Tranexamic acid has been used to reduce intraoperative bleeding; however, its effect on anti-inflammation and the amount of drainage after orthognathic surgery is yet to be determined. Therefore, we aimed to examine the effect of tranexamic acid on intraoperative bleeding volume and operation time, amount of drainage, and anti-inflammation after orthognathic surgery. Forty healthy women who underwent bilateral sagittal split ramus osteotomy under general anesthesia participated in this study. The amount of intraoperative bleeding, the operation time, the amount of drainage, and the C-reactive protein level were compared between patients intravenously administered with tranexamic acid before surgery (before-surgery group) and those administered with the drug after surgery (after-surgery group). All data were analyzed using the Student t-test. Results were considered to be statistically significant when P < 0.05. Although no significant difference was found in the amount of drainage between the groups (P > 0.05), significant variations were detected in the amount of bleeding during surgery (before-surgery group: 161.7 ± 45.3 mL versus after-surgery group: 270.2 ± 24.0 mL; P = 0.0009), operation time (before-surgery group: 141.3 ± 16.8 min versus after-surgery group: 166.8 ± 24.9 min; P = 0.03), and postoperative C-reactive protein level (before-surgery group: 3.77 ± 0.40 mg/dL versus after-surgery group: 5.02 ± 0.75 mg/dL; P = 0.012) between the groups. In conclusion, administering tranexamic acid before surgery was found to significantly decrease bleeding, reduce operation time, and suppress postoperative inflammation.

Phospholipase C-related catalytically inactive protein (PRIP) was first identified as an inositol 1,4,5-trisphosphate-binding protein, and was later found to be involved in a variety of cellular events, particularly those related to protein phosphatases. We previously reported that Prip knock-out (KO) mice exhibit a lean phenotype with a small amount of white adipose tissue. In the present study, we examined whether PRIP is involved in energy metabolism, which could explain the lean phenotype, using high-fat diet (HFD)-fed mice. Prip-KO mice showed resistance to HFD-induced obesity, resulting in protection from glucose metabolism dysfunction and insulin resistance. Energy expenditure and body temperature at night were significantly higher in Prip-KO mice than in wild-type mice. Gene and protein expression of uncoupling protein 1 (UCP1), a thermogenic protein, was up-regulated in Prip-KO brown adipocytes in thermoneutral or cold environments. These phenotypes were caused by the promotion of lipolysis in Prip-KO brown adipocytes, which is triggered by up-regulation of phosphorylation of the lipolysis-related proteins hormone-sensitive lipase and perilipin, followed by activation of UCP1 and/or up-regulation of thermogenesis-related genes (e.g. peroxisome proliferatoractivated receptor-␥ coactivator-1␣). The results indicate that PRIP negatively regulates UCP1-mediated thermogenesis in brown adipocytes.Obesity, which develops due to chronic excess food intake that exceeds total energy expenditure, is becoming an epidemic worldwide. Obesity is a risk factor for many chronic diseases, such as type 2 diabetes mellitus, cardiovascular disease, dyslipidemia, obstructive sleep apnea, and certain forms of cancer, which is decreasing both the quality and length of life, and increasing individual and national healthcare costs (1). To maintain energy homeostasis at the appropriate level for a given environmental condition, a complex interplay exists between the central nervous system and the peripheral organs. In the periphery, nutrient levels are regulated in key storage organs (e.g. fat in adipose tissue and glycogen in the liver and elsewhere) as well as in the blood (e.g. blood glucose) (2).In mammals, adipose tissue exists as mainly as two different types: white adipose tissue (WAT) 3 and brown adipose tissue (BAT). As the major form of energy storage, fat in white adipocytes provides a buffer for energy imbalances when energy intake is not equal to energy output; i.e. excessive energy is stored as triglyceride (TAG) and is supplied to the body by lipolysis in a nutrient-starved state. Brown adipocytes directly dissipate the chemical energy in fatty acids through uncoupling protein 1 (UCP1); i.e. the enzyme uncouples respiration from ATP synthesis and dissipates the energy as heat (3).Recently, many studies have shown that BAT participates in adult human obesity, and activation of UCP1-mediated thermogenesis in BAT prevents obesity and diabetes (3-5). Therefore, BAT has attracted much attention as a target for the treat...

Phosphorylation of hormone-sensitive lipase (HSL) and perilipin by protein kinase A (PKA) promotes the hydrolysis of lipids in adipocytes. Although activation of lipolysis by PKA has been well studied, inactivation via protein phosphatases is poorly understood. Here, we investigated whether phospholipase C-related catalytically inactive protein (PRIP), a binding partner for protein phosphatase 1 and protein phosphatase 2A (PP2A), is involved in lipolysis by regulating phosphatase activity. PRIP knockout (PRIP-KO) mice displayed reduced body-fat mass as compared with wild-type mice fed with standard chow ad libitum. Most other organs appeared normal, suggesting that mutant mice had aberrant fat metabolism in adipocytes. HSL in PRIP-KO adipose tissue was highly phosphorylated compared to that in wild-type mice. Starvation of wild-type mice or stimulation of adipose tissue explants with the catabolic hormone, adrenaline, translocated both PRIP and PP2A from the cytosol to lipid droplets, but the translocation of PP2A was significantly reduced in PRIP-KO adipocytes. Consistently, the phosphatase activity associated with lipid droplet fraction in PRIP-KO adipocytes was significantly reduced and was independent of adrenaline stimulation. Lipolysis activity, as assessed by measurement of non-esterified fatty acids and glycerol, was higher in PRIP-KO adipocytes. When wild-type adipocytes were treated with a phosphatase inhibitor, they showed a high lipolysis activity at the similar level to PRIP-KO adipocytes. Collectively, these results suggest that PRIP promotes the translocation of phosphatases to lipid droplets to trigger the dephosphorylation of HSL and perilipin A, thus reducing PKA-mediated lipolysis.

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Objectives: Daily assessments of swallowing function and interventions such as rehabilitation and dietary adjustments are necessary to improve dysphagia. Cervical auscultation is convenient for health care providers for assessing swallowing ability.Although this method allows for swallowing sound evaluations, sensory evaluations with this method are difficult. Thus, we aimed to assess swallowing sound by the combined use of an electronic stethoscope and an artificial intelligence (AI) system that incorporates sound recognition.Material and Methods: Herein, 20 fifth-year dentistry student volunteers were included; each participant was drank 10 ml and then 20 ml of water in different positions (sitting and supine). We developed an algorithm for indexing bolus inflow sounds using AI, which compared the swallowing sounds and created a new index. Results:The new index value used for swallowing sound was significantly higher in men than in women and in the sitting position than in the supine position. A software for acoustic analysis confirmed that the swallowing index was significantly higher in men than in women as well as in the sitting position than in the supine position.These results were similar to those obtained using the new index. However, the new index substantially differed between sexes in terms of posture compared with effective sound pressure. Conclusions:We developed a new algorithm for indexing swallowing sounds using a stethoscope and an AI system, which could identify swallowing sounds. For future research and development, evaluations of patients with dysphagia are necessary to determine the efficacy of the new index for bedside screening of swallowing conditions.