Dihydromyricetin improves Parkinson's disease-like lesions in T2DM rats by activating AMPK/ULK1 pathway / 生理学报

The purpose of this study was to explore the effect and mechanism of dihydromyricetin (DHM) on Parkinson's disease (PD)-like lesions in type 2 diabetes mellitus (T2DM) rats. The T2DM model was established by feeding Sprague Dawley (SD) rats with high-fat diet and intraperitoneal injection of streptozocin (STZ). The rats were intragastrically administered with DHM (125 or 250 mg/kg per day) for 24 weeks. The motor ability of the rats was measured by balance beam experiment, the changes of dopaminergic (DA) neurons and the expression of autophagy initiation related protein ULK1 in the midbrains of the rats were detected by immunohistochemistry, and the protein expression levels of α-synuclein (α-syn), tyrosine hydroxylase (TH), as well as AMPK activation level, in the midbrains of the rats were detected by Western blot. The results showed that, compared with normal control, the rats with long-term T2DM exhibited motor dysfunction, increased α-syn aggregation, down-regulated TH protein expression, decreased number of DA neurons, declined activation level of AMPK, and significantly down-regulated ULK1 expression in the midbrain. DHM (250 mg/kg per day) treatment for 24 weeks significantly improved the above PD-like lesions, increased AMPK activity, and up-regulated ULK1 protein expression in T2DM rats. These results suggest that DHM may improve PD-like lesions in T2DM rats by activating AMPK/ULK1 pathway.

DHM improves cognitive dysfunction in T2DM rats by inhibiting hippocampal endoplasmic reticulum stress / 中国药理学通报

Aim To investigate the effeet of dihydro- myricetin ( DHM ) on cognitive dysfunction in type 2 diabetes mellitus ( T2DM) rats and its mechanism.Methods SD rats were randomly divided into the normal control group ( n = 56) : normal diet and citrate buffer solution (30 mg • kg 1 ) ; T2DM model group (n =60) : high glucose, fat and low dose STZ ( 30 mg • kg 1 ) ( Four unsuccessful rats were eliminated ).Then rats in the above two groups were treated with or without DHM (250 mg • kg 1 • d intragastric).After 12 weeks, eight rats in each group were randomly selected to perform Morris water maze and Y maze test to observe the effect of DHM on cognitive function of rats.The remaining rats in each group were injected ERS antagonist tauroursodeoxycholic acid ( TUDCA ) 10 jxg • d 1 or ERS activator tunicamycin (TUN) 10 jxL, respectively.After the behavioral analysis, the hippocampal tissues of rats were taken out.The expressions of EH stress related proteins GRP78 and P- PERK were detected by Western blot.Results Both DHM and TUDCA could improve cognitive dysfunction in T2DM rats.On the contrary, TIJN reduced the effect of DHM on cognitive dysfunction in T2DM rats.TUDCA decreased the expression of GRP78 and p- PERK proteins in T2DM rats, while TUN increased the expression of GRP78 and p-PERK proteins in T2DM rats treated by DHM.Conclusion DHM improves cognitive dysfunction in T2DM rats, and the mechanism may be related to the inhibition of endoplasmic reticulum stress.

Automated Assessment System for Neonatal Endotracheal Intubation Using Dilated Convolutional Neural Network.

Neonatal endotracheal intubation (ETI) is an important, complex resuscitation skill, which requires a significant amount of practice to master. Current ETI practice is conducted on the physical manikin and relies on the expert instructors' assessment. Since the training opportunities are limited by the availability of expert instructors, an automatic assessment model is highly desirable. However, automating ETI assessment is challenging due to the complexity of identifying crucial features, providing accurate evaluations and offering valuable feedback to trainees. In this paper, we propose a dilated Convolutional Neural Network (CNN) based ETI assessment model, which can automatically provide an overall score and performance feedback to pediatric trainees. The proposed assessment model takes the captured kinematic multivariate time-series (MTS) data from the manikin-based augmented ETI system that we developed, automatically extracts the crucial features of captured data, and eventually provides an overall score as output. Furthermore, the visualization based on the class activation mapping (CAM) can automatically identify the motions that have significant impact on the overall score, thus providing useful feedback to trainees. Our model can achieve 92.2% average classification accuracy using the Leave-One-Out-Cross-Validation (LOOCV).

[Impaired glucose metabolism in patients with obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To investigate the prevalence of impaired glucose-insulin metabolism in obstructive sleep apnea hypopnea syndrome (OSAHS); to examine the relation between severity of OSAHS and impaired glucose metabolism; and to evaluate the effectiveness of continuous positive airway pressure (CPAP) on impaired glucose metabolism. METHODS: A total of 214 patients who were free of diabetes at baseline underwent both nocturnal polysomnography (PSG), and 2-h oral glucose-tolerance test, insulin and hemoglobin A1c test. CPAP treatment for glucose-insulin metabolism (+) was given to OSAHS group after informed consent had been obtained. RESULTS: Eighty-eight patients and 17 patients with impaired glucose-insulin metabolism were found in OSAHS group and the control group respectively. Impaired glucose-insulin metabolism was present in 54.3% of OSAHS group and 32.7% of control group. Logistic regression analysis showed a significant positive correlation with OSAHS (AHI ≥ 10 times/h) and impaired glucose-insulin metabolism in all patients (OR = 2.440, 95%CI 1.201 - 4.958). Plasma glucose level changes had no significant differences between before and after CPAP treatment (P > 0.05). CONCLUSION: OSAHS is associated with a high frequency of impaired glucose metabolism. The relationship between OSAHS and impaired glucose metabolism is independent of obesity. Longest apnea time (LAT) and AHI are important contributors to impaired glucose metabolism in OSAHS patients. Short-term CPAP therapy has no significant improvement on glucose metabolism in patients with OSAHS.