Is there Two-Way Information Transmission between Stock Markets and Stock Discussion Boards?

This research investigates information transmissions between stock returns and abnormal posting volumes using a total of 1,031,206 messages posted on Chinese stock message boards. Based on a multivariable GARCH (1, 1) model and causality in variance test, the study shows that there are significant two-way volatility spillovers effects: a positive volatility spillover effect from stock returns to abnormal posting volume, and a negative volatility spillover effect from abnormal posting volume to stock returns. The information exchange and communication on stock message boards have a certain role to stabilize financial markets and to improve the investment rationale

Chronic intermittent fasting improves cognitive functions and brain structures in mice.

Obesity is a major health issue. Obesity started from teenagers has become a major health concern in recent years. Intermittent fasting increases the life span. However, it is not known whether obesity and intermittent fasting affect brain functions and structures before brain aging. Here, we subjected 7-week old CD-1 wild type male mice to intermittent (alternate-day) fasting or high fat diet (45% caloric supplied by fat) for 11 months. Mice on intermittent fasting had better learning and memory assessed by the Barnes maze and fear conditioning, thicker CA1 pyramidal cell layer, higher expression of drebrin, a dendritic protein, and lower oxidative stress than mice that had free access to regular diet (control mice). Mice fed with high fat diet was obese and with hyperlipidemia. They also had poorer exercise tolerance. However, these obese mice did not present significant learning and memory impairment or changes in brain structures or oxidative stress compared with control mice. These results suggest that intermittent fasting improves brain functions and structures and that high fat diet feeding started early in life does not cause significant changes in brain functions and structures in obese middle-aged animals

Isoflurane induces learning impairment that is mediated by interleukin 1β in rodents.

Postoperative cognitive decline is a clinical syndrome. Volatile anesthetics are commonly used during surgery. It is conceivable that volatile anesthetics may contribute to postoperative cognitive decline. Isoflurane can impair cognitive functions of animals under certain conditions. However, the mechanisms for this impairment are not clear. Here, male 18-month old Fisher 344 rats or 10-week old mice were exposed to 1.2 or 1.4% isoflurane for 2 h. Our studies showed that isoflurane impaired the cognitive functions of the rats in Barnes maze. Isoflurane-exposed rats had reduced freezing behavior during the training sessions in the fear conditioning test. This isoflurane effect was attenuated by lidocaine, a local anesthetic with anti-inflammatory property. Rats that had training sessions and were exposed to isoflurane 30 min later had freezing behavior similar to that of control animals. Isoflurane increased the expression of interleukin 1β (IL-1β), interleukin-6 and activated caspase 3 in the hippocampus of the 18-month old rats. IL-1β positive staining was co-localized with that of NeuN, a neuronal marker. The increase of IL-1β and activated caspase 3 but not interleukin-6 was attenuated by lidocaine. Isoflurane also impaired the cognitive functions of 10-week old C57BL/6J mice and increased IL-1β in their hippocampi. However, isoflurane did not affect the cognitive functions of IL-1β deficient mice. Our results suggest that isoflurane impairs the learning but may not affect the recall of the aged rats. IL-1β may play an important role in this isoflurane effect

Glutamate transporter type 3 knockout reduces brain tolerance to focal brain ischemia in mice

Excitatory amino-acid transporters (EAATs) transport glutamate into cells under physiologic conditions. Excitatory amino-acid transporter type 3 (EAAT3) is the major neuronal EAAT and also uptakes cysteine, the rate-limiting substrate for synthesis of glutathione. Thus, we hypothesize that EAAT3 contributes to providing brain ischemic tolerance. Male 8-week-old EAAT3 knockout mice on CD-1 mouse gene background and wild-type CD-1 mice were subjected to right middle cerebral artery occlusion for 90 minutes. Their brain infarct volumes, neurologic functions, and brain levels of glutathione, nitrotyrosine, and 4-hydroxy-2-nonenal (HNE) were evaluated. The EAAT3 knockout mice had bigger brain infarct volumes and worse neurologic deficit scores and motor coordination functions than did wild-type mice, no matter whether these neurologic outcome parameters were evaluated at 24 hours or at 4 weeks after brain ischemia. The EAAT3 knockout mice contained higher levels of HNE in the ischemic penumbral cortex and in the nonischemic cerebral cortex than did wild-type mice. Glutathione levels in the ischemic and nonischemic cortices of EAAT3 knockout mice tended to be lower than those of wild-type mice. Our results suggest that EAAT3 is important in limiting ischemic brain injury after focal brain ischemia. This effect may involve attenuating brain oxidative stress

