Metabolic Brain Disease - Schizophrenia is a debilitating mental illness. Levels of oxytocin have been proposed as a biomarker of schizophrenia; however, the observed levels of oxytocin in... 相似文献
The prevalence of Barrett's esophagus has been calculated at between 1.3 and 1.6%. There is little information with respect to this in Mexico.
Aim
To determine the frequency and characteristics of Barrett's esophagus in patients that underwent endoscopy at a national referral center, within a 10-year time frame.
Material and methods
The databases of the pathology and gastrointestinal endoscopy departments of the Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán” were analyzed, covering the period of January 2002 to December 2012. Patients with a histologic diagnosis of Barrett's esophagus were included. The variables of age, sex, the presence of dysplasia/esophageal adenocarcinoma, Barrett's esophagus length, and follow-up were analyzed.
Results
Of 43,639 upper gastrointestinal endoscopies performed, 420 revealed Barrett's esophagus, corresponding to a frequency of 9.6 patients for every 1,000 endoscopies. Of those patients, 66.9% (n = 281) were men, mean patient age ± SD was 57.2 ± 15.3 years, 223 patients (53%) presented with long-segment Barrett's esophagus, and 197 (47%) with short-segment Barrett's esophagus. Dysplasia was not present in 339 patients (80.7%). Eighty-one (19.3%) patients had some grade of dysplasia or cancer: 48/420 (11.42%) presented with low-grade dysplasia, 20/420 (4.76%) with high-grade dysplasia, and 13/420 (3.1%) were diagnosed with esophageal cancer arising from Barrett's esophagus. Mean follow-up time was 5.6 years.
Conclusions
The frequency of Barrett's esophagus was 9.6 cases for every 1,000 upper gastrointestinal endoscopies performed. Dysplasia was not documented in the majority of the patients with Barrett's esophagus and they had no histopathologic changes during follow-up. A total of 19.3% of the patients presented with dysplasia or cancer. 相似文献
Introduction: Eosinophilic esophagitis (EoE) is a chronic, allergen-driven inflammatory esophageal disease characterized by predominantly eosinophilic inflammation leading to esophageal dysfunction. Recent efforts to understand EoE have increased our knowledge of the disease.
Areas covered: Multiple cells, molecules, and genes interplay with early life environmental factors in the pathophysiology of EoE to converge in the esophageal epithelium at the center of disease pathogenesis. Epithelial cells constitute a mayor cytokine source for TSLP and Calpain-14; an impaired epithelial barrier function allowing penetration of food and microbiota-derived antigens is involved in triggering and maintaining inflammation. Eosinophil and mast cell-derived products, including TGFβ, together with IL-1β and TNFα, promote epithelial mesenchymal transition in EoE, contributing to tissue remodeling by synthetizing and depositing extracellular matrix in subepithelial layers. This article aims to provide a state-of-the-art update on the pathophysiology of EoE applied to clinical practice, and latest research and developments with potential interest to improve the diagnosis and treatment of patients with EoE are revised.
Expert commentary: Preliminary approaches have provided promising results toward incorporating minimally invasive methods for patient diagnosis and monitoring in clinical practice. Early diagnosis and optimized therapies will allow for personalized medicine in EoE. 相似文献
Transdermic administration by electroporation has developed over recent years for applying drugs in a variety of pathological processes. However, mechanisms are still not finally settled. India ink was applied to the backs of guinea pigs and for the transdermic transport short, high-voltage pulses (TDES, Dencort Dell) were administrated. Punch biopsies (4 mm) immediately taken after 24, 48, 72, 96 and at 26 days were studied by light and electronic microscopy. The ultrastructural characteristics and image pigment particles were reported. Particles of India ink were observed in the stratum corneum and in the epidermic keratinocytes of samples studied immediately after treatment. Particles were also seen in the epidermic and folicular keratinocytes, and in the papillary and reticular dermis (among collagen fibers, vessel walls, and macrophages) in all the subsequent biopsies; but not in the controls, which were conducted with electromagnetic waves alone. No tissue alterations were observed. The efficacy and noninvasive nature of electroporation for the transdermic administration of macromolecules is confirmed. 相似文献
Journal of Autism and Developmental Disorders - The objective of our study was to evaluate the frequency of treatable inborn errors of metabolism (IEM) in a clinical sample of Mexican children and... 相似文献
Nerve growth factor (NGF) is an important modulator of rat pancreatic β-cell physiology in vitro. In this study, we analysed the expression of NGF, TrkA and insulin in human pancreatic islets from normal, ductal adenocarcinoma and insulinoma-afflicted samples, using double immunofluorescent labelling and confocal microscopy.We found that in normal human pancreas, insulin and NGF are co-expressed in β cells. Moreover, similar to previous observations in rat, the high affinity NGF receptor TrkA is also expressed in β cells.Pancreatic β cells in normal islets from adenocarcinoma and mucinous cystadenocarcinoma patients also expressed NGF. In 2 out of 15 exocrine tumour samples, NGF was detected also in the tissue surrounding the islets, while 2 out of 13 adenocarcinoma tumours expressed this growth factor.In five insulinoma samples, we observed weaker immunofluorescent labelling of insulin and NGF in the neoplastic tissue, compared to the islets not afflicted by the tumour, which may be a consequence of increased hormone secretion rate.We demonstrate that human β cells express TrkA and NGF. These findings are consistent with the hypothesis that NGF modulates insulin secretion through a paracrine/autocrine loop, similar to the one observed in cultured rat β cells. 相似文献
