Abstract:A fibre-optic strain sensor based on a gourd-shaped joint multimode fibre (MMF) sandwiched between two single-mode fibres (SMFs) is described both theoretically and experimentally. The cladding layers of the two MMFs are reshaped to form a hemisphere using an electrical arc method and spliced together, yielding the required gourd shape. The gourd-shaped section forms a Fabry-Perot cavity between the ends of two adjacent but noncontacting multimode fibres' core. The effectiveness of the multimode interference based on the Fabry-Perot interferometer (FPI) formed within the multimode inter-fibre section is greatly improved resulting in an experimentally determined strain sensitivity of −2.60 pm/με over the range 0-1000 με. The sensing characteristics for temperature and humidity of this optical fibre strain sensor are also investigated.

Neuroinflammation has been recognized as a major contributor to brain injury caused by intracerebral hemorrhage (ICH). Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome acts as an important mediator of inflammatory response in various inflammation-related diseases including hemorrhagic insults. Cordycepin has recently been shown to possess anti-inflammatory effect; however, its role and the possible underlying mechanisms in ICH remain unclear. This study was designed to investigate the neuroprotective effect of cordycepin in mice models of ICH and to elucidate the underlying molecular mechanisms. ICH was induced in male ICR mice by injecting autologous blood infusion stereotactically. Cordycepin was then given intraperitoneally (i.p.) at 30 min after ICH induction. The results demonstrated that NLRP3 inflammasome was activated and exacerbated the inflammatory progression after ICH. Cordycepin treatment significantly alleviated neurological deficits, brain edema, and perihematomal tissue damage following ICH. These changes were accompanied by downregulated NLRP3 inflammasome components expression and a reduction of production and release of inflammasome substrates interleukin-1beta (IL-1β) and interleukin-18 (IL-18). Furthermore, cordycepin ameliorated neuronal death in the perihematomal regions, accompanied by a large reduction in the expression of high-mobility group protein B 1 (HMGB1) post-ICH. In conclusion, this study provides in vivo evidence that cordycepin confers neuroprotective effect in the models of ICH, possibly through the suppression of NLRP3 inflammasome activation.

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OBJECTIVE The purpose of this study was to evaluate whether intraoperative monitoring of lateral spread response (LSR) improves the efficacy of microvascular decompression (MVD) for hemifacial spasm (HFS). METHODS In this prospective study, patients undergoing MVD for HFS were assigned to one of 2 groups, Group A (MVD with intraoperative LSR monitoring) or Group B (MVD without LSR monitoring). Clinical outcome at 12 months after surgery was assessed through telephone survey. Data analysis was performed to investigate the effect of intraoperative LSR monitoring on efficacy of MVD. RESULTS A total of 283 patients were enrolled in the study, 145 in Group A and 138 in Group B. There was no statistically significant difference between the 2 groups with respect to the percentage of patients who had spasm relief at either 1 week (Group A 87.59% vs Group B 83.33%; p = 0.317) or 1 year (93.1% vs 94.2%; p = 0.809) after surgery. A clear-cut elimination of LSR during surgery was observed in 131 (90.34%) of 145 patients; LSR persisted in 14 patients (9.66%) at the end of the surgical procedure. Disappearance of LSR correlated with spasm-free status at 1 week postoperatively (p = 0.017) but not at 1 year postoperatively (p = 0.249). CONCLUSIONS Intraoperative LSR monitoring does not appear to provide significant benefit with respect to the outcome of MVD for HFS in skilled hands. Persistence of LSR does not always correlate with poor outcome, and LSR elimination should not be pursued in all patients after verification of complete decompression.

Objective: To construct a prediction model for more precise evaluation of prognosis which will allow personalized treatment recommendations for adjuvant therapy in patients following resection of ESCC. Background: Marked heterogeneity of patient prognosis and limited evidence regarding survival benefit of various adjuvant therapy regimens pose challenges in the clinical treatment of ESCC. Methods: Based on comprehensive clinical data obtained from 4129 consecutive patients with resected ESCC in a high-risk region in China, we identified predictors for overall survival through a 2-phase selection based on Cox proportional hazard regression and minimization of Akaike information criterion. The model was internally validated using bootstrapping and externally validated in 1815 patients from a non-high-risk region in China.Results: The final model incorporates 9 variables: age, sex, primary site, T stage, N stage, number of lymph nodes harvested, tumor size, adjuvant treatment, and hemoglobin level. A significant interaction was also observed between N stage and adjuvant treatment. N1+ stage patients were likely to benefit from addition of adjuvant therapy as opposed to surgery alone, but adjuvant therapy did not improve overall survival for N0 stage patients. The C-index of the model was 0.729 in the training cohort, 0.723 after bootstrapping, and 0.695 in the external validation cohort. This model outperformed the seventh edition American Joint Committee on Cancer staging system in prognostic prediction and risk stratification. Conclusions: The prediction model constructed in this study may facilitate precise prediction of survival and inform decision-making about adjuvant therapy according to N stage.

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Intestinal barrier dysfunction remains a critical problem in patients with intracerebral hemorrhage (ICH) and is associated with poor prognosis. Ghrelin, a brain-gut peptide, has been shown to exert protection in animal models of gastrointestinal injury. However, the effect of ghrelin on intestinal barrier dysfunction post-ICH and its possible underlying mechanisms are still unknown. This study was designed to investigate whether ghrelin administration attenuates intestinal barrier dysfunction in experimental ICH using an intrastriatal autologous blood infusion mouse model. Our data showed that treatment with ghrelin markedly attenuated intestinal mucosal injury at both histomorphometric and ultrastructural levels post-ICH. Ghrelin reduced ICH-induced intestinal permeability according to fluorescein isothiocyanate conjugated-dextran (FITC-D) and Evans blue extravasation assays. Concomitantly, the intestinal tight junction-related protein markers, Zonula occludens-1 (ZO-1) and claudin-5 were upregulated by ghrelin post-ICH. Additionally, ghrelin reduced intestinal intercellular adhesion molecule-1 (ICAM-1) expression at the mRNA and protein levels following ICH. Furthermore, ghrelin suppressed the translocation of intestinal endotoxin post-ICH. These changes were accompanied by improved survival rates and an attenuation of body weight loss post-ICH. In conclusion, our results suggest that ghrelin reduced intestinal barrier dysfunction, thereby reducing mortality and weight loss, indicating that ghrelin is a potential therapeutic agent in ICH-induced intestinal barrier dysfunction therapy.

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