Aim: To evaluate the feasibility and utility of confocal laser endomicroscopy (CLE) in the description of normal gastrointestinal (GI) mucosa and in the diagnosis of GI disorders in children, in comparison to histology.
Methods: Forty-four patients (19 female) median age 10.9 years (range 0.7-16.6 years) with suspected or known GI pathology underwent esophago-gastro-duodenoscopy (OGD) (n = 36) and/or ileocolonoscopy (IC) (n = 31) with CLE using sodium fluorescein and acriflavine as contrast agents. Histological sections were compared with same site confocal images by two experienced pediatric and GI histopathologists and endoscopists, respectively.
Results: Duodenum and ileum were intubated in all but one patient undergoing OGD and IC. The median procedure time was 16.4 min (range 7-25 min) for OGD and 27.9 min (range 15-45 min) for IC. A total of 4798 confocal images were compared with 153 biopsies from the upper GI tract from 36 procedures, and 4661 confocal images were compared with 188 biopsies from the ileocolon from 31 procedures. Confocal images were comparable to conventional histology both in normal and in pathological conditions such as esophagitis, Helicobacter pylori gastritis, celiac disease, inflammatory bowel disease, colonic heterotopia, and graft versus host disease.
Conclusion: CLE offers the prospect of targeting biopsies to abnormal mucosa, thereby increasing diagnostic yield, reducing the number of biopsies, decreasing the burden on the histopathological services, and reducing costs.
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http://dx.doi.org/10.3748/wjg.15.2214 | DOI Listing |
Alzheimers Dement
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Pacific Brain Health Center, Pacific Neuroscience Institute Foundation, Santa Monica, CA, USA.
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Method: RNAseq, immunochemistry of the brain, immunofluorescence, and confocal microscopy of macrophages.
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Alzheimers Dement
December 2024
Interdisciplinary Institute for Neuroscience (UMR 5297), University of Bordeaux, Bordeaux, Gironde, France.
This is a maximal intensity projection of CA1 pyramidal cell transfected with plasmid with the reporter GFP using single cell electroporation technique. In this particular case the organotypic slices were prepared from p5-7 pups in a tissue chopper (McIlwain). And maintained in MEM bases media with added glutamax with a change in 2 alternative dyas at 37°C and 5% CO for 4 days in-vitro (DIV) before electroporating with a glass pipette of 7-10mΩ resistance by applying 4 square pulses of -ve voltage of -2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Arizona, Tucson, AZ, USA.
Background: Cerebral microvascular dysfunction and nitro-oxidative stress are present in patients with Alzheimer's disease (AD) and may contribute to disease progression and severity. A pro-nitro-oxidative environment can lead to post-translational modifications of ion channels central to microvascular regulation in the brain, including the large conductance Ca-activated K channels (BK). Nitro-oxidative modulation of BK can resulting in decreased activity and vascular hyper-contractility, thus compromising neurovascular regulation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Background: Alzheimer's disease (AD) is a neurological disorder marked by progressive cognitive decline, memory deficits, and neuronal cell loss (Knopman, 2021). A brain region significantly impacted by the progression of AD is the subiculum, a structure responsible for spatial navigation, cognitive processes, and the modulation of emotional and affective behaviors within the hippocampus (Fanselow and Dong, 2010). Although subiculum cell loss has been well-established as an early indicator of AD (Carlesimo et al.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The University of Sydney, Sydney, NSW, Australia.
Background: SMOC1 has recently emerged as one of the most significant and consistent new biomarkers of early Alzheimer's disease (AD). SMOC1 is one of the earliest changing proteins in AD, with SMOC1 cerebrospinal fluid levels increasing 29 years before symptom onset in autosomal dominant AD. Despite this clear association with disease, very little is known about the role of SMOC1 in AD or its function in the brain.
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