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Biomedical subjects

M Wu

Publications and source records attributed to M Wu.

At least 109 records · Page 6Linked to original sources

[Linkage disequilibrium analysis of chromosome 22 and schizophrenia in a Chinese population].

OBJECTIVE: To explore the molecular genetic relations of chromosome 22 and schizophrenia and locate the susceptibility gene of schizophrenia. METHODS: Six dinucleotide tandem repeat loci on chromosome 22 were chosen to analyze 126 affected sib-pair nuclear families of schizophrenia in Chinese population by fluorescent labeled auto-mated genotyping and transmission/ disequilibrium test(TDT). RESULTS: The TDT-chi square value of IL2Rbeta was 25.30(P=0.01), which suggests there is linkage disequilibrium between IL2R beta and schizophrenia. The P vaules of the other five loci (D22S944, D22S264, D22S303, D22S278 and CYP2D6) were greater than 0.05. CONCLUSION: A susceptive gene of schizophrenia may be located in IL2Rbeta locus or adjacent region.

Chromosomes, Human, Pair 22↗

Transgenic mice with overexpression of human scavenger receptor A on endothelial cells.

OBJECTIVES: To establish a new transgenic mouse model for determining the function and role of human scavenger receptor A (SR-A) in atherosclerosis in vivo. METHODS: Human scavenger receptor minigene-driven mouse tie-1 promoter was constructed and confirmed by endonuclease digestion and sequence analysis. Transgenic mice were generated via the microinjection method. PCR and Southern blot were used to screen the positive transgenic mice. RT-PCR and immunohistochemical analysis were used to detect the level and location of human SR-AI expression in transgenic mice. The activity of human SR-AI was determined by morphologic observation of aortic endothelial cells of transgenic mice under transmission electron microscopy. RESULTS: The electrophoresis assay showed the expected 4 fragments of 0.9 kb, 1.1 kb, 1.2 kb and 4.2 kb in the Sma I digest and 2 fragments of 0.8 kb and 6.7 kb in Bgl II digest of plasmids pTie-1/hSR-A. The fragment sequence of tie-1 promoter and human SR-A cDNA in plasmids pTie-1/hSR-A was correct and no ATG before the translation initiation sites of human SR-A was found by sequence analysis. 561 injected and surviving embryos with the purified human SR-A minigene were implanted into the oviducts of 19 ICR pseudopregnant mice. Among the 54 surviving pups from 13 foster mothers, 7 were identified by PCR and Southern blot analysis. The results of RT-PCR and immunohistochemical analysis showed human SR-A was specifically expressed on vascular endothelial cells of the aorta and renal artery, as well as hepatic sinusoidal endothelial cells in transgenic mice. Transmission electron microscope (TEM) of aorta of transgenic mice showed that a large number of vesicles, multivesicle bodies and swollen mitochondria filled the plasma of endothelial cells. CONCLUSIONS: A transgenic mouse model with overexpression of human SR-A in endothelial cells was successfully established. The transgene was integrated and transmitted into the chromosome of transgenic mice. Tie-1 promoter controlled the transgene to express in endothelial cells in mice. Pinocytic activity of aortic endothelial cells in transgenic mice was higher than that of C57BL/6J mice. Our studies will provide a new transgenic model for investigation of atherosclerosis and functions of human SR-A.

Animals↗

Effects of methylprednisolone and aprotinin on phospholipase D activity of leukocytes in systemic inflammatory response induced by cardiopulmonary bypass.

AIM: To investigate the role of leukocyte phospholipase D (PLD) in systemic inflammatory response induced by cardiopulmonary bypass (CPB) and the effects of methylprednisolone and aprotinin on leukocyte PLD activity. METHODS: Forty-two patients who received CPB open heart surgery were divided into 3 groups: methylprednisolone group, aprotinin group, and control group. Arterial blood (10 mL) was collected for assay of leukocyte PLD activity, myeloperoxidase (MPO) activity, and CD11b expression at 8 different time points in perioperative period. Plasma IL-6, IL-8, and C-reactive protein levels were also determined. RESULTS: At the time point of ascending aorta declamped, leukocyte PLD activity for control group was (18 +/- 8) nmol choline . h-1 . mg-1, which was higher than that of pre-CPB (P < 0.01); the PLD activity for methylprednisolone group was (10 +/- 6) nmol choline . h-1 . mg-1 that was lower than control (P < 0.05), while it had no statistical difference compared with that of pre-CPB. In methylprednisolone group, PLD activity elevation was postponed to the time point of CPB stopped. There was no statistical difference in PLD activity between aprotinin group and control (P > 0.05). After administration of methylprednisolone or aprotinin, leukocyte CD11b expression, plasma IL-6, IL-8, C-reactive protein levels, and MPO activity decreased by different extent. CONCLUSION: Leukocyte PLD activity was elevated significantly in systemic inflammatory response induced by CPB and methylprednisolone partially blunted the CPB-induced inflammatory response by inhibiting PLD activity.

