Kinetic Study on Palm Oil Waste Decomposition

No abstract available

Diagnosis of biliary tract and ampullary carcinomas

Diagnostic methods for biliary tract carcinoma and the efficacy of these methods are discussed. Neither definite methods for early diagnosis nor specific markers are available in this disease. When this disease is suspected on the basis of clinical symptoms and risk factors, hemato-biochemical examination and abdominal ultrasonography are performed and, where appropriate, enhanced computed tomography (CT) and/or magnetic resonance cholangiopancreatography (MRCP) is carried out. Diagnoses of extrahepatic bile duct cancer and ampullary carcinoma are often made based on the presence of obstructive jaundice. Although rare, abdominal pain and pyrexia, as well as abnormal findings of the hepatobiliary system detected by hemato-biochemical examination, serve as a clue to making a diagnosis of these diseases. On the other hand, the early diagnosis of gallbladder cancer is scarcely possible on the basis of clinical symptoms, so when this cancer is found with the onset of abdominal pain and jaundice, it is already advanced at the time of detection, thus making a cure difficult. When gallbladder cancer is suspected, enhanced CT is carried out. Multidetector computed tomography (MDCT), in particular — one of the methods of enhanced CT — is useful for decision of surgical criteria, because MDCT shows findings such as localization and extension of the tumor, and the presence or absence of remote metastasis. Procedures such as magnetic resonance imaging, endoscopic ultrasonography, bile duct biopsy, and cholangioscopy should be carried out taking into account indications for these procedures in individual patients. However, direct biliary tract imaging is necessary for making a precise diagnosis of the horizontal extension of bile duct cancer

Design and baseline characteristics of the finerenone in reducing cardiovascular mortality and morbidity in diabetic kidney disease trial

Background: Among people with diabetes, those with kidney disease have exceptionally high rates of cardiovascular (CV) morbidity and mortality and progression of their underlying kidney disease. Finerenone is a novel, nonsteroidal, selective mineralocorticoid receptor antagonist that has shown to reduce albuminuria in type 2 diabetes (T2D) patients with chronic kidney disease (CKD) while revealing only a low risk of hyperkalemia. However, the effect of finerenone on CV and renal outcomes has not yet been investigated in long-term trials. Patients and Methods: The Finerenone in Reducing CV Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD) trial aims to assess the efficacy and safety of finerenone compared to placebo at reducing clinically important CV and renal outcomes in T2D patients with CKD. FIGARO-DKD is a randomized, double-blind, placebo-controlled, parallel-group, event-driven trial running in 47 countries with an expected duration of approximately 6 years. FIGARO-DKD randomized 7,437 patients with an estimated glomerular filtration rate >= 25 mL/min/1.73 m(2) and albuminuria (urinary albumin-to-creatinine ratio >= 30 to <= 5,000 mg/g). The study has at least 90% power to detect a 20% reduction in the risk of the primary outcome (overall two-sided significance level alpha = 0.05), the composite of time to first occurrence of CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. Conclusions: FIGARO-DKD will determine whether an optimally treated cohort of T2D patients with CKD at high risk of CV and renal events will experience cardiorenal benefits with the addition of finerenone to their treatment regimen. Trial Registration: EudraCT number: 2015-000950-39; ClinicalTrials.gov identifier: NCT02545049

Complicated intra-abdominal infections worldwide : the definitive data of the CIAOW Study

Peer reviewe

Acid Ceramidase Deficiency is characterized by a unique plasma cytokine and ceramide profile that is altered by therapy