Up until fairly recently, it was thought that sciatic pain in the lumbar herniated disc was caused by compression on the nerve root. However, the lumbar herniated disc shows mixed pictures which are difficult to explain by simple mechanical compromise. In recent years various immunology, immunohistochemistry and molecular biology studies have shown that the herniated tissue is not an inert material, but rather it Is biologically very active with the capability of expressing a series of inflammatory mediators: cytokines such as interleukin-1, interleukin-6, interleuquin-8 and tumor necrosis factor being the ones which stand out. The inflammation is not only induced by the chemical irritation of the bioactive substances released by the nucleus pulposus but also by an autoimmune response against itself. Thus, in addition to the mechanical factor, the biomechanical mediation plays an important role in the pathophysiology of sciatic pain and of radiculopathy. Through a review of a wide range of literature, we researched the cellular molecular mediators involved in this inflammatory process around the lumbar herniated disc and its involvement in sciatic pain. 相似文献
The genetic variability of 24 Trypanosoma cruzi isolates from humans (11) and triatomines (13) in northeastern Brazil was analyzed by random amplified polymorphic DNA (RAPD) and compared with taxonomic groups, host, and geographical origin of the parasite. TcI (12.5 %), TcII (45.8 %), and TcIII (41.6 %) showed a similarity coefficient (SC) of 0.74 using the mean of three primers and 0.80, 0.75, and 0.66 for λgt11-F, M13-40F, and L15996 primers, respectively. The samples were clustered according to their phylogenetic origin in two polymorphic and divergent branches: one associated with TcI and the other with two subbranches corresponding to TcII and TcIII. TcI was only identified in humans and correlated with the Id homogenous group (0.80 SC). TcII from humans and Triatoma brasiliensis showed 0.86 SC and was clustered according monoclonal or polyclonal populations with similar RAPD profiles detected among the vector and/or humans in different municipalities. TcIII was isolated exclusively in sylvatic cycles from T. brasiliensis and Panstrongylus lutzi and showed low variability (0.84 SC) and high homology mainly among isolated populations at the same locality. The homology of T. cruzi among different hosts and locations suggests the distribution of principal clones circulating and reveals an overlapping between the sylvatic and domestic cycles in this area, where T. brasiliensis infected with TcII acts as link in both environments. This species is important to maintain TcII and TcIII in wild cycles and deserves particular attention due an emergent risk of these populations being introduced into the domestic cycle; moreover, its clinical and epidemiological implications remain unknown. 相似文献
Acute gastroenteritis (AGE) is a leading cause of disease worldwide. The aim of this prospective observational study is to describe the epidemiology of AGE in closed and semi-closed institutions in Catalonia. In 2017, 151 outbreaks were reported; 30.5% occurred in closed and semi-closed institutions; 71.7% caused by norovirus (NoV) (1532) cases. Person-to-person transmission accounted for 75.8% of NoV outbreaks vs 46.1% in non-NoV outbreaks (p?<?0.001). Attack rate for NoV outbreaks was 33.1% vs 14.3% for non-NoV outbreaks (RR?=?2.3; 95%CI: 2.0–2.7). The high number of affected underscores prompt and intense preventive measures to avoid the extension and perpetuation of outbreaks in these settings.
SARS-CoV-2 infection causes an abrupt response by the host immune system, which is largely responsible for the outcome of COVID-19. We investigated whether the specific immune responses in the peripheral blood of 276 patients were associated with the severity and progression of COVID-19. At admission, dramatic lymphopenia of T, B, and NK cells is associated with severity. Conversely, the proportion of B cells, plasmablasts, circulating follicular helper T cells (cTfh) and CD56–CD16+ NK-cells increased. Regarding humoral immunity, levels of IgM, IgA, and IgG were unaffected, but when degrees of severity were considered, IgG was lower in severe patients. Compared to healthy donors, complement C3 and C4 protein levels were higher in mild and moderate, but not in severe patients, while the activation peptide of C5 (C5a) increased from the admission in every patient, regardless of their severity. Moreover, total IgG, the IgG1 and IgG3 isotypes, and C4 decreased from day 0 to day 10 in patients who were hospitalized for more than two weeks, but not in patients who were discharged earlier. Our study provides important clues to understand the immune response observed in COVID-19 patients, associating severity with an imbalanced humoral response, and identifying new targets for therapeutic intervention. 相似文献