Recently, stem cell like side population (SP) cells have been found in many normal organizations and malig?nant tumors, which have the proficiency of differentiation and self-renewal. These cells play an important role in cancer stem cell research, though they occupy a low proportion in total cells. Here, we reviewed the foundation of SP cells, and their rela?tionship with stem cells, and the clinical application in the future.

As one of the serious complications of diabetes, diabetic retinopathy( DR) has become a main eye disease which causes blindness. The occurrence and development of DR is related to many factors. The pathogenesis is complicated, and the mechanism has not been clear. Early data suggest that the occurrence and development of DR has relations with many factors such as blood sugar level, diabetes duration and the environment. Among the factors, mitochondrial dysfunction and oxidative stress is the important mechanisms of DR and has become research focus in recent years. Consequences of mitochondrial dysfunction within cells include elevation of the rate of reactive oxygen species( ROS) production due to damage of electron transport chain proteins, mitochondrial DNA ( mtDNA ) damage, and loss of metabolic capacity. Clear understanding on the mechanism of mitochondrial functional change under high sugar level and oxidative stress response in the occurrence and development of DR is of great significance on prevention and cure of DR. ln this article, the development of mitochondrial metabolism and oxidative stress of DR is reviewed.

Objective:To investigate the existence of side population cells with the potency of stem cells in human gallbladder carcinoma cell line GBC-SD and the differences in ABCG2,Oct-4 and CD34 expression among SP cells,non-SP cells and GBC-SD cells.Methods:SP and non-SP cells were sorted from GBC-SD cells by fluorescence-activated cell sorting(FACS).The expression of ABCG2,Oct-4 and CD34 in SP cells,non-SP cells,and GBC-SD cells was detected by reverse transcription-polymerase chain reaction(RT-PCR),Western blot,flow cytometry(FCM)and immunofluorescence chemistry.Results:SP cells with stem cell potency were isolated from GBC-SD cells with a proportion of(0.64±0.08)%.The metastatic ability of SP cells was obviously higher than that of non-SP cells and GBC-SD cells(P<0.05).The expression of ABCG2 was significantly higher in SP cells than in non-SP cells and GBC-SD cells[(89.56±3.86)%vs.(1.32±0.49)%and(12.37±1.61)%,P=0.001].The expression of Oct-4 in these cells was(94.87±1.40)%,(88.16±2.34)%and(90.17±1.61)%,respectively(P>0.05).CD34 was neady absent in these cells on protein level[(1.78±0.51)%vs.(0.63±0.21)%and(0.96±0.381)%,P>0.05)],but it was highly expressed in non-SP cells and GBC-SD cells and absent in SP cells off mRNA leve;.Conclusion:SP calls which hava the potency of stem cells,exist in human gallbladder carcinoma GBC-SD cell line and have the phenotype of ABCG2+Oct-4+CD34-.

Pathogen-associated molecular patterns (PAMPs) are conservative molecules associated with groups of pathogens or their products. These molecules are recognized by relevant receptors. PAMPs induce the expression of inflammatory cytokines through the signal cascade. The role of PAMPs in the initiation and development of periodontitis is recently attracting attention. PAMPs induce the expression of inflammatory mediators after they are recognized in the periodontium. This process damages the periodontal soft tissue and osseous tissue, thus resulting in periodontitis. The results of this study will provide an excellent resolution for the treatment of periodontitis by blocking the pathogenic pathway of PAMPs.
Cytokines ; Humans ; Pathogen-Associated Molecular Pattern Molecules ; Periodontitis ; Periodontium

Schistosomiasis is a kind of zoonosis with serious hazard,which is popular in many countries and regions in the world. One of the efforts for schistosomiasis prevent and control is developing new drugs and vaccines,and knowing the tran?scription regulation mechanism and the function of transcription factors will help us find the targets of new drugs and vaccines as soon as possible. This article reviews the progress of Schistosoma transcription factors and research methods.

Objective To explore the influences of age and duration of status convulsion (SC) on hippocampal neuron apoptosis by observing the dynamic change of neuron apoptosis in rats with different age when SC terminates. Methods Seizures were induced in infant rats (IRs) and adult rats (ARs) injected with lithium and pilocarpine intraperitoneally. Rats were sacrificed at 6 time points (3, 6, 12 hours and 1, 3, 7 days) after 30 minutes of SC, or 2 time points (3 hours and 1 day ) after 3 hours of SC respectively. The location and type of apoptotic cells were assessed by using terminal deoxynucleotidyl dUTP nick end-labeling (TUNEL) of brain sections in situ. The proportion of apoptotic cells was quantified by Annexin-Ⅴ-FITC apoptosis detecting method and analysed by flow cytometer. Results (1) SC induced neuronal apoptosis and necrosis mainly in the CA_1 and CA_3 regions of hippocampus. (2) As compared to the time point before SC, the proportion of apoptotic cells in IRs and ARs hippocampus was increased obviously at 3 hours point after 30 minutes of SC (IRs 0.55%?0.21%, ARs 0.53%?0.06%), and with a maximal induction at 12 hours in IRs (0.67%?0.18%) and 1 day in ARs (0.98%?0.38%). The apoptotic process continued at least for 3—7 days. (3) In IRs, the proportion of apoptotic cells was lower than in ARs at different time points after 30 minutes of SC, except 3 hours point. There was a significant difference between the two age groups at 1 day and 7 days after SC respectively. The age-related difference was more obvious after 3 hours SC. Conclusions (1) Severe seizure induces neuronal apoptosis in hippocampus. (2) Age and duration of SC might be the important factors in influencing the neuronal apoptosis. The neuronal apoptosis in hippocampus after SC would have a positive correlation with age and duration of SC.

The correct pairing of disulfide bonds maintains the correct folding mode and high-level structure formation of peptides and protein drugs, which is crucial for the quality control of products. In order to ensure that the disulfide bonds are correctly paired, disulfide bond analysis is an essential part of peptides and protein drug characterization. Mass spectrometry can be used to analyze disulfide bonds. However, insulin and its analogues have two pairs of disulfide bonds without restriction enzyme cutting site. Conventional collision-induced dissociation (CID) and high-energy induced cleavage (HCD) cannot accurately locate the complex disulfide bond. In our study, three methods were used to localize the complex disulfide, including enzyme digestion combined with key peptide fragment in source decay (ISD) fragmentation method, enzyme digestion combined with partial reduction alkylation method, intact protein source ISD and electron transfer dissociation (ETD) cleavage method, The applicability of insulin aspart, insulin lispro and insulin glargine were also investigated. This study provides a new way for the quality control of disulfide bonding mode of insulin and its analogues, and also provides a reference for the disulfide bond localization of peptides or proteins containing this complex disulfide bond.

Objective To analyze the clinical features and gene mutation in mthylmalonic acidemia (MMA) accompanied by homocysteinemia (cblC), and review the relevant literatures. Methods The clinical features of 3 cases of MMA diagnosed by gene detection were retrospectively analyzed, and meanwhile the pertinent literatures of pathogenesis of MMA, especially combined with late-onset cblC and its gene detection, were reviewed. Results Patient 1 (26 days old) suffered from intermittent convulsions for 3 days, with isosuccinic acid 175.8 μmol/L, C3/C2 rate 1.363, homocysteine >?65 μmol/L and abnormal EEG. MMACHC gene detection found an exon deficiency (delEXON1), which has not been reported. Patient 2 ( 12 year old) was hospitalized for limb shaking, hyperspasmia and vomiting. His isosuccinic acid level was 334.3 μmol/L, C3/?C2 rate was 0.37, homocysteine >?65 μmol/L, and had abnormal EEG. MMACHC gene detection found the mutations of c.482G?>?A and c.609G?>?A. Patient 3 was hospitalized for intermittent convulsions for 20 days, whose isosuccinic acid, C3/?C2 rate, and homocysteine were increased. MMACHC gene detection found the mutations of c.394C?>?T and c.540del8 and c.540del8 had not been reported. Review of literatures discovered that MMA was combined with epileptic seizure in some patents, which further validate that the mutation in MMACHC gene c.482G?>?A may be related to the late-onset of cblC. Conclusions Gene detection contributes to the diagnosis of MMA; the mutation of MMACHC gene c.482G>A may be related to the late-onset of cblC; delEXON1 and c.540del8 are new mutations which have not been reported.

Objective To investigate the clinical features of paroxysmal kinesigenic dyskinesia (PKD) and the mutation features of its pathogenic gene proline-rich transmenbrane protein 2 (PRRT2). Method The clinical manifestations and genetic tests of one case of PKD were retrospectively analyzed, and the related literatures were reviewed. Results A 10 year and 9 month male patient was recruited. The age of dyskinesias onset was 7 year and 6 month. The descriptions of the attacks were abnormal involuntary movements which were induced by sudden voluntary movements and presented with dystonia. The frequency of the attacks was three to ifve times per day with the duration lasting ten to twenty seconds, and there is no loss of consciousness. Treatment with oxcarbazepine is effective. A heterozygous mutation in PRRT2 gene, c.649_650insC (p. 217fs224X), was found by genetic testing, and the mutation was inherited from the patient’s mother who showed no symptom of PKD. Conclusion The onset age of PKD could be in the childhood and adolescence. The attack is provoked by sudden movements and the duration time is short. Treatment with antiepileptic drug is effective. The test of PRRT2 gene may help diagnosis. Mutation c.649_650insC is the hotspot mutation of the gene.