Alzheimers disease is the most common cause of progressive decline of mental function. Recent years there is a large development in the early diagnosis and therapeutic progress in Alzheimer disease. The article reviews the progress in the pathogenesis, early diagnosis and new therapies in Alzheimers disease.

AIM:To evaluate the diagnostic value of co-detection of ischemia modified albumin (IMA) and treadmill exercise test (TET) for silent myocardial ischemia (SMI).METHODS:80 patients [55 males and 25 females;mean age (54?8) years] with suspected SMI were selected.All patients were examined with TET and coronary arteriongraphy(CAG) in one week.IMA was detected before TET and two hours after TET.All patients were divided into CHD and NCHD groups combined with the results of CAG.Changes in the concentration of IMA were observed of two groups before and after TET.The diagnostic value of co-detection of ischemia modified albumin and treadmill exercise test was evaluated for SMI.RESULTS:Among the 80 patients,it was diagnosed as CHD 33 cases,NCHD 47 cases.There were significant higher levels of IMA after TET in CHD group (P0.05).IMA levels were significantly higher in the patients of CHD after TET than those patients of NCHD[(13.3?3.5) vs (4.7?1.8) ng/mL,P0.05).The sensitivity value was 81.8% for IMA after TET,specificity was 76.6%,positive predictive value was 71.1%,negative predictive value was 85.7%.The sensitivity was 93.8% with the co-detection of IMA and TET,specificity was 87.5%,positive predictive value was 83.3%,negative predictive value was 95.5%.CONCLUSION:IMA is a useful biochemical marker for the early myocardial ischemia.There is a high sensitivity and negative predictive value for IMA two hours after TET in the diagnosis of SMI.There is much higher diagnostic value with the co-detection of IMA and TET.

Objective To observe the expression of aquaporin 4 (AQP-4) in contused brain tissue and its relationship with brain edema following brain trauma.Methods A retrospective case control analysis was made on 42 patients with severe brain trauma admitted from January 2015 to March 2016.There were 23 males and 19 females,aged from 23 to 62 years [(35.5 ± 5.6) years].Glasgow coma score (GCS) was 3-5 points in 7 patients,6-8 points in 23 and 9-10 points in 12.Brain tissue removed from the area 1 cm near the contusion during the cranial surgery were allocated to study group (n =42),while brain tissue removed far from the contusion after internal decompression were used as control (n =8).Ultrastructure of brain tissues was observed under electron microscope.Water content of brain tissue was measured by dry-wet weight method and expression of AQP-4 was measured by immunohistochemical method at postinjury hours ＜ 6,6-12,12-24,24-72,72-96 and ＞ 96.Results Morphology and structure of brain tissue in control group were normal.Whereas in study group,the intracellular and interstitial edema were obvious and morphological structure were damaged.Water content and AQP-4 expression in control group showed no obvious increase after operation(73.55 ±0.10,0.193 ±0.016).Water content in study group increased significantly compared to control group and reached the peak value (81.28 ± 0.56) at postinjury 24-72 hours (P ＜ 0.01).AQP-4 expression in study group increased at postinjury 6 hours (0.242 ±0.023) and reached a peak at postinjury 24-72 hours (0.338 ± 0.013),with significant difference compared to control group (P ＜ 0.05).Correlation analysis showed change of brain water content was positively correlated with expression level of AQP-4 (r =0.931,P ＜ 0.01).Conclusion Expression of AQP-4 in the injured area of brain trauma is significantly increased along with the increase of water content,suggests that the upregulation of AQP-4 plays an important role in traumatic brain edema.

To express Pleurocidin in Escherichia coli and to enhance the secretory efficiency of the fusion protein, the gene encoding Pleurocidin was ligated with Cherry DNA sequence via blunt-end ligation. Then this fusion gene was cloned into pET22b (+) vector and the recombinant plasmid was transformed into E. coli BL21 (DE3). Lactose was used to induce expression of fusion protein. The recombinant plasmid pET22b (+) -CP was successfully constructed and high-level expression of fusion protein was induced with lactose. Statistics showed that addition of glycine after 16 h of induction significantly enhanced the secretory efficiency of the fusion protein. After hydrolysis of the fusion protein by diluted hydrochloric acid and some further purification steps, r-Pleurocidin was obtained with antibacterial activity against E. coli DH5α and Bacillus subtilis BS168. In conclusion, the fusion protein was expressed in E. coli and biologically active r-Pleurocidin was obtained after hydrochloric acid cleavage and purification.
Animals ; Cloning, Molecular ; Escherichia coli ; metabolism ; Fish Proteins ; biosynthesis ; Flounder ; Recombinant Fusion Proteins ; biosynthesis

