A new enzymatic biosensor worn on eyeglasses has been developed for low-noise and noninvasive determination of lactate in human sweat during physical exercise. The Os (osmium)-complex, the electron mediator between the enzyme and the electrode, was first immobilized on a flexibly printed carbon electrode. Then, a gel membrane with the stereoscopic reticular structure of lactate oxidase and horseradish peroxidase was casted on the electrode to form the biosensor. Linearity of the biosensor was observed for up to 25 mM lactate in a phosphate buffered solution of pH 7.0. Chemical selectivity was evaluated by adding common interferent species such as ascorbic acid, glucose and uric acid to the lactate. The negligible current interference indicated excellent discriminatory selectivity of the biosensor. Applied to an analysis of the real sweat lactate dynamics of healthy subjects during cycling exercise, the amperometric profiles of the biosensors reflected changes in sweat lactate that depended on physical exercise intensity. Compared with other reported epidermal biosensors attached to the arm or leg, our biosensor not only exhibited a similar current change tendency but also rarely suffered from deformational interference due to their forehead measurement position. Such a successful application of real-time monitoring of sweat lactate means that eyeglass-bound biosensors hold considerable promise in the physical exercise and biomedical fields.

The impact of magnolol on cerebral ischemic stroke in rats and the molecular mechanism were explored. Sprague-Dawley rat models were studied. Cerebral indexes, hematoxylin and eosin staining, TUNEL staining assay, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were applied. The cerebral index in model group was significantly higher than that in sham operation group, and the cerebral index was obviously decreased after magnolol administration. Inflammatory cells accumulated in the brain tissue of rats in the model group. Abundant apoptotic cells were produced in the model group, which was overtly improved after rats were given magnolol. RT-PCR and western blot analysis showed that expression of mRNA and protein of brain-derived neurotrophic factor (BDNF) were distinctly decreased in model group, and increased after rats were given magnolol; while mRNA and protein expression of Bcl-2-associated X protein (Bax) were significantly raised in model group, and reduced after rats were given magnolol. The results showed that there were statistically significant differences in expression of BDNF and Bax among sham operation, model and magnolol administration groups (p<0.01). In conclusion, magnolol can increase the expression of BDNF and decrease the expression of Bax, thereby inhibiting apoptosis to protect the nerves, and magnolol can improve cerebral ischemic stroke in rats.

Objectives To evaluate the impact of cerebrovascular disease deaths on life expectancy (LE) of Chinese residents in 2010 and its change compared with 2005, and then to find the high risk population (age, gender and region) whose deaths caused by cerebrovascular disease made the main impact on the LE Methods LE and cause-eliminated LE were calculated by standard life table techniques using the adjusted mortality data from National Disease Surveillance System: The Death Surveillance Data Sets in 2005 and 2010. Decomposition method was used to quantitatively evaluate the impact of cerebrovascular disease. Results The LE of Chinese residents was 73.24 years in 2010, which was higher in women and urban residents compared with men and rural residents. The LE loss caused by cerebrovascular disease deaths in Chinese residents was 2.26 years, it was higher in men and rural residents compared with women and urban residents, and more than 30% of LE loss came from the premature deaths of cerebrovascular disease in people who were less than 65 years old. Compared with 2005, The LE of Chinese residents increased 0.92 years, and the change of cerebrovascular disease deaths contributed 0.04 years to the increase of LE (0.45 years for urban residents), but the increase of cerebrovascular disease deaths made 0.12-year LE loss for rural residents. Conclusions The cerebrovascular disease deaths had a tremendous impact on LE in Chinese population, and the impact was significant different between urban residents and rural residents. LE is likely to be further increased by reducing deaths caused by cerebrovascular disease, and the special attention should be paid to reduce the premature cerebrovascular disease deaths in people who were less than 65 years old.

To observe and analyze the clinical efficacy of nimodipine and edaravone combination in the treatment of acute cerebral hemorrhage, a total of 180 patients definitely diagnosed as acute cerebral hemorrhage and treated in Shandong Jiyang Public hospital were enrolled. The patients were divided into the control group and the research group with 90 patients in each group. Of those, patients of the control group were treated with edaravone, while a combination of nimodipine and edaravone was administered to patients in the research group. Therapeutic efficacy, neurologic impairment score, life quality score, hematoma volume and edema volume were compared between both the groups. Results obtained showed that the total therapeutic efficacy of the research group was better than that of the control group (P<0.05). Measurement of patients' hematoma volume and edema volume before and after treatment indicated that the research group after drug administration demonstrated significant improvement over the control group (P<0.05). Moreover, there was a greater decrease in the neurologic impairment score of the research group than that of the control group (P<0.05). Combination of nimodipine and edaravone in the treatment of acute cerebral hemorrhage achieved better outcomes indicating greater therapeutic efficacy.