Broad bandwidth of perceptual learning in second-order contrast modulation detection

Comparing characteristics of learning in first- and second-order systems might inform us about different neural plasticity in the two systems. In the current study, we aim to determine the properties of perceptual learning in second-order contrast modulation detection in normal adults. We trained nine observers to detect second-order gratings at an envelope modulation spatial frequency of 8 cycles/8 with their nondominant eyes. We found that, although training generated the largest improvements around the trained frequency, contrast sensitivity over a broad range of spatial frequencies also improved, with a 4.09-octave bandwidth of perceptual learning, exhibiting specificity to the trained spatial frequency as well as a relatively large degree of generalization. The improvements in the modulation sensitivity function (MSF) were not significantly different between the trained and untrained eyes. Furthermore, training did not significantly change subjects' ability in detecting firstorder gratings. Our results suggest that perceptual learning in second-order detection might occur at the postchannel level in binocular neurons, possibly through reducing the internal noise of the visual system

What Are the New Challenges of the Current Cancer Biomarkers?

Biomarkers are emerging research filed in the past decade. Even though numerous biomarkers were reported, the efficiency of cancer therapy remains low. So the question emerges as to how much can we trust the current biomarkers on cancer therapy? In this upcoming chapter, we would like to illustrate the outcomes of classical cancer therapies on advanced pancreatic cancer disclosed successful, neutral and failed in clinical trials. The analysis will be carried on the perspective interdisciplinary on the biomarkers including anatomy, physiology, pharmacology, biochemistry, history path and development of pharmacy. Particular in-depth insight may open a window for new researches and lighting the therapies

Mesenchymal Stem Cell Transplantation for Liver Cell Failure: A New Direction and Option

Background and Aims. Mesenchymal stem cell transplantation (MSCT) became available with liver failure (LF), while the advantages of MSCs remain controversial. We aimed to assess clinical advantages of MSCT in patients with LF. Methods. Clinical researches reporting MSCT in LF patients were searched and included. Results. Nine articles (n=476) related with LF patients were enrolled. After MSCT, alanine aminotransferase (ALT) baseline decreased largely at half a month (P<0.05); total bilirubin (TBIL) baseline declined to a certain stable level of 78.57 μmol/L at 2 and 3 months (P<0.05). Notably, the decreased value (D value) of Model for End-Stage Liver Disease score (MELD) of acute-on-chronic liver failure (ACLF) group was higher than that of chronic liver failure (CLF) group (14.93 ± 1.24 versus 4.6 ± 5.66, P<0.05). Moreover, MELD baseline of ≥20 group was a higher D value of MELD than MELD baseline of <20 group with a significant statistical difference after MSCT (P=0.003). Conclusion. The early assessment of the efficacy of MSCT could be based on variations of ALT at half a month and TBIL at 2 and 3 months. And it had beneficial effects for patients with LF, especially in ACLF based on the D value of MELD

Spatiotemporal Scan and Age-Period-Cohort Analysis of Hepatitis C Virus in Henan, China: 2005–2012

Background: Studies have shown that hepatitis C virus (HCV) infection increased during the past decades in China. However, little evidence is available on when, where, and who were infected with HCV. There are gaps in knowledge on the epidemiological burden and evolution of the HCV epidemic in China. Methods: Data on HCV cases were collected by the disease surveillance system from 2005 to 2012 to explore the epidemic in Henan province. Spatiotemporal scan statistics and age-period-cohort (APC) model were used to examine the effects of age, period, birth cohort, and spatiotemporal clustering. Results: 177,171 HCV cases were reported in Henan province between 2005 and 2012. APC modelling showed that the HCV reported rates significantly increased in people aged > 50 years. A moderate increase in HCV reported rates was observed for females aged about 25 years. HCV reported rates increased over the study period. Infection rates were greatest among people born between 1960 and 1980. People born around 1970 had the highest relative risk of HCV infection. Women born between 1960 and 1980 had a five-fold increase in HCV infection rates compared to men, for the same birth cohort. Spatiotemporal mapping showed major clustering of cases in northern Henan, which probably evolved much earlier than other areas in the province. Conclusions: Spatiotemporal mapping and APC methods are useful to help delineate the evolution of the HCV epidemic. Birth cohort should be part of the criteria screening programmes for HCV in order to identify those at highest risk of infection and unaware of their status. As Henan is unique in the transmission route for HCV, these methods should be used in other high burden provinces to help identify subpopulations at risk

