Pain Control by Co-adaptive Learning in a Brain-Machine Interface.

Innovation in the field of brain-machine interfacing offers a new approach to managing human pain. In principle, it should be possible to use brain activity to directly control a therapeutic intervention in an interactive, closed-loop manner. But this raises the question as to whether the brain activity changes as a function of this interaction. Here, we used real-time decoded functional MRI responses from the insula cortex as input into a closed-loop control system aimed at reducing pain and looked for co-adaptive neural and behavioral changes. As subjects engaged in active cognitive strategies orientated toward the control system, such as trying to enhance their brain activity, pain encoding in the insula was paradoxically degraded. From a mechanistic perspective, we found that cognitive engagement was accompanied by activation of the endogenous pain modulation system, manifested by the attentional modulation of pain ratings and enhanced pain responses in pregenual anterior cingulate cortex and periaqueductal gray. Further behavioral evidence of endogenous modulation was confirmed in a second experiment using an EEG-based closed-loop system. Overall, the results show that implementing brain-machine control systems for pain induces a parallel set of co-adaptive changes in the brain, and this can interfere with the brain signals and behavior under control. More generally, this illustrates a fundamental challenge of brain decoding applications-that the brain inherently adapts to being decoded, especially as a result of cognitive processes related to learning and cooperation. Understanding the nature of these co-adaptive processes informs strategies to mitigate or exploit them.

MoS2 QDs-Based sensor for measurement of fluazinam with triple signal output.

In this study, direct detection of fluazinam was realized using a fluorescent sensor using disulfide quantum dots (MoS2 QDs) via inner filter effect (IFE). The maximum excitation of as-prepared MoS2 QDs presented a complementary spectral-overlap with the maximum absorption of fluazinam. Thus the occurrence of inner filter effect led to the significant fluorescence quenching of MoS2 QDs. Additionally, fluorescent quenching efficiency of MoS2 QDs could be enhanced by the effects of π-π stacking, hydrogen bond and electrostatic interaction between fluazinam and MoS2 QDs, and these non-chemical bond responses also promoted the selectivity for fluazinam detection. Under the optimum conditions, the IFE-based fluorescent sensor exhibited a relative wide linear range from 50 nM to 25 µM with the LOD of 2.53 nM (S/N = 3). In addition, a paper-based sensor was established by cross-linking the MoS2 QDs into cellulose membrane for naked-eyed detection and digital analysis of fluazinam. The paper-based sensor presented a liner range from 10 µM to 800 µM for fluazinam detection with the LOD of 2.26 µM. Additionally, the acceptable recoveries were obtained for fluazinam detection in the spiked samples of tomato, potato and cucumber, indicating that the proposed method provided an effective sensing platform for real applications of fluazinam detection in food safety.

Modulation of expression of p16 and her2 in rat breast tissues of mammary hyperplasia model by external use of rupifang extract.

OBJECTIVE: To observe the effect of Rupifang Extract in external use on expression of proto-oncogenes her2 and tumor suppression genes p16 in rat breast tissues of mammary hyperplasia model. To explore the mechanisms of Rupifang Extract in external use for preventing and treating mammary hyperplasia. METHODS: Thirty virginal female Wistar rats were randomized into 5 groups, 6 in each, A: blank control group; B: model group; C: the low dose group of Rupifang; D: the middle dose group of Rupifang; and E: The high dose group of Rupifang. The mammary hyperplasia rat models were produced by injecting estradiol benzoate and progesterone and irritating by tail nipping. Drug intervention was also launched during the model formation. After 30 days, the expression of her2 and p16 in breast tissues of rats in each group were detected by the SP immunohistochemical method. RESULTS: Compared with Blank control group, the expression of her2 in breast tissues in Model group was higher, and the expression of p16 was lower (P < 0.05 or P < 0.01). After intervention with Rupifang Extract, compared with Model group, the expression of her2 in breast tissues in Rupifang groups was lower, and the expression of p16 higher (P < 0.05 or P < 0.01). CONCLUSION: The mechanisms of Rupifang Extract in external application for preventing and treating mammary hyperplasia may be reducing the expression of proto-oncogenes her2 and increasing the expression of tumor suppression genes p16.