Aim Toinvestigatetheroleofhyperglyce-mia in cerebral ischemia/reperfusion(I/R)injury with a middle cerebral artery occlusion(MCAO)rat model anditsmechanism.Methods EightyhealthymaleSD rats were randomly assigned into sham group, I/R group (normoglycemia),hyperglycemic I/R groupⅠ(HG1 )and hyperglycemic I/R groupⅡ(HG2 ).The cerebral I/R model was established by occluding the middle cerebral artery(MCA)in rats.Hyperglycemia was induced by intraperitoneal injection of 50% glu-cose solution.Neurological deficit was determined by Ludmila Belayev test;infarct size and brain edema were measured by TTC staining;mitophagy was ob-served by double immunofluorescent staining and elec-tron microscope.The expressions of autophagy-related proteins(LC3 and Beclin-1 )and apoptosis-related pro-teins(Cyt-C,AIF,caspase-9 and caspase-3 )were ex-aminedbyWesternblotfurtherly.Results Bloodglu-cose level was controlled at 4 mmol·L-1 (normoglyce-mia),10 mmol · L-1 (HG1 ) and 20 mmol · L-1 (HG2)respectively.There were no significant differ-ences between model group and HG1 group in neuro-logical deficit scores,infarct volume and edema size(P>0. 05 ).However,these indications in HG2 group were significantly increased compared with model group (P<0. 05 ).After 3 days of reperfusion,the level of mitophagy was significantly reduced accompanied with increased mitochondria damages in HG 2 group (P <0. 05 ),and the expressions of mitochondrial related ap-optotic proteins(Cyt-C,AIF,caspase-9 and caspase-3 ) were significantly increased accordingly compared to modelgroup.Conclusions Mildhyperglycemiacan not intensify the cerebal ischemic injury.In contrast, severe hyperglycemia significantly aggravates the brain ischemic injury by inhibiting the removal of injured mi-tochondria in a manner of mitophagy,thus amplifying the mitochondrial mediated cascade damage responses.

Parkinson's disease (PD) is a common neurodegenerative disorder with typical motor symptoms and a variety of non-motor symptoms,including neuropsychiatric symptoms,autonomic dysfunctions,abnormal sense,sleep disorders and fatigue.Studies showed that several non-motor symptoms,such as olfactory dysfunction,constipation,rapid eye movement sleep behavior disorder,depression and fatigue,can occur before the onset of motor symptoms.Fatigue has been considered as one of the most disabling symptoms,and it has a significant impact on activity of daily living and quality of life,and brings heavy burdens to caregivers.However,fatigue in PD has no special biomarkers,so clinicians are lack of the recognition and intervention.Here,we will expound the prevalence,risk factors,rating scales and potential mechanism relating to neuropathology,neuroinflammation and neurobiochemistry in PD patients with fatigue.

Current resource of medical morality is in shortage.When emphasizing the exterior supervision of the government,we should put more emphasis on the exterior restricting factors which are more profound,such as the excursion of the norm to the experts,the excessive market-orientation of medical innovation,the shortage of financial devotion,the deficiency of hospital management system.To solve the above problems,a fair medical surrounding is to be built,a patients association be established,and the social honesty and credit mechanism be rebuilt.

Abstract?AlM:To analyze the blindness causes of 1854 cases in our hospital hospitalized patients, and explore the strategy and direction of blindness prevention according to the different treatment efficacy.?METHODS: Cluster sampling was used to select from September 2010 to August 2013 in our hospital department of ophthalmology patients 5 473 cases, in which total of 1 854 cases of blind patients, accounting for 33. 88% of hospitalized patients. According to the WHO's criteria of blindness. The BCVA enacted <0. 05 or vision radius less than 10 degrees are for the blind, and the exclusion of less than 3 years old children don't cope with visual inspection of the inclusion criteria for age and cause of blindness blind patients were analyzed. To the blind to patient age and etiology were analyzed, the main cause of blindness and statistics of all ages, records of the blind patients after treatment eye sight;and calculating the blindness of the literacy rate, on the blindness through analysis of the causes of the risk treatment.?RESULTS:ln 1 854 cases of blind patients, including 728 people right-eye blinding, 767 people left-eyes blinding, 359 people total blinding, adding up to 2 213 eyes, aged from 60~80 years old were in the majority. The top three diseases resulting blindness were cataract, diabetic retinopathy and glaucoma. ln 2 213 blind eyes, the eyes treated were 2 172, of which 1 762 eyes ( 81. 12%) were succeeded, 410 eyes ( 18. 88%) failed. ln the failed cases, the first three diseases were diabetic retinopathy, glaucoma and retinal detachment.?CONCLUSlON: ln recent years, disease etiology of blinding eye has changed, but cataracts, diabetic retinopathy and glaucoma are still high incidence of blindness due, so the treatment of diabetic retinopathy, glaucoma and retinal detachment should be the emphasis for blindness prevention and treatment in the future.

There were 12 patients who were all type C1 or C3 epipod comminuted fracture.By means of the internal fixation,all patients were transplanted with the nanometer artificial bones,comprising hydroxyapatite and ?-tricalcium phosphate.The 12 patients used the bacteriophages preoperation,during operation and 3 days postoperation.They were free from pressure dressing and started to take exercises 48 hours postoperatively.Followed up for 6-12 months,all of the 12 patients healed well.So nanometer artificial bone is an effective method for the epipodite comminuted fracture,without any severe toxicity or complications.

