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Filter by:During last years, non-caloric sweeteners (NCSs) have been increasingly incorporated into foodstuffs in replacement of sucrose in Chile. This situation has reached a point where it is currently difficult to find sugary foods without NCSs. As a result, the voluntary and involuntary consumption of these additives is growing significantly in the population, increasing the risk of exceeding the acceptable daily intake (ADI), especially for children. This situation is worrying as recent evidence suggests that NCSs are not inert in the body and can trigger adverse metabolic effects. For example, the consumption of beverages with NCSs has been shown to favor the development of obesity and type-2 diabetes in children and adults, and a recent study reported that the intake of NCSs during pregnancy was associated with a greater weight gain of the child at one year. It is likely that certain NCSs pass into the amniotic fluid and that the fetus is exposed to some of these compounds during pregnancy. This situation would persist in the infant through breast milk, as some studies detected sucralose and acesulfame-K in this fluid, even in mothers who claimed not to consume them. However, the real impact of NCS exposure during the neonatal period on the child health has been few studied. Therefore, the aim of this study is to determine the concentration of NCSs in samples of amniotic liquid and breastmilk and to correlate these data with the NCS intake by the mothers. Mothers/children will be classified in quintiles according to the results obtained. In the children from quintiles 1 and 5, we will also study whether neonatal exposure to NCSs may affect the sweet taste threshold and the preferences for this taste, the levels of salivary insulin and the weight gain in the first year. Breastmilk microbiota and child fecal microbiota will be also evaluated.
We hypothesize that combined critical care ultrasound and PAC monitoring-oriented therapy protocol (CUP protocol), would improve prognosis of patients of ARDS with right ventricular dysfunction. Therefore, the overall goal of the study is: 1) To build the combined critical care ultrasound and PAC monitoring-oriented therapy protocol （CUP Protocol）in detail for patients of ARDS with RV dysfunction. Advantage of CUP protocol is that it directly aims at key parameters that we need for the prevention and treatment of such patients; we could improve the mechanical ventilation protocol, unequal pulmonary lesions, hemodynamics management and reduce pulmonary artery pressure according to these parameters, so that to improve the prognosis of the patients.2) To verify the value of CUP Protocol in ARDS with ACP.
The advent of high throughput genomic DNA sequencing has led to major advances in the diagnosis of genetic diseases of heterogeneous origin. Thus, our hospital laboratory has developed in recent years several diagnostic tests based on the targeted sequencing of coding sequences of gene panels (from about twenty genes for DNA repair diseases to nearly five hundred genes for the intellectual disability). These targeted analyzes, carried out by capture, have thus solved 25 to 80% of the cases according to the indications, without allowing the diagnosis of the totality of the patients. For these negative cases, the search for mutations in the coding sequences was then extended to Whole Exome Sequencing, thus providing several additional diagnoses. Patients still remain without diagnosis after this exome study. These could be complex cases of genetic or even non-genetic origin, but also monogenic pathologies linked to mutations that are not identifiable by coding sequence analyzes, and especially affecting messenger RNAs.
The prognosis of extensive-stage small cell lung cancer is still very poor, even for those who received platinum-based chemotherapy and chest radiotherapy. 2-year survival rate of these patients is only about 10%. Therefore, this study aims to explore a comprehensive treatments with low toxicity to further improve the efficacy for these paitents with PD-1 inhibitor.
Sepsis is a dysregulated host response to severe life-threatening infections, leading to organ failure and death in up to 40% of patients with septic shock. Pulmonary infections are the main cause of community-acquired sepsis and frequently lead to the development of acute respiratory distress syndrome(ARDS). Features of immunosuppression, including diminished cell surface monocyte human leukocyte antigen DR (mHLA-DR) expression, are strongly associated with hospital mortality. Such decrease in HLA-DR expression on antigen-presenting cells has been associated with impairment of microbial antigens to Tcells. Septic patients also show elevated expression of inhibitory receptors associated with cell exhaustion.. Yet, biochemical, flow cytometric and immunohistochemical findings consistent with immunosuppression have been observed in lungs and spleen of patients died of sepsis and multiple organ failure, demonstrating the relevance of studying these defects directly in organ tissues. A novel approach aimed to characterize the role and prognostic value of alveolar biomarkers measured directly in the injured lungs is warranted and supported by: -disappointing results of previous clinical trials attempting to restore the level of biomarkers measured on circulating cells; -evidences of regional immunosuppression in lungs of ARDS patients; -lung is the main site of hospital-acquired infections with a prevalence of ventilator-associated pneumonia in 30% over the course of Intensive Care Unit(ICU) stay in ARDS patients. Investigators speculate that biomarkers measured on alveolar leukocytes (AL) surface, are important predictors of outcome and potential therapeutic targets in ICU patients with pneumonia-associated ARDS. Investigators aim to explore whether biomarkers measured directly on AL from patients with pneumonia-associated ARDS are associated to regional pulmonary immunosuppression using leukocyte functional tests; and predictors of outcomes. Bronchoalveolar lavage fluid(BALF) and blood samples will be collected in ARDS patients. Leukocyte populations and cell membrane biomarkers will be quantified using flow cytometry. Leukocyte functional tests will be performed ex vivo on leukocytes collected from BALF and blood samples. Pharmacological interventions will be performed ex vivo. This project aims to identify biomarkers associated with outcomes and potential therapeutic targets.
