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Shuta Morishige,1 Yoshikazu Yamaguchi,1 Kei Nakajima,1 Sayaka Tsuboi,1 Yoh Sugawara,2 Hajime Hayami,1 Joseph D Tobias,3 Gaku Inagawa1 1Department of Anesthesiology, Yokohama Municipal Citizen’s Hospital, Yokohama, Japan; 2Department of Anesthesiology, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; 3Department of Anesthesiology and Pain Medicine, Nationwide Children’s Hospital and The Ohio State University, Columbus, OH, USACorrespondence: Yoshikazu Yamaguchi, Department of Anesthesiology, Yokohama Municipal Citizen’s Hospital, 1-1 Mitsuzawanishimachi, Kanagawa-ku, Yokohama-shi, Kanagawa, 221-0855, Japan, Tel +81-45-316-4580, Fax +81-45-316-6580, Email yoshikaz@yokohama-cu.ac.jpAbstract: Cardiac surgery-associated acute kidney injury may require postoperative renal replacement therapy. Although the right internal jugular vein and femoral veins are generally the preferred insertion sites for the hemodialysis catheter for continuous renal replacement therapy, the presence of other indwelling catheters or prior thrombotic events from previous catheters may preclude use of these sites. We present a case in which the hemodialysis catheter was inserted into the distal femoral vein using point-of-care ultrasound in a patient with multiple catheter insertions after coronary artery bypass grafting. Although the tip of the dialysis catheter was more distal than the classic femoral approach, renal replacement therapy was performed without problems. Moreover, it was easier for the nurses to keep the insertion site clean and to change the patient’s position.Keywords: central venous catheter, renal replacement therapy, femoral vein

It is well known that retinoic acid (RA) suppresses adipogenesis, although there are some contradicting reports. In this study, we examined the effect of extracellular glucose on RA-induced suppression of adipogenesis in 3T3L1 cell culture. When the cells were cultured in normal glucose medium (NG), the addition of RA suppressed lipid accumulation. However, when cultured in high glucose medium (HG), addition of RA to the cells enhanced lipid accumulation. These changes were accompanied by parallel alterations in fatty acid synthase (FAS) and sterol regulatory element-binding protein (SREBP)-1 gene expression. Transfection of SREBP-1 siRNA suppressed RA-induced enhancement of lipid accumulation and FAS expression in the cells cultured with HG. Transfection of the nuclear form of SREBP-1a cDNA into the cells cultured with NG inhibited RA-induced suppression of lipid accumulation and FAS expression. Moreover, RA- and HG-induced SREBP-1a expression occurred at the early phase of adipogenesis and was dependent on glucocorticoid to induce liver X receptor (LXR) , peroxisomal proliferator-activated receptor (PPAR) and retinoid X receptor (RXR), the key nuclear factors influencing the SREBP-1a gene expression. These results suggest that RA suppresses and enhances lipid accumulation through extracellular glucose concentration-dependent modulation of SREBP-1 expression.

Kei Nakajima,1 Haruki Oshida,1 Toshitaka Muneyuki,2 Masafumi Kakei21Division of Clinical Nutrition, Department of Medical Dietetics, Faculty of Pharmaceutical Sciences, Josai University, Keyakidai, Sakado, 2First Department of Comprehensive Medicine, Saitama Medical Center, Jichi Medical University School of Medicine, Amanuma, Omiya, Saitama, JapanAbstract: Pancreatic exocrine insufficiency (PEI) is often observed in patients with pancreatic diseases, including chronic pancreatitis, cystic fibrosis, and tumors, or after surgical resection. PEI often results in malnutrition, weight loss and steatorrhea, which together increase the risk of morbidity and mortality. Therefore, nutritional interventions, such as low-fat diets and pancreatic enzyme replacement therapy (PERT), are needed to improve the clinical symptoms, and to address the pathophysiology of pancreatic exocrine insufficiency. PERT with delayed-release pancrelipase is now becoming a standard therapy for pancreatic exocrine insufficiency because it significantly improves the coefficients of fat and nitrogen absorption as well as clinical symptoms, without serious treatment-emergent adverse events. The major adverse events were tolerable gastrointestinal tract symptoms, such as stomach pain, nausea, and bloating. Fibrosing colonopathy, a serious complication, is associated with high doses of enzymes. Several pancrelipase products have been approved by the US Food and Drug Administration in recent years. Although many double-blind, placebo-controlled trials of pancrelipase products have been conducted in recent years, these studies have enrolled relatively few patients and have often been less than a few weeks in duration. Moreover, few studies have addressed the issue of pancreatic diabetes, a type of diabetes that is characterized by frequent hypoglycemia, which is difficult to manage. In addition, it is unclear whether PERT improves morbidity and mortality in such settings. Therefore, large, long-term prosp

Recently it has been reported that the estimated glomerular filtration rate (eGFR) is higher in habitual coffee consumers than in noncoffee consumers. However, the causality remains unclear. Therefore, we conducted a clinical trial to investigate the effects of coffee consumption on kidney function. Nineteen asymptomatic nonsmokers aged 21-27 years old participated in this study. They consumed coffee (18?g coffee beans/450?mL per day) or green tea as a comparator for 2 weeks in a crossover design. Although creatinine-based eGFR was not affected after consuming either beverage, all cystatin-C-based eGFRs determined using five different equations were significantly increased after coffee consumption (means: 5.0-7.7%), but not after green tea consumption (means: 0.1-1.6%). Serum adiponectin and magnesium levels increased significantly after coffee consumption (means: 13.6% and 4.3%, resp.), but not after green tea consumption. These findings suggest that even a short period of coffee consumption may increase cystatin-C-based eGFR, along with favorable changes in serum adiponectin, in healthy young adults.