Empirical Calculation Method of Bypass Leakage in Scroll Compressors

This study presents an empirical method to calculate the bypass leakage mass flow rate along the tip seal in a scroll compressor. The leakage flows through small axial and radial clearances between the orbiting and fixed scrolls of scroll compressor were previously studied by Ishii et al. In these earlier studies, the pressure decay in the pressurized vessel due to leakage through the axial and radial clearances was measured using a maximum pressure of 3 MPa for CO2 and 0.6 MPa for R22. The Darcy-Weisbach equation for incompressible, viscous fluid flow through the thin rectangular cross-section was applied to calculate the leakage mass flow rate that matched the pressure decay characteristics. The empirical friction factors were determined and plotted on a Moody diagram. As a result, the empirical friction factors for both axial and radial clearance leakage flows have been determined and shown to take on essentially the same value for both CO2 and R22, despite the significantly different working pressures. In contrast, the flow patterns in bypass leakage along the tip seal are so complicated that not even the leakage characteristics are known definitively. No method exists for calculating the bypass leakage mass flow rate. In the present study, a bypass leakage model was constructed, compatible with a production-type scroll compressor with a large cooling capacity. A similar test of the pressure decay in the pressurized vessel due to bypass leakages were conducted with the refrigerant gas R410A. The measured pressure decay characteristics were then simulated by the Darcy-Weisbach equation with the empirical friction factors from our previous study for the leakage flow through the axial clearance. In the present simulations of the measured pressure decay, the complicated flow patterns through bypass clearances were classified into two representative rectangular thin cross-section leakage passes, one with an equivalent width and the other with an equivalent length. Empirical friction factor values for the equivalent pass width and length were determined to match the measured pressure decays. As a result, the calculation of the bypass leakage flow rate along the tip seal in scroll compressors can be accomplished using a simple scheme in terms of the equivalent pass width and equivalent pass length for two representative leakage passes forming a thin rectangular cross-section and applying empirically determined friction factors,

Effects of ferric citrate on intracellular oxidative stress markers after hydrogen peroxide treatment of human U937 monocytes

Phosphate binders, such as iron （III） citrate hydrate （FCH）, are essential medications for hemodialysis patients. Some in vivo studies have demonstrated that FCH prevented induction of oxidative stress in the presence of transferrin. However, how FCH affects iron-related oxidative stress in the absence of transferrin remains unclear. In the current study, we investigated the effects of ferric citrate （FC） on oxidative stress in the absence of transferrin in vitro to address this question. Human U937 monocytes were pretreated with FC, iron （II） chloride tetrahydrate （FeCl2・4H2O）, iron （III） chloride hexahydrate （FeCl3・6H2O）, or saccharated ferric oxide for 24 h and then treated with 10-mM hydrogen peroxide （H2O2） for 30 min. The final Fe concentrations were adjusted to approximately 200µg/dl. Iron concentration, intracellular reactive oxygen species （ROS） levels, and intracellular lipid peroxidation of the cell membrane were measured. After treatment with FC, iron concentration and ROS levels increased. Change in lipid peroxidation after treatment with FC was not observed. However, after treatment with H2O2, no change was observed in the intracellular ROS levels in FC-pretreated cells, whereas lipid peroxidation of the cell membrane was decreased. Despite the high iron concentration in FC-pretreated cells, neither intracellular ROS nor cell membrane lipid peroxidation levels were increased with H2O2 treatment. Their results might represent antioxidative effects of FC. The results of this study may contribute to a better understanding of the effects of oxidative stress in hemodialysis patients treated with FCH

TRAIL Team Description Paper for RoboCup@Home 2023

Our team, TRAIL, consists of AI/ML laboratory members from The University of Tokyo. We leverage our extensive research experience in state-of-the-art machine learning to build general-purpose in-home service robots. We previously participated in two competitions using Human Support Robot (HSR): RoboCup@Home Japan Open 2020 (DSPL) and World Robot Summit 2020, equivalent to RoboCup World Tournament. Throughout the competitions, we showed that a data-driven approach is effective for performing in-home tasks. Aiming for further development of building a versatile and fast-adaptable system, in RoboCup @Home 2023, we unify three technologies that have recently been evaluated as components in the fields of deep learning and robot learning into a real household robot system. In addition, to stimulate research all over the RoboCup@Home community, we build a platform that manages data collected from each site belonging to the community around the world, taking advantage of the characteristics of the community

Effect of Hydrogen Peroxide and High Glucose on the Glucose Metabolism of Lymphoma-derived U937 Cells

Our study aimed to clarify specific oxidative stress and glucose metabolic disorders in hemodialysis patients, by examining hydrogen peroxide (H2O2) - and high glucose-induced oxidative stress, glucose transport and the failure of glycolysis. As an in vitro blood cell model of end-stage renal disease (ESRD) in patients with diabetes, human monocytic U937 cells of malignant lymphoma origin were exposed to high glucose (28.9mM) for 6 days, with 5mM H2O2 added on the last day. The generation of intracellular reactive oxygen species (ROS), glucose levels, lactate levels, AMP-activated protein kinase (AMPK) activity and Glut4 levels were examined. Exposure of U937 cells to H2O2 resulted in a significant increase in intracellular ROS generation and glucose levels. Under high glucose conditions, treatment with H2O2 significantly promoted these actions. In H2O2-induced U937 cells, AMPK activity and Glut4 levels were significantly increased, but lactate and pyruvate levels were significantly decreased. Thus, exposure of U937 cells to H2O2 and a high glucose load promoted an increase in intracellular ROS, and exposure to H2O2 induced increased glucose transport and high intracellular glucose due to reduced glycolytic metabolism. This suggests that reduced glycolytic metabolism might be induced in states of high oxidative stress in hemodialysis patients with diabetes

