debajo de la media reportada para América Latina (9.5 pmp). 2) El número de pacientes en espera de trasplante de un órgano sólido pasó de 4,993 en 2007 a 15,448 en 2018 (incremento del 309%). 3) En 2017, México reportó tener 255 centros autorizados para trasplante renal, más que cualquier país en el mundo. Para el caso de otros órganos, como hígado, corazón, pulmón y páncreas, México es el país que tiene más centros autorizados en América Latina. Conclusión: La evolución de las cifras de donación cadavérica y de trasplante de órganos sólidos en el período de estudio explica una escasez cada vez mayor de órganos para trasplante en México, a pesar de una aparente gran capacidad instalada. El sistema nacional de donación y trasplante de órganos es ineficaz e ineficiente.
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