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Cell migration refers to the ability of cells to translocate across a substrate or through a matrix. To achieve net movement requires spatiotemporal regulation of the actin cytoskeleton. Computational approaches are necessary to identify and quantify the regulatory mechanisms that generate directed cell movement. To address this need, we developed computational tools, based on stochastic modeling, to analyze time series data for the position of randomly migrating cells. Our approach allows parameters that characterize cell movement to be efficiently estimated from cell track data. We applied our methods to analyze the random migration of Mouse Embryonic Fibroblasts (MEFS) and HeLa cells. Our analysis revealed that MEFs exist in two distinct states of migration characterized by differences in cell speed and persistence, whereas HeLa cells only exhibit a single state. Further analysis revealed that the Rho-family GTPase RhoG plays a role in determining the properties of the two migratory states of MEFs. An important feature of our computational approach is that it provides a method for predicting the current migration state of an individual cell from time series data. Finally, we applied our computational methods to HeLa cells expressing a Rac1 biosensor. The Rac1 biosensor is known to perturb movement when expressed at overly high concentrations; at these expression levels the HeLa cells showed two migratory states, which correlated with differences in the spatial distribution of active Rac1.Derangements in bilirubin metabolism and/or dysfunctions in the hepato-biliary system lead to the unhealthy buildup of bilirubin in blood, resulting in jaundice. During the course of this disorder, circulating red cells are invariably subjected to toxic effects of serum bilirubin and an array of inflammatory compounds. This study aimed to investigate the vibrational spectroscopy of live red cells in jaundice using micro-Raman spectroscopy combined with optical-trap. Red cells from blood samples of healthy volunteers and patients with jaundice were optically immobilized and micro-Raman probed using a 785 nm diode laser. Raman signatures from red cells in jaundice exhibited significant variations from the normal and the spectral-markers were obtained from multivariate analytical methods. This research gives insightful views on how different pathologies can act as “stress-milieus” for red cells in circulation, possibly impeding their normal functions and also exasperating anemia. Raman spectroscopy, an emerging bio-analytical technique, is sensitive in detecting molecular-conformations in situ, at cellular-levels and in real-time. This study could pave way in understanding fundamental red cell behavior in different diseases by analyzing Raman markers.It is known that nitric oxide (NO) may affect myosin heavy chain (MyHC) isoform mRNA transcription in skeletal muscles. The content of NO in soleus muscles decreases during rat hindlimb unloading as well as slow MyHC mRNA transcription. We aimed to detect which signaling pathways are involved in NO-dependent prevention of hindlimb-suspension (HS)-induced changes in MyHCs’ expression pattern. Male Wistar rats were divided into four groups cage control group (C), hindlimb suspended for 7 days (7HS), hindlimb suspended for 7 days with L-arginine administration (7HS+A) (500 mg/kg body mass), and hindlimb suspended for 7 days with both L-arginine (500 mg/kg) and NO-synthase inhibitor L-NAME administration (50 mg/kg) (7HS+A+N). L-arginine treatment during 7 days of rat HS prevented HS-induced NO content decrease and slow MyHC mRNA transcription decrease and attenuated fast MyHC IIb mRNA transcription increase; it also prevented NFATc1 nuclear content decrease, calsarcin-2 expression increase, and GSK-3β Ser 9 phosphorylation decrease. Moreover, L-arginine administration prevented the HS-induced myh7b and PGC1α mRNAs content decreases and slow-type genes repressor SOX6 mRNA transcription increase. see more All these slow fiber-type protective effects of L-arginine were blocked in HS+A+N group, indicating that these effects were NO-dependent. Thus, NO decrease prevention during HS restores calcineurin/NFATc1 and myh7b/SOX6 signaling.Woody breast (WB) myopathy in modern broilers is causing major meat quality issues and consumer complaints. The poultry industry is sorting out WB filets through the inconsistent manual hand-palpation method. Bioelectrical impedance analysis (BIA) method was evaluated as a rapid and objective WB detection method. Freshly deboned broiler breast filets (15 filets × 2 categories × 3 trials) were sorted (hand-palpation) into severe woody (SW) and normal (N) categories were analyzed for BIA values, cook loss, texture (BMORS) method. SW filets had significantly (P less then 0.05) higher resistance and reactance compared to N indicating BIA can be used to detect WB filets. In another experiment, we determined the ability of the BIA to differentiate between four WB severity levels using the whole filet. Significant differences were observed in resistance and reactance of normal and other WB categories, however, there were no significant differences among mild, moderate and severe WB categories. Segmental BIA of those filets indicated that BIA can be used to separate cranial, medial and caudal region of the breast filet based on the presence of WB myopathy. Accidental discovery of spaghetti breast in the samples demonstrated the significance of compounding different factors in analyzing WB meat using BIA.Sishen Pill (SSP) is a typical prescription in the pharmacopeia of traditional Chinese medicine (TCM), and is usually used to treat inflammatory bowel disease (IBD). It is known that inflammatory dendritic cells (DCs) and imbalance of gut microbiota play significant roles in the pathogenesis of IBD. However, it is not clear whether SSP can treat IBD by regulating interaction of DCs and gut microbiota. In the present study, the levels of inflammatory DCs and gut microbiota were analyzed by flow cytometry and 16S rDNA analysis. SSP relieved the pathological damage to the colon of mice with colitis induced by dextran sodium sulfate (DSS). As typical indicators of inflammatory DCs, the levels of CD11c+CD103+E-cadherin+ cells and pro-inflammatory cytokines [interleukin (IL)-1β, -4, -9, and -17A] were decreased in mice with colitis treated by SSP for 10 days. Simultaneously, the gut microbiota composition was regulated, and beneficial bacteria were increased and pathogenic bacteria were reduced. The results indicated that SSP regulated the interaction between inflammatory DCs and gut microbiota to treat DSS-induced colitis.