Aged ; Humans ; Male ; Palatal Neoplasms ; pathology ; Uvula ; pathology

Background and purpose: Protein kinase P1k3 could increase the transcriptional activity of p53. However, the effect of P1k3 on the transcriptional activity of p73 is still unknown. Our study was to investigate the effect of P1k3 on the transcriptional activity of p73. Methods: Luciferase reporter assay, RT-PCR and colony formation assay were adopted to study the effect of P1k3 and kinase-deficient P1k3 (K52R) on the transcriptional activity of p73 in p53-deficient human lung carcinoma H1299 cells. Results: Luciferase reporter assay showed that p73 increased the luciferase activities induced by p21~(WAF1) and Bax promoters (P<0.05). After co-transfection with p73 and P1k3, the luciferase activities induced by p21~(WAF1) and Bax promotors were significantly decreased in a dose-dependent manner as compared with the group that transfected p73 only (P<0.05). However, kinase-deficient Plk3 (K52R) had no significant effect on the luciferase activities induced by p21~(WAF1) and Bax promoters (P>0.05). RT-PCR showed that p73 increased the mRNA expressions of p21~(WAF1) and BAX (P<0.05). P1k3 decreased the expressions of p21~(WAF1) and Bax induced by p73 (P<0.05). Kinase-deficient P1k3 (K52R) had no significant effect on the expressions of p21~(WAF1) and Bax induced by p73 (P>0.05). Colony formation assay revealed that p73 decreased the colony formation of H1299 cells (P<0.05). P1k3 decreased the inhibitory effect of p73 on the colony formation of H1299 cells (P<0.05). Kinase-deficient P1k3 (K52R) had no significant effect on the inhibitory effect of p73 on the colony formation of H1299 cells (P>0.05).Conclusion: P1k3 can inhibit the transcriptional activity of p73, where as kinase-deficient P1k3 has no effect on the transcriptional activity of p73.

Objective To study effects and other related problems of surgery for patients with cervical spine fracture and ankylosing spondylitis.Methods Twelve patients with cervical spine fracture and ankylosing spondylitis were treated with surgery from April 1986 to April 2004.All eases were studied retrospectively.They were followed up for an average of 67.5 months and their complete clinical data were kept.The neurological function was evaluated by ASIA (American Spinal Injury Association) impairment scale,and the image analyzing software (Image-Pro Plus 5.1) was used to measure the angles of superior and inferior vertebral bodies of the fusion segment at flexion and extension positions.The difference between flexion and extension angles,?,served as the parameter of interspinal movement.According to the definition of spinal fusion by FDA (Food and Drug Administration),the?≥4?was considered as nonfusion.Other related problems were discussed by descriptive study.Results The average improvement in the nine patients with neurological injury was 1.3 ASIA grades.The injured segments in 10 cases were treated with fusion,of whom nine were fused by internal fixation.The fusion rate was 100%.Three cases were scheduled to have laminoplasty,but two had to receive laminectomy instead because of intraoperative complete fracture at the hinged side.Ten patients were complicated by insufficient function of major organs preop- eratively,and endotracheal intubation was difficult to perform in eight cases.Postoperative complications occurred in three cases,but fortunately healed completely.There were no deaths or fatal complications.Conclusions The neurological function can be improved by surgery for patients with cervical spine fracture and ankylosing spondylitis. Although the cervical spine is instable for most of the patients,fusion with internal fixation is indicated and can be successful.Those who had preoperative systemic diseases are likely to suffer from postoperative complications.The difficult endotracheal intubation is a common intraoperative problem.

Objective:To examine the serum proteomic spectra of human esophagial carcinoma by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS),so as to set up a diagnostic model of esophagial carcinoma and to investigate its clinical value. Methods:Thirty-two esophagial carcinoma patients and 28 healthy controls were obtained from Fourth Affiliated Hospital of Hebei Medical University during May to September of 2008. Serum protein was extracted by weak cation exchange (WCX) protein chip system,and proteomic spectra was examined by MALDI-TOF MS. The obtained data were analyzed by ZUCI-protein chip data analyze system (ZUCI-PCDAS) and an esophagial carcinoma diagnostic model was established by genetic arithmetic (GA) combined support vector machine (SVM). The above 60 samples were randomly divided into training set and blinding test set,with training set including 21 esophagial carcinoma patients and 19 healthy controls and blinding test set including 11 esophagial carcinoma patients and 9 healthy controls,so as to examine the specificity and sensitivity of this diagnostic model. Results:Serum proteomic spectra of esophagial carcinoma patients and healthy controls were obtained by MALDI-TOF MS,and m/z (mass to charge) peaks of 44 differential proteins were obtained after analyzed by ZUCI-PCDAS software package (P

Previous researches showed that the expression level of E-Cad in most infiltrating cancer cells was reduced or negative. This study explored whether 4HPR restrained the infiltration of bladder cancer cells through regulating the expression of E-Cad. The infiltrating bladder cancer cells T24 were cultured, and then treated by a proper dosage of drug. Their viability was a determined by MTT method. Western blotting and RT-PCR were adopted to detect the changes of E-Cad gene expression at both protein and mRNA levels. Moreover, immunofluorescent staining and confocal fluorescence microscopy were employed for the observation of the expression of E-Cad. The result showed that, at both mRNA and protein levels, the expression level of E-Cad in T24 cells treated by 4HPR was significantly higher than that of control group, while the β-Cat expression was also relocated from the cell nucleus to cytoplasm. Our findings suggested that the regulatory function of 4HPR on infiltration of bladder cancer cells T24 is at least partly achieved by regulating the expression of E-Cad.