Objective To verify the variation of mitogen-activated protein kinase kinase kinase 5 (MAPKKK5) gene expression in patients with cryptogenic refractory temporal lobe epilepsy (TLE) and to evaluate the possible molecular pathogenesis of intractable TLE. Methods Reverse transcription polymerase chain reaction (RT-PCR) and Western-blot analysis were used to measure the expression alterations of MAPKKK5 mRNA as well as its protein product MAPKKK5 in temporal cortex samples from patients who had undergone temporal lobectomy for intractable epilepsy (n=10). Tissues from 10 subjects who did not have epilepsy served as controls. Results The expression of MAPKKK5 mRNA (1.001?0.321) and its protein MAPKKK5 (0.359?0.299) were significantly increased in epileptic brain compared with the controls (0.648?0.157, 0.137?0.084, respectively) (all P

Objective To observe the effect of Professor Deng Tietao’s Brain-strengthening Recipe 1 on learning and memory abilities of rats with vascular dementia, and to explore its molecular biology mechanism. Methods The vascular dementia rat model was established by permanent occlusion of the bilateral arteria carotis communis. Sixty male SD rats were randomly divided into 5 groups, namely sham-operation group, model group, nimodipine (5.4 mg·kg-1·d-1) group, and high-and low-dose Chinese medicine groups (57.6 and 14.4 g·kg-1·d-1, respecitvely) . After medication for 30 days, the learning and memory abilities were evaluated by Morris water maze test. The histological changes of the rat hippocampal tissues were observed after HE staining, and the mRNA expression of N-methyl-D-aspartate receptor subunit 2B ( NR2B) in rat hippocampus was measured by real-time fluorescence quantitative polymerase chain reaction (RT-PCR) . Results The water maze test results showed that the escape latency of the rats in the sham-operation group was significantly decreased on the third day, and was significantly decreased in the high-dose Chinese medicine group on the fourth day ( P<0.05 compared with the model group). The results of spatial probe test showed that the times of rats passing through the platform within 60 seconds were significantly higher in high-dose Chinese medicine group ( P<0.01compared with the model group) , but the time for rat staying at the quadrant of the platform in the other four groups did not differ from that in the model group ( P>0.05). HE staining results for the model group were presented as the absence of neural cells in hippocampus CA1 region, karyorrhexis of nerve cells, indistinctness of nuclear membrane, disappearance of nucleolus, shrinkage of nerve cells, increase of cytoplasm acidophily, and reactive hyperplasia of astrocytes. And in the hippocampal CA1 region of high- and low-dose Chinese medicine groups, the injured neural cells were found, and the lesions were slighter than those of the model group. Compared with the model group, the mRNA expression of NR2B was increased in nimodipine group and high-dose Chinese medicine group ( P<0.05) . The mRNA expression of NR2B showed a increasing trend in low-dose Chinese medicine group, but the differences were insignificant compared with that of the model group ( P>0.05). Conclusion Brain-strengthening Recipe 1 has obvious effects on improving the learning and memory abilities of vascular dementia rats, and the therapeutic mechanism is associated with reduction of the degree of neuronal damage in hippocampus and with the upregulation of the mRNA expression of NR2B.

miRNA is a kind of endogenous non-coding short RNA. Mature miRNA was formed through the process of shearing and transporting after genetic transcription. miRNA exhibits many important biological functions through regulating expression and translation of target mRNAs. Different miRNAs may act as oncogenes or antioncogenes, and have tissue specificity. The progress of the tumorigenesis is usually accompanied by expression-profile changes of miRNAs. MiRNA regulates many tumor biological behaviors such as differentiation, proliferation, apoptosis, invasion, metastasis, and drug resistance of tumors. Furthermore, some miRNAs have clinical significance in predicting prognosis of tumor patients.

Based on the word-formation of Medical English terms,this paper gives a comprehensive analysis of their transformation and adaptation in Chinese language and culture.Three major factors are discussed for the application and diversification of medical English terms,including the language family in translation,linguistic context,situational context and cultural context.

BACKGROUND:Al ogeneic penetrating keratoplasty is the most effective method for treating corneal blindness. However, the incidence of rejections is high after keratoplasty, so it is urgent to develop an immunosuppressive drug with high efficacy and low toxicity. OBJECTIVE:To establish al ogeneic penetrating keratoplasty models and monitor the expression of tumor necrosis factor-αin blank control group and after transforming growth factor-β1 eyedrop during acute rejection period of corneal grafts. METHODS:Al ogeneic penetrating keratoplasty models were established and were randomly divided into blank control group, ciclosporin A group (1%ciclosporin A), and transforming growth factor-β1 group (1μg/ml transforming growth factor-β1 eyedrop). The medications from each group commenced at 1 day after surgery, one eyedrop once, three eyedrops per day. Al the operated eyes were given 0.3%ofloxacin ophthalmic solutions and 0.5%tropicaide ophthalmic solution, three times per day, for 12 days. The corneal grafts were harvested for hematoxylin-eosin staining and immunihistochemical staining (SABC method), to detect tumor necrosis factor-αexpression in corneal grafts. RESULTS AND CONCLUSION:Hematoxylin-eosin staining showed that, corneal grafts were significantly thickened, a large number of histoleucocytes and lymphocytes infiltrated in the blank control group;corneal grafts showed normal thickness and no inflammatory cel s infiltrated in the transforming growth factor-β1 group. Immunohistochemical staining showed that, there were less cel s positive for tumor necrosis factor-αin the transforming growth factor-β1 group compared with the blank control group (P<0.05). Transforming growth factor-β1 eyedrops can reduce the expression of tumor necrosis factor-αin the corneal grafts during acute rejection period, and reduce the inflammatory cel s infiltration in the corneal grafts, which is probably the mechanism of transforming growth factor-β1 to prevent and treat corneal al ograft rejection.