Adolescent↗

[Detection of proteins and mRNA of p16, p53 and nm23 in mucoepidermoid carcinoma of salivary glands and their prognostic significance].

OBJECTIVE: To disclose the relationship between the expression of p16, p53 and nm23 and the significant morphologic characteristics in mucoepidermoid carcinoma. METHODS: The proteins and mRNA in paraffin blocks from 41 mucoepidermoid carcinoma patients were studied with immunohistochemical methods and in situ hybridization respectively. RESULTS: The negative expression of p16 was found in 62.5% (15/24) of the low differentiation grade and in 29.4% (5/17) of the high differentiation grade (P = 0.037). The positive p53 expression was detected in 70.8% (17/24) of the low grade neoplasms and in 23.5% (4/17) of the high grade (P = 0.003), while positive nm23 protein was present in 37.5% (9/24) and 64.7% (11/17) respectively (P = 0.086). However, no relationship was found between positive mRNA of p16, p53, nm23 and WHO pathologic grade. CONCLUSIONS: There is a significant correlation between expression of p16 and p53 and WHO pathologic grade of mucoepidermoid carcinoma, which indicates clinical prognostic significance. No correlation is noticed between the pathologic grade and the expression of nm23 protein and mRNAs of p16, p53 and nm23.

Adult↗

[Relationship between growth potential of pine, population density of Monochamus alternatus and pathogenicity of Bursaphlenchus xyloophilus].

The results showed that the growth potential of pine (x) is negative related to the population density of Monochamus alternatus (y) and the pathoyenecity of Bursaphlenchus xyloophilus (z). But the population density of Monochamus alternatus is positively related to the pathogenicity of Bursaphlenchus xyloophilus. Three linear equations regression line were established as y = 1793.771 - 16404.47x, z = 31.80989 - 241.9274x, y = -407.611 + 70.51478z. Correlation coefficient is -0.8139, -0.8770 and +0.9864 respectively.

Animals↗

[Effect of hypoxia-ischemia on cysteinyl aspartate-specific proteinases activity in cerebral tissue of neonatal rat].

OBJECTIVE: To study the effect of hypoxia-ischemia on cysteinyl aspartate-specific proteinases (caspase-3) activity in cerebral tissue of neonatal rat and probe into its significance. METHODS: To induce hypoxio-ischemic brain damage (HIBD), the left carotid artery of rats at day 7 was ligated and animals were exposed to 8% oxygen for 2 hours. 0.5, 12, 24, and 48 hours after HIBD, both ipsilateral and contralateral cerebral tissue were ditected and homogenized, caspase-3 activity was measured by cleavage of the colorimetric substrate DEVD-pNA. RESULTS: Caspase-3 activity in ipsilateral cerebral tissue increased gradually after HIBD and peaked at 24 hours, and then decreased significantly at 48 hours(P < 0.001). There were no significant changes in caspase-3 activity in the contralateral tissue at all time points (P > 0.05). CONCLUSIONS: Significant activation of caspase-3 after cerebral hypoxia-ischemia strongly suggests that apoptosis is involved in HIBD. Application of caspase inhibitors or other anti-apoptotic agents may become a new therapeutics of HIBD.

Animals↗

Pressure changes in spinal canal and evaluation of spinal cord injuries in spinal section subjected to impact.