Acid Ceramidase Deficiency (Farber disease, FD) is an ultra-rare Lysosomal Storage Disorder that is poorly understood and often misdiagnosed as Juvenile Idiopathic Arthritis (JIA). Hallmarks of FD are accumulation of ceramides, widespread macrophage infiltration, splenomegaly, and lymphocytosis. The cytokines involved in this abnormal hematopoietic state are unknown. There are dozens of ceramide species and derivatives, but the specific ones that accumulate in FD have not been investigated. We used a multiplex assay to analyze cytokines and mass spectrometry to analyze ceramides in plasma from patients and mice with FD, controls, Farber patients treated by hematopoietic stem cell transplantation (HSCT), JIA patients, and patients with Gaucher disease. KC, MIP-1 alpha, and MCP-1 were sequentially upregulated in plasma from FD mice. MCP-1, IL-10, IL-6, IL-12, and VEGF levels were elevated in plasma from Farber patients but not in control or JIA patients. C16-Ceramide (C16-Cer) and dhC16-Cer were upregulated in plasma from FD mice. a-OH-C18-Cer, dhC12-Cer, dhC24:1-Cer, and C22:1-Cer-1P accumulated in plasma from patients with FD. Most cytokines and only a-OH-C18-Cer returned to baseline levels in HSCT-treated Farber patients. Sphingosines were not altered. Chitotriosidase activity was also relatively low. A unique cytokine and ceramide profile was seen in the plasma of Farber patients that was not observed in plasma from HSCT-treated Farber patients, JIA patients, or Gaucher patients. The cytokine profile can potentially be used to prevent misdiagnosis of Farber as JIA and to monitor the response to treatment. Further understanding of why these signaling molecules and lipids are elevated can lead to better understanding of the etiology and pathophysiology of FD and inform development of future treatments. (C) 2016 Elsevier B.V. All rights reserved.Rare Disease FoundationBC Children's Hospital FoundationNational Institutes of HealthVaincre les Maladies LysosomalesPlexcera TherapeuticsUniv Toronto, Inst Med Sci, Toronto, ON M5G 1L7, CanadaUniv Toronto, Dept Med Biophys, Toronto, ON M5G 1L7, CanadaMed Univ South Carolina, Dept Microbiol & Immunol, Hollings Canc Ctr, Charleston, SC 29425 USAUniv Calgary, Alberta Childrens Hosp, Med Genet & Pediat, Calgary, AB T3B 6A8, CanadaCtr Hosp Univ Sherbrooke, Dept Genet, Sherbrooke, PQ J1G 2E8, CanadaMcGill Univ, Dept Med Genet, Montreal, PQ H3A 0G4, CanadaMcGill Univ, Dept Pediat, Montreal, PQ H3A 0G4, CanadaUniv Milano Bicocca, San Gerardo Hosp, Dept Pediat, I-20126 Monza, ItalyG Gaslini Childrens Hosp, I-16148 Genoa, ItalyGerman Ctr Paediat & Adolescent Rheumatol, D-82467 Garmisch Partenkirchen, GermanyKagoshima Univ, Grad Sch Med & Dent Sci, Div Hematol & Immunol, Ctr Chron Viral Dis, Kagoshima 8908544, JapanKarolinska Univ Hosp, Pediat Rheumatol, S-17176 Stockholm, SwedenDokuz Eylul Univ, Pediat Rheumatol, TR-35210 Izmir, TurkeyDokuz Eylul Univ, Gastroenterol & Metab Dis, TR-35210 Izmir, TurkeyUniv Cordoba, Metab Dis, RA-14002 Cordoba, ArgentinaMed Univ Greifswald, Dept Paediat Oncol & Haematol, D-17475 Greifswald, GermanyGoethe Univ, Dept Paediat Oncol & Haematol, D-60323 Frankfurt, GermanyUniv Glasgow, Pediat Rheumatol, Glasgow G12 8QQ, Lanark, ScotlandNotre Dame De Secours Univ Hosp, Pediat Rheumatol, Byblos, LebanonUniv Fed Sao Paulo, Pediat Rheumatol, BR-04023900 Sao Paulo, BrazilUniv Sao Paulo, Hosp Ribeirao Preto, Neurogenet, BR-04023900 Sao Paulo, BrazilBernard & Millie Duker Childrens Hosp, Albany Med Ctr, Pediat Rheumatol, Albany, NY 12208 USAChildrens Natl Hlth Syst, Metab Dis, Washington, DC 20010 USAPlexcera Therapeut, New York, NY 10029 USAIcahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USACHU Purpan, Inst Federatif Biol, Lab Biochim Metab, F-31037 Toulouse 1, FranceUniv Hlth Network, Toronto, ON M5G 1L7, CanadaMed Coll Wisconsin, 8701 Watertown Plank Rd,CRI C4540, Milwaukee, WI 53226 USAUniv Fed Sao Paulo, Pediat Rheumatol, BR-04023900 Sao Paulo, BrazilNIH: 1R21NS078191-01A1NIH: R01 DK54830Web of Scienc