The G13 domain derived from granulysin shows high antimicrobial activities against Gram-positive and Gram-negative bacteria but does not lyse Jurkat cells or liposomes. To explore a new approach for high expression of the G13 domain, we fused the sequence encoding G13 to thioredoxin (Trx) gene to construct the recombinant expression vector (pThioHisA-G13). A cyanogen bromide (CNBr) cleavage site was introduced between the Trx and G13 to facilitate final release of the recombinant G13. The recombinant expression vector, pThioHisA-G13, was transformed into E. coli BL21 (DE3). Upon induction by IPTG Trx-G13 fusion protein was expressed and took the form of inclusion bodies counting 58% (W/W) of total cellular proteins. The inclusion body was solved by urea (8 mol/L) and then cleaved by CNBr. We purified the recombinant peptide G13 by one-step cation exchange chromatography. Results of agarose diffuse assay analysis indicated that the recombinant G13 exhibited antibacterial activity. The procedure described in this study will provide a reliable and simple method for highly efficient production of some cationic antimicrobial peptides.
Anti-Infective Agents ; metabolism ; Antigens, Differentiation, T-Lymphocyte ; genetics ; Cyanogen Bromide ; pharmacology ; Escherichia coli ; genetics ; metabolism ; GTP-Binding Protein alpha Subunits, G12-G13 ; biosynthesis ; genetics ; Inclusion Bodies ; metabolism ; Protein Structure, Tertiary ; genetics ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; Thioredoxins ; genetics ; Transfection

To investigate the effects of NDUFS7 gene mutation on neurons, the mutant plasmid of pcDNA3.1(+)-NDUFS7 Q208STOP was constructed and transfected into differentiated SH-SY5Y cells. The effect of transfecting mutant plasmid on the viability of dopaminergic neural cells was detected by MTT assay. The effect of transfection of mutant plasmid on apoptosis was detected by Annexin Ⅴ-FITC/PI staining followed by flow cytometry assay. The changes in the expression levels of apoptosis-related proteins Bax and Bcl-2 in cells after transfection of mutant plasmid were detected by Western blot. The effects of transfection of mutant plasmid on the mitochondrial membrane potential in differentiated SH-SY5Y cells and the intervention effect of antioxidant Trolox were examined using JC-1 fluorescent probe. The intervention effect of Trolox on the apoptosis of differentiated SH-SY5Y cells transfected with mutant plasmid was detected by PI/Hoechst staining. The results showed that the subunit mutation of mitochondrial complex I in dopaminergic neurons could lead to decreased neuronal viability and increased apoptosis, while antioxidants could alleviate the abnormal mitochondrial membrane potential and apoptosis caused by transfection of mutant plasmids, suggesting that transfection of mutant plasmid of NDUFS7 gene could lead to apoptosis by causing abnormal mitochondrial function in dopaminergic neurons.

To investigate the effects of VHL (von Hippel-Lindau) inhibitor on Caenorhabditis elegans (C.elegans) model of Parkinson''s disease (PD),C.elegans were exposed to rotenone and treated with VHL inhibitor VH298.The death,dopaminergic neurodegeneration and mitochondrial unfolded protein response (mito-UPR) of transgenic strains with the markers zcIs9 and otIs181 exposed to different concentrations of rotenone were investigated. The death,dopaminergic neurodegeneration,and changes of behaviors including head thrashes,body bends and foraging behavior of C.elegans model of PD treated with different concentrations of VH298 were explored.The results showed that different concentrations of rotenone can lead to the death,dopaminergic neurodegeneration and abnormal mito-UPR of transgenic nematodes with zcIs9; otIs181,while the VHL inhibitor can decrease the death rate and alleviate dopaminergic neurodegeneration of rotenone-induced C.elegans model of PD.The VHL inhibitor can also attenuate the behavioral abnormalities of head thrashes,body bends and foraging behavior of C.elegans model.These results suggest that rotenone may cause mitochondrial damage in the transgenic nematodes with zcIs9; otIs181, and then destroy mitochondrial homeostasis,thereby resulting in dopaminergic neurodegeneration and death of the nematodes. The VHL inhibitor VH298 may promote the survival of rotenone-induced C.elegans model of PD,and alleviate dopaminergic neurodegeneration,thereby improving the behavioral abnormalities of C.elegans model of PD.