OBJECTIVE: To observe pressure changes in the spinal canal of the vertebrarium subjected to impact. From the point of view of impact, pressure changes and spinal cord injuries, the relationship between the type of spinal fracture and the severity of spinal cord injuries were analyzed and some experimental data were provided for early evaluation of severity of spinal cord injuries. METHODS: An experimental model of spinal burst fracture was made with Type BIM-I bio-impact machine and techniques of high velocity vertical loading in static pattern and stress shielding were adopted. Vertebral sections T10-L4 taken from fresh cadavers were impacted and pressure changes in the spinal canal were observed. The types and severity of spinal fracture were studied with gross and radiography examination. RESULTS: Great positive pressure wave (wave A) in the spinal canal of the 4 vertebral specimens with burst fracture was recorded. The peak value of pressure was correlated with the severity of posterior column injuries. Generally, the peak value of pressure was low in the samples with posterior column injuries, but high in the samples without injuries. The predominant features of fractures were burst fractures of vertebral body and severe destruction of the skeletal and fiber structure of the spinal canal. Positive and negative pressure waves (wave B) were recorded in 2 vertebral samples in which no significant abnormal changes were found by radiography examination, however, a little liquid effusion in the vertebral body was found by gross examination. CONCLUSIONS: The type of pressure wave in the spinal canal is related to the deformation or the destruction of the spinal canal structure. The peak value of the pressure is non-linearly related to the obstruction in the spinal canal, but related to posterior column injuries.

Biomechanical Phenomena↗

[Relationship between genetic alterations and clinicopathological features in intrahepatic cholangiocarcinoma].

OBJECTIVE: To evaluate the pedigree of genetic alterations during the tumorigenesis of intrahepatic cholangiocarcinoma (ICC) and their correlation with clinicopathological features by analysis of loss of heterozygosity (LOH) in 6 tumor suppressor genes (APC, MCC, DCC, OGG1, p53 and RB1) and point mutations in Ki-ras-2 oncogene. METHODS: Genomic DNA was isolated from paraffin-embedded slides of 22 surgically resected ICC cases by microdissection-based PCR amplification and agarose gel electrophoresis. Genetic alterations were analyzed by direct DNA sequencing. RESULTS: The total frequency of alterations in 7 genes studied was 86.4% (19/22). Based on the pattern of altered genes and their correlation with clinicopathological parameters, the genetic alterations were classified into two groups: Group I (9/19, 47.4%): alterations in APC, MCC, DCC and Ki-ras-2,); Group II (10/19, 52.6%): alterations in p53, OGG1 and RB1. The average age of patients in Group I (mean age, 57.2 years) was significantly younger than those in Group II (mean age, 69.1 years) (P < 0.05). CONCLUSIONS: The occurrence and development of ICC was closely related with the accumulation and cooperation of multiple genetic alterations. The genetic alterations of APC, MCC, DCC and Ki-ras-2 may play crucial roles in the early stage of development of ICC, and the genetic alterations of p53, OGG1 and RB1 may play important roles in accelerating advanced progression of ICC. The detection of the pedigree of genetic alterations in ICC may provide useful information for evaluating the state of tumor progression and clinic prognosis.

Adult↗

Cystic fibrosis transmembrane conductance regulator and H+ permeability in regulation of Golgi pH.

This paper reviews experiments from this lab that have tested the hypothesis that pH of the Golgi (pH(G)) of cystic fibrosis (CF) airway epithelial cells is alkaline compared to normal, that this altered pH affects sialyltransferase and other Golgi enzymes controlling biochemical composition of the plasma membrane and that altered surface biochemistry increases bacterial binding. We generated a plasmid encoding a modified green fluorescence protein-sialyltransferase (GFP-ST) chimera protein that was pH-sensitive and localized to the Golgi when transfected into HeLa cells and also CF and normal or cystic fibrosis transmembrane conductance regulator- (CFTR)-corrected airway epithelial cells. Digital imaging microscopy of these Golgi-localized probes showed that there was no correlation between pH(G) (6.4-7.0) and the presence of CFTR, whether cells were in HCO(3)(-)/CO(2)-containing or in HCO(3)(-)/CO(2)-free solutions. Activation of CFTR by raising cell [cAMP] had no effect on pH(G). Thus, CFTR seemed not to be involved in controlling pH(G). Experiments on HeLa cells using an avidin-sialyltransferase chimera in combination with a pH-sensitive fluorescent biotin indicated that even in cells that do not express CFTR, Cl(-) and K(+) conductances of the Golgi and other organelle membranes were large and that pH(G) was controlled solely by the H(+) v-ATPase countered by a H(+) leak. A mathematical model was applied to these and other published data to calculate passive H(+) permeability (P(H+)) of the Golgi, endoplasmic reticulum, trans-Golgi network, recycling endosomes and secrety granules from a variety of cells. An organelle's acidity was inversely correlated to its calculated P(H+). We conclude that the CFTR plays a minor role in organelle pH regulation because other (Cl(-) and K(+)) channels are present in sufficient numbers to shunt voltages generated during H(+) pumping. Acidity of the Golgi (and perhaps other organelles) appears to be determined by the activity of H(+) pumps countered by H(+) leaks.