This is a randomized, double-blind study of MSDC-0602K or placebo in subjects with pre-T2D or T2D and evidence of NAFLD/NASH.
Many people with symptomatic Osteoarthritis (OA) report chronic joint pain, especially if those patients are older than 50 years. In Europe OA is the most common form of chronic pain condition (34%) reported and entails a high economic and social burden for society. Probiotic treatment has been shown to promote bone metabolism, reduce pain and inflammatory responses of age-related musculoskeletal disorders, including OA. Gut microbiota has been proven to be of crucial importance in maintaining human health. However, the microbiota profile changes with aging, while the loss of microbiota diversity and the alterations in the optimal composition and quantity of beneficial microbes are believed to increase the risk of many diseases. Interestingly, emerging evidence leads to the hypothesis that alterations in the gut microbiome could also be considered as possible triggering factors in the onset of musculoskeletal disorders such as OA. We hypothesize that these patients with pain-OA will demonstrate an alteration of the gut microbiota to associated with the intensity of pain.
Non-alcoholic fatty liver diseases (NAFLD) include several entities ranging from simple steatosis to hepatic fibrosis or cirrhosis. Steatosis, considered benign and the first stage of the disease, is characterized by the accumulation of triglycerides in the liver. It may in some cases progress to nonalcoholic steatohepatitis (NASH), which is characterized by the presence of a marked inflammation with or without fibrosis. NAFLD is the most common liver disease in the world and is particularly associated with type 2 diabetes (T2D) (80% in the diabetic population). While NASH is characterized by a higher prevalence of mortality from a cardiac and hepatic (cirrhosis and cancer) origin, therapeutic resources are almost non-existent. RANK (receptor activator of NF-kB) and its ligand RANKL (a member of the TNFalpha family) have emerged in recent years as new players in bone pathophysiology. By binding to its receptor, RANKL induces a number of signaling pathway and in particular the NF-kB pathway (Nuclear factor-kB), a major player in inflammation. Recent literature shows that the role of RANK / RANKL is not confined to the bone but may be involved in the genesis of inflammation in other tissues. It has been shown recently that a high circulating level of RANKL was a risk factor predictor of T2DM. Furthermore, the invalidation of RANK specifically in hepatocytes protects from insulin resistance and hepatic steatosis induced by a high fat diet in mice. The aim of our project is to provide a proof of concept that the RANKL / RANK system plays an important role in the pathogenesis of NAFLD and in the progression of this disease to NASH. The aim of our project is to provide a proof of concept that the RANKL / RANK system plays an important role in the pathogenesis of NAFLD and in the progression of this disease to NASH. The investigator propose to study the RANKL / RANK expression in serum and liver biopsies of type 2 diabetic patients at different stages of NAFLD.
Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is still the only treatment available to cure acute myeloid leukemia and high risk myelodysplasia. Allo-HSCT has an anti-tumor effect (called the graft versus leukemia effect= GVL) mediated by donor lymphocytes. This GVL effect is often associated with graft-versus-host disease (GVHD). Several studies have shown that the relapse incidence is lower in patients developing chronic GVHD. These studies confirm the impact of donor immune system on leukemic residual cells. In fact, the relapse incidence increased in patients with no sign of GVHD. The investigators assume that leukemic cells probably use mechanisms to inhibit the allogeneic response. These escape mechanisms to immunosurveillance have been described in other malignancies. Out of context of the allo-HSCT, in acute myeloid leukemias and myelodysplasia, correlations between the severity of the disease and the presence of regulatory T cells (Tregs) or exhausted T cells (PD1 positive) in the bone marrow and in the blood of patients were described at the time of diagnosis or relapse. Myeloid Derived Suppressive Cells (MDSCs) have been described as capable of inducing Tregs and exhausted T cells in the tumor microenvironment.The investigators want to evaluate the role of myeloid suppressive cells in bone marrow after allo HSCT. They hypothesize that their presence in bone marrow and / or blood recipient is correlated to the relapse incidence.
The aim of this study is to investigate the efficacy, safety, and survival benefit of etoposide plus cisplatin and irinotecan plus cisplatin in first-line therapy of non-primary pancreatic metastatic and/or unresectable gastrointestinal neuroendocrine tumor G3 type. In addition, the investigators will explore the resistance mechanisms of gastrointestinal neuroendocrine tumor G3, and screen out biomarkers that can predict the efficacy of chemotherapy.