To understand the distribution and accumulation rules of polydatin, resveratrol, anthraglycoside B, emodin and physicion in different tissue structure of rhizome and root of Polygonum cospidatum, the content of 5 active compounds were analyzed simultaneously by HPLC, based on plant anatomy and histochemistry. The rhizome and root consist of different tissues, with an increased diameter, the proportions of the secondary xylem and phloem have increased. Resveratrol and polydatin mainly distributed in the pith, the secondary phloem and periderm of rhizome, and the secondary phloem and periderm of the root, while emodin and anthraglycoside B concentrated in the secondary structure and pith of rhizome mostly. In different thickness of the measured samples, the total contents of 5 compounds were correspondingly higher in thinner rhizome and root than those in the coarse ones.
Plant Roots ; chemistry ; Polygonum ; chemistry ; Rhizome ; chemistry

Parkinson's disease(PD) is the most common neurodegenerative movement disorder and ?-synuclein plays an important role in its development.Using the genetically tractable Saccharomyces cere-visiae as a model system,the phenotypic repercussions and potential mechanisms of ?-synuclein-induced cytotoxicity are characterized through modulating its expression level and other cellular factors.Aggrega-tion-induced toxicity is more dramatic upon elevated expression of ?-synuclein than that induced at moder-ate levels of expression.The induced toxicity is also enhanced by reagents such as dimethyl sulfoxide,which increase intracellular levels of phospholipid and membrane,as well as ferrous ions and hydrogen peroxide,both of which cause oxidative stresses in yeast cells.In contrast,over-expression of yeast homologue of hu-man chaperone DJ-1,YDR533C,markedly alleviate the inhibition of growth afflicted by exogenous expres-sion of ?-synuclein.Taken together,the data presented suggest a role for protein folding machinery together with quality control system in dealing with the aggregation of ?-synuclein.

Breast Neoplasms ; metabolism ; pathology ; Cadmium Compounds ; Cell Line, Tumor ; Female ; Humans ; Quantum Dots ; Receptor, ErbB-2 ; analysis ; metabolism ; Selenium Compounds ; Spectrometry, Fluorescence ; Tellurium ; Zinc Compounds

BACKGROUND: The effect of pituitary adenylate cyclase activating polypeptide (PACAP) during traumatic brain injury (TBI) and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI. METHODS: Male Sprague Dawley rats were randomly divided into 3 treatment groups (n=6, each): sham-operated, vehicle (normal saline)+TBI, and PACAP+TBI. Normal saline or PACAP (1g/5L) was administered intracerebroventricularly 20 minutes before TBI. Right parietal cortical contusion was produced via a weight-dropping method. Brains were extracted 24 hours after trauma. Histological changes in brains were examined by HE staining. The numbers of CD4+ and CD8+ T cells in blood and the spleen were detected via flow cytometry. RESULTS: In injured brain regions, edema, hemorrhage, inflammatory cell infiltration, and swollen and degenerated neurons were observed under a light microscope, and the neurons were disorderly arrayed in the hippocampi. Compared to the sham group, average CD4+ CD8– lymphocyte counts in blood and the spleen were significantly decreased in rats that received TBI+vehicle, and CD4– CD8+ were increased. In rats administered PACAP prior to TBI, damage was attenuated as evidenced by significantly increased CD4+, and decreased CD8+, T lymphocytes in blood and the spleen. CONCLUSION: Pretreatment with PACAP may protect against TBI by influencing periphery T cellular immune function.

AIM:To research the effects of lithium chloride on transforming growth factor beta (TGF-β) and connective tissue growth factor (CTGF) in cultured human Tenon capsule fibroblasts (HTFs) and explore its mechanism.METHODS:HTFs were cultured and identified by vimentin staining with immunofluorescence and the morphological characteristics.The experimental group was processed 48h with LiCl in concentration of 80mmol/L, the control group without LiCl.The mRNA expression of TGF-β and CTGF in two groups were analyzed with real-time fluorescent quantitative polymerase chain reaction (real time-qPCR) and the protein expression was detected with Western blot.RESULTS:The cultured HTFs expressed TGF-β and CTGF.The mRNA expression of TGF-β and CTGF significantly decreased compared with the control group(t=20.042, 14.995, P<0.05).the protein expression of TGF-β and CTGF also decreased significantly compared with the control group(t=46.058、12.452, P<0.05)CONCLUSION:The cultured HTFs can express TGF-β and CTGF in mRNA and proteins' level.LiCl can reduce the expression of TGF-β and CTGF both in gene and proteins' level.LiCl has the potential to modulate wound healing for glaucoma filtration surgery.