Photocatalytic Nitrogen Oxide Removal Activity Improved Step-by-Step through Serial Multistep Cu Modifications

Previous research has evidenced the insufficient efficiency in a one-step modified photocatalyst for NO removal. In this article, a serial multistep modification was explored to improve the NO removal activity of g-C3N4. In the experiment, a g-C3N4 photocatalyst has been successfully modified by Cu elements three times on one continuous process. Meanwhile, results showed that the serial multistep modifications could improve NO removal activity by g-C3N4 step by step. The main active species in the g-C3N4 system were h(+) and O-center dot(2)- but they were h(+) and (OH)-O-center dot in the three-modified g-C3N4 systems. Moreover, different mechanisms of activity improvement caused by the modified Cu in the serial-modified samples were identified. In the first modified sample, Cu2+ can decompose H2O2 molecules into (OH)-O-center dot via a Fenton-like reaction. In the second modified sample, the H2O2 molecule is activated by Cu-0 and decomposed into (OH)-O-center dot by the generated photoelectrons. After the third modification, the synergistic effects of the N vacancy and Cu-0 were identified, which significantly enhanced the photocatalytic NO removal activity of g-C3N4. This study proposed that the serial multistep modification can be a promising method to improve the NO removal activity of g-C3N4 stage-by-stage

The effects of various feeding protocols on oxidative stress status in the brain.

<p>Seven-week old male mice had free access to regular chow or high fat diet or were allowed to have free access to regular chow every other day (intermittent fasting) for 11 months. Their brains were then harvested to measure glutathione (GSH), glutathione disulfide (GSSG), 4-hydroxy-2-nonenal (HNE) and nitrotyrosine containing proteins. The levels of GSH and GSSG and ratio of GSH/GSSG in the cerebral cortex and hippocampus are presented in panels A and B, respectively. The levels of HNE and nitrotyrosine containing proteins in the cerebral cortex and hippocampus are shown in the panels C and D. Results are means ± S.E.M (n = 8). * P<0.05 compared with mice on regular chow <i>ad libitum</i>.</p

The effects of various feeding protocols on CA1 pyramidal cell layer thickness, neuron-specific proteins and brain derived neurotrophic factor (BDNF) in the brain.

<p>Seven-week old male mice had free access to regular chow or high fat diet or were allowed to have free access to regular chow every other day (intermittent fasting) for 11 months. Their brains were then harvested to measure CA1 pyramidal cell layer thickness (panel A) and expression of NeuN, drebrin and synaptophysin in the cerebral cortex (panel B) and hippocampus (panel C) as well as the BDNF levels in the cerebral cortex and hippocampus (panel D). The protein abundance results in each mouse were normalized by the mean value of the corresponding protein in the regular diet-fed mice. Results are means ± S.E.M (n = 7 – 12). * P<0.05 compared with mice on regular diet ad libitum. GAPDH: glyceraldehydes 3-phosphate dehydrogenase; Hippo: hippocampus; SP: synaptophysin; RD: regular diet; IF: intermittent fasting; HFD: high fat diet.</p

Isoflurane-induced cognitive impairment measured by Barnes maze and fear conditioning.

<p>Eighteen-month-old Fisher 344 rats were exposed to or were not exposed to 1.2% isoflurane for 2 h. They were subjected to Barnes maze 2 weeks later or fear conditioning 27 days later. A: performance in the training sessions of Barnes maze test. There is a significant effect of training sessions on the latency to identify the target hole (P<0.001 by two-way repeated measures analysis of variance). B: latency to identify the target hole at 1 day or 8 days after the training sessions. C: number of other hole searched before identifying the target hole at 1 day or 8 days after the training sessions. D: performance in fear conditioning test. Results are mean±S.D. (n = 6). *P<0.05 compared with the corresponding control in panels B, C and D by t-test.</p