Lentinula edodes Cultured Extract and Rouxiella badensis subsp. acadiensis (Canan SV-53) Intake Alleviates Immune Deregulation and Inflammation by Modulating Signaling Pathways and Epigenetic Mechanisms.

Puberty is a critical developmental period of life characterized by marked physiological changes, including changes in the immune system and gut microbiota development. Exposure to inflammation induced by immune stressors during puberty has been found to stimulate central inflammation and lead to immune disturbance at distant sites from the gut; however, its enduring effects on gut immunity are not well explored. Therefore, in this study, we used a pubertal lipopolysaccharides (LPS)-induced inflammation mouse model to mimic pubertal exposure to inflammation and dysbiosis. We hypothesized that pubertal LPS-induced inflammation may cause long-term dysfunction in gut immunity by enduring dysregulation of inflammatory signaling and epigenetic changes, while prebiotic/probiotic intake may mitigate the gut immune system deregulation later in life. To this end, four-week-old female Balb/c mice were fed prebiotics/probiotics and exposed to LPS in the pubertal window. To better decipher the acute and enduring immunoprotective effects of biotic intake, we addressed the effect of treatment on interleukin (IL)-17 signaling related-cytokines and pathways. In addition, the effect of treatment on gut microbiota and epigenetic alterations, including changes in microRNA (miRNA) expression and DNA methylation, were studied. Our results revealed a significant dysregulation in selected cytokines, proteins, and miRNAs involved in key signaling pathways related to IL-17 production and function, including IL-17A and F, IL-6, IL-1ß, transforming growth factor-ß (TGF-ß), signal transducer and activator of transcription-3 (STAT3), p-STAT3, forkhead box O1 (FOXO1), and miR-145 in the small intestine of adult mice challenged with LPS during puberty. In contrast, dietary interventions mitigated the lasting adverse effects of LPS on gut immune function, partly through epigenetic mechanisms. A DNA methylation analysis demonstrated that enduring changes in gut immunity in adult mice might be linked to differentially methylated genes, including Lpb, Rorc, Runx1, Il17ra, Rac1, Ccl5, and Il10, involved in Th17 cell differentiation and IL-17 production and signaling. In addition, prebiotic administration prevented LPS-induced changes in the gut microbiota in pubertal mice. Together, these results indicate that following a healthy diet rich in prebiotics and probiotics is an optimal strategy for programming immune system function in the critical developmental windows of life and controlling inflammation later in life.

Human-in-the-loop active electrosense.

Active electrosense is a non-visual, short range sensing system used by weakly electric fish, enabling such fish to locate and identify objects in total darkness. Here we report initial findings from the use of active electrosense for object localization during underwater teleoperation with a virtual reality (VR) head-mounted display (HMD). The advantage of electrolocating with a VR system is that it naturally allows for aspects of the task that are difficult for a person to perform to be allocated to the computer. However, interpreting weak and incomplete patterns in the incoming data is something that people are typically far better at than computers. To achieve human-computer synergy, we integrated an active electrosense underwater robot with the Oculus Rift HMD. The virtual environment contains a visualization of the electric images of the objects surrounding the robot as well as various virtual fixtures that guide users to regions of higher information value. Initial user testing shows that these fixtures significantly reduce the time taken to localize an object, but may not increase the accuracy of the position estimate. Our results highlight the advantages of translating the unintuitive physics of electrolocation to an intuitive visual representation for accomplishing tasks in environments where imaging systems fail, such as in dark or turbid water.

The insulin sensitivity, glucose sensitivity, and acute insulin response to glucose load in adolescent type 2 diabetes in Taiwanese.

BACKGROUND: Insulin sensitivity (SI), glucose sensitivity (SG), acute insulin response to glucose load (AIR), and obesity in adolescent type 2 diabetes patients (young diabetes, YDM) in Taiwan were studied. METHODS: Forty patients diagnosed at <22 years of age were enrolled and divided into non-obese (NOYDM, BMI < 27 kg/m(2)) and obese groups (OBYDM BMI > 27 kg/m(2)). Adult-onset type 2 diabetes patients (ADM) >40 years old (n = 41) and nondiabetic young adults (N) (n = 23) served as controls. Fasting plasma lipids, insulin, and glucose were measured. Homeostasis model assessment was calculated to estimate insulin sensitivity and beta-cell function. A frequent-sampled intravenous glucose tolerance test was performed to evaluate SI, SG, and AIR. RESULTS: SI and AIR were significantly lower in YDM and ADM than in N (0.92 +/- 0.13, 0.8 +/- 0.15 and 3.24 +/- 0.47 x 10(-4)/U/mL for SI; 40.3 +/- 20.3, 107.3 +/- 50.2, 1208 +/- 306.3 uU/min for AIR). SG of YDM and ADM were lower compared with N (0.014 +/- 0.00138, 0.0292 +/- 0.0058 vs 0.034 +/- 0.0086 min(-1) respectively). No difference was noted between YDM and ADM. SI and SG were not different in NOYDM and OBYDM. AIR was higher in OBYDM (83.6 +/- 34.3 vs -7.6 +/- 13.66 uU/min). CONCLUSIONS: YDM had defects in SI, SG, and AIR compared to N, which was similar to the pathophysiology of ADM. The results imply that YDM may be either a different subtype of diabetes or the same type of diabetes as ADM, with severe defects associated with earlier age of onset. OBYDM had higher AIR than NOYDM.

The insulin sensitivity, glucose effectiveness and acute insulin response to glucose load of non-obese adolescent type 2 diabetes.

To determine the clinical characteristics in adolescent type 2 diabetes (young diabetes, YDM) in Taiwan, we enrolled 11 males who were diagnosed with YDM before 19 years of age into our study. Another 11 patients with adult type 2 diabetes (mature age diabetes, MADM) who were diagnosed after the age of 40 were enrolled as compare group. Subjects from both groups were being treated with oral hypoglycemic agents only at the time of enrollment, and none of the subjects had a history of diabetic ketoacidosis. Plasma lipid levels were measured from the fasting plasma sample. A homeostasis model assessment was used to estimate insulin sensitivity (HOMA-S) and beta-cell function (HOMA-B). Frequent-sampled intravenous glucose tolerance test was also performed to measure the insulin sensitivity (S(I)), glucose effectiveness (E(G)), and acute insulin response after glucose load (AIR). After adjusting for age and BMI, fasting plasma glucose, total cholesterol, HDL-cholesterol, triglycerides, and HOMA-B levels were similar between two groups. The fasting plasma insulin and HOMA-S were significantly higher in YDM. However, the S(I), E(G) and AIR in both groups were also not significantly different. In conclusion, the early onset of diabetes in YDM may be due to the early deterioration of the S(I), E(G) and AIR with similar severity compared with MADM. The role of E(G) might be more important than previously thought in these patients. Finally, the YDM might be a subtype of type 2 diabetes.