Objective To study the distribution of Jk(a-b-) phenotype in the blood donors of Panyu district. Methods Negative samples were screened by U type 96 well microplate technology, and then confirmed by routine serologic testing. The Jk(a-b-) phenotypes were genotyped and the genomic DNA coding region covering 4-11 exons and their flanking region were expanded and sequenced. Results Ten Jk(a-b-) phenotypes were found out of 50034 donors from June 2004 to August 2006, with the frequency of 0.02%. Three kinds of mutation sequences were detected: 1) AG to AA in the 3' splice site of intron 5; A to G at 588 site, and AA196CCA to CCG in exon 7. The genotype presumed to be JKb(△6)/ JKb(△6).2) C to A at 222 site of exon 5, and AA74AAC to AAA ; C to G at 536 site of exon 7, and AA179CCT to CGT; A to G at 588 site of exon 7,and AA196CCA to CCG. The genotype is presumed to be JKb(222A)/JKb(536G).3) AG to AA in the 3' splice site of intron 5;A to G at 499 site of exon 7,and AA167ATG to GTG; A to G at 588 side of exon 7,and AA196CCA to CCG. The genotype is presumed to be JKb(△6)/JKb(499G). Conclusions Two novel mutations, A to G at 499 side of exon 7 and C to G at 536 site of exon 7, are first discovered.

Objective To investigate the genotypes and encoding resistance genes differences of Acinetobacter baumannii and analyze their interrelations with multi-drug resistance.Methods A total of 77strains Acinetobacter baumannii were collected random from the second Xiangya Hospital during September 2008 to September 2009.The K-B method which was WHO recommended was adopted to Acinetobacter baumannii drug sensitivity test to 15 kinds of antibiotics to establish susceptibility spectrum.At the same time,random amplified polymorphic DNA(RAPD)technique was used to establish DNA fingerprinting.The genes of β-lactamase(TEM-1,IMP,OXA-23,OXA-24,AmpC),aminoglycoside-modifying enzymes[aac(3')-Ⅰ ,aac(6')-Ⅰ ,ant(3")-Ⅰ]and 16S rRNA methylase(armA,rmtA,rmtB)were detected by PCR and sequenced,and find the relationship between the gene encoding and multi-drug resistance.In addition,we compared the rates of resistance genes of Acinetobacter baumannii and the relations with the genotype and the multi-resistance.Results Thirty-one sensitive strains and 46 multi-drug resistance strains(10 Pan-drug resistances)were isolated.Seventeen types from A to Q were separated using RAPD technique.E genotype widely popular in the ICU was the advantage type in multi-drug resistance strains,and the rate was 47.1%.While the various types scattered in sensitive strains.The positive rates of TEM-1,IMP,OXA-23,OXA-24,AmpC,aac(3')-Ⅰ ,aac(6')-Ⅰ ,ant(3")-Ⅰ ,armA in the multi-drug resistance strains and the sensitive strains were 95.7%,39.1%,84.8% ,54.3%,87.0%,89.1%,84.8%,45.7%,63.0% and 58.1%,9.7%,32.3%,48.4%,48.4%,29.0%,45.2%,12.9%,9.7%,respectively,and there was significant difference except for OXA-24 using the X2 test(P ＜ 0.05).All isolates were negative for rmtA gene and rmtB gene.Drug susceptibility analysis showed that the resistant rate was significantly higher of the strains carrying resistant genes than that of the resistance negative strains.When the strains were resistant to gentamicin and amikacin,the rate of three aminoglycoside genes positive was 34.8%.The trains containing all the measured β-lactamase genes were all resistant strains.Conclusion Compared with the sensitive Acinetobacter baumannii strains,a broad resistance spectrum and a high drug resistance rate were showed in multidrug resistance strains isolated from clinic,which harboring many kinds of β-lactamase genes and aminoglycosides genes with a high separation rate,and the same clone of multiple drug-resistant strains may be transmitted in and among wards.

Objective:To establish the bacterial endotoxin test for HSSYO-001-3S. Methods: HSSYO-001-3S was dissolved in dimethylsulfoxide,diluted by BET water and centrifuged,and then the supernatant was used for the bacterial endotoxin test. The ex-periment was carried out according to the gel-clot technique for bacterial endotoxin inspection and the related regulations in Chinese Pharmacopoeia (2015 edition,volumeⅣ,general rule 1443). Results:HSSYO-001-3S was added with cosolvent and diluted by BET water to 1 mg·ml-1,and there was no interference effects to bacterial endotoxin test from the supernatant diluted four times or more. Conclusion:Bacterial endotoxin test can be used to control the quality of HSSYO-001-3S.

Mitochondrial shape rapidly changes by dynamic balance of fusion and fission to adjust to constantly changing energy demands of cancer cells. Mitochondrial dynamics balance is exactly regulated by molecular motor consisted of myosin and actin cytoskeleton proteins. Thus, targeting myosin-actin molecular motor is considered as a promising strategy for anti-cancer. In this study, we performed a proof-of-concept study with a natural-derived small-molecule J13 to test the feasibility of anti-cancer therapeutics

Diabetes have been shown to cause progressive neuronal injury with pain and numbness via advanced glycation end-products (AGEs)-induced neuronal cell apoptosis; however, the valuable drug targets for diabetic neuropathy have been poorly reported so far. In this study, we discovered a natural small-molecule schisandrol A (SolA) with significant protective effect against AGEs-induced neuronal cell apoptosis. ATP6V0D1, a major subunit of vacuolar-type ATPase (V-ATPase) in lysosome was identified as a crucial cellular target of SolA. Moreover, SolA allosterically mediated ATP6V0D1 conformation via targeting a unique cysteine 335 residue to activate V-ATPase-dependent lysosomal acidification. Interestingly, SolA-induced lysosome pH downregulation resulted in a mitochondrial-lysosomal crosstalk by selectively promoting mitochondrial BH3-only protein BIM degradation, thereby preserving mitochondrial homeostasis and neuronal cells survival. Collectively, our findings reveal ATP6V0D1 is a valuable pharmacological target for diabetes-associated neuronal injury via controlling lysosomal acidification, and also provide the first small-molecule template allosterically activating V-ATPase for preventing diabetic neuropathy.