Objective To explore whether stromal cell-derived factor 1 (SDF-1) can promote the clearance of β-amyloid deposition in the brain of APP/PS1 mice and the possible underlying mechanism.Methods Twelve 28-week-old APP/PS1 mice were divided into two groups:a treatment group and a control group.Animals were given the intracerebroventricular injection weekly with PBS or mouse recombinant SDF-1 α for eight weeks.Microglia and Aβ in cerebral cortex and hippocampal region of APP/PS1 mice were detected by immunofluorescence.Results After 8-week treatment,both the relative number and the relative area of Aβ deposits in the mice of treatment group were less than those in the control group.The relative number of plaque associated microglia increased to a significantly greater extent in the cortex and hippocampus in treatment group than those in the control group.Conclusion Injecting SDF-1α significantly reduced amyloid burden in APP/PS1 mice.This effect might associated with the improvement of the chemotoxis of microglia,which promote the phagocytosis of Aβ by microglia.

Objective To retrospectively analyze the clinical effect of 131 I in the treatment of hyperthyroid heart disease.Methods 269 cases who received nuclear medicine 131 I therapy for hyperthyroid heart disease were selected.Clinical laboratory and related examinations,including determination of serum thyroid hormones and antibod-ies (FT3 ,FT4 ,TSH,TRAb,TGAb and TPOAb),biochemical indicators,analysis of blood,electrocardiogram,thyroid ultrasonography,thyroid 131 I uptake rate determination,static imaging and color Doppler ultrasound of the heart were condutced.After diagnosis clear integrated touch technique,thyroid color Super and the thyroid static imaging deter-mine thyroid weight.131 I dose by following formula calculation determine:131 I dose =(each grams thyroid plans vol-ume)×thyroid weight (g)/thyroid 24h or highest 131 I rate (%),each grams thyroid plans volume for 2.96-4.44MBq,calculation 131 I dose,application SPSS 17.0 statistics software for statistics,used paired t test to analyze serum hormone levels of FT3 ,FT4 ,sTSH before treatment,3,6 and 12 months after treatment.Results After 131 I treatment 3,6,12 months,serum FT3 ,FT4 ,sTSH levels significantly declined compared with before treatment (t =36.03,23.88,17.81,45.01,24.85,13.95,49.97,25.66,10.28,all P <0.01).Of 269 patients received 131 I treat-ment,hyperthyroidism cured in 220 cases (81.8%),improved in 42 cases (15.6%),invalid in 7 cases (2.6%);hyperthyroidism heart recovered in 226 cases (84.0%),effective rate was 97.0%(261 /269).Conclusion The treatment of hyperthyroid heart disease as soon as possible is the key to control hyperthyroid,reduced thyroid hormone in the peripheral circulation,131I can be fast and effective treatment of hyperthyroidism,hyperthyroid abnormal ECG and cardiac anomalies symptom relief for time is the ideal treatment of hyperthyroid heart disease recovery as soon as possible,with normal thyroid function,hyperthyroid can return to normal or part of normal.

In order to investigate the neuroprotective effects of cyclin-dependent kinase-5 (cdk-5) inhibition in mice with Niemann-Pick disease type C (NPC) (npc(-/-)), recombinant adeno-associated virus (rAAV) carrying the small interfering RNA (siRNA) specific for cdk-5 gene was injected into 3-day-old npc(-/-) mice intracerebroventricularly. The rAAV-GFP-injected age-matched npc(-/-) mice and non-surgery age-matched npc(-/-) mice were employed as controls (n=6-10/group). From the 4th to 8th week after the treatment, mice were weighed, and evaluated for limb motor activity by using the coat hanger test once a week. Eight-week-old npc(-/-) mice were sacrificed by decapitation, and brains were quickly dissected and halved sagittally. Immunohistochemistry, Western blotting, and HE staining were used to evaluate the neuropathology in npc(-/-) mice. The results showed that rAAV-cdk-5-siRNA-GFP significantly reduced the number of axonal spheroids, delayed the death of Purkinje neurons, ameliorated motor defects in npc(-/-) mice, and significantly attenuated the hyperphosphorylation of tau proteins. These data suggested that inhibition of cdk-5 activity has neuroprotective effect on neurons in NPC mice.

Objective:To analyze the practical situation of clinical college tutorial system teaching from the perspective of students'needs,and provide reference for optimizing the teaching mode of clinical college tutorial system.Method:A total of 79 undergraduate students who participated in the tutorial system teaching in the clinical college of our university were selected as the research subjects.Through questionnaire surveys and one-to-one in-depth interviews,the current implementation status of the tutorial system teaching mode and students'needs and expectations for the tutorial system teaching mode were understood.Results:The overall satisfaction with the teacher-student relationship was 86.07%,and students'willingness to communicate internally was the main factor affecting communication.And 1.27%of students believed that they had no obstacles in teacher-student communication,and 98.73%of students did not want mentors to teach more than 5 students.And 69.62%of students preferred mentors to provide teaching guidance through clinical practice.Binary logistic regression analysis showed that students'perception that mentorship had no significant effect was a negative factor in teaching effectiveness(OR=0.045,95%CI:0.003-0.598).Conclusions:Taking students'needs as the starting point,strengthening the preaching of the mentorship teaching mode,reinforcing the confidence in learning,and improving the teaching programme and teaching quality evaluation system are conducive to enhancing the quality of mentorship teaching in clinical college.

significantly attenuated the hyper-phosphorylation of tau proteins. These data suggested that inhibition of cdk-5 activity has neuropro-tective effect on neurons in NPC mice.

The glymphatic system plays a pivotal role in maintaining cerebral homeostasis. Chronic cerebral hypoperfusion, arising from small vessel disease or carotid stenosis, results in cerebrometabolic disturbances ultimately manifesting in white matter injury and cognitive dysfunction. However, whether the glymphatic system serves as a potential therapeutic target for white matter injury and cognitive decline during hypoperfusion remains unknown. Here, we established a mouse model of chronic cerebral hypoperfusion via bilateral common carotid artery stenosis. We found that the hypoperfusion model was associated with significant white matter injury and initial cognitive impairment in conjunction with impaired glymphatic system function. The glymphatic dysfunction was associated with altered cerebral perfusion and loss of aquaporin 4 polarization. Treatment of digoxin rescued changes in glymphatic transport, white matter structure, and cognitive function. Suppression of glymphatic functions by treatment with the AQP4 inhibitor TGN-020 abolished this protective effect of digoxin from hypoperfusion injury. Our research yields new insight into the relationship between hemodynamics, glymphatic transport, white matter injury, and cognitive changes after chronic cerebral hypoperfusion.
Animals ; Brain Ischemia ; Carotid Stenosis/drug therapy* ; Cognitive Dysfunction/etiology* ; Digoxin ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; White Matter