RESUMEN
The utilization rates of laparoscopic gastric banding (LAGB) declined worldwide from 42.3% in 2008 to 1.8% in 2018. Rates of complications requiring removal may reach 40-50% in the medium to long term. Bowel obstruction is a rare but severe complication that occurs after LAGB. A comprehensive literature search in PubMed was carried out to identify all available case reports of intestinal obstruction after gastric banding. The search terms were as follows: "intestinal obstruction", "small bowel obstruction", "gastric band", "gastric banding", "gastric band complications", and "laparoscopic gastric band obstruction". The Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) flowchart was used. Forty-three case reports were included in our review. Laparotomy was necessary in 18/43 (41%) of patients. Vomit was not always reported, while abdominal pain was constantly present. A CT scan was the preferred diagnostic tool. The main causes of occlusion were found to be the erosion of the gastrointestinal tract or internal hernia due to a loose tube loop. Forty-six percent of cases occurred within 5 years from insertion. Even if rare, small bowel obstruction after LAGB requires surgical intervention often with an open approach. The absence of vomit masks symptoms, but an obstruction must be always suspected in the case of severe colicky abdominal pain. A CT scan is recommended for making diagnoses.
RESUMEN
Layer 1 (L1) of the neocortex acts as a nexus for the collection and processing of widespread information. By integrating ascending inputs with extensive top-down activity, this layer likely provides critical information regulating how the perception of sensory inputs is reconciled with expectation. This is accomplished by sorting, directing, and integrating the complex network of excitatory inputs that converge onto L1. These signals are combined with neuromodulatory afferents and gated by the wealth of inhibitory interneurons that either are embedded within L1 or send axons from other cortical layers. Together, these interactions dynamically calibrate information flow throughout the neocortex. This review will primarily focus on L1 within the primary sensory cortex and will use these insights to understand L1 in other cortical areas.
Asunto(s)
Neocórtex , Neocórtex/fisiología , Interneuronas/fisiología , Axones , Movimiento Celular , Técnicas de Placa-ClampRESUMEN
Human induced pluripotent stem cells (hiPSCs) have been used extensively in vitro to model early events in neurodevelopment. Because of a number of shortcomings, previous work has established a potential to use these cells in vivo after transplantation into the mouse brain. Here, we describe a systematic approach for the analysis of transplanted hiPSC-derived neurons and glial cells over time in the mouse brain. Using functional two-photon imaging of GCaMP6f- expressing human neural cells, we define and quantify the embryonic-like features of their spontaneous activity. This is substantiated by detailed electron microscopy (EM) of the graft. We relate this to the synaptic development the neurons undergo up to 7 months in vivo. This system can now be used further for the genetic or experimental manipulation of developing hiPSC-derived cells addressing neurodevelopmental diseases like schizophrenia or Autism Spectrum Disorder.
RESUMEN
Altered glutamatergic neurotransmission is thought to play a crucial role in the progression of Alzheimer's disease (AD). Accordingly, the identification of peculiar biochemical patterns reflecting AD-related synaptopathy in blood and cerebrospinal fluid (CSF) could have relevant diagnostic and prognostic implications. In this study, we measured by High-Performance Liquid Chromatography the amount of glutamate, glutamine and glycine in post-mortem brain samples of AD patients, as well as in CSF and blood serum of drug-free subjects encompassing the whole AD clinical spectrum (pre-clinical AD, n = 18, mild cognitive impairment-AD, n = 29, dementia AD, n = 30). Interestingly, we found that glutamate and glycine levels, as well as total tau protein content, were significantly reduced in the superior frontal gyrus of patients with AD, compared with non-demented controls. No significant change was also found in glutamate, glutamine and glycine CSF concentrations between AD patients and neurological controls. Remarkably, serum glutamate levels were significantly higher in patients affected by early AD phases compared to controls, and were negatively correlated with CSF total tau levels. Conversely, serum glutamine concentration was significantly increased in AD patients, with a negative correlation with MMSE performances. Finally, we reported a significant correlation between serum L-glutamate concentrations and CDR score in female but not in male cohort of AD subjects. Overall, our results suggest that serum glutamate and glutamine levels in AD patients could vary across disease stages, potentially reflecting the progressive alteration of glutamatergic signaling during neurodegenerative processes.