Pleiotropic Effects of Linagliptin Monotherapy on Levels of Nitric Oxide, Nitric Oxide Synthase, and Superoxide Dismutase in Hemodialysis Patients with Diabetes

Linagliptin is an anti-diabetic drug and the only bile-excreted dipeptidyl peptidase-4 inhibitor. Malnutrition-inflammation-atherosclerosis syndrome is an important prognostic factor for hemodialysis patients, and we previously reported anti-inflammatory effects of linagliptin in hemodialysis patients with diabetes. Inflammation can accelerate oxidative stress, vasoconstriction, and platelet aggregation. However, few studies have investigated the pleiotropic effects of linagliptin treatment on inflammation in hemodialysis patients. In this study, we have extended our previous investigations of these effects in a longer and more thorough follow-up of hemodialysis patients with diabetes. We examined 20 hemodialysis patients with diabetes who were not receiving oral diabetes drugs or insulin therapy and who exhibited inadequate glycemic control (glycated albumin levels＞20%). Linagliptin (5mg) was administered daily, and we evaluated the patients’ superoxide dismutase, 8-hydroxydeoxyguanosine, nitric oxide, nitric oxide synthase, and asymmetric dimethylarginine levels in serum at baseline and after 1, 3, and 6 months of treatment. After 6 months of treatment, superoxide dismutase levels had significantly decreased from 8.8±0.5U/ml to 7.0±0.5U/ml. Nitric oxide synthase levels were significantly increased at 3 and 6 months (maximum, 94.2±13.2µg/ml; baseline, 31.6±5.5µg/ml). After 3 months of treatment, nitric oxide levels had significantly increased from 64.5±6.6µmol/l to 104±15.4µmol/l, and remained significantly elevated at 6 months. Asymmetric dimethylarginine and 8-hydroxydeoxyguanosine levels did not change during the 6-month treatment course, and no patients exhibited hypoglycemia or other significant adverse effects. Linagliptin treatment significantly changed various markers of inflammation relevant to the atherosclerosis in malnutrition-inflammation-atherosclerosis syndrome. Therefore, linagliptin monotherapy has pleiotropic effects on inflammation in hemodialysis patients with diabetes, and may improve their prognosis

The Effectiveness of Combined Medical Therapy and Hemodialysis for Hypercalcemia in Anaplastic Lymphoma Kinase-negative Anaplastic Large Cell Lymphoma

A 71-year-old man with a right lower abdominal quadrant epithelial tumor developed gradually worsening lumbago and dysbasia. He became comatose and was admitted to our hospital. He had swelling of the left axillary lymph nodes and necrosis of the 4.0-cm diameter abdominal tumor, which infiltrated the subcutaneous tissues. He was hypercalcemic (16.7mg/dl), and had elevated levels of soluble interleukin-2 receptor (24,090U/ml) and parathyroid hormone-related protein (5.4pmol/l). Computerized tomography (CT) showed left axillary lymphadenopathy, splenomegaly, and a right abdominal-wall mass that was described as anaplastic large cell lymphoma upon pathology. Brain radiography and CT revealed multiple lesions infiltrating the cranium. Magnetic resonance imaging showed diffuse low signal intensity throughout the vertebral spine. The patient was diagnosed with anaplastic lymphoma kinase (ALK) -negative anaplastic large cell lymphoma with hypercalcemia. Fluid replacement and drug therapies including calcitonin had no effect on the hypercalcemia or the coma. The patient\u27s serum calcium concentration decreased after hemodialysis (calcium dialysate concentration, 5mg/dl) and subsequent zoledronic acid hydrate therapy. His consciousness improved by the fifth day of treatment. This rare case of hypercalcemia in ALK-negative anaplastic large cell lymphoma improved with combined medical and hemodialysis therapy

MiR-33a is a therapeutic target in SPG4-related hereditary spastic paraplegia human neurons

Recent reports, including ours, have indicated that microRNA (miR)-33 located within the intron of sterol regulatory element binding protein (SREBP) 2 controls cholesterol homeostasis and can be a potential therapeutic target for the treatment of atherosclerosis. Here, we show that SPAST, which encodes a microtubule-severing protein called SPASTIN, was a novel target gene of miR-33 in human. Actually, the miR-33 binding site in the SPAST 3′-UTR is conserved not in mice but in mid to large mammals, and it is impossible to clarify the role of miR-33 on SPAST in mice. We demonstrated that inhibition of miR-33a, a major form of miR-33 in human neurons, via locked nucleic acid (LNA)-anti-miR ameliorated the pathological phenotype in hereditary spastic paraplegia (HSP)-SPG4 patient induced pluripotent stem cell (iPSC)-derived cortical neurons. Thus, miR-33a can be a potential therapeutic target for the treatment of HSP-SPG4