Cannabinoid Receptor Subtype 2 (Cb2R) Agonist Gw405833 Reduces Agonist-Induced Ca2+ Oscillations In Mouse Pancreatic Acinar Cells

Emerging evidence demonstrates that the blockade of intracellular Ca 2+ signals may protect pancreatic acinar cells against Ca 2+ overload, intracellular protease activation, and necrosis. The activation of cannabinoid receptor subtype 2 (CB 2 R) prevents acinar cell pathogenesis in animal models of acute pancreatitis. However, whether CB 2 Rs modulate intracellular Ca 2+ signals in pancreatic acinar cells is largely unknown. We evaluated the roles of CB 2 R agonist, GW405833 (GW) in agonist-induced Ca 2+ oscillations in pancreatic acinar cells using multiple experimental approaches with acute dissociated pancreatic acinar cells prepared from wild type, CB 1 R-knockout (KO), and CB 2 R-KO mice. Immunohistochemical labeling revealed that CB 2 R protein was expressed in mouse pancreatic acinar cells. Electrophysiological experiments showed that activation of CB 2 Rs by GW reduced acetylcholine (ACh)-, but not cholecystokinin (CCK)-induced Ca 2+ oscillations in a concentration-dependent manner; this inhibition was prevented by a selective CB 2 R antagonist, AM630, or was absent in CB 2 R-KO but not CB 1 R-KO mice. In addition, GW eliminated L-arginine-induced enhancement of Ca 2+ oscillations, pancreatic amylase, and pulmonary myeloperoxidase. Collectively, we provide novel evidence that activation of CB 2 Rs eliminates ACh-induced Ca 2+ oscillations and L-arginine-induced enhancement of Ca 2+ signaling in mouse pancreatic acinar cells, which suggests a potential cellular mechanism of CB 2 R-mediated protection in acute pancreatitis

Dcf1 Deficiency Attenuates the Role of Activated Microglia During Neuroinflammation

Microglia serve as the principal immune cells and play crucial roles in the central nervous system, responding to neuroinflammation via migration and the execution of phagocytosis. Dendritic cell-derived factor 1 (Dcf1) is known to play an important role in neural stem cell differentiation, glioma apoptosis, dendritic spine formation, and Alzheimer’s disease (AD), nevertheless, the involvement of the Dcf1 gene in the brain immune response has not yet been reported. In the present paper, the RNA-sequencing and function enrichment analysis suggested that the majority of the down-regulated genes in Dcf1-/- (Dcf1-KO) mice are immune-related. In vivo experiments showed that Dcf1 deletion produced profound effects on microglial function, increased the expression of microglial activation markers, such as ionized calcium binding adaptor molecule 1 (Iba1), Cluster of Differentiation 68 (CD68) and translocator protein (TSPO), as well as certain proinflammatory cytokines (Cxcl1, Ccl7, and IL17D), but decreased the migratory and phagocytic abilities of microglial cells, and reduced the expression levels of some other proinflammatory cytokines (Cox-2, IL-1β, IL-6, TNF-α, and Csf1) in the mouse hippocampus. Furthermore, in vitro experiments revealed that in the absence of lipopolysaccharide (LPS), the majority of microglia were ramified and existed in a resting state, with only approximately 10% of cells exhibiting an amoeboid-like morphology, indicative of an activated state. LPS treatment dramatically increased the ratio of activated to resting cells, and Dcf1 downregulation further increased this ratio. These data indicated that Dcf1 deletion mediates neuroinflammation and induces dysfunction of activated microglia, preventing migration and the execution of phagocytosis. These findings support further investigation into the biological mechanisms underlying microglia-related neuroinflammatory diseases, and the role of Dcf1 in the immune response