Cystic Fibrosis Transmembrane Conductance Regulato↗

[The antioxidative effect of procyanidins from pine bark in vitro].

OBJECTIVE: To assess the antioxidative effect of procyanidins from pine bark on free radical damage. METHODS: Hemolysis, Malonaldehyde(MDA) level of mice liver homogenates, the conformation changes of irradiated plasmid PUC18 were used as indexes. RESULTS: Procyanidins could reduce the hemolysis degree of human RBC induced by H2O2 significantly(P < 0.01), reduce the MDA level of mice liver homogenate initiated by VitC/Fe2+ remarkably(P < 0.01), and reduce the degree of single-strain break of plamid PUC18 induced by 60Co gamma significantly(P < 0.01). CONCLUSION: Procyanidins had good antioxidative function. It can prevent RBC membrane, plasmid DNA suffering from oxygen free radical damage in vitro.

Animals↗

[Research on DNA molecular marker of Magnolia officinalis Rehd. et Wils.--RAPD study on certified species].

AIM: To discuss the intraspecific relationship in Magnolia officinalis and the genuineness of Cortex Magnoliae officinalis, and to find some DNA characters of certified "Houpo". METHODS: Thirty-three samples from eleven locations, which can represent most of the distribution of M. officinalis, were selected. The total DNA was extracted. Severty-four random primers were tried to get good amplification. RESULTS: One hundred and sixteen bands amplified from seventeen primers, were clustered by NTSYS-pc software. Three branches were obtained. Some distinctive primers and bands, which represent certified species or fine breed, were obtained also. CONCLUSION: 1) M. officinalis should be divided into three geographic clans instead of two subspecies or varieties, they are, a) typical officinalis, b) typical biloba and c) Middle type. This conclusion agrees with the leaf form and other characters. 2) The genetic difference between "Chuanpo" and "Wenpo" is evident and the difference is in correspondence with the quantities of their chemical constituents. So, the genetic difference is the main reason of the genuineness of Cortex Magnoliae officinalis. 3) These results may be used to establish DNA database for identification of Cortex Magnoliae officinalis.

DNA Fingerprinting↗

[Surgery of substernal goiter].

OBJECTIVE: To study the surgical approaches and operative techniques for substernal goiter. METHOD: A retrospective study of 27 cases with substernal thyroid nodules was made in our hospital. RESULT: The operations on 27 patients with substernal nodules have been successfully carried out. Among them, 10 were goiters, 9 adenomas, 4 malignancy and 4 were thyroid cancer metastasizing to paratracheal or substernal nodes. Resection via cervical collar incision was adequate in 23 cases. Three thyroid cancers with paratracheal node metastasis were completely resected by sternotomy and only one thyroid cancer with paratracheal and substernal nodes metastasis was resected by combined thoracotomy and cervical collar incision. CONCLUSION: Resection via cervical collar incision for all retrosternal thyroid nodules were advised. The preliminary experience with this procedure suggests that it has some advantages in the management of substernal goiter, including: 1. ease of operation compared to both sternotomy and thoracotomy; 2. relatively low morbidity; 3. safe and reliable.

Adult↗

Surgical treatment of malignant esophageal tumors in PUMC Hospital.

To study how to prolong the postoperative survival time of the patients with malignant esophageal tumors. The clinical data of 1098 patients with malignant esophageal tumors from 1961 to 1992 were retrospectively analyzed. The deletion of fragile histamine triplet (FHIT) gene (a tumor suppressor gene) in 30 fresh esophageal samples obtained in 1996 was detected with PCR and RT-PCR method. The resectability was raised gradually and the operative morbidity and mortality decreased year by year, but there was no significant improvement on the postoperative 5-year survival rate. Delayed diagnosis and irradical resection influenced the long-term survival. The deletion of cDNA of FHIT gene was 64. 2% in esophageal cancer and 20% in the resected margin of the cancer. We believe that high-grade atypical hyperplasia in esophageal epithelium and deletion of FHIT gene in esophageal cancer and its resected margin are pathological and molecular markers for early diagnosis of esophageal cancer respectively, and the latter may be one of the molecular markers for the resection. Early diagnosis and treatment, radical, resection, and postoperative nutritional support are very important for the improvement of the postoperative survival time of the patients.

Acid Anhydride Hydrolases↗

[Calculation of spectroscopic parameters of Ho3+ in Ho:YVO4 crystal].

The intensity parameters omega lambda of Ho3+ in Ho:YVO4 crystal were calculated with J-O theory according to the absorption spectrum. Based on these omega lambda values, the oscillator strength of excited energy state, spontaneous radiation rate, branching ratio and integrated emission cross section were estimated. A discussion on potentiality of application in the infrared laser material is given.

Chemical Phenomena↗

[Percutaneous radiofrequency ablation of liver malignancies].

OBJECTIVE: To describe the safety and efficacy of percutaneous radiofrequency ablation (PRFA) to treat liver cancer. METHODS: One hundred patients with histologically or clinically confirmed primary or metastatic malignancies were treated percutaneously under ultrasound guidance using LeVeen multipolar array needle electrode and RF 2000 generator between October, 1999 and October, 2000. All patients were followed up to assess complication, treatment response, recurrence and curative effect. RESULTS: PRFA was performed in 76 patients with primary liver cancer and 24 patients with metastatic liver cancer. AFP positive of small hepatic cancer (inoperative) became AFP negative in 75.0% patient (21/28). The rate of completely concrete necrosis of small hepatic malignancies shown by MRI was 85.9%(61/71). CONCLUSIONS: PRFA as a local thermal therapy is a kind of new palliative treatment for hepatic malignancies. It is minimally invasive, safe and effective especially for small hepatic tumors and can also be used in conjunction with TACE for larger ones.

Adult↗

PPARalpha agonists reduce 11beta-hydroxysteroid dehydrogenase type 1 in the liver.

11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) is an enzyme that converts cortisone to the active glucocorticoid, cortisol. Cortisol-cortisone interconversion plays a key role in the regulation of glucose metabolism, since mice deficient in 11betaHSD1 are resistant to diet-induced hyperglycemia. Peroxisome proliferator activator receptors (PPAR) are key regulators of glucose and lipid homeostasis. We observed a striking downregulation of murine hepatic 11betaHSD1 expression and activity after chronic treatment of wild-type mice with PPARalpha agonists, while 11betaHSD1 in the livers of PPARalpha knockout mice, or in mice treated for only 7 h with PPARalpha agonists, was unaltered. Our results are the first to show PPARalpha agonists can affect glucocorticoid metabolism in the liver by altering 11betaHSD1 expression after chronic treatment. Regulation of active glucocorticoid levels in the liver by PPARalpha agonists may in turn affect glucose metabolism, consistent with reports of their antidiabetic effects.

11-beta-Hydroxysteroid Dehydrogenases↗

Transglutaminase-3, an esophageal cancer-related gene.

Transglutaminase-3 (TGase-3) is an enzyme with the ability to catalyze the irreversible cross-linking of peptide-bound glutamine residues either with peptide-bound lysines or with primary amines. It has been implicated in the formation and assembly of the cornified cell envelope of the epidermis, hair follicle and perhaps other stratified squamous epithelia. We show here the involvement of TGase-3 in human esophageal cancer. In an initial study, mRNA differential display was performed with 3 pairs of esophageal cancer tissues and matched normal adjacent mucosa by a 10-mer arbitrary primer and mixed anchored primers (GT15N, N = A, C and G). Four differentially expressed cDNA bands were consistently observed in all 3 normal tissues but barely detected in their tumor counterparts. One of them was identified to be the 3; end of TGase-3. Northern blot and dot blot analyses of 14 samples confirmed the down-regulation of TGase-3 in malignant tissues compared with normal epithelia. RT-PCR revealed that TGase-3 expression was lost in 3 esophageal carcinoma cell lines and decreased in 35/38 tumors compared with adjacent normal mucosa. Taken together, 49/52 (94.2%) esophageal tumors presented down-regulation of the gene. Our data suggest that alteration of TGase-3 expression is a common event in the development of human esophageal cancer.

Adenocarcinoma↗