Dental Enamel Hypoplasia ; classification ; etiology ; genetics ; Humans ; Molecular Biology

This study is to investigate the influence and mechanism of action of asymmetrical dimethylarginine (ADMA) and the induced oxidative stress level on Alzheimer's disease (AD) incidence. ADMA concentration, nitric oxide, Abeta(40)/Abeta(42) ratio, inducible NO synthase (iNOS) activity and the concentrations of the induced free radicals including malondialdehyde (MDA), 3-nitrotyrosine (3-NT) and peroxynitrite (ONOO-) in the cerebrospinal fluid (CSF) from 34 neurologically normal controls and 37 AD patients were quantitatively determined and statistically compared. The results showed that the ADMA concentration significantly decreased in AD patients, and it showed negative correlation with the NO, iNOS activity, and showed positive correlation with MMSE score. ADMA concentration was negatively correlated with Abeta(40)/Abeta(42) ratio (P<0.01) with the observation that Abeta(40)/Abeta(42) ratio increased while ADMA level decreased in CSF in AD patients. The concentration levels of MDA, 3-NT and ROS significantly increased compared with the control with all the P values less than 0.05. These findings suggested that the ADMA disorder and the oxidative damage effect of the induced free radicals in CSF of AD patients are an important mechanism of AD incidence, and their joint regulation may provide new idea for the prevention and clinical treatment of AD.

Child, Preschool ; Female ; Humans ; Multiple Acyl Coenzyme A Dehydrogenase Deficiency ; pathology ; Rett Syndrome ; pathology

Prostatic artery of 12 elder and 9 younger cadavers were isolated and transected.Vascular inner diameter and thickness of vascular wall of these cross sections were observed microscopically.Atherosclerotic plaque could be seen in the prostatic artery of 12 elders.And there were the thickening of tunica intima and the narrowing of inner diameter.The inner diameter of elderly prostatic artery was (452 ± 97) μm,the thickness of their tunica intima (228 ± 82) μm and inner diameter/thickness 3.14 ± 0.68.Tunica intima of 9 younger prostatic arteries were glabrate.The inner diameter of younger prostatic artery was (864 ± 17)μm,the thickness of their tunica intima (57 ± 4)μm and inner diameter/thickness 15.52 ± 0.18.Statistically significant differences existed between elder and younger cadavers in the above 3 parameters.As compared with younger counterpart,prostatic artery of elders was more stenotic and its tunica intima tended to he thicker.

Objective To determine the risk factors for emergence agitation (EA) during the recovery period after general anesthesia.Methods One thousand and thirty-four patients of both sexes aged 18-89 yr undergoing general anesthesia were divided into EA group and non-EA group.EA occurring during recovery from general anesthesia was assessed by using Riker sedation-agitation scale.Age,sex,complication,education,medical history,ASA physical status,type and duration of anesthesia and operation,volume of blood loss,fluid replacement,urine volume,duration of stay in PACU,number of drainage tubes and so forth were recorded.Multivariate logistic regression was used to analyze the risk factors for the occurrence of EA.Results Thirty-six patients developed EA during recovery from anesthesia.The incidence of EA was 3.5 ％.Logistic regression indicated that high risk operation,premedication with diazepam,induction of anesthesia without midazolom and fluid replacement during operation were the risk factors for EA (P ＜ 0.05).Conclusion High-risk operation,premedication with diazepam,induction of anesthesia without midazolom and fluid replacement during operation are the risk factors for EA during recovery from general anesthesia.

Objective To observe the different expression of somatomedin-receptor in cell membrane of prostate epithelial cells at anoxic or normoxic condition.Methods Human prostate epithelial cells line RWPE-1 were cultured in vitro.At 4,8,12,24,48 h after cells had been seeded,the gene and protein expression of epidermal growth factor receptor (EGFR),fibroblast growth factor receptor (FGFR),transforming growth factor β1 receptor (TGF- β 1R),insulin-like growth factor-1 receptor (IGF-1 R) and vascular endothelial growth factor receptor (VEGFR) in prostate epithelial cells were tested by RT-PCR and immunohistochem-istry methods,respectively.Results The expression of mRNA and protein of EGFR,FGFR,IGF-1R,TGF- β1R,VEGFR were significantly increased in anoxic and normoxic prostate epithelial cells (P ＜ 0.01 ).At different time point,the expression of mRNA and protein of EGFR,FGFR,IGF-1R,TGF- β1R,VEGFR significantly higher in anoxic than those in normoxic prostate epithelial cells (P＜ 0.01 )besides 4 h EGFR mRNA,12 h EGFR protein,4 h IGF-1R mRNA,4 and 8 h IGF-1R protein,4 and 8 h TGF-β 1R mRNA,4 and 8 h TGF-β 1R protein,4 h VEGFR mRNA (P ＞ 0.05).Conclusion Anoxic prostate epithelial cell can up-regulate the expression of somatomedin-receptor.

Aged ; Giant Cells ; pathology ; Humans ; Male ; Stomach Neoplasms ; pathology

Adenosine Triphosphatases ; genetics ; Cation Transport Proteins ; genetics ; Copper-transporting ATPases ; Gene Deletion ; Humans ; Infant ; Male ; Menkes Kinky Hair Syndrome ; genetics ; Polymorphism, Single Nucleotide

This study was aimed to investigate the activation of P38MAPK/STAT3 and expression of telomerase reverse transcriptase during sodium nitroprusside (SNP) inducing apoptosis of human leukemia cell line K562 and to explore the molecular mechanisms of SNP-inducing apoptosis in K562 cells. The K562 cell were treated with different concentrations of SNP and were cultured for different time. Cell apoptosis was analysed by cell morphology, DNA agarose gel electrophoresis, DNA content, and Annexin-V/PI labeling method. The TdT-mediated dUTP nick end labeling (TUNEL) assay was used to quantitate the in situ cell apoptosis. The expressions of phosphorylated p38MAPK or STAT3 were analysed by flow cytometry, while the expression of hTERT mRNA in transcriptional level was measured by fluorescence quantitative RT-PCR. The results showed that SNP inhibited K562 cell growth. The K562 cell apoptosis was confirmed by typical cell morphology and DNA fragment, peak of sub-G1 phase, TUNEL and Annexin-V/PI labeling. A majority of K562 cells were arrested in G0/G1 phase. After treatment with SNP at 0.5-3.0 mmol/L, the expression of phosphorylated-P38MAPK and phosphorylated-STAT3 increased first and decreased afterwards. Incubation of K562 cell with SNP (2 mmol/L) could increase the expression of phosphorylated-P38MAPK and phosphorylated-STAT3 at 12 hours and 24 hours respectively, and down-regulated at 72 hours and 48 hours. SNP could decrease the expression of hTERT-mRNA in time-and dose-dependent manner. It is concluded that SNP can significantly induce K562 cells apoptosis, its mechanism may be related to the activation of P38MAPK and suppression of phosphorylated-STAT3 and hTRET-mRNA.
Apoptosis ; drug effects ; Humans ; K562 Cells ; Nitroprusside ; pharmacology ; RNA, Messenger ; biosynthesis ; genetics ; STAT3 Transcription Factor ; genetics ; metabolism ; Telomerase ; biosynthesis ; genetics ; p38 Mitogen-Activated Protein Kinases ; genetics ; metabolism

To study the molecular mechanisms of nitric oxide donor sodium nitroprusside (SNP) -induced apoptosis in K562 human leukemia cell line, the different concentrations of SNP and different time of culture were used to treat K562 cell. At the same time, potassium ferricyamide (PFC) was used as control, blank was designed in experiment. Cell apoptosis was analysed by cell morphology, DNA agarose gel electrophoresis, DNA content, and annexin-V/PI labeling method. The TdT-mediated dUTP nick end labeling (TUNEL) assay was used to quantify in situ cell apoptosis. Reactive oxygen species (ROS) in cells and mitochondrial transmembrane potential (DeltaPsim) were labeled by dihydrorhodamin 123, 2', 7'-dichlorodihydrofluorescein diacetate and rhodamin 123/PI. bcl-2, bax, bad, p53 gene proteins and mitochondrial membrane protein were analysed by flow cytometry. The results showed that the K562 cell apoptosis was confirmed by typical cell morphology, DNA fragment, sub-G(1) phase, TUNEL and annexin-V/PI labeling. A majority of K562 cells were arrested in G(0)/G(1) phase. During the process of SNP-induced apoptosis in K562 cell, the mean fluorescence intensity of ROS in cells was significantly higher than those in blank and PFC control, while the DeltaPsim reduced. The expression of p53, bax, bad, Fas protein and mitochondrial membrane protein increased and bcl-2 protein decreased after SNP treatment. It is concluded that SNP induces K562 cell apoptosis through increasing ROS in cells, expressing the p53, bax, bad, Fas protein and mitochondrial membrane protein and decreasing bcl-2 protein, opening the mitochondrial permeability transition pore and reducing DeltaPsim. Furthermore, the Fas was activated during the apoptosis process.
Apoptosis ; drug effects ; Dose-Response Relationship, Drug ; Humans ; In Situ Nick-End Labeling ; K562 Cells ; Membrane Potential, Mitochondrial ; drug effects ; Nitric Oxide Donors ; pharmacology ; Nitroprusside ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Reactive Oxygen Species ; metabolism ; Tumor Suppressor Protein p53 ; metabolism ; bcl-2-Associated X Protein ; metabolism ; fas Receptor